Tracing volitional recovery in post-stroke akinetic mutism using longitudinal microstructure imaging: Insights from a single case study
Jie ZhangYingqiao WangZhenyu ShuYao OuyangXingru ZhangHuiqi WangLi ZhangShan FangXiangming YeJuebao Li
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Akinetic mutism
Stroke
Tracing
Akinetic mutism
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• Brain-injured children who progress from coma to a sleeplike state of akinetic mutism are often misinterpreted by their parents as having improved. In children with akinetic mutism caused by extensive destruction of the cerebral gray matter, the computed tomographic scan may demonstrate the irreversible nature of the pathologic changes. (AJDC1984;138:166-167)
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Akinetic mutism
Anterior cerebral artery
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Akinetic mutism is a clinical syndrome in which the patient is unable to speak (mutism) or move (akinesia). Various brain lesions can induce akinetic mutism. We attended a 71-year-old woman who presented with akinetic mutism caused by bilateral anterior cerebral artery infarction. The patient improved after the administration of levodopa combined with carbidopa, in response to visual and verbal stimuli. Increased verbal output and spontaneous motor activities were also noted. Levodopa may be helpful to the treatment of akinetic mutism. (J Korean Acad Rehab Med 2007; 31: 238-242)
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Carbidopa
Anterior cerebral artery
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Methionine/methionine type 1 (MM1-type) sporadic Creutzfeldt-Jakob disease (sCJD), known as the 'classic type,' shows typical clinicopathological sCJD findings. In general, patients reach an akinetic mutism state within a few months of disease onset and die soon after if supportive therapies are not administered. Here, we describe remarkable neuropathologic observations of MM1-type sCJD in a 48-year-old, Japanese man with an unusually prolonged akinetic mutism state. In the early disease stages, the patient exhibited abnormal behaviour with gait disturbance and rapidly progressive cognitive dysfunction. Diffusion-weighted magnetic resonance imaging revealed extensive cerebral cortical hyperintensity. Prion protein (PrP) gene analysis revealed no mutations, and the polymorphic codon 129 exhibited methionine homozygosity. Although the patient remained stable with tube feeding for more than 2 years after reaching the akinetic mutism state, he died because of central respiratory failure 30 months after disease onset. Neuropathologic investigation showed extensive devastating lesions, such as status spongiosus, and typical spongiform changes could no longer be observed in the cerebral neocortex. Conspicuous pyramidal tract degeneration was observed. However, the regions commonly preserved in MM1-type sCJD pathology were still relatively preserved. Immunostaining revealed extensive diffuse synaptic-type PrP deposition in the grey matter. The pathological findings suggested that sCJD is a neurodegenerative disease that shows system degeneration; there are primary and secondary degenerative regions and distinct preserved regions, even in cases with prolonged disease duration. In addition, it is considered that there is a limited survival period for MM1-type sCJD, even if active symptomatic treatment is provided.
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Degeneration (medical)
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Akinetic mutism is a syndrome caused by various etiologies, and characterized by silent immobility and preserved alertness. The repetitive ventriculoperitoneal shunt for the recurrent hydrocephalus can be a forerunner of that. We present a man with akinetic mutism following two times of ventriculoperitoneal shunt revision. Akinetic mutism of the patient may be caused by the damage on the ascending dopaminergic projections. Symptoms were not alleviated by the normalization of ventricular size but by a large dose of bromocriptine.
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A 25-year-old woman with multiple sclerosis and an affective disorder probably secondary to MS presented with multiple neurological signs and symptoms suggestive of active MS, most prominently akinetic mutism. Spinal fluid analysis and MRI supported a diagnosis of active MS. SPECT and EEG were nonspecifically abnormal. After 6 weeks of severe akinetic mutism refractory to one ECT treatment and trials of steroids and stimulants, the patient recovered spontaneously over a 2-month period. An acute brainstem lesion seen on MRI may explain this patient's akinetic mutism.
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Refractory (planetary science)
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Akinetic mutism
Perseveration
Frontal lobe
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Akinetic mutism is described in various clinical presentations but typically is defined as a state wherein the patient appears awake but does not move or speak. It can be divided into two different subtypes; the most common subtypes depend on the lesion location, mesencephalic-diencephalic region, also called apathetic akinetic mutism (somnolent mutism), and those involving the anterior cingulate gyrus and adjacent frontal lobes called hyperpathic akinetic mutism. The pathway of akinetic mutism is believed to originate from circuits that link the frontal and subcortical structures. This case reports a 48-year-old African American female with bilateral anterior cerebral artery stroke and akinetic mutism with coexisting thyroid storm. This patient with bilateral anterior cerebral artery infarcts presented with characteristics that are typical for akinetic mutism such as having intact eye movements but an inability to respond to auditory or visual commands. With the incidence of bilateral anterior cerebral artery (ACA) ischemic stroke being rare and the incidence of akinetic mutism secondary to ischemic stroke even rarer, we suspect that this patient potentially had a unilateral occlusion of anomalous anterior cerebral vasculature.
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Stroke
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Akinetic mutism
Perseveration
Disinhibition
Apathy
Apraxia
Stroke
Frontal lobe
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