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)

At the Department of Neurology and Internal Medicine at our hospital, there are 22 outpatients who are nursed at home. Their diseases are Parkinson's disease, spinal cerebellar degeneration, dementia and other diseases. The problem is how we should care for and support these patients in the future, now that the official Care Insurance System has started. We discuss how we could support such patients, through the case of a patient suffering from Parkinson's disease. The patient was a 69-year-old female. In 1991, she developed Parkinson's disease, accompanied with trembling in her right upper limb. Her condition was controlled at our hospital. Is April 1999, she lost strength in her right thigh without any previous notice, so she was hospitalized for treatment. For a period, she became aggressive from hallucinations and delusions and she had to be taken care of all day. Her only daughter lived apart and her 72-year-old husband was also suffering from Parkinson's disease. In spite of such conditions, she hoped to receive home care and her husband accepted that. We asked what they would want us to do. We had meetings together with the staff of the local administration, doctors, nurses, and pharmacists. The report from our hospital staff says, "It may be difficult for only her family to support her. She needs other supporting systems." She came to our hospital twice a month. We made an effort to understand her condition with the help of the report of a visiting nurse. However, her illusions and delusions made it difficult even to utilize the short-stay. Her husband sometimes uses violence and says. "I can't stand this any more--her unrest, micturition at night and refusal to eat." Nevertheless, she continues to say "I want to stay at home." They have had considerable trouble. The following are necessary for home care of some patients. 1. Understanding what a patient and her family want to do. Cooperating with the staff of the administration, in consideration of the Care Insurance System. 2. Studying with incurable neurology patients using pamphlets or other materials and supporting them, 3. Discussing how to act in concert with patients at home and outpatients at the hospital involving a risk without MSW.
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PMID:[Continuous nursing of incurable patients at home--the case of a patient with Parkinson's disease]. 1119 Mar 7

Neuropsychiatric symptoms are common in basal ganglia disorders and may have severe clinical consequences. The authors compared the neuropsychiatric manifestations of patients with Parkinson's disease (PD) and progressive supranuclear palsy (PSP). All 103 PD patients and 27 of the 61 PSP patients were taking dopaminergic agents. PSP patients showed significantly more apathy and disinhibition. Patients with PD had higher frequency of hallucinations, delusions, and depression. These results suggest that PSP patients show symptoms compatible with lesioned orbitofrontal and medial frontal circuits, such as disinhibition and apathy, whereas PD patients show symptoms associated with monoaminergic disturbances, such as psychosis and depression.
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PMID:Neuropsychiatric symptoms of patients with progressive supranuclear palsy and Parkinson's disease. 1120 28

Dementia with Lewy bodies (DLB), the second most frequent cause of primary degenerative dementias following Alzheimer's disease, has been increasingly recognized since the proposal of the consensus name and clinical diagnostic criteria. Although DLB overlaps in clinical, pathological, and genetic features with Alzheimer's disease and Parkinson's disease, DLB should be understood as an entity with the essential feature of the presence of Lewy bodies in the brain stem and cerebral cortex. From the clinical point of view, DLB is characterized by the presence of progressive dementia without severe memory disorders at the early stage, with significant cognitive fluctuations, well-formed recurrent visual hallucinations, and spontaneous Parkinsonism. This article reviews recent clinical and research findings, including our own, to facilitate clinical recognition of DLB. In addition to the supportive features described in the consortium clinical diagnostic criteria for DLB such as falls and great sensitivity to neuroleptic drugs, our studies found other frequent disorders including disproportionately severe visuoconstructive and visuoperceptual disturbances, transitory alterations in consciousness with reduplication phenomena, misidentification delusions, and non-aphasic misnamings. Neuroimaging features include relatively preserved hippocampal volume on MRI and occipital involvement on metabolic and blood flow imagings. The correct diagnosis of DLB is important to administer adequate treatment, to avoid adverse effects with neuroleptic drugs, and to establish precise prognosis. The present summary of the clinical features is hopefully helpful for clinical diagnosis of DLB. From a therapeutic point of view, cholinesterase inhibitors seemingly show some efficacy in the treatment of cognitive alterations. Further research would result in advances in diagnostic methods and therapeutic approaches in the near future.
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PMID:[Dementia with Lewy bodies]. 1121 12

Delusional jealousy has been reported in organic and "functional" psychotic disorders. In organic psychoses, delusional jealousy is usually associated with impaired orientation or other cognitive disturbances. Delusional jealousy in Parkinson's disease has rarely been reported in the scientific literature. A case of a 49-year-old man suffering from this pathology in the course of Parkinson's disease is presented as to clinical picture, therapy, course, and outcome.
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PMID:[A case of delusional jealousy in Parkinson disease ]. 1126 67

Psychosis arises with considerable frequency in a number of neurologic conditions. The treatment of such patients is often challenging, as many of the treatments for psychosis pose some risk of worsening the underlying neurologic condition. Although psychosis may emerge in the context of any neurologic condition that sufficiently disrupts the functioning of or connections between limbic, paralimbic, frontal, subcortical areas mediating complex sensory perception, interpretation, and thought or language organization, secondary psychoses are most often encountered in patients with Alzheimer's disease (Parkinson's disease receives dopaminomimetic therapies) and epilepsy. Psychosis, and particularly delusions and visual hallucinations, may arise in Alzheimer's disease. Based on the available literature, the first-line therapy for this problem is risperidone 0.5 to 3 mg per day. If this treatment proves unsuccessful, low-dose haloperidol or olanzapine should be considered next. If these treatments prove unsuccessful, quetiapine should then be considered. Finally, clozapine may be useful for treatment-refractory psychosis due to Alzheimer's disease, but due caution is warranted given its considerable anticholinergic properties and potential for worsening cognition in these patients. Although disease-emergent psychosis (paranoid delusions and visual hallucinations) may develop in patients with Parkinson's disease, psychosis due to dopaminomimetic therapy is much more common. When such symptoms develop, the accepted first step is to taper anti-parkinsonian medications were possible. Anticholinergic medications, amantadine, selegiline, and dopamine receptor agonists should be reduced or discontinued, provided that the patient can tolerate changes in motor symptoms attendant to such reductions. When these reductions are not feasible or fail to improve treatment-emergent psychosis, low-dose quetiapine or clozapine may be useful. The greatest body of evidence supports the effectiveness of these treatments and their relative lack of adverse effects on motor function. When psychosis develops in the context of epilepsy, the generally accepted first step is to maximize anticonvulsant therapy in an effort to reduce the possible contribution of electrophysiologic disturbances in the described areas to psychotic symptoms. When interictal psychosis persists despite such adjustments, initiation with low-dose atypical antipsychotics carries the least risk of lowering seizure threshold and should be considered.
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PMID:Psychosis Due to Neurologic Conditions. 1138 5

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

Psychosis is quite common in Parkinson's disease (approximately 25% of patients) and therefore constitutes a serious public health problem. All patients suffering from idiopathic Parkinson's disease, and especially elderly and demented patients, are at risk of developing delusions or hallucinations. The most prominent psychotogenic factors are dopaminomimetic agents, which may induce dopamine hypersensitivity in the frontal and limbic dopamine projection regions, and consequently, either directly or indirectly, elicit psychotic signs and symptoms. A Parkinson's disease-related cholinergic deficit in combination with an age-related further loss of cholinergic integrity also plays a prominent role. Psychosis in Parkinson's disease patients appears to be a more important contributor to caregiver distress than motor parkinsonism. Psychosis therefore probably represents the single greatest risk factor for nursing home placement. Typical antipsychotic drugs, because of their selective dopamine receptor antagonistic effects, can reduce psychotic signs but at the cost of an increase in parkinsonism. As a consequence of a non-selective antagonism at both serotonergic and dopaminergic receptors, atypical antipsychotic drugs are associated with fewer extrapyramidal side-effects. On the other hand, hypersensitivity to these agents may induce delirium or a malignant neuroleptic syndrome. Atypical antipsychotic agents such as clozapine, quetiapine and olanzapine should therefore be started at very low doses that are increased gradually. Cholinomimetic therapy may prove to be helpful in the prevention and treatment of psychotic manifestations in Parkinson's disease patients, given the effects observed in patients suffering from dementia with Lewy bodies.
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PMID:Management of psychosis in Parkinson's disease. 1147 Sep 67

Chronic delusional psychosis with hallucinations (CDHP) is commonly assumed to complicate the later stages of Parkinson's disease, as a side effect of antiparkinsonian medication. We studied 7 patients with early onset PD, who had developed psychiatric manifestations consisting in CDHP after a few years of antiparkinsonian therapy. All patients underwent a neurological, psychiatric and brain imaging (CT or MRI) evaluation. Detailed clinical history was recorded in order to reveal prior psychiatric illness and to analyse the relationship between neurological disease, cognitive impairment and psychosis. Our findings suggest that CDHP occurring in patients with early onset PD, normal or slightly impaired cognitive functions and normal CT/MRI scans is invariably the expression of a coexisting psychiatric illness which prior to onset of the neurologic disease had not been correctly diagnosed and which has been disclosed by dopaminergic therapy.
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PMID:Chronic delusional hallucinatory psychosis in early-onset Parkinson's disease: drug-induced complication or sign of an idiopathic psychiatric illness? 1148 98

Direct and indirect signs and symptoms of Parkinson's disease are a major cause of disability in the elderly. Intrinsic symptoms comprise not only the well-known clinical hallmarks of this disease with motor behavioral abnormalities, such as bradykinesia, hypokinesia, rigidity and tremor, but also autonomic failure with orthostatic hypotension, urinal incontinence and impotence as well as non-motor behavioral abnormalities: mental dysfunction characterized by mood disorders, cognitive dysfunction and, sporadically, delusions and hallucinations. These symptoms are caused by a progressive abnormal degeneration of the dopamine (DA) producing cells in the substantia nigra (SN) and ventral tegmentum area (VTA) in combination with an interindividual fluctuating degree of decay in the noradrenergic (locus coeruleus), cholinergic forebrain (nucleus basalis of Meynert) and serotoninergic (dorsal raphe nuclei) systems. Extrinsic symptoms, induced by pharmacotherapy, mainly manifest with (un)predictable motor response fluctuations and dopaminomimetic psychosis. Psychological and psychiatric symptoms in Parkinson's disease (PD) are important predictors of the patient's quality of life. As these symptoms are potentially treatable, identification is of major clinical importance both for the patients and their caregivers and may enable to maintain Parkinson's disease patients at home for a longer period.
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PMID:Intrinsic and extrinsic psychosis in Parkinson's disease. 1169 84

Psychotic symptoms develop in 20-30% of patients with Parkinson's disease (PD) receiving chronic anti-PD medications, and visual hallucinations with or without delirium and paranoid delusions are the most frequent symptoms. Psychotic symptoms disturb ADL and QOL of PD patients and tax caregivers far more than the motor disabilities do, and good management of drug-induced psychotic symptoms is potentially important. Withdrawal of anti-PD drugs relieves the patients from psychotic side effects, but worsens the parkinsonian motor symptoms. The first step of treatment is to eliminate triggering factors other than anti-PD drugs, such as infections, metabolic disorders, subdural hematoma, and hallucinogenic drugs. The second step is to eliminate anti-PD drugs in the following order; first anticholinergics, amantadine and selegiline, second dopamine agonists, and finally levodopa/carbidopa. Anti-PD medications should be reduced to the point of improving psychotic side effects without drastically worsening parkinsonian motor symptoms. When the above adjustments fail to sufficiently alleviate psychotic side effects, the third step is consideration of antipsychotic drugs although they have potential capacity to antagonize dopamine D2 receptors and worsen parkinsonism. Atypical antipsychotics such as clozapine and olanzapine are recommended, though the former is not available in Japan.
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PMID:Drug-induced psychotic symptoms in Parkinson's disease. Problems, management and dilemma. 1169 85


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