Mania a Potu: Review of the literature

BACKGROUND: The concept of Mania a Potu (MAP) also known as alcohol idiosyncratic reaction or pathologic alcohol intoxication is a controversial one. However, the literature from the beginning of the XX century, particularly the German, contains many descriptions of the condition. Krafft-Ebing first described the features of Pathologische Alkoholreaction in 1869. Later Magnan classified both MAP and delirium tremens under “Acute Alcoholic Insanity” (Bevan Lewis, 1899). This condition has been described as a state of pathological intoxication, characterized by extreme excitement, sometimes accompanied by extreme aggressive behaviour and clouding of consciousness and resulting from the ingestion of small amounts of alcohol by a susceptible individual. It is usually followed by a prolonged period of sleep and amnesia for the episode. The quantity of alcohol consumed to induce this reaction is a controversial issue. In the field of forensics, the significance of this condition becomes particularly pronounced, especially in the legal defence of individuals accused of violent crimes committed in the midst of intense excitement or rage.
METHODS: We conducted a literature review using the PubMed and Google Scholar databases on the aetiology of Mania a Potu/ alcohol idiosyncratic reaction. 
RESULTS: The aetiology of this disorder is mostly uncomprehended. Several risk factors have been described such as exhaustion (Keller & McCormick, 1968), emotional distress (Heilbronner, 1901) and disturbances of sleep or malnourishment (Rozhnov, 1970). Hypoglicaemia, brain damage and increased cerebrospinal fluid pressure may also play a role (Slater & Roth, 1969; Lishman, 1978; Morozov et al.,1974). Some authors theorize that alcohol idiosyncratic reaction may be regarded as an atypical form of epilepsy and some studies have documented ECG changes such as cortical irritability with paroxysmal frontal slow wave activity or generalized slowing and disorganization of the pattern with occasional spiking in the temporal, frontal or occipital regions (Skelton, 1970; Marinacci, 1963; Maletsky, 1976; Thompson, 1944). Jellinek (1942) suggested that MAP primarily manifested in individuals with psychopathic personalities, characterized by spontaneous episodes of anger, even during periods of abstinence.
CONCLUSIONS: Most experimental studies have been unable to successfully identify a foundational etiological explanation for MAP. The intricate combination of alcohol's neurotoxic effects, emotional stress, sleep deprivation, nutritional deficiencies, and individual susceptibility may contribute to the manifestation of MAP. The likelihood that MAP is an alcohol-induced epileptic phenomenon has been investigated but remains unconfirmed.  Further research is essential to elucidate the specific mechanisms and risk factors that contribute to the development of this condition, paving the way for more targeted prevention and intervention strategies.