Acute polyradiculopathy secondary to idelalisib in Relapsed Classical Hodgkin's lymphoma.

Patients with relapsed or refractory Hodgkin's lymphoma are likely incurable with standard treatment. Idelalisib, a delta-isoform specific Phosphatidyl-inositol-3-kinase (PI3K) inhibitor has shown its efficacy in other hematopoietic B malignancies. We report the case of a 51-years old patient with relapsed and refractory Hodgkin's Lymphoma receiving idelalisib after several regimens of chemotherapy. He achieved a good partial response for several months, unfortunately, idelalisib had to be stopped because of the onset of a severe polyradiculoneuritis attributed to this treatment. We assume here that the polyradiculoneuritis could be caused by T cell mediated autoimmunity to myelin proteins. To our knowledge, this adverse event has never been described so far with idelalisib.

Motor polyradiculopathy during pembrolizumab treatment of metastatic melanoma.

INTRODUCTION: Pembrolizumab, a monoclonal antibody directed against the immune checkpoint programmed cell death-1 receptor (PD-1), has improved survival in patients with advanced melanoma. Neuromuscular immune-mediated side effects have been rarely reported. METHODS: We describe a 44-year-old man with metastatic melanoma who presented with progressive muscle weakness after 23 doses of pembrolizumab. RESULTS: The patient developed asymmetric, proximal muscle weakness and atrophy in all four limbs. Cerebrospinal fluid examination showed albuminocytologic dissociation. MRI revealed contrast enhancement of the lumbosacral roots. Electrodiagnostic studies demonstrated widespread fibrillation potentials in all four limbs, suggesting a generalized motor polyradiculopathy. Despite pembrolizumab discontinuation and treatment with steroids and intravenous immunoglobulin, limb weakness worsened. Electrodiagnostic studies were repeated, and showed marked and diffuse axonal motor damage. Seven weeks after clinical onset the patient was treated with plasma exchanges. He showed no further deterioration. DISCUSSION: We report a severe motor polyradiculopathy associated with an anti-PD-1 agent that expands the spectrum of neuromuscular complications of this class of drugs. Muscle Nerve 56: E162-E167, 2017.

A patient with postpolio syndrome developed cauda equina syndrome after neuraxial anesthesia: A case report.

Combined spinal anesthesia and postoperative epidural analgesia is widely used in orthopedic surgery. Uncommon but serious neurologic complications of neuraxial anesthesia (NA) include direct trauma during needle or catheter insertion, central nervous system infections, and neurotoxicity of local anesthetics. Cauda equina syndrome (CES) is a rare complication after NA but can result in severe neurologic deterioration that may require surgical intervention. We present a case of a 69-year-old woman with postpolio syndrome who developed CES after combined spinal anesthesia and postoperative epidural analgesia. Perioperative observations and follow-up examinations, including magnetic resonance imaging, revealed no evidence of direct needle- or catheter-induced trauma, spinal hematoma, spinal ischemia, intraneural anesthetic injection, or infection. We speculate that CES symptoms were observed because of enhanced sensitivity to a combination of regional anesthetic technique-related microtrauma and neurotoxicity of bupivacaine and ropivacaine. Thus, practitioners should be aware that patients with preexisting neurologic diseases may be at increased risk for CES after NA.

Protective effect of ginsenoside Rg1 on lidocaine-induced apoptosis.

Lidocaine, as an anesthetic substance, is often used for surface and spinal anesthesia. However, studies have shown that lidocaine may induce transient neurological symptoms and cauda equina syndrome. In the present study the effects of the ginsenoside Rg1 (Rg1) on lidocaine­induced apoptosis were assessed in Jurkat cells using flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The data showed that incubation with Rg1 provides protection against lidocaine­induced apoptosis in cultured Jurkat cells. In order to investigate the effect of Rg1 on the apoptosis pathway, caspase 3 gene expression was determined. The results suggested that the protective effect of Rg1 on lidocaine­induced apoptosis is mediated by altering the level of B­cell lymphoma­2 (BCL­2) family proteins and downregulating caspase­3 expression. In conclusion, the present study demonstrated that incubation with Rg1 provides protection against lidocaine­induced apoptosis in cultured Jurkat cells. In addition, the study demonstrated that Rg1 is a notable antiapoptotic molecule that is capable of blocking the caspase­dependent signaling cascade in Jurkat cells, and that the protective effect of Rg1 on lidocaine­induced apoptosis is mediated by altering levels of BCL­2 family proteins and downregulating caspase­3 expression. The present study provides the basis for understanding and evaluating the effect of Rg1 in the in vivo treatment of lidocaine-induced transient neurological symptoms and cauda equina syndrome by lidocaine.

Successful treatment of infliximab-associated immune-mediated sensory polyradiculopathy with intravenous immunoglobulin.

Infliximab, a tumor necrosis factor-alpha antagonist, is used to treat many inflammatory diseases. Various forms of demyelinating neuropathies have been reported as neurological complications associated with infliximab use. There have been few reports of pure sensory neuropathy associated with infliximab. We report the clinical, electrophysiological, and pathological findings of a patient with subacute sensory polyradiculopathy 1 month after infliximab therapy for psoriasis vulgaris. Immune-mediated pathogenesis was suggested by positive anti-ganglioside antibodies and rapid response to intravenous immunoglobulin. This is the first reported case of sensory polyradiculopathy with positive anti-ganglioside antibodies following infliximab therapy. Our findings suggest the clinical importance of immunological investigations and treatment in demyelinating neuropathies following infliximab therapy.

Cauda equina syndrome following combined spinal and epidural anesthesia: a case report.

PURPOSE: To describe a case of complete neurological recovery from cauda equina syndrome lasting ten months following spinal anesthesia with 0.5% hyperbaric bupivacaine and epidural anesthesia with ropivacaine, and to discuss the possible mechanisms involved. CLINICAL FINDINGS: A 79-yr-old man with Paget's disease was scheduled for surgery to remove a skin tumour below his scrotum. He had no history of radicular pain or back pain and no pre-existing neurologic disorder. Surgery was performed with the patient in the supine position. He received 0.5% hyperbaric bupivacaine intrathecally for the procedure and ropivacaine through an epidural catheter for postoperative pain management. After catheter removal, the patient developed urinary retention, fecal incontinence, and perianal hypoesthesia. A lumbosacral magnetic resonance imaging (MRI) revealed no tumour, infarction, degeneration, spinal stenosis, or compression on the cauda equina nerve roots. A diagnosis of cauda equina syndrome was made, and the etiology was thought to be toxicity of bupivacaine either alone or in combination with ropivacaine. After three months, the patient reported some return of sensation at the perianal area, with complete resolution at four months. At the ten-month follow-up visit, the patient had recovered from his urinary retention and fecal incontinence. CONCLUSION: This case suggests that spinal anesthesia, even with an ordinary dose of hyperbaric 0.5% bupivacaine, might induce cauda equina syndrome in older patients.

Anterior lumbosacral polyradiculopathy after intrathecal administration of methotrexate.

Transient paraparesis has been reported with intrathecal chemotherapy agents and the most common cause is an incomplete inflammatory myelopathy. We report a case of a 30-year-old man diagnosed with acute lymphoblastic leukaemia who developed subacute anterior lumbosacral polyradiculopathy following intrathecal methotrexate, an unusual complication of intrathecal chemotherapy in adults. Spinal magnetic resonance discarded myelopathy. Cerebrospinal fluid exam showed elevation of protein, mononuclear pleocytosis and immunoglobulin synthesis. Electrodiagnostic study showed alterations of sensory and motor conductions only in lower limbs, consistent with multilevel radiculopathy. Differential diagnosis included toxic and neoplastic polyradiculopathy, and axonal variant of acute inflammatory demyelinating polyradiculoneuropathy. The authors review possible pathogenic mechanisms and propose several therapeutic and preventive options.

Síndrome de Cauda Equina: publicación de tres casos: Holguín: 2006 / Syndrome caudan horses: publication of three cases: Holguin: 2006

La lidocaina es un anestésico local que se ha utilizado ampliamente por vía subaracnoidea para obtener anestesia raquídea; sin embargo, con su uso pueden aparecer complicaciones entre las que se encuentra el síndrome de cauda equina. Definir una complicación presentada en tres pacientes ocurridos post anestesia raquídea con lidocaina hiperbárica al 5 por ciento. Se describe el cuadro clínico y la evolución de tres pacientes que presentaron alteraciones sugestivas de síndrome de cauda equina, paraplejia ó, paraparesia, insensibilidad en miembros inferiores, no control de los esfínteres, TAC de columna normal después de operaciones de abdomen inferior con anestesia raquídea. Impresionaron como una complicación neurotóxica causada por el anestésico empleado. Se aplicó tratamiento medicamentoso y fisioterapia con evolución favorable en dos pacientes. Las complicaciones neurológicas post raquianestesia están descritas, reportes de neurotóxicidad a la lidocaina hiperbárica al 5 por ciento unido a otros factores se incluyen dentro de las posibles causas del síndrome de cauda equina. La presentación de estos casos nos hace considerar el origen del síndrome de cauda equina y otras circunstancias que pudieran incidir en su aparición(AU)

Neurologic complications associated with intrathecal liposomal cytarabine given prophylactically in combination with high-dose methotrexate and cytarabine to patients with acute lymphocytic leukemia.

Central nervous system (CNS) prophylaxis has led to a significant improvement in the outcome of patients with acute lymphocytic leukemia (ALL). Liposomal cytarabine (Enzon Pharmaceuticals, Piscataway, NJ; Skye Pharma, San Diego, CA), an intrathecal (IT) preparation of cytarabine with a prolonged half-life, has been shown to be safe and effective in the treatment of neoplastic meningitis. Liposomal cytarabine was given for CNS prophylaxis to 31 patients with newly diagnosed ALL. All patients were treated concurrently with hyper-CVAD chemotherapy (fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) including high-dose methotrexate (MTX) and cytarabine on alternating courses. Liposomal cytarabine 50 mg was given intrathecally on days 2 and 15 of hyper-CVAD and day 10 of high-dose MTX and cytarabine courses until completion of either 3, 6, or 10 IT treatments, depending on risk for CNS disease. Five patients (16%) experienced serious unexpected neurotoxicity, including seizures, papilledema, cauda equina syndrome (n = 2), and encephalitis after a median of 4 IT administrations of liposomal cytarabine. Toxicities usually manifested after the MTX and cytarabine courses. One patient died with progressive encephalitis. After a median follow-up of 7 months, no isolated CNS relapses have been observed. Liposomal cytarabine given via intrathecal route concomitantly with systemic chemotherapy that crosses the blood-brain barrier such as high-dose MTX and cytarabine can result in significant neurotoxicity.