Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levodopa-induced dyskinesias (LID) in Parkinson's disease (PD) may be classified into three main categories: "On" dyskinesias, diphasic dyskinesias (DD), and "off" periods. The study of 168 parkinsonian patients showed that about half (n = 84) showed one pattern of LID only. A combination of two was present in 68, and 16 had the three presentation patterns. A fairly good correlation between type of dyskinesia and presentation pattern was established. Chorea, myoclonus, and dystonic movements occurred during the "on" period. Dystonic postures, particularly affecting the feet, were mainly present in the "off" period, but a few patients had a diphasic presentation. Repetitive stereotyped movements of the lower limbs always corresponded to DD. Acute pharmacological tests using dopamine agonists (subcutaneous apomorphine 3-8 mg; intravenous lisuride 0.1-0.15 mg) and dopamine antagonists (intravenous sulpiride 200-400 mg and intravenous chlorpromazine 25 mg) were performed in 40 patients. Dopamine agonists enhanced "on" dyskinesias and markedly reduced or abolished "off" period dystonia and DD. Dopamine antagonists reduced all types of LID but usually aggravated parkinsonism. These clinical and pharmacological results indicate that LID in PD are a heterogeneous phenomenon difficult to explain on the basis of a single pathophysiological mechanism.
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PMID:Levodopa-induced dyskinesias in Parkinson's disease: clinical and pharmacological classification. 135 58

Milacemide, a glycine prodrug that is able to enter the brain readily, has been shown to have an antimyoclonic property in the p,p'-DDT-induced myoclonus syndrome. Milacemide increased regional 5-HT and dopamine and decreased 5-HIAA, DOPAC and HVA levels in naive rats. In p,p'-DDT-treated rats, 5-HT levels were unchanged at the time the rats experienced spontaneous myoclonus in all brain regions except in the striatum, where it increased. 5-HIAA levels increased but did not reach significant levels except in the striatum. Dopamine, DOPAC, HVA and norepinephrine were unchanged. When rats were treated concurrently with both p,p'-DDT and milacemide, regional 5-HT levels were increased and NE levels in the brainstem and cerebellum decreased. Depletion of brain serotonin by pretreatment with PCPA or with 5,7-DHT, or blocking 5-HT receptors with different 5-HT antagonists, failed to eliminate the antimyoclonic property of milacemide. This antimyoclonic effect of milacemide may be mediated through other mechanisms besides its ability to increase brain 5-HT levels. Possible mechanisms to be considered are its antiepileptic property, and its ability to increase brain glycine levels. Milacemide may have potential for therapeutic trials in patients with myoclonus.
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PMID:Milacemide increases 5-hydroxytryptamine and dopamine levels in rat brain--possible mechanisms of milacemide antimyoclonic property in the p,p'-DDT-induced myoclonus. 257 9

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.
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PMID:Neuroleptic malignant syndrome: a review and report of six cases. 1721 72

Dystonias can be classified as primary or secondary, as dystonia-plus syndromes, and as heredodegenerative dystonias. Their prevalence is difficult to determine. In our experience 80-90% of all dystonias are primary. About 20-30% of those have a genetic background; 10-20% are secondary, with tardive dystonia and dystonia in cerebral palsy being the most common forms. If dystonia in spastic conditions is accepted as secondary dystonia, this is the most common form of all dystonia. In primary dystonias, the dystonic movements are the only symptoms. In secondary dystonias, dystonic movements result from exogenous processes directly or indirectly affecting brain parenchyma. They may be caused by focal and diffuse brain damage, drugs, chemical agents, physical interactions with the central nervous system, and indirect central nervous system effects. Dystonia-plus syndromes describe brain parenchyma processes producing predominantly dystonia together with other movement disorders. They include dopa-responsive dystonia and myoclonus-dystonia. Heredodegenerative dystonias are dystonic movements occurring in the context of other heredodegenerative disorders. They may be caused by impaired energy metabolism, impaired systemic metabolism, storage of noxious substances, oligonucleotid repeats and other processes. Pseudodystonias mimic dystonia and include psychogenic dystonia and various orthopedic, ophthalmologic, vestibular, and traumatic conditions. Unusual manifestations, unusual age of onset, suspect family history, suspect medical history, and additional signs may indicate nonprimary dystonia. If they are suspected, etiological clarification becomes necessary. Unfortunately, potential etiologies are legion. Diagnostic algorithms can be helpful. Treatment of nonprimary dystonias, with few exceptions, does not differ from treatment of primary dystonias. The most effective treatment for focal and segmental dystonias is local botulinum toxin injections. Deep brain stimulation of the globus pallidus internus is effective for generalized dystonia. Antidystonic drugs, including anticholinergics, tetrabenazine, clozapine, and gamma-aminobutyric acid receptor agonists, are less effective and often produce adverse effects. Dopamine is extremely effective in dopa-responsive dystonia. The Bertrand procedure can be effective in cervical dystonia. Other peripheral surgery, including myotomy, myectomy, neurotomy, rhizotomy, ramizectomy, and accessory nerve neurolysis, has largely been abandoned. Central surgery other than deep brain stimulation is obsolete. Adjuvant therapies, including orthoses, physiotherapy, ergotherapy, behavioral therapy, social support, and support groups, may be helpful. Analgesics should also be considered where appropriate.
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PMID:Nonprimary dystonias. 2149 5

Dopamine transporter (DaT) single-photon emission computed tomography (SPECT) and [18F]fluoro-L-DOPA ([18F]DOPA) positron emission tomography (PET) facilitate the investigation of dopaminergic hypofunction in neurodegenerative diseases. DaT SPECT and [18F]DOPA PET have been adopted as survey tools in clinical trials. In a large study on Parkinson's disease, 4-15% of subjects clinically diagnosed with early-stage Parkinson's disease had normal dopaminergic functional imaging scans. These are called Scans without Evidence of Dopamine Deficit (SWEDDs), and are considered to represent a state different from Parkinson's disease. Neurological diseases that exhibit parkinsonism and have normal dopaminergic cells in the nigrostriatal system (e.g., essential tremor, psychogenic parkinsonism, DOPA-responsive dystonia, vascular parkinsonism, drug-induced parkinsonism, manganism, brain tumor, myoclonus-dystonia (DYT11), and fragile X syndrome) might be diagnosed with SWEDDs. True bradykinesia with fatigue or decrement may be useful for distinguishing between Parkinson's disease and SWEDDs. However, because SWEDDs encompass many diseases, their properties may not be uniform. In this review, we discuss DaT SPECT, the concept of SWEDDs, and differential diagnosis.
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PMID:[Scans without Evidence of Dopamine Deficit (SWEDDs)]. 2676 1