M P Alexander1. 1. Memory Disorders Research Center, Boston University, Department of Neurology, Massachusetts, USA.
Abstract
OBJECTIVE: Akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. METHODS: The effects of dopaminergic treatment of a patient with chronic AKM after discrete bilateral infarctions of the mesencephalic ventral tegmental area and the lateral hypothalamus were studied with motor measures, the Functional Independence Measure (FIM), and neuropsychological tests. RESULTS: Treatment with a combination of carbidopa/levodopa and pergolide produced prompt amelioration of AKM with dramatic and rapid improvement in FIM. An apathetic, amotivational state persisted despite resolution of akinesia and normal frontal executive functions. CONCLUSIONS: AKM may respond to dopaminergic treatment even after months of severe akinesia. The mechanism of abulia is more complex than simply a partial dopaminergic deficiency state and may persist even when AKM is treated and frontal cognitive functions are normal.
OBJECTIVE:Akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. METHODS: The effects of dopaminergic treatment of a patient with chronic AKM after discrete bilateral infarctions of the mesencephalic ventral tegmental area and the lateral hypothalamus were studied with motor measures, the Functional Independence Measure (FIM), and neuropsychological tests. RESULTS: Treatment with a combination of carbidopa/levodopa and pergolide produced prompt amelioration of AKM with dramatic and rapid improvement in FIM. An apathetic, amotivational state persisted despite resolution of akinesia and normal frontal executive functions. CONCLUSIONS: AKM may respond to dopaminergic treatment even after months of severe akinesia. The mechanism of abulia is more complex than simply a partial dopaminergic deficiency state and may persist even when AKM is treated and frontal cognitive functions are normal.