A CONTRIBUTION TO THE ANATOMICAL BASIS OF THALAMIC AMNESIA

TLDR

Damage to diencephalic structures, especially vascular lesions in the ventral thalamus, is known to cause memory dysfunction. The study examined CT findings of 11 thalamic vascular lesion cases to identify the critical structures involved in human memory. CT imaging of these cases was used to map lesion locations relative to memory‑related structures. Thalamic amnesia depends more on intrathalamic white matter lesions—particularly the mamillothalamic tract and ventral lamina medullaris interna—than on nuclear lesions, with lesions sparing these structures not producing memory deficits, supporting a disconnection syndrome model.

Abstract

Damage to diencephalic structures is stated to give rise to memory dysfunction. Amnesia is likely to occur following vascular lesions in the ventral portion of the thalamus. The CT findings of 6 of our own cases and 5 patients reported in the literature, all with selective vascular lesions of the thalamus, were studied to determine the critical structures involved in human memory processes more closely. Thalamic amnesia probably depends on intrathalamic white matter lesions more than on nuclear lesions. The mamillothalamic tract and the ventral portion of the lamina medullaris interna are the most likely candidates in the mediation of memory processes and a combined lesion of these structures may be responsible for thalamic amnesia in man. Two patients without significant memory dysfunction had lesions in the ventrobasal portion of the mediodorsal nucleus sparing the mamillothalamic tract and the ventral part of the lamina medullaris interna. Our findings correspond well with the understanding of amnesia as a 'disconnection syndrome' stressed recently by Warrington and Weiskrantz (1982) and with Mishkin's (1982) model of the memory system in monkeys.