It has been previously shown that patients with achalasia may have motor abnormalities of the stomach, small bowel and biliary system. This study investigates whether a disturbance of extraintestinal autonomic function occurs. Autonomic function studies were performed in 15 patients with achalasia and 15 age- and sex-matched healthy controls. Pupillograms were obtained during darkness, light exposure and after pilocarpine administration. Cardiovascular function studies included determinations of heart rate variation during deep breathing and orthostasis. In addition, we determined blood pressure changes in response to sustained handgrip, cold exposure and orthostasis. Neurohormonal function was investigated by measuring serum pancreatic polypeptide (PP) levels prior to and following sham feeding. Pupillary function did not differ in patients as compared with controls. However, 9 of 15 patients (95% CI: 32-84%) and none of the controls showed at least one abnormal autonomic cardiovascular response. A significant difference between the two groups was observed in sympathetic function (P = 0.023). More patients than controls did not respond to sham feeding with a PP increase. It is concluded that some patients with achalasia exhibit an abnormality of the autonomic nervous system that extends beyond the gastrointestinal tract. These abnormalities mainly concern cardiovascular function but may also involve neurohormonal responses.
PCDD has a mild toxic effect on the peripheral nervous system manifesting as mild sensory neuropathy of the legs in a minority of the most severely exposed persons.
The chemiluminescence activity (CL-A; synonym = burst activity, BA) and the percentage of OKT3-, OKT4- and OKT8-positive peripheral blood cells were serially examined in four control persons and in eight patients with multiple sclerosis. When the OKT values obtained in phases of increased CL-A (clinical remission) were compared with those of the control group, the percentage of OKT3-positive cells was reduced (P = 0.014), and that of OKT4-positive cells increased (P = 0.014); there were no significant changes in the percentage of OKT8-positive cells (P = 0.171). After the CL-A had returned to normal values, the OKT4-positive cells remained elevated (P = 0.029), whereas the OKT3- (P = 0.342) and OKT8-positive cells (P = 0.443) showed no significant changes. When in the same patients, phases of increased CL-A were compared with phases in which values were not elevated, a reduced percentage of OKT3-positive cells was found in phases with increased CL-A (P = 0.031); however, the OKT4-positive and OKT8-positive cells did not differ significantly (P = 0.156 and 0.281).
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