Cases reported "Akinetic Mutism"

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1/8. Recovery of children after severe head injury. Psychoreactive superimpositions.

    After the regaining of consciousness and awareness in the strange environment of an intensive care unit, an injured child is exposed to a situation of extreme psychological impact. This situation, in addition to a probably organically changed reactivity, is liable to provoke a particular, abnormal psychic response. The abnormal reaction can follow the pattern of a feigned-death response and thus mimic an organic coma vigile (apallic state). The resulting psychoreactive stuporous state ("Sleeping beauty syndrome") may lead to a misjudgement of the recovery degree and may delay early rehabilitation. With the help of a representative case, the clinical manifestation, course, and treatment of this reactive juvenile syndrome are presented. The interaction of physiogenic and psychogenic factors responsible for some psychiatric sequelae during the early period after head injury is emphasized.
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2/8. Preserved auditory cognitive ERPs in severe akinetic mutism: a case report.

    kinetic mustism is a dramatic deficit in spontaneous initiation of voluntary motor and speech acts, usually secondary to bilateral lesions of the anterior cingulate cortices and supplementary motor areas [Principles of neurology, McGraw-Hill, new york, 1989]. Given the obvious limitations of traditional neuropsychological testing in this clinical context, the use of neurophysiological tools such as bedside auditory cognitive event-related potentials (ERPs), recently proven to be relevant to evaluate comatose and vegetative patients [Clin. Neurophysiol. 110 (9) (1999) 1601; news Physiol. Sci. 17 (2002) 38], may constitute an interesting alternative. Here, we present the ERPs of a 38-year-old right-handed woman with severe akinetic mutism recorded in a passive auditory odd-ball paradigm. In spite of this severe clinical state, we could observe the presence of a "Mismatch Negativity", and of a larger P300 in rare trials than in frequent ones. By revealing a high level of cognitive integration of environmental auditory information, our study emphasizes the potential clinical relevance of MMN and P300 recordings in akinetic mutism to assess patient cognitive functioning.
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3/8. 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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4/8. MRI findings from a case of fulminating adult-onset measles encephalitis.

    We report a rare case of fulminating adult-onset measles encephalitis. A 34-year-old man developed a comatose state after measles eruptions and ultimately akinetic mutism. Titers of anti-measles IgM antibodies were elevated in both serum and cerebrospinal fluid. brain magnetic resonance imaging (MRI) 3 months after onset revealed widespread hyperintense lesions in the periventricular white matter and marginal hyperintense lesions in the brainstem on fluid-attenuated inversion recovery and diffusion-weighted images. The marginal lesions in the brainstem are similar to subpial demyelinating lesions seen in postinfectious encephalomyelitis. This case of encephalitis may be related to an autoimmune-mediated process triggered by measles infection.
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5/8. Coma vigil masquerading as psychiatric illness.

    A patient is described who had the hyperpathic variety of akinetic mutism (coma vigil), which was mistaken for a dissociative state. The case discussion emphasizes the importance of differentiating neuropsychiatric syndromes from those which are purely psychiatric in nature in order that appropriate treatment may be given.
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6/8. Computed tomographic findings in akinetic mutism.

    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.
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7/8. Bilateral symmetrical softening of the thalamus.

    The clinical and pathological data of a 48 year old patient who survived 40 days are reported. Her disturbance of consciousness corresponded to an apallic syndrome, which 12 days later bacame akinetic mutism. Symmetrical softening involving the medial thalamic nuclei from the plane of the corpora mamillaria to the red nuclei was found. The ischemic lesion might be explained by transient circulatory collapse combined with hypoplasia of the vertebrobasialr arteries. On the EEG slight irregular alpha activity was recorded (alpha coma) and external stimuli elicited theta-delta waves (paradox activation). A survey of the literature of akinetic mutism is included and the correlation between non-hypnoid unconsciousness and EEG is discussed.
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8/8. Locked-in syndrome caused by a tumor.

    A case of locked-in syndrome is described. Clinical and radiologic evidence suggested the presence of a brain-stem tumor. autopsy showed that the patient had a reticulum cell sarcoma. This is the first reported case of locked-in syndrome caused by a tumor.
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