Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0426980 (motor symptom)
 471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies of spontaneous extrapyramidal symptoms, dyskinesia and parkinsonism, in unmedicated schizophrenia are of importance in understanding their underlying pathology and relation to the psychosis. This is a study of extrapyramidal symptoms using Abnormal Involuntary Movements Scale for dyskinesia and Simpson-Angus Scale for parkinsonism in 143 schizophrenia patients who never received antipsychotic medication. Psychopathology was measured using the Positive and Negative Syndrome Scale. Dyskinesia was present in 35% of patients and parkinsonism in 15%. The two disorders coexisted in 11 subjects. Orofacial dyskinesia, rigidity and tremor were common symptoms noted. There was no significant change in the rates and total scores of dyskinesia and parkinsonism with gender, age, duration of illness or age at onset of psychosis. Dyskinesia was unrelated to psychopathology. Parkinsonism score correlated positively with the motor symptom cluster of psychopathology. Dyskinesia and parkinsonism scores correlated positively with each other and parkinsonism score discriminated presence of dyskinesia. The associations between the spontaneous abnormal movements and other aspects of schizophrenia differed from those described in treated patients. Dyskinesia and parkinsonism are an integral part of the schizophrenia disease process whose relationship with other factors could be influenced by antipsychotic drug treatment.
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PMID:Extrapyramidal symptoms in unmedicated schizophrenia. 1572 24

Parkinson's disease (PD) is a progressive disease that usually affects the motor system but is also associated with a non-motor symptom (NMS) complex that ranges from dribbling saliva, constipation, depression, sleep disorders, apathy, hallucinations, and dementia. These features contribute significantly to morbidity and institutionalization, more than quadrupling the cost of care. Furthermore, recent evidence suggests that NMS such as constipation, olfaction, rapid eye movement behavior disorder, fatigue, and depression may be markers of a preclinical stage of PD. PD-NMS are not well recognized in clinical practice and part of the reason is the lack of any instrument that aims to assess the complex range of NMS of PD in a unified and integrated manner. Recently, an international, multidisciplinary PD-NMS group has developed an integrated questionnaire and scale to assess NMS of PD in a comprehensive manner. This will help improve care and treatment of PD in the future.
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PMID:The non-motor symptom complex of Parkinson's disease: a comprehensive assessment is essential. 1598 11

PD (Parkinson's disease) is an aetiologically heterogeneous disorder characterized by a clinical phenotype consisting of resting tremor, rigidity and bradykinesia. Motor symptoms are associated with a progressive loss of dopaminergic neurons, with Lewy body inclusions within surviving neurons. Although heritability studies have shown evidence of familial aggregation, twin studies have provided limited support for a genetic aetiology. Nevertheless, classical linkage methods have nominated 11 regions of the genome and pathogenic mutations have been identified in several genes, including alpha-synuclein, parkin, ubiquitin C-terminal hydrolase L1, oncogene DJ-1, PTEN-induced protein kinase 1 and microtubule-associated protein tau. Most recently, heterozygous mutations in LRRK2 (leucine-rich repeat kinase 2) were found to cause late-onset, autosomal-dominant PD. Despite their consistent clinical phenotype, family members with LRRK2 mutations can have variable alpha-synuclein and tau pathologies. Lrrk2 is a member of the Roc (Ras of complex proteins) family, with Ras GTPase and MAPKKK (mitogen-activated protein kinase kinase kinase) catalytic domains. Thus its discovery highlights vesicle dynamics and secondary-messenger signalling in disease pathophysiology. To diagnose a disease accurately and effectively treat it, requires an understanding of its molecular pathogenesis. Herein, we provide an overview of the genetics of PD, how these discoveries are revolutionizing long-held beliefs and more importantly how this knowledge may be translated into patient therapy.
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PMID:Pathophysiology, pleiotrophy and paradigm shifts: genetic lessons from Parkinson's disease. 1604 50

The mental rotation of objects requires visuospatial functions mediated by the parietal lobes, whereas the mental rotation of hands also engages frontal motor-system processes. Nondemented patients with Parkinson's disease (PD), a frontostriatal disorder, were predicted to be impaired on mentally rotating hands. Side of PD motor symptom onset was investigated because the left motor cortices likely have a causal role in hand mental rotation. The prediction was that patients with right-side onset (RPD, greater left-hemisphere dysfunction) would commit more errors rotating hands than patients with left-side onset (LPD). Fifteen LPD, 12 RPD, and 13 normal control adults (NC) made same/different judgments about pairs of rotated objects or hands. There were no group differences with objects. When rotating hands, RPD, but not LPD, made more errors than the NC group. A control experiment evaluated whether visual field of presentation explained differences between PD subgroups. In the first experiment (1A), the hand to be mentally rotated was presented in the right visual field, but here (1B) it was presented in the left visual field. Only the LPD group made more errors than the NC group. The evidence suggests a double dissociation for the RPD and LPD groups between tasks differing in visual-field presentation. The findings indicate that hemifield location of a to-be-rotated hand stimulus can cause the hemispheric frontoparietal networks to be differentially engaged. Moreover, frontostriatal motor systems and the parietal lobes play a necessary role during the mental rotation of hands, which requires integrating visuospatial cognition with motor imagery.
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PMID:Frontostriatal circuits are necessary for visuomotor transformation: mental rotation in Parkinson's disease. 1606 Dec 63

Parkinson's disease (PD) is a basal ganglia disorder. Motor symptoms develop insidiously following substantial neurodegeneration of the dopamine (DA) neurons in the nigrostriatal system and produce slowed, infrequent movements, postural instability, and gait changes. A thorough understanding of neurochemical compensations occurring in the striatum during early stages of PD is crucial in identifying components that are altered initially as the DA is depleted. Producing an incomplete lesion of the nigrostriatal DA system in rats would mimic the principal early neurochemical features of human PD. We infused 6-hydroxydopamine unilaterally into the substantia nigra to reach a target of approximately 50% depletion in striatal DA at 4 weeks. This was evaluated by HPLC analysis of tissue DA content and monitored behaviorally by forepaw use reflecting asymmetries in striatal DA levels. DA loss was assessed by using tyrosine hydroxylase immunohistochemical staining, and the data were conjoined with the behavioral assessments. We found that activated caspase-3, its actin cleavage product fractin, and components of the apoptosome were increased significantly in DA-depleted striatum. Thus mobilization of the intrinsic programmed cell death pathway occurred, without cell loss. Elevations in apoptogenic proteins were pronounced in enkephalinergic striatopallidal neurons compared with the substance P-containing striatonigral neurons. Our findings suggest that cellular homeostatic imbalances that accompany even mild striatal DA depletion take time to develop, differentially affect the striatal output pathways, and may be an important feature of early-stage PD. These observations could be capitalized upon to develop therapeutic interventions in the preclinical phases of the disorder.
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PMID:Partial dopamine loss enhances activated caspase-3 activity: differential outcomes in striatal projection systems. 1618 Feb 25

The short plasma half-life limits the antiparkinsonian efficacy of levodopa/carbidopa (LD/CD). Administration of LD/CD with the catechol-O-methyltransferase inhibitor entacapone in one tablet (LCE) may extend plasma half-life of LD and thus its effect on motor symptoms in patients with Parkinson's disease (PD). The objectives of this study were to monitor the motor response to a switch from LD/CD to LCE by a simultaneous performance of an instrumental motor test and rating of motor symptoms and to compare the LD plasma behavior between both conditions in terms of stability. Twenty-one treated PD patients received LD/CD and then the identical oral LD dosage of LCE within a standardized setting on 2 consecutive days. Rating better reflected the motor improvement after LD application than the instrumental test. Motor symptoms of PD patients decreased significantly more during the LCE than the LD/CD condition, probably due to significantly higher LD plasma levels and a significantly less pronounced fall of the LD concentrations following the second LD intake. Our study shows a more stable LD plasma behavior during LCE intake and accordingly a better effect on motor symptoms according to rating outcomes and motor test results to a lesser extent.
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PMID:Inhibition of catechol-O-methyltransferase contributes to more stable levodopa plasma levels. 1621 93

Oxaliplatin, an effective cytotoxic treatment in combination with 5-fluorouracil for colorectal cancer, is associated with sensory, motor and autonomic neurotoxicity. Motor symptoms include hyperexcitability while autonomic effects include urinary retention, but the cause of these side-effects is unknown. We examined the effects on motor nerve function in the mouse hemidiaphragm and on the autonomic system in the vas deferens. In the mouse diaphragm, oxaliplatin (0.5 mM) induced multiple endplate potentials (EPPs) following a single stimulus, and was associated with an increase in spontaneous miniature EPP frequency. In the vas deferens, spontaneous excitatory junction potential frequency was increased after 30 min exposure to oxaliplatin; no changes in resting Ca(2+) concentration in nerve terminal varicosities were observed, and recovery after stimuli trains was unaffected. In both tissues, an oxaliplatin-induced increase in spontaneous activity was prevented by the voltage-gated Na(+) channel blocker tetrodotoxin (TTX). Carbamazepine (0.3 mM) also prevented multiple EPPs and the increase in spontaneous activity in both tissues. In diaphragm, beta-pompilidotoxin (100 microM), which slows Na(+) channel inactivation, induced multiple EPPs similar to oxaliplatin's effect. By contrast, blockers of K(+) channels (4-aminopyridine and apamin) did not replicate oxaliplatin-induced hyperexcitability in the diaphragm. The prevention of hyperexcitability by TTX blockade implies that oxaliplatin acts on nerve conduction rather than by effecting repolarisation. The similarity between beta-pompilidotoxin and oxaliplatin suggests that alteration of voltage-gated Na(+) channel kinetics is likely to underlie the acute neurotoxic actions of oxaliplatin.
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PMID:Oxaliplatin induces hyperexcitability at motor and autonomic neuromuscular junctions through effects on voltage-gated sodium channels. 1623 Oct 11

The effect of drug treatment and its adverse effects confound studies on symptoms and associated factors in schizophrenia. Knowledge of psychopathology in the untreated state would identify the natural state of the illness and is relevant to understand pathology underlying the illness. We report here symptoms of schizophrenia as measured by Positive and Negative Syndrome Scale in 143 patients with schizophrenia living in the community never treated with antipsychotic drugs. Positive symptoms were more frequent than negative ones. Negative subscale scores correlated negatively with positive subscale scores and positively with general psychopathology subscale scores. Age correlated negatively with negative and general psychopathology subscale scores independent of duration of illness. Duration of illness and the proportion of life spent in psychosis did not correlate with any Positive and Negative Syndrome Scale scores. The factors (negative, positive, anxiety-depression, motor, and excitement) extracted by a forced 5-factor analysis explained 56% of variance. This factor structure resembled that of treated patients reported in most studies except for the identification of a motor symptom cluster. Psychopathology in the never-treated schizophrenia varied in some aspects from descriptions in the treated state. The differences can be said to demarcate the natural features of the illness from medication effects on the relationship of symptoms with one another and to sex, age, duration of illness, and age at onset.
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PMID:Psychopathology in never-treated schizophrenia. 1632 96

It is well known that applying vibrations to men influences multiple physiological functions. The authors analysed post effects of whole-body-vibration (WBV) on motor symptoms in Parkinson's disease (PD). Sixty-eight persons with PD were randomly subdivided into one experimental and one control group. Motor symptoms were assessed by the UPDRS (Unified Parkinson's Disease Rating Scale) motor score. A cross-over design was used to control treatment effects. The treatment consisted of 5 series of whole-body-vibration taking 60 seconds each. On average a highly significant (p<0.01) improvement of 16.8% in the UPDRS motor score was found in the treatment group. Only marginal changes (p>0.05) were found in the control group. The cross-over procedure showed comparable treatment effects (14.7% improvement after treatment). With respect to different symptom clusters only small changes were found in limb akinesia and cranial symptoms. By contrast, tremor and rigidity scores were improved by 25% and 24%, respectively. According to the structure of symptom changes it is unlikely that these effects are explainable on peripheral sensory level, exclusively. With respect to the findings of other studies one can speculate about changes in activation of the supplementary motor area and in neurotransmitter functions.
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PMID:The effects of random whole-body-vibration on motor symptoms in Parkinson's disease. 1672 Sep 35

Freezing of gait (FOG) is a disabling episodic gait disturbance that is common among patients with Parkinsonism. FOG typically lasts a few seconds and is associated with a unique sensation: the patient feels that his feet are glued to the ground, causing him to remain in place despite making a concerted effort to overcome the motor block and move forward. Traditionally, FOG has been viewed as a motor symptom of advanced Parkinson's disease. Here we describe evidence which demonstrates that mental conditions also likely play an important role in the pathogenesis of FOG. Stress, anxiety, depression and cognitively challenging situations are associated with FOG, and may set the stage for and increase the likelihood that FOG occurs. A conceptual model that explains how mental conditions may modulate FOG is developed.
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PMID:The role of mental function in the pathogenesis of freezing of gait in Parkinson's disease. 1678 Aug 86


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