Neurological Disorders

Introduction: Scabies is a skin infection caused by the Sarcoptes scabiei (variety hominis) mite. The classic variant produces pruritic lesions with intense, persistent itching. Immunosuppressed patients develop a more aggressive form of the infection known as crusted (Norwegian) scabies.

Clinical cases: We present four episodes of ocrelizumab-treated multiple sclerosis patients with B-cell lymphopenia who developed the classic variant of scabies.

Conclusion: To our knowledge, no cases have been published in the literature, which relate ocrelizumab with the development of scabies. The maintenance of cellular immune response protects of development of crusted scabies.

Introduction: Alemtuzumab produces a total depletion and posterior repopulation of T and B cells. Autoimmunity is an important adverse event of this drug. In recent years, other autoimmune diseases, different to thyroid, kidney and platelets alterations have been described.

Clinical Case: We present one case of alemtuzumab-treated multiple sclerosis patient who develops ulcerative colitis after two cycles of alemtuzumab.

Conclusion: To our knowledge, no cases have been published in the literature, which relate alemtuzumab with the development of ulcerative colitis. The different kinetics in B and T cells repopulations and the change in the gut microbiota induced by alemtuzumab or by changes in diet to prevent listeriosis, could increase the risk of developing this autoimmune phenomenon.

We present the case of a healthy 32-year-old woman who came to our hospital due to fever and left otalgia. She subsequently developed dizziness and gait instability, opsoclonus-myoclonus syndrome, and altered level of consciousness. She was admitted to the intensive care unit, developing status epilepticus, which was refractory to third-line treatment with propofol and barbiturates. A thorough assessment including autoimmunity studies, viral testing, and mitochondrial disease testing yielded negative results. A brain magnetic resonance imaging scan revealed signal hyperintensities in both caudate nuclei and putamina, and gadolinium-enhancing small punctiform lesions in the left hemisphere and left cerebellar tonsil. Suspecting an immune-mediated disorder, we started treatment with high-dose steroids and plasmapheresis, in addition to different combinations of antiepileptic drugs. The patient was refractory to these treatments; electroconvulsive therapy improved the EEG tracing and may have helped manage status epilepticus. Subsequent examinations revealed paralysis of left cranial nerves IX, X, and XII, which resolved nearly completely in the final days of hospitalisation, leaving the patient practically asymptomatic. Our findings point to encephalitis with brainstem involvement and manifesting as cryptogenic new-onset refractory status epilepticus.