Monday, 19 February 2018

PSY 2016 Abnormal Psychology and Psychiatry 2017-2018


PSY 2016-1 - Abnormal Psychology and Psychiatry 2017 - 2018
Professor Bruce G Charlton






May 8 2018 - complete set of lecture notes

  1. Introduction to Psychiatric disorders
  2. Features of psychosis
  3. Catatonia
  4. Schizophrenia
  5. Sedatives/ hypnotics
  6. Neuroleptics/ Antipsychotics
  7. Mania & Bipolar Disorder
  8. Lithium
  9. Mood stabilizers
  10. Depression (Melancholia & Psychotic)
  11. Tricyclic Antidepressants
  12. Electroconvulsive Therapy & ketamine

  13. Benzodiazepines & SSRIs
  14. SAD, Neurotic Depression, Generalised anxiety, Panic, Phobias, PTSD, OCD

  15. Revision lecture





    16. Core texts:

  • Psychiatric Drugs Explained – David Healy
  • Plus specific reference online – given for each lecture 
    What is psychiatry?
    Medicine - psychological causes, signs, symptoms, treatments
    Conc on ill health - qv psychology
    Mainly therapeutic and human orientated
    Who are psychiatrists?
    Who are clinical psychologists?
    How do people get to see psych/psychols?
    What kind of people become psychiatric patients?
    What do psych/psychols actually do?
    New areas of psychiatry
    Lifestyle management eg sexual function, effectiveness at work, sleep problems etc.
    Cognitive enhancement - ‘smart drugs’.
    New problems in Psychiatry

  1. Invention of new diagnoses to sell drugs/ create work
  2. Widening of diagnostic categories to sell drugs/ create work
  3. Widening drug indications from where they are overall effective to where they overall do more harm than good – e.g. SSRI antidepressants.
  4. Widening drug use to new groups – eg antidepressants and antipsychotics in children and young teenagers
  5. Increase in psych problems caused by psych drugs – side effects, dependence (‘Iatrogenic’ problems)


NATURE OF PSYCHIATRIC ILLNESS

What is it? No clear answer - a collection of problems united by history

  1. Historical - public health function wrt behavior– ‘safety’, asylum -
  2. ‘Suffering’ psychological symptoms – majority are milder/ functional (but mania, dementia)
  3. Pathological brain process - but not always diagnosable - usually presumed rather than proven. Definite brain diseases ‘organic’ often treated by physicians - neurologists or geriatricians
  4. Of exclusions - no physical disease can be found eg. hysteria
  5. Psychopathology - disturbance in basic psychological function - concentrations or memory - hallucinations or thought disorder.
  6. Social deviance and control - crime, psychopaths, USSR schiz.
  7. Evolutionary perspective – fitness-reducing problems of social functioning


Psychiatric Disorders

PSYCHOSIS – In hospital unable to function or suicide risk; qualitative abnormality; lack insight - signs (‘inside’ the disorder) – schizophrenia, mania, psychotic/ endogenous depression…

NEUROSIS – Outside hospital, GP, at work; quantitative exaggeration of normal symptoms – anxiety, obsessive ruminations, misery/ depression, hypochondria, fatigue…


Physical treatments

NOTE: Psychological treatments (NOT in this course)


Drugs – six main types

  1. Hypnotics/ Sedatives
  2. Stimulants
  3. Tranquillizers
  4. Neuroleptics/ Antipsychotics
  5. Antidepressants
  6. Mood stabilizers - lithium


Physical treatments

ECT – electroconvulsive therapy




PSY 2016-2 Abno Psych and Psychiatry – 2017-2018

Bruce G Charlton

Psychotic features: Hallucinations, Delusions and Thought Disorder


Reference: Mellar CS, First rank symptoms of schiz. BJ Psych 1970; 117: 15-23



Search youTube ‘schizophrenia’ ‘gerald’ https://www.youtube.com/watch?v=gGnl8dqEoPQ


Hallucinations

Sensory perception when there is no real object to perceive - a false perception (NOT a distortion of a real perception or a misinterpretation).

Halluc appears to the patient as a normal sensory experience, indistinguishable from real.

Occur in: Schizophrenia, Mania, Psychotic depression, Brain disease, dysfunction, some drugs.

Also (normal) Hypnagogic (going to sleep) and hypnopompic (waking-up) hallucinations. Some studies have shown high prevalence of hallucinations – around 10% population?


Any sensory modality - hearing, vision, touch, taste, smell.

  1. Bodily sensations (being touched, fluid inside – maybe a fluid level, formication)
  2. Delusions of smell or taste - eg smell/ taste poison or taste a poison, or depressive (rotting, disgusting smell etc). eg. led to suicide, or avoidance.
  3. Visual hallucinations - usually assoc with brain disease

  • Delirium – from general disease (eg infection with temperature) – e.g. dust falling through air. Delirium tremens –snakes and elephants. 
  • Hallucinogenic drugs – lights, colours, shapes, or complex scenes.

  1. Auditory hallucinations – hearing voices when nobody is there. A classic sign of madness. With mania and psychotic depression hallucinations are Mood Congruent


Delusions

Delusion = A false belief – that is an idea (not a perception)

  1. False, unshakeable and dominating belief – feels true and usually evokes emotional response and action
  2. Out of keeping with personal and cultural background
  3. No insight – only ‘diagnosed’ by other people
    Eg. A primary delusion Not caused by hallucination: Light turned green and I knew I was the son of God.
    Many delusions are secondary to hallucinations – i.e. false beliefs to ‘explain’ hallucinations – hallucinated sensation in skin explained in terms of insects crawling under the skin.
    A persecutory delusion: Middle-aged unmarried woman believed that men unlock doors of her home, anaesthetize, sexually interfere with her. Meanwhile police using rays to keep her under surveillance.
    Delusions in mania and psychotic depression are mood congruent – eg depressed patient guilty of a serious crime, a manic patient is a god.  
    Thought Disorder (TD)
    Subjectively – thought disorder refers to the subject’s report of their thinking processes which they perceive as abnormal – this relies on introspection and the subject’s ability to describe this.
    Thought disorder is also associated with observed behavioural abnormalities – mainly of speech, sometimes of movements, facial expressions presumably indicate thought processes.
    TD is similar to what happens in dreams – cannot follow a line of reasoning, bizarre things seem plausible, strange twists and turns of dreaming.

  1. Psychotic Depression – Retardation. Part of ‘psychomotor retardation’.
  2. Accelerated thinking/ Flight of ideas – mania. Pressure of speech. Makes sense, but thought is experienced as rapid, ideas follow in quick succession and direction of thought determined by chance associations, distractions and ‘clang’ associations.
    “they thought I was in the pantry at home – peekaboo – there’s a magic box – poor darling Catherine - you know, Catherine the great – the fire grate – I’m always up the chimney – I want to scream with joy – halleluiah!”  
  3. Schizophrenia: Thought-blocking –. Thought and speech suddenly stop in the middle of a theme or mid-sentence – and a new and unconnected subject takes over. May be described as thought-withdrawal (a delusional explanation – a Schneiderian first rank symptom). Or thoughts can be derailed 
    Concrete thinking – schizophrenia.
    Acts out literal meaning of words - Shoes off – why?
    ‘I like to keep my feet on the ground’,
    Walking sideways – due to drug ‘side’-effects
    PSY 2016-3 – Abno. Psychol. and Psychiatry – 2017-18
    Bruce Charlton
    Catatonia
    M. Fink, MA Taylor. Catatonia: Subtype or Syndrome in DSM? Am J Psychiatry 2006; 163: 1875-1876
    YouTube – search and watch Symptoms of Schizophrenia (1940) Lasts 13.08 minutes. Note – the masks are to preserve anonymity.
    Catatonia
    Used to be wrongly regarded as a subtype of schizophrenia.
    Not a disorder/ disease, but a group of abnormal movements (motor features) that can be regarded as a type of psychopathology (like hallucinations or delusions).
    Usually found with other psychotic disorders – but catatonia needs to be regarded separately because:
    1. Requires specific treatment.
    2. Is made worse by some common treatments for psychoses especially antipsychotics, and
    3. With the proper treatment is usually completely and rapidly curable.
    Catatonia can occur in several psychiatric disorders esp affective disorders – mania, melancholia/ psychotic depression, schizophrenia. Also, after brain infections such as syphilis or encephalitis lethargica.
    Catatonia can also be a drug side effect e.g.:
    Dopamine-blocking drugs – e.g. antipsychotics.
    SSRIs – indirectly dopamine-blocking
    Withdrawal of L-dopa
    Catatonic features:
    Patient may go through phases displaying various of these signs

  1. Immobility, Rigidity-statue, Waxy flexibility
  2. Mutism, verbally unresponsive – may still move etc – Stupor – generally unresponsive, may not visibly respond to pain, but may later remember.
  3. Catalepsy = posturing – upper and lower body at right angles/ arms above head/ psychological pillow
  4. Mannerisms – saluting, caricatured normal movements - hands and fingers oddly.
  5. Interaction with people: Copying/ Echoing movements and speech. Or Negativism – physical resistance, psychological negativism.
  6. Meaningless, unprovoked excitement, violence, talking/ singing/ undressing
    About 10 percent of emergency psychiatric admissions have catatonia – usually mild - about 0.1 percent (one in a thousand) prevalence in population.
    Untreated catatonia could be rapidly fatal, usually lasts months- year-plus, sometimes catatonia was permanent.
    Should treat as early as possible.
    Cause: ? How psychiatric phenomena/ brain altering drugs may cause movement disorder.
    Similar to Tonic Immobility – imminent predation
    Response to extreme, inescapable, unlocalisable anxiety.
    Treatment of catatonia

  1. High dose benzodiazepines eg lorazepam
  2. Most powerful treatment ECT – electroconvulsive therapy / electroshock
    Note – it is important to diagnose C. because it may happen in schizophrenia or mania, but is made worse by neuroleptics/ antipsychotics. May provoke the neuroleptic malignant syndrome
    Antipsychotics are given to many patients with ‘psychotic’ symptoms such as hallucinations and delusions, but usually worsen catatonia and may cause it – this can be fatal - Neuroleptic Malignant Syndrome
    Serotonin-enhancing drugs e.g. SSRIs. Serotonin syndrome.
    PSY 2016 – 4 Abnormal Psychol and Psychiatry 2017-18
    Bruce G Charlton
    Schizophrenia
    MA Taylor et al. The failure of the schizophrenia concept… Acta Psychiatrica Scandinavica 2012; 122: 173-83]
    Schizophrenia
    The classic form of ‘madness’.
    Usually stated to be about 1% of population everywhere – but nature, prevalence and prognosis does vary by time and place.
    May have originated in 1700s, became common through the 1800s equal incidence in men and women; seems to be getting rarer over recent years and becoming mainly a Male disorder.
    Schizophrenia is not one ‘disease’ with one cause – it is a collection of several diseases with – probably – several causes - that produce broadly characteristic symptoms, and have different outcomes.
    Clinical features – characteristic symptoms
    Usually post-puberty, insidious onset late teens early twenties, both sexes.
    Poor prognosis/ outcome, the patient never returning fully to normal – if persists more than six months.
    (But brief psychotic episodes may be the clinically identical to schizophrenia in terms of psychotic features – yet improve in days and the patient returns to normal and many never have another episode.)
    In general un-understandability – perplexed mood, not serve any purpose. No insight into condition.
    Hebephrenia
    Core schizophrenia is Hebephrenia/ Disorganized subtype – original and most characteristic schizophrenia syndrome.
    Dominated by thought-disorder – Disorganized speech, subjective experiences of abnormal thought processes.
    Fatuous affect/ emotions, silly facial expressions, progresses to apathy and indifference
    Also hallucinations – typically hearing voices, and delusions – often of paranoid ‘self-reference’.
    ‘Pane of glass’ – lack of empathic contact
    ‘Paranoid Schizophrenia’ is much comment diagnosis dominated by hallucinations and delusions. May be almost the same as manic-depressive disorder ‘Bipolar Type 1’
    ? “Negative symptoms” – these are usually a side effect of antipsychotics =

  1. Affective flattening/ blunted emotions;
  2. Avolia reduced drive/ motivation;
  3. Asocial;
  4. Alogia = ‘poverty’ of thought, and little speech;
  5. Anhedonia – inability to feel pleasure


Distinctive ‘Schneiderian’ First Rank symptoms – Hallucinations and Delusions

Specific types of auditory hallucinations – spoken thoughts, arguing, running commentary


Primary delusion

A period of perplexity, paranoid suspiciousness about ‘something going-on’ - The primary delusion is regarded as the explanation.


Secondary delusions to explain thought disorder

Broadcasting of thought & insertion of thought – delusions which explain the experience of thought disorder. Controlled thoughts and movements - delusions which explain the experience of thought disorder



Prognosis

Duration of at least 6 months before diagnosis – to diff from mania in type I bipolar disorder and Brief Psychotic Disorder – episode less than a month with complete recovery.

When schiz. Is chronic, usually progressive with relapses and remissions. The longer it goes on, the worse the prognosis. The more gradual the onset, the worse the prognosis.

Evidence that the prognosis has become worse over recent decades especially in developed countries – linked to the increased usage of, and dependence on, and damage from antipsychotic drugs.



Treatment  

Antipsychotic/ Neuroleptic drugs – tranquillize/ demotivated (?self treat by heavy smoking)

ECT

Minor tranquillizers/ sedation e.g. benzodiazepines 


Causes

Unknown – many theories - probably many causes for many different but overlapping disorders

Probably some cases caused by new genetic mutations – but low fertility means these are usually not passed-on.

If core schizophrenia was a disorder of the industrial revolution era, but is now disappearing, the cause may be linked to some aspect of this era - ? infection, toxin.  


PSY 2016-5 Abnormal Psychology and Psychiatry 2017-18

Bruce G Charlton

Tranquillisation, Sedatives and Hypnotics

Ref Laura Allison and Joanna Moncrieff. ‘Rapid tranquillisation’… History of Psychiatry. 2014; 25: 57-69 


Tranquilliser - a drug which calms, reduces anxiety and agitation.

Sedative – tends to induce sleep, but not always.

Hypnotic – drug given specifically to cause sleep.

Sedatives and Hypnotics are often the same drug in different doses – low dose sedation/ tranquillisation and higher doses cause sleep.

But some particular drugs are only marketed or prescribed specifically to induce sleep (e.g. zopliclone or zolpidem) – and some drugs tranquillise without sedation (flupenthixol, haloperidol).  

These drugs are usually given over the short term – especially in the day time – i.e. days or weeks 


Behavioural control in Psychiatry

Probably the original function of psychiatry – to prevent suicide, or protect the public.

  1. Physical restraints

All kinds of restraints were used in the past – straps, ropes, chains, cages, restraining chairs, strait jacket, padded cell.

2. Sedative/ hypnotic (sleep-inducing) drugs which made patient drowsy/ sleepy less motivated to be violent. Sleep may also be curative in psychosis.

e.g

Paraldehyde from 1880s

Barbiturates from around 1900

Antihistamines eg promethazine from 1940s

Benzodiazepines eg diazepam/ Valium from 1960s

Sedation still remains a very important mode of controlling behaviour – most acutely agitated patients continue to receive e.g. benzodiazepines (e.g. lorazepam) or sedative antihistamines (e.g. promethazine).  


  1. The neuroleptic/ antipsychotic effect - causing demotivation, indifference to environment, and blunting of emotions e.g. chlorpromazine (1950). Will discuss in the lecture on these drugs.


Sleep

Sleep is, obviously, biologically necessary. Insufficient sleep must have deleterious effects. Sleep is disrupted in many psychiatric disorders, especially those with psychotic symptoms. Patients with mania may stop sleeping for several days, getting worse and worse.



Hypnotics

Early drugs late 19th century included bromide and barbiturates, meprobamate/ Miltown 1955.

Benzodiazepines – e.g. Diazepam/ Valium. Variably effective. Safe in overdose. Suppress deep NREM sleep (stages III and IV).

So – with benzos you may fall asleep earlier and sleep longer – but less deeply, less satisfying sleep. Effects wear off with repeated us (tolerance). Produce rebound insomnia if stopped suddenly.

Nowadays ‘Z-drugs’ such as zopiclone, or zolpidem instead of BZs – work on BZ receptors, but less effective, more prone to dependence.

Antihistamines – promethazine (Phenergan), diphenhydramine (Nytol), or trimeprazine (Vallergan) available without prescription. Problem with hang-over.


Melatonin – A natural hormone, elevated at night. Doesn’t work for everyone, but may be able to produce more normal sleep architecture (i.e. with both deep sleep and REM sleep)


Sleep is very important. Drugs may help in the short term, or even be necessary when people are over-active, but so far all hypnotic drugs have significant problems.  





PSY 2016-6 – Abno Psychology & Psychiat 2017-18


Bruce G Charlton


Neuroleptics/ Antipsychotics




a.k.a. major tranquillizers

Neuroleptic = seizes and holds stable the nervous system - true

Antipsychotic implies specific effect on psychosis – false

Major tranquillizers used in psychotic disorders – contrasted with ‘minor’ tranquillizers used in neurotic disorders such as Miltown/ meprobamate – or Valium/ diazepam


References

Healy D - Psychiatric Drugs Explained

www.mentalhealth.com for information on specific drugs

Joanna Moncrieff. Magic bullets for mental disorders: the emergence of the concept of an ‘antipsychotic’ drug. Journal of the History of the Neurosciences. 2013; 22: 30-46. (joannamoncrieff.com)


Chlorpromazine (first neuroleptic - 1950)

Risperidone (first marketed ‘atypical’ from mid-1990s)


Major therapeutic effect of neuroleptics

Neuroleptics– specific effect is to ‘calm’ agitation & reduce behaviour activity even when not patient was not sleepy.

Induces state of psychic indifference (tranquillization) by blunting of emotion (neuroleptic) – induces dose dependent Parkinsonism.

But not truly ‘anti-psychotic’. Usually people can’t be bothered to respond-to hallucinations, delusions; become ‘indifferent’ to psychotic symptoms, rather than actually alleviating the psychotic symptoms.

Note: Antipsychotics make catatonia worse, can induce malignant catatonia = neuroleptic malignant syndrome.


Mechanism of action

Traditional neuroleptics – e.g. chlorpromazine Primarily D2 blockers.

Meso-limbic dopamine system concerned with motivation and pleasure centre – neuroleptics reduce drive and emotional responsiveness.

Atypical neuroleptics e.g risperidone.

Weaker D2/ plus S2 receptor blockers – are usually less neuroleptic, and cause more sedation and weight gain.


Clinical uses

  1. Used in schizophrenia, mania, psychotic major depressive disorder
  2. Calming agitation from any cause
  3. Suppress undesired behavior (along wth all forms motivated behaviour) in demented and delirious old people – eg elderly homes, and in non-psychotic violent people eg. in prisons/ political prisoners in USSR. 
  4. Now prescribed as ‘mood stabilizers’ in ‘bipolar disorder’ including children, suppresses ‘hyperactive’ behaviour. Increasing rates of prescription, including children and teens – most profitable recent drug ‘Ablify’/ aripirazole
      
    Side effects

  1. Dysphoric – make many people ‘feel bad’, patients often dislike taking them – not abused. All patients experience ‘negative symptoms’ demotivation and emotional blunting, anhedonia, asocial. Akathisia – inner turmoil & agitation – can provoke suicide
  2. Long term usage creates dependence – too-rapid withdrawal causes  psychotic breakdown
  3. ‘Dyskinesias’ = abnormal movements (rigidity, tremor, tongue protrusion, upward gaze). Tardive Dyskinesia often permanent ie. brain damage.
    Conclusion - General view - antipsychotics suppress symptoms, do not cure disease. Unpleasant to take, impair normal functioning, produce dependence.
    Should therefore minimize antipsychotic prescription except as a last resort, low doses as possible, and in short term.
    But the opposite is happening – antipsychotics more prescribed than ever, often being marketed as mood-stabilizers or supposedly for prevention of future problems.
    PSY 2016-7 Abnormal Psychology and Psychiatry 2017-18
    Bruce G Charlton
    Mania and Bipolar Disorder
    Joanna Moncrieff. The medicalisation of ‘ups and downs’. Transcultural society; 51: 581-98. (joannamoncrieff.com)
    Jules ANGST – The bipolar spectrum. British Journal of Psychiatry 2007; 190: 189-91
    Bipolar Disorder is nowadays a common diagnosis – around 5%-plus of the population including all ages down to toddlers. A disorder that is of mild-moderate severity, usually treated outside of hospital. Often diagnosed with 1 week or less of sustained mood change/ or swinging moods through the day. Treated with multidrug ‘cocktails’.
    Until about 20 years ago Bipolar Disorder was an alternative name for the diagnosis of Manic Depressive Disorder, which was regarded as rare (0.1% percent of the population) adult disorder: severe (typically needing weeks/ months of treatment in hospital) and implying LT preventive treatment mostly with lithium) and restricted to adults.
    Expansion of diagnosis
    Therefore, since then the category Bipolar Disorder has been expanded into a ‘Bipolar Spectrum’ it includes about fifty times more people.
    So only approx. 2 percent of modern Bipolar Disorder are equivalent to the old Manic Depressive Disorder.
    Officially – Bipolar Disorder is regarded as a ‘spectrum’ of type I and II – type I is more like the old/ rare/ severe/ hospitalised Manic Depressive disorder (but nowadays not requiring such LT mood change or hospitalisation)  
    Bipolar II
    Type two Bipolar is probably more than 90% of Bipolar diagnoses and includes a mixed bag of people with short term mood swings.
    Previously Bipolar II would have been diagnosed as mixed bag of ‘Nervousness’, anxiety states, Major Depressive Dis., acute psychoses, personality disorders, and psychoactive drug responses.
    e.g. drug induced mania as a side-effect of antidepressants, drug-withdrawal reactions – eg from antipsychotic withdrawal, other drug abuses (as with cocaine-caused celebrity bipolar disorder).
    Note – officially cannot diagnose Bipolar in the situation of psychotropic drug use – cocaine, psychostimulants etc. But it happens anyway, and ‘drugs’ tend to ignore prescribed agents with very similar effects.
    Bipolar II probably not a milder version of Bipolar I – although presumably a gray area/ overlap. ‘Bipolar Spectrum’ idea is probably a wrong and harmful concept. 
    HYPOMANIA and MANIA (approx. = severe BIPOLAR I)
    Mania = Severe Hypomania plus Psychotic Features
    Mania is a serious psychosis characterized by a ‘high’ mood and over-talkativeness, over-activity, overbearing attitude; where the sufferer does not realize that they are ill (no insight) – indeed feels exceptionally well.
    Clinical Features of Hypomania (less-than mania)
    Manic mood: ‘high’ – elated/ happy, irritable, angry, hostile
    Increased energy/ activity - decreased desire for sleep therefore hyperactivity - over-talkative, racing speech
    Poor concentration and distractible attention
    Inflated Self-Esteem (Grandiosity)
    Reckless or Impulsive Behavior / Suicide
    Over-work, spending money, novel illegal or criminal behaviour, promiscuity or sexual aggressiveness, violence, alcohol/ drug abuse.
    Hypomanic patients usually lack insight.
    Mania = hypomania plus psychotic features
    Mood congruent delusions & hallucinations
    ‘Flight of Ideas’ thought disorder
    Catatonia common
    Overactivity without treatment (olden days) may lead to exhaustion, collapse, even death.
    Requires compulsory hospital treatment due to potential for suicide, harm to life and due to lack of insight – non-compliance with treatment.
    Prognosis – Bipolar I is regarded as typically a life-long, relapsing and remitting disorder – but with full functional recovery between episodes (assuming no significant drug side effects)
    Treatment
    Acute:
    Emergency tranquillisation/ sedation –e.g. Antihistamines – e.g. promethazine; Benzodiazepines e.g. Lorazepam
    Neuroleptics/ Antipsychotics
    ECT
    Long term:
    Traditionally Lithium carbonate; Modern practice multi-drug cocktails – often five or even more agents - including
    Increasingly multi-drug ‘cocktails’ including (sometimes several): Anticonvulsants; Antipsychotics; Antidepressants; Psychostimulants; Anxiolytics and Hypnotics. -> SFX and dependence
    PSY 2016-8 Abnormal Psychology & Psychiatry 2017-18
    Lithium
    Bruce Charlton
    Edward Shorter. The history of lithium therapy. Bipolar Disorder. 2009; 11:4-9
    Lithium
    One of the most important psychiatric drugs
    Probably the only true ‘mood stabilizer’ by a rigorous definition
    Used both to treat acute mania and to reduce frequency of breakdowns in manic-depressive/ bipolar disorder. 
    An ion, prescribed as a salt - lithium carbonate.
    Cannot be patented, therefore has never been heavily marketed. 
    History of lithium usage
    Initially recognized as a calming, or tranquilizing drug - used as a sedative in acute mania.
    Discovered 19th century lithium water (naturally occurring, eg Perrier, Vichy - used as treatment for gout. 7-up was a lithium drink until 1950.
    Gout was thought to be related to mania and melancholia, and late 1000s Li used to treat these, including periodic depression by Lange (of James-Lange theory of emotion fame).
    But Li slipped out of usage and was forgotten. Effective treatment quite often fail to be widely adopted or are forgotten - may currently be happening to lithium
    Cade 1949 (Australia) working on urine of manic patients in guinea pigs, found that lithium seemed to sedate the GPs. But problems of toxicity including deaths.
    Re-launched and championed in 1960s esp by Dane called Mogens Schou – with regular blood level monitoring. 
    Initially led to great resistance and controversy in British psychiatry, but eventually widely adopted. 

  1. Lithium first discovered as a tranquillizer or antidepressant.
  2. Later lithium used mainly as prophylactic (preventive) for manic depressive illness - prevents or reduces frequency of recurrences of both mania and (probably, but not so effectively) depression.
  3. Unknown mode of action. But probably can be conceptualized as providing continuous combined treatment both tranquillizing & anti-depressant (ie mood stabilization).
  4. Narrow therapeutic range. Ineffective in low doses, toxic in high doses.
    Each person must have dosage ‘titrated’ against blood levels - must monitor blood levels weekly or monthly until stable.

  1. Dangerous in overdose, toxic to fetus.
  2. Often bad side effects –

  • Tremor
  • dry mouth (thirst)
  • Weight gain
  • May make people feel dulled and unresponsive - or they may miss the excitement of mania.

  1. Probably, lithium maintenance significantly reduces suicide rate in BPI, which is high.
    However, rapid withdrawal from Li significantly increases suicide rate. Must withdraw slowly (if possible)
    So, lithium creates a dependence state – pro - the drug may be both helpful in prevention but - con - also hard to stop taking it safely.
    Due to many SFX of Li in 1980s psychiatrists began trying out different type of drugs – the anti-epileptic ‘mood stabilizers’. 
    These were patented drugs and led to a huge expansion in the diagnostic category of bipolar disorder.
    But none seem to be as effective as lithium and only lithium is capable of treating and preventing both mania and depression.
     PSY 2016-9 Abnormal Psychology & Psychiatry 2017-18
    The so-called ‘mood stabilizers’
    Bruce G Charlton

    www.mentalhealth.com
    Healy – Psychiatric drugs explained

    GUY M. GOODWIN a1 and GIN S. MALHI What is a mood stabilizer? Psychological Medicine (2007), 37:609–614

    Lithium is the only true mood stabilizer: only agent that treats both mania and depression…


    Mood stabilizer cocktails/ Multi-drug combinations
    But cocktails of three or more ‘mood stabilizers’ often used
    These include selections of one or more of the following:

    1.    Lithium (declining use)
    2.    Anticonvulsants
    3.    SSRI antidepressants
    4.    Antipsychotics
    5.    Benzodiazepines
    6.    Psychostimulants

    In other words, variable combinations of variable numbers of all of the main classes of drugs used in psychiatry except tricyclic antidepressants.

    One example (from internet discussion group) seven drugs: lithium, two antipsychotics, and two psychostimulants, an antidepressant, a benzodiazepine.
    Why? Mostly trying but failing to achieve control (several-fold increased admissions for BPD), system destabilization, chasing side-effects, emerging interacting dependence/ tolerance/ withdrawal.
    Widely prescribed incl. being given to young children and teenagers. Multiple side effects, dependence, possible permanent long term damage from antipsychotics

    Mood Stabilizers
    Essentially – ‘mood stabilizer’ is scientifically so vague as to be almost meaningless – but because applied to patented drugs the vagueness has been very useful and successful for marketing purposes.
    So-called ‘mood stabilizers’ were originally anticonvulsant/ anti-epileptic drugs used first off-label, then on license.
    Retrospective scientific rationale for use was the BPD was analogous to epilepsy due to ‘kindling’ – theory of Robert Post. One affective episode was supposed to make it more likely that there would be another. Theory found Not to be true – episodes do Not tend to be more rapid, most anticonvulsants are not effective in treating or preventing MDD.
    Anti-epileptics don’t help MDD as a class of drugs, only certain non-epileptic effects may be helpful.

    Carbamazepine
    Discovered in Japan in 1960s (Li not available).
    Carbamazepine is mainly effective in controlling mania – probably works as a kind of tranquillizer. Anti-irritability, anti-aggression.
    Common side effects: sedation, impaired coordination. Rare blood side effects – eg. may switch of WBCs - monthly bloods.
    Conclusion – Carbamazepine is an anti-irritability, anti-aggression, anti-manic agent.

    Sodium Valproate/ Valproex/ Valproic Acid/ Semisodium Valproate
    Used in children as anti-epileptic fewer psychological side effects ?improve personality problems in epilepsy.
    Began to be used in psychiatry in France 1960s
    Became much more popular in 1990s – as newly patented forms became available – therefore now widely used.
    Sedative action, useful at controlling acute mania, perhaps useful at preventing mania – but not depression.
    Side effects include: sedation, weight gain
      
    Lamotrigine
    Anticonvulsant. Not effective against mania, but has stimulant (dopaminergic) actions and may be an effective antidepressant. Few side effects. Patient often feels good.

    Gabapentin
    Anticonvulsant. Anti-anxiety agent similar to benzodiazepines, but misleadingly marketed as mood stabilizer – had to pay several billion dollar fine.  

    Neuroleptics/ Antipsychotics
    Given to control agitated behaviour in acute mania – also schizophrenia, and psychotic depression.
    May also be given to prevent MD episodes, especially mania, in lower doses than used for acute behavioural control. Continuous treatment.

    None of these drugs are truly preventive, but actually a form of continuous and potentially treatments – with all the problems, plus.


PSY 2016-10  Abnormal Psychology and Psychiatry 2017-18
Bruce G Charlton
Depression: Melancholia & Psychotic Depression

Ref: Fink, M; Taylor MA – Resurrecting Melancholia. Acta Psychiatrica Scandinavica. 2007; 115 (supplement 433) 14-20. 

Severe melancholic/ psychotic depression is perhaps the worst psychiatric illness to experience. Has a high death rate from dehydration/ starvation and suicide.
But if you survive a complete recovery is usual.
And quite likely you will never get it again - although the risk of future episodes is higher than for average population.

Definitions – Two types of ‘depression
Major Depressive Disorder is a large, imprecise category. But evidence is that DSM ‘Major Depressive Disorder’ should be split into at least two different categories.
MDD divides into: Melancholic and non-melancholic (‘Neurotic’) depression.

Only approx 1% of MDD is Melancholia including Psychotic Depression – a disease state.
Severe and rare, an emergency, requires hospital.
Most effectively treated with TCAs and ECT.

Melancholia
Melancholia is the same thing as Endogenous Depression.
Helpless, often suicidal patients requiring prolonged care and hospitalization – about a year – but typically making a full recovery.
Melancholia plus Psychotic features = Psychotic depression.
Same basic illness but more severe and with hallucinations and delusions.

Melancholia - Clinical Features
Depressed mood: misery, fatigue, aches and pains. Guilt. Anhedonia – emotional numbness, inability to experience pleasure, demotivation

Other features:
Disturbed sleep EMW = early morning wakening.
Diurnal (=daily) variation, depression worse in the morning
Blames self/ ideas self-harm/ intention suicide – highest incidence
Reduced appetite/ stop drinking - weight loss, dehydation
Psychomotor retardation – very slowed up in movement and speech.

Vital symptoms – fatigue, aches and pains, heaviness, washed-out – feels ill.
Feels like a bodily illness – such as an infection (flu, glandular fever), autoimmune illness (rheumatoid arthritis), or disseminated cancer

Treated with Tricyclic Antidepressants e.g. Imipramine
Second line Monoamine Oxidase Inhibitors eg Phenelzine
ECT is the fastest and most effective treatment of Melancholia
 (SSRIs do not work)
Ketamine by 2-3Xweek intravenous infusion is a new treatment – may be the quickest and fastest treatment of all.

Psychotic Depression – Clinical features
Typically patient is wretched, agitated, constant movement, repeated phrases of misery; ‘insane’ - experiencing hallucinations, delusions, catatonia; no insight, hope-less and actively suicidal.  
i.e. Psychotic depression is Melancholia plus delusions, hallucinations, catatonia.

Delusions =  false beliefs about guilt, sin, poverty, or imminent disasters – rotten inside, nothingness/ dead etc.  – ie mood-congruent
Hallucination= Usually hearing voices - nasty comments, accusing of crimes or sins – guilt; or accused of rotting, decomposing, smelling etc – ie mood-congruent

Severe melancholia or psychotic depression may progress to unresponsive stupor - dehydration, starvation - potentially fatal.
ECT has been the only really effective treatment for Psychotic Depression – perhaps ketamine too.

Aetiology­ – i.e. cause
Mysterious – like a disease, often out of the blue.
No single cause, probably many causes and sub-types – not usually explicable by psychological cause.

Epidemiology
Melancholia (including Psychotic Depression): Incidence of c100 new cases per million population per year (Prevalence about 0.1% of population at any given time)
Major Depressive Disorder – About 100 times more commonly diagnosed than melancholia - 10,000 new cases MDD per million population (Prevalence about 10% of population at any given time.

Melancholia is rare but a medical emergency – high risk of suicide, probably needs urgent hospitalization.

PSY 2016-11 Abno Psychology and Psychiat – 2017-18
Bruce G Charlton
Tricyclic antidepressants (TCAs)

Healy – strongly recommend.
Ref: EF Domino. History of Modern Psychopharmacology Psychosomatic Medicine 1999 61:591-598

Name refers to a chemical structure - three circles.
In terms of usage, TCAs are a family of drugs, with different main effects but similar side effects.

For Melancholia:
Imipramine – discovered by Roland Kuhn – 1956.
Amitriptyline – was most widely prescribed. Marketed in modern way – marketed the concept of depression in a book given free to doctors, and the drug was associated with the diagnosis.
Usually sedative effect (especially Amitriptyline)

For stimulant effect – eg demotivation, sleepiness
Desipramine (mainly norepinephrine re-uptake blocking effect – stimulant. Similar clinical uses to psychostimulants or MAOIs.

For emotion-stabilising (including anti-anxiety):
Clomipramine (mainly serotonin reuptake-blacking effect)
Gave Arvid Carlsson the idea for SSRIs – similar clinical uses to SSRIs.


Probably the most effective class of drugs used to treat moderate to severe depression of the kind leading to hospitalization (eg especially malaise and perhaps demotivated subtypes).  

Psychological action
Perhaps their core action is to treat physical /‘vital’ symptoms of depression, not the psychological symptoms - ie affect body primarily, rather than brain (malaise theory). This is what Kuhn used imipramine for.
This effect on physical symptoms can be conceptualized as an analgesic (painkilling) effect – removal of unpleasant (including painful) sensations.

Imipramine and Amitriptyline are effective in treating various types of pain – in cancer/ terminal care, in migraine, in chronic pain.
Acts on vital symptoms as soon as absorbed:
Within hours may increase sleep and appetite. Act like a ‘tonic’.

Noradrenergic enhancing effect may increase drive and energy. Acts like a ‘tonic’ is supposed to act: ‘helps you sleep, builds you up, and gives you energy’.
Effect on overall mood is slow and gradual – may take weeks – some patients may not be aware of it, or they may not experience an improved mood even though vital symptoms have improved.

Chemical mechanism of action of TCAs
Antideps act on receptors in brain; but relatively weakly compared with some other psychiatric drugs. Effects on the body may therefore be more significant.
Core action is considered to be amine reuptake inhibition – usually acting to various degrees on norepinephrine, serotonin and/ or dopamine.
Catecholamine hypothesis of depression, 1965 Jospeh Schildkraut - emphasized deficiency of norepinephrine action. (He also worked on subtypes of depression, but this was not influential despite prestigious publication).
Nowadays more general ‘amine hypothesis’ – includes 5-HT is the most fashionable cause, or possibly dopamine.



Tricyclic side effects
· Weight gain (females don’t like, unless mod-sev dep with weight loss)
· Impotence or difficult orgasm (males don’t like, unless mod sev dep with loss of libido) – but similar effects also occur with SSRIs, especially in older people.
· Dry mouth, constipation
· Cardiotoxic, care with elderly people, arrhythmias
· Dangerous in overdose

Do not work on psychotic depression.
Make schizophrenia and mania worse – can trigger mania

SSRIs are mostly very different effects and side effects, and are not interchangeable with TCAs (except for clomipramine) – do not work for melancholia.






PSY 2016 – 12 Abnormal Psychology and Psychiatry 2017-18

Bruce Charlton

ECT and Ketamine

ECT – electroconvulsive therapy or ECS – electroshock/ electroshock therapy aka ‘Shock therapy’ (but not exactly a shock)

References

Max Fink. Convulsive therapy: a review of the first 55 years. Journal of Affective Disorder. 2001; 63: 1-15.

 

JB Singh et al. A double-blind, randomized…study of intravenous ketamine. American Journal of Psychiatry. 2016; 173: 816-26.

*

An example of psychiatry at the centre of social controversy. Extreme views – 1. The single most effective and important treatment in psychiatry; 2. A damaging fake treatment actually being used as a punishment//

 

Definitions

Use of electrical current passed through the brain to induce a ‘grand mal’ general epileptic seizure.

Main public knowledge of procedure and outcome are from fictional depictions – eg One flew over the cuckoo’s nest; Zen and the Art of Motorcycle Maintenance. Fictional depictions are fictional!

 

Describe procedure ‘modified ECT’

General anaesthetic, pre-oxygenation – patient asleep

Muscle relaxant – patient ventilated

Application of electrical current via moistened electrodes on scalp, usually applied to temples. Epileptic seizure usu. tens of seconds

Anaesthetic and muscle relaxant wears off – patient wakes, goes to rest and recover. Usually somewhat groggy for a while, more rarely confused.

2 or 3 Tx per week, a few weeks - +ve sigs are rapid (3-5 Tx) improvement in mood, increase energy and appetite, return to usual sleep patterns

 

Side effects

For about an hour immediately after awakening – may be ‘acute confusional state’ of disorientation, transient memory loss, and headache.

Laying-down of new memory may be impaired for several weeks after ECT course. (can be an effect of the illness; or sedative drugs time of ECT).

?Longer term memory problems – probably not, but some are reported. May be due to severe depression, mania etc.

Point is to compare severity of ECT side effects with those of alternative treatments, and with the effects of no treatment (bearing in mind that some illnesses are self-limiting) Eg ECT versus Antipsychotics, ECT versus deep brain stimulation in Parkinson’s

 

 

Indications

1.    psychotic depression

2.    mania

3.    acute schizophrenia

4.    delirium

5.    Parkinson’s disease and Lewy body dementia.

6.    Catatonia

 

 

Ketamine

Intravenous infusion ketamine over 40 minutes – approx. twice a week for about 4 weeks.

May provide relief from psychotic depression (probably melancholia) within minutes – fades over a few days – but after a few weeks seems to be lasting.

Greatest breakthrough since ECT and tricyclics.

 

Ketamine is >40 year old (off patent) anaesthetic (in high doses), analgesic, stimulant and quite often produces dissociative and sometimes ‘mystical/ psychotic’ dreamy states. Previously used as a single anaesthetic agent in third world countries.

 

Chemically ketamine is classified as an NMDA receptor blocker.

N-methyl-D-aspartate – an important neurotransmitter.

Ketamine finding has been downplayed and ‘concerns’ have been raised about off-label use, side effects etc… Caution advised…

 

But melancholia is rare and ketamine is off patent – so Big Pharma is looking at new me-too NMDA blockers to be delivered by intranasal spray for ‘Major Depressive Disorder’ in outpatient/ primary health care (much bigger market).

 

Similar to what happened with SSRIs – 15 year lag between discovery and new drugs. And new drugs have new side effects – but not necessarily as clinically effective.

 

 

 

 

 

PSY2016-13 – Abnormal Psychology and Psychiatry 2017-18

Bruce G Charlton

Selective Serotonin-Reuptake Inhibitors – SSRIs & Benzodiazepines

 

Healy, D – Psychiatric Drugs Explained

Charlton BG. A model for self-treatment of four sub-types of symptomatic 'depression' Medical Hypotheses. 2009; 72: 1-7

 

Fluvoxamine - Luvox

Fluoxetine - Prozac

Citalopram - Cipramil 

 

As benzodiazepines were for the 70s and 80s, so the SSRIs are for the 90s and 00s – main class of drugs used to treat anxiety symptoms and mild-moderate outpatient depression. Similar patients but drugs have different pharmacological and clinical effects.

Chemical structure – derived from antihistamines – like TCAs and antipsychotics. Diphenhydramine (Nytol) is an SSRIS 

Similar biochemical action to TCAs but act ‘selectively’ to inhibit serotonin re-uptake more strongly than norepinephrine.  

 

Clinical effects

Clinical effect is similar to, weaker than antipsychotics: main effect is emotional stabilization/ drugs are ‘serenic’.

Therefore may make unstable people more stable: less shy - more sociable, less anxious, less prone to downward/ depressive mood swings

– but others may be less motivated, hardening of personality – less caring and empathic. 

 

Clinical uses

Does not work in moderate to severe hospital depression – not really an ‘antidepressant’.

Effective in some outpatient ‘Neurotic depression’ especially when anxiety or mood swings are a problem. Effective in all forms of anxiety – GAD, panic, social phobia, agoraphobia and other generalized phobias, OCD.

Also delays orgasm – used for this purpose in men to treat ‘premature ejaculation’. May prevent women having orgasm.

 

Unwanted side effects

Usually mild and temporary

Suicide warning. Rarely (< 1:1000) people feel acute mental turmoil, acutely suicidal with bizarre violent fantasies (eg about violent death) –suicide, sometimes out of the blue – perhaps especially suicides by hanging in kneeling position. Stop drug if agitated/ violent fantasy

Evidence that SSRI-type drugs may be associated with mass shootings.

 Dependence – withdrawal symptoms when stopping. A serious problem for some people.

 

St John’s Wort seems to function like an SSRI but may be better – fewer side effects and equally or more effective.

 

Benzodiazepines - BZs

1954 - synthesized chlordiazepoxide (Librium) - long-acting

Diazepam - (Valium)

Lorazepam

 

Mode of action

Act to modulate GABA neurotransmitter - major NT responsible for inhibition of neurons.

BENZ may be synthetic equivalent of natural brain chemicals called beta-carbolines.

 

Clinical Effects – among the most useful ever drugs

1.    Subjective effect – pleasant, soothing, relaxing like alcohol.

2.    Anti-anxiety - especially when anxiety due to muscle tension. Diazepam is one of the best muscle relaxant drugs, used for spasm and spasticity. Slipped disc, muscle spasms, cerebral palsy.

3.    Hypnotic - usually produces sleep in high enough doses - but variable between individuals.

4.    Anti-convulsant - used in treatment of acute epilepsy and in withdrawal of alcohol or heroin

5.    Control of violent behavior and acute psychosis  - eg acute schizophrenia or mania. Usually lorazepam.

6.    Treatment of catatonia.

 

SIDE EFFECTS

Rebound anxiety and insomnia for several days following withdrawal.

Addictive dependence - ? susceptible minority– month Rx.

Abuse - especially IV e.g. temazepam.

 

 

SSRIs versus BZs

 

1.    Similar range of uses

2.    Different mode of action

3.    Different side effects – but similar withdrawal effects

4.    BZs pleasant to take, more addictive

5.    SSRIs not addictive - dulling, but worse dependence than BZs


 
Lecture notes for the last two lectures of PSY 2016 – 2017-2018

These complete the syllabus

 

Bruce G Charlton

 

 

Seasonal Affective Disorder (SAD). Light therapy

 

SAD - Eagles JM, British Journal of Psychiatry. 2003;182:174-6

 

Example of disorder mostly discovered, diagnosed and treated outside of medical profession and without prescriptions – not much about it in the research literature. 

 

Winter depression/ blues, linked with treatment with bright light therapy given in the mornings.

Increased incidence of depressive symptoms/ major depressive disorder during winter months.

Typical clinical picture varies in severity in a continuum, with symptoms such as:

 

  1. Fatigue & Reduced motivation
  2. Excessive sleeping (hypersomnia)
  3. Increased appetite (carbohydrate) - weight gain 
  4. Irritable mood
  5. Reduced sociability

 

Think of dozy, idle, overweight person who loses their temper whenever anybody bothers them: ‘I can’t be bothered - get me some cake then leave me alone to sleep!’

 

Main theory is that people with SAD are unable to adapt to shorter photo-period in winter.

 

 

Pathology – Lack of early morning light in winter. 

Humans evolved Africa +/-30 degrees latitude – similar day length in summer and winter.

But at extreme latitude day length varies widely between summer and winter.

 

Texas 30 degrees N

Naples/ Boston 40 N

Canada (most of population) 40-50 N

Newcastle 54 N

Iceland 65 N

Arctic Circle 66.5 N

 

SAD seems to be caused by the shorter day in winter – maybe reduced intensity of light/ cloudy weather.

 

Epidemiology

Prevalence varies from 0-10 percent with increasing latitude.

Commoner in women, especially in childbearing years

Acclimatization occurs in individuals who move to more extreme latitudes, SAD worse in recent migrants.

Longer-term adaptation (by natural selection) of populations who have been at extreme latitude for many generations (eg Iceland) – seem to have lower prevalence SAD than expected. This implies some genetic element – and SAD (or resistance to SAD) probably heritable.

 

Treatment

Acclimatisation - a proportion of people get better with time – c. one third?

 

Light therapy

Seems very effective, although it is hard to compare with placebo

Indoor lighting c 100-400 lux (evening at home - office)

Outdoor cloudy winter day – 4000 lux

Outdoor bright sun – 40 000 lux plus

 

Treatment with ‘light boxes’ before sunrise.

Administered in the morning e.g 10 000 lux for 30 mins for severe SAD.

‘Light visor’ - close proximity of light source

Dawn simulators go from darkness to c 400 lux.

 

Problem of funding trials of non-pharmacological treatments, and blinded controls. 

Or can ‘go south’ for the winter – that works within a few days, but only for as long as you stay near the equator, relapse about a week after return…

 

 

Neurotic/ Reactive Depression

Refs: Shorter E. The doctrine of two depressions in historical perspective. Acta Psychiatrica Scandinavica 2007; 115 (suppl 433): 5-13

 

Neurotic Depression = those people diagnosed with DSM Major Depressive Disorder who do NOT have melancholia (or psychotic depression) – maybe 98 percent of MDD patients?

Major group of outpatient/ community psychopathology treated by GPs/ family doctors, and also by psychotherapitsts and clinical psychologists.

Neurotic depressives include people who suffer from psychiatric symptoms with depression, and often seek treatment – but seldom go to hospital, commit suicide only at about the same rate as the general population (unless from drug side effects – eg SSRIs and Antipsychotics cause suicide, but as a rare side effect). 

MDD  is perhaps 10% of population – and neurotic depression is about 98% of modern ‘depression’ / Major Depressive Disorder. Increasingly MDD is diagnosed as part of ‘Bipolar Disorder Type II/ Spectrum.

No precise definitions of Neurotic/ Reactive depression – the group includes many types of people with 1. depression as a mood - but also often 2. anxiety, 3. fatigue, 4. obsessional symptoms, 5. aches/ pains/ hypochondria.

Tendency to blame others/ circumstances (not self)

Commoner in women

 

 

ANXIETY AND ITS MANIFESTATIONS

 

IM Marks, RM Nesse. Fear and Fitness. Ethology and Sociobiology. 1994; 15: 247-261.

 

GENERALIZED ANXIETY DISORDER (GAD)

REFERENCE

H-U Wittchen & J Hoyer. (2001) Generalized Anxiety Disorder: nature and course. Journal of Clinical Psychiatry 62 (supplement 11) pp 15-21.

 

Anxiety is a kind of fear, unpleasant increase in arousal - probably a universal experience - although magnitude is very variable.

A universal biological category, cross-cultural, once of the basic emotions an adaptive response – improves reproduction/ survival: increases arousal.

GAD describes (approximately) long-term anxiety-about-everything

(DSM defines as several months anxiety about more than one theme).

 

Evolved fears

Many fears are evolved eg. fear of the dark, of being alone, of strangers – we do not learn these fears – on the contrary we learn to overcome them.

Anxiety disorders may be more a failure to learn to overcome fears, rather than learning of fears.

In modern life anxiety is very common – is this an example of evolutionary mismatch?

 

GENERALIZED ANXIETY DISORDER (GAD)

Used to be termed just Anxiety or Anxiety State, overlaps with Neuroticism and Neurotic depression.

Chronic unrealistic or excessive anxiety (about 2 or more themes) - for most of the time and for several months).

NOT phobic, obsessive, hypochondriac or panic.

The person may have good reason to be anxious, but the anxiety has become maladaptive, prevents them doing anything constructive. Or else the causal problems may be intractable.

Usually begins in childhood or adolescence and continues through life waxing and waning.

Epidemiology depends on definition; USA 1 year prevalence supposedly > 15 percent for all anxiety disorders. Twice as common in women as men.

 

Treatment:

1.      Relaxation - especially self-hypnosis, learned muscle relaxation; and Supportive discussion, explanation, advice

2.      Cognitive-behavioral - difficult, no specific ‘entry point’ for therapy to work on.

3.      Drugs :

  • Alcohol (self-medication) - more dangerous than most of the drugs. Impairs cognitive function, performance, causes violence and accidents. ?
  • Beta-blockers - eg propranolol - peripheral effects – reduce heart rate, blood pressure… reduce feedback to brain. Unpleasant in high doses.
  • Benzodiazepines – muscle relaxation, tranquillizing/ calming
  • SSRIs - emotional buffering/ stabilizing – serenic agents. Self-medicate St John’s Wort to get similar effect?

 

 

Phobic Anxiety/ Phobias

Anxiety in relation to particular circumstances (i.e. about just one theme)

Avoids situation

Anticipatory anxiety

 

Specific/ Simple phobia - Eg: spiders, snakes, heights, dentists, flying.

General phobia - Eg. Agoraphobia, Social phobia/ anxiety 

 

Evolutionary significance - Fear that is on average adaptive in ancestral environment may be maladaptive under modern conditions - Eg fear of snakes or spiders and social phobia/ anxiety

Treatment  Typically Behavioural Therapy (BT) for simple phobia; or drug therapy for General Phobias. 

 

Panic, Depersonalisation

 

PP Roy-Byrne et al, Michelle G Craske, Murray B Stein Panic disorder. Lancet. 2006; 368: 1023-32

 

Panic disorder

Characterised by:

1.      Episodes of acute, severe anxiety – anxiety building up rapidly over a timescale of seconds.

2.      Prominent physical symptions:

-          Chest pain, hyperventilation, breathlessness

-          Dizziness, faintness, unreality, tingling

3.      Sense of impending doom – fear of heart attack, epileptic fit, stroke, death.

4.      Attack ends with lying down, collapsing, or frantic running into air outside - or back into home. 

5.      Patient identifies whatever preceding event as a cause, and tries to avoid that situation. Fear of panicking becomes a restriction – may develop agoraphobia.

 

In sum – Panic is a disabling anxiety. Not obviously a defence mechanism – e.g. not for increased vigilance, fight or flight.

Panic often found with other anxiety disorders, and depression.

Prevalence – at any time, about 2.5% population could be diagnosed as Panic Disorder.

 

Treatments

1.      Explanation - reassurance

2.      BT or CBT

3.      Antidepressants – SSRIs, TCAs, MAOIs

4.      Anxiolytics – Benzodiazepines. 

 

 

Depersonalisation

 

A strange and unusual type of anxiety symptom

A feeling of detachment

An alteration in the perception of the self, so that the patient feels detached from himself – his mental process or his body – feels like an observer of himself. 

(Feeling as if in a dream.)

 

A related phenomenon, which overlaps, is Derealisation – which means feeling detached from the external world, the environment to that it seems strange and unreal.

Sometimes called ‘Dissociation’ phenomena – based on an idea that mental functions might have become detached from each other - and may be a complex state of feeling things are unreal, emotional numbing, heightened self-observation.

Cause? Sierra and Berrios, 1998 suggest caused by simultaneous:

1.      Inhibition of emotional processing

2.      Heightened state of alertness

May happen in high anxiety states such as panic (especially with hyperventilation), in PTSD, also Temporal Lobe Epilepsy.

 

Treatment – If related to anxiety, usually treated with benzodiazepines such as diazepam.

But paradoxically, BZs can themselves cause depersonalisation as a side effect.

 

PTSD – Post-traumatic Stress Disorder

 

Ref: DJ Stein et al. Post-traumatic stress disorder. Lancet. 2007; 369: 139-44

 

Long lasting but delayed psychological effects of severe trauma.

Main similarity is with ‘combat fatigue/ shell shock’. Especially in 1914-18 war.

PTSD introduced in 1980 DSM III, following return of veterans from Vietnam War.

 

Diagnosis

  1. Delayed/ protracted response to severely stressful or traumatic event (war, disaster, torture, violence) – latency of weeks/ months < 6 months
  2. Symptoms of re-living, intrusive memories, flashback, nightmares cued by reminders
  3. Avoidance of possible cues
  4. High arousal, hyper-vigilance, low startle threshold

 

Prevalence approx.. 4% of adult population at any one time with PTSD (but can occur in all ages).

Twice as many women as men

 

Treatment

CBT – prevent response

SSRIs

? ‘mood stabilizers’ (eg sodium valproate)

 

Obsessive Compulsive Disorder – OCD

Reference: Stein D.J.  Obsessive Compulsive Disorder. Lancet. 2002; 360: 397-405.

 

Not a true anxiety disorder, although anxiety may be a prominent symptom. However the drug treatment is the same as for anxiety disorders.

Epidemiology – c 2% population prevalence and 2% chance of having it in lifetime – (unusually) same prevalence in men and women.

 

Obsessions – cognitive

Subjective unwanted/ distressing/ inappropriate thoughts (alien but recognized as personal)

Obsessions -

1.  Thoughts - words, phrases, rhymes

2.  Images - eg violent, disgusting

3.  Impulses - eg violent, shameful

A fear that they will act on these obsessions

 

Compulsions – behavioural

Objective actions - quasi-rituals, performed unwillingly, with anxiety and inner struggles, to get relief from…maybe specific number of repetitions

 

Treatments

1.  Explanation, reassurance, support.

2.  Behavioural therapy may be effective for for compulsions.

3.  SSRIs, clomipramine.

 

NOTE: Drug treatment of Neurotic depression and the various types of anxiety is mostly identical:

e.g. Tranquillizing, sedative type drugs – such as benzodiazepines eg. diazepam; rapidly effective in reducing anxiety – minutes-hours.

Or: SSRI-type ‘antidepressants, have emotion-stabilizing effects – slower onset over days-weeks?

In the past psychostimulant type drugs (e.g. amphetamines) – alone or in combination with sedatives such as barbiturates - were sometimes used in both Neurotic Depression and some of the anxiety disorders, or drugs with stimulant effects (e.g. MAOIs). Seldom used at present, mainly due to problems of addiction.

 

 

 






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