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At least 19 recordsLinked to original sources
PubMed1991

Mutism after removal of a vermian medulloblastoma: cerebellar mutism.

A case of mutism after removal of a vermian medulloblastoma from a 4-year-old girl is reported. Postoperatively, the patient was mute without disturbance of consciousness, language comprehension, or lower cranial nerve function. Computed tomography scans demonstrated no abnormal findings except for the surgical lesion in the posterior fossa. The mutism lasted for 78 days, followed by a period of dysarthria, but she gradually became fluent. The mechanism of "cerebellar mutism" is briefly discussed.

Cerebellar Neoplasms↗
PubMed1992

[Hereditary unilateral deaf-mutism as a variable manifestation of bilateral deaf-mutism or hearing loss].

A total of 2,519 patients with bilateral severe congenital deafness (deaf-mutism) from Central Switzerland were recorded during the period between 1834 to 1979. More recently, 31 persons with unilateral severe deafness were examined. By constructing genealogical charts going back to the 17th century, at least ten of these unilaterally deaf persons were shown to be related to patients with bilateral deafness (pedigrees I-IV). Some of them exhibited a more or less marked Klein- Waardenburg syndrome. The unilateral deafness of those patients was inherited and not acquired. Congenital unilateral deafness may be understood to be the result of the broad variability of the expressivity of acoustic defects.

Deafness↗
PubMed1992

Elective mutism as a variant of social phobia.

To examine the relationship between the syndromes of elective mutism and social phobia, a case of elective mutism associated with social phobia in a 12-year-old girl is presented, and the clinical literature regarding the syndrome of elective mutism is reviewed. Elective mutism or reluctance to speak in unfamiliar social situations may be a symptom of social phobia. Social anxiety is a nearly universal characteristic of children manifesting the syndrome of elective mutism. Elective mutism may respond to treatment with medications that also are effective in the treatment of social phobia. Elective mutism may be a manifestation of social phobia rather than a separate diagnostic syndrome. Pharmacologic treatment may be effective.

Child↗
PubMed1991

Mechanism of mutism following the transcallosal approach to the ventricles.

Transient mutism has been known as a common manifestation following callosotomy for medically intractable epilepsy, but its cause has not been clearly elucidated. In this paper, we report three cases of mutism following a transcallosal approach to tumours in the lateral and third ventricles and retrospectively analyze the surgical, neurological and radiological features which may suggest the cause of this type of mutism. Mutism may be a result of division of the corpus callosum. Suppression of the limbic system caused by lesions in the anterior cingulate gyrus, septum pellucidum, and fornix may have been of importance in at least two of these three cases. Impairments of the supplementary motor cortex, thalamus and basal ganglia may also be factors reducing speech production. The mechanism of such transient mutism seems to be a complex of two or more of these factors, and their combinations may be different from one case to the other.

Adult↗
PubMed1990

[Capsular pseudobulbar mutism in a patient of lacunar state].

A patient of mutism with pseudobulbar palsy and frontal lobe syndrome resulting from lacunar state was reported. The patient, a 64-year-old man, was admitted to Gifu University Hospital because of a decrease in spontaneous activity, lack of volition and anorexia. The CT scan, performed on July 29, 1987, demonstrated lacune in the right internal capsule (IC), periventricular lucency especially around the anterior horn of lateral ventricles, and ventricular dilatation. He was transferred to a medical ward because of repeated aspiration pneumonia. Neurological examination revealed mutism, pseudobulbar palsy, and frontal lobe signs. The CT scan, performed on March 30 1988, demonstrated the newly developed lacune in the left IC. The MRI also showed two coinciding lacunes, one in the genu of the right IC and the other in the anterior limb of the left IC. The SPECT with 123I iodoamphetamine showed decreased blood supply predominantly to the frontal lobes. A mechanism by which the mutism occurs is discussed from two points of view, pseudobulbar palsy and frontal lobe syndrome. He developed initially frontal lobe syndrome in which paucity of spontaneous speech was noted. The CT scan at that time demonstrated lacune in the right IC. About eight months later when he became mute, the CT scan showed lacunes in bilateral ICs without any other low density areas in frontal language areas such as Broca's area, subcortical area and supplementary motor area. As the MRI showed that the right lacune was in the genu but the left lacune was in the anterior limb of IC, the left cortico-bulbar tract was thought to be not directly involved. The SPECT showed decreased blood supply predominantly to the frontal lobes. Although dysphagia improved, mutism did not improve at all. Therefore it is postulated that both pseudobulbar palsy and frontal lobe dysfunction might play a role in producing the mutism of this patient.

Akinetic Mutism↗
PubMed1990

Cyclosporin-associated akinetic mutism and extrapyramidal syndrome after liver transplantation.

Three patients developed akinetic mutism on the third day after the introduction of intravenous cyclosporin A, given for immunosuppression after liver transplantation. One patient in addition developed a florid orofacial dyskinesia, which resolved completely, as did the akinetic mutism, after withdrawal of cyclosporin. In these patients the time course of the akinetic mutism and extrapyramidal syndrome, which developed in the absence of any other identifiable cause, suggests cyclosporin A was the precipitating factor. Subsequently, two of the patients showed signs of pseudobulbar palsy with abnormalities in the pons on MRI scanning, suggesting central pontine myelinolysis (CPM). None of the patients had experienced significant fluctuations in serum sodium or other risk factors for central pontine myelinolysis and the exact relationship to the earlier cyclosporin related mutism was not clear.

Adult↗
PubMed1975

[Akinetic mutism and bicingular softening. 3 anatomo-clinical cases].

The authors describe three pathological cases of akinetic mutism with, as a common basic lesion, bilateral infarction of the cingulate gyrus secondary to aneurysm of the anterior communicating artery (case n degrees 1), to a huge olfactory meningioma (case n degrees 2), both operated on, and to atheromatous occlusion of the anterior cerebral arterial system (case n degrees 3). These three cases enable a variety of "anterior and waking" akinetic mutism to be described which is unusual enough to be compared with other mesencephalic and diencephalic aspects of this syndrome. It is in fact an akinetic mutism characterized by: a certain dissociation in its non-response to various stimuli, a particularly marked appearance of wakefulness when day-time alertness is considered, conservation of the waking-sleeping rhythm, perception and reaction unpredictable and paradoxical in both degree and quality, complete absence of any spontaneous verbal communication in contrast to relative break-down of solicited communication which is infrequent, uncertain and unresponsive to the usual methods of stimulation, without any possibility of a code. In addition, there is a remarkable mimic and segmental general akinesia, resistant to the usual nociceptive stimuli, but sensitive to slight excitation of the manual and oral zones. Besides this special akinetic mutism, there are variously systematised signs, mostly asymmetrical, indicating lesion of the cortico-sub-cortical frontal structures bordering on the gyrus cinguli. This unusual behaviour pattern corresponds in these three cases to extensive anterior bilateral ischemic lesions of the cingulate gyrus regularly associated with bilateral infarctions confined to the medial aspect of F1 in the superficial territory of the two anterior cerebral arteries, to possible neurosurgical changes (ablation of the right frontal pole) and to compressive or ischaemic lesions of the gyrus rectus. These exclusively cortico-sub-cortical associated lesions are in contrast with the remarkably intact caudate nuclei, the pallidal, thalamic, hypothalamic and septal formations and the anterior pillars of the fornix. These findings compared with the results of experimental research carried out by M. Kennard, help, if help is needed, to resolve the apparent contradictions between the effects of therapeutic cingulectomies or cingulotomies and the scanty pathological data already available in cerebral vascular pathology.

Adult↗
PubMed1992

Acquired mutism: physiopathy and assessment.

The speechless patient presents a unique challenge to the clinician working with neurologically impaired adults. Acquired speechlessness, or mutism, has been associated with a variety of clinical states and syndromes after damage to central and peripheral nervous system structures. The intent of this paper is to summarize the reported states and syndromes associated with acquired mutism (eg, persistent vegetative state, akinesia), and to organize this information in a framework for clinical assessment of the speechless patient. For the purpose of discussion, speech production is divided into five interrelated processes: arousal; cognitive processing; affect and drive; motor initiation, planning, programming, and coordination; and execution of movement. Disorders characterized by mutism are classified according to the process or processes of speech production that primarily are affected. Each subtype of acquired mutism is characterized by a cluster of neurologic signs, which has been incorporated into a decision-making framework for use in a clinical setting.

Affect↗
PubMed1989

Transient mutism following removal of a cerebellar tumor. A case report and review of the literature.

A 14-year-old boy developed mutism 24 h after the removal of a vermian low-grade astrocytoma. The mutism was not accompanied by long tract signs or cranial nerve palsies. He started to regain his speech 3 weeks postoperatively, and 4 months after the operation he was minimally dysarthric. Seven similar cases of transient muteness following cerebellar operations and not accompanied by long tract signs or cranial nerve palsies have been reported in the literature. In most of them there was delayed postoperative onset of the mutism. In all patients the recovery of speech started to appear 2 weeks to 3 months postoperatively and passed through a dysarthric phase. The absence of long tract or other brain stem signs, together with the presence of dysarthria during the recovery of speech, suggests a cerebellar cause for the transient muteness.

Adolescent↗
PubMedDate not supplied

Cerebellar mutism after posterior fossa surgery.

A large midline posterior fossa medulluloblastoma and a cerebellar arteriovenous malformation with associated clot were moved with postoperative mutism. Mutism was immediate and resolved into an ataxic dysarthria with residual mild dysarthria at 3 months. The literature is reviewed, and the clinicopathological and neurophysiological data of cerebellar function in speech are discussed. Acute injury to the midportion of the cerebellum with or without dentate nuclear involvement can cause a spectrum of speech disturbances. The more widespread the injury to the midportion of the cerebellum with dentate nuclei involvement the greater the risk of developing postoperative mutism.

Adolescent↗
PubMed1992

Controlled investigation of the amobarbital interview for catatonic mutism.

OBJECTIVE: Clinical reports over the last 60 years suggest that the amobarbital interview is effective in relieving catatonic symptoms. This has never been substantiated with methodologically sound trials. The authors postulated that a randomized blind comparison of intravenous amobarbital and saline would demonstrate the superiority of amobarbital in relieving catatonic mutism. METHOD: The subjects were 20 inpatients with catatonic mutism. They were randomly assigned to either saline (N = 10) or a 5% amobarbital solution (N = 10), and the infusions were administered intravenously at a rate of 1 cc/min or less over 10 minutes by a blinded physician. A second blinded physician administered a semistructured interview during the infusion to control for the effect of suggestion. A third blinded physician rated patient responsiveness, reactivity, and arousal. Any patient who was unresponsive to the initial infusion was crossed over to the other infusion. Interviews were videotaped for determination of interrater reliability. RESULTS: In the initial infusions, six of 10 patients responded to amobarbital and zero of 10 responded to saline. Four of the saline nonresponders responded when given amobarbital. Response was evident by the 4th minute of the amobarbital infusion. Interrater reliability was high. The responders and nonresponders differed significantly in the variance of the weight-adjusted amobarbital dose, and the responders tended to be older and female. CONCLUSIONS: Intravenous amobarbital is superior to saline in relieving catatonic mutism, although only 50% of these patients responded. The nonresponders were distinguished from the responders by a greater variance in the weight-adjusted dose of amobarbital.

Adult↗
PubMedDate not supplied

Unexpected recovery of functional communication following a prolonged period of mutism post-head injury.

A case is presented of a seven-year-old female who showed an unexpected recovery of functional communication skills following a prolonged period of traumatic mutism subsequent to a severe closed head injury. The patient initially presented as comatose. A period of mutism subsequent to the coma extended for ten months. Following this protracted period of mutism the child demonstrated rapid and unexpected recovery of functional communication skills, despite the persistence of higher level language deficits. The findings of a neurological assessment, neuroradiological assessment and battery of speech/language tests are described. The present case is discussed in light of the existing literature on recovery from paediatric head trauma.

Brain Damage, Chronic↗
PubMed1991

Elective mutism: origins in stranger anxiety and selective attention.

Through a focus on the events of early infancy, the author interprets elective mutism on the basis of the infant's responses to discrepancies from expected stimuli. Initially, the child's silence derives from a "freezing" of action when exposed to perceived danger. Subsequently, aberrant or fearful stimuli are minimized by the child's apparent unresponsiveness. Through identification with the parent, the child imbues elective mutism with information value as a pause to signal impending communication. Mutism later represents an identification that is displaced from the parent to "stranger" adults.

Attention↗
PubMedDate not supplied

[Post-traumatic mutism. A report of five cases (author's transl)].

After a review of current concepts about post-traumatic mutism, the authors describe five patients with this unusual symptom. The study extends on a long follow-up period. Differential diagnosis and possible neurological and psychopathological factors are discussed. Analysis of their personal observations leads the authors to think that there is a relationship between the length of coma and the duration of mutism. Frontal and/or bilateral lesions seem to be more likely to produce post-traumatic mutism, as does the existence of emotional disturbances or depressive symptoms in past history.

Adolescent↗
PubMed1992

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.

Adult↗
PubMed1992

Mutism after cerebellar medulloblastoma surgery.

The case of a 9-year-old boy is presented, who developed transient mutism after removal of a medulloblastoma in the region of the cerebellar vermis. The mutism disappeared within 6 months. Neither reduction of consciousness nor disturbances of caudal cranial nerves or phonation ever appeared. The case is discussed with regard to its phenomenology, pathogenesis, and etiology, corresponding case reports are also taken into consideration.

Brain Edema↗
PubMed1989

Methylphenidate in amytal-resistant mutism.

Methylphenidate eliminated mutism in a catatonic schizophrenic after Amytal had failed. Response permitted an adequate clinical evaluation and temporary resumption of eating, self-care and sociability. This suggests that methylphenidate has a useful role in the clinical evaluation of the mute patient who fails to respond to Amytal and that 2 psychopharmacological varieties of catatonic mutism may exist.

Adult↗