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PubMed2003

[Cerebellar mutism syndromes with subsequent dysarthria: a study of three children and a review of the literature].

Cerebellar mutism and subsequent dysarthria (MSD) is a possible complication of posterior fossa surgery. It is usually seen in children after resection of a cerebellar mass lesion. Most patients become mute after a period of (near)normal postoperative speech, and are dysarthric once speech resumes. The pathophysiological mechanisms underlying MSD are most probably multifactorial, combining neuroanatomical, neurophysiological, neuropsychological, and psychological factors. The aim of the present article is to better define the MSD syndrome. The cerebellum is not only involved in motor control. It is also part of a distributed neural circuitry which underlies higher cognitive functions such as, for instance, those associated with the programming of kinetic parameters before motor initiation of a movement. We hypothesize that it could also be involved in the mental initiation which precedes the programming of any intentional bucco-phonatory movements to be performed in order to express oneself.

Brain Neoplasms↗
PubMed2005

[Akinetic mutism related to hydrocephalus and cerebellar surgery treated with bromocriptine and ephedrine. A pathophysiological review].

Akinetic mutism (AM) is a behavioral disorder characterized by impossibility to move or speak in awake patients. lt has been typically described as a transient disorder following posterior fossa tumour resection. Besides, AM may also appear after recurrent shunt failures in hydrocephalic patients, with no tendency towards improvement, either spontaneously or with shunt revisions. However successful treatment of this second type of AM has been achieved with bromocriptine. We present a patient who developed AM after a posterior fossa surgery complicated by ventriculitis and multiple hydrocephalic events. AM only improved with bromocriptine. We review AM pathophysiology. Although not well known, it appears to be quite different, depending on its cerebellar or hydrocephalic origin. Damage to dentate nucleus or its efferents (mainly of glutamate) should promote AM of cerebellar origin, while damage to paraventricular monoaminergic pathways could explain AM related to repeated shunt failures which has successful response to bromocriptine treatment. However, a more complete study of this disorder is required to ascertain its aetiology.

Akinetic Mutism↗
PubMed1995

Risk factors related to deaf-mutism among pupils attending the Alexandria governmental deaf-mute schools.

Childhood deafness interferes with the cognitive development of the child, so it is considered a major handicap. The present work was carried out to reveal possible risk factors of deaf-mutism and the magnitude of each. The case control design was chosen as a research methodology. A 50% sample of deaf-mute pupils at the primary level were selected at random from each of the two governmental schools for the deaf-mutes in Alexandria (boys=96, & girls=76). A control group chosen at random from a main stream governmental school and matched by age and sex of the pupils as well as with education and occupation of the father. Matching was carried out at the sampling phase, pairing each case to its control. Data were collected by interviewing the mothers using an interviewing schedule. Matched analysis was carried out where pairing of cases and controls was retained. The likelihood estimate of Odds ratio conditional on the number of discordant pairs was estimated using McNemer's test. The 5% level was chosen as the level of significance. The study revealed 172 deaf-mute pupils. Their mean age was 9.48+/-1.981 years. Boys outnumbered girls (55.8% and 44.2% respectively). In 59.4% parents were cousins. Deafness was first noticed at 6 to 60 months of age with a mean of 14.70+/-10.2 months. Most fathers and mothers were illiterate (48.84% and 61.63%). Heredity was a risk factor, where 84.82% of cases had a positive family history compared to none of the controls. Moreover, in case of consanguinity the Odds ratio=5.60. Acquired deafness constituted the second important group of all causes of deafness. Meningitis featured as the most important cause of acquired deafness with an estimated relative risk of 18.5, followed by fever (Odds ratio=4.67), then repeated attacks of acute tonsillitis and ear disease where the case control percent difference was 8.72% and 4.65% respectively.

Case-Control Studies↗
PubMed1990

Persistent mutism and dysphagia of acute onset due to bilateral internal capsule infarction.

Acute mutism with paralysis of the bulbar and facial muscles following discrete bilateral internal capsular infarction is a rare stroke syndrome. We describe a 62 year-old male who suddenly became unable to speak or swallow. The paucity of facial expression and inability to voluntarily move the facial, lingual and pharyngeal muscles were persistent and contrasted with a relatively mild limb paresis which recovered. High resolution CT scan revealed infarcts in the posterior limbs of both internal capsules. It is important to recognise this stroke syndrome because of the permanence of dysarthria and dysphagia associated with it.

Bulbar Palsy, Progressive↗
PubMed1989

[Hyperkinetic mutism within the scope of consciousness disorder in a case of systemic lupus erythematosus].

A thirty-year-old housewife, who had been diagnosed as SLE, had been hyperkinetic and mute for 13 months after reiteration of manic-depressive episodes. In this condition she walked around without aim, ate and drank only with nursing help, and could not understand the circumstances around her; she was incontinent of urine and feces. Serological examination did not show any abnormal results during psychic exacerbation. She recovered dramatically by electroconvulsive therapy, and was completely amnestic about the past 15 months. Because her mental state was considered to be limited consciousness, it might be possible that her hyperkinetic and mute state is situated between twilight state and akinetic mutism.

Adult↗
PubMed1989

Spontaneous bilateral anterior cerebral artery occlusion resulting in akinetic mutism. A case report.

An unusual case concerning a patient with akinetic mutism (AM) due to spontaneous bilateral anterior cerebral artery occlusion is reported. Brain CT scan revealed the presence of mild low density foci presenting an irregular enhancement, which followed the distribution of mesial frontal gyri and paracentral lobulus, bilaterally. Right and left carotid angiographies showed bilateral occlusion of the anterior cerebral artery. Our case is characterized by an exclusive localization of the infarction in the frontal cortex. This finding suggests that a limited damage involving the anterior cerebral arteries territory could be, on its own, responsible for the AM syndrome.

Aged↗
PubMed1987

Elective mutism: a case study of a disorder of childhood.

This paper reviews a number of treatment strategies utilized in the treatment of a 6-year-old boy with a history of multiple parental separations. When the patient presented to the child psychiatric clinic, he had a history of not speaking in the preceding four months, following the arrival of a stepmother in the household and a move to a new house in a new locality. Developmental and psychometric assessments are presented and their utility in early diagnosis and later prognosis are discussed. Reluctant speech is differentiated from, and compared with, elective mutism.The management of elective mutism is often complicated by these children not speaking to anyone in certain environments, and very frequently the persons with whom they do speak are not available for participation in treatment programs. Consequently, if a child does not speak to anyone who can participate in the early mapping of treatment modalities, the use of treatment strategies such as stimulus fading is impossible. Suggestions for future management to overcome this difficulty are presented and discussed.

Affective Symptoms↗
PubMedDate not supplied

Akinetic mutism and locked-in syndrome: the functional-anatomical basis for their differentiation.

The accurate location and extent of brainstem lesions that cause akinetic mutism (a.m.) and/or locked-in syndrome (LiS) are reviewed. We compared the data of our morphological analysis with recent neurochemical findings and speculated on the possible pathomechanism that results in the clinical state. There seems to be an anatomic correspondence between pathways of dopamine containing neurons and the lesions associated with a.m. We argue that mesocoeruleo, diencephalospinal and/or mesocorticolimbic dopaminergic systems are selectively damaged in a.m. but spared in LiS.

Adult↗
PubMed1985

Akinesia and mutism following a methylphenidate challenge test.

A case of akinesia and mutism is described in a menopausal, depressed woman with onset following a mood challenge with 40 mg of methylphenidate taken orally over a 3-hour period. Various diagnoses are considered with preference given on clinical grounds to conversion disorder precipitated by drug-induced dysphoria. It is suggested that increased susceptibility to dysphoria may have been related to prior clomipramine administration and hypoestrogenism.

Adult↗
PubMed1982

[An autopsy case of Parkinson's disease associated clinically with dementia terminating in akinetic mutism and pathologically with multiple Lewy's Bodies in the cerebral cortex].

An autopsy case of a 50 year-old male with Parkinson's disease associated with multiple Lewy bodies in the cerebral cortex was reported. His clinical symptoms began at the age of 26 with the speech and actions indicative of a persecution complex accompanied by irritability and were followed by progressive dementia from the age of 37 and Parkinsonism since the age of 41. He was in a state of akinetic mutism thereafter till his death at the age of 50. Autopsy disclosed in addition to the typical findings of Parkinson's disease in the brain stem multiple intracytoplasmic Lewy bodies in medium-sized neurons of the fifth and sixth layers of the cerebral cortex. They were atypical in the sense that they did not have any haloes. They were especially numerous in the cingulate gyrus. In addition, findings of non-specific neuronal degeneration were obtained in the cerebral cortex such as cellular atrophy with massive deposition of lipofuscin pigments, central chromatolysis, cell loss and cellular gliosis in the third, fifth and sixth layers. These neuronal findings were also prominent in the cingulate gyrus. Such senile changes as senile plaques or granulo-vacuolar degeneration were not found, although there were a few foci of neurofibrillary degeneration in the hippocampal gyrus. Histochemically and electron microscopically, no difference was observed in the constituents of Lewy bodies between the brain stem and the cerebral cortex. Such autopsy findings and a review of the literature indicate that the dementia in this case may be related not only to the presence of Lewy bodies but also to the above-described, non-specific neuronal degeneration in the bilateral cingulate gyri and surrounding frontal gyri. The standpoint of regarding a Parkinson's disease with multiple Lewy bodies in the cerebral cortex as an independent disease entity was criticized.

Akinetic Mutism↗
PubMed1983

Mutism: loss of neocortical and limbic vocalization.

A patient with complete mutism of 5 years duration was studied to determine the cause of the defective phonation. The patient had neurological findings indicative of pseudobulbar palsy, but he had lost emotional vocalization and emotional facial expression, as well as propositional speech. Phylogenetic, ontogenetic, and anatomic evidence indicates that propositional speech and volitional facial movements are mediated by corticobulbar tracts descending from neocortical areas, whereas emotional vocalization and emotional facial expression are dependent on intact limbic system connections. The findings suggest that the patient's impaired faciovocal expression was the result of lesions involving both limbic system and descending neocortical connections.

Bulbar Palsy, Progressive↗
PubMed1995

Silent eulogy. Elective mutism in a six-year-old Hispanic girl.

A case of elective mutism in a six-year-old Hispanic girl treated in a public mental health setting is presented. The central feature of the case was the facilitation of a delayed grieving process in a little girl who had witnessed her father's death. The presentation stresses the critical need to integrate the unfolding clinical material with the realities of the stresses of parental distress and resistance. An attempt is made to understand this "resistance" in the context of cultural and social realities, while attending to the possible underlying psychodynamic meaning.

Child↗
PubMed1994

Dilantin toxicity presenting as mutism following severe head injury: case report.

A case is presented in which a patient was placed on phenytoin following open depressed skull fracture. He subsequently was lost to follow-up, and then presented with several complaints, among them mutism, found to be related to phenytoin toxicity. There are no reports to date of this condition being caused by phenytoin. The issue is again raised of the risk versus benefits of long-term anticonvulsant prophylaxis following severe head injury.

Adolescent↗
PubMed1994

Post-traumatic mutism.

We report on the infrequent verbalisation disorder called "post-traumatic mutism" observed in 12 subjects with severe traumatic head injuries. These patients during the recovery of their conditions showed for a certain period a speechlessness even though some of them could communicate through gestures and writing. The nature and the possible mechanism of the disorder are discussed.

Adult↗
PubMedDate not supplied

[An unusual coincidence: elective mutism and sleep-related bioelectric seizure status syndrome].

A case study of a 9-year-old girl is presented which suffers from elective mutism and a rare, special form of cerebral seizures (ESES). After a brief review of the literature concerning these two rare diseases diagnosis, psychotherapy and anticonvulsive treatment as well as a follow-up are described. It is argued that in this case there are two independent, very rare diseases, and problems are discussed which arise from the necessity to integrate two heterogeneous therapeutic concepts.

Anticonvulsants↗
PubMed1993

Total mutism--a case report of a rare psychiatric disorder and approaches for behaviour therapy.

Total mutism, which is an extremely rare psychiatric disorder, was observed in an 11-year-old boy. He refused to speak a few weeks after starting school. Behavioural analysis showed that learning by model as well as positive and negative reinforcements were involved in the pathogenesis and maintenance of the disorder. The treatment followed principles of behaviour therapy by the use of operant techniques in the sense of contingency management methods. White noise, transmitted by earphones, was utilized to interrupt auditory feedback. It has been suggested that by this method anxiety would be diminished in the case of speech phobia. Within a few months of hospital admission the boy developed speaking behaviour progressing from barely audible breaths to sibilants of normal loudness. Short dialogues were possible after 18 months. The additional conduct disorder improved simultaneously with the increase in verbal and social skills. One year after hospitalization some social uncertainty persisted with tendencies to avoid demands.

Behavior Therapy↗
PubMedDate not supplied

Akinetic mutism due to diphenylhydantoin toxicity.

Akinetic mutism (AM) is a rare, specific, unconscious state. An AM patient seems to be awake, lacks mental activity, is unable to speak, and does not respond to any environmental stimulus. Cyclical sleep and awake states are maintained, and incontinence is present. Various factors such as tumor, vascular events, drug use and radiotherapy are responsible for the development of AM. A 12-year-old epileptic patient displayed AM and diphenylhydantoin toxicity (DPH). She seemed awake, was unable to speak or to understand, and had no movements with either spontaneous or noxious stimuli. Her serum DPH level was greater than 40 micrograms/ml. Magnetic resonance imaging (MRI) showed mild cerebellar atrophy. All known causes of AM were excluded. The AM state in this patient was considered to be due to toxic DPH levels. She regained her motor and mental activity within two months after carbamazepine was administered to replace DPH. She was symptom-free when examined at the two-year follow-up. No similar adverse effect of DPH has been reported to date.

Akinetic Mutism↗