Akinetic mutism


Akinetic mutism

Description, Causes and Risk Factors:

akinetic mutism

Subacute or chronic state of altered consciousness, in which the patient appears alert intermittently, but is not responsive, although his/her descending motor pathways appear intact; due to lesions of various cerebral structures.

Akinetic mutism describes a situation where a patient is alert but unable to move or talk. These symptoms are caused by brain damage, and the functioning of the rest of the body is unaffected. The brain damage can be caused by various issues such as infections, toxins, or degenerative brain disease. This condition is a symptom of a problem and not a disease in itself.

Types:

    Hyperpathic akinetic mutism: When the frontal lobe is involved, the akinetic mutism is known as hyperpathic akinetic mutism.

  • Somnolent akinetic mutism: When the mesencephalic region is damaged, the condition is called somnolent akinetic mutism.

Akinetic mutism may be caused by toxins such as carbon monoxide or drugs. The condition can also result from infections from agents like multiple sclerosis or from swellings caused by diseases such as measles or HIV. Hydrocephalus, which is also known as water in the brain, a condition which can be present at birth or as a result of trauma, can be another cause.

Degenerative diseases like Creutzfeld-Jakob disease or other forms of dementia can also cause it. Tumors that affect the brain regions involved can also be a cause, as can trauma to the frontal lobes. Problems with the circulatory system supplying the brain, such as blood clots or hemorrhages, can also damage the brain.

Risk Factors:

    Olfactory groove meningioma.

  • Bilateral infiltration of the fornix.

  • Environmental.factors.

  • Biological.factors.

  • Interpersonal factors.

  • Anxiety.

This is an appraisal of the varied clinical presentation and the neural substrate for akinetic mutism following stroke. This is a descriptive study of eight selected patients with akinetic mutism following infarction/hemorrhage in different regions of the brain with characteristic syndromes. They involved the critical areas namely, the frontal (cingulate gyrus, supplementary motor area and dorsolateral 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 behavior. Akinetic mutism could be explained by damage to the frontal lobe and or interruption of the complex frontal subcortical circuits.

Symptoms:

Symptoms may include:

    Whispering speech.

  • Dementia.

  • Ataxia.

  • Behavioral disturbance.

  • Seizures.

Diagnosis:

The diagnosis is important as akinetic mutism is often misdiagnosed as depression, delirium and locked-in-syndrome. Doctors diagnose the condition through magnetic resonance imaging techniques and may take cerebrospinal fluid samples to look for an infectious cause.

Treatment:

Treatment involves treating the causal agent, and a patient may also receive medication to support brain signaling, such as a dopamine agonist. A patient with akinetic mutism shows symptoms that are similar to other recognized conditions, such as catatonia in psychiatric patients and locked-in state in paralysis patients, but it is a distinct medical condition.

The case study of a 53-year-old male patient who developed akinetic mutism for a period of 7 months after a subarachnoid hemorrhage. The hemorrhage was caused by a ruptured aneurysm in the right anterior communicating artery, followed by a secondary infarction in the territory of the right anterior cerebral artery. Baseline brain F-18 fluorodeoxyglucose positron emission tomographic images revealed decreased glucose metabolism in both frontal lobes. Treatment with atomoxetine, a selective norepinephrine reuptake inhibitor, for a period of 8 weeks led to a clinically significant improvement in the patient's cognitive function and activities of daily living. A subtraction brain positron emission tomographic analysis after atomoxetine medication revealed increased cerebral glucose metabolism in both the premotor and visual association cortices. Thus, we suggest that atomoxetine can be a useful therapeutic option in the treatment of chronic akinetic mutism.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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