The understanding of alcohol-induced psychotic disorder (AIPD) as an illness phenomenon is becoming is increasingly important for the clinician. AIPD is often described as a “rare complication” [1] of alcohol use disorders. Despite this description, it was noted that the number of persons’ diagnosed with alcohol psychosis has escalated by four times in certain countries [2] and for patients diagnosed with AIPD there is 68% risk of re-admission [3]. There is a 37% co-morbidity of AIPD with other mental disorders [4] and a 5–30% risk that patients with AIPD will develop a chronic schizophrenia-like syndrome [5]. Patients who develop AIPD are at risk of becoming suicidal and need to be carefully monitored [3].
Recent research [1, 6] concurs with earlier findings [7] that AIPD is a distinct diagnostic entity that can be distinguished from schizophrenia. Most commonly, AIPD mostly occurs with auditory hallucinations but also delusions, often of a paranoid nature. Whilst AIPD resembles paranoid schizophrenia, it generally occurs without negative symptoms [1, 7]. The psychotic episode reportedly often lasts no more than a month [8] to 6 months [6, 9], but during that time, reality testing is impaired. The person suffering from AIPD related auditory hallucinations has no insight into the fact that hallucinations are substance-induced [10] especially during the episode.
There are inconsistent reports regarding the outcome of this disorder [2, 5]. Some authors [2, 5] noted that AIPD may become prolonged and schizophrenia-like symptoms may develop. Other authors [9, 11] noted that the outcome of AIPD is usually good if abstinence is achieved. There is some indication that AIPD is a severe psychiatric disorder with poor prognosis [4]. This study [4] however included in their sample persons who suffered from alcohol-withdrawal delirium. A fifty year follow-up study [12] concurred with the previous study [4] and found that alcohol-induced psychotic syndrome (AIPS) is associated with increased risk for premature death. This study included sample persons with delirium tremens as well as AIPD, hence the use of the term AIPS. The authors however conclude that AIPD is a severe mental illness with poor prognosis [4].
The age of onset of alcoholism reported in AIPD varied between 21.4 [2] and 29.1 years [13] with the latter study showing a significantly younger age of onset of alcoholism for AIPD patients than their non-psychotic alcohol-dependent male counterparts. There were no significant differences [13] with reference to age, education, marital status and employment between male alcoholic patients with and without a history of psychosis. In this study [13] however there was a significant difference between the number of Caucasian men diagnosed with AIPD and the number of non-Caucasian men. AIPD was diagnosed more in the Caucasian men. A previous study [4] reported that low socio-economic status, paternal mental health or alcohol related difficulties, early onset of alcohol dependence and numerous hospitalizations increase the risk for developing AIPD.
Although a number of reports [2, 14, 15] addressed the phenomenological expression of AIPD, the nuanced clinical presentation received very little scientific attention [16]. This paucity of interest is deemed unjustified as the correct diagnosis of this condition is key to accurate treatment and improved prognosis [16]. This paucity of literature highlights the lack of scientific evidence addressing the cognitive deficits of this disorder. There is some evidence suggesting that cognitive deficits as measured by the mini-mental state examination (MMSE) [17] may be greater in AIPD compared to uncomplicated AD [1].
The present introductory study compared the neuropsychological functioning of patients who were diagnosed with AIPD with the neuropsychological functioning of alcohol dependent patients in order to differentiate between these two conditions from a neuropsychological perspective. Additionally, this paper aims to expose the associated brain region which is potentially at the genesis of AIPD. Understanding the underlying pathophysiology may lead to more effective treatment of AIPD and prevent relapse, including recurrent re-admissions and possibly the development of more severe pathology.
Neuropsychological deficits associated with alcohol use
The susceptibility to acquire neuropsychological deficits resulting from alcohol use or abuse is multifactorial [18]. In addition to alcohol use, there are several contributory elements to cognitive decline such as current age, age at which alcohol consumption started, the period of time over which alcohol was consumed, family history of alcoholism, nutrition, and conditions related to birth and pregnancy [18]. The literature concurs that increasing age and medical co-morbidity exacerbates the negative cognitive sequelae of alcohol use disorders [19]. On the other hand, there seems to be little support for the hypothesis that gender, specifically being female, is a risk factor for cognitive decline despite the fact that women appear to be more prone to alcoholism than men [18]. Chronic malnutrition, in the presence of alcohol dependence or abuse, is considered a consequence of alcohol abuse, specifically thiamine deficiency which again may lead to neurological deficits [20]. These neurological deficits, acquired through thiamine deficiency may be reversible given improved nutrition or treatment.
Alcohol misuse may cause diffuse brain damage therefore most domains of neuropsychological assessment may be affected [21]. Even alcohol-dependent patients without dementia may have mild cognitive deficits in neuropsychological functioning [21, 22]. Alcohol dependent subjects often have deficits of working memory, immediate and delayed memory as well as recognition; visual-constructive ability and verbal fluency [21].
Vocabulary is usually not affected by alcohol abuse [19, 23], but other language functions such as abstraction and comprehension were found to be impaired [19]. There is evidence showing that alcohol misuse may cause difficulties in attention and concentration [22,23,24]. Motor control difficulties such as impairment of gait, balance and speed were also reported in the presence of alcohol abuse [20].
Alcohol abuse is often detrimental to memory function [19, 20, 22, 25, 26]. Mild deficits in explicit memory were found in individuals who abused alcohol [20] and difficulties in short term memory and learning problems were described [27]. Chronic excessive alcohol intake was associated with difficulties in learning of new and complex verbal material [27]. Alcohol misuse harms word recognition but not the ability to identify distractor words [28]. Impairments in episodic memory, that is memory for autobiographical information, were specifically noted for persons with AD [29, 30].
A number of authors [20, 23, 26] reported poor visuospatial functioning and visuospatial processing associated with alcoholism. One author [23] asserted that patients with AD demonstrate deficiency on new tasks that involves integration and manipulation of material. Alcohol dependent persons’ performed poorer on tasks of response inhibition, executive function and attentional control [31].
Neuropsychological deficits of uncomplicated alcohol use disorders include mild cognitive deficits in executive functions [20]. Specific executive functions impaired in this population include planning, switching, correction, self-monitoring and decision-making [20]. More distinct impaired decision-making is associated with more severe alcoholism [32]. Alcohol dependent patients demonstrated deficits on tasks of rule detection, inhibition of dominant responses, coordination of dual tasks [32], and difficulties in problem-solving ability [26].
Although numerous studies elaborated on the complexity and diversity of the neuro-cognitive fall-out associated with alcohol use, there has been very little focus on AIPD. Earlier reports by Bleuler 1916 [14] generally noted that for patients suffering from AIPD; memory, attention and concentration are intact. These were based on observation, rather than neuropsychological assessments. Reporting on a retrospective review of hospital admission records, Surawics [33] noted that patients with AIPD demonstrated deficits in arithmetic, figure drawing and matching sets. These patients only occasionally exhibited fleeting memory difficulties which were associated with the duration and severity of alcohol abuse history. Both patients with schizophrenia [34] and alcohol-dependent patients with a history of hallucinations [35] have demonstrated similar deficits in source-monitoring of information. It was reported that alcohol-dependent patients with a history of hallucinations were prone to confuse imagination with reality (e.g. discriminating external versus internal source of information) [35]. Apart from these reports [33,34,35], we found no previous reports assessing neuropsychological differences between patients with uncomplicated AD and AIPD.
This introductory study formed part of a larger study aimed at differentiating alcohol-induced psychotic disorder (AIPD) from uncomplicated AD and Schizophrenia [1]. In particular, this study aimed to explore the neuro-cognitive deficits of AIPD as compared to the cognitive deficits of uncomplicated alcohol dependence (AD). We postulated that cognitive deficits in AIPD would be more severe than in uncomplicated AD [1].
