The results failed to show an association between post-discharge multinutrient supplementation and development in the assessed infants.

Plasma exchange (PLEX) is a therapeutic apheresis modality in which the plasma is separated from inflammatory factors such as circulating autoreactive immunoglobulins, the complement system, and cytokines, and its therapeutic effect is based on the removal of these mediators of pathological processes. Plasma exchange is well established for various neurological disorders, and it is applied successfully in central nervous system inflammatory demyelinating diseases (CNS-IDD). It mainly modulates the humoral immune system; thus, it has a greater theoretical effect in diseases with prominent humoral mechanisms, such as neuromyelitis optica (NMO). However, it also has a proven therapeutic effect in multiple sclerosis (MS) attacks. Several studies have suggested that patients with severe attacks of CNS-IDD have poor response to steroid therapy but show clinical improvement after the PLEX treatment. Currently, PLEX is generally established only as a rescue therapy for steroid unresponsive relapses. However, there are still research gaps in the literature regarding plasma volume, number of sessions, and how early the apheresis treatment needs to started. Thus, in the present article, we summarize the clinical studies and meta-analyses, especially about MS and NMO, outlining clinical data regarding the experience with therapeutic PLEX in severe attacks of CNS-IDD, the clinical improvement rates, the prognostic factors of a favorable response, and highlighting the likely role of the early apheresis treatment. Further, we have gathered this evidence and suggested a protocol for the treatment of CNS-IDD with PLEX in the routine clinical practice.

ObjectiveWe report a case of biopsy-proven giant cell arteritis after an initial presentation of area postrema syndrome.MethodsA 65-year-old man was evaluated using MRI, temporal artery biopsy, and ultrasound.ResultsThe patient presented with refractory nausea, vomiting, and hiccups that caused weight loss without any other neurologic or clinical symptoms. His MRI scan 15 days later revealed a hyperintense sign on the area postrema with no abnormal diffusion or contrast enhancement, compatible with isolated area postrema syndrome. An extensive workup for inflammation and other etiologies including neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody disorder, and multiple sclerosis (MS) showed negative results. The patient responded to treatment with methylprednisolone. Two months after the initial clinical manifestation, the patient developed fatigue, headache, and scalp tenderness. He was diagnosed with giant cell arteritis after ultrasonography and biopsy were performed. He responded well to oral glucocorticoids and had only 1 relapse during tapering. He has not had arteritic ischemic optic neuropathy or any new episodes of area postrema syndrome.DiscussionThis case demonstrates the importance of expanding the differential diagnosis in patients with area postrema syndrome and no other signs of NMOSD.

Background Evidence is insufficient to show whether fortification has any effect on growth in preterm infants after discharge. Objective to verify whether VLBW preterm infants who are supplemented with multicomponent present greater anthropometric measurements than those not supplemented. Study Design Parallel randomized controlled trial. A computer-generated random number table was used to allocate the participants. Participants Preterm infants discharged from the NICU of a University Hospital from northeast, Brazil, weighing less than 1,500 g exclusively breastfed at discharge and followed up until they reached 6 months corrected gestational age.  Intervention intervention group received Nestlé® PreNan® formula, fractionated in 2 g of powder, mixed with the mother's milk twice a day. Control group was exclusively breastfed. Follow-up was conducted until the infants reached 6 months corrected gestational age (CGA). Outcomes Growth of the anthropometrics parameters weight, head circumference (HC) and lenth with 6 months of corrected age.  Mixed effects model for longitudinal data was used. Interaction according to sex was detected and ajusted. Results Weight gain was significantly higher in the intervention group. This effect was verified only for males (p = 0.001). No statistically significant association was observed between the intervention and the head circumference or length (p = 0.211; 0.597). The weaning rate at the end of follow-up was similar in both groups. Conclusions Breastmilk supplementation may improve the weight gain of very low birthweight preterm infants up to six months corrected gestational age. This effect differed by sex and was considered significant only for males.

Case report: A 62-year-old patient was transferred from another hospital with complaints of subacute torpor and fever two months after an allogeneic bone marrow transplant. He had the diagnosis of chronic myelomonocytic leukemia type 2 four years before the beginning of the neurological symptoms. The disease remained stable for two years after the diagnosis, but progressed and he was submitted to a bone marrow transplant. The complications during the procedure were a febrile neutropenia, that resolved with a cycle of antibiotics, and a reactivation of cytomegalovirus (CMV) infection (he had a high risk to reactivation due to the status of antibodies of the donator, that was negative, and he had positive antibodies). He remained stable and was discharged from the hospital 30 days after the transplant. Two months after the transplant, the fever and torpor began, and he went to the emergency department in his hometown. There, he was diagnosed with a positive coronavirus disease 2019 (COVID-19) infection and reactivation of cytomegalovirus, with prescription of endovenous ganciclovir, without clinical improvement. His clinical symptoms evolved to loss of balance and progressive torpor, and was transferred to our hospital for clinical evaluation. In the initial examination, he was febrile, torporous, he was not collaborative to the neurological examination due to the level of consciousness. He was hypotonic and had withdrawal from a painful stimulus on four limbs. His tendinous reflexes were hyperactive and symmetrical. Due to his level of consciousness, the cerebellar maneuvers were not testable. He was then submitted to orotracheal intubation due to neurological deterioration. In his complementary investigation, the serum polymerase chain reaction (PCR) for CMV was already negative and his PCR for COVID-19 was also negative. The electroencephalogram showed slow generalized periodic discharges. His computerized tomography showed no abnormalities, so he was submitted to a lumbar puncture that showed 8 cells, with 97% lymphocytes, 74 mg/dL of protein, 26 mg/dL of glucose with no neoplasic cells and a positive PCR for Toxoplasma gondii. The PCR for mycobacterium tuberculosis, cryptococcosis, and viruses were negative. After the results, we started sulfadiazine and pyrimethamine and he was submitted to a magnetic resonance imaging that showed multiple nodular foci of hypersignal in T2/FLAIR (T2-weighted-Fluid-Attenuated Inversion Recovery) and diffusion abnormalities on the cortical surface of the cerebellar hemispheres, thalamus, basal ganglia and subcortical white matter of the cerebral hemispheres, being more evident in the cerebellum and basal ganglia. Besides the atypical radiological findings for neurotoxoplasmosis, his serologic testing on the serum showed an positive immunoglobulin M and immunoglobulin G for Toxoplasma gondii. He had no clinical improvement with the antibiotics, and so, ten days after he was submitted to a new magnetic resonance imaging showing increase in the size and number of multiple small focal lesions with hypersignal on T2/FLAIR in the brain parenchyma, highlighting confluent lesions in the basal ganglia and focal lesions in the cerebellar hemispheres, which show contrast uptake, as well as in the thalamus and midbrain. His neurological symptoms evolved and he showed a minimally conscious state, with spasticity in the four limbs. He was submitted to a new lumbar puncture that showed 1 cell, 78 mg/dL of protein and 50 mg/dl of glucose, an improvement, despite clinical and radiological worsening. Because of the clinical worsening, he was submitted to a brain biopsy. His cerebral biopsy was negative for neoplasic infiltration of the cerebral nervous system, viral infections, cryptococcus and toxoplasmosis. It showed an interstitial CD3 lymphocytic inflammation with vasculitis and frequent macrophages, very rare CD20 lymphocytes and p24 and SV-40 negative. His neuropathological criteria were compatible with CLIPPERS (chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids). The patient was submitted to five days of metilprednisolone and with oral prednisone after, with slow clinical improvement, but probably due to the lack of systemic clinical status of the patient and delayed diagnosis because of the atypical presentation, the patient died of pneumonia.

Introduction: The investigation of hemorrhagic demyelinating cerebral lesions is challenging with diverse etiologies. We report a case of varicella zoster virus (VZV) infection with prominent hemorrhagic demyelinating component and systemic thrombosis. Objectives: Describe a case of hemorrhagic demyelinating lesions and systemic thrombosis secondary to varicella zoster central nervous system infection. Case report: A 45-year-old man presented with a one-week history of left leg strength loss associated with pyramidal liberation on the left side. Brain MRI showed two expansive hemorrhagic lesions, in the frontoparietal lobe and in the cingulate gyrus region. There were T2/FLAIR hypersignal in the subcortical area of both cerebral hemispheres and in the cervical cord, suggestive of demyelination. His arterial magnetic resonance imaging with vessel wall imaging showed focal tapering on the pial branches of the middle cerebral artery, but his digital angiography showed no abnormalities. The lumbar puncture had 8 cells, (lymphocyte predominance), 52 proteins/ dL, and 53 mg/dL of glucose. In two days, he developed a left side hemiplegia associated with seizures and pulmonary thromboembolism, demanding lung mechanical thrombectomy and anticoagulation. He had a positive lupus anticoagulant and a positive VZV IgG in the cerebrospinal fluid associated with positive oligoclonal bands. He received intravenous acyclovir with complete resolution of the symptoms. Conclusion: The clinical manifestations of VZV infection are wide, and we should suspect of this infection in patients with central nervous system demyelinating lesions, even without other skin lesions.

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