Site icon almostadoctor

Depression

Dr Tom Leach
Depression

Depression

Introduction

Depression is one of a group of disorders known as the affective mood disorders, and the internalising disorders – other examples include:
The symptoms of these conditions are often similar, and there is considerable overlap. The actual combination of symptoms will determine the diagnosis.
Depression can occur as a single episode, or as ongoing condition with periods of ‘relapse’ and ‘remission’.
Depressed patients have a decreased quality of life, as well as increased mortality.
The exact terminology for the diagnosis of depression can be a little confusing. Major depression (also sometimes called major depressive disorder) is defined by the DSM-V criteria for the diagnosis of major depression (see below). Generally when we refer to depression, we are talking about major depression (consider the two terms synonymous for this article unless otherwise stated). There are also subsets of patients whom may have depressed mood but do not meet these criteria. Sometimes we might define these patients as suffering from minor depression, or if there is an obvious recent event that has precipitated the mood disturbance, we might define the condition as adjustment disorder with depressed mood.

Aetiology

Epidemiology

Differentials – for low mood

Investigations

At the time of a first / new presentation, the following investigations may be considered to rule out an underlying case

Diagnosis

It is recommended that depression be diagnosed in line with the DSM-V diagnostic criteria for major depression.

DSM-V Diagnostic criteria

Diagnosing depression requires a relative short history of at least 2 weeks.

At least FIVE of the following almost every day for the last 2 weeks. Numbers ONE and TWO are essential.

  1. Depressed mood
  2. Loss of interest or pleasure in previously enjoyed activities
  3. Change in weight (>5% in <1 month) OR change in appetite
  4. Changes in sleep – insomnia or hypersomnia
  5. Psychomotor agitation (e.g. symptoms of anxiety) or retardation
  6. Fatigue or low energy
  7. Feelings of worthlessness or guilt
  8. Reduced concentration or decisiveness
  9. Suicidal ideation or attempt

PLUS ALL of the following:

  1. Symptoms cause significant distress or impair functioning
  2. Symptoms not due to a medication, other substance or other underlying illness
  3. Symptoms are not better explained by a schizophrenia spectrum disorder or psychotic disorder
  4. No history of a manic or hypomanic episode (if present – consider bipolar disorder)

There may also be:

An assessment of severity also depends on the impact on normal functioning.

Previously, depression had been thought of in terms of major and minor symptoms. It can still be useful to think in these terms.

Major Symptoms

The three core symptoms
‘More than 2 weeks’ means that the patient would have experienced the symptoms for at least part of the day on everyday for the last two weeks.

Minor symptoms

Cognitive

Functional

Other clinical characteristics
Some patients may experience melancholia – this is where the patient feels unable to experience any emotions at all – emotional numbness.

Screening Tools

In general practice, screening tools are often used to assess if a patient is suffering from depression, as well as to track the course of the condition over time. Examples of screening tools are:

Other variations may be used. Patients may complete these as questionnaires on paper, or they may complete them on the computer. The second method is more widely used, as you are able to easily and quickly compare progress over time.
These methods are able to give a rough guide to the severity of the depression, as well as to assess risk.

History

Questions to ask when taking a history

Mental State
DEAD SWAMP – depression history taking made easy!

Assessing suicidal ideation

Although the predictive power of assessing suicide risk is sometimes controversial (evidence is poor that it is possible to truly predict suicidal risk), it is still important to undertake a suicidal risk assessment.

Ask about:

Management

Basic Principles

The basic principles of management are:

Mild Depression
Advise patient about the diagnosis and explain what it means.
Watchful waiting, psychology / CBT (often long waiting lists to see psychologist on NHS), computerised CBT, self-help, exercise, short psychological interventions (e.g. advise about activity scheduling, structured problem solving, negative though channelling), sleep hygiene.
Moderate and severe depression
All of the above, PLUS:
Medication (see below), psychological interventions, consider getting social support
Treatment-resistant, atypical/psychotic depression, those at risk
All of the above, PLUS:
Medication, complex psychological interventions, combined drug treatment
High risk
All the above, plus consider ECT
 

Psychological interventions

Drug treatments

SSRI’s – 1st line. E.g. fluoxetine, citalopram, sertraline, paroxetine. Side effects include:

If these are unsuccessful you can consider the following types of medication:

Medications are effective 70% of patients – but you need to trial them for at least 4-6 weeks. If this is unsuccessful try another drug in the same class, before trying a drug in a different class.

General effects of drug treatment

  • Increased monoamine levels in the brain
  • Reversed damaged intracellular signalling pathways
  • Reduced CRF production
  • Inhibition of NMDA release
  • BEWARE of serotonin syndrome – which is more likely if more than one drug with serotonerigc effects are given concurrently

Continuation of drug treatments

  • If medication is successful, and remission is achieved, it is recommended to continue medication for at least 12 months
  • If there are subsequent further episodes – continue treatment for 2-3 years when it is restarted
  • Risk factors for relapse include:
    • More than 2 episodes int he last 5 years
    • More than 3 previous episodes in total
    • History of severe or prolonged depression
    • Co-morbid medical problems
    • Life stressors

Summary of drug treatments

Drug
Mechanism
Effect
Tricyclic antidepressants
Block NA and 5-HT re-uptake
↑Mood
MAO inhibitors
Increase stores of NA and 5-HT
↑Mood
Reserpine
Increase NA and 5-HT storage
↑Mood
α Methotyrosie
Inhibits NA synthesis
↓Mood*
Methyldopa
Inhibits NA synthesis
↓Mood*
ECT
Increases CNS responsiveness to 5-HT and NA
↑Mood
Tryptophan
Increases 5-HT synthesis
↑Mood
*used to help calm manic patients
Complimentary medicines
  • The evidence for the effectiveness of any other agents (e.g. St John’s Wort, or other herbal treatments) is lacking
  • However – up to 50% of the general population have taken an alternative medication int he last 12 months
  • Public perception differ substantially from the evidence:
    • 80% of people believe that complimentary therapies are likely to help with depression
    • Only 30% of people believe that antidepressants are effective for depression

ECT – electroconvulsive therapy

Still sometimes controversial, ECT has been proven in several studies to be more effective than antidepressant medication.

Indications include:

Mechanism
It is thought that it induces grand mal type seizures, and that these are necessary for anti-depressant effect. It is also thought that seizures that originate in lower brain areas are less effective than seizures that originate in higher brain areas at reducing depression.
Using a high electrical current increases the therapeutic effect, but increases the risk of memory loss and confusion.
Practicalities
It is given under a short acting general anaesthetic. Patients are also given a muscle relaxant to reduce the risk of injury. Patients are usually starved from at least midnight the night before. They are also given Atropine (anticholinergic) to reduce salivary and bronchial secretions, and to prevent bradycardia.
Before the treatment begins, patients are ventilated with 100% O2. This has been proven to reduce amnesia. Electrodes are placed:
They are moistened to allow good contact with the skin. Almost all patients have bilateral ECT.
Unwanted effects
ECT is relatively safe, but there is a mortality associated with it (1 in 20,000). However, this is extremely low, roughly equal to that of a minor procedure involving a short-acting general anaesthetic (e.g. some dental treatments).
Physical complications
General physiological effects include; increase in BP, massive increase in cerebral bloodflow, altered pulse rate. This means that ECT is contraindicated in patients with previous MI, arryhtmias, aneutysms, previous cerebral haemorrhage and raised ICP.
Although rare, serious physical complications can include:

Psychological side effects

ECT is useful in the short-term, but does not give an indication as to what treatments might be useful in the longer term.
TMS – transcranial magnetic stimulation – this does not provide proven benefit in depression, nor does electrical stimulation of the vagus nerve.
 
Risk
Managing risk is important in depression. The risk to others is usually low, but risk of self-harm is increased. You need to specifically ask about thoughts of self harm and suicide.As well as active self harm, many depressed patients suffer self neglect, secondary to the core symptoms of depression (loss of interest in normal activities). In many cases, this can be managed with carers and home support, but in severe cases, where the patient’s physical well-being is at risk, then inpatient care may be necessary.
 

Prognosis

Prognosis for depression is very good. Most patients will make a good recovery. The greatest risk is usually death from suicide before treatment has had time to take effect.
Outcome and timescales are very varied, but many patients on anti-depressant drugs will be symptom free within just 4-6 weeks. However, treatment should be continued for a minimum of 9 months, otherwise there is an 80% risk of relapse. Even despite this, recurrence is common, especially in those with previous depressive episodes in the last 5 years. Clinicians have to make decisions on an individual basis as to whether or not to continue treatment beyond the 9 month period.
 Factors that point to a good outcome are:

Theories of Pathology Depression

The pathology of depression is not well understood. However, one way of thinking about depression is with the stress vulnerability model. This states that individuals have a genetically defined level at which excessive stress will result in a mood disorder (i.e. depression). Subject any given individual to enough stress, and they will surpass this threshold, and begin to suffer from a mood disorder.

At a cellular level, prolonged “stress” results in neuron cell death via two pathways:

  • Mitochondrial dropout
    • Increased glucocorticoids (i.e. cortisol) in response to stress leads to excessive mitochondrial activity, leading to “burnout” of the mitochondria, and subsequent neuronal death
  • Glional dropout
    • Brain-derived neurotrophin factor (BDNF) is a protein in the brain that protects neurons from damage
    • The neurotransmitter serotonin, noradrenalines, and to a lesser extent dopamine all cause increased synthesis of BDNF
    • In depression, there are reduced levels of BDNF and this leads to neuronal cell death
  • The end result of these factors is decreased brain activity in the prefrontal cortex, and increased activity in the limbic system
  • Microscopically, the brains of those with chronic depression can be seed to have neuronal cell death
  • Macroscopially, on MRI, there may be seen up a 1/3 reduction in side of the hippocampus
  • Therefore – real and significant physical brain changes can be seen in depression – it is not just “all in the mind”
The Monoamine theory
This is widely accepted, although it isn’t without its flaws.
It states that depression results from underactivity of monoamine transmitters, and conversely, that mania results from overactivity of monoamine transmitters. The main transmitter involved is serotonin although it is thought that noradrenaline is also involved.
Evidence for the theory comes from the fact that:
The theory is also generally supported by the medications used to treat the condition, although there are some anomalies. In clinical practice, both noradrenaline and 5-HT treatments are equally effective, although some people will respond better to some types of drugs than others.
It is also worth noting that when patients take medications the level of the NT in the brain is altered very quickly, but the clinical effect takes weeks to appear. This tells us that there is some secondary adaptive changes in the brain which are responsible for the condition, and not just the actual level of NT present. These changes probably involve the downregulation of receptors.
There are also probably altered signalling pathways in response to 5-HT in depressed patients – basically G-coupling may no longer function properly.
Hypothalamic Involvement
Hypothalamic neurons receive 5-HT input, which alters their output (in this case it looks like 5-HT is inhibitory of these neurons). In turn, they release CRH (corticotropic releasing hormone), which controls ACTH, and ultimately, steroid levels. In depressed patients, cortisol levels are often high, because the hypothalamic neurons are not suppressed as much as normal, and just like in Cushing’s, these patients will fail to be suppressed by the dexamethasone suppression test.
Even more interesting is that CRH itself in excess quantities actually causes some of the symptoms of depression – such as anxiety, loss of appetite, reduced activity etc. and CRH levels are also usually raised in depression.
Neuroplasticity and Hypotrophy
In depressed patients, there is often neuron loss in the hippocampus and prefrontal cortex. Also, many of the therapies used to treat depression, and thus ultimately 5-HT itself actually promote neurogenesis.

Depression and pregnancy

Depression around the time of pregnancy (“perinatal depression”) is extremely common, and affects about 10% of women during pregnancy, and 15% of women after birth.

It typically starts in the first few weeks, and peaks at about 12 weeks after birth. Particularly common symptoms are anxiety and agitation, mood swings, and other features typical of depression. In very severe cases, the wellbeing of the baby may be at risk – ask about infanticidal ideation and well as suicidal ideation.

Risk factors

  • Previous perinatal depression
  • Previous mental health problems
  • Social or cultural isolation
  • Abusive relationship (past or present)
  • Family history of mental health disorder
  • Other life stressors as for depression at any time

It is recommend to screen every pregnant women for depression, both before and after birth, using the Edinburgh Postnatal depression scale (EPNDS). Explain the process before jumping in and asking the questions. Those with a high score (10+), typically require more regular further screening. Those with a score of 13+ require urgent psychological or psychiatric referral. SSRIs can be used in pregnancy, but specialist advice should be sought.

Management

Is typically the same as major depression – a combination of basic lifestyle factors, psychological therapies and medication.

Medications most likely used in the perinatal periods include:

  • SSRIs – sertraline, paroxetine
  • Other – amitriptyline, nortriptyline

Postnatal blues  is a milder form of low mood, that typically 80% of new mothers, typically in the first two weeks after giving birth, and lasts <2 weeks.

Typical features include:

  • Feeling down or depressed
  • Mood swings
  • Irritability
  • Feeling emotional
  • Feeling inadequate
  • Tiredness
  • Muscle aches and pains
  • Headaches

Management

  • Reassurance
  • Get as much rest as possible – ovoid over-tiredness
  • Accept help around the house
  • Share the workload of a new baby with your partner
  • If symptoms last >14 days – consider post-natal depression

Depression in children and adolescents

Depression is common in teenagers, and probably under-diagnose in younger childhood age groups. In children, it is more likely to manifest as irritability and loss of interest in usual activities. Suicidal ideation and attempt is rare before adolescence.

Assessing for depression and other mental health disorders in teenagers can be difficult. Try not to be judgemental. An curious, non-intrusive approach is best.

A useful framework for history taking is the HEADS-ED assessment tool:

  • H – Home
    • How does your family get along with each other?
  • E – Educations / employment
    • How are you doing at school?
    • Do you have a lot of school friends?
    • Are you working?
  • A – Activities and peers
    • What do you do in your spare time?
    • How are your relationships with friends?
  • D – Drugs and alcohol
    • Do you drink alcohol?
    • Do you take any drugs?
  • S – Suicidality
    • Do you have any thoughts of wanting to kill yourself?
  • E – Emotions, behaviours and thought disturbance
    • How have you been feeling lately?
  • Discharge plan
    • Do you have any help? Do you want any help? Are you on a waiting list to see somebody (e.g. psychologist) ?

 

Depression in the elderly

Depression in the elderly is extremely common and often underdiagnosed. It is also often confused with, and associated with dementia.

Symptoms of depression in the elderly can be different to other age groups, and it more commonly associated with psychosis. It also commonly causes a change in sleep pattern.

Elderly patients are less likely to respond to medical therapies.

 

Adjustment disorder

Adjustment disorder is a less severe type of depression, with depressed mood which doesn’t meet the DSM-V criteria, and typically occurs in response to a major life stressor – such as losing your job, or death of a close friend or relative. It typically lasts <6 months, and is not a chronic relapsing and remitting disorder – unlike depression. If symptoms do not resolve within the time frame, then the likely true diagnosis is depression

Related Articles

Exit mobile version