The natural history of diabetic neuropathy and its risk factors are not well understood, apart from the recognition that prevalence increases with duration and, in many studies, degree of glycemia. The role of potential risk factors was therefore evaluated in a cross-sectional analysis from the baseline examination of the Pittsburgh Epidemiology of Diabetes Complications Study. We present results from the first 400 subjects seen at baseline examination. Neuropathy was determined by a trained internist with a standardized examination and was defined as the presence of at least two of three criteria: abnormal sensory or motor signs, symptoms consistent with neuropathy, and decreased tendon reflexes. The prevalence of neuropathy in this cohort was 34% (18%, 18-29 yr old, 58% greater than or equal to 30 yr old) with no difference by sex. By focusing on subjects greater than or equal to 18 yr old, all significant univariate variables (e.g., duration, glycosylated hemoglobin [HbA1]) were analyzed in 3 multiple logistic regression models: all subjects greater than or equal to 18 yr old and separating the same subjects into two groups based on age (18-29 and greater than or equal to 30 yr). Duration, HbA1, smoking status, and high-density lipoprotein cholesterol were found to be associated with neuropathy in the models for the greater than or equal to 18-yr-old group and the greater than or equal to 30-yr-old group. In the 18- to 29-yr-old group, duration, HbA1, and hypertension status were found to be significantly associated with neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied 62 patients with hemifacial spasm to test the presence of ephaptic transmission and ectopic excitation. The zygomatic and mandibular branches of the facial nerve were stimulated separately, recording simultaneously from the orbicularis oculi and mental muscles. Antidromic impulses were transmitted bidirectionally between the two branches. Transmission took place in a fraction of slow conducting motor nerve fibers. After-activity and late-activity were recorded as single potentials or trains, suggesting autoexcitation of fibers. The interspike frequency was 250 to 350 Hz. Hyperventilation produced synchronous clonic-tonic activity, suggesting ectopic excitation caused by hypocalcemia. Ectopic excitation and ephaptic transmission are important pathophysiologic factors in hemifacial spasm.

Pathologic and pathophysiologic findings in hemifacial spasm are reviewed in connection with recent theoretical and experimental studies of ectopic/ephaptic excitation. The intracranial segment of the normal facial nerve is ensheathed by an arachnoid membrane only and shows no fascicular organization. In hemifacial spasm, this segment shows signs of demyelination. Several electrical phenomena relating to ectopic excitation, ephaptic transmission between facial nerve fibers, and autoexcitation can be reproduced in clinical electrophysiologic studies of hemifacial spasm. These abnormalities gradually disappear after facial nerve decompression in the cerebellopontine recess. It is concluded that the normal facial nerve is vulnerable to minor compression, the primary pathophysiologic mechanism in hemifacial spasm is ectopic/ephaptic excitation due to compression and demyelination of the intracranial segment of the facial nerve, and the facial nerve in hemifacial spasm is a useful model for the study of ephaptic transmission, which has provided new information about the resolution of abnormal electrical events after decompression.

The need for a standardized and valid means of assessing diabetic neuropathy has been increasingly recognized. To identify potential components of such an assessment, interobserver variation (neurologist and internist) of a standard neurologic examination and the comparability of this examination with vibratory and thermal sensitivity testing was studied. The study population comprised the first 100 participants in a neuropathy substudy of 25- to 34-yr-old subjects with insulin-dependent diabetes mellitus taking part in a cohort follow-up study. Symptoms of dysesthesias, paresthesias, and burning, aching, or stabbing pain revealed good interobserver agreement. Signs of neuropathy, more prevalent in the great toe than index finger, showed poor interobserver agreement for vibration, but fair interobserver agreement for touch and pinprick. Mean quantitative sensory thresholds differed significantly by clinical category of abnormal vibratory and pinprick sensations. Threshold testing showed twice the prevalence of abnormality compared with clinical examination. It is concluded that components of the clinical examination can be identified that, along with quantitative sensory-threshold testing, may provide a satisfactory core assessment for use both in epidemiologic studies and incorporation into more in-depth protocols required for clinical research and practice. The clinical relevance of the greater prevalence of abnormalities on threshold testing will be established by long-term follow-up.