Cases reported "Akinetic Mutism"

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1/10. Event-related brain potentials in a patient with akinetic mutism.

    The clinical pattern of complete akinetic mutism (AM) was observed in a patient with a bilateral infarction of the anterior cerebral arteries extending to the rostral cingulate cortex and the supplementary motor areas. Since the patient was unable to produce any overt response, event-related brain potentials (ERPs) were used to obtain information about cortical processing of stimuli. Oddball tasks with simple acoustical stimuli and semantic categories were used. Verbal processing was further assessed by comparing event-related potentials to words compatible versus incompatible to the semantic context. Although the pattern of cortical responses was abnormal, differential responses were clearly obtained to semantically different word classes. Thus, the hypothesis about cortical non-responsivity of AM patients, drawn from several previous reports, was not supported. An ERP examination in AM patients can deliver information about their mental state, provided that the stimuli and tasks possess a wide range of informational complexity and motivational value.
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2/10. Posterior encephalopathy subsequent to cyclosporin A presenting as irreversible abulia.

    A case of cyclosporin A (Cys A)-induced posterior encephalopathy developed into persistent abulia despite rapid and marked improvement of abnormal T2- and FLAIR MRI hyperintense regions. diffusion-weighted MRI signal intensity was also high at the onset. This change is atypical in Cys A-induced encephalopathy and was thought to predict poor recovery from the encephalopathy. Persistent abulia was probably due to marked hypoperfusion in the whole cortex including bilateral frontal lobes and basal ganglia as detected by SPECT. Apart from the breakdown of the blood-brain barrier, direct toxicity of Cys A to the brain may play a role in the pathogenesis of chronic, irreversible encephalopathy.
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3/10. frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning.

    A middle-aged man suffering from acute carbon monoxide intoxication was clinically assessed to be in an akinetic and mute state. In order to elucidate regional cerebral disturbances, brain metabolism was investigated with fluoro-deoxyglucose positron emission tomography ((18)FDG-PET) 5.5 months after intoxication. Significantly reduced metabolic rates of glucose were revealed in selected brain regions, especially in both the frontal and anterior cingulate cortices, as well as in the subcortical white matter. Frontal and cingulate cortices showed a preserved metabolism of 35-53%, whereas the regional glucose consumption in cerebral white matter was reduced by more than 70%. In contrast, other areas of the brain such as the sensory-motor cortex, parts of the temporal lobes, basal ganglia and brainstem disclosed normal metabolic values. This lesion topography is discussed in relation to the development of akinetic mutism in the present case and in comparison with recent reports on the topic. Considering a plausible pathophysiology, akinetic mutism appears to be based on a different structural neuropathology when compared with the locked-in syndrome and the vegetative state. It is suggested that akinetic mutism is regarded as a specific condition characterized by injury of the frontal neuronal systems which promote executive functions.
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4/10. akinetic mutism in bilateral necrotizing leucoencephalopathy after radiation and chemotherapy: electrophysiological and autopsy findings.

    In a patient with akinetic mutism, extensive circumscribed bilateral lesions in the precentral part of the centrum semiovale, due to delayed necrotizing leucoencephalopathy after combined intravenous polychemotherapy and radiation, were found at autopsy. CT and somatosensory evoked potentials were normal and a slow alpha rhythm was present, but there was a lack of EEG desynchronization. akinetic mutism and the loss of desynchronization in this case are thought to result from interrupted thalamofrontal and extrathalamic reticulofrontal projections and the disconnection of the anterior limbic cortex.
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5/10. Cyanide-induced akinetic rigid syndrome: clinical, MRI, FDG-PET, beta-CIT and HMPAO SPECT findings.

    A 35-year-old female ingested a lethal dose of potassium cyanide in a suicide attempt. She survived following antidote therapy and intensive care. Following artificial coma she presented with an agitative state for several days followed by akinetic mutism, buccofacial and ideomotoric aphasia. Severe rigid-akinetic syndrome, dysarthria, dysphagia and generalized dystonia developed weeks later. MRI revealed lesions in the caudate and lentiform nuclei, precentral cortex, and cerebellum. SPECT by [123-I] 2 beta-carbomethoxy-3-beta-(4-iodophenyl)-Tropan on two occasions revealed progressive loss of dopamine transporter suggestive of nigral neuronal apoptosis. Striatal and frontal hypometabolism and hypoperfusion were found by FDG-PET and HMPAO SPECT.
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6/10. Spontaneous bilateral anterior cerebral artery occlusion resulting in akinetic mutism. A case report.

    An unusual case concerning a patient with akinetic mutism (AM) due to spontaneous bilateral anterior cerebral artery occlusion is reported. Brain CT scan revealed the presence of mild low density foci presenting an irregular enhancement, which followed the distribution of mesial frontal gyri and paracentral lobulus, bilaterally. Right and left carotid angiographies showed bilateral occlusion of the anterior cerebral artery. Our case is characterized by an exclusive localization of the infarction in the frontal cortex. This finding suggests that a limited damage involving the anterior cerebral arteries territory could be, on its own, responsible for the AM syndrome.
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7/10. akinetic mutism associated with bicingular lesions: clinicopathological and functional anatomical correlates.

    The clinical symptoms and neuropathological findings of three patients suffering from akinetic mutism were summarized. The patients showed almost absolute mutism and immobility and were unable to communicate in any way. The neurological signs varied from case to case. The pathological features common to all of the cases were bilateral lesions of the rostral part of the anterior cingulate gyri which overlapped onto the neighboring supplementary motor area, while differing as regards other damage. With the help of more recent neurobiochemical findings we tried to analyze the pathomechanism of akinetic mutism on the basis of the structures damaged. There seems to be an anatomic correspondence between the mesolimbocortical dopaminergic system and the circumscribed bilateral lesions of the medial prefrontal cortex. The study suggests that damage of the mesolimbocortical dopaminergic terminal fields in the anteromedial frontal cortex is essential for this specific type of akinetic mutism.
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8/10. akinetic mutism and parkinsonism associated with obstructive hydrocephalus.

    We report the case of a patient with idiopathic aqueductal stenosis and hydrocephalus who had several episodes of akinetic mutism, each preceded by shunt malfunction, that resolved with shunt revision. She also developed a parkinson's syndrome resistant to shunt revision but responsive to antiparkinsonian medications. The parkinson's syndrome and the episodes of akinetic mutism may be related to a reduction of dopaminergic input to the striatum and to the cingulate and frontal cortex brought about or worsened by ventricular dilatation.
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9/10. Mutism developing after bilateral thalamo-capsular lesions by neuro-Behcet disease.

    We described a 44-year old right-handed man showing mutism, left hemiplegia and pseudobulbar palsy after CT and MRI documented bilateral thalamo-capsular lesions by neuro-Behcet disease. Single photon emission tomography (SPECT) and xenon CT revealed hypoperfusion of the bilateral frontal lobes. The pathophysiological mechanism of mutism was discussed and we postulate that mutism might occur as the result of frontal lobe dysfunction due to the disconnection of thalamocortical fiber from thalamus to frontal cortex and that it could be interpreted as an incomplete form of akinetic mutism.
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10/10. akinetic mutism: a report of three cases.

    OBJECTIVES: To report 3 new cases of akinetic mutism, a clinical syndrome defined by silent immobility with preserved visual alertness not accountable by lesion of the areas and/or effector pathways of speech and voluntary movements. MATERIAL AND methods: Anatomopathological studies were performed in Cases 1 and 2; clinical follow-up, EEG, angiography and CT scans in Case 3. RESULTS: Case 1: Bipallidal necrosis; Case 2: Left pallidal necrosis with right frontoparietal cortico-subcortical infarction; Case 3: Striato-capsular infarction on the left side, involving the caudate nucleus and the anterior arm of the internal capsule, together with obstructive hydrocephalus. CONCLUSION: The roles of both globus pallidus and prefrontostriatal circuits in the onset of voluntary movements are discussed.
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