PT  - JOURNAL ARTICLE
AU  - Claude M.J. Braun
AU  - Mathieu Dumont
AU  - Julie Duval
AU  - Isabelle Hamel-Hébert
AU  - Lucie Godbout
TI  - Brain modules of hallucination: an analysis of multiple patients with brain lesions
DP  - 2003 Nov 01
TA  - Journal of Psychiatry and Neuroscience
PG  - 432--449
VI  - 28
IP  - 6
4099  - http://jpn.ca/content/28/6/432.short
4100  - http://jpn.ca/content/28/6/432.full
SO  - JPN2003 Nov 01; 28
AB  - We systematically reviewed the localization of focal brain lesions that cause isolated hallucination in a single sensory modality. Case reports of post-lesion nonparoxysmal hallucination in 1 (and only 1) of 3 sensory modalities (i.e., visual, auditory, somatic) were reviewed, and the content of the qualitative descriptions was analyzed for each modality. The lesion is practically always located in the brain pathway of the sensory modality of the hallucination. There seem to exist localized sensory brain circuits that in healthy people diminish the intensity of internal sensory representation. After a lesion, hallucinosis seems to be caused also by compensatory overactivation of tissue in the nearby brain sensory pathway. This type of hallucination may indeed be termed a “release” form, whereby patients are aware of the hallucinatory nature of their experience, but not usually of “dream centres” as proposed by Lhermitte. Instead, we propose that it is dreaming that should be considered a special case of neural “release.”