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Poliomyelitis-like syndrome associated with Epstein-Barr virus infection
Poliomyelitis-like Syndrome Associated With Epstein-Barr Virus Infection Michael Wong, MD, PhD, Anne M. Connolly, MD, and Michael J. Noetzel, MD A 20-month-old male presented with an acute clinical syndrome resembling poliomyelitis, characterized by a flaccid monoplegia, areflexia of the involved limb, and preserved sensation. Electrophysiologic studies supported a neuronopathic localization involving the anterior horn cells. Although laboratory evidence for a poliovirus infection was absent, serologic and polymerase chain reaction studies documented an active central nervous system infection with Epstein-Barr virus, indicating that a poliomyelitis-like syndrome may be produced by infectious agents other than enteroviruses. © 1999 by Elsevier Science Inc. All rights reserved. Wong M, Connolly AM, Noetzel MJ. Poliomyelitis-like syndrome associated with Epstein-Barr virus infection. Pediatr Neurol 1999;20:235-237.
Introduction Epstein-Barr virus (EBV) infections may be associated with a variety of neurologic disorders and complications, including encephalitis, transverse myelitis, and neuropathies [1,2]. Although a poliomyelitis-like syndrome has been reported to occur with infectious agents other than polioviruses, most cases have been limited to the enterovirus family [3-5]. This case report describes a patient who presented with clinical, laboratory, and electromyographic evidence of a poliomyelitis-like syndrome associated with an active EBV central nervous system infection.
From the Division of Pediatric Neurology; Department of Neurology; Washington University School of Medicine; St. Louis Children’s Hospital; St. Louis, Missouri.
© 1999 by Elsevier Science Inc. All rights reserved. PII S0887-8994(98)00142-8 ● 0887-8994/99/$20.00
Case Report A 20-month-old previously healthy male presented with a 1-week history of progressive gait difficulties. Seven days before hospitalization, he developed rhinorrhea, cough, and a temperature of 38.4°C. Concurrently he started limping, favoring his right leg. This impairment progressed over 3 days until he was unable to walk or move the right leg. There was no history of arm or left leg weakness, bulbar dysfunction, bowel or bladder dysfunction, or mental status changes. He was seen initially in the emergency department at St. Louis Children’s Hospital and admitted for evaluation. The patient’s past medical history was unremarkable. He began walking at 12 months. He was not taking any medications, and his immunizations were current, including oral polio vaccine at 2, 4, and 12 months. There were no sick contacts, except a paternal grandfather who had Guillain-Barre´ syndrome 2 months earlier. Physical examination at admission revealed that he was afebrile and had a blood pressure of 120/70 mm Hg. General examination was noteworthy for apparent back tenderness on passive movement of either leg. Neurologic examination revealed normal mental status and cranial nerves. Strength and tone in both upper extremities and left lower extremity were normal, except for mild (4/5) weakness in his left iliopsoas and quadriceps. He had a complete flaccid monoplegia of his right leg, with no movement even to noxious stimuli. Deep tendon reflexes were just elicitable in the left leg and both arms; they were absent in his right patellar and achilles tendons. Plantar responses were flexor on the left and absent on the right. Rectal tone was normal and anal wink and cremasteric reflexes were present. Sensation was intact to pinprick in all extremities. Normal laboratory studies during his initial evaluation included electrolytes, glucose, liver function tests, hemogram, sedimentation rate, plain radiographs of the pelvis, spine, and lower extremities, bone scan, and abdominal computed tomography. Cerebrospinal fluid (CSF) analysis revealed a protein of 69 mg/dL, glucose of 64 mg/dL, 10 erythrocytes/ mm3, and 60 leukocytes/mm3, with 71% lymphocytes and 29% monocytes. Repeat CSF 2 weeks later revealed a protein of 41, glucose of 71, 0 erythrocytes, and 7 leukocytes, with 91% lymphocytes and 9% monocytes. Serum IgG and IgM to the viral capsid antigen of EBV were positive at greater than 1:40. Polymerase chain reaction to EBV was positive in the CSF. Serologic studies for poliovirus, cytomegalovirus, mycoplasma, and syphillis were negative. Viral cultures of CSF, stool, and nasopharynx and bacterial cultures of CSF and blood had no growth. This combination of viral cultures is designed to detect a variety of viruses, including adenovirus, influenza, parainfluenza, respiratory syncytial virus, cytomegalovirus, herpes simplex virus, poliovirus, and other enteroviruses. Immunoglobulin and T-cell subpopulation analysis presented no evidence of an immunodeficient state in the patient. Serologic testing of family members, including the grandfather with Guillain-Barre´ syndrome, found no evidence of recent EBV infection. Electrophysiologic studies were performed on hospital days 2 and 15. On day 2 the right tibial motor nerve conduction study (NCS) revealed no compound muscle action potential (CMAP) recorded from the abductor hallucis. The right peroneal motor NCS recorded from the tibialis anterior demonstrated a normal onset latency and proximal conduction velocity, with a small CMAP amplitude (0.71 mV). Electromyogram
Communications should be addressed to: Dr. Wong; Division of Pediatric Neurology; Campus Box 8111; St. Louis Children’s Hospital; One Children’s Place; St. Louis, MO 63110-1093. Received June 10, 1998; accepted October 27, 1998.
Wong et al: EBV-Poliomyelitis Syndrome 235
(EMG) of the right tibialis anterior had no fibrillations but markedly reduced numbers of motor unit potentials. The right gastrocnemius and vastus medialis had no motor unit potentials. In contrast, left tibial and peroneal NCSs and left tibialis anterior EMG, as well as upper extremity studies, were within normal limits. Bilateral sural and right superficial peroneal sensory nerve action potentials and conduction velocities were normal. Somatosensory-evoked responses from the lower extremities revealed normal bilateral cortical latencies. In the repeated electrophysiologic studies on hospital day 15, EMG of the right tibialis anterior revealed fibrillations and positive sharp waves, consistent with a denervating process, and the right peroneal CMAP recording from the tibialis anterior demonstrated some recovery, but the remainder of the findings were unchanged. Magnetic resonance imaging (MRI) of the thoracic and lumbosacral spine with and without gadolinium revealed no abnormalities on hospital day 1. Two weeks later a repeated study revealed nonspecific meningeal enhancement with gadolinium involving the anterior thecal sac around the cauda equina but no other signal abnormalities. Because initial diagnostic considerations included atypical transverse myelitis and Guillain-Barre´ syndrome, the patient received intravenous methylprednisolone (1 gm/1.73 m2/day) for 5 days and intravenous immunoglobulin (1 gm/kg/day) for 2 days. During the first week of a 3-week hospitalization, including transfer to the neurorehabilitation unit, he manifested no change in his neurologic findings, with a persistent flaccid monoplegia. During the second week, he started to demonstrate some recovery of function in his right leg, improving to 2/5 strength in the right iliopsoas and anterior tibialis by the third week. At follow-up visits at 3 and 6 months, he demonstrated modest additional improvement of his right leg with 2 to 3/5 strength in most right leg muscle groups, but tendon reflexes remained absent, and he required a full knee-ankle-foot orthosis to walk.
Discussion The clinical picture of asymmetric flaccid paralysis, mononuclear inflammation and EBV present in the CSF, and electromyographic evidence of a neuronopathy is consistent with a poliomyelitis-like syndrome in this patient. Although it is difficult to definitely localize the precise neuroanatomic defect, the EMG-NCS data strongly suggest involvement of the anterior horn cells innervating the right leg. Furthermore the marked asymmetry of the paralysis, the normal sensory examination, and the normal conduction velocities and somatosensory-evoked potentials make a polyradiculoneuropathic process (i.e., Guillain-Barre´ syndrome) or myelopathic process unlikely. Although MRI signal changes in the ventral spinal cord have been reported in some cases of poliomyelitis-like syndromes [6], the absence of specific MRI abnormalities in the authors’ patient was not helpful in localization. This difference may be the result of the timing of the MRI changes, which may require at least 1 month to be detected, because this patient only received MRI scans during the acute period. Although poliomyelitis resulting from wild type poliovirus has not been reported in the United States since 1979, approximately 10 patients per year still contract vaccine-related poliomyelitis in this country [7]. Vaccineassociated paralytic poliomyelitis generally occurs within 2 months after immunization. In addition to polioviruses, other infectious etiologies of poliomyelitis-like syndromes have been identified, almost all of which also belong to the
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enterovirus family, such as the Coxsackie and the enteric cytopathogenic human orphan viruses [3-5]. One previous case report also linked herpes simplex virus-1 to a patient with probable Hopkins syndrome, a poliomyelitis-like paralysis associated with asthma [8]. In the authors’ patient the negative viral cultures and serologies to poliovirus and the 8-month interval since his last oral polio vaccine immunization make the wild type of poliomyelitis or vaccine-associated poliomyelitis unlikely, whereas the positive serologic findings and presence of EBV DNA in the CSF support the notion that active EBV infection was etiologic. Despite the diverse neurologic sequelae of EBV infections the authors believe that this is the first report of EBV causing a poliomyelitis-like syndrome. EBV infections have also been associated with a number of other neurologic complications involving different parts of the neural axis [1,2], including meningoencephalitis [9], cranial nerve palsies [10], transverse myelitis [11,12], and mono- and polyneuropathies, especially Guillain-Barre´ syndrome [13]. Furthermore, EBV infection can affect multiple levels of the nervous system concurrently or sequentially [14,15]. In some cases an infectious mononucleosis illness can be identified before, simultaneously with, or after the neurologic deficit occurs. Alternatively, neurologic findings may be the sole manifestation of the EBV infection. Pathophysiologically, EBV has been proposed to induce neurologic damage through a number of direct infectious or indirect postinfectious inflammatory mechanisms. In this patient the authors hypothesize that an active EBV infection in the CSF caused either direct viral invasion of or immunologic/ inflammatory reaction to anterior horns cells or their proximal roots, resulting in his monoplegia. In conclusion, a poliomyelitis-like syndrome can result from various etiologies, which may be difficult to distinguish purely on clinical grounds. A detailed immunization history, including timing and type of polio vaccination, is useful in determining the likelihood of vaccine-associated and the wild type of poliomyelitis. If a patient with a poliomyelitis-like syndrome lacks evidence of a poliovirus infection, it is recommended that other infectious etiologies be investigated, including other members of the enterovirus and herpes virus families, such as Coxsackie, enteric cytopathogenic human orphan, herpes simplex, and EBV. References [1] Connelly KP, DeWitt LD. Neurologic complications of infectious mononucleosis. Pediatr Neurol 1994;10:181-4. [2] Grose C, Henle W, Henle G, Feorino P. Primary Epstein-Barr virus infections in acute neurologic diseases. N Engl J Med 1975;292: 392-5. [3] Hayward JC, Gillepie SM, Kaplan EM, et al. Outbreak of poliomyelitis-like paralysis associated with enterovirus 71. Pediatr Infect Dis J 1989;8:611-6. [4] Kopel FB, Shore B, Hodes HL. Non-fatal bulbospinal paralysis due to ECHO 4 virus. J Pediatr 1965;67:588-94. [5] Jarcho LW, Fred HL, Castles CH. Encephalitis and poliomyeli-
tis in the adult due to Coxsackie virus group B, type 5. N Engl J Med 1963;268:235-7. [6] Kornreich L, Dagan O, Grunebaum M. MRI in acute poliomyelitis. Neuroradiol 1996;38:371-2. [7] Querfurth H, Swanson PD. Vaccine-associated paralytic poliomyelitis. Arch Neurol 1990;47:541-4. [8] Kyllerman MG, Herner S, Bergstrom TB, Ekholm SE. PCR diagnosis of primary herpesvirus type I in poliomyelitis-like paralysis and respiratory tract disease. Pediatr Neurol 1993;9:227-9. [9] Domachowske JB, Cunningham CK, Cummings DL, Crosley CJ, Hannan WP, Weiner LB. Acute manifestations and neurologic sequelae of Epstein-Barr virus encephalitis in children. Pediatr Infect Dis J 1996;15:871-5. [10] Snyder R. Bell’s palsy and infectious mononucleosis. Lancet 1973;2:917-8.
[11] Junker AK, Roland EH, Hahn G. Transverse myelitis and Epstein-Barr virus infection with delayed antibody response. Neurology 1991;41:1523-4. [12] Caldas C, Bernicker E, Dal Nogare A, Luby JP. Case report: Transverse myelitis associated with Epstein-Barr virus infection. Am J Med Sci 1994;307:45-8. [13] Grose C, Feorino PM. Epstein-Barr virus and Guillain-Barre´ syndrome. Lancet 1972;2:1285-7. [14] Merelli E, Bedin R, Sola P, et al. Encephalomyeloradiculopathy associated with Epstein-Barr virus: Primary infection or reactivation? Acta Neurol Scand 1997;96:416-20. [15] Tsutsumi H, Kamazaki H, Nakata S, et al. Sequential development of acute meningoencephalitis and transverse myelitis caused by Epstein-Barr virus during infectious mononucleosis. Pediatr Infect Dis J 1994;13:665-7.
Wong et al: EBV-Poliomyelitis Syndrome 237
Introduction Epstein-Barr virus (EBV) infections may be associated with a variety of neurologic disorders and complications, including encephalitis, transverse myelitis, and neuropathies [1,2]. Although a poliomyelitis-like syndrome has been reported to occur with infectious agents other than polioviruses, most cases have been limited to the enterovirus family [3-5]. This case report describes a patient who presented with clinical, laboratory, and electromyographic evidence of a poliomyelitis-like syndrome associated with an active EBV central nervous system infection.
From the Division of Pediatric Neurology; Department of Neurology; Washington University School of Medicine; St. Louis Children’s Hospital; St. Louis, Missouri.
© 1999 by Elsevier Science Inc. All rights reserved. PII S0887-8994(98)00142-8 ● 0887-8994/99/$20.00
Case Report A 20-month-old previously healthy male presented with a 1-week history of progressive gait difficulties. Seven days before hospitalization, he developed rhinorrhea, cough, and a temperature of 38.4°C. Concurrently he started limping, favoring his right leg. This impairment progressed over 3 days until he was unable to walk or move the right leg. There was no history of arm or left leg weakness, bulbar dysfunction, bowel or bladder dysfunction, or mental status changes. He was seen initially in the emergency department at St. Louis Children’s Hospital and admitted for evaluation. The patient’s past medical history was unremarkable. He began walking at 12 months. He was not taking any medications, and his immunizations were current, including oral polio vaccine at 2, 4, and 12 months. There were no sick contacts, except a paternal grandfather who had Guillain-Barre´ syndrome 2 months earlier. Physical examination at admission revealed that he was afebrile and had a blood pressure of 120/70 mm Hg. General examination was noteworthy for apparent back tenderness on passive movement of either leg. Neurologic examination revealed normal mental status and cranial nerves. Strength and tone in both upper extremities and left lower extremity were normal, except for mild (4/5) weakness in his left iliopsoas and quadriceps. He had a complete flaccid monoplegia of his right leg, with no movement even to noxious stimuli. Deep tendon reflexes were just elicitable in the left leg and both arms; they were absent in his right patellar and achilles tendons. Plantar responses were flexor on the left and absent on the right. Rectal tone was normal and anal wink and cremasteric reflexes were present. Sensation was intact to pinprick in all extremities. Normal laboratory studies during his initial evaluation included electrolytes, glucose, liver function tests, hemogram, sedimentation rate, plain radiographs of the pelvis, spine, and lower extremities, bone scan, and abdominal computed tomography. Cerebrospinal fluid (CSF) analysis revealed a protein of 69 mg/dL, glucose of 64 mg/dL, 10 erythrocytes/ mm3, and 60 leukocytes/mm3, with 71% lymphocytes and 29% monocytes. Repeat CSF 2 weeks later revealed a protein of 41, glucose of 71, 0 erythrocytes, and 7 leukocytes, with 91% lymphocytes and 9% monocytes. Serum IgG and IgM to the viral capsid antigen of EBV were positive at greater than 1:40. Polymerase chain reaction to EBV was positive in the CSF. Serologic studies for poliovirus, cytomegalovirus, mycoplasma, and syphillis were negative. Viral cultures of CSF, stool, and nasopharynx and bacterial cultures of CSF and blood had no growth. This combination of viral cultures is designed to detect a variety of viruses, including adenovirus, influenza, parainfluenza, respiratory syncytial virus, cytomegalovirus, herpes simplex virus, poliovirus, and other enteroviruses. Immunoglobulin and T-cell subpopulation analysis presented no evidence of an immunodeficient state in the patient. Serologic testing of family members, including the grandfather with Guillain-Barre´ syndrome, found no evidence of recent EBV infection. Electrophysiologic studies were performed on hospital days 2 and 15. On day 2 the right tibial motor nerve conduction study (NCS) revealed no compound muscle action potential (CMAP) recorded from the abductor hallucis. The right peroneal motor NCS recorded from the tibialis anterior demonstrated a normal onset latency and proximal conduction velocity, with a small CMAP amplitude (0.71 mV). Electromyogram
Communications should be addressed to: Dr. Wong; Division of Pediatric Neurology; Campus Box 8111; St. Louis Children’s Hospital; One Children’s Place; St. Louis, MO 63110-1093. Received June 10, 1998; accepted October 27, 1998.
Wong et al: EBV-Poliomyelitis Syndrome 235
(EMG) of the right tibialis anterior had no fibrillations but markedly reduced numbers of motor unit potentials. The right gastrocnemius and vastus medialis had no motor unit potentials. In contrast, left tibial and peroneal NCSs and left tibialis anterior EMG, as well as upper extremity studies, were within normal limits. Bilateral sural and right superficial peroneal sensory nerve action potentials and conduction velocities were normal. Somatosensory-evoked responses from the lower extremities revealed normal bilateral cortical latencies. In the repeated electrophysiologic studies on hospital day 15, EMG of the right tibialis anterior revealed fibrillations and positive sharp waves, consistent with a denervating process, and the right peroneal CMAP recording from the tibialis anterior demonstrated some recovery, but the remainder of the findings were unchanged. Magnetic resonance imaging (MRI) of the thoracic and lumbosacral spine with and without gadolinium revealed no abnormalities on hospital day 1. Two weeks later a repeated study revealed nonspecific meningeal enhancement with gadolinium involving the anterior thecal sac around the cauda equina but no other signal abnormalities. Because initial diagnostic considerations included atypical transverse myelitis and Guillain-Barre´ syndrome, the patient received intravenous methylprednisolone (1 gm/1.73 m2/day) for 5 days and intravenous immunoglobulin (1 gm/kg/day) for 2 days. During the first week of a 3-week hospitalization, including transfer to the neurorehabilitation unit, he manifested no change in his neurologic findings, with a persistent flaccid monoplegia. During the second week, he started to demonstrate some recovery of function in his right leg, improving to 2/5 strength in the right iliopsoas and anterior tibialis by the third week. At follow-up visits at 3 and 6 months, he demonstrated modest additional improvement of his right leg with 2 to 3/5 strength in most right leg muscle groups, but tendon reflexes remained absent, and he required a full knee-ankle-foot orthosis to walk.
Discussion The clinical picture of asymmetric flaccid paralysis, mononuclear inflammation and EBV present in the CSF, and electromyographic evidence of a neuronopathy is consistent with a poliomyelitis-like syndrome in this patient. Although it is difficult to definitely localize the precise neuroanatomic defect, the EMG-NCS data strongly suggest involvement of the anterior horn cells innervating the right leg. Furthermore the marked asymmetry of the paralysis, the normal sensory examination, and the normal conduction velocities and somatosensory-evoked potentials make a polyradiculoneuropathic process (i.e., Guillain-Barre´ syndrome) or myelopathic process unlikely. Although MRI signal changes in the ventral spinal cord have been reported in some cases of poliomyelitis-like syndromes [6], the absence of specific MRI abnormalities in the authors’ patient was not helpful in localization. This difference may be the result of the timing of the MRI changes, which may require at least 1 month to be detected, because this patient only received MRI scans during the acute period. Although poliomyelitis resulting from wild type poliovirus has not been reported in the United States since 1979, approximately 10 patients per year still contract vaccine-related poliomyelitis in this country [7]. Vaccineassociated paralytic poliomyelitis generally occurs within 2 months after immunization. In addition to polioviruses, other infectious etiologies of poliomyelitis-like syndromes have been identified, almost all of which also belong to the
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enterovirus family, such as the Coxsackie and the enteric cytopathogenic human orphan viruses [3-5]. One previous case report also linked herpes simplex virus-1 to a patient with probable Hopkins syndrome, a poliomyelitis-like paralysis associated with asthma [8]. In the authors’ patient the negative viral cultures and serologies to poliovirus and the 8-month interval since his last oral polio vaccine immunization make the wild type of poliomyelitis or vaccine-associated poliomyelitis unlikely, whereas the positive serologic findings and presence of EBV DNA in the CSF support the notion that active EBV infection was etiologic. Despite the diverse neurologic sequelae of EBV infections the authors believe that this is the first report of EBV causing a poliomyelitis-like syndrome. EBV infections have also been associated with a number of other neurologic complications involving different parts of the neural axis [1,2], including meningoencephalitis [9], cranial nerve palsies [10], transverse myelitis [11,12], and mono- and polyneuropathies, especially Guillain-Barre´ syndrome [13]. Furthermore, EBV infection can affect multiple levels of the nervous system concurrently or sequentially [14,15]. In some cases an infectious mononucleosis illness can be identified before, simultaneously with, or after the neurologic deficit occurs. Alternatively, neurologic findings may be the sole manifestation of the EBV infection. Pathophysiologically, EBV has been proposed to induce neurologic damage through a number of direct infectious or indirect postinfectious inflammatory mechanisms. In this patient the authors hypothesize that an active EBV infection in the CSF caused either direct viral invasion of or immunologic/ inflammatory reaction to anterior horns cells or their proximal roots, resulting in his monoplegia. In conclusion, a poliomyelitis-like syndrome can result from various etiologies, which may be difficult to distinguish purely on clinical grounds. A detailed immunization history, including timing and type of polio vaccination, is useful in determining the likelihood of vaccine-associated and the wild type of poliomyelitis. If a patient with a poliomyelitis-like syndrome lacks evidence of a poliovirus infection, it is recommended that other infectious etiologies be investigated, including other members of the enterovirus and herpes virus families, such as Coxsackie, enteric cytopathogenic human orphan, herpes simplex, and EBV. References [1] Connelly KP, DeWitt LD. Neurologic complications of infectious mononucleosis. Pediatr Neurol 1994;10:181-4. [2] Grose C, Henle W, Henle G, Feorino P. Primary Epstein-Barr virus infections in acute neurologic diseases. N Engl J Med 1975;292: 392-5. [3] Hayward JC, Gillepie SM, Kaplan EM, et al. Outbreak of poliomyelitis-like paralysis associated with enterovirus 71. Pediatr Infect Dis J 1989;8:611-6. [4] Kopel FB, Shore B, Hodes HL. Non-fatal bulbospinal paralysis due to ECHO 4 virus. J Pediatr 1965;67:588-94. [5] Jarcho LW, Fred HL, Castles CH. Encephalitis and poliomyeli-
tis in the adult due to Coxsackie virus group B, type 5. N Engl J Med 1963;268:235-7. [6] Kornreich L, Dagan O, Grunebaum M. MRI in acute poliomyelitis. Neuroradiol 1996;38:371-2. [7] Querfurth H, Swanson PD. Vaccine-associated paralytic poliomyelitis. Arch Neurol 1990;47:541-4. [8] Kyllerman MG, Herner S, Bergstrom TB, Ekholm SE. PCR diagnosis of primary herpesvirus type I in poliomyelitis-like paralysis and respiratory tract disease. Pediatr Neurol 1993;9:227-9. [9] Domachowske JB, Cunningham CK, Cummings DL, Crosley CJ, Hannan WP, Weiner LB. Acute manifestations and neurologic sequelae of Epstein-Barr virus encephalitis in children. Pediatr Infect Dis J 1996;15:871-5. [10] Snyder R. Bell’s palsy and infectious mononucleosis. Lancet 1973;2:917-8.
[11] Junker AK, Roland EH, Hahn G. Transverse myelitis and Epstein-Barr virus infection with delayed antibody response. Neurology 1991;41:1523-4. [12] Caldas C, Bernicker E, Dal Nogare A, Luby JP. Case report: Transverse myelitis associated with Epstein-Barr virus infection. Am J Med Sci 1994;307:45-8. [13] Grose C, Feorino PM. Epstein-Barr virus and Guillain-Barre´ syndrome. Lancet 1972;2:1285-7. [14] Merelli E, Bedin R, Sola P, et al. Encephalomyeloradiculopathy associated with Epstein-Barr virus: Primary infection or reactivation? Acta Neurol Scand 1997;96:416-20. [15] Tsutsumi H, Kamazaki H, Nakata S, et al. Sequential development of acute meningoencephalitis and transverse myelitis caused by Epstein-Barr virus during infectious mononucleosis. Pediatr Infect Dis J 1994;13:665-7.
Wong et al: EBV-Poliomyelitis Syndrome 237