No abstract

No abstract

Patients who have had stroke are at significant risk for various neuropsychiatric illnesses. The most common and important of these are poststroke depression and poststroke dementia (attributable to vascular dementia, Alzheimer's dementia, or a combination of mechanisms). Poststroke neuropathology may lead some patients to experience concurrent and "overlapping" mood and cognitive symptoms. Less frequently, poststroke anxiety disorders, psychosis, isolated pathologic expressions of emotions, and apathy or fatigue may be encountered. The authors review the current literature on poststroke neuropsychiatry and offer an integrated approach to pathophysiologic concepts and clinical surveillance, screening, diagnosis, and evidence-based pharmacologic and nonpharmacologic intervention for these clinical problems on the clinical boundary between neurology and psychiatry.

The effect of mild to moderate arterial occlusive disease on peripheral nervous system conduction was prospectively investigated in 18 subjects and 18 control subjects, aged 40 to 85 years. Experimental and control subjects underwent a thorough history and physical followed by vascular and electrophysiologic studies. The primary outcome measure was the sensory nerve action potential. Although 33% of the subjects with peripheral arterial disease had experienced paresthesias, the clinical evaluation of sensation was relatively unaffected. Sensory conduction studies revealed 30% absent sural responses and 56% absent superficial peroneal nerve responses in subjects with peripheral arterial disease compared with 3 and 14% absent responses in control subjects, respectively (P = 0.044; 0.025). There were no differences in distal latency or sensory amplitude, although the superficial peroneal amplitude did approach significance (P = 0.06). No significant differences were found in motor distal latency, amplitude, or conduction velocity. Age, leg length, temperature, disease severity, presence of paresthesias, cholesterol levels, and past alcohol or tobacco ingestion did not account for the difference in sensory responses. These results support the presence of a mild sensory axonopathy in subjects with peripheral arterial disease. Electromyographers should be cognizant of absent distal responses from peripheral arterial disease so as not to ascribe the findings to an alternative pathology and should not attribute abnormal motor conduction results to the presence of this degree of peripheral arterial disease.

No abstract