Regarding sleep terror, which of the following statements is false?
A. Sleep terrors occur in slow-wave sleep (stage 3 and 4) unlike nightmares which occur in REM sleep. Sleep terrors are characterized by a sudden arousal with intense fearfulness, often associated with a sharp scream. The subject may sit up in bed, may vocalize unintelligibly, and waking the individual leads to confusion. There is amnesia for the episode and unlike nightmares it is very rarely associated with vividly recalled dreams and images. A familial pattern has been reported. In children, night terrors may be transient but in adults they may be associated with other psychopathology.
Reference:
A 25-year-old man complains of excessive daytime sleepiness. He loses balance and falls down every time he laughs at a joke. He also complains of seeing ‘ghosts’ while falling asleep.
Which of the following is likely to be found in this patient?
D. This patient is likely to have narcolepsy. Narcolepsy is a disorder of unknown aetiology. It consists of the tetrad of excessive day time sleepiness, cataplexy, sleep paralysis, and hypnagogic hallucinations. Polysomnography typically shows sleep-onset REM stage. Cataplexy refers to sudden loss of muscular tone, often seen in association with emotional reactions in those with narcolepsy. An abnormality in the hypocretin neurones in the lateral hypothalamus has been noted in those with narcolepsy. Hypocretin (orexin) is a highly excitatory peptide hormone secreted from the hypothalamus. This is necessary to maintain wakefulness and it also increases appetite. Narcolepsy, especially cataplexy, is considered to be a hypocretin deficiency syndrome. SSRIs and TCAs remain the treatment of choice currently. Modafinil is also being tried as a treatment.
All of the following increases the risk of developing dementia in those with Parkinson’s disease except:
D. Dementia is estimated to occur in 27% of patients with Parkinson’s disease (PD). Dementia has been associated with older age, greater PD severity, hallucinations, longer duration of PD, greater disability, and male gender. Causes of dementia in PD include Lewy body pathology, dopamine depletion, coexisting AD, and other conditions. Reduced fluorodopa uptake in the frontal cortex and caudate nucleus, and in mesolimbic pathways are predictors of cognitive impairment. Temporoparietal cortical hypometabolism also predicts cognitive impairment. Donepezil has been found to be useful in two separate double-blind trials in patients with PD.
Which of the following is considered as a ‘Parkinson plus’ syndrome?
C. Progressive supranuclear palsy is considered as a Parkinson plus syndrome. It is distinguished from Parkinson’s disease by the presence of early broad-based and stiff gait disorder (axial greater than limb rigidity in extension) with backward falls, and supranuclear gaze palsy with slow vertical saccades and difficulty looking down (and hence the falls). Falls are very common in these patients and are an important cause of morbidity. Patients are prone to develop various psychiatric complications, including cognitive dysfunction and mood disorders. Cholinesterase inhibitors have not been particularly useful in treating patients with progressive supranuclear palsy associated dementia. Other Parkinson plus syndromes include multisystem atrophy (called Shy–Drager syndrome when associated with autonomic failure), olivopontocerebellar atrophy, and cortico-basal degeneration.
A 64-year-old man presents with sudden-onset blindness that started as a ‘curtain coming down’ and he lost his vision completely for a few minutes. Within 15 minutes this improved and was restored to full, normal vision.
The origin of emboli in this case is most likely to be at:
C. In this case the origin of emboli must be at the internal carotid artery. The ophthalmic artery, a branch of the internal carotid artery, is blocked transiently, producing the symptoms described in the question. This is called as amaurosis fugax which translates to ‘fleeting darkness’. It is related to transient but sudden monocular visual loss as a result of decreased retinal circulation. It is a type of transient ischaemic attack and could be a harbinger of a cerebrovascular accident. Compromise of posterior circulation usually leads to cortical blindness, often with macular sparing.
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