indication

For therapeutic neurolysis of nerves or ganglia for the relief of intractable chronic pain in such conditions as inoperable cancer and trigeminal neuralgia (tic douloureux), in patients for whom neurosurgical procedures are contraindicated.

pharmacology

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.

mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes.

toxicity

Oral, rat LD₅₀: 5628 mg/kg. Symptoms and effects of overdose include nausea, vomiting, CNS depression, acute respiratory failure or death and with chronic use, severe health problems, such as liver and brain damage.

biotransformation

Hepatic. Metabolized by cytochrome P450 enzyme CYP2E1.

absorption

Rapidly absorbed.

drug interactions

Abacavir: Abacavir is partly metabolized through the alcohol dehydrogenase enzyme system. Alcohol increases the area under the curve (about 41%) of Abacavir. Interaction does not appear to be clinically significant.

Tizanidine: Ethanol increases the adverse effects of Tizanidine. The CNS depressant effects of these agents are additive.

Triprolidine: Triprolidine may enhance the CNS depressant effects of Ethanol.