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)

Parkinson's disease patients are frequently impaired in a variety of neuropsychological tasks involving memory, perceptual motor performance and cognitive flexibility. Although various theories have been forwarded to explain specific impairments, few attempts have been made to account for all the deficits within a single theoretical framework. Furthermore, the frequent occurrence of dementia, the adverse side effects of medication and the motor symptoms of the disease tend to interfere with neuropsychological performance. This has hindered the clear delineation of the neuropsychological profile of Parkinsonian patients. The present paper examines the evidence for intellectual deficits in non-demented Parkinson's disease patients. A number of problems inherent in cognitive research on Parkinson's disease are discussed. The contribution of dementia, motor symptom severity and medication in the expression of these intellectual impairments is examined. It is suggested that many of the neuropsychological deficits described in Parkinson's disease may result from a common underlying deficit in some aspect of information processing. Although it is not possible to pinpoint the precise mechanism(s) involved on the basis of the available evidence, several possibilities are suggested by cognitive and electrophysiological data.
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PMID:Parkinson's disease: a conceptualization of neuropsychological deficits within an information-processing framework. 269 79

Juvenile Huntington disease (JHD) patients are distinguished from adult patients by an age at onset of less than 20 years. Investigating patients in our own database, we examined the proposition derived from studies in world literature that JHD should not be viewed as a separate clinical entity but rather as a manifestation of the rigid variant of the disease. Of 53 patients with JHD recorded in the Leiden Roster for Huntington Disease, relationships between sex, age at onset, duration of illness, maternal or paternal inheritance, motor symptom, first clinical features, and characteristics during the disease course, were obtained from the patients' files, and investigated. Although chorea is present in JHD, patients more often developed rigidity. Paternal inheritance, early dementia, epilepsy/myoclonus, and tremor during the disease course are confined for the most part to the rigid cases. A shorter duration of illness was evident in male patients with rigid JHD who inherited the disease from their father and developed their first disease feature at a younger age. The recognition of JHD as a distinct clinical entity does not appear to be warranted. Therefore, we propose, in accordance with other investigators, that rigid JHD be considered a clinical variant with special features.
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PMID:Juvenile Huntington disease in the Netherlands. 930 74

Huntington's disease is a dominantly inherited progressive autosomal disease that affects the basal ganglia. Symptoms appear later in life and manifest as progressive mental deterioration and involuntary choreiform movements. Patients with Huntington's disease develop a progressive but variable dementia. Dysphagia, the most significant related motor symptom, hinders nutrition intake and places the patient at risk for aspiration. The combination of involuntary choreoathetoid movements, depression, and apathy leads to cachexia. Factors of considerable concern to the anesthesiologist who treats patients with Huntington's disease may include how to treat frail elderly people incapable of cooperation, how to treat patients suffering from malnourishment, and how to treat patients with an increased risk for aspiration or exaggerated responses to sodium thiopental and succinylcholine. The successful anesthetic management of a 65-yr-old woman with Huntington's disease who presented for full-mouth extractions is described.
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PMID:Huntington's disease: review and anesthetic case management. 1048 87

The relationship between dementia with Lewy bodies (DLB) and Parkinson's disease with dementia (PDD) has been insufficiently described, and it is still problematic. Twenty-nine cases of DLB and 10 cases of PDD were investigated in the present study. DLB cases disclosed a significantly older disease onset and shorter disease duration than PDD cases (p<0.01 each). However, they showed no significant difference in dementia onset or dementia duration (p>0.05 each). Motor symptoms (parkinsonism) were suspected as the cause of the younger disease onset in PDD cases. Compared with 10 age-matched cases of definite Alzheimer's disease, both 19 DLB cases and 6 PDD cases had significantly better scores in the final test of mini-mental state examination (MMSE) and revised version of Hasegawa's Dementia Scale (HDSR) within 12 months before death, although no significant differences between DLB and PDD were indicated. DLB and PDD were suspected to show cognitive impairment of similar severity in the terminal stage. They would thus be difficult to classify as completely different entities.
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PMID:Cognitive conditions of pathologically confirmed dementia with Lewy bodies and Parkinson's disease with dementia. 1460 10

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

It is well known that many patients with Parkinson's disease experience neuropsychological decline. However, the nature and extent of mental status change varies widely, with some patients showing mild or no cognitive impairments and others exhibiting frank dementia. Research has shown that several clinical disease parameters may differentially correlate with patterns of neuropsychological dysfunction. The present study examined side and type of motor symptom at disease onset and their relationship to cognition in idiopathic Parkinson's disease (PD). We identified 58 patients who initially presented with one of the following symptom profiles: right-side tremor onset (RSO-T; n = 15), right-side bradykinesia/rigidity onset (n = 12), left-side tremor onset (n = 19), and left-side bradykinesia/rigidity onset (n = 12). There were no differences between groups in disease duration, overall mental status, education, or depression severity. We administered a battery of neuropsychological measures to the four PD subgroups and a group of matched control subjects (n = 40). MANCOVAs controlling for age revealed patients with RSO-T performed significantly better than the other three PD subgroups across the entire neuropsychological battery. Further, the RSO-T subgroup performed comparably to controls. In contrast, the other three PD subgroups showed widespread cognitive deficits. These findings suggest an intricate relationship between motor symptom and side of disease onset and it is the combination of these factors that may influence the disease course and extent of cognitive deterioration. Furthermore, patients who develop tremor on the right side of their body represent a distinct subgroup of PD patients who exhibit relative sparing of cognitive function.
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PMID:Side and type of motor symptom influence cognition in Parkinson's disease. 1699 Nov 55

Parkinson's disease is classically characterised as a motor neurodegenerative disorder. Motor symptoms in the disorder are secondary to an altered dopamine-acetylcholine balance due to reduced striatal dopaminergic tone and subsequent cholinergic overactivity. In the past, anticholinergic drugs were given to improve motor aspects of the disease. There is now an increasing interest in the cognitive and non-motor symptoms of Parkinson's disease and in cholinesterase-inhibitor therapy for dementia associated with Parkinson's disease. In this Personal View, we reconsider the dopamine-acetylcholine balance theory and look at recent clinical findings and the possible cooperative role of dopamine and acetylcholine in the induction and maintenance of the long-lasting changes of striatal and cortical synaptic plasticity. We also discuss a convergent versus parallel model to explain cognitive dysfunctions in Parkinson's disease according to dopamine-acetylcholine dependent alterations in synaptic plasticity.
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PMID:A convergent model for cognitive dysfunctions in Parkinson's disease: the critical dopamine-acetylcholine synaptic balance. 1705 64

Depression is a common comorbid condition in Parkinson's disease (PD) and a major contributor to poor quality of life and disability. However, depression can be difficult to assess in patients with PD due to overlapping symptoms and difficulties in the assessment of depression in cognitively impaired patients. As several rating scales have been used to assess depression in PD (dPD), the Movement Disorder Society commissioned a task force to assess their clinimetric properties and make clinical recommendations regarding their use. A systematic literature review was conducted to explore the use of depression scales in PD and determine which scales should be selected for this review. The scales reviewed were the Beck Depression Inventory (BDI), Hamilton Depression Scale (Ham-D), Hospital Anxiety and Depression Scale (HADS), Zung Self-Rating Depression Scale (SDS), Geriatric Depression Scale (GDS), Montgomery-Asberg Depression Rating Scale (MADRS), Unified Parkinson's Disease Rating Scale (UPDRS) Part I, Cornell Scale for the Assessment of Depression in Dementia (CSDD), and the Center for Epidemiologic Studies Depression Scale (CES-D). Seven clinical researchers with clinical and research experience in the assessment of dPD were assigned to review the scales using a structured format. The most appropriate scale is dependent on the clinical or research goal. However, observer-rated scales are preferred if the study or clinical situation permits. For screening purposes, the HAM-D, BDI, HADS, MADRS, and GDS are valid in dPD. The CES-D and CSDD are alternative instruments that need validation in dPD. For measurement of severity of depressive symptoms, the Ham-D, MADRS, BDI, and SDS scales are recommended. Further studies are needed to validate the CSDD, which could be particularly useful for the assessment of severity of dPD in patients with comorbid dementia. To account for overlapping motor and nonmotor symptoms of depression, adjusted instrument cutoff scores may be needed for dPD, and scales to assess severity of motor symptoms (e.g., UPDRS) should also be included to help adjust for confounding factors. The HADS and the GDS include limited motor symptom assessment and may, therefore, be most useful in rating depression severity across a range of PD severity; however, these scales appear insensitive in severe depression. The complex and time-consuming task of developing a new scale to measure depression specifically for patients with PD is currently not warranted.
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PMID:Depression rating scales in Parkinson's disease: critique and recommendations. 1739 34

Levodopa has been the mainstay of symptomatic therapy for Parkinson Disease (PD) for 40 years providing benefit to virtually all patients. Levodopa therapy results in improved activities of daily living, enhanced quality of life, and improved mortality. However, the long-term use of levodopa is associated with the development of motor fluctuations and dyskinesia. In addition, levodopa therapy has further limitations. It has little or no effect on certain motor features (e.g. gait and balance dysfunction) and a non-motor symptom complex (autonomic dysfunction, pain syndromes, sleep disorders, mood disturbances, dementia). Further, multiple case reports illustrate the potential of levodopa and other dopaminergic agents to cause or reveal a series of impulse control disorders. This review highlights the levodopa unresponsive symptoms in PD.
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PMID:Levodopa unresponsive symptoms in Parkinson disease. 1878 79

Non-motor symptoms, such as psychiatric symptoms and autonomic dysfunction, are common co-morbid conditions in Parkinson's disease (PD) and major contributors to poor quality of life and disability. Within the group of neuropsychiatric conditions, depressive symptoms are the most common condition. Despite their frequency and importance, depressive symptoms can be difficult to assess and diagnose and thus depression in PD is frequently unrealized. Diagnostic challenges include the overlap of depressive symptoms with motor and non-motor symptoms of PD, such as dementia and apathy. Furthermore, there are no definite standards to assess and diagnose depression in PD leading also to the lack of exact data on the epidemiology of this non-motor symptom in PD. Depending on the diagnostic test and the study design the prevalence of depression in PD is reported between 7 and 72% of PD patients with approximately 40% in most cross-sectional studies. In contrast, the pathogenesis and long-term course of depression in PD remain elusive. Current hypothesis, however, includes that depressive symptoms are part of the core condition of PD when regarded as an entity. The present review summarizes the current knowledge on epidemiology, pathogenesis and diagnosis of depression in PD and proposes on this data base a standard procedure for screening and diagnosis of depressive symptoms in PD.
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PMID:[Depression in Parkinson's disease. Part 1: epidemiology, signs and symptoms, pathophysiology and diagnosis]. 1901 23


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