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At least 271 records · Page 15Linked to original sources
PubMed1997

Akinetic mutism: disconnection of frontal-subcortical circuits.

Akinetic mutism may result from anterior cingulate lesions or a disconnection of the limbic connections projecting from the cingulate through subcortical circuits. Based on nonhuman primate primate tracer studies, ventral pallidal lesions should disrupt the anterior cingulate frontal-subcortical circuit. A patient developed a rigid akinetic mute state caused by bilateral lesions of the globus pallidus interna with ventral extension. The anatomic basis of the patient's clinical findings support a similarity in frontal-subcortical anatomy between humans and nonhuman primates. Isolated pallidal lesions are rare. Future studies should document whether ventral extension below the anterior commissure is associated with a loss of motivation.

Aged↗
PubMed1998

[Significance of single photon emission computed tomography and akinetic mutism].

Akinetic mutism is a reactive status with permanent opening of the eyes. The accountable lesions are always bilateral. The injured cerebral structures include the frontal gyri, the thalami or the mesencephalic areas. In one case of a 44-year-old patient, magnetic resonance imaging and computed tomography were not contributive. Tc99m brain SPECT imaging was performed and displayed bilateral frontal hypoactivity. This case suggests that this technique could be helpful for diagnosis when clinical features and radiological pattern are opposite.

Adult↗
PubMed1989

A case of pure word mutism: don't be fooled!

A case of pure word mutism, often called "small Broca's aphasia," in a 44-year-old woman with a psychiatric history and a long history of unresolved, vague neurologic symptoms is presented. Although hysterical reaction was high on the list of differential diagnoses due to the patient's medical history, cranial computed tomography performed in the emergency department revealed an infarct in the distribution of the middle cerebral artery, which probably caused her condition. The patient improved slightly during hospitalization and was discharged on the sixth hospital day with a moderate expressive aphasia for which she received intensive speech therapy.

Adult↗
PubMed1975

Goiter and deaf mutism.

The occurrence of deaf-mutism and goiter unassocaited with creatinism or mental retardation in euthyroid patients is known as Pendred's Syndrome. It is considered due to a single mutant recessive gene responsible for both the goiter and deafness. The penetrance is high, the intenseness of expressivity may vary within the same family and only one generation is affected. The extremely atypical hyperplasia seen in such goiters has been considered malignant. In 1956 the author reported a family in which 4 of 6 sibilings demonstrated Pendred's Syndrome. Three of the 4 had undergone thyroidectomy, two were considered to have carcinoma. Nineteen years later the family is again reported. The fourth sibling has recently undergone thyroidectomy. This thyroid demonstrated the same atypical hyperplasia as seen in the elder two siblings. The 19 year followup of this family has shown no evidence of recurrence or metastases, indicating that the atypical hyperplasia is probably not malignant. Pendred's Syndrome is described and certain suggestions are made for the counseling of the parents and the treatment and counseling of those children so afflicted.

Adolescent↗
PubMed1978

Abnormal neutrophil chemotaxis in a syndrome of unusual facies, proportionate small stature and sensorineural deafness-mutism.

Two of 5 children in one family presented with unique facies, proportionate small stature and sensorineural deafness-mutism. One of the children who had a history of recurrent infections, was shown to have a defect of leukocyte chemotaxis. Although impairment of chemotaxis could not be demonstrated in the other affected sibling, it is unlikely that the association of a previously undescribed syndrome and a rare disorder of chemotaxis is a chance occurrence.

Abnormalities, Multiple↗
PubMed1987

Prevalence and genetic aspects of deaf mutism in Shanghai.

Two hundred and eighty-five cases of congenital deaf mutism were ascertained in a population of 483,611 in Zhabei District in Shanghai. The prevalence was 0.059% (1:1697). Inherited cases accounted for 84.83% of all cases. The mode of inheritance was autosomal recessive with complete penetrance and heterogeneity (consisting of at least five different loci). The fitness was 77.63%, the coefficient of selection was 0.2237, the mutation rate was 1.119 x 10(-4) mutation/gamete, and no heterozygote advantage was proven.

China↗
PubMed1991

Goitre and deaf-mutism.

The occurrence of congenital deafness, mutism and goitre unassociated with cretinism or mental retardation in euthyroid patients is known as Pendred's Syndrome. It has been estimated that 4-10 % of children with congenital deafness suffer from this condition. The perceptive hearing loss is considered to be present at birth although it is frequently not recognized for several years. The cause of the hearing defect is a congenital bilateral malformation of the cochlea of the Mondini type. The goitre is not recognized clinically at birth or in early childhood. It becomes apparent in the pre-pubertal years when it presents as a colloid enlargement progressing to a nodular goitre. The thyroid defect has been shown to be a partial defect in iodine organification leading to the underproduction of thyroxine and subsequent thyroid hyperplasia. The syndrome is caused by a single mutant recessive gene responsible for both the deafness and goitre. Its autosomal mechanism gives an equal incidence in both sexes, unusual in thyroid disease. This article reviews the current aspects of pathogenesis and treatment of this syndrome and reports its occurrence in two Sudanese siblings.

Adolescent↗
PubMed1979

[Deaf-mutism, lymphedema of the lower limbs and hematological abnormalities (acute leukemia, cytopenia) with autosomal dominant transmission].

Report of a syndrome constituted from sensorineural deaf mutism, lymphoedema of lower limbs with early onset and haematological anomalies (aucte myeloblastic leukaemia, cytopenia) in four individuals (three boys and two girls from two generations). This observation suggest autosomal dominant transmission, however recessive transmission cannot be formelly excluded.

Child↗
PubMed1981

Inner ear pathology in deaf mutism.

This is a report of the inner ear pathology found in a pair of temporal bones from a deaf mutism case. This patient's spouse and four of six children were deaf mutes. Some members in the succeeding generation were also known to be deaf mutes. The temporal bones (horizontally sectioned) showed the cochleo-saccular degeneration with exactly similar extent bilaterally. The scala media and the saccular space were atrophied, and displaced membranes were attached onto the degenerated sensory epithelia in many areas, but some portion of the scala media exhibited an ectatic view. The cochlear and saccular nerves were severely reduced. In addition to the pathology found in the pars inferior, the internal auditory canal and the cochlear aqueduct were enlarged. All end organs and nerves in the pars superior were intact.

Aged↗
PubMed1993

[Symptomatology of language disorders in cerebral palsy with mutism].

Language disturbances in cerebral palsy with mutism. The analysis of the afferent side of language in 18 cerebral palsy children with no oral expression shows that they form a very heterogeneous population. The semiological analysis concerning comprehension leads to their classification into four main groups akin to the classical dysphasia syndromes. Major agrammatism occurring in phonologico-syntactic dysphasia. Sensory dysphasias (or verbal deafness). Mixed (or global) dysphasias. Motor dysphasias: phonological programmation disturbances (anarthria) and motor production disturbances (dysarthria). The disclosure of these various dysphasias allows for specific rehabilitation and for education procedures suitable for each individual patient.

Adolescent↗