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PubMed2006

[MM1 variant of sporadic Creutzfeldt-Jakob disease with long duration akinetic mutism state].

INTRODUCTION: When patients present with a characteristic clinical picture of Creutzfeldt-Jakob disease (CJD) associated with positive 14-3-3 assay, periodic sharp wave complexes, high-signal of the striatum on magnetic resonance imaging, and homozygosis methionine (M) in codon 129, the median survival is 4 to 6 months. CLINICAL CASE: We report a 58-year-old woman with these typical features who survived 21 months, 19 of them in an akinetic mutism state. The autopsy confirmed the diagnosis of the most common CJD phenotype (MM1), usually associated with a shorter survival, and demyleinitation of the white matter (panencephalopathic form). CONCLUSIONS: The MM1 variant of CJD, with a rapidly progressive course leading into an akinetic mutism shortly after disease onset can be followed by a long akinetic mutism state. This profile is suggestive of panencephalopathic form and should be taken into account when counselling about survival.

Akinetic Mutism↗

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↗

PubMed1989

Elective mutism: report of a case successfully treated by a family doctor.

Elective mutism is a rare psychological disorder of multiple etiology, wherein intellectually normal, nonpsychotic children, who can talk, remain silent with all individuals except a small group of intimate relatives and peers. Certain characteristics and relationship patterns are typically found in the family of the affected child. This report details elective mutism in a young girl in the author's family medicine practice and the treatment attempted by different therapists over a period of several years. Only when all other treatment had failed did the author, by default, accept responsibility for the case. Based on his special relationship as the child's family doctor, and one hypothetically valid interpretation of the function played by the girl's silence, the child's speech was unblocked within a short time and is the first reported case of elective mutism successfully treated by a family doctor.

Child, Preschool↗

PubMed1987

[Akinetic mutism from recurrent hydrocephalus: successful treatment with levodopa, bromocriptine and trihexyphenidyl].

A case of akinetic mutism was reported with reference to a marked improvement by levodopa, bromocriptine and trihexyphenidyl. A 39-year-old male, first seen on February 2, 1981, had an occipitalgia, accompanied by nausea and vomiting. For several months before this consultation, the patient had suffered from asthenopia. Brain CT scan and cerebral angiogram demonstrated internal hydrocephalus due to aqueduct stenosis of unknown etiology. After a ventriculoperitoneal shunt operation on February 20, 1981, he completely recovered. Two years and a half after the shunt insertion he had no difficulty in his daily life. He reentered the hospital on December 21, 1983, because of personality change, mental deterioration and bradykinesia. Brain CT scan showed recurrent hydrocephalus resulting from shunt blockage. Following the shunt revision, hydrocephalus was resolved. Nevertheless, the patient did not return to his previous state. And he became bed-ridden, incontinent of urine, and unable to take fluids or foods, following which he went into a state of akinetic mutism. Other neurological findings were as follows: upward gaze palsy, impaired convergence, convergence nystagmus, plastic rigidity of neck and all four limbs, and diffuse hyperreflexia with right Babinski's sign. Abnormal involuntary movement was not seen. On March 27, 1984, levodopa therapy was instituted and on April 2, trihexyphenidyl was combined with levodopa. Shortly after administration of levodopa and trihexyphenidyl, akinetic mutism began to improve, but upward gaze palsy was not affected. He began to speak and could walk unassisted by the end of July.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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↗

PubMed1995

[Transient cerebellar mutism after removal of a posterior fossa tumor in two cases].

We have reported the cases of two young patients who presented transient mutism in the course of recovery from removal of a cerebellar medulloblastoma. Although cerebellar symptoms were observed immediately after surgery, neither consciousness disturbance nor sensory aphasia was observed when the patients were mutic. From the analysis of serial magnetic resonance imaging (MRI). Gd-enhanced regions were noticed in the dentate nucleus and the cerebellar peduncle when mutism appeared, and they disappeared when mutism was gone. Although the mechanism of this interesting symptom is not clear, these MRI findings may indicate that focal ischemia or edema associated with surgical procedure may play a role in the appearance of this symptom.

Adolescent↗

PubMed1993

Transient "cerebellar" mutism in lesions of the mesencephalic-cerebellar region.

Four patients aged from 20 to 48 years with transient mutism are presented: 3 patients underwent surgery for midline tumours of the mesencephalic-cerebellar region (medulloblastoma in two cases and pinealoblastoma in one), at times attached to one or both lateral recesses of the IV ventricle. One patient was hospitalized and treated for brain-stem ischemia. All patients developed mutism 48 to 72 hours after surgery; in the patient with brain-stem softening mutism appeared 72 hours after admission. All the patients had unimpaired consciousness and no deficits of lower cranial nerves. Speech, always normal in the first hours after surgery, was regained after a period of 6-16 weeks. Various hypotheses for this speech disorder are analyzed.

Adult↗

PubMedDate not supplied

A case of childhood shigellosis with mutism.

Bacillary dysentery, an acute infection caused by various strains of Shigella, is characterized by abdominal pain, tenesmus, and diarrhea with mucus, pus and blood. Neurologic manifestations including meningismus, delirium and convulsions may accompany the infection. We describe a thirteen-year-old girl who presented with headache, convulsion and loss of consciousness at the onset and developed diarrhea with blood and pus after hospitalization. The diagnosis of shigellosis was based on clinical data and isolation of the microorganism in the stool specimen. After improved physical functions, the patient developed mutism that continued for two days in the course of her illness, despite having no history of neurologic or psychological problems. She was diagnosed by a psychiatrist with organic mental syndrome NOS (Not Otherwise Specified) according to DSM-III-R criteria. None of the conditions that may cause mutism could be confirmed. This is the first reported case of mutism accompanying shigellosis.

Adolescent↗

PubMed1997

Mutism in 36 patients who underwent callosotomy for drug-resistant epilepsy.

Thirty-six drug-resistant epileptic patients submitted to callosotomy were studied. Anterior callosotomy was performed in 27 patients, total two-stage callosotomy was performed in 8 patients and 1 patient had only posterior callosotomy. We found mutism in 10 patients (2 after complete callosotomy and 8 after anterior section). The patients did not speak, but the comprehension was present: they were able to carry out orders and to write. Their attitude to the environment was characterized by complete indifference. The mutism was always transient, lasting from 4 to 25 days (mean 7 days). Regression of mutism was always complete. We think that this complication should be chiefly attributed mainly to surgical manipulation, even if it is impossible to completely exclude a multi-factorial etiology.

Adolescent↗

PubMed1987

Hypertrophic cardiomyopathy associated with congenital deaf-mutism.

A family is presented in which there is a high incidence of hypertrophic cardiomyopathy and congenital deaf-mutism. The two abnormalities occurred together in 2 cases, and the syndrome was strongly suspected in a third individual. Hypertrophic cardiomyopathy without deaf-mutism was observed in a further 2 cases. Hypertrophic cardiomyopathy is inherited by an autosomal dominant mode; that occurring together with deaf-mutism is also probably inherited dominantly.

Adult↗

PubMed1995

Familial mitochondrial encephalomyopathy with deaf-mutism, ophthalmoplegia and leukodystrophy.

We report two sisters (32 and 36 years old) with familial deaf-mutism, progressive external ophthalmoplegia, leukodystrophy and mitochondrial myopathy. T2-weighted brain MRI demonstrated diffuse symmetrical high intensity areas in the white matter. Their muscle biopsies showed ragged-red fibers and cytochrome c oxidase (CCO)-negative fibers. CCO activity in biopsied muscle decreased to about 20% of normal control. They had no deletions of the mitochondrial DNA and no point mutations in mitochondrial tRNA. Their brother was diagnosed as having Kugelberg-Welander disease, grand mal seizures and urinary dysfunction. Their parents and grandparents had consanguinity. Three relatives were found to have deaf-mutism without accompanying ophthalmoplegia. This rare combination of mitochondrial encephalomyopathy and familial deaf-mutism might be caused by a nuclear DNA mutation in these sisters.

Adult↗

PubMed1987

Akinetic mutism in a bone marrow transplant recipient following total-body irradiation and amphotericin B chemoprophylaxis. A positron emission tomographic and neuropathologic study.

We describe a case of akinetic mutism associated with diffuse cerebral leukoencephalopathy, which developed in a bone marrow transplant recipient following total-body irradiation and amphotericin B chemoprophylaxis. A trial of high-dose bromocriptine did not stimulate purposeful verbal or motor activity. Fluorine 18-fluorodeoxyglucose/positron emission tomographic studies, performed before and during bromocriptine therapy, demonstrated cerebral hypometabolism and treatment-related decreases in regional cerebral blood volume. We conclude that whole-brain or total-body irradiation may increase blood-brain barrier permeability to polyene antibiotics, and that high-dose therapy with dopamine agonists is unlikely to benefit patients with akinetic mutism due to diffuse white-matter lesions.

Adult↗

PubMed1984

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.

Akinetic Mutism↗

PubMed1997

Elective mutism--associated with developmental disorder/delay. Two case studies.

Elective mutism (EM) is not regarded as a separate diagnostic category in the ICD-9, but is included under the heading "313: Disturbance of emotions specific to childhood and adolescence." In the ICD-10 EM is acknowledged as a separate diagnosis defined as "a marked, emotionally determined lack of speech in certain situations in a child with a normal or near normal speech/language ability." The diagnosis excludes pervasive developmental disorder and specific developmental disorders of speech and language. Two patients referred for EM to a child and adolescent psychiatry outpatient clinic, showed specific developmental delays and assessment indicated slight mental retardation in one of them. The question arose regarding how extensively EM is reported in the literature as associated with developmental disorder/delay. A search was carried out in four data-bases where most references were listed under the keyword "mutism". This paper presents the two case studies, and the results of the literature inventory. It concludes that EM may be associated with developmental disorder/delay and suggests that this could be a predisposing factor for an emotionally determined lack of speech in certain situations.

Causality↗

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↗

PubMed1997

Postoperative mutism after the clipping of a distal anterior cerebral artery aneurysm. A case report.

A 40-year-old man with mutism developed after clipping a left distal anterior cerebral artery aneurysm is presented. The most characteristic presenting symptom was complete absence of speech with unimpaired consciousness which occurred on the fourth day after operation. The patient recovered spontaneously within three weeks. In this paper we discuss the possible pathogenesis and anatomical location of mutism related to a distal anterior cerebral aneurysm in view of the literature.

Adult↗

PubMed2001

A follow-up study of 45 patients with elective mutism.

Forty five patients (23 boys and 22 girls) with elective mutism (8.7 +/- 3.6 years old), who were referred to a university department and a child guidance clinic within a 15-year-period, were followed up on average 12 years later. For 41 of them, sufficient information could be obtained at follow-up, and 31 patients could be investigated personally. At follow-up, an interview and a standardized psychopathological examination were carried out as well as two standardized biographic inventories. The main results were: 1) a high load of individual and family psychopathology was characteristic of the patients. The disorder started already at age 3 to 4 and referral age was 8 years on average. 2) In 16 out of 41 patients (39%), a complete remission could be observed. All other patients still revealed some communication problems. 3) The formerly mute patients described themselves as less independent, less motivated with regard to school achievement, less self-confident and less mature and healthy in comparison to a normal reference group. 4) A poor outcome could be best predicted by the variable "mutism within the core family"at the time of referral.

Age of Onset↗

PubMed2005

Long-term effects of transient cerebellar mutism after cerebellar astrocytoma or medulloblastoma tumor resection in childhood.

BACKGROUND: Following cerebellar tumor resection, some patients develop transient cerebellar mutism (TCM). Although the mutism resolves, it is not known whether there are long-term motor speech deficits in patients with TCM that are in excess of those in individuals with cerebellar tumors who had not developed postoperative TCM. METHODS: Long-term survivors of cerebellar tumors resected in childhood who developed TCM were matched to survivors without TCM and to controls. Speech samples were formally analyzed by two speech pathologists. RESULTS: Tumor survivors who had TCM had significantly more ataxic dysarthric speech and slower speech than either those without TCM or controls and were more dysfluent than controls. Tumor survivors without TCM did not differ from controls on ataxic dysarthria or speech rate. CONCLUSIONS: Survivors who had TCM showed more speech deficits than controls or survivors without TCM. The data suggest that speech deficits are chronic if not permanent sequelae of TCM.

Adolescent↗