Early diagnosis of n‐hexane–caused neuropathy

Abstract

n-Hexane neuropathy was studied in 20 workers exposed for prolonged periods to this solvent, and with urinary 2,5-hexanedione concentrations exceeding the biological exposure index recommended by the American Conference of Governmental Industrial Hygienists (5 mg/L) with a mean of 11.02 mg/L (range 5.3-24.2 mg/L). Although neurological examination did not detect significant anomalies in any of the patients, and the conduction velocity and F waves of all the nerves tested were normal, neurographic studies revealed significant differences in the amplitude of sensory nerve action potentials (SNAP) recorded from the sural (mean 14.0 microV), median (mean 17.3 microV), and ulnar (mean 7.9 microV) nerves when compared with normal values from healthy adults of the same age range, examined under identical conditions. The amplitude of the SNAP in sural and median nerves correlated significantly with the number of years worked. The notable decrease in mean amplitude of the SNAP appeared to reflect the primary neurotoxic effects of 2,5-hexanedione.

n-Hexane Neuropathy Caused by Addictive Inhalation: Clinical and Electrophysiological Features

“…Our findings show that the clinical manifestations of n-hexane abuse neuropathy are similar, although of a severer degree, to those seen in patients suffering from chronic industrial exposure [1, 2, 3, 4, 5, 6, 7, 8]. n-Hexane abuse results in subacute motor-dominant polyneuropathy associated with anorexia and body weight loss; the duration of disease progression after the withdrawal of the chemicals was maximally 4 months.…”

“…The neurological manifestations of n-hexane neuropathy are uniform and predominantly characterized by motor polyneuropathy, disease progression despite discontinuance of the chemicals, and slow recovery [3, 4, 5, 6, 7, 8]. Nerve conduction studies have shown reduced conduction velocities and amplitudes of both motor and sensory responses [2, 3, 7, 8], suggesting mixed axonal and demyelinating features.…”

N-hexane neuropathy with vertigo and cold allodynia in a silk screen printer: A case study

“…In our patient, the reflexes were preserved, probably due to the short duration of the disease. According to the previous studies, significant decrements in sensory action potential (SAP) amplitudes for the median and sural nerves have been shown to be indicators for early detection of n-hexane-induced peripheral neuropathy in asymptomatic workers with exposure to n-hexane [4,11]. Also a decrease in motor and sensory conduction velocities in people exposed to n-hexane has been shown in the previous studies [12].…”

Electrophysiological Studies of Shoemakers Exposed to Sub‐TLV Levels of n‐hexane

“…In occupationally exposed workers following a sufficient level of exposure to HEX, subjects gradually experience weakness and/or numbness and paresthesia in their distal extremities 2,4,6) . The severity of the neuropathy and the related clinical signs and symptoms are proportional to the intensity, duration and frequency of exposure 9,11,12) . Following continued exposure or recurrent episodic exposures to higher concentrations, motor signs and symptoms can also appear 4,13) .…”

“…Furthermore, conventional needle electromyographic examinations may show some abnormalities such as minimal signs of denervation 2,14) . In asymptomatic workers exposed to HEX, a subclinical neuropathy can be detected by certain abnormalities in nerve conduction studies (NCS) such as diminished amplitudes of sensory nerve action potentials (SAP) in the sural, median and ulnar nerves compared with age-matched normal controls 12) . In patients with clearly established neuropathy, all the above changes became much more pronounced, and marked decreases in MCV and SCV and obvious prolongation of distal and F-wave latencies (DL) also occur 2,4,5) , suggesting that the primary neurotoxic effect of 2,5-hexanedione (2,5-HD) is axonal with secondary demyelination 7,11) .…”