Clinical study
Akinetic mutism following stroke

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Abstract

This is an appraisal of the varied clinical presentation and the neural substrate for akinetic mutism following stroke. The diagnosis is important as akinetic mutism is often misdiagnosed as depression, delirium and locked-in-syndrome.This is a descriptive study of eight selected patients with akinetic mutism following infarction/haemorrhage in different regions of the brain with characteristic syndromes. They involved the critical areas namely, the frontal (cingulate gyrus, supplementary motor area and dorso-lateral border zone), basal ganglia (caudate, putamen), the mesencephalon and thalamus. The disorders of speech and communication took different forms. The speech disorder included verbal inertia, hypophonia, perseveration, softened and at times slurred. The linguistic disturbances were fluent, non-fluent, anomia and transcortical (motor, mixed) aphasias. The findings were related to what is known about the neuroanatomic location of the lesions and the role of the frontal-subcortical circuitry in relation to behaviour. Akinetic mutism could be explained by damage to the frontal lobe and or interruption of the complex frontal subcortical circuits.

Introduction

Akinetic mutism (AM), abulia and apathy are terms that have been used to describe behavioural abnormalities relating to reduced activity and slowness. Several investigators proposed that these clinical states are simply a continuum of severity of reduced behaviour and AM may be an extreme form.1

Following the landmark case report of Cairns et al.,2 the term AM had been used to describe a syndrome characterised by marked reduction of nearly all motor functions including facial expression, gestures and speech output but with some degree of alertness. They described a patient with an epidermoid cyst in the third ventricle whom after several evacuations of the cyst became more alert and responsive. Since then AM had been used in situations with similar clinical picture associated with different aetiologies and pathologies. There is considerable variation in the presentation of such patients and the clinical features of AM correspond more closely to the functional anatomy of the brain regions affected rather to the pathology.

This paper will appraise (i) stroke patients with AM selected to illustrate the variability in the clinical presentation, speech and language characteristics and course of the disease process and (ii) the likely pathophysiological mechanisms that underlie the diverse locations associated with AM.

Section snippets

Right supplementary area and cingulate gyrus

A 77-year-old right handed woman was seen with left-sided hemiplegia on day two. She was drowsy and responded poorly to verbal commands. She had a right gaze palsy with total weakness of the left arm and leg. The tone was decreased and the left plantar was extensor. She was in atrial fibrillation. On day 8 she was alert and non-communicative but seemed to comprehend. Three weeks later although she was alert, she was markedly akinetic with no speech output except for an occasional word. There

Discussion

Eight patients with AM involving different anatomical sites and of maximal importance the frontal lobe (supplementary motor area, cingulate gyrus), basal ganglia (caudate, putamen/globus pallidus) and the mesencephalothalamic regions were selected for consideration. The diagnosis of AM requires certain criteria for this is not only important scientifically but also for use in clinical practice and in research. Furthermore the heterogeneity among the patients with akinetic mutism may raise the

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