Psychotic pregnancy denial: a review of the literature and its clinical considerations.

BACKGROUND: Pregnancy denial can be broken into two major types, non-psychotic and psychotic deniers, and further classified into pervasive, affective and persistent sub-types. It can lead to increased morbidity and mortality of the mother and neonate. Psychotic pregnancy denial is rare and the medical literature existing on the subject is limited to a small number of case reports and case series. No formal recommendation exists on the clinical management of psychotic pregnancy denial in the antenatal or postpartum period. The authors provide a comprehensive review of the literature regarding psychotic pregnancy denial, present an example of an unpublished case and provide suggestions for clinical management. CASE: A 33-year-old primigravida at 37 6/7 weeks gestation presented with new-onset psychotic pregnancy denial with no prior history of psychosis. She had a negative medical work-up for organic causes of psychosis. Using a multidisciplinary approach, the decision was made to deliver the fetus at 38 1/7 weeks via cesarean section due to concerns for patient and fetal safety. Following delivery, she was admitted to an inpatient psychiatric facility and underwent 16 bilateral electroconvulsive therapy (ECT) treatments to which she showed complete response. CONCLUSION: Psychotic pregnancy denial is rare and potentially dangerous. Delivery prior to 39 weeks gestation is reasonable for worsening psychiatric disease but careful consideration of the risk-benefit analysis and ethical framework must be deliberated.Teaching points: In cases of worsening psychiatric disease in pregnancy, a multidisciplinary approach is necessary for comprehensive care. Psychotic denial of pregnancy leads to increased maternal and neonatal morbidity and mortality. Delivery prior to 39 weeks gestational age is reasonable to expedite psychiatric treatment.PrecisUsing a multidisciplinary approach, the decision to deliver before 39 weeks gestation is reasonable for worsening psychiatric disease.

Neocortical and thalamic spread of amygdala kindled seizures.

PURPOSE: Amygdala kindling is an epilepsy model involving long-term network plasticity in the nervous system. In this model, repeated weak stimulation of the amygdala eventually leads to severe motor seizures. The mechanisms for worsening behavioral seizures, and the possible role of enhanced connectivity between the amygdala and other structures have not been thoroughly investigated. METHODS: We performed simultaneous field potential recordings from the amygdala, frontal cortex, and medial thalamus during kindling in rats. Seizures were analyzed for signal power compared with baseline and for correlation between recording sites. Interictal signals were analyzed for changes in coherence between electrode contacts in kindled animals compared with sham kindled controls. RESULTS: We found that increased behavioral severity of seizures was related to increased seizure duration and to increased signal power in the frontal cortex and medial thalamus. Kindling was associated with increased connectivity between the amygdala and frontal cortex, based on increased amygdala-frontal signal correlation during seizures. In addition, during the interictal period, increased coherence was noted between amygdala and frontal contacts in kindled animals compared with controls. CONCLUSIONS: We found evidence for increased connectivity between the amygdala and frontal cortex both during seizures and in the interictal period, as a result of kindling. Enhanced connections between limbic and neocortical circuits may be important for the development of epilepsy, as well as for normal long-range network plasticity in the nervous system.