Horizontal saccades and smooth pursuit eye movements were studied in 26 patients with myotonic dystrophy. Clinical neuro-ophthalmological investigations in 1 patient revealed an inability to achieve a full range of eye movements. Electro-oculography showed a significant decrease of the maximum velocity of the visually-guided saccades in 83% of the patients. Smooth pursuit eye movements were not significantly different from age-matched controls. Visual evoked potential (VEP) latencies (P100) were significantly prolonged compared with controls in 64% of the patients. The saccadic latency of the visually-guided saccades was correlated with the prolonged VEP latencies, indicating that lesions in the primary visual pathways probably contribute to the oculomotor dysfunction. The isolated decrease of the maximum velocity of the saccades in combination with EMG findings favours a peripheral (dystrophic) pathophysiological mechanism.

The case reports presented so far, concerning a possible causative relationship between the ophthalmological use of chloramphenicol (O-CAP) and blood dyscrasias, are few in number, not always fully documented and therefore not always convincing. The overall use of this drug in a restricted area in the Netherlands was assessed. On a yearly basis 1:29 people used O-CAP. In a four-year period in the same area, 12 patients with aplastic anemia and 190 patients with other cytopenic dyscrasias were found. After exclusion of all cases with other possible causes of the dyscrasia, e.g. cancer and related therapy, other drugs than O-CAP and infectious diseases, 59 cases remained in which a definite cause could not be established. We traced back the use of O-CAP in the relevant period. No dyscrasias were found that unequivocally were caused by O-CAP. The rate of O-CAP use in the dyscrasia-group was approximately equal to that in the population as a whole. Hence we concluded that it is highly improbable that O-CAP played a part in the etiology of blood dyscrasias in the region. Statistical evaluation of material derived from a much larger region may, however, lead to a more differentiated conclusion.

No abstract

In 204 adult, white diabetics the palpebral fissure was measured and related to the state of metabolic control of the diabetes. A control group was formed of 204 persons matched by age and sex. The average palpebral fissure in the control group was 9.9 mm: there was a slight, but not significant, difference between the age groups and the sexes. In diabetics who were not insulin dependent the average width of the palpebral fissure was found to be 9.4 mm; in severe chronic deregulation of the diabetes, however, an average palpebral fissure of 8.0 mm was found, a significant narrowing. In insulin-dependent diabetics the average width of the palpebral fissure was 8.3 mm. This significant narrowing also increased if there was severe chronic deregulation of the diabetes. The average palpebral fissure associated with proliferative retinopathy in insulin-dependent type 1 diabetics was 6.0 mm (nearly 4 X standard deviation). This ptosis in diabetes is very probably due to chronic tissue hypoxia, to which the levator palpebrae muscle is probably extra sensitive, and in which thickening of the basal membrane of the capillaries may be one of the most important factors.

Key words: chordoma of the base of the skull, chondroid chordoma, orbital ap_ex syndrome due to chordoma, ophthalmoplegia dolorosa due to chordoma Abstract. Chondroid chordoma of the base of the skull has a significantly more favourable prognosis than the classical chordoma. The clinical and radiological symptoms of this relatively benign form, and its histological and therapeutic aspects, are discussed in connection with the case of a 50-year-old patient.