A Case of the Cauda Equina Syndrome Associated With the Intrathecal Chemotherapy in a Patient With Primary Central Nervous System Lymphoma
A 58-year-old male patient who had no past medical history presented with fatigue, subjective feeling of the left lower-extremity weakness for 1 month, and the left facial palsy for 3 days. Brain MRI was preformed after admission to the Department of Neurosurgery at the Konkuk University Medical Center. A brain tumor was revealed at corpus callosum and septum pellucidum. On the physical examination was observed was the central type left facial palsy without other neurological abnormalities. He underwent craniotomy and a tumor removal operation, and didn't show any changes in the neurological examination following the surgery. After the diagnosis of the diagnosed as diffuse large B-cell lymphoma on the tissue biopsy, the patient he was transferred to the Department of Internal Medicine for chemotherapy. He received one treatment of the systemic chemotherapy, with MTX, thiopeta, and vincristine, 16 days after the surgery. Five weeks after the surgery, the patient he underwent the IT chemotherapy 9 times, with MTX 15 mg, Ara-C 40 mg, and hydrocortisone 50 mg over a 4-week period, followed by the intracranial radiation therapy with 30 Gy doses. After 4 weeks from the initiation of the IT chemotherapy, he developed a gradual weakness of the bilateral lower extremities, and then dysuria 4 days later. The cerebrospinal fluid (CSF) study was normal with a pressure of 13.0 cm H2O, the protein level 78.1 mg/dL, and the glucose level more than 70% of blood sugar. There were no findings of white blood cells nor malignant cells in the CSF. The patient was transferred to the Department of Rehabilitation Medicine for the evaluation and treatment of the bilateral lower extremities weakness. He demonstrated a Medical Research Council (MRC) grade III weakness of the right hip flexor and knee extensor, MRC grade II weakness of the right hip extensor, knee flexor, ankle dorsiflexor and plantarflexor, and big toe extensor and flexor, and general MRC grade II weakness of the left lower extremity. There was hypesthesia to the pain, temperature, vibration, and proprioception at the dermatome below L2 level bilaterally. There were no responses of the bilateral knee and the ankle deep tendon reflexes, and the pathologic reflexes including Babinski sign and ankle clonus were absent. He received a Foley catheter insertion, as he did not have any urination sense and was not able to void at all. He also could not sense anal mucosa touch or deep anal pressure, and showed weakness of the anal sphincter muscle. There were no responses of the bilateral bulbocavernosus reflexes (BCR). However, the bilateral upper extremities and trunk had normal neurological findings. Electrodiagnostic examination was performed 5 weeks after the onset of the bilateral lower extremities weakness. It revealed a decreased compound muscle action potential (CMAP) amplitude of the right common peroneal nerve, measured from the extensor digitorum brevis (EDB) and the left tibial nerve from the abductor hallucis (AH) muscles. No CMAP response was detected from the left EDB muscle. There were normal sensory findings of the bilateral superficial peroneal and sural nerves. Late response studies showed the delayed F-wave latency of the left tibial nerve, with no F-wave of the left common peroneal nerve. The H-reflex was absent in the bilateral tibial nerves (). The motor-evoked potentials recorded from the bilateral AH muscles following the stimulation of the bilateral primary motor cortices showed delayed latencies, 46.00 ms in the right and 45.85 ms in the left side. However, the recordings of the bilateral upper extremities were normal. The somatosensory evoked potentials which were recorded on the bilateral somatosensory cortices had no responses when the bilateral tibial nerves were stimulated, but showed normal findings when the bilateral upper extremities were stimulated. The needle electromyogram revealed abnormal spontaneous activities in the bilateral iliopsoas, vastus medialis, tibialis anterior, peroneus longus, gastrocnemius, gluteus maximus, and the 1st sacral paraspinalis muscles, along with the polyphasic motor unit potentials in the left tibialis anterior and the peroneus longus muscles (). The electrodiagnostic study findings were consistent with the bilateral lumbosacral polyradiculopathy from the 2nd lumbar to the 1st sacral spinal nerve. The urodynamic study revealed the areflexic neurogenic bladder which may present the 2nd to the 4th sacral nerves dysfunction. He also presented a decreased sense of the anus and a weakness of the anal sphincter muscle. He was diagnosed with the cauda equina syndrome based on his clinical presentation and the results of the electrodiagnostic and urodynamic studies. The lumbar computed tomography (CT) did not show other lesions except the central spinal stenosis at the L4-5 intervertebral disc level to a mild degree, which was not significant enough to induce a nerve injury (). He received a rehabilitation program regimen including the wheelchair transfer training, strengthening of the upper extremities, activities of daily living training, and management of neurogenic bladder and bowel. There were no neurological improvements upon discharge and at 14 months follow-up visit after the onset.