Acute psychotic states
The manifestation of acute psychoses is usually closely associated with the development of withdrawal syndrome. Depending on the leading syndrome, several forms are distinguished.
Severe delirium An extremely dangerous condition requiring treatment in an intensive care unit. Prognostically unfavorable signs include:
- Inability to move independently due to severe weakness.
- Critical homeostasis shifts: drop in blood pressure, hyperthermia (above 40 °C), dehydration, pronounced tachyarrhythmia, and oliguria.
- Neurological deficit: from muscle atonia and ataxia to the onset of epileptiform seizures and hyperkinesia (including stereotyped picking movements of the hands).
- Transformation of consciousness: development of mussitant (muttering) or professional delirium with complete disorientation.
Acute hallucinosis Unlike delirium, it occurs against the background of clear consciousness. The patient hears true verbal hallucinations (voices perceived from outside). They are often commentary or threatening in nature, arguing among themselves. The patient retains memory of events but is impervious to reasoning (lack of suggestiveness). Symptom amplification in the evening is typical. A 'pursued pursuer' type reaction is possible, where the patient attempts to take revenge on imaginary enemies.
Acute paranoid Debuts with sensory delusions and unsystematized ideas of reference. Affectogenic illusions are characteristic: in real conversations of casual passersby, the patient hears threats and accusations. Behavior is dictated by intense fear: patients flee, barricade themselves in rooms. Symptom regression during treatment occurs strictly in stages: first, fear subsides, then perceptual disorders disappear, and only at the end does insight into the past delusion emerge.
Chronic psychoses and encephalopathies
Prolonged intoxication and vitamin deficiency (especially thiamine) lead to irreversible organic lesions of the central nervous system.
Korsakoff's amnestic psychosis First described in the late 19th century. The disease develops either as an outcome of severe delirium or gradually. The classical clinical triad includes:
- Fixation amnesia — total inability to memorize current events.
- Disorientation in place and time (a consequence of amnesia).
- Polyneuropathy (the severity of neurological deficit does not always coincide with the severity of cognitive impairment).
Patients with this syndrome exhibit a specific loss of insight: they formally acknowledge memory problems but remain passive, experiencing no anxiety or shame. The prognosis is unfavorable: working capacity is permanently lost. With prolonged sobriety, only minimal adaptation is possible (memorizing their ward, attending physician).
Wernicke-Korsakoff acute encephalopathy The most severe variant of acute alcohol-induced psychoses (hemorrhagic brain lesion). It begins with deep delirious clouding of consciousness, accompanied by the rapid buildup of somatic decompensation. The risk of death is extremely high.
Rarer forms include alcoholic cerebellar atrophy, Marchiafava-Bignami disease, and central pontine myelinolysis (the latter two forms frequently result in the patient's death).
Dependency diagnostic criteria
The diagnosis of dependence can only be established by a specialized professional (psychiatrist or narcologist). General practitioners record signs of prolonged abuse, which are divided into clinical manifestations of withdrawal and indirect markers.
Withdrawal syndrome (abstinence syndrome) An absolute sign of established dependence. Often masked as somatic pathology (hypertensive crisis, ischemic attack). Its specifics:
- Combination of tachycardia and transient hypertension with purple-cyanotic hyperemia of the upper torso.
- Profuse hyperhidrosis (sweating), tremor, nystagmus.
- Sleep disturbances: stubborn insomnia, vivid nightmares (harbingers of psychosis).
- Onset of epileptic seizures exclusively on days 1–3 after cessation of use.
Indirect signs and anamnesis In conversations with the doctor, patients often demonstrate anosognosia (denial of illness), yet fixate on periods of sobriety ("I haven't drank all month"). Loss of dose control despite social and medical problems is characteristic. The doctor's questions should be neutral (e.g., "How do you tolerate alcohol?"), as direct accusations provoke dissimulation.
Laboratory markers There are no 100% specific tests, but a complex is evaluated:
- Increase in mean corpuscular volume (MCV).
- Liver function tests: AST predominance over ALT, isolated GGT elevation.
- Elevated uric acid, IgA, and HDL concentrations.
Briefly: answers to topical questions
Which brain structures are specifically affected in acute Wernicke's encephalopathy?
In acute Wernicke's encephalopathy, structures of the deep gray matter and periventricular areas are specifically affected. The most frequently involved in the pathological process are:
- Mammillary bodies (mammillary bodies) — characterized by a high-intensity signal transforming into atrophy.
- Thalami — predominantly medial and dorsomedial regions are affected.
- Periaqueductal spaces — including the periaqueductal gray matter.
- Walls of the third ventricle — periventricular zones are involved.
- Tectum of the midbrain (quadigeminal plate) — as well as the roof of the fourth ventricle.
- Brainstem structures and basal ganglia — pons, medulla oblongata.
The cerebral cortex and dentate nuclei are less frequently involved in the pathological process.
What pharmacological agents are used to manage severe alcohol delirium?
To manage severe alcohol delirium, GABAergic agents are predominantly used as pathogenetic therapy. The main drug groups include:
- Benzodiazepine tranquilizers — diazepam, bromdihydrochlorophenylbenzodiazepine (phenazepam).
- Barbiturates — sodium thiopental, hexobarbital (hexenal).
- Other GABAergic agents — zopiclone, zolpidem, sodium oxybate.
For florid psychosis, injectable drugs are used; available injectable agents include diazepam, phenazepam, sodium thiopental, and hexobarbital. Due to high tolerance in patients with alcoholism, high doses are required. Neuroleptics (e.g., haloperidol) have only a symptomatic effect and are ineffective without GABAergic agents, while drugs with pronounced anticholinergic action are contraindicated.
What clinical manifestations are characteristic of opioid withdrawal syndrome?
Clinical manifestations of opioid withdrawal syndrome develop sequentially and include psychopathological, autonomic, somatic, and behavioral disorders. The following symptoms are characteristic:
- Initial manifestations — anxiety and restlessness.
- Autonomic disorders — rhinitis, lacrimation, relentless sneezing, excessive sweating, chills, tachycardia, elevated blood pressure, cold and cyanotic extremities, mydriasis.
- Sleep disturbances — persistent insomnia.
- Pain syndrome — body aches ('withdrawal pains'), predominantly in the lower back, spine, and lower extremities.
- Gastrointestinal disorders — recurrent vomiting, spastic abdominal pain, and diarrhea with tenesmus.
- Behavioral disorders — loss of behavioral control and an extreme increase in drug craving.
The triad of Korsakoff's psychosis: 'FOP' — Fixation amnesia, Orientation impaired, Polyneuropathy.
Class and exam questions
How to distinguish alcohol hallucinosis from delirium?
The main difference is the state of consciousness. In hallucinosis, consciousness remains clear, the patient is fully oriented to the environment, but hears true voices. In delirium, consciousness is clouded, with massive disorientation and suggestibility.
Can Korsakoff's psychosis be completely cured?
No. The prognosis in most cases is unfavorable. Even with complete cessation of alcohol and adequate therapy, severe memory disorders persist for life, and working capacity is lost.
In what sequence do symptoms disappear in acute paranoid states?
The resolution of psychosis occurs in stages: first, the affect regedes (fear disappears), then perceptual disorders vanish, and last of all, the patient develops insight into the past delusion.
How long do laboratory parameters take to normalize after alcohol cessation?
The lipid profile normalizes within 2 weeks, while markers of liver damage (enzymes and IgA) recover within 1–2 months. Erythrocyte macrocytosis persists the longest — up to 4–6 months.
What else to study on this topic
- Pathogenesis of alcoholic jealousy delirium
- Features of somatic damage (cardiomyopathy, pancreatitis, giant sialadenitis)
- Rare encephalopathies: Marchiafava-Bignami disease and central pontine myelinolysis
- Rules for taking an anamnesis in patients with suspected addiction
- Legal aspects of diagnosing addiction by a general practitioner
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