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.
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