Chapter 8: Common Patterns of Abnormal Sensation

Total Unilateral Loss of All Forms of Sensation

This occurs in the great majority of cases with lesions of the thalamus (ventral posteromedial and posterolateral thalamic nuclei (VPM and VPL)) or as a posterior one-third of the internal capsule lacunar stroke. If this is the case, there is an updraft of the arm with a thalamic hand (adduction and the flexion of the fingers) or a parietal updraft with undulating movement of the fingers (polyminimyoclonus). No extremity moves with normal facility, with absent proprioceptive feedback to the motor cortex. There is a loathness to move with thalamic or parietal lesions, although strength may be intact. In thalamic lesions, motor function may return prior to complete sensory restitution. Rarely, an SI lesion may cause devastating loss of all primary modality sensation on the contralateral side of the body (Fig. 8.1). Another site for this sensory deficit is a partial lesion of the thalamus (VPL and VPM primarily), or a lesion of the upper brain stem that occurs in the dorsal pons, but will be accompanied by cranial nerve deficits and a contralateral hemiparesis. If it occurs with a thalamic lesion, the leg is often affected first and the motor deficit most often clears prior to the sensory deficit. At the red nucleus level of the midbrain, a rubral tremor or postural kinetic tremor will be associated. The spinothalamic-mediated sensations of pain and temperature are dorsal to the red nucleus, while proprioception and lemniscal sensation are lateral. The third nerve nuclear complex is medial to the red nucleus and in the same arterial territory of the thalamic intrapeduncular artery that arises from the tip of the basilar artery and is often involved by a cardiac embolus. Thus, a third nerve lesion associated with spinothalamic sensory loss would suggest a midbrain lesion.