89. Headache Disorders Flashcards

(104 cards)

1
Q

What is a migraine?

A

recurrent attacks of severe headache, autonomic nervous system dysfunction, and, in some patients, an aura causing visual, sensory, motor, or other neurologic symptoms. It is a primary headache disorder with a genetic basis.

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2
Q

What are demographics of people who tend to get migraines?

A

attacks typically begin in the sec- ond decade of life and peak in prevalence in the fourth decade, affect- ing about 1 of 4 women and 1 of 12 men

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3
Q

What is the pathophysiology of migraines?

A

abnormal trigeminal nerve and thalamic activity, possibly triggered by a sterile neuropeptide-induced inflammatory process, leads to activity and sensitization of higher order neurons in the brainstem and thalamus. Descending modulation is likely to be compromised as well

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4
Q

What is the mechanism behind migraine aura?

A

Cortical spreading depression, a neuro- electrical event characterized by a slow wave of depolarization

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5
Q

What is the defn of a migraine?

A

chronic and recurrent disease with a gradual onset of a unilateral pulsatile headache moderate to severe in intensity, exacerbated by routine activities
- lasts 4-72h

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6
Q

List 4 primary migraines via the international headache society classification of headaches

A
  1. Migraine
  2. Tension-typeheadache
  3. Cluster headache and trigeminal autonomic cephalalgias
  4. Other primary headaches
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7
Q

List 5 secondary migraines via the international headache society classification of headaches

A
  1. Headache attributed to trauma or injury to the head or neck
  2. Headache attributed to cranial or cervical vascular disorder
  3. Headache attributed to nonvascular intracranial disorder
  4. Headache attributed to a substance or its withdrawal
  5. Headache attributed to infection
  6. Headache attributed to disorder of homeostasis
  7. Headache or facial pain attributed to disorder of cranium, neck, eyes,
    ears, nose, sinuses, teeth, mouth, or other facial or cranial structures
  8. Headache attributed to psychiatric disorder
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8
Q

List the A-E criteria of migraine without aura

A

A. At least five attacks fulfilling criteria in B, C, D, and E
B. Attack lasts 4 to 72 hours (untreated or unsuccessfully treated) C. Headache has at least two of the following characteristics:
1. Unilateral location
2. Pulsating quality
3. Moderate to severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity (e.g.,
walking or climbing stairs)
D. During headache, at least one of the following:
1. Nausea or vomiting (or both)
2. Photophobia and phonophobia
E. Not attributable to another disorder

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9
Q

List the A-E criteria of migraine WITH aura

A

A. At least two attacks that fulfill criterion B
B. Presence of at least three of the following four characteristics for a diag-
nosis of classic migraine:
1. One or more fully reversible aura symptoms indicating focal cerebral
cortical or brainstem dysfunction (or both)
2. At least one aura symptom developing gradually over more than 4 min-
utes, or two or more symptoms occurring in succession
3. No single aura symptom lasting longer than 60 minutes
4. Headache beginning during aura or afterward, with a symptom-free
interval of less than 60 minutes (also may begin before aura)
C. Exclusion of related organic diseases by means of an appropriate history, physical examination, and neurologic examination with appropriate diag-
nostic tests

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10
Q

How many migraines per month does it take to consider being chronic?

A

15

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11
Q

What is the mc aura and what might it include?

A

visual; features may include scintillating sco- toma (bright rim around an area of visual loss), teichopsia (subjective visual image perceived with eyes open or closed), fortification spectra (zigzagged lines that slowly drift across the visual field), photopsias (poorly formed brief flashes or sparks of light), and blurred vision

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12
Q

What is a retinal migraine?

A

are syndrome consisting of recurrent attacks of monocular visual dysfunction, including positive features (such as scintillations) or negative features (such as blindness). As with aura, these symptoms are completely reversible.

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13
Q

What is the classic presentation of a hemiplegic migraine?

A

characterized by a motor aura consisting of hemiparesis or hemiplegia. The progression of the motor deficit is gradual and, in most cases, is accompanied by a visual, sensory, or speech disturbance. The neurologic symptoms last up to 60 minutes, followed by headache

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14
Q

What is a migraine with brainstem aura?

A

aura referable to the brainstem. Common neurologic findings include dysarthria, tinnitus, vertigo, diplopia, and altered level of consciousness.

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15
Q

What is the defn of status migrainosus?

A

severe unremitting migraine headache that persists unabated for more than 72 hours.

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16
Q

Name 5 factors that can trigger migraine?

A

sleep deprivation, stress, hunger, hormonal changes, including menstruation, and use of certain drugs, including oral contraceptives and nitroglycerin. In addition, some patients report specific food sensitivities to chocolate, caffeine, and foods rich in tyramine, monosodium glutamate, and nitrates. Alcohol, specifically red or port wine, has also been implicated. In others, cer- tain sensory stimuli, such as a strong glare or strong odors, loud noises, and weather changes, can trigger an attack.

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17
Q

Which patients with migraine should consider getting a ct?

A

older or immunocompromised patients with new-onset headaches, headaches associated with unexplained neurologic abnormalities, and new head- aches with an abrupt onset

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18
Q

What are 5 oral migraine medications and doses?
- list 1 SE/consideration per

A

Ibuprofen
400 mg PO
Gastrointestinal upset
Naproxen sodium
500 mg PO
Gastrointestinal upset
Acetaminophen + metoclopramide
650 mg + 10 mg PO
Combination therapy has better efficacy than acetaminophen alone
Sumatriptan
50–100 mg PO
Use cautiously in patients with cardiovascular risk factors
Eletriptan
40 mg PO
Use cautiously in patients with cardiovascular risk factors
Ubrogepant
50–100 mg
may cause transaminitis

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19
Q

What are 3 FIRST-line parenteral migraine medications and doses?
- list 1 SE/consideration per

A

Prochlorperazine
10 mg IV
Sedation and dystonic reaction
Metoclopramide
10 mg IV
Dystonic reaction
Droperidol
2.5 mg IV
QT prolongation; dystonic reaction
Ketorolac
15 mg IV or 15 mg IM
Gastrointestinal upset; avoid this medication in elderly patients and in patients with renal insufficiency
Sumatriptan
6 mg SC
Chest pain, throat tightness, flushing
Contraindicated with hypertension, coronary artery disease,
peripheral vascular disease, and pregnancy Cannot be used within 24 hours of ergot use

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20
Q

What are 2 second-line parenteral migraine medications and doses?
- list 1 SE/consideration per

A

Dihydroergotamine (DHE)
1 mg IV or IM; may be repeated in 1 hour
Nausea (pretreat with antiemetic)
Often causes chest pain
Caution in inhibitors of enzyme CYP450 3A4
Magnesium sulfate
2 g IV
More efficacious in migraine with aura

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21
Q

What is a procedure one may consider for migraine?

A

greater occipital nerve with 6ml bupivicaine 0.5% inj bilaterally

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22
Q

What additional medication for migraine may be considered in pt with recurrence?

A

dex 10mg IV

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23
Q

Describe how to complete a greater occipitial nerve block for migraine

A

injector identified the appropriate location using landmarks on the patient’s head. The medial landmark was the occipital protuberance. The lateral landmark was the mastoid process. Using these landmarks to form a line, the injector identified the correct location, which was one-third of the distance from the occipital protuberance along this line (two-thirds of the distance away from the mastoid process). The injector felt for pulsation of the occipital artery and attempted to elicit pain or paresthe- sia in the distribution of the GON by pressing slightly. The injector then used a fan technique, placing 1 mm of anesthetic at the correct spot, 1 mm slightly medial of the correct spot, and 1 mm slightly lateral to the correct spot.

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24
Q

What are common side effects of triptans

A

tingling, flushing, warm or hot sensations, heaviness in the chest, and initial worsening of the underlying headache

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25
Who CANNOT have sumatriptan?
coronary artery disease and should not be used within hours of administration of an ergotamine containing meds
26
Which patients tend to get cluster headaches
men >wo smoke almost always pre age 50 defined time interval (can last wk - mo) precipated by etoh
27
What is the pathophys of a cluster headache?
abnormal activation of the trigeminal nerve contrib- utes to headache nociception. Typically, secondary parasympathetic activation causes ipsilateral lacrimation and rhinorrhea, a characteris- tic of cluster headache syndrome.
28
Cluster headache duration
multiple episodes can occur within a 24-hour period. Each headache lasts from 15 minutes up to 3 hours, with a mean duration of about two hours.
29
Cluster headache classic sx
unilateral sharp, stabbing pain in the eye, which may awaken the patient from sleep. The attacks occur exclusively in the territory of the trigeminal nerve. Unlike the patient with migraine, the patient with cluster headache presents agitated and anxious, rocking, rubbing the head, and pacing. The attack subsides rapidly, often leaving the patient exhausted. Accompanying the headache are ipsilateral autonomic symptoms, such as ptosis, miosis, and forehead or facial sweating. The eye often is injected and tearing, and many patients have unilateral nasal conges- tion or rhinorrhea.
30
Acute first line tx of cluster headache
First-Line Sumatriptan 6 mg SQ Oxygen At least 6–12 L/ min until h/a gone
31
Second line tx of cluster headache
Octreotide 100 micrograms SQ GI symptoms Metoclopramide 10 mg IV Dystonic reaction
32
Discharge tx consideration for cluster headache pt
Dexamethasone 10 mg IM or IV Most efficacious dose unknown, some notes also say 10d predn taper starting with 60mg for at least 2d Verapamil 240–480 mg/day PO in 2–4 divided doses May cause constipation, use cautiously if BP or HR are low Melatonin 10 mg qHS Well tolerated
33
Name 3 ddx for cluster headache?
carotid a dissection trigeminal neuralgia rare trigeminal autonomic cephalagias
34
Carotid a dissection vs cluster headache considerations?
CA diss: particu- larly neck pain, Horner syndrome, or unilateral neurologic deficit, should undergo neurovascular imaging
35
Describe clinical features of a tension headache
tight, bandlike discomfort or pressure around the head that is nonpulsating and dull. They also may experi- ence tightening of the neck muscles. headache does not worsen with physical activity, and accompanying symptoms (such as nausea, vomiting, phonophobia, and photophobia)
36
Why do most pt get headache and meningismus in SAH?
activation of meningeal nociceptors
37
What are mc nontraumatic SAH cause?
ruptured saccular/berry aneurysm (sm <15mm) near or at major junction of cerebral vessels (particularly circle of Willis)
38
If not a saccular aneurysm, what are the other 20% in nontraumatic SAH?
posterior circ - basilar a
39
What is perimesencephalic hemorrhage? How is it treated?
a benign form of SAH, in which a localized hemorrhage occurs anterior to the midbrain, with- out extension, and with no vascular abnormalities on cerebral vascular imaging. These hemorrhages resolve spontaneously and do not require intervention.
40
List 5 RF for aneursymal SAH
age (typ 40-60) rate of growth of the aneurysm and increases with aneurysmal size hypertension, smoking, excessive alcohol consumption, and use of sympathomimetic drugs. Both genetic and familial associations of cerebral aneurysms Marfan, Ehlers Danlos syndrome type IV/CTD AD polycystic kidney disease Coarctation of aorta
41
Headaches that peak over __ mins tend not to be SAH
60 mins
42
What are the 6 grades and condition of the Hunt and Hess Clinical Grading Scale for Cerebral Aneurysms and SAH
0 Unruptured aneurysm 1 Asymptomatic or minimal headache and slight nuchal rigidity 2 Moderate or severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy 3 Drowsiness, confusion, or mild focal deficit 4 Stupor, moderate to severe hemiparesis 5 Deep coma, decerebrate posturing, moribund appearance
43
List the 6 comonents of the Ottawa Subarachnoid clinical decision rule
Age ≥ 40 years Neck pain or stiffness Loss of consciousness Onset during exertion Thunderclap (instantly peaking) headache Limited neck flexion on examination
44
What is the Hunt and Hess scale used for in pt with SAH
stratifies pt according to clinical sx and signs at presentation, predictive of outcome ie 1-2 good px; grade 4-5 do poorly; 3 are just at risk for clinical deterioration
45
What is the ddx for SAH
cervical artery dissection (CAD), cere- bral venous thrombosis (CVT), reversible cerebral vasoconstriction syndrome, hemorrhagic or ischemic stroke, and primary headache disorders, including migraine and cluster headache
46
Sn and sp of Ottawa SAH rule
high (near 100%) sensitivity is achieved, but with low (less than 20%) specificity.
47
Diagnostic imaging for SAH suspected
acute hemorrhages less than 24 hours old, the sensitivity of third-generation multidetector row CT scanners in identifying hemorrhage is greater than 90%; however, sensitivity decreases to approximately 50% by the end of the first week, as blood is resorbed. ensitivity of non–contrast- enhanced head CT performed within 6 hours of headache onset approaches 100%
48
When to LP in determing SAH
patient preference, local availability, and what else is on the differen- tial diagnosis. xanthochromia secondary to metabolism of hemoglobin to pigmented oxyhbg and bilirubin - which takes 12h to go SAH cannot be ruled out if a substantial number of RBCs persist in tube 4; however, an RBC count of less than 100 in tube 4 indicates that aneurysmal SAH does not need to be pursued further
49
What ecg findings can you see with SAH? List 4
cardiac arrh Typical electrocardiographic findings include ST-T wave changes, U waves, and QT prolongation.
50
Management of SAH
1. airway management of hunt and hess 3 or more 2. sbp <160 or map 95-130 (labetalol, nicardipine 60mg po/ng q4h if high) 3. antinausea prn 4. agitated - sedate fentanyl/midaz 5. seizure - keppra 6. definitive: endovascular coil embolization vs neurosurg clip
51
name 5 of the most common types of intracranial malignancy causing headache
Metastatic: Breast Lung Gastrointestinal Melanoma Meningioma Glioblastoma Primary CNS lymphoma Pituitary adenoma
52
Clinical features of an intracranial neoplasm causing headache:
present for weeks to months. The headache may have been present initially only on awak- ening (most likely in patients with increased ICP), gradually becoming continuous. The classic triad of brain tumor headache—sleep distur- bances, severe pain, and nausea and vomiting any valsalva makes it worse
53
If there is ICP in an intracranial neoplasm, what med tends to be given?
dex 10mg IV then 4mg q6h
54
What is giant cell arteritis?
inflammatory vasculopathy that occurs in medium and large arteries with well-developed wall layers and adventitial vasa vaso- rum. It typically involves the major branches of the aorta and has a predilection for the extracranial branches of the carotid artery (e.g., temporal and occipital arteries). It can involve the ophthalmic, verte- bral, and distal subclavian arteries,
55
Who tends to get GCA?
wo mean age 71 (so think of if over 50)
56
Why does GCA occur?
inflammatory infiltrate in the arterial wall resulting in intimal hyperplasia and subsequent stenosis and occlusion, leading to a variety of ischemic complications
57
Why does GCA needed to be tx (ie feared complication of undiagnosed)
loss of vision is due to anterior ischemic optic neuropathy.
58
Physical exam findings consistent with GCA
Headache is the most common initial manifestation and occurs in more than 70% of patients. The headache often is of 2 to 3 months’ duration and can be continuous or intermittent; it can worsen at night or on exposure to cold. The pain may be described as sharp, throbbing, boring, or aching and usually is localized to the temporal region but may occur anywhere in the head. The physical examination may reveal tenderness over the scalp in the area of the temporal artery, with exacerbation of the pain by wearing a hat or resting the head on a pillow. Patients also can experience jaw claudication secondary to vascular insufficiency of the masseter and temporalis muscles. Systemic signs and symptoms are often present, including fever, anorexia, and weight loss. Approximately 40% of patients develop symptoms of polymyalgia rheumatica, pain in their large proximal joints,
59
List the diagnostic criteria for GCA (box 89.6)
Age ≥ 50 years old New headache type, particularly in association with visual loss or jaw clau- dication Temporal artery tenderness or tenderness of other extracranial arteries ESR ≥ 50 mm/h or CRP ≥ 10 mg/L Positive imaging finding or temporal artery biopsy
60
What vision issue can occur in GCA before A ION
amarosis fugax
61
List 4 complications of GCA
amarosis fugax AION peripheral neuropathies, transient isch- emic attacks, and stroke.
62
What is a marcus - gunn pupil and increases concern for GCA?
elative afferent pupillary defect
63
DDX of GCA
Takayasu arteritis can affect the aorta and its primary branches as well, but it affects younger patients and visual loss is uncommon. Polyarteritis nodosa, microscopic polyangiitis, and granulomatosis with polyangiitis (formerly known as Wegener gran- ulomatosis) can rarely affect the temporal artery but have different histopathology and vascular involvement. Ischemic stroke can cause headache with visual loss or amaurosis fugax. Pituitary apoplexy clas- sically presents with thunderclap headache and bitemporal visual field loss.
64
Tx of GCA
we recommend methylprednisolone 1000 mg per day for 3 consecutive days to optimize immunosuppression and sup- press tissue edema. For patients without visual symptoms, lower doses of steroids, in the range of 40 to 60 mg/day of prednisone should be used.
65
What med might be given in outpt setting to pervent relapse of GCA during steroid taper?
tocilizumab
66
What is the mc cause of ischemic stroke in pt <50 yoa?
cervical a dissection
67
What are risks/mechanisms related to carotid a dissection?
sudden neck movement or trauma preceding the event. Reported mechanisms include neck torsion, chiro- practic manipulation, coughing, minor falls, heavy lifting, various sports including basketball and volleyball, sexual intercourse, childbirth, and motor vehicle collisions.
68
What is the pathologic lesion in cervical a dissection?
intramurla hemorhage within media of arterial wall - The hematoma can be localized or extend circumferentially along the length of the vessel, resulting in partial or complete occlusion. Damage to the intima results in platelet aggregation and thrombus formation further compromis- ing vessel patency or causing distal embolization.
69
What is typical presentation signs and sx for cervical a dissection?
(1) unilateral headache or neck pain, sometimes radiating to the ipsilateral eye; (2) ipsilateral ptosis and miosis (a partial Horner syndrome) ; and (3) either blindness, due to retinal ischemia, or contralateral motor deficits, caused by cerebral ischemia. However, this complete triad is only present in a minority of patients.
70
What factors are associated with worse carotid a dissection prognosis? List 3
older age, occlusive disease on angiography, and stroke as the initial presenting symptom.
71
What is the classic presentation of a vertebral a dissection?
relatively young person with severe, unilateral posterior headache and a rapidly progressive neurologic deficit with symptoms of brainstem and cerebellar ischemia. Common findings include vertigo, severe vomiting, ataxia, diplopia, hemiparesis, unilateral facial weakness, and tinnitus.
72
Compared to carotid a dissection, is vertebral a dissection rare or common?
rare
73
What is the prognosis for vertebral a dissection?
Approximately 10% of patients who develop a vertebral dissection die during the acute phase, secondary to mas
74
What is the preferred imaging for carotid a and vertebral a dissection?
CTA
75
Patients with cervical a dissection presenting as ischemic troke are considered candidates (most of the time) for what two possible therapies?
thrombolytic therapy endovascular thrombectomy
76
For pt with cervical a dissection without acute ischemic stroke signs what is tx?
Antiplatelet agents including aspirin, clopi- dogrel, or dipyridamole, and anticoagulation with unfractionated or low–molecular-weight heparin
77
List 5 RF for cerebral venous thrombosis
Classically linked to the Virchow triad of blood stasis, blood vessel wall abnor- malities, and a hypercoagulable state. Both genetic and acquired prothrombotic conditions have been associated with CVT. Inherited thrombophilias such as antithrombin III, protein C and protein S defi- ciencies, and factor V Leiden mutation are the most common genetic causes. Acquired causes for CVT include pregnancy and the puerpe- rium, malignancy, head trauma, surgery, parameningeal infections, and exogenous hormones, such as oral contraceptives. Other causes include systemic inflammatory disorders, including vasculitis, inflam- matory bowel disease and connective tissue disorders, and neurosur- gical procedures.
78
What two "types" of findings are classic for cerebral venous trhombosis:
1) Those that are related to increased ICP due to impaired venous drainage, and (2) those related to focal brain injury from venous occlusion resulting in ischemia, infarction, or hemorrhage.
79
List 5 possible findings in pt with CVT
diffuse headache increasing over days to weeks mc sx focal neuro findings seizure ocular: orbital pain, proptosis, chemosis, EOM paralysis, papilledema
80
Recommended testing when considering CVT
cbc chem esr clotting studies - pt, ptt ddimer MRA vs MRI best but typically CTA and CTV faster to get
81
Tx for CVT
anticoagulated. with unfractionated heparin or w based LMWH tx seizure with antiepileptic drug as required tx underlying etiology for thrombus if possible
82
What is idiopathic IC HTN?
een primarily in young, obese women of childbearing age - unclear mechanism but perhaps imbalance between csf production and reabsorption
83
Idiopathic IC HTN: RF list 3
including anti- biotics (most commonly tetracyclines), vitamin A and retinoids, and human growth hormone. yo female obesity
84
What is the diagnostic criteria for IIH
Headache that remits with normalization of CSF pressure *worsened with valsalva Papilledema (may not be appreciable in all patients) May have CN VI palsy Increased CSF opening pressure: >250 mm in adults; >280 mm in children Normal CSF diagnostic studies Normal neuroimaging studies No other cause of increased ICP identified
85
What are ultrasound findings consistent with IIH?
diameter of the optic nerve sheath, 3 mm behind the optic disc, is consistent with elevated intra- cranial pressure if greater than 5 mm.
86
CSF findings sp to IIH: adult vs child
If neuroimaging is normal, an LP should be performed in the lateral decubitus position to measure CSF opening pressure and to obtain CSF diagnostic studies. An opening pressure of 250 mm H2O or more (normal is 70 to 180 mm H2O) is necessary to make the diagnosis. child >280mm
87
Tx for IIH
actually may not feel better with significant csf removal nsaids antidopa med - metoclopramide visual field loss - acetazolamide 250-500mg bid if not improving with this, consider optic nerve sheath decompression or csf diversion procedure
88
What is the probable csf pathophysiology in a low csf pressure/post dural puncture headache?
persistent CSF leak that exceeds CSF production, resulting in CSF hypotension. If sufficient CSF is lost, the brain descends in the cranial vault when the patient assumes the upright posi- tion, leading to increased traction on the pain fiber
89
What things actually reduce post dural puncture headache?
noncutting needle use likea whitaker or sprotte postulated bevel up in LLDP LP, 20-22g needle use
90
What are cardinal features of post LP headache?
rthostatic or positional headache that is precipitated by the upright position and relieved when the patient lies down. About 90% occur within the first 72 hours after the LP and typically resolve within 1 week, though headaches may persistent for months.
91
What are possible tx options for post dural puncture headaches?
bed rest, hydration and analgesia within 5-7d if not: methylxanthine agents (such as caffeine 500 mg IV drip over 1 hour) and corticosteroids may be of benefit. For severe headaches that do not respond to these conservative measures, an epidural blood patch (EBP) should be used. This procedure involves the injection of 15 to 30 mL of autologous blood into the epidural space near the site of the original dural puncture resulting in a blood clot that seals off the dural hole.
92
What is the mc sx following concussion/tbi?
headache
93
What is the defn of post traumatic headache?
PTH develops within 7 days of the injury or regaining consciousness. Acute PTH resolves within 3 months, whereas persistent PTH persists beyond 3 months.
94
What are two hypertensive headaches you should worry about?
preeclampsia *>20 weeks, proteinuria posterior reversible encephalopathy syndrome *abnormal MRI white matter changes hypertensive emergency ICH - abnormal neuroimaging
95
What is reversible cerebral vasoconstriction syndrome (RCVS)?
cerebral arteriopathy characterized by segmental areas of vasoconstriction within large- and medium-sized vessels. RCVS causes recurrent thun- derclap headache in susceptible patients and may cause ischemic or hemorrhagic stroke
96
What are the clinical features of RCVS?
thunderclap headache abrupt severe robbing and associated with nausea, vomiting, and photophobia. The headache may be provoked by use of vasoactive medications or substances such as recreational sym- pathomimetics or nasal decongestants
97
Recommended diagnostic testing for RCVS
ct lp to r/o sah repeat neurovascular imaging/angio if recurs
98
Tx of RCVS
prevention of ischemic and hemorrhagic stroke and elimination of headache. To date, the natural history of this disorder is incompletely understood. Treatment with calcium channel blockers, such as nimodipine 30 to 60 mg PO q4h, has been described and we recommend that it be offered to patients with progressive or refractory symptoms.
99
DDX "thunderclap" headache - list 5
SAH RCVS CVT cervical a dissection hemorrhagic stroke pituitary apoplexy post coital headache
100
A 29-year-old female presents within 1 hour of the sudden onset of a severe, diffuse headache accompanied by meningismus and vomiting. Emergent computed tomography (CT) scan is negative. Lumbar puncture (LP) reveals 50,000 red blood cells (RBCs) in tube 1 and 30,000 RBCs in tube 4. Opening pressures are normal, and the sample is negative for xanthochromia. What would be the most appropriate next step? a. Admission and observation b. Cerebrovascular imaging study c. Hydration,analgesics d. Magnetic resonance imaging (MRI) scan with gadolinium
B
101
A 69-year-old male presents with several months of intermittent left-sided headaches that have been worse at night and occasion- ally on exposure to cold air. On several occasions, he has noted increased pain while eating. He has had no other symptoms other than modest fatigue. Physical examination is unremarkable with normal vital signs and ophthalmologic and neurologic survey. Lab- oratory evaluation shows only a mild anemia, with a hemoglobin of 11 mg/dL and normocytic indices. What would be the most appro- priate next step? a. Computed tomography (CT) scan of the brain b. Electrocardiogram c. Erythrocyte sedimentation rate (ESR) d. Neurology consultation
C
102
With cavernous sinus thrombosis, the clinical picture is usually dominated by which of the following? a. Facialpain b. Lethargy c. Nausea and vomiting d. Ocular findings such as pain and proptosis
D
103
A 28-year-old man with a history of migraine and no other med- ical history presents with a pounding, bilateral 9/10 headache associated with nausea and vomiting that has lasted for 48 hours. The patient reports experiencing a similar headache about once every few months. Physical exam is noteworthy for a blood pres- sure of 180/110 mm HG in his right arm and 178/111 mm HG in his left arm. Physical exam, including a detailed neurologic exam, is otherwise completely normal. The most appropriate first step in the management of this patient is the following: a. Non-contrast CT scan of the head b. Metoclopramide 10 mg IV c. Labetalol 20 mg IV d. CT angiography of the head and neck
B
104
An obese 37-year-old female reports worsening headache × 3 months, which first responded to ibuprofen but now no longer does. The headache is bilateral, pulsating, associated with nausea, and improves when she assumes an upright position. She reports 5-second blackouts of her vision, which occur occasionally when she changes position. A neurologic exam is unremarkable. Retinal exam is deferred because of marked photophobia. Non-contrast head CT scan is normal. The most appropriate next step in the diag- nostic workup is: a. MRV b. D-dimer c. CTangiography d. Lumbar puncture
D