headache Flashcards
Recognize the epidemiological implications of headache
. Migraine is the third most common disease on the planet
Know the difference between a primary and secondary headache syndrome
primary (90%): with no known cause (i.e. migraine) and can be episodic (coming and going) or chronic (present on most days for at least 3 months). Secondary: attributed to a systemic or cephalic disorder and are often constant.
Which intracranial structures can “hurt”
Three basic structures that carry pain fibers include the meninges, certain blood vessels (dural veins or sinuses, meningeal arteries, extracranial and proximal intracranial arteries, and extracranial veins), and the dermis. These structures are innervated by the trigeminal sensory system
List most common primary headache syndromes
Tension type (93% one year prevalence), migrane (12% prevalence), and trigeminal autonomic cephalagias (<0.5% prevalance)
List most common/threatening causes of secondary headache
meningitis, hemorrhage (subarachnoid, subdural, epidural), intracranial hypertension (idiopathic, brain tumor, brain abscess), and giant cell (temporal) arteritis
HIS criteria for migraine
at least 5 recurring headaches that last 4-72 hours and are characterized by at least 2 of the following: unilateral in location, pulsating in character, moderate or severe in intensity, and pain that increases with physical activity. They must also be associated with at least one of the following: nausea and/or vomiting, OR photophobia and phonophobia.
Phases of a migraine
A. PREMONITORY -may include alterations in mood, alertness and appetite up to 24 hours prior to headache
B. AURA – Various neurologic symptoms preceding headache (about 30% experience an aura)
C. HEADACHE AND ASSOCIATED SYMPTOMS
D. RESOLUTION – post-event exhaustion and lethargy
A. PREMONITORY -may include alterations in mood, alertness and appetite up to 24 hours prior to headache
B. AURA – Various neurologic symptoms preceding headache (about 30% experience an aura)
C. HEADACHE AND ASSOCIATED SYMPTOMS
D. RESOLUTION – post-event exhaustion and lethargy
A. PREMONITORY -may include alterations in mood, alertness and appetite up to 24 hours prior to headache
B. AURA – Various neurologic symptoms preceding headache (about 30% experience an aura)
C. HEADACHE AND ASSOCIATED SYMPTOMS
D. RESOLUTION – post-event exhaustion and lethargy
Triggers for migraine
missed meals or lack of adequate sleep, alcohol consumption, caffeine withdrawal, perimenstruation, “relief” of stress, and certain food [MSG, nitrites (hot dogs), tyramine (cheese)].
Migraine treatment - abortive
Abortives include aspirin, acetaminophen, NSAIDs, combination medication such as ibuprofen/caffeine/ aspirin or caffeine/aspirin/acetaminophen, serotonin receptor agonists, either selective (triptans-such as sumatriptan, naratriptan, rizatriptan, eletriptan), or non-selective (ergotamine derivatives).
Migraine treatment - prophylactic and alternatives
prophylactic medications include beta blockers, calcium channel blockers, tricyclic antidepressants, and anti-epileptics. Alternatives or non-pharmacologic treatments include supplements (i.e. Magnesium, Vitamin B2- riboflavin, Butterbur), sleep, acupuncture, and biofeedback. Botox injections are used for chronic migraine (occurring >15days/month, >4 hours/day, for at least 3 months).
Classifications for migraine aura
Criteria for aura include 2 episodes with reversible symptoms of at least one of the following: visual, sensory, language, motor, brainstem, retinal changes AND with 2 of the following: unilateral symptoms, gradual development over 5 minutes or greater, symptom lasting 5-60 minutes, accompanied or followed by headache.
Migraine pathogenesis
. Before or simultaneously with the onset of aura symptoms, regional cerebral blood flow is decreased in the cortex corresponding to the clinically affected area and often over a wider area. In contrast, regional cerebral blood flow imaging shows no changes suggestive of cortical spreading depression (CSD) during attacks of migraine without aura. Most likely, migraine headache depends both on activation of the trigeminovascular pathway by pain signals that originate in peripheral intracranial nociceptors, and on dysfunction of CNS structures involved in the modulation of neuronal excitability and pain.
HIS criteria for tension type headache
include at least 10 episodes of headache that last 30 minutes to 7 days, and each episode must be characterized by at least 2 of the following: pressing or tightening sensation, mild to moderate in severity, bilateral, and not aggravated by physical activity. Patients must not have nausea or vomiting and they can have only one or none of the following: photophobia or phonophobia
Tension type headache treatment - not LO
aborting the headache with over-the-counter medications like aspirin, acetaminophen, and non-steroidal anti-inflammatory drugs (NSAIDS). Prophylactic medications include tricyclic antidepressants, selective serotonin reuptake inhibitors (i.e. Prozac), psychotherapy, and physical therapy
HIS criteria for cluster headache
at least 5 episodes of severe, unilateral, periorbital and/or temporal pain that lasts 15-180 min. The pain should recur at least every other day up to 8 times per day. One of the following must be present ipsilaterally: conjunctival injection, lacrimation, nasal congestion, rhinorrhea, eyelid edema, ptosis, miosis, facial swelling, ear fullness; restlessness/agitation is diagnostic
Who are more prone to cluster headaches
men (4:1 men to women)
Triggers of cluster headaches
alcohol or drugs with vasodilator properties
Therapy of cluster headaches - no a LO
Abortive therapy includes oxygen, triptans, ergotamine derivative, lidocaine, corticosteroids, nerve blocks, which can often break a “cluster” period. Prophylaxis includes calcium channel blockers, lithium, and anti-epileptics
What is unique about trigeminal neuralgia
can be primary or secondary headahce
Trigeminal neuralgia HIS criteria
very brief pain in the trigeminal nerve distribution lasting <1 second to up to 2 min. The pain must be of one of the following characteristics: intense, sharp, superficial, or stabbing. It is triggered by sensory stimulation of a particular area within the trigeminal sensory innervation or by a factor such as chewing or brushing teeth
secondary causes of trigeminal neuralgia
vascular compression (by a tortuous artery) of the trigeminal nerve or by demyelination of the trigeminal nerve within the pons (i.e. multiple sclerosis)
treatment of tigeminal neuralgia- not a LO
Treatment is often incompletely successful, but includes anti-epileptics (gabapentin, pregabalin, carbamazepine, topiramate) or baclofen. Surgical decompression of the nerve is often recommended for medically intractable pain, contraindication to medical treatment, and/or vascular compression of the nerve noted on neuroimaging with neuropathy on examination.
Clinical presentation of head injury with headache
Typically the pain will develop within 7 days of the injury and resolve by 3 months. Most patients experience dizziness, poor concentration, irritability and insomnia associated with the concussion and headache. Younger age patients and men are less likely to develop a clinically significant or persistent headache after a concussion.
clinical presentation of meningitis
Typically the pain is acute (hours for bacterial meningitis and 1-2 days for viral) onset and is associated with fever, neck stiffness (meningismus), nausea and/or vomiting, altered consciousness (especially with bacterial meningitis) and signs of meningeal irritation (Kernig/Brudzinski signs).
What is kernig and brudzinski signs
Both occur in meningitis. Kernig’s sign: Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. Brudzinski’s sign: Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed
Diagnosis of meningitis
LP: elevated nucleated cells (white blood cells) in the cerebrospinal fluid (CSF), normal or low CSF glucose (low glucose in bacterial meningitis), normal or elevated CSF protein, and CSF gram stain or culture indicating the organism (in bacterial meningitis).
subarachnoid hemorrhage presentation
most common cause of a sudden, intense, incapacitating (“thunderclap”) headache. Many patients with SAH report their headache as the “worst headache of my life”. The pain is typically diffuse. Associated symptoms include neck stiffness, photophobia, nausea, vomiting, and neurologic signs on examination. Depressed arousal or obtundation is a common finding
subarachnoid hemorrhage mechanisms
Mechanisms include trauma, ruptured aneurysm and arteriovenous malformation. A sentinel headache may precede in aneurysms.
Diagnosis of subarachnoid hemorrhage
. An immediate CT scan is warranted in all cases of suspected SAH. A lumbar puncture is needed if SAH is suspected and the CT scan is negative, but sensitivity of an LP is potentially poor within the first few hours and becomes the most sensitive at 12 hours. Cerebral angiography is performed immediately to confirm the presence of an aneurysm or other vascular malformation
Giant cell arteritis population
affects elderly in 80-90, women and men equally
giant cell arteritis presentatioin
Associated symptoms include jaw claudication, temporal artery region scalp tenderness, blindness, joint pain, and constitutional symptoms such as fever, malaise, and weight loss.
giant cell arteritis diagnosis
Erythrocyte sedimentation rate and C-reactive protein are usually both elevated. Temporal artery biopsy
giant cell arteritis treatment
steroids- must do temporal artery biopsy within 7 days. High dose and > or = 1 year when vision loss is present
Describe symptoms that occurs with increased intracranial pressure
headache that occurs or worsens with exertion, retrobulbar pain, associated nausea and/or vomiting, pulsatile intracranial noises, transient visual obscurations, photopsias (flashes of light), diplopia, and vision loss. Headache that is worse upon awakening or awakens the patient from sleep is classically associated with increased ICP but is not always present in people with mild to moderate elevation of ICP.
signs that occur with elevated intracranial pressure
sixth nerve palsies from distention of the nerves in the subarachnoid space, papilledema (edema of the optic nerve), and vision loss from optic nerve dysfunction
What is idiopathic intracranial hypertension
aka pseudotumor cerebri. normal CSF constituents, normal neuroimaging, normal neurological examination except for papilledema and sixth nerve palsies, and no other causes to explain the increased ICP. Obesity is the most common risk factor and women are 9 times more likely to develop the disease than men.
