Cases reported "Mutism"

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1/6. Bilateral crossed cerebello-cerebral diaschisis and mutism after surgery for cerebellar medulloblastoma.

    A 7-year-old boy developed mutism after surgery for cerebellar medulloblastoma. Postoperative magnetic resonance imaging (MRI) showed atrophy of the cerebellar vermis and both cerebellar hemispheres, predominantly on the right side. Single photon emission computed tomography (SPECT) with technetium-99m-ethyl cysteinate dimer (Tc-99m ECD) revealed decreased cerebral blood flow (CBF) in the bilateral thalami, bilateral medial frontal lobes, and left temporal lobe in addition to the cerebellar vermis and both cerebellar hemispheres when mutism was manifest, indicating the existence of bilateral crossed cerebello-cerebral diaschisis (BCCCD). Circulatory disturbance in both cerebellar hemispheres secondary to tumor resection probably caused BCCCD in both cerebral hemispheres, predominantly in the left, via the dentatothalamocortical pathway (DTCP). With recovery of his mutism, CBF increased in the right thalamus, bilateral medial frontal lobes and left temporal lobe. Thus BCCCD was improved, with only a slight decrease in CBF still persisting in the left thalamus. The mechanism of mutism may have involved damage to the cerebellar vermis (the site of incision at operation), the left dentate nucleus (heavily infiltrated by the tumor) and the right dentate nucleus of the cerebellum (affected by circulatory disturbance secondary to acute postoperative edema). The SPECT findings suggested that mutism was associated with BCCCD-induced cerebral circulatory and metabolic hypofunction in the supplementary motor area mediated via the DTCP.
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2/6. mutism after evacuation of acute subdural hematoma of the posterior fossa.

    CASE REPORT: A 7-year-old boy was involved in a road traffic accident. A computed tomography scan revealed an acute subdural hematoma (ASDH) of the posterior fossa, traumatic subarachnoid hemorrhage, and distortion of the brain stem. Removal of the ASDH was completed 3.5 h after injury. After extubation, the patient rapidly recovered consciousness. He was able to follow commands, although he did not speak. He began to utter 14 days after the injury. His speech became normal 39 days after injury. A magnetic resonance imaging scan revealed a post-contusional change in the right cerebellum and an ischemic lesion in the pons. DISCUSSION: Immediate removal of the hematoma is the only therapy for patients with ASDH of the posterior fossa. Although any lesions of the dentate nucleus, red nucleus, thalamus, cerebral cortex, and pons, all of which are involved in this case, are able to cause mutism, his mutism was primarily caused by the severe ASDH of the posterior fossa. The transient nature of this syndrome suggests that the cause of the mutism is trauma-related edema and/or transient ischemia of these structures.
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3/6. Transient cerebellar mutism caused by bilateral damage to the dentate nuclei after the second posterior fossa surgery. Case report.

    The authors report on the case of a 6-year-old boy who underwent resection of a midline cerebellar tumor. The boy was able to speak fluently after the operation. Magnetic resonance (MR) imaging showed that the right dentate nucleus had been partially removed along with the tumor, but that the left dentate nucleus remained with the residual tumor. A second operation was performed to remove the residue, after which the child suffered mutism. Three weeks post-surgery, he could only communicate through gestures. He started speaking I week later and regained normal speech 2 months after the operation. Final MR imaging revealed gross-total removal of the tumor and dentate nucleus on the injured left side. The cerebellar mutism was considered to have been caused by bilateral damage to the dentate nuclei and not by unilateral damage.
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4/6. Pure mutism due to simultaneous bilateral lenticulostriate artery territory infarction.

    A case of pure mutism without pseudobulbar palsy and other neurological findings resulting from simultaneous bilateral lenticulostriate artery territory infarction is presented. A 45-year-old woman suffered a transient ischemic attack with nonfluent aphasia and right hemiparesis. Six months later, she developed pure mutism without oral apraxia, pseudobulbar signs, and motor deficits. magnetic resonance imaging revealed bilateral infarction in the lentiform nucleus regions. In the available data, there is only one report of simultaneous bilateral lenticulostriate infarction. To date, in all reported cases of mutism of subcortical vascular origin there are also various degrees of pseudobulbar signs and motor deficits and the responsible lesions are mostly consecutive. The case presented here is the first to show pure vascular mutism without other neurological findings.
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5/6. Postoperative mutism in neurosurgery. Report of two cases.

    mutism is defined as a state in which a patient is conscious but unwilling or unable to speak. It has been reported to occur in association with a multitude of conditions, including trauma, epilepsy, tumors, stroke, psychoses, and brain surgery. The cases of two patients who became mute in the immediate postoperative period are presented. The first patient developed mutism following removal of a parasagittal meningioma, and the second following removal of a posterior fossa medulloblastoma. It is believed that transient injury may have occurred to the supplementary motor cortex in the first case and to the dentate nuclei in the second case. It is interesting that these two areas are connected via pathways involving the ventrolateral nucleus of the thalamus, and that lesions of this thalamic nucleus can also lead to mutism. It therefore appears plausible that interruption of these pathways may be involved in the pathogenesis of mutism. Although mutism is an infrequent complication of brain surgery, neurosurgeons should be aware that it may occur following removal of lesions in these areas and that it is generally a transient condition.
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6/6. Reversible cerebral perfusion alterations in children with transient mutism after posterior fossa surgery.

    mutism is an infrequent and transitory complication observed following posterior fossa surgery. patients become mute in the immediate postoperative period, with restoration of speech within a few weeks in the absence of additional neurological alterations. The anatomical structures thought to be involved are the connections between the cerebellar dentate nucleus, the ventrolateral nucleus of the contralateral thalamus and the supplementary motor area. In an attempt to understand the pathophysiology of this syndrome, and to depict the perfusion of different brain areas semiquantitatively, in two children who had become mute after posterior fossa surgery we performed a Tc99M-HM-PAO SPECT study during the period of mutism and again when normal speech had returned. In one patient, who had a left cerebellar astrocytoma, the SPECT study showed a marked reduction of cerebral perfusion in the right fronto-parietal region, and in the other, who had a medulloblastoma, a left fronto-temporo-parietal perfusion alteration was observed. When the patients regained normal speech, the follow-up SPECT studies revealed normalization of the cerebral perfusion. This study demonstrates the occurrence of a focal dysfunction of cerebral perfusion in children with cerebellar mutism after posterior fossa surgery. These observations are useful in extending our understanding of the pathophysiology of this postoperative clinical syndrome.
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