N-hexane is a component of a number of glues. Therefore, exposure is likely to come from inhalant abuse. With acute exposure, N-hexane causes euphoric effects. Pronounced peripheral polyneuropathy may occur after chronic intoxication. Hexane is metabolized to 2,5-hexanedione (2,5-HD), which is responsible for much of the neurotoxicity related to this compound.
Unlike toluene, hexane does not produce significant central neurological symptoms. Lightheadedness, headache, decreased appetite, and mild euphoria as well as occasional hallucinations may occur acutely, but seizures and delirium are not associated with N-hexane exposure. The predominant neurological feature of N-hexane exposure appears to be peripheral neuropathy. Symmetrical sensory dysfunction in the hands and feet is the usual presenting complaint. Decreased response to pin, vibration, and thermal stimulation is found on examination. Glue huffers may develop proximal weakness. The most prominent electrophysiological feature is slowing of motor and nerve conduction velocities, which occurs in proportion to the intensity of clinical disease. y
Methyl-N-butyl ketone (MBK) is used as a paint thinner, cleaning agent, and solvent for dye printing. Exposure to MBK is associated with sensorimotor polyneuropathy, which may begin several months after continued chronic exposure. In the later stages, axonal degeneration occurs distally.
There is no specific treatment for N-hexane and MBK neuropathy other than removal from the source of exposure. After removal, recovery (regeneration of peripheral nerve axons) may occur over a period of weeks.
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