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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic neuroleptic therapy may be associated with the development of diverse movement disorders including Tardive dyskinesia (TD), Parkinsonism, dystonia, and akathisia in a subset of schizophrenic patients. It is presently unknown why only a proportion of neuroleptic-treated patients develop these movement disorders. In the following communication, we present a series of studies which demonstrate that the development of these movement disorders may be facilitated by certain risk factors including disturbances in pineal melatonin functions, diabetes mellitus, cognitive deficits, suicidal behavior, and disturbances in the functions of the choroid plexus. Recognition of these biological factors may prove useful in: (a) further understanding of the pathophysiology of these disorders, and (b) identifying patients at risk for these movement disorders.
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PMID:Risk factors for neuroleptic-induced movement disorders. 168 14

A computer-assisted staged system of a follow-up of factory workers with CHD and diabetes mellitus was developed. It included automated screening by questionnaire, ECG and biochemical screening, physical examination, investigation of the basic carbohydrate-lipid indices, more detailed examination in out- or inpatients settings using up-to-date diagnostic methods (bicycle ergometry, monitoring after Holter, etc.), identification of groups for a follow-up, and therapeutic and sanitary measures. A total of 27750 persons were investigated. The most important group was that including persons with risk factors: vegetovascular dystonia developing into CHD (6%) or essential hypertension (20%). Sanitary measures by unified methods caused a decrease in temporary disability with the economic effect of 197,000 rubles.
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PMID:[Characteristics of the dynamic outpatient observation of workers at an industrial enterprise]. 297 90

C57BL/KsJ db/db inbred mice have an hereditary autosomal recessive disease resembling in some respects maturity onset human diabetes mellitus. At 8--11 months of age, they displayed intermittent symptoms suggestive of a mild sensory neuropathy. These symptoms consisted of adduction of their hind limbs and flexing hind paws when raised by the tail, and inability to maintain their position on the roto wheel. Peripheral nerves and sensory ganglia of the diabetic mice were compared with those of the unafflicted littermates and studied with respect to Schwann cell counts and myelinated nerve fiber diameter measurements. In addition, teased fibers of peripheral nerves were compared for obvious changes in internodal distance and demyelination. Chromatolytic neurons were moe abundant in lumbosacral spinal ganglia of diabetic mice than in corresponding ganglia of controls or in more anterior spinal ganglia and trigeminal ganglia of diabetics. Histologic studies showed an increase in Schwann cell counts in longitudinal sections of peripheral nerves. A similar but larger increase was observed in peripheral nerves of mice affected with an hereditary sensory neuropathy, dystonia musculorum. A small but general decrease in myelinated fiber diameter was observed in sensory and motor nerves.
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PMID:Peripheral neuropathy in mouse hereditary diabetes mellitus. I. Comparison of neurologic, histologic, and morphometric parameters with dystonic mice. 696 18

This is the first reported case of dystonia with a partial deletion of the long arm (q) of chromosome 18. Neurologic findings in the 18q- syndrome include mental retardation, seizures, nystagmus, incoordination, tremor, and chorea. A 36-year-old woman with an 18q terminal deletion [karyotype 46,XX,del(18)(q22.2)] had hypothyroidism, diabetes mellitus, borderline intelligence, short stature, short neck, sensorineural hearing loss, and sensorimotor axonal neuropathy. Parents' karyotypes were normal. She had had incoordination and writing difficulty since childhood. Posturing and tremor of the head began at age 16, followed by arm tremors. She had jaw deviation and tremor, neck tremor with retrocollis, involuntary pronation of the right arm, coarse postural and severe action tremor, and tight pen grip with dystonic wrist extension on writing. The 18q- syndrome should be added to the list of genetic causes of secondary dystonia. A karyotype analysis should be considered in secondary dystonias, particularly when there are associated features such as short stature and endocrinopathies.
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PMID:Dystonia in a patient with deletion of 18q. 756 32

A variety of degenerative diseases involving deficiencies in mitochondrial bioenergetics have been associated with mitochondrial DNA (mtDNA) mutations. Maternally inherited mtDNA nucleotide substitutions range from neutral polymorphisms to lethal mutations. Neutral polymorphisms are ancient, having accumulated along mtDNA lineages, and thus correlate with ethnic and geographic origin. Mildly deleterious base substitutions have also occurred along mtDNA lineages and have been associated with familial deafness and some cases of Alzheimer's Disease and Parkinson's Disease. Moderately deleterious nucleotide substitutions are more recent and cause maternally-inherited diseases such as Leber's Hereditary Optic Neuropathy (LHON) and Myoclonic Epilepsy and Ragged-Red Fiber Disease (MERRF). Severe nucleotide substitutions are generally new mutations that cause pediatric diseases such as Leigh's Syndrome and dystonia. MtDNA rearrangements also cause a variety of phenotypes. The milder rearrangements generally involve duplications and can cause maternally-inherited adult-onset diabetes and deafness. More severe rearrangements frequently involving detections have been associated with adult-onset Chronic Progressive External Ophthalmoplegia (CPEO) and Kearns-Sayre Syndrome (KSS) or the lethal childhood disorder, Pearson's Marrow/Pancreas Syndrome. Defects in nuclear-cytoplasmic interaction have also been observed, and include an autosomal dominant mutation causing multiple muscle mtDNA deletions and a genetically complex disease resulting in the tissue depletion of mtDNAs. MtDNA nucleotide substitution and rearrangement mutations also accumulate with age in quiescent tissues. These somatic mutations appear to degrade cellular bioenergetic capacity, exacerbate inherited mitochondrial defects and contribute to tissue senescence. Thus, bioenergetic defects resulting from mtDNA mutations may be a common cause of human degenerative disease.
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PMID:Mitochondrial DNA mutations in diseases of energy metabolism. 807 79

The natural history of cervical dystonia (spasmodic torticollis) was investigated in a population-based study in Rochester, Minnesota. Eleven new cases were identified with onset during the 20-year period 1960-1979. The overall incidence rate was 1.2 per 100,000 person-years (95% confidence interval 0.5-1.9) with a female:male ratio of age-adjusted incidence rates of 3.6:1. A unitary etiology was not apparent: injury antedated onset in four of the 11 patients, whereas six had documented thyroid disease and four had diabetes. A family history of movement disorder was recorded for only one subject. Only one of the cases would have been classified as moderate in severity; the others were mild. In follow-up through 1993, progressive disability was noted in only two patients, and two others went into remission. Three cases of intracranial aneurysm were confirmed, two of which produced fatal subarachnoid hemorrahage. A third death was due to amyotrophic lateral sclerosis.
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PMID:Epidemiology and outcome of cervical dystonia (spasmodic torticollis) in Rochester, Minnesota. 855 13

Recently botulinum toxin has been used with increasing frequency as a safe and effective treatment for many previously refractory conditions associated with excessive muscle activity. The indications for use of botulinum toxin injection continue to expand. This report describes the case of an 83-year-old woman with a history of diabetes mellitus and lumbar spinal stenosis who developed a severe focal dystonia of the left great toe, such that the toe maintained the extended position. Functionally, the resultant deformity prevented the patient from wearing shoes. In addition, the patient had significant pain in the left great toe. Under needle electromyographic localization, 50 units of botulinum toxin were injected into the left extensor hallucis longus muscle. Two weeks after the injection the patient was symptom free and could place her left foot into a shoe. Seven months later, she remained symptom free. This case illustrates that localized injection of botulinum toxin to a specific lower limb muscle can effectively result in decreased muscle activity and functional improvement.
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PMID:Management of focal dystonia of the extensor hallucis longus muscle with botulinum toxin injection: a case report. 977 89

We present a boy of eight years of age with symptoms of Kearns-Sayre syndrome (KSS) characterised by ophthalmoparesis, palpebral ptosis, mitochondrial myopathy, pigmentous retinitis, associated to short stature, cerebellar signs, cardiac blockade, diabetes mellitus, elevated cerebrospinal fluid protein concentration, and focal hand and foot dystonia. The skeletal muscle biopsy demonstrated ragged red fibers, cytochrome C oxidase-negative and succinate dehydrogenase-positive fibers. The magnetic resonance imaging showed symmetrical signal alteration in tegmentum of brain stem, pallidum and thalamus. Mitochondrial DNA analysis from skeletal muscle showed a deletion in heteroplasmic condition. The association of dystonia to KSS, confirmed by molecular analysis, is first described in this case, and the importance of oxidative phosphorylation defects in the physiopathogenesis of this type of movement disorder is stressed.
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PMID:Kearns-Sayre syndrome "plus". Classical clinical findings and dystonia. 1068 96

The clinical features, outcomes, differential diagnoses, epidemiology, risk factors, and treatment approaches to tardive drug-induced extrapyramidal syndromes (EPS) are reviewed. Tardive forms of dyskinesia (TD), dystonia (TDt), akathisia (TA), Gilles de la Tourette syndrome (TGTS), myoclonus (TM), and parkinsonism (TP) are described. Moreover, pharmacological and topographical subtypes of TD are discussed. While TD, TDt, and TA are clearly delineated syndromes, there are limited data on TGTS, TM, and the questionable TP. TDt is distinguished from TD by clinical and treatment-related variables. Epidemiological studies provide evidence of better prognosis for TD compared with both TDt and TA. Two distinct groups of variables were found to be associated with a higher risk for TD: an exogenous factor (neuroleptic treatment variables and alcohol or drug abuse) and a factor of predisposition (elderly, female, affective disorder diagnosis, presence of EPS, diabetes mellitus type II, and signs of central vulnerability). In contrast, being younger and male was associated with TDt. A significant relationship between the hyperkinetic forms of tardive EPS was confirmed. Therapeutic strategy differs for the mild, moderate, and severe forms of tardive EPS. Using low doses of antipsychotics is a good preventive approach. Reducing the dose or switching to an atypical antipsychotic is the usual, but not yet fully explored, first therapeutic step. Clozapine, an antipsychotic with antidyskinetic and antidystonic effectiveness, is the second treatment step. Various suppressors of tardive movements were tested in controlled trials, mainly in TD. GABAergic benzodiazepines (clonazepam), adrenergic antagonists (propranolol, clonidine), antioxidants (alpha-tocopherol), and calcium channel blockers (nifedipine) are useful in the third step of treatment of more severe tardive EPS. Unlike TD, TDt and (partially) TA improve on higher doses of anticholinergic medication. Local injection of botulinum A toxin markedly ameliorates focal tardive dystonia over several months. Less verified therapeutic interventions are discussed.
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PMID:Tardive drug-induced extrapyramidal syndromes. 1107 62

We review epidemiological data on primary blepharospasm (BSP). There is a large variation in the stated prevalence of BSP, with crude estimates ranging from 16 to 133 per million in different studies. A large proportion of this variability may be the result of differences in physician education on BSP. Age and female gender may increase the risk of developing BSP. The few case-control studies focusing on adult dystonias including BSP showed an increased risk in association with family history of dystonia and/or postural tremor, prior head and face trauma, and prior eye disease (e.g., blepharitis and keratoconjunctivitis), and a decreased risk associated with cigarette smoking. No association was found with age-related medical conditions such as hypertension and diabetes, family history of parkinsonism, and a history of anxiety or depression. Broocks et al. [Am J Psychiatry, 1998;155:555-557] found a significantly higher frequency of obsessive-compulsive symptoms in BSP than hemifacial spasm despite the clinical similarity. Among putative risk factors for BSP, age at onset, female gender, and prior head or face trauma may affect spread of dystonia to adjacent body regions. While limited, the body of epidemiological data support the idea that environmental and familial, possibly genetic, factors may both be important in the etiology of BSP.
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PMID:Epidemiology of primary blepharospasm. 1183 33


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