Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 38 patients with Parkinson's syndrome Madopar preparation was used (L-dopa with peripheral decarboxylase inhibitor) in 33 cases as the main drug and in 5 cases as an addition to L-dopa. In the group of 33 patients 39 could complete the treatment, one patient died suddenly, three had the treatment withdrawn in view of side effects. The effectiveness of Madopar was assessed by means of five-rate scoring systems NUDS and ART. Clinical improvement was found in 22 cases (about 67%). The improvement included mainly bradykinesia and rigidity, while tremor was only slightly improved. Side effects developed in about 40% of patients and were slight and transient (apart from 3 cases). The main contraindications seem to be psychotic disturbances. In the group of 5 cases treated with Madopar as an additional drug in low doses improved the result of long-term treatment with L-dopa.
Neurol Neurochir Pol
PMID:[Treatment of parkinsonism with L-dopa and peripheral decarboxylase inhibitor]. 116 36

On the basis of observations of 18 patients the authors evaluated clinically the action of Sinement preparation (Merch, Sharp and Dohme) containing L-dopa 250 mg and carbidopa 25 mg in the treatment of Parkinson's disease. In the evaluation particular attention was given to side effects. Therapeutic results of Sinemet and L-dopa alone were compared in patients receiving these drugs alternatively. The observations of authors indicate that Sinemet gives the same therapeutic results as L-dopa, but in much lower doses and with less frequent side effects. Sinemet, similarly as L-dopa exerts the best effect on bradykinesia and muscular rigidity and less on tremor.
Neurol Neurochir Pol
PMID:[Comparison between results achieved by administering L-dopa and Sinemet in parkinsonism in the light of our records]. 118 52

Four patients with severe form of Parkinson's disease received transplantation of fetal dopaminergic cells into the caput of the caudate nucleus. The operation was done by an original method using a device designed specially for this purpose. In all cases the duration of the disease was 10 to 15 years, and the predominating signs were tremor, bradykinesia, and markedly pronounced side effects of the treatment (on-off syndrome and involuntary movements). One patients died 5 weeks after the operation. Autopsy demonstrated good survival of the transplanted cells with good integration with the brain of the recipient and traces of positive immunocytochemical reaction for tyrosine hydroxylase. In the other patients a significant clinical improvement was noted after the operation, with reduced intensity of parkinsonian symptomatology, shortening of the duration of the off phase, improved motor ability and reduced intensity of the involuntary movements. The longest follow-up was 24 months.
Neurol Neurochir Pol 1992
PMID:[Transplantation of fetal dopaminergic cells in Parkinson disease]. 140 86

Extrapyramidal signs were assessed in 112 patients satisfying NINCDS/ADRDA criteria for probable Alzheimer's disease. They were present in 50% of the patients. The most common features of them were bradykinesia and rigidity. Resting tremor was rarely encountered. There were no significant differences in age of onset, symptom duration, presence of primitive reflexes and psychotic symptoms between cases with and without extrapyramidal signs, while the presence of extrapyramidal signs was associated with statistically significant greater dementia severity.
Neurol Neurochir Pol
PMID:[Extrapyramidal signs in Alzheimer's disease]. 896 73

The pharmacological profile of the novel serotonin-dopamine antagonists (SDA)-type antipsychotic, perospirone, was compared with other SDA and typical antipsychotics, and a potential role of 5-HT2 and D2 receptor interaction in the atypical antipsychotic property of SDA was discussed based on the findings with selective 5-HT2 antagonists. Our study revealed that perospirone, like other SDA, differed from the typical antipsychotics by exhibiting 1) putative anxiolytic and/or antidepressant actions in some animal models (e.g., conditioned fear stress-induced freezing model and rat social interaction), 2) reduced extrapyramidal side effects (EPS) liability (catalepsy and bradykinesia induction), 3) weaker blocking actions at striatal D2 receptors as revealed by c-fos expression and dopamine turnover and 4) lower propensity to induce supersensitivity of dopamine receptors after repeated treatments (e.g., dopamine agonist-induced stereotyped behavior and vacuous chewing movement). The 5-HT2 antagonists mimicked the action of SDA antipsychotics in the animal models of mood disorder. In addition, combined treatments of 5-HT2 antagonists with typical antipsychotic could attenuate EPS induction and striatal c-fos expression associated with D2 receptor blockade, and could prevent the sensitization of D1 receptor function after repeated treatments. These findings suggest that the blockage of 5-HT2 receptors contributes to the broad efficacy profile of SDA (i.e., antipsychotic and mood stabilizing actions) and may counteract the D2 (and/or D1) blocking activities of antipsychotics in the striatum to reduce EPS.
Pol J Pharmacol 1997 Aug
PMID:Potential role of 5-HT2 and D2 receptor interaction in the atypical antipsychotic action of the novel succimide derivative, perospirone. 943 64

Degeneration of dopaminergic neurons that project from substantia nigra to striatum is the primary mechanism that causes Parkinson disease (PD). This death of dopaminergic cells disturbs control over impulses sent from the motor cortex and hence results in the presence of three cardinal motor signs: tremor, rigidity, bradykinesia. The cause of Parkinson disease is unknown. Current treatments relieve symptoms but do not halt the progression of the disease. It is not yet known what causes neurons to degenerate. Influences of aging, environmental toxins, genetic susceptibility have been pointed out by researchers, but the theory of oxidative stress seems to be the most convincing. It is supposed that SN neurons are exposed to oxidative reactions from dopamine metabolism (production) during which hydrogen peroxide and toxic semiquinones are formed. Additionally, in brains of PD patients there are decreased concentrations of defence mechanisms such as glutathion and compensatory ferritin that binds iron, maintaining it in its safe state (Fe2+ iron takes part in Fenton reaction that leads to free radicals production). However, we have to admit that Parkinson disease is probably multifactorial, and the combination of the above stated factors may cause the disease.
Neurol Neurochir Pol
PMID:[Factors which can play important role in pathogenesis of Parkinson disease]. 1061 5

Cortico-basal degeneration (CBD) or cortico-basal ganglionic degeneration is a condition characterised by selective cortical atrophy of parietal and in a lesser extent, frontal lobe associated with dysfunction of the basal ganglia. The clinical symptoms of CBD, predominantly extrapyramidal signs (bradykinesia and rigidity) and apraxia, affect often only one body side in the onset phase, with the left one being more frequent. Neuropathological studies reveal neuronal loss, gliosis, and achromasia chiefly in frontal and parietal cortex, as well as in basal ganglia and substantia nigra. Functional investigations, such as SPECT, disclose similar distribution of abnormalities (hypometabolism). The aetiology and causative treatment of CBD are unknown. The authors highlight the diagnostic difficulties in CBD including a necessity of a prolonged patient's observation in order to ascertain the differential diagnosis of other neurodegenerative disorders, in particular progressive supranuclear palsy, Alzheimer's disease and Parkinson's disease.
Neurol Neurochir Pol
PMID:[Cortico-basal degeneration]. 1084 10

The paper reports 4-years results of a pilot study concerning the influence of a stereotactic pallidotomy on somatosensory evoked potentials in idiopathic Parkinson's disease. Potentials were recorded through the scalp surface from sensorimotor cortex of both hemispheres. Amplitudes and latencies of early and late waves were compared before and after the surgery. The surgery was recommended after 4 years of L-dopa therapy when bradykinesia and rigidity of right leg led to gait difficulty and postural instability. The dominant features of the syndrome were accompanied by tremor, micrography, chorea and lower responsiveness to L-dopa. Following the surgery a clear improvement of motor activity was observed. Increase of 20-90 ms waves amplitudes and P45 latency prolongation of 6-11 ms appeared due to the attenuation of pallidal inhibition exerted upon the thalamo-cortical transmission and a new arrangement of a cortical motor program. These electrophysiological changes, correlated with a clinical amelioration, may indicate as a favourable prognosis for a patient. Five months after pallidotomy a slight decrease of amplitudes occurred in relation to the previous examinations. Four years after surgery increase of most amplitudes and latencies and reconfiguration of later waves were related to deterioration of clinical course and worsening of left-side signs. We believe that somatosensory evoked potentials change may be a sensible indicator of motor state in Parkinson's disease. As far as we know the present study is one of the first presentation of somatosensory evoked potentials after pallidotomy.
Neurol Neurochir Pol
PMID:[Cryopallidotomy in Parkinson disease. Effect on somatosensory potentials]. 1096 25

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by high instability and extension of CAG sequences within the coding region of IT15 gene. It affects both sexes and age at onset of the disease may be different but usually occurs in midlife. The term Juvenile Huntington's disease is generally applied to 10% of the cases with onset before 20. We present clinical features and results of DNA analysis in 16 patients from 14 families aged 9 to 36. The age of onset was between 5 to 20 years; duration of the disease was from 2 to 16 years. In 10 cases the mutated gene was transmitted by the affected father; only in two cases by the mother. In all cases anticipation manifested by earlier onset of the disease in subsequent generations and expansion of CAG repeats was documented. The number of CAG repeats was between 50 and 92 (mean 67.3). Progressive mental deterioration, declining school performance, hyperactivity and emotional disturbances were the first symptoms of juvenile HD. Neuropsychological assessment showed mean IQ in Wechsler test 59.6 and Mini-Mental State Examination scores 22.8. Rigidity and bradykinesia were predominant features in the cases with juvenile onset, the remaining ones developed choreatic movements. Three persons had epileptic seizures; two (both females) revealed behaviour and psychiatric disturbances. Amplitudes of somatosensory evoked potentials, visual evoked potentials and brainstem auditory evoked potentials were markedly reduced. MRI of the brain showed atrophy of heads of the caudate nuclei, putamen and globus pallidus.
Neurol Neurochir Pol
PMID:[Clinical and genetic study of juvenile form of Huntington's disease]. 1204 2

Surgical treatment of Parkinson's disease (PD) is indicated in patients with severe neurological symptoms (tremor, bradykinesia, rigidity)--who do not benefit from nor tolerate pharmacological therapy. Surgery for PD modifies the motor system function by lesioning or electrostimulation of thalamic, pallidal or subthalamic nuclei. The technological progress together with refined CNS monitoring enabled wider application of deep brain stimulation (DBS). The efficacy of DBS is comparable with lesioning techniques (thalamotomy or pallidotomy) however bears less adverse effects. Both lesioning and DBS are generally well tolerated by patients. The side effects are mostly transient and neurological complications, if occur, usually do not affect quality of patient's life. Unfortunately, the modern surgery for PD is still very expensive and demanding for a large team of specialists and high technology.
Neurol Neurochir Pol
PMID:[Current therapies for parkinson's disease. Part II: surgical treatment]. 1459 61


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