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

Neuroanatomic Correlates

The frontal lobe plays an important role in behaviour and speech.

The supplementary motor areas (SMAs) have extensive afferent and efferent connections with the motor and premotor cortex.[35] The SMAs are concerned with programming motor subroutines before voluntary movements can be executed. The right SMA is concerned with activation of the motor output[36] and the left SMA is less involved with motor activation but is more concerned with sequencing of primary motor routines. Impaired functioning of the SMA could give rise to abnormalities of Parkinsonian motor programme, and the SMA acts as the "energizer unit."[37] Tremor, rigidity, and akinesia have been described following a low grade glioma involving the left SMA.[38] Petrovic[39] described eight patients with tumours of the SMA who could be categorized into two types: one with speech block, aphemia (mutism), and reiteration, and the other group with dysphasic manifestations occurring with lesions of the speech dominant hemisphere.

The anterior cingulate gyrus is very similar to the SMA which has connections with the cingulate gyrus.[37] The anterior cingulate gyrus has short connections with the dorso-lateral prefrontal cortex. Lesions of the cingulate gyrus, SMA, or both give rise to akinesia and mutism with restriction of spontaneous activity.[36] The anterior cingulate influences goal-directed behaviour through the cortical gateway for limbic motivation.[40] AM is typically associated with bilateral anterior cingulate lesions.[41,42]

AM has been reported following bilateral globus pallidal lesions.[43,44] De Long and Georgepolous[45] proposed a relationship between basal ganglia and the frontal cortical areas through a concept of motor and complex loops (Figure 4A). Lesions of the loop may therefore cause SMA dysfunction, and SMA dysfunction may lead to akinesia.[46]

a: Basic Neural Pathways, b: Major Dopaminergic tracts

AM also results from bilateral subcortical paramedian diencephalic and midbrain lesions.[8,23] The mesencephalic-diencephalic reticular activating system--which includes the midbrain, reticular formation, thalamus, and hypothalamus--has projections to the frontal lobe.[9,13]

Alexander et al.[48] described five frontal-subcortical circuits according to their function or cortical site. The motor and oculomotor circuits are associated with sensorimotor functions; the dorsolateral prefrontal and the orbitofrontal circuits are associated with cognitive functions, and the anterior cingulate circuit (medial frontal) with limbic mechanisms,[45] featuring reduced motivation, interest activity, maintenance, and apathy. Each circuit includes the frontal lobe, striatum, globus pallidus/substantia nigra thalamus, and connecting links between these structures.[50] The dorsal-lateral prefrontal circuit originates from the lateral convexity of the frontal lobe anterior to the premotor area and the circuit structures include the caudate nucleus, globus pallidus, substantia nigra, and ventral anterior dorsal medial nuclei of the thalamus. The medial frontal circuit begins in the anterior cingulate cortex and the circuit includes the nucleus accumbens (also known as the limbic striatum), globus pallidus, substantia nigra, and the medial dorsal nucleus of the thalamus. Damage to these areas or interruption of the circuit either by focal lesions or by diffuse brain damage could give rise to mutism and akinesia.

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