headache

Question 1

Recognize the epidemiological implications of headache

Answer 1

. Migraine is the third most common disease on the planet

Question 2

Know the difference between a primary and secondary headache syndrome

Answer 2

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.

Question 3

Which intracranial structures can “hurt”

Answer 3

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

Question 4

List most common primary headache syndromes

Answer 4

Tension type (93% one year prevalence), migrane (12% prevalence), and trigeminal autonomic cephalagias (<0.5% prevalance)

Question 5

List most common/threatening causes of secondary headache

Answer 5

meningitis, hemorrhage (subarachnoid, subdural, epidural), intracranial hypertension (idiopathic, brain tumor, brain abscess), and giant cell (temporal) arteritis

Question 6

HIS criteria for migraine

Answer 6

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.

Question 7

Phases of a migraine

Answer 7

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

Question 8

Triggers for migraine

Answer 8

missed meals or lack of adequate sleep, alcohol consumption, caffeine withdrawal, perimenstruation, “relief” of stress, and certain food [MSG, nitrites (hot dogs), tyramine (cheese)].

Question 9

Migraine treatment - abortive

Answer 9

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).

Question 10

Migraine treatment - prophylactic and alternatives

Answer 10

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).

Question 11

Classifications for migraine aura

Answer 11

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.

Question 12

Migraine pathogenesis

Answer 12

. 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.

Question 13

HIS criteria for tension type headache

Answer 13

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

Question 14

Tension type headache treatment - not LO

Answer 14

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

Question 15

HIS criteria for cluster headache

Answer 15

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

Question 16

Who are more prone to cluster headaches

Answer 16

men (4:1 men to women)

Question 17

Triggers of cluster headaches

Answer 17

alcohol or drugs with vasodilator properties

Question 18

Therapy of cluster headaches - no a LO

Answer 18

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

Question 19

What is unique about trigeminal neuralgia

Answer 19

can be primary or secondary headahce

Question 20

Trigeminal neuralgia HIS criteria

Answer 20

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

Question 21

secondary causes of trigeminal neuralgia

Answer 21

vascular compression (by a tortuous artery) of the trigeminal nerve or by demyelination of the trigeminal nerve within the pons (i.e. multiple sclerosis)

Question 22

treatment of tigeminal neuralgia- not a LO

Answer 22

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.

Question 23

Clinical presentation of head injury with headache

Answer 23

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.

Question 24

clinical presentation of meningitis

Answer 24

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).

Question 25

What is kernig and brudzinski signs

Answer 25

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

Question 26

Diagnosis of meningitis

Answer 26

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).

Question 27

subarachnoid hemorrhage presentation

Answer 27

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

Question 28

subarachnoid hemorrhage mechanisms

Answer 28

Mechanisms include trauma, ruptured aneurysm and arteriovenous malformation. A sentinel headache may precede in aneurysms.

Question 29

Diagnosis of subarachnoid hemorrhage

Answer 29

. 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

Question 30

Giant cell arteritis population

Answer 30

affects elderly in 80-90, women and men equally

Question 31

giant cell arteritis presentatioin

Answer 31

Associated symptoms include jaw claudication, temporal artery region scalp tenderness, blindness, joint pain, and constitutional symptoms such as fever, malaise, and weight loss.

Question 32

giant cell arteritis diagnosis

Answer 32

Erythrocyte sedimentation rate and C-reactive protein are usually both elevated. Temporal artery biopsy

Question 33

giant cell arteritis treatment

Answer 33

steroids- must do temporal artery biopsy within 7 days. High dose and > or = 1 year when vision loss is present

Question 34

Describe symptoms that occurs with increased intracranial pressure

Answer 34

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.

Question 35

signs that occur with elevated intracranial pressure

Answer 35

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

Question 36

What is idiopathic intracranial hypertension

Answer 36

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.