Cerebrovascular Ischemia
Authors: Flaherty, Alice W.; Rost, Natalia S.
Title: Massachusetts General Hospital Handbook of Neurology, The, 2nd Edition
Copyright 2007 Lippincott Williams & Wilkins
> Table of Contents > Adult Neurology > Cerebrovascular Ischemia
Cerebrovascular Ischemia
A. Acute stroke evaluation
Always an emergency because aggressive emergent rx is available (see below).
1. The ABBA of acute stroke: Determines whether pt is eligible for intervention. Emergent CT/CTA helps with the last two.
a. Acuity? When did symptoms start?
b. Badness? How severe are they?
c. Bleeding? Intracranial blood is an absolute contraindication for tPA
d. Anterior vs. posterior? I.e., carotid vs. vertebrobasilar territory.
2. Acuity: If pt. awoke with sx, count time from when last seen normal. Time of onset cutoffs for acute stroke rx vary with vascular source.
a. Anterior circulation: Acute usually defined as sx beginning <3 h ago, but rx now available for anterior circulation strokes up to 9 h (or more if sx fluctuate, esp. with BP).
b. Posterior circulation: Up to 24 h for posterior circulation strokes.
3. NIH Stroke Scale: This standardized exam will answer the first two questions of ABBA. Add scores for total. Higher score is worse.
a. Level of consciousness: 0 = alert and responsive; 1 = arousable to minor stimuli; 2 = arousable only to pain; 3 = reflex responses or unarousable.
b. Orientation: Ask pt.'s name and month. Must be exact. 0 = both correct; 1 = one correct (or dysarthria, intubated, foreign language); 2 = neither correct.
c. Commands: Open/close eyes, grip and release nonparetic hand (mimicry or another 1-step command okay). 0 = both correct (okay if impaired by weakness); 1 = one correct; 2 = neither correct.
d. Best gaze: Horizontal EOM by voluntary or Doll's test. 0 = normal; 1 = partial palsy (abnormal in one or both eyes); 2 = forced eye deviation or total paresis that cannot be overcome by Doll's.
e. Visual field: Use visual threat if necessary. If monocular, score field of good eye. 0 = normal; 1 = quadrantanopia, partial hemianopia, or extinction; 2 = complete hemianopia; 3 = blindness.
f. Facial palsy: If stuporous, check grimace to pain. 0 = normal; 1 = minor paralysis (flat nasolabial fold, asymmetric smile); 2 = partial paralysis (lower face); 3 = complete paralysis (lower and upper face).
g. Motor arms: Arms outstretched 90 degrees (sitting) or 45 degrees (supine) for 10 sec. Encourage best effort. 0 = no drift 10 sec; 1 = drift but does not hit bed; 2 = some antigravity effort, but cannot sustain; 3 = no antigravity effort, but even minimal movement counts; 4 = no movement at all; X = cannot assess due to amputation, fracture, etc.
h. Motor legs: Score like motor arms (see above).
i. Limb ataxia: Check finger-nose and heel-shin; score only if out of proportion to paresis. 0 = no ataxia (or aphasia, hemiplegic); 1 = ataxia in arm or leg; 2 = ataxia in arm AND leg; X = unable to assess, as above.
j. Sensory: Use pin. Check grimace or withdrawal if stuporous. Score only stroke-related losses. 0 = normal; 1 = mild-moderate unilateral loss but pt. aware of touch (or aphasic or confused); 2 = total unilateral loss, pt. unaware of touch; 3 = bilateral loss or coma.
k. Best language: Describe cookie jar or picture; name objects; read sentences. May use repeating, writing, stereognosis. 0 = normal; 1 = mild-mod aphasia (but comprehensible); 2 = severe aphasia (almost no info exchanged); 3 = mute, no one-step commands, coma.
l. Dysarthria: Read list of words. 0 = normal; 1 = mild-mod slurring; 2 = severe, unintelligible, or mute; X = intubation or mechanical barrier.
m. Extinction/neglect: Simultaneously touch pt on both hands, show fingers in both visual fields, ask about deficit, left hand. 0 = normal; 1 = neglects or extinguishes to double stimulation in any modality; 2 = profound neglect in more than one modality.
4. Bleed risk: Ask about anticoagulant use, HA, neck/eye pain, recent trauma, rectal bleeding. Visible stroke on CT increases bleed risk.
5. Anterior vs. posterior circulation stroke: Save more precise localization for later. The following sx are a rough guide.
a. Anterior: Preserved alertness, aphasia; neglect; both weak and numb in face + arm without leg OR in leg without face + arm; horizontal gaze palsy in which pt. looks away from paretic side.
b. Posterior: Ataxia; vertigo, N/V; cranial nerve deficits; altered consciousness; bilateral or crossed sensory and motor deficits; crossed dissociation of proprioception from pain sensation, horizontal gaze palsy in which pt looks towards paretic side.
6. The rest of the H&P: Do this only after the NIH Stroke Scale and getting pt at top of queue for emergent CT.
a. Other causes and complications: LOC, seizure-like activity, previous strokes and their deficits, etc.
b. Vascular risk factors: HTN, smoking, obesity, DM, hyperlipidemia, male sex, age, angina, MIs, PVD, pregnancy, oral contraceptive use, family history of early MIs or strokes.
c. Detailed exam: See sx of specific stroke syndromes, p. 26.
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B. See also
venous sinus thrombosis, p. 126; transient monocular blindness, p. 45; hemorrhagic strokes, p. 61.
C. Tests
1. Blood:
a. General: Glucose, BUN/Cr, CBC, PTT (q6h on heparin until in range), PT, INR, ESR, Hgb A1c, RPR, homocysteine.
1) False positives: Glucose, WBC, ESR, and CRP are all mildly high post stroke. Check Hgb A1c if glucose >130. CPK rises 4-7 d post stroke.
b. Lipids: Total cholesterol, LDL, HDL, triglycerides.
c. Hypercoagulability panel for pts <60 (lupus anticoagulant and anticardiolipin Ab, D-dimer, fibrinogen, Lp(a), protein C&S, factor V Leiden, prothrombin gene mutation, antithrombin III Ab).
2. Imaging: (See imaging, p. 179.)
a. Emergent head CT: To rule out bleed. Best to do head and neck CTA at same time; it may detect persistent clot or arterial stenosis (contraindications: confirmed contrast allergy, Cr >1.7). Consider CT perfusion scan to assess area at risk for further ischemia.
b. Follow-up scan: To assess stroke territory, e.g., MRI with diffusion-weighted image (DWI), or repeat CT in 6-12 h. Consider diffusion-perfusion MRI to look for territory at risk in pts whose exam fluctuates or iron-susceptibility sequence to rule out small bleeds from amyloid angiopathy.
c. Vascular studies: Carotid ultrasound, anterior and posterior transcranial Doppler (TCD), MRA (time-of-flight or with gadolinium), or CT angiogram. Consider conventional angiogram [diagnostic or therapeutic (IA tPA)].
3. Cardiac workup: EKG; echocardiogram + bubble study, or TEE, to rule out LV clot, patent foramen ovale, atrial septal aneurysm. Consider bubble TCD. Holter to rule out A fib.
D. DDx of stroke
Cerebral bleed, TIA, postictal (Todd's) paralysis, spinal cord lesion, peripheral nerve injury (e.g., Bell's palsy, Saturday night
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palsy), MS flare, vasculitis, hemiplegic migraine, transient global amnesia, venous infarct, acute illness causing flare of an old stroke's sx, hypoglycemia.
E. Mechanisms of ischemic stroke
1. Thrombus: ~40% of strokes
a. Large artery: (~15% of strokes) Arterial dissection, atherosclerosis.
b. Penetrating artery: (~25%) Lacunar, from hypertensive lipohyalinosis.
c. Venous thrombosis: (see p. 126.)
2. Embolus:
a. Cardiac: About 20% of all ischemic strokes. Causes: A fib, sustained A flutter, rheumatic valve dz/mechanical valves, LV clot (recent MI, dilated cardiomyopathy), endocarditis, myxoma, hypercoagulable state (see p. 192).
b. Paradoxical embolus: Via patent foramen ovale, atrial septal aneurysm, atrial or ventricular septal defect; or clot from lung.
c. Artery-to-artery embolus: E.g., from carotid plaque.
d. Other: Fat, air, or septic embolus.
3. Coagulopathy or platelet disorder: <5%. see p. 192.
4. Low flow: <5%; border-zone ischemia during systemic hypotension, often in the setting of pre-existing large-artery atherosclerosis.
5. Vasculopathy: <5%; infectious (e.g., syphilis, TB, VZV), vasospasm (e.g., cocaine, migraine), collagen vascular dz, primary CNS vasculitis, moya-moya dz, fibromuscular dysplasia, homocystinuria, Fabry's dz.
6. Cryptogenic: ~30% of all ischemic strokes. A dx of exclusion.
F. Transient ischemic attack (TIA) vs. stroke
TIA was originally defined as a deficit lasting <24 h; now defined as a brief deficit, typically lasting <1 h, caused by a focal CNS ischemia without evidence of infarction. Treat TIA as an impending stroke (10% of TIA develop stroke within 90 d, of which 50% occur in the first 2 d).
1. Predictive factors for stroke after TIA: Age >60, DM, sx duration >10 mins, weakness and/or speech impairment. Diagnostic workup for TIA is similar to stroke and warrants an admission to expedite. Management is guided by underlying etiology.
2. Embolic TIA: Sx usually of vascular territory ischemia, last minutes to hours before embolus breaks up.
3. Lacunar TIA: Sx often of white matter ischemia, often stuttering or stereotyped.
4. Low-flow TIA: Sx usually of watershed ischemia, often blood pressure dependent, stereotyped, or crescendo, with evidence of large-artery atherosclerosis.
5. Amyloid angiopathy: Sx usually of cortical ischemia, often spreading across to adjacent body parts over a few minutes.
G. Rx of acute stroke
1. Emergent thrombolysis: Use NIH tPA protocol for acute stroke in every pt. <3 hours of witnessed (confirmed) symptom onset. Can be given by any physician and does not require informed consent (standard of practice).
a. Contraindications: Large stroke on noncontrast head CT (>1/3 arterial territory); blood on CT; minor (except aphasia) or
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resolving deficit; history of ICH; recent stroke, head trauma, or intracranial procedure (<3 mo); seizure at symptom onset; suspicion of SAH; recent trauma or surgery (<14 d); active internal bleeding; history of GI/UT bleeding (<21 d); recent LP or noncompressible arterial puncture; bleeding diathesis (INR >1.2, abnormal PTT, plts <100); uncontrollable HTN; serum glucose <50 or >400.b. IV tissue plasminogen activator (tPA): Give <3 h after symptom onset. 0.9 mg/kg up to 90 mg, 10% of total dose as IV bolus (over 1 min), and remainder IV over 60 min.
c. Intra-arterial tPA: Experimental, multiple agents and variations used. Informed consent required by family. IA tPA is given with angiographic guidance at site of clot, less than 6 h after symptom onset for anterior circulation clot; 12 h (and up to 24 h if no MR/CT evidence of infarct and/or hemorrhagic transformation) for posterior circulation clot.
1) Pre-op and post-op angio orders: see p. 177.
2) Blood pressure management after lysis: Keep SBP <180, DBP <105, with labetalol or nitroprusside if necessary.
2. Mechanical clot disruption or retrieval: up to 9 (ant)- 24 (post) hrs.
3. Intracranial stents or bypass.
4. Anticoagulants: See also p. 160.
a. Contraindications: Recent CNS bleed, surgery (relative).
b. Aspirin: If no bleed on CT and pt is not a candidate for thrombolysis, have pt chew 325 mg.
c. Other antiplatelet agents: If pt has had stroke on aspirin or cannot tolerate it.
1) Clopidogrel: Indicated alone for secondary stroke prevention but showed higher risk of bleeding complications when combined with ASA.
2) Aspirin-dipyridamole: combination (25/200) is protective, but cost and HA may be problems.
d. IV heparin:
1) Indications: Symptomatic carotid stenosis, neck artery dissection, cerebral venous thrombosis, intracardiac clot. Less evidence for anticoagulation in acute new-onset A fib, intracranial atherosclerosis, lacunar infarcts, etc.
2) Administration: Avoid loading boluses (e.g., 3,000-5,000 units) except if systemic indication (e.g., DVT with paradoxical embolism, unstable angina with MI and cardiac thrombus). In septic emboli, anticoagulation can be initiated after infection has been sufficiently treated with antibiotics.
e. Heparin alternatives: If h/o heparin-induced thrombocytopenia.
f. Consider warfarin: INR goal usually 2-3, but 3-4.5 for metal heart valves.
1) Short-term warfarin: For cerebral venous thrombosis, carotid or vertebral dissection. Warfarin for 3-6 months; then may discontinue if cause no longer present and vessel reconstitution is confirmed by imaging.
2) Long-term warfarin:
a) Indication: Atrial fibrillation (including paroxysmal), mechanical heart valve, hypercoagulable disorder.
b) No evidence for warfarin in these: Prevention of stroke recurrence, embolus of unknown origin, intracranial stenosis, and inoperable extracranial stenosis is not currently supported by evidence.
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5. Maintain blood pressure: Allow or even assist HTN in acute strokes the brain needs a higher perfusion pressure.
a. Exceptions: Evidence of end-organ damage MI, CHF, aortic dissection, h/o severe CAD, large stroke, hemorrhagic transformation of stroke.
1) In non-tPA pts.: Avoid sustained (2 readings 5 min apart) SBP >185 or DBP >110
2) In pts. with a procedure (tPA, thromborrhexis, CEA): Avoid SBP >140 to prevent reperfusion syndrome.
b. Hold routine BP meds: As long as the above exceptions are not present.
c. Avoid dehydration: When giving IV fluids to avoid dehydration, use D5NS to avoid cerebral edema.
d. Hypertensive therapy: Consider IV pressors in pts with diffusion-perfusion mismatch and variation of sx with SBP.
1) Pressor trial: Use peripheral neosynephrine to see if HTN helps stroke sx. If sx improve at SBP 180, pt. will require ICU monitoring for the duration of treatment.
2) Contraindications: Active or history of severe coronary dz; SBP >180 required to show benefit; large infarct or evidence of hemorrhagic transformation.
e. Antihypertensives: Short acting is better, so use IV drugs if possible
1) Order of use: -blocker first, then add calcium channel blockers, then ACEI, then nitrates, then hydralazine, then 1-blockers.
a) IV: Labetalol nicardipine enalapril nitroprusside hydralazine.
b) PO: Lopressor diltiazem captopril isosorbide hydralazine.
2) Avoid: Drugs that can make BP plummet (nifedipine) or directly dilate arteries (hydralazine, nitrates). The latter could hinder autoregulation of cerebral vasculature. Clonidine can be too sedating (sometimes useful for agitation).
6. Prevent cerebral edema: IVF of choice is D5NS to aim for hypertonic isovolemia. If there is progressive mass effect or signs of brainstem herniation, treat high ICP aggressively; see p. 68. See also Herniation, p. 181.
7. Oxygen:
a. Hyperbaric oxygen: For ischemia related to carbon monoxide poisoning, air emboli, etc.
b. O2 via nasal cannula in the EW.
8. Treat fever: If temperature >100.4 F, treat with acetaminophen, ice packs, cooling blankets.
9. Treat hyperglycemia: Keep glucose <130, with insulin drip if needed, to decrease oxidative metabolism.
10. Drugs to avoid: haloperidol, benzodiazepines, opiates, -antagonists, nifedipine.
11. Aspiration precautions: Keep NPO until bedside swallow or official S&S evaluation is done; may need NGT early on for meds.
12. Monitor coagulation factors: If on heparin, PTT q6h until therapeutic. If on warfarin, PT/INR qd.
13. Physical, occupational, and speech/swallow therapy evaluation: Wait until pt is hemodynamically stable and can cooperate with therapist.
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H. Surgical interventions for secondary stroke prevention
1. Carotid endarterectomy (CEA): Indications are:
a. Carotid stenosis: Greater than 70% (from NASCET study); debatable between 50%-70%.
b. Deficit: TIA or infarct in vascular territory distal to lesion ( symptomatic stenosis ).
c. No severe distal stenoses: Downstream from lesion.
d. Good surgical candidate: Age <75, no serious cardiac disorders. (see preoperative cardiac evaluation, p. 210.)
e. Stable CNS: No intracerebral hemorrhage or extensive fresh infarct (may postpone operation 2+ weeks to prevent reperfusion injury ).
2. Carotid stenting: An option for those who cannot get CEA. Higher risk of reocclusion but fewer intraoperative complications.
3. Patent foramen ovale closure:
a. Indications: Young patients with PFO-associated stroke (large PFO/atrial septal aneurysm; temporal evidence of clot by DVT/MRV of pelvic veins, etc.).
b. Alternatives: ASA vs. warfarin for PFO with associated atrial septal aneurysm in young patients.
I. Vascular territories and stroke syndromes
1. See also: Angiographic anatomy, p. 175.
2. Anterior vs. posterior circulation: The latter are more dangerous. see p. 22.
3. Middle cerebral artery (MCA):
a. Superior division: Weak face/arm > leg, expressive aphasia.
b. Inferior division: Mild or transient motor/sensory deficit, fluent aphasia, neglect, sometimes field cut (Meyer's loop infarct causes superior quadrantanopia, not hemianopsia), Gerstmann's syndrome (dominant inferior parietal lobule, with acalculia, L-R dissociation, finger agnosia, agraphia).
4. Anterior cerebral artery (ACA): Contralateral leg weak, grasp reflex, gegenhalten, abulia, gait disorder, perseveration, urinary incontinence. Sometimes bilateral if both ACAs have common origin.
5. ACA-MCA watershed: Contralateral trunk > weakness. Bilateral watershed gives man-in-the-barrel syndrome, with proximal > distal weakness.
6. MCA-PCA watershed: Parietal lobe dysfunction, Balint syndrome (if bilateral).
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Figure 5. Cerebrovascular territories. (From Greenberg MS. Handbook of Neurosurgery. 3rd ed. Lakeland, FL: Greenberg Graphics; 1994, with permission.)
7. Posterior cerebral artery (PCA): Contralateral field cut. Sometimes memory loss, color anomia, alexia without agraphia, hemisensory loss, mild hemiparesis. Spatial disorientation is nondominant superior parietal lobule. Complications of PCA stroke include:
a. Brainstem ischemia: PCA stroke can be the beginning of a top-of-the-basilar syndrome.
b. Uncal herniation can pinch off PCAs.
c. Hemorrhagic transformations are common after PCA infarcts.
8. Subcortical arteries:
a. Heubner and other medial striates: AKA recurrent artery of Heubner. See expressive aphasia, mild hemiparesis arm > leg, proximal > distal. Comes off ACA or A-comm to anterior hypothalamus, globus pallidus, putamen, head of caudate nucleus.
b. Anterior choroidal and other lenticulostriates: Contralateral sensorimotor loss, homonymous hemianopsia. The anterior choroidal comes off ICA to posterior limb of int. capsule, cerebral peduncle, and medial globus pallidus.
9. Basilar artery: Infarct causes pontine and cerebellar signs.
a. Occlusion: Frequently bilateral signs, e.g., quadriplegia, conjugate horizontal gaze palsies, coma, locked-in syndrome.
b. Top of the basilar embolus:
1) Sx: Usually see oculomotor problems, altered mental status, dorsal midbrain syndrome, bilateral thalamic stroke.
2) Embolic complications: Emboli from basilar clot can cause occipital, thalamic, cerebellar, and brainstem infarcts with contralateral hemiplegia but ipsilateral horizontal gaze palsy (opposite of cerebral lesion), INO, palatal myoclonus, etc.
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c. Basilar scrape syndrome:
1) Sx: Progressive brainstem and cerebellar sx as basilar thrombosis sequentially occludes PICA, AICA, paramedian basilar aa., perforators, SCA, etc. Often bilateral or alternating sides.
2) Prognosis: Usually ends with complete occlusion, top-of-the-basilar syndrome, and infarct.
10. Midbrain strokes: From occlusion of basilar branches. Damage to oculomotor, Edinger-Westphal, red, trochlear, or lateral geniculate nuclei; reticular activating system.
a. Dorsal midbrain syndrome: (Parinaud's syndrome) see p. 48.
b. Rostral interstitial nucleus: From branch of PCA. Infarct of single side can give a bilateral upgaze palsy because the infarct catches crossing fibers en passant.
c. Ventral midbrain syndrome: Bilateral down gaze paralysis, paralysis of convergence, obtundation.
d. Named midbrain syndromes: Varying degree of CN III palsy and contralateral motor system dysfunction, namely Weber's, with contralateral weakness; Claude's, with contralateral rubral tremor; and Benedikt's, with both.
1) Eponym rant: Why immortalize very dead guys when you could use descriptive names? That would spare the energy wasted on keeping similar eponyms straight (e.g., Bell's palsy, Bell's reflex, Bell's nerve, and Bell's law), the problem of diseases named after Nazis (e.g., Hallervorden-Spatz), etc.
2) Syndrome rant: But, you protest, it's hard to find descriptive names that distinguish syndromes as similar as Benedikt's, Claude's, and Weber's. Why even bother? Simply describing the sx helps pt management more and makes your notes clearer to nonneurologists.
11. Pontine strokes: From occlusion of basilar branches. Damages nuclei of V, VII, and VIII, reticular activating system.
a. Locked-in syndrome: From basis pontis lesion, sparing tegmentum. Frequently, the only motor function preserved is vertical gaze. Sx may be mistaken for coma or nonconvulsive status epilepticus.
b. Pontine rigors: The jerking movements sometimes seen in bilateral pontine strokes.
12. Cerebellar strokes: Vertigo, N/V, nystagmus, ataxia, poor smooth pursuit, often headache; often with brainstem signs including ipsilateral hearing loss, ipsilateral Horner's, contralateral pain, and temperature loss. SCA and AICA are off basilar; PICA off vertebral.
a. Large cerebellar strokes are an emergency because of the risk of herniation. Consider neurosurgical decompression if >3 cm or
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if edema/hemorrhagic transformation. Pt. can die within hours of first brainstem signs.b. Superior cerebellar artery (SCA): Ataxia. Usually embolic. Rarely causes hydrocephalus (7%).
c. Posterior inferior cerebellar artery (PICA): Vertigo, N/V. Often with lateral medullary syndrome (see below). Embolus and stenosis are equally likely. If whole territory is infarcted, there is a 25% risk of hydrocephalus.
d. Anterior inferior cerebellar artery (AICA): Hearing loss, weak/numb face, ataxia, vertigo. Rare; usually thrombotic; usually with brainstem infarct too.
13. Medullary stroke: From vertebral artery lesion. Signs of damage to VIII, IX-XII, spinal tract, and nucleus of V. Hemiparesis implies more medial involvement or higher lesion.
a. Lateral medullary syndrome (Wallenberg's):
1) Vestibular sx: Vertigo, N/V, nystagmus, diplopia.
2) Crossed sensory loss: Sensory loss on ipsilateral face; poor pain and temperature sensation on contralateral body.
3) Horner's syndrome: Ipsilateral.
4) Poor speech and swallow: Dysphagia, hoarseness, hiccups, ipsilateral poor gag. From cranial nerve IX, X palsies.
5) Ataxia: Ipsilateral.
b. Medial medullary syndrome (D j rine's): Ipsilateral tongue weakness and deviation, contralateral hemiparesis and poor proprioception, but cutaneous sensation spared.
14. Lacunar syndromes: Thought to be from hypertensive lipohyalinosis; probably not helped by heparin.
a. Typical locations: In order of decreasing frequency: putamen, caudate, thalamus, pons, internal capsule, corona radiata.
b. Pure sensory: Ventral posterolateral or posteromedial nucleus of the thalamus.
c. Pure motor: Posterior limb of internal capsule, corona radiata, basis pontis, or cerebral peduncle.
d. Sensorimotor: Contralateral face, arm, and leg involvement due to a lesion in the thalamus and adjacent posterior limb of internal capsule.
e. Ataxic hemiparesis: Ataxia weakness on same side. Often leg > arm > face. From basis pontis (upper third, midline), or ventral anterior thalamus + adjacent internal capsule, or superior cerebellar peduncle.
f. Dysarthria-clumsy hand: Weak face, dysphagia, and ipsilateral clumsy hand. From lesion of basis pontis, genu of internal capsule, or immediately subcortical white matter.
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