PubMed · 6520102
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M C Maheshwari. 1984. Transient global amnesia.. https://pubmed.ncbi.nlm.nih.gov/6520102/
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The intralaminar thalamic nuclei are characterized by their prominent projections to striatum. Lesions of the intralaminar nuclei have been found to impair delayed matching trained with retractable levers. Comparable impairments have been observed for rats with lesions of the olfactory tubercle, involving ventral areas of striatum and pallidum. We conducted two experiments to test the functional dependence of thalamic and striatal lesions on the delayed matching task. In experiment 1, we determined the effects of inactivating the intralaminar nuclei with bilateral lidocaine infusions. In experiment 2, we compared the effects of unilateral thalamic inactivations in rats with unilateral olfactory tubercle lesions. We trained rats to perform the delayed matching task to criterion and then implanted dual cannulas aimed at the bilaterally symmetrical areas in the intralaminar nuclei. Rats in experiment 2 were also given a unilateral olfactory tubercle lesion. The results of experiment 1 showed dose-dependent impairments for bilateral infusions that were qualitatively similar, although of lesser severity than delayed matching impairments observed in previous studies for rats with lesions involving extensive areas of the intralaminar nuclei. A comparable impairment was observed in experiment 2 when thalamus was inactivated on the side opposite the olfactory tubercle lesion. Performances were significantly worse when thalamus was inactivated on the contra-lesion than on the ipsi-lesion side of the brain. These results are discussed in terms of the role of ventral striatum and related thalamic nuclei in memory.
The traditional explanation of dense amnesia after medial temporal lesions is that the amnesia is caused by damage to the hippocampus and related structures. An alternative view is that dense amnesia after medial temporal lesions is caused by the interruption of afferents to the temporal cortex from the basal forebrain. These afferents travel to the temporal cortex through three pathways, namely the anterior temporal stem, the amygdala and the fornix-fimbria, and all these three pathways are damaged in dense medial temporal amnesia. In four experiments using different memory tasks, we tested the effects on memory of sectioning some or all of these three pathways in macaque monkeys. In a test of scene-specific memory for objects, which is analogous in some ways to human episodic memory, section of fornix alone, or section of amygdala and anterior temporal stem sparing the fornix, each produced a significant but mild impairment. When fornix section was added to the section of anterior temporal stem and amygdala in this task, however, a very severe impairment resulted. In an object recognition memory task (delayed matching-to-sample) a severe impairment was seen after section of anterior temporal stem and amygdala alone, with or without the addition of fornix section; this impairment was significantly more severe than that which was seen in the same task after amygdalectomy leaving the temporal stem intact, with or without fornix section. Animals with combined section of anterior temporal stem, amygdala and fornix were also impaired in object-reward association learning. However, the retention of pre-operatively acquired object-reward associations was at a high level. These results show that the pattern of impairments after section of anterior temporal stem, amygdala and fornix in the monkey, leaving hippocampus intact, resembles human dense amnesia and is different from the effects of hippocampal lesions in the monkey.
OBJECTIVE: The clinical significance of heparin coating in cardiopulmonary bypass has previously been investigated. However, few studies have addressed the possible influence on brain function and memory disturbances. METHODS: Three hundred low-risk patients exposed to coronary bypass surgery were randomised into three groups according to type of heparin coating: Carmeda Bioactive Surface, Baxter Duraflo II and a control group. Outcome was determined from a number of clinically oriented parameters, including a detailed registry of postoperative deviations from the normal postoperative course. Brain damage was assessed through S100 release and memory tests, including a questionnaire follow-up. RESULTS: Clinical outcome was similar for all groups. Blood loss (Duraflo only), transfusion requirements and postoperative creatinine elevation were reduced in the heparin-coated groups. A lower incidence of atrial fibrillation was noted in the Duraflo group. Heparin coating did not uniformly attenuate the release of S100 or the degree of memory impairment. CONCLUSIONS: Cardiopulmonary bypass (CPB) with heparin coating and a reduced dose of heparin seems to be safe. Clinical outcome and neurological injury seem not to be associated with type of heparin coating used for CPB. However, blood loss and transfusion requirements may be reduced.