All of the following are sleep changes associated with depression except:
B. Disrupted sleep architecture is a long-recognized feature of mood disorders. Several sleep-related electroencephalogram (EEG) changes have been noted in around 90% of those with depression. Short REM latency, increased amount of REM sleep, increased REM density, especially in the first REM episode, prolonged sleep latency, increased frequency of awakenings with low arousal threshold, reduced slow-wave sleep, and shifting of delta sleep to second-stage NREM sleep are some of the notable changes. Some reports have suggested that bipolar depression may be atypical with respect to sleep changes in that daytime sleepiness and increased sleep efficiency are reported. In hypomania/mania, short REM latency, inability to fall asleep, short sleep duration, and reduced delta sleep are seen. In patients who have secondary depression due to a chronic medical condition, REM sleep may be reduced.
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A 60-year-old man has episodes of disturbed sleep. He experiences unusual movements associated with singing and talking to unseen people during some of these episodes. He recalls vivid dreams when he wakes up.
The most appropriate diagnosis would be:
C. Normally REM sleep is associated with loss of muscle tone (atonia) and dreaming. In some patients, as an isolated condition or as a prodrome for later neurodegenerative disorders such as Lewy body dementia/Parkinson’s disease, this normal atonia is absent. This then leads to ‘dreams being acted out’ with uncontrolled limb movements. This is called REM sleep behavioural disorder. Patients can recall dreams when awakened, unlike sleep terror. The behaviours may be more complex than simple sleepwalking. Periodic limb movement disorder is characterized by periodic episodes of repetitive and stereotyped limb movements that occur during sleep. These movements can cause clinical sleep disturbance expressed by insomnia or excessive daytime sleepiness. This is not a dream-related behaviour, unlike REM sleep behavioural disorder. Restless legs syndrome, in simplistic terms, is the daytime extension of periodic limb movement disorder wherein episodic akathisia and motor restlessness are seen during the day and at night.
All of the following are recognized treatment options for restless legs syndrome except:
D. Pharmacological treatment options for restless leg syndrome include dopaminergic agents (L-dopa, pergolide, pramipexole), anticonvulsants (gabapentin, carbamazepine), certain opioid drugs, and clonazepam. Amitriptyline has no role in the management of restless leg syndrome. An increase in periodic limb movements observed during sleep has been reported as a side-effect of tricyclics. Some patients may report new-onset restless leg syndrome in association with SSRIs or tricyclics when treated for depression.
A 29-year-old man presents with erectile dysfunction. His history reveals excessive stress at work.
Which of the following indicates a psychogenic rather than an organic cause for his sexual dysfunction?
A. It is important to realize that clear-cut demarcations between psychogenic or organic erectile dysfunctions are difficult to ascertain in clinical practice. But certain clues that may favour a psychogenic origin/overlay of erectile dysfunction include sudden onset of the problem, early collapse of erection (as against complete absence of tumescence), preserved spontaneous (early morning) and self-stimulated erections, antecedent (temporally related) problems or changes in relationship, a history of significant preceding or ongoing life events, and evidence of psychological problems. Clues that may indicate an organic aetiology include preserved ejaculation in spite of impaired erection, unperturbed libido (in the early stages), and a history of antecedent physical injury, surgeries, or vascular risk factors in the medical history, smoking, and other prescribed or recreational drug use.
Which of the following drugs used for erectile dysfunction acts via the dopaminergic mechanism?
D. Apomorphine is a dopamine receptor agonist which stimulates both dopamine D1 and D2 receptors and is sometimes used in male erectile dysfunction. Phosphodiesterase-5 (PDE-5) is an enzyme found in the trabecular smooth muscle of the penis. It catalyses the degradation of cGMP, which results in an elevated cytosolic calcium concentration and muscular contraction leading to erection. PDE-5 inhibitors such as sildenafi l, vardenafi l, and tadalafi l block this biochemical pathway to promote erection. Sildenafi l and vardenafi l must be taken 1 hour before sexual activity to enable their action. Alprostadil is prostaglandin E1 , which causes smooth muscle relaxation and subsequent vasodilation by acting on adenylate cyclase to increase the intracellular cyclic adenosine monophosphate (cAMP) concentration. Yohimbine is not commonly used for erectile dysfunction; it is an adrenergic antagonist relatively selective for alpha-2 receptors. The site of action of yohimbine when used for erectile dysfunction is suspected to be central rather than peripheral as the predominant subtype of alpha-adrenoceptor in penile erectile tissue is alpha-1 type rather than alpha-2 type.
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