Increased endoneurial fluid pressure in experimental lead neuropathy

Abstract

THE endoneurial compartment of peripheral nerve is relatively inaccessible because of its small size and is maintained in a specialised environment by means of a perineurial barrier¹, a blood–nerve barrier² and a cerebrospinal fluid barrier. We have gained access to the endoneurial compartment of mammalian peripheral nerve by means of small polyethylene matrix (PEM) capsules and have recorded endoneurial fluid pressure (EFP) using an active servo null system³. The solid PEM capsules have pores of approximately 60 µm which facilitate entry of fluid into the interstices and connecting polyethylene tubing, but unlike hollow capsules⁴, are not invaded by connective tissue. We have used PEM capsules to make serial measurements of EFP in control and lead-fed rats and watched the pathological changes. We did this because of the prominence of endoneurial oedema in, for example, inflammatory polyradiculoneuropathy⁵, diabetic neuropathy⁶, acromegalic neuropathy⁷ and experimental lead⁸ and galactose^9,10 neuropathies, and because external pressure causes segmental demyelination and even axonal degeneration of peripheral nerve fibres¹¹. We found that EFP increased progressively in lead-fed rats and preceded the onset of fibre pathology. The time course of the increase and of fibre pathology suggests that increased EFP is a cause of segmental demyelination in lead neuropathy.