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BMJ Case Reports 2012; doi:10.1136/bcr.11.2011.5267
  • Findings that shed new light on the possible pathogenesis of a disease or an adverse effect

Status of memory loss

  1. Norman Delanty1
  1. 1Neurology Department, Beaumont Hospital, Dublin, Dublin, Ireland
  2. 2Neurophysiology Department, Beaumont Hospital, Dublin, Ireland
  3. 3Neuropathology Department, Beaumont Hospital, Dublin, Ireland
  1. Correspondence to Dr Parameswaran Mahadeva Iyer, parames68{at}gmail.com

Summary

A 72-year-old woman presented with first onset of seizure with no prior history of cognitive dysfunction. EEG revealed focal non-convulsive status epilepticus. MRI brain showed a left temporal non-enhancing lesion. Temporal pole biopsy showed acute neuronal necrosis and astrocyte hyperplasia together with extensive amyloid plaques and neurofibrillary tangles. Perivascular oligodendroglial hyperplasia was present. Postmortem examination revealed extensive plaque and tangle disease. Perivascular oligodendroglial hyperplasia was limited to the left temporal area. The presence of focal perivascular oligodendroglial hyperplasia in the left temporal cortex, combined with extensive plaque and tangle disease may have contributed to the focal status epilepticus in this patient. Although the presence of focal perivascular oligodendroglial hyperplasia has been reported in cases of temporal lobe epilepsy, it has not been reported as a cause of seizure in patients with Alzheimer’s disease previously. Further studies for clinical-pathologic correlation would be required to confirm this hypothesis.

Footnotes

  • Competing interests None.

  • Patient consent Obtained.

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