Cancer

Cancer. prevent paraplegia, especially in patients with hematologic neoplasia. Intrathecal (it) chemotherapeutic regimens such as methotrexate (MTX) combined with cytarabine arabinoside (Ara\C) are used as treatment and prophylaxis of central nervous system (CNS) leukemia.1, 2 Neurological complications of this chemotherapy vary from asymptomatic chemical arachnoiditis to stroke\mimics, leukoencephalopathy, myelopathy, and/or Maackiain cauda equina syndrome.3, 4, 5, 6, 7 MXT is a dihydrofolate reductase inhibitor that induces experimental demyelination.8 Despite the mechanisms of Maackiain MXT toxicity are unclear, some authors suggested to be dose dependent and related to a possible reduce clearance9 in cerebrospinal fluid while others related to a local depletion of folate due to MTX consumption folate10 and the improvement after folic acid supplementation.11, 12 Electrophysiological studies may help in useful in this setting. Among all the findings, the F wave latency measures the conduction time in motor fibers from the stimulus site to the spinal cord and subsequent return to the peripheral site of recording. Its absence provides evidence of conduction block of anterior rami at specific root level and has been considered specific for demyelination.13 We reported two cases of acute neurotoxicity related to MTX\it with an early neurophysiological screening that help to define poor prognosis and review of previous clinical and neurophysiological cases published in the literature. 2.?MATERIALS AND METHODS Two patients were referred to the Neurology Department of Hospital Clinic in Barcelona. The neurophysiological assessments were performed with Dantec KeyPoint Net G4 electromyograph (Natus Medical Inc., Pleasanton, CA, USA) following conventional methods for routine electrodiagnostic testing. The study was approved by the Ethical Committee of the Hospital Clinic of Barcelona, and all patients gave their written informed consent which included image permission for publication. 2.1. Case report 1 A 58\year\old man with high\grade B lymphoma received treatment with cyclophosphamide and rituximab, and triple intrathecal therapy Maackiain (MTX, Ara\C, and dexamethasone) as CNS prophylaxis. He received three doses of MTX\it, with a total dose of 36?mg in three non\consecutive days. Ten days after the last lumbar puncture, he complained with lower limb weakness, which evolved into paraplegia and urinary retention. Neurological examination revealed absence of deep tendon reflexes in lower limbs and a sensory level at T1. Cerebrospinal fluid (CSF) parameters were within normal limits. Nerve conduction studies (NCS) and electromyography (EMG) performed 1?week after neurological onset showed the absence of the F wave in both lower limbs with a minimal amplitude decrease and normal latency in CMAP responses suggesting a lumbosacral polyradiculoneuropathy. No abnormalities were found in upper limbs (see Table ?Table11 and Figure ?Physique1A,B).1A,B). Lumbosacral magnetic resonance imaging (MRI) with gadolinium revealed no abnormalities. MTX\it treatment Maackiain was stopped and the patient was empirically treated with intravenous Maackiain methylprednisolone without improvement. One week later NCS and EMG studies showed a dramatic decrease of motor amplitudes with relatively normal latencies in peroneal and tibial posterior nerves of both sides ( 1?mV) and moderate denervation in proximal and distal muscles of lower limbs (see Table ?Table1).1). Thoracic spinal cord MRI revealed no abnormalities 2?months from onset. No improvement was observed after 6?months of physiotherapy and he remained with flaccid paraplegia and sensory level. Table 1 Results on nerve conduction and EMG studies thead valign=”top” th align=”left” rowspan=”2″ valign=”top” colspan=”1″ /th th align=”left” colspan=”2″ style=”border-bottom:solid 1px #000000″ valign=”top” rowspan=”1″ Patient 1 /th th align=”left” colspan=”2″ style=”border-bottom:solid 1px #000000″ valign=”top” rowspan=”1″ Patient 2 /th th align=”left” valign=”top” rowspan=”1″ colspan=”1″ Onset /th th align=”left” valign=”top” rowspan=”1″ colspan=”1″ After 1?wk /th th align=”left” valign=”top” rowspan=”1″ colspan=”1″ Onset /th th align=”left” valign=”top” rowspan=”1″ colspan=”1″ After 3?wk /th /thead Median nerveMotor distal latency (3.9?ms)3.23.12.92.8CMAP amplitude (6.0?mV)7.47.41513Motor CV (50.0?m/s)60616061SNAP amplitude (21?V)2322ND26F wave latency (31?ms)29292423Peroneal nerveMotor distal latency (5.0?ms)4000CMAP amplitude (2.0?mV)1.1000Motor CV (42.0?m/s)45\\\SNAP Amplitude (4.0?V)6682F wave latency (57.0?ms)NONENONENONENONETibial Posterior nerveMotor distal latency (6.0?ms)5.55.25.10CMAP amplitude (3.0?mV)20.310Motor CV (38.0?m/s)404152\F wave latency (57.0?ms)NONENONENONENONESural nerveSensory distal latency (3.0?ms)2,6ND2,52.6SNAP amplitude (7.0?V)8ND2520Sensory CV (38.0?m/s)53ND6252Tibialis AnteriorFibrillation potentials+++++++++MUP recruitmentRRRRQuadricepsFibrillation potentials+++++++++MUP recruitmentRRRR Open in a separate window 1?wk, one week; CMAP, compound muscle action potential; CV, conduction velocity; MUP, motor unit potential; ND, not done; NONE, no response; R, Rabbit polyclonal to AMACR reduced; SNAP, sensory nerve action potential; Fibrillation qualitative measurement: + minimum; ++ moderate; +++ moderate; ++++ severe. Open in a separate window Physique 1 Case 1: Nerve conduction study at the initial phase (A) showed a relatively preserved compound motor action potential (CMAP) together with absent proximal F wave for the same nerve (proximal motor conduction block). The same study was repeated 1?wk after (B) and it showed severely decreased amplitudes without latencies delay at lower limbs. Case 2: Lumbosacral magnetic resonance imaging (MRI) at T1\weighted with gadolinium in sagittal sequences showed an enhancement of spinal cord roots at L2 level (C, arrow) 2.2. Case report 2 A 26\year\old woman previously diagnosed with acute lymphocytic leukemia in 2017 was treated with dexamethasone, vincristine, MTX,.