| Akinetic mutism | |
|---|---|
| Specialty | Neurology,Psychiatry |
Akinetic mutism is amedical condition wherepatients tend neither to move (akinesia) nor speak (mutism). It is the most extremedisorder of diminished motivation. Akinetic mutism was first described in 1941 as a mental state where patients lack the ability to move or speak.[1] However, their eyes may follow their observer or be diverted by sound.[1] Patients lack most motor functions such as speech, facial expressions, and gestures, but demonstrate apparent alertness.[2] They exhibit reduced activity and slowness, and can speak in whisperedmonosyllables.[1][3] Patients often show visual fixation on their examiner, move their eyes in response to anauditory stimulus, or move after often repeated commands.[1][2] Patients with akinetic mutism are notparalyzed, but lack thewill to move.[1] Many patients describe that as soon as they "will" or attempt a movement, a "counter-will" or "resistance" rises up to meet them.[4]
Akinetic mutism varies across all patients. Its form, intensity, and clinical features correspond more closely to its functional anatomy rather than to its pathology. However, akinetic mutism most often appears in two different forms: frontal and mesencephalic.[2]
Akinetic mutism can occur in the frontal region of the brain and occurs because of bilateralfrontal lobe damage. Akinetic mutism as a result of frontal lobe damage is clinically characterized ashyperpathic.[5] It occurs in patients with bilateral circulatory disturbances in the supply area of theanterior cerebral artery.[2]
Akinetic mutism can also occur as a result of damage to themesencephalic region of the brain. Mesencephalic akinetic mutism is clinically categorized assomnolent orapathetic akinetic mutism.[5] It is characterized byvertical gaze palsy andophthalmoplegia. This state of akinetic mutism varies in intensity, but it is distinguished by drowsiness, lack of motivation, hyper-somnolence, and reduction in spontaneous verbal and motor actions.[2][5]
Akinetic mutism can be caused by a variety of things. It often occurs after brain injury or as a symptom of other diseases.
Akinetic mutism is often the result of severefrontal lobe injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.[citation needed]
Many cases of akinetic mutism occur after a thalamic stroke.[3] Thethalamus helps regulate consciousness and alertness.[citation needed]
Another cause of both akinesia and mutism isablation of thecingulate gyrus. Destruction of the cingulate gyrus has been used in the treatment ofpsychosis. Such lesions result in akinesia, mutism,apathy, and indifference to painful stimuli.[7] Theanterior cingulate cortex is thought to supply a "global energizing factor" that stimulates decision making.[8] When the anterior cingulate cortex is damaged, it can result in akinetic mutism.[citation needed]
Akinetic mutism is a symptom during the final stages ofCreutzfeldt–Jakob disease (a rare degenerativebraindisease) and can help diagnose patients with this disease.[2][9] It can also occur in a stroke that affects bothanterior cerebral artery territories.[citation needed] Another cause isneurotoxicity due to exposure to certain drugs such astacrolimus andcyclosporine.
Other causes of akinetic mutism are as follows:
Akinetic mutism can be misdiagnosed asdepression,delirium, orlocked-in syndrome, all of which are common following a stroke.[3] 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.[3] 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.[citation needed]
Treatments using intravenousmagnesium 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.[11]
As seen in the case of Elsie Nicks, the puncture or removal of a cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst fills up again, the symptoms can reappear.[1]
Symptoms of akinetic mutism suggest a possible presynaptic deficit in thenigrostriatal pathway, which transmits dopamine. Some patients with akinetic mutism have shown to improve withlevodopa ordopamine agonist therapy,[12] or by repleting dopamine in the motivational circuit withstimulants,antidepressants, oragonists such asbromocriptine oramantadine.[6]
Other treatments includeamantadine,carbidopa-levodopa,donepezil,memantine, and oralmagnesium oxide.[6][11]
Fourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic mutism byHugh Cairns in 1941. She suffered from severe headaches her entire life and was eventually givenmorphine 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 rightlateral 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.[1]