Chronic neurological sequelae of acute organophosphate pesticide poisoning.

To evaluate the latent neurological effects of organophosphate pesticide poisoning, this epidemiologic study examined 100 matched-pairs of individuals with previous acute organophosphate pesticide poisoning and nonpoisoned controls. No significant difference between poisoned subjects and controls was found on audiometric tests, ophthalmic tests, electroencephalograms, or the clinical serum and blood chemistry evaluations. Of the more than 50 scores from the neurological examination, abnormalities were demonstrated among the cases only on measures of memory, abstraction, and mood, and on one test of motor reflexes. Differences between the two cohorts were much more apparent in the neuropsychological tests. The differences occurred on tests of widely varying abilities including intellectual functioning, academic skills, abstraction and flexibility of thinking, and simple motor skills. Twice as many cases as controls (24 vs. 12) had Halstead-Reitan Battery summary scores in the range characteristic of individuals with cerebral damage or dysfunction. Results from the Minnesota Multiphasic Personality Inventory and the Patient's and Relative's Assessment of Patient Functioning Inventories also revealed greater distress and complaints of disability for the poisoned subjects.

Hyponatremia and central pontine myelinolysis.

Autopsy in a patient with severe hyponatremia showed central pontine myelinolysis. Review of our patients with central pontine myelinolysis and those described in the English literature to data disclosed that 61 percent had documented hyponatremia. While the exact mechanism involving hyponatremia and central pontine myelinolysis cannot be defined, a circumstantial relationship is apparent. The purpose of this paper is to emphasize this relationship and to suggest that the possibility of central pontine myelinolysis be considered in any patient with hyponatremia and neurologic dysfunction.

Detection of canine Batten disease with the EEG.

Although it has been suggested that EEG changes appear early in the course of human Batten disease, these observations have been made only after the onset of clinical abnormalities and without immediate pathological correlation. In this brief report we have been able to document for the first time, abnormal EEGs in a strain of dogs proposed as a model for Batten disease. The degree of abnormality in the canine EEG correlated with the degree of clinical involvement and with the presence of pathological inclusions, resembling those seen in human Batten disease. In younger dogs, abnormal EEGs were obtained even before clinical manifestations of the disease. The large amplitude discharges reported with photic stimulation in children with the late infantile form of Batten disease were not elicited in the dog model. However, this dog strain is a model for the juvenile rather than the late infantile form although similarities between dogs and both forms of human Batten disease were seen. It is proposed that the EEG is both a method for early detection of this disease as well as a tool ot measure the degree of involvement. This information may be of use in relation to future therapeutic trials.

Sodium humate solution studied with small-angle x-ray scattering.

Small-angle x-ray scattering analyses of sodium humate solutions indicate either that particles of two or more different sizes exist in solution or that all of the particles are the same size but consist of a dense core and a less dense outer shell. Fractionation on a molecular sieve chromatographic column suggests that the first possibility is the more likely of the two. The radius of gyration and molecular weight of the larger particles are respectively 110 A and 1 x 10(6) and those of the smaller particles 38 A and 2.1 x 10(5). These particles are ellipsoidal.