Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 114 patients who had been previously diagnosed as Parkinson's disease, we diagnosed six cases as clinically definite "diffuse Lewy body disease (DLBD)" according to McKeith's criteria with more strict modifications. Besides a central feature, dementia, and core features including parkinsonism, fluctuating cognition, and recurrent visual hallucinations, the patients presented some of supportive features, that is, repeated falls (4 cases), syncope (5 cases), and transient loss of consciousness (all cases). Autopsy, which was performed in 2 of the cases, revealed Lewy bodies in various nervous tissues including autonomic nervous systems in both cases. 7 cases of probable DLBD and 8 cases of possible DLBD, which lacked fluctuating cognition and/or visual hallucinations, demonstrated neither of repeated falls, syncope, nor transient loss of consciousness. Episodes of these supportive features, which seem to be associated with autonomic dysfunctions and/or fluctuating cognition, should be important in the differential diagnosis of DLBD.
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PMID:[Diffuse Lewy body disease searched out from 114 patients with parkinsonism]. 1096 48

DLBD is also called Dementia with Lewy bodies(DLB) which was proposed by the consortium on DLB international workshop(CDLB) in 1995. CDLB criteria of clinical diagnosis contain progressive cognitive decline as a mandatory feature, and fluctuating cognition, recurrent visual hallucinations and parkinsonism as 3 core features. Supportive features include repeated falls, syncope, transient loss of consciousness, neuroleptic sensitivity, and systematized delusions. CDLB pathologic criteria include the presence of Lewy bodies as the only essential feature, and associated features included Lewy-related neurites, senile plaques, neurofibrillary tangles, and regional neuronal loss in the areas vulnerable to Parkinson's disease. Lewy bodies are counted and scored from 0 to 2 in 5 designated cortical areas. Total Lewy body score of 7-10 indicates DLBD.
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PMID:[Diagnostic criteria of diffuse Lewy body disease]. 1106 44

We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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PMID:[A-56-year-old woman with parkinsonism, whose mother had Parkinson's disease]. 1142 77

On the basis of current literature, clinical and neuropathologic features of idiopathic autonomic neuropathy is presented. Idiopathic autonomic neuropathy is a disease characterized by acute or subacute onset, monophasic course over a period of several years, it is often preceded by an infection. The spectrum of autonomic changes ranges from cholinergic or adrenergic dysfunction to pandysautonomia, leading to heterogeneity of its clinical features. Possible sympathetic system abnormalities found in autonomic neuropathy are: poor pupillary response to light in darkness, orthostatic hypotension leading to syncope, hypotension without compensatory tachycardia, ejaculation disturbances and vasomotor instability. Possible parasympathetic dysfunctions are: salivation and lacrimation disturbances, absent pupillary constriction to light and near gaze, gastrointestinal tract immobility and impairment of gastrointestinal function, atonic bladder with large residual volume, erectile impotence. Pandysautonomia is thought to result from an immune mediated mechanism and responds well to plasmaferesis and intravenous immunoglobin therapy leading to gradual, sometimes not full, recovery. Moreover in this article we pay attention to the clinical value of many tests like cardiovascular or pharmacological studies in the diagnosis of pandysautonomia and in differentiation of pre- and postganglionic changes. In order to diagnose idiopathic autonomic neuropathy one has to rule out a large number of diseases with autonomic dysfunction e.g.: diabetes, malignant neoplasms, acute intermittent porphyria, Shy-Drager syndrome, Riley-Day's dysautonomia, Parkinson's disease, amyloidosis and others.
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PMID:[Idiopathic autonomic neuropathy (pandysautonomia)]. 1173 67

In patients with Idiopathic Parkinson's Disease (IPD) without a history of syncope the cardiovascular and cerebrovascular response to orthostatic stress was studied to search for subclinical impairment of autoregulatory mechanisms. Fifteen patients with IPD and 15 healthy age-matched controls were studied at rest and during head-up tilt (HUT). Heart rate, mean arterial blood pressure (MAP) and mean blood flow velocity (MBFV) in the middle cerebral artery were measured simultaneously. Changes of MAP and MBFV and the relationship between both were assessed. During HUT, heart rate increased less in patients than in healthy subjects (16.3% versus 24.2%, p=0.03). In the first minute of orthostasis MAP decreased more in patients than in healthy subjects (-4.0% versus -0.6%, p=0.04). MAP reached the pre-tilt values within 2 min in healthy subjects and 5 min in patients. Cerebral blood flow velocities fell to a similar degree and with similar time characteristics in patients and controls (-15.4% versus -16.7%, p=0.3). In both groups, patients and controls, changes of MAP did not correlate with changes of MBFV. It can be concluded that in IPD patients without symptoms of orthostatic dysregulation the autonomic circulatory control is impaired while the cerebral hemodynamic regulation during orthostasis is unaffected.
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PMID:Normal cerebral hemodynamic response to orthostasis in Parkinson's disease. 1203 20

The prevalence of falls among neurological patients is unknown, although disturbances of gait and posture are common. Falls may lead to burdens for the patient, the caregivers and the health system. We designed a prospective study and investigated all patients for a history of falls admitted to a neurological hospital during a 100-day period. Clinical investigation was carried out and several disease specific rating scales were applied. A total of 548 patients were investigated. Of all patients 34% had fallen once or more often during the last twelve months. A disturbance of gait was blamed for the fall in 55%, epileptic seizures in 12%, syncope in 10 % and stroke in 7%. Intrinsic risk factors for falls were high age, disturbed gait, poor balance and a fear of falling. As extrinsic factors we identified the treatment with antidepressants, neuroleptics and different cardiovascular medications, adverse environmental factors in the patients' home and the use of walking aids. Within the diagnoses, falls were most frequent in Parkinson's disease (62 %), syncope (57%) and polyneuropathy (48 %). According to these findings falls in neurological in-patients are twice as frequent as in an age-matched population living in the community. Falls in neurological patients are particularly linked to medication and disorders affecting gait and balance.
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PMID:Falls in frequent neurological diseases--prevalence, risk factors and aetiology. 1499 93

The aim of this study is to present a clinical role for 123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy in the differential diagnosis in patients with parkinsonian syndromes. We present a 51-year-old woman with parkinsonian syndrome and syncope occurrence. She reproduced spontaneous syncope in the tilt test. We present also a 60-year-old man with parkinsonian syndrome and syncope and presyncope occurrence. He also reproduced spontaneous syncope in the tilt test. Cardiac 123I-MIBG scintigraphy was performed in both patients. In the former patient, the H/M ratio of MIBG uptake was within normal ranges, in the latter, it was abnormally impaired. The results of the 123I-MIBG cardiac scintigraphy confirm results of the other studies. In the patient with Parkinson's disease the H/M ratio of MIBG uptake was abnormally impaired. The patient with the multiple system atrophy was within normal ranges.
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PMID:[123I-metaiodobenzylguanidine myocardial scintigraphy in the differential diagnosis of patients with parkinsonian syndromes -- case reports]. 1627 70

Parkinson's disease (PD), multiple system atrophy (MSA) and pure autonomic failure (PAF) are neurodegenerative disorders frequently associated with orthostatic hypotension and syncope, though with different underlying mechanisms. Cerebral hemodynamic responses in these three neurodegenerative diseases are still incompletely studied and it is possible that they would be differentially affected. We measured blood flow velocity (BFV) in the middle cerebral artery (MCA) and vertebral artery (VA) in patients with these disorders and investigated whether cerebral vasomotor reactivity (VMR) differs in these three disorders. Twenty-four patients (9 with PD, 10 with MSA and 5 with PAF) were studied. VMR was assessed in the MCA and VA, using transcranial Doppler (TCD) and Diamox test (injection of 1 g acetazolamide i.v.) with the patients in a recumbent position. The percent difference between BFV before and after acetazolamide injection was defined as VMR% and the results were compared by ANOVA. The mean MCA and VA blood flow velocities were similar in the three disorders and within normal limits for our laboratory. The mean MCA VMR values were 37.5+/-24.0%, 27.9+/-28.0% and 38.0+/-33.9% in PD, MSA and PAF, respectively. The VA VMR values were 22.9+/-23.6%, 32.4+/-38.0% and 18.9+/-18.3%, respectively, with no significant differences between the groups. We conclude that BFV is normal in PD, MSA and PAF and that the VMR, as investigated by TCD and the Diamox test, did not disclose differences in cerebral vasomotor responses between these conditions.
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PMID:Cerebral vasomotor reactivity in Parkinson's disease, multiple system atrophy and pure autonomic failure. 1643 86

Dementia with Lewy bodies appears to be the second most common form of dementia, accounting for about one in five cases. The condition is characterized by dementia accompanied by delirium, visual hallucinations, and parkinsonism. Other common symptoms include syncope, falls, sleep disorders, and depression. The presence of both Lewy bodies and amyloidplaques with deficiencies in both acetylcholine and dopamine neurotransmitters suggests that dementia with Lewy bodies represents the middle of a disease spectrum ranging from Alzheimer's disease to Parkinson's disease. The diagnosis of dementia with Lewy bodies is based on clinical features and exclusion of other diagnoses. Individualized behavioral, environmental, and pharmacologic therapies are used to alleviate symptoms and support patients and their families. Cholinesterase inhibitors are more effective in patients who have dementia with Lewy bodies than in those with Alzheimer's disease. Conversely, patients who have dementia with Lewy bodies do not respond as well to antiparkinsonian medications. Anticholinergic medications should be avoided because they exacerbate the symptoms of dementia. Traditional antipsychotic medications can precipitate severe reactions and may double or triple the rate of mortality in patients who have dementia with Lewy bodies.
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PMID:Dementia with Lewy bodies: an emerging disease. 1662 10

Cholinesterase inhibition in patients with Alzheimer's disease (AD) may affect heart rate, sometimes inducing bradycardia. Additional cardiac safety considerations apply in patients with dementia with Lewy bodies (DLB) and Parkinson's disease (PDD), in whom cardiovascular autonomic nervous system dysfunction is common. We conducted a review of the safety data available for rivastigmine in these two conditions. A modest reduction in the mean heart rate of 1.5-2 bpm was seen. No clinically meaningful treatment differences in bradycardia or ECG abnormalities were apparent. Compared with placebo, rivastigmine appeared to be associated with fewer vascular disorder adverse events (AEs) (p = 0.002) and fewer AEs of syncope (p = 0.018) in PDD patients (n = 541). A smaller randomised, placebo-controlled study of rivastigmine in DLB (n = 120) showed similar findings. Rivastigmine appears to have a favourable cardiac safety profile in PDD and DLB patients.
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PMID:Cardiac safety of rivastigmine in Lewy body and Parkinson's disease dementias. 1680 45


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