Pure sensory stroke

Fisher CM (1965b) Pure sensory stroke involving face, arm, and leg. Neurology 15 76-80... 

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). 

Pure sensory stroke constitutes about 5% of cases. It has the same distribution as pure motor stroke but the symptoms are of sensory loss, with or without sensory signs affecting all modalities equally, or sparing proprioception. The lesion is usually in the thalamus (see Fig. 10.3) but can be in the brainstem. 

Small thalamic lesions may cause a pure sensory stroke or sensorimotor stroke, sometimes with ataxia in the same limbs (Schmahmann 2003). However, other deficits may occur in isolation, or in combination depending on which thalamic nuclei are involved. These include paralysis of upward gaze, small pupils, apathy, depressed consciousness, hypersomnolence, disorientation, visual hallucinations, aphasia and impairment of verbal memory attributable to the left thalamus, and visuospatial dysfunction attributable to the right thalamus. Occlusion of a single small branch of the proximal posterior cerebral artery can cause bilateral paramedian thalamic infarction with severe retrograde and anterograde amnesia. 

Fig. 10.3. Images with T2-weighted (a) and diffusion-weighted (b) MRI in a 70-year-old man who presented with a history of sudden-onset numbness and tingling in the left face arm and leg. On examination there was sensory loss over the left hand but nothing else. The diffusion-weighted images confirm a thalamic infarct consistent with the clinical diagnosis of pure sensory stroke.

Pure motor stroke constitutes about 50% of lacunar cases. It consists of a unilateral motor deficit involving two or three areas, the face, upper arm and/or leg, including the whole of each area that is affected. There are often sensory symptoms but no sensory signs. The lesion occurs at locations where the motor pathways are closely packed together and separate from other pathways usually in the internal capsule or pons, sometimes the corona radiata or cerebral peduncle, and rarely in the medullary pyramid. There may be a flurry of immediately preceding TIAs, the so-called capsular warning syndrome (Donnan et al. 1996). 

Sensorimotor stroke constitutes about 35% of cases. It is the combination of a pure motor stroke with sensory signs in the affected body parts. The lesion is usually in the thalamus or internal capsule, but it can be in the corona radiata or pons. A similar clinical picture can be caused by cortical infarcts, leading to misclassification (Blecic et al. 1993). 

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). 

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