N-hexane Polyneuropathy Research Articles

P956: N-hexane polyneuropathy: clinical and electrophysiological review with five patients

P956: N-hexane polyneuropathy: clinical and electrophysiological review with five patients

Central nervous system involvement in n-hexane polyneuropathy demonstrated by MRI and proton MR spectroscopy

Central nervous system involvement in n-hexane polyneuropathy demonstrated by MRI and proton MR spectroscopy

Glue sniffing polyneuropathy: an under recognized aspect of a public health hazard

Glue sniffing polyneuropathy: an under recognized aspect of a public health hazard

Focal conduction block in n-hexane polyneuropathy

Focal conduction block in n-hexane polyneuropathy

Focal conduction block in n‐hexane polyneuropathy

A 19-year-old man with an asymptomatic history of recreational gasoline vapor inhalation presented with subacute progressive quadriparesis. For 2 weeks, he had intensely inhaled Coleman® fuel oil vapor, which contains n-hexane. Nerve conduction studies including near-nerve needle stimulation showed focal conduction block in the bilateral median and ulnar nerves. Sural nerve biopsy was consistent with giant axonal neuropathy. Conduction block as seen in this case has not heretofore been described in n-hexane polyneuropathy. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:964–969, 1998.

Magnetic nerve root stimulation in two types of brachial plexus injury: Segmental demyelination and axonal degeneration

Magnetic cervical nerve root stimulation was performed in 9 patients with plexopathies secondary to suspension (SP) and in 12 cases with neurogenic thoracic outlet syndrome (NTOS). The findings were compared with those of the previously reported case groups: n-hexane polyneuropathy (HPNP), inflammatory demyelinating polyneuropathy (IDP), and motor neuron disease (MND). Muscle responses elicited by magnetic stimulation had very high rates of amplitude and area loss in the neck-axilla segments of the 6 SP patients. This, along with the other electrophysiological findings, suggested the presence of segmentally demyelinating plexus lesions. In NTOS patients, magnetic stimulation findings were not significantly different from those of the controls. Neck-axilla segment amplitude and are reduction rates in SP and IDP patients were significantly higher than those found in NTOS, HPNP, and MND groups, implying that magnetic nerve root stimulation may have a role in the demonstration of segmentally demyelinating lesions involving proximal nerve segments.

N-Hexane Polyneuropathy in Japan: A Review of n-Hexane Poisoning and Its Preventive Measures

n-Hexane Polyneuropathy in Japan: A Review of n-Hexane Poisoning and Its Preventive Measures

Determination of urinary 2,5-hexanedione concentration by an improved analytical method as an index of exposure to n-hexane.

2,5-Hexanedione is a main metabolite of n-hexane and is considered as the cause of n-hexane polyneuropathy. Therefore, it is useful to measure 2,5-hexanedione for biological monitoring of exposure to n-hexane. The analytical methods existing for n-hexane metabolites, however, were controversial and not established enough. Hence, a simple and precise method for determination of urinary 2,5-hexanedione has been developed. Five ml of urine was acidified to pH 0.5 with concentrated hydrochloric acid and heated for 30 minutes at 90-100 degrees C. After cooling in water, sodium chloride and dichloromethane containing internal standard were added. The sample was shaken and centrifuged. 2,5-Hexanedione concentration in an aliquot of dichloromethane extract was quantified by gas chromatography using a widebore column (DB-1701). Urinary concentration of 2,5-hexanedione showed a good correlation with exposure to n-hexane (n = 50, r = 0.973, p less than 0.001). This method is simple and precise for analysis of urinary 2,5-hexanedione as an index of exposure to n-hexane.

An electrophysiological follow up of patients with n-hexane polyneuropathy.

Electroneurographic (ENeG) and evoked potential (EP) studies were regularly performed on 11 printing workers with n-hexane polyneuropathy after cessation of exposure. At the initial examination, the ENeG studies simulated a demyelinative process. Further slowing of nerve conduction velocity, or further decreasing of action potential amplitude, or both in the follow up ENeG study were found in about half the patients. The motor distal latency did not worsen. Nerve conduction returned to normal earlier in the sensory than in the motor nerves. After the patients had regained full motor capability, conduction velocities in motor nerves were still significantly slowed. These ENeG characteristics correlate with the pathological and pathophysiological changes in experimental hexa-carbon neuropathies. The initial findings from the EP studies indicated a conduction abnormality in the central nervous system (CNS). Delayed worsening occurred in the amplitude of visual EPs in three patients. On serial follow up, the interpeak latency and interpeak amplitude of visual EPs improved little. Residual abnormalities were also found in the interpeak latency of auditory EPs in the brainstem and in the absolute latency of scalp somatosensory EPs from the peroneal nerve. Astroglial proliferation in the CNS probably impedes recovery of the abnormalities in EP.

Biphasic recovery in n-hexane polyneuropathy A clinical and electrophysiological study

We studied the course of recovery in n-hexane polyneuropathy in 4 patients by quantitatively assessing clinical and electrophysiological features. The electrophysiological study included measures of motor conduction of the median, ulnar, tibial and peroneal nerves and sensory conduction of the median, ulnar and sural nerves. After cessation of exposure, there was an initial worsening in muscle strength, sensory deficit and nerve conduction for up to 2-5 months. This deterioration was more severe and prolonged in the lower limbs than in the upper limbs. The period of deterioration was followed by a slow recovery studied for 1 year.

Neurotoxic effects of n-hexane on the human central nervous system: evoked potential abnormalities in n-hexane polyneuropathy.

An outbreak of n-hexane polyneuropathy as a result of industrial exposure occurred in printing factories in Taipei area from December 1983 to February 1985. Multimodality evoked potentials study was performed on 22 of the polyneuropathy cases, five of the subclinical cases, and seven of the unaffected workers. The absolute and interpeak latencies of patterned visual evoked potential (pVEP) in both the polyneuropathy and subclinical groups were longer than in the normal controls. The pVEP interpeak amplitude was also decreased in the polyneuropathy cases. Brainstem auditory evoked potentials (BAEP), showed no difference of wave I latency between factory workers and normal controls, but prolongation of the wave I-V interpeak latencies was noted, corresponding with the severity of the polyneuropathy. In somatosensory evoked potentials (SEPs), both the absolute latencies and central conduction time (CCT) were longer in subclinical and polyneuropathy cases than in the unaffected workers and normal controls. From this evoked potentials study, chronic toxic effects of n-hexane on the central nervous system were shown.