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S E Bundey

Publications and source records attributed to S E Bundey.

15 recordsLinked to original sources

A syndrome of severe mental retardation, spasticity, and tapetoretinal degeneration linked to chromosome 15q24.

Nine affected individuals are described from a large extended Pakistani family manifesting a syndrome characterized by a triad of varying degrees of spasticity, severe mental retardation, and visual impairment resulting from tapetoretinal degeneration. In all cases, the parents were at least first cousins, since there was complex consanguinity within the pedigree. The clinical features differ from previously reported syndromes involving pigmentary retinal degeneration and appear to represent a new recessively inherited neurodegenerative condition. Linkage to a 4-5 cM-region between markers D15S211 and D15S152 on 15q24 has been established by autozygosity mapping.

Abnormalities, Multiple↗

Autozygosity mapping, to chromosome 11q25, of a rare autosomal recessive syndrome causing histiocytosis, joint contractures, and sensorineural deafness.

We describe a highly consanguineous family, originating from Pakistan, displaying histiocytosis, joint contractures, and sensorineural deafness. The form of histiocytosis exhibited by this family does not fit readily into any of the recognized classes of this disease. It appears to represent a novel form of familial histiocytosis demonstrating autosomal recessive inheritance. Using autozygosity mapping, we have identified a homozygous region of approximately 1 cM at chromosome 11q25, in affected individuals. A maximum two-point LOD score of 3.42 (recombination fraction straight theta = .00) was obtained with marker D11S968. This is the first genetic locus to be described that is involved in the molecular pathogenesis of histiocytosis.

Abnormalities, Multiple↗

Optic atrophy in Wolfram (DIDMOAD) syndrome.

Wolfram syndrome is the association of diabetes mellitus and optic atrophy, also called DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy and deafness). Incomplete characterisation has caused diagnostic confusion; we therefore undertook a nation-wide cross-sectional case finding study. We identified 45 patients with Wolfram syndrome, median age 29 years. All patients fulfilled the ascertainment criteria (juvenile onset diabetes mellitus and optic atrophy). Optic atrophy presented in 38 patients with reduced visual acuity and colour vision defect (median age 11 years), progressing to visual acuity of 6/60 or less in 35 patients (median time 8 years, range 1-25 years). Visual field examinations recorded before acuity deteriorated showed central scotomas with peripheral constriction. Blind patients had absent pupillary reflexes. Horizontal nystagmus was seen in patients with other signs of cerebellar degeneration. There was no pigmentary retinal dystrophy; only 3 patients had background diabetic retinopathy, despite a median duration of diabetes of 24 years. Electroretinography was normal in 3 patients and showed reduced amplitude in 3 patients; visual evoked responses were abnormal (10/10 patients: reduced amplitude to both flash and pattern stimulation). Magnetic resonance imaging showed generalised brain atrophy with reduced signal from the optic nerves and chiasm. A postmortem brain specimen from one patient revealed atrophy of the optic nerves, chiasm, cerebellum and brainstem. We found no evidence of mitochondrial genome defects or rearrangements. This primary neurogenerative disorder presents with diabetes mellitus and progressive optic atrophy, probably due to pathology in the optic nerve.

Adolescent↗

Wolfram (DIDMOAD) syndrome.

Wolfram syndrome (MIM 222300) is the association of juvenile onset diabetes mellitus and optic atrophy, also known as DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy, and Deafness). Patients present with diabetes mellitus followed by optic atrophy in the first decade, cranial diabetes insipidus and sensorineural deafness in the second decade, dilated renal outflow tracts early in the third decade, and multiple neurological abnormalities early in the fourth decade. Other abnormalities include primary gonadal atrophy. Death occurs prematurely, often from respiratory failure associated with brainstem atrophy. Most patients eventually develop all complications of this progressive, neurodegenerative disorder. The pathogenesis is unknown, but the prevalence is 1 in 770000 in the UK and inheritance is autosomal recessive. A Wolfram gene has recently been mapped to chromosome 4p16.1, but there is evidence for locus heterogeneity, and it is still possible that a minority of patients may harbour a mitochondrial genome deletion. The best available diagnostic criteria are juvenile onset diabetes mellitus and optic atrophy, but there is a wide differential diagnosis which includes other causes of neurodegeneration.

Humans↗

Neurodegeneration and diabetes: UK nationwide study of Wolfram (DIDMOAD) syndrome.

Wolfram syndrome is the association of diabetes mellitus and optic atrophy, and is sometimes called DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). Incomplete characterisation of this autosomal recessive syndrome has relied on case-reports, and there is confusion with mitochondrial genome disorders. We therefore undertook a UK nationwide cross-sectional case-finding study to describe the natural history, complications, prevalence, and inheritance of the syndrome. We identified 45 patients with Wolfram syndrome--a prevalence of one per 770,000. Non-autoimmune, insulin-deficient diabetes mellitus presented at a median age of 6 years, followed by optic atrophy (11 years). Cranial diabetes insipidus occurred in 33 patients (73%) with sensorineural deafness (28, 62%) in the second decade; renal-tract abnormalities (26, 58%) presented in the third decade followed by neurological complications (cerebellar ataxia, myoclonus [28, 62%]) in the fourth decade. Other abnormalities included gastrointestinal dysmotility in 11 (24%), and primary gonadal atrophy in seven of ten males investigated. Median age at death (commonly central respiratory failure with brain-stem atrophy) was 30 years (range 25-49). The natural history of Wolfram syndrome suggests that most patients will eventually develop most complications of this progressive, neurodegenerative disorder. Family studies indicate autosomal recessive inheritance with a carrier frequency of one in 354, an absence of a maternal history of diabetes or deafness, and an absence of the mitochondrial tRNA Leu (3243) mutation. Juvenile-onset diabetes mellitus and optic atrophy are the best available diagnostic criteria for Wolfram syndrome, the differential diagnosis of which includes other causes of neurodegeneration.

Adolescent↗

A clinical and molecular genetic study of dentatorubropallidoluysian atrophy in four European families.

Dentatorubropallidoluysian atrophy is a neurodegenerative disorder with characteristic pathology, chiefly described in reports from Japan, and is associated with an unstable CAG trinucleotide repeat in a gene on chromosome 12. We describe four European families, three British and one Maltese, with this mutation. All exhibited autosomal dominant inheritance, and there was evidence for anticipation associated with an increase of the expansion with paternal transmission in two families. Affected chromosomes from patients with dentatorubropallidoluysian atrophy had CAG expansions of 58 to 74 repeats, compared to 7 to 26 in control chromosomes, and the size of repeat was significantly inversely correlated with age of onset. The clinical features were diverse, even within individual families, and comprised a combination of a movement disorder (chorea, myoclonus, dystonia, or parkinsonism), cerebellar ataxia, epilepsy, psychosis, and dementia. A clinical diagnosis of Huntington's disease had been made in affected individuals from all families. Neuropathological examination of 2 patients showed no specific abnormality in one and degenerative changes predominantly affecting the spinal cord in the other. Investigation of 55 patients who might represent sporadic examples of dentatorubropallidoluysian atrophy did not detect any expanded alleles. Dentatorubropallidoluysian atrophy is likely to be more common than previously recognized in non-Japanese populations, and should be considered in any patient with a dominantly inherited neurodegenerative disorder with the above-mentioned clinical features.

Adolescent↗

Unusual features in the inheritance of ataxia telangiectasia.

A prevalence study of ataxia telangiectasia was conducted in the West Midlands, with a population of over 5 million. The prevalence in those aged 50 or less was found to be 1 in 514,000 and the birth frequency to be about 1 in 300,000. A genetic study of 47 families ascertained throughout the United Kingdom was carried out concurrently. A low parental consanguinity rate was found, no parents being first cousins or more closely related, whereas 10% had been expected. The incidence of ataxia telangiectasia in the 79 sibs of index cases was 1 in 7. These two features demonstrate that ataxia telangiectasia may not always be an autosomal recessive condition. Other possible explanations are that some cases are double heterozygotes or new dominant mutations.

Adolescent↗

Frequency and replication status of the fragile X, fra(X)(q27-28), in a pair of monozygotic twins of markedly differing intelligence.

Chromosome analysis using conventional staining, G banding, and, after BUdR incorporation, two R banding methods, one using Hoechst and one acridine orange, were performed on lymphocytes from a pair of female monozygotic twins. The culture conditions were designed to show the presence of the fragile X (q27-28) which had previously been found to be segregating in the family. One twin was of higher than normal intelligence and the other had been diagnosed as mentally retarded. The frequency of the occurrence of the early/active fragile X compared to the overall total of informative fragile X was determined using both methods described above and was also compared with previous published data in the form of a graph showing percentage of early/active fragile X against intelligence.

Adult↗

Population incidence and segregation ratios in the Martin-Bell syndrome.

A clinical and cytogenetic study of children attending schools for the educationally handicapped has been carried out in the City of Coventry. As a result of this an estimate of the population incidence of the Martin-Bell syndrome among schoolchildren has been made. Among school-boys the incidence of mental retardation due to the fra (X) was found to be 0.73 per 1000 and among schoolgirls 0.48 per 1000. The overall prevalence is 0.61 per 1000. Genetic and cytogenetic analysis of 14 families ascertained in an unbiased manner showed that the expected 50% ratio of affected to unaffected relatives was disturbed, the possible result of a segregation distortion.

Child↗