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Biomedical subjects

J E Bos

Publications and source records attributed to J E Bos.

9 recordsLinked to original sources
PubMed1992

Eye movements in myotonic dystrophy.

Smooth pursuit eye movements were studied with infrared reflection equipment in 10 patients with myotonic dystrophy and in 10 age- and sex-matched controls. Smooth pursuit gain, measured after correction for catch-up saccades, was decreased in the patient group. Normal latencies of saccadic eye movements made a lack of attention an unlikely explanation for this low gain. Likewise, presence of catch-up saccades and normal fixation made it unlikely that extra-ocular myopathy explained the low smooth pursuit gain. We suggest that periventricular white matter abnormalities represent a more likely explanation.

Adult↗
PubMed1991

Detection of the pupil constriction latency.

Two methods to accurately determine the moment of pupil constriction onset are discussed. For data sampled at a high rate (approximately 200 Hz) pupil velocity deviations from zero can simply be used, giving a satisfactory inaccuracy of about 5 ms. For data sampled at a low rate (less than 50 Hz), e.g. using a TV pupillometer, curve-fitting can be applied. It is demonstrated that curve-fitting, based on a second-order mathematical model, preceded by a linear trend, can result in an inaccuracy of less than 5 ms. Both methods give latencies independent of signal amplitude. This implies that a pupillometer yielding a relative measurement of the pupil area can be used for the detection of pupil constriction latencies. Furthermore it is demonstrated that the averaging of pupil constrictions results in an advanced moment of onset. Where latency differences of less than 25 ms are concerned, raw pupil data should therefore not be averaged.

Algorithms↗
PubMed1991

The cause of increased pupillary light reflex latencies in diabetic patients: the relationship between pupillary light reflex and visual evoked potential latencies.

In 42 diabetic patients the relationship between the latency of the pupillary light reflex and the pattern reversal visual evoked potential (P100) was examined. Fifty-five percent of diabetic patients had pupillary light reflex latencies above the normal range. In 19% the visual evoked potentials were prolonged when compared to the normal range. Latencies of pupillary light reflexes and VEPs showed no correlation. There was a minimal correlation between the presence of retinopathy and prolongation of both the pupillary light reflex and the visual evoked response latency (kappa coefficients respectively: 0.31, P less than 0.01 and 0.36, P less than 0.02). The presence of an increased pupillary light reflex latency was positively correlated with a reduced respiratory sinus arrhythmia (kappa coefficient: 0.58, P less than 0.0001). Increased VEP latencies showed no correlation with signs of cardiovascular autonomic neuropathy. We conclude that the afferent optic pathway can be affected in diabetic patients. However, prolongation of pupillary light reflex latency in diabetic patients is primarily due to an efferent pupillary defect and represents parasympathetic dysfunction.

Adult↗
PubMed1991

Assessment of autonomic function in myotonic dystrophy.

Published reports suggested autonomic nervous system dysfunction in myotonic dystrophy but were inconclusive partly due to small patient numbers and because only a limited number of tests was used. Autonomic nervous system function with noninvasive tests was assessed in ten myotonic dystrophy patients and age and sex matched healthy controls. Statistically significant differences included reduction in the heart rate response to standing and in the blood pressure response to sustained handgrip. Latency of the pupillary light reflex was not different from controls but the time to reach peak velocity of contraction was significantly longer in the myotonic dystrophy group. It is argued that these results reflect dysfunction of voluntary and iris smooth muscle rather than autonomic nervous system dysfunction.

Adult↗
PubMed1990

Assessment of pupillary light reflex latency and darkness adapted pupil size in control subjects and in diabetic patients with and without cardiovascular autonomic neuropathy.

Increased pupillary light reflex latencies were found more often than a reduced darkness pupil size in diabetic patients with and without abnormal cardiovascular reflexes. This finding suggests that parasympathetic pupillary dysfunction precedes sympathetic pupillary denervation in diabetic autonomic neuropathy.

Adolescent↗