Temporary partial amnesia is a variety which is frequently observed in normal persons, even the most gifted. A word or fact escapes us, seems wholly lost for a few minutes, hours, or days; the more we strive to recall it, the less we succeed; yet later, when not sought for, the fact or word appears in our consciousness as if spontaneously, but more probably by some effect of the law of association. Such partial and momentary forgetfulness may assume proportions which render it pathological. What is known as transitory aphasia may be classed in this group. In a few minutes or hours a person without apoplectic, epileptic, or paralytic phenomena loses all power to express his thoughts by speaking or writing; there is verbal amnesia and agraphia. The subject is conscious of his condition and of the wholly futile or incorrect attempts he makes to communicate with others.
Temporary complete amnesia is almost equivalent to loss of consciousness, yet not strictly so. For example, after a sharp blow upon the head a person may perform complicated acts, reply to questions, and apparently act normally, yet after a variable time he will declare that he remembers absolutely nothing of the injury and what he did or said for hours or days afterward. The same phenomenon is observed in the course of psychoses, neuroses (epilepsy), in some acute diseases, and in certain states of intoxication.
Permanent partial amnesia occurs in states of dementia, such as senile dementia, paralytic dementia, and in certain cases of aphasia. Great gaps exist in the patient's memory; some things are well recalled, others wholly and for ever effaced. The psychological law governing the failure of memory in these cases is that the earliest and strongest impressions survive, while recent and less forcible (i.e. less interesting) ones are lost. Substantives or names are especially liable to obliteration, as are also many of the delicate residua which lie at the basis of the subject's ethical conceptions and acts.
Permanent complete amnesia is observed at the end of degenerative cerebral diseases, as organic dementia, whether of the form termed secondary or that designated as paralytic. Sometimes after acute general diseases the memory may be a perfect blank for a considerable length of time, and education has to be repeated. Memory may be so completely absent that cases are known in which the patient gave a fresh greeting to the asylum physician every two or three minutes indefinitely, as if each were a first meeting. Momentary perception and automatic (reflex) response are there, but no impression is made; there is no residuum left in the cortical centres. In these cases amnesia is accompanied by degeneration of the visual, auditory, etc. cortical areas or centres.
An interesting form of amnesia, not generally recognized as such, is the loss of acquired skill in muscular movements, such as are necessary for writing, for using tools, and for doing various delicate professional movements. Here the motor residua acquired by laborious education or training are gradually lost without actual paralysis or ataxia. This variety is exquisitely illustrated by certain cases of dementia paralytica where long before marked intellectual symptoms occur there is loss of skill in mechanical arts and in handwriting.
In testing a subject's memory due attention should be paid to the law of the survival of older and more interesting residua, as well as to the power of the law of association. Such questions should be asked as pertain to recent events in the patient's experience, and about matters which are not closely related logically. A patient who might tell us nearly all about his early personal experiences, his business and family relations, incidents of his childhood, etc., would fail to remember what he had for breakfast, what he did the day before, etc.
The physiological cause of real amnesia is impairment in the vitality (nutrition) of ganglion-cells in the various cerebral sensory areas or centres, and of the motor area as well (motor residua). In cases of transitory amnesia we suppose this to be due to the action of toxic agents, to anæmia, and impaired molecular or chemical nutrition, as after acute diseases, in extreme debility, in psychoses, etc. In cases of terminal permanent dementia, autopsies afford us evidence of degeneration and disappearance of ganglion-cells: we find granular and fatty pigmentation, atrophy, calcarous degeneration of these bodies, thickening and shrinkage of the neuroglia, and degenerative changes in blood-vessels. Doubtless degeneration or destruction of association fasciculi of nerve-fibres in the cortex cerebri or in the white substance plays a considerable part in the production of permanent amnesia, but we are as yet unable to give a clear demonstration of this. Theoretically, we may admit an organic loss of memory with the following conditions of the brain: (1) diseased perceptive (sensory) centres or motor area with normal association fasciculi; (2) normal perceptive centres and motor area with degenerate or broken association fasciculi, connecting these parts with one another and with the more strictly ideational or expressive (centrifugal) areas and parts of the brain and spinal cord.
Amnesia—or, more properly speaking, dulness of perception and feebleness of retention of residua—occurs as a strictly congenital condition from imperfect cerebral development, or a little later in life from infantile diseases, constituting one of the aspects of idiocy.