Steps of Clinical Assessment of Depression

Steps of Clinical Assessment  

Step 1: Listen to the patient carefully, establish rapport, and develop a therapeutic alliance.

Step 2: Confirm the diagnosis by identifying the full spectrum of signs and symptoms of depression and anxiety, and confirm a lack of a history of mania. Also exclude organicity especially hyper/hypothyroidism, Cushing disease, brain tumors, and any other physical conditions that can induce or mimic the symptoms of depression. A detailed medical history, physical examination, and relevant laboratory investigations (TFTs,  Cortisol, DST, brain imaging, ECG, etc.) Should be obtained for this purpose. Exclude (depression/anxiety as) the impact of medications (e.g. propranolol), substances of abuse, and alcohol.  

Step 3: Assess the severity clinically and to monitor, with a standard scale, (HAMD/HAM-A, BDI/BAI, etc). Severity also influences the choice of treatment.

Step 4: Assess the impact of the condition on the patient and family, including personal distress, work difficulties, social life, financial matters, etc. A needs assessment scale and global functioning scale may also help. 

Step 5: Assess the risk of suicide, deliberate self-harm, self-neglect, and harm to others. 

Step 6: Assess for etiological factors, confirm the absence of genetic predisposition, and identify any long-term difficulties, recent stressful circumstances, cognitive distortions and dysfunctional beliefs, socioeconomic status, social support, substance abuse, personality factors e.g. sociotropy and neuroticism, borderline personality disorder, dysthymic personality, etc. 

Step 7: For long-term management and patient education, a prognostic assessment is also mandatory. Apart from the short course, and lack of bipolarity, other prognostic factors will be revealed as the assessments above are carried out, e.g. comorbid substance use and personality disorder, social support, etc.  

Step 8: Finally Assess for medical comorbidities, especially atrial fibrillation, other cardiac conditions, hypo/hyperthyroidism, hypertension,  metabolic syndrome (influences drug choice and management) in liaison with a physician.  

Step 9: Determine whether the patient needs admission, based on severity, social support, risks, and patient preference 

Classification of Depression According to the International Classification Diseases, Tenth Revision (ICD-10)

Waleed Ahmad

The ICD-10 has comprehensively sub-classified into various categories based on the clinical profile of symptoms and the course of symptoms. 

Based on the course, it may be a depressive episode, recurrent (major) depressive disorder, persistent depressive disorder or dysthymia, recurrent brief depression, etc. Depression may also be either unipolar or bipolar or it may occur in  

1. A first depressive episode, duration of at least15 days, is classified as a depressive episode (F32). If the first depressive episode severe and rapid onset, duration less than 15 days still depressive episode (F32).  
2. A depressive episode can be
1. mild (2 core symptoms, 2 other symptoms from the list) (32.0)
2. moderate (2 core symptoms, 3 or preferably 4 other symptoms) (32.1)
3. Severe (3 core symptoms, 4 other symptoms) without psychotic symptoms (32.2) (no delusion, hallucination or stupor)
4. Severe with psychotic symptoms (above plus either delusions, hallucinations or stupor) (F32.3)
5. Delusions can be mood-congruent or incongruent (neutral delusions e.g. delusions of reference are considered mood incongruent. None of them counts towards schizoaffective disorder unless one of the first-rank) 
6. A mild and moderate depressive episode can be 
1. with somatic syndrome (four or more somatic symptoms, or three very severe somatic symptoms)
2. without somatic syndrome (three or less somatic symptoms, not severe) 
7. A severe depressive episode always has a somatic syndrome 
8. Psychotic symptoms occur only in severe depression 
9. An episode of melancholic depression and agitated depression is coded under the severe depressive episode 
10. A single episode with atypical features→Other depressive episodes (F32.8)
11. An episode of masked depression NOS also coded under Other depressive episodes (F32.8) 
12. If depressive symptoms fluctuate/alternate with non-depressive symptoms e.g. worry, tension, distress also coded under F32.8
13. The second episode of depression changes the diagnostic category to recurrent depressive disorder (F33) 
14. A long history of typical depressive episodes, current episode hypomanic, the category remains recurrent depressive disorder (F33) 
15. Few brief hypomanic episodes but most of the episodes were depressive, the category remains the same
16. A long history of depressive episodes, current episode manic, category changes to bipolar 
17. A patient develops an episode that persists for long, fulfils criteria of depression, →persistent depression (F33.8 other recurrent mood disorders) 
18. An episode of subthreshold depressive symptoms persists for two years→dysthymia 
19. An episode of mild or moderate depression, followed by a two-year history of subthreshold depressive symptoms →dysthymia 
20. An episode of subthreshold depressive symptoms, current episode mild/moderate depression, → NOT dysthymia. Call it double depression? recurrent depressive disorder (? not clarified) current episode mild/moderate depression
21. Seasonal affective disorder coded under F33 (current mild or moderate episode only i.e. Cannot be severe) 
22. A patient has monthly episodes of depression that last less than two weeks, usually 2-3 days. Symptomatic criteria for d episode only depressive episodes can be fulfilled →recurrent be monthly episodes if depressive disorder F38.10
23. A patient has symptoms of both mania and depression which are equally prominent and fulfil criteria for depression and mania or hypomania by the number and severity of symptoms, last for two weeks→mixed affective episode 
24. A patient has symptoms of both mania and depression which alternate within hours, and fulfil criteria for depression as well as mania or hypomania by the number and severity of symptoms, the episode lasts for two weeks→mixed affective episode

Is alertness always normal in dementia?

Impaired alertness is generally a feature of delirium. In one form of dementia, however, 'fluctuating alertness' is a striking feature.

Can you name it?

Lewy body dementia

The Safest NSAID for a patient on lithium

What is the most suitable non-steroidal anti-inflammatory drug (NSAID) you can prescribe to a patient who is on Lithium therapy?

>> Aspirin or Sulindac. 

Visual perception

Can you answer any one or two of these right?

1. In visual perception, the recurrence or prolongation of a visual phenomenon beyond the customary limits of the appearance of the real event in the world is termed ___________

2. The size of the perception can be either larger '________' or smaller ' ___________' than expected.

3. In some cases, there can be apparent reduction in one hemifield of vision '_____________'

4. These anomalies are common in ______________.

5. Alteration in the customary shape of the perceived object is termed __________ .

6. ‘One woman saw people upside down, on their heads’ (Bleuler, 1950). This is an example of ___________

7. When metamorphopsia affects faces, it is referred to as __________.

8. , ____________, is the complete absence of colour

9. ______________ refers to the perversion of colour perception

10. . ___________ involves the object appearing far away,

11. __________ is the term used when the object is appearing nearer than it should.

12. ____________ is the term for when the perceived object is in a different position from what is expected, so that the patient, for example, experiences the transposition of objects from left to right.

13. __________ is the impairment of visual perception of motion in which the individual is unable to perceive the motion of objects.

’

Immunity in depression

What happens to cellular immune responses in depression?

exaggerated

reduced

Neuropathology of Alzheimer's Disease

Neuropathology of Alzheimer's Disease

Gross Brain Changes

The following are the gross changes in the brains of the people with Alzheimer’s disease:

1. Reduced weight of the brain
2. Reduced cortical volume
3. Dilated ventricles
4. Deepening of sulci

Magnetic Resonance Imaging

On magnetic resonance imaging, the diagnostically most important finding is atrophy, especially of the medial temporal lobe. It affects the entorhinal cortex the earliest but then it spreads to other regions of the temporal lobe and limbic lobe for example hippocampus, amygdala, and parahippocampus. Later, the pathology extends to parietal lobe and eventually global atrophy. It spares frontal lobes until the late stage. The progression of atrophy occurs in a similar pattern as the progression of the neuropathology.

Dilated ventricles can show global atrophy, but the most reliable method is a direct measurement of volume. Expansion of the fissures is the indirect, and less reliable way to measure the atrophy. For Alzheimer’s disease, fissures/sulci in the temporal lobe and parietal lobe are more important.

 Parietal atrophy relates to the early onset subtype of Alzheimer’s Dementia.

It begins in the Entorhinal Cortex. 

References

Johnson, K. A., Fox, N. C., Sperling, R. A., & Klunk, W. E. (2012). Brain imaging in Alzheimer disease. Cold Spring Harbor perspectives in medicine, 2(4), a006213. doi:10.1101/cshperspect.a006213

Alzheimer disease | Radiology Reference Article | Radiopaedia.org. (n.d.). Retrieved January 17, 2020, from https://radiopaedia.org/articles/alzheimer-disease-1

Neurobiology of Panic Disorder

"There is most evidence for changes in Gamma-aminobutyric acid, with lowered cortical Gamma-aminobutyric acid type levels measured by magnetic resonance spectroscopy, and diminished benzodiazepine-receptor binding in the parietotemporal regions in unmedicated patients with panic disorder (Hasler et al., 2008)."

This happens in panic disorder. Gamma-aminobutyric acid is the major inhibitory neurotransmitter in the brain. Benzodiazepine also binds to Gamma-aminobutyric acid type A receptors and increases its firing rate, thus resulting in hyperpolarisation of the cell because of increased chloride influx. So, specific regions in the brain are hyperexcitable in patients with panic disorder.

Summary of Hasler et al. 

Context

Studies have implicated the benzodiazepine receptor system in the pathophysiologic mechanism of panic disorder  by indirect evidence from pharmacological challenge studies and by direct evidence from single-photon emission computed tomography and positron emission tomography neuroimaging studies

1. The benzodiazepine receptor binding potential was decreased in multiple areas of the frontal, temporal, and parietal cortices and was increased in the hippocampus/ parahippocampal region in subjects with panic disorder vs controls
2. The most significant decrease was in the dorsal anterolateral prefrontal cortex; the most significant increase in the hippocampus/parahippocampal gyrus
3. In subjects with panic disorder, the severity of panic and anxiety symptoms correlated positively with benzodiazepine receptor binding in the dorsal anterolateral prefrontal cortex but negatively with binding in the hippocampus/parahippocampal gyrus
4. These data provide evidence of abnormal benzodiazepine–Gamma-aminobutyric acid type A receptor binding in panic disorder, suggesting that basal and/or compensatory changes in inhibitory neurotransmission play roles in the pathophysiologic mechanism of panic disorder.