Handler Lectures Flashcards
Migraine, tension, cluster, & chronic daily headache=
primary headache
Post-traumatic, e.g post concussion; space occupying lesions (tumors); HA associated with CVD; hypertensive encephalopathy=
secondary headache
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
Migraine HA
End pathway- activation of afferent sensory fibers that innervate meningeal and/or cerebral blood vessels; fibers arise from the Trigeminal nerve (CN V)
Migraine HA
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
Neurogenic theory
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
Serotonin (5-HT)
Abort HAs when taken early
Serotonin antagonists
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
Migraine with AURA
Some of these suggest decreased blood flow in the distribution of the internal carotid artery, mimicking TIA’s
Aura
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
Aura
Prolonged aura with neurologic deficits lasting 1h-1 week; uncommon
Complex migraine
Can happen, but rare, there are permanent neuro deficits consistent with a localized stroke (w/ defect on CT or MRI)
Complex migraine
Potent serotonin agonist and vasoconstrictor
Ergotamine
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
5-HT1 Receptors
Activation of these receptors in pial/dural vessels leads to vasoconstriction
5-HT1
Activation of these receptors in the brain stem may inhibit further activation of trigeminal neurons responsible for migraine attacks
5-HT1
A very potent NSAID that may be useful in preventing relapse of the acute headache
Indomethacin
Useful as migraine prophylaxis; drugs that cross BBB
Beta adrenergic blockers (propranolol & metoprolol) & Tricyclic antidepressants (amitriptyline, nortriptylene)
MC type of HA; poorly understood pathophys; includes vascular, muscular, and myofascial components
Tension headaches
Episodic and chronic forms; symmetric tightness/pressure; mild-moderate pain; DO NOT worsen with physical exertion, no N/V or other neuro symptoms
Tension headaches
AKA Migrainous neuralgia; 6x more common in males; likely vascular with activation of trigeminal-vascular system
Cluster headaches
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
Cluster Headaches
Tx with 100% O2
Cluster Headaches
Any HA occurring >15 days/month (often for 3+ months); Develops over time in a pt with intermittent HA’s
Chronic Daily Headaches
Can cause HAs related to displacement of vascular structures
Intracranial Mass Lesions
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)
Intracranial Mass Lesions
50% of intracranial mass lesions are=
Gliomas
Signs= Neuro defects, papilledema, personality changes, intellectual decline, seizures and emotional lability
Intracranial mass lesions
Can cause brain herniation through tentorial hiatus d/t increased pressure, leading to stupor and coma often followed by death
Intracranial mass lesions
“Brain Attack”: The sudden or rapid onset of a neurological deficit in the distribution of a vascular territory lasting >24hrs
Stroke
The sudden or rapid onset of a neurologic deficit in the distribution of a vascular territory lasting
TIA
85% of strokes=
ischemia/infarct
15% of strokes=
hemorrhage
MC cause of death in pts with cerebrovascular disease=
myocardial infarction
Most POWERFUL RF of a stroke=
HTN
Pathological outcomes depend on: adequacy of collateral circulation, development of Circle of Willis, and duration of insult/restoration of blood flow
Stroke
Major RF for a stroke; cardiac emboli
AFib
With ischemic strokes, 50% of all strokes d/t=
atherosclerosis
When a blood clot forms in an artery and stays in that same spot=
thrombus in situ
Blood clot can form in carotid bifurcation and break off and move distally=
Embolus
aka lipohyalinosis: small vessel disease; deep penetrating arterioles occlude/thrombose:
Lacunar infarcts
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
Cerebral emboli
Often lodge in medium sized vessels
Cerebral emboli
~20% of ischemic strokes; AFib very common (importance of prevention with anticoagulation); MI, dilated cardiomyopathy
cardioembolism
Stroke syndromes; contralateral hemiparesis or hemisensory loss; hemianopsia (visual field defect); if dominant hemisphere (aphasia), if non-dominant (speech preserved)
Middle cerebral artery (MCA)
Stroke syndromes; less common; sxs more pronounced in leg, associated with language and gait disturbance
Anterior cerebral artery (ACA)
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
Posterior circulation
HTN; deep penetrating arterioles (small vessels; small infarcts up to 1.5 cm on CT/MRI
Lacunar stroke/infarcts
Carotid disease present; transient monocular blindness; embolism to ophthalmic artery (off of carotid)
Amaurosis fugal
Most ACCURATE-invasive; “gold standard” or extra and intracranial disease; complications include contrast rxn, kidney failure, plaque rupture stroke.
Arteriography
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
TIA
Etiology likely: embolic from carotid stenosis/plaque or embolic from cardiac source; severe carotid stenosis with transient hypotension; small vessel occlusion
TIA
Removes plaque; best results if SYMPTOMATIC blockage and >70% stenosis; significantly reduces risk of subsequent ipsilateral stroke; risks include stroke and complications of surgery
Carotid endarterectomy
These agents prevent platelet aggregation and release of vasoactive substances like thromboxaneA2
Anti-platelet agents
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
Aspirin
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
Clopidogrel (Plavix)
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
Cerebral infarct
Loose mesh stent placed in thrombus obstructing cerebral vessel-removes thrombus and restores blood flow
Solitaire FR Revascularization device
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
Full anticoagulation
Used for immediate and short term anticoagulation (days); Work by inhibiting the ACTION of clotting factors
Heparin
LONG TERM oral anticoagulation; inhibits PRODUCTION of clotting factors in liver; decr subsequent stroke risk; monitored by INR
Warfarin
Intracerebral (HTN, AVM, and Trauma); Subarachnoid space (aneurysm, AVM); CT scan diagnostic; spinal tap if CT negative to r/o SAH
Hemorrhagic stroke
Rupture of small arteritis or micro aneurysms of the perforating vessels ; HTN major RF; hematologic and bleeding disorders; trauma, anticoagulant therapy, liver disease
Intracerebral hemorrhage
RAPID evolution of euro deficit often progressing to hemiparesis, hemiplegia or hemisensory loss; 50% mortality; LOC in 50%; Vomiting and HA common
intracerebral hemorrhage
Tx is by surgical decompression (limited usefulness)-best in cerebellar bleeds
Hemorrhagic stroke
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)*
Subarachnoid Hemorrhage (SAH)
If this is suspected and CT is negative, do CSF tap and look for blood or xanthochromia
SAH
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
Arterial venous malformations (AVM)
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
MCA
Contralateral hemiplegia (arm/face>leg) + hemianesthesia; gaze preference towards infarcted side of brain
MCA
If located in DOMINANT hemisphere: global aphasia (involves both receptive and motor areas)
MCA
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)
MCA
Abulia (slowness to respond), lack of spontaneous movement +/- confusion; impairment of gait and stance (gait apraxia); behavioral changes, memory disturbance; urinary incontinence
ACA occlusion DISTAL to anterior communicating artery (acoma)
Occlusion of single vertebral after often asymptomatic if COW intact
Posterior circulation stroke
