What alcohol-related cognitive impairments occur? - Chapter 18

What is an alcohol-related disorder?

How often do alcohol-related disorders occur?

Of all patients, almost half have a primary alcohol-related problem. The average age is around 45 years old, and three-quarters of those seeking help are male. Almost 50% of the people who seek treatment for their alcohol addiction also have cognitive impairments due to prolonged and excessive alcohol consumption. 10% have a serious disorder such as Korsakoff's syndrome. Alcohol results in three simultaneous processes that can be classified into direct neurotoxic effects, indirect neurotoxic effects and an irreversible influence on physiological processes due to chronic B1 deficiency. The acute effects of alcohol influence prospective memory, explicit memories, reduced ability to perceive (the intensity of) emotions, less response inhibition and loss of control. The chapter only deals with chronic effects.

Neurotoxicity

By stimulating the GABA system, the overall neurotransmission is slowed down, causing disorders. The inhibition on NMDA receptors (glutamate) mainly cause memory disorders. As a counter-reaction, more NMDA receptors come and become more sensitive. The brain is particularly sensitive to alcohol effects in adolescence.

Neuropathology

The neocortex (especially the frontal lobes), the hippocampus, the cerebellum and the limbic system (especially the hypothalamus) are the structures that are most sensitive to alcohol. In the frontal lobes there is a loss of volume due to less frontal blood flow and metabolism. The hypothalamus has less volume due to white matter changes and within the cerebellum there is much atrophy in the white matter. The hypothalamus has less volume also due to changes in the white matter. If the patient completely stops using alcohol, the volume loss is partially reversible.

Which cognitive impairments can occur?

What general impairments are caused by alcohol?

After a short abstinence period (less than a month), patients had problems in the areas of impulsiveness, risk taking, problem-solving, cognitive flexibility, attention, and perceptuomotor speed. In a group of patients with alcohol use disorder (AUD) who had been abstinent for 32 days, only changes in verbal episodic memory were demonstrated (Errico, King, Lovallo & Parsons, 2002), while after six years most of them no longer had cognitive impairments (Fein, Torres, Price & Di Sclafani, 2006). Those who still experience problems, experience this mainly in the field of visual-spatial skills, decision-making and executive functioning. Ihara, Berrios and London (2000) distinguish four patterns of cognitive impairment:

1. Impaired executive functions with spared intelligence and memory.

2. Combined executive impairments and memory deficits with spared intelligence.

3. Global cognitive deterioration.

4. Unimpaired cognitive capabilities.

Two-thirds of the patient group studied fell into one of the last two categories. Alcoholics mainly look at their chance of winning in the short term; not to the long-term consequences. Furthermore, they know what is expected of them in social problem situations, but they cannot inhibit their inappropriate behaviour. There are also indications that they are less accurate in recognizing facial expressions (they experience a sad face as a hostile face directed at them). The continuity hypothesis assumes a dose-response relationship with social drinkers at one end and patients with Korsakoff at the other end.

Korsakoff's syndrome

Korsakoff's syndrome is an amnestic syndrome in which the patient has great difficulty learning new information and digging up present information. A long-term poor diet leads to Korsakoff's syndrome. This makes Korsakoff an indirect effect of alcohol abuse: the cause is a long-term deficiency of thiamine (B1). Sometimes Korsakoff's syndrome is called Wernicke-Korsakoff syndrome because 80 to 90% of all alcoholics with Wernicke's encephalopathy develop a Korsakov syndrome. Wernicke's encephalopathy is an acute syndrome characterized by ataxia, nystagmus, ophthalmoplegia, confusion, and apathy (not all characteristics need to be present). Neuropathological abnormalities are mainly found in the nuclei of the thalamus, the mammillary bodies (part of the hypothalamus) and structures around the third and fourth ventricle.

Confabulations in Korsakoff's syndrome

Korsakoff patients have little or awareness of their disease and the confabulate spontaneously. There are disturbances in the anterograde memory, the retrograde memory (note the temporal gradient: more recent years are remembered worse) and in the executive functions (and the working memory). The classic syndrome is based on an isolated memory disorder and the inability to live independently. The implicit memory is intact. Relatively speaking, the visual functions, the abstraction capacity and the general intelligence are also spared (although subtle deviations are revealed on tests). The spontaneous confabulations are not caused by a tendency to fill in memory gaps. Three possible causes are:

• Decreased executive control, as a result of which incorrect memories are retrieved (impairment in the 'retrieval strategy').

• Temporal confusion, as a result of which correct memories are associated with the wrong time.

• Impaired reality monitoring, which causes a discrepancy between the ongoing reality and retrieved memories. Fragments of memories from the past are erroneously activated and not suppressed, and are consequently distorted and then linked to the ongoing reality.

• The spontaneous confabulations are mainly present in the acute phase of Korsakoff's syndrome, and gradually decrease (or sometimes disappear completely).

Alcohol-related dementia

The differential diagnosis between Korsakov's syndrome and alcohol dementia is difficult. Alcohol related dementia is expressed by memory deficits, but there are no validated criteria on which a diagnosis should be based. An alcohol dementia is different from other dementias for several reasons, because:

• There is no clear pathophysiological process or underlying neuroanatomical substrate. It is for this reason that there is talk of an 'alcohol-related dementia' (ARD).

• There is no further progression of cognitive functioning in abstinence.

• According to Oslin, Atkinson, Smith and Hendrie (1998), the dementia must still be present sixty days after the last drop of alcohol has been consumed, which should have been preceded by a history of at least five years of excessive alcohol use.