There menstrual psychosis It is an interesting picture both for the phenomenal presentation and for the type of drugs used for treatment.
Clinically this disorder manifests itself with episodes of confusion, typical of the delirium, which often present themselves near the menarca or childbirth, probably linked to the presence of anvulatory cycles. If the complete psychopathological framework appears relatively not very frequent and often unrecognized, it is not so for all those variants of the sub -face disorder.
It manifests itself as a psychotic disorder that usually occurs between the third previous day and 3 days following the cycle (1,3). Unlike the psychotic disorders Classics, this form presents a complete remission between one crisis and another and does not cause cognitive deterioration typical of chronic paintings (1).
We find a first description of this disorder at the end of the 1800s by Kraft Ebing (4.5) who later published a monograph on the topic. In 1998 Brockington (6) presented data that attracted attention again on this Psychotic form linked to the menstrual cycle However, over time, it was forgotten again in clinical practice, despite a fair amount of work on the correlation between psychosis and menstrual cycle (1,3,6).
The current pathophysiological hypothesis suggests an increased receptor sensitivity during the menstrual phase characterized by the estrogen drop. This hypothesis is supported by the data detected in schizophrenic patients that high levels of estrogen correlate with low scores of positive symptoms (7.9).
It seems that estrogen levels interfere with the levels of dopamine and with the degree of sensitivity of its receptors called D2. In the monkeys that during the follicular phase (which is associated with low estrogen levels), the receptors for type D2 dopamine, at the level of that cerebral nucleus called striped body, have a sensitivity of 12% greater than the receptor sensitivity detected in the luteinic phase (characterized instead of high levels of estrogen) (10), has been associated with low -follicular phase (
The implication is that in periods with low levels of estrogen a higher dopaminergic activity could correlate with the appearance of Positive symptoms of psychosis.
Estrogen modulates the synthesis of tyrosine-hydroxylase (enzyme involved in the synthesis of dopamine) in dopaminergic systems: according to Deuchar and Brockington (12) during the anovulator cycles the brain is exposed to high levels of estrogen that block the D2 receptors; The hypothesis is that when, physiologically, the levels of estrogen descend, exposure to D2 receptors that have become hypersensitive to dopamine can constitute a triggering factor for the psychotic crisis.
Hitonized neurobiological etiology suggests for treatment the use of sex hormones. In fact, antipsychotics manage to make the crisis of minor duration but do not interfere with the cyclicality of the disorder (13).
In literature it is suggested to use as treatment, off label, extruporgestin combinations (2.8); The use of modulators of estrogen receptors (2) and thyroid hormones (13) also seems encouraging.
Given the correlation of the disorder with anovulator cycles, those antipsychotics which determine an increase in prolactin levels (among these: old generation antipsychotics, sulpirids and Risperidone).
Remembering this psychopathological framework can help the clinician, making him pay more attention to those paintings in which the history of symptoms is linked to the phases of the menstrual cycle.
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