When Should Professional Help Be Sought
Don’t let a mood disorder hold you back from following your dreams and living a happy and fulfilled life. Taking the first step and asking for help, although very worrying and daunting at first, is a very small step to take in comparison to letting the years of your life pass by – going through the motions of living, but not really enjoying life to the full.
Many people often delay seeking professional help due to uncertainty about what is happening, what might be achieved and at what cost.
It is important to take action before the mood disorder impairs every day functioning. The earlier help is sought, the better the chances of a successful recovery.
Would you delay seeking help if you had a melanoma?
An untreated mood disorder can become much worse and potentially life threatening.
Depression Impacts Many Australians
Many people will go through times of clinical depression during their life.
Depression is certainly no cause for shame; however unfortunately, clinical depression is so often under-diagnosed and untreated. Sometimes, doctors or health professional do not recognise depression for what it is. Also, people can feel a sense of fear of disgrace if they come forward and admit that they are suffering or alternatively do not recognise their own depression.
Depression can start physically with feelings of aches and pains (indirectly) or commence with a conviction that “this is the way the world is”. Just as diabetes and migraines tend to run in families so too does depression although for many, there is no family history.
Depression can be minor or transient and not require intervention, however when it is more intrusive and persistent, professional assistance should be sought from a psychiatrist.
It is important to diagnose the depressive illness correctly so that the most appropriate treatment/s (whether biological or psychological) can be implemented to ensure recovery and long term remission.
In a small percentage of cases, depression can become persistent or treatment resistant. The Lawson Clinic psychiatrists address treatment resistant depression based on the research of the Black Dog Institute which suggests four principal causes of persistent and treatment-resistant mood disorders:
- Under-treatment of the more biological conditions such as melancholic depression;
- Excessive physical treatments (medication) for those with the less biological (e.g. non-melancholic) depressive disorders;
- Failure to identify bipolar disorder, in particular bipolar II;
- Failure to identify an underlying contributory condition (whether medical or another psychiatric condition such as an anxiety or personality disorder).
It is important to recognise that depression can be biological in its origin, but psychological in its experience. Those suffering from depression may have to push themselves or be encouraged by someone else to seek advice or treatment. They may feel that nothing much can be done about the way they feel but, in fact, even the most acute depressions can be successfully treated.
Oversimplifying Depression – A Diagnosis is Only Half The Answer
In trying to inform the Australian community about the prevalence of depression, definitions of depression have been progressively redefined and oversimplified in communications to patients and the public.
The Black Dog Institute and The Lawson Clinic are of the perspective that the world wide view of depression as a ‘single disease’ (rather than a set of conditions), varying only in severity, not being related to an individual’s personality and brought about by chemical changes in the brain, thus requiring antidepressant medication – with all antidepressant drugs being equally effective – is fundamentally flawed. So too we suggest is the view that the numerous psychotherapies can assist all expressions of depression and are of comparable effectiveness to antidepressant medication.
But, by lumping multiple potentially different depressive disorders under one ‘single disease’, by not respecting multiple causes triggering a person to become unwell (whether genetic, psychological or environmental) and by testing treatments as if they have universal rather than specific application, we have a non-specific model of depression and an “All roads lead to Rome’ therapeutic paradigm. Such a model is like viewing all cancers as the same and applying any one of multiple treatments to them, whereas we know that there are many types of cancer (some benign, some malignant), all triggered by different factors, some environmental, some genetic. We also know that there are many different treatments for cancer, each specific to the type of cancer diagnosed.
Research at the world famous Black Dog Institute in Sydney – has challenged many of the current assumptions about depression. The Institute and The Lawson Clinic do not view depression as a ‘single disease’ but suggest that there are different types of depression that can represent diseases, disorders or reactions. For some depressive diseases, chemical changes in the brain may be the primary cause, with the depression occurring independently of personality and temperament; for other depressive disorders, the individual’s personality style may be all-important.
We also argue against the view that each of the available antidepressant drugs are equally effective and suggest that the most effective therapies are not the same for each principal depressive type, with some expressions of depression most likely to respond to antidepressant medication and others quite unlikely to respond. Similarly, we suggest that the usefulness of some of the psychotherapies (such as cognitive behavioural therapy) is not equivalent across the depressive types.
A diagnosis of depression, therefore, is only half the answer. The first question should be ‘What type?’ Once the specific ‘type’ of depression has been identified, patients (and their families) can be better informed about the specific cause of the depression and the treatments for it. Patients are thus offered a much better chance of managing, or beating, their depression.
The Biology Of Depression
While our knowledge of the working brain is still limited, in most instances of clinical depression it is likely that neurotransmitter function is disrupted. Another term for neurotransmission is ‘nerve conduction’ – but what does this mean?
The human brain is extremely sophisticated; indeed it is far more complicated and versatile than even the most powerful modern computer. It contains in excess of 100 billion brain cells, known as neurons, each of which is connected to many other neurons. If you look at them under a microscope, neurons appear as thin wires connecting little blobs of brain tissue. However, even with strong magnification the neurone-to-neurone connections, known as synapses, are not apparent. Synapses can be electrical but the majority are chemical. A signal from one part of the brain travels to another – as a series of electrical impulses – along neurons.
When two neurons meet, the signal is carried across the synapse by the release of a tiny balloon-like packet of ‘neurotransmitter’, in which a message-carrying chemical is carefully packaged. Once released into the synapse this balloon immediately ruptures, releasing its chemical contents, which are then free to quickly migrate across the synapse and attach themselves to unique docking stations called receptors. Receptors are like light switches waiting to be switched on or off. When an appropriate chemical successfully docks with a receptor, the switch is thrown and this initiates a complex series of reactions in the next neurone that culminates in the reproduction of the original signal. In this manner, information is passed from one neurone to another and, in healthy brain function, the signal remains as strong in the second and subsequent neurons as it was in the first.
There are many different neurotransmitters in the brain, of which 100 or so have been identified. Each neurotransmitter serves a variety of purposes. Mood regulation involves many neurotransmitters, including some brain hormones such as cortisol. However, there are three neurotransmitters that are particularly important in relation to depression and bipolar disorder.
The first of these, serotonin, is the most well known and often talked about. It is found in the blood, gut and almost all parts of the brain. Serotonin neurons have their “home” in the base of the brain, and their connections travel upwards to other parts of the brain including the hypothalamus (the hormone centre of the brain), the hippocampus (the memory centre of the brain) and the amygdala (a region thought to be involved strongly in emotions such as fear and anger). Neurons containing serotonin make lots of connections and therefore serotonin is involved in regulating blood pressure, temperature, sleep, appetite, sexual behaviour, pain, learning and, last but not least, mood. To serve these many functions there are several kinds of serotonin receptors into which serotonin ‘docks’, allowing the same signal to have different meanings depending on which kind of receptor a neurone possesses.
The second neurotransmitter important to mood regulation is noradrenaline. Its home is also in the base of the brain and, like serotonin connections, noradrenaline neurones extend to virtually all areas of the brain. Noradrenaline is, however, better known for its role in the ‘fight or flight’ response; it puts the brain and body on high alert in the face of imminent danger so that the individual prepares to either fend off any threat or escape it altogether. Noradrenaline therefore regulates arousal, the cardiovascular system and primes the brain to alarm signals in the environment. Interestingly, in addition to acting as a neurotransmitter, noradrenaline also regulates other neurotransmitters, in particular serotonin, and as such is thought to play an important role in regulating mood both directly and indirectly.
The third neurotransmitter of particular relevance to mood is dopamine. Dopamine is closely related to noradrenaline in that one chemical reaction converts dopamine into noradrenaline, and much of the noradrenaline in the brain is made in this way. However, unlike noradrenaline and serotonin neurones, dopamine neurones are found in several locations in the brain and, although the connections are still quite widespread, they are much less diffuse. Like noradrenaline and serotonin, dopamine has many types of receptors and is involved in a range of processes such as reward, emotion and movement. Indeed, it is most well known for its role in Parkinson’s disease, in which a lack of dopamine in a specific part of the brain eventually leads to disordered movement. It is interesting to note, then, that many patients with Parkinson’s disease also develop depression. Furthermore, depression in Parkinson’s disease often occurs before any movement changes become apparent, suggesting that dopamine is equally and perhaps independently critical in the development of depression.
It has been known for more than half a century that these three principal neurotransmitters play a role in regulating mood, a fact that has been convincingly demonstrated time and time again by experiments in animals and the successful use of antidepressants in humans. However, bringing together our knowledge of the brain’s chemistry and our understanding of clinical depression has largely failed to respect their differential impact on key depressive subtypes.
In general, and especially over the last decade, all types of depression have been equated to a lack of serotonin or disruption in its neurotransmission. This is reflected in the development of antidepressants (selective serotonin reuptake inhibitors or SSRIs) that act selectively on serotonin alone. By comparison, noradrenaline and dopamine have attracted much less attention, partly because they are judged to have greater contributions to anxiety and psychosis respectively.
Consequently, antidepressants having specific noradrenaline or dopamine actions are far fewer and have only recently been developed and made available. The ‘serotonin model of depression’ has been useful in that many of the antidepressants it has spawned are much better tolerated and so many more people have been treated. However, such a model is limited in terms of understanding and managing the varying types of clinical depression.
An alternative view, developed at the Black Dog Institute, is illustrated below, and suggests that there is a broad association between the three principal subtypes of clinical depression and the three neurotransmitters described above.
In this model, we suggest that all three neurotransmitters contribute to each subtype of clinical depression, rather than one only. However, we also suggest that their proportional influence varies, such that dysfunction in one neurotransmitter clearly underpins the illness pattern in each subtype and so shapes the differing depressive symptoms and clinical pictures.
There are major implications for treatment.
In non-melancholic depression, we suggest that the admixture of anxiety and depressive symptoms is largely the consequence of altered serotonin neurotransmission. This can be seen as the first line of chemical adjustment that takes place in a person, in terms of their mood, when clinically depressed. There may, in some instances, be evidence of additional noradrenaline and dopamine-related symptoms but, even then, these are often submerged within serotonin-driven abnormalities. Classic symptoms include changes in sleep, appetite and libido along with symptoms and signs of anxiety.
In melancholic depression there are additionally clear psychomotor changes (or PMD as described earlier). Patients have difficulty initiating thoughts and movements which, if executed, are slowed. Pleasurable experiences are limited, and attention and concentration are often severely compromised. These symptoms are derived largely from noradrenaline neurotransmission disruption, although dopamine abnormalities also contribute significantly. Serotonin-driven symptoms may also be present but do not determine the clinical picture.
In psychotic melancholia, the presence of delusions and hallucinations along with marked melancholic symptoms signify the primary role of dopamine neurotransmission dysfunction. Serotonin and particularly noradrenaline still contribute, but the clinical picture predominantly reflects a dopaminergic contribution.
This model is, of course, limited in only touching on the chemistry and chemical treatment of depression. However, it is useful as it provides a model for the specific neurotransmitters, linking them to each other and to the key clinical subtypes.
The Influence of Personality Style
Our clinical observation and research has identified eight different personality styles that are relevant to either predisposing, precipitating and / or perpetuating a depressive episode. Having one or more of these personality styles can make an individual more susceptible to the impact of certain stressors.
Anxious worrying & depression – this person has an internalizing style and tends to be highly strung , tense, nervy and prone to stewing over things.
Irritability & depression – this person also has high levels of trait anxiety, but they externalize their anxiety by being irritable, crabby, and easily rattled under stress.
Self-criticism & depression – this person has a ‘self critical’ personality style and tends to have low self esteem, often reflecting a lack of parental care or even abuse in childhood, or other deprivational experiences in their early years.
Sensitivity to rejection & depression – this person tends to be hypersensitive to the nuances in inter-personal relationships, and is inclined to magnify minor criticism or misinterpret others as being critical, and thus readily feels rejected and abandoned.
Self-focused & depression – this person tends to lack consideration and empathy for others, is often hostile and volatile in interacting with other people, and has a low threshold for frustration.
Perfectionism & depression – this person will tend to externalize their self image, judging their success from meeting very high standards, and if they think that they have failed to meet such high standards, or if somebody criticizes their performance, they feel demeaned and crushed.
Socially avoidant & depression – this person tends to be shy and will avoid social situations for fear of their imagined limitations being exposed, like saying something stupid, or blushing and thereby risking ridicule.
Personal reserve & depression – this person tends to be wary of others getting too close and feels vulnerable and depressed when their inner world is exposed to others.
These personality styles are not pure types; most people who develop a personality driven non-melancholic depression will have some combinations of such styles.
Being Diagnosed With Bipolar Disorder
The getting of wisdom in bipolar disorder establishes itself over time, largely through learning from past experiences with the illness, as strategies for identifying warning signs of a relapse emerge with growing self-knowledge.
In many cases, the management of bipolar disorder becomes easier over time as the individual and their support network learn more about the particular vulnerabilities.
An accurate diagnosis may become the turning point in an individual’s life, ultimately changing them from ‘victim t’ to ‘victor’.
One Australian study (Access Economics, 2003, p. 6) found that the average time between the onset of the first symptoms of bipolar disorder and its accurate identification was more than ten years. This time-lag builds, in effect, to a cumulative mass of hardship. Diagnosis is the first step in helping the individual and others to identify symptoms and begin to learn about the disorder.
If the illness is familial, there is some precedent for further illness within that particular family, but if it is isolated within an individual, the learning experience becomes rather more ambiguous for those involved.
I am the ‘bipolar black sheep’ of my family, so our learning curve has been quite steep, and we were initially unprepared for the trials which the illness presented to us. But I am increasingly hopeful about my future given that I have now received a diagnosis, and have found a good team of mental health workers to help me understand and manage the illness.
Acting On Early Warning Signs
Pre-emptive strategies for walking the fine line to avoid bipolar mood swings include protecting the sleep-wake cycle (as sleep disruption is both a contributor to and a consequence of bipolar mood swings) and imposing steady routines. Also keeping a mood chart can help identify the build-up of a mood swing.
Triggers that can put a person at risk of an episode include: skipping medication, stress and frustration at home and work, life changes and taking drugs and alcohol – or other stimulants such as cough suppressants or too much coffee. Late nights or changes to circadian (body clock) rhythms can also be a stress. In this regard, the onset of spring is a trigger for many, as is changing work shifts or overseas travel.
Individualised ‘relapse signatures’ can be collated from each episode to help the person with bipolar disorder and others involved in their care to recognise the triggers and early warning signs of an impending high (or low). Many signatures are well-recognised: sleep changes, irritability, flighty or obsessive ideas, mysticism and profound and synchronic ideas, changed eating habits, being intrusive or paranoid, multi-tasking (in talk and at work), increased libido, driving faster and spending more.
Other early warning signs … include feeling a quiver or glow or flame, hand and body tremors, cleaning during the night, excessive washing, increased heart rate, generalised itch, increased metabolism and more frequent bowel movements.
If a person with bipolar disorder is faced with unavoidable life and work changes, then strategies for normalising sleep as well as self-calming techniques such as medication and exercised are often useful remedies.
Depression Case Studies
These case studies consider the role of biological, social and other factors in depression.
Gillian had been a shy and somewhat quiet child. She was 22 when she first saw a psychiatrist at her mother’s insistence, but had experienced depression since the onset of adolescence. After being retrenched from her job as a research assistant she became increasingly withdrawn. She was worried, anxious and afraid to go out of her house. She would cry often and retreat to her room and stay in bed, asking her family to tell anyone who phoned that she was not at home.
It was clear to Gillian’s family that something was upsetting her, but she just kept to herself and would not let on. Her family would sometimes find her crying. Gillian was usually very reliable, however she started letting responsibilities lapse, and felt guilty at the same time for letting her family down.
Sensitive to criticism, she informed her doctors that she avoided relationships. Her first boyfriend just dumped her and she felt that her life was not worth living. She used to worry about things a fair bit but now she was worrying all the time.
Kate’s husband Anthony brought her into hospital. He told the doctors that Kate during the last few weeks was behaving like she had been after the birth of their first son 10 years earlier. Although the baby was eagerly anticipated, after the birth Kate became deeply depressed and was not able to look after her son. Kate had experienced several episodes of depression since that time, but those episodes had lifted without the need to take antidepressant medication.
Anthony first thought that Kate’s constant tears and withdrawal was caused by menopause. She said that she had no energy and, even though she was tired, she could not sleep through the night. She was lethargic, moved slowly and hardly spoke. Formerly an excellent hostess, she had stopped contacting friends, and lost both her interest in cooking and her appetite.
One night, Anthony found Kate with a bottle of tablets and, although she assured him that she wouldn’t harm herself, she confessed that she had been thinking of suicide.
Peter was a true extrovert requiring a lot of stimulation and moved from one interest to another. He was the life of the party, eager to meet people and warmed quickly to new friendships. He had been in several relationships but was a bit indecisive. He would fall intensively in love, but then find his partner monotonous after a while.
He took many ‘sickies’ and as a result lost his job and became depressed. He started to take his frustrations out on his girlfriend, snapping at her constantly. He also got into arguments with his family and friends.
He explained to his GP that he had become very irritable and felt that he couldn’t control his feelings. He had recently smashed a window to ‘let off some steam’. It had made him feel somewhat better, temporarily.
Trevor, a 69 year old widower, was admitted to a hospital after a concerned neighbour and his GP had found him unkempt and very agitated.
In hospital he stated that his insides had rotted away and refused to eat. Preoccupied and distressed by this delusion, he was unable to be reassured by the staff. He paced constantly, wringing his hands and saying over and over ‘What will become of me?’
He told staff that he was being punished for his failures and indiscretions. His guilt was out of proportion to the incidents he then described: for instance, he felt he deserved to go to jail for failing to include a minor payment on his tax return twenty years ago.
When the doctors spoke to a relative, it came out that Trevor had been like this before, once soon after he had returned from the war, and twice in the last few years. One episode came on after Trevor thought he had sped through a police radar. He was convinced that this incident had caused his depression. A cousin had been hospitalised for a similar setback.
In the absence of specific markers for melancholic and psychotic depression, both Gillian and Peter are more likely to have a non-melancholic depression. Gillian’s symptoms are indicative of an internalising anxious worrying personality style, while Peter’s are of an externalising irritable and self-focused personality style. Both styles contribute to the onset and persistence of the depression following particular stressors.
Kate’s and Trevor’s depressions appear more biologically based, with evidence of psychomotor disturbance (retardation and agitation respectively). Trevor is also experiencing psychotic episodes. Kate is likely to have melancholic depression and Trevor, with his delusions, a psychotic melancholia. Their depressions appear unrelated to personality style – the biological stressors are hormonal in Kate’s case and genetic in Trevor’s.
Diagnostic sub-typing is assisted by considering type-specific clinical features such as psychomotor disturbance and evidence of psychosis, and further helped by other clues presented in the vignettes. Treatment recommendations would be expected to differ for each one.
Psychiatrists vs Psychologists: what is the difference?
Psychiatrists are medical doctors who have completed at least 12-13 years of study to obtain Fellowship to the Royal Australian and New Zealand College of Psychiatrists.
It is firstly necessary to undertake 6 years of university study which includes basic psychiatric training. Once their tertiary medical qualifications are obtained, they then work as an intern for an additional 12 months in a general hospital so as to obtain registration as a medical practitioner. This is followed by another 12 months as Resident Medical Officers.
Upon completing this term, a doctor may undertake specialist training as a psychiatrist. Training in this regard is conducted by the Royal Australian and New Zealand College of Psychiatrists. A panel of psychiatrists for the Psychiatric Training Program interviews a doctor wishing to become a psychiatrist and extensive references regarding their work performance and suitability are taken into consideration.
The training program for post-graduate training in psychiatry takes a minimum of 5 years, during which time doctors work under supervision in community clinics and private/public hospitals with adults, families, children, adolescents, and the elderly on a full range of psychiatric problems. Trainees in psychiatry are supervised by experienced, qualified psychiatrists and undergo rigorous examinations throughout their training during which their experience and competence are tested.
Doctors can only be elected Fellows of The Royal Australian and New Zealand College of Psychiatrists if they have successfully completed these strict training and examination requirements.
Psychiatrists are trained both to recognise and treat the effects of emotional disturbances on the body as a whole, as well as the effects of physical conditions on the mind. Psychiatrists may prescribe medications and use a variety of psychological techniques to improve the wellbeing of their patients.
Clinical psychologists are specialists in the assessment, diagnosis and treatment of psychological and mental health problems. Clinical psychologists have usually completed a minimum of 6 years full-time university training. This includes postgraduate study in a recognised clinical psychology training program, a substantial research thesis, and supervised practice in health and mental health settings. Clinical psychologists follow strict guidelines for professional conduct that cover client privacy and confidentiality. Various psychological techniques such as CBT, interpersonal therapy, psychotherapy, mindfulness and counselling are applied by clinical psychologists to assist patients who are impacted by a mental health concern. Clinical psychologists do not prescribe medication such as antidepressants.