Effects of Alcohol

Alcohol acts as a CNS depressant, which, in small doses interferes with cortical function, but in larger doses may depress medullary processes. The apparent stimulatory effects of alcohol occur because it acts first on the so-called higher centers of the brain that govern inhibition (141).

Although there is general agreement on the sequence of clinical effects caused by drinking alcohol, the blood alcohol concentrations at which these effects occur vary in different subjects. The difference in susceptibility is most marked between habituated and nonhabituated drinkers, but tolerance to the effects remains variable even within these broad categories (142,143).

Table 15

Sequence of Central Nervous Depressant Effects of Alcohol

Table 15

Sequence of Central Nervous Depressant Effects of Alcohol

Stage of influence

Blood alcohol concentration mg/100 mL

Clinical effect

Sobriety

10-50

• Often no obvious effect; may feel "relaxed"

Euphoria

30-120

• Mild euphoria with increased talkativeness

• Decreased inhibitions

• Increased self-confidence

• Impaired fine motor skills

Excitement

• Poor sensory perception

• Impaired memory and comprehension

• Incoordination and loss of balance

Drunkenness

150-300

• Disorientation, mental confusion

• Decreased pain sense

• Increased incoordination with staggering gait

• Slurred speech

Stupor

250-400

• General inertia approaching paralysis

• Marked lack of response to stimuli

• Inability to stand or walk

• Vomiting, incontinence of urine and feces

Coma

• Depressed or absent reflexes

• Cardiovascular and respiratory depression

• Possible death

Death

Over 450

• Death from respiratory depression

Table 15 provides a guide to the general effects. It should be noted that the effects are more pronounced when blood alcohol levels are rising than when falling. This is known as the Mellanby effect and is believed to result from an acute tolerance to alcohol that develops during intoxication (144). Some specific effects are discussed.

4.2.1. Nystagmus

Because the eye is effectively part of the CNS, it is one of the easiest parts of the body to examine to detect the effects of alcohol; the most extensively studied ocular effect of alcohol intoxication is nystagmus. Alcohol can cause nystagmus through at least two mechanisms. By acting on the vestibular system, it can cause positional alcohol nystagmus (PAN) (145), detected when the patient is lying supine with the head turned to either the left or right. Horizontal gaze nystagmus (HGN) results from the inhibition of the smooth pursuit system and the impaired ability to maintain eccentric gaze (146) brought about by alcohol's effect on ocular movements via neural mechanisms (147).

Positional alcohol nystagmus occurs in two stages (148). The first stage, PAN I, is associated with acute elevation of blood alcohol, tending to occur approx 30 minutes after alcohol ingestion. In PAN I, the fast phase of nystagmus is in the direction toward which the head is turned. PAN II normally occurs at approx 5-6 hours after drinking and is characterized by nystagmus in the opposite direction to that seen in PAN I.

HGN is a jerky eye movement noted when gaze is directed to one side. The fast phase of HGN is in the direction of gaze, and it becomes intensified at a more eccentric gaze position (147). Although HGN can be seen in normal individuals at extreme lateral gaze (149), when detected at lesser deviations, it is considered pathological. An angle of onset of 40° or less from the midline is a sensitive indicator of a blood alcohol level in excess of 100 mg/100 mL (143). Although some authors have maintained that blood alcohol levels of more than 80 mg/100 mL are consistently associated with HGN (150), others have found that it is absent in just less than 40% of drivers with an average blood alcohol of 120 mg/100 mL (range 9-218 mg/100 mL) (151). Because HGN may be noted in several pathological conditions, including the ingestion of sedative and tranquilizing drugs (152), its presence should not be taken as proof of alcohol intoxication. It is perhaps for these reasons that the Kansas Supreme Court, when assessing the admissibility of HGN evidence in drink driving prosecutions decided that "the reliability of HGN evidence is not currently a settled proposition in the scientific community" (153).

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