A 40-year-old man with severe H1N1 influenza infection with prolonged hypoxia and critical illness who remained comatose after withdrawal of sedatives and paralytics. Interventions: Clinical examination and magnetic resonance imaging. Results: Brain imaging revealed multifocal T2 hyperintense lesions, edema, and hemorrhages consistent with acute hemorrhagic leukoencephalitis (AHL) and restricted diffusion in the basal ganglia consistent with hypoxic brain injury. The patient remained in a severely disabled state following treatment with plasma exchange and high-dose corticosteroids. Conclusions: This is the first study of neurologic complications associated with H1N1 influenza infection in adults. Severe brain injury can occur by 2 distinct mechanisms: a fulminant autoimmune demyelinating insult (AHL) and hypoxic brain injury. Clinicians should be aware of these potential complications so that appropriate imaging and treatment can be considered.
Sleep disorders in myotonic dystrophy type 1 (DM1) are common and include sleep-disordered breathing, hypersomnia, and fatigue. Little is known regarding the occurrence of sleep disturbance in myotonic dystrophy type 2 (DM2). We hypothesized that DM2 patients may frequently harbor sleep disorders. We reviewed medical records of all genetically confirmed cases of DM2 seen at our sleep center between 1997 and 2010 for demographic, laboratory, overnight oximetry, and polysomnography (PSG) data. Eight patients (5 women, 3 men) with DM2 were identified. Excessive daytime sleepiness was seen in 6 patients (75%), insomnia in 5 (62.5%), and excessive fatigue in 4 (50%). Obstructive sleep apnea was diagnosed in 3 of 5 patients (60%) studied with PSG. Respiratory muscle weakness was present in all 6 patients (100%) who received pulmonary function testing. Four of 8 (50%) met criteria for diagnosis of restless legs syndrome. The clinical spectrum of DM2 may include a wide range of sleep disturbances. Although respiratory muscle weakness was frequent, sustained sleep-related hypoxia suggestive of hypoventilation was not seen in our patients. Further prospective studies are needed to examine the frequency and scope of sleep disturbances in DM2.
RLS, EDS, and fatigue are frequent sleep disturbances in patients with DM2, while OSA and pRBD symptoms are not. EDS was independently associated with DM2 diagnosis, suggesting possible primary CNS hypersomnia mechanisms. Further studies utilizing objective sleep measures are needed to better characterize sleep comorbidities in DM2.
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