Headaches.txt

• Occurrence: acute/subacute/chronic?
• Location: unilatera/bilatera?
• Duration: seconds/minutes/days
• Severity: how severe is the pain on a scale of 1-10? - does it fluctuate?
• Character: type of pain it causes - throbbing, pulsating, steady pressure, squeezing, tight feeling, dull, sharp. Lancinating, electric, shock feeling, feel like my head might blow up.
• Frequency: and temporality
• Associated symptoms: N/V, photophobia, sonophobia, visual disturbances, focal neurologica deficits, fever, myalgias, lacrimation, rhinorrhea, etc.?
• Precipitating factors: foods/alcohol? chewing/exercise/medication/specific part of menstrual cycle? tired/stressed/hungry
• Exacerbating factors: coughing sneezing/light/noise, body postuure?
• Alleviating factors: lying down in a quiet dark room/medication/after vomiting?

• Intracranial hemorrhage
• Occlusion/distention of cerebral vessels
• Meningitis/Encephalitis
• Hypertensibe headache
• Postlumbar puncture headache

blood in the cranial cavity can produce headache, altered consciousness, focal neurological deficits specific to location of the bleed, and seizures

• Usually arterial
• Associated with linear skull fracture which crosses/tears middle meningeal artery
• Tx: evacuation of hematoma

• Usually venous bleed
• shearing of bridging veins in the subdural space, more common in the young and the elderly
• Acute SDH appears hyperdense (white) on CT scan. Associated with head trauma (acute SDH develops within 4-7 days of head trauma( or anticoagulation
• Tx: evacuation of the hematoma

• traumatic or spontaneous
• Spontaneous: usually due to rupture of an aneurysm or arteriovenous malformation (AVM)
• Increased Intracranial pressure
• Classic presentation: pt comes to ER with "the worst headache of my entire life"
• Associated symptoms: loss of consciousness of altered mental status, vomiting and nuchal rigidity
• CT scan of the brain will demonstrate the SAH in 90% of patients if done within the first 24 hours.
• IF CT NEGATIVE, then LP
• If blood is present for the first 24 hours after the SAH the CSF will be pink.
• CSF later becomes yellow (xanthochromic) due to enzymatic breakdown of Hb to bilirubin
• Delayed onset vasospasm: can produce focal neurological deficits (most commonly 5-9 days after SAH)
• Tx: reduction of intracranial pressure; bp control/ nimodipine (a Ca2+ channel blocker) to reduce ischemic sequelae form cerebral vasospasm in pts with a ruptured aneurysm, prophylactic anticonvulsant therapy, and surgical therapy

can be due to HTN, vascular malformation, trauma, anticoagulation, intracranial tumor, sympathomimetic agents (amphetamines, cocaine) and amyloid angiopathy

can cause acure obstructive hydrocephalus

• headache can accompany TIAs and thrombotic or embolic strokes due to pain sensitive receptors in large cerebral arteries
• Carotid dissection: causes headache and facial pain ipsilateral to the dissecting artery (ptosis, meiosis, anhydrous) in 50% due to stretching or compression of the sympathetic fibers in the carotid sheath
• 20% of strokes in pts < 40 yers old caused by carotid or vertebral dissection

• Pain due to inflammation which can be cause by infection (bacterial, viral, fungal), granulomatous processes, neoplasms or chemical irritants
• headache usually develops over a period of hours (or even days)
• Dx: by CSF examination
• Tx: specific to causative agent
• Note: most common viral encephalitis is due to herpes - Tx: acyclovir
• Hypertensive headache
• seen with malignant hypertension, and conditions causing a sudden elevation of blood pressure such as pheochromocytoma, sexual intercourse, or ingestion of tyramine-containing foods while taking a monoamine oxidase (MAO) inhibitor

• cause by a persistent spinal subarachnoid fluid leak with resultant traction on pain-sensitive structures at the base of the brain
• more commone in women
• peak incidence in 18-30yr olds
• Throbbing occipital headache: precipitated by standing and relieved by lying down
• usually beins 24-48 hrs post LP and lasts 1-2 days
• Treatments for prolonged post LP headache: oral or IV caffeine, epidural saline, epidural blood patch

• decreased by using a smaller gauge needle (22G), inserting bevel parallel rather than perpendicular to dural fibers, replacing stiletto before withdrawing needle, and using a noncutting or atraumatic needle.
• It was previously thought that risk of a post LP headache was minimized by removing a low volume of CSF, remaining recumbent after the LP for up to 24 hrs, and increasing fluids post LP, but studies have failed to substantiate these as risk factors

• brain tumor, abscess or subdural hematoma: can cause headache
• new onset of headache in the middle or later life always warrants ruling out mass lesion!
• Headache is typically worse in the morning, has associated N/V and is worse tih maneuvers that increase intracranial pressure
• Dx: neuroimaging (CT or MRI)

• aka giant cell arteritis: systemic vasculitis of unknown etiology characterized by subacute granulomatous inflammation most pronounce along the internal elastic lamina of the arterial wall
• Usually affects branches of the external carotid artery, most commonly the superficial temporal artery
• usually seen in older women and is often associated with polymyalgia rheumatic 9Sx include malaise, weight loss, fever, myalgias and arthalgias)
• headache pain is severe, unilateral or bilateral, boring quality
• Clinical findings: due to decreased blood flow: include jaw/tongue claudication (pain with chewing), scalp tenderness and jaw stiffness
• Opthalmic artery involvement: can result in visual changes or sudden loss of vision, leading to blindness in up to 60% (half of those will have bilateral blindness)

• age>50
• new onset localized headache
• temporal artery tenderness or decreased pulsation
• increased sedimentation rate >50mm/hr
• arterial biopsy showing necrotizing arteritis characterized by predominance of mononuclear cell infiltrates or granulomatous process
• if patient meets 3 out of 5: study showed Ds. sensitivity 93.5% Specificity 91.2%
• Temporal artery biopsy standard for Dx, but negative biopsy: does not exclude
• Tx: corticosteroids (prednisone)

• sharp, stabbing, electric shock-like, burning pain in the distribution of one or more branches of the trigeminal nerve
• usually maxillary and/or mandibular, only 5% opthalmic
• pain usually does not cross sides during episode but: occurs bilaterally in 3-5%
• Individual pains brief, but can occur many times a day or in flurries
• Pain: spontaneously or triggered by chewing, talking, touching the face (washing, shaving, stroking face), cold air or wind.
• Can trigger reflex spasm of the face - "tic doloreaux": usually pain-free between attacks, but can have chronic ach ein region between attacks

• idiopathic
• symptomatic: compromise of the trigeminal root by tumor (acoustic neuroma, cholesteatoma, osteoma), aneurysm, chronic meningitis
• symptomatic cause may produce sensory deficit in distribution of affected branches of trigeminal nerve.
• In younger individuals: often a presenting symptom of MS, MRI of brain should be done

• Medical treatments: carbamazepine (usually first choice), other anticonvulsants (phenytoin, valproic acid, gabapentin, lamotrigine, topiramate, clonazepan), baclofen and tricyclic antidepressants
• Surgical interventions: percutanous block with alcohol or glycerol, microbascular decompression, percutanous stereotactiv radiofrequency thermal rhizotomy, and gamma knife surgery

• Same type of pain as trigeminal neuralgia, but in glossopharyngeal distribution
• can also have continuous burning aching pain in the oropharynx, base of the tongue, tonsillar pillars, and auditory meatus
• more common in men
• age of onset: slightly earlier than trigeminal neuralgia
• medical treatment: same as trigeminal neuralgia

• most cases idiopathic
• association with: obesity, recent weight gain, pregnancy, oral contraceptives, corticosteroids, withdrawal from steroids, endocrine dysfunction (menstrual irregularities, Cushing's disease, addison's disease, hypoparathyroidism), hypervitamenosis A, tetracycline (in infants), and obstruction of intracranial venous drainage (venous sinus thrombosis, polycythemia, thrombocytosis, head trauma)
• Most commonly affected: women in their 20's
• Thought to be due to: increased resistance to CSF reabsorption at the arachnoid granulations
• have increased IP resulting in headaches and papilledema
• May have associated blurry vision, intermittent visual obscurations, pain with eye movement (extremes of gaze), horizontal diplopia, tinnitus, dizziness, and nausea and vomiting
• pressure on the on the optic nerves can result in optic atrophy and blindness
• CT/MRI may show slit-like ventricles.
• Opening pressure is elevated on LP
• Tx: acetazolamide, prednisone, repeated LPs or lumboperitonieal shunt and optic nerve sheath fenestration

• follows a vesicular skin eruption in a dermatomal distribution caused by herpes zoster (shingles)
• 10-15% of cases involve the trigeminal nerve
• characterized by: constant severe burning dysesthetic pain
• Opthalmic division of the trigeminal nerve: most commonly affected in the head (80%)!
• Acute skin eruption treated with antivirals (acyclovir, valcyclovir, famcyclovir)

• trycyclic antidepressants, antiepileptic drugs
• lydocaine cream or gel
• capsaicin cream
• prevalence increases with advancing age: affects 50% of those over age 50 following acute herpes zoster

• migraine
• Cluster headaches
• Tension-type headaches

• throbbing/pulsatile headache, usually unilateral, lasting hours to days
• may have associated N/V, photophobia and sonophovia
• affects about 12% of the population (18% of women, 6% of men)
• Onset: in youth/early adulthood
• often family history
• usually thought to be due to vasodilation from transiently decreased cerebral blood flow
• Classic migraine headaches: preceded by an "aura" most commonly fibula symptoms, including flashing bright zigzags of light, and scintillating scotomata
• less commone: paresthesias, speech disturbance, hemiplegia, or opthalmoplegia

not preceded by an aura and is commonly bilateral and periorbital

• skipping meals
• bright of flickering lights
• strong odors such as perfume
• weather changes
• too much or too little sleep
• stress
• or relaxation after stress
• drugs (vasodilators such as nitroglycerine, oral contraceptives)
• caffeine withdrawal, the menstrual cycle
• certain foods: red wine, MSG, food high in tyramine such as sharp cheese, foods with nitrite preservatives such as hotdogs and bacon, and chocolate containing phenylethylamine
• migraine headaches are exacerbated by physical activity
• patients seek to lie down in a quiet dark room
• Vomiting and sleep may alleviate the headache

• eliminate precipitating factors
• Medication: symptomatic (analgesics) fir infrequend mild migraines NSAIDs, isometheptene or butalbital
• Moderate to sever headaches: triptans, narcotics, ergot preparations/ antiemetic

• selective serotonin 1B,D receptor agonists (5-HT agonists)
• are thought to constrict cranial vessels and activate peripheral terminals of the trigeminal nucleus caudal causing neuronal inhibition and blockade of release of CRGP
• Vasoconstrictors are contraindicated in pregnancy and in patients with significant hypertension, coronary artery disease or peripheral vascular disease

• chronic prophylactic medication should be initiated
• anti-inflammatory agents : ASA, naproxen
• TCAs: amitriptyline, nortriptyline
• beta-blockers: propranolol, atenolol, metoprolol, nadolol, timolol
• calcium channel blockers: verapamil, nicardepine
• cyproheptadine: used primarily in children
• anticonvulsants (valproic acid, gabapentin, tipirimate
• methysergide
• often continue to use symptomatic treatments as well

• much less common than migraine headaches (prevalence 0.4%)
• affects men more often than women (6:1)
• age of onset typically 20-40
• positive family hx in 7%
• Cluster headaches are always unilateral and usually occur on the same side in subsequent bouts

• excruciating, constant, nonthrobbing
• occurs in periorbital region, eye, or temple
• Headache lasts from 10 mins - 2 hrs, average 45 mins
• peaks in within first 15 minutes of headache
• associated autonomic sx: on side of headache - autonomic - lacrimation, conjunctival injection, nasal congestion, rhinorrhea, facial flushing, ptosis, meiosis
• pt agitated, and may restlessly pace: during an attack

• alcohol or vasodilating drugs (nitroglycerine, histamines)
• etiology unknown

• Acute: 100% oxygen at 7-10 L/min for 15-30 mins; SQ or nasal lidocaine
• should also receive daily prophylactic medications: steroids, vorapamil, lithium carbonate, methysergide, divalproex sodium or combinations

• bilateral, steady, nonthrobbing headaches
• occur in occipiptical/nuchal region: may feel like a tight band around the head
• no associated visual symptoms or N/V
• More common in women
• can occur occasionally or frequently (even daily)
• underlying pathophysiology: unknown = contraction of scalp and neck muscles now thought to be secondary phenomenon rather than cause
• patients may have emitted features of migraine and tension - type headaches
• Acute attacks are treated with OTC meeds, NSAIDs and analgesics

• glaucoma
• sinusitis
• temporomandibular joint dysfunction
• Cervical spine disease
• chronic SDH
• postconcussive syndrome