Delusions Flashcards
Hersh et al
TLE = change med = delusion of identity. SPECT = hypo-perfusionof L temporal lobe. Ventral parts of temporal lobe = face perception and visual input of who is who = out of balance
Su et al
Cerebrovascular disease = extensive white matter lesions (subfrontal and subcortical). Assume delusions = interruption of neural circuits inc. AC loop, dlPFC loop with connections to basal ganglia. If connections to frontal lobe disrupted = involuntary actions
Chen et al
PD. DBS in STN to trigger dopamine release = accidentally stimulated limbic not motor part of STN = delusions
Duggal
Fregoli, AH and delusions. 8 yrs earlier = road accident and seizures = EEG = L temporal spike and sharp waves
Melca et al
Delusional misidentification in OCD
Dejode et al
Left hemiparesis after stroke in RH = Capgras (ICU physicians) = EEG and CT = lesions in posterior RH
Horikawa et al
Pre-capgras = temporal lobe atrophy. Pre- and post-capgras = hypo-perfusion in entire RH getting worse. Hypo-perfusion decreased after remission of delusions.
Mechanisms for Capgras
Hypo-RH and hyper-LH = imbalance?
Working memory damage = dissociation between recognition and identification
RH face processing deficits = right temporo-limbic-frontal disconnection
Association between limbic system and visual areas damaged BUT capgras with inanimate objects
Frontal lobe and reality monitoring damaged = Cipriani et al = capgras found in patients with dementia and frontal disinhibition
Blanke et al (1)
Stimulated points of seizure around angular gyrus = feel like falling. As increase stimulation = different delusions
Blanke et al (2)
Abnormalities of vestibular system? = body-reference frame and balance
Patients with damage to temporo-parietal junction = OBE
Price we pay for visuo-spatial perspective taking?
Blanke and Mohr
Heautoscopy and OBE more likely in temporal lobe
Heautoscopy more likely in LH
Autoscopic hallucination equally likely in temporal, parietal and occipital lobes
