出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/07/31 11:52:16」(JST)
Akinetic mutism is a medical term describing patients tending neither to move (akinesia) nor speak (mutism). Akinetic mutism was first described in 1941 by Cairns et al. 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 whispered monosyllables.[1][3] Patients often show visual fixation on their examiner, move their eyes in response to an auditory stimulus, or move after often repeated commands.[1][2] Patients with akinetic mutism are not paralyzed, but lack the will 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 bilateral frontal lobe damage. Akinetic mutism as a result of frontal lobe damage is clinically characterized as hyperpathic.[5] It occurs in patients with bilateral circulatory disturbances in the supply area of the anterior cerebral artery.[2]
Akinetic mutism can also occur as a result of damage to the mesencephalic region of the brain. Mesencephalic akinetic mutism is clinically categorized as somnolent or apathetic akinetic mutism.[5] It is characterized by vertical gaze palsy and ophthalmoplegia. 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]
Symptoms of akinetic mutism progress over time.[2] The occurrence of akinetic mutism takes place approximately four months after the symptoms first appear.[2]
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 severe frontal lobe injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.
Many cases of akinetic mutism occur after a thalamic stroke.[3] The thalamus helps regulate consciousness and alertness.
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.[7] The anterior 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.
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.[2][9] 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:
Akinetic mutism can be misdiagnosed as depression, delirium, or locked-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.
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.[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 the nigrostriatal pathway, which transmits dopamine. Some patients with akinetic mutism have shown to improve with levodopa or dopamine agonist therapy,[12] or by repleting dopamine in the motivational circuit with stimulants, antidepressants, or agonists such as bromocriptine or amantadine.[6]
Other treatments include amantadine, carbidopa-levodopa, donepezil, memantine, and oral magnesium oxide.[6][11]
Fourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic mutism by Cairns in 1941. She suffered from severe headaches her entire life and was eventually given morphia 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.[1]
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リンク元 | 「日本昏睡尺度」「無動性無言症」「無動無言」 |
関連記事 | 「akinetic」 |
1.覚醒している(confusion, senselessness, delirium) | ||
1 | だいたい意識清明だが、今ひとつはっきりしない | |
2 | 見当識障害あり | |
3 | 名前、生年月日がいえない | |
2.刺激すると覚醒する(stupor, lethargy, hypersomnia, somnolence, drowsiness) | ||
10 | 呼びかけで容易に開眼する 合目的的な運動(例えば、右手を握れ、離せ)をするし、言葉も出るが、間違いが多い | |
20 | 大きな声、または体をゆさぶることにより開眼する 簡単な命令に応ずる(例えば、何らかの理由で開眼できない場合の離握手) | |
30 | 痛み刺激で辛うじて開眼する 痛み刺激をくわえつつ呼びかけを繰り返すとかろうじて開眼する | |
3.刺激しても覚醒しない(deep coma, coma, semicoma) | ||
100 | はらいのける動作をする | |
200 | 手足を少し動かしたり顔をしかめたりする(除脳硬直を含む) | |
300 | 全く動かない |
間脳から上部脳幹にかけての網様体や脳梁・帯状回の損傷によるもので、四肢の自発運動はみられず無言であるが、嚥下機能は保たれ、対象を注視したり、追視するなどの眼球運動もみられる。睡眠覚醒のリズムも保たれる。
失外套症候群 | 無動性無言症 | 閉じ込め症候群 | |
障害部位 | 両側大脳半球の広範な障害 | 視床下部・脳幹 | 両側の橋底腹側部・延髄 |
障害の原因 | 変性疾患・無酸素症・一酸化炭素 | 梗塞・腫瘍 | 梗塞(脳底動脈血栓症)・損傷 |
脳波 | 低振幅徐波 | 高電位徐波 | 正常パターン |
意識障害 | 有 | 有(軽度) | 無 |
睡眠覚醒リズム | 有(覚醒時開眼) | 有 | 有 |
周囲の状況認知 | 不可 | 不可 | 可能 |
意思伝達 | 不可 | 不可 | 眼球運動や開閉眼で可 |
発話 | 不可 | 不可 | 不可 |
.