Akinetic mutism

Symptoms and signs

• Lack of motor function (but not paralysis)
• Lack of speech
• Apathy
• Slowness
• Disinhibition

Causes

Akinetic mutism can be caused by a variety of things. It often occurs after brain injury or as a symptom of other diseases.

Frontal lobe damage

Akinetic mutism is often the result of severe frontal lobe injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.

Thalamic stroke

Many cases of akinetic mutism occur after a thalamic stroke.

Ablation of cingulate gyrus

Another cause of both akinesia and mutism is ablation of the cingulate gyrus. Destruction of the cingulate gyrus has been used in the treatment of psychosis. Such lesions result in akinesia, mutism, apathy, and indifference to painful stimuli. The anterior cingulate cortex is thought to supply a "global energizing factor" that stimulates decision making. When the anterior cingulate cortex is damaged, it can result in akinetic mutism.

Other

Akinetic mutism is a symptom during the final stages of Creutzfeldt–Jakob disease (a rare degenerative brain disease) and can help diagnose patients with this disease. It can also occur in a stroke that affects both anterior cerebral artery territories. Another cause is neurotoxicity due to exposure to certain drugs such as tacrolimus and cyclosporine.

Other causes of akinetic mutism are as follows:

• Respiratory arrest and cerebral hypoxia
• Acute cases of encephalitis lethargica
• Meningitis
• Hydrocephalus
• Trauma
• Tumors
• Aneurysms
• Olfactory groove meningioma
• Cyst in third ventricle
• Toxical lesions and infections of central nervous system
• Delayed post-hypoxic leukoencephalopathy (DPHL)
• Creutzfeldt–Jakob disease (mesencephalic form)
• Gerstmann–Sträussler–Scheinker syndrome

Diagnosis

Akinetic mutism can be misdiagnosed as depression, delirium, or locked-in syndrome, all of which are common following a stroke. Patients with depression can experience apathy, slurring of speech, and body movements similar to akinetic mutism. Similarly to akinetic mutism, patients with locked-in syndrome experience paralysis and can only communicate with their eyes. Correct diagnosis is important to ensure proper treatment. A variety of treatments for akinetic mutism have been documented, but treatments vary between patients and cases.

Treatment

Magnesium sulfate

Treatments using intravenous magnesium sulfate have shown to reduce the symptoms of akinetic mutism. In one case, a 59-year-old woman was administered intravenous magnesium sulfate in an attempt to resolve her akinetic mutism. The patient was given 500 mg of magnesium every eight hours, and improvement was seen after 24 hours. She became more verbal and attentive, and treatment was increased to 1000 mg every eight hours as conditions continued to improve.

Epidermoid cyst puncture

As seen in the case of Elsie Nicks, the puncture or removal of an intracranial epidermoid cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst recurs, the symptoms can reappear.

Dopamine agonist therapy

Symptoms of akinetic mutism suggest a possible presynaptic deficit in the nigrostriatal pathway, which transmits dopamine. Some patients with akinetic mutism have shown to improve with levodopa or dopamine agonist therapy, or by increasing dopaminergic transmission in the motivational circuit with stimulants, antidepressants, or agonists such as bromocriptine or amantadine.

Other treatments include amantadine, carbidopa-levodopa, donepezil, memantine, and oral magnesium oxide.

History

Fourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic mutism by Hugh Cairns in 1941. She suffered from severe headaches her entire life and was eventually given morphine to help with treatment. She began to enter a state of akinetic mutism, experiencing apathy and loss of speech and motor control. A cyst on her right lateral ventricle was tapped, and as soon as the needle advanced toward the cyst, she let out a loud noise and was able to state her name, age, and address. After her cyst was emptied, she regained her alertness and intelligence, and she had no recollection of her time spent in the hospital. The cyst was drained two more times over the next seven months and was eventually removed. After eight months of rehabilitation, Elsie no longer experienced headaches or akinetic mutism symptoms.