Mutism in the Older Adult

Nages Nagaratnam, MD, FRCP, FRACP, FRCPA, FACC; Gowrie Pavan, MBBS, FRAGP

Disclosures

Geriatrics and Aging. 2005;8(8):61-68. 

In This Article

Akinetic Mutism

Following the landmark case report of Cairns et al.,[8] the term akinetic mutism (AM) has been used to describe a syndrome characterized by marked reduction of nearly all motor functions, including facial expression, gestures, and speech output, but with some degree of alertness. Following this report, the term AM has been used in situations with similar clinical pictures associated with different etiologies and pathologies. Depending on the clinical picture, AM had been subdivided into two pathology types based on the anatomic location of the lesion. One is related to the mesencephalic region and is described as apathetic akinetic mutism or somnolent mutism. The other is known as hyperpathic akinetic mutism and is associated with bilateral frontal damage (Figure 2).[9]

The Neural Pathways in Akinetic Mutism

The critical areas involved are the frontal lobe (cingulate gyrus, supplementary motor area [SMA], and the dorso-lateral border zones), basal ganglia (caudate and putamen), and the mesencephalus and thalamus.[10] The vascular syndromes giving rise to AM are the most striking, particularly those related to the anterior cerebral artery (ACA) which could be either unilateral or bilateral, transient or prolonged. Neuroimaging is an important diagnostic test (Figure 3). Apart from cerebral infarction or hemorrhage,[11] a variety of focal pathologies can produce AM.[8,12,13,14,15] CJD is a rapidly progressive disease, characterized by dementia and myoclonus, and is highly protean in its manifestations. AM has been described as a symptom of CJD and included as a classification criterion for its diagnosis.[14] AM commences within an average of 7.5 weeks in CJD.[16]

Demonstration of a Cerebral Infarction

Lim et al.[15] described AM with findings of white matter intensities. There are two types of white matter changes: periventricular and deep white matter lesions. The deep matter lesions are separate from the ventricles; they have a different pathogenesis.[17] There are several causes for these lesions apart from normal aging, but the more severe types can be associated with atherosclerotic disease.[18,19] According to some investigators, these changes detected by computed tomography or solely by magnetic resonance imaging have different meanings, and when these changes are seen on the CT they may indicate associated dementia.[20]

Somnolent AM of the mesencephalic type can vary in intensity.[9,21] AM has been reported after thalamic lesions[22,23] and thalamocapsular lesions.[13] Brown[24] identified two broad classes of disturbances with unilateral left thalamic lesions: one showing AM, often with a stuporose state, and the other with a fluent type of speech disorder.

AM is often erroneously diagnosed as locked-in syndrome or persistent vegetative state. Distinguishing between them is important because management differs. The distinguishing characteristics are shown in Table 1 . The blunted emotional expression and apathy in patients with severe depression, together with psychomotor retardation such as slurred speech and body movements, may mimic AM.

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