Akinetic Mutism - Causes, Symptoms & Treatment

Akinetic mutism is a medical term describing patients who tend neither to speak ( mutism ) nor move ( akinesia ). Akinetic mutism is often due to damage to the frontal lobes of the brain. Mutism is a rare childhood condition characterized by a consistent failure to speak in situations where talking is expected. It results from bilateral damage to the orbital surface of the frontal lobes. The patient appears awake and has normal ocular movement but does not speak, is incontinent, and has minimal motor response to painful stimulation. 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. The syndrome of akinetic mutism is typically the result of bilateral hemispheric injury, usually involving the anterior cingulate gyri.

Diffuse brain damage underlies akinetic mutism in patients with Creutzfeldt-Jakob disease. It can also occur in a stroke that affects both anterior cerebral territories. Other locations for lesions producing akinetic mutism include the thalami, globus pallidus, internal capsule, and frontal white matter. These lesions are thought to disrupt anterior frontal subcortical circuits that subserve motivation. In our patient, the syndrome of akinetic mutism appears to be the result of a lesion in the body of the cingulate gyrus in one hemisphere in combination with the extension of the stroke into the body of the corpus callosum, effectively disconnecting the functional contralateral cingulate gyrus. In effect, this unilateral lesion disrupted bilateral pathways that are necessary in order to sustain normal motivation. The involvement of bilateral callosal fibers in the regions of the anterior cingulate may also explain the profound hemineglect that emerged as the akinetic mutism improved. The anterior cingulate cortex is part of a bihemispheric network of cortical, subcortical, and white matter structures that are involved in attention, including spatial attention. The left cingulate lesion and callosal disconnection may have sufficiently disrupted the patient's spatial attention network such that right visual neglect and anosognosia resulted.

Causes of Akinetic Mutism

Common Causes and Risk factors of Akinetic Mutism:

• Olfactory groove meningioma.
• Bilateral infiltration of the fornix.
• Environmental.factors
• Biological.factors
• Interpersonal factors
• Anxiety.

Signs and Symptoms of Akinetic Mutism

Common Sign and Symptoms of Akinetic Mutism

• Whispering speech.
• Demetia.
• Ataxia.
• Behavioral disturbance.
• Seizures.

Treatment for Akinetic Mutism

Common Treatment of Akinetic Mutism

• Treatment of akinetic mutism with bromocriptine.
• Behavior modification therapy is also helpful for akinetic mutism.
• Antidepressant medication such as , amphotericin B and zolpidem.