The Amnesic Syndrome

Perhaps the most well-known amnesic patient is H.M., who was treated surgically in 1953 to relieve the symptoms of severe epileptic seizures. The operation involved lesioning of the hippocampus bilaterally, which did help with the epileptic seizures, but also produced a profound memory deficit. Animal researchers have since discovered that the memory deficit suffered by H.M. was not entirely attributable to hippocampus damage; cortical areas adjacent to the hippocampus (entorhinal, perirhinal, and parahippocampal cortices) were also damaged during the surgery, as was the amygdala. Stuart Zola-Morgan and Larry Squire have since conducted studies on monkeys to determine which of the damaged structures is most critical to healthy memory performance. One of the tasks that they use is called the "delayed non-matching to sample" task. The monkey is first shown an object, under which is hidden a reward (e.g., a raisin). The monkey lifts up the object and receives the reward. Then, after varying delays, the monkey is presented with two objects, one of which is the same as the first object, and the other different. This time, the reward is hidden beneath the new object. The critical question is whether the monkey will remember which object he/she lifted before, because the reward is now situated under the other object. Presumably, the reward is situated under the new object to rule out successful performance based on perseveration of the prior response (an influence not unrelated to the automatic influence in Jacoby's work; in a way, the task pits automatic and recollective influences in opposition). The critical results from these studies are that memory performance for the monkey deteriorates with increases in the time interval between the single object and two object trials. By lesioning different parts of the brain, researchers also discovered that damage to the amygdala does not play an important role in the amnesic syndrome, but that damage to the cortical areas surrounding the hippocampus, as well as damage to the hippocampus itself, does play an important role. Perhaps most interesting is that a severe amnesia can occur without damage to the hippocampus, if the cortical areas surrounding the hippocampus are lesioned (perirhinal and parahippocampal cortices).

The amnesic syndrome can result from damage to other structures as well. In particular, patients with Korsakoff's syndrome exhibit behaviors that are quite similar to those with medial temporal lobe damage (e.g., H.M.), although the damage in Korsakoff's syndrome is to the diencephalon rather than to the hippocampus and adjacent medial temporal areas. The implication of this is that the amnesic syndrome occurs as a result of damage to a memory system, where damage to any number of parts of the system can result in the same pattern of deficits. Or, alternatively, the amnesic syndrome may not be a pure deficit, and medial temporal lobe amnesics should perhaps be studied separately from those with other types of damage. To substantiate this view, you would want to show that medial temporal lobe amnesics show different patterns of impairment than Korsakoff patients. Larry Squire has reported one such finding, where Korsakoff patients were shown not to produce a release from proactive interference effect, while patients given electro-convulsive therapy to treat depression (which also causes a short-lived amnesia) did produce a release from proactive interference effect. However, a critical control subject in this study was an amnesic who had been injured in an accident with a pointed instrument. The injury was specific to the diencephalic area (thalamus, hypothalamus). Although one might expect this patient to produce data similar to the Korsakoff patients, this patient did produce a normal release from proactive interference effect. The implication of this result is that the failure to produce the release from proactive interference effect may have been due to damage in other parts of the brain in the Korsakoff patients (e.g., the frontal lobes). The possibility that there are differences among amnesic patient types remains an open question.