[Amnesic episodes].

The L1/NgCAM cell adhesion molecule is involved in neurite outgrowth, axonal fasciculation and cell migration in the nervous system. We studied the effects of antibodies against L1 injected intracranially at various times before and after training 2-day-old chicks in a visual categorization task. Memory retention was tested 24 h post-training. Anti-L1 antibodies impaired task retention only when administered in three restricted time windows: immediately before training, at about 5.5 h after training and from 15 to 18 h after training. No amnesia was produced by injections before, between or after these sensitive periods (from -1 to +21 h relative to training). These results indicate that there are multiple post-training periods during which L1 is involved in the formation of long-term memory.

Amnesia↗

PubMed1998

Visual memory-deficit amnesia: a distinct amnesic presentation and etiology.

We describe a form of amnesia, which we have called visual memory-deficit amnesia, that is caused by damage to areas of the visual system that store visual information. Because it is caused by a deficit in access to stored visual material and not by an impaired ability to encode or retrieve new material, it has the otherwise infrequent properties of a more severe retrograde than anterograde amnesia with no temporal gradient in the retrograde amnesia. Of the 11 cases of long-term visual memory loss found in the literature, all had amnesia extending beyond a loss of visual memory, often including a near total loss of pretraumatic episodic memory. Of the 6 cases in which both the severity of retrograde and anterograde amnesia and the temporal gradient of the retrograde amnesia were noted, 4 had a more severe retrograde amnesia with no temporal gradient and 2 had a less severe retrograde amnesia with a temporal gradient.

Amnesia↗