Hemiparesis

FIGURE 4.2 Seventy-three-year-old female with sudden right hemiparesis, left facial weakness, dysarthria, nausea, and downheat nystagmus. Posterior circulation angioplasty demonstrated occlusion of the proximal hasilar artery (arrows— a and b). Note the retrograde opacification of the superior cerebellar arteries through postero-inferior cerebellar to superior cerebellar arteries collaterals (b). 

Toni D, Del Duca R, FiorelU M, Sacchetti ML, Bastianello S, Giubilei F, Martinazzo C, Argentino C. Pure motor hemiparesis and sensorimotor stroke accuracy of very early clinical diagnosis of lacunar strokes. Stroke 1994 25(l) 92-96. 

Hemiparesis or monoparesis occur commonly, as does a hemisensory deficit. 

Signs and symptoms Headache, vomiting, stupor, hemiparesis, aphasia, visual disturbances, and seizure transient ischemic attack is a strong predictor for stroke. Behavioral and performance changes may be present in patients with asymptomatic infarction. 

Hemiparesis, aphasia, papilledema, weakness, seizure, nausea and vomiting... 

Hemiparesis Weakness or slight paralysis involving one side of the... 

The possibility of cerebrovascular action of PCP was raised by the development of focal seizures and hemiparesis in a 6-year-old boy who had ingested what was presumed to be PCP (18). Hypertensive encephalopathy with a blood pressure of260/160 occurred in an 18-year-old woman who used PCP (43). These clinical findings are compatible with in vitro studies indicating that cerebral artery spasms can be produced by PCP as well as by LSD and mescaline (4). Whether such cerebrovascular actions are pertinent to the mental effects of these drugs is questionable. 

Neurologic - A transient acute neurologic syndrome has been observed in patients treated with high-dosage regimens. Manifestations of this stroke-like encephalopathy may include confusion, hemiparesis, transient blindness, seizures, and coma. 

A previously healthy 34-year-old woman who underwent ovulation induction with leuprorelin acetate and FSH developed abdominal ascites due to OHSS, followed by acute aphasia and right hemiparesis (76). The stroke was caused by a large intracardiac thrombus. 

Blockade of the anterior choroidal artery may cause infarction of the lateral geniculate body causing hemianopia with preserved central vision and a prominent sensory loss with hemiparesis (Bruno et al. 1989). 

In blockade of the anterior spinal artery, ischemia of the medial medulla may occur with contralateral hemiparesis, ipsilateral tongue weakness and contralateral loss of posterior column sensation (Ho and Meyer 1981). 

Isolated cerebellar infarction withoutinvolvement of the medulla is often difficult to identify, since gait ataxia, vomiting and dizziness may not be accompanied by typical brainstem symptoms (Barth et al. 1994). Cerebellar edema may compress the medulla and the pons leading to conjugate eye deviation to the side opposite the lesion without contralateral hemiparesis. This sign is probably pathognomonic for severe cerebellar mass effect and requires immediate intervention. 

Clinically stereotyped TIAs or the opticocerebral symptom with simultaneous amaurosis and contralateral hemiparesis due to critically low blood supply through an occluded or almost occluded ICA herald a pending borderzone ischemia (Tsiskaridze et al. 2001). Rarely so-called limb shaking TIAs may point to a hemodynamic ischemia in ICA occlusive disease (Baquis et al. 1985). 

J Neurol Neurosurg Psychiatry 40 1182-1189 Fisher CM (1978) Ataxic hemiparesis. A pathologic study. Arch Neurol 35 126-128... 

Fig. 3.1a,b. a The ischaemic penumbra. The perfusion (PI) lesion delineates the extent of hypoperfusion and the diffusion (DWI) lesion outlines the infarct core. The difference between the two lesions (perfusion-diffusion mismatch) represents the ischaemic penumbra, tissue at risk of progression to infarction, b Patient imaged at 3 h after onset of left hemiparesis and neglect with large PI (time to peak - TTP) lesion and smaller DWI lesion. At day 3 reperfusion has not occurred and the infarct core (diffusion lesion) has expanded greatly into the region of acute perfusion-diffusion mismatch. This is consistent with the perfusion-diffusion mismatch area representing the ischaemic penumbra... 

While physicians may not recognize up to 80% of lacunes (Tuszynski et al. 1989), several clinical syndromes have been correlated with relevant lacunes detected at subsequent autopsy. Five of these are regarded as the classic lacunar syndromes pure motor hemiparesis, sensorimotor stroke, pure sensory hemiparesis, dysarthria clumsy hand syndrome, and ataxic hemiparesis (Donnan et al. 2002 Fisher 1982 Bamford 2001). Pure motor stroke is the commonest lacunar syndrome in clinical practice, while pure sensory stroke is encountered less frequently. The involvement of the face, arm and leg of one side is the characteristic feature of the first three syndromes while reductions of consciousness, cognitive or visual field defects are absent. Even though lacunar infarcts have been linked to lacunar syndromes, the latter are of course not specific for this stroke subtype and mimicked by cortical infarcts, intracerebral hematomas, and non-vascular causes (Bogousslavsky et al. 1988 Bamford 2001). 

Precentral artery territory infarcts result in a hemiparesis with predominant proximal arm involvement. In left sided strokes, non-fluent aphasia, usually transcortical motor aphasia, apraxia and agraphia are present, while in right sided strokes, neglect and motor impersistence can be found. 

Subcortical white matter infarcts may mimic a superficial MCA infarct causing a partial anterior circulation syndrome or present as a lacunar syndrome (pure motor, ataxic hemiparesis or sensori motor stroke). Superficial perforating artery infarcts (medullary branches) are often accompanied by cortical spotty lesions. Borderzone and white matter medullary branches infarctions are usually caused by hypoperfusion due lo large vessel occlusion or stenosis (Bogousslavsky 1993 Donnan and Yasaka 1998), but white matter medullary branches infarction can also be caused by cardioembolism (Lee et al. 2003). 

Aphasia and neglect can be found following respectively dominant and non-dominant anterior choroidal artery infarcts. Anterior choroidal artery infarcts usually cause the classical 3H syndrome hemiparesis, hemihypesthesia, hemianopia. Pure motor hemiparesis and isolated hemianopia can also occur (Han et al. 2000). Anterior choroidal artery territory infarcts are rarely caused by small vessel occlusion. In general they are caused by cardioembolism or large artery disease with occlusion or artery-to-artery embolism (Leys et al. 1994). 

Bogousslavsky et al. 1988). Posterior choroidal artery infarcts result in visual field defects, variable sensory loss, hemiparesis, dystonia, hand tremor and occasionally amnesia and aphasia. Visual field defects, commonly quadrantanopia or hemianopia, are found if the lateral posterior choroidal arteries branches are involved in isolation. Unusual field defects such as homonymous horizontal sec-toranopia or wedge shaped homonymous hemianopia, may also be found and may be explained by the dual blood supply to the lateral geniculate body by... 

---