Acrylamide neurotoxicity and mechanism of action Acrylamide acute toxicity tests in rats, mice and rabbits showed oral LD50 of 150-180 mg/kg, which indicates that it is only moderately toxic, but its high neurotoxicity to humans has been recognized, and its toxic effects on the heart, liver, kidney and other systems are gradually being recognized. As early as 1956, it was found that occupational exposure to acrylamide caused contact dermatitis, erythema, desquamation, and phytodysfunction due to direct skin irritation in exposed areas of workers. Further peripheral nerve damage occurred. The epidermal peeling caused by dermatitis can promote further absorption of acrylamide, thus aggravating the skin lesions. The main symptoms of long-term occupational exposure to acrylamide are numbness, weakness, sweaty hands and feet, headache and dizziness, and diminished distal tactile sensation, etc. When the cerebellum is involved, hobbling, tremor sensation of the limbs, and diminished deep reflexes may also occur. Mechanisms of neurological damage: Acrylamide is an accumulative neurotoxin that damages both the central and peripheral nervous systems. It can inhibit the enzymes related to axonal transport in the axon, which leads to swelling and degeneration of the axon and degeneration of the Schwann cells, and eventually leads to degeneration and loss of the myelin sheath. This results in different degrees of damage to the cerebral cortex, cerebellum, and optic thalamus. The distal peripheral nerves are more affected than the proximal ones, and the axons of the circumferential lamina propria of the foot, which is innervated by thick nerve fibers, and the peroneal nerve endings are usually the first to show axonal degeneration. In addition, a large number of nerve fibers in the long tracts of the spinal cord, such as the cerebellar tract of the spinal cord, can be degenerated. The distal involvement of these centripetal central fibers coexisted with the distal degeneration of peripheral nerves, which LOPACHIN called central-peripheral distal axonopathy. Upon further study, he suggested that the same damage to the end plate and Purkinje fibers also played an important role. Clinical manifestations of acrylamide poisoning After long-term exposure to low concentrations of acrylamide, the exposed local skin becomes sweaty, wet and cold, peeling and erythematous. Patients complain of general weakness, numbness of the limbs, swelling of the hands, sweating, peeling, movement disorders, and sexual dysfunction in married patients. This may be followed by numbness and tingling in the extremities, weakness of the lower limbs, and drowsiness. Cerebellar dysfunction can occur within a month or so after exposure to high levels of acrylamide, even if it is short-term. The symptoms include horizontal nystagmus, slurred speech, reduced muscle tone in the limbs, unstable finger, nose and knee movements, dysmotility, and staggering gait. In severe cases, cerebellar dysfunction may subside after a few weeks of exposure, followed by peripheral nerve damage. Multiple peripheral neuropathies are the main manifestations of chronic acrylamide poisoning. The onset is usually insidious. In mild acrylamide poisoning, the early manifestations include impaired vibration sensation in the extremities and blunted Achilles tendon reflexes. In mild to moderate acrylamide poisoning, the sensory impairment gradually extends to the elbow and knee level or ataxia due to deep sensory impairment, inability to walk in a straight line with both feet, inability to stand on one foot and difficulty in standing with eyes closed. Neuro-electromyography is important for early diagnosis. Treatment of acrylamide poisoning We have treated hundreds of patients with acute and chronic acrylamide poisoning in the past decade, and all of them have been successfully cured without any sequelae. Poisoned patients can call 13864459864 for consultation.