First Report of SARS-CoV-2 Detection in Cerebrospinal Fluid in a Child With Guillain-Barré Syndrome.

Underlying mechanisms on the association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and neurologic complications are still poorly understood. Cases of Guillain-Barré Syndrome (GBS) have been linked to the SARS-CoV-2 infection as the result of dysregulated immune response with damage in neuronal tissues. In the current report, we present the first pediatric case of GBS with detection of SARS-CoV-2 in the cerebrospinal fluid (CFS). This unique case of COVID-19-associated GBS with detection of SARS-CoV-2 RNA in the CSF indicates direct viral involvement inducing peripheral nerve inflammation.

Progressive leg pain and weakness.

A 54-year-old man presented with progressive asymmetric leg pain and weakness. He had a history of invasive squamous cell carcinoma that was fully treated 2 years earlier. His leg symptoms progressed relentlessly during several months. Imaging studies demonstrated enhancement of the cauda equina and leptomeninges of the lower spinal cord. Initial cerebrospinal fluid examination showed an elevated protein concentration and lymphocytic pleocytosis with no malignant cells on cytological analysis. There was short-term improvement in symptoms and cerebrospinal fluid abnormalities with intravenous steroids. Two additional cerebrospinal fluid studies showed normal cytological findings, elevated IgG synthesis, and elevated antibody titers to varicella-zoster virus. Over time, the patient worsened, developed cranial neuropathies, and ultimately died. The pathological diagnosis and the approach to the clinical data are discussed.

Description of six cases of child cauda equina leptomeningitis: an emerging disease.

Child cauda equina leptomeningitis (CCEL) is a typical clinical example of aseptic meningitis with patterns of an emerging disease, and it affects children aged 2-9. Here we will describe six cases of CCEL. After the prodromes, all children underwent an acute phase with hypoasthenia of the lower limbs, hyporeflexia, staggering and ataxia with steppage. Only in one case there were generalized fits and coma of grade 1-2 too. All children underwent a spinal magnetic resonance imaging (MRI), proving pathologic enhancement of cauda equina and conus medullaris leptomeningitis. At the same time, MRI made possible the differential diagnosis between cauda equina leptomeningitis and isolated minor forms of Guillain-Barre syndrome involving the lower limbs. Three hypotheses will be formulated for understanding the pathogen mechanism(s) of CCEL. The first one is based on the presence of an immediate viral damage on the meninges, the second one, the more likely, contemplates the occurrence of an immunomediated mechanism in a host genetically prone to react in an abnormal way from an immune viewpoint. The third hyphotesis consists in a two-time damage: an early immediate damage from the virus, and a later immunomediated reaction.

[Lesions of the conus medullaris and the cauda equina caused by cytomegalovirus in HIV infection. 7 cases]. / Atteintes du cône terminal et de la queue de cheval dues au cytomégalovirus au cours de l'infection à VIH. 7 observations.

OBJECTIVES: Neurologic infections caused by cytomegalovirus are common in patients with acquired immunodeficiency syndrome (AIDS). The prognosis is particularly severe when the infection is localized in the conus medullaris and/or the cauda equina. METHODS: Among the 861 patients with AIDS treated in our unit from 1991 to 1993, 7 cases involving cytomegalovirus infection of the conus medullaris and/or the cauda equina were studied retrospectively. RESULTS OF THE CASE REPORTS: Clinical manifestations were nearly always the same: low back pain, motor deficiency in the lower limbs progressing to flaccid paraplegia and sphincter failure. The cerebrospinal fluid contained a high cell count with unaltered polynuclears and increased protein levels. In 6/7 patients virus cultures and search for the viral genome in the cerebrospinal fluid were positive. The clinical course was favourable in 6 patients after 3 weeks treatment with ganciclovir and/or foscarnet. Virology tests became negative in three-fourths of the patients. Nevertheless, relapse occurred after 4.2 weeks despite long-term therapy. CONCLUSION: The severe clinical course of this disease and the gravity of constantly fatal relapse requires highly adapted treatment and overall health care.