Biomedical subjects
R Marttila
Publications and source records attributed to R Marttila.
[Infrequent causes of cerebral ischemic disease].
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[Subdural hematoma--an insidious complication of spinal anesthesia].
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[Electrolyte imbalance and central pontine myelinolysis].
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[Bannwarth's syndrome--a spirochetal cause of meningoradiculitis].
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[Treatment of tremor].
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Penetration of lidocaine and its active desethylated metabolite into cerebrospinal fluid in man.
Penetration into lumbar cerebrospinal fluid (CSF) of lidocaine and its active desethylated metabolite, monoethylglycinxylidide (MEGX), has been studied in 10 neurological patients after a single subcutaneous injection of 2 mg/kg prior to lumbar puncture. An HPLC method was used to assay lidocaine, MEGX and glycinxylidide (GX) in serum and CSF. The serum protein unbound fraction of lidocaine was determined by equilibrium dialysis. The mean peak serum lidocaine concentration was found 25 minutes after injection, and the corresponding peak CSF level occurred after 70 min. A similar slow penetration of MEGX into CSF was observed, which indicates low membrane permeability for these two agents. No GX was found. The steadily increasing CSF lidocaine/serum total lidocaine ratio throughout the period of study up to 120 min and the higher level in CSF than the corresponding unbound fraction of the total serum lidocaine indicate that serum protein binding is not the sole determinant of the penetration of lidocaine into lumbar CSF. Rapid accumulation in brain tissue and diffusion back into cerebral extracellular fluid and to lumbar CSF may also occur. The apparent slow membrane penetration of lidocaine and its desethylated metabolite may be one reason for the difficulty of controlling lidocaine infusion rates according to therapeutic effectiveness and side-effects.
Vestibular neuronitis; a neurological and neurophysiological evaluation.
Neurological and neurophysiological findings were retrospectively reviewed in a group of 50 patients with vestibular neuronitis (VN). The onsets of VN were found to be clustered in the period from August to January. A preceding infection was reported by 36% of the patients. Neurological examinations did not reveal any other relevant signs than a spontaneous nystagmus during the acute phase. The results of routine laboratory tests and cerebrospinal fluid tests were within normal limits. EEG was recorded in 37 patients; 15 patients had a definitely abnormal EEG, with a slowing of the dominant occipital rhythm or more generalized diffuse slowing in 12 cases. 5 patients, 3 of them without slowing of the background activity, had a distinct focal disturbance of intermittent slow activity in the temporal region. In control recordings, an improvement was seen in the slowing of the background activity but not in the focal disturbances. Brainstem auditory evoked responses (BSER) were recorded in 12 patients, 5 of whom had abnormal responses. The seasonal clustering of VN onsets and the association of VN with overt infections further suggest its infectious pathogenesis. The observed EEG and BSER disturbances suggest a subclinical brainstem involvement in some cases of VN.
[Tardive dyskinesia].
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[Rare extrapyramidal disorders: progressive supranuclear paralysis and striato-nigral degeneration].
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Long-term responses of Parkinson's disease to levodopa therapy.
The long-term responses of Parkinson's disease to levodopa therapy were studied in the patient material followed-up for 9 years. Levodopa treatment alleviated the parkinsonian symptoms to a considerable degree and substantially improved the quality of life of the parkinsonian patients. However, after treatment for 2 to 3 years, a progressive deterioration of parkinsonian symptoms was observed accompanied by an increase in the incidence of dyskinesias, on-off phenomena, postural instability and dementia. An analysis of the mortality rates in the follow-up material of 349 patients showed that initially levodopa treatment decreased the excess mortality due to Parkinson's disease. The ratios of observed to expected deaths ranged from 1.10 to 1.67. However, during the ninth year of treatment the ratio increased to 1.95 almost reaching the values obtained in the first years of levodopa treatment. Thus it appears that levodopa has only a limited period of usefulness in the treatment of Parkinson's disease. Although levodopa very significantly improves parkinsonian symptoms, it does not arrest the pathological progress and modify the natural course of the disease.
Immunoglobulin G antibodies to herpes simplex type 1 virus detected by radioimmunoassay in serum and cerebrospinal fluid of patients with schizophrenia.
Serum and CSF specimens from 16 schizophrenic patients and 18 nonpsychiatric controls were tested by radioimmunoassay for immunoglobulin G antibody of capsid, envelope and excreted antigens of herpes simplex type 1 virus. There were no significant differences in the antibody levels between the schizophrenic patients and the controls. The etiological role of viruses and virus-like agents in schizophrenia and some methodological aspects are discussed.
Brain dopamine receptor stimulation and the relief of Parkinsonism: relationship between bromocriptine and levodopa.
The relationship between dopamine receptor stimulation by bromocriptine or levodopa and the relief of parkinsonism was studied in 24 patients with Parkinson disease. Bromocriptine, 30 mg daily for 20 weeks, elicited an improvement in the parkinsonian clinical features, but this was less than the subsequent improvement with levodopa and benserazide, 800 mg and 200 mg daily, respectively. There was a negative correlation between the pretreatment severity of the disease or changes in cerebrospinal fluid homovanillic acid (HVA) and improvement in parkinsonian disability during bromocriptine treatment. Futhermore, it was found that clinical improvement and HVA responses in the cerebrospinal fluid after dopamine receptor stimulation by bromocriptine may predict the clinical response to levodopa.
Cephalic motor responses in brain death.
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Brain dopamine turnover and the relief of parkinsonism.
The relationship between dopamine receptor activation and the relief of parkinsonian clinical features was studied in 40 patients with Parkinson's disease. Treatment with dopamine receptor agonists, piribedil or bromocriptine, decreased significantly both the basal level and probenecid-induced accumulations of homovanillic acid (HVA) in the CSF. But there were no changes in the concentrations of 5-hydroxyindole acetic acid (5-HIAA). Correlation analyses showed that patients who improved with both the dopamine agonists used had significantly lower probenecid response of HVA in the CSF and a less severe disease condition than those without beneficial effect. This relationship between dopamine receptor activation and improvement of parkinsonian disability suggests that the therapeutic efficacy of dopamine receptor agonists depends on the functional capacity of brain dopaminergic mechanisms.
Brain dopamine turnover and the relief of parkinsonism.
Levodopa alone or combined with a decarboxylase inhibitor elevated the concentration of homovanillic acid (HVA) in the cerebrospinal fluid (CSF). This increase correlated significantly with the dose of the drug but not with the clinical improvement, although some correlations with clinical side effects were evident. Nevertheless, the concentrations of HVA in the CSF during combined treatment were considerably lower than with therapeutically equivalent doses of levodopa alone. Obviously, a part of the HVA found in the CSF during levodopa treatment originates from the capillary walls. Treatment with dopamine receptor agonists, Piribedil or Bromocriptine decreased significantly both the basal level and probenecid- induced accumulations of HVA and CSF. But there were no changes in concentrations of 5-hydroxyindoleacetic acid (5-HIAA). Correlation analyses showed that patients who improved with both dopamine agonists used had significantly lower probenecid response of HVA in the CSF and less severe disease than those without beneficial effect. This relationship between dopamine receptor activation and improvement of parkinsonian disability suggests that the therapeutic efficacy of dopamine receptor agonists depends on the functional capacity of brain dopaminergic mechanisms.