There were no differences in the other alleles that have been described in MS subjects, such as HLA-DRB1*04, HLA-DRB1*08 and HLA-DRB1*13. These findings may support the hypothesis that implicated immune-genetics as a key factor in development of this type of disease.

Klüver-Bucy syndrome (KBS), described originally in monkeys and later in humans, is associated with bilateral anterior damage on the temporal poles, amygdala, or mediodorsal thalamic nucleus, 1,2 which are part of Yakovlev's circuit or lateral limbic circuit. 1 The uncinate fasciculus and other tracts are critical parts of this network 3 ; however, it is uncertain if white matter lesions could produce KBS. We present the case of a young woman who attended the National Institute of Neurology and Neurosurgery of Mexico with acute disseminated encephalomyelitis, a clinical entity with relevant white matter damage, presenting with acute catatonia and chronic KBS. CASE REPORTCatatonic Syndrome in a Patient With Acute Disseminated Encephalomyelitis At age 26 years, patient "M" was a married woman, graduated as a physician, had one daughter, and did not have relevant pathological, psychiatric, or family antecedents. She received a seasonal influenza vaccine and H1N1 vaccine on November 2009. Her illness began on January 2010, with rhinorrhea, nonproductive cough, 40°C fever, headache, hypersomnia, dysarthria, and left pyramidal syndrome. Neurological examination findings at the National Institute of Neurology and Neurosurgery revealed somnolence and ophthalmoplegia, left ptosis, and left facial paralysis. Her muscle strength was 4/5 on all four extremities; generalized hyperreflexia, a dystonic posture of all four extremities, bilateral dysmetria, and indistinct lateropulsion were also documented. Laboratory testing ruled out renal, hepatic, or endocrine impairments and electrolyte imbalance. HIV, VDRL, and antinuclear antibody test results were negative. Results on adenosine deaminase, India ink microscopy, and JC virus (or John Cunningham virus) polymerase chain reaction were also negative. Results on MRI scan (February 2010) showed hyperintense lesions on T2/fluidattenuated inversion recovery sequences on the right-sided caudate nucleus, globus pallidus, putamen, anterior thalamus, and cerebral peduncle. A second MRI scan (March 2010) showed new lesions on the contralateral side, with a similar topography. After excluding other causes, we concluded that she fulfilled criteria for acute disseminated encephalomyelitis, due to previous viral infection symptomatology; multifocal neurological involvement and encephalopathy; generalized

No abstract