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Cerebellar mutism is a rare phenomenon often described in children following surgical intervention in the posterior fossa. In this report we present a very unusual case of pre-operative cerebellar mutism in an adult in the context of cognitive-affective syndrome caused by cystic hemangioblastoma.
A 3.7-year-old girl presented with an anterior neck injury followed by progressive subcutaneous emphysema and loss of consciousness. After resuscitation, a laceration on the first tracheal cartilage was closed surgically. As she was extubated one week later, she was found to have right hemiplegia and muteness. MRI showed a T2-bright lesion on the tegmentum of the left midbrain down to the upper pons. Right vertebral angiography disclosed an intimal flap with stenosis at the C3 vertebral level presumably caused by a fracture of the right C3 transverse process later confirmed in a cervical 3D-CT scan. Her muteness lasted for 10 days, after which she began to utter some comprehensible words in a dysarthric fashion. Her neurological deficits showed improvement within 3 months of her admission. Transient mutism after brain stem infarction has not been reported previously. We discuss the anatomical bases for this unusual reversible disorder in the light of previous observations and conclude that bilateral damage to the dentatothalamocortical fibers at the decussation of the superior cerebellar peduncle may have been responsible for her transient mutism.
Mutism occurring after posterior fossa surgery has been reported in children. We report an adult case of transient mutism after resection of a large tumor in the right cerebellar hemisphere. Although the patient was fully alert and without lower cranial nerve palsies and long tract signs, he had been mute for 4 days after surgery. Postoperative magnetic resonance imaging scan showed a slight hemorrhage in the region of the resected tumor. The relevant literature is reviewed.
Mutism following brain trauma is quite common, is usually transient, and recovery of speech is essentially the rule. Lasting total absence of speech without aphasia is highly unusual. Three such patients, two of traumatic and one due to vascular origin showing buccofacial apraxia (BFA) and computerized tomography (CT) evidence of bilateral frontal lesions are reported. It is suggested that complete lasting mutism associated with BFA is a result of bihemispheric lesions affecting mainly the opercular part of the inferior frontal gyrus and immediate adjacent regions.
Four children who exhibited akinetic mutism during the course of their neurologic diseases were treated with bromocriptine. Reversal of the akinetic mute states was evident in all patients. Pathways of the dopaminergic neurons are reviewed and a clinically useful mechanism which causes akinetic mutism is postulated.
BACKGROUND: Selective mutism is a psychiatric disorder of childhood characterized by consistent inability to speak in specific situations despite the ability to speak normally in others. The objective of this study was to test whether reduced auditory efferent activity, which may have direct bearings on speaking behavior, is compromised in selectively mute children. METHODS: Participants were 16 children with selective mutism and 16 normally developing control children matched for age and gender. All children were tested for pure-tone audiometry, speech reception thresholds, speech discrimination, middle-ear acoustic reflex thresholds and decay function, transient evoked otoacoustic emission, suppression of transient evoked otoacoustic emission, and auditory brainstem response. RESULTS: Compared with control children, selectively mute children displayed specific deficiencies in auditory efferent activity. These aberrations in efferent activity appear along with normal pure-tone and speech audiometry and normal brainstem transmission as indicated by auditory brainstem response latencies. CONCLUSIONS: The diminished auditory efferent activity detected in some children with SM may result in desensitization of their auditory pathways by self-vocalization and in reduced control of masking and distortion of incoming speech sounds. These children may gradually learn to restrict vocalization to the minimal amount possible in contexts that require complex auditory processing.
kinetic mustism is a dramatic deficit in spontaneous initiation of voluntary motor and speech acts, usually secondary to bilateral lesions of the anterior cingulate cortices and supplementary motor areas [Principles of Neurology, McGraw-Hill, New York, 1989]. Given the obvious limitations of traditional neuropsychological testing in this clinical context, the use of neurophysiological tools such as bedside auditory cognitive event-related potentials (ERPs), recently proven to be relevant to evaluate comatose and vegetative patients [Clin. Neurophysiol. 110 (9) (1999) 1601; News Physiol. Sci. 17 (2002) 38], may constitute an interesting alternative. Here, we present the ERPs of a 38-year-old right-handed woman with severe akinetic mutism recorded in a passive auditory odd-ball paradigm. In spite of this severe clinical state, we could observe the presence of a "Mismatch Negativity", and of a larger P300 in rare trials than in frequent ones. By revealing a high level of cognitive integration of environmental auditory information, our study emphasizes the potential clinical relevance of MMN and P300 recordings in akinetic mutism to assess patient cognitive functioning.
This study describes the successful treatment of a seventh grade boy who had selective mutism in school since kindergarten. Treatment consisted of systematic desensitization, consultation with school personnel, and training in social speaking skills. The student made significant gains with respect to frequency of verbalizations to teachers and peers, number of individuals spoken to, anxiety related to speaking, school attendance, and involvement in school-based extracurricular activities. At one year follow-up, the student's rate of speech was indistinguishable from his classmates'. Special issues concerning the treatment of long-term selective mutism are discussed.
A 54-year-old man developed somnolent akinetic mutism and acute mixed transcortical aphasia following a left thalamo-mesencephalic infarction. He also exhibited behavioural changes, namely apathy, slowness, lack of spontaneity, disinhibition, perseveration, gait apraxia and incontinence consistent with frontal lobe dysfunction. Presumably the akinetic mutism and language dysfunction were due to the thalamic stroke. All the manifestations could be related to interruption of the frontal-subcortical circuitry.
Transient mutism after posterior fossa surgery in children or associated with cerebellar hemorrhage or trauma is a recognized phenomenon. However, its association with parainflammatory cerebellitis has been rarely described. We report on a previously healthy 3-year-old child with severe cerebellitis after acute gastroenteritis of unidentified cause. Severe ataxia and transient mutism were the prevailing clinical features. Magnetic resonance imaging revealed swelling of the cerebellum with protruding cerebellar tonsils at the level of the occipital foramen. Recovery from the acute illness was slow and incomplete. Residual cerebellar dysfunction manifested with dysphonic and dysarthric speech, as well as motor coordination problems and was associated with atrophy of the vermis and cerebellar hemispheres in follow-up studies.
Acquired neurologic mutism in childhood is a complex phenomenon occurring in various neurologic conditions with different etiologies. We illustrate its clinical heterogeneity as reflected in a wide range of concomitant behavioral features by presenting 4 children with acquired neurologic mutism. Neuropsychologic examinations revealed differential patterns of defective or preserved phonation, orofacial movements, communicative behavior, and linguistic functions. We propose that detailed neuropsychologic analysis contributes to descriptions of the evolution of the speech impairment beyond the mute phase and the long-term disability. A framework for the clinical evaluation of children is therefore presented.
We report the case of a patient with idiopathic aqueductal stenosis and hydrocephalus who had several episodes of akinetic mutism, each preceded by shunt malfunction, that resolved with shunt revision. She also developed a parkinson's syndrome resistant to shunt revision but responsive to antiparkinsonian medications. The parkinson's syndrome and the episodes of akinetic mutism may be related to a reduction of dopaminergic input to the striatum and to the cingulate and frontal cortex brought about or worsened by ventricular dilatation.
BACKGROUND AND OBJECTIVES: The postoperative cerebellar mutism syndrome (CMS) is an unique acute postoperative complication characterized by transient decrease in speech output (often mutism), apathy, irritability as well as global cerebellar dysfunction. As much as 25% of patients undergoing a resection of a cerebellar or IV ventricular tumor may develop such a syndrome. In this retrospective study we characterize the clinical features of the CMS and explore potential etiologic mechanisms. METHODS: We conducted a retrospective analysis of medical records and imaging tests of 8 consecutive patients with the CMS identified through the database of the Children's Hospital and Dana-Farber Cancer Institute, Boston, and compared with a control group of 8 unaffected children undergoing a comparable tumor resection. RESULTS: In contrast to the control group, children in the affected group had marked decrease in speech output and comprehension, apathy and lack of initiative, inattention, persistent eye closure, flaccid hemiparesis and a severe global cerebellar dysfunction. Swallowing difficulties and bowel and bladder dysfunction were also observed. The median duration of the syndrome as judged by the persistence of the communication abnormalities was 4 weeks. The recovery was near complete with exception for a persistent global cerebellar dysfunction. A comparison of CT and MRI scans of children in both groups failed to identify distinguishing features. CONCLUSION: A surgical lesion of the midline cerebellum can cause a complex neurological dysfunction such as the CMS. Thus, we postulate that the cerebellum and its connections function as a 'modulatory system' in control of both motor and non-motor functions, including attention and language.
OBJECTIVES: This case report deals with the day care treatment of two seven- and eight-year-old siblings with elective mutism. Their treatment entails a combination of psychopharmacological and intensive behavior therapy. The multimodal therapeutic process is presented together with continuing psychosocial steps. Behavioral intervention focuses on building verbal expressive capacity, reducing speech anxiety in social situations and generalization to non-therapeutic situations. The case report is discussed in the context of the current literature on elective mutism.
This longitudinal case study challenges the assumption that individuals with autism who have severely restricted speech and language skills have a poor prognosis for further development of expressive oral language. The study follows the development of a woman with autism from mutism at age 10 to acquisition of a range of spoken and written language skills at age 26. The intervention in which the woman participated and her skills pre- and post-intervention and at two follow-up assessments are documented. The results support the hypotheses that speech and language development may proceed after mutism associated with limited verbal imitation and phoneme production skills, that some skills may plateau or decline, and that both spoken and written language may become viable forms of communication.
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.
Selective mutism is a disorder characterized by a persistent failure to speak in certain social situations. It is typically diagnosed in childhood, and the disorder can last from just a few months to several years in some individuals. Debate surrounds the origins and causes of this disorder. Recent literature suggests that selective mutism may be a form of social phobia. The present article is a brief review of the literature on the etiology, assessment, comorbid diagnoses, and treatment perspectives from several theoretical orientations, including behavioral, family systems, and psychopharmacological.
Two rare cases of akinetic mutism induced by aneurysmal subarachnoid haemorrhage are reported. The literature is reviewed, the possible pathophysiological mechanism of akinetic mutism is considered and the association between these two conditions is explored with an attempt to address the roles of medical treatment and surgery and to discuss prognosis.