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)

A group of 71 patients with Parkinson's disease were treated with L-Dopa and benserazide during periods ranging from 27 to 60 months. In 28% of cases a decline in therapeutic effects and or delayed appearance or increase of secondary actions were observed constituting a long-term syndrome. Its most complex and dramatic expression, the on-off effect, was present in 11% of cases. Those patients with more severe symptoms were studied by means of continuous clinical observation enabling the design of daytime follow-up curves. Observations were repeated with varying dosage patterns, showing variations but no substantial changes or disappearance of the symptoms described. Electromyographic recordings and films were taken in certain cases defining the characteristics of on and off effects. Several procedures were implemented in an attempt to control Long-Term Syndrome manifestations: Change of dosage, variation of L-dopa/decarboxilase inhibitor ratio, association of anticholinergic agents with antidepressants, hypoprotein diets. Improvement was moderate and/or transient, with the exception of Nortriptilline which permitted total or partial control of certain symptoms, especially hypokinetic periods, bouts of tremor and dystonic attitudes. It was occasionally necessary to interrupt administration of L-Dopa, readministering it later with recovery of the therapeutic effect and/or avoidance of undesirable effects for varying periods of time. Loss than optimal doses proved beneficial in reducing or postponing Long-Term Syndrome manifestations. Although L-Dopa does not detain the course of the disease, the persistence of favourable results in most patients for prolonged periods of treatment confirms the long-term therapeutic value of this drug.
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PMID:[Long-term syndrome in the treatment of parkinsonism with L-dopa]. 124 97

Most of Parkinson's disease patients treated with Levodopa develop the Long Treatment Levodopa Syndrome. Many authors showed a correlation between clinical features and plasma level of Levodopa. In our study, five parkinsonian patients with severe clinical response fluctuations, oral levodopa treatment was replaced by repeated continuous infusions of Levodopa (with oral carbidopa). Our results confirm that repeated intravenous infusion are very effective in PD patients with LTS.
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PMID:[Intravenous infusion of L-dopa: current prospective therapies]. 180 80

The Kraepelinian subtypes, developed early in the century, recognize the heterogeneity of schizophrenia but do not reliably predict differences in response to classical neuroleptics. The newer distinction of positive and negative syndromes in schizophrenia carry promise as an approach to identifying meaningful clinical and neurobiological dimensions. The present review summarizes the supportive evidence from a series of investigations using the Positive and Negative Syndrome Scale (PANSS), and a hypothesis on the pathophysiology of negative and positive symptoms is advanced. Our data suggest that: (a) positive and negative syndromes in schizophrenia represent stable, independent dimensions and not co-exclusive subtypes; (b) both are unrelated to the progression of illness; (c) they are differentially related to fundamental aspects of schizophrenia, including premorbid adjustment, cognitive development, family psychiatric history, the cognitive and neuropsychiatric profiles, dopaminergic functions, drug response, and subsequent course; (d) together with depression and excitement, they comprise the fundamental symptomatic components of schizophrenia, which, in their interaction, can account for the specific Kraepelinian subtypes. We have proposed that negative symptoms represent the core pathology in schizophrenia and may be understood as a variant of parkinsonism, hence characterized by dopaminergic deficiency and increased cholinergic activity. This view is supported by the striking overlap with Parkinsonism in regard to clinical features, neurochemistry, pharmacology, neuropathology, and neuroradiology. Positive symptoms are thought to reflect increased dopaminergic activity, which may arise as a compensatory adaptive mechanism to overcome the progressive dopamine loss in the maturing brain. The early onset of schizophrenia by comparison to Parkinson's disease may explain why schizophrenia entails more pronounced positive symptoms, development deficits, and cognitive, social, and emotional impairments. We describe evidence that pineal calcification, which may reflect disturbance of melatonin functions, appears to be a nongenetic factor in schizophrenia associated with perinatal injury. This may in part underlie the negative syndrome and its response to antipsychotic compounds with serotonergic (5-HT) antagonism.
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PMID:Experimental models of schizophrenia. 193 75

A variety of degenerative diseases involving deficiencies in mitochondrial bioenergetics have been associated with mitochondrial DNA (mtDNA) mutations. Maternally inherited mtDNA nucleotide substitutions range from neutral polymorphisms to lethal mutations. Neutral polymorphisms are ancient, having accumulated along mtDNA lineages, and thus correlate with ethnic and geographic origin. Mildly deleterious base substitutions have also occurred along mtDNA lineages and have been associated with familial deafness and some cases of Alzheimer's Disease and Parkinson's Disease. Moderately deleterious nucleotide substitutions are more recent and cause maternally-inherited diseases such as Leber's Hereditary Optic Neuropathy (LHON) and Myoclonic Epilepsy and Ragged-Red Fiber Disease (MERRF). Severe nucleotide substitutions are generally new mutations that cause pediatric diseases such as Leigh's Syndrome and dystonia. MtDNA rearrangements also cause a variety of phenotypes. The milder rearrangements generally involve duplications and can cause maternally-inherited adult-onset diabetes and deafness. More severe rearrangements frequently involving detections have been associated with adult-onset Chronic Progressive External Ophthalmoplegia (CPEO) and Kearns-Sayre Syndrome (KSS) or the lethal childhood disorder, Pearson's Marrow/Pancreas Syndrome. Defects in nuclear-cytoplasmic interaction have also been observed, and include an autosomal dominant mutation causing multiple muscle mtDNA deletions and a genetically complex disease resulting in the tissue depletion of mtDNAs. MtDNA nucleotide substitution and rearrangement mutations also accumulate with age in quiescent tissues. These somatic mutations appear to degrade cellular bioenergetic capacity, exacerbate inherited mitochondrial defects and contribute to tissue senescence. Thus, bioenergetic defects resulting from mtDNA mutations may be a common cause of human degenerative disease.
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PMID:Mitochondrial DNA mutations in diseases of energy metabolism. 807 79

The Long-Term Dopa Syndrome (LTDS) is one of the main problems in the management of advanced parkinsonian patients. A transient L-Dopa withdrawal (Drug Holiday, DH) can be useful to improve the drug response after DH, even if this approach presents risks due to patient akinesia. We tried to verify if Apomorphine sc administration during DH (DH with Apomorphine, DHA) can: a) reduce the risks connected with DH: b) maintain the benefits of DH: c) standardize the duration of DH. Twenty-five parkinsonian patients with LTDS were treated with Apomorphine sc during DH (14 days). No patient had any severe side effects. The follow-up at 180 days, conducted using the Unified Parkinson's Disease Rating Scale, demonstrated a significant improvement in the clinical conditions of about 70% of the patients, allowing a 27.1% reduction in daily L-dopa dosage. DHA can represent a valid therapeutical approach for parkinsonian patients with LTDS.
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PMID:Apomorphine SC treatment in parkinsonian patients with long-term L-dopa syndrome during L-dopa drug holiday. 874 22

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions, and a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotions. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The aims of this study were: first to establish some correlations between alexithymia and some symptoms of schizophrenia, and second to estimate the intensity of alexithymia in negative versus positive and undifferentiated schizophrenic patients. Twenty-nine patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients were assessed by one trained psychiatrist (IN) using six rating scales: Beth Israel Questionnaire (BIQ) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Depressive Retardation Rating Scale (DRRS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). In the total sample, the mean score of BIQ was 4.79 +/- 1.68 (mean +/- SD). Significant correlations were found between alexithymia and blunted affect (r = 0.376; p < 0.05), poverty of speech (r = 0.471; p < 0.01), anxiety (r = 0.370; p < 0.05), total score of DRRS (r = 0.370; p < 0.05), and motor subscore of DRRS (r = 0.429; p < 0.05). The patients with negative symptoms of schizophrenia had significantly higher total scores in alexithymia (p < 0.05), blunted affect (p < 0.0001), poverty of speech (p < 0.0001), anxiety (p < 0.05), total score of DRRS (p = 0.01) and his motor subscore (p < 0.0001) as compared to positive and undifferentiated subtypes. In our study, alexithymia seems to be correlated with negative and depressive symptoms in negative forms of schizophrenia, regardless of medication status.
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PMID:[Negative symptoms, depression, anxiety and alexithymia in DSM III-R schizophrenic patients]. 941 92

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions and, a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotion. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The purpose of this study was to estimate and compare the prevalence of alexithymia in deficit and non-deficit schizophrenia. The term "deficit symptoms" may be used as Carpenter, to refer specifically to those negative symptoms that are not considered secondary. The influence of patients' symptoms has also been studied on alexithymia scores: negative and positive symptoms of schizophrenia, depression, anxiety, anhedonia and effects of neuroleptics. Twenty-five patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients have been categorized into deficit (n = 12) and non-deficit (n = 13) subgroups by one trained psychiatrist (SD), using the Schedule for the Deficit Syndrome. The subjects have been assessed by the same rater (IN), blind to deficit status, using six rating scales: Beth Israel Questionnaire (BIQ) and Toronto Alexithymia Scale (TAS) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). Using TAS, alexithymic characteristics were more prevalent in the deficit subgroup as compared to non-deficit subgroup (83% versus 30.76%; p < 0.01). Significant correlations were observed in the non-deficit subgroup between: TAS and anxiety (r = 0.743; p < 0.01), TAS and depression (r = 0.568; p < 0.05), BIQ and blunted affect (r = 0.636; p < 0.02), BIQ and poverty of speech (r = 0.629; p < 0.02). These correlations were not significant in the deficit group of patients. Alexithymia in schizophrenic patients seems to be a trait characteristic in deficit patients, and a state related to many symptoms, such as flattening of affect, poverty of speech, depression and anxiety in nondeficit patients.
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PMID:[Alexithymia in negative symptom and non-negative symptom schizophrenia]. 945 28

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

Encoding action phrases by enacting leads normally to better memory performance than verbal encoding. In order to gain additional insight into the representational basis of the enactment effect, neurological patients are contrasted with healthy participants. Persons suffering from Parkinson's disease, which primarily impairs the motor system, and patients suffering from Frontal Lobe Syndrome, which primarily affects action-related planning processes, were involved. We investigated whether the enactment effect would be differentially affected by these disorders. In addition, the characteristics of information processing after encoding by enacting was analyzed by varying memory material (unrelated versus clusterable actions) and by adding an encoding condition that included obligatory action planning (director condition). The findings indicate that the impact of motor information for the enactment effect is not dominant compared to the role of action-related cognitive and motivational processes, in particular planning processes. The findings of the two experiments are explained within traditional conceptual memory theories.
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PMID:Memory for action events: findings in neurological patients. 1566 Jun 29

The preliminary results obtained by the Study Group for Treatment of Involuntary Movements by Extradural Motor Cortex Stimulation (EMCS) of the Italian Neurosurgical Society, are reported. The series includes 16 cases of very advanced Parkinson's Disease (PD), aged 46-81; 15 of them were not eligible for Deep Brain Stimulation. Ten cases have been evaluated at 3-30 months after implantation. Unilateral, sub-threshold extradural motor cortex stimulation (2 8 Volt, 100-400 microsec., 20-120 Hz) by chronically implanted electrodes, relieves, at least partially, but sometime dramatically, the whole spectrum of symptoms of advanced PD. Tremor and rigor bilaterally in all limbs and akinesia are reduced. Standing, gait, motor performance, speech and swallowing are improved. Benefit is marked as far as axial symptoms is concerned. Also the symptoms of Long Term Dopa Syndrome -dyskinesias, motor fluctuations - and other secondary effect of levodopa administration psychiatric symptoms - are improved. Levodopa dosage may be reduced by 50%. The effect seems persistent and does not fade away with time. Improvement ranged, on the basis of the UPDRS scale, from <25% to 75%. There was only one case of complete failure. Quality of life is markedly improved in patients who were absolutely incapable of walking and unable arise out of chair. After stimulation they could walk, even if assistance was necessary. Improvement was observed also in those with disabling motor fluctuation and dyskinesias which could be abolished.
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PMID:Extradural motor cortex stimulation (EMCS) for Parkinson's disease. History and first results by the study group of the Italian neurosurgical society. 1598 39


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