Reversible Parietal Hypometabolism in Late-Onset Psychosis

A 74-year-old woman with a history of depression, craniocerebral trauma during adulthood, and a TIA, was admitted to the neurosurgery department because of pain in the right lower limb due to lumbosacral plexopathy. While undergoing examinations, she became convinced that her hospital stay was part of a conspiracy, that she was being used for medical experiments, and was to be poisoned by medication. She accused one physician of maltreating her, sent secret messages by phone, accused caregivers of theft, and believed that walls were permeable through invisible holes. A disturbance of consciousness was never observed. Subjective memory complaints were present before admission, and cognitive difficulties were observed during hospitalization, confirmed by MMSE (15/30). An antipsychotic drug was started, and she was referred to the geriatric psychiatry ward. Mental examination at admission revealed a conscious, cooperative, but suspicious woman with paranoid delusions without hallucinations, incoherent formal thinking, and disorganized speech. Neuropsychological testing revealed poor sustained attention, executive dysfunction, and episodic memory impairment. MRI showed periventricular leukomalacia, but no recent ischemia. 18F-FDG PET revealed severe hypometabolism of bilateral parietal, posterior temporal and frontal cortex (Figure 1), a pattern suggestive of AD. Psychotic symptoms improved gradually, as well as cognitive status, with an MMSE score of 25 after 15 weeks of hospitalization. A follow-up 18F-FDG PET, 3 months after the initial one, showed a relative increase of parietal metabolism. During 4 years of follow-up, cognitive status remained stable despite memory complaints. An 11C-PIB PET did not show abnormal cortical amyloid deposition (Figure 1). However delusional ideas persisted, allowing a diagnosis of very-late-onset schizophrenia-like psychosis.²

Late-onset delusions may be an early symptom of AD. On the other hand, psychotic disorders in elderly persons are often associated with cognitive impairment. Because of the clinical overlap, neuroimaging is considered an important diagnostic tool, with temporoparietal hypometabolism and a positive 11C-PIB PET being supportive of AD diagnosis.¹ In contrast, neuroimaging findings in late-onset psychotic disorders that have been described so far, are generally nonspecific, including enlarged ventricles, white-matter changes,³ and hypoperfusion of frontal and temporal cortex measured by SPECT.^4,5 Until now, no 18F-FDG PET studies have been reported in late-onset psychosis. Our case report illustrates that, in addition to frontal metabolic changes, late-onset psychosis can be associated with severe parietal hypometabolism. In contrast with the natural evolution of AD, we observed a partial recuperation of parietal hypometabolism over time associated with improvement of cognitive status and reduction of psychotic symptoms.