Disruption or disorganisation of biological rhythm is observed in

Ans. c (Depression) (Harrison's medicine 17th ed., Chapter 386)ETIOLOGY AND PATHOPHYSIOLOGY OF DEPRESSION# Although evidence for genetic transmission of unipolar depression is not as strong as in bipolar disorder, monozygotic twins have a higher concordance rate (46%) than dizygotic siblings (20%), with little support for any effect of a shared family environment. There is some evidence that a functional polymorphism in the serotonin transporter (5- HTT) gene may interact with stressful life events to markedly increase risk of depression and suicide. Positron emission tomography (PET) studies show decreased metabolic activity in the caudate nuclei and frontal lobes in depressed patients that returns to normal with recovery. Single-photon emission computed tomography (SPECT) studies show comparable changes in blood flow.# Postmortem examination of brains of suicide victims indicate altered noradrenergic activity.# Diurnal variations in symptom severity and alterations in circadian rhythmicity of a number of neurochemical and neurohumoral factors suggest that biologic differences may be secondary to a primary defect in regulation of biologic rhythms. Patients with major depression show consistent findings of a decrease in rapid eye movement (REM) sleep onset (REM latency), an increase in REM density, and, in some subjects, a decrease in stage IV delta slow-wave sleep.