Psychostimulants: clinical presentation and dependence
This group includes cocaine, amphetamines, illicit derivatives (from ephedrine or phenylpropanolamine), and MDMA. Intoxication manifests as a manic-like syndrome.
Symptoms of intoxication:
- Psychiatric: unnatural vivacity, talkativeness, overestimation of one's abilities, hypersexuality. Patients feel no need for sleep or food, experiencing a sense of lightness throughout the body.
- Autonomic: dry mucous membranes, marked pupillary dilation, skin pallor with red dermographism, tachycardia, and elevated blood pressure. A specific sign is the sensation of hair moving and goosebumps («crawling skin»).
With increased dosages or chronic use, severe hallucinatory-delusional psychoses develop. Delusions of persecution, auditory callouts, and tactile hallucinations occur (patients scratch their skin in search of imaginary insects).
Dependence develops rapidly, especially with intravenous administration. The craving is compulsive in nature: the drug is used continuously until supplies are completely exhausted. The withdrawal syndrome is not life-threatening, but is accompanied by severe dysphoria, anhedonia, somnolence, and insatiable appetite.
Cannabinoids (cannabis products)
The use of marijuana and hashish is the most widespread form of substance abuse in the world. Behavior during intoxication directly depends on the dose taken.
Features of intoxication:
- In high doses, motor disinhibition, silly behavior, irrepressible laughter, and distortion of time and space perception are observed.
- Visual images and sounds become unnaturally vivid, and tinnitus occurs.
- Somatic findings include tachycardia, facial flushing with a pale nasolabial triangle, conjunctival injection, and mydriasis.
Although episodic social smoking may not lead to dependence for a long time, transitioning to daily solitary use results in stable addiction in about three months. Withdrawal is mild (similar to nicotine cessation), accompanied by irritability, insomnia, chills, and resolves spontaneously in 4–6 days. However, high doses can provoke acute psychosis resembling schizophrenia or oneiroid state.
Hallucinogens and anticholinergics
These drugs radically distort reality perception and emotional background. Dependence on them is less common because the effects frequently induce fear.
- Hallucinogens (LSD, ketamine, phencyclidine):
Cause derealization, depersonalization, and synesthesia (the ability to «see» sounds). Tolerance to LSD develops within 2–3 days but rapidly drops after a pause. A physical withdrawal syndrome is not characteristic of this group.
- Anticholinergics (trihexyphenidyl, atropine):
In toxic doses, they provoke severe delirious clouding of consciousness. The initial excitation phase is rapidly replaced by depressed consciousness and slowed speech. Somatic signs include tachypnea, urinary retention, dry skin, and muscle twitching. Chronic use leads to profound encephalopathy with cognitive decline.
Treatment approaches (using stimulants as an example)
Treatment of dependence begins with the simultaneous discontinuation of the substance. Therapy is divided into three stages depending on the phase of remission.
1. Recovery (acute period) Basically, the patient requires rest. Pharmacological support includes short courses of tranquilizers and mood stabilizers (carbamazepine). To relieve the autonomic storm, adrenoceptor blockers (propranolol, pyroxan) are used. Nootropics with a sedative component (phenibut), B vitamins (thiamine), and hepatoprotectors are indicated.
2. Abatement of pathological craving As physical recovery progresses, aggression and drug craving increase. Antipsychotics are prescribed (chlorprothixene, risperidone, quetiapine). Important: they must not be used as monotherapy due to the risk of dopamine deficiency, so antidepressants (mirtazapine, mianserin) must be included in the regimen. If chorea is present, amantadine is used.
3. Maintenance outpatient therapy The basis of this stage is intensive individual and group psychotherapy. Medications include bromocriptine to support monoamine systems (with a categorical ban on alcohol and a warning about reduced concentration) or long-term courses of antidepressants.
Briefly: answers to topical questions
What drugs belong to the group of sedatives and hypnotics?
The group of sedatives and hypnotics includes derivatives of benzodiazepine, barbituric acid, meprobamate, methaqualone, glutethimide, sodium oxybate, chlormethiazole, chloral hydrate, and other drugs. Their effects share a high similarity with hypnotics and alcohol.
What are the main clinical manifestations of sedative intoxication?
Mild intoxication with sedatives presents with drowsiness, coordination impairment, slurred speech, tachycardia, constricted pupils, and shallow breathing. Severe intoxication is characterized by coma with absent pupillary light reflex, as well as respiratory and cardiac dysfunctions.
How does the withdrawal syndrome manifest in hypnotic and sedative dependence?
The withdrawal syndrome clinically resembles alcohol withdrawal and is accompanied by increasing anxiety, persistent insomnia, tremor, agitation, irritability, headache, and loss of appetite. At the peak of the condition, severe complications in the form of delirium, hallucinatory-delusional psychoses, and epileptic seizures are possible.
What internal organ complications arise from chronic sedative use?
Chronic use of sedatives leads to immunosuppression, the development of hepatitis and fatty liver disease, myocardiodystrophy, as well as gastrointestinal lesions in the form of hyperacid gastritis and a tendency to constipation. Practically all patients develop somatic and neurological consequences, including encephalopathy.
How does the development of tolerance to sedatives differ from tolerance to psychostimulants?
Tolerance to sedatives develops unevenly: it rapidly develops to the hypnotic effect, but does not develop to the neurological effects, which is why the lethal dose increases only slightly. At the same time, tolerance to psychostimulants changes dynamically and depends on the depletion of monoamine stores, requiring a substantially higher dose for a new rush of activity.
To remember the symptoms of anticholinergic poisoning: «Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter».
Class and exam questions
Why is it impossible to use only antipsychotics when treating stimulant dependence?
Antipsychotic monotherapy exacerbates dopamine deficiency in the central nervous system, leading to severe treatment dissatisfaction and provoking relapse. They must be combined with antidepressants.
How quickly does tolerance to LSD develop?
Tolerance to LSD increases rapidly — already by the 2-3rd day of continuous intake, the drug stops working, but it returns to baseline just as quickly after a break.
What are the specific features of cannabinoid withdrawal syndrome?
The withdrawal syndrome is physically safe and resembles the reaction to tobacco cessation: insomnia, irritability, mild tremor, and chest discomfort. It lasts 4-6 days.
What else to study on this topic
- Pathogenesis of monoamine system depletion in chronic cocaine use
- Differential diagnosis of cannabinoid psychosis and schizophrenia debut
- Mechanisms of manganese encephalopathy and chorea development from illicit stimulants
- Features of dependence development in individuals with psychopathic personality traits
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