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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↗

PubMed1997

Mutism in an adult following hypertensive cerebellar hemorrhage: nosological discussion and illustrative case.

Mutism after cerebellar injury has been associated with tumors, hemorrhage, and surgery of midline cerebellar structures. Literature review identified 54 cases, primarily in children after surgical splitting of the inferior vermis. We present a 47-year-old who developed transient mutism after cerebellar hemorrhage. This represents the first report of transient mutism in an adult with neither tumor nor brainstem infarction and documents the importance of cerebellar structures for initiation and production of speech in adulthood. This case further differs from those previous because of the long mute period and the subsequent return of continued ataxic and dysarthric speech.

Adolescent↗

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↗

PubMed2004

Mutism after evacuation of acute subdural hematoma of the posterior fossa.

CASE REPORT: A 7-year-old boy was involved in a road traffic accident. A computed tomography scan revealed an acute subdural hematoma (ASDH) of the posterior fossa, traumatic subarachnoid hemorrhage, and distortion of the brain stem. Removal of the ASDH was completed 3.5 h after injury. After extubation, the patient rapidly recovered consciousness. He was able to follow commands, although he did not speak. He began to utter 14 days after the injury. His speech became normal 39 days after injury. A magnetic resonance imaging scan revealed a post-contusional change in the right cerebellum and an ischemic lesion in the pons. DISCUSSION: Immediate removal of the hematoma is the only therapy for patients with ASDH of the posterior fossa. Although any lesions of the dentate nucleus, red nucleus, thalamus, cerebral cortex, and pons, all of which are involved in this case, are able to cause mutism, his mutism was primarily caused by the severe ASDH of the posterior fossa. The transient nature of this syndrome suggests that the cause of the mutism is trauma-related edema and/or transient ischemia of these structures.

Accidents, Traffic↗

PubMed1998

Reversible cerebral perfusion alterations in children with transient mutism after posterior fossa surgery.

Mutism is an infrequent and transitory complication observed following posterior fossa surgery. Patients become mute in the immediate postoperative period, with restoration of speech within a few weeks in the absence of additional neurological alterations. The anatomical structures thought to be involved are the connections between the cerebellar dentate nucleus, the ventrolateral nucleus of the contralateral thalamus and the supplementary motor area. In an attempt to understand the pathophysiology of this syndrome, and to depict the perfusion of different brain areas semiquantitatively, in two children who had become mute after posterior fossa surgery we performed a Tc99M-HM-PAO SPECT study during the period of mutism and again when normal speech had returned. In one patient, who had a left cerebellar astrocytoma, the SPECT study showed a marked reduction of cerebral perfusion in the right fronto-parietal region, and in the other, who had a medulloblastoma, a left fronto-temporo-parietal perfusion alteration was observed. When the patients regained normal speech, the follow-up SPECT studies revealed normalization of the cerebral perfusion. This study demonstrates the occurrence of a focal dysfunction of cerebral perfusion in children with cerebellar mutism after posterior fossa surgery. These observations are useful in extending our understanding of the pathophysiology of this postoperative clinical syndrome.

Adolescent↗

PubMed1998

Transient cerebellar mutism after evacuation of a spontaneous vermian haematoma.

Cerebellar mutism after surgery for posterior fossa tumours in children is a well-described, though rare, entity. Most of these tumours are located in the region of the cerebellar vermis extending to the hemispheres. The authors report a case of cerebellar mutism in an 8-year-old boy who underwent surgical evacuation of a spontaneous vermian haematoma. We feel that his mutism was an extreme form of cerebellar dysarthria.

Cerebellar Diseases↗

PubMed2005

Visual disturbance associated with postoperative cerebellar mutism.

Cerebellar mutism is an uncommon complication of posterior fossa surgery. Manifestations include disturbances of articulation, prosody, and pitch, and, if severe, complete mutism. Symptoms are independent of recognizable cortical or brainstem injury, and recovery is variable, with permanent deficits frequently observed. Cerebellar dysfunction is commonly invoked as an etiology, although controversy remains concerning the mechanism. Visual impairment has been reported only once before in the setting of this disorder. We report a confirmatory case of sudden, severe visual loss in association with cerebellar mutism after resection of a midline medulloblastoma in a 7-year-old.

Cerebellar Neoplasms↗

PubMed2005

Mixed neuronal-glial tumor of the fourth ventricle and successful treatment of postoperative mutism with bromocriptine: case report.

BACKGROUND: Tumors composed of both neurocytic and astrocytic cells are uncommon and poorly understood. We describe the clinicopathologic features of a very rare rosette-forming glioneuronal tumor of the fourth ventricle and propose bromocriptine as a useful therapeutic agent for cerebellar mutism after posterior fossa surgery. CASE DESCRIPTION: A fourth ventricle tumor was incidentally discovered in an 18-year-old woman. Magnetic resonance imaging revealed ventriculomegaly and a solid tumor with low-intensity signals on T1-weighted images and high-intensity signals on T2-weighted images. There was slight gadolinium enhancement. The tumor was subtotally resected. Although its lower half was well circumscribed, its upper half manifested invasive growth. Histologically, 2 components were identified, synaptophysin-positive neurocytic cells forming perivascular pseudorosettes and glial fibrillary acidic protein-positive astrocytic cells with Rosenthal fibers. Overall, cellular atypia was minimal and the MIB-1 labeling index was low. On the basis of these histologic findings, the tumor bore striking similarity to the recently described rosette-forming glioneuronal tumors of the fourth ventricle. Postoperatively, the patient manifested cerebellar mutism. The administration of bromocriptine improved her neurological status dramatically. CONCLUSION: The natural history of rosette-forming glioneuronal tumors of the fourth ventricle is not yet fully understood. Therefore, careful and long-term follow-up monitoring of the tumor hosts is necessary. Bromocriptine therapy may promote recovery from mutism after posterior fossa surgery.

Adolescent↗

PubMed2001

Mutism after posterior fossa surgery. Review of the literature.

Adolescent↗

PubMed2001

BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction.

INTRODUCTION: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. CASE REPORT: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. DISCUSSION: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction.

Aged↗

PubMed2004

Consanguinity, caste and deaf-mutism in Punjab, 1921.

The effects of religion, population sub-division and geography on the prevalence of deaf-mutism were investigated using information collected in the 1921 Census of Punjab. The total sample size was 9.36 million, and comprised data on thirteen Hindu castes, seventeen Muslim biraderis and two Sikh castes. A two-way analysis of variance comparing males in Hindu castes in which consanguineous marriage was prohibited, with males in Muslim biraderis which favoured first cousin marriage, indicated major differences with respect to the patterns of deaf-mutism within each religion. In the Muslim population 9.1% of the relative variation in the prevalence of deaf-mutism was inter-biraderi, 36.8% between geographical regions, and 48.8% an interaction between biraderi and region, whereas among Hindus 46.8% of the observed variation was inter-caste, 12.8% inter-region and 33.6% due to caste region interaction. From a wider disease perspective the results obtained with the Hindu community indicate the significant genetic differentiation associated with caste endogamy. As the overwhelming majority of Hindu marriages continue to be within-caste, it can be predicted that similar levels of inter-caste differences in disease frequency currently exist. By comparison, the lower level of inter-biraderi variation among Muslims is probably indicative of the dissolution of pre-existing caste boundaries and the resultant gene pool mixing that followed the large-scale conversion of Hindus to Islam during Muslim rule in North India from the 13th to the 19th centuries.

Catchment Area, Health↗

PubMed2002

Akinetic mutism caused by bilateral infiltration of the fornix in a patient with astrocytoma.

In a 59-year-old female patient, a World Health Organization (WHO) grade II astrocytoma had been diagnosed 16 years ago, which finally progressed into WHO grade III. Several right frontal neurosurgical resections, local radiation and a local radioimplant had been applied. Despite this long record, she was reported alert with a Karnofsky index of 90% until admission. Within a few weeks she rapidly developed akinetic mutism. Upon admission, computed tomography (CT) scan showed a large cystic right frontal defect and a suggested small tumor recurrence. White matter of the frontal lobe appeared to be translucent and compatible with previous radiation. The severe mental changes were initially attributed to a delayed radiation encephalopathy. Neuropathologically, the white matter of the frontal lobe showed mild elevated cell density consistent with gliosis; however, a tumor recurrence invading the tip of the corpus callosum and invading the entire length both fornices appeared. From the neuropathological findings of massive local tumor recurrence in both fornices, together with the acute clinical onset, it seems unlikely that the sequel of radiotherapy caused akinetic mutism, but the symmetric and severe involvement of the limbic system. We conclude that the rapid progression from a state of alertness to a full clinical picture of akinetic mutism was because of infiltration of both fornices.

Akinetic Mutism↗

PubMedDate not supplied

Cerebellar mutism syndrome.

Since 1980, a growing number of pediatric patients with mutism following posterior fossa surgery have been recognized. This syndrome typically affects children and in rare cases young adults who become mute one or two days after tumor operation but do not show disturbances of consciousness or language comprehension. The disorder persists for 1 to 4 months. The pathogenesis is still unknown. Of 21 children who underwent surgery for large posterior fossa tumors between 1991 and 1995, 6 developed cerebellar mutism. Histologically the tumors were classified as astrocytoma WHO grade I, astrocytoma WHO grade II and ependymoma WHO grade III in one case and medulloblastoma WHO grade IV in three cases. Besides the clinical course, intraoperative findings and CT or MRI data are evaluated and discussed considering possible etiological hypotheses. Our own experience and also literature reviews suggest that the lesion of the cerebellar hemispheres might be the most important one of multiple factors causing cerebellar mutism. Generally the syndrome is transient. The diagnosis should not delay adjuvant therapy in patients with a malignancy.

Adolescent↗

PubMed2002

Two sets of twins with selective mutism: neuropsychological findings.

Neuropsychological data are reviewed from two sets of dizygotic twins presenting with selective mutism characterized by situation specific anxiety, extreme passive behavior, lack of responsivity, lack of peer interaction, and a chronic course of selective mutism. Both sets of twins had a history of prematurity and delayed speech development. One set of twins presented with normal intelligence and normal receptive language skills but with expressive language and oral motor sequencing difficulties. The second set of twins presented with Verbal IQ deficits and significant receptive and expressive language deficits. A summary of current conceptualizations regarding etiology and treatment of selective mutism is provided.

Child↗

PubMed2004

Frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning.

A middle-aged man suffering from acute carbon monoxide intoxication was clinically assessed to be in an akinetic and mute state. In order to elucidate regional cerebral disturbances, brain metabolism was investigated with fluoro-deoxyglucose positron emission tomography ((18)FDG-PET) 5.5 months after intoxication. Significantly reduced metabolic rates of glucose were revealed in selected brain regions, especially in both the frontal and anterior cingulate cortices, as well as in the subcortical white matter. Frontal and cingulate cortices showed a preserved metabolism of 35-53%, whereas the regional glucose consumption in cerebral white matter was reduced by more than 70%. In contrast, other areas of the brain such as the sensory-motor cortex, parts of the temporal lobes, basal ganglia and brainstem disclosed normal metabolic values. This lesion topography is discussed in relation to the development of akinetic mutism in the present case and in comparison with recent reports on the topic. Considering a plausible pathophysiology, akinetic mutism appears to be based on a different structural neuropathology when compared with the locked-in syndrome and the vegetative state. It is suggested that akinetic mutism is regarded as a specific condition characterized by injury of the frontal neuronal systems which promote executive functions.

Acute Disease↗

PubMed2001

Mutism after surgical removal of a cerebellar tumor: two case reports.

The authors report two pediatric cases of transient mutism that occurred after surgical removal of a medulloblastoma and a pilocytic astrocytoma of the vermis and discuss the pathophysiology of this syndrome. Transient mutism has been described for the first time quite recently, even in cases where these tumors were also surgically removed before. Perhaps improvement in imaging and in surgical techniques made neurosurgeons more daring and some interventions that were judged impossible are routinely performed today. If this is the case, postoperative transient cerebellar mutism might be considered the price that must be paid in order to cure more patients with cerebellar tumors.

Astrocytoma↗

PubMed1999

Phenelzine treatment of selective mutism in four prepubertal children.

Four children, ages 5 1/2 to 7 years, diagnosed with selective mutism and successfully treated with phenelzine are presented. All four children were anxious and extremely shy and had family histories of anxiety and shyness. The first three children were treated with phenelzine prior to reports that fluoxetine was helpful in some cases. The fourth child was treated initially with fluoxetine and had shown only minimal improvement after 10 months of doses up to 16 mg daily. Phenelzine doses ranged from 30 to 60 mg/day and treatment, including medication taper, lasted from 24 to 60 weeks. The phenelzine was generally well-tolerated and weight gain was the most common side effect. No hypertensive reactions or serotonin syndromes occurred. There was no recurrence of mutism after medication discontinuation. The authors conclude that phenelzine can be an effective treatment for selective mutism, but because of the possibility of serious food and drug interactions and the necessary dietary restrictions, it should be reserved for cases that do not respond to behavior therapy and fluoxetine or other specific serotonin reuptake inhibitors.

Child↗

PubMed1993

Elective mutism and mental retardation.

The association of elective mutism and mental retardation is noted. Two cases of elective mutism associated with mental retardation are presented. Both individuals had long-standing patterns of inhibition, shyness, and anxiety manifested by general refusal to talk outside the home, particularly at school. The importance of assessment of intellectual functioning and linguistic skills for the establishment of intervention priorities and clinical management is discussed. The possibility of the presence of mental retardation in individuals with elective mutism should be considered.

Adolescent↗