Combined evaluation of pupillary and cardiovascular responses to cold pressor test in cluster headache patients

Little is known about the structures and mechanisms involved in the pathophysiology of cluster headache (CH). In this study, pupillary and cardiovascular responses to the cold pressor test (CPT) were monitored in CH patients during either an active phase of disease or a remission period in order to evaluate the oculocephalic and cardiovascular functioning of the autonomic nervous system in this form of idiopathic headache. CH patients showed a specific pattern of pupillary response on both sides during both phases of the disease. This response differed from that of controls because of an absent miosis. The pressor response to CPT was more marked in CH patients than in controls. Naloxone pretreatment caused specific and selective changes in both the pupillary and cardiovascular responses of CH patients. These data suggest a systemic sympathetic hyperactivation in response to CPT in CH patients. An oculocephalic sympathetic hypofunction is possibly associated as well as an altered opioid neuromodulation.     

Sarcoidosis: 25-year clinical follow-up

Based on the follow-up of 1,600 patients with sarcoidosis from 1971 to 1996, the authors analyzed the value of various methods for identifying the disease, the frequency and nature of misdiagnoses. They showed the efficiency of basic treatments in patients with sarcoidosis: corticosteroidal hormones, nonhormonal antiinflammatory drugs, plasmapheresis, and physiotherapy. Recurrencies and progression were seen in 23.85% of patients. The likely causes of recurrent sarcoidosis are considered. It is concluded that recurrencies are one of the important problems of modern sarcoidosis.     

The gene encoding protein-tyrosine phosphatase RPTP epsilon (PTPRE) is assigned to human chromosome 10q26

In suspected Horner's syndrome, cocaine eye drops are applied to verify the diagnosis. Subsequent application of hydroxyamphetamine or pholedrine eye drops allows localization of the site of the interruption in the oculosympathetic pathway. In the present study the influence of cocaine on subsequent pholedrine testing was examined. Cocaine 5% and pholedrine 5% eye drops were applied to eight (72-h interval only six) normal volunteers with light-colored irides. The ages of the subjects ranged from 23 to 40 years. Eye drops were applied to the same eye at varying intervals of up to 72 h, with the cocaine being given between 8:30 and 9:30 a.m. Pupil diameters were recorded by means of a frame-grabber card in a personal computer and were subsequently measured before and at 50-60 min after each drug application in 1.7 cd/m2 ambient light. In the absence of pretreatment with cocaine, pholedrine changed the mean pupil diameter from 6.89 to 8.57 mm. At 12 h after cocaine pretreatment the pupil remained dilated. Pholedrine dilated the pupil further, from 7.69 to 8.61 mm. When cocaine was given 24 h before pholedrine, the pupil dilated from 6.75 to 8.25 mm; at 48 h after cocaine application, pholedrine dilated the pupil from 6.14 to 8.20 mm; and at 72 h after cocaine pretreatment, pholedrine dilated the pupil from 5.74 to 8.00 mm. As compared with the mean diameter of the untreated contralateral pupil, the pholedrine-induced dilation amounted to 2.32 mm in the absence of cocaine pretreatment, 1.04 mm at 12 h after cocaine application, 1.29 mm at 24 h after cocaine administration, 1.89 mm at 48 h after cocaine pretreatment, and 2.18 mm at 72 h after cocaine application. The residual cocaine effect interfered with the mean pupil dilation produced by pholedrin for at least 48 h. To ensure that the sensitivity of the pholedrine test is maximal, the examiner should delay its use for more than 48 h after the cocaine test.