Prominent neuroleptic sensitivity in a case of early-onset Alzheimer disease due to presenilin-1 G206A mutation

Cogn Behav Neurol. 2008 Sep;21(3):190-5. doi: 10.1097/WNN.0b013e31817d74bf.

Abstract

Objective: We describe atypical motor and cognitive features in a case of familial Alzheimer disease (FAD) due to presenilin-1 (PS-1) mutation.

Background: Extrapyramidal signs (EPS) typically are a late-presenting feature of sporadic Alzheimer disease (AD), but relatively little data are available regarding EPS in FAD.

Method: A 59-year-old, right-handed man of Caribbean-Hispanic descent underwent brain imaging studies, laboratory tests for AD, and serial neurologic and neuropsychologic evaluations.

Results: The patient presented with recent-onset delusional ideation associated with cognitive decline. Prominent EPS developed soon after initiation of an atypical neuroleptic agent. Neuropsychologic evaluation revealed global cognitive deficits; he was found to be a carrier of a PS-1 point mutation at position G206A. EPS resolved completely after discontinuing the neuroleptic agent and coincided with improved motor speed, set initiation, and verbal fluency.

Conclusions: Severe neuroleptic sensitivity and associated deficits of cognitive speed occurred in response to a dopaminergic antagonist agent; both responded readily to withdrawal of the offending agent. Patients with PS-1 AD may be at substantially increased risk of neuroleptic-induced EPS. That feature underscores the heterogeneity of the FAD clinical phenotype.

Publication types

  • Case Reports

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / physiopathology
  • Antipsychotic Agents / adverse effects*
  • Basal Ganglia Diseases / chemically induced
  • DNA Mutational Analysis
  • Drug Hypersensitivity / etiology*
  • Humans
  • Male
  • Middle Aged
  • Pedigree
  • Point Mutation / genetics*
  • Presenilin-1 / genetics*

Substances

  • Antipsychotic Agents
  • Presenilin-1