We can increase our knowledge about human memory by studying brain-damaged patients suffering from amnesia. Such patients generally have extensive memory problems, which can be so great that they cannot remember that they read a newspaper or ate a meal within the previous hour. Over the past 30 years or so, there has been a dramatic increase in the amount of research that cognitive psychologists and cognitive neuropsychologists have carried out on amnesic patients.

Why are amnesic patients of interest? One reason is that the study of amnesia provides a good test-bed for existing theories of normal memory. Data from amnesic patients can strengthen or weaken the support for memory theories. For example, the notion that there is a valid distinction between short-term and long-term memory stores has been tested with amnesic patients. Some patients have severely impaired long-term memory but intact short-term memory, whereas a few patients show the opposite pattern. This is what is known as a double dissociation, and is good evidence that there are separate short-term and long-term stores.

Another reason for studying amnesic patients is that such research has led to new theoretical developments. Studies of amnesia have suggested theoretical distinctions that have proved relevant to an understanding of memory in normal individuals. Some examples are discussed later in the chapter.

Progress in this area has been slow. Some of the main reasons for this were identified by Hintzman (1990, p. 130):

The ideal data base on amnesia would consist of data from thousands of patients having no other disorders, and having precisely dated lesions [injuries] of known location and extent, and would include many reliable measures spanning all types of knowledge and skills, acquired at known times ranging from the recent to the distant past. Reality falls near the opposite pole of each dimension of this description.

Amnesic patients often have fairly widespread brain damage. This makes it hard to interpret the findings. It is especially hard to know which brain area is mainly responsible for a given memory deficit if, say, three different brain areas are all damaged.

In order to make sense of the findings from amnesic patients, it is necessary to have some background understanding of the amnesic condition. The reasons why patients have become amnesic are very varied. Bilateral stroke is one factor causing amnesia, but closed head injury is the most common cause. However, patients with closed head injury often have a range of cognitive impairments, and this makes it hard to interpret their memory deficit. As a result, most experimental work has focused on patients who have become amnesic because of chronic alcohol abuse (Korsakoff's syndrome). The symptoms of Korsakoff patients tend to become worse over time, whereas those of patients with closed head injury do not. It remains a matter of controversy whether there are enough similarities among these various groups to justify considering them together.

Amnesic syndrome

Those who think most amnesic patients form a similar or homogeneous group often refer to the "amnesic syndrome". Its main features are as follows:

• There is a marked impairment in the ability to remember new information which was learned after the onset of the amnesia; this is antero-grade amnesia.

• There is often great difficulty in remembering events occurring prior to amnesia; this is known as retrograde amnesia, and is pronounced in patients with Korsakoff's syndrome.

• Patients suffering from the amnesic syndrome generally have only slightly impaired short-term memory on measures such as digit span (the ability to repeat back a random string of digits). This is also shown by the fact that it is possible to have a normal conversation with an amnesic patient.

• Patients with the amnesic syndrome have some remaining learning ability after the onset of the amnesia.

The amnesic syndrome can be produced by damage to various brain structures. These structures are in two separate areas of the brain: a sub-cortical region called the diencephalon; and a cortical region known as the medial temporal lobe. It can be hard to pinpoint the precise location of damage in any given patient. Attempts to do so often used to rely on post-mortem examination, but the development of neuroimaging techniques has allowed accurate assessment of the damaged areas while the patient is alive.

Some of the brain areas that can produce the amnesic syndrome when damaged are shown in Figure 7.5. Chronic alcoholics who develop Korsakoff's syndrome have brain damage in the diencephalon, especially the medial thalamus and the mammillary nuclei, but typically the frontal cortex is also damaged. Other amnesics have damage in the medial-temporal region. This can happen as a result of herpes simplex encephalitis, anoxia (lack of oxygen), infarction, or sclerosis (involving a hardening of tissue or organs). There are other cases in which some of the temporal lobe was removed from epileptic patients to reduce the incidence of epileptic seizures. As a result, many of these patients (including the much-studied HM) became severely amnesic (Scoville & Milner, 1957). The exact extent of HM's brain damage was not known for many years. However, Corkin et al. (1997, p. 3978) carried out MRI on HM. They found that his brain damage was less extensive than had been believed previously. However, they "confirmed that the lesions responsible for the amnesic syndrome in HM are confined to the medial temporal lobe" (Corkin et al., 1997, p. 3978).

In most areas of cognitive neuropsychology, broad categories or syndromes have been replaced by a larger number of more specific categories. Why has this failed to happen with the amnesic syndrome? One possible reason is because nearly all amnesic patients exhibit the same pattern of symptoms. However, this seems very unlikely. As Downes and Mayes (1997, pp. 301-302) argued, "The [amnesic] syndrome almost certainly comprises several functional deficits with their own distinctive neuroanatomies."

A more convincing reason why most theorists have failed to identify sub-types of amnesia is because of the problems of identifying the precise area of brain damage in any given patient. The main brain structures that can be damaged in amnesics are close together, and this has made it hard to associate particular patterns of memory impairment with specific brain structures. However, Parkin and Hunkin (1997, p. 100) divided amnesic patients into those with lesions in the temporal lobe and those with lesions in the diencephalon, and concluded as follows: "We have examined the value of the contextual processing deficit hypothesis [the notion that amnesic patients have special problems in processing contextual information] and have shown that a contextual processing deficit only offers a means of explaining diencephalic amnesia."

Aggleton and Brown (1999) favoured a rather different theoretical position. According to Aggleton and Brown (1999, p. 426), "The traditional distinction between temporal lobe and diencephalic amnesics is

Some of the brain structures involved in amnesia (indicated by asterisks). Figure from "Clinical symptoms, neuropathology and etiology" by Nelson Butters and Laird S.Cermak in Alcoholic Korsakoff's syndrome: An information-processing approach to amnesia. Copyright © 1980 by Academic Press, reproduced by permission of the publisher.

Beat The Battle With The Bottle

Beat The Battle With The Bottle

Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.

Get My Free Ebook

Post a comment