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Background: Vasculitic peripheral neuropathy (VPN) is caused by vessel inflammation leading to peripheral nerve injury of acute-to-subacute onset. When VPN occurs in the context of systemic disease it is classified as Systemic Vasculitic Neuropathy (SVN) and as Non-Systemic Vasculitic Neuropathy (NSVN) when restricted to the nerves. Objective: This study aimed to compare the clinical characteristics, biopsy findings and disease outcome in patients with VPN. Methods: Clinical records of adult patients with VPN diagnosed at our institution between June-2002 and June-2019 were retrospectively reviewed. Demographic characteristics, clinical manifestations, nerve conduction studies, nerve biopsies, treatment and clinical evolution were analyzed in all patients with at least 6 months follow-up. Results: Twenty-five patients with VPN were included (SVN, n = 10; NSVN, n = 15). No significant differences in demographic or clinical features were found between groups. The median delay between symptom onset and nerve biopsy was significantly longer in NSVN patients (10 vs 5.5 months, p = 0.009). Erythrocyte sedimentation rate (ESR) values over 20 mm/h were significantly more common in SVN patients (100% vs. 60%, p = 0.024). Nerve biopsies showed active lesions more frequently in treatment-naive patients compared to those who had received at least 2 weeks of corticosteroids (92% vs 38%; p = 0.03), with a higher proportion of definite VPN cases (92 vs 46%; p = 0.04). Conclusions: Although the clinical manifestations are similar, ESR is an important tool to help distinguish between both conditions. Early nerve biopsy in untreated patients increases diagnostic accuracy, avoiding misdiagnosis.

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Background: A treatment-related fluctuation (TRF) in a patient with Guillain-Barré syndrome (GBS) is defined as clinical deterioration within two months of symptom onset following previous stabilization or improvements with treatment. Objective: To investigate the clinical characteristics and factors that could increase the risk of relapse of GBS in patients with and without TRFs. Methods: Retrospective review of medical records of patients (>18 years) with GBS evaluated between January/2006 and July/2019. Demographic and clinical characteristics, ancillary studies, treatment received, and the clinical course of patients with and without TRFs were analyzed. Results: Overall, 124 cases of GBS were included; seven (5.6%) presented TRFs. GBS-TRF cases were triggered more frequently by infectious mononucleosis (28.57 vs. 8.55%; p=0.01). GBS-TRF were initially treated with plasmapheresis more frequently than those without TRF (14.29 vs. 1.70%; p=0.0349). Combined treatment (71.43 vs. 4.27%; p<0.001) and corticosteroids (42.86 vs. 1.71%; p<0.001) were more commonly used in the GBS-TRF group. GBS-TRF patients presented a higher median initial disability score (4 vs. 2; p=0.01). Conclusions: Patients with GBS triggered by infectious mononucleosis and a high degree of initial disability have higher chances of developing TRFs. Although patients with TRF were treated with plasmapheresis more often, the total number was too low to suggest a link between plasma exchange and TRF.

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.