Alcohol-induced Persisting Amnestic Disorder
Continuous heavy alcohol consumption can lead to several neu-rological deficits caused by thiamin deficiency. Among them, al-cohol-induced persisting amnestic disorder (AIPAD, also known as a Korsakoff’s psychosis, due to the fantastic confabulatory sto-ries described by patients suffering this condition) is prominent. Profound deficits in anterograde memory and some deficits in retrograde memory characterize this condition. Patients cannot retain or learn new information and experience profound disori-entation to time and place. The severity of anterograde memory deficits typically leads Korsakoff’s patients, who are unaware of their deficit, to reconstruct forgotten events by confabulating. Korsakoff’s amnestic disorder is usually preceded by several episode of Wernicke’s encephalopathy, characterized by confu-sion, ataxia, nystagmus and gaze palsies. When this condition subsides, the characteristic memory deficits of Korsakoff’s psy-chosis become prominent.
Cessation of drinking can lead to an improvement in memory with approximately 20% of the cases demonstrating complete recovery. However, in most cases memory deficits re-main unchanged, and in some instances long-term care is needed despite sobriety.
Continuous heavy drinking is also associated with progressive and gradual development of multiple cognitive deficits character-ized by memory impairment, apraxia, agnosia, or disturbances in executive functioning. These deficits cause serious impairment in social and occupational functioning and persist beyond the du-ration of alcohol intoxication and alcohol withdrawal. History, physical exam and laboratory tests should be utilized to deter-mine whether these deficits are etiologically related to the toxic effects of alcohol use. Other factors associated with this condition are poor nutritional status and vitamin deficiencies, as well as history of head trauma. It is believed that this condition is associ-ated with the repeated occurrence of Wernicke’s encephalopathy. Atrophy of frontal lobes and increased ventricular size have been described in this condition. Continuous alcohol consumption ex-acerbates the dementia, whereas drinking cessation is associated with improvement and even recovery of cognitive deficits.
Alcohol-induced mood disorder (AIMD), characterized by de-pressed mood and anhedonia, as well as elevated, expansive, or irritable mood, frequently develops as a consequence of heavy drinking. Onset of symptoms can occur during episodes of al-cohol intoxication or withdrawal, and may resemble a primarymajor depressive, manic, hypomanic, or a mixed episode. In contrast to the dysphoria and lack of energy observed during episodes of alcohol withdrawal, severity and duration of alcohol-induced mood symptoms is greater than is usually expected, war-ranting independent attention by the clinician. Although mood disturbances are common among alcoholic patients entering treatment (80%), alcohol-induced mood symptoms tend to sub-side within 2 to 4 weeks following alcohol cessation. Evidence that the mood disturbances are not better explained by a primary mood disorder should be sought by the clinician. Evidence sug-gesting a primary mood disorder includes onset of mood symp-toms preceding onset of alcohol abuse and persistence of mood symptoms after alcohol cessation or during extended periods of abstinence. Regardless of the primary or secondary nature of mood symptoms, given the high prevalence of suicide among al-coholics, clinicians should closely monitor the patient for emerg-ing suicidal thoughts, implementing more intensive treatment (discussed later) if necessary.
Although alcohol has anxyolitic properties at low doses, heavy alcohol consumption can induce prominent anxiety symptoms. Alcohol-induced anxiety (AIA) symptoms more commonly in-clude generalized anxiety symptoms, panic attacks and phobias. In order to establish this diagnosis, clinicians must rule out other general medical conditions or psychiatric disorders that can mimic this problem. AIA may develop during alcohol intoxica-tion or withdrawal, but its severity and duration are typically worse than the anxiety normally observed during the course of these conditions. An onset of drinking preceding the anxiety syndrome, and improvement or remission of anxiety during peri-ods of abstinence, suggest AIAD. Monitoring the course of these symptoms for several weeks after alcohol cessation can be use-ful in determining their nature. Usually, a substantial improve-ment of anxiety will be observed during this period, suggesting a direct relationship of anxiety to alcohol. In some cases, a full remission of symptoms is not observed until after 3 to 4 weeks of abstinence.
This disorder is characterized by prominent hallucinations or de-lusions that are judged by the clinician to be due to the effects of alcohol. The psychotic symptoms usually occur within a month of an alcohol intoxication or withdrawal episode, and the patient is characteristically fully alert and oriented, lacking insight that these symptoms are alcohol-induced. Although onset of psy-chotic symptoms can occur during or shortly after alcohol intoxi-cation, delirium or alcohol withdrawal delirium, alcohol-induced hallucinations, and/or delusions do not occur exclusively during the course of these conditions. Evidence that hallucinations and delusions are not part of a primary psychotic disorder include: atypical or late age of onset of psychotic symptoms, onset of alcohol drinking preceding the onset of psychiatric symptoms, and remission of psychotic episodes during extended periods of abstinence. Usually, alcohol-induced psychotic symptoms tend to subside within a few weeks of abstinence, although in a sub-set of patients psychotic symptoms can become chronic, requir-ing long-term treatment with antipsychotic medication. In these cases clinicians are obligated to consider a schizophrenic or a delusional disorder as part of the differential diagnosis.
Heavy alcohol consumption can be associated with a prominent disturbance of sleep. At intoxicating BALs, especially when blood alcohol levels are declining, sedation and sleepiness can be observed. Alcohol intoxication induces an increase in nonrapid eye movement (NREM) sleep, whereas rapid eye movement (REM) sleep density decreases. Subsequently, there is an increase in wakefulness, restless sleep, and vivid dreams or nightmares related to a reduction in NREM sleep and a rebound in REM sleep density. During alcohol withdrawal, sleep is fragmented and dis-continuous with an increase in REM sleep. After withdrawal, patients frequently complain of sleep difficulties and may experi-ence superficial and fragmented sleep for months or years.
In contrast to the primary sleep disorders (PSD), alcohol-induced sleep disorder (AISD) is characterized by an onset of drinking preceding the sleep disturbance and by remission of symptoms during the course of sustained abstinence. AISD can occur during the course of a typical alcohol intoxication or alco-hol withdrawal episode. However, duration and severity of the sleep disturbances exceed those typically observed during these conditions. Given that protracted alcohol-withdrawal symptoms are frequent among abstinent alcoholics, onset of AISD can oc-cur up to 4 weeks after initiation of alcohol abstinence. History of a previous PSD and/or persistence of sleep disturbances for more than 4 weeks following intoxication or acute withdrawal are highly suggestive of a PSD. Differential diagnosis is com-plicated by the fact that heavy alcohol consumption can cooccur and exacerbate other psychiatric disorders that present with sleep disturbances (e.g., mood disorders, anxiety). Alcohol consump-tion can also intensify other sleep problems such as narcolepsy or breathing-related sleep disorders BRSD.
Although small doses of alcohol in healthy individuals appear to enhance sexual receptivity in women and facilitate arousal to erotic stimuli in men, continuous and/or heavy drinking may cause significant sexual impairment. Alcohol-induced sexual dysfunction is characterized by impaired desire, impaired arousal and impaired orgasm, or sexual pain. It is also associated with marked distress or interpersonal conflicts. Onset of these impairments usually occurs during alcohol intoxication but du-ration of symptoms exceeds the uncomplicated course of alco-hol intoxication. Symptoms usually subside after 3 to 4 weeks of alcohol abstinence. Persistence of symptoms beyond this time may suggest a primary sexual dysfunction (PSD) or a sexual dys-function due to the medical complications of alcoholism (e.g., neuropathy, alcoholic-liver disease). Onset of a recurrent sexual dysfunction preceding the onset of alcohol abuse also suggests a primary disorder. Use of other substances, particularly those prescribed for the treatment of alcohol withdrawal such as ben-zodiazepines or barbiturates, should be ruled out as a cause of the sexual dysfunction.