Psychiatry A Flashcards
What is the definition of substance abuse?
This requires excessive use of a substance which causes pleasure and causes a low when absent. There must be a cycle of high and low for a substance to be able to be abused.
How is dependency diagnosed?
Three of more of these:
- C: Compulsion to take the substance
- C: Impaired control of substance taking behaviour in terms of onset, termination, or levels of use
- P: Physiological withdrawal when stopped or reduced
- P: Pre-occupation with use to the exclusion of other pleasures (salience)
- T: Tolerance to effects causing increased use for same effect
- H: Persistent use despite clear harm
What is salience/primacy?
Obtaining and using the substances takes over so that other interests and pursuits are neglected.
What is tolerance?
Increased doses of the psychoactive substance are required to achieve the effects originally produced by lower doses which contributes to the escalation of use.
What does ‘narrowing of repertoire’ mean?
Loss of variation in the use of the substance. This is common in alcoholism where they get the same brand, shop and drinking bodies.
What is intoxication?
The overloading of the body with the substance causes disturbances in level of consciousness, cognition, perception, affect, and behaviour. The disturbance is directly related to the effect of the substance and resolves with time.
What is a withdrawal state?
There is clear evidence of recent cessation or reduction of use which correlates with symptoms and signs compatible with known features of withdrawal of the substance (depending on the substance). These symptoms must not be attributable to another disorder and in some will be abortable by re-instating the substance.
Define harmful use
The pattern of psychoactive substance use that is causing damage to health. There is clear evidence of physical or psychological harm and the nature of the harm should be identifiable. The pattern of use has persisted for at least one month, or has occurred repeatedly over a 12 month period.
Define abstinence
Period during which no substance is used
What does reinstatement mean in substance abuse?
Occurs after a period of abstinence, when a patient restarts the substance and rapidly increases use to previously harmful levels.
What does detoxification mean?
The process of reducing and stopping the use of an additive substance. Medical assistance may be required for some substances. Benzodiazepines are used in the treatment of alcohol withdrawal.
What are the stages of change in substance addiction?
Outlined by Prochaska and DiChlemente
- Pre-contemplation: Person feels there is no problem though others recognise it
- Contemplation: Person weighs up pros & cons and considers if change is necessary
- Decision: Person decides whether to act or not
- Action: Person chooses strategy for change & pursues it
- Maintenance: Gains are maintained and consolidated
- Relapse: Return to previous pattern, but relapse may help learning
How should a substance misuse history be taken?
Remember age of starting drug, types, quantities, frequency, route of administration, overdoses, abstinence, relapse, triggers, withdrawal symptoms, medical complications, psychiatric and forensic history. The uncover the relationship of the substance of abuse to the presenting complaint such as acute intoxication, harmful use, dependence syndrome, withdrawal state, psychotic disorder, or amnesic syndrome.
Explore the physical health, psychological wellbeing, social and family relationships, and economic/employment status. Determine the level of patient motivation to change. Offer appropriate intervention.
Dual diagnosis of mental illness and comorbid substance misuse. Diagnosing mental illness becomes challenging in the face of substance misuse. Primary psychiatric illnesses often precipitate substance misuse, and the substance may worsen the psychiatric illness.
What are the normal and harmful levels of alcohol use?
Safe levels are defined as 2-3 units a day or 14 units a week.
Harmful levels for women are over 6 units a day or 35 units a week.
Harmful levels for men are more than 8 units a day and 50 units a week.
What are the risk factors for alcohol dependence?
This is more common in men and there is between 25-50% genetic predisposition. It is more common in publicans, doctors, journalists, salesmen, actors, entertainers, and seamen. Social factors which contribute to development include childhood difficulties, parental separation, and low educational achievement.
What are the features of alcohol intoxication?
Relaxation & euphoria followed by disinhibition, various emotional states (irritable, weepy, morose), impulsive, and irresponsible behaviour. There may be slurred speech, ataxia, sedation, confusion, flushed face, nystagmus, and conjunctival injection.
How does alcohol withdrawal present?
This can present with headache, nausea, retching, vomiting, sweating, insomnia, anxiety, agitation, tachycardia, hypotension, delirium tremens, and seizures.
What are the complications of alcohol dependence?
This can include hepatitis/cirrhosis, pancreatitis, oesophageal varices, gastritis, and peptic ulceration. Neurological complications can include peripheral neuropathy, seizures, or dementia. Alcohol misuse increases the risk of bowel, breast, oesophageal and liver cancer. Cardiovascular complications include HTN and cardiomyopathy.
Patients are also prone to head injuries from falls/accidents/fights and there is a risk of foetal alcohol syndrome.
Psychological complications can include worsening anxiety/depression, self-harm, increased suicide risk, amnesia/blackouts, cognitive impairment (alcohol dementia and Korsakoff’s), alcoholic hallucinations, and morbid jealousy.
Social complications include poor work performance, unemployment, domestic violence, marital & family breakdown, drink driving/assault/theft, childhood neglect and childhood abuse.
How is alcohol dependence managed?
Assess the motivation to change. Detoxification can be done with benzodiazepines and thiamine. Relapse prevention is with psychological support such as AA and medical options include acamprosate (reduces craving) or disulfiram (induces flushing if alcohol is taken).
What are alcohol-related emergencies?
Delirium Tremens occurs 48 hours after abstinence. It presents with confusion, hallucinations, illusions, agitation, sweating, tachycardia, tremor, and seizures. It should be treated with reducing benzodiazepine regime & parenteral B vitamins (Pabrinex) to avoid Wernicke-Korsakoff’s syndrome.
How does Wernicke’s encephalopathy present and how is it managed?
This presents with the classic triad of confusion, ataxia and ophthalmoplegia. It is caused by an acute thiamine (B1) deficiency and should be treated with a course of Pabrinex (parenteral B vitamins) given as IV or IM. If untreated it will lead to Korsakoff’s psychosis which is irreversible anterograde amnesia with confabulation.
How are benzodiazepines abused?
Benzodiazepines are usually taken orally but can be injected. They produce sedation, euphoria, disinhibition, lability of mood, anterograde amnesia, unsteady gait, slurred speech, nystagmus, reduced consciousness, and respiratory depression. Withdrawal can cause delirium tremens. Treatment is to convert diazepam equivalent dose and gradually withdraw over 8+ weeks.
How is cocaine abused?
Cocaine is a stimulant which causes alertness, confidence, sense of strength, and disinhibition. It is very short acting. The ‘come down’ comes with fatigue, depression, dysphoria, paranoia, and depersonalisation. There are two forms of cocaine; powder (hydrochloride) and crack (alkaloid which is heated and inhaled through a pipe or injected with vitamin C and heroin to create a speedball).
Cocaine withdrawal presents with intense craving and there is no replacement therapy available. They can have acute psychotic episodes that may require antipsychotics & benzodiazepines for symptom control short term. There are groups available such as cocaine anonymous.
How is cannabis abused?
This produces a high, but this is generally an exaggeration of previous mood sate such as anxiety, paranoia, distortion of time, or mild hallucinogenic effect. Signs can include conjunctival injection, dry mouth, tachycardia, and respiratory tract symptoms. There is an associated with schizophrenia.
How is heroin abused?
This is an opiate derivative which is highly addictive. This is known as brown sugar, smack, or gear. If injected, it is combined with cocaine into a speedball. It can also be smoked or snorted. The high is a strong sense of relaxation and wellbeing. Withdrawal symptoms include vomiting, diarrhoea, cramps, sweats, and dysphoria. There is a big risk of overdose.
Physical effects include pin-point pupils, track marks, constipation, poor nutrition, poor dental state from reduced saliva flow, respiratory depressants, and comorbidity with blood borne viruses such as hepatitis C/B/HIV.
How is heroin abuse managed?
Management of heroin abuse is with harm reduction through needle exchanges, encourage smoking rather than injecting, and raise awareness of overdose and how to manage it, provide naloxone to those at risk. Narcotics anonymous is a useful group.
Opioid stimulation treatment (OST) can be with:
- Methadone: Full agonist which prolongs QT interval (monitor ECG 6 monthly). It is cheap and has a large evidence base.
- Buprenorphine (Subutex) is a partial agonist which is less sedating and less risk of OD
- Other options include dihydrocodeine (stop gap treatment only)
There should be a patient choice of OST and the aim is maintenance and detoxification.
How are amphetamines abused?
These are stimulants known as speed and whizz. They can be snorted, injected, or put on gums. Effects include cardiovascular strain, enlarged pupils, talkativeness, agitation, irritation, and psychosis (schizophreniform).
Ecstasy (MDMA) is sold in tablet or powder form. It causes increased energy, hyperaesthesia, increased feeling of wellbeing and love but also panic, dysphoria and depression. It has been associated with raised temperatures, dehydration, tachycardia, and DIC.
What is Khat?
Khat is a plant grown in east African regions which has to be taken fresh. It produces a simulant like effect and has been known to precipitate psychosis. It has been used to make “miaow-miaow.”
How is ketamine abused?
This is an anaesthetic agent and is commonly powder or tablet. It produces hallucinations, reduced pain sensation, drowsiness, sedation, and respiratory depression. Prolonged use can cause ketamine bladder which presents with haematuria, scarring and severe pain (removal of bladder required).
How is LSD abused?
LSD is taken as a tab on a square of paper. It produce hyperaesthesia, hallucinations, or other altered perceptions. Flashbacks can occur days/months later. It can precipitate mental illness in people with a predisposition.
How are novel psychoactive substances abused?
Known as legal highs they can come in many forms. They can be stimulants, sedatives, synthetic cannabinoids, or hallucinogens. Spice is a synthetic cannabinoid which is more potent than cannabis. It’s a class B drug which is usually smoked. Typical effects include euphoria, giggles, hunger pangs, drowsiness, and talkativeness. It is more likely to cause hallucinations that cannabis.
Some people have bad reactions such as paranoia, panic attacks, or forgetfulness and can even make users freeze.
What are the features and symptoms of puerperal psychosis?
Otherwise known as postpartum psychosis, this is a severe mental illness that begin in the days or weeks after having a baby. Symptoms can vary and change rapidly. They include mania, depression, confusion, hallucinations, and delusions. This is a psychiatric emergency as should be seen ASAP. If the family report a sudden change in personality this should be taken seriously.
For a diagnosis it must occur within the first 2 weeks after birth and symptoms will usually appears within the first few days. Very rarely it can occur after a few weeks. It occurs in 1/1000 women (0.1%). There is a genetic link for puerperal psychosis but is also associated with hormonal changes after birth and significant sleep deprivation. Women who have a past medical history of puerperal psychosis, bipolar affective disorder, or schizoaffective disorder are high risk.
How should puerperal psychosis be managed?
Puerperal psychosis responds well to prompt treatment and has a good prognosis. Preventative measures for high-risk mothers include preconception counselling, specialist support during pregnancy and a pre-birth planning care plan. Treatment is with urgent assessment and diagnosis, specialist support, transfer to a mother and baby unit, antipsychotics and mood stabilisers.
Severe symptoms response in 2-12 weeks but full recovery may take 6-12 months. Most women make a full recovery.
What is postnatal depression?
This is a depressive illness affecting 10-15 women in every 100 who have a baby. The symptoms are similar to depression at other times.
What are the symptoms of postnatal depression?
Symptoms include persistent low mood, insomnia, loss of appetite, anhedonia, loss of energy, reduced motivation, neglect of self-care, and feelings of hopelessness. There may be suicidal ideation or thoughts to harm the baby. Psychotic symptoms may be seen in severe cases. Onset is anywhere in the first year of the babies life but some (1/3) experience depression while pregnant and should be treated on initial presentation.
Over 50% of new mothers will experience ‘baby blues’ within 3-4 days but these usually settle after 10 days. This settling means it is not PND. There is no known cause but there are associations with depression/anxiety during pregnancy, previous mental illness, poor support, a recent emotional or psychological trauma, domestic violence, previous abuse, and refugees. Always rule out anaemia and hypothyroidism as these can cause depression.
How is postnatal depression managed?
Management is with support, severe cases may need referral, self-help, talking therapies and medications (antidepressants or antipsychotics).
How are anxiety disorders classified?
- Anxiety disorders: Phobic disorders (agoraphobia – with or without panic disorder, specific phobia, or social phobia)
- Non-situational disorders: Generalised anxiety disorder and panic disorder
- Reaction to stress: Acute stress reaction, PTSD, and adjustment disorder
- OCD
- Secondary to other psychiatric disorders (depression, psychosis, neurodevelopmental disorder or personality disorders)
- Secondary to a general medical condition (organic anxiety disorder)
- Secondary to psychoactive substance use, especially alcohol use
What is pathological anxiety?
This is not always pathological as it avoids harm in fearful situations. When anxiety becomes excessive it can be pathological as it impacts the level of function. According to the Yerkes-Dodson law the relationship between performance and anxiety has an inverted U shape. Mild to moderate levels of anxiety results in improved performance but high anxiety impairs performance.
Clinical Features: There are two inter-related components:
1. Thought of being apprehensive
2. Awareness of a physical reaction to anxiety (autonomic or peripheral anxiety)
Physical signs of anxiety can include tachycardia, palpitations, high BP, SOB, chest discomfort, dry mouth, sweating, cold skin, muscle tension, dizziness, choking sensation, and nausea/vomiting.
How is pathological anxiety subcategorized?
Pathological anxiety can be defined by pattern as either generalised or paroxysmal.
Generalised: Does not occur in discrete episodes and tends to last for hours-days or even longer. It is not associated with any specific external threat or situation (free floating).
Paroxysmal: This has an abrupt onset and occurs in discrete short-lived episodes. It tends to be severe and in the most severe form will present as a panic attack.
Differential diagnosis for anxiety should consider the rate of onset, severity, duration (generalised or paroxysmal), acquired or life-long, spontaneous or threat related, and are there other psychiatric conditions or medical conditions (hyperthyroidism).
What is agoraphobia?
This means fear of the marketplace and is used to refer to fear of entering crowded spaces. In extreme cases it will leave patients housebound or unable to leave the house without the company of someone they know. There is a close relationship between agoraphobia and panic disorder. If they feel they cannot escape the place they may experience a panic attack. Agoraphobia can be coded in ICD-10 as with or without panic disorder.
What is social phobia?
Also known as social anxiety disorder. The patient fears being in social situations where they may be exposed to scrutiny by others that would lead to humiliation or embarrassment. This may be limited to an isolated fear (public speaking or interaction with opposite sex) or may involve all social situations outside the patient’s own home. It often starts in adolescence and can dictate the choice of employment (night shifts and isolated jobs).
What are specific phobias?
Also known as simple phobias, these are restricted to a clearly specific and discernible object or situation. Examples include situational (public transport, flying, driving, tunnels, bridges, or elevators), natural environment (heights, storms, water, or darkness), blood-injection-injury, animals or insects (spiders or dogs) and others (choking, vomiting, or contracting an illness (HIV)).
What are non-situational anxiety disorders?
Generalised anxiety disorder and panic disorder
What is generalised anxiety disorder?
This is a long-standing free-floating anxiety. The patient may describe excessive worry about minor things and should be apprehensive on most days for about six months. There is usually a mild to moderate severity and three key elements are:
- Apprehension
- Motor tension (restlessness, fidgeting, tension headaches, or inability to relax)
- Autonomic overactivity
What is panic disorder?
Characterised by the presence of panic attacks that occur spontaneously and unpredictably and that are not restricted to any particular situation or objective danger. The patient typically exhibits anticipatory anxiety (fear of further panic attacks) but between panic attacks the patient is relatively free of anxiety symptoms. There may be a fear of impending doom and can co-exist with agoraphobia.
What anxiety disorders are known as reactions to stress?
Acute stress reaction, PTSD, and adjustment disorder
What is acute stress reaction?
Symptoms develop immediately after, or within minutes of, a traumatic stressor. Typically, the patient experiences an initial ‘dazed’ state, followed by possible deterioration and a narrowing of attention, with inability to process external stimuli. The patient may have amnesia of the episode and symptoms usually diminish after 24-48 hours. This is no longer considered a mental disorder as it is part of normal existence.
What is post-traumatic stress disorder?
Symptoms usually develop after one month, and within 6 months, of a traumatic stressor. This leads to significant impairment or distress. Symptoms include repetitive re-experiencing of the traumatic event (flashbacks/hallucinations/illusions and external cues resembling the stressor), avoidance behaviours, increased arousal (insomnia, anger, hypervigilance, exaggerated startle reactions and poor concentration).
The biggest risk factor is experiencing past trauma, especially childhood trauma. Complex PTSD is a series of severe trauma (repeated childhood sexual abuse) and development of persistent difficulties in regulating affect, relationships, with others, guilt, shame, and worthlessness. It is closely related to symptoms seen in EUPD.
What is adjustment disorder?
Symptoms are considered to be significant enough as to be out of proportion to the psychosocial stressor (becoming a parent or breakdown of a relationship) or cause disturbance of social or occupational functioning. Emotional or behavioural symptoms occur within three months (DSM-V) or one month (ICD-10) of the stressor.
The patient’s personality and vulnerability play an important contributing role. Symptoms usually fully resolve within six months of onset and if not, it requires a reassessment of the initial diagnosis. Symptoms are usually mood-related or anxious. It can be associated with suicidal ideation.
Define the obsessions in OCD?
Obsessions are defined as involuntary thoughts, images, or impulses which have the following characteristics:
- Recurrent and intrusive (experienced as unpleasant or distressing)
- Enter the mind against the conscious resistance
- Patient recognises them as being of their own mind
These are not excessive concerns about everyday life problems. Patient usually retains insight into recognising that the thoughts are irrational. This is Ego-dystonic (as opposed to ego-syntonic)
What are the compulsions in OCD?
Compulsions are repetitive mental operations (counting, praying, repeating a mantra silently) or physical acts (checking, handwashing, or rituals). They have the following characteristics:
- Patient feels compelled to perform them in response to their own obsessions or irrationally defined rules
- Performed to reduce anxiety through the belief they will prevent a “dreaded event” occurring
They are experienced as unpleasant and serve no realistically useful purpose despite their tension-relieving properties. They patient will try to resist carrying out the compulsion which will cause increased anxiety.
How is OCD diagnosed?
ICD-10 stipulated that OCD is diagnosed if obsessions or compulsions are present for at least two successive weeks and are a source of distress or interfere with the patient’s functioning. They are acknowledged to come from the patient’s own mind. Obsessions are unpleasantly repetitive and at least one thought or act is resisted unsuccessfully. Compulsive act is not in itself pleasurable excluding the relief of anxiety. OCD can be categorised as predominantly obsessive thoughts, predominantly compulsive acts or mixed.
What differentials should be considered for OCD?
Differentials for obsessional: Depressive disorder, hypochondriasis, and schizophrenia
Differentials for compulsive: Habit or impulse control disorders (pathological gambling/ trichotillomania/kleptomania)
Differentials for mixed: Eating disorder, ASD, or obsessive-compulsive (anankastic) personality disorder
What physical conditions can cause anxiety?
This should always be actively sought and ruled out. A medical condition should predate the development of the anxiety and symptoms should resolve with treatment of the medical condition. Examples include congestive cardiac failure, PE, COPD, asthma, hypoglycaemia, pheochromocytoma, Cushing’s disease, hyperthyroidism, cerebral trauma, vitamin deficiencies, and temporal lobe epilepsy. Often symptoms can arise from a combination of a general medical condition and anxiety as each predispose to the other.
How can anxiety be related to psychoactive drug use?
This should always be actively sought and ruled out. Intoxication with alcohol, amphetamines, cannabis, cocaine, hallucinogens, ketamine, caffeine, novel psychoactive substances, phencyclidine, or inhalants can cause anxiety.
Withdrawal from substances such as alcohol, nicotine, benzodiazepines, cocaine, opiates, sedatives, and hypnotics can cause anxiety.
Anxiety can occur as a side effect from drugs such as antidepressants, antipsychotics, anticholinergics, thyroid hormones, corticosteroids, and sympathomimetics.
What is the epidemiology of anxiety?
Anxiety is the most prevalent type of mental disorder with a 1-year prevalence of 12-17%. It is typically under-diagnosed in primary care settings where 90% of cases are managed. It is often only recognised after years and only 1/3 of those with significant clinical anxiety disorders receive any kind of treatment.
What is the aetiology of anxiety disorders?
Heritability in anxiety disorders is approximately 30-50% but especially panic disorder and OCD in which 1/3 have a first degree relative with the same diagnosis. There is likely a genetic overlap with depression. OCD shares a genetic link with Tourette syndrome. The three main neurotransmitter systems implicated are GABA, serotonin, and noradrenaline.
There is a genome-wide association with calcium-dependent neural signalling in causing anxiety. Damage to the caudate nucleus can cause obsessive-compulsive symptoms. Hyper-activation of the amygdala in response to anxiety-provoking stimuli is found in PTSD, social phobias, and others. It is hypothesised that anxiety disorders likely represent abnormalities of brain regions, rather than of individual regions alone.
Social and psychological factors can include stressful life events, traumatic events (PTSD), and over-estimation of dangers which will respond to exposure response prevention (ERP).
What psychological treatment can be used in anxiety disorders?
Psychological treatment is recommended as first line treatment (especially in milder forms). CBT is the most effective for anxiety disorders. CBT is first line for specific phobias which may involve systemic desensitisation, flooding, or modelling. In panic disorder, CBT may help the patient understand how to recognise normal stimuli and thus prevent panic attacks. In PTSD, effective treatments are trauma focussed CBT and EMDR. Debriefing immediately after the trauma is not recommended.
Applied relaxation is used in generalised anxiety disorder. This focusses on being able to relax the muscles during situations in which the patient is or may be anxious. Supportive psychotherapy, psychodynamic psychotherapy and family therapy may also be helpful in the treatment of anxiety but there is less evidence. Counselling may be helpful for patients experiencing stressful life events, illness, or bereavement. Psychoeducation can also be helpful.
What pharmacological treatments are available for anxiety disorder?
SSRIs are the first-line treatment for most anxiety disorders due to proven efficacy and tolerable side-effect profile. Venlafaxine has proven efficacy in generalised anxiety disorder. In general, higher doses and longer duration is required for depression and up to 12 weeks SSRI use is required for improvement in OCD. Restlessness, jitteriness, and an initial increase in anxiety symptoms can occur in the first few days following the initiation of an SSRI. They can use a benzodiazepine for the first few days or titrate the SSRI slowly.
Benzodiazepines are highly effective in reducing anxiety and can be used short-term n PTSD or for PRN use is a social phobia or specific phobia. They are not recommended for generalised anxiety disorder, panic disorder, or OCD.
Pregabalin is licensed for use in generalised anxiety disorder (often after a trial of an SSRI).
Tricyclic antidepressants (TCAs) are generally considered only after other treatments have been tried owing to their increased frequency of adverse events. Clomipramine (the most serotonergic of the TCAs) has proven efficacy in OCD.
Propranolol can be used (regular or PRN) to reduce autonomic arousal to anxiety-provoking stimuli.
What are the basic activities of daily living?
These include walking, feeding, dressing/grooming, toileting, bathing, and transferring.
What should the risk assessment for a patient with dementia consider?
This should include behavioural concerns, wandering, getting lost, fire, financial exploitation by others, abuse from caregivers, aggression, or accidentally hurting themselves.
What is pseudodementia?
Depression causing memory problems.
What is dementia and how is it diagnosed?
Dementia is an umbrella term describing a clinical syndrome. It is an acquired global impairment of intellect, memory, and personality, but without impairment of consciousness. The impairment in intellectual function affecting more than one cognitive domain. This interferes with social or occupational function and is a decline from a previous level. This deterioration cannot be explained by delirium or major psychiatric disease.
The DSM-5 and ICD-10 definitions require impairment in two or more cognitive domains, sufficient to interfere with social or occupational functioning. Deficits which are too mild or circumscribed to fulfil this definition are called Mild Cognitive Impairment (MCI).
What are the four cognitive domains?
- Executive function (frontal, hemispheric white matter)
- Memory (medial temporal lobes/hippocampus)
- Language (left hemisphere)
- Visuospatial (occipital and parietal)
What is mild cognitive impairment?
Cognitive decline abnormal for age and education but does not interfere with function and activities. They are at risk to develop degenerative dementia. When memory loss predominates it is termed amnestic MCI. There is a 10-15% per year conversion to Alzheimer’s dementia.
What are the causes of cortical dementia?
Alzheimer’s disease and frontotemporal dementias
What are the causes of subcortical dementia?
Huntington’s disease, Parkinson’s disease, Focal Thalamic & Basal Ganglia Lesions, and MS
What are the mixed causes of dementia?
Vascular dementia, Dementia with Lewy bodies, corticobasal degeneration, and neurosyphilis
What are the epidemiology and risk factors for Alzheimer’s disease?
This is the most common neurodegenerative and dementing disease. Prevalence doubles every 5 years after the age of 65 and over 50% of those older than 85.
Risk factors include age, mild cognitive impairment, ApoE4 positivity, family history in first degree relative (especially early onset), vascular risk (dementia and heart disease), low education, low physical and social activity, and being female.
What are the features and symptoms of Alzheimer’s disease?
Clinical features of AD: Early symptoms include poor short-term memory and loss of orientation, there will be a smooth slow decline without dramatic short term fluctuations and other domains become involved with time.
Behavioural and psychological symptoms include depression, anxiety, irritability, hostility, apathy, delusions, hallucinations, sleep-wake changes, “sundowning”, and agitation.
What are the aetiology and features of Lewy body dementia?
This has relatively early occipital and basal ganglia degeneration and presents similarly to Parkinson’s disease. Alpha-synuclein aggregates into Lewy Bodies. Concurrent AD is common.
Clinical features include dementia (visuospatial and executive), parkinsonism, recurrent early visual hallucinations, fluctuation (recurrent delirium evaluations). Suggestive features include REM sleep disorder (dream enactment) and neuroleptic sensitivity.
What are the aetiology and features of Frontotemporal dementia?
Average age of onset is 58 and it is often familial (30-50%). There is an overlap with progressive supranuclear palsy (PSP), ALS and corticobasal degeneration. There are pathological aggregates of Tau or TDP-43.
Clinical features include behaviour and personality change (may be misdiagnosed as a psychiatric disorder), executive function, progressive non-fluent aphasia, parkinsonism, or muscle weakness.
What are the aetiology and features of Vascular dementia?
This should be suspected when there is an abrupt onset or stepwise deterioration, fluctuating course, history of stroke, focal neurological symptoms or signs, bilateral infarcts, and executive dysfunction/gait disorder/apathy/incontinence.
On imaging there may be evidence of chronic small vessel ischaemic disease involving subcortical white matter. This is non-diagnostic as it is very common with age and changes may or may not be symptomatic.
What are the differentials for dementia?
Structural brain lesion (subdural bleed), thyroid disease, vitamin B12 deficiency, untreated OSA, depression, anxiety, alcoholism, and medications (benzodiazepines, opioids, anticholinergics, neuroleptics, dopaminergic, and other sedatives).
How should suspected dementia be investigated?
Examination should include a general neurological exam, gait assessment, cognitive screen bloods, mini-mental state examination (MMSE), ACE-R (Addenbrooke’s), Mini-cog, and Montreal Cognitive Assessment (MoCA).
Diagnostic testing:
For slowly progressive dementia in >65s: Vitamin B12, TFTs, and neuroimaging with a CT. Neuropsychology testing can help but is not mandatory. FDG-PET is approved to differentiate AD from FTD. PET has little value. Younger patients or rapid/atypical course of dementia should be assessed with a tiered approach to target a range of diagnoses emphasising treatable causes.
The head turning test: Patient turns to loved one to help answer a question is highly sensitive for dementia. Turning up to memory clinic alone usually means no dementia but not always.
What are the treatment options for dementia?
No current pharmacological treatment slows down neuronal loss in the brain. Modest symptom improvement in AD and sometimes PDD/LBD can be achieved by cholinesterase inhibitors like donepezil/rivastigmine/galantamine. Memantine has modest benefit in AD.
Non-pharmacological management is with assessment of care needs, carer support, EMI residential or nursing homes, OT assessment, and psychological interventions such as CBT/behaviour management therapy/support groups/ cognitive stimulation groups/light/massage/aromatherapy may be beneficial.
What are neurotransmitters?
These are used for cell-to-cell communication. Examples include acetylcholine, dopamine, GABA, glutamate, noradrenaline, and serotonin.
Describe the types of neuro-receptors
These excite through the opening of Na/K+ channels in response to binding to a neurotransmitter. This leads to depolarisation of the post-synaptic membrane. The binding of a neurotransmitter to an inhibitory receptor causes K+/Cl channels to open which leads to the hyperpolarisation of the post-synaptic membrane which inhibits the generation of an action potential. The same neurotransmitter can produce an excitatory response in some postsynaptic cells and an inhibitory response in others.
There are two types of receptors:
1. Ionotropic/ligand-gated: Contain two functional domains – an extracellular site that binds neurotransmitters, and a membrane-spanning domain that forms an ion channel and causes membrane potential change in <2ms.
- Metabotropic/G-protein coupled: These affect channels by the activation of intermediate molecules (G proteins). The response is slower but longer lasting such as seconds to minutes.
What is the relationship between dopamine and Parkinson’s disease?
D1 receptors are excitatory (D1 +D5) whereas D2 receptors are inhibitory (D2, D3 +D4). PD is characterised by bradykinesia which is due to degeneration of dopamine-secreting neurones within the substantia nigra. There is dysfunction of the nigrostriatal pathway. Dopamine receptors are GPCRs. Dopamine can be increased (LDOPA) or the breakdown of dopamine can be inhibited (MOA inhibitors/amantadine/D2 receptor agonists or COMT inhibitors).
What is the relationship between dopamine and schizophrenia?
Mesolimbic-mesocortical pathways are involved in emotions and organisation of thoughts. This is implicated in schizophrenia. D2-receptor antagonists are used in the treatment of schizophrenia (opposite to PD) such as Haloperidol.
What is the relationship between serotonin and depression?
Serotonin and 5-HT receptors are possible involved which are targeted by SSRIs. The serotonin pathways run from the raphe nuclei of the brainstem to the cortex, thalamus, limbic system, and spinal cord.
What is the relationship between GABA and epilepsy?
GABA (gamma-Aminobutyric acid) is the chief inhibitory neurotransmitter in the CNS and plays the principal role in reducing neuronal excitability throughout the nervous system. It is involved in inhibitory motor control in the spinal cord and the regulation of muscle tone. GABAa receptors are ligand gated and are responsible for inhibitory action in the CNS whereas GABAb receptors are GPCR and responsible for motor control in the spinal cord and regulation of muscle tone.
GABAa positive allosteric modulators include alcohol, benzodiazepines (anxiolytic and antiepileptic), and barbituates such as phenobarbital (antiepileptic).
What is the relationship between acetylcholine and dementia?
95% of CNS receptors are muscarinic GPCRs and the rest nicotinic ligand-gated. Cholinergic projection from the nucleus basalis of Meynert (in the basal forebrain) to the forebrain neocortex and associated limbic structures is involved in learning and memory and thus been implicated in AD. There is a dramatic loss of cholinergic neurons in the cortex of AD patients.
What is the function of Glutamate in the neurological system?
This is a major excitatory neurotransmitter and the most abundant neurotransmitter. There are 3 types of inotropic receptors (NMDA, AMPA, and Kainate). These are metabotropic GPCRs.
What is the function of Noradrenaline in the neurological system?
The major concentration of noradrenergic neurons is in the locus of ceruleus of the caudal pons. Fibres from the locus ceruleus form part of the reticular activating system which is responsible for behavioural arousal and levels of awareness. GPCRs include a1/a2/b1/b2/b3 where a2 is inhibitory. There is an a2 agonist clonidine which is an anxiolytic & sedative.
Acetylcholine and noradrenaline play important roles within the autonomic nervous system and acetylcholine is the neurotransmitter at the neuromuscular junction.
What are the drugs options available for anxiolytics?
- Benzodiazepines are GABAs receptor agonists. There is no enzyme induction, and they use phase 1 metabolism to form active metabolites although lorazepam/temazepam undergo direct phase 2 reactions. Clinical effects include anxiolytic, hypnotic and anticonvulsants. Adverse effects include drowsiness, dizziness, confusion, cleft lip and palate and respiratory depression in foetus, cognitive and psychomotor impairment, tolerance and cross-tolerance with alcohol, withdrawal, and discontinuation symptoms.
- Antidepressants are generally 5-HT reuptake blockers. SSRIs are 1st line pharmacological treatment for anxiety disorders (clomipramine in OCD).
- Buspirone (Azapirones) are 5-HT1a receptor partial agonists and have a short elimination half-life. It is effective in GAD but less effective for acute anxiety and social phobia. They should not be used as an augmenting agent with an SSRI in anxiety disorders. Adverse effects include dizziness, nausea and akathisia.
- Pregabalin: MOA is through a high affinity for voltage gated calcium channels and is eliminated via the kidney. It is effective in GAD and social phobia. It is also useful as an augmenting agent for antidepressant treated anxiety disorders. It is well tolerated but is a drug of abuse and discontinuation syndrome can occur. Deranged LFTs, vertigo, dizziness, and weight gain are also seen.
- Beta blockers: MOA is through blockage of beta adrenoceptors. Clinical effects include reduction in physical symptoms of anxiety, akathisia and lithium induced fine tremor. Adverse effects include bradycardia and hypotension, be wary of bronchospasm in asthma patients.
Describe the uses, consequences, and mechanism of action of benzodiazepines
These vary in their duration of action. Short acting agents such as lorazepam and temazepam have a greater potential for abuse and dependence but may be safer in acute situations. Long-acting agents include diazepam. Benzodiazepines can be used for short term management of severe anxiety. Bispirone can be used in the longer-term but may be less efficacious than alternative strategies and is rarely used in clinical practice.
Benzodiazepine addiction should be treated with conversion to a longer acting drug (diazepam) before starting a very slow reducing regimen. The non-benzodiazepine Z drugs (zopiclone, zaleplon and zolpidem) are not used as anxiolytics though they act on the same receptors. They are commonly prescribed as hypnotics.
Benzodiazepine metabolism is through phase 1 metabolism via CYP450, and phase 2 metabolism (conjugation) occurs in lorazepam, oxazepam and temazepam.
How are antipsychotics classified?
They are broadly defined as first or second generation.
1st generation antipsychotics: Effects predominantly on D2 receptors (antagonism) requires about 70% D2 receptor occupancy for efficacy. Extrapyramidal side effects include dystonia, drug-induced parkinsonism, akathisia, and tardive dyskinesia. There may also be prolactin elevation, muscarinic (cholinergic) blocking properties and there is limited efficacy on the negative symptoms of schizophrenia. Examples include chlorpromazine, haloperidol, trifluoperazine, fluphenazine, zuclopenthixol, and flupentixol.
2nd generation antipsychotics: These have a lower D2 receptor affinity and a high serotonin/dopamine-binding ratio. These have a greater efficacy for both positive and negative symptoms and a reduced risk for the development of extrapyramidal symptoms. Examples include clozapine, amisulpride, risperidone, olanzapine, quetiapine, and aripiprazole (this exhibits unique dopamine modulatory effects). 2nd generation antipsychotics are linked to the development of metabolic abnormalities more than conventional agents. These include obesity (truncal), hypercholesterolaemia/dyslipidaemia, elevated BP, and diabetes.
What are the dopamine pathways?
- Mesolimbic pathway: Linked to positive symptoms: Delusions, hallucinations, disorganised speech/thinking and disorganised or catatonic behaviour
- Mesocortical pathway: Linked to negative symptoms: Alogia, affective flattening and avolition
- Nigrostriatal pathway: Controls motor movement
- Tuberoinfundibular pathway: Controls prolactin secretion
Give some examples of antipsychotics and their mechanism of action
Olanzapine: This is a multi-receptor antagonist (histamingeric/muscarinic/serotonergic/adrenergic/dopaminergic). It has D2 receptor selectivity. It is used for the treatment of positive, negative and mood stabilising symptoms. Short-acting injections are effective for the treatment of agitation and behavioural control. Long-acting injections require post injection monitoring for post-injection syndrome. Side effects include sedation, weight gain, metabolic syndrome, dry mouth, and constipation.
Paliperidone: This is a metabolite of risperidone but with lesser bioavailability. It has less affinity for D4 receptors than risperidone. It antagonises 5HT2A/5HT2C/D2/H1/adrenergic receptors. It comes in oral and long-acting injectable form. It is licenced for the treatment of schizophrenia. Side effects include severe EPSEs, hyperprolactinaemia, weight gain, but a lower risk of QTc interval changes.
Risperidone: 5HT2A/5HT2C/D2/Adrenergic receptor antagonist. It has a low-moderate H1 affinity. It is used for the treatment of schizophrenia and acute treatment of mania. Side effects include akathisia, dystonia, weight gain, hyperprolactinaemia, and tachycardia.
What are the side effects of antipsychotics?
General side effects of antipsychotics are extrapyramidal side effects (EPSEs), neuroleptic malignant syndrome (NMS), prolonged QTc interval (risk factor for fatal ventricular arrhythmia so If QTc interval is over 500 ms the refer the patient for cardiovascular assessment), hyperprolactinaemia, osteoporosis, sexual dysfunction, and metabolic syndromes.
Other side effects include a reduced seizure threshold, anticholinergic effects (constipation), hyponatraemia (SIADH), photosensitivity, agranulocytosis and myocarditis (clozapine).
When should clozapine be prescribed?
This is licensed for treatment-resistant schizophrenia but can also improve positive and negative symptoms of psychosis, affective symptoms, cognitive symptoms and manic symptoms in bipolar disorder. These effects are due to the clozapine’s receptor affinity binding profile (histaminergic/muscarinic/serotonergic/dopaminergic).
All patients MUST be registered with a clozapine monitoring service. They should have an FBC done weekly for the first 18 weeks to assess neutropenia/agranulocytosis, and then fortnightly until 52 weeks of treatment, and then monthly from then on.
What are the side effects of clozapine?
Side effects include increased appetite, weight gain, constipation, hypersalivation, tachycardia, seizures, neutropenia, agranulocytosis (concurrent use of lithium can increase WCC), myocarditis and cardiomyopathy.
Dystonic reactions such as oculogyric spasm and torticollis have a higher risk in the early stages of treatment or after a dose increase. It may also occur on drug withdrawal. Treatment of this side effect is with oral or IM anticholinergics such a procyclidine 5-10 mg.
Drug-induced parkinsonism: This presents with tremor, bradykinesia, and rigidity. It can be treated with an anticholinergic agent, but this should not be routine. Most patients will cope with the symptoms without active treatment.
Akathisia: This is the subjective unpleasant state of motor restlessness which is linked to violence and suicide. It responds poorly to anticholinergics but can be treated by changing to a drug with lower liability for akathisia – usually atypical. There is a place for the use of a non-selective beta blocker (propranolol), small dose of clonazepam, or the antihistamine cyproheptadine, have been suggested and tried.
Tardive dyskinesia: This involves a wide variety of movements such as lip-smacking, chewing, tongue protrusion, choreiform hand movements, pelvic thrusting, and severe orofacial movements. This is caused by super-sensitivity of dopamine receptors due to prolonged therapy with dopamine-blocking drugs. This should be managed with the discontinuation or reduction of any anticholinergics, reduction to the minimum effective antipsychotics, or the use of atypical antipsychotics (clozapine has little or no association with TD). FDA has approved deutetrabenazine and valbenazine.
SIADH: This is commonly associated with the use of haloperidol, risperidone, quetiapine, olanzapine, and clozapine. Mild – moderate hyponatraemia presents as confusion, epilepsy, cramps, nausea, headache, and lethargy. As the plasma sodium falls these symptoms become increasingly severe and seizures/coma can develop.
Hyperprolactinaemia: Antipsychotic-related serum prolactin elevation occurs in 40% of men and 60% of women. This can lead to galactorrhoea, gynaecomastia, hypogonadism, infertility, oligomenorrhoea/amenorrhoea, and sexual dysfunction. Risperidone and paliperidone have potent prolactin-elevating effects. Quetiapine, aripiprazole, and clozapine have no effect on prolactin.
Reduced seizure threshold: Seizure is recognised as a side effect of antipsychotic therapy, the higher the dose the higher the risk. Clozapine has the highest risk of reducing seizure threshold.
Postural hypotension: Mediated through the adrenergic alpha-1 blockade. It is a particular risk when phenothiazine is prescribed for the elderly or when high doses of antipsychotics are used. Atypical antipsychotics (clozapine/risperidone/quetiapine) have important affinity for alpha-1 receptors making dosing titration necessary.
Anticholinergic side effects: Dry mouth, blurred vision, urinary retention, and constipation. Clozapine has been associated with severe constipation which can lead to intestinal obstruction. Therefore, chlorpromazine and clozapine are not advised for patients with closed angle glaucoma. Olanzapine and quetiapine only have mild side effects of this kind.
Metabolic syndromes: This usually presents as truncal obesity, diabetes, impaired glucose tolerance, hyperlipidaemia, and elevated BP. Clozapine has the highest risk of weight gain, followed by olanzapine, quetiapine, and risperidone. In some cases, an oral hypoglycaemic or insulin is required. Advice should be provided on increased appetite, diet, and exercise. Weight should be monitored regularly.
Describe neuroleptic malignant syndrome and what are the risk factors?
Neuroleptic Malignant Syndrome: This is a life-threatening medical emergency occurring in 0.5% of patients newly treated with antipsychotics. Clinical features rapidly progress over 72 hours including hyperthermia, muscular rigidity, decreased consciousness, and labile BP. They may have an elevated CK level, leucocytosis, abnormal LFTs, and myoglobinuria. Usual causes of death are PE, DIC, aspiration, and renal failure secondary to rhabdomyolysis.
Risk factors for NMS include rapid antipsychotic dose increase, IM medication, medical illnesses, male gender, and dehydration. Treatment is with cessation of the antipsychotic, hydration, antipyretics, dopamine agonists (bromocriptine/dantrolene) to help reduce the muscle spasms, and ICU may be required. Investigations should include serum CK, temperature, pulse and BP.
SSRIs: Examples, indications, MOA, and side effects
Examples include fluoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil), Citalopram (Celexa), Escitalopram (Lexapro), and Fluvoxamine (Luvox). The therapeutic effect may not appear for 3-8 weeks after treatment initiation.
SSRIs are absorbed into the GI tract and then bind to proteins to cross the blood-brain barrier. Peak plasma levels occur between 1-8 hours. They are metabolised in the liver and the half-life is around 1 day. SSRIs, except citalopram and escitalopram, inhibit P450 so cause many drug-drug interactions.
SSRIs are first-line antidepressants because of their efficacy, tolerability, and general safety in overdose. They are used for anxiety, panic disorder, OCD, PTSD, eating disorders, and premenstrual syndrome. Between 28-55% of patients fail to respond to SSRI therapy and many continue to experience residual symptoms. The efficacy of SSRI treatment increases with the severity of the depression and may not be beneficial in mild-moderate disease. CYP26 and CYP2C19 polymorphisms affect SSRI efficacy and safety.
Side effects include GI symptoms, dizziness, headache, sexual dysfunction, drowsiness, weight changes, insomnia, syndrome of hyponatremia, movement disorders, QT prolongation, suicidal ideation, and discontinuation syndrome (dysphoria, dizziness, GI distress, fatigue, and myalgia). Fluoxetine is safe to use in pregnancy.
Give an example and side effects of noradrenaline reuptake inhibitors (SNRIs)
Reboxetine is used in major depressive disorder (MDD) and is safe in combination therapy as it has few interactions. Side effects include uncertainty, paralysis, powerlessness and avoidance.
Give an example and side effects of noradrenaline and serotonin reuptake inhibitors (NSRIs)
Duloxetine and Venlafaxine which has similar uses to SSRIs but also used for chronic pain syndromes. It has an improved potency and onset of action. Shorter half lide than SSRIs at 5 hours. Duloxetine is a moderately potent CYP2D6 inhibitor. Side effects include HTN (not duloxetine), loss of appetite, and hepatic failure.
What is the MOA, side effects and indications for monoamine oxidase inhibitors (MAOI)?
These prevent the catabolism of NE, DA and 5-HT neurotransmitters by blocking monoamine oxidase irreversibly. Serious and potentially lethal adverse events include hypertensive crises so there is a requirement for strict dietary restrictions.
Selegiline is a selective MAOb which is used in low doses as a transdermal patch in Parkinson’s disease. Side effects include hypotension, dry mouth, headache, GI upset, and myoclonic jerks. These should never be co-prescribed with an SSRI or NSRI due to the risk of serotonin syndrome.
What is serotonin syndrome?
This is usually the result of an interaction between multiple medications that increase serotonergic neurotransmission. It will present within 6-24 hours of a drug initiation or dose increase. Symptoms include agitation, tachycardia, hypertension, tremor, rigidity, clonus, hyperthermia, and dilated pupils. It should be treated with support, benzodiazepines, and cyproheptadine (serotonin antagonist).
Describe the MOA, indications and side effects of tricyclic antidepressants
These include amitriptyline and its metabolite nortriptyline, imipramine and its metabolite desipramine, and clomipramine. Uses include depression, anxiety, bulimia nervosa, neuropathic pain, and smoking cessation. The half-life is around 1 day. Mechanism of action includes serotonin reuptake blockage, norepinephrine reuptake blockage, histamine receptor antagonists, muscarinic & alpha-adrenergic receptor antagonists, and Na and Ca channel blockage.
Side effects include anti-histaminic effect (sedation, weight gain, and confusion), anticholinergic action (dry mouth, blurred vision (dilated pupils), urinary retention, and constipation), antiadrenergic action (orthostatic hypotension and dizziness), voltage sensitive sodium channels in the heart and brain are blocked in overdose causing coma, seizures, cardiac arrhythmias, and cardiac arrest. Other side effects include lowering the seizure threshold, bone marrow and lover toxicity, and cardiotoxic effects. Not all TCAs have the same affinity for all receptors as nortriptyline is well tolerated whereas amitriptyline has a potent antihistaminic action.
Give some examples of atypical antidepressants
The mechanism of action for these drugs is unclear.
Bupropion (dopamine and norepinephrine reuptake inhibitor) is used for smoking cessation as well as depression. It inhibits P450. Side effects include seizures (dose-dependent), dry mouth, nausea, insomnia, hypertension, sexual dysfunction, and weight gain.
Mirtazapine (presynaptic alpha-2 adrenergic and postsynaptic serotonin blockade) has antihistamine properties via H1 receptors and is thus sedative. There are no significant drug-drug interactions. Side effects include dry mouth, drowsiness, weight gain, and rarely agranulocytosis. In OD there is a risk of fatal arrhythmia and sedation.
Vilazodone and vortioxetine block serotonin reuptake in addition to various effects on 5-hydroxytryptamine receptor subtypes.
Research is now ongoing into the use of kappa opioid receptor antagonists, CB1 cannabinoid receptor antagonists or agonists, cytokines, histone deacetylase inhibitors, and tissue plasminogen activator.
What is addiction?
Addiction is a diseased state of the brain and nerve centres characterised by an irresistible impulse to indulge in intoxicating liquors or other narcotics, for the relief these afford, at any peril (Kerr, 1884).
Addiction is a chronic condition involving a repeated powerful motivation to engage in rewarding behaviour, acquired as a result of engaging I that behaviour, that has significant potential for unintended harm. (West and Brown 2013).
DSM-5 and ICD-11 definitions of substance use disorder:
What are the theories of psychopathology of addiction?
There is evidence of a neurobiological pattern in the brain when substances are consumed in individuals at risk of addiction. There is a biological change in the brain with tolerance and withdrawal. The nucleus accumbens and dopamine pathways are often cited when discussing the pathophysiology of addiction. Drugs of abuse do cause the release of dopamine in the nucleus accumbens, but there is also a release whenever a person engages in something they enjoy.
Positive reinforcement: People take drugs because they get pleasure from doing so via the dopamine reward pathway.
Negative reinforcement: People take drugs to alleviate negative symptoms such as mental or physical pain or to remove withdrawal symptoms.
The opponent process theory states that there is an initial euphoria with intoxication, but future dosing does not give them same reward. The B process is the low after substance intoxication before returning to normal. When the drug has been used for some time, the euphoria is minimal but the come down is bigger and longer lasting.
Incentive sensitisation is the idea that we want to use a substance rather than like it. Drug cues are salient and draw attention which can be implicit or explicit so the cues end up causing dopamine release rather than the substance itself. As the dopamine pathway becomes sensitised the cues become pathologically salient so there is increase dopamine release and density of dendritic spines in the NA.
Impaired decision making: This is the theory that after taking a substance for an extended period of time we develop an impaired ability to inhibit responses to drug cues, even when associated with longer term negative consequences. Frontal striatal dopamine pathways are involved in inhibitory control, planning and working memory.
What are the psychological theories of addiction?
Classical conditioning: Pavlov’s dog states that unrelated things become linked with substance use. This is observed as cue reactivity.
Operant conditioning: This is positive reinforcement and negative reinforcement which states that we do something and learn from it. This explains the initial motivation of using a substance and then negative reinforcement maintains the addiction. This does not explain relapse.
Social learning theory: This states that we learn behaviours through observing others and our social norms so others enjoying smoking conditions us to smoke.
What are the social theories of addiction?
Risk and resilience:
Adverse Childhood experiences such as abuse, neglect, or household dysfunction reduces the ability to be resilient which makes them vulnerable to use and dependence on drugs. This is evidenced in the literature. 5 or more ACEs are associated with significant increased risk.
Vietnam veterans’ study: This was a response to heroin abuse in US soldiers after the war. They found that the context of the opiate use was very important and changing to a supportive place rather than the war zone allowed patients to quit.
Rat Park: Rats become addicted easily, but they are experimented on outside of their normal societies. When rats were allowed to live in a large community as they would in the wild it was found that they abused drugs less. This suggested that societal issues are possibly causative for addition issues.
What are behavioral addictions?
Gambling and Gaming are the only behavioral addictions. These behaviors meet the definition of ICD11 addiction.
