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Biomedical subjects

R Marttila

Publications and source records attributed to R Marttila.

At least 37 records · Page 2Linked to original sources
PubMed1994

Lyme borreliosis associated with complete flaccid paraplegia.

We report the case of a patient with concomitant Lyme borreliosis and acute paraplegia. The paraplegia was complete, flaccid and of upper motor neurone type. The diagnosis of borreliosis was based on the detection of large amounts of IgM and IgG borrelia antibodies in the acute phase serum and on the complete disappearance of IgM antibody during the review period. IgG borrelia antibodies were also detected in the CSF, but leakage of antibodies from the blood to the intrathecal space could not be ruled out. Lymphocytosis and increased total protein concentration in the CSF were signs compatible with neuroborreliosis. Ceftriaxone therapy effected dramatic recovery of the patient. This case suggests that borreliosis should be considered a possible cause of acute flaccid paraplegia.

Acute Disease↗
PubMed1993

Receptor occupancy in lumbar CSF as a measure of the antagonist activity of atenolol, metoprolol and propranolol in the CNS.

1. The antagonist activity of atenolol, metoprolol and propranolol in the CNS was estimated by determining the extent to which the drugs occupy animal beta 1- and beta 2-receptors in CSF ex vivo at the time of lumbar puncture. 2. Five CSF and plasma samples were obtained 4 h after drug intake from subjects treated for hypertension with atenolol, 100 mg once daily and five from subjects treated with metoprolol, 50 mg three times daily. Twenty-four samples were obtained 1, 2, 4 or 12 h after drug intake from subjects receiving a single 40 mg dose of propranolol. 3. The receptor occupancy in the samples was determined by adding beta 1-receptors of rabbit lung and beta 2-receptors of rat reticulocytes into the samples and labeling the receptors with a nonselective beta-adrenoceptor antagonist, (-)-[3H]-CGP-12177. 4. Atenolol and metoprolol occupied, as expected, larger fractions of beta 1- than beta 2-receptors in CSF and plasma samples. The receptor fraction occupied by atenolol in CSF was significantly (P < 0.05) lower than that occupied by metoprolol. The differences in occupancy between the drugs in plasma, however, were not statistically significant. 5. Propranolol occupied larger fractions of beta 2- than beta 1-receptors in the samples. Although propranolol concentrations in CSF were only 1/20-1/40 of those in plasma, the receptor occupancy of propranolol in CSF was similar to that in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1984

[Tremor].

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Diagnosis, Differential↗
PubMed1983

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.

Adult↗
PubMed1983

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.

Adolescent↗
PubMed1982

[Tardive dyskinesia].

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Dyskinesia, Drug-Induced↗
PubMed1980

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.

Aged↗