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What are the short-term effects of drug addiction? A clinician’s perspective on substance dependency

15th July 2025 / Written by Harbor London

Understanding the short-term effects of drug addiction is critical for clinicians involved in acute care, primary care, psychiatry, and addiction rehabilitation services.

These effects – ranging from cardiovascular instability and altered mental status to psychomotor impairment and behavioural dysregulation – can present rapidly and with varying severity, often mimicking or exacerbating pre-existing medical or psychiatric conditions¹.

From a clinical standpoint, distinguishing between the pharmacological effects of acute intoxication, the onset of withdrawal syndromes, and underlying mental health issues is central. For example, stimulant-induced paranoia may resemble a primary psychotic episode², while opioid-induced sedation could be mistaken for a post-ictal state³. Accurate identification is vital not only for effective triage and risk assessment, but also for tailoring intervention strategies and mitigating harm.

Moreover, short-term substance effects frequently precipitate acute psychiatric crises⁴, self-harm incidents, or emergency department admissions. Recognising these patterns allows clinicians to implement early interventions and to initiate discussions around long-term treatment pathways, including detoxification, harm reduction, and integrated mental health support.

Ultimately, a clear grasp of these acute presentations helps to reduce morbidity, prevent escalation, and improve outcomes for patients with substance use disorders, especially within a multidisciplinary care model.

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Central nervous system depressants

Central Nervous System (CNS) depressants – including opioids, benzodiazepines, barbiturates, and certain sedative-hypnotics – act primarily by enhancing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA)⁵ or, in the case of opioids, by binding to mu-opioid receptors.

Their short-term effects are clinically significant due to their rapid onset, dose-dependent impact on respiratory and cognitive function⁶, and high potential for synergistic toxicity when combined.

Short-term clinical effects

Neurological: drowsiness, sedation, impaired coordination, slurred speech, and cognitive dulling are common⁷. High doses may induce stupor or coma.
Respiratory: CNS depressants, particularly opioids and barbiturates, pose a high risk of respiratory depression⁸. This can lead to hypoventilation, hypoxia, and death in the absence of timely intervention.
Cardiovascular: mild hypotension and bradycardia are typical, though severe hypotension may occur with overdose or polydrug use.
Psychiatric: paradoxical reactions such as agitation or aggression can occasionally arise, particularly with benzodiazepines in susceptible individuals.

Withdrawal considerations

Even short-term, high-dose use can induce a withdrawal syndrome upon cessation⁹.

Symptoms include rebound anxiety, tremors, insomnia, tachycardia, and – especially with long-term benzodiazepine use – seizures and psychosis. These require careful tapering under medical supervision.

Clinical relevance

Clinicians must remain vigilant to the signs of acute depressant intoxication, particularly in patients presenting with altered mental status or respiratory compromise. Co-ingestion of multiple depressants significantly increases the risk of fatal overdose¹⁰. According to the UK Office for National Statistics, opioid-related deaths often involve benzodiazepines¹¹, highlighting the need for integrated substance misuse and mental health assessment.

Central nervous system stimulants

Central Nervous System (CNS) stimulants – including substances such as cocaine, amphetamines¹² (e.g. dexamphetamine, methamphetamine), methylphenidate, and synthetic cathinones – exert their effects primarily by increasing extracellular concentrations¹³ of dopamine, noradrenaline, and serotonin via enhanced release and reuptake inhibition.

Powerful in their effects, and sometimes used by individuals in high-demand work environments¹⁴, these agents can be associated with a distinct spectrum of short-term physiological and psychological effects that may have acute implications for clinical assessment and intervention.

Short-term clinical effects

Neurological and psychiatric:

Heightened alertness, euphoria, increased energy, and reduced fatigue.
Restlessness, agitation, anxiety, panic attacks, and insomnia are common¹⁵, particularly with higher doses or prolonged use.
Acute psychotic symptoms (e.g., paranoia, hallucinations, delusions) can manifest even after brief use¹⁶, particularly in individuals with underlying vulnerability.
Seizures, especially in cases of high-dose cocaine or methamphetamine ingestion.

Cardiovascular:

Tachycardia, hypertension, and vasoconstriction are routine effects¹⁷.
Increased risk of cardiac arrhythmias, myocardial infarction, and cerebrovascular accidents, even in young individuals with no prior history of cardiovascular disease.
Hyperthermia and rhabdomyolysis are serious potential complications, particularly with amphetamines and MDMA.

Gastrointestinal and other somatic:

Anorexia, dry mouth, nausea, and abdominal cramps.
Bruxism and dehydration are frequent in MDMA use.
Sudden onset of severe headache may indicate hypertensive crisis or stroke.

Withdrawal and crash phase

Stimulant withdrawal often presents as a ‘crash’ – characterised by profound fatigue, hypersomnia, dysphoria, irritability, and intense drug cravings¹⁸. While not typically life-threatening, it carries a high risk of relapse and, in some cases, suicidal ideation.

Repeated cycles of use and withdrawal contribute to neuroadaptive changes associated with long-term cognitive and emotional dysregulation.

Clinical relevance

In acute presentations, stimulant intoxication should prompt careful evaluation of cardiovascular status, hydration, and mental state. Management may include benzodiazepines for agitation or seizures, and aggressive cooling for hyperthermia.

Hallucinogens and dissociatives

Hallucinogens and dissociatives constitute a diverse group of psychoactive substances that exert profound alterations in perception, mood, and cognition¹⁹.

While historically associated with recreational or illicit use, there is a growing body of clinical research²⁰ exploring their controlled therapeutic potential in treating conditions such as depression, PTSD, and substance use disorders. Agents such as psilocybin and ketamine are currently being studied – and in some cases prescribed²¹ – under carefully controlled protocols for their rapid-acting antidepressant and neuroplasticity-promoting effects.

Despite this emerging evidence, unsupervised or non-clinical use of these compounds carries significant risks, particularly in acute settings. It’s important to note that this research is still in its infancy and, though showing early promise, no firm conclusions can be drawn yet.

Short-term clinical effects

Psychological and perceptual:

Altered visual and auditory perception, synaesthesia, time distortion, and changes in sensory integration²².
Acute anxiety, depersonalisation, and dysphoria, especially in unfamiliar or uncontrolled environments.
Transient psychosis or panic states may occur²³, especially in individuals with underlying vulnerability.
Dissociative agents (e.g., ketamine, PCP) can produce detachment from body or reality, confusion, and loss of sense of identity.

Neurological and somatic:

Nystagmus, ataxia, mydriasis, and muscle tension.
Short-term memory disruption²⁴, dizziness, and in high doses, catalepsy or mutism.
Seizures have been reported, particularly with high-dose PCP.

Autonomic and cardiovascular:

Tachycardia, hypertension, nausea, and hyperreflexia.
Mild hyperthermia may occur. In rare cases, cardiovascular instability can result from polysubstance use or underlying conditions.

Complications and acute risks

Behavioural risk: perceptual distortion and impaired judgment increase the risk of trauma or hazardous behaviour. PCP intoxication, in particular, is associated with psychomotor agitation and aggression²⁵.
Hallucinogen Persisting Perception Disorder (HPPD): though rare, HPPD presents as recurring visual disturbances long after drug use²⁶, and has been primarily linked to LSD and psilocybin.
Ketamine-induced cystitis: although more often seen in chronic use, acute presentations of urinary urgency or discomfort may begin to emerge early in high-frequency use.

Clinical relevance

While ongoing trials suggest potential for these substances in neuropsychiatric care, acute presentations in emergency or general practice settings continue to warrant careful assessment and management. Clinicians should be alert to the possibility of hallucinogen or dissociative intoxication in patients presenting with sudden onset perceptual abnormalities, unexplained agitation, or altered sensorium.

Initial treatment remains supportive, often requiring environmental de-escalation, IV fluids, and benzodiazepines in cases of severe anxiety or agitation. A clear distinction must be drawn between medically supervised psychedelic therapy and unregulated use – the latter of which can result in serious physical and psychological complications.

Cannabis and synthetic cannabinoids

Cannabis is one of the most commonly used psychoactive substances in the UK – 7.4% of adults between 16- to 59-years-old reported using cannabis within the last year²⁷ – with increasing social acceptability and ongoing debates around its therapeutic use²⁸.

The primary psychoactive component, Δ⁹-tetrahydrocannabinol (THC), acts on the endocannabinoid system, particularly CB₁ receptors in the central nervous system²⁹.

Synthetic cannabinoids (e.g., “Spice,” “K2”), though structurally different, often bind with higher affinity to the same receptors³⁰ and can elicit more potent and unpredictable effects.

Short-term clinical effects

Cannabis:

Cognitive and psychological:

Impaired short-term memory, attention, and executive functioning³¹.
Euphoria, altered time perception, and heightened sensory experience.
Anxiety, paranoia, and in some cases acute psychosis, particularly with high-potency THC strains or in vulnerable individuals.

Somatic and neurological:

Conjunctival injection (“red eyes”), dry mouth, increased appetite.
Mild ataxia, slowed reaction time, and dizziness.
Tachycardia is common; occasional hypotension may occur.

Respiratory:

Bronchodilation acutely, but chronic use (particularly when smoked) contributes to cough, phlegm, and airway inflammation.

Synthetic cannabinoids:

Marked variability:

Unpredictable potency and pharmacokinetics lead to a wide range of clinical presentations³², often more severe than natural cannabis.
Delirium, agitation, seizures, acute kidney injury, and cardiovascular complications have all been reported.

Neuropsychiatric risk:

Acute psychosis is significantly more common and severe³³.
Cases of suicidal ideation, hallucinations, and aggression are more prevalent, particularly in adolescent and homeless populations.

Clinical considerations

While low-to-moderate THC cannabis use may result in mild or self-limiting symptoms, the increasing THC:CBD ratio in modern strains poses heightened psychiatric risks. The potential for triggering or exacerbating schizophrenia-spectrum disorders³⁴ in genetically susceptible individuals remains a key concern, particularly among adolescent users.

Synthetic cannabinoids, due to their potency and lack of regulation, represent a significant clinical challenge. Patients may present with symptoms that mimic stimulant toxicity, psychosis, or seizure disorders, necessitating careful differential diagnosis.

Initial management for both cannabis and synthetic cannabinoid intoxication is primarily supportive:

For mild presentations: reassurance and monitoring.
For severe agitation or psychosis: benzodiazepines may be required; antipsychotics used cautiously.
For synthetic toxicity: consider hospital admission due to risk of multi-organ effects.

Inhalants and volatile substances

Inhalants and volatile substances refer to a diverse group of chemicals that produce psychoactive effects when their vapours are inhaled³⁵.

Common agents include solvents (e.g., toluene, acetone), aerosols, nitrites (“poppers”), and gases such as butane or nitrous oxide. These substances are typically inhaled for their rapid onset of euphoria or disinhibition, often by younger individuals³⁶ (although not exclusively³⁷), or those with limited access to other drugs.

Short-term clinical effects

CNS and neuropsychiatric:

Rapid onset of dizziness, euphoria, and disinhibition³⁸.
Cognitive impairment – slurred speech, ataxia, visual distortion, and reduced coordination.
Disorientation, hallucinations, and, at higher doses, delirium or stupor.
Seizures have been reported with volatile hydrocarbon use.

Cardiovascular:

Arrhythmias: sensitisation of the myocardium to catecholamines can lead to sudden cardiac arrest (“sudden sniffing death syndrome”)³⁹, particularly with butane or propane.
Hypotension or tachycardia, depending on the specific agent.

Respiratory:

Airway irritation, wheezing, and cough⁴⁰.
Hypoxia and respiratory depression with high or prolonged exposure.
Risk of chemical pneumonitis if aspiration occurs, especially when substances are ingested or inhaled from plastic bags.

Other systemic effects:

Gastrointestinal upset, including nausea and abdominal pain.
Renal or hepatic toxicity, particularly with chronic toluene exposure.
Frostbite injuries to the face or airways from pressurised gases⁴¹.

Clinical considerations

Diagnosis of acute inhalant intoxication relies heavily on clinical suspicion – especially as these substances are often used covertly, and are undetectable via standard toxicology screens.

Presentation can mimic alcohol or sedative intoxication, but with a much shorter duration and distinctive chemical odour on the breath or clothing. Key clinical priorities include:

1. Airway management and oxygenation.

2. Cardiac monitoring, given the high risk of ventricular arrhythmias.

3. Observation for neurotoxicity, especially in adolescents with repeated use, where long-term cognitive sequelae have been documented.

Withdrawal effects vs short-term intoxication

Clinicians must distinguish between the immediate effects of drug intoxication and the often-overlapping, yet mechanistically distinct, symptoms of withdrawal. While intoxication reflects the pharmacodynamic actions of the substance on the central nervous system (CNS), withdrawal represents the neuroadaptive rebound once that substance is removed or reduced⁴², particularly after sustained use.

Short-term intoxication

Short-term intoxication is characterised by a substance-specific enhancement or suppression of CNS activity. For example:

– Opioids produce euphoria, analgesia, and respiratory depression.

– Stimulants trigger hypervigilance, tachycardia, and reduced appetite.

– Depressants cause drowsiness, slurred speech, and impaired motor coordination.

– Hallucinogens may provoke perceptual distortions and paranoia.

These effects are generally dose-dependent and resolve as the drug is metabolised, though toxicity or overdose may result in life-threatening complications requiring urgent medical intervention.

Withdrawal effects

In contrast, withdrawal symptoms reflect compensatory physiological responses:

– Opioid withdrawal includes mydriasis, piloerection, diarrhoea, and severe dysphoria.

– Alcohol or benzodiazepine withdrawal may cause seizures, delirium tremens, and death if unmanaged.

– Stimulant withdrawal is marked by anhedonia, hypersomnia, and suicidal ideation.

Clinically, withdrawal symptoms often emerge 6–24 hours after cessation (depending on the substance’s half-life), peak within 48–72 hours, and may last several days.

Clinical red flags: when to intervene

While some mild intoxication symptoms may resolve spontaneously, healthcare practitioners must remain vigilant for specific clinical red flags that demand immediate intervention:

Respiratory depression (particularly with opioids or sedatives).
Cardiac arrhythmias or chest pain in stimulant or inhalant users.
Delirium, hallucinations, or seizures indicating severe CNS involvement.
Hyperthermia, muscle rigidity, or rhabdomyolysis (e.g., in serotonin syndrome or stimulant toxicity).
Suicidal ideation or acute psychosis, often seen in withdrawal from stimulants or synthetic cannabinoids.
Polysubstance use where pharmacological interactions may be unpredictable and severe.
Repeated presentations to emergency or primary care, suggesting escalating dependence.

In these cases, urgent medical stabilisation, psychiatric evaluation, and referral to specialist addiction services are warranted. In all scenarios, documentation and a clear discharge plan – preferably with psychosocial follow-ups – are essential to reducing the likelihood of recurrence or harm.

Applying clinical insight to early intervention

Understanding the short-term effects of drug addiction is more than academic; it’s a clinical imperative. These early physiological and psychological signs, whether intoxication or withdrawal-related, offer valuable diagnostic windows through which healthcare professionals can identify substance use disorders at an earlier stage.

Recognising the nuanced presentation of substance use or misuse allows for:

Informed clinical decisions
Timely referrals
Person-first care planning

Importantly, differentiating acute intoxication from withdrawal can guide appropriate pharmacological and psychosocial responses, prevent avoidable complications, and reduce the risk of progression to severe substance use disorder.

With many patients presenting through emergency, primary, or mental health care channels, clinicians can play a critical role in flagging high-risk cases⁴³ and initiating conversations about substance use in a non-judgmental, evidence-informed manner.

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What are the short-term effects of drug addiction? A clinician’s perspective on substance dependency

Central nervous system depressants

Short-term clinical effects

Withdrawal considerations

Clinical relevance

Central nervous system stimulants

Short-term clinical effects

Withdrawal and crash phase

Clinical relevance

Hallucinogens and dissociatives

Short-term clinical effects

Complications and acute risks

Clinical relevance

Cannabis and synthetic cannabinoids

Short-term clinical effects

Cannabis:

Synthetic cannabinoids:

Clinical considerations

Inhalants and volatile substances

Short-term clinical effects

Clinical considerations

Withdrawal effects vs short-term intoxication

Short-term intoxication

Withdrawal effects

Clinical red flags: when to intervene

Applying clinical insight to early intervention

References

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Contact

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