Abstract

AbstractBackgroundAkinetic mutism (AM) is characterized by sparse volitional motor and speech activation with reasonably preserved arousal and vigilance functions. Akinetic mutism, the most severe of these disorders, is most commonly associated with bilateral hemispheric pathology, although unilateral lesions may produce this condition as well.MethodCase: Our patient is a 42‐year‐old right handed man who presented to the emergency department with an acute onset of akinetic mutism. His family described him as a calm and intelligent individual with a good cultural knowledge level and without any evident cognitive abnormality before he suddenly experienced akinetic mutism. On examination, he was alert but produced no spontaneous speech and had only rare, spontaneous movement of his arm and leg. With repeated prompting, he followed single‐step commands.ResultMagnetic resonance imaging demonstrated an infarction in the distribution of the left posterior inferior cerebellar artery. During the course of 7 days, as the patient became more interactive, he demonstrated normal language function. As he became more communicative, cognitive impairment became apparent. Neuropsychological evaluation were performed after approximately 12 days after onset because of the impossibility of test administration during the acute phase. Impaired performances were evident on executive function testing with difficulties in planning, abstract reasoning, set‐shifting and perseveration. Furthermore, attention disorders and memory dysfunction were mild observed and were probably due to the poor ability of planning and organization. Language tests revealed mild deficits in the semantic sphere with paraphasia, anomia and circumlocutory expressions. During psychometric testing, the patient presented agitated and anxious behavior with affective air hunger and episodes of crying. Brain SPECT were performed after approximately 14 days after onset. Brain SPECT demonstrated hyporperfusion in Lt. cerebellar and frontal cortex.ConclusionThe syndrome of akinetic mutism is typically the result of bilateral hemispheric injury, usually involving the anterior cingulate gyri. Other locations for lesions producing akinetic mutism include the thalami, globus pallidus, internal capsule, and frontal white matter. We describe a man with akinetic mutism and cognitive impairment due to an ischemic stroke in the distribution of the left PICA.

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