Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight patients developed a syndrome marked by features of catatonia (including posturing, waxy flexibility, withdrawal and regression) and parkinsonism (including bradykinesia and rigidity) while receiving high-potency neuroleptic drugs. The syndrome had a gradual onset, responded slowly to withdrawal of the neuroleptic or use of an anticholinergic agent, but seemed to respond more rapidly to amantadine. The syndrome may easily be confused with a worsening of schizophrenic symptoms.
Arch Gen Psychiatry 1977 Aug
PMID:Catatonic reactions to high-potency neuroleptic drugs. 88 19

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
Gen Pharmacol 1990
PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Extrapyramidal symptoms are frequently found in patients with schizophrenia. Most are attributed as drug-induced parkinsonism, but comorbidity of idiopathic Parkinson's disease is also possible. We report a 59-year-old male with a diagnosis of schizophrenia for 32 years. Progressive hand tremor was noted from age 53; and then masked face, bradykinesia, dysphagia, sialorrhea; and unsteady shuffling gait became markedly exacerbated, even after discontinuing all antipsychotics for 6 months. The diagnosis of idiopathic Parkinson's disease was confirmed by Tc99m TRODAT SPECT. The dilemma of psychopharmacological treatment to control both disorders was encountered. Based on the review of treatment for Parkinson's disease psychosis (PDP), the recommended treatments suggest the utilization of quetiapine, clozapine, or aripiprazole. However, monotherapy with each of the three atypical antipsychotics failed due to poor efficacy or worsening of parkinsonism symptoms. After a 2-month cautious titration, a combination of quetiapine 50 mg/day and clozapine 37.5 mg/day finally achieved satisfactory efficacy. This case report illustrates the dilemma of treating a patient with schizophrenia and comorbid idiopathic Parkinson's disease, which differed from PDP and required more clinical data for a proper treatment recommendation.
Gen Hosp Psychiatry
PMID:Treatment dilemma in comorbidity of schizophrenia and idiopathic Parkinson's disease. 2176 41

Parkinson disease (PD) is a chronic neurodegenerative movement disorder characterized by selective loss of nigrostriatal dopaminergic neurons and formation of Lewy bodies. Clinical manifestations include motor impairments involving tremor, bradykinesia, postural instability and rigidity. Using dHPLC method we screened exons 31, 35, 41, 48 of the Leucine-rich repeat kinase 2 (LRRK2) gene and exons 2, 6 and 7 of Parkinson protein 2 (parkin, PARK2) genes in a cohort of 216 consecutive, unrelated Slovak patients with familial or sporadic PD, including early and late onset. By this means we aimed to detect the most common pathogenic mutations within LRRK2 (Arg1441Cys, Arg1441Gly, Arg1628Pro, Tyr1699Cys, Gly2019Ser, Ile2020Thr, Gly2385Arg) and parkin genes responsible for late and early onset forms of disease, respectively. However, none of these mutations was identified in our cohort. Heterozygous point mutation p.Arg275Trp in exon 7 of parkin gene was identified in one patient with age at onset 61 years. Furthermore, we observed the presence of one exonic (LRRK2 ex 48: 7155A>G) and eight intronic polymorphisms (in LRRK2: IVS35+23T>A, IVS47-91insGCCAT, IVS47-91insGCAT, IVS47-41A>G, IVS47-9delT, IVS47-20C>T, IVS47-90A>G, in parkin: IVS2+25T>C), three of which were novel.
Gen Physiol Biophys 2013 Mar
PMID:Analysis of Leucine-rich repeat kinase 2 (LRRK2) and Parkinson protein 2 (parkin, PARK2) genes mutations in Slovak Parkinson disease patients. 2353 35