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This chapter discusses the case of a 27-year-old male who was admitted to the hospital with right arm numbness. It presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on the patient. His vital signs were normal. There was mild expiratory wheezing at the bases bilaterally related to an upper respiratory infection. There was reduced sensation to light touch, pinprick and vibration in the right upper extremity in C6-C7 distribution. MRI of the brain showed multiple small hyperintense lesions in white matter throughout both cerebral hemispheres and the brainstem. An overnight sleep study followed by a multiple sleep latency test (MSLT) revealed REM sleep without atonia and abundant myoclonic jerks in REM sleep. A diagnosis was made of probable parasomnia overlap disorder in the context of multiple sclerosis. Parasomnia overlap disorder responds favorably to the administration of clonazepam.
This chapter discusses the case of a 43-year-old male having problems with his nocturnal sleep at the age of 23 when he started to present recurrent nocturnal awakenings from sleep associated with involuntary eating. It presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on the patient. Actigraphic recordings for 2 weeks disclosed persistent muscular activity during the nocturnal period and two to five episodes per night of further enhanced muscular activity that corresponded to the eating episodes noted by the patient in his diary. The sleep medicine specialist established a diagnosis of sleep-related eating disorder (SRED) based on the clinical history and on the results of the video-polysomnography (PSG) recording. Low-dosage dopaminergic agents such as levodopa/carbidopa at bedtime, sometimes combined with codeine and/or clonazepam, bromocriptine and pramipexole, have been shown to reduce the eating episodes.
This chapter presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on a 24-year-old man who was admitted with the chief concern of abnormal breathing sounds during sleep for the past 5 years. Physical examination and vital signs were normal with a BMI of 28 kg/m2. His Epworth Sleepiness Scale score, for subjective assessment of excessive daytime somnolence, was 9. The patient entered sleep through NREM sleep stages, had recognizable NREM/ REM sleep alternations and physiological muscle atonia during REM sleep, with a total sleep time of 222 minutes. The groaning sounds lasted between 5 and 15 seconds and recurred in clusters, 16 minutes in net duration but spanning across 30 minutes. The overall clinical and polygraphic features in this patient were felt to be consistent with the diagnosis of catathrenia, a syndrome whose etiology remains unclear.
This chapter presents the history, clinical findings, pathology, differential diagnosis and management of propriospinal myoclonus. Propriospinal myoclonus at sleep onset consists of sudden axial jerks arousing during drowsiness preceding falling asleep and during intra-sleep relaxed wakefulness and upon awakening in the morning. The jerks may be variable in frequency, recurring in clusters separated by long gaps of time or quasi-periodically every 10-20 sec during transition from wakefulness to sleep. For patients with suspected propriospinal myoclonus, multiple muscle EMGs from cranial, axial and limb muscles are essentials at polysomnographic investigation. According to the evidence available, propriospinal myoclonus at sleep onset must originate at the spinal level, but it must be set into motion by neurophysiological mechanisms specific to the transitional period between wake and sleep. Propriospinal myoclonus at wake-sleep transitions remains idiopathic condition, often lifelong one, in which no structural abnormality of the brain or spinal cord has been demonstrated.
Four patients had a positive personal history for parasomnias and two- a positive family history. Personal history was positive for parasomnias in two patients. Family history was positive for parasomnias in two patients, for nocturnal groaning in one patient, and for sudden infant death syndrome in one patient. Eight patients were reporting a family history positive for parasomnias and three for nocturnal groaning. Catathrenia is associated with a positive personal or familial history for other parasomnias. There is no drug medication available for catathrenia. Empirical pharmacological treatments with dosulepine, trazodone, clonazepam, paroxetine, carbamazepine, gabapentin, and pramipexole have been unsuccessful or refused. The efficacy of the nCPAP ventilation is still debated. In particular, nCPAP treatment seems effective only when noisy breathing during sleep, diagnosed as catathrenia, is related to the co-existence of expiratory and inspiratory flow limitation with obstructive apneas or hypopneas and consequent intermittent hypoxia.
Rapid eye movement (REM) sleep behavior disorder (RBD) was first formally identified in 1986 by Schenck and Mahowald in five elderly subjects presenting similar motor behavioral patterns during REM sleep consisting of violent dream-enacting behaviors. The clinical manifestations of RBD are typically dream-related motor-behavioral manifestations that appear to be the enactment of a fight. Subclinical or preclinical RBD, status dissociatus and parasomnia overlap syndrome are the clinical-pathophysiological subtypes of RBD, according to ICSD-2. The literature contains anecdotal reports of co-existing RBD and narcolepsy in both adults and children, in some cases with the RBD episodes as the presenting symptoms. The parasomnia and non-parasomnia disorders are taken into account in the differential diagnosis of RBD. In humans, RBD has been associated with several etiologies and abnormalities. Anecdotal reports and uncontrolled, retrospective studies of small patient series suggest that levodopa and pramipexole (D3 agonist) reduce RBD manifestations.
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