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

Movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.
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PMID:Movement disorders as a manifestation of nonketotic hyperglycemia. 260 Mar 93

Three patients with hemiballism-hemichorea caused by non-ketotic hyperglycaemia are presented, two of whom had hyperosmolar non-ketotic hyperglycaemic syndrome. In two of the three patients, the hyperkinesia was the initial presenting symptom of their diabetes mellitus. The hypersensitivity of the postmenopausal dopamine receptor, decreased gamma-aminobutyric acid in the brain in non-ketotic hyperglycaemia, coexisting lacunar infarct in the basal ganglion, and pre-existing metabolic dysfunction in the basal ganglion may all have played a part in the pathogenesis of this movement disorder.
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PMID:Hemiballism-hemichorea and non-ketotic hyperglycaemia. 800 61

Autoimmune polyglandular syndrome is characterized by a failure of multiple endocrine organs and the presence of circulating organ-specific autoantibodies targeted against the failing organs. Here we describe a patient with autoimmune polyglandular syndrome type I with the endocrine manifestations of hypoparathyroidism, adrenocortical insufficiency, and insulin-dependent diabetes mellitus. Long-standing hypoparathyroidism led to extensive calcification of the basal ganglia which resulted in the clinical presentation of an extrapyramidal movement disorder (choreoathetotic and hemiballistic hyperkinesia of the left extremities). Interestingly, parallel to rehydration and the initiation of cortisol replacement therapy a complete reversion of the hyperkinetic signs was achieved. This case shows a rare multiendocrine organ failure with complex metabolic interactions resulting in marked neurological signs. Furthermore, this case demonstrates for the first time that a hyperkinetic syndrome--most likely due to hypoparathyroidism-induced basal ganglia calcification--can be reversed solely by adequate treatment of the concomitant endocrine failures.
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PMID:Reversible hyperkinesia in a patient with autoimmune polyglandular syndrome type I. 831 86

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

The periodic limb movements (PLM) are defined as stereotyped, periodic movements of the legs and/or upper limbs during sleep. The patient exhibits dorsifilexion of the ankle and extension of the big toe with occasional flexion of the knee and hip. PLM originally was described as "nocturnal myoclonus" by Symonds in 1953. Recently, the term "nocturnal myoclonus" has been replaced with PLM, because the movements are slower than true myoclonic movement. The appearance of PLM was reported in sleep apnea syndrome, delayed sleep phase syndrome, narcolepsy, spinal cord tumor, diabetes mellitus and uremia. The prevalence of PLM statistically increase with age. Patients with PLM show excessive daytime sleepiness or insomnia. Several reports show the difficulty recognizing periodic limb movement disorder (PLMD) without polysomnography (PSG). The diagnosis of PLMD is established only by PSG.
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PMID:[Periodic limb movement disorder]. 950 40

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

Restless legs syndrome (RLS) is a perplexing, debilitating, and fairly common condition that can be challenging to manage. Hallmark symptoms include an increase in the severity of sensations during rest and an irresistible urge to move the affected limbs. RLS often occurs concomitantly with periodic limb movement disorder. There are no known causes of RLS, but likely triggers include heredity, iron and vitamin deficiencies, caffeine, and alcohol. Chronic conditions such as diabetes, peripheral neuropathy, and Parkinson's disease can worsen and prolong RLS symptoms. Symptom management begins by establishing proper nutrition intake and improved sleep hygiene. If these fail, conservative pharmacologic treatment is appropriate, with regimens chosen from dopaminergic agents, benzodiazepines, opioids, and anticonvulsants.
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PMID:Restless legs syndrome. How to provide symptom relief with drug and nondrug therapies. 1077 1

Since the introduction of chlorpromazine in the 1950s, antipsychotics have been used for the treatment of schizophrenia. The phenothiazines were followed by the butyrophenones, particularly haloperidol. With all the movement disorder side effects of these medications (extrapyramidal syndrome, akathisia, tardive dyskinesia), the pharmaceutical industry has gradually released atypical antipsychotics. This class includes clozapine (released in the USA in 1990), risperidone (1994), olanzapine (1996), quetiapine (1998) and ziprasidone (2001). However, the rate of diabetes mellitus in patients with schizophrenia appeared to increase with the availability of this class of medications. In reviewing rate and degree of changes in weight, glucose control and lipid levels induced by typical and atypical antipsychotics, it was found that in contrast to case reports, there is a dearth of retrospective, open and controlled studies. However, in studies as early as 1964, significant weight increases were found to be associated with use of chlorpromazine. While the phenothiazines may have some effect on patients with chemical diabetes, there is little evidence of the typical antipsychotics producing diabetes mellitus de novo, or worsening diabetes that is already been discovered. Ziprasidone appears to be the antipsychotic with the most beneficial combination of effects: no weight gain, no change in glucose utilisation and reductions in cholesterol and serum triglycerides (TGs).
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PMID:Antipsychotic medication: effects on regulation of glucose and lipids. 1182

Movement disorders such as chorea and ballism rarely occur in diabetes mellitus. We report the case of 26-year-old man with a 13-year-history of type 1 diabetes mellitus. He presented with a right side hemichorea. Brain CT-scan and MRI showed an infarction of the head of the caudate nucleus and the anterior part of the putamen. Presence of microangiopathy affecting retina, kidneys and peripheral nerves suggest a similar involvement of the lenticulo-striatal arteries. Hemichorea and hemiballism usually occur in older patients presenting type 2 diabetes mellitus. Non-ketotic hyperglycaemia is the common cause in such situation. Striatal infarct, as seen in our patient, is rarely reported.
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PMID:[Hemichorea caused by striatal infarct in a young type 1 diabetic patient]. 1188 23

Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini-Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA- groups. Since the presence of ACLA in individuals with stroke is usually treated by full-scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive.
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PMID:Anticardiolipin antibody in vascular parkinsonism. 1236 May 48


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