Substance-induced anxiety disorder – Anxiety states by substances
28 Nov 2018

Substance-induced anxiety disorder – Anxiety states by substances

Post by radars

The American diagnosis scheme DSM-IV also introduces anxiety disorders as substance-induced anxiety disorder, which can consist of pronounced anxiety, panic attacks, compulsive thoughts or compulsions. The symptoms of anxiety occur during or within one month after a substance intoxication (poisoning) or after withdrawal and are causally related to the intake of substances (alcohol, caffeine, nicotine, drugs, drugs or other substances).

Alcohol, nicotine, coffee, medication, and drugs can cause panic attacks due to cardiovascular changes (collapse or recirculation of the circulatory system) as well as by a blood glucose drop. Panic patients are often found to have alcohol or drug (tranquilizer) abuse, increased smoking, and excessive coffee consumption. After the occurrence of panic attacks, the excessive consumption of alcohol or tranquilizers will be increased even more. When a drug with a calming effect is suddenly stopped, the adrenaline level increases, causing a panic attack.

Stimulating drugs can cause an excessive circulatory reaction, which is experienced as a panic attack, so that anxiety persists, even if substances have not been taken for a long time.

Overdosing or psychological and physical withdrawal symptoms can lead to anxious physical observation due to the effects experienced.

Many drugs (cocaine, amphetamines, LSD, for example) develop their biochemical effects precisely in those brain structures that have to do with emotional reactions and memory processes (mediobasal congestion with the associated limbic system). This explains the emotional changes, abnormal excitement, and anxiety (“horror trips”) and panic attacks.

The suspicion of a substance-induced anxiety disorder may result from the presence of features which are untypical for a primary anxiety disorder (e.g., atypical age at onset of the disorder or atypical course). In case of a panic disorder, these are:

Beginning after 45 years (which is rare),

Presence of atypical symptoms during a panic attack (primary dizziness, loss of equilibrium, awareness, bladder or bowel control, headaches, slurred speech, amnesia, etc.).

On a primary anxiety disorder, which already existed before the substance abuse, the following circumstances indicate:

Anxiety symptoms before the substance use, stopping the anxiety symptoms for a considerable time (over a month) after the end of the substance or the acute withdrawal,

Development of symptoms that are more pronounced than expected due to the nature and quantity of the substance or due to the intake, the earlier presence of a primary anxiety disorder.

The DSM-IV identifies the following 10 classes of substances that can cause a specific substance-induced anxiety disorder by abuse, poisoning, side effects or withdrawal symptoms (nicotine and opiates are not mentioned):

  1. Caffeine
  2. Alcohol
  3. Sedatives, hypnotics, anxiolytics
  4. Amphetamines or similar sympathomimetic
  5. Cocaine
  6. Cannabis
  7. Hallucinogens
  8. Phencyclidines or similar substances (not discussed here)
  9. Inhalants, i. Snuffles (not discussed here)
  10. Other substances (drugs)


Caffeine removes fatigue, exhaustion and general weakness in small doses (50-250 mg) and makes thinking and feeling livelier. There is a shortened reaction time, a slight euphoria, a stimulation of the breathing and an increased performance. Increased coffee consumption (more than 3-4 cups of coffee per day) can easily trigger panic attacks in people who are prone to anxiety.

Highly high daily doses (250-600 mg) can cause the following symptoms: cardiac arrhythmias, cardiac arrhythmias, reddened face, gastrointestinal discomfort, restlessness, restlessness, nervousness, agitation, psychomotor agitation, trembling, muscle twitching, sleep disturbance, insomnia, insensibility.

High doses (over 600 mg in a short time or over 1000 mg per day) cause heart rash, sleep disorders, restlessness and nausea, nausea and vomiting.

The elimination half-life is 3-7 hours. Caffeine binds to the adenosine receptors in the central nervous system and inhibits the soothing effect of adenosine, which results in the stimulating effect of coffee. There is an increase in excitatory neurotransmitters, especially dopamine. After some cups of coffee, about 50% of the adenosine receptors are caffeinated.

In pure, concentrated form, caffeine is present in many drugs (50-200 mg per tablet). After overcoming the panic disturbance, the moderate coffee consumption should be possible once it was experienced as pleasant.

The caffeine content of beverages and medicines is very different:

  • 1 cup roasted coffee (approx. 225 ml) =125 mg caffeine
  • 1 cup instant coffee (about 225 ml) = 90 mg caffeine
  • 1 cup decaffeinated coffee = 4 mg caffeine
  • 1 cup of tea (leaf or bag) = 60 mg caffeine
  • 1 cup of cocoa (150 ml) =5 mg caffeine
  • 1 can Coca-Cola (333 ml) =40 mg caffeine
  • 1 can of energy drink (e.g., Red Bull) = 80 mg caffeine
  • 1 caffeine-containing painkillers (e.g., thomapyrin) = 50 mg


Alcohol, depilatory sedatives, and various drugs have an anxiety-suppressing effect at first, but lead later to long-term intake, paradoxical effects or withdrawal symptoms to massive anxiety states, so that the same means are again used for the control if those concerned are not known.

The potential abuse potential of alcohol is based on the activation of dopaminergic neurotransmitter systems, in particular, dopaminergic nerve tracts, which extend from the ventral area (a region of the medial lobe), the nucleus accumbens (an accumulation of nerve cells in the forebrain) and the frontal cortex (anterior cerebral cortex). The desired effect of alcohol is caused by an excitatory (excitatory) effect of alcohol on the dopaminergic neurons in the tegmental is ventral region due to inhibition of the inhibitory (inhibitory) interneurons mediated by GABAA receptors. However, ethanol could also directly increase the activity of the dopaminergic neurons without the intermediary of internal neurons.

Anxiety in the context of alcohol withdrawal is caused by two factors:

Reduced GABA activity. Ethanol enhances the effect of the most important natural inhibitory transmitter substance GABA at certain GABAA receptors. The relaxing and anxiety-dissolving effect of alcohol is due to an amplification of the GABA-ergogenic mechanisms of action. Chronic alcohol consumption lowers the GABA level in the plasma, which causes a rise in excitement when alcohol is discontinued. In the case of alcohol withdrawal or reduced alcohol consumption of addicts, there is a longer lasting excitability increase in the central nervous system, which is associated with anxiety and can continue for a month even when the alcohol is completely stopped.

Increased noradrenergic activity. In the case of an alcohol withdrawal, an overactivity occurs in the locus coeruleus, the central noradrenergic structure, resulting in a general excitation, especially anxiety. Frequently, therefore, alcohol withdrawal symptoms are treated with tranquilizers or the doctor describes the symptoms of a panic attack without reporting any previous abuse of alcohol, so that tranquilizers are used as a (wrong) treatment method.

In an alcohol withdrawal after excessive and long-lasting alcohol consumption, at least two of the following symptoms occur within a few hours or less: anxiety, hyperactivity of the vegetative nervous system (perspiration or pulse above 100), psychomotor agitation, insomnia, increased tremor , temporary visual, tactile or acoustic hallucinations or illusions, grand mal seizures (epileptic seizures).

Long-standing alcohol abuse can damage the heart muscle due to its damping effect and the heart in its pumping power can be impaired by the frequent vitamin B1 deficiency. Consumption of alcohol also stimulates the adrenal glands to increase the release of cortisol, the stress hormone, which increases the blood pressure by inhibiting the excretion of water by the kidneys.

In people with high blood pressure the stress hormones, which are already elevated, are degraded more slowly because of the alcohol so that the blood pressure rises even more and symptoms occur (a headache, dizziness, dyspnea, chest pressure, heart problems, performance impairment, restlessness, etc.). At low blood pressure, the blood vessel dilating effect of the alcohol becomes noticeable, so that on standing, especially a lot of blood in the wide-spread veins of the legs. The counter-regulation causes heart rashes and sweating.

Sedatives, hypnotics, anxiolytics

Sedatives, hypnotics, and anxiolytics include benzodiazepines, carbamates (e.g., Meprobamat®), barbiturates and barbiturate-like hypnotics. This substance class includes all sleeping pills and almost all immediate acting anxiety-relieving drugs. These agents have a similar effect as alcohol: they can dampen substance-induced anxiety disorders and show the same withdrawal symptoms as with alcohol dependency when a severe or long-lasting consumption is ended or reduced.

According to the DSM-IV, an amphetamine intoxication has the following symptoms:

Inadequate behavioral or psychological changes: anxiety, tension, aggressiveness, euphoria or affective flattening, hypervigilance (excessive alertness), change in sociability, diminished judgment, reduced social and professional function.

At least two of the following symptoms: tachycardia (heart rash) or bradycardia (slow heartbeat), increased or decreased blood pressure, perspiration or chills, nausea or vomiting, loss of weight, psychomotor agitation or slowing, muscle weakness, respiratory rate (respiratory depression), chest pain, Confusion among others

In the case of amphetamine dependence, severe anxiety and paranoid symptoms often occur, as with regular cocaine intake. Today’s highly sophisticated designer drugs also belong to the amphetamine-like substances. These are chemically prepared mixtures of amphetamine-like and hallucinogenic substances, which can have different effects depending on the composition.

The proportion of amphetamine leads to increased drive, sleep and loss of appetite, inner unrest, increased red blood pressure, and speed of thought. The most recent designer drug is Ecstasy, which is ultimately an amphetamine. Amphetamine effects can lead to massive circulatory reactions, in extreme cases to overheating and cardiovascular failure due to insufficient cooling and the lack of fluid supply (e.g., in rave parties). Occurring panic attacks can trigger an ecstasy-induced anxiety disorder, at least for vulnerable persons.


Cocaine was recommended in 1884 by Sigmund Freud as a remedy for depression and anxiety and was tested in years of self-experimentation, but later became very dangerous. Cocaine is a natural substance from the leaves of the cocaine smoke, which is called “coke” or “snow” in the drug scene.

Cocaine urges the neurotransmitters norepinephrine, dopamine and serotonin from the synaptic end-buttons of the nerve endings in the brain and, through their rise in the corresponding synapses, induce an artificial high-spiritedness and vigor. At the same time, a longer duration of the stimulus conduction is made possible by the reuptake inhibition of noradrenaline, dopamine, and serotonin in the presynaptic nerve termination. The decisive behavioral enhancing and psychostimulatory effects of cocaine are due to its influence on the mesolimbic dopaminergic nerve endings (localized in the medial prefrontal cortex, nucleus accumbens, amygdala complex, and hippocampus).

The enhancement of dopamine activity can trigger or worsen schizophrenia-like psychoses. Serotonin is also involved in the effects of cocaine (a serotonin deficiency enhances the efficacy of cocaine as a positive enhancer).

Cocaine has the strongest effect of all stimulants. Because of the short elimination half-life (30-90 minutes), frequent intake is required to remain “high”. Cocaine is currently spreading. It is often used as a means to increase performance.

Cocaine has three central pharmacological effects: local anesthetic, constriction of the blood vessels, strong psychostimulants with pronounced reinforcing properties.

Cocaine activates the sympathetic nervous system with all its consequences: increased attention, motor hyperactivity, increase in pulse frequency, vasoconstriction, increased blood pressure, enlargement of the bronchi and bronchioles, increase in body temperature, dilated pupils, increased glucose availability and displacement of the blood flow from the inner Organs to the muscles.

The withdrawal occurs within one hour for short-acting drugs (e.g., triazolam), and for long-acting drugs (e.g., diazepam) only after 1-2 days or later. These drugs are discussed extensively as the classical sedative in the chapter on psych – pharmacotherapy.

Amphetamines and similarly acting sympathomimetic

This substance class includes the following:

Amphetamine preparations (often called “wake-up”);

Methamphetamine: amphetamine-like substances, e.g. “Speed” and “Ice” (acting quickly and intensively by smoking, similar to “crack” cocaine), the preparation Pervitin® was taken in the second world war by soldiers of many countries;

Substances having a different structure, but with an anti-amphetamine effect (e.g., methylphenidate: Ritalin®, fenetylline: Captagon®);

Some appetite suppressants (“diet pills”).

The main representatives of this substance group are the amphetamine derivatives, which are now banned in Austria and are only available illegally. In the FRG, the amphetamine preparations are also no longer commercially available, structurally related substances are subject to prescription or are used to a limited extent within the scope of the narcotics prescription regimen (for example the preparations Ritalin® and Captagon®).

Amphetamines are included in the group of psychostimulants comprising natural substances (e.g., cocaine) and synthetic substances (e.g., amphetamines).

Amphetamines and amphetamine-like drugs (aside from the lack of anesthetic effect) are similar to cocaine, only longer, but may have more intense peripheral sympathomimetic effects (sympathetic excitation).

Psychostimulants of all kinds have the following effects:

Dopamine reuptake inhibition. Psychostimulants cause eruption of the neurotransmitter dopamine into the presynaptic cleft and thus a longer dopamine dwell in the synaptic cleft, thereby increasing and extending the dopamine effect on the mesolimbic system in the brain (seat of the “reward system”).

Distribution of stress hormones. Many stimulants cause a release of the stimulant catecholamines (adrenaline, norepinephrine, and dopamine).

Inhibition of monoamine oxidase (MAO). The MAO builds catecholamines in the presynaptic neuron. The stimulants inhibit this process and thus cause a higher amount of catecholamine in the presynaptic nerve ending.

Some stimulants have an effect on postsynaptic catecholamine receptors, including dopamine receptors.

The various possibilities of action make the subjectively rewarding effect (“kick”) in the mesolimbic system of the brain, although depending on the substance a somewhat different mode of action is given.

Amphetamine and its derivatives release dopamine and norepinephrine from the presynaptic nerve endings and at the same time inhibit the reuptake into the presynaptic neuron, which increases their efficacy. These substances suppress fatigue and drowsiness due to better circulation and oxygen supply, eliminate physical fatigue and laxity, create general well-being and a slight euphoria (“high” -feel) and improve the concentration and performance in the short term. Some amphetamines are “appetite suppressants” because they suppress the feeling of hunger.

Side effects of the amphetamine use are heart palpitations, heart stumbling, increased blood pressure, insomnia, nightmares, trembling, headache, mouth dryness, diarrhea, and the like.

Psychostimulants are becoming increasingly important as part of the service society. The “new dependents” want to be successful. They often have failures and try to keep fit through “speed” preparations.

Cocaine users are in the following dilemma:

Appetite, sleep, and fatigue are suppressed, but they return later.

The motor activity is increased, which soon manifests itself in excitement, restlessness and movement impulses.

Consciousness and mental presence increase as desired but later go into exhaustion.

There are the desired immediate and intense euphoria and increased self-assurance, but later a pronounced state of anxiety, which lasts several hours, in addition, depressions and in extreme cases, delusions occur. The need for restoration of euphoria rapidly leads to psychological dependence.

Chronic cocaine consumption in the sense of a psychological dependency leads to fear, depression, persecution ideas, aggressive behavior, and weight loss.

Cocaine withdrawal after discontinuation or reduction of the substance causes a dysphoric (depressive) detuning as well as at least two of the following physiological changes: fatigue, psychomotor restlessness or slowing, vigorous and unpleasant dreams, insomnia or excessive sleep need, increased appetite. On the other hand, physical dependence with withdrawal symptoms does not occur.

According to the DSM-IV, cocaine intoxication is shown in the following symptoms:

Unsuitable behavioral or psychological changes: euphoria or affective flattening, anxiety, tension or anger, hypervigilance, changes in social behavior, impaired judgment or impairment in the social or professional field. There may also be perceptual disturbances (hallucinations).

At least two physical symptoms: tachycardia or bradycardia, increased or decreased blood pressure, perspiration or chills, nausea or vomiting, weight loss, pupillary dilatation, psychomotor agitation or slowing, muscle weakness, shallow breathing, chest pain, cardiac arrhythmia, confusion, seizures, dystonia, dyskinesia.


Cannabis is the world’s most commonly consumed illegal substance. Cannabis is obtained from the feminine hemp plants, as marijuana (a mixture of dried leaves, stems and flowers) and hashish (from the more powerful resin of the hemp plant).

The active substance THC (tetrahydrocannabinol) activates the dopaminergic neurons and causes a massive increase in serotonin levels in the brain. Serotonin has a function in the transmission of stimuli in the limbic system and in the reticular system and thus affects emotions, perception, and attention.

The simultaneous attenuation and excitation of different areas of the brain lead to mood fluctuations and emotional lability (unmotivated change of cheerfulness and deep sadness). The existing mood is amplified. The serotonin action causes, inter alia, a narrowing of the peripheral blood vessels (cold hands and feet) and an increase in pulse rate by 20-30 beats per minute. One-third of cannabis users experience mild forms of anxiety, depression or irritability. At high doses, “Horrortrips” can be used. These may appear similar to hallucinogen-induced “bad trips”: as mild to moderate anxiety states, as severe anxiety states in the extent of a panic attack, as paranoid ideas and hallucinations.

In the case of psychological dependence, discontinuation of the substance causes mental withdrawal symptoms: anxiety, restlessness, irritability, sleep disturbances, and vegetative disturbances. A cannabis intoxication has the following symptoms:

Unreasonable behavioral or psychological changes: first euphoria (desired), then anxiety, social withdrawal, impairment of motor coordination, impaired judgment.

At least two physical symptoms: heart rash, mouth dryness, increased appetite, visualization of vessels in the eye.


The inhomogeneous group of hallucinogens comprises natural or chemical substances which, for a certain time, alter the consciousness and the mood and cause schizophrenia-like conditions. The most famous hallucinogen is LSD (lysergic acid diethylamide), an active ingredient of the mother grain, a fungus that grows on cereals, followed by mescaline and psilocybin. Designer drugs (e.g., ecstasy) consist of different mixtures of hallucinogens and amphetamines.

Hallucinogen intoxication has the following symptoms:

Unconcerned behavioral or psychological changes: clear anxiety or depression, relationships of ideas, fear of losing the mind, paranoid ideas, impaired judgment, impaired social or professional functioning.

Changes in perceptions: Perception of perception, depersonalization, derealization, illusions, hallucinations, synesthesia (co-excitation of a sense organ in the case of irritation of another, for example, color vision in the case of sounds).

At least two physical symptoms (as a result of the stimulating effect): cardiac tears, heart stumbling, perspiration, blurred vision, trembling, coordination disorders, rapid change of the pupil width (mydriasis).

Chronic hallucinogen consumption often causes the following anxiety states:

  • Horrortrips: massive acute anxiety attacks with paranoid hallucinatory staining,
  • Flashback phenomena: without new drug ingestion unexpectedly a new noise effect, accompanied by intense anxiety and disorientation.
  • Other substances (drugs)

Anxiety can be triggered by numerous drugs:

Antibiotics: the intramuscular administration of procaine-penicillin G trigger strong anxiety and panic states,

Antihistamines (allergy products)

Antisympathotonics (antihypertensive agents): the abrupt discontinuation of the substance clonidine, preparation Catapresan®, results in an overreaching release of catecholamines, which is associated with the previously imposed noradrenergic release inhibition as well as with receptor changes,

Alpha-sympathomimetics (vasoconstrictive agents for the treatment of hypotensive blood pressure disorders and mucosal swelling in inflammation): after prolonged use, the abrupt discontinuation of vasoconstricting alpha-sympathomimetic nasal drops, especially oxymetazoline, can lead to anxiety and panic states due to the elimination of the natural inhibition processes in the locus coeruleus, in which a high norepine concentration is given,

  • Antiarrhythmic drugs (against cardiac arrhythmia): the substance lidocaine can have a pronounced and specific death,
  • Asthma means
  • Anabolic steroids (male sex hormone to increase athletic performance),
  • Glucocorticoids (e.g., cortisone),
  • Thyroid preparations,
  • Certain colds,
  • Antiparkinsonian drugs with anticholinergic effects,
  • Cytostatics (against tumor cells), e.g. ifosfamide,
  • Analgesics (painkillers),
  • oral contraceptives: certain preparations can cause anxiety-depressive mood disorders.

Heavy metals and toxins (e.g.., volatile substances such as gasoline or paints, organophosphate insecticides, nerve gases, carbon monoxide, carbon dioxide) can also cause anxiety symptoms.


Nicotine is not mentioned in the DSM-IV among the substances that can cause an anxiety disorder. The research results are currently insufficient to be able to speak of an intoxication by nicotine (and resulting anxiety). However, the possible occurrence of anxiety is indicated in the presentation of the nicotine tract.

Nicotine stimulates specific acetylcholine receptors in the brain and thus enhances psychomotor activity, mental performance, sensorimotor performance, attention, and memory.

At the same time, nicotine activates the sympathetic nervous system via the increased adrenaline discharge and puts the body in an alarm state like a stress reaction.

Nicotine accelerates the heartbeat and narrows the blood vessels, increasing the blood pressure. However, the initial increase in performance soon leads to a reduction in performance (by blood pressure drop and oxygen deficiency).

In the long term, too much nicotine causes a disturbance of the serotonin storage distribution, an inhibition of protein synthesis, a blood vessel constriction, and an arterial calcification.

In stressful situations, nicotine deprives the body of the necessary oxygen and the appetite inhibition the necessary energy, so that the physical capacity is ultimately lowered, especially if there is an additional demand for oxygen due to physical or psychological stress. Nicotine transport via the bloodstream affects oxygen transport.

Oxygen is transported to the red blood cells by binding oxygen molecules. The toxic carbon monoxide contained in the smoke binds in the same way to the red blood cells (erythrocytes), 200 times lighter than oxygen. Even with a low carbon monoxide concentration, 15-20% of all erythrocytes are “occupied” with carbon monoxide and are responsible for their actual task as oxygen carriers. The carbon monoxide in the blood prevents adequate oxygen supply to the brain and to other organs, in particular to the heart, which can result in cardiac arrhythmias and angina pectoris-like seizures.

In the case of nicotine contraction (sudden cessation of smoking within 24 hours), at least four of the following symptoms occur according to the DSM-IV: anxiety, restlessness, decreased heart rate, difficulty concentrating, distractibility, disappointment or anger weight gain.

Opiate withdrawal

In the DSM-IV, opiate-related anxiety states cannot be coded as substance-induced anxiety disorders, because they occur not through the substance as such, but only through their withdrawal. There are also frequent anxiety and restlessness among the many rightful and painful symptoms of opiate withdrawal (for example, nausea, vomiting, diarrhea, sweating, fever, muscle pain, goosebumps, lacrimation, insomnia, dysphoric distress).

Anxiety is not only one of the first withdrawal symptoms, but also occurs within the context of the less acute symptoms of withdrawal lasting weeks and months, often associated with dysphoric-depressive mood, joylessness, and sleep disturbance. Anxiety and restlessness occur in a similar way to a withdrawal of alcohol, sedatives, hypnotics and anxiolytics.