Generalized Anxiety Disorder: Revisited.

Generalized Anxiety Disorder (GAD) from an official recognition as a residual category in DSM-III has come a long way to be appreciated as a common underlying anxiety pathway in the literature. Despite still being defined as extreme anxiety and worry upon performance and about one's health, GAD seems to be a general umbrella of anxiety, covering even social anxiety and panic disorder (PD) and even when not treated and chronic, leading to major depressive disorder (MDD). Along the line of some other similar studies and contentions, in the present study we sought to validate the hypothesis of GAD encompassing social anxiety as well as performance anxiety and its extension to PD and MDD. We also examined the onset of each diagnostic category of GAD, PD and MDD and their developmental course in our clinical sample. 113 patients with Generalized Anxiety Disorder (GAD) out of 295 referrals to our mood and anxiety clinic during the three months of May-July 2019, were identified and included in this research. We expanded the definition of GAD as per our clinical observation to include any situations triggering the anxiety including any performance and social situations and did not exclude if the anxiety led to panic attacks. The results of our study showed that an encompassing GAD (including performance and social anxiety) has an early onset, recognized partially in childhood, but mostly during adolescence. An untreated GAD was complicated with panic disorder and episodes of major depression, each with an onset later in life. GAD in our study was also found to be familial and genetic, while its post-morbid depression seemed to be more a reaction to a long-standing untreated anxiety. The findings of our study if replicated has research implication of better understanding the developmental course of mood disorders and hold the promise of more targeted treatments of anxiety, panic and depression in clinical practice.

Reactive Depression: Lost in Translation!

The old classification of depression as reactive and endogenous, which are still observed in clinical practice, both cannot be accommodated under the current rubric of major depression. This is because psychiatric nosology under the Diagnostic and Statistical Manual of Mental Disorders (DSM) and its latest fifth edition (DSM-V) is still descriptive and not etiologic. The aim of this review was to revisit reactive and endogenous categories of depression from the perspective of today's understanding of etiological pathways. From an epigenetic perspective, the old dichotomy of reactive versus endogenous is interrelated through the impact of the environment (e.g., stress). This includes familial or prenatal depression, where the environmental impact is before birth, or childhood depression, where the early life stress is the precipitating factor to genetic susceptibility. In conclusion, searching for both environmental impact (e.g., stressors) and genetic predispositions in depression, even at a clinical level, could help clinicians with better therapeutic decisions.

Pregabalin in the treatment of depression.

Although studies have demonstrated the efficacy of the new anti-epileptic on the block, Pregabalin, in the treatment of Generalized Anxiety Disorder and Social Anxiety Disorder, there is no study so far of such efficacy for the treatment of depression. This case study in a patient with chronic major depression demonstrates that Pregabalin could be an effective augmenting agent to other anti-depressants, e.g. SSRI's and SNRI's. This added property of Pregabalin may be related to its probable GABA-ergic mechanism of action that could be soon the emerging treatment pathway for achieving better remission in chronic depression that is yet clinically problematic.