**4.4 Visual symptoms**

Typically, vision loss occurs as a direct result of a toxic or corrosive material striking the cornea and conjunctiva or because the lens loses its transparency due to cataract formation. Direct attacks on the neuronal components of the visual system are less common than indirect attacks. Mydriasis and miosis are two distinct symptoms caused by exposure to or use of parasympathomimetic medications, anticholinesterase inhibitors, and parasympatholytics such as atropine. Nystagmus can develop as a side effect of certain medications, including phenytoin and antibiotics (aminoglycoside). Neurotoxic exposure is rarely associated with direct retinal injury despite a possible association with specific therapeutic medications. Both toluene (which induces demyelination) and hexachlorophene can cause optic nerve injury (leading to deformation of myelin). Alcohol addiction (methanol or ethanol) is also associated with widespread damage of the neuronal components of the visual system. Nonetheless, the etiology is suspected to be compounded by many chronic alcoholics' nutritional deficiencies [6, 7].

## **4.5 Peripheral nervous system neuropathies**

These are frequently mistaken with axonopathies. However, the terms do not refer to the same thing. Peripheral neuropathy can develop within the neuron, resulting in the death or dysfunction of cells (in which case we call a neuronopathy). Axon degeneration (axonopathy) or loss of neuronal or axonal function may occur when the myelin sheath is disrupted. Channelopathy may develop from a change in the function of ion channels, or the toxin may target nerve terminals (leading to a neuromuscular transmission syndrome). Neuronopathies are easily recognized since they are much more likely to be sensory in origin and affect areas supplied by the injured neurons. The mechanisms by which they cause harm are not well understood. Methyl mercury is the neurotoxin most frequently connected with this illness. Proprioception may be compromised before or more severely than subsequent pain, whereas nerve conduction velocity and muscular strength are preserved. Healing is unpredictable, as neurons may survive or perish as a result of the toxic insult. Demyelinating neuropathies affect the peripheral nervous system when the Schwann cell or internode's myelin sheath is damaged. Diphtheria toxin can cause segmental demyelination by damaging the Schwann cell. Hexachlorophene and perhexiline have also been associated with myelin disturbance. Recovery is dependant upon the activation and replication of surviving Schwann cells. Regenerated internodes are slightly shorter than typical in length, myelin sheaths are thinner, and nodes can be somewhat longer than usual. Remyelinated axons conduct at a slower pace in general. Axonopathies are lesions of the peripheral nervous system produced by axon

destruction. The presenting signs and symptoms typically manifest gradually and initially impact the long axons and distant locations. Sensory symptoms predominate over motor problems, and ankle reflexes degrade fast. The signs and symptoms then spread proximally for the duration of the axon's "regeneration." Healing occurs as a result of damaged axon regrowth. Recovery is often slow due to the 0.5–3.0 mm per day rate of axonal development. Numerous industrial chemicals, such as acrylamide, arsenic, carbon disulfide, n-hexane, lead, organic mercury, and thallium, have been shown to cause axon damage. While recovery is often uncomplicated, chronic ataxia, stiffness, and hyperreflexia can occur following severe poisoning. Axonal channelopathies are caused by aberrant ion channel activity and manifest as faulty axonal conduction. These are typically made up of natural toxins. The motor nerve terminal is a major target for a range of natural neurotoxins (clostridial toxins, cone snail toxins, snake, spider, and scorpion venoms), all of which induce harm to the nerve terminal. What is unknown is the involvement of the nerve terminal in the expression of toxic insult induced by a variety of harmful substances, including organophosphates and acrylamide, both of which have been shown to cause considerable nerve terminal damage. It is unsurprising that most axonopathies that die back originate at the nerve terminal [6, 7, 9].
