Brain tissue is non sensitive structure
From where headache appearPain-Sensitive Cranial Structures
(1) skin, subcutaneous tissue, muscles, extracranial arteries, and periosteum of the skull (2) delicate structures of the eye, ear, nasal cavities, and paranasal sinuses (3) intracranial venous sinuses and their large tributaries 4) parts of the dura at the base of the brain and the arteries within the dura, particularly the proximal parts of the anterior and middle cerebral arteries and the intracranial segment of the internal carotid artery (5) the middle meningeal and superficial temporal arteries (6) the optic, oculomotor, trigeminal, glossopharyngeal, vagus, and first three cervical nerves.INSENSITIVE TO PAIN.
The brain parenchyma, Pial arteries over the convexities, The cerebral ventricles Choroid plexusHEADACHE
the most common reason for seeking medical help a detailed history will determine the diagnosis more often than the physical examination or imagingHISTORY TIPS
onset quality, severity, location, duration, time course the conditions that produce, exacerbate, or relieve it.Onset of Headaches
A stable headache disorder of many years’ duration is almost always of benign origin.“Recent onset "newly onset headache :range is from 1 to 12 months. In general, the more recent the onset, the more worrisomeThe “worst ever” headache: change in an existing headache pattern all raise the possibility of an intracranial lesionThunderclap headache : Headaches of instantaneous onset reaching maximum severity over a minute usually seen in SAH ICH Onset of a new headache in patients older than 50 years raises suspicion of an intracranial lesion (e.g.,subdural hematoma) or giant cell (temporal or cranial) arteritis
THUNDERCLAP HEADACHE” may be defined as an abrupt onset, often a “worst ever” headache that is maximal in seconds but may develop in minutes. Vascular causes• SAH• Carotid and vertebral artery dissection• Cerebral venous thrombosis• Arterial hypertension• Temporal arteritis Nonvascular causes• Meningoencephalitis• Intermittent hydrocephalus (colloid cyst of the 3rd ventricle)• Spontaneous intracranial hypotension only one person in eight who has such a 'thunderclap' headache will have had a subarachnoid hemorrhage = other symptoms including vomiting and neck stiffness
Frequency and Periodicity
Episodic = migraine Chronic migraine: occurring 15 or more days per month Episodic = cluster headaches typically occur daily for several weeks or months and are followed by a lengthy headache-free interval. Chronic cluster headaches occur at least every other day for more than 1 year.chronic daily headache without migrainous or autonomic features is likely to be a chronic tension-type headache Untreated migraine pain usually peaks within 1 to 2 hours of onset and lasts 4 to 72 hours. Headache coming on over a matter of hours is less likely to be associated with structural disease and more likely to be due to migraine, unless accompanied by other significant symptoms or signs. Patients with bacterial meningitis are usually generally ill and pyrexial
Frequency and Periodicity
Temporal Profile
Cluster headache is typically maximal immediately or peaks within minutes . Cluster headaches can last 15 to 180 minutes2 to 30 minutes and occurring several times a day are typical of episodic or chronic paroxysmal hemicrania, both of which are more common in women and are prevented by INDOMETHACINTension -type headaches commonly build up over hours and last hours to days to years.Primary stabbing headaches (“ice-pick pains”) are momentary, lasting only seconds. Stabbing pains are more common in patients with migraine and cluster headaches.New daily-persistent headache: headache that is daily and unremitting from onset, usually in patients without prior headaches A chronic, continuous, unilateral headache of moderate severity with superimposed attacks of more intense pain, associated with autonomic features, suggests the diagnosis of hemicrania continua Brief shocklike pains, often triggered by stimulation in the territory served by the affected nerve
Time of Day and Precipitating Factors
awaken patients from a sound sleep Hypnic headaches typically affect older patients and regularly awaken the patient at a particular time of night. Unlike cluster headaches, they are usually diffuse and not associated with autonomic phenomena worse on waking may be caused by increased intracranial pressure Migraine headaches can occur at any time but often begin in the morning.Location
Headaches so well localized by the patient that a finger is used to locate the exact spot on the skull are never associated with significant disease. patient over 60 years with head pain localized to one or both temples, giant cell arteritis should be considered, especially if the temporal pulses are not palpable and/or the arteries are enlarged and tender.Migraine pain often has a pulsating quality that may be superimposed on a more continuous pain. The pain of cluster headache characteristically is severe, boring, and steady and often is described as a “hot poker.” SUNCT produces moderately severe pain in the orbital or temporal region and may be described as sharp and stabbing or (rarely) pulsatile. Tension-type headaches usually are described as a steady feeling of fullness, tightness, or pressure, or like a cap, band, or vise. Quality and Severity
Quality and Severity
Headaches caused by meningeal irritation, whether related to infectious meningitis or blood are typically severe. Trigeminal neuralgia is severe, brief, sharp, electric shock–like, or stabbing; pains can occur up to several times per minute, and a milder ache may persist between paroxysms of pain. Glossopharyngeal neuralgia pain is similar in character to that of trigeminal neuralgia.Accompanying Symptoms
premonitory symptoms that precede a migraine headache by hours. These can include psychological changes (e.g., depression, euphoria, irritability) or somatic symptoms (e.g., constipation, diarrhea, abnormal hunger, fluid retention, increased urination) The aura: refers to focal cerebral symptoms associated with a migraine attack. These symptoms typically last 20 to 30 minutes but can last 1 hour and usually precede the headache.Aura
Visual aura symptoms are most common and may consist of either Positive (flickering lights, spots, or lines) or Negative (scotomas or visual field loss) The visual symptoms characteristically affect both eyes but can affect one eye alone. Other hemispheric aura symptoms, such as somatosensory disturbances (tingling and/or numbness) or dysphasic language disturbance, may occur with or without visual symptoms. brainstem aura , such as vertigo, dysarthria, ataxia, auditory symptoms, diplopia, bilateral visual symptoms in both eyes, bilateral paresthesias, and decreased level of consciousness, may accompany basilar-type migraineAccompanying features
Nausea, vomiting, photophobia, phonophobia,and osmophobia characteristically accompany migraine attacks lacrimation, rhinorrhea, and nasal congestion Ipsilateral miosis, ptosis, lacrimation, conjunctival injection, and nasal stuffiness commonly accompany cluster headache Temporomandibular joint dysfunction includes jaw pain precipitated or aggravated by movement of the jaw or clenching of the teeth and is associated with reduction in the range of jaw movement, joint clicking, and tenderness over the joint. Headache accompanied by fever suggests an infection Jaw claudication, or tenderness of the scalp arteries in an older person strongly suggests GCA.Aggravating Factors
Routine physical activity, light, sound, and smells typically aggravate migraine headaches. marked worsening of headache in the upright position suggests intracranial hypotension
Family History of Headaches
Migraine often is an inherited disorder, and a family history of migraine (sometimes referred to as “sick headaches”) is present in about two-thirds of patients. Tension-type headaches also can be familial. Cluster headache characteristically is not inherited. Familial hemiplegic migraine is a rare autosomal dominant variant of migraine with aura, wherein the aura includes hemiparesis lasting minutes to 24 hours.WORRISOME CLINICAL FEATURES
“Worst-ever” headache Onset with exertion (20% of SAH occur with exertion) Impaired alertness or conscious level, neck stiffness, Progressive neurological deteriorationAbnormal neurological examination (3rd or 6th nerve palsy),papilledema, subhyaloid hemorrhage, hemiparesis, diplegia (anterior communicating aneurysm)Loss of visual acuity or visual fields tenderness to palpation and hardeneded temporal arteriesAuscultation of the skull disclose a bruit ( AVM), sensitive areas overlying a cranial metastasis, an inflamed paranasal sinusMigraine
Epidemiology• Migraine is a common episodic neurological condition. It occurs in up to 11% of the adult population, usually with onset in late adolescence or the early third decade. Approximately 70% of migraine sufferers are females.• There is a tendency for migraine to become less severe or even remit in the fifth and sixth decades.• Forty-six percent of patients have a family history of migraine. The risk of a child developing migraine is about 70% if both parents are affected, and 45% when one parent is affected.Pathophysiology
activation of the trigeminovascular network in the dorsal midbrain and dorsolateral pons (especially serotoninergic projections).presumably causes: impaired regional blood flow to the brain, perimeningeal vasodilatation neurogenic inflammation, [seritonin, and dopamine ] cortical spreading depression,A migraine attack can be divided into four components: prodrome,aura, headache, resolutionThe occurrence of an aura distinguishes two major types of migraine episode: Migraine with aura (“classic migraine”) Migraine without aura (“common migraine”).
Migraine auravisual phenomena such as fortification spectra, scotomata, scintillating scotomata, visual or auditory hallucinations.Less commonly, visual distortions such as macropsia and micropsia may be described.Somatosensory phenomena, usually paresthesias, Hemiparesis, sometimes with a “march, olfactory and gustatory hallucinations distortions of body image are unusual but sometimes reported.The aura may occur without evolution into a headache; this is referred to as “migraine equivalent.
Headache phase
• Headache may be unilateral, bilateral, or shift sides during the course of an attack. It is often throbbing in character, although it may be more continuous felt in a periorbital or retroorbital distribution. There is often a “referred tension” component, with occipital and cervical pain being prominent.• Most important associated features include exacerbation by routine physical activity, nausea, vomiting, photophobia, and phonophobia
Migraine triggers
Stress and relaxation after stress Sleep: sleep deprivation, “sleeping in,” interruption of usual sleeppattern Trauma and mild closed head injury Sensory stimulation: glare, flickering lights, smells (e.g., certain perfumes) Irregular eating habits: missing a meal (hypoglycemia) Foods: red wine, cheese, chocolate, caffeine Food additives: monosodium glutamate Exercise Excessive heat and dehydration Drugs: vasodilators such as nitroglycerin psychological stressMIGRAIN VARIANT
Migraine without aura (“common migraine”)At least five attacks fulfilling criteria a–d:a. Headache lasting 4 hours to 72 hoursb. Nausea/vomiting and/or light and noise sensitivityc. Two of the following:• Unilateral pain• Moderate or severe intensity pain• Aggravation by simple physical activity• Pulsating paind. Not attributable to another disorderMigraine with aura (“classic migraine”)• Aura develops over >4 minutes or two or more symptoms occur insuccession• Each aura <60 min• Headache <60 min following aura
Basilar migraine: characterized by a visual prodrome, ataxia, vertigo, diplopia, tinnitus, and nausea/vomiting. nystagmus, dysarthria and altered level of consciousness may be present. Sometimes an acute confusional episode, often in children. Ophthalmoplegic migraine: Migrainous headache with 3rd or 6th nerve paresis, which may persist for days to weeks, sometimes requiring exclusion of intracranial hypertension or aneurysm.
Hemiplegic migraine: Usually begins in childhood and remits in adulthood; may be sporadic or familial. Hemiplegia may last less than 1 hour, or it can persist for days to weeks. Attacks are often precipitated by minor head injury, and changes in consciousness may be present. Many cases of familial hemiplegic migraine have been mapped to chromosome 19p13 . Status migrainosus: Attacks of migraine lasting longer than 72 hours, usually with prolonged nausea and vomiting.
Menstrual migraine +Sixty percent of women report an increase in migraine frequency around menstruation; 14% have migraine exclusively related to the menstrual period. The hormonal stimulus is thought to be exposure to high estrogen levels, followed by the sharp decline in estrogen immediately prior to ovulation. Estrogen may increase the sensitivity of some 5-HT receptors. Release of uterine prostaglandins at the time of menstruation may also play a role in the development of migraine.
Menstrual migraine/TREATMENT
Non-hormonal prophylaxis• NSAIDS: Naproxen 550 mg daily beginning 2 days prior to predicted menstruation and continuing for 3 days into period.• Triptans: Frovatriptan 2.5 mg bid for 6 days starting 2 days prior to anticipated onset of menstruation. Naratriptan 1 mg bid for 6 days, starting 2 days prior to onset of mensesHormonal prophylaxis• Continuous hormone treatment The most common agent used for hormonal prophylaxis is perimenstrual estrogen, given as estradiol gel at a dose of 1.5 mg, or transdermal estrogen 100 μg, to be given 3 days prior to onset of menses and then continued for 1 week.• Combination oral contraceptive pills (OCPs) may also be given; if a 1-week hormone-free interval after a 3-week cycle is consistently associated with recurrent headache, three consecutive hormonal cycles can be attempted, followed by 1 week of hormone withdrawal.
Migraine therapy
Identification and avoidance of precipitants or exacerbating factors (such as the contraceptive pill) may prevent attacksAcute (abortive) migraine therapySimple analgesia with antiemetics Useful only if nausea and vomiting are not major symptoms during a migraine attack; effect may be limited by reduced gastric motility.Acetaminophen, 500–1000 mg or an NSAID (ibuprofen, naproxen, diclofenac) + metoclopramide, 10 mg.Triptans (selective 5-HT1 antagonists)• All drugs of this class (sumatriptan, zolmitriptan, naratriptan, rizatriptan, eletriptan, almotriptan, frovatriptan; have a high efficacy with up to 70% having a response within 2 hours and 40% being pain free at 2 hours.• Early therapy will optimize therapeutic response.• Headache recurrence within 12–24 hours occurs in 30% of patients; a second dose of triptan may be attempted. If this is ineffective,administration of a “rescue medication” such as a narcotic analgesic, NSAID, corticosteroid, or neuroleptic may be considered .
• If two trials of a particular triptan at high therapeutic doses areunsuccessful, a trial of another triptan should be considered.• Overuse may result in rebound headaches in 10% of patients.• Contraindications include coronary artery disease, cerebrovascular disease, uncontrolled hypertension, peripheral vascular disease, significant hepatic impairment, and pregnancy.• Common adverse effects include chest discomfort or heaviness; jaw, shoulder, and neck tightness; paraesthesias, fatigue, and dizziness.• Concurrent MAOI administration is contraindicated. Serotonin syndrome is an occasional adverse event.
Ergot group
5-HT agonists that are potent vasoconstrictors of the extra-cranial arteries. These can be administered orally, sublingually, by subcutaneous injection or by nasal spray. Ergotamine preparations should be avoided since they easily lead to dependence. This is less likely to happen with the triptans, but it can occurErgotamine preparations• Ergotamine tartrate is still sometimes useful in patients who do not respond to triptans and who do not have any contraindications to treatment with vasoactive medications. A dosage of 1–2 mg alone or in combination with caffeine may be given orally at onset. It may also be administered by inhaler or suppository.• Overdosage results in nausea, rebound headache, and peripheral vasoconstriction. The recommended maximum dose per week is 10 mg.• Dihydroergotamine (DHE) is used intravenously in patients with intractable migraine or status migrainosus at doses of 0.3–1.0 mg every 8 hours up to a total dose of 10 mg.
Migraine prophylaxis• Prophylactic therapy should be considered if more than two attacks per month are reported, or if attacks become markedly debilitating.• A headache diary is useful to monitor frequency and patterns, including relationship to menses, sleep patterns, and other triggers. It is critical to determine if analgesic or triptan overuse is ongoing; these problems will render prophylaxis ineffective.• Prophylactic drug therapy includes :• Beta-blockers• Tricyclic antidepressants• Anticonvulsants• Calcium channel antagonists (less effective than other prophylactic regimens but useful when other agents are contraindicated)
TENSION/MUSCLE CONTRACTION
• Most common type• Usu bilateral, often described as a tight band, squeezing• Not aggravated by physical activity, no prodrome/aura• May be associated w/ nausea or photophobia• Usu waxes and wanes• May last for several days• Tx: tylenol or NSAIDsCLUSTER headache
• Much less common• More common in men (9:1), onset in late 20s• Severe, stabbing, periorbital pain• Associated w/ ipsilateral tearing, nasal congestion, rhinorrhea, conjucntival injection, ptosis, eyelid swelling, flushing of forehead, can see horner’s• Precipitants: alcohol, heavy smoking, NTG• Onset frequently at night, usually lasts 30min - 3hrs• Each attack is similar, often occurring at the same time of day (“alarm - clock headache”)• Pt prefers to pace and keep active during attack• Cluster refers to the seasonal occurrence of episodes• Acute tx: 02 > 7 L/min (90% effective), intranasal DHE, sumitriptan• Prophylaxis: CCBs, valproate, lithium carbonate
GIANT CELL ARTERITIS
• Over 50 yo and average is 70: 4 females to 1 male• Headache + visual loss, jaw claudication, tenderness of scalp over temporal arteries• Pain is piercing or buring quality, usually unilateral• Note: pain can be located more in jaw than temporal skull region• Fundoscopy: can see edema or papillitis but usually are normal• Association with PolyMyalgia Rheumatica (50%)• ESR elevated, mild anemia, mild leukocytosis• Risks: blindness,, basilar artery infarct• Tx: prednisone 60 - 100 mg po od• Treat with steroids even b/f lab results if you suspect this dx87 ys Hemicrania ESR 100
TRIGEMINAL NEURALGIA• Tic Douloreux = sudden wincing of facial muscles in response to severe facial pain• Facial pain that occurs suddenly, lasts seconds to minutes, lancating/electrical quality, progression to constant ache, UNILATERAL 95%• V2 and V3 more common distribution than V1• May have “trigger spot” on face, may be precipitated by talking, chewing, facial movement, or tapping on the trigger zone to reproduce symptoms• 2 females: 1 male, most > 50yo• Theories: HSV irritation of CNV, dental disease, anatomic nerve lesion, vascular compression by adjacent vessels, MS, cerebellopontine angle mass• Diagnosis: history with NORMAL physical examination (CNV: normal sensation to face, muscles of mastication normal, normal corneal reflex)•
Ddx: glossopharyngeal neuralgia, post - herpetic neuralgia, TMJ pain, dental dz,sinusitis, trauma, cluster h/a, GCA• CT/MRI: normal, should be done to r/o posterior fossa tumor• Management• Tegretol: 100 - 200 mg/day and titrate up (some start at 200 mg po tid)• Alternative: dilantin• Failure of medical Rx: injections, peripheral neurectomy, radiation, orsurgical decompression
PSEUDOTUMOR CEREBRI
• Also called idiopathic intracranial HTN• Typical patient: overweight, young adult females• Etiology Unknown is most common Steroid Rx Birth control pill Coagulation disorders Venous sinus thrombosis (must r/o) Tetracycline Pregnancy? Obesity? Ear infections?History• Overweight, young femal with h/a, diplopia, blurry vision, papilledema• Headache/neck ache• Transient visual obscuration• N/V• Blurred vision and/or diplopia• Menstrual irregularities• Normal level of consciousness• Physical• severe papilledema (decreased axonal transport)• VI nerve palsy (seen as medially deviated eye with inability to abduct)•
Investigations• MUST do CT b/f Lp • LP shows elevated CSF pressure • r/o etiology: medications, endocrine, venous thrombosis (MR venography• Treatment• repeat LP• acetazolamide (carbonic anhydrase inhibitor)• dexamethasone• weight reduction• optic nerve fenestrations if vision is a threatenedShunting CSF