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* mcq15
 #136222  
  sinagrida - 11/07/06 09:55
 
  15. An infarct causes a pure motor herniparesis . This infarct is likely to be secondary to occlusion in the territory of the :

a) the Posterior Cerebral Artery
b) deep penetrating lacunar artery
c) The superior cerebellar artery
d) The anterior inferior cerebellar artery
e) The posterior inferior cerebellar artery

 
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* Re:mcq15
#547215
  ulise - 11/07/06 10:22
 
  15ddd?????????????? not really sure  
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* Re:mcq15
#547224
  sinagrida - 11/07/06 10:25
 
  Correct!!!

The right answer is B

Lacunes are caused by occlusion of a single penetrating artery. The deep penetrating arteries are small nonbranching end arteries (usually smaller than 500 mm in diameter), which arise directly from much larger arteries (eg, the middle cerebral artery, anterior choroidal artery, anterior cerebral artery, posterior cerebral artery, posterior communicating artery, cerebellar arteries, basilar artery). Their small size and proximal position predispose them to the development of microatheroma and lipohyalinosis.
Lacunar strokes, which comprise the most common paradigm of small vessel infarction, account for 10% of all strokes. Several distinct lacunar syndromes are recognized: the most common is pure motor herniparesis. The clinical characteristics of this syndrome include severe herniparesis or herniplegia involving the limbs, face and trunk often with associated dysarthria. Notably absent are sensory disturbance, visual or language deficits. The site of such infarctions are within the corona radiata, internal capsule, cerebral peduncle, pons and rarely the medullary pyramid. The pure sensory stroke produces hemisensory deficits involving the face, limbs and trunk contralateral to the small infarction in the ventral posterior thalamic nucleus which causes the syndrome. Lacunar infarction in the genu or anterior limb of the internal capsule or pontine base produce clumsy hand-dysarthria syndrome which manifests clinically as clumsiness of the contralateral hand and tongue with contralateral facial paresis. Homolateral ataxia and crural paresis result from pontine lacunes involving post-decussating cerebellar tracts and pre-decussating corticospinal tracts. The resultant signs are of mild contralateral hemiparesis involving leg more than arm or face with more marked ataxia of the weak limbs. Bilateral lacuries within the internal capsule in perithalamic locations may result in a mutism syndrome. The accrual of multiple lacunae within the internal capsules of both hemispheres may result in a pseudobulbar syndrome in which there is dysarthria, hyperactive gag reflex with dysphagia, spasticity especially of the lower limbs extensor plantar reflexes, gait apraxia with small hesitant steps and emotional incontinence. This lacunar state is a major part of subcortical atherosclerotic encephalopathy. There is evolving evidence that microvascular occlusive disease can be due not only to thrombotic or obliterative disease but also to embolic processes. Intra. and extracranial arterial sources are implicated as is cardioembolism of microparticulate matter.

 
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