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PubMed1995

[Akinetic mutism--a review of the literature].

Cairns and coworkers (1941) introduced the term "akinetic mutism" to denote a syndrome characterised by lack of responsiveness in the presence of apparently preserved vigilance. The present paper reviews clinical data as well as results of animal experimentation to outline the functional-neuroanatomic basis of this constellation. The clinical literature following the original publication of Cairns et al. (1941) reported syndromes of "akinetic mutism" in bilateral mesodiencephalic or frontal lesions of various aetiology. At least two pathomechanisms of akinetic mutism can be differentiated: (a) reduced "arousal" of cortical functions due to lesions at or rostral to the mesodiencephalic junction; (b) impaired activation of the motor system following bilateral damage to the frontal lobes. Since perceptual and cognitive functions are disturbed as well in mesodiencephalic akinetic mutism, the latter notion does not seem to be adequate. The terms "apallic syndrome" or "vegetative state" are rather more appropriate in these instances. The label "akinetic mutism" can then be restricted to a pathophysiologically distinct syndrome, i.e. reduced motor activation following bilateral frontal damage.

Akinetic Mutism↗
PubMed1994

[Mutism in central motor disorders--a review of the literature].

Mutism can be defined as "a condition in which there is no, or very little, oral-verbal expression, whereas comprehension of speech ... is normal or at least at a considerably higher level" (Lebrun, 1990). Benson (1979) enumerates five neuroanatomical correlates of mutism: (a) damage to the Broca region, (b) lesion of the supplementary motor area of the dominant hemisphere, (c) dysfunction of the mesencephalic reticular system, (d) thalamotomy, and (e) bilateral pathology of cortical and subcortical motor structures. The last item refers to syndromes of mutism resulting from central motor disorders. Depending on location and size of the lesion this pathophysiological interpretation should hold true for the fourth point as well. In mutism due to central motor disturbances lacking verbal expression represents the most severe degree of dysarthria, i.e. anarthria. The present review provides a detailed description of mutism following corticobulbar, striatal, and cerebellar dysfunctions.

Brain↗
PubMed1999

Sertraline treatment of 5 children diagnosed with selective mutism: a single-case research trial.

In this single-case research study, we examined the efficacy and acceptability of sertraline treatment in children diagnosed with selective mutism. We utilized a double-blind, placebo-controlled trial of sertraline within a replicated multiple baseline/across participants research design (n = 2; n = 3). Multiple methods of assessment involving across-setting informants were completed repeatedly throughout the 16-week study. Follow-up data was collected at 4 and 20 weeks poststudy. Assessment measures failed to demonstrate group changes in mutism, anxiousness, and shyness. All individuals realized considerable improvement on some of these variables. Two of the five participants no longer met diagnostic criteria for selective mutism following less than 10 weeks of 100 mg sertraline treatment. A third participant was reported asymptomatic at 20 weeks poststudy. Treatment compliance was high. Parent treatment acceptability ratings were highly favorable. Single-case research methodology has considerable clinical utility in the medication treatment of selective mutism. Frequent and repeated measurement across phases helped to highlight varying levels of participant improvement across situationally specific settings. Additional investigation of the use of selective serotonin reuptake inhibitors in treating selective mutism is warranted.

Antidepressive Agents↗
PubMed1994

Treatment of elective mutism with fluoxetine: a double-blind, placebo-controlled study.

OBJECTIVE: To evaluate the efficacy of treatment with fluoxetine in reducing symptoms associated with elective mutism. METHOD: Sixteen subjects with elective mutism were treated with placebo (single-blind) for 2 weeks. Fifteen placebo nonresponders were then randomly assigned to double-blind treatment with fluoxetine at a dose of 0.6 mg/kg/day (N = 6) or continued placebo (N = 9) for an additional 12 weeks. Outcome ratings were completed by the treating psychiatrist, parents, and teachers. RESULTS: Significant improvements over time on ratings of elective mutism, anxiety, and social anxiety, rated by clinician, parents, and teachers, were demonstrated in both fluoxetine- and placebo-treated subjects. Subjects treated with fluoxetine were significantly more improved than placebo-treated subjects on parent's ratings of mutism change and global change. Clinician and teacher ratings did not reveal significant differences between treatment groups. Although improved, most subjects in both treatment groups remained very symptomatic at the end of the study period. Side effects were minimal. CONCLUSION: Fluoxetine may be beneficial and safe in the treatment of children with elective mutism. Longer periods of treatment may yield more substantial therapeutic benefits. Further study is indicated.

Adolescent↗
PubMed1998

Akinetic mutism as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease.

OBJECTIVES: Among the classification criteria for the diagnosis of Creutzfeldt-Jakob disease, akinetic mutism is described as a symptom which helps to establish the diagnosis as possible or probable. Akinetic mutism has been anatomically divided into two forms--the mesencephalic form and the frontal form. The aim of this study was to delimit the symptom of akinetic mutism in patients with Creutzfeldt-Jakob disease from the complex of symptoms of an apallic syndrome and to assign it to the individual forms. METHODS: Between April and December 1996, 25 akinetic and mute patients with Creutzfeldt-Jakob disease were consecutively examined. The patients were classified according to the definition of akinetic mutism by Cairns and secondly in accordance with the features constituting the complete picture of an appalic syndrome (defined by Gerstenbrand). RESULTS: From 25 patients with definite Creutzfeldt-Jakob disease, 24 patients showed impoverishment of speech and, after a mean duration of four (range 1.1-11.2) months, almost complete absence of voluntary movements and speech. Seven patients were classified as being mute and akinetic and assigned to the mesencephalic form whereas 13 patients were classified as apallic. One patient was mute without being akinetic and four patients were comatose. CONCLUSION: Diffuse brain damage underlies akinetic mutism in patients with Creutzfeldt-Jakob disease. The term can be used as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease; however, it should be applied very carefully and delimited clearly from the apallic syndrome.

Adult↗
PubMed1997

Cerebellar mutism after posterior fossa surgery--two case reports.

Two adults (aged 71 and 74 years) developed cerebellar mutism after posterior fossa surgery for a mass lesion in the superior cerebellar hemisphere or upper vermis. Histological examination showed one was a hemangioblastoma, the other a metastatic brain tumor. The tumors were totally removed via the occipital transtentorial approach. Both patients developed mutism on the 2nd postoperative day, which persisted for 3-4 weeks and was followed within 2-4 months by cerebellar dysarthria. Thereafter, their condition improved. Transient cerebellar mutism usually occurs in pediatric patients after the removal of a mass lesion in the upper vermis. Cerebellar mutism in adults is rare. The predominance of cerebellar mutism in children may be attributable to the predilection for vermian tumor and their tendency to experience personality and behavioral changes after posterior fossa surgery.

Aged↗
PubMed1998

Cerebellar mutism after basilar artery occlusion--case report.

A 30-year-old female became comatose due to embolic occlusion of the basilar artery, caused by surgical injury to the origin of the vertebral artery during removal of a neurinoma in the upper thoracic paravertebral region. The basilar artery occlusion was treated by local fibrinolysis through a microcatheter. Two weeks later she recovered her consciousness but suffered mutism. Her speech disturbance was characterized by severe ataxic dysarthria known as "cerebellar mutism" but without cranial nerve paresis. The mutism gradually improved during the following 3 months. This is case of cerebellar mutism was apparently due to ischemic stroke. Disturbance by hypoperfusion of the cerebellum and brain stem may have been involved in the pathogenesis of cerebellar mutism.

Adult↗
PubMed1994

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.

Brain Neoplasms↗
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↗
PubMed1987

Mutism, malingering, and competency to stand trial.

Mutism and mental illness have had a long-standing historical relationship with regard to the issue of competence to stand trial. This article reports a defendant who remained mute for 10 months and describes his use of the symptom of mutism in his malingering. Although mutism is frequently used by defendants for malingering, clinicians must have a high index of suspicion for the possibility. We recommend a comprehensive evaluation including neurologic workup, repeat interviews, observation of the defendant at unsuspected times for communicative speech with other inmates, study of handwriting sample, collateral nursing documentation, and, if necessary, Pentothal interviews to establish authenticity of mutism. The authors review the historical background and legal considerations of the relationship between mutism and malingering.

Forensic Psychiatry↗
PubMedDate not supplied

[Elective mutism in children: literature review].

This paper presents contemporary opinions about selective mutism in children, including epidemiology, etiology, clinical features and therapy. This is the first extensive review on this topic in Polish literature. The essential feature of selective mutism is persistent failure to speak in social situations, where speaking is expected (e.g., in school), despite speaking in other situations (e.g., at home). The authors present the diagnostic criteria according do DSM-IV and suggested by other authors. Clinical characteristics of this disorder were also presented, including personality traits and behaviour of mutistic children (different at home and in unfamiliar environment) and comorbidity of selective mutism. Etiology of this disorder seems to be multifactorial. The important etiological factors are: minimal brain dysfunction, somatic or psychological trauma, particularly during the speech development and a family structure, especially the mother-child relation. The authors emphasize that mutism in children is a heterogeneous symptom and present several models of mutism. The paper describes also different methods of treatment (e.g., behavioral, psychodynamic, family therapy and some case reports on pharmacotherapy); and long-term prognosis.

Age of Onset↗
PubMed1996

Cerebellar mutism after posterior cranial fossa surgery.

Mutism is a rare sequel of PCF tumor removal. Three patients aged 5 to 20 years old with mutism after posterior fossa surgery are presented. Suboccipital craniectomy was performed in all patients with grossly total removal of a medulloblastoma. The mutism that may occur after an operation for a PCF lesion has been explained in functional and/or organic terms. To date, 24 similar cases of mutism following cerebellar operations have been reported in the literature. We review the features of the syndrome in the light of the published cases and speculate on the underlying physiopathology. The absence of long tract or other brain stem signs, together with a presence of dysarthria during the recovery of speech, suggested a organic cerebellar cause of the mutism.

Adult↗
PubMed1994

Transient mutism following posterior fossa surgery in children.

We report 3 patients, ages 5, 9 and 13 years, with mutism following posterior fossa surgery (PFS). All presented with headache of 10-180 days duration, excellent premorbid learning performance and paucity of neurologic signs. Radiographic studies demonstrated large posterior fossa tumor occupying the fourth ventricle, and hydrocephalus, leading to gross total resection of the tumor. Within 24-48 hr, all patients were mute. None had problems with swallowing and coughing. All were able to nod "yes or no," follow commands, point to body parts, and make their wants known by gestures. Jaw, gag, snout and palmomental reflexes were normal. CT scan and MRI Brain showed no cerebral hemispheric lesions. All children regained speech although dysarthric, within 5-12 weeks. Twenty-two previously reported cases are similar to ours. We conclude that this post-surgical mutism syndrome is unique and must be differentiated from aphemia, Broca's aphasia, hysterical mutism and elective mutism. The cerebellum, in a way not yet understood, does play a role in speech production.

Adolescent↗
PubMed1994

Transient mutism after posterior fossa surgery.

An 8-year-old girl developed mutism after removal of a vermian medulloblastoma. The mutism was not accompanied by long tract signs or cranial nerve palsy. The girl started to regain her speech 2 weeks postoperatively, showing marked improvement 2 months after the operation, after passing through a dysarthric phase. Magnetic resonance imaging showed only normal postoperative changes without abnormalities of dentate nuclei or supranuclear region. Nineteen similar cases of transient mutism following cerebellar operations have been reported in the literature, most of them with a delayed postoperative onset. In all patients the recovery of speech started to appear 4 days to 4 months postoperatively, and all patients passed through a monotonous, dysarthric phase. The absence of long tract or other brain stem signs, together with the presence of dysarthria during the recovery of speech, suggested a cerebellar cause of the transient mutism. Various hypotheses advanced to explain the pathogenesis of this speech disorder are analyzed.

Cerebellar Neoplasms↗
PubMed1993

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions.

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Akinetic Mutism↗
PubMed1988

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.

Aged↗
PubMed2004

Cerebellar mutism--report of four cases.

The aim of the present study was to investigate the manifestations of mutism after surgery in children with cerebellar tumors. Speech impairment following cerebellar mutism in children was investigated based on standardized acoustic speech parameters and perceptual criteria. Mutistic and non-mutistic children after cerebellar surgery as well as orthopedic controls were tested pre-and postoperatively. Speech impairment was compared with the localization of cerebellar lesions (i. e. affected lobules and nuclei). Whereas both control groups showed no abnormalities in speech and behavior, the mutistic group could be divided into children with dysarthria in post mutistic phase and children with mainly behavioral disturbances. In the mutistic children involvement of dentate and fastigial nuclei tended to be more frequent and extended than in the nonmutistic cerebellar children. Cerebellar mutism is a complex phenomenon of at least two types. Dysarthric symptoms during resolution of mutism support the anarthria hypothesis, while mainly behavioral changes suggest an explanation independent from speech motor control.

Age Factors↗
PubMed1998

Selective mutism among second-graders in elementary school.

OBJECTIVE: This study assessed the prevalence of selective mutism among second graders in elementary school, and examined related issues such as the situations in which the children refuse to speak, their performance level at school, and some temperamental/behavioural characteristics of these children. METHOD: A definition of selective mutism (according to the DSM-IIIR) was sent to all second grade teachers in the study area, asking them if there were any children with these symptoms in their class. If a positive answer, the teacher was asked to fill in a questionnaire concerning the child. RESULTS: The prevalence rate for selective mutism was found to be 2%, with girls outnumbering boys. Selective mutism had been in progress more than a year in most cases. Most often, the children refused to speak to the teacher (58%), and one-fifth spoke to nobody at school. One-third of the mute children were performing at a lower level than average. Fewer of these children were reluctant to speak to the teacher than were mute children with an average or higher than average performance level. The children were characterized as shy, withdrawn and serious, with only some being hyperactive or aggressive. About one third of the children had had contact with health services.

Child↗