Levetiracetam can be effective in the treatment of restless legs syndrome with periodic limb movements in sleep: report of two cases.
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Biomedical subjects
Publications and source records attributed to G F Mennuni.
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Attempts to analyse the sleep structure of patients with eating disorders have so far led to conflicting results. Polygraphic findings suggest that patients with bulimia nervosa are not easily distinguishable from age-matched controls, whereas anorexic patients show some abnormalities in sleep efficiency and sleep architecture. Nevertheless, both bulimic and anorexic patients complain of poor quality sleep. The aim of this study was to evaluate the microstructure of sleep in anorexia and bulimia by analysing arousal (following the rules of the American Sleep Disorders Association) and the cyclic alternating pattern (CAP). The results confirmed the presence of sleep disturbances in eating disordered patients: an increase in arousal length and the CAP rate. They also seem to confirm the findings of previous studies suggesting that altered sleep in eating disordered patients may be related to their body mass index (BMI) and psychopathological status.
Geriatric patients often complain about sleep disorders, but many of the typical sleep disturbances in the elderly are thought to be normal consequences of old age and go underdiagnosed and undertreated. Sleep disorders are estimated to affect nearly 50% of older persons. Most frequently the elderly suffer from Sleep Disordered Breathing (SDB), Periodic Limb Movements in Sleep (PLMS), Restless Legs Syndrome (RLS), morning headaches, circadian rhythm disorders, excessive daytime sleepiness, Obstructive Sleep Apnea Syndrome (OSAS), and insomnia. This review describes all these common sleep problems in the older population and their possible treatment.
OBJECTIVE: A high prevalence of sleep disorders is reported in patients affected by Mucopolysaccharidosis III (Sanfilippo syndrome). These disorders have never been investigated by prolonged, objective, and instrumental evaluations. The present work is based on sleep duration and structure in Sanfilippo patients. STUDY DESIGN: The features of sleep/wake cycle in 6 Sanfilippo patients and 6 healthy controls were evaluated by means of sleep diaries and 48 hour ambulatory EEG and polygraphic recordings. Statistical analysis was performed by means of the U-test (Mann-Whitney). RESULTS: Four out of six Sanfilippo patients, the oldest patients in our sample, showed an extremely irregular sleep pattern, with several sleep episodes of inconstant duration, irregularly distributed along 24 hours. The two younger patients showed sleep maintenance insomnia with several nocturnal awakenings. CONCLUSIONS: These results suggest that sleep disruption in Sanfilippo syndrome consists of an irregular sleep/wake pattern, which at its onset might appear as a disorder of initiating or maintaining sleep. This could explain why same patients do not respond to conventional hypnotics. The present observation might suggest attempting therapies aimed at resynchronization, such as behavioral treatment, light therapy or melatonin.
A woman affected by multiple cranial nerve palsy developed several episodes of total insomnia and respiratory crises resulting from central breathing depression associated with dysautonomic symptoms. Oligoclonal IgG bands were present in her cerebrospinal fluid, and immunohistochemistry showed increased binding of serum and cerebrospinal fluid on gamma-aminobutyric acid-ergic, synapse-rich neuronal cells. Immunosuppressive treatment and plasma exchange were followed by clinical improvement, with restoration of sleep architecture and disappearance of respiratory crises, suggesting autoimmune pathogenesis of the syndrome.
OBJECTIVES: We report on a case of ESES/CSWS observed in a patient of 21 years and still persisting at the age of 25. Cases of ESES/CSWS have never been previously described in adult patients. ESES/CSWS is considered to be related to the degree of maturation of the central nervous system, and therefore strictly age-related. METHODS: Our case of ESES/CSWS was observed in a 2 1 year old woman referred for cognitive and behavioral disorders. She had previously had epileptic fits, but was seizure free at that time. The patient underwent a full-night polygraphic recording , which showed typical ESES/CSWS pattern, with a Spike-and-Wave Index >8 5%. Polysomnography was repeated 9 times in a 4 year follow-up, during which the ESES/CSWS condition persisted, despite the pharmacological treatments. The patient also underwent cerebral magnetic resonance imaging and fludeoxyglucose F 18 positron emission tomography (PET). RESULTS: The PET study revealed reduced metabolic activity within the lower gyrus of the right parietal lobe, but no significant difference between subcortical structures and cortical mantle was seen. MRI scans were normal. CONCLUSIONS: This observation suggests that ESES/CSWS might not always be an age-related condition. Sleep EEG recordings should always be performed in patients with behavioral disorders and a history of epileptic fits.
The "distal myopathies" include autosomal dominant, autosomal recessive, and sporadic disorders. Two of the recessive disorders are considered to be definitive entities: Miyoshi's myopathy, which has an early adult onset and first involves the calf muscles, and distal myopathy with rimmed vacuoles. We here describe the cases of two sisters and compare them with previously reported cases. The disorder in our patients is characterised by: a) autosomal recessive inheritance; b) onset in early adult life; c) initial involvement of the tibialis anterior and peroneal muscles; d) subsequent involvement of the calf muscles spreading to the proximal muscles of the legs and, later, the arms; e) a moderately disabling evolution over a period of 10-12 years; f) marked and stably high serum levels of CK and other enzymes; g) EMG evidence of myopathic damage, with fibrillation at rest; and h) a histological picture of dystrophic myopathy, with atrophy of mainly type 2 fibres. We think that this syndrome is different from the two forms of autosomal recessive distal myopathy mentioned above.