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)

Parkinson's disease can present as a progressive hemiparesis without tremor. The presence of mild cogwheel rigidity in a hemiparetic patient may suggest the diagnosis, as may the normal findings on brain scan and electroencephalogram in a patient with gradually evolving hemiparesis. The response to appropriate medication has been prompt and excellent. It is important that Parkinson's disease be considered in the differential diagnosis of a progressively evolving hemiparesis.
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PMID:A pseudohemipharetic form of Parkinson's disease. 7 43

The two-compartment pharmacokinetics of theophylline in ten hospitalized elderly patients with apparently normal renal, hepatic and cardiopulmonary functions was investigated after intravenous administration of the drug. Nine patients suffered from slight hemiparesis and one from Parkinson's disease. Biological theophylline half-lives of 5.4--9.0 hours and plasma clearence values of 28--42 ml kg-1hr-1 were found. The apparent volumes of distribution during the beta-phase, Vdbeta, were 0.33--0.43 1 kg-1. It is concluded that a therapeutic concentration of about 10 microgram theophylline per ml serum could be established in the investigated group of elderly patients following an intravenous initial loading dose of 3.7 mg theophylline per kg followed by a continuous infusion of 0.35 mg per kg body weight per hour. In the therapeutic use of theophylline monitoring of the serum theophylline concentration is generally advised because of the elsewhere reported variability in the biological half-life of the compound.
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PMID:Pharmacokinetics of theophylline in ten elderly patients. 58 Mar 50

In recent muscle metabolic studies, patients with moderate upper motor neuron lesions showed marked difficulty in performing an equal submaximal work load (bilaterally) in two-legged exercise. For a better evaluation of these patients, studies were performed on each leg separately. Six patients with Parkinson's disease and six with moderate hemiparesis were studied. During one-legged submaximal and maximal exercise heart rate, oxygen uptake, and blood lactate were determined. Maximal voluntary contraction in knee and ankle flexion and extension for each leg was measured. Succinate dehydrogenase (SDH) activity in the thigh muscles was determined. During submaximal exercise, oxygen uptake, heart rate and blood lactate increased more in the paretic leg of hemiparetic patients and in the more affected leg of the Parkinson patients. In hemiparetic patients maximal voluntary contraction of flexors and extensors of the knee was significantly reduced in the paretic leg but was reduced even in the nonparetic knee flexors. SDH activity was very low in both legs in all patients and lowest in the paretic and more affected leg, respectively. It is concluded that (a) the general muscle inactivity per se, secondary to the neurological disorder, may lead to a reduced work capacity; (b) the increased heart rate and blood lactate level seem to be correlated to the relative exercise level of each leg; and (c) in patients with impaired muscle function of one or both legs, evaluation of each leg separately with regard to work capacity and muscle metabolism is of value.
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PMID:Work capacity, muscle strength and SDH activity in both legs of hemiparetic patients and patients with Parkinson's disease. 119 56

Between 1985 and 1990, the authors performed stereotactic posteroventral pallidotomies on 38 patients with Parkinson's disease whose main complaint was hypokinesia. Upon re-examination 2 to 71 months after surgery (mean 28 months), complete or almost complete relief of rigidity and hypokinesia was observed in 92% of the patients. Of the 32 patients who before surgery also suffered from tremor, 26 (81%) had complete or almost complete relief of tremor. The L-dopa-induced dyskinesias and muscle pain had greatly improved or disappeared in most patients, and gait and speech volume also showed remarkable improvement. Complications were observed in seven patients: six had a permanent partial homonymous hemianopsia (one also had transient dysphasia and facial weakness) and one developed transitory hemiparesis 1 week after pallidotomy. The results presented here confirm the 1960 findings of Svennilson, et al., that parkinsonian tremor, rigidity, and hypokinesia can be effectively abolished by posteroventral pallidotomy, an approach developed in 1956 and 1957 by Lars Leksell. The positive effect of posteroventral pallidotomy is believed to be based on the interruption of some striopallidal or subthalamopallidal pathways, which results in disinhibition of medial pallidal activity necessary for movement control.
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PMID:Leksell's posteroventral pallidotomy in the treatment of Parkinson's disease. 150 2

Between 1986 and 1988 a door-to-door survey was conducted on a stable rural population of 60,820 in central Ethiopia. Trained lay health workers made a complete census and identified cases with symptoms and signs of neurological disorders, using specially designed questionnaires which, in a previous pilot study, were found to have a sensitivity of 91% and specificity of 85%. Neurological disorders in the rural population were epilepsy, postpoliomyelitis paralysis, mental retardation, peripheral neuropathy (mainly due to leprosy), and deaf-mutism with prevalence rates (cases/100,000 population) of 520, 240, 170, 150 and 130, respectively. The prevalence rates of the other less common neurological disorders were 62 for hemiparesis (15 of which were for cerebrovascular accidents), 20 for cerebral palsy, 16 for optic atrophy, 12 for perceptive deafness, 10 for tropical spastic paraparesis, 7 for Parkinson's disease and 5 for motor neuron disease, ataxia and chorea/athetosis. Among related non-neurological conditions, blindness, locomotor disability and deafness were predominant. The significance and role of such a neuroepidemiological study in laying the strategies for the prevention of neurological disorders and rehabilitation of patients are discussed in the context of a developing country.
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PMID:Community-based study of neurological disorders in rural central Ethiopia. 208 51

The reflex responses in the abductor pollicis brevis muscle were examined in 22 patients with mild central hemiparesis and in nine patients with Parkinson's disease. In the group of patients with central hemiparesis there were 15 subjects with a spastic and seven subjects with a flaccid type of affection. The reflex responses in the abductor pollicis brevis muscle were evoked during isometric contraction. The recorded muscular potentials were unidirectionally rectified and averaged. The reflex responses were then identified as excitatory and inhibitory modulations of basal activity of the muscle after the evoking stimulus. The reflexes were evoked by percussion with a hammer on the lateral area of the base of the distal digit of the thumb, by electrical stimulation of the median nerve on the wrist and by electric stimulation of the cushion of the thumb and the superficial radial nerve on both sides. On the side of the spastic or flaccid central hemiparesis the long-latency parts of the reflex responses after percussion on the distal digit of the thumb and after electrical stimulation of the median nerve were either not elicitable or had a lower amplitude than on the non-paretic extremity. In three subjects on the affected side also the of long-latency part of the reflex response was prolonged after percussion of the distal digit of the thumb. The short-latency parts of the reflex response on the side of the spastic hemiparesis were more expressed, contrary to the finding on the side with the flaccid hemiparesis where suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Reflex reaction in the abductor pollicis brevis muscle after mechanical and electrical stimulation in patients with central hemiparesis and Parkinsonism. Electromyographic study]. 279 Oct 67

Twenty-eight cases of mirror writing were seen during a period of three and a half years. These consisted of 12 patients with essential tremor, nine with Parkinson's disease, three with spino-cerebellar degeneration and four other cases. There were no cases of hemiparesis, aphasia, apraxia, agnosia or confusion. Fragmentary reversals were excluded from this study. Since essential tremor, Parkinsonian tremor and cerebellar tremor can be abolished by a stereotaxic produce applied to the thalamus, a common neural pathway via the thalamic nuclei may exist in these disorders. The existence is therefore proposed of some neural mechanism that controls the higher cerebral function of writing via the thalamus.
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PMID:The aetiology of mirror writing: a new hypothesis. 343 91

In 58 patients with progressive supranuclear palsy (PSP), 19 (32.8%) had CT, MRI, or autopsy evidence of a multi-infarct (MI) state. The clinical findings in the infarct syndrome were similar to idiopathic PSP. Five MI-PSP patients had had a stroke, four had focal dystonia, two had hemiparesis, and one had an intention tremor of recent onset. In contrast, only 5.9% (12.9% of those with CT or MRI) of 426 Parkinson's disease patients had evidence of strokes. One case of PSP studied pathologically was attributed to cerebral amyloid angiopathy.
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PMID:Progressive supranuclear palsy and a multi-infarct state. 356 71

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64

Posteroventral pallidotomy (PVP) was carried out in 86 patients with Parkinson's disease, who presented marked bradykinesia, freezing of gait and postural defect associated with rigidity and tremor in 82 patients (bradykinesia type), and similar gait and postural problems with minimum signs of rigidity and tremor in 4 (pure akinesia type). The stereotactic coordinates of Leksell's device were calculated from MRI and conventional ventriculography. The final target was defined by microelectrode techniques in the basal ganglia. The microrecording study revealed a very high background activity in the internal pallidum in patients of the bradykinetic type, however, a much lower pallidal activity in patients of the pure akinesia type. Fifty-eight patients underwent unilateral PVP, and 28 underwent bilateral surgery. Following PVP, rigidity tremor and poor reciprocal movements were significantly improved especially in the contralateral extremities. The most dramatic findings were the reversal of akinetic symptoms and wearing-off phenomena. The patients were followed up for 3-30 months (mean = 8) after surgery. Of the 82 bradykinesia type patients, good result were obtained in 48 (58%), fair results in 26 (32%), and minor improvement or no change in 8 (10%). In all the 4 patients of the pure akinesia type, recurrence of the akinetic symptoms occurred after a temporal improvement lasting a few days to 3 month after surgery. There was worst dysarthria in 3 patients, hemiparesis in 1 and partial motor aphasia in 1. The visual field problem was not complicated in any patients. These findings suggest that akinetic symptoms in PD are implicated in overactive pallidal outputs with putative GABAergic modulator by excessively inhibiting pedunculopontine nucleus activity (midbrain locomotor and posture regions) as well as thalamic activity. Partial interruption of the pallidal efferents eliminates the akinetic symptoms by disinhibitory effects on the target structures. The pathology of PD of the pure akinesia type is supposedly in the brainstem and should be excluded from indication of pallidotomy.
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PMID:Surgical control of akinesia in Parkinson's disease. 879 Oct 23


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