Article Text

This article has a correction. Please see:

Download PDFPDF
Regional cerebral glucose metabolism in akinetic catatonia and after remission
  1. X De Tiége1,
  2. S Laureys1,
  3. S Goldman1,
  4. X De Tiége2,
  5. I Massat2,
  6. F Lotstra2,
  7. J Mendlewicz2,
  8. J-C Bier3,
  9. J Berré4
  1. 1PET/Biomedical Cyclotron Unit, Erasme Hospital, Free University of Brussels, Brussels, Belgium
  2. 2Department of Psychiatry, Erasme Hospital, Free University of Brussels
  3. 3Department of Neurology, Erasme Hospital, Free University of Brussels
  4. 4Intensive Care Unit, Erasme Hospital, Free University of Brussels
  1. Correspondence to:
 Dr X De Tiége, PET/Biomedical Cyclotron Unit and Department of Psychiatry, Erasme Hospital, Free University of Brussels, Brussels, Belgium;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

K L Kahlbaum published in 1874 the first recorded description of catatonia. Akinetic catatonia is now defined as a neuropsychiatric syndrome principally characterised by akinesia, mutism, stupor, and catalepsy.1 Even if some advances have been made in the recognition of catatonia, in particular by the development of different rating scales,1 the pathophysiology of this syndrome is not clearly established.

A right handed 14 year old girl presented with akinetic catatonia during an episode of depression in the context of a bipolar type I disorder. Her catatonic status was characterised by akinesia with brief episodic spontaneous stereotyped movements, mutism, no spontaneous oral intake, catalepsy, waxy flexibility, and stupor with brief occasional eye contacts. This corresponded to a total score of 19 on the Northoff Catatonia Scale.1 Electroencephalogram performed one day after onset of symptoms showed diffuse theta activity with sporadic diffuse delta activity. Cerebral magnetic resonance imaging was normal. Brain positron emission tomographies (PET) were obtained on a CTI-Siemens HR+ tomograph. A first PET (PET1) using [18F]-fluorodeoxyglucose (FDG) was performed on day 2 in a drug free state. Thereafter, intramuscular injection of 2 mg of lorazepam induced rapid clinical remission of the akinetic phase. Oral lorazepam was then given (3.75 mg/day) during five days. On day 8, a second PET with FDG was performed while the patient was treated by olanzapine (15 mg/day) and presented hyperactivity, logorrhoea, and disinhibition characterised …

View Full Text

Linked Articles

  • Correction
    BMJ Publishing Group Ltd