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Published 28 September 2009
Cite this as: BMJ Case Reports 2009 [doi:10.1136/bcr.04.2009.1754]
Copyright © 2009 by the BMJ Publishing Group Ltd.

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Cerebral single photon emission computer tomography in thalamic lacunar infarction presenting with amnesia

Kiyotaka Nakamagoe, Akira Tamaoka

Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Tennodai 1-1-1, Tsukuba, Ibaraki, 305-8575, Japan

Correspondence to:
Kiyotaka Nakamagoe, Nakamagoek{at}md.tsukuba.ac.jp

A 62-year-old right handed woman experienced a sudden decrease in spontaneity and a concurrent deterioration of memory. Her consciousness was clear. Some points, such as recalling the names of three simple preregistered objects after 5 mins and calculation, were deducted from the Mini-Mental State Examination (MMSE) score (23/30). She was oriented to time and place. The Wechsler Memory Scale-Revised showed verbal rather than spatial memory impairment (the spatial memory index/verbal memory index difference score was 26, a significant value). No abnormalities were observed in any other neurological findings. Her electroencephalogram was normal. Magnetic resonance imaging (MRI) showed a regional lacunar infarction in the thalamus (fig 1). MR angiography showed stenosis of the left posterior cerebral artery, but there was no sign of obstruction or stenosis of the internal carotid arteries. Her single photon emissions computed tomography (SPECT) scan Z score decreasing image showed decreased blood flow in the frontal, temporal, and parietal lobes (fig 2). Her memory improved at 6 months from onset (MMSE score 29/30).


 


 

The patient had a thalamic infarction in the dominant left hemisphere. The SPECT images revealed extensive blood flow defects in the corresponding cerebral hemisphere where the afferent fibres from the thalamus terminate. She described recent memory disturbances with a substantial decline in verbal memory performance, which is consistent with the symptoms of thalamic amnesia. In view of these facts, it could be concluded that her amnesia resulted from thalamic lacunar infarction.2,3

It is therefore necessary to consider thalamic lacunar infarction as a potential underlying aetiology of amnesia.

Competing interests: none.

Patient consent: Patient/guardian consent was obtained for publication

References

  1. Minoshima, S, Frey, KA, Koeppe, RA, et al. A diagnostic approach in Alzheimer’s disease using three-dimensional stereotactic surface projections of fluorine-18-FDG PET. J Nucl Med 1995; 36: 1238–48.[Abstract/Free Full Text]
  2. Clarke, S, Asssal, G, Bogousslavsky, J, et al. Pure amnesia after unilateral left polar thalamic infarct: topographic and sequential neuropsychological and metabolic (PET) correlations. J Neurol Neurosurg Psychiatery 1994; 57: 27–34.[CrossRef]
  3. Stenset, V, Grambaite, R, Reinvang, I, et al. Diaschisis after thalamic stroke: a comparison of metabolic and structural changes in a patient with amnesia syndrome. Acta Neurol Scand 2007; 115: 68–71.[CrossRef]

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