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Casey: Neurology > Handler Lectures > Flashcards

Handler Lectures Flashcards

1
Q

Migraine, tension, cluster, & chronic daily headache=

A

primary headache

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2
Q

Post-traumatic, e.g post concussion; space occupying lesions (tumors); HA associated with CVD; hypertensive encephalopathy=

A

secondary headache

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3
Q

2nd MC HA disorder; May cause motion sickness with N/V; Worse w/ physical activity; post-consumption of small amounts of colored wine or liquor

A

Migraine HA

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4
Q

End pathway- activation of afferent sensory fibers that innervate meningeal and/or cerebral blood vessels; fibers arise from the Trigeminal nerve (CN V)

A

Migraine HA

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5
Q

The brain activates or sensitized trigeminal nerve fibers wishing the meninges initiating the headache via neurogenic inflammation; the vascular changes that occur during the attack are the result of vascular inflammation

A

Neurogenic theory

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6
Q

A NT which activates pain fibers (brainstem) contributes to vasoconstriction and inflammation; the release of peptides and NT at trigeminal nerve branches lead to inflammation and vasodilation of meningeal and dural blood vessels

A

Serotonin (5-HT)

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7
Q

Abort HAs when taken early

A

Serotonin antagonists

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8
Q

Transient episodes of focal neurologic dysfunction that appear before the HA phase begins; these include expanding scotoma (blind spot) with scintillating margin (visual hallucinations), visual field defects, unilateral paresthesias, numbness, weakness, dysphasia

A

Migraine with AURA

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9
Q

Some of these suggest decreased blood flow in the distribution of the internal carotid artery, mimicking TIA’s

A

Aura

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10
Q

Contributed to by activation of a wave of electrical activity that spears throughout the brain, depressing cortical activity and resulting in visual and other symptoms; Initiated by the CNS. “Spreading depression of Lao” seen on PET scans

A

Aura

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11
Q

Prolonged aura with neurologic deficits lasting 1h-1 week; uncommon

A

Complex migraine

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12
Q

Can happen, but rare, there are permanent neuro deficits consistent with a localized stroke (w/ defect on CT or MRI)

A

Complex migraine

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13
Q

Potent serotonin agonist and vasoconstrictor

A

Ergotamine

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14
Q

Predominant serotonin receptors in the CNS; function as presynaptic auto receptors whose activation inhibits release of serotonin & related NTs that cause vasodilation, inflammation and pain

A

5-HT1 Receptors

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15
Q

Activation of these receptors in pial/dural vessels leads to vasoconstriction

A

5-HT1

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16
Q

Activation of these receptors in the brain stem may inhibit further activation of trigeminal neurons responsible for migraine attacks

A

5-HT1

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17
Q

A very potent NSAID that may be useful in preventing relapse of the acute headache

A

Indomethacin

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18
Q

Useful as migraine prophylaxis; drugs that cross BBB

A

Beta adrenergic blockers (propranolol & metoprolol) & Tricyclic antidepressants (amitriptyline, nortriptylene)

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19
Q

MC type of HA; poorly understood pathophys; includes vascular, muscular, and myofascial components

A

Tension headaches

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20
Q

Episodic and chronic forms; symmetric tightness/pressure; mild-moderate pain; DO NOT worsen with physical exertion, no N/V or other neuro symptoms

A

Tension headaches

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21
Q

AKA Migrainous neuralgia; 6x more common in males; likely vascular with activation of trigeminal-vascular system

A

Cluster headaches

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22
Q

Unilateral Horner’s syndrome (miosis, ptosis, anhydrosis); Recurrent episodes of intense unilateral orbital, supraorbital, or temporal head pain along with ipsilateral partial cervical sympathetic paralysis (conjunctival injection, lacrimation, rhinorrhea, nasal congestion, eyelid edema, loss of facial sweating

A

Cluster Headaches

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23
Q

Tx with 100% O2

A

Cluster Headaches

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24
Q

Any HA occurring >15 days/month (often for 3+ months); Develops over time in a pt with intermittent HA’s

A

Chronic Daily Headaches

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25
Q

Can cause HAs related to displacement of vascular structures

A

Intracranial Mass Lesions

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26
Q

Sxs: usually dull bifrontal or occipital HA that begin in morning; are worsened by exertion or postural change and may be associated with N/V; usually associated with other neurologic findings (generalized disturbance of cerebral function)

A

Intracranial Mass Lesions

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27
Q

50% of intracranial mass lesions are=

A

Gliomas

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28
Q

Signs= Neuro defects, papilledema, personality changes, intellectual decline, seizures and emotional lability

A

Intracranial mass lesions

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29
Q

Can cause brain herniation through tentorial hiatus d/t increased pressure, leading to stupor and coma often followed by death

A

Intracranial mass lesions

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30
Q

“Brain Attack”: The sudden or rapid onset of a neurological deficit in the distribution of a vascular territory lasting >24hrs

A

Stroke

31
Q

The sudden or rapid onset of a neurologic deficit in the distribution of a vascular territory lasting

A

TIA

32
Q

85% of strokes=

A

ischemia/infarct

33
Q

15% of strokes=

A

hemorrhage

34
Q

MC cause of death in pts with cerebrovascular disease=

A

myocardial infarction

35
Q

Most POWERFUL RF of a stroke=

A

HTN

36
Q

Pathological outcomes depend on: adequacy of collateral circulation, development of Circle of Willis, and duration of insult/restoration of blood flow

A

Stroke

37
Q

Major RF for a stroke; cardiac emboli

A

AFib

38
Q

With ischemic strokes, 50% of all strokes d/t=

A

atherosclerosis

39
Q

When a blood clot forms in an artery and stays in that same spot=

A

thrombus in situ

40
Q

Blood clot can form in carotid bifurcation and break off and move distally=

A

Embolus

41
Q

aka lipohyalinosis: small vessel disease; deep penetrating arterioles occlude/thrombose:

A

Lacunar infarcts

42
Q

Embolism rom heart or artery to the brain; important role in pathology of strokes and TIA’s; Blood clot breaks off, occludes more distant/distal vessel

A

Cerebral emboli

43
Q

Often lodge in medium sized vessels

A

Cerebral emboli

44
Q

~20% of ischemic strokes; AFib very common (importance of prevention with anticoagulation); MI, dilated cardiomyopathy

A

cardioembolism

45
Q

Stroke syndromes; contralateral hemiparesis or hemisensory loss; hemianopsia (visual field defect); if dominant hemisphere (aphasia), if non-dominant (speech preserved)

A

Middle cerebral artery (MCA)

46
Q

Stroke syndromes; less common; sxs more pronounced in leg, associated with language and gait disturbance

A

Anterior cerebral artery (ACA)

47
Q

Stoke syndromes; LEAST common; vertebral artery (branch of subclavian); crossed contralateral dysfunction (motor/sensory) plus ipsilateral bulbar/cerebellar signs: vertigo, dizziness, gait disturbance, diplopia, facial palsy, dysarthria

A

Posterior circulation

48
Q

HTN; deep penetrating arterioles (small vessels; small infarcts up to 1.5 cm on CT/MRI

A

Lacunar stroke/infarcts

49
Q

Carotid disease present; transient monocular blindness; embolism to ophthalmic artery (off of carotid)

A

Amaurosis fugal

50
Q

Most ACCURATE-invasive; “gold standard” or extra and intracranial disease; complications include contrast rxn, kidney failure, plaque rupture stroke.

A

Arteriography

51
Q

Abrupt onset of symptoms with transient focal neuro deficit dependent on involved anatomy (anterior, posterior circulation); sxs may vary during episodes; warning for subsequent stroke

A

TIA

52
Q

Etiology likely: embolic from carotid stenosis/plaque or embolic from cardiac source; severe carotid stenosis with transient hypotension; small vessel occlusion

A

TIA

53
Q

Removes plaque; best results if SYMPTOMATIC blockage and >70% stenosis; significantly reduces risk of subsequent ipsilateral stroke; risks include stroke and complications of surgery

A

Carotid endarterectomy

54
Q

These agents prevent platelet aggregation and release of vasoactive substances like thromboxaneA2

A

Anti-platelet agents

55
Q

Inhibits cyclooxygenase and synthesis of thromboxaneA2, decreasing both platelet aggregation and vasoconstriction; 325mg daily (GI SE and bleeding); decreases frequent of TIA’s and risk of subsequent stroke

A

Aspirin

56
Q

75mg/day; inhibits platelet aggregation and prevents activation of glycoprotein IIb/IIIa (a fibrinogen binder); decreases atherosclerotic events; for pts with recurrent TIA’s or ASA intolerance/allergy

A

Clopidogrel (Plavix)

57
Q

Thrombotic or embolic occlusion of major vessel; tx dependent on timing! MUST FIRST obtain head CT to r/o hemorrhage; if onset of symptoms thrombolytic therapy with t-PA o

A

Cerebral infarct

58
Q

Loose mesh stent placed in thrombus obstructing cerebral vessel-removes thrombus and restores blood flow

A

Solitaire FR Revascularization device

59
Q

Indicated if: embolus from heart (stroke or TIA); or A Fib >72hrs; risk is cerebral hemorrhage; must do CT to r/o hemorrhage before use

A

Full anticoagulation

60
Q

Used for immediate and short term anticoagulation (days); Work by inhibiting the ACTION of clotting factors

A

Heparin

61
Q

LONG TERM oral anticoagulation; inhibits PRODUCTION of clotting factors in liver; decr subsequent stroke risk; monitored by INR

A

Warfarin

62
Q

Intracerebral (HTN, AVM, and Trauma); Subarachnoid space (aneurysm, AVM); CT scan diagnostic; spinal tap if CT negative to r/o SAH

A

Hemorrhagic stroke

63
Q

Rupture of small arteritis or micro aneurysms of the perforating vessels ; HTN major RF; hematologic and bleeding disorders; trauma, anticoagulant therapy, liver disease

A

Intracerebral hemorrhage

64
Q

RAPID evolution of euro deficit often progressing to hemiparesis, hemiplegia or hemisensory loss; 50% mortality; LOC in 50%; Vomiting and HA common

A

intracerebral hemorrhage

65
Q

Tx is by surgical decompression (limited usefulness)-best in cerebellar bleeds

A

Hemorrhagic stroke

66
Q

Most d/t bleeding from SACCULAR ANEURYSMS; highest risk if >6mm; SUDDEN onset of severe HA followed by N/V, impaired or LOC, +/- neuro deficit; Meningeal signs often present (KERNIGS AND BRUDZINSKI SIGNS)*

A

Subarachnoid Hemorrhage (SAH)

67
Q

If this is suspected and CT is negative, do CSF tap and look for blood or xanthochromia

A

SAH

68
Q

MC vascular malformation of CNS often involving MCA and branches; tangled web of arteries connected directly to veins (congenital); angiography necessary to dx (CT may confirm hemorrhage); Tx with surgery

A

Arterial venous malformations (AVM)

69
Q

Stroke syndromes: occlusion often means embolus from carotid artery or heart (LV); degree of damage can vary depending on collaterals and whether occlusion is at proximal MCA or one of it’s 2 major divisions

A

MCA

70
Q

Contralateral hemiplegia (arm/face>leg) + hemianesthesia; gaze preference towards infarcted side of brain

A

MCA

71
Q

If located in DOMINANT hemisphere: global aphasia (involves both receptive and motor areas)

A

MCA

72
Q

If located in NON-DOMINANT hemisphere: anosognosia (denial/neglect and unawareness of the euro deficit) constructional apraxia (unable to draw or construct 2 or 3D figures)

A

MCA

73
Q

Abulia (slowness to respond), lack of spontaneous movement +/- confusion; impairment of gait and stance (gait apraxia); behavioral changes, memory disturbance; urinary incontinence

A

ACA occlusion DISTAL to anterior communicating artery (acoma)

74
Q

Occlusion of single vertebral after often asymptomatic if COW intact

A

Posterior circulation stroke

Casey: Neurology (7 decks)

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