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Neurology 1999;53:344
© 1999 American Academy of Neurology


Articles

Postencephalitic focal retrograde amnesia after bilateral anterior temporal lobe damage

Y. Tanaka, MD, Y. Miyazawa, MD, R. Hashimoto, MD, I. Nakano, MD and T. Obayashi, MD

From the Departments of Neurology (Drs. Tanaka, Miyazawa, Hashimoto, and Nakano) and Clinical Pathology (Dr. Obayashi), Jichi Medical School, Tochigi, Japan.

Address correspondence and reprint requests to Dr. Yasufumi Tanaka, Department of Neurology, Jichi Medical School, 3311-1 Yakushiji, Minamikawachi, Tochigi, 329-0498, Japan.

BACKGROUND: Marked retrograde amnesia with no or almost no anterograde amnesia is rare. Recently, a combination of ventrolateral prefrontal and temporopolar cortical lesions has been suggested as the cause of such isolated or focal retrograde amnesia. It is also assumed that when the right-sided cortical structures are damaged, autobiographical episodic memories are affected.

OBJECTIVE: To search for new anatomic substrates for focal retrograde amnesia.

METHODS: We performed extensive neuropsychological tests and obtained detailed neuroimages on a 43-year-old woman who showed a severe, persistent retrograde amnesia but only a limited anterograde amnesia after probable herpes simplex encephalitis.

RESULTS: Tests of autobiographical memory revealed that she had a memory loss extending back to her childhood for both semantics and incidents; however, the ability to recall specific episodes appeared much more severely impaired than the ability to recall factual information about her past. The patient also showed profound impairments in recalling public memories; however, her scores improved nearly to a control level on forced-choice recognition memory tasks, although the recall of memories for a decade just before her illness remained mildly impaired. MRI revealed focal pathologies in the temporal poles and the anterior parts of the inferotemporal lobes on both sides, predominantly on the left, with some extension to the anterior parts of the medial temporal lobes. There was additional damage to the left insular cortex and its surrounding structures but no evidence of frontal lobe damage on MRIs or cognitive tests.

CONCLUSIONS: A profound retrograde amnesia may be produced by damage to the bilateral temporal poles and anterior inferotemporal lobes in the absence of frontal lobe pathologies, and a dense and persistent episodic old memory loss can arise even with a relatively small lesion in the right anterior temporal lobe if it is combined with extensive damage to the left.




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