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)

Patients with Parkinson's Disease display a number of orofacial manifestations. These manifestations are secondary to motor and sensory deficits, resulting in bradykinesia, muscle rigidity and tremor, and difficulties with speech, swallowing, proprioception, tactile sensitivity, and hard- and soft-tissue trauma. This case describes the use of a bruxism splint which benefited a PD patient by diminishing the occurrence of orofacial pain secondary to muscle tremor and rigidity while reducing the cumulative damage to the oral structures common with the disease. The impact of therapy on sleep, speech, and swallowing difficulties is also discussed.
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PMID:Management of orofacial manifestations of Parkinson's disease with splint therapy: a case report. 830 10

The neural mechanism of parkinsonian motor symptoms, i.e., rigidity, tremor and akinesia, which are the result of nigrostriatal dopamine deficiency, is interpreted from long-term observations on the effect of surgical and pharmacological treatment of the disease in relation to the neuropathological findings within the substantia nigra zona compacta (SNc). Rigidity, tremor and secondary akinesia start first with degeneration of the ventral tier of the SNc followed by spread of the pathology to the dorsal tier, which may produce primary akinesia. Later, locus ceruleus pathology will be added. Spread of pathology is extremely slow in the juvenile or early onset parkinsonism (JP) compared with that in Parkinson's disease (PD). This spreading of pathology from one functional system to another might be one of the key factors responsible for the progressive worsening of the disease, which is different in speed between JP and PD.
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PMID:The neural mechanisms and progressive nature of symptoms of Parkinson's disease--based on clinical, neurophysiological and morphological studies. 861 10

Familial polyneuropathy mimicking Charcot-Marie-Tooth disease associated with parkinsonism and dementia has been reported in literature. We present with similar peroneal muscular atrophy, rigidity of upper extremities, severe peripheral neuropathy, mental retardation and diabetes mellitus. The patient, a 42-year-old man, developed progressive muscle weakness, mental retardation and difficulty in walking in childhood. Because of his pes cavus, he had three surgical operations. At the age of 20 years, he developed distal muscular atrophy of lower limbs. On neurological examination, all limb muscles were atrophic, especially in lower one third of the thigh. Rigidity was noted in the upper extremities. Deep tendon reflexes were hyperactive in the upper and diminished in the lower extremities. Muscle CT revealed low density areas in all the muscles examined, specially in the gastrocnemius and anterior tibial muscles. Needle EMG showed neurogenic change in the forearm, but not in the lower limbs, because of no voluntary contractions obtained due to severe muscle atrophy. Marked slowing of motor conduction velocity with muscle action potentials of very low amplitude was found in the ulnar nerve. Muscle action potentials were not elicited in the median and peroneal nerves. Sensory action potentials were not elicited from the median, ulnar and sural nerves. These findings were consistent with axonal polyneuropathy. In the sural nerve biopsy, the densities of myelinated fibers were markedly decreased. However, unmyelinated fiber densities were relatively preserved. Onion bulb formation was not found. This patient may be classified into hereditary motor-sensory neuropathy (HMSN) type II based on the clinical findings delayed nerve conduction velocities and axonal degeneration in the sural nerve. He has also diabetes mellitus. CT of the brain revealed nothing particular. He is one of members with familial Parkinson's disease (PD) developed in Sagamihara. Peroneal muscular atrophies are not necessarily associated with PD, though it has been occasionally complicated in various neuro-degenerative diseases including parkinsonism. We are now following the patient to detect the symptom of Parkinson's disease for early treatment.
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PMID:[An unusual case of peroneal muscular atrophy with rigidity, polyneuropathy, mental retardation, and diabetes mellitus developed in familial Parkinson's disease]. 866 30

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

Stereotactic operations have long been used to relieve agitation and muscle rigidity in Parkinson disease. Because of its high-density resolution, CT is quite effective to portray the location, size, shape and density of the thermocoagulative focus. The foci were classified into different types according to their changes in different time periods. Correlation with pathological changes was discussed.
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PMID:CT analysis of postoperative changes after thalamotomy for Parkinson's disease. 874

Twenty de novo patients with Parkinson's disease (Hoehn-Yahr stages I, II, III) were studied in a double blind trial after introducing (--)-deprenyl monotherapy. The parkinsonian symptoms were assessed by a novel graded clinical rating scale, by UPDRS and by the North Western self-rating scale. A significant change was observed in motor behaviour and daily activity (UPDRS) after 3 weeks of treatment with (--)-deprenyl at 10 mg/day. The total scores using UPDRS and the North Western ratings were changed significantly after 4 weeks. The greatest changes observed were in walking and in hypokinesia. Rigidity was not modified by (--)-deprenyl.
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PMID:Delayed development of symptomatic improvement by (--)-deprenyl in Parkinson's disease. 874 57

Pulmonary dysfunction was investigated in fifty-eight Parkinson's patients. Clinical disability was assessed by the Unified Parkinson's Disease Rating Scale. Pulmonary dysfunction was studied by spirometry with flow-volume loops, body plethysmography with lung volumes computation and maximal inspiratory and expiratory static mouth pressures. Forced vital capacity (FVC), forced expiratory volume in 1 min (FEV1), FEV1/FVC% and arterial PO2 and PCO2 were significantly below normal values. Residual volume (RV) and total rows were above normal values. Thirty-six had upper airway obstruction as judged by inspiratory flow peaks (PIF) < 3 l/s and FEV1/PEF (expiratory flow peak) > 8.5 l/min and MEF50/MIF50 > 1. Eighteen patients had a central (FEV1 < 80% and FEV1/FVC% < 80% of normal values) or peripheral (maximal expiratory flow between 75% and 25% of FVC and maximal expiratory flow after expiration of 50% below 70% of normal values) obstructive pattern. Sixteen patients had a restrictive dysfunction as judged by a total lung capacity < 85% or FVC < 80% with FEV1/FVC% > 80%. Sixteen patients had air trapping (RV > 120% and RV/TLC > 40%) and seven patients had lung insufflation (TLC > 120%). Rigidity, Rx signs of cervical arthrosis and limitations for passive movement of neck were higher in patients with central or peripheral airway obstruction. Bradykinesia and Rx signs of dorsal arthrosis was higher in patients with upper airway obstruction. Restrictive dysfunction was not related to tremor, rigidity or bradykinesia. The present data support the hypothesis that Parkinson patients present a high risk for pneumologic disturbances. These pulmonary dysfunctions are induced by the simultaneous action of a group of factors including the degree of bradykinesia or rigidity and the musculoskeletal limitations of vertebral column probably induced by chronic anomalous posture.
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PMID:Obstructive and restrictive pulmonary dysfunctions in Parkinson's disease. 879 Dec 48

Recent neuropathological findings define that 10-20% of the Parkinson patients belong to the atypical Parkinson's syndrome due to multi-system disease marked by typical Parkinsonian symptoms such as rigor, tremor and akinesia and early onset of severe autonomic, cerebellar or pyramidal disorders. Symptoms like postural hypotension, dysphagia, hypersalivation, urinary bladder dysfunction, thermodysregulation, abnormalities in eye movement, early falls or dementia etc. are frequently seen in these patients. In these patients dopamin depletion in the nigrostriatal pathway is combined with degeneration of other cerebral structures like olivopontocerebellar and intermediolateral columns. Patients need high dosages of L-dopa and other antiparkinsonian drugs with poor prognosis in general. First, we report on an atypical Parkinson patient who developed acute dyspnoea and muscle rigidity after general anaesthesia; second, on another patient who took a long time to recover from general anaesthesia. Both responded to antiparkinsonian drugs, the first to orally applied L-dopa, the second to intravenous amantadine. Most probably the interruption of the treatment with high dosages of L-dopa (in these patients given in 2-4 hours intervals) had caused these complications. The special nature of the anaesthesiological management of atypical Parkinson patients is reviewed.
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PMID:[Perioperative management of the patient with atypical Parkinson disease]. 886 35

Parkinson's disease, a chronic incurable disorder, has a significant impact on quality of life. Parkinson's disease results from chronic degeneration of cells in the basal ganglia that produce dopamine. It typically affects elderly individuals producing muscle rigidity and akinesia. Traditionally, Parkinson's disease has been controlled by medications. However, for some patients, medications may no longer be effective, or may produce drug-related complications. For this group of patients, pallidotomy is gaining support as an intervention to control the debilitating symptoms of Parkinson's disease, thus enabling a person to perform everyday tasks. Although the procedure was developed in the 1950s, contemporary technology has allowed a resurgence of the intervention. With the focus on relief of two of the major symptoms of Parkinson's disease, the pallidotomy procedure is gaining support as a surgical intervention for this disease. Therefore, it is important for the health care team to have an understanding of the disease process, surgical intervention and postoperative care to enhance quality outcomes for this patient population.
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PMID:Pallidotomy: a surgical intervention for control of Parkinson's disease. 888 May 95

We report a 43-year-old woman who died after 18 years history of parkinsonism. She was well until 25 years of the age (1976) when she noted a difficulty in stepping her feet. In the next year, she started to drag her feet. She was treated with levodopa with good response, however, she developed dyskinesia when she was 33 years of the age. She was evaluated in another hospital in 1984. She showed normal intelligence, normal ocular movement, masked face, small voice, small step gait, stooped posture, freezing of the gait, retropulsion, and cogwheel rigidity in limbs. No tremor or ataxia was noted. She received left ventrolateral thalamotomy at that time. Rigidity on the right side markedly reduced, however, she continued to show bradykinesia and motor fluctuations. On August 1 of 1994, she developed fever of 40 degrees C and dyspnea. On the next day, she expired from acute respiratory distress. She was able to walk unsupported until just before her last admission. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that this patient had Lewy body-positive young onset Parkinson's disease. Opinions were divided into two groups, i.e., young onset Lewy-body positive Parkinson's disease and Lewy-body negative young onset parkinsonism. Post-mortem examination revealed moderate loss of pigmented neurons in the substantia nigra more in the ventro-lateral part. Lewy bodies were found in the remaining neurons. Lewy bodies were more frequently seen in the locus coeruleus, although neuronal loss was less prominent in the locus coeruleus. The dorsal vagal motor nucleus showed moderate loss of neurons. Otherwise, the central nervous system was unremarkable. To our knowledge, this patient had the second youngest age of the onset so far reported in the literature for Lewy-body positive typical Parkinson's disease.
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PMID:[A 43-year-old woman with 18 years history of parkinsonism]. 892 38


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