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)

Subcortical dementia is a clinical syndrome incorporating disorders of cognitive and affective sphere, which is caused by organic damage to subcortical structures. The syndrome is usually connected with Progressive Supranuclear Palsy, Huntington Disease, Parkinson's Disease. Subcortical dementia is mainly characterized by: slowing down of psychic functions and impairment of their precision, disorders in the ability to use achieved knowledge and personality changes. Most authors stress the fact that similar cognitive and emotional personality defects are observed in cases of frontal cortex damage. Recent research points to the existence of functional subcortical-prefrontal circuits which regulate human behaviour. There is a link between subcortical dementia and functional or structural break of one or more cortical-subcortical connections. Attention is also called to disorders in certain neurotransmitting systems (dopaminergic, acetylcholinergic) as well as to brain hypometabolism in basal ganglia, thalamus and prefrontal cortex.
Neurol Neurochir Pol
PMID:[Subcortical dementia and the frontal lobe syndrome]. 951 60

Idiopathic Parkinson Disease accounts for approximately 75% of all cases of parkinsonism. The described case of Corticobasal Degeneration (CBD), until now not presented in Polish medical literature is a relatively rare example of so-called "parkinson plus" syndrome. The authors present the case of a 56 years old woman with asymmetric onset of rigidity and atypical tremor of upper extremity followed by gait disturbances (gait apraxia), dysarthria, bilateral pyramidal signs and myoclonus. Complete lack of clinical improvement after treatment with L-dopa and progressive character were observed from the onset of the disease. The presented case seems to be helpful in differential diagnosis of parkinson plus syndromes and specially CBD, which seems to be difficult in the first stages of the disease. Although the case was not neuropathologically verified (patient is still alive) the diagnosis seems to be almost true.
Neurol Neurochir Pol
PMID:[Cortico-basal degeneration. Diagnosis and differentiation and the description of the first case in Poland]. 1035 40

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

The relationship between genetically determined polymorphic oxidation and acetylation and susceptibility to some disease has aroused much interest. The aim of our study was to evaluate whether patients with Parkinson's disease differ from healthy persons in their ability to oxidize sparteine and acetylate sulfadimidine as model drugs. Oxidation and acetylation phenotypes were estimated in 50 patients with Parkinson's disease. The control group consisted of 160 healthy volunteers for comparison of oxidation phenotype and 60 healthy volunteers for comparison of acetylation phenotype. The phenotyping of oxidation revealed two distinct populations among 50 patients with Parkinson's disease: 47 persons (94%) were extensive metabolizers of sparteine and 3 persons (6%) were poor metabolizers. In 160 healthy persons, 146 persons (91.2%) were extensive metabolizers of sparteine and 14 persons (8.8%) were poor metabolizers. The difference between frequency distribution of PMs and EMs in healthy persons and in patients with Parkinson's disease was not statistically significant. The phenotyping of acetylation showed among 50 patients with Parkinson's disease 38 persons (76%) slow acetylators and 12 persons (24%) rapid acetylators. In 60 healthy volunteers the phenotype of slow acetylation was observed in 29 persons (48.3%) and rapid acetylation in 31 persons (51.7%). The prevalence of slow acetylators among patients with Parkinson's disease in comparison to healthy volunteers was statistically significant (chi 2 = 8.7677/p < 0.003). The results of our study may suggest that the slow acetylation phenotype is associated with increased risk of the development of Parkinson's disease.
Neurol Neurochir Pol
PMID:[Clinical significance of oxidation and acetylation genetic polymorphism in patients with Parkinson's disease]. 1067 54

Apomorphine is a non-specific dopamine agonist, most similar to it, with a strong action on D2, D3, D4 receptors and weaker action on D1 and D5 receptors. It has been known since 100 years, and in Parkinson's disease it was used first in 1970 by Schwab and Cotzias. Apomorphine is used in Parkinson's disease with high-grade fluctuations of symptoms which cannot be controlled by oral drugs, especially in off" periods resistant to levodopa. After subcutaneous administration it changes the "off" to "on" period within 5-10 minutes. Unfortunately, its effect is short-lasting and wears off after 40-90 minutes. Apomorphine is administered in repeated single subcutaneous injections or in continuous subcutaneous infusion, if more than 7-9 single injections are required daily. Before beginning of treatment the optimal dose of apomorphine should be determined. For counteracting its emetic action domperidon (Motilium) is given additionally 20 mg t.d.s. Apomorphine produces no tolerance and is not losing its effectiveness with continued treatment. The most frequent adverse effects during long-term treatment are local cutaneous reactions, increased intensity of dyskinesia during the "on" period, visual hallucinations whose illusory character is clear to the patient, psychoses, orthostatic hypotension. The authors treated 8 patients with marked fluctuations in Parkinson's disease treated with levodopa. In 7 cases the effects was good--6 of them received 2-3 mg s.c. 3-4 times in 24 hours for 7-12 days. One patient has been treated 9 months with good result. In one case the intensity of dyskinesia made impossible treatment continuation.
Neurol Neurochir Pol
PMID:[Apomorphine in treatment of Parkinson's disease with fluctuations]. 1079 Oct 32

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

Bromocriptine is applied for treatment of patients with hyperprolactinaemic disorders, Parkinson's disease and acromegaly. Sometimes, this drug can be useful as adjuvant in patients with prostate hypertrophy, cocaine and alcohol abuse, or neuroleptic malignant syndrome. Recently, bromocriptine was found to improve memory. In randomized trials bromocriptine demonstrated improvement of prefrontal cortex function in traumatic brain injury patients. These informations suggest a potential possibility of this drug to therapy for patients with prefrontal damage.
Neurol Neurochir Pol
PMID:[Bromocriptine: uses until now and prospects of new therapeutic applications]. 1097 49

The author presents current views on neuroprotective strategies in therapy of idiopathic Parkinson's disease. They are the result of different aetiopathogenetic concepts of Parkinson's disease. The concepts of loss of nigral cells as a result of aging, apoptosis or genetic defect (alpha-synucleine) are not sufficiently proven and their role is only hypothetic. Therapeutic use of nerve growth factors seems to be a promising novel strategy but there are technical problems how to deliver them to the brain. One of the most and widely acceptable concept is the theory of the role of oxidative stress in pathogenesis of Parkinson's disease. It was a scientific basis for clinical trials with selegiline (DATATOP, SINDEPAR, PDRG) which results were unfortunately disappointing, mostly because of symptomatic effect of selegiline. Another interesting concept seems to be the excitotoxicity of amino acids (like glutamate) and amantadine is the well known drug with recently discovered antagonism to NMDA receptors. In only one retrospective clinical trial in humans its neuroprotective effect was proven, but we need now well prepared prospective trials with this drug to confirm this result. So far, despite the hopes concerning selegiline no one effective neuroprotective agent is available in treatment of Parkinson's disease.
Neurol Neurochir Pol
PMID:[Is there an effective neuroprotective treatment of Parkinson's disease? (therapeutic possibilities against the background of etiopathogenetic concepts]. 1110 5

Only in the second half of the 20th century a breakthrough occurred in the traditional neurological therapeutic methods based up to that time mainly on bromine with valerian extract and vitamins B. Later on in that century several great discoveries were made which improved greatly the effectiveness of the neurological therapy: psychopharmacology which began with the introduction of chlorpromazine and reserpine, the use of corticosteroids for which the Nobel award was given, levodopa introduction for Parkinson's disease, non-steroid antiinflammatory agents and the demonstration of their action mechanism /also Nobel award/, immunotherapy, botulin toxin for the treatment of dystonias and thrombolytic drugs possibly the drugs of the future. The main disappointment is the broad chasm between the progress made in diagnostic methods and the low effectiveness of therapy in strokes, amyotrophic lateral sclerosis, Alzheimer's disease and other degenerative neurological diseases. Many problems arose with the introduction of levodopa changing the course and clinical pattern of Parkinson's disease. The problem of our times are the adverse effects of pharmacotherapy. The low effectiveness of the new drugs used in epilepsy is also disappointing. A hope for the future is the new direction in therapy--the use of genes and also the use of monoclonal antibodies and neurotrophic agents. It is to be expected that in the near future medicine will find effective methods for the treatment of malignant neoplasms.
Neurol Neurochir Pol 1999
PMID:[Achievements, disappointments and hopes in neurological therapy in the 20th century]. 1110 59


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