Narcolepsy with cataplexy and hyperthyroidism sudden appeared after H1N1 vaccination.

Narcolepsy type 1 (NT1) is a chronic sleep disorder, characterized by excessive daytime sleepiness, cataplexy and fragmented nocturnal sleep. It is caused by a hypocretin deficiency due to a significant reduction of the neurons producing it. In the last years, it has been postulated that an autoimmune mechanism would be responsible for the destruction of these neurons in those genetically predisposed patients. The increased incidence of narcolepsy after the pandemic H1N1 influenza vaccination campaign in 2009-2010 is known. We present below the case of an adult patient who, 10 days after receiving H1N1 vaccination, suffers a traffic accident after falling asleep. Subsequent studies revealed hyperthyroidism due to Graves disease. In spite of the treatment, the patient persisted with daily and disabling daytime sleepiness, sleep attacks and episodes of generalized muscle atony with preservation of consciousness. A nocturnal polysomnography and multiple sleep latency test (MSLT) were performed with a diagnosis of NT1. The particularity of this case is the presentation of 2 autoimmune diseases triggered by an H1N1 vaccine without adjuvant, so far there is only evidence of NT1 associated with vaccines with adjuvant and viral infection. The association of both entities has made us reflect on the autoimmune mechanism, reinforcing the theory of its role in the onset of the disease.

[Kleine Levin syndrome: Review of diagnosed cases of Buenos Aires, Argentina]. / Síndrome de Kleine Levin: reporte de casos de Buenos Aires, Argentina.

Kleine-Levin syndrome is an uncommon disorder with recurrent episodes of hypersomnia, and behavioral abnormalities such as binge-eating and hypersexuality. Our aims were to report cases of the Kleine-Levin syndrome diagnosed in Buenos Aires, Argentina and to characterize the clinical presentation of these patients. We evaluated patients with Kleine-Levin syndrome according to the International Classification of Sleep Disorders. Psychiatric, physical and neurological symptoms were present. Some patients were investigated with brain Magnetic Resonance Imaging, Single Photon Emission Computed Tomography, electroencephalogram and some with polysomnography. Seven patients (2 female, 5 male), ages from 8 to 47 years (median 20.7 years) were included in the study. The duration of symptoms was 1.5-20 days with a mean of 8. The range of interval between episodes: 2.5-24 months, median=13. All seven patients had a history of hypersomnia (one of them post head injury); 5 reported hyperphagia and 2 reduced appetite. Brain MRI was performed in 6 patients: 1 showed non-specific abnormalities and another presented diencephalic hematoma; the rest were normal. Our paper is the first one in Buenos Aires reporting Kleine-Levin syndrome of different ethiologies. The prevalence is difficult to estimate in our country.

Recurrent hypersomnia following traumatic brain injury.

BACKGROUND: Recurrent hypersomnia (RH) following a traumatic brain injury (TBI) is a rare form of RH. According to the International Classification of sleep disorders, 2nd edition (ICSD-2), RH must be considered in the differential diagnosis as secondary to an organic insult of the central nervous system and not as the clinical subtype of RH, Kleine-Levin syndrome (KLS). The aim of our study was to investigate if cases of RH following TBI should be considered in the differential diagnosis of RH as indicated by the International classification of sleep disorders, 2nd edition or as genuine, or indicated by ICSD-2, RH must cases of KLS. METHODS: Twelve cases of RH developed after TBI were collected and analyzed for circumstance at onset, severity of TBI, delay between TBI and occurrence of first episode of RH, symptoms of RH, duration and cycle length of episodes of hypersomnia, physical signs, and brain morphological imaging at the time of hypersomnia episodes. RESULTS: Factors such as the delay between TBI and the first episode of RH, the presence of other triggering factors and potential genetic factors, the degree of the severity of TBI, the presence or absence of any consistent brain imaging abnormality, provided the following results: (1) two of the cases could be considered as symptomatic of the underlying pathological brain process, (2) eight of the cases could be considered as simply triggered by TBI in patients at risk for KLS, and (3) two cases could be considered neither symptomatic nor triggered by TBI, due to the long delay between TBI and occurrence of symptoms. CONCLUSION: Cases of RH following TBI do not present under a single mechanism. Clinical assessment and laboratory tests are necessary to correctly classify them.

Kleine-Levin syndrome in a 14-year-old girl: CSF hypocretin-1 measurements.

CSF hypocretin-1 measurements were performed during a period of hypersomnia and during an asymptomatic interval in a 14-year-old girl affected with severe Kleine-Levin syndrome. A twofold decrease in hypocretin-1 was evidenced during the period of hypersomnia in comparison with the asymptomatic interval. Together with previous data, this result is in favour of recurrent dysfunction at the hypothalamic level in Kleine-Levin syndrome.