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Biomedical subjects

J D Meerwaldt

Publications and source records attributed to J D Meerwaldt.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of stimulus orientation on contrast sensitivity in Parkinson's disease.

We studied the effect of stimulus orientation on contrast sensitivity function in 21 patients with Parkinson's disease and in 10 normal subjects. This was done by measuring contrast sensitivity over a range of spatial frequencies for vertical and horizontal sine wave grating stimuli. There was a great test-retest consistency in normal subjects and patients. Fifteen of the 21 patients showed contrast sensitivity deficit in at least one eye. Orientation-specific loss was demonstrated in 17 of the 25 "affected" eyes. The most frequent type of orientation-specific loss was a notch defect, which preferentially affected the middle spatial frequencies. We attribute orientation-specific and spatial frequency-selective loss in Parkinson's disease to a functional disruption of neurons on the visual cortex.

Aged↗
PubMed1987

Factors that influence the occurrence of response variations in Parkinson's disease.

Retrospective study of 129 patients treated with dopamine substitution showed that the occurrence of response variations is related to the duration of therapy and not to the nature of the predominant symptom (tremor or hypokinesia and rigidity) or the age of onset of the disease. A relationship was found between the occurrence of response variations and the severity of the disease when levodopa therapy was started. Patients fared worst who were in Hoehn and Yahr stages I and II when levodopa therapy was begun.

Activities of Daily Living↗
PubMed1987

Effect of levodopa treatment on contrast sensitivity in Parkinson's disease.

We studied contrast sensitivity function in 10 parkinsonian patients before and after levodopa treatment. Pretreatment contrast sensitivity function was abnormal in 16 of the 20 eyes. After treatment, only high-frequency loss was observed in 6 eyes. All other types of deficit disappeared under treatment. These changes of contrast sensitivity function following treatment suggest that dopamine is a functional transmitter in the visual pathways.

Aged↗
PubMed1987

Open multicenter trial with Madopar HBS in parkinsonian patients. Preliminary assessment after short-term treatment.

In 23 patients with idiopathic Parkinson's disease presenting with severe fluctuations in motor performance and 'on-off' phenomena after long-term treatment with levodopa, the standard form of Madopar was replaced by the controlled-release form Madopar HBS. The Meerwaldt's patient card has been used to evaluate the frequency and intensity of response swings. Only 2 patients, who suffered from clear-cut 'end-of-dose' deterioration, significantly benefited by this switch from standard Madopar to Madopar HBS. Eight patients had a minimal or not essential improvement of the parkinsonian symptomatology and/or of the response fluctuations. Thirteen patients returned to their previous standard Madopar treatment after deterioration of parkinsonian symptoms or increase of dyskinesia under the HBS treatment. The overall increase in dosage of levodopa with Madopar HBS was 54% in comparison with the initial standard Madopar dosage.

Aged↗
PubMed1987

Spatial disorientation as an early symptom of Parkinson's disease.

In 44 consecutive outpatients with idiopathic Parkinson's disease (PD) without levodopa substitution therapy, we tested spatial orientation. Spatial orientation was impaired on the rod orientation test in 43 patients, on the line orientation test in 7 patients, and on the facial recognition test in 17 patients. There was no correlation between severity of spatial disorientation and age, length of illness, verbal WAIS score, or severity of PD. Impairment of spatial orientation is part of PD even in mild cases.

Aged↗
PubMed1987

Long-term treatment with high-dosage bromocriptine in advanced Parkinson's disease.

Long-term follow-up indicated that levodopa as a replacement therapy merely improves the parkinsonian symptoms, and does so for only a limited number of years. The reason for this tachyphylaxis or declining efficacy in levodopa therapy and the increasing number and intensity of various distressing difficulties in the management of Parkinson's disease, such as dyskinesias and on-off phenomena, is the main subject of many recent studies. It is still widely accepted that levodopa provides the best therapeutic tool for Parkinson's disease. Bromocriptine, an ergot derivative, is the main clinically used dopamine agonist, and it has been established as a valuable adjunct in the treatment of Parkinson's disease. Bromocriptine is most useful in patients with a declining efficacy of levodopa treatment, in patients with diurnal oscillations in motor performance, especially in patients with wearing-off phenomena, and in patients with onset and end-of-dose dyskinesias. The question of bromocriptine dosage, required to obtain an optimal benefit and a decreased rate of late adverse reactions, is quite controversial. The trend has been to lower daily dosage of bromocriptine, i.e., low doses suffice in patients with mild, early disease. Higher doses of bromocriptine seem to be required in patients with severe parkinsonian deficits. In this retrospective study of 8 years experience with high dosage of bromocriptine in levodopa response-losing parkinsonian patients, the adjunction of bromocriptine had a clear-cut but short-lasting beneficial effect on the disability scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Apnoea testing to confirm brain death in clinical practice.

In six patients an apnoea test was carried out to confirm brain death according to a protocol recommended in the USA. After ten minutes' apnoea the pCO2 did not reach the target value of 7.98 kPa (60 mm Hg) in any of these patients. This was caused by the low initial value and the slow increase of the pCO2. Moreover, we could not confirm the belief that the necessary duration of the apnoea test can be predicted by assuming a rise of the pCO2 of 0.33 kPa (2.5 mm Hg) per minute.

Adult↗
PubMed1986

Contrast sensitivity in Parkinson's disease.

We studied contrast-sensitivity function in 39 patients with Parkinson's disease. Sixty-four percent of the patients showed contrast-sensitivity loss in one or both eyes. The abnormality was not related to the first symptom or the severity of disease. Sensitivity loss at intermediate frequencies (notch loss) in 30% of the "affected" eyes suggested a cortical component. These findings support the belief that there is a widespread neurotransmitter deficiency in Parkinson's disease.

Adult↗
PubMed1984

Balint's syndrome in a man with border-zone infarcts caused by atrial fibrillation.

A 70-year-old man showed Balint's syndrome and other signs of bilateral posterior-hemisphere dysfunction of acute onset without initial unconsciousness. A computerized tomographic scan showed bilateral infarcts in the posterior arterial border-zone areas. Clinical evidence suggests that hypotension at the onset of atrial fibrillation caused these infarcts. There was a marked difference in the time course of recovery between the left and the right infarct which demonstrated that the elements of Balint's syndrome disappeared together with the left-hemisphere symptoms while the right-hemisphere symptoms were still present.

Aged↗
PubMed1984

Response variations in the treatment of Parkinson's disease.

The problems of long-term levodopa therapy tend to occur earlier if levodopa is combined from the start with a decarboxylase inhibitor. We conducted a retrospective study of 123 patients. Among patients treated with levodopa without a decarboxylase inhibitor, only 25% had response variations (end-of-dose deterioration, on-off response fluctuation) after 6 years of treatment. Among patients treated with both levodopa and a decarboxylase inhibitor, 90% showed response variations after 6 years of therapy.

Carboxy-Lyases↗