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)

Tremor can be categorized into three general types: resting, action, and intention, Each requires different therapy. Resting tremor is present when the hands are at rest; it disappears with movement. It is characteristic of Parkinson's disease and responds to treatment with L-dopa either alone or in combination with a decarboxylase inhibitor. Action tremor is maximal when the hands are outstretched to the front; it may persist during movement. It is not rare and is often misread as a sign of Parkinson's disease. Propranolol is beneficial. Intention tremor occurs with movement and is characteristic of cerebellar disease. Pharmacologic agents are not helpful. The only known effective treatment is stereotaxic surgery.
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PMID:The shaking patient. Diagnosis and management of tremor. 83 91

We describe the clinical features of parkinsonism in 25 patients whose age of onset was under 40 years. Among them, 17 patients, whose age of onset was after their 21st birthday, were classified as young onset Parkinson's disease (YOPD), and the remaining 8 whose age of onset was before their 21st birthday were classified as juvenile parkinsonism (JP). Rigidity and akinesia were revealed in all 25 patients. Resting tremor was observed in only 5 patients; 3 in the YOPD group and 2 in the JP group. There were 8 of the 25 patients (32%) who experienced an aching sensation in the leg before or at the onset of the parkinsonian features. In 6 of these 8 cases, the sensory symptoms were on the same side where the clinical manifestations of parkinsonism later developed. In the JP group, 2 patients had right foot dystonia, which improved with levodopa. Diurnal fluctuations in parkinsonian symptoms were found in 9 of the 25 cases. The familial incidence of parkinsonism was higher in the JP group. The parkinsonian disabilities in all 25 cases responded dramatically to levodopa therapy. Unfortunately, 10 cases, 5 in the YOPD group and 5 in the JP group, developed dyskinesia. The longer they took levodopa, the greater the chance of developing dyskinesia. The cumulative percentage of dyskinesia was 100% in the YOPD group and 83% in the JP group by the seventh and fourth year of treatment, respectively. A positive correlation was found between the prevalence of dyskinesia and the duration of treatment in both groups.
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PMID:Early onset parkinsonism in Chinese. 168 78

Dementia and extrapyramidal signs combine in both Alzheimer's disease (AD) and Parkinson's disease (PD) to produce various degrees of clinical overlap between the two diseases. Rest tremor, positive motor response to dopaminergic drugs, bradyphrenia and disproportionate deficits in visuospatial function, dating capacity, recency discrimination, sequencing and set-shifting are specific features of PD; myoclonus, orofacial dyskinesia, aphasia and rapidly progressive global dementia favours AD. A clearer analysis of the underlying brain-behaviour relationships is necessary to advance our understanding of the origin of cognitive and motor impairment and its treatment.
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PMID:Clinical similarities and differences between Alzheimer's disease and Parkinson's disease. 331 3

Premortem diagnosis of diffuse Lewy body disease (DLBD) is difficult, and knowledge of the parkinsonian features of DLBD might facilitate the diagnosis. In this study, we compared the parkinsonian syndrome of DLBD and Parkinson's disease (PD). We retrospectively reviewed the charts of Columbia-Presbyterian Medical Center (CPMC) Brain Bank cases (1989-1993) with pathologically diagnosed DLBD or PD, and the literature on the parkinsonian features in DLBD patients presenting with parkinsonism. Parkinsonism accompanied or preceded cognitive/psychiatric changes in most CPMC cases (DLBD 100%, PD 88%). DLBD had an earlier mean age of onset than PD did (57 versus 64 years), a similar male:female ratio (1.7:1 versus 1.9:1), and similar mean disease duration (12-13 years). Cognitive/psychiatric changes were less frequent in PD than in DLBD (65 versus 100%) (p = 0.025). Rest tremor was specifically mentioned in 29% of DLBD versus 56% of PD (p = 0.10). Bradykinesia was less common in PD (56% versus 86%) (p = 0.05). All those with PD responded to L-Dopa, as did all those with DLBD who received L-Dopa. In conclusion, there are subtle differences between PD and DLBD in age of onset, frequency of cognitive/psychiatric changes, bradykinesia, and rest tremor. However, even when taken together, these cannot be used to distinguish these entities.
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PMID:Parkinsonian features of eight pathologically diagnosed cases of diffuse Lewy body disease. 775 61

Resting tremor is one of the characteristic features of Parkinson's disease. However, there are a number of patients who typically have resting tremor alone for at least 5 years without development of other parkinsonian signs or symptoms. The etiology of an isolated resting tremor is still obscure. Recently, positron emission tomography was used to study these patients with isolated resting tremor, and demonstrated a markedly decreased striatal uptake of fluoro-dopa to the range of Parkinson's disease. These findings suggested the existence of a separate subtype, namely, tremulous Parkinson's disease with a manifestation of resting tremor alone. In order to confirm the existence of this subgroup of tremulous Parkinson's disease and further investigate its morphological changes and the usefulness of magnetic resonance imaging, we collected 5 patients who typically have resting tremor for at least 8 years in the absence of other features of Parkinson's disease. MRI was performed and the results of the images showed typical findings of Parkinson's disease with smudging or decreased distance between substantia nigra and red nucleus. Quantitative analysis also demonstrated a significant decrease of the above-noted distance when the resting tremor group was compared to the essential tremor group. Therefore, patients with an isolated resting tremor can have morphological abnormalities in addition to functional disturbances shown by positron emission tomography. To our knowledge, this is the first paper to report that resting tremor is a variant of Parkinson's disease rather than essential tremor, by using a double-blind method, with magnetic resonance imaging to support.
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PMID:Resting tremor only: a variant of Parkinson's disease or of essential tremor. 858 89

The object of the present study was to evaluate the hand tremor occurring under various conditions in 81 patients with Parkinson's disease (PD) and to statistically analyze their relation to clinical rating items. We found that resting and action tremor have to be separated, whereas postural tremor can be related to either one of them. Resting tremor does not correlate with disability items or performance items except for an item rating social handicaps. Action tremor shows some influence on performance items. Current rating scales of PD represent a valid measure of resting tremor but are less valid for the measurement of action tremor.
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PMID:Tremors in Parkinson's disease: symptom analysis and rating. 931 77

Parkinson's disease (PD) is characterized by progressive neuronal loss associated with Lewy bodies in many subcortical nuclei leading to multiple biochemical and pathophysiological changes of clinical relevance. Loss of nigral neurons causing striatal dopamine deficiency is related to both the duration and clinical stages (severity) of the disease. The clinical subtypes of PD have different morphological lesion patterns: a) The akinetic-rigid type shows more severe cell loss in the ventrolateral part of substantia nigra zona compacta (SNZC) that projects to the dorsal putamen than the medial part projecting to caudate nucleus and anterior putamen, with negative correlation between SNZC cell counts, severity of akinesia-rigidity, and dopamine loss in the posterior putamen. Reduced dopaminergic input causes overactivity of the GABA ergic inhibitory striatal neurons projecting via the "indirect loop" to SN zona reticulata (SNZR) and medial pallidum (GPI) leading to inhibition of the glutamatergic thalamo-cortical motor loop and reduced cortical activation. b) The tremor-dominant type shows more severe neuron loss in medial than in lateral SNZC and damage to the retrorubral field A8 containing only few tyrosine hydroxylase and dopamine transporter immunoreactive (IR) neurons but mainly calretinin-IR cells. A8 that is rather preserved in rigid-akinetic PD (protective role of calcium-binding protein?) projects to the matrix of dorsolateral striatum and ventromedial thalamus. Together with area A10 it influences the strial efflux via SNZR to thalamus and from there to prefrontal cortex. Rest tremor in PD is associated with increased metabolism in the thalamus, subthalamus, pons, and premotor-cortical network suggesting an increased functional activity of thalamo-motor projections. In essential tremor, no significant pathomorphological changes but overactivity of cerebello-thalamic loop have been observed. c) In the akinetic-rigid forms of multisystem atrophy, degeneration is more severe in the lateral SNZC with severe loss of calbindin-IR cells reflecting initial degeneration of the striatal matrix in the caudal putamen with transsynaptic degeneration of striatonigral efferences that remain intact in PD. This fact and loss of striatal D2 receptors--as in advanced stages of PD--are reasons for negative response to L-dopa substitution. These data suggest different pathophysiological mechanisms of the clinical subtypes of PD that have important therapeutic implications. d) Involvement of extranigral structures in PD includes the mesocortical dopaminergic system, the noradrenergic locus coeruleus, dorsal vagal nucleus and medullary nuclei, serotonergic dorsal raphe, nucleus basalis of Meynert and other cholinergic brainstem nuclei, e.g. Westphal-Edinger nucleus (controlling pupillomotor function), posterolateral hypothalamus and the limbic system, e.g. amygdaloid nucleus, part of hippocampal formation, limbic thalamic nuclei with prefrontal projections, etc. Damage to multiple neuronal systems by the progressing degenerative process causing complex biochemical changes may explain the variable clinical picture of PD including vegetative, behavioural and cognitive dysfunctions, depression, pharmacotoxic psychoses, etc. Future comparative clinico-morphological and pathobiochemical studies will further elucidate the pathophysiological basis of specific clinical symptoms of PD and related disorders providing a broader basis for effective treatment strategies. Parkinson's disease (PD) is characterized by progressive degeneration of the nigrostriatal dopaminergic system and other subcortical neuronal systems leading to striatal dopamine deficiency and other biochemical deficits related to the variable clinical signs and symptoms of the disorder. (ABSTRACT TRUNCATED)
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PMID:Post mortem studies in Parkinson's disease--is it possible to detect brain areas for specific symptoms? 1037 Sep 1

The manner in which characteristics of time series in the frequency domain can enhance discrimination between physiologic and parkinsonian tremor when tremor amplitude is low was examined. Rest tremor and postural tremor with and without visual feedback were recorded twice in the two hands of a group of patients with Parkinson's disease (PD) (n = 21) and a group of healthy control subjects (n = 30) using displacement laser systems. Recordings were analyzed quantitatively using amplitude and seven frequency domain characteristics. Postural tremor with no visual feedback allowed the most efficient discrimination between the two groups of subjects especially in velocity and acceleration (derived from displacement) and allowed identification of more patients with PD as separate from the range observed in the control group. Moreover, the frequency domain characteristics that were investigated identified the majority of the patients even when amplitude did not. After eliminating redundant (correlated) characteristics, it was found that the frequency composition of tremor in PD can be described adequately with four characteristics, which are the most reliable, independent, and discriminative elements for detecting early or subtle modifications in tremor. Also, a series of finger flexions was found to enhance physiologic tremor but not tremor in PD. Discrimination of low-amplitude tremor in PD from normal physiologic tremor is enhanced by examining the median frequency of oscillations, the concentration of power in the power spectrum, and the distribution of power in particular ranges. Tremor measurement should not be limited to acceleration data as some information is more visible in velocity time series.
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PMID:Using frequency domain characteristics to discriminate physiologic and parkinsonian tremors. 1057 31

Tremor is defined as rhythmic oscillatory activity of body parts. Four physiological basic mechanisms for such oscillatory activity have been described: mechanical oscillations; oscillations based on reflexes; oscillations due to central neuronal pacemakers; and oscillations because of disturbed feedforward or feedback loops. New methodological approaches with animal models, positron emission tomography, and mathematical analysis of electromyographic and electroencephalographic signals have provided new insights into the mechanisms underlying specific forms of tremor. Physiological tremor is due to mechanical and central components. Psychogenic tremor is considered to depend on a clonus mechanism and is thus believed to be mediated by reflex mechanisms. Symptomatic palatal tremor is most likely due to rhythmic activity of the inferior olive, and there is much evidence that essential tremor is also generated within the olivocerebellar circuits. Orthostatic tremor is likely to originate in hitherto unidentified brainstem nuclei. Rest tremor of Parkinson's disease is probably generated in the basal ganglia loop, and dystonic tremor may also originate within the basal ganglia. Cerebellar tremor is at least in part caused by a disturbance of the cerebellar feedforward control of voluntary movements, and Holmes' tremor is due to the combination of the mechanisms producing parkinsonian and cerebellar tremor. Neuropathic tremor is believed to be caused by abnormally functioning reflex pathways and a wide variety of causes underlies toxic and drug-induced tremors. The understanding of the pathophysiology of tremor has made significant progress but many hypotheses are not yet based on sufficient data. Modern neurology needs to develop and test such hypotheses, because this is the only way to develop rational medical and surgical therapies.
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PMID:The pathophysiology of tremor. 1136 Feb 55

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


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