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)

Potential risk factors for various types of stroke were studied using a case-control study design. All 1978 US death certificates for which the registered underlying cause of death was subarachnoid hemorrhage (SAH), cerebral hemorrhage (CH), or cerebral infarction (CI) were identified. The frequency with which other conditions appeared on the death certificates of cases with and without hypertension was compared with controls. These data provide new information, such as the occurrence of peripheral vascular disease in association with SAH, the risk of CH in epileptic and cirrhotic patients, and the association of benign neoplasms of the nervous system, motor neuron disease, and 'paralysis agitans' with CI.
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PMID:Conditions associated at death with specific types of completed stroke in patients with and without hypertension: a case-control study. 291 91

Catecholamines and indolealkylamines are of clinical interest in neurological and psychiatric disorders. We measured 3-methoxy-DOPA, 3-methoxy-4-hydroxyphenylglycol, dihydroxyphenylacetic acid, tryptophan, 5-hydroxyindoleacetic acid and homovanillic acid in human cerebrospinal fluid with a simple, sensitive , inexpensive, rapid and accurate procedure using high performance liquid chromatography coupled to an electrochemical detector. Patients with Parkinson's disease have a decrement in homovanillic acid that is reversed by treatment with L-3,4-dihydroxyphenylalanine. After this medication, 3-methoxy-DOPA is measurable in cerebrospinal fluid. Patients with depression show a decrease in serotonin turnover expressed by diminished 5-hydroxyindoleacetic acid content in cerebrospinal fluid. Depressed patients also show low levels of tryptophan. Monoamine metabolites are augmented in patients with subarachnoid hemorrhage.
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PMID:Monoamine metabolites in human cerebrospinal fluid. HPLC/ED method. 620 98

Immunoreactive vasoactive intestinal peptide (VIP) was measured in lumbar and ventricular cerebrospinal fluid (CSF) from patients with various neurological disorders and in 2 hour aliquots of cisternal fluid removed continuously from rhesus monkeys. Although most of the VIP in concentrated pools of human ventricular fluid and of monkey cisternal fluid co-eluted with synthetic porcine VIP28 on a column of Sephadex G-25 superfine, there was evidence that smaller immunoreactive fragments were also present. A circadian pattern of CSF VIP concentration was observed in 2 of the 3 monkeys studied, with highest levels occurring at night and lowest during the day. Ventricular fluid VIP levels were highest in hydrocephalic children and lowest in patients with multiple sclerosis or epilepsy, while VIP was not detectable in ventricular fluid from patients in coma following a severe head injury. There were no significant differences in VIP concentrations in CSF from patients with dystonia. Parkinson's disease, or Alzheimer's disease, suggesting that VIP containing neurons are not affected in these disorders. Lumbar fluid VIP levels were low in patients undergoing aneurysm surgery. Since VIP is a potent vasodilator, these findings may have important implications in relation to the development of vasospasm following subarachnoid hemorrhage.
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PMID:Vasoactive intestinal peptide in cerebrospinal fluid. 647 66

Parkinson's disease has been associated with heavy occupational exposure to carbon disulfide, and this solvent, as well as other organic solvents, may cause neurotoxic effects. Therefore, the hypothesis was raised that organic solvents in general may be associated with Parkinson's disease. A case-referent study design was applied, and some other suspected exposures were studied as well. The diagnosis registers of two Swedish hospitals were used as the source of subjects. Male in-patients with Parkinson's disease (the cases) or subarachnoid hemorrhage (referents), with symptom appearance between 35-69 a of age and residence in the vicinity of the hospitals, were included in the study. Occupational exposure to the chemicals under study were determined from questionnaire answers of 91 cases and 75 referents. No differences in exposure frequency to organic solvents in general were observed, but three cases had been exposed to carbon disulfide compared to none of the referents. Six cases, but only two referents, had been exposed to mercury, and further exploration of a possible association between exposure to mercury and Parkinson's disease is recommended. The outcome of the study does not support the hypothesis that occupational exposure to organic solvents in general increases the risk of Parkinson's disease, but the confidence intervals of the odds ratios do not rule out such possibilities.
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PMID:Parkinson's disease and occupational exposure to organic solvents, agricultural chemicals and mercury--a case-referent study. 734 10

In-vivo microdialysis has been used extensively to study the neurochemical mechanisms of ischemia, epilepsy and hypoglycemia. It is also being increasingly used to document the response of neurons to various medications. Most of the work to date has been done in small animals. In the last 2 years, the technique has been adapted for use in patients with subarachnoid hemorrhage, head trauma, Parkinson's disease, brain tumors and epilepsy. Two of the major limiting factors are the invasiveness of the technique and the resultant potential for CNS infection. We describe a simple, safe and reliable method to measure neurochemical changes in the human brain with in-vivo microdialysis. We were able to easily monitor for 4-6 h daily for up to 4 days in awake or comatose patients with subarachnoid hemorrhage or head trauma. Cerebral concentrations of glutamate, GABA, other amino acids and catecholamines were measured. This technique thus has a potential for on-line measurements of neurotoxins in patients with unstable neurological conditions.
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PMID:A new method of in-vivo microdialysis of the human brain. 854 74

Rapid eye movement (REM) sleep behavior disorder (RBD) involves complex behavior and a loss of muscle atonia occurring during REM sleep. Half of these patients with RBD have an underlying neurologic disorder including dementia, olivopontocerebellar atrophy, subarachnoid hemorrhage, and cerebrovascular disease. Clonazepam is the drug of choice for RBD. RBD has been rarely reported to precede the onset of Parkinson's disease (PD). Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment. It is postulated that levodopa ameliorates RBD by suppressing REM sleep, and it remains to be seen whether levodopa can be an alternative to clonazepam in idiopathic RBD without PD.
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PMID:Rapid eye movement sleep behavior disorder preceding Parkinson's disease with therapeutic response to levodopa. 868 94

A 51-year-old male was transferred to our hospital just after traffic accident. On admission, the patient was comatose (Glasgow Coma Scale of 6) and showed a left hemiparesis with a left oculomotor nerve palsy. Computed tomography demonstrated a traumatic subarachnoid hemorrhage without mass lesion. Magnetic resonance imaging showed high intensity lesions on the left dorsolateral midbrain and the right cerebral peduncle. The distribution of lesions implied diffuse axonal injury involving dopaminergic systems such as the substantia nigra and the ventral tegmental area. After several months of conservative management, the patient showed no recovery and was diagnosed as persistent vegetable state. The administration of L-dopa was then started and the patient showed remarkable neurological improvement. Therefore the patient's neurological status was thought to be modified with primary brain stem injury and accompanying traumatic Parkinson's syndrome. It is important to understand "pseudo" persistent vegetative state in the management of patients showing prolonged consciousness disturbance. L-dopa should be considered as the drugs of pharmacological intervention for the patients of masked parkinsonism behind "pseudo" persistent vegetative state whose dopaminergic systems might have been damaged.
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PMID:[A case of primary brain-stem injury recovered from persistent vegetative state after L-dopa administration]. 1065 5

The effect of brain injury and disease on the output of established artists is an object of much study and debate. The emergence of de novo artistic behaviour following such injury or disease, while very rare, has been recorded in cases of frontotemporal dementia, epilepsy, subarachnoid haemorrhage and Parkinson's disease. This may be an underdiagnosed phenomenon and may represent an opportunity to further understand the neural bases of creative thought and behaviour in man and those of cognitive change after brain injury. There is clearly an important role for hemispheric localization of pathology, which is usually within the temporal cortex, upon the medium of artistic expression, and a likely role for mild frontal cortical dysfunction in producing certain behavioural and cognitive characteristics that may be conducive to the production of art. Possible mechanisms of 'artistic drive' and 'creative idea generation' in these patients are also considered. The increased recognition and responsible nurturing of this behaviour in patients may serve as a source of great comfort to individuals and their families at an otherwise difficult time.
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PMID:De novo artistic behaviour following brain injury. 1749 6

Erythropoietin (EPO) was first identified as a hematopoietic cytokine that stimulates proliferation and differentiation of erythroid progenitor cells and was approved by the Food and Drug Administration as a treatment for chronic renal disease patients with anemia. In neural tissues, EPO is working via EPO receptors and induces non-hematopoietic effects. Recent studies have demonstrated that EPO exerts therapeutic potentials on neurological disorders such as ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, traumatic brain injury, and Parkinson's disease. EPO treatment has been shown to reduce the ischemic infarct and hemorrhage volume, decrease neuronal death including apoptosis, and improve survival rates in animal models. The mechanism of EPO action in neurological disorders involves neuroprotection and promotion of neurogenesis and angiogenesis. Clinical trials of EPO treatments in neurological diseases have accumulated positive results. In stroke patients, EPO treatment may reduce infarct volume and improve functional outcomes. EPO administration has proven safe in animal studies and adult human patients, although safety and efficacy data in neonates and infants are incomplete and long-term multi-center patient evaluations are necessary. Available information suggests that EPO is a promising therapeutic drug for the treatment of neurological diseases.
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PMID:Therapeutic strategy of erythropoietin in neurological disorders. 1867 7

Sildenafil, a phosphodiesterase-5 inhibitor commonly used for erectile dysfunction, may also have a beneficial therapeutic effect in the treatment of stroke, subarachnoid hemorrhage, dementia, learning, and neurodegenerative disorders by enhancing angiogenesis and neurogenesis. It also favorably influences the nitric oxide-cyclic guanosine monophosphate pathways, which are involved in the pathogenesis of a number of neurological diseases. Its potential therapeutic role in the treatment of the neurological disorders mentioned above is still under preclinical investigation. Sildenafil is currently being used to treat erectile dysfunction in patients with multiple sclerosis, Parkinson disease, multisystem atrophy, and spinal cord injury by improving their neurologically related erectile dysfunction. Conversely, it has been implicated in a number of neurological problems, such as intracerebral hemorrhage, migraine, seizure, transient global amnesia, nonarteritic anterior ischemic optic neuropathy, macular degeneration, branch retinal artery occlusion, and ocular muscle palsies. Thus, preclinical and very limited clinical data suggest that sildenafil may have therapeutic potential in selected neurological disorders. However, numerous reports are available regarding neurological adverse events ascribed to the drug. Although sildenafil shows some promise as a therapeutic agent in selected neurological disorders, well-designed clinical trials are needed before the agent can be recommended for use in any neurological disorder.
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PMID:Role of sildenafil in neurological disorders. 1905 Apr 13


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