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PubMed1986

Mutism: review, differential diagnosis, and report of 22 cases.

Mutism is a common manifestation of both psychiatric and neurologic illness. Psychiatric disturbances associated with mutism include schizophrenia, affective disorders, conversion reactions, dissociative states, and dementias. Neurologic disorders producing mutism involve the basal ganglia, frontal lobes, or limbic system structures. In psychiatric and neurologic conditions, mutism is often associated with other signs of catatonia. The authors review the literature on mutism, including psychiatric, neurologic, toxic-metabolic, and drug-induced causes. Methods to discriminate among the many causes of mutism in the clinical setting are discussed, and 22 new cases of mutism are reported to emphasize the wide differential diagnosis.

Adolescent↗
PubMedDate not supplied

[Mutism in children].

INTRODUCTION: Mutism is absence of verbal expression with conservation of language comprehension. The origin of mutism is multifactorial and may followed from cranial trauma surgery of the posterior fossa, acquired epileptic syndromes and psychogenic origin. OBJECTIVE: To refer patients who had presented mutism of diverse etiology. CLINICAL CASES: We analysed three children who had presented mutism originated by diverse causes. Case 1. A child with family and school problems, attention deficits and limited communication resources. Neurological examination and other auxiliary test (EEG) were normal. He presented no alteration in language or speech. We recommended the change of the school and a psychotherapeutic orientation. Case 2. A 4 year old female child who has suffered varicella 15 days earlier and presented limitations in her verbal expression despite maintain her linguistically capacity. She showed a indifferent behavior and her movements were without finality. Neurological examination was normal. The girl understood and followed instruction properly. However her verbal communication was absent. Total recuperation occurred in 72 hours. Case 3. A 12 years old child who had suffered a cranial traumatism with loss of consciousness ten days earlier. After this traumatism, he presented behavior changes, disorientation and blurred vision. Additionally he presented stereotypies and limitations in psychosocial connections. Despite his mutism, he conserved the structure and content of language. SPECT showed hypoperfusion in orbitotemporal region. Improvement was total 20 days after his traumatism. CONCLUSIONS: The mutism has multifactorial etiology. References were made to three cases who's mutism was related to emotional causes, post-varicella complications and posttraumatic events.

Attention Deficit Disorder with Hyperactivity↗
PubMed1995

Transient mutism following a posterior fossa approach to cerebellar tumors in children: a critical review of the literature.

Transient mutism has been known as a rare complication following a posterior fossa approach to cerebellar tumors and its cause has not been clearly elucidated. The cerebellar mutism is not accompanied by cranial nerve deficits and disorders of consciousness. Since 1985 only 23 cases of mutism following removal of a cerebellar tumor in children have been reported in the literature. Two additional cases have been operated upon in our department. Extensive injury to the vermian and paravermian cerebellar area, involving the hemispheric cortex, cerebellar peduncles, fibers from the dentato-thalamocortical pathway, and dentate and interpositum nuclei may be the most important anatomical substrate of mutism. The mechanism of such transient mutism seems to be a complex of two or more factors (vascular disturbances due to manipulation or retraction of the cerebellar region around the IV ventricle and emotional factors). On the basis of these 25 cases the major features of the cerebellar mutism are discussed.

Ataxia↗
PubMed1988

A procedural distinction between elective and progressive mutism.

This paper introduces a procedural distinction between elective and progressive mutism. In elective mutism, a child elects to talk freely with intimates (e.g. family members); in progressive mutism a child does not communicate verbally with anyone (including intimates). This analysis argues that clinicians' therapeutic goals and parents' expectations of treatment outcomes for elective mutism would differ from those applied to a case of progressive mutism and that the selection of the appropriate concept (elective vs progressive) to name the type of mutism prior to intervention would enhance treatment outcomes.

Behavior Therapy↗
PubMed2005

Cerebellar mutism in adults after posterior fossa surgery: a report of 2 cases.

BACKGROUND: Mutism has been associated with injury to midline cerebellar structures secondary to degenerative disease, tumors, hemorrhage, or surgery. Typically, cerebellar mutism syndrome (CMS) has been seen in children and only rarely described in adults after surgery of the posterior fossa. This syndrome typically arises 48 hours after the initiating event and resolves approximately 7 to 8 weeks later. Characteristics of CMS include complete absence of speech without impaired consciousness, other cranial nerve deficits, or long tract signs. CASE DESCRIPTION: The authors report on 2 patients each of whom developed cerebellar mutism after tumor resection using a posterior fossa approach. The first patient underwent gross total resection of a pineal region tumor via a supracerebellar approach. The second patient underwent posterior fossa decompression for a left cerebellar hemispheric renal cell carcinoma metastasis with adjacent hemorrhage. One patient displayed a variant of cerebellar mutism with severe ataxic dysarthria without complete absence of speech, whereas the other demonstrated frank mutism. After neuroimaging studies confirmed the absence of a surgically treatable postoperative cause for the patients' symptoms, they were managed in a supportive fashion (eg, speech therapy) and improved within 3.5 months and 1 year, respectively. CONCLUSION: It is paramount that neurosurgeons be aware of cerebellar mutism with regard to its very rare occurrence in adults, its time of onset, and typical self-limiting course.

Adult↗
PubMed2001

Mutism: elective or selective, and acquired.

When a child does not speak, this may be because there is no wish to do so (elective or selective mutism), or the result of lesions in the brain, particularly in the posterior fossa. The characteristics of the former children are described, especially their shyness; and it is emphasized that mild forms are quite common and a definitive diagnosis should only be made if the condition is significantly affecting the child and family. In the case of mutism due to organic causes, the commonest of these is trauma to the cerebellum. Operations on the cerebellum to remove tumours can be followed by mutism, often after an interval of a few days, and it may last for several months or longer, to be followed by dysarthria. Other rarer causes are discussed, and also the differential diagnosis. The so-called posterior fossa syndrome consists of mutism combined with ataxia, cranial nerve palsies, bulbar palsies, hemiparesis, cognitive impairment and emotional lability, but the post-operative symptoms are often dominated by the lack of speech. The most accepted cause for the condition is vascular spasm with involvement of the dentate nucleus and the dentatorubrothalamic tracts to the brain-stem, and subsequently to the cortex. Diaschisis may be involved in causing the loss of higher cerebral functions, and possibly, complicating hydrocephalus. The treatment of elective mutism is reviewed, either using a psychotherapeutic approach or a variety of drugs, or both. These may well be ineffective, and it must be remembered that the condition often resolves on its own. The former treatment must concentrate on the training of social skills and activities of daily life and must be targeted to both the child, the family, and the school. Also, all kinds of punishment and insistence on speech must be discouraged. The drug, which seems to be most effective, is fluoxetine. Discovering more about the causes of mutism due to organic causes may well depend on studies using such techniques as magnetic resonance imaging and single photon emission tomography.

Cerebellar Diseases↗
PubMed2001

Cerebellar mutism caused by arteriovenous malformation of the vermis.

Transient mutism following posterior fossa tumour resection in children is well known in the literature. To our Knowledge, this phenomenon has never been reported without surgical intervention. We report a case of cerebellar mutism secondary haemorrhage from a vermian arteriovenous malformation (AVM), which resolved to ataxic dysarthria after 6 weeks. Embolization of the AVM was performed and the patient's clinical status continued to improve gradually till she became normal 6 months from the insult. The mutism was due to rupture of the AVM which might correlate the cerebellar mutism with the transient vasospasm of the blood vessels supplying the cerebellum. It is possible for a spontaneus posterior fossa bleed to result in transient mutism similar to post surgical mutism.

Adolescent↗
PubMed1995

Practical guidelines for the assessment and treatment of selective mutism.

OBJECTIVE: To provide practical guidelines for the assessment and treatment of children with selective mutism, in light of the recent hypothesis that selective mutism might be best conceptualized as a childhood anxiety disorder. METHOD: An extensive literature review was completed on the phenomenology, evaluation, and treatment of children with selective mutism. Additional recommendations were based on clinical experience from the authors' selective mutism clinic. RESULTS: No systematic studies of the phenomenology of children with selective mutism were found. Reports described diverse and primarily noncontrolled treatment approaches with minimal follow-up information. Assessment and treatment options for selective mutism are presented, based on new hypotheses that focus on the anxiety component of this disorder. Ongoing research suggests a role for behavior modification and pharmacotherapy similar to the approaches used for adults with social phobia. CONCLUSION: Selectively mute children deserve a comprehensive evaluation to identify primary and comorbid problems that might require treatment. A school-based multidisciplinary individualized treatment plan is recommended, involving the combined effort of teachers, clinicians, and parents with home- and clinic-based interventions (individual and family psychotherapy, pharmacotherapy) as required.

Anxiety Disorders↗
PubMed2003

Clinical distinctions between selective mutism and social phobia: an investigation of childhood psychopathology.

OBJECTIVE: To investigate the hypothesis that children with selective mutism are more socially anxious than children with social anxiety disorder but who are not selectively mute. METHOD: Twenty-three children with comorbid selective mutism and social phobia and 23 age-matched controls with social phobia alone and their parents participated in a comprehensive assessment of social anxiety and related aspects of psychopathology. RESULTS: The results do not uniformly support previous suggestions that children with selective mutism refuse speech because they are "frozen with fear." Although clinician and observer ratings for children with selective mutism revealed higher ratings of social distress than for children with social phobia alone, self-report data do not support this conclusion. Furthermore, although there were no group differences on measures of trait anxiety, general fears, or scores on the Child Behavior Checklist broadband Internalizing or Externalizing scales, children with selective mutism scored higher than children with social phobia alone on the Child Behavior Checklist Delinquency subscale, suggesting the presence of a broader clinical syndrome. CONCLUSION: It remains unclear whether children with selective mutism have extreme levels of social anxiety. Potential areas that might shed further light on this interesting disorder are discussed.

Case-Control Studies↗
PubMed1995

Mutism and cerebellar dysarthria after brain stem surgery: case report.

Transient mutism resolving to cerebellar speech after posterior fossa surgery is a well-recognized phenomenon, particularly in pediatric patients. The anatomic basis for this postoperative functional change is unclear but may reside in the dominant superior cerebellar hemisphere or the medial deep cerebellar nuclei. We report a case of an 8-year-old girl who presented for surgical resection of a cavernous malformation of the right pons (at the level of the middle cerebellar peduncle) after hemorrhage. Preoperatively, her complaints consisted of contralateral motor deficits. She had normal speech. Her lesion was resected through a subtemporal approach to the pons. She awoke unable to speak. She was able to communicate through a variety of verbal cues, including sign language. Her mutism lasted 12 days after which she underwent a prolonged period of slowly resolving cerebellar dysarthria. Her preoperative motor deficits also slowly resolved. This is the first reported case of mutism resolving to cerebellar dysarthria after a supratentorial approach to the brain stem. We discuss the anatomic basis for postoperative mutism in light of previous observations combined with the unusual finding of mutism after pontine surgery. In particular, reports of mutism after bilateral cerebellar hemispheric injury, bilateral or unilateral medial deep nuclear injury, and, now, pontine tegmental injury implicate the superior cerebellar hemispheres, the deep cerebellar nuclei, and the nuclear outflow through the superior cerebellar peduncle as the anatomic bases for cerebellar participation in the production of human speech.

Brain Neoplasms↗
PubMed1995

Mutism and pseudobulbar symptoms after resection of posterior fossa tumors in children: incidence and pathophysiology.

MUTISM AND A variety of other neurobehavioral symptoms have been reported anecdotally after the removal of posterior fossa mass lesions. To determine the incidence and clinical spectrum of this syndrome, a detailed review was performed of patients undergoing resection of infratentorial tumors at our institution during the last 9 years; 12 of 142 patients (8.5%) manifested this syndrome, the largest series of such patients reported to date. Each child had a lesion that involved the vermis; seven had medulloblastomas, three had astrocytomas, and two had ependymomas. The incidence among children with vermian neoplasms was 13%. Ten children underwent division of the inferior vermis during tumor resection, and three had a superior vermian incision; one child underwent both superior and inferior vermian incisions. In 10 children, mutism developed in a delayed fashion postoperatively. The speech disturbance was associated with poor oral intake in 9 children, urinary retention in 5, long-tract signs in 6, and bizarre personality changes, emotional lability, and/or decreased initiation of voluntary movements in all 12. Neuropsychiatric testing, performed in seven children, confirmed impairments not only in speech but also in initiation of other motor activities. Ten children regained normal speech, bladder control, and neurological functioning, other than ataxia and mild dysarthria, within 1 to 16 weeks; two children had significant residual deficits. Characteristically, affect and oral intake returned to their preoperative baseline before the speech difficulties began to resolve. A detailed radiological review of these cases in parallel with 24 cases of vermian tumors without mutism identified only one factor that was significantly associated with the mutism syndrome, bilateral edema within the brachium pontis (P < 0.01). Neither the size of the tumor nor the length of vermian incision was associated with the development of mutism. The clinical features of this syndrome in the context of these imaging findings suggest that the mutism syndrome results from transient impairment of the afferent and/or efferent pathways of the dendate nuclei that are involved in initiating complex volitional movements. The clinical courses of our patients are presented and compared with those of similar cases in the literature in an attempt to evaluate the validity of this hypothesis.

Adolescent↗
PubMed1995

Transient cerebellar mutism after posterior fossa surgery in children.

Cerebellar mutism has been reported after surgery for posterior fossa tumors in children and, rarely, in adults. The pathogenesis of this syndrome remains unclear, and controversy exists regarding whether it is a purely psychogenic disorder or an organic syndrome. The anatomical substrate for the mutism also remains unknown. We encountered five cases of postoperative transient cerebellar mutism in a consecutive series of 63 children with posterior fossa tumors. These cases were analyzed and compared with the patients without mutism to find predictive factors for the occurrence of mutism, with the hope of elucidating further the pathophysiological mechanism. The most significant finding was the presence in all cases of a period of cerebellar dysarthria after resolution of the muteness. We, therefore, believe that cerebellar mutism is an extreme form of dysarthria, rather than a real cognitive deficit or a psychological disturbance.

Adolescent↗
PubMed1997

The family history of children with elective mutism: a research report.

The family history was studied in children with elective mutism. The samples comprised a series of N = 38 children with elective mutism and a control group of N = 31 children with a similar behavioural phenotype, i.e., the combination of an emotional disorder and a developmental disorder of articulation or expressive language. Interviews were performed with the respective mothers. There was a clear excess of the personality trait of taciturnity in first-, second-, and third-degree relatives. Although mutism was reported almost exclusively in the group of relatives of children that manifested elective mutism, the differences between the two samples were not significant probably due to low frequencies. Disorders of speech and language were quite common in the relatives of subjects in both samples. Psychiatric disorders were more frequently reported in the families with an electively mute child. The study lends some evidence for the assumption that genetic factors may play a role in the etiology of elective mutism.

Case-Control Studies↗
PubMed1991

Mechanism of mutism following the transcallosal approach to the ventricles.

Transient mutism has been known as a common manifestation following callosotomy for medically intractable epilepsy, but its cause has not been clearly elucidated. In this paper, we report three cases of mutism following a transcallosal approach to tumours in the lateral and third ventricles and retrospectively analyze the surgical, neurological and radiological features which may suggest the cause of this type of mutism. Mutism may be a result of division of the corpus callosum. Suppression of the limbic system caused by lesions in the anterior cingulate gyrus, septum pellucidum, and fornix may have been of importance in at least two of these three cases. Impairments of the supplementary motor cortex, thalamus and basal ganglia may also be factors reducing speech production. The mechanism of such transient mutism seems to be a complex of two or more of these factors, and their combinations may be different from one case to the other.

Adult↗
PubMed2001

Bilateral crossed cerebello-cerebral diaschisis and mutism after surgery for cerebellar medulloblastoma.

A 7-year-old boy developed mutism after surgery for cerebellar medulloblastoma. Postoperative magnetic resonance imaging (MRI) showed atrophy of the cerebellar vermis and both cerebellar hemispheres, predominantly on the right side. Single photon emission computed tomography (SPECT) with technetium-99m-ethyl cysteinate dimer (Tc-99m ECD) revealed decreased cerebral blood flow (CBF) in the bilateral thalami, bilateral medial frontal lobes, and left temporal lobe in addition to the cerebellar vermis and both cerebellar hemispheres when mutism was manifest, indicating the existence of bilateral crossed cerebello-cerebral diaschisis (BCCCD). Circulatory disturbance in both cerebellar hemispheres secondary to tumor resection probably caused BCCCD in both cerebral hemispheres, predominantly in the left, via the dentatothalamocortical pathway (DTCP). With recovery of his mutism, CBF increased in the right thalamus, bilateral medial frontal lobes and left temporal lobe. Thus BCCCD was improved, with only a slight decrease in CBF still persisting in the left thalamus. The mechanism of mutism may have involved damage to the cerebellar vermis (the site of incision at operation), the left dentate nucleus (heavily infiltrated by the tumor) and the right dentate nucleus of the cerebellum (affected by circulatory disturbance secondary to acute postoperative edema). The SPECT findings suggested that mutism was associated with BCCCD-induced cerebral circulatory and metabolic hypofunction in the supplementary motor area mediated via the DTCP.

Cerebellar Neoplasms↗
PubMedDate not supplied

Transient "cerebellar" mutism.

The term "cerebellar mutism" refers to a specific disorder in which a complete but transient loss of speech, followed by dysarthria, occurs following resection of intrinsic posterior cranial fossa tumors or cerebellar hemorrhages, or upon trauma. Although it is well known that the lack of long-tract findings and cranial nerve (CN) involvement is the rule, the pathophysiology of cerebellar mutism has not been clearly elucidated. A review of the relevant literature disclosed 93 patients with this condition, the majority of these being in the pediatric age group. The neuropathological findings were as follows: 57 primitive neuroectodermal tumors (PNET), 19 astrocytomas, 10 ependymomas, 5 vascular malformations, 1 metastatic tumor, and 1 traumatic injury. The interval before the onset of mutism ranged from 0 to 168 h (mean 40.9 h). The mutism lasted from 1 to 168 days (mean 37.6 days). Subsequent dysarthria was present in 75 (80%) of the 93 patients. In this article, some specific recent illustrative reports are presented, and the concept of the role of the cerebellum in language and cognition is discussed. With these data as our point of departure, various hypotheses that have been advanced to explain the pathogenesis of this transient speech disorder are analyzed. The findings of the study suggest that the cause of the cerebellar mutism is the ischemia caused by vasospasm, as it usually developed after a latent period.

Arteriovenous Malformations↗
PubMed1999

Akinetic mutism after fourth ventricle choroid plexus papilloma: treatment with a dopamine agonist.

BACKGROUND: Akinetic mutism is a behavioral state wherein a patient seems to be awake but does not move or speak. Several patients are reported to have developed mutism after posterior fossa surgery. We present a patient who developed akinetic mutism after total excision of a choroid plexus papilloma of the fourth ventricle, and who was treated with bromocriptine. CASE DESCRIPTION: An 18-year-old woman was admitted with akinetic mutism, which had developed 6 days after posterior fossa surgery. She had had no neurologic deficit in the first 5 days after surgery and could communicate with her family. Despite antioedematous therapy and daily lumbar punctures to drain cerebrospinal fluid, there was no clinical improvement after she entered the akinetic mute state. Brain magnetic resonance revealed ventriculomegaly; brain single photon emission computed tomography revealed bilateral reduction of perfusion in the frontal region. Because daily lumbar drainage did not result in clinical improvement, shunt placement was not considered. Bromocriptine therapy was begun at a dose of 2x2.5 mg; 24 hours later, the patient started to speak and move her upper extremities. Further improvement occurred over the following week when the dose was increased to 3x2.5 mg. Bromocriptine was replaced with a placebo to determine whether the neurologic improvement was caused by the medicine. The patient's neurologic status deteriorated progressively; therefore, bromocriptine was restarted and she was discharged from the hospital. During the 6 months of follow-up, the patient has remained in good health. CONCLUSIONS: The etiology of akinetic mutism is not clear. Monoaminergic pathways, particularly dopaminergic cell groups, are most probably involved in this syndrome, because bromocriptine has a dramatic effect on these patients, as demonstrated in our case.

Adolescent↗
PubMed1997

Role of cavum septum pellucidum in akinetic mutism of hydrocephalic children.

Two children 9 and 13 years of age with histories of aqueductal stenosis developed akinetic mutism after multiple shunt revisions. The girl had spontaneous relief of her akinetic mutism 1 month later, after parenteral antibiotics and multiple shunt revisions. The akinetic mutism of the boy was resistant to antiparkinsonian therapy before megadosage of bromocriptine (120 mg/day). Both children had a prominent cavum septum pellucidum (CSP), which has rarely been involved in the pathogenesis of akinetic mutism. Because of the rapid shrinkage of the girl's CSP after shunt revision, but not that of the boy even after stereotactic fenestration of the wall of his CSP, their eventual outcomes were different. Wide CSP (WCSP) may play an important role in the occurrence of akinetic mutism in hydrocephalic patients.

Adolescent↗