This is not to be confused with "meth", a common abbreviation for methamphetamine and for methadone in Britain and the United States. Mechanism
Methanol is toxic by two mechanisms. First, methanol (whether it enters the body by ingestion, inhalation, or absorption through the skin) can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning. Second, in a process of toxication, it is metabolized to formic acid (which is present as the formate ion) via formaldehyde in a process initiated by the enzyme alcohol dehydrogenase in the liver. Methanol is converted to formaldehyde via alcohol dehydrogenase and formaldehyde is converted to formic acid (formate) via aldehyde dehydrogenase. The conversion to formate via ALDH proceeds completely, with no detectable formaldehyde remaining. Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances. Treatment
Methanol poisoning can be treated with fomepizole, or if unavailable, ethanol may be used. Both drugs act to reduce the action of alcohol dehydrogenase on methanol by means of competitive inhibition. Ethanol, the active ingredient in alcoholic beverages, acts as a competitive inhibitor by more effectively binding and saturating the alcohol dehydrogenase enzyme in the liver, thus blocking the binding of methanol. Methanol is excreted by the kidneys without being converted into the very toxic metabolites formaldehyde and formic acid. Alcohol dehydrogenase instead enzymatically converts ethanol to acetaldehyde, a much less toxic organic molecule.
Congenital oculomotor palsy
The origins of the vast majority of congenital oculomotor palsies are idiopathic. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma. Acquired oculomotor palsy
Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm, particularly of the posterior communicating artery
Space occupying lesions or tumours, both malignant and non-malignant
Inflammation and infection
Trauma
Demyelinating disease (multiple sclerosis)
Autoimmune disorders such as myasthenia gravis
Post-operatively as a complication of neurosurgery
Cavernous sinus thrombosis

Mechanism
As the pair of oculomotor nerves arises from different subnuclei in the midbrain, courses through different structures in the brain and branches into superior and inferior divisions after exiting the cavernous sinuses, any lesions along its path will produce different pathological features of the third nerve palsy. The parasympathetic aspect of the nerve (which constricts pupils and thicken the lens) is located on the nerve surface, supplied by pial blood vessels. The nerves core contains the main trunk of the oculomotor nerve, supplied by vasa vasorum. Thus pathologies affecting the nerves core without affecting the superficial part of the nerve (thus sparing the pupillary reflex) are known as "medical" oculomotor nerve palsy.