Depressive disorders

Psychiatry Lecture / 5th yr

Dr. Sami Adil Al-Badri / Psychiatrist
11th October 2015
MOOD DISORDERS:
DEPRESSIVE DISORDER
(UNIPOLAR DEPRESSION) part 1
Case 1: a 40-year-old woman presented to her GP complaining of feeling tired and “washed-out”منتهية . She has had difficulty getting off to sleep for about 4 weeks, but has felt restless during the day. Straightforward, everyday tasks have become a challenge and sometimes provoke a dry mouth and churning تقلب stomach, but she occasionally feels tearful. The GP is aware that the woman’s mother died 3 months prior to the presentation. The patient describes no thoughts of self-harm.
(discuss: diagnosis and treatment)

Mood disorder is a term applied to a range of condition in which the most prominent symptom is elevation or depression of mood. All of us can be sad or happy for a while. Mood can show extreme manifestations, like other natural biological phenomena such as the level of blood pressure or blood sugar.

The mood, like blood pressure, is regarded disordered and need treatment when it is beyond control, prolonged, causes functional disturbance, and can be treated.

Untreated depression can lead to personal, familial, and social disasters. Living close to a depressed person can be one of the most traumatic experiences threatening infants and young children.

CONCEPT

Before 20th century:
All mental illnesses were considered one condition.
Melancholia (Black Bile): theories with no evidence about depression.
20h century:
Kraepelin--- differentiated two types of insanity, 1. Deteriorating (Dementia Praecox=Schizophrenia) and 2. Periodic (Manic Depressive Insanity).
Freud: psychological explanation of depression (functional disorder). At that time no organic lesions were found in the brain of depressed patients, hence the disorder was said to be functional, i.e. problem in the function, not in the structure.
In the 1960s: Reactive Depression Vs. Endogenous Depression.
Isoniazid (INH) was the first drug to be called as an antidepressant (Reactive and Endogenous types both respond to antidepressants)--- biological explanation of depression.
Pharmaceutical companies, driven by profit rather than by science, exaggerated the benefits of medications (medicalization of loneliness, relationship difficulties, day-to-day stress, etc.) and this led to over-prescription of antidepressants in the world while still those with severe depression (e.g. melancholic) do not receive treatment.
New concepts like PTSD, adjustment disorder, dysthymia are found not responsive to antidepressants like severe (melancholic) or psychotic major depressive disorder.


EPIDEMIOLOGY
Life time prevalence= 5-10% (some studies found it as low as 1% and others as high as 30%). The Iraqi Mental Health Survey (IMHS) found lifetime prevalence of depression in males around 5% and in females around 10%. The prevalence rate of depression is not fixed between studies.
Sex ratio male to female = 1:2
First episode typically in mid-20s but can occur at any age.

ETIOLOGY

There are predisposing, precipitating, and perpetuating factors.
Genetic: Heritability estimates range from 40-70% and families also have high rates of anxiety disorders and neuroticism. Prevalence in first degree is higher than general population, concordance rate is higher in the MZ than in the DZ twins.
Childhood experiences: Loss of a parent, lack of parental care, parental alcoholism / antisocial traits, childhood sexual abuse.
Personality traits: Neuroticism / anxiety, impulsivity, obsessionality.
Social circumstances:
Marital status: low rates associated with marriage, high rates with separation or divorce.
It was found that, for women, having 3 or more children under the age of 11, lack of paid employment, and lack of a confiding relationship were associated with increased risk of depression (recent studies support the lack of a confiding relationship, but not the other factors).
Adverse life events: particularly “loss” events (increased risk 2-3 months after event) in vulnerable individuals.
Physical illness: Especially if chronic, severe, or painful. Neurological disorders (e.g. Parkinson's disease, MS, stroke, epilepsy) have higher risk (perhaps due to “shared” pathology). Higher rates also noted in post-MI, diabetic, and cancer patients, although family or personal history of depression are important determinants of occurrence.

Monoamine theory: depression is caused by decrease concentration of monoamines (i.e. Serotonin, Noradrenalin, and Dopamine) in the brain. The theory is supported by the mechanism of action of antidepressant drugs, and by the finding of low 5-HIAA (a metabolite of serotonin) in CSF.
Disturbance in neuroendocrine function: high CSF levels of CRF (Corticotropin-Releasing Factor).
Other findings and theories: e.g. Changes in sleep pattern Reduced total SWS and shortened REM latency (secondary to increased cholinergic and/or reduced serotonergic/ noradrenergic drive. hypoperfusion in some parts of the brain in some of the cases, and many psychological theories (one of the most important psychological theories is the cognitive theory which stresses on the thinking errors on which is based a type of therapy called: Cognitive Behavioral Therapy CBT).
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Diagnostic Criteria
DSM-IV criteria of Major Depressive Disorder:
Four of these eight with depressed mood or anhedonia for 2 weeks= major depressive disorder
Mnemonic: SIGECAPS: 1. Sleep changes (typically decrease), 2. Interest (Anhedonia=no interest), 3. Guilt, 4. Energy (decrease), 5. Concentration (decrease), 6. Appetite and weight changes (typically decrease), 7. Psychomotor changes (retardation or agitation), and 8. Suicidal ideation and/or attempts.

N.B. in every diagnostic criteria in psychiatry add these two points at the end: (i) not caused by the direct physiological effect of a substance (e.g. drug or alcohol) or a general medical condition; (ii) causes significant distress or impairment of function.-------------------------------------------------------------------------------------------------------
Subtypes (there are different classifications but can be summarized as follows):
Non-melancholic or called "without somatic symptoms". Essentially, defined as absence of psychotic or marked somatic symptoms. Previously known as neurotic depression or reactive depression. Life events appear to be provoking factors, but only in those with a predisposition to depression, and treatment should focus on the underlying disorder as well as managing any significant provoking factors. Onset at any age.
Major Depressive Disorder (MDD) with melancholic features, or called "with somatic symptoms". There are somatic symptoms: early morning wakening, diurnal variation of mood, significant weight loss, reduced libido, amenorrhoea, constipation and psychomotor retardation. The presence of somatic symptoms defines what is regarded as a more "biological" or "endogenous" depressive episode, which is more severe (and more responsive to antidepressant treatment). Starts in 5th decade or later. Usually there is no precipitating stress.
Dysthymia : Less severe, but more chronic than depression (2-20yrs, median 5yrs). Also called Neurotic Depression. Starts in 2nd and 3rd decade. Poor response to medication.
MDD with catatonic features: there is marked psychomotor disturbance which can manifest as one or few of the following: (immobility, mutism, peculiar movements, excessive movements, echolalia or echopraxia). This subtype is especially responsive to ECT and benzodiazepine (especially lorazepam).
MDD with psychotic symptoms (mood congruent) (Delusions: e.g. nihilisticعدميّة , hallucinations: e.g. derogatory إزدرائيّة auditory or olfactory of bad smell, and catatonia)
Postnatal depression
Premenstrual dysphoric disorder
MDD with atypical features (Atypical depression): Hypersomnia, hyperphagia. Best treatment: phenelzine.
Seasonal affective disorder (SAD): also called "winter depression". Treatment: Light therapy (drugs also effective).
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Clinical Features

Patients may describe their mood as depressed, sad, or irritable. Anhedonia indicates an inability to take pleasure in formerly pleasurable activities, associated with lack of interest. In addition to other symptoms such as loss of energy and fatigue, difficulty in concentration which appears when the patient cannot read of follow a conversation or count money, sometimes so severe that it resembles dementia and called pseudodementia. Appetite and weight are often lost; however at times these may increase. Loss of appetite is sometimes so severe to a degree that threatens life and hospital admission is indicated as an emergency. Sleep is often lost, and insomnia may be initial (trouble falling asleep), middle (awakening in the middle of the night and having trouble getting back to sleep), or terminal (awakening early and being unable to get back to sleep); in a minority, patients may become hypersomnic and experience an increased need for sleep, sometimes sleeping 12 or 16 h a day. Psychomotor change: either agitation or retardation (psychomotor retardation= slow movements). Suicide: may be a death wish (I wish that I die(, or may put a plan to kill the self (e.g. buying a poison and hiding it and preparing for the death by paying the debts and making apologies in advance, and maybe writing a letter), suicidal attempt means a genuine trial to end the life (to be differentiated by attention seeking behavior by history, for example in the genuine suicidal attempt the patient take caution not to be saved (e.g. waiting everybody to go out from the home, and lock the door on the self) and the method used is believed to be highly fatal by the patient (e.g. taking 3 sheets or more of a medication). Psychotic symptoms occur in some patients but they are mood-congruent. Bizzare delusions do not occur. Occasionally, the depressive episode will evolve into a catatonic stupor.


In mental retardation and in elderly with dementia depression presents with the somatic symptoms and here it is not melancholic but is called “masked depression.”

Transcultural factors: while somatic features are found in all societies, they are more frequent & prominent in non-western cultures. However, it is necessary to distinguish between somatization and somatic metaphors مجاز for an emotional state e.g. Iraqis tend to use expressions such as “hemmed in حصرة”, or “pressure in the chest” to express emotional suffering.

In MSE (mental status examination):

Appearance: downturned eyes, sagging corners of the mouth, vertical furrows between the eyebrows, poor eye contact, weight loss (sagging clothes), dehydration, unkempt, poor personal hygiene.
Behavior: psychomotor retardation typically occurs.
Speech: slow, long delay before answering questions.
Mood: low and sad, hopeless, future seems bleak. Sometimes anhedonia. Anxiety and irritability can occur.
Thought form: normal.
Thought speed: slow.
Thought content: pessimistic thoughts, suicidal &/or homicidal thoughts. Sometimes in psychotic depression there are mood congruent delusions like delusion of poverty, delusion of illness.
Perception: mood congruent auditory hallucinations e.g. “you should die.”
Cognition: poor attention, concentration, and memory (psydodementia).
Co-morbidity
There is increased risk of anxiety disorders and substance abuse.

Differential diagnosis

Other psychiatric disorders: Stress-related disorders (adjustment disorders/bereavement, PTSD), bipolar disorder.
Neurological disorders: Dementia, Parkinson's disease, Others.
Endocrine disorders: hypothyroidism, others.
Metabolic disorders: hypercalcaemia, porphyria.
Haematological disorders: Anaemia.
Inflammatory conditions: SLE.
Infections: Syphilis, Lyme disease, and HIV encephalopathy.
Sleep disorders: especially sleep apnoea.
Medication-related e.g. antihypertensives (beta-blockers, methyldopa); steroids; interferon, and psychiatric medication (esp. antipsychotics)
Substance misuse, e.g. alcohol, benzodiazepines, opiates, marijuana.
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Answer to Case 1:
Dx. Preferred diagnosis: mild depressive episode. Alternative dx.: adjustment disorder/ bereavement, generalized anxiety disorder, physical problem (hypothyroidism, anemia, diabetes), and drug or alcohol misuse.
Treatment: no indication for admission. No role of antidepressants. Short-term course of hypnotics may help. Reassurance, supportive and educative psychotherapy.
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REFERENCES
Bazzoui, W. (1970) Affective Disorders in Iraq. Brit. J. Psych., 117, 195-203
Clark, T., Day, E., & Fergusson, E. C. (2005) Core Clinical Cases in Psychiatry. Hodder Arnold
Gelder, M., Harrison, P., Cowen, P. (2006) Shorter Oxford Textbook of Psychiatry. 5th Ed. Oxford University Press.
Iraqi Mental Health Survey (IMHS) done by the Ministry of Health in collaboration with the World Health Organization (WHO) in 2006-2007
Jacob, K. S. (2009) Major Depression: Revisiting the Concept and Diagnosis. Advances in Psychiatric Treatment. Vol. 15 279-285
Moore, D. P. (2006) The Little Black Book of Psychiatry. 3rd Ed. Jones and Bartlett Publishers.
Sadock, B. J., Sadock, V. A., (2014) Synopsis of Psychiatry. 11th Ed. Lippincott William & Wilkins