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.
Signs and Symptoms of Akinetic Mutism
Common Sign and Symptoms of Akinetic Mutism
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.