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)

The study was finished according to schedule with 32 of the 49 examined patients, i.e. without changes in neuroleptic medication. The antiparkinson medication had been suddenly withdrawn in all patients. No patient had to be given another antiparkinson treatment due to reappearing Parkinson symptoms. Slight and constant deterioration in their condition occurred in four patients within 1-3 weeks following withdrawal of the antiparkinson medication; this fact justified recommencement of the antiparkinson therapy. All but seven patients had been given antiparkinson drugs for more than 1 year. All patients were on neuroleptic drugs. The neuroleptic dose was increased in seven patients, a slight transient deterioration of the Parkinson symptoms occurring in two cases. Investigation into the longitudinal course of the diseases revealed that the intensity of symptoms is not always steady, but that certain variations occur. An equable course was observed in paranoid schizophrenics. In cases of catatonia and hebephrenia variations in the symptoms and their intensity must be expected. However, these variations need not inevitably call for recommencement of the antiparkinson treatment. Thus, our results confirm similar available studies in that the incidence of relapses in cases of neuroleptically conditioned Parkinson's disease is very low in patients who had been receiving antiparkinson medication for long periods; this incidence of relapses amounts to 8% in our study. Our figures are lower than those referred to in literature up to now. Within 1-3 weeks following withdrawal it becomes obvious whether another antiparkinson therapy will be necessary or not. Within the scope of our study, we cannot comment on the statement that antiparkinson drugs may be withdrawn, without any risk of a relapse, after 3-month administration.
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PMID:Open withdrawal of antiparkinson drugs in the neuroleptic- induced Parkinson syndrome. 124 94

Ten patients with advanced Parkinson's disease, presenting with tremor, rigidity and akinesia had autologous adrenal medullary transplantation taken from the left adrenal gland to the head of the right caudate nucleus. Particular attention was taken to avoid prolonged exposure of the adrenal tissue before transplantation and to separate the medullary from the cortical adrenal tissues. Postoperative CT scans confirmed the correct position of the transplants. Differences between pre- and 1-year postoperative clinical conditions were statistically evaluated, with patients under medical (L-dopa) treatment and after the medication was temporarily discontinued. Performance of motor tasks was tested to differentiate slowness of movements imposed by excessive muscular tension (rigidity) from that secondary to delayed reaction time to sensory demands (akinesia). Two deaths occurred 35 and 69 day after surgery for causes not related to the surgical procedures. One of those patients had remained stable neurologically and the other had deteriorated to progressive dementia and catatonia. At autopsy, no lesions in the CNS other than those expected from the surgical procedure were evident, and histological examination failed to reveal chromaffin cells in the head of the right caudate nucleus. Evaluation of the 8 cases that survived for 1 year revealed no significant improvement in their clinical or motor task performance, when considered as a group. However, cases with mild akinesia did better than cases with moderate to advanced akinesia, suggesting that transplantation is indicated in cases with rigidity, but not in cases with 'negative' symptoms of Parkinson's disease. All cases required postoperative medication.
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PMID:Autologous adrenal medullary transplants in advanced Parkinson's disease with particular attention to the selective improvement in symptoms. 184 77

1. The tetradecapeptide somatostatin (SS) has a widespread, uneven distribution within several organs including the central nervous system (CNS), with particularly high concentration in the hypothalamus. 2. The SS-related peptides (SS28, SS28(1-12), SS28(15-28)) are originated from the precursor pre-prosomatostatin. 3. SS is suggested to be involved in a large number of CNS functions, locomotion, sedation, excitation, catatonia, body temperature, feeding, nociception, paradoxical sleep, self-stimulation, seizure, learning and memory. 4. SS influences central neurochemical processes. 5. It is possible that SS is related to various neurological and psychiatric illnesses, like Huntington's disease, multiple sclerosis, Parkinson's disease, epilepsy, eating disorders, Alzheimer's disease, schizophrenia and major depressive illness.
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PMID:Preclinical and clinical studies with somatostatin related to the central nervous system. 197 75

Parkinsonism is an uncommon movement disorder in childhood. Six unusual cases of acquired parkinsonism in hospitalized children are described. Clinical manifestations included an akinetic-rigid syndrome with and without tremor, the combination of parkinsonism and dystonia, and a parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia, and sialorrhea were frequent associations. Etiologies included hypoxic-ischemic encephalopathy; haloperidol treatment with and without neuroleptic malignant syndrome; toxicity of cytosine arabinoside, cyclophosphamide, amphotericin B, and methotrexate; St. Louis encephalitis and other encephalitides; and a pineal tumor with hydrocephalus. Cranial magnetic resonance imaging results ranged from normal to profound cerebral and cerebellar atrophy with chemotherapeutic toxicity. The illnesses usually were severe enough to require pharmacotherapy. Incorrect diagnoses of depression or catatonia delayed treatment or aggravated the problem. Acute treatment included amantadine, levodopa/carbidopa with or without selegiline, diphenhydramine, or benztropine. The concentration of CSF homovanillic acid was normal in a neuroleptic-associated patient, but the level was low in an encephalitic patient. All patients demonstrated dramatic improvement, including two who were not treated; some had complete resolution of symptoms and none required continued antiparkinsonian drugs despite poor scores on the Unified Parkinson's Disease Rating Scale and the Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism described are more common in a general pediatric hospital than the parkinsonism associated with the popularized Segawa syndrome.
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PMID:Clinical spectrum of secondary parkinsonism in childhood: a reversible disorder. 802 61

Retinoic acid is synthesized from retinaldehyde by several different dehydrogenases, which are arranged in conserved spatial and developmentally regulated patterns. Here we show for the mouse that a class-1 aldehyde dehydrogenase, characterized by oxidation and disulfiram sensitivity, is found in the brain at high levels only in the basal forebrain. It is present in axons and terminals of a subpopulation of dopaminergic neurons of the mesostriatal and mesolimbic system, forming a retinoic acid-generating projection from the ventral tegmentum to the corpus striatum and the shell of the nucleus accumbens. In the striatum the projection is heaviest to dorsal and rostral regions, declining gradually toward ventral. The enzyme is expressed early in development, shortly after appearance of tyrosine hydroxylase. Other dopaminergic neurons in the brain, as well as the chromaffin cells of the adrenal medulla, do not contain this dehydrogenase. The presence of this enzyme may be a factor in the long-term success of transplants of dopaminergic cells to the corpus striatum in Parkinson disease, and it may play a role in parkinsonism and catatonia due to disulfiram (Antabuse) neurotoxicity.
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PMID:High levels of a retinoic acid-generating dehydrogenase in the meso-telencephalic dopamine system. 805 59

This paper presents 6 patients with catatonia and subthalamic mesencephalic tumors with hydrocephalus involving the third and the lateral ventricles. This anatomic and psychiatric anomaly is investigated on the basis of personal observations and a review of the literature. These cases allow an interesting parallel to be traced between neurological clinical signs and psychiatric signs. Various anatomic and physiological models are discussed which emphasize specialized neuronal circuits (somewhat similar to those involved in Parkinson's disease) and certain specific neurotransmitters such as dopamine, together with the reactivity of these circuits to intracranial pressure variations. Once more, clinical and laboratory data on schizophrenia concur to suggest that organic etiology is the causal factor in a known psychiatric pathology.
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PMID:Schizophreniform catatonia on 6 cases secondary to hydrocephalus with subthalamic mesencephalic tumor associated with hypodopaminergia. 890 36

Depression is a common condition that often responds to a variety of treatment modalities. Concerns about antidepressant medications' safety and efficacy and individuals' lack of response or their problems complying with medication regimens have prompted a resurgence in electroconvulsive therapy (ECT) for specific mental health conditions. Outpatient maintenance ECT, performed under general anesthesia, is a safe, effective follow-up treatment for individuals with major depression who have undergone inpatient ECT. Individuals with bipolar disorders, catatonia, mania, and schizophrenia and those with Parkinson's disease also can benefit from outpatient ECT. Perioperative nursing care for individuals who undergo outpatient ECT is similar to the care provided to patients scheduled for ambulatory surgery. Successful performance of outpatient ECT requires collaboration by skilled perioperative nurses, psychiatrists, anesthesia care providers, affected individuals, and family members.
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PMID:Treatment of depression with outpatient electroconvulsive therapy. 906 Nov 52

Electroconvulsive therapy (ECT) is an efficacious treatment for a variety of neuropsychiatric conditions including major depression, mania, catatonia, Parkinson's disease, and neuroleptic malignant syndrome. However, ECT-induced memory dysfunction complicates the treatment and is a major concern for both patients and providers. We briefly review ECT-induced memory dysfunction and propose a glutamatergic model for it. (Articles examined were retrieved by a Medline search on the terms electroconvulsion and glutamate, with language limited to English.) Specifically, we hypothesize that ECT-induced memory dysfunction results from neuronal insults due to excessive release of excitatory amino acids and activation of their receptors, which produce cation and water flux and reversible oxidative stress. This model offers multiple testable hypotheses; exploring them may help to identify the risk factors for this significant side effect of ECT treatment and may thus yield effective agents for its prevention and treatment.
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PMID:A glutamatergic model of ECT-induced memory dysfunction. 955 49

The present review describes findings and clinical indications for the dopamine D2 receptor scintigraphy. Methods for the examination of D2 receptors are positron emission tomography (PET) using 11C- or 18F-labelled butyrophenones or benzamides or single photon emission tomography (SPECT) using 123l-iodobenzamide (IBZM) respectively. The most important indication in neurology is the differential diagnosis of Parkinsonism: patients with early Parkinson's disease show an increased D2 receptor binding (D2-RB) compared to control subjects. However, patients suffering from Steele-Richardson-Olszewski-Syndrome or Multiple System Atrophy show a decreased D2-RB and are generally non-responsive to treatment. Postsynaptic blockade of D2 receptors results in a drug induced Parkinsonian syndrome, which can be diagnosed by D2 scintigraphy. Further possible indications occur in psychiatry: the assessment of receptor occupancy is useful in schizophrenic patients treated with neuroleptics. Additionally, D2 receptor scintigraphy might help to clarify the differential diagnosis between neuroleptic malignant syndrome and lethal catatonia. The method might be useful for supervising neurobiochemical changes in drug dependency and during withdrawal. Assessment of dopamine D2 receptor binding can simplify the choice of therapy in depressive disorder: patients showing a low D2 binding are likely to improve following an antidepressive drug treatment whereas sleep deprivation is promising in patients with high D2 binding.
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PMID:[Clinical impact of cerebral dopamine-D2 receptor scintigraphy]. 983 Jun 15

There is a now a substantial body of evidence that suggests the new antipsychotic agent, risperidone, may be safe and effective for treating psychotic, affective or behavioural symptoms associated with various disorders other than schizophrenia, schizophreniform disorder or schizo-affective disorder. These conditions include bipolar disorder, obsessive-compulsive disorder, Tourette's syndrome, dementia, Lewy body disease, mental retardation, Parkinson's disease, idiopathic segmental dystonia and organic catatonia. Although much of the data is anecdotal or in the form of open studies, there is now emerging a small number of well controlled investigations supporting efficacy for mania, dementia, behavioural disturbance in mental retardation and conduct disorder. Conventional antipsychotics have long been used, either in a primary capacity or as an adjunct to treat these disorders; however, they have limited benefit, pose significant risks of extrapyramidal side-effects, and may cause the potentially life-threatening neuroleptic malignant syndrome. In contrast, risperidone at the recommended low doses may be efficacious and pose reduced risk of motor side-effects. This article reviews the evidence that risperidone may be an effective new treatment for disorders other than schizophrenia.
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PMID:Does risperidone have a place in the treatment of nonschizophrenic patients? 1119 55


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