Persistent anterograde amnesia due to the artery of Percheron occlusion: a case report.

Bilateral thalamic infarction involving the artery of Percheron (AOP) can cause diagnostic difficulties due to the varying clinical presentations. AOP infarcts presented with isolated memory impairment are not common and the factors affecting the persistence of memory disorders are still unknown. A 41-year-old male patient was hospitalized with acute unconsciousness. MRI disclosed bilateral paramedian thalamic infarction The patient had isolated memory deficit and his anterograde amnesia continued without any change in the past decade. More cases might answer the questions concerning the intra- and extra-thalamic structures responsible for the amnesic syndrome and the factors affecting the persistence of the symptoms.

Item recognition is less impaired than recall and associative recognition in a patient with selective hippocampal damage.

This article explores the recall, item recognition, and associative recognition memory of patient B.E., whose pattern of retrograde amnesia was reported by Kapur and Brooks (1999; Hippocampus 9:1-8). Structural magnetic resonance imaging (MRI) has shown that B.E. has bilateral damage restricted to the hippocampus. The structural damage he had sustained was accompanied by bilateral hypoperfusion of the temporal lobe, revealed by positron emission tomography (PET), and which single photon emission computed tomography (SPECT) suggested was greater in the left than the right temporal lobe. B.E. showed a global anterograde amnesia for verbal material, but he displayed some sparing of nonverbal item recognition relative to nonverbal recall and associative recognition. His performance on an item recognition task that used the remember/know procedure and another that involved repetition of the test phase, to reduce the difference between the familiarity of the targets and foils, suggested that his relatively spared nonverbal item recognition may have been mainly supported by familiarity. This finding is consistent with the view that the anterior temporal lobe, including the perirhinal cortex, can support familiarity-based memory judgments (Brown and Bashir, 2002; Philos Trans R Soc Lond B 357:1083-1095). B.E.'s data also highlight the importance of functional as well as structural scan information for interpreting the pattern of memory deficits shown by patients with selective hippocampal structural lesions.

Brain SPECT evaluation of amnestic ED patients after mild head trauma.

A short period of amnesia is a common complaint after mild head injury. In this study we compare the duration of amnesia after mild head trauma to single photon emission computed tomography (SPECT) perfusion imaging shortly after admission to the emergency department (ED). Sixteen patients consecutively admitted to the ED were prospectively evaluated. The amnesia was scored according to the Extended Glasgow Coma Score. A computed tomography (CT) scan was performed to all patients. All patients had anterograde amnesia. Eleven patients had amnesia of grade 2 (69%) and 5 patients of grade 3 (31%). All patients had a normal CT scan. Twelve of sixteen patients (75%) showed regional perfusion abnormalities on the SPECT study. Decreased perfusion was observed at least in one region (8/12 patients had 2 abnormal regions). The logistic regression analysis showed that SPECT results significantly predicted the severity of amnesia (r = 0.9, P <.0001). Additionally, the SPECT accounted for approximately 84% of the variation in amnesia. We conclude that amnesia after mild head injury is associated with a high incidence of early regional cerebral perfusion abnormalities. Amnesia lasting more than half an hour is associated with bilateral cerebral hypoperfusion. SPECT evaluation in the ED may by a useful additional tool in the objective assessment of posttraumatic amnesia.

Profound amnesia and confabulation following traumatic brain injury.

Amnesia and confabulation may persist following acute aneurysmal hemorrhage of the anterior communicating artery, chronic alcoholic Korsakoff's syndrome, and late-stage dementia of the Alzheimer type. However, there is a paucity of information regarding the persistence of these symptoms following traumatic brain injury. We present the case of JL, a 43-year-old male with persistent and severe anterograde amnesia for verbal and visual information with co-occurring provoked confabulation which persists well into the chronic phase of recovery after a severe traumatic brain injury. Neuropsychological testing at 7 weeks post-injury demonstrated severe anterograde amnesia with co-occurring confabulation. Follow-up testing at 9.5 months post-injury showed persistent and severe anterograde amnesia and provoked confabulation despite superior non-verbal intelligence and above average attentional and perceptual abilities. Late computed tomography showed chronic hypodense regions in the temporal lobes, bilaterally (L > R), and in the region of the left ventrolateral frontal lobe. This case demonstrates that anterograde amnesia and provoked confabulation may persist long after the acute phase of recovery after traumatic brain injury, and also supports previous research which asserts that medial temporal lobe damage must be accompanied by ventral frontal lobe pathology to produce the amnestic-confabulatory syndrome.