Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 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

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

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

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

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

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

There is a renewed interest in basal ganglia surgery for improvement of motor symptoms in cerebral palsy. Rigidity, choreoathetosis, and tremor can be improved or abolished by a well-placed radiofrequency lesion, either in the ventrolateral nucleus of the thalamus or ventroposterior pallidum. The target is chosen based on the predominance of the symptoms in a given patient. A review of the main reports on surgery of the basal ganglia for cerebral palsy, as well as the author's data, shows that the surgery can have a remarkable impact on patients' quality of life when motor dysfunction is improved. An update of the physiopathology of cerebral palsy motor symptoms related to anatomic findings on experimental work, magnetic resonance imaging, and autopsy is used to rationalize surgery of the basal ganglia. Modern stereotactic technique based on exquisite demonstration of the basal ganglia anatomy by magnetic resonance imaging is described and supported by intraoperative electricophysiologic studies. The author stresses the importance of a multidisciplinary approach to provide the cerebral palsy patient with a comprehensive treatment plan before stereotactic surgery.
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PMID:Role of stereotaxis in the treatment of cerebral palsy. 895 61

Rigidity, tremor, akinesia and disorder of postural reflex are the main clinical features of Parkinson's disease. We presented the mechanism underlying rigidity and assessed central motor conduction time (CMCT) using magnetic, with or without vibratory, stimulations. Basal ganglia, especially, the internal pallidum, and the thalamus play major roles in the mechanism of rigidity in Parkinson's disease. Hyperexcitability of the spinal motor nucleus due to low threshold has been recognized. Magnetic stimulation is painless and is simpler than electric stimulation. Therefore, this method is used clinically for evaluating conduction disturbance of the upper motor neurons in multiple sclerosis, cerebrovascular disease and so on. CMCT measured by magnetic and/or electric stimulation may be abbreviated or normal in Parkinson's disease, according to the literature, though controversy persists in this regard. In our study, CMCT was normal in Parkinson patients. However, CMCT was reduced in patients with rigidity and tremor. Furthermore, in a portion of the patients, CMCT was further abbreviated by also applying vibratory stimulation. These observations support the hypothesis that cells in the thalamus, cortex and spinal cord and/or pathways in these portions of the central nervous system are excitable or activated in Parkinson patients with rigidity and tremor. However, elucidation of the mechanisms underlying rigidity and tremor awaits further investigation.
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PMID:[Central motor conduction time using magnetic and vibratory stimulation in Parkinson's disease, especially in patients with rigidity]. 901 45

From September 1994 to June 1995, eight patients with intractable parkinsonism underwent gamma thalamotomy in our hospital. All of these patients were male, with an average age of 59.3 years. The duration of the disease from initial diagnosis was 2-10 years (mean 6.8 years). All had failed or had serious side effects with antiparkinsonian medicine. Seven cases had tremor-dominant symptoms, while the other had mainly rigidity. Six cases had bilateral symptoms. Computed tomography or magnetic resonance imaging (MRI) was undertaken prior to treatment in all cases to exclude focal brain lesions. Stereotactic MRI was taken with the Leksell frame in place and both T1- and T2-weighted images were obtained. The targets were located in the area of Vim/Voa/Vop based on the Schaltenbrand atlas. In seven cases, two plugged 4-mm-collimator shots were used. The maximum dose was 160 Gy in six cases and 180 Gy in one case. In another case, a single 4-mm-collimator shot was used, and a maximum dose of 160 Gy was delivered to the target center. The border of the internal capsule was outside the 20-30% isodose line. We intended the 50% isodose line to have an oval-shaped region with the use of two shots and should correspond to the shape of Vim. Follow-up data were available for six patients (mean: 4.5 months, range: 2-9 months). Tremor disappeared in three cases and improved in the other three. In one of these six cases, the tremor disappeared just 3 days after gamma thalamotomy. Rigidity improved in four of these six cases. In only one patient, treated with a maximum dose of 180 Gy, was there any contralateral limb weakness, which developed 3 months after treatment and has been recovering gradually. Follow-up MRI T2-weighted images in this case showed that the diameter of the lesion was larger than intended and there was a region of diffuse edema in the thalamus and upper brain stem. No other complications occurred in this series.
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PMID:Stereotactic Gamma thalamotomy for the treatment of parkinsonism. 903 76


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