What Is Memory Disorders:And What Causes Memory Loss

What is memory disorders.Memory describes the processes by which past experience is stored and retrieved. Disorders of memory include anterograde amnesia, i.e., the failure to store new memories, or retrograde am­nesia, i.e., disorders of storage or retrieval of memories laid down in the past.

Certain separable stages in memory storage have become clear from clinical observation. There is a stage of immediate memory, which is the ability to retain material presented as long as attention is not distracted. This is examined by such tests as digit span, i.e., the ability to repeat a series of digits spoken by the examiner. Most normal persons can immediately repeat a series of seven such digits. The next step is trans­fer to the long-term memory store. The first step in this is intermediate memory storage, and the later step is called remote memory. The reasons for separating these steps will become clear when we discuss the clinical syndromes.

ANATOMY OF MEMORY

Memories are probably held in short-term store simply by continuation of nervous activity. The transfer to the long-term store probably involves some molecular change either in the nerve mem­brane or in the intracellular organelles. The structures most involved appear to lie in the inner ring of the limbic system, including the hippo­campus, fornix, mammillary body, mammillothalamic tract (or bundle of Vicq d’Azyr) antero- ventral thalamic nucleus, and cingulate gyrus. The most important structures appear to be the hippocampus and mammillary bodies. The intact­ness of these structures appears to be important, in some as yet undefined way, in the transfer of memories from the immediate to the long-term stores. The memories are probably not laid down in these limbic structures since their destruction does not lead to loss of remote memories. They must therefore act on the structures which are the sites of storage. The limbic structures are also impor­tant, as will be seen below, in retrieval from the intermediate store.

Clinical Memory Disorders And Memory Process In Human Brain

Memory disorder may be evident in widespread disorder of the brain such as may be produced by drugs or metabolic disorders. On the other hand, memory may be relatively or dramatically spared in many of the dementias. Thus memory is much less impaired than such functions as calculation and abstraction in general paresis or Huntington’s chorea. By contrast, in Alzheimer’s disease, in which involvement of hippocampus is prominent, memory disorder is a salient feature of the initial stages.

Disease processes predominantly affecting the hippocampal-mammillary system will produce significant memory disorder with little or no ef­fect on other intellectual functions. This clinical state is called Korsakoff’s syndrome. When due to thiamine deficiency, the most striking lesions are in the mammillary bodies. The hippocampus may be involved in Alzheimer’s disease, head in­jury, or tumors. Disease of the posterior cerebral artery may cause infarction of the hippocampus. Herpes simplex encephalitis, has a predilection for all the structures of the limbic system. Occa­sional cases of severe memory loss have been re­ported following bilateral removal of the medial temporal structures surgically.

In order to produce a permanent memory deficit, bilateral lesions of the mamillo-hippocampal system are required. However, a unilateral lesion of the left hippocampus will produce a transient memory disorder, which may last as long as three months.

The memory disorder that sometimes follows head injury illustrates well the different states of the memory process outlined above. A patient who shows this disorder let us say a week after the episode may exhibit the following picture. He will be alert, awake, and cooperative and may, on a standard IQ test, score in a normal or even superior range. In addition his immediate mem­ory, as shown, for example, by digit span, will be normal. By contrast he shows an anterograde amnesia, i.e., an inability to learn new material.

He also shows a retrograde amnesia extending back from 3 to 20 years. More remote memories, in particular most of what was learned before the age of 12, are much better preserved. Over the next two or three months the condition improves. The ability to learn new material reappears (but the patient will have a permanent gap in his memory for the period in which he lacked this ability). The retrograde amnesia gradually shrinks until it reaches its

permanent form, with a duration of seconds to minutes. The long retrograde amnesia must therefore have been a disorder of retrieval, rather than storage. It thus appears that the integrity of the limbic structures is necessary for the retrieval from intermediate, but not remote memory. In cases of persistent KorsakofF’s syn­drome, such as occur frequently with other forms of disorders that produce permanent bilateral limbic system damage, the retrograde amnesia does not improve significantly.

A prominent feature of many but not all cases of KorsakofF’s syndrome, especially in the early stages, is confabulation, i.e., the tendency of the patient to invent fanciful replies to questions whose answers he doesn’t know.

Functional amnesia occurs in hysteria (usually young women) or in older patients who are de­pressed. A similar clinical picture seen in malin­gerers is usually easy to recognize. The patient may show either a highly selective memory dis­order, e.g., denying that he is married, although all other recent and remote facts are preserved, or a global disorder, e.g., professing total amnesia for all events of his life.

Failure of a patient with­out aphasia to state his own name is invariably not organic in origin. Another common syndrome is the fugue state in which the patient denies any memory of his activities for a period of time ranging from hours to weeks, during which his external activities appeared normal or during which he disappeared and traveled extensively. Although some short-lasting fugue states may occasionally be the result of temporal lobe epi­lepsy, the author’s experience has been that these are nearly all functional in origin.

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