Ptosis, miosis and cats.

Horner's syndrome (HS) is caused by a disruption in the oculosympathetic pathway. Both congenital and acquired HS are unusual in children. Acquired HS can be caused by trauma, surgical intervention, tumours, vascular malformations or infection.We describe the case of a 6-year-old boy who was brought to our emergency department with ptosis, miosis, painful cervical lymphadenopathy and a cat scratch on a hand. The diagnosis of a cat scratch disease was confirmed by serology. A full recovery was observed on antibiotic treatment and cervical lymphadenomegaly reduction 3 weeks later.

Bilateral oculosympathetic paresis associated with loss of nocturnal melatonin secretion in patients with spinal cord injury.

BACKGROUND: Lesions along the sympathetic pathway to the eye produce oculosympathetic paresis (OSP, Horner's syndrome). The oculosympathetic pathway descends from the hypothalamus through the cervical spinal cord and ascends to the superior cervical ganglion (SCG), which innervates sympathetic targets in the ipsilateral face and eye. This pathway appears to closely co-localize with a similar retino-pineal neural pathway from the hypothalamus through the cervical spinal cord and SCG to the pineal gland. As such, lesions along this shared pathway, such as occur in neurologically complete injury to the cervical spinal cord (tetraplegia), would be predicted to result in simultaneous OSP and loss of pineal melatonin production. Loss of melatonin production may contribute to the pervasive sleep disruption observed in patients with tetraplegia. METHODS: We assessed the presence of OSP by photographic documentation of ptosis and pupillary dilation response to cocaine eye drops in 5 individuals with neurologically complete damage to their upper thoracic or lower cervical spinal cord. We correlated these results with an analysis of the pattern of melatonin production in these same individuals. RESULTS: Bilateral OSP was present in individuals with cervical spinal cord injury; each also lacked significant production of melatonin. No evidence of OSP was observed in the 2 individuals with thoracic spinal cord injury below the level of the oculosympathetic pathway. Both had normal circadian rhythms of melatonin production, with timing and amplitude of the rhythm within normal parameters. CONCLUSION: The presence of bilateral oculosympathetic paresis can be predictive of the complete loss of the nocturnal production of melatonin.

Serum leucine-enkephalin in bronchial carcinoma and its relation to tumour location.

Serum concentrations of the opioid peptide leucine-enkephalin were measured by radioimmunoassay in 30 patients with histologically confirmed bronchial carcinoma and 10 control subjects. This peptide, which is present in greatest amounts in the central and autonomic nervous systems, has previously been found in bronchial neoplasms. The mean serum concentration of leucine-enkephalin was significantly greater in the patients with carcinoma (1035 pg/ml) than in the control subjects (426 pg/ml). In the 23 patients with a tumour in non-apical regions of the lung, however, the mean concentration of the peptide (422 pg/ml) did not differ significantly from that in control subjects; serum concentrations in the seven patients with an apical neoplasm (mean 3050 (range 1259-5820) pg/ml) were significantly greater than values in either the control subjects or the patients with non-apical lung tumours. All seven subjects with an apical tumour had one or more features of Horner's syndrome and the three with all four components of the syndrome had the highest serum concentrations. Serum concentrations of leucine-enkephalin were unrelated to tumour type or presence of metastatic disease. No patient had evidence of metastases in the central nervous system or adrenal glands. Raised serum concentrations of leucine-enkephalin in patients with an apical tumour probably reflect invasion of cervical sympathetic ganglia with release of the peptide into the circulation rather than elaboration of the peptide by the neoplasm.