1/133. 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.- - - - - - - - - - ranking = 1keywords = mutism (Clic here for more details about this article) |
2/133. Transient mutism resolving into cerebellar speech after brain stem infarction following a traumatic injury of the vertebral artery in a child.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.- - - - - - - - - - ranking = 0.66666666666667keywords = mutism (Clic here for more details about this article) |
3/133. Progressive catatonia.We present the case of a young man with a diagnosis of a childhood-onset pervasive developmental disorder who developed a progressive neurologic deterioration with persistent catatonia and right hemiparesis. On his initial evaluation approximately three years after the onset of mutism, he manifested right hemiparesis and catalepsy. Two years later, although catalepsy had subsided, motor function had deteriorated so that he could not use his hands to feed or dress himself. Oral-facialbuccal dyskinesia manifested by blepharospasm and grimacing were present constantly during waking hours. Quantitative electroencephalography demonstrated markedly decreased amplitude, a finding associated with catatonia. Left sural nerve biopsy indicated large axon cylinder degeneration. Left deltoid biopsy demonstrated perimysial fibrosis and type II fiber predominance. Although magnetic resonance imaging of the head without contrast was normal, positron emission tomography indicated hypometabolism of the right cerebral and the right cerebellar hemispheres. The patient continues to deteriorate despite a course of 25 electroconvulsive treatments. He continues to manifest criteria for catatonia including motoric immobility, mutism, and peculiarities of voluntary movement such as prominent grimacing. We suspect an inherited neurodegenerative disorder. Since catatonia is a treatable condition frequently associated with medical and neurological diseases, examination for the features of catatonia must be included in the assessment of patients with progressive brain degeneration. This report is an attempt to clarify the traits of a serious variant of progressive brain degeneration.- - - - - - - - - - ranking = 0.22222222222222keywords = mutism (Clic here for more details about this article) |
4/133. fragile x syndrome and selective mutism.This is the first report that details an association between fragile x syndrome (FXS) and selective mutism (SM). This 12-year-old girl with heterozygous full mutation at FMR1 has a long history of social anxiety and shyness in addition to SM. Her sister also has the full mutation and a history of SM that resolved in adolescence. A beneficial response to fluoxetine and psychotherapy is described. The FMR1 mutation appears to be the first gene mutation associated with SM and further studies are recommended to assess what percentage of patients with SM have the FMR1 mutation.- - - - - - - - - - ranking = 61188.619802503keywords = selective mutism, mutism (Clic here for more details about this article) |
5/133. Complete mutism after midbrain periaqueductal gray lesion.Several neurophysiological studies have highlighted the role of the midbrain periaqueductal gray matter (PAG) in the initiation of vocalization in various animal species, from frogs to primates. With regard to humans, only two cases of complete mutism following a lesion to the PAG have been reported so far. This article describes a new case of a patient (GM) who, following an ischemic lesion to the periaqueductal gray region of the midbrain, presented with complete and irreversible mutism, though her language comprehension functions and her non-verbal expression capacity were preserved. This clinical case provides evidence that in humans the PAG also acts as a link between different vocalization-eliciting external and internal stimuli (which reach the PAG from sensory and emotional structures) and the vocal-motor coordinating mechanisms in the lower brain stem.- - - - - - - - - - ranking = 0.66666666666667keywords = mutism (Clic here for more details about this article) |
6/133. akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction.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.- - - - - - - - - - ranking = 0.83007231065243keywords = mutism, aphasia (Clic here for more details about this article) |
7/133. Elective mutism: effect of dental treatment with N2/O2-inhalation sedation: review and report of case.Elective mutism in children is characterized by a marked, emotionally determined selectivity in speaking, such that the child demonstrates his or her language competence in some situations but fails to speak in other situations. An eight-year-old boy with elective mutism had to undergo restorative dental treatment. It was chosen to use relative analgesia to perform this treatment. The sedation with oxygen and nitrous oxide resulted in complete symptom remission as long as the sedation lasted.- - - - - - - - - - ranking = 0.66666666666667keywords = mutism (Clic here for more details about this article) |
8/133. Selective mutism--the child who doesn't speak at school.Selective mutism is a syndrome in which there is a consistent failure to speak in social situations where speech is expected, despite speaking in other situations. The problem is most common in the child who speaks actively and well at home but who refuses to speak in school. This paper describes 2 young children from the author's practice who refuse to speak at school and a short summary of recent changes in the thinking about the cause and therapy of selective mutism. This is the first article on selective mutism to appear in an American pediatric journal.- - - - - - - - - - ranking = 24476.003476557keywords = selective mutism, mutism (Clic here for more details about this article) |
9/133. A case of mutism subsequent to cocaine abuse.The authors report a case of mutism that was ultimately found to be associated with chronic cocaine use in an adult woman. Brain dysfunction was confirmed by SPECT scan, which revealed reduced cerebral blood perfusion and areas of infarction, presumably consequent to the cocaine addiction. This is the first reported case of such an association.- - - - - - - - - - ranking = 0.55555555555556keywords = mutism (Clic here for more details about this article) |
10/133. 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.- - - - - - - - - - ranking = 73426.454874115keywords = selective mutism, mutism (Clic here for more details about this article) |
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