Senin, 06 Oktober 2008
headache,diagnosis and teratmen
n General Statistics
n Second most common complaint after back pain
n “Everyone” has headaches (HA)
n More than 80 million ER visits in U.S. per year
n Frequency of HA due to rich nerve supply and psychological implications of head pain
n General Statistics
n Nerves responsible for HA have their source from myelinated C fibers and A-delta fibers in cranial nerves V, IX, X, and roots C1, C2, C3
n Pain sensitive structures include the eye, ear, paranasal sinuses, large extra and intra cranial arteries, dural sinuses, periosteum of the skull skin, cranial muscles, and the upper cervical spine
n Etiologies
n Commonly overlooked etiologies include: food, fever, viral, metabolic, withdrawal, and pharmaceutical
n International Headache Society Classifications (see attachment)
n History: Questions to ask
n Character of pain
n Mode of onset
n Mode of offset
n Time of onset
n Relieving factors
n Aggravating factors
n History: Questions to ask
n Precipitating factors
n Frequency of attacks
n Duration of attacks
n Associated symptoms
n Family history of headache
n Allergies
n Seven danger signals of an ominous headache
n A “first” headache
n Headache due to exertion
n Headache with fever
n Headache in a drowsy or confused patient
n Seven danger signals of an ominous headache
n Headache in a patient with nuchal rigidity or meningeal signs
n Headache in a patient with abnormal physical signs
n Headache in a patient who “looks ill”
n Physical Exam
n Gait assessment
n Vital signs
n Fundoscopic exam
n Facial symmetry
n Head & Neck structures
n Deep tendon reflexes
n Plantar response
n Limb strength
n Relevant Muscles
n Trapezius
n Sternocleidomastoid
n Temporalis
n Occipitofrontalis
n Suboccipital muscles
n Masseter
n Relevant Muscles
n Medial & Lateral Pterygoid
n Anterior & Posterior Digastric
n Fascial muscles
n Splenius Capitis
n Posterior Cervical musculature
n Deep Anterior Cervical musculature
n Cervical Dysfunction
n Upper cervical nerves posses fibers for pain from the lower part of the occipital sinus, vertebral and posterior meningeal arteries, and the dural floor of the posterior fossa (C1, C2, C3)
n Differential Diagnosis:Migraine Headache
Etiology:
n Hereditary component
n Not correlated with personality types “A” or neuroses
n The worsening or migraine that occurs during periods of intense nervousness, anxiety, and depression is usually due to the superimposition of a tension headache
n Vascular spasm followed by vasodilatation
n Migraine Headache:Signs & Symptoms
Classic Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: preceded with visual disturbances and less often with hemi-sensory disturbances, hemiparesis, or aphasia
n Migraine Headache:Signs & Symptoms
Classic & Common Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: photophobia and or phonophobia; tension headache often concomitant
n Aggravated: red wine, nuts, aged cheese, chocolate and caffeine containing beverages
n Risk factor: women are more affected than men
n Migraine Headache:Diagnosis & Treatment
n Response to ergot therapy
n Drug treatment is widely varied (caffeine, NSAIDS, barbiturates, narcotics, beta blockers, calcium channel blockers, sedatives, and more…)
n Prevention by avoiding predisposing factors, decreasing stress, maintaining sleep regularity
n Osteopathic treatment would include stabilizing vasculature and associated concomitant tension headache
n Differential Diagnosis:Cluster Headache
Etiology
n Disturbed hypothalamic biorhythm
n Excess smoking and drinking may precipitate via sphenopalatine irritation
n Hemicranial (unilateral) cranial dysfunction
n Cervical somatic dysfunction with irritation of the spinal accessory nerve
n Cluster Headache:Signs & Symptoms
n Character: excruciating pain often stabbing
n Location: usually near one eye
n Associated: tearing, flushed face, nasal congestion, conjunctival congestion (ANS)
n Risk factor: males affected more than females
n Onset: begins at 20 – 40 years of age
n Cluster Headache:Signs & Symptoms
n Attacks last 30 – 90 minutes daily for days and then disappear for months (Headache “vacation”)
n Alcohol can precipitate but only during an active cycle, not during “vacations”
n Some are so painful that they can lead to suicide
n Cluster Headache: Prevention & Treatment
n Drug treatment is widely varied
n Osteopathic treatment would include a thorough cranial assessment
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Etiology
n Ruptured aneurysm
n Arteriovenous malformation
n Trauma
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Signs & Symptoms
n Character: full-blown catastrophic headache
n Location: Holocaine
n Duration: continuous
n Associated: photophobia, retinal hemorrhages, nuchal rigidity, Brudzinski’s sign, Kernig’s sign, obtunded collapse
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Diagnosis
n CT may show blood and aneurysm
n Lumbar puncture may show bloody CSF
n MRI
n Differential Diagnosis:Organic origin, Meningitis
Etiology
n Virus
n Bacteria
n Fungus
n Tuberculous
n Differential Diagnosis:Organic origin, Meningitis
Signs & Symptoms
n Character: cephalgia is intense, steady, and deep
n Location: holocranial pain associated with retro-orbital pain which is aggravated with eye movement
n Onset: sub-acute or acute
n Associated: fever, generalized convulsions, varied levels of consciousness, nuchal rigidity, Brudzinski and Kernig’s signs
n Differential Diagnosis:Organic origin, Meningitis
Diagnosis
n Headache with fever and nuchal rigidity
n LP reveals pleocytosis, increased protein, and low glucose
n CT scan after Tx is underway to R/O brain abscess and subdural empyema
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Etiology
n Increased volume
n Increased venous pressure
n Obstruction to flow/absorption of CSF
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Signs & Symptoms
n HA is severe
n HA occur with coughing, sneezing, valsalva effort
n Associated findings include papilledema, obtunded, focal neurologic signs & symptoms
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Diagnosis
n CT
n MRI
n Avoid LP
n Differential Diagnosis:Organic origin, Hypertension
n Usually no HA’s until DBP > 120 mm Hg
n 3 major causes of acute severe hypertension: drugs, pheochromocytoma, neurogenic (paraplegia)
n Associated findings include: retinopathy, convulsions, confusion or stupor evolving over several days
n Differential Diagnosis:Organic origin, Vasculopathies
Etiology
n Temporal (giant cell) arteritis
n Dissection of a vessel
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms of Temporal Arteritis
n Character: throbbing and sharp, burning pain
n Location: focal headache in the temporal or frontal-occipital region
n Onset: gradual and progressive
n Aggravated: headache worse at night and with cold
n Risk: most common in white females > 50 years old
n Associated: weight loss, fever, fatigue, polymyalgia rheumatica, monocular visual loss, jaw claudication
n Differential Diagnosis:Organic origin, Vasculopathies
Diagnosis of Temporal arteritis
n Increased sed rate
n Biopsy
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms (Dissection of vessel)
n Severe, localized HA
n History of trauma or vigorous exertion
n Diagnosis with CT
n Differential Diagnosis:Organic origin, Acute Purulent Sinusitis
n Involving the frontal, maxillary, sphenoidal, or ethmoidal sinuses
n True “sinus HA” is rare; if present, the patient is usually very ill, with a severe localized HA for hours or days, PND & tender sinuses; often misdiagnosed as tension HA or common migraine but may have these as concomitant HA
n Diagnosis: CT
n Differential Diagnosis:Tension HeadacheEtiology
Skeletal components
n Somatic dysfunctions of the upper cervical unit are going to impinge on the upper cervical nerves which have afferents in the cranium and dura
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Can be explained by trigger point reflex mechanisms. A myofascial trigger point is a focus of hyperirritability within a taut band of skeletal muscle or the associated fascia that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness, and sometimes to referred autonomic phenomena and distortion of proprioception
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Trigger points can result directly from ischemia due to chronically tense muscles, acute overload, overwork fatigue, direct trauma, and chilling.
n Trigger points can result indirectly from other trigger points (a.k.a. latent trigger points), visceral disease, arthritic joints, and by emotional distress
n Differential Diagnosis:Tension HeadacheEtiology
Soft tissue components
n Ligaments can refer pain to sclerotomes which need to be addressed to completely resolve the somatic dysfunction
Lymphatics
n Need to free up the thoracic inlet to allow drainage of fluids
n Trapezius
n The trapezius can have many trigger points but the ones located in the upper fibers are most relevant for cephalgia
n Pain referral pattern: Posterolateral aspect of the neck, mastoid process, temple and back of the orbit, and the angle of the jaw
n Trapezius
n The patient can often be misdiagnosed as having cervical radiculopathy or atypical facial neuralgia. The normally minimal antigravity function of the upper trapezius is overstressed by any position or activity in which the trapezius helps to carry the weight of the arm for a prolonged period
n The muscle can also be strained by chronic injury due to overload, carrying a heavy backpack, long telephone calls, and sleeping prone with the head turned to one side
n Trapezius
n The trapezius can also entrap the greater occipital nerve which enervates the skin of the scalp and the semispinalis capitis muscle
n Sternocleidomastoid Sternal division
n Pain referral pattern: supra-orbital and deep within the orbit, occipital ridge, and vertex
n Associated autonomic findings: excessive lacrimation, reddening of the conjunctiva, apparent “ptosis,” and visual disturbances
n Sternocleidomastoid Clavicular division
n Pain referral pattern: frontal area which extends across the forehead to the other side, and posterior auricular
n Associated proprioceptive findings: spatial disorientation
n Sternocleidomastoid
n The SCM trigger points can be activated by sleeping on two pillows and keeping the neck in a flexed position, or by keeping the neck in an extended position as in painting a ceiling or sitting in the front row of a theater with a high screen or elevated stage. The SCM is often injured in a “whiplash” injury that might occur in an automobile crash.
n Temporalis
n Pain referral pattern: widely throughout the temple, along the eyebrow, and behind the eye
n Temporalis trigger points may be activated by bruxism, direct trauma such as a fall or an impact to the cranium. The temporalis muscle can also be activated secondary to spasm in the masseter muscle
n Occipitofrontalis
n Frontal division pain referral pattern: upward and over the forehead on the ipsilateral side
n Occipital division pain referral pattern: laterally, diffusely over the back of the head and with pain deep in the orbit
n Second most common complaint after back pain
n “Everyone” has headaches (HA)
n More than 80 million ER visits in U.S. per year
n Frequency of HA due to rich nerve supply and psychological implications of head pain
n General Statistics
n Nerves responsible for HA have their source from myelinated C fibers and A-delta fibers in cranial nerves V, IX, X, and roots C1, C2, C3
n Pain sensitive structures include the eye, ear, paranasal sinuses, large extra and intra cranial arteries, dural sinuses, periosteum of the skull skin, cranial muscles, and the upper cervical spine
n Etiologies
n Commonly overlooked etiologies include: food, fever, viral, metabolic, withdrawal, and pharmaceutical
n International Headache Society Classifications (see attachment)
n History: Questions to ask
n Character of pain
n Mode of onset
n Mode of offset
n Time of onset
n Relieving factors
n Aggravating factors
n History: Questions to ask
n Precipitating factors
n Frequency of attacks
n Duration of attacks
n Associated symptoms
n Family history of headache
n Allergies
n Seven danger signals of an ominous headache
n A “first” headache
n Headache due to exertion
n Headache with fever
n Headache in a drowsy or confused patient
n Seven danger signals of an ominous headache
n Headache in a patient with nuchal rigidity or meningeal signs
n Headache in a patient with abnormal physical signs
n Headache in a patient who “looks ill”
n Physical Exam
n Gait assessment
n Vital signs
n Fundoscopic exam
n Facial symmetry
n Head & Neck structures
n Deep tendon reflexes
n Plantar response
n Limb strength
n Relevant Muscles
n Trapezius
n Sternocleidomastoid
n Temporalis
n Occipitofrontalis
n Suboccipital muscles
n Masseter
n Relevant Muscles
n Medial & Lateral Pterygoid
n Anterior & Posterior Digastric
n Fascial muscles
n Splenius Capitis
n Posterior Cervical musculature
n Deep Anterior Cervical musculature
n Cervical Dysfunction
n Upper cervical nerves posses fibers for pain from the lower part of the occipital sinus, vertebral and posterior meningeal arteries, and the dural floor of the posterior fossa (C1, C2, C3)
n Differential Diagnosis:Migraine Headache
Etiology:
n Hereditary component
n Not correlated with personality types “A” or neuroses
n The worsening or migraine that occurs during periods of intense nervousness, anxiety, and depression is usually due to the superimposition of a tension headache
n Vascular spasm followed by vasodilatation
n Migraine Headache:Signs & Symptoms
Classic Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: preceded with visual disturbances and less often with hemi-sensory disturbances, hemiparesis, or aphasia
n Migraine Headache:Signs & Symptoms
Classic & Common Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: photophobia and or phonophobia; tension headache often concomitant
n Aggravated: red wine, nuts, aged cheese, chocolate and caffeine containing beverages
n Risk factor: women are more affected than men
n Migraine Headache:Diagnosis & Treatment
n Response to ergot therapy
n Drug treatment is widely varied (caffeine, NSAIDS, barbiturates, narcotics, beta blockers, calcium channel blockers, sedatives, and more…)
n Prevention by avoiding predisposing factors, decreasing stress, maintaining sleep regularity
n Osteopathic treatment would include stabilizing vasculature and associated concomitant tension headache
n Differential Diagnosis:Cluster Headache
Etiology
n Disturbed hypothalamic biorhythm
n Excess smoking and drinking may precipitate via sphenopalatine irritation
n Hemicranial (unilateral) cranial dysfunction
n Cervical somatic dysfunction with irritation of the spinal accessory nerve
n Cluster Headache:Signs & Symptoms
n Character: excruciating pain often stabbing
n Location: usually near one eye
n Associated: tearing, flushed face, nasal congestion, conjunctival congestion (ANS)
n Risk factor: males affected more than females
n Onset: begins at 20 – 40 years of age
n Cluster Headache:Signs & Symptoms
n Attacks last 30 – 90 minutes daily for days and then disappear for months (Headache “vacation”)
n Alcohol can precipitate but only during an active cycle, not during “vacations”
n Some are so painful that they can lead to suicide
n Cluster Headache: Prevention & Treatment
n Drug treatment is widely varied
n Osteopathic treatment would include a thorough cranial assessment
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Etiology
n Ruptured aneurysm
n Arteriovenous malformation
n Trauma
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Signs & Symptoms
n Character: full-blown catastrophic headache
n Location: Holocaine
n Duration: continuous
n Associated: photophobia, retinal hemorrhages, nuchal rigidity, Brudzinski’s sign, Kernig’s sign, obtunded collapse
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Diagnosis
n CT may show blood and aneurysm
n Lumbar puncture may show bloody CSF
n MRI
n Differential Diagnosis:Organic origin, Meningitis
Etiology
n Virus
n Bacteria
n Fungus
n Tuberculous
n Differential Diagnosis:Organic origin, Meningitis
Signs & Symptoms
n Character: cephalgia is intense, steady, and deep
n Location: holocranial pain associated with retro-orbital pain which is aggravated with eye movement
n Onset: sub-acute or acute
n Associated: fever, generalized convulsions, varied levels of consciousness, nuchal rigidity, Brudzinski and Kernig’s signs
n Differential Diagnosis:Organic origin, Meningitis
Diagnosis
n Headache with fever and nuchal rigidity
n LP reveals pleocytosis, increased protein, and low glucose
n CT scan after Tx is underway to R/O brain abscess and subdural empyema
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Etiology
n Increased volume
n Increased venous pressure
n Obstruction to flow/absorption of CSF
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Signs & Symptoms
n HA is severe
n HA occur with coughing, sneezing, valsalva effort
n Associated findings include papilledema, obtunded, focal neurologic signs & symptoms
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Diagnosis
n CT
n MRI
n Avoid LP
n Differential Diagnosis:Organic origin, Hypertension
n Usually no HA’s until DBP > 120 mm Hg
n 3 major causes of acute severe hypertension: drugs, pheochromocytoma, neurogenic (paraplegia)
n Associated findings include: retinopathy, convulsions, confusion or stupor evolving over several days
n Differential Diagnosis:Organic origin, Vasculopathies
Etiology
n Temporal (giant cell) arteritis
n Dissection of a vessel
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms of Temporal Arteritis
n Character: throbbing and sharp, burning pain
n Location: focal headache in the temporal or frontal-occipital region
n Onset: gradual and progressive
n Aggravated: headache worse at night and with cold
n Risk: most common in white females > 50 years old
n Associated: weight loss, fever, fatigue, polymyalgia rheumatica, monocular visual loss, jaw claudication
n Differential Diagnosis:Organic origin, Vasculopathies
Diagnosis of Temporal arteritis
n Increased sed rate
n Biopsy
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms (Dissection of vessel)
n Severe, localized HA
n History of trauma or vigorous exertion
n Diagnosis with CT
n Differential Diagnosis:Organic origin, Acute Purulent Sinusitis
n Involving the frontal, maxillary, sphenoidal, or ethmoidal sinuses
n True “sinus HA” is rare; if present, the patient is usually very ill, with a severe localized HA for hours or days, PND & tender sinuses; often misdiagnosed as tension HA or common migraine but may have these as concomitant HA
n Diagnosis: CT
n Differential Diagnosis:Tension HeadacheEtiology
Skeletal components
n Somatic dysfunctions of the upper cervical unit are going to impinge on the upper cervical nerves which have afferents in the cranium and dura
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Can be explained by trigger point reflex mechanisms. A myofascial trigger point is a focus of hyperirritability within a taut band of skeletal muscle or the associated fascia that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness, and sometimes to referred autonomic phenomena and distortion of proprioception
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Trigger points can result directly from ischemia due to chronically tense muscles, acute overload, overwork fatigue, direct trauma, and chilling.
n Trigger points can result indirectly from other trigger points (a.k.a. latent trigger points), visceral disease, arthritic joints, and by emotional distress
n Differential Diagnosis:Tension HeadacheEtiology
Soft tissue components
n Ligaments can refer pain to sclerotomes which need to be addressed to completely resolve the somatic dysfunction
Lymphatics
n Need to free up the thoracic inlet to allow drainage of fluids
n Trapezius
n The trapezius can have many trigger points but the ones located in the upper fibers are most relevant for cephalgia
n Pain referral pattern: Posterolateral aspect of the neck, mastoid process, temple and back of the orbit, and the angle of the jaw
n Trapezius
n The patient can often be misdiagnosed as having cervical radiculopathy or atypical facial neuralgia. The normally minimal antigravity function of the upper trapezius is overstressed by any position or activity in which the trapezius helps to carry the weight of the arm for a prolonged period
n The muscle can also be strained by chronic injury due to overload, carrying a heavy backpack, long telephone calls, and sleeping prone with the head turned to one side
n Trapezius
n The trapezius can also entrap the greater occipital nerve which enervates the skin of the scalp and the semispinalis capitis muscle
n Sternocleidomastoid Sternal division
n Pain referral pattern: supra-orbital and deep within the orbit, occipital ridge, and vertex
n Associated autonomic findings: excessive lacrimation, reddening of the conjunctiva, apparent “ptosis,” and visual disturbances
n Sternocleidomastoid Clavicular division
n Pain referral pattern: frontal area which extends across the forehead to the other side, and posterior auricular
n Associated proprioceptive findings: spatial disorientation
n Sternocleidomastoid
n The SCM trigger points can be activated by sleeping on two pillows and keeping the neck in a flexed position, or by keeping the neck in an extended position as in painting a ceiling or sitting in the front row of a theater with a high screen or elevated stage. The SCM is often injured in a “whiplash” injury that might occur in an automobile crash.
n Temporalis
n Pain referral pattern: widely throughout the temple, along the eyebrow, and behind the eye
n Temporalis trigger points may be activated by bruxism, direct trauma such as a fall or an impact to the cranium. The temporalis muscle can also be activated secondary to spasm in the masseter muscle
n Occipitofrontalis
n Frontal division pain referral pattern: upward and over the forehead on the ipsilateral side
n Occipital division pain referral pattern: laterally, diffusely over the back of the head and with pain deep in the orbit
chronic headache
Chronic Daily Headaches
David V. Lardizabal, M.D.
Assistant Professor, Kirksville College of Medicine
Objectives
To learn the systematic approach in the diagnosis of chronic daily headaches
To present different cases of chronic daily headaches
Basic Components of the History
Onset
Location
Quality
Duration
Frequency
Associated Symptoms
Triggers
Relieving Factors
Medication: dose/frequency
General and Neurologic Examination
Case #1
A previously healthy 38 year old man presented with 4 month history of daily headache. The headache began gradually and without provocation. The pain was continuous and became progressively more severe and disabling. The headache was moderately intense holocranial pressure that lasted throughout the day and was not associated with gastrointestinal or autonomic symptoms.
Case #1 continued
He tried over-the-counter analgesics without relief prior to receiving acetaminophen with codeine from his family physician. A prior neurological examination and non-enhanced MRI of the head were unremarkable. His alleviating factors was “resting and relaxing” were the only thing that helped. His headache was improved when he is supine i.e. resting in bed, resting in the sofa, or mid-day naps. When he rises from bed, his headache would invariably intensity.
Diagnosis?
Diagnosis?
Case #2
15 year old boy has been having daily headaches for the past 6 months. It is a constant pressure. He has incontinence and difficulty in looking up. He has tried different analgesics without relief. He wakes up in the morning vomiting. The neurologic examination showed no upgaze and papilledema.
Diagnosis?
Diagnosis?
Case #3
18 year old female had a minor head trauma from an altercation. She has daily headaches and posterior neck pain for 2 weeks. She vomits daily. She has no nausea, light or sound sensitivity. Her neurological examination is normal. The CT scan was negative. She was told to have post-traumatic headache.
Diagnosis?
Diagnosis?
Lesson Number 1
Secondary Headaches should be vigilantly investigated in daily headache patients.
Neurologic Examination is important
CT is not the diagnostic test of choice
MRI with/without contrast should be performed in new daily headaches.
Secondary Chronic Daily Headaches
Post-Traumatic Headache
Cervical Spine Disorders
Headaches associated with Vascular Disorders; AVM; arteritis including GCA, dissection, subdural hematoma
Headache associated with Non-Vascular disorders (EBV, HIV, tumor)
TMJ, Sinus infections (sphenoid), Chronic CNS infections
Intracranial Hypotension or hypertension
Primary Chronic Daily Headaches
Definition of CDH
> 15 or more headache days
> 3 or more months
Chronic Daily Headaches
Duration of head pain
Autonomic Features
Medication History
Neurologic Examination
Duration of the Head Pain
More than 4 hours
Less than 4 hours
Autonomic Features
Eyelid swelling
Ptosis “drooping”
Miosis or Mydriasis
Conjunctival injection
Lacrimation “Tearing”
Rhinorrhea “runny nose”
Medication History
What are the medication used for abortive and/or prophylactic therapy?
What is the monthly consumption?
Case #4
23 year old woman presented for evaluation of intractable and disabling daily headache of 6 months duration. Her headache began 3 years ago, occurring one to 3 times per month. Initially, her headache were left temporal in location and were severe and throbbing and associated with prominent nausea and photo- or phonophobia.
Case #4 continued
Over the past 6 months, she has had a moderate intensity, diffuse, daily, and continuous headache with only mild photophobia and occasional nausea. To allow herself to function at school, throughout the past year, she escalated her abortive medication use, initially using 4 to 8 acetaminophen-aspirin-caffeine tablets daily and in the past 6 months, 4 to 8 perscription acetaminophen-caffeine-butalbital tablets daily.
Case #4 continued
Prophylactic therapy with tricyclic antidepressant and anticonvulsant was unhelpful. Her neurological examination and brain MRI were normal.
Case #4
Fulfills criteria for CDH
Normal MRI and exam
Secondary causes excluded.
Diagnosis?
Chronic Daily Headaches?
Lesson Number 3
Chronic Daily Headache is a Symptom
It is NOT a Diagnosis
Migraine
Medication Overuse Headaches ( MOH)
Medication Overuse Headaches (MOH)
Simple analgesics
> 15 days for > 3 months
Opiods, Ergotamines, Triptans or Combination of medications
> 10 days/month > 3 months
Frequent/regular use 2-3 times per week
Lesson Number 4
Medication Overuse Headaches should be excluded or Treated before diagnosing Primary CDH disorders
What are the Primary Chronic Daily Headache Disorders?
Case #5
A 50 year old female has been complaining of right supraorbital pain for the past 1 year. The pain is brief, typically 15 minutes. It is stabbing, and electric-like. The attacks are sporadic and she can have 5 to 40 exquisitely painful episodes for 5 days every week. The neurologic examination is normal and MRI brain is normal.
Case #5 Continued
Anticonvulsants failed.
Microvascular Decompression failed
Gamma Knife Therapy failed.
What was the presumptive diagnosis in this case?
Case #5 continued
The patient had tearing, ptosis, and rhinorrhea on the same side of the pain.
Diagnosis?
This is not Trigeminal Neuralgia
Trigeminal Autonomic Cephalalgia
Chronic Paroxysmal Hemicrania
Case #6
50 year old woman. She has been having right sided headache for the past 10 years. It is a dull pain that last almost the whole day. She has no nausea, no photophobia, no phonophobia, or vomiting. At times, there are “stabbing” pains just above the eyebrow. She has tearing in the right eye and ptosis in these acute stabbing headaches. She has tried “all the headache medications made by man.” Her examination and MRI, LP were normal.
Lesson Number 5
The presence of autonomic features is an important differential
Chronic Paroxysmal Hemicrania (< 4 hrs HA)
Hemicrania Continua (> 4 hours HA)
Patients with CDH with autonomic features should be therapeutically tried with Indomethacin
Primary Variety
Headache Duration < 4 hours
Cluster Headache
Chronic Paroxysmal Hemicrania
SUNCT
Hypnic Headache
Criteria of Chronic Cluster
Attacks occurs for more than 1 year without remission or with remission lasting less than 1 month.
Frequency: one every second day to eight day.
Associated with one of:
Lacrimation, nasal congestion, rhinorrhea, forehead/facial sweating, miosis, eyelid edema, conjunctival injection, sense of restlessness or agitation during headache.
Hypnic Headache
Attacks of pain may be unilateral/bilateral and always occur after falling asleep.
15-180 minutes
15 times per month
None or one of the following:
Nausea, photophobia, phonophobia
Not attributable to another disorder
SUNCT
Short-Lasting Unilateral Neuralgiform Headache with Conjunctival injection and Tearing
At least 20 attacks
Unilateral moderately severe orbital or temporal stabbing or throbbing pain lasting 10-120 seconds
Not attributable to another disorder
At least one: nasal congestion, rhinorrhea, or eyelid edema.
Primary CDH
Headache Duration > 4 hours
Chronic Migraine
Chronic Tension-Type Headache
New Daily Persistent Headache
Hemicrania Continua (indomethacin responsive)
Chronic Migraine (CM)
“transformed migraine”
Migraine without aura with CDH features in the absence of medication overuse.
When CM is associated with medication oversue, only a diagnosis of probable Chronic mgraine and probable MOH.
Only after withdrawal of overused medications and the persistence of migraine on more than 15 days per month can a diagnosis of CM be made.
Chronic Tension-Type HA
Fulfills CDH definition
At least 2 of of the pain characteristics
Pressing/tightening quality
Mild to moderate severity
Bilateral location
No aggravation by walking stairs or similar routine physical activity
Historyof episodic TT HA
No vomiting, no more than one: nausea, photophobia
Does not meet criteria for NDPH or HC
New Daily Persistent Headache
Abrupt development (< 3 days) of headache that does not remit.
Summary
Chronic Daily Headache should be approached in a systematic manner
Secondary HA should be excluded
It must fulfill CDH definition
Do no over-medicate patients or educate them in avoiding overmedication
Always remember the associated symptoms; not just the pain
Thank You
DIHYDROERGOTAMINE PROTOCOL
DIHYDROERGOTAMINE PROTOCOL
DIHYDROERGOTAMINE PROTOCOL
David V. Lardizabal, M.D.
Assistant Professor, Kirksville College of Medicine
Objectives
To learn the systematic approach in the diagnosis of chronic daily headaches
To present different cases of chronic daily headaches
Basic Components of the History
Onset
Location
Quality
Duration
Frequency
Associated Symptoms
Triggers
Relieving Factors
Medication: dose/frequency
General and Neurologic Examination
Case #1
A previously healthy 38 year old man presented with 4 month history of daily headache. The headache began gradually and without provocation. The pain was continuous and became progressively more severe and disabling. The headache was moderately intense holocranial pressure that lasted throughout the day and was not associated with gastrointestinal or autonomic symptoms.
Case #1 continued
He tried over-the-counter analgesics without relief prior to receiving acetaminophen with codeine from his family physician. A prior neurological examination and non-enhanced MRI of the head were unremarkable. His alleviating factors was “resting and relaxing” were the only thing that helped. His headache was improved when he is supine i.e. resting in bed, resting in the sofa, or mid-day naps. When he rises from bed, his headache would invariably intensity.
Diagnosis?
Diagnosis?
Case #2
15 year old boy has been having daily headaches for the past 6 months. It is a constant pressure. He has incontinence and difficulty in looking up. He has tried different analgesics without relief. He wakes up in the morning vomiting. The neurologic examination showed no upgaze and papilledema.
Diagnosis?
Diagnosis?
Case #3
18 year old female had a minor head trauma from an altercation. She has daily headaches and posterior neck pain for 2 weeks. She vomits daily. She has no nausea, light or sound sensitivity. Her neurological examination is normal. The CT scan was negative. She was told to have post-traumatic headache.
Diagnosis?
Diagnosis?
Lesson Number 1
Secondary Headaches should be vigilantly investigated in daily headache patients.
Neurologic Examination is important
CT is not the diagnostic test of choice
MRI with/without contrast should be performed in new daily headaches.
Secondary Chronic Daily Headaches
Post-Traumatic Headache
Cervical Spine Disorders
Headaches associated with Vascular Disorders; AVM; arteritis including GCA, dissection, subdural hematoma
Headache associated with Non-Vascular disorders (EBV, HIV, tumor)
TMJ, Sinus infections (sphenoid), Chronic CNS infections
Intracranial Hypotension or hypertension
Primary Chronic Daily Headaches
Definition of CDH
> 15 or more headache days
> 3 or more months
Chronic Daily Headaches
Duration of head pain
Autonomic Features
Medication History
Neurologic Examination
Duration of the Head Pain
More than 4 hours
Less than 4 hours
Autonomic Features
Eyelid swelling
Ptosis “drooping”
Miosis or Mydriasis
Conjunctival injection
Lacrimation “Tearing”
Rhinorrhea “runny nose”
Medication History
What are the medication used for abortive and/or prophylactic therapy?
What is the monthly consumption?
Case #4
23 year old woman presented for evaluation of intractable and disabling daily headache of 6 months duration. Her headache began 3 years ago, occurring one to 3 times per month. Initially, her headache were left temporal in location and were severe and throbbing and associated with prominent nausea and photo- or phonophobia.
Case #4 continued
Over the past 6 months, she has had a moderate intensity, diffuse, daily, and continuous headache with only mild photophobia and occasional nausea. To allow herself to function at school, throughout the past year, she escalated her abortive medication use, initially using 4 to 8 acetaminophen-aspirin-caffeine tablets daily and in the past 6 months, 4 to 8 perscription acetaminophen-caffeine-butalbital tablets daily.
Case #4 continued
Prophylactic therapy with tricyclic antidepressant and anticonvulsant was unhelpful. Her neurological examination and brain MRI were normal.
Case #4
Fulfills criteria for CDH
Normal MRI and exam
Secondary causes excluded.
Diagnosis?
Chronic Daily Headaches?
Lesson Number 3
Chronic Daily Headache is a Symptom
It is NOT a Diagnosis
Migraine
Medication Overuse Headaches ( MOH)
Medication Overuse Headaches (MOH)
Simple analgesics
> 15 days for > 3 months
Opiods, Ergotamines, Triptans or Combination of medications
> 10 days/month > 3 months
Frequent/regular use 2-3 times per week
Lesson Number 4
Medication Overuse Headaches should be excluded or Treated before diagnosing Primary CDH disorders
What are the Primary Chronic Daily Headache Disorders?
Case #5
A 50 year old female has been complaining of right supraorbital pain for the past 1 year. The pain is brief, typically 15 minutes. It is stabbing, and electric-like. The attacks are sporadic and she can have 5 to 40 exquisitely painful episodes for 5 days every week. The neurologic examination is normal and MRI brain is normal.
Case #5 Continued
Anticonvulsants failed.
Microvascular Decompression failed
Gamma Knife Therapy failed.
What was the presumptive diagnosis in this case?
Case #5 continued
The patient had tearing, ptosis, and rhinorrhea on the same side of the pain.
Diagnosis?
This is not Trigeminal Neuralgia
Trigeminal Autonomic Cephalalgia
Chronic Paroxysmal Hemicrania
Case #6
50 year old woman. She has been having right sided headache for the past 10 years. It is a dull pain that last almost the whole day. She has no nausea, no photophobia, no phonophobia, or vomiting. At times, there are “stabbing” pains just above the eyebrow. She has tearing in the right eye and ptosis in these acute stabbing headaches. She has tried “all the headache medications made by man.” Her examination and MRI, LP were normal.
Lesson Number 5
The presence of autonomic features is an important differential
Chronic Paroxysmal Hemicrania (< 4 hrs HA)
Hemicrania Continua (> 4 hours HA)
Patients with CDH with autonomic features should be therapeutically tried with Indomethacin
Primary Variety
Headache Duration < 4 hours
Cluster Headache
Chronic Paroxysmal Hemicrania
SUNCT
Hypnic Headache
Criteria of Chronic Cluster
Attacks occurs for more than 1 year without remission or with remission lasting less than 1 month.
Frequency: one every second day to eight day.
Associated with one of:
Lacrimation, nasal congestion, rhinorrhea, forehead/facial sweating, miosis, eyelid edema, conjunctival injection, sense of restlessness or agitation during headache.
Hypnic Headache
Attacks of pain may be unilateral/bilateral and always occur after falling asleep.
15-180 minutes
15 times per month
None or one of the following:
Nausea, photophobia, phonophobia
Not attributable to another disorder
SUNCT
Short-Lasting Unilateral Neuralgiform Headache with Conjunctival injection and Tearing
At least 20 attacks
Unilateral moderately severe orbital or temporal stabbing or throbbing pain lasting 10-120 seconds
Not attributable to another disorder
At least one: nasal congestion, rhinorrhea, or eyelid edema.
Primary CDH
Headache Duration > 4 hours
Chronic Migraine
Chronic Tension-Type Headache
New Daily Persistent Headache
Hemicrania Continua (indomethacin responsive)
Chronic Migraine (CM)
“transformed migraine”
Migraine without aura with CDH features in the absence of medication overuse.
When CM is associated with medication oversue, only a diagnosis of probable Chronic mgraine and probable MOH.
Only after withdrawal of overused medications and the persistence of migraine on more than 15 days per month can a diagnosis of CM be made.
Chronic Tension-Type HA
Fulfills CDH definition
At least 2 of of the pain characteristics
Pressing/tightening quality
Mild to moderate severity
Bilateral location
No aggravation by walking stairs or similar routine physical activity
Historyof episodic TT HA
No vomiting, no more than one: nausea, photophobia
Does not meet criteria for NDPH or HC
New Daily Persistent Headache
Abrupt development (< 3 days) of headache that does not remit.
Summary
Chronic Daily Headache should be approached in a systematic manner
Secondary HA should be excluded
It must fulfill CDH definition
Do no over-medicate patients or educate them in avoiding overmedication
Always remember the associated symptoms; not just the pain
Thank You
DIHYDROERGOTAMINE PROTOCOL
DIHYDROERGOTAMINE PROTOCOL
DIHYDROERGOTAMINE PROTOCOL
cephalgia
n IMAGING OF CEPHALGIA
n Dr. Patricia Jorizal, SpRad
n Radiology Department
n Siloam Hospitals Kebon Jeruk
n Cephalgia ?
n Pain in the head that located above the eyes or the ears, behind the head or in the back of the upper neck.
n Type :
1. Primary (migraine, tension, cluster)
2. Secondary (tumors, stroke, meningitis, etc)
n Causes ?
n Primary : not associated with (caused by) other disease
v Migraine à vasodilatation & release of chemicals from nerve fibers around blood vessels.
v Tension excess stress/hectic day.
v Cluster no clear cause, precipitate by alcohol & cigarettes.
n Causes ?
n Secondary : caused by associated disease
v Tumor or metastasis in the brain
v Subdural hematoma à ruptured veins after trauma ; elderly
v Epidural hematoma ruptured arteries as the results of skull fractures
v Infections meningitis, tuberculosis
v Strokes
v Subarachnoid hemorrhage aneurysm
v Sinusitis
v Sudden onset of severe high blood pressure
n Radiology Imaging
n Conventional X-ray
n Computed Tomography (CT) Scan
n Magnetic Resonance Imaging (MRI)
n Waters
n DSCT (Dual Source CT)
n CT Contrast Agents
n Intravenous contrast à iodinated
Differentiate blood vessels vs. vascular internal organs
What is MRI?
n MRI is short for Magnetic Resonance Imaging. MRA [Magnetic Resonance Angiography] is also a kind of MRI.
n MRI is an advanced technology that lets the doctor see internal organs, blood vessels, muscles, joints, tumors, areas of infection, and more -- without x-rays, surgery, or pain. MRI is very safe, no known harmful effects. It's important to know that MRI will not expose to any radiation.
n How should patient get ready for the exam?
n No special preparation is needed.
n However, there may be some circumstances in which you'll be given specific instructions to follow before the exam à fasting 4 hours for abdominal examination
Make a appointment 1 day before the exam …
n Disadvantages
* Slow scan acquisition produce an artifacts due to biological motion i.e. cardiac, vascular respiratory excursion, etc
* Patient experience claustrophobia due to small bore of the magnet
* Strong static magnetic field interferes the proper function of the usual life-support equipment
n Restrictions for the exam ?
n A pacemaker
n Aneurysm clips
n Cochlear implants
n A neuro-stimulator (Tens-unit)
n Metal implants
n Steel surgical staples or clips
n An implanted drug infusion device
n Any implant made partially or wholly of iron or steel
n Coins
n Jewelry
n Watches
n Keys
n Dentures or partial plates
n Hearing aids
à Metal objects made of iron or steel can interfere with the exam
à Magnetic waves can also erase the code on bank cards and credit cards
n How long does the scan take?
n The exam can last from 30 minutes to usually no more than an hour.
n Dr. Patricia Jorizal, SpRad
n Radiology Department
n Siloam Hospitals Kebon Jeruk
n Cephalgia ?
n Pain in the head that located above the eyes or the ears, behind the head or in the back of the upper neck.
n Type :
1. Primary (migraine, tension, cluster)
2. Secondary (tumors, stroke, meningitis, etc)
n Causes ?
n Primary : not associated with (caused by) other disease
v Migraine à vasodilatation & release of chemicals from nerve fibers around blood vessels.
v Tension excess stress/hectic day.
v Cluster no clear cause, precipitate by alcohol & cigarettes.
n Causes ?
n Secondary : caused by associated disease
v Tumor or metastasis in the brain
v Subdural hematoma à ruptured veins after trauma ; elderly
v Epidural hematoma ruptured arteries as the results of skull fractures
v Infections meningitis, tuberculosis
v Strokes
v Subarachnoid hemorrhage aneurysm
v Sinusitis
v Sudden onset of severe high blood pressure
n Radiology Imaging
n Conventional X-ray
n Computed Tomography (CT) Scan
n Magnetic Resonance Imaging (MRI)
n Waters
n DSCT (Dual Source CT)
n CT Contrast Agents
n Intravenous contrast à iodinated
Differentiate blood vessels vs. vascular internal organs
What is MRI?
n MRI is short for Magnetic Resonance Imaging. MRA [Magnetic Resonance Angiography] is also a kind of MRI.
n MRI is an advanced technology that lets the doctor see internal organs, blood vessels, muscles, joints, tumors, areas of infection, and more -- without x-rays, surgery, or pain. MRI is very safe, no known harmful effects. It's important to know that MRI will not expose to any radiation.
n How should patient get ready for the exam?
n No special preparation is needed.
n However, there may be some circumstances in which you'll be given specific instructions to follow before the exam à fasting 4 hours for abdominal examination
Make a appointment 1 day before the exam …
n Disadvantages
* Slow scan acquisition produce an artifacts due to biological motion i.e. cardiac, vascular respiratory excursion, etc
* Patient experience claustrophobia due to small bore of the magnet
* Strong static magnetic field interferes the proper function of the usual life-support equipment
n Restrictions for the exam ?
n A pacemaker
n Aneurysm clips
n Cochlear implants
n A neuro-stimulator (Tens-unit)
n Metal implants
n Steel surgical staples or clips
n An implanted drug infusion device
n Any implant made partially or wholly of iron or steel
n Coins
n Jewelry
n Watches
n Keys
n Dentures or partial plates
n Hearing aids
à Metal objects made of iron or steel can interfere with the exam
à Magnetic waves can also erase the code on bank cards and credit cards
n How long does the scan take?
n The exam can last from 30 minutes to usually no more than an hour.
migraine
n General Statistics
n Second most common complaint after back pain
n “Everyone” has headaches (HA)
n More than 80 million ER visits in U.S. per year
n Frequency of HA due to rich nerve supply and psychological implications of head pain
n General Statistics
n Nerves responsible for HA have their source from myelinated C fibers and A-delta fibers in cranial nerves V, IX, X, and roots C1, C2, C3
n Pain sensitive structures include the eye, ear, paranasal sinuses, large extra and intra cranial arteries, dural sinuses, periosteum of the skull skin, cranial muscles, and the upper cervical spine
n Etiologies
n Commonly overlooked etiologies include: food, fever, viral, metabolic, withdrawal, and pharmaceutical
n International Headache Society Classifications (see attachment)
n History: Questions to ask
n Character of pain
n Mode of onset
n Mode of offset
n Time of onset
n Relieving factors
n Aggravating factors
n History: Questions to ask
n Precipitating factors
n Frequency of attacks
n Duration of attacks
n Associated symptoms
n Family history of headache
n Allergies
n Seven danger signals of an ominous headache
n A “first” headache
n Headache due to exertion
n Headache with fever
n Headache in a drowsy or confused patient
n Seven danger signals of an ominous headache
n Headache in a patient with nuchal rigidity or meningeal signs
n Headache in a patient with abnormal physical signs
n Headache in a patient who “looks ill”
n Physical Exam
n Gait assessment
n Vital signs
n Fundoscopic exam
n Facial symmetry
n Head & Neck structures
n Deep tendon reflexes
n Plantar response
n Limb strength
n Relevant Muscles
n Trapezius
n Sternocleidomastoid
n Temporalis
n Occipitofrontalis
n Suboccipital muscles
n Masseter
n Relevant Muscles
n Medial & Lateral Pterygoid
n Anterior & Posterior Digastric
n Fascial muscles
n Splenius Capitis
n Posterior Cervical musculature
n Deep Anterior Cervical musculature
n Cervical Dysfunction
n Upper cervical nerves posses fibers for pain from the lower part of the occipital sinus, vertebral and posterior meningeal arteries, and the dural floor of the posterior fossa (C1, C2, C3)
n Differential Diagnosis:Migraine Headache
Etiology:
n Hereditary component
n Not correlated with personality types “A” or neuroses
n The worsening or migraine that occurs during periods of intense nervousness, anxiety, and depression is usually due to the superimposition of a tension headache
n Vascular spasm followed by vasodilatation
n Migraine Headache:Signs & Symptoms
Classic Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: preceded with visual disturbances and less often with hemi-sensory disturbances, hemiparesis, or aphasia
n Migraine Headache:Signs & Symptoms
Classic & Common Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: photophobia and or phonophobia; tension headache often concomitant
n Aggravated: red wine, nuts, aged cheese, chocolate and caffeine containing beverages
n Risk factor: women are more affected than men
n Migraine Headache:Diagnosis & Treatment
n Response to ergot therapy
n Drug treatment is widely varied (caffeine, NSAIDS, barbiturates, narcotics, beta blockers, calcium channel blockers, sedatives, and more…)
n Prevention by avoiding predisposing factors, decreasing stress, maintaining sleep regularity
n Osteopathic treatment would include stabilizing vasculature and associated concomitant tension headache
n Differential Diagnosis:Cluster Headache
Etiology
n Disturbed hypothalamic biorhythm
n Excess smoking and drinking may precipitate via sphenopalatine irritation
n Hemicranial (unilateral) cranial dysfunction
n Cervical somatic dysfunction with irritation of the spinal accessory nerve
n Cluster Headache:Signs & Symptoms
n Character: excruciating pain often stabbing
n Location: usually near one eye
n Associated: tearing, flushed face, nasal congestion, conjunctival congestion (ANS)
n Risk factor: males affected more than females
n Onset: begins at 20 – 40 years of age
n Cluster Headache:Signs & Symptoms
n Attacks last 30 – 90 minutes daily for days and then disappear for months (Headache “vacation”)
n Alcohol can precipitate but only during an active cycle, not during “vacations”
n Some are so painful that they can lead to suicide
n Cluster Headache: Prevention & Treatment
n Drug treatment is widely varied
n Osteopathic treatment would include a thorough cranial assessment
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Etiology
n Ruptured aneurysm
n Arteriovenous malformation
n Trauma
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Signs & Symptoms
n Character: full-blown catastrophic headache
n Location: Holocaine
n Duration: continuous
n Associated: photophobia, retinal hemorrhages, nuchal rigidity, Brudzinski’s sign, Kernig’s sign, obtunded collapse
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Diagnosis
n CT may show blood and aneurysm
n Lumbar puncture may show bloody CSF
n MRI
n Differential Diagnosis:Organic origin, Meningitis
Etiology
n Virus
n Bacteria
n Fungus
n Tuberculous
n Differential Diagnosis:Organic origin, Meningitis
Signs & Symptoms
n Character: cephalgia is intense, steady, and deep
n Location: holocranial pain associated with retro-orbital pain which is aggravated with eye movement
n Onset: sub-acute or acute
n Associated: fever, generalized convulsions, varied levels of consciousness, nuchal rigidity, Brudzinski and Kernig’s signs
n Differential Diagnosis:Organic origin, Meningitis
Diagnosis
n Headache with fever and nuchal rigidity
n LP reveals pleocytosis, increased protein, and low glucose
n CT scan after Tx is underway to R/O brain abscess and subdural empyema
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Etiology
n Increased volume
n Increased venous pressure
n Obstruction to flow/absorption of CSF
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Signs & Symptoms
n HA is severe
n HA occur with coughing, sneezing, valsalva effort
n Associated findings include papilledema, obtunded, focal neurologic signs & symptoms
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Diagnosis
n CT
n MRI
n Avoid LP
n Differential Diagnosis:Organic origin, Hypertension
n Usually no HA’s until DBP > 120 mm Hg
n 3 major causes of acute severe hypertension: drugs, pheochromocytoma, neurogenic (paraplegia)
n Associated findings include: retinopathy, convulsions, confusion or stupor evolving over several days
n Differential Diagnosis:Organic origin, Vasculopathies
Etiology
n Temporal (giant cell) arteritis
n Dissection of a vessel
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms of Temporal Arteritis
n Character: throbbing and sharp, burning pain
n Location: focal headache in the temporal or frontal-occipital region
n Onset: gradual and progressive
n Aggravated: headache worse at night and with cold
n Risk: most common in white females > 50 years old
n Associated: weight loss, fever, fatigue, polymyalgia rheumatica, monocular visual loss, jaw claudication
n Differential Diagnosis:Organic origin, Vasculopathies
Diagnosis of Temporal arteritis
n Increased sed rate
n Biopsy
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms (Dissection of vessel)
n Severe, localized HA
n History of trauma or vigorous exertion
n Diagnosis with CT
n Differential Diagnosis:Organic origin, Acute Purulent Sinusitis
n Involving the frontal, maxillary, sphenoidal, or ethmoidal sinuses
n True “sinus HA” is rare; if present, the patient is usually very ill, with a severe localized HA for hours or days, PND & tender sinuses; often misdiagnosed as tension HA or common migraine but may have these as concomitant HA
n Diagnosis: CT
n Differential Diagnosis:Tension HeadacheEtiology
Skeletal components
n Somatic dysfunctions of the upper cervical unit are going to impinge on the upper cervical nerves which have afferents in the cranium and dura
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Can be explained by trigger point reflex mechanisms. A myofascial trigger point is a focus of hyperirritability within a taut band of skeletal muscle or the associated fascia that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness, and sometimes to referred autonomic phenomena and distortion of proprioception
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Trigger points can result directly from ischemia due to chronically tense muscles, acute overload, overwork fatigue, direct trauma, and chilling.
n Trigger points can result indirectly from other trigger points (a.k.a. latent trigger points), visceral disease, arthritic joints, and by emotional distress
n Differential Diagnosis:Tension HeadacheEtiology
Soft tissue components
n Ligaments can refer pain to sclerotomes which need to be addressed to completely resolve the somatic dysfunction
Lymphatics
n Need to free up the thoracic inlet to allow drainage of fluids
n Trapezius
n The trapezius can have many trigger points but the ones located in the upper fibers are most relevant for cephalgia
n Pain referral pattern: Posterolateral aspect of the neck, mastoid process, temple and back of the orbit, and the angle of the jaw
n Trapezius
n The patient can often be misdiagnosed as having cervical radiculopathy or atypical facial neuralgia. The normally minimal antigravity function of the upper trapezius is overstressed by any position or activity in which the trapezius helps to carry the weight of the arm for a prolonged period
n The muscle can also be strained by chronic injury due to overload, carrying a heavy backpack, long telephone calls, and sleeping prone with the head turned to one side
n Trapezius
n The trapezius can also entrap the greater occipital nerve which enervates the skin of the scalp and the semispinalis capitis muscle
n Sternocleidomastoid Sternal division
n Pain referral pattern: supra-orbital and deep within the orbit, occipital ridge, and vertex
n Associated autonomic findings: excessive lacrimation, reddening of the conjunctiva, apparent “ptosis,” and visual disturbances
n Sternocleidomastoid Clavicular division
n Pain referral pattern: frontal area which extends across the forehead to the other side, and posterior auricular
n Associated proprioceptive findings: spatial disorientation
n Sternocleidomastoid
n The SCM trigger points can be activated by sleeping on two pillows and keeping the neck in a flexed position, or by keeping the neck in an extended position as in painting a ceiling or sitting in the front row of a theater with a high screen or elevated stage. The SCM is often injured in a “whiplash” injury that might occur in an automobile crash.
n Temporalis
n Pain referral pattern: widely throughout the temple, along the eyebrow, and behind the eye
n Temporalis trigger points may be activated by bruxism, direct trauma such as a fall or an impact to the cranium. The temporalis muscle can also be activated secondary to spasm in the masseter muscle
n Occipitofrontalis
n Frontal division pain referral pattern: upward and over the forehead on the ipsilateral side
n Occipital division pain referral pattern: laterally, diffusely over the back of the head and with pain deep in the orbit
n Second most common complaint after back pain
n “Everyone” has headaches (HA)
n More than 80 million ER visits in U.S. per year
n Frequency of HA due to rich nerve supply and psychological implications of head pain
n General Statistics
n Nerves responsible for HA have their source from myelinated C fibers and A-delta fibers in cranial nerves V, IX, X, and roots C1, C2, C3
n Pain sensitive structures include the eye, ear, paranasal sinuses, large extra and intra cranial arteries, dural sinuses, periosteum of the skull skin, cranial muscles, and the upper cervical spine
n Etiologies
n Commonly overlooked etiologies include: food, fever, viral, metabolic, withdrawal, and pharmaceutical
n International Headache Society Classifications (see attachment)
n History: Questions to ask
n Character of pain
n Mode of onset
n Mode of offset
n Time of onset
n Relieving factors
n Aggravating factors
n History: Questions to ask
n Precipitating factors
n Frequency of attacks
n Duration of attacks
n Associated symptoms
n Family history of headache
n Allergies
n Seven danger signals of an ominous headache
n A “first” headache
n Headache due to exertion
n Headache with fever
n Headache in a drowsy or confused patient
n Seven danger signals of an ominous headache
n Headache in a patient with nuchal rigidity or meningeal signs
n Headache in a patient with abnormal physical signs
n Headache in a patient who “looks ill”
n Physical Exam
n Gait assessment
n Vital signs
n Fundoscopic exam
n Facial symmetry
n Head & Neck structures
n Deep tendon reflexes
n Plantar response
n Limb strength
n Relevant Muscles
n Trapezius
n Sternocleidomastoid
n Temporalis
n Occipitofrontalis
n Suboccipital muscles
n Masseter
n Relevant Muscles
n Medial & Lateral Pterygoid
n Anterior & Posterior Digastric
n Fascial muscles
n Splenius Capitis
n Posterior Cervical musculature
n Deep Anterior Cervical musculature
n Cervical Dysfunction
n Upper cervical nerves posses fibers for pain from the lower part of the occipital sinus, vertebral and posterior meningeal arteries, and the dural floor of the posterior fossa (C1, C2, C3)
n Differential Diagnosis:Migraine Headache
Etiology:
n Hereditary component
n Not correlated with personality types “A” or neuroses
n The worsening or migraine that occurs during periods of intense nervousness, anxiety, and depression is usually due to the superimposition of a tension headache
n Vascular spasm followed by vasodilatation
n Migraine Headache:Signs & Symptoms
Classic Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: preceded with visual disturbances and less often with hemi-sensory disturbances, hemiparesis, or aphasia
n Migraine Headache:Signs & Symptoms
Classic & Common Migraine
n Character: throbbing pain
n Location: hemicranial
n Associated: photophobia and or phonophobia; tension headache often concomitant
n Aggravated: red wine, nuts, aged cheese, chocolate and caffeine containing beverages
n Risk factor: women are more affected than men
n Migraine Headache:Diagnosis & Treatment
n Response to ergot therapy
n Drug treatment is widely varied (caffeine, NSAIDS, barbiturates, narcotics, beta blockers, calcium channel blockers, sedatives, and more…)
n Prevention by avoiding predisposing factors, decreasing stress, maintaining sleep regularity
n Osteopathic treatment would include stabilizing vasculature and associated concomitant tension headache
n Differential Diagnosis:Cluster Headache
Etiology
n Disturbed hypothalamic biorhythm
n Excess smoking and drinking may precipitate via sphenopalatine irritation
n Hemicranial (unilateral) cranial dysfunction
n Cervical somatic dysfunction with irritation of the spinal accessory nerve
n Cluster Headache:Signs & Symptoms
n Character: excruciating pain often stabbing
n Location: usually near one eye
n Associated: tearing, flushed face, nasal congestion, conjunctival congestion (ANS)
n Risk factor: males affected more than females
n Onset: begins at 20 – 40 years of age
n Cluster Headache:Signs & Symptoms
n Attacks last 30 – 90 minutes daily for days and then disappear for months (Headache “vacation”)
n Alcohol can precipitate but only during an active cycle, not during “vacations”
n Some are so painful that they can lead to suicide
n Cluster Headache: Prevention & Treatment
n Drug treatment is widely varied
n Osteopathic treatment would include a thorough cranial assessment
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Etiology
n Ruptured aneurysm
n Arteriovenous malformation
n Trauma
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Signs & Symptoms
n Character: full-blown catastrophic headache
n Location: Holocaine
n Duration: continuous
n Associated: photophobia, retinal hemorrhages, nuchal rigidity, Brudzinski’s sign, Kernig’s sign, obtunded collapse
n Differential Diagnosis:Organic origin, Subarachnoid hemorrhage
Diagnosis
n CT may show blood and aneurysm
n Lumbar puncture may show bloody CSF
n MRI
n Differential Diagnosis:Organic origin, Meningitis
Etiology
n Virus
n Bacteria
n Fungus
n Tuberculous
n Differential Diagnosis:Organic origin, Meningitis
Signs & Symptoms
n Character: cephalgia is intense, steady, and deep
n Location: holocranial pain associated with retro-orbital pain which is aggravated with eye movement
n Onset: sub-acute or acute
n Associated: fever, generalized convulsions, varied levels of consciousness, nuchal rigidity, Brudzinski and Kernig’s signs
n Differential Diagnosis:Organic origin, Meningitis
Diagnosis
n Headache with fever and nuchal rigidity
n LP reveals pleocytosis, increased protein, and low glucose
n CT scan after Tx is underway to R/O brain abscess and subdural empyema
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Etiology
n Increased volume
n Increased venous pressure
n Obstruction to flow/absorption of CSF
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Signs & Symptoms
n HA is severe
n HA occur with coughing, sneezing, valsalva effort
n Associated findings include papilledema, obtunded, focal neurologic signs & symptoms
n Differential Diagnosis:Organic origin, Increased Intracranial pressure
Diagnosis
n CT
n MRI
n Avoid LP
n Differential Diagnosis:Organic origin, Hypertension
n Usually no HA’s until DBP > 120 mm Hg
n 3 major causes of acute severe hypertension: drugs, pheochromocytoma, neurogenic (paraplegia)
n Associated findings include: retinopathy, convulsions, confusion or stupor evolving over several days
n Differential Diagnosis:Organic origin, Vasculopathies
Etiology
n Temporal (giant cell) arteritis
n Dissection of a vessel
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms of Temporal Arteritis
n Character: throbbing and sharp, burning pain
n Location: focal headache in the temporal or frontal-occipital region
n Onset: gradual and progressive
n Aggravated: headache worse at night and with cold
n Risk: most common in white females > 50 years old
n Associated: weight loss, fever, fatigue, polymyalgia rheumatica, monocular visual loss, jaw claudication
n Differential Diagnosis:Organic origin, Vasculopathies
Diagnosis of Temporal arteritis
n Increased sed rate
n Biopsy
n Differential Diagnosis:Organic origin, Vasculopathies
Signs & Symptoms (Dissection of vessel)
n Severe, localized HA
n History of trauma or vigorous exertion
n Diagnosis with CT
n Differential Diagnosis:Organic origin, Acute Purulent Sinusitis
n Involving the frontal, maxillary, sphenoidal, or ethmoidal sinuses
n True “sinus HA” is rare; if present, the patient is usually very ill, with a severe localized HA for hours or days, PND & tender sinuses; often misdiagnosed as tension HA or common migraine but may have these as concomitant HA
n Diagnosis: CT
n Differential Diagnosis:Tension HeadacheEtiology
Skeletal components
n Somatic dysfunctions of the upper cervical unit are going to impinge on the upper cervical nerves which have afferents in the cranium and dura
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Can be explained by trigger point reflex mechanisms. A myofascial trigger point is a focus of hyperirritability within a taut band of skeletal muscle or the associated fascia that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness, and sometimes to referred autonomic phenomena and distortion of proprioception
n Differential Diagnosis:Tension HeadacheEtiology
Muscular components
n Trigger points can result directly from ischemia due to chronically tense muscles, acute overload, overwork fatigue, direct trauma, and chilling.
n Trigger points can result indirectly from other trigger points (a.k.a. latent trigger points), visceral disease, arthritic joints, and by emotional distress
n Differential Diagnosis:Tension HeadacheEtiology
Soft tissue components
n Ligaments can refer pain to sclerotomes which need to be addressed to completely resolve the somatic dysfunction
Lymphatics
n Need to free up the thoracic inlet to allow drainage of fluids
n Trapezius
n The trapezius can have many trigger points but the ones located in the upper fibers are most relevant for cephalgia
n Pain referral pattern: Posterolateral aspect of the neck, mastoid process, temple and back of the orbit, and the angle of the jaw
n Trapezius
n The patient can often be misdiagnosed as having cervical radiculopathy or atypical facial neuralgia. The normally minimal antigravity function of the upper trapezius is overstressed by any position or activity in which the trapezius helps to carry the weight of the arm for a prolonged period
n The muscle can also be strained by chronic injury due to overload, carrying a heavy backpack, long telephone calls, and sleeping prone with the head turned to one side
n Trapezius
n The trapezius can also entrap the greater occipital nerve which enervates the skin of the scalp and the semispinalis capitis muscle
n Sternocleidomastoid Sternal division
n Pain referral pattern: supra-orbital and deep within the orbit, occipital ridge, and vertex
n Associated autonomic findings: excessive lacrimation, reddening of the conjunctiva, apparent “ptosis,” and visual disturbances
n Sternocleidomastoid Clavicular division
n Pain referral pattern: frontal area which extends across the forehead to the other side, and posterior auricular
n Associated proprioceptive findings: spatial disorientation
n Sternocleidomastoid
n The SCM trigger points can be activated by sleeping on two pillows and keeping the neck in a flexed position, or by keeping the neck in an extended position as in painting a ceiling or sitting in the front row of a theater with a high screen or elevated stage. The SCM is often injured in a “whiplash” injury that might occur in an automobile crash.
n Temporalis
n Pain referral pattern: widely throughout the temple, along the eyebrow, and behind the eye
n Temporalis trigger points may be activated by bruxism, direct trauma such as a fall or an impact to the cranium. The temporalis muscle can also be activated secondary to spasm in the masseter muscle
n Occipitofrontalis
n Frontal division pain referral pattern: upward and over the forehead on the ipsilateral side
n Occipital division pain referral pattern: laterally, diffusely over the back of the head and with pain deep in the orbit
headache
What is a headache? Headache is defined as pain in the head that is located above the eyes or the ears, behind the head (occipital), or in the back of the upper neck. Headache, like chest pain or dizziness, has many causes.
What are the causes of headaches? There are two types of headaches: primary headaches and secondary headaches. Primary headaches are not associated with (caused by) other diseases. Examples of primary headaches are migraine headaches, tension headaches, and cluster headaches. Secondary headaches are caused by associated disease. The associated disease may be minor or serious and life threatening.
How common are primary and secondary headaches? Tension headaches are the most common type of primary headache; as many as 90% of adults have had or will have tension headaches. Tension headaches are more common among women than men.
Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches. Migraine headaches affect children as well as adults. Before puberty, boys and girls are affected equally by migraine headaches, but after puberty, more women than men are affected. An estimated 6% of men and up to 18% of women will experience a migraine headache.
In the United States, migraine headaches often go undiagnosed or are misdiagnosed as tension or sinus headaches. As a result, many migraine sufferers do not receive effective treatment.
Cluster headaches are a rare type primary headache, affecting 0.1% of the population. An estimated 85% of cluster headache sufferers are men. The average age of cluster headache sufferers is 28-30 years, although headaches may begin in childhood.
Secondary headaches have diverse causes, ranging from serious and life threatening conditions such as brain tumors, strokes, meningitis, and subarachnoid hemorrhages to less serious but common conditions such as withdrawal from caffeine and discontinuation of analgesics.
Many people suffer from "mixed" headache disorders in which tension headaches or secondary headaches trigger migraine headaches.
What are the symptoms of tension headaches? Tension headaches often begin in the back of the head and upper neck as a band-like tightness or pressure. Tension headaches also are described as a band of pressure encircling the head with the most intense pain over the eyebrows. The pain of tension headaches usually is mild (not disabling) and bilateral (affecting both sides of the head). Tension headaches are not associated with an aura (see below) and are seldom associated with nausea, vomiting, or sensitivity to light and sound. Tension headaches usually occur sporadically (infrequently and without a pattern) but can occur frequently and even daily in some people. Most people are able to function despite their tension headaches.
What are the symptoms of migraine headaches? Migraine is a chronic condition of recurrent attacks. Most (but not all) migraine attacks are associated with headaches. Migraine headaches usually are described as an intense, throbbing or pounding pain that involves one temple. (Sometimes the pain can be located in the forehead, around the eye, or the back of the head). The pain usually is unilateral (on one side of the head), although about a third of the time the pain is bilateral. The unilateral headaches typically change sides from one attack to the next. (In fact, unilateral headaches that always occur on the same side should alert the doctor to consider a secondary headache, for example, one caused by a brain tumor). A migraine headache usually is aggravated by daily activities like walking upstairs. Nausea, vomiting, diarrhea, facial pallor, cold hands, cold feet, and sensitivity to light and sound commonly accompany migraine headaches. As a result of this sensitivity to light and sound, migraine sufferers usually prefer to lie in a quiet, dark room during an attack. A typical attack lasts between 4 and 72 hours.
An estimated 40%-60% of migraine attacks are preceded by premonitory (warning) symptoms lasting hours to days. The symptoms may include sleepiness, irritability, fatigue, depression or euphoria, yawning, and cravings for sweet or salty foods. Patients and their family members usually know that when they observe these warning symptoms that a migraine attack is beginning.
An estimated 20% of migraine headaches are associated with an aura. Usually, the aura precedes the headache, although occasionally it may occur simultaneously with the headache. The most common auras are 1) flashing, brightly colored lights in a zigzag pattern (fortification spectra), usually starting in the middle of the visual field and progressing outward and 2) a hole (scotoma) in the visual field, also known as a blind spot. Some elderly migraine sufferers may experience only the visual aura without the headache. A less common aura consists of pins-and-needles sensations in the hand and the arm on one side or pins-and-needles sensations around the mouth and the nose on the same side. Other auras include auditory (hearing) hallucinations and abnormal tastes and smells.
Complicated migraines are migraines that are accompanied by neurological dysfunction. The part of the body that is affected by the dysfunction is determined by the part of the brain that is responsible for the headache. Vertebrobasilar migraines are characterized by dysfunction of the brainstem (the lower part of the brain that is responsible for automatic activities like consciousness and balance). The symptoms of vertebrobasilar migraines include fainting as an aura, vertigo (dizziness in which the environment seems to be spinning) and double vision. Hemiplegic migraines are characterized by paralysis or weakness of one side of the body, mimicking a stroke. The paralysis or weakness is usually temporary, but sometimes it can last for days.
For approximately 24 hours after a migraine attack, the migraine sufferer may feel drained of energy and may experience a low-grade headache along with sensitivity to light and sound. Unfortunately, some sufferers may have recurrences of the headache during this period.
What are the symptoms of cluster headaches? Cluster headaches are headaches that come in groups (clusters) lasting weeks or months, separated by pain-free periods of months or years. During the period in which the cluster headaches occur, pain typically occurs once or twice daily, but some patients may experience pain more than twice daily. Each episode of pain lasts from 30 minutes to one and one-half hours. Attacks tend to occur at about the same time every day and often awaken the patient at night from a sound sleep. The pain typically is excruciating and located unilaterally around or behind one eye. Some patients describe the pain as feeling like a hot poker in the eye. The affected eye may become red, inflamed, and watery. The nose on the affected side may become congested and runny. Unlike patients with migraine headaches, patients with cluster headaches tend to be restless. They often pace the floor, bang their heads against a wall, and can be driven to desperate measures. Cluster headaches are much more common in males than females.
What causes primary headaches? Migraine headache is caused by a combination of vasodilatation (enlargement of blood vessels) and the release of chemicals from nerve fibers that coil around the blood vessels. During a migraine attack, the temporal artery enlarges. (The temporal artery is an artery that lies on the outside of the skull just under the skin of the temple.) Enlargement of the temporal artery stretches the nerves that coil around the artery and causes the nerves to release chemicals. The chemicals cause inflammation, pain, and further enlargement of the artery. The increasing enlargement of the artery magnifies the pain.
Migraine attacks commonly activate the sympathetic nervous system in the body. The sympathetic nervous system is often thought of as the part of the nervous system that controls primitive responses to stress and pain, the so-called "fight or flight" response. The increased sympathetic nervous activity in the intestine causes nausea, vomiting, and diarrhea. Sympathetic activity also delays emptying of the stomach into the small intestine and thereby prevents oral medications from entering the intestine and being absorbed. The impaired absorption of oral medications is a common reason for the ineffectiveness of medications taken to treat migraine headaches. The increased sympathetic activity also decreases the circulation of blood, and this leads to pallor of the skin as well as cold hands and feet. The increased sympathetic activity also contributes to the sensitivity to light and sound sensitivity as well as blurred vision.
Tension headache does not have a clear cause. Many physicians attribute tension headaches to excess stress or a hectic day. There is also evidence that some tension headaches may have a cause that is similar to the cause of migraine headaches.
Cluster headache also does not have a clear cause, although alcohol and cigarettes can precipitate attacks.
Are primary headaches dangerous? Tension headaches have not been shown to lead to neurological dysfunction or brain damage. In general, this is true of migraine headaches. However, there is a rare association of migraine headaches and stroke, particularly in sufferers of complicated migraines. While cluster headaches need to be differentiated from more serious neurological conditions, there is no known danger of cluster headaches leading to stroke.
What diseases cause secondary headaches? Important examples of diseases causing secondary headaches include:
· Tumors in the brain, including tumors that have spread (metastasized) to the brain from another organ such as the lung or breast
· Subdural hematomas, which are collections of blood underneath the dura (the covering of the brain) due to bleeding from ruptured veins. Subdural hematomas typically occur in elderly individuals after a fall or other trauma to the head. Sometimes the fall can precede the visit to the doctor by weeks, and the elderly patients may not even recall the fall. Symptoms of subdural hematomas include chronic headaches, change in personality, and weakness of the extremities.
· Epidural hematomas, which are rapid collections of blood due to the rupture of arteries that run on the inner surface of the skull. Epidural hematomas usually are the result of skull fractures. The typical story is a head injury that causes a concussion with loss of consciousness and a skull fracture. The return of consciousness is followed by the sudden development of coma caused by an expanding hematoma.
· Infections such as meningitis caused by bacteria (meningococcus and pneumococcus), tuberculosis, Lyme disease, or cryptococcus
· Strokes due either to blood clots within the arteries of the brain or rupture of the blood vessels in the brain
· Subarachnoid hemorrhages which are caused by bleeding into the space between the brain and its outer arachnoid lining. The most common source of subarachnoid hemorrhage is an aneurysm, a ballooning of the weakened wall of an artery inside the head.
· Sudden onset of severe high blood pressure. (Chronic mild to moderate high blood pressure is not a common cause of headache).
· Temporal arteritis, a vasculitis (inflammation) of the temporal artery which runs beneath the skin of the temple. Temporal arteritis occurs primarily in older people and may be associated with fatigue, body aches, and anemia. Without proper treatment, temporal arteritis may lead to blindness and strokes.
· Acute angle glaucoma with sudden elevation of pressures inside the eyes
· Infections of the sinuses (sinusitis), ear (otitis), and teeth
· Hypothyroidism, a condition in which the thyroid gland does not produce enough thyroid hormone
· Repeated carbon monoxide poisoning
· Parkinson's disease
· Medications such as indomethacin, estrogen, progestins, calcium channel blockers (commonly used for treating high blood pressure), and selective serotonin reuptake inhibitors (commonly used to treat depression)
· Overuse of over-the-counter or prescription pain relievers. Overuse of pain relievers causes the pain relievers to become less effective. As the effect of the pain reliever wears off, headaches recur (rebound headache).
· Cardiac ischemia (lack of blood supply to the muscles of the heart caused by coronary artery disease). Although cardiac ischemia is best known as a cause of either heart attacks or angina, it also may cause a headache. The headache may occur with or without the accompanying chest pain of a heart attack or angina. As with angina, in some individuals the headache may occur with exertion and subside with rest.
How are secondary headaches diagnosed? Conditions causing secondary headaches, such as bacterial meningitis, subarachnoid hemorrhage, severe (malignant) high blood pressure, epidural or subdural hematomas, can cause serious brain damage or even death. Therefore, timely and accurate diagnosis of secondary headaches is crucial. Special blood tests, brain scans, CT scans or MRI, and lumbar puncture (spinal tap) are necessary to establish these diagnoses (see below). The challenge for doctors is to decide which patients should undergo these special tests. To make such decisions, doctors rely upon information obtained from the initial patient interview and physical examination. Information that is important to the doctor include:
1. The mode of onset of the headache. For example, patients with a subarachnoid hemorrhage typically report having a sudden onset of severe headache ("the worst headache ever"). The pain of recurrent migraine headaches tends to build up gradually. Sometimes the headache of subarachnoid hemorrhage is triggered by exertion such as sex.
2. The age of the patient. Temporal arteritis typically occurs in older people and is extremely rare in individuals younger than 50. Patients with primary headaches (for example migraine headaches) typically have many years of similar headaches, often starting at a young age. Therefore, new onset of a headache after 50 years of age or onset of a new type of headache suggests a secondary headache and should prompt testing.
3. The location of the headache (on one side or both sides of the head). Headaches that persistently occur on the same side often are secondary headaches associated with, for example, brain tumors or arteriovenous malformations (abnormal clusters of blood vessels in the brain).
4. Associated fever and neck stiffness. Bacterial meningitis is a rapidly progressive and life-threatening disease with fever, headaches, stiff neck, and deterioration in mental function. Herpes simplex encephalitis is a virus infection of the brain that causes death of brain tissue. Symptoms include fever, headache, and deterioration in mental function. Early treatment with antibiotics and anti-viral agents can decrease the extent of brain damage and improve survival.
5. Associated mental deterioration, seizures, or weakness of the extremities or face, which can be symptoms of brain tumors.
6. Associated temporary weakness of the extremities or facial muscles, which can be symptoms of transient ischemic attack (TIAs). Transient ischemic attacks are caused by temporary interruptions in the flow of blood to small areas of the brain. Transient ischemic attacks are warning signals for future strokes that can cause permanent brain damage. Headache also can accompany strokes and intracerebral bleeding (bleeding into the substance of the brain).
7. Recent head trauma. Headaches soon after trauma to the head may be caused by subdural or epidural hematomas.
What are the tests for secondary headaches? The patient history and physical examination provide the best means for determining the cause of secondary headaches. Therefore, it is extremely important that patients with severe headaches undergo examination by a doctor experienced in diagnosing and treating headaches. A few tests may be useful in diagnosing the presence and cause of secondary headaches including blood tests, computerized tomography (CT Scan) and magnetic resonance imaging (MRI) scans of the head, and lumbar puncture.
Blood testsAn elevated white blood cell count suggests infection such as meningitis. An elevated erythrocyte sedimentation rate suggests temporal arteritis. Abnormal thyroid tests suggest thyroid disorders. Blood tests also may detect kidney failure and abnormally elevated calcium levels as the cause of headaches.
CT scan of the headA CT scan of the head is useful for detecting accumulation of blood such as subdural hematomas and subarachnoid hemorrhages. It is moderately useful in detecting brain tumors and strokes not due to hemorrhage.
MRI scan of the headAn MRI scan of the head can detect subdural and epidural hematomas, herpes simplex infection of the brain, strokes, tumors, and arterial aneurysms.
Lumbar punctureCerebro-spinal fluid, the fluid that surrounds the brain and spinal cord, can be removed with a needle that is inserted into the spine in the lower back. Examination of the fluid can reveal infection (such as meningitis due to bacteria or tuberculosis) or blood from hemorrhage. In some patients with subarachnoid hemorrhage, CT scans are normal, and lumbar punctures are necessary to demonstrate blood from the hemorrhage that has spread throughout the cerebro-spinal fluid.
When should one consult a doctor for headaches? Many people who suffer from mild headaches medicate themselves with over-the-counter analgesics, and they usually do not seek medical care. Nevertheless, the symptoms of primary headaches and secondary headaches can overlap. Furthermore, a person with a long history of migraine or tension headaches can develop a new secondary headache. Many tension or sinus headaches probably are migraine headaches and will respond to treatments that are specific for migraine. Therefore, a doctor should be consulted if the headache is:
· Severe ("the worst ever")
· Different than the usual headaches
· Starts suddenly during exertion
· Aggravated by exertion, coughing, bending, or sexual activity
· Associated with persistent nausea and vomiting
· Associated with stiff neck, fever, dizziness, blurred vision, slurred speech, unsteady gait, weakness or unusual sensations of the arm or leg, excessive drowsiness or confusion
· Associated with seizures
· Associated with recent head trauma or a fall
· Not responding to treatment and is getting worse
· Disabling, and interfering with work and the quality of life
· Requires more than the recommended dose of over-the-counter analgesics for relief
What is the treatment for tension headaches? Individuals with occasional tension headaches or mild migraine headaches that do not interfere with daily activities usually medicate themselves with over-the-counter (OTC, non-prescription) pain relievers (analgesics). Many OTC analgesics are available. OTC analgesics have been shown to be safe and effective for short-term relief of headache (as well as muscle aches, pains, menstrual cramps, and fever) when used according to the instructions on their labels.
There are two major classes of OTC analgesics: acetaminophen (Tylenol) and non-steroidal anti-inflammatory drugs (NSAIDs). The two types of NSAIDs are aspirin and non-aspirin. Examples of non-aspirin NSAIDs are ibuprofen (Advil, Nuprin, Motrin IB, and Medipren) and naproxen (Aleve). Some NSAIDs are available by prescription only. Prescription NSAIDs are usually prescribed to treat arthritis and other inflammatory conditions such as bursitis, tendonitis, etc. The difference between OTC and prescription NSAIDs may only be the amount of the active ingredient contained in each pill. For example, OTC naproxen (Aleve) contains 220 mg of naproxen per pill, whereas prescription naproxen (Naprosyn) contains 375 or 500 mg of naproxen per pill.
Acetaminophen reduces pain and fever by acting on pain centers in the brain. Acetaminophen is well tolerated and generally is considered easier on the stomach than NSAIDs. However, acetaminophen can cause severe liver damage in high (toxic) doses or if used on a regular basis over extended periods of time. In individuals who regularly consume moderate or large amounts of alcohol, acetaminophen can cause serious damage to the liver in lower doses that usually are not toxic. Acetaminophen also can damage the kidneys when taken in large doses. Therefore, acetaminophen should not be taken more frequently or in larger doses than recommended on the label.
NSAIDs relieve pain by reducing the inflammation that causes the pain (They are called non-steroidal anti-inflammatory drugs or NSAIDs because they are different from corticosteroids such as prednisone, prednisolone, and cortisone which also reduce inflammation). Corticosteroids, though valuable in reducing inflammation, have predictable and potentially serious side effects, especially when used long-term. NSAIDs do not have the same side effects that corticosteroids have.
Aspirin, Aleve, Motrin, and Advil all are NSAIDs and are similarly effective in relieving pain and fever. The main difference between aspirin and non-aspirin NSAIDs is their effect on platelets. Platelets are small particles in the blood that cause blood clots to form. Aspirin prevents the platelets from forming blood clots. Therefore, aspirin can increase bleeding by preventing blood from clotting though it also can be used therapeutically to prevent clots from causing heart attacks and strokes. The non-aspirin NSAIDs also have anti-platelet effects, but their anti-platelet action does not last as long as aspirin.
Aspirin, acetaminophen, and caffeine also are available combined in OTC analgesics for the treatment of headaches. Examples of such combination analgesics are Pain-aid, Excedrin, Fioricet, and Fiorinal.
Finding an effective analgesic or analgesic combination often is a process of trial and error because individuals respond differently to different analgesics. In general, a person should use the analgesic that has worked in the past. This will increase the likelihood that an analgesic will be effective and decrease the risk of side effects.
There are several precautions that should be observed with OTC analgesics:
· Children and teenagers should not use aspirin for the treatment of headaches, other pain, or fever, because of the risk of developing Reye's Syndrome, a life-threatening neurological disease that can lead to coma and even death.
· Patients with balance disorders or hearing difficulties should avoid using aspirin because aspirin may aggravate these conditions.
· Patients taking blood thinners such as warfarin (Coumadin) should not take aspirin and non-aspirin NSAIDs without a doctor's supervision because they add further to the risk of bleeding that is caused by the blood thinner.
· Patients with active ulcers of the stomach and duodenum should not take aspirin and non-aspirin NSAIDs because they can increase the risk of bleeding from the ulcer and impair healing of the ulcer.
· Patients with advanced liver disease should not take aspirin and non-aspirin NSAIDs because they may impair kidney function. Deterioration of kidney function in these patients can lead to rapid and life-threatening deterioration of their liver disease.
· Patients should not overuse OTC or prescription analgesics. Overuse of analgesics can lead to the development of tolerance (increasing ineffectiveness of the analgesic) and rebound headaches (return of the headache as soon as the effect of the analgesic wears off, usually in the early morning hours). Thus, overuse of analgesics can lead to a vicious cycle of more and more analgesics for headaches that respond less and less to treatment and occur more frequently.
What is the treatment for moderate to severe migraine headaches? Migraine-specific abortive medications usually are necessary for moderate to severe migraine headaches. The abortive medications for moderate or severe migraine headaches are different than OTC analgesics. Instead of relieving pain, they abort headaches by counteracting the cause of the headache, dilation of the temporal arteries. In fact, they cause narrowing of the arteries. Examples of migraine-specific abortive medications are the triptans and ergot preparations.
Triptans The triptans attach to serotonin receptors on the blood vessels and nerves and thereby reduce inflammation and constrict the blood vessels. This stops the headache. The triptan with the longest history of use is sumatriptan (Imitrex). Sumatriptan is available in the United States as an injection, oral tablet, and nasal spray. Zolmitriptan (Zomig) and rizatriptan (Maxalt) are newer triptans that are available as oral tablets and as tablets that melt in the mouth. Naratriptan (Amerge), almotriptan (Axert) and frovatriptan (Frovalan) are available only as oral tablets.
Traditionally, triptans were prescribed for moderate or severe migraines after OTC analgesics and other simple measures failed. Newer studies suggest that triptans can be used as the first treatment for patients with migraines that are causing disability. (Significant disability is defined as more than 10 days of at least 50% disability during a three-month period.). Triptans should be used early after the migraine begins, before the onset of pain or when the pain is mild. Using a triptan early in an attack increases its effectiveness, reduces side effects, and decreases the chance of recurrence of another headache during the following 24 hours. Used early, triptans can be expected to abort more than 80% of migraine headaches within 2 hours.
What are the side effects of triptans? The most common side effects of triptans are facial flushing, tingling of the skin, and a sense of tightness around the chest and throat. Other less common side effects include drowsiness, fatigue, and dizziness. These side effects are short-lived and are not considered serious.
The most serious side effects of triptans are heart attacks and strokes. Triptans are effective in migraine headaches because they narrow arteries in the head; however, they also can narrow arteries in the heart. In individuals without existing carotid or coronary artery disease, the narrowing caused by triptans usually does not cause problems. However, in patients whose carotid and coronary arteries are narrowed by atherosclerosis or who suffer from intermittent spasm of the coronary arteries (a condition called Prinzmetal's or variant angina), the narrowing caused by triptans can further reduce the flow of blood through the arteries and have been reported to cause heart attacks and strokes. Therefore, triptans should not be given to patients who have had heart attacks and strokes, or to patients who have symptoms of atherosclerosis such as angina, transient ischemic attacks, and intermittent claudication.
Healthy adults may have atherosclerosis and narrowing of the coronary arteries that are "silent", that is, without past strokes, transient ischemic attacks, heart attacks, or angina. Therefore, before prescribing a triptan, a doctor should evaluate patients for possible atherosclerosis if they have one or more risk factors for developing atherosclerosis. These risk factors include cigarette smoking, diabetes mellitus, high blood pressure, high levels of LDL ("bad") cholesterol in the blood, obesity, male and over 40 years of age, female and postmenopausal, or a family member(s) who have had heart attacks at an early age. Some patients who are at risk should receive their first dose of a triptan in the doctor's office while being monitored with an electrocardiogram (EKG).
Triptans can interact with other drugs. For example, there have been rare reports of triptans causing a "serotonin syndrome" when given together with a selective serotonin reuptake inhibitor. Selective serotonin reuptake inhibitors (SSRIs) are a class of medications widely used to treat depression. The symptoms of serotonin syndrome include confusion, fever, tremor, high blood pressure, diarrhea, and sweating. Certain triptans such as sumatriptan, zolmitriptan, and rizatriptan can interact with monoamine oxidase inhibitors. Propranolol (Inderal) can raise rizatriptan blood levels. Cimetidine (Tagamet) can increase zolmitriptan blood levels.
Triptans should not be used in pregnant women and are not generally used in young children.
Ergots Ergots, like triptans, are medications that abort migraine headaches. Examples of ergots include ergotamine preparations (Ergomar, Wigraine, and Cafergot) and dihydroergotamine preparations (Migranal, DHE-45). Ergots, like triptans, cause constriction of blood vessels, but ergots tend to cause more constriction of vessels in the heart and other parts of the body than the triptans, and their effects on the heart are more prolonged than the triptans. Therefore, they are not as safe as the triptans. The ergots also are more prone to cause nausea and vomiting than the triptans. The ergots can cause prolonged contraction of the uterus and miscarriages in pregnant women.
Midrin Midrin is used to abort migraine and tension headaches. It is a combination of isometheptene (a blood vessel constrictor), acetaminophen (a pain reliever), and dichloralphenazone (a mild sedative). It is most effective if used early during a headache; however, because of its potent blood vessel constricting effect, it should not be used in patients with high blood pressure, kidney disease, glaucoma, atherosclerosis, liver disease, or taking monoamine oxidase inhibitors.
What other medications are used for treating migraine headaches? Narcotics and butalbital-containing medications sometimes are used to treat migraine headaches; however, these medications are potentially addicting and are not used as initial treatment. They are sometimes used for patients whose headaches fail to respond to OTC medications but who are not candidates for triptans either due to pregnancy or the risk of heart attack and stroke.
In patients with severe nausea, a combination of a triptan and an anti-nausea medication, for example, prochlorperazine (Compazine) or metoclopramide (Reglan) may be used. When nausea is severe enough that oral medications are impractical, intravenous medications such as DHE-45 (dihydroergotamine), prochlorperazine (Compazine), and valproate (Depacon) are useful.
How are migraine headaches prevented? There are two ways to prevent migraine headaches: 1) by avoiding factors ("triggers") that cause the headaches, and 2) by preventing headaches with medications (prophylactic medications). Neither of these preventive strategies is 100% effective. The best one can hope for is to reduce the frequency of headaches.
What are migraine triggers? A migraine trigger is any factor that causes a headache in individuals who are prone to develop headaches. Only a small proportion of migraine sufferers, however, clearly can identify triggers. Examples of triggers include stress, sleep disturbances, fasting, hormones, bright or flickering lights, odors, cigarette smoke, alcohol, aged cheeses, chocolate, monosodium glutamate, nitrites, aspartame, and caffeine. For some women, the decline in the blood level of estrogen during the onset of menstruation is a trigger for migraine headaches. The interval between exposure to a trigger and the onset of headache varies from hours to two days. Exposure to a trigger does not always lead to a headache. Conversely, avoidance of triggers cannot completely prevent headaches. Different migraine sufferers respond to different triggers, and any one trigger will not induce a headache in every person who has migraine headaches.
Sleep and migraineDisturbances such as sleep deprivation, too much sleep, poor quality of sleep, and frequent awakening at night are associated with both migraine and tension headaches, whereas improved sleep habits have been shown to reduce the frequency of migraine headaches. Sleep also has been reported to shorten the duration of migraine headaches.
Fasting and migraineFasting possibly may precipitate migraine headaches by causing the release of stress-related hormones and lowering blood sugar. Therefore, migraine sufferers should avoid prolonged fasting.
Bright lights and migraineBright lights and other high intensity visual stimuli can cause headaches in healthy subjects as well as patients with migraine headaches, but migraine patients seem to have a lower than normal threshold for light-induced pain. Sunlight, television, and flashing lights all have been reported to precipitate migraine headaches.
Caffeine and migraineCaffeine is contained in many food products (cola, tea, chocolates, coffee) and OTC analgesics. Caffeine in low doses can increase alertness and energy, but caffeine in high doses can cause insomnia, irritability, anxiety, and headaches. The over-use of caffeine-containing analgesics causes rebound headaches. Furthermore, individuals who consume high levels of caffeine regularly are more prone to develop withdrawal headaches when caffeine is stopped abruptly.
Chocolate, wine, tyramine, MSG, nitrites, aspartame and migraineChocolate has been reported to cause migraine headaches, but scientific studies have not consistently demonstrated an association between chocolate consumption and headaches. Red wine has been shown to cause migraine headaches in some migraine sufferers, but it is not clear whether white wine also will cause migraine headaches. Tyramine (a chemical found in cheese, wine, beer, dry sausage, and sauerkraut) can precipitate migraine headaches, but there is no evidence that consuming a low-tyramine diet can reduce migraine frequency. Monosodium glutamate (MSG) has been reported to cause headaches, facial flushing, sweating, and palpitations when consumed in high doses on an empty stomach. This phenomenon has been called Chinese restaurant syndrome. Nitrates and nitrites (chemicals found in hotdogs, ham, frankfurters, bacon and sausages) have been reported to cause migraine headaches. Aspartame, a sugar-substitute sweetener found in diet drinks and snacks, has been reported to trigger headaches when used in high doses for prolonged periods.
Female hormones and migraineSome women who suffer from migraine headaches experience more headaches around the time of their menstrual periods. Other women experience migraine headaches only during the menstrual period. The term "menstrual migraine" is used mainly to describe migraines that occur in women who have almost all of their headaches from two days before to one day after their menstrual periods. Declining levels of estrogen at the onset of menses is likely to be the cause of menstrual migraines. Decreasing levels of estrogen also may be the cause of migraine headaches that develop among users of birth control pills during the week that estrogens are not taken.
What should migraine sufferers do? Individuals with mild and infrequent migraine headaches that do not cause disability may require only OTC analgesics. Individuals who experience several moderate or severe migraine headaches per month or whose headaches do not respond readily to medications should avoid triggers and consider modifications of their life-style. Life-style modifications for migraine sufferers include:
· Go to sleep and waking up at the same time each day.
· Exercise regularly (daily if possible). Make a commitment to exercise even when traveling or during busy periods at work. Exercise can improve the quality of sleep and reduce the frequency and severity of migraine headaches. Build up your exercise level gradually. Over-exertion, especially for someone who is out of shape, can lead to migraine headaches.
· Do not skip meals, and avoiding prolonged fasting.
· Limit stress through regular exercise and relaxation techniques.
· Limit caffeine consumption to less than two caffeine-containing beverages a day.
· Avoid bright or flashing lights and wearing sunglasses if sunlight is a trigger.
· Identify and avoid foods that trigger headaches by keeping a headache and food diary. Review the diary with your doctor. It is impractical to adopt a diet that avoids all known migraine triggers, however, it is reasonable to avoid foods that consistently trigger migraine headaches.
What are prophylactic medications for migraine headaches? Prophylactic medications are medications taken daily to reduce the frequency and duration of migraine headaches. They are not taken once a headache has begun. There are several classes of prophylactic medications: beta blockers, calcium-channel blockers, tricyclic antidepressants, antiserotonin agents and anticonvulsants. Medications with the longest history of use are propranolol (Inderal), a beta blocker, and amitriptyline (Elavil), an antidepressant. When choosing a prophylactic medication for a patient the doctor must take into account the drug side effects, drug-drug interactions, and co-existing conditions such as diabetes, heart disease, and high blood pressure.
Beta blockersBeta-blockers are a class of drugs that block the effects of beta-adrenergic substances such as adrenaline (epinephrine). By blocking the effects of adrenaline, beta-blockers relieve stress on the heart by slowing the rate at which the heart beats. Beta-blockers have been used to treat high blood pressure, angina, certain types or tremors, stage fright, and abnormally fast heart beats (palpitations). They also have become important drugs for improving survival after heart attacks. Beta-blockers have been used for many years to prevent migraine headaches.
It is not known how beta-blockers prevent migraine headaches. It may be by decreasing prostaglandin production, though it also may be through their effect on serotonin or a direct effect on arteries. The beta-blockers used in preventing migraine headaches include propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor, Lopressor LA, Toprol XL), nadolol (Corgard), and timolol (Blocadren).
Beta-blockers generally are well tolerated. They can aggravate breathing difficulties in patients with asthma, chronic bronchitis, or emphysema. In patients with who already have slow heart rates (bradycardias) and heart block (defects in electrical conduction within the heart), beta-blockers can cause dangerously slow heartbeats. Beta-blockers can aggravate symptoms of heart failure. Other side effects include drowsiness, diarrhea, constipation, fatigue, decrease in endurance, insomnia, nausea, depression, dreaming, memory loss, impotence.
Tricyclic antidepressantsTricyclic antidepressants (TCAs) prevent migraine headaches by altering the neurotransmitters, norepinephrine and serotonin, that the nerves of the brain use to communicate with one another. The tricyclic antidepressants that have been used in preventing migraine headaches include amitriptyline (Elavil), nortriptyline (Pamelor, Aventyl), doxepin (Sinequan), imipramine (Tofranil), and protriptyline.
The most commonly encountered side effects associated with TCAs are fast heart rate, blurred vision, difficulty urinating, dry mouth, constipation, weight gain or loss, and low blood pressure when standing.
TCAs should not be used with drugs that inhibit monoamine oxidase such as isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate), and procarbazine (Matulane), since high fever, convulsions and even death may occur. TCAs are used with caution in patients with seizures, since they can increase the risk of seizures. TCAs also are used with caution in patients with enlargement of the prostate because they can make urination difficult. TCAs can cause elevated pressure in the eyes of some patients with glaucoma. TCAs can cause excessive sedation when used with other medications that slow the brain's processes, such as alcohol, barbiturates, narcotics, and benzodiazepines, e.g. lorazepam (Ativan), diazepam (Valium), temazepam (Restoril), oxazepam (Serax), clonazepam (Klonopin), zolpidem (Ambien). Epinephrine should not be used with amitriptyline, since the combination can cause severe high blood pressure
Antiserotonin medicationsMethysergide (Sansert) prevents migraine headaches by constricting blood vessels and reducing inflammation of the blood vessels. Methylergonovine is related chemically to methysergide and has a similar mechanism of action. They are not widely used because of their side effects. The most serious side effect of methysergide is retroperitoneal fibrosis (scarring of tissue around the ureters that carry urine from the kidneys to the bladder). Retroperitoneal fibrosis, though rare, can block the ureters and cause backup of urine into the kidneys. Backup of urine into the kidneys can cause back and flank (the side of the body between the ribs and hips) pain and ultimately can lead to kidney failure. Methysergide also has been reported to cause scarring around the lungs that can lead to chest pain, and shortness of breath.
Calcium channel blockersCalcium channel blockers (CCBs) are a class of drugs that block the entry of calcium into the muscle cells of the heart and the arteries. By blocking the entry of calcium, CCBs reduce contraction of the heart muscle, decrease heart rate, and lower blood pressure. CCBs are used for treating high blood pressure, angina, and abnormal heart rhythms (e.g., atrial fibrillation). CCBs also appear to block a chemical within nerves, called serotonin, and have been used occasionally to prevent migraine headaches. The CCBs used in preventing migraine headaches are diltiazem (Cardizem, Dilacor, Tiazac), verapamil (Calan, Verelan, Isoptin), and nimodipine.
The most common side effects of CCBs are constipation, nausea, headache, rash, edema (swelling of the legs with fluid), low blood pressure, drowsiness, and dizziness. When diltiazem or verapamil are given to individuals with heart failure, symptoms of heart failure may worsen because these drugs reduce the ability of the heart to pump blood. Verapamil and diltiazem may reduce the elimination and increase the blood levels of carbamazepine (Tegretol), simvastatin (Zocor), atorvastatin (Lipitor), and lovastatin (Mevacor). This can lead to toxicity from these drugs.
AnticonvulsantsAnticonvulsants (antiseizure medications) also have been used to prevent migraine headaches. Examples of anticonvulsants that have been used are valproic acid, phenobarbital, gabapentin, and topiramate. It is not known how anticonvulsants work to prevent migraine headaches.
Who should consider prophylactic medications to prevent migraine headaches? Not all migraine sufferers need prophylactic medications; individuals with mild or infrequent headaches that respond readily to abortive medications do not need prophylactic medications. Individuals who should consider prophylactic medications are those who:
1. Require abortive medications for migraine headaches more frequently than twice weekly.
2. Have two or more migraine headaches a month that do not respond readily to abortive medications.
3. Have migraine headaches that are interfering substantially with their quality of life and work.
4. Cannot take abortive medications because of heart disease, stroke, or pregnancy, or cannot tolerate abortive medications because of side effects.
How effective are prophylactic medications?Prophylactic medications can reduce the frequency and duration of migraine headaches but cannot be expected to eliminate migraine headaches completely. The success rate of most prophylactic medications is approximately 50%. Success in preventing migraine headaches is defined as more than a 50% reduction in the frequency of headaches. Prophylactic medications usually are begun at a low dose that is increased slowly in order to minimize side effects. Individuals may not notice a reduction in the frequency, severity, or duration of their headaches for 2-3 months after starting treatment.
What is the proper way to use preventive medications?
· Doctors familiar with the treatment of migraine headaches should prescribe preventive medications.
· Decisions about which preventive medication to use are based on the side effects of the medication and the medical conditions that the patient may have.
· Propranolol (Inderal) often is used first, provided that the patient does not have asthma, COPD or heart disease. Amitriptyline (Elavil) also is used commonly.
· Preventive medications are begun at low doses and gradually increased to higher doses if needed. This minimizes side effects from the medications. Preventive medications are to be taken daily for months to years. When they are stopped, the dose needs to be gradually reduced rather than abruptly stopped. Abruptly stopping preventive medications can lead to headaches.
· In some instances, more than one drug may be needed. Non-medication and behavioral therapies also may be needed.
What is the treatment of cluster headaches? As with migraine headaches, there are two approaches to treating cluster headaches: abortive and prophylactic. Abortive treatment is taken to stop the headaches. Prophylactic treatment is used to abolish or shorten the cycle of headaches.
Abortive treatments include inhalation of 100% oxygen at 8-10 liters/minute using a non-rebreathing facemask for 10-15 minutes along with a triptan such as sumatriptan (nasally, or under the skin) or an ergot such as DHE (intravenously, under the skin, or intramuscularly).
A calcium channel blocker, verapamil (Calan, Verelan, Isoptin) is the medication of choice for prophylactic treatment of cluster headaches. Other prophylactic medications include valproate, ergotamine, lithium, and methysergide. On occasion, verapamil may be combined with another prophylactic medication. Prophylactic medications usually are begun early during a cycle of cluster headaches and continued for two weeks longer than the usual cycle. The dose of medication then is reduced gradually. Because prophylactic medications may take two weeks to be effective, prednisone (a corticosteroid) often is used in decreasing doses for the first two weeks of treatment. Prednisone often can quickly abolish the headaches.
What is the treatment for menstrual migraine? There are several aspects to treating menstrual migraines:
1. To abort menstrual migraine, take medications after the onset of menstrual migraine. Generally, medications that are effective in aborting non-menstrual migraines are effective at aborting menstrual migraines.
2. To prevent menstrual migraine, take medications just before the onset of menstruation and continue for the duration of the expected headache. Taking hormones such as estrogens or estrogen related medications also help to prevent migraine.
3. To reduce the frequency and duration of menstrual migraine, take prophylactic medications (such as beta blockers, calcium channel blockers, anticonvulsants, tricyclic antidepressants) that are normally used on a continuous basis to prevent non-menstrual migraines.
NSAIDs such as naproxen sodium (Aleve) or ibuprofen (Advil, Motrin) have been used effectively to abort menstrual migraines. A combination analgesic containing acetaminophen, aspirin, and caffeine (ACC) can also be used to treat menstrual migraines. For women whose menstruation and menstrual migraines occur on a regular and predictable pattern, NSAIDs may be used 24 hours before the expected onset of menstrual migraine and continued for the expected duration of the headache. Since NSAIDs inhibit prostaglandins, they have the added benefit of relieving menstrual cramps as well. For NSAIDs side effects and precautions, please read the "Medication therapies for migraine" section of this article.
Triptans (naratriptan, rizatriptan, sumatriptan, zolmitriptan) have been found to be effective in aborting menstrual migraines, as well as controlling the associated nausea and vomiting. Sumatriptan given 2-3 days before and continued for the duration of the expected headache was found to be effective in reducing the frequency and severity of menstrual migraine. Naratriptan used in the same manner has also been found to be effective in preventing menstrual migraine. However, in those cases where breakthrough headaches occurred, they were just as severe as in patients taking placebo. For side effects and precautions of triptans, please read the "What are side effects of triptans" section of this article.
Dihydroergotamine (DHE) can be used as a nasal spray or given intramuscularly or intravenously to abort menstrual migraines. Ergotamine (oral, rectal, or intranasal) and DHE (intranasal, intramuscular, or intravenous) can be used around the time of menstruation (several days before and continued for the duration of the expected headache) to prevent menstrual migraines. For ergot side effects and precautions, please read the "What are the ergots?" section in this article.
If these medications are ineffective, doctors may try daily preventive medications such as beta-blockers, anticonvulsants, calcium channel blockers, and tricyclic antidepressants to reduce the frequency and the severity of menstrual migraines. The choice of the preventive medications is based on the experiences and preferences of the doctor, the medication side effects, and the woman's other associated medical conditions.
For women already taking preventive medications and yet still experience headaches, the doses of preventive medications can be increased around the time of the menstruation (some doctors use preventive medications only around the time of the menstruation). Alternatively doctors may try hormone treatment.
Since a drop in estrogen level just prior to menstruation is the trigger for menstrual migraines, estrogen replacement before menstruation has been used in preventing menstrual migraines. For some women with menstrual migraine, Estradiol skin patches (such as TTS 50, TTS 100) applied 2 days before menstrual migraine and continued for 7 days during the expected headache period is effective. However, the dose of estrogen must be closely monitored, as too high of a dose can actually trigger migraine in susceptible individuals.
Some women with difficult to treat menstrual migraines may be helped by using low dose oral contraceptives to reduce the estrogen fluctuations. Other less frequently used medications for menstrual migraines include tamoxifen, bromocriptine, danazol and gonadotropin-releasing hormone (GnRH). Reference: The medical clinics of North America "Headache", Ninan T. Mathew, MD, July 2001
Medically Reviewed by: Joseph Carcione, D.O., M.B.A., Board Certified Neurology Last Editorial Review: 3/23/2007
What are the causes of headaches? There are two types of headaches: primary headaches and secondary headaches. Primary headaches are not associated with (caused by) other diseases. Examples of primary headaches are migraine headaches, tension headaches, and cluster headaches. Secondary headaches are caused by associated disease. The associated disease may be minor or serious and life threatening.
How common are primary and secondary headaches? Tension headaches are the most common type of primary headache; as many as 90% of adults have had or will have tension headaches. Tension headaches are more common among women than men.
Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches. Migraine headaches affect children as well as adults. Before puberty, boys and girls are affected equally by migraine headaches, but after puberty, more women than men are affected. An estimated 6% of men and up to 18% of women will experience a migraine headache.
In the United States, migraine headaches often go undiagnosed or are misdiagnosed as tension or sinus headaches. As a result, many migraine sufferers do not receive effective treatment.
Cluster headaches are a rare type primary headache, affecting 0.1% of the population. An estimated 85% of cluster headache sufferers are men. The average age of cluster headache sufferers is 28-30 years, although headaches may begin in childhood.
Secondary headaches have diverse causes, ranging from serious and life threatening conditions such as brain tumors, strokes, meningitis, and subarachnoid hemorrhages to less serious but common conditions such as withdrawal from caffeine and discontinuation of analgesics.
Many people suffer from "mixed" headache disorders in which tension headaches or secondary headaches trigger migraine headaches.
What are the symptoms of tension headaches? Tension headaches often begin in the back of the head and upper neck as a band-like tightness or pressure. Tension headaches also are described as a band of pressure encircling the head with the most intense pain over the eyebrows. The pain of tension headaches usually is mild (not disabling) and bilateral (affecting both sides of the head). Tension headaches are not associated with an aura (see below) and are seldom associated with nausea, vomiting, or sensitivity to light and sound. Tension headaches usually occur sporadically (infrequently and without a pattern) but can occur frequently and even daily in some people. Most people are able to function despite their tension headaches.
What are the symptoms of migraine headaches? Migraine is a chronic condition of recurrent attacks. Most (but not all) migraine attacks are associated with headaches. Migraine headaches usually are described as an intense, throbbing or pounding pain that involves one temple. (Sometimes the pain can be located in the forehead, around the eye, or the back of the head). The pain usually is unilateral (on one side of the head), although about a third of the time the pain is bilateral. The unilateral headaches typically change sides from one attack to the next. (In fact, unilateral headaches that always occur on the same side should alert the doctor to consider a secondary headache, for example, one caused by a brain tumor). A migraine headache usually is aggravated by daily activities like walking upstairs. Nausea, vomiting, diarrhea, facial pallor, cold hands, cold feet, and sensitivity to light and sound commonly accompany migraine headaches. As a result of this sensitivity to light and sound, migraine sufferers usually prefer to lie in a quiet, dark room during an attack. A typical attack lasts between 4 and 72 hours.
An estimated 40%-60% of migraine attacks are preceded by premonitory (warning) symptoms lasting hours to days. The symptoms may include sleepiness, irritability, fatigue, depression or euphoria, yawning, and cravings for sweet or salty foods. Patients and their family members usually know that when they observe these warning symptoms that a migraine attack is beginning.
An estimated 20% of migraine headaches are associated with an aura. Usually, the aura precedes the headache, although occasionally it may occur simultaneously with the headache. The most common auras are 1) flashing, brightly colored lights in a zigzag pattern (fortification spectra), usually starting in the middle of the visual field and progressing outward and 2) a hole (scotoma) in the visual field, also known as a blind spot. Some elderly migraine sufferers may experience only the visual aura without the headache. A less common aura consists of pins-and-needles sensations in the hand and the arm on one side or pins-and-needles sensations around the mouth and the nose on the same side. Other auras include auditory (hearing) hallucinations and abnormal tastes and smells.
Complicated migraines are migraines that are accompanied by neurological dysfunction. The part of the body that is affected by the dysfunction is determined by the part of the brain that is responsible for the headache. Vertebrobasilar migraines are characterized by dysfunction of the brainstem (the lower part of the brain that is responsible for automatic activities like consciousness and balance). The symptoms of vertebrobasilar migraines include fainting as an aura, vertigo (dizziness in which the environment seems to be spinning) and double vision. Hemiplegic migraines are characterized by paralysis or weakness of one side of the body, mimicking a stroke. The paralysis or weakness is usually temporary, but sometimes it can last for days.
For approximately 24 hours after a migraine attack, the migraine sufferer may feel drained of energy and may experience a low-grade headache along with sensitivity to light and sound. Unfortunately, some sufferers may have recurrences of the headache during this period.
What are the symptoms of cluster headaches? Cluster headaches are headaches that come in groups (clusters) lasting weeks or months, separated by pain-free periods of months or years. During the period in which the cluster headaches occur, pain typically occurs once or twice daily, but some patients may experience pain more than twice daily. Each episode of pain lasts from 30 minutes to one and one-half hours. Attacks tend to occur at about the same time every day and often awaken the patient at night from a sound sleep. The pain typically is excruciating and located unilaterally around or behind one eye. Some patients describe the pain as feeling like a hot poker in the eye. The affected eye may become red, inflamed, and watery. The nose on the affected side may become congested and runny. Unlike patients with migraine headaches, patients with cluster headaches tend to be restless. They often pace the floor, bang their heads against a wall, and can be driven to desperate measures. Cluster headaches are much more common in males than females.
What causes primary headaches? Migraine headache is caused by a combination of vasodilatation (enlargement of blood vessels) and the release of chemicals from nerve fibers that coil around the blood vessels. During a migraine attack, the temporal artery enlarges. (The temporal artery is an artery that lies on the outside of the skull just under the skin of the temple.) Enlargement of the temporal artery stretches the nerves that coil around the artery and causes the nerves to release chemicals. The chemicals cause inflammation, pain, and further enlargement of the artery. The increasing enlargement of the artery magnifies the pain.
Migraine attacks commonly activate the sympathetic nervous system in the body. The sympathetic nervous system is often thought of as the part of the nervous system that controls primitive responses to stress and pain, the so-called "fight or flight" response. The increased sympathetic nervous activity in the intestine causes nausea, vomiting, and diarrhea. Sympathetic activity also delays emptying of the stomach into the small intestine and thereby prevents oral medications from entering the intestine and being absorbed. The impaired absorption of oral medications is a common reason for the ineffectiveness of medications taken to treat migraine headaches. The increased sympathetic activity also decreases the circulation of blood, and this leads to pallor of the skin as well as cold hands and feet. The increased sympathetic activity also contributes to the sensitivity to light and sound sensitivity as well as blurred vision.
Tension headache does not have a clear cause. Many physicians attribute tension headaches to excess stress or a hectic day. There is also evidence that some tension headaches may have a cause that is similar to the cause of migraine headaches.
Cluster headache also does not have a clear cause, although alcohol and cigarettes can precipitate attacks.
Are primary headaches dangerous? Tension headaches have not been shown to lead to neurological dysfunction or brain damage. In general, this is true of migraine headaches. However, there is a rare association of migraine headaches and stroke, particularly in sufferers of complicated migraines. While cluster headaches need to be differentiated from more serious neurological conditions, there is no known danger of cluster headaches leading to stroke.
What diseases cause secondary headaches? Important examples of diseases causing secondary headaches include:
· Tumors in the brain, including tumors that have spread (metastasized) to the brain from another organ such as the lung or breast
· Subdural hematomas, which are collections of blood underneath the dura (the covering of the brain) due to bleeding from ruptured veins. Subdural hematomas typically occur in elderly individuals after a fall or other trauma to the head. Sometimes the fall can precede the visit to the doctor by weeks, and the elderly patients may not even recall the fall. Symptoms of subdural hematomas include chronic headaches, change in personality, and weakness of the extremities.
· Epidural hematomas, which are rapid collections of blood due to the rupture of arteries that run on the inner surface of the skull. Epidural hematomas usually are the result of skull fractures. The typical story is a head injury that causes a concussion with loss of consciousness and a skull fracture. The return of consciousness is followed by the sudden development of coma caused by an expanding hematoma.
· Infections such as meningitis caused by bacteria (meningococcus and pneumococcus), tuberculosis, Lyme disease, or cryptococcus
· Strokes due either to blood clots within the arteries of the brain or rupture of the blood vessels in the brain
· Subarachnoid hemorrhages which are caused by bleeding into the space between the brain and its outer arachnoid lining. The most common source of subarachnoid hemorrhage is an aneurysm, a ballooning of the weakened wall of an artery inside the head.
· Sudden onset of severe high blood pressure. (Chronic mild to moderate high blood pressure is not a common cause of headache).
· Temporal arteritis, a vasculitis (inflammation) of the temporal artery which runs beneath the skin of the temple. Temporal arteritis occurs primarily in older people and may be associated with fatigue, body aches, and anemia. Without proper treatment, temporal arteritis may lead to blindness and strokes.
· Acute angle glaucoma with sudden elevation of pressures inside the eyes
· Infections of the sinuses (sinusitis), ear (otitis), and teeth
· Hypothyroidism, a condition in which the thyroid gland does not produce enough thyroid hormone
· Repeated carbon monoxide poisoning
· Parkinson's disease
· Medications such as indomethacin, estrogen, progestins, calcium channel blockers (commonly used for treating high blood pressure), and selective serotonin reuptake inhibitors (commonly used to treat depression)
· Overuse of over-the-counter or prescription pain relievers. Overuse of pain relievers causes the pain relievers to become less effective. As the effect of the pain reliever wears off, headaches recur (rebound headache).
· Cardiac ischemia (lack of blood supply to the muscles of the heart caused by coronary artery disease). Although cardiac ischemia is best known as a cause of either heart attacks or angina, it also may cause a headache. The headache may occur with or without the accompanying chest pain of a heart attack or angina. As with angina, in some individuals the headache may occur with exertion and subside with rest.
How are secondary headaches diagnosed? Conditions causing secondary headaches, such as bacterial meningitis, subarachnoid hemorrhage, severe (malignant) high blood pressure, epidural or subdural hematomas, can cause serious brain damage or even death. Therefore, timely and accurate diagnosis of secondary headaches is crucial. Special blood tests, brain scans, CT scans or MRI, and lumbar puncture (spinal tap) are necessary to establish these diagnoses (see below). The challenge for doctors is to decide which patients should undergo these special tests. To make such decisions, doctors rely upon information obtained from the initial patient interview and physical examination. Information that is important to the doctor include:
1. The mode of onset of the headache. For example, patients with a subarachnoid hemorrhage typically report having a sudden onset of severe headache ("the worst headache ever"). The pain of recurrent migraine headaches tends to build up gradually. Sometimes the headache of subarachnoid hemorrhage is triggered by exertion such as sex.
2. The age of the patient. Temporal arteritis typically occurs in older people and is extremely rare in individuals younger than 50. Patients with primary headaches (for example migraine headaches) typically have many years of similar headaches, often starting at a young age. Therefore, new onset of a headache after 50 years of age or onset of a new type of headache suggests a secondary headache and should prompt testing.
3. The location of the headache (on one side or both sides of the head). Headaches that persistently occur on the same side often are secondary headaches associated with, for example, brain tumors or arteriovenous malformations (abnormal clusters of blood vessels in the brain).
4. Associated fever and neck stiffness. Bacterial meningitis is a rapidly progressive and life-threatening disease with fever, headaches, stiff neck, and deterioration in mental function. Herpes simplex encephalitis is a virus infection of the brain that causes death of brain tissue. Symptoms include fever, headache, and deterioration in mental function. Early treatment with antibiotics and anti-viral agents can decrease the extent of brain damage and improve survival.
5. Associated mental deterioration, seizures, or weakness of the extremities or face, which can be symptoms of brain tumors.
6. Associated temporary weakness of the extremities or facial muscles, which can be symptoms of transient ischemic attack (TIAs). Transient ischemic attacks are caused by temporary interruptions in the flow of blood to small areas of the brain. Transient ischemic attacks are warning signals for future strokes that can cause permanent brain damage. Headache also can accompany strokes and intracerebral bleeding (bleeding into the substance of the brain).
7. Recent head trauma. Headaches soon after trauma to the head may be caused by subdural or epidural hematomas.
What are the tests for secondary headaches? The patient history and physical examination provide the best means for determining the cause of secondary headaches. Therefore, it is extremely important that patients with severe headaches undergo examination by a doctor experienced in diagnosing and treating headaches. A few tests may be useful in diagnosing the presence and cause of secondary headaches including blood tests, computerized tomography (CT Scan) and magnetic resonance imaging (MRI) scans of the head, and lumbar puncture.
Blood testsAn elevated white blood cell count suggests infection such as meningitis. An elevated erythrocyte sedimentation rate suggests temporal arteritis. Abnormal thyroid tests suggest thyroid disorders. Blood tests also may detect kidney failure and abnormally elevated calcium levels as the cause of headaches.
CT scan of the headA CT scan of the head is useful for detecting accumulation of blood such as subdural hematomas and subarachnoid hemorrhages. It is moderately useful in detecting brain tumors and strokes not due to hemorrhage.
MRI scan of the headAn MRI scan of the head can detect subdural and epidural hematomas, herpes simplex infection of the brain, strokes, tumors, and arterial aneurysms.
Lumbar punctureCerebro-spinal fluid, the fluid that surrounds the brain and spinal cord, can be removed with a needle that is inserted into the spine in the lower back. Examination of the fluid can reveal infection (such as meningitis due to bacteria or tuberculosis) or blood from hemorrhage. In some patients with subarachnoid hemorrhage, CT scans are normal, and lumbar punctures are necessary to demonstrate blood from the hemorrhage that has spread throughout the cerebro-spinal fluid.
When should one consult a doctor for headaches? Many people who suffer from mild headaches medicate themselves with over-the-counter analgesics, and they usually do not seek medical care. Nevertheless, the symptoms of primary headaches and secondary headaches can overlap. Furthermore, a person with a long history of migraine or tension headaches can develop a new secondary headache. Many tension or sinus headaches probably are migraine headaches and will respond to treatments that are specific for migraine. Therefore, a doctor should be consulted if the headache is:
· Severe ("the worst ever")
· Different than the usual headaches
· Starts suddenly during exertion
· Aggravated by exertion, coughing, bending, or sexual activity
· Associated with persistent nausea and vomiting
· Associated with stiff neck, fever, dizziness, blurred vision, slurred speech, unsteady gait, weakness or unusual sensations of the arm or leg, excessive drowsiness or confusion
· Associated with seizures
· Associated with recent head trauma or a fall
· Not responding to treatment and is getting worse
· Disabling, and interfering with work and the quality of life
· Requires more than the recommended dose of over-the-counter analgesics for relief
What is the treatment for tension headaches? Individuals with occasional tension headaches or mild migraine headaches that do not interfere with daily activities usually medicate themselves with over-the-counter (OTC, non-prescription) pain relievers (analgesics). Many OTC analgesics are available. OTC analgesics have been shown to be safe and effective for short-term relief of headache (as well as muscle aches, pains, menstrual cramps, and fever) when used according to the instructions on their labels.
There are two major classes of OTC analgesics: acetaminophen (Tylenol) and non-steroidal anti-inflammatory drugs (NSAIDs). The two types of NSAIDs are aspirin and non-aspirin. Examples of non-aspirin NSAIDs are ibuprofen (Advil, Nuprin, Motrin IB, and Medipren) and naproxen (Aleve). Some NSAIDs are available by prescription only. Prescription NSAIDs are usually prescribed to treat arthritis and other inflammatory conditions such as bursitis, tendonitis, etc. The difference between OTC and prescription NSAIDs may only be the amount of the active ingredient contained in each pill. For example, OTC naproxen (Aleve) contains 220 mg of naproxen per pill, whereas prescription naproxen (Naprosyn) contains 375 or 500 mg of naproxen per pill.
Acetaminophen reduces pain and fever by acting on pain centers in the brain. Acetaminophen is well tolerated and generally is considered easier on the stomach than NSAIDs. However, acetaminophen can cause severe liver damage in high (toxic) doses or if used on a regular basis over extended periods of time. In individuals who regularly consume moderate or large amounts of alcohol, acetaminophen can cause serious damage to the liver in lower doses that usually are not toxic. Acetaminophen also can damage the kidneys when taken in large doses. Therefore, acetaminophen should not be taken more frequently or in larger doses than recommended on the label.
NSAIDs relieve pain by reducing the inflammation that causes the pain (They are called non-steroidal anti-inflammatory drugs or NSAIDs because they are different from corticosteroids such as prednisone, prednisolone, and cortisone which also reduce inflammation). Corticosteroids, though valuable in reducing inflammation, have predictable and potentially serious side effects, especially when used long-term. NSAIDs do not have the same side effects that corticosteroids have.
Aspirin, Aleve, Motrin, and Advil all are NSAIDs and are similarly effective in relieving pain and fever. The main difference between aspirin and non-aspirin NSAIDs is their effect on platelets. Platelets are small particles in the blood that cause blood clots to form. Aspirin prevents the platelets from forming blood clots. Therefore, aspirin can increase bleeding by preventing blood from clotting though it also can be used therapeutically to prevent clots from causing heart attacks and strokes. The non-aspirin NSAIDs also have anti-platelet effects, but their anti-platelet action does not last as long as aspirin.
Aspirin, acetaminophen, and caffeine also are available combined in OTC analgesics for the treatment of headaches. Examples of such combination analgesics are Pain-aid, Excedrin, Fioricet, and Fiorinal.
Finding an effective analgesic or analgesic combination often is a process of trial and error because individuals respond differently to different analgesics. In general, a person should use the analgesic that has worked in the past. This will increase the likelihood that an analgesic will be effective and decrease the risk of side effects.
There are several precautions that should be observed with OTC analgesics:
· Children and teenagers should not use aspirin for the treatment of headaches, other pain, or fever, because of the risk of developing Reye's Syndrome, a life-threatening neurological disease that can lead to coma and even death.
· Patients with balance disorders or hearing difficulties should avoid using aspirin because aspirin may aggravate these conditions.
· Patients taking blood thinners such as warfarin (Coumadin) should not take aspirin and non-aspirin NSAIDs without a doctor's supervision because they add further to the risk of bleeding that is caused by the blood thinner.
· Patients with active ulcers of the stomach and duodenum should not take aspirin and non-aspirin NSAIDs because they can increase the risk of bleeding from the ulcer and impair healing of the ulcer.
· Patients with advanced liver disease should not take aspirin and non-aspirin NSAIDs because they may impair kidney function. Deterioration of kidney function in these patients can lead to rapid and life-threatening deterioration of their liver disease.
· Patients should not overuse OTC or prescription analgesics. Overuse of analgesics can lead to the development of tolerance (increasing ineffectiveness of the analgesic) and rebound headaches (return of the headache as soon as the effect of the analgesic wears off, usually in the early morning hours). Thus, overuse of analgesics can lead to a vicious cycle of more and more analgesics for headaches that respond less and less to treatment and occur more frequently.
What is the treatment for moderate to severe migraine headaches? Migraine-specific abortive medications usually are necessary for moderate to severe migraine headaches. The abortive medications for moderate or severe migraine headaches are different than OTC analgesics. Instead of relieving pain, they abort headaches by counteracting the cause of the headache, dilation of the temporal arteries. In fact, they cause narrowing of the arteries. Examples of migraine-specific abortive medications are the triptans and ergot preparations.
Triptans The triptans attach to serotonin receptors on the blood vessels and nerves and thereby reduce inflammation and constrict the blood vessels. This stops the headache. The triptan with the longest history of use is sumatriptan (Imitrex). Sumatriptan is available in the United States as an injection, oral tablet, and nasal spray. Zolmitriptan (Zomig) and rizatriptan (Maxalt) are newer triptans that are available as oral tablets and as tablets that melt in the mouth. Naratriptan (Amerge), almotriptan (Axert) and frovatriptan (Frovalan) are available only as oral tablets.
Traditionally, triptans were prescribed for moderate or severe migraines after OTC analgesics and other simple measures failed. Newer studies suggest that triptans can be used as the first treatment for patients with migraines that are causing disability. (Significant disability is defined as more than 10 days of at least 50% disability during a three-month period.). Triptans should be used early after the migraine begins, before the onset of pain or when the pain is mild. Using a triptan early in an attack increases its effectiveness, reduces side effects, and decreases the chance of recurrence of another headache during the following 24 hours. Used early, triptans can be expected to abort more than 80% of migraine headaches within 2 hours.
What are the side effects of triptans? The most common side effects of triptans are facial flushing, tingling of the skin, and a sense of tightness around the chest and throat. Other less common side effects include drowsiness, fatigue, and dizziness. These side effects are short-lived and are not considered serious.
The most serious side effects of triptans are heart attacks and strokes. Triptans are effective in migraine headaches because they narrow arteries in the head; however, they also can narrow arteries in the heart. In individuals without existing carotid or coronary artery disease, the narrowing caused by triptans usually does not cause problems. However, in patients whose carotid and coronary arteries are narrowed by atherosclerosis or who suffer from intermittent spasm of the coronary arteries (a condition called Prinzmetal's or variant angina), the narrowing caused by triptans can further reduce the flow of blood through the arteries and have been reported to cause heart attacks and strokes. Therefore, triptans should not be given to patients who have had heart attacks and strokes, or to patients who have symptoms of atherosclerosis such as angina, transient ischemic attacks, and intermittent claudication.
Healthy adults may have atherosclerosis and narrowing of the coronary arteries that are "silent", that is, without past strokes, transient ischemic attacks, heart attacks, or angina. Therefore, before prescribing a triptan, a doctor should evaluate patients for possible atherosclerosis if they have one or more risk factors for developing atherosclerosis. These risk factors include cigarette smoking, diabetes mellitus, high blood pressure, high levels of LDL ("bad") cholesterol in the blood, obesity, male and over 40 years of age, female and postmenopausal, or a family member(s) who have had heart attacks at an early age. Some patients who are at risk should receive their first dose of a triptan in the doctor's office while being monitored with an electrocardiogram (EKG).
Triptans can interact with other drugs. For example, there have been rare reports of triptans causing a "serotonin syndrome" when given together with a selective serotonin reuptake inhibitor. Selective serotonin reuptake inhibitors (SSRIs) are a class of medications widely used to treat depression. The symptoms of serotonin syndrome include confusion, fever, tremor, high blood pressure, diarrhea, and sweating. Certain triptans such as sumatriptan, zolmitriptan, and rizatriptan can interact with monoamine oxidase inhibitors. Propranolol (Inderal) can raise rizatriptan blood levels. Cimetidine (Tagamet) can increase zolmitriptan blood levels.
Triptans should not be used in pregnant women and are not generally used in young children.
Ergots Ergots, like triptans, are medications that abort migraine headaches. Examples of ergots include ergotamine preparations (Ergomar, Wigraine, and Cafergot) and dihydroergotamine preparations (Migranal, DHE-45). Ergots, like triptans, cause constriction of blood vessels, but ergots tend to cause more constriction of vessels in the heart and other parts of the body than the triptans, and their effects on the heart are more prolonged than the triptans. Therefore, they are not as safe as the triptans. The ergots also are more prone to cause nausea and vomiting than the triptans. The ergots can cause prolonged contraction of the uterus and miscarriages in pregnant women.
Midrin Midrin is used to abort migraine and tension headaches. It is a combination of isometheptene (a blood vessel constrictor), acetaminophen (a pain reliever), and dichloralphenazone (a mild sedative). It is most effective if used early during a headache; however, because of its potent blood vessel constricting effect, it should not be used in patients with high blood pressure, kidney disease, glaucoma, atherosclerosis, liver disease, or taking monoamine oxidase inhibitors.
What other medications are used for treating migraine headaches? Narcotics and butalbital-containing medications sometimes are used to treat migraine headaches; however, these medications are potentially addicting and are not used as initial treatment. They are sometimes used for patients whose headaches fail to respond to OTC medications but who are not candidates for triptans either due to pregnancy or the risk of heart attack and stroke.
In patients with severe nausea, a combination of a triptan and an anti-nausea medication, for example, prochlorperazine (Compazine) or metoclopramide (Reglan) may be used. When nausea is severe enough that oral medications are impractical, intravenous medications such as DHE-45 (dihydroergotamine), prochlorperazine (Compazine), and valproate (Depacon) are useful.
How are migraine headaches prevented? There are two ways to prevent migraine headaches: 1) by avoiding factors ("triggers") that cause the headaches, and 2) by preventing headaches with medications (prophylactic medications). Neither of these preventive strategies is 100% effective. The best one can hope for is to reduce the frequency of headaches.
What are migraine triggers? A migraine trigger is any factor that causes a headache in individuals who are prone to develop headaches. Only a small proportion of migraine sufferers, however, clearly can identify triggers. Examples of triggers include stress, sleep disturbances, fasting, hormones, bright or flickering lights, odors, cigarette smoke, alcohol, aged cheeses, chocolate, monosodium glutamate, nitrites, aspartame, and caffeine. For some women, the decline in the blood level of estrogen during the onset of menstruation is a trigger for migraine headaches. The interval between exposure to a trigger and the onset of headache varies from hours to two days. Exposure to a trigger does not always lead to a headache. Conversely, avoidance of triggers cannot completely prevent headaches. Different migraine sufferers respond to different triggers, and any one trigger will not induce a headache in every person who has migraine headaches.
Sleep and migraineDisturbances such as sleep deprivation, too much sleep, poor quality of sleep, and frequent awakening at night are associated with both migraine and tension headaches, whereas improved sleep habits have been shown to reduce the frequency of migraine headaches. Sleep also has been reported to shorten the duration of migraine headaches.
Fasting and migraineFasting possibly may precipitate migraine headaches by causing the release of stress-related hormones and lowering blood sugar. Therefore, migraine sufferers should avoid prolonged fasting.
Bright lights and migraineBright lights and other high intensity visual stimuli can cause headaches in healthy subjects as well as patients with migraine headaches, but migraine patients seem to have a lower than normal threshold for light-induced pain. Sunlight, television, and flashing lights all have been reported to precipitate migraine headaches.
Caffeine and migraineCaffeine is contained in many food products (cola, tea, chocolates, coffee) and OTC analgesics. Caffeine in low doses can increase alertness and energy, but caffeine in high doses can cause insomnia, irritability, anxiety, and headaches. The over-use of caffeine-containing analgesics causes rebound headaches. Furthermore, individuals who consume high levels of caffeine regularly are more prone to develop withdrawal headaches when caffeine is stopped abruptly.
Chocolate, wine, tyramine, MSG, nitrites, aspartame and migraineChocolate has been reported to cause migraine headaches, but scientific studies have not consistently demonstrated an association between chocolate consumption and headaches. Red wine has been shown to cause migraine headaches in some migraine sufferers, but it is not clear whether white wine also will cause migraine headaches. Tyramine (a chemical found in cheese, wine, beer, dry sausage, and sauerkraut) can precipitate migraine headaches, but there is no evidence that consuming a low-tyramine diet can reduce migraine frequency. Monosodium glutamate (MSG) has been reported to cause headaches, facial flushing, sweating, and palpitations when consumed in high doses on an empty stomach. This phenomenon has been called Chinese restaurant syndrome. Nitrates and nitrites (chemicals found in hotdogs, ham, frankfurters, bacon and sausages) have been reported to cause migraine headaches. Aspartame, a sugar-substitute sweetener found in diet drinks and snacks, has been reported to trigger headaches when used in high doses for prolonged periods.
Female hormones and migraineSome women who suffer from migraine headaches experience more headaches around the time of their menstrual periods. Other women experience migraine headaches only during the menstrual period. The term "menstrual migraine" is used mainly to describe migraines that occur in women who have almost all of their headaches from two days before to one day after their menstrual periods. Declining levels of estrogen at the onset of menses is likely to be the cause of menstrual migraines. Decreasing levels of estrogen also may be the cause of migraine headaches that develop among users of birth control pills during the week that estrogens are not taken.
What should migraine sufferers do? Individuals with mild and infrequent migraine headaches that do not cause disability may require only OTC analgesics. Individuals who experience several moderate or severe migraine headaches per month or whose headaches do not respond readily to medications should avoid triggers and consider modifications of their life-style. Life-style modifications for migraine sufferers include:
· Go to sleep and waking up at the same time each day.
· Exercise regularly (daily if possible). Make a commitment to exercise even when traveling or during busy periods at work. Exercise can improve the quality of sleep and reduce the frequency and severity of migraine headaches. Build up your exercise level gradually. Over-exertion, especially for someone who is out of shape, can lead to migraine headaches.
· Do not skip meals, and avoiding prolonged fasting.
· Limit stress through regular exercise and relaxation techniques.
· Limit caffeine consumption to less than two caffeine-containing beverages a day.
· Avoid bright or flashing lights and wearing sunglasses if sunlight is a trigger.
· Identify and avoid foods that trigger headaches by keeping a headache and food diary. Review the diary with your doctor. It is impractical to adopt a diet that avoids all known migraine triggers, however, it is reasonable to avoid foods that consistently trigger migraine headaches.
What are prophylactic medications for migraine headaches? Prophylactic medications are medications taken daily to reduce the frequency and duration of migraine headaches. They are not taken once a headache has begun. There are several classes of prophylactic medications: beta blockers, calcium-channel blockers, tricyclic antidepressants, antiserotonin agents and anticonvulsants. Medications with the longest history of use are propranolol (Inderal), a beta blocker, and amitriptyline (Elavil), an antidepressant. When choosing a prophylactic medication for a patient the doctor must take into account the drug side effects, drug-drug interactions, and co-existing conditions such as diabetes, heart disease, and high blood pressure.
Beta blockersBeta-blockers are a class of drugs that block the effects of beta-adrenergic substances such as adrenaline (epinephrine). By blocking the effects of adrenaline, beta-blockers relieve stress on the heart by slowing the rate at which the heart beats. Beta-blockers have been used to treat high blood pressure, angina, certain types or tremors, stage fright, and abnormally fast heart beats (palpitations). They also have become important drugs for improving survival after heart attacks. Beta-blockers have been used for many years to prevent migraine headaches.
It is not known how beta-blockers prevent migraine headaches. It may be by decreasing prostaglandin production, though it also may be through their effect on serotonin or a direct effect on arteries. The beta-blockers used in preventing migraine headaches include propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor, Lopressor LA, Toprol XL), nadolol (Corgard), and timolol (Blocadren).
Beta-blockers generally are well tolerated. They can aggravate breathing difficulties in patients with asthma, chronic bronchitis, or emphysema. In patients with who already have slow heart rates (bradycardias) and heart block (defects in electrical conduction within the heart), beta-blockers can cause dangerously slow heartbeats. Beta-blockers can aggravate symptoms of heart failure. Other side effects include drowsiness, diarrhea, constipation, fatigue, decrease in endurance, insomnia, nausea, depression, dreaming, memory loss, impotence.
Tricyclic antidepressantsTricyclic antidepressants (TCAs) prevent migraine headaches by altering the neurotransmitters, norepinephrine and serotonin, that the nerves of the brain use to communicate with one another. The tricyclic antidepressants that have been used in preventing migraine headaches include amitriptyline (Elavil), nortriptyline (Pamelor, Aventyl), doxepin (Sinequan), imipramine (Tofranil), and protriptyline.
The most commonly encountered side effects associated with TCAs are fast heart rate, blurred vision, difficulty urinating, dry mouth, constipation, weight gain or loss, and low blood pressure when standing.
TCAs should not be used with drugs that inhibit monoamine oxidase such as isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate), and procarbazine (Matulane), since high fever, convulsions and even death may occur. TCAs are used with caution in patients with seizures, since they can increase the risk of seizures. TCAs also are used with caution in patients with enlargement of the prostate because they can make urination difficult. TCAs can cause elevated pressure in the eyes of some patients with glaucoma. TCAs can cause excessive sedation when used with other medications that slow the brain's processes, such as alcohol, barbiturates, narcotics, and benzodiazepines, e.g. lorazepam (Ativan), diazepam (Valium), temazepam (Restoril), oxazepam (Serax), clonazepam (Klonopin), zolpidem (Ambien). Epinephrine should not be used with amitriptyline, since the combination can cause severe high blood pressure
Antiserotonin medicationsMethysergide (Sansert) prevents migraine headaches by constricting blood vessels and reducing inflammation of the blood vessels. Methylergonovine is related chemically to methysergide and has a similar mechanism of action. They are not widely used because of their side effects. The most serious side effect of methysergide is retroperitoneal fibrosis (scarring of tissue around the ureters that carry urine from the kidneys to the bladder). Retroperitoneal fibrosis, though rare, can block the ureters and cause backup of urine into the kidneys. Backup of urine into the kidneys can cause back and flank (the side of the body between the ribs and hips) pain and ultimately can lead to kidney failure. Methysergide also has been reported to cause scarring around the lungs that can lead to chest pain, and shortness of breath.
Calcium channel blockersCalcium channel blockers (CCBs) are a class of drugs that block the entry of calcium into the muscle cells of the heart and the arteries. By blocking the entry of calcium, CCBs reduce contraction of the heart muscle, decrease heart rate, and lower blood pressure. CCBs are used for treating high blood pressure, angina, and abnormal heart rhythms (e.g., atrial fibrillation). CCBs also appear to block a chemical within nerves, called serotonin, and have been used occasionally to prevent migraine headaches. The CCBs used in preventing migraine headaches are diltiazem (Cardizem, Dilacor, Tiazac), verapamil (Calan, Verelan, Isoptin), and nimodipine.
The most common side effects of CCBs are constipation, nausea, headache, rash, edema (swelling of the legs with fluid), low blood pressure, drowsiness, and dizziness. When diltiazem or verapamil are given to individuals with heart failure, symptoms of heart failure may worsen because these drugs reduce the ability of the heart to pump blood. Verapamil and diltiazem may reduce the elimination and increase the blood levels of carbamazepine (Tegretol), simvastatin (Zocor), atorvastatin (Lipitor), and lovastatin (Mevacor). This can lead to toxicity from these drugs.
AnticonvulsantsAnticonvulsants (antiseizure medications) also have been used to prevent migraine headaches. Examples of anticonvulsants that have been used are valproic acid, phenobarbital, gabapentin, and topiramate. It is not known how anticonvulsants work to prevent migraine headaches.
Who should consider prophylactic medications to prevent migraine headaches? Not all migraine sufferers need prophylactic medications; individuals with mild or infrequent headaches that respond readily to abortive medications do not need prophylactic medications. Individuals who should consider prophylactic medications are those who:
1. Require abortive medications for migraine headaches more frequently than twice weekly.
2. Have two or more migraine headaches a month that do not respond readily to abortive medications.
3. Have migraine headaches that are interfering substantially with their quality of life and work.
4. Cannot take abortive medications because of heart disease, stroke, or pregnancy, or cannot tolerate abortive medications because of side effects.
How effective are prophylactic medications?Prophylactic medications can reduce the frequency and duration of migraine headaches but cannot be expected to eliminate migraine headaches completely. The success rate of most prophylactic medications is approximately 50%. Success in preventing migraine headaches is defined as more than a 50% reduction in the frequency of headaches. Prophylactic medications usually are begun at a low dose that is increased slowly in order to minimize side effects. Individuals may not notice a reduction in the frequency, severity, or duration of their headaches for 2-3 months after starting treatment.
What is the proper way to use preventive medications?
· Doctors familiar with the treatment of migraine headaches should prescribe preventive medications.
· Decisions about which preventive medication to use are based on the side effects of the medication and the medical conditions that the patient may have.
· Propranolol (Inderal) often is used first, provided that the patient does not have asthma, COPD or heart disease. Amitriptyline (Elavil) also is used commonly.
· Preventive medications are begun at low doses and gradually increased to higher doses if needed. This minimizes side effects from the medications. Preventive medications are to be taken daily for months to years. When they are stopped, the dose needs to be gradually reduced rather than abruptly stopped. Abruptly stopping preventive medications can lead to headaches.
· In some instances, more than one drug may be needed. Non-medication and behavioral therapies also may be needed.
What is the treatment of cluster headaches? As with migraine headaches, there are two approaches to treating cluster headaches: abortive and prophylactic. Abortive treatment is taken to stop the headaches. Prophylactic treatment is used to abolish or shorten the cycle of headaches.
Abortive treatments include inhalation of 100% oxygen at 8-10 liters/minute using a non-rebreathing facemask for 10-15 minutes along with a triptan such as sumatriptan (nasally, or under the skin) or an ergot such as DHE (intravenously, under the skin, or intramuscularly).
A calcium channel blocker, verapamil (Calan, Verelan, Isoptin) is the medication of choice for prophylactic treatment of cluster headaches. Other prophylactic medications include valproate, ergotamine, lithium, and methysergide. On occasion, verapamil may be combined with another prophylactic medication. Prophylactic medications usually are begun early during a cycle of cluster headaches and continued for two weeks longer than the usual cycle. The dose of medication then is reduced gradually. Because prophylactic medications may take two weeks to be effective, prednisone (a corticosteroid) often is used in decreasing doses for the first two weeks of treatment. Prednisone often can quickly abolish the headaches.
What is the treatment for menstrual migraine? There are several aspects to treating menstrual migraines:
1. To abort menstrual migraine, take medications after the onset of menstrual migraine. Generally, medications that are effective in aborting non-menstrual migraines are effective at aborting menstrual migraines.
2. To prevent menstrual migraine, take medications just before the onset of menstruation and continue for the duration of the expected headache. Taking hormones such as estrogens or estrogen related medications also help to prevent migraine.
3. To reduce the frequency and duration of menstrual migraine, take prophylactic medications (such as beta blockers, calcium channel blockers, anticonvulsants, tricyclic antidepressants) that are normally used on a continuous basis to prevent non-menstrual migraines.
NSAIDs such as naproxen sodium (Aleve) or ibuprofen (Advil, Motrin) have been used effectively to abort menstrual migraines. A combination analgesic containing acetaminophen, aspirin, and caffeine (ACC) can also be used to treat menstrual migraines. For women whose menstruation and menstrual migraines occur on a regular and predictable pattern, NSAIDs may be used 24 hours before the expected onset of menstrual migraine and continued for the expected duration of the headache. Since NSAIDs inhibit prostaglandins, they have the added benefit of relieving menstrual cramps as well. For NSAIDs side effects and precautions, please read the "Medication therapies for migraine" section of this article.
Triptans (naratriptan, rizatriptan, sumatriptan, zolmitriptan) have been found to be effective in aborting menstrual migraines, as well as controlling the associated nausea and vomiting. Sumatriptan given 2-3 days before and continued for the duration of the expected headache was found to be effective in reducing the frequency and severity of menstrual migraine. Naratriptan used in the same manner has also been found to be effective in preventing menstrual migraine. However, in those cases where breakthrough headaches occurred, they were just as severe as in patients taking placebo. For side effects and precautions of triptans, please read the "What are side effects of triptans" section of this article.
Dihydroergotamine (DHE) can be used as a nasal spray or given intramuscularly or intravenously to abort menstrual migraines. Ergotamine (oral, rectal, or intranasal) and DHE (intranasal, intramuscular, or intravenous) can be used around the time of menstruation (several days before and continued for the duration of the expected headache) to prevent menstrual migraines. For ergot side effects and precautions, please read the "What are the ergots?" section in this article.
If these medications are ineffective, doctors may try daily preventive medications such as beta-blockers, anticonvulsants, calcium channel blockers, and tricyclic antidepressants to reduce the frequency and the severity of menstrual migraines. The choice of the preventive medications is based on the experiences and preferences of the doctor, the medication side effects, and the woman's other associated medical conditions.
For women already taking preventive medications and yet still experience headaches, the doses of preventive medications can be increased around the time of the menstruation (some doctors use preventive medications only around the time of the menstruation). Alternatively doctors may try hormone treatment.
Since a drop in estrogen level just prior to menstruation is the trigger for menstrual migraines, estrogen replacement before menstruation has been used in preventing menstrual migraines. For some women with menstrual migraine, Estradiol skin patches (such as TTS 50, TTS 100) applied 2 days before menstrual migraine and continued for 7 days during the expected headache period is effective. However, the dose of estrogen must be closely monitored, as too high of a dose can actually trigger migraine in susceptible individuals.
Some women with difficult to treat menstrual migraines may be helped by using low dose oral contraceptives to reduce the estrogen fluctuations. Other less frequently used medications for menstrual migraines include tamoxifen, bromocriptine, danazol and gonadotropin-releasing hormone (GnRH). Reference: The medical clinics of North America "Headache", Ninan T. Mathew, MD, July 2001
Medically Reviewed by: Joseph Carcione, D.O., M.B.A., Board Certified Neurology Last Editorial Review: 3/23/2007
