Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parkinson's disease (PD) is primarily a disease of elderly individuals with a peak age at onset of 55 to 66 years. It is characterized by bradykinesia, rigidity, tremor, and postural instability; and affects approximately 1 million individuals in the US and is the second most common neurodegenerative disease next to Alzheimer's disease. The motor symptoms of PD are the focus of pharmacotherapy, yet the nonmotor symptoms (e.g., dementia, psychosis, anxiety, insomnia, autonomic dysfunction, and mood disturbances) can be the most disturbing, disabling, and misunderstood aspects of the disease. Depressive symptoms occur in approximately half of PD patients and are a significant cause of functional impairment for PD patients. There is accumulating evidence suggesting that depression in PD is secondary to the underlying neuroanatomical degeneration, rather than simply a reaction to the psychosocial stress and disability. The incidence of depression is correlated with changes in central serotonergic function and neurodegeneration of specific cortical and subcortical pathways. Understanding comorbid depression in PD may therefore add to the understanding of the neuroanatomical basis of melancholia.
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PMID:Prevalence, etiology, and treatment of depression in Parkinson's disease. 1289 11

Diagnostic accuracy has been addressed previously for Parkinson's disease in a brain bank collection, but accuracy of progressive supranuclear palsy (PSP) has not been addressed in a similar setting. Clinical and genetic features of pathologically confirmed cases of PSP were compared with misdiagnosed cases to determine ways to improve diagnostic accuracy. Medical records were reviewed for 180 cases sent to the Society of Progressive Supranuclear Palsy Brain Bank that had standardized neuropathologic evaluations as well as determination of apolipoprotein E and tau genotypes. Of the 180 cases studied, 137 had PSP and 43 had other pathologic diagnoses. Corticobasal degeneration (CBD), multiple system atrophy (MSA), and diffuse Lewy body disease (DLBD) accounted for 70% of the misdiagnosed cases. History of tremor, psychosis, dementia, and asymmetric findings were more frequent in misdiagnosed cases. The frequency of H1 tau haplotype (93 vs. 80%) and H1H1 genotype (86 vs. 66%) were significantly greater and APOE epsilon4 carrier state was significantly less (17 vs. 41 %) in PSP compared with misdiagnosed cases. Pathologic evaluation of clinically diagnosed PSP remains important for definitive diagnosis, and CBD, MSA, and DLBD are the disorders most likely to be misdiagnosed as PSP. Tremor, psychosis, early dementia, asymmetric findings, absence of H1 haplotype, and presence of APOE epsilon4 should raise questions about a diagnosis of PSP.
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PMID:Diagnostic accuracy of progressive supranuclear palsy in the Society for Progressive Supranuclear Palsy brain bank. 1450 69

Parkinson's disease (PD) is a neurodegenerative disorder that affects an estimated 1 million people in the US and tens of millions worldwide. Medication therapy has made significant advances and improvements especially over the last 10 years. A number of new treatments and new strategies have emerged and the quality of life for the average sufferer has improved. This review will describe the rationale and strategies for current medical therapies in PD, with special emphasis on the use of antipsychotic agents. Levodopa remains the most efficacious medication for the management of PD. Long-term use of levodopa, however, is associated with the development of motor fluctuations including dyskinesia. Trials with dopamine agonists have demonstrated a delay in the onset of dyskinesia with the use of this therapy. There is also active, ongoing investigation to determine whether a neuroprotective effect may be present with agonist therapy. Anticholinergics have been successfully used to treat tremor as well as sialorrhoea and urinary urgency. Catechol-O-methyltransferase inhibitors increase 'on time', decrease 'off time,' and improve motor scores. Continuous stimulation of dopamine receptors may decrease the fluctations observed with pulsatile delivery of anti-Parkinsonian medications, but this will require more study. Monoamine oxidase-B inhibitors, specifically selegiline, may provide symptomatic improvement; the question as to whether a neuroprotective benefit is present remains unanswered. Amantadine has demonstrated both symptomatic benefit and dyskinesia benefit in some patients. Selective dopamine blockers such as clozaril and quetiapine, have been shown to be effective in the treatment of psychosis. This class of medications is particularly useful as an adjunctive to levodopa and dopamine agonists. Doses of dopaminergic drugs can be escalated to treat Parkinsonian symptoms, whereas selective dopamine blockers can be added to block psychosis. Old management strategies required a reduction in dopaminergic therapy and therefore worsened Parkinsonian symptoms. Even though there have been great advances in the medical options for symptomatic management of PD, there are still many unmet needs for this patient population.
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PMID:Rationale for current therapies in Parkinson's disease. 1452 85

Parkinson's disease is often recognised as a motor disease characterised by rest tremor, rigidity, bradykinesia, and postural disturbances. However, there are several non-motor aspects of the disease that are of at least equal importance in the management of patients with Parkinson's disease. They include depression, cognitive impairment, anxiety, and psychosis among others. It is important to recognise them, as they are common and they contribute significantly to patients' morbidity, quality of life, and institutionalisation to long term care homes. In addition to the disease duration and severity, other factors including drugs may contribute to their occurrence. Pathogenesis of these aspects is not fully understood, though there has been a significant increase in the knowledge in recent years. Management of these aspects involves a multidisciplinary approach.
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PMID:Neuropsychiatric non-motor aspects of Parkinson's disease. 1461 97

Comparative investigation of motor and neuropsychological functions was conducted in 17 patients with clinically established diagnosis of dementia with Lewy bodies (DLB), 21 patients with Parkinson's disease (PD) without dementia and 26 patients with dementia (PDD). No significant differences were found in overall severity of parkinsonian features. However, comparing to PD, patients with DLB rarely had resting tremor, bilateral parkinsonism onset and good response to levadopa medication but more frequently exhibited gaze up palsy and myoclonus. Patients with PDD had more prominent akinesia, rigidity and axial disturbances, as compared to the PD patients without dementia, but there were no significant differences in these variables between patients with DLB and PDD. Comparing to PDD patients, those with DLB poorly performed on the tests measuring attention, verbal fluency and visual-spatial functions. Behavioral disturbances (especially apathy, aspontaneity, euphoria, obsessive-compulsive syndrome, dysinhibition, environment dependence) were severer in the patients with DLB and PDD, but no significant differences were found between these two groups. All the patients with DLB, 14 patients with PDD (53.8%) and 2 patients without dementia (7.4%) had psychotic disorders, which emerged later and were less pronounced in the patients with DLB compared to PDD patients. However, no significant differences were found in motor and neuropsychological impairment between DLB and PDD with psychotic disorders. The results may indicate a typological similarity of clinical manifestations of DLB and PDD that suggest nosologic proximity of these conditions included to synucleinopathies group.
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PMID:[Comparative study of Parkinson's disease and dementia with Lewy bodies]. 1487 Jun 86

Parkinson's disease (PD) is a chronic neurodegenerative disease, in which mainly dopaminergic neurons in the substantia nigra in the brain degenerate, leading to a depletion of dopamine (DA) in the striatum. The most important motor disturbances of the disease are bradykinesia (slowing down of movement), hypokinesia (poverty of movement), rigidity (muscle stiffness), tremor and postural instability. Besides these well-known motor symptoms, non-motor symptoms may develop, such as depression, cognitive impairment and psychosis. Psychotic symptoms constitute a relatively common but nevertheless serious complication, with visual hallucinations and paranoid delusions often being most prominent. These symptoms are important contributors to patient and caregiver distress and are often important risk factors for nursing home placement. Exogenous (related to therapeutic interventions) factors are of major importance but endogenous (related to the disease process itself) factors might also contribute to the development of psychotic symptoms in PD. Therapeutic strategies comprise reduction of antiparkinsonian treatment, cholinesterase inhibitors and atypical antipsychotics. As psychotic symptoms in PD are often influenced by both endogenous and exogenous factors, a combination of strategies may be chosen.
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PMID:Psychotic symptoms in Parkinson's disease: pathophysiology and management. 1515 49

We report a 53-year-old male patient with late onset mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes(MELAS) with hallucination and delusion. The patient manifested various neurological symptoms including perceptive deafness, muscle weakness of limbs with loss of consciousness, sensory abnormalities in hands, feet and a face, abnormal sense of taste, tremor, palsy of upward eye movement and weak deep tendon reflexes prior to the psychotic episode. He was diagnosed as MELAS, because of high serum lactic acid and pyruvic acid, and the point mutation in the mitochondrial DNA 3243. SPECT imaging showed decreased perfusion in occipital cortex and thalamus. These SPECT changes improved after disappearing visual hallucination. Hallucination might be caused by delirium due to stroke-like episode. Dysfunction in the occipital cortex and thalamus might be involved with this perfusion change.
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PMID:[A case with late-onset MELAS with hallucination and delusion]. 1523 27

Clozapine is the gold standard treatment for Parkinson's disease (PD) psychosis based on double blinded, placebo controlled trials, and has also been shown to alleviate tremor and dyskinesia. There is accumulating data suggesting that clozapine may be associated with increased frequency of diabetes mellitus (DM) compared to conventional neuroleptic drugs in treating schizophrenia. Forty-four predominantly geriatric parkinsonian subjects on clozapine for psychosis, tremor or dyskinesia, on an average dose of 50.6 mg/d for a mean duration of 41 months were reviewed. The prevalence of DM in this cohort was 18.1% (8/44). This rate was similar to that reported in the aged-matched general population (prevalence = 19.3% for ages > or = 60 years). In this small study, parkinsonian patients on long-term, low dose clozapine were not at increased risk for developing DM. Larger controlled prospective studies are needed to confirm this.
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PMID:Diabetes mellitus among parkinsonian patients treated chronically with clozapine. 1546 3

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42

We report a 75-year-old Japanese woman with probable dementia with Lewy bodies (DLB). At the age of 64, she showed left hand resting tremor, and gradually developed bradykinesia, and rigidity. She was diagnosed as having parkinsonism and took medication. At the age of 70, she showed hallucination and dementia. As she had developing cognitive dysfunction and hallucination and parkinsonism, she was diagnosed to have probable DLB. At the age of 75, after administration of donepezil, she showed severe psychosis and worsened parkinsonism, and was admitted to hospital. On neurological examination, she showed severe rigidity and akinesia, and behavioral immobility like "waxy flexibility" or motiveless resistance to maintenance of rigid posture against attempts to be moved. The phenomena, she presented as motor abnormalities, were thought to be catatonia. In consideration of clinical course, her catatonia and worsened parkinsonism was thought to be induced by donepezil and she was stopped the administration of donepezil. After treatment with trihexiphenizil, she had improvement of motor abnormalities and worsened parkinsonism. It is important to recognize that donepezil may induce catatonia on the patients of parkinsonism with severe dementia.
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PMID:[A patient with probable dementia with Lewy bodies, who showed catatonia induced by donepezil: a case report]. 1560 76


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