The term “amnesia” is used generally to describe impairment or loss of memory. It is often subclassified as being either retrograde or anterograde. With retro- grade amnesia, memories that had previously been stored are no longer available. With anterograde amnesia, information occurring in real time does not enter long-term storage. Memory is a complex process comprising three different functions: (1) registration of information, (2) storage by reinforcement, and (3) retrieval.
Registration of Information. If information is not registered initially, it will not be remembered later. Failure to register is the explanation for absentminded- ness, probably the most common abnormality of memory.
Storage by Reinforcement. Repetition of information to be remembered or relating such information to other factors or events enhances later recall.
Retrieval. To recall the information, a person must search the “memory bank,” where it has been stored. Inability to recall information on request could result from a defect in any of the three aspects of memory function.
The key anatomic regions for registration and storage of memory traces are in an area often referred to as the Papez circuit, in which the fornix connects the hippo- campus to the mammillary bodies, which, in turn, are connected to the anterior nuclei of the thalamus by the mammillothalamic tract. The anterior thalamic nuclei project to the cingulate gyri, which then connect with the hippocampus, completing the circuit. The memory system is primarily cholinergic. The left medial temporal lobe is most concerned with verbal memory and the right temporal lobe with visual recall.
The prototype of amnestic disorders is Korsakoff syndrome, seen in chronic alcoholism and other states of vitamin B deficiency. This syndrome affects the medial thalamus and mammillary bodies and is characterized by an inability to record new memories and recall events of the recent past. Some patients confabulate to fill in gaps in their memory. Any bilateral destructive lesion of the thalami and medial temporal lobes can cause a similar syndrome. Such lesions include gliomas that spread bilaterally over the fornix and splenium of the corpus callosum; bilateral posterior cerebral artery infarctions, often caused by embolism of the top of the basilar artery; and herpes simplex encephalitis, a viral disease with predilection for temporal lobe damage. Lesions within the Papez circuit affect the “memory bank.” The patient is unable to recall items despite being given cues or being asked to select the correct item to be recalled from a group of alternatives. Uni- lateral lesions of the left medial temporal lobe and thalamus can produce amnesia that may last up to 6 months.
Head trauma often disrupts functions of memory. The severity of a head injury or concussion is often classified by the degree of retrograde amnesia that results; the longer the period of retrograde amnesia, the worse the injury. Head injury victims may also experience a period of anterograde amnesia.
Transient Global Amnesia. Total global amnesia is a particularly common memory disorder. In this benign syndrome, the patient seems bewildered and asks repetitive questions about the environment and activities, and, despite appropriate replies, asks the same questions moments later. The patient cannot form new memories and is often unable to recall events of the past days, months, and even years. Speech, reading, writing, calculations, drawing, and copying are normal, as are the results of the rest of the neurologic examination. Behavior and memory usually return to normal within 24 hours, but the patient is never able to recall events during the period of amnesia. Such attacks may recur, but the cause of the syndrome remains obscure.