Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A regional technique for the study of curare sensitivity has been applied to patients with Duchenne type muscular dystrophy, myotonic disorders, certain lower motor neurone disorders, to patients with weakness in the arm after hemiplegia, to patients with hyper-reflexia and hypertonia without weakness, and to Parkinsonism. In the dystrophy patients, sensitivity to curare differs from normal controls in that the neuromuscular block persists. The possibilities that this latent defect of neuromuscular transmission is the result of acetylcholine deficiency due to a prejunctional defect or the result of alterations in the property of the postjunctional membrane are discussed. In the myotonic and lower motor neurone disorders, curare sensitivity was similar to that of normal controls. After hemiplegia, the affected side shows resistance to curare when compared with the unaffected side. In states of hyper-reflexia and hypertonia, however, the sensitivity to curare is greater than in normal controls. In Parkinsonism, sensitivity is similar to that of the controls. The results in upper motor neurone lesions are discussed in relation to the dependence of neuromuscular transmission upon the motor neurone, which, in turn, is dependent upon descending impulses.
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PMID:Study of sensitivity to curare in certain neurological disorders using a regional technique. 16 92

Toxic metals encountered industrially or environmentally may produce the following syndromes: 1) Peripheral neuropathy: which is mainly sensory in arsenic and entirely motor with inorganic lead, organophosphorus compounds and tallium produce a mixed form of peripheral neuropathy. 2) Encephalopathy: usually with lead poisoning where ataxia and hemiplegia or optic atrophy may occur. 3) Optic neuritis: transient or permanent impairment of vision in arsenic poisoning and blurring of vision followed by field fedects with thallium poisoning. 4) Cerebellar disturbances: in the form of ataxia in organic mercury. 5) Parkinsonism: extrapyramidal signs occurs in manganese poisoning shown as mask face and rigidity of muscles. 6) Mental changes: as acute psychosis in organic lead and erethism in organic mercury.
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PMID:Neurological syndromes produced by some toxic metals encountered industrially or environmentally. 35 38

The 159 patients with Parkinson's disease with onset after the age of 50 (mean: 62.3 years) were studied with reference to diagnosis and treatment. The results were as follows: 1. Other than the characteristic features, the symptoms at onset were depression (6% of the patients), lumbago (4%), hemiplegia-like (4%) and dizziness (3%), causing misdiagnoses in some of the patients. Among 159 patients studied, the severity most frequent was Yahr stage 3 (63%) at first examination, indicating the necessity of earlier diagnosis. 2. Magnetic resonance imaging (MRI) of the substantia nigra and striatum was investigated using a 1.5 Tesla field and T2-weighted images, which gave no specific results concerning diagnosis and severity. However, it was useful in differential diagnosis between this disease and parkinsonism caused by multiple system atrophy and cerebrovascular diseases. 3. With 123I-IMP SPECT, decrease in blood flow in the frontal and temporal lobes correlated with the severity (Yahr stage) of the disease. Regarding cognitive functions the scores of Hasegawa's Dementia Scale and Mini-Mental State showed a highly significant correlation with the amount of blood flow in frontal and parietal lobes, suggesting that dementia might be caused by dysfunction of these lobes. 4. In 98 patients treated with levodopa mixed with dopa-economizers for more than a year, the maximum improvement was small in severely disabled patients of Yahr stage 5 and 4 because none improved to stage 3A or below (3A is an arbitrary criterion meaning mild involvement in stage 3 with 3P meaning more severe cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis and treatment of Parkinson's disease in the elderly]. 187 Feb 74

The recruitment pattern of single motor units (SMUs) was studied in the early (R1) and late (R2) blink reflex components in normal subjects (15), patients with parkinsonism (10) and with hemiplegia due to hemispheral lesions (5). Reflexes were evoked by constant current stimuli applied to the supraorbital nerve. SMU discharges were recorded in the preseptal part of the lower eyelid using a bipolar needle electrode. Thresholds of R1 and R2, latencies at the thresholds and the number of discharges in R2 were determined. In parkinsonism, the recruitment of SMUs in R1 was impaired, suggesting that the malfunction of the basal ganglia in this disorder is associated with a reduced excitability of neurons in the pontine brain-stem. In hemiplegia, the recruitment in both R1 and R2 could be impaired. The orderly function of neurones in the pontine and medullary pathways of these components appears to require facilitatory hemispheral influences. Signs of disinhibition occasionally found in R1 may point to an imbalance between facilitatory and inhibitory hemispheral influences upon the pontine pathway.
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PMID:Changes in the recruitment pattern of single motor units in the blink reflex of patients with parkinsonism and hemiplegia. 240 58

As a tool for the study of normal and pathological motor manifestations, the experimental models of motor alterations are discussed. Here, we present particularly the neural and ethological characteristics of experimental models as hemiplegia, akinesia, parkinsonism and epilepsy.
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PMID:[Neural and ethological relations in the evaluation of motor control changes. II. Experimental models]. 268 7

Diagnosis of brucella meningitis was made in 10 patients by serological tests on blood and cerebrospinal fluid using Rose Bengal, standard agglutination, indirect immunofluorescent and enzyme-linked immunosorbent assay (ELISA) tests and by blood and CSF culture. All patients had significantly elevated antibody titres. In three Br. melitensis was isolated both from blood and CSF and in a further three from blood only. Eight patients were 30 years old or less and seven were female. Seven patients had a history of contact with livestock and had consumed raw milk. Meningitis occurred in five, meningoencephalitis with hemiplegia in one, paraplegia and cranial nerve palsies in one and psychosis and/or nightmares in three. Transient Parkinsonism was seen in one patient and generalized rigidity and non-Parkinsonian tremors in another. Computerized tomography revealed ventricular dilation in one patient and punctate hyperdense, non-enhancing shadows in the lentiform nuclei in two others. Treatment with a combination of tetracycline, rifampicin and streptomycin was successful.
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PMID:Brucella meningitis: presentation, diagnosis and treatment--a prospective study of ten cases. 362 3

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54

Surgical treatment for Parkinson's disease began by blocking of the pyramidal system in early part of this era. In 1942, Meyers performed Ansotomy for the treatment of Parkinsonism without leaving hemiplegia, leading subsequent operating target to blocking of pallidofugal fiber. Then, the development of stereotaxy in 1947 caused an operative progress to Pallidotomy and further to Thalamotomy. Although the spread of levodopa therapy gradually brought about decline of surgical treatment, Thalamotomy became to be reexamined in view of not a little problems about and side effects of levodopa therapy. With the development of CT, MRI and the like, Thalamotomy via MRI-stereotaxy was developed, making operations safer and surer. Besides, transplantation of dopamine neurons into the striatum was tried as an essential treatment and is in clinical application via animal experiments. Fetal ventral mesencephalic tissue and adrenal medullary tissue are available therefore, but demerits are such that the former poses some ethical problem and the latter is poor and short-lived response. The transplantation of stellate ganglion into the striatum, which we have recently developed is safe and more effective than the adrenal medullary tissue. The respective one thirds of the cases did without levodopa following transplantation, needed half as much as the preoperative levodopa dose and needed the same as the latter. Although Horner's syndrome was noted in all cases following transplantation, no Parkinson syndrome became aggravated in any one of the cases.
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PMID:[Surgical treatment of Parkinson's disease]. 827 75

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

At present, there are three major surgical approaches to Parkinson's disease (PD): (1) Ablative surgery (i.e. pallidotomy, thalamotomy); (2) deep brain stimulation (DBS) of the thalamus, internal globus pallidus (GPi) and subthalamic nucleus (STN); and (3) grafting fetal mesencephalic cells into the striatum. As a result of increasing understanding of the pathophysiology of the basal ganglia and the demonstration of surgical alleviation of experimental parkinsonism, surgery has regained a paramount importance in the management of PD. The aim of pallidotomy and DBS is to reduce the excessive inhibitory output from the GPi and substantia nigra reticulata (SNr). Pallidotomy and DBS of the STN or GPi aim to reverse the pathophysiological consequences of dopamine deficiency in PD, and should be considered entirely symptomatic treatments. The ideal candidates for pallidotomy are young patients in good general health in whom dyskinesias are the main reasons for disability. Patients with severe bilateral problems uncontrollable with present pharmacological tools are candidates for DBS. As yet, there are no formal data to help decide how to choose between GPi and STN stimulation. In our practice, patients are allocated to GPi stimulation when 'on' dyskinesias are extremely severe. In most other instances, we prefer to perform STN stimulation. At present there is almost no reason to decide for the thalamic stimulation since tremor is equally arrested by STN stimulation, which in addition improves all other features of PD. Equally the only indication for thalamotomy would be a patient with long-standing tremor as the main clinical manifestation, which can not be controlled with drugs. The proportion of patients in whom the thalamus will be the preferable target for either DBS or thalamotomy is small (less than 5%). Grafting aims to repair the nigrostriatal pathway and restore dopaminergic function in the striatum. In the future implants containing not only dopaminergic cells but also growth factors and a variety of other substances could become a method to not only functionally compensate the biochemical abnormalities of PD but also to arrest its progression. This technique is limited to a few centres around the world owing to the technical, logistical and ethical problems of obtaining and handling embryonic cells. At present, grafting of dopaminergic cells is perhaps best suited for patients with young-onset PD (less than 45 years old) who are at high risk of developing complications within a short time of beginning pharmacological treatment and in whom the idea of making lesions or implanting electrodes into the brain for decades seems less appealing. Consideration of surgery in any given patient should be weighed against the risks (about 1% mortality and 2-6% of severe morbidity-hemiplegia, cognitive deficit, speech problems, etc.) associated with these techniques. The development of better imaging methods and the growing expertise of multidisciplinary teams will undoubtedly make surgery for PD safer and more effective in the future.
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PMID:Surgical treatment of Parkinson's disease. 942 72


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