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Showing posts from January, 2018

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 distre

Classification of Depression According to the ICD-10

A first depressive episode, duration at least15 days →depressive episode (F32)  A first depressive episode, severe and rapid onset, duration less than 15 days →still depressive episode (F32) A depressive episode can be mild (2 core symptoms, 2 other symptoms from the list) (32.0) moderate (2 core symptoms, 3 or preferably 4 other symptoms) (32.1) Severe (3 core symptoms, 4 other symptoms) without psychotic symptoms (32.2) (no delusion, hallucination or stupor) Severe with psychotic symptoms (above plus either delusions, hallucinations or stupor) (F32.3) Delusions can be mood-congruent or incongruent (neutral delusions e.g. delusions of reference are considered mood incongruent. None of them count towards schizoaffective disorder unless one of the first-rank)  A mild and moderate depressive episode can be  with somatic syndrome (four or more somatic symptoms, or three very severe somatic symptoms) without somatic syndrome (three or less somatic symptoms, not severe)  A severe depressi

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 t

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: Reduced weight of the brain Reduced cortical volume Dilated ventricles 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 Alzheime

Neurobiology of Panic Disorder

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