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Guillain-Barré syndrome and optic neuritis after Mycoplasma pneumoniae infection
Brain & Development xxx (2018) xxx–xxx www.elsevier.com/locate/braindev
Case Report
Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection Manaka Matsunaga a, Yuichi Kodama a,⇑, Shinsuke Maruyama a, Akinori Miyazono a, Shunji Seki a, Takayuki Tanabe a, Michiyoshi Yoshimura b, Junichiro Nishi c, Yoshifumi Kawano a b
a Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan c Department of Microbiology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
Received 3 April 2017; received in revised form 9 January 2018; accepted 19 January 2018
Abstract We report the case of a 12-year-old girl who developed Guillain-Barre´ syndrome (GBS) and optic neuritis (ON) following Mycoplasma pneumoniae infection. Her symptoms, including bilateral vision impairment and tingling in her hands and right foot, were resolved after methylprednisolone pulse therapy. Serum anti-galactocerebroside (Gal-C) IgM antibodies were detected in our patient. This is the first report of a child with GBS and ON associated with M. pneumoniae infection. Ó 2018 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Keywords: Mycoplasma pneumoniae; Optic neuritis; Guillain-Barre´ syndrome, anti-Gal-C
1. Introduction Neurological manifestations have been reported to occur in 1–10% of Mycoplasma pneumoniae infections [1]. Some adults have reportedly developed GuillainBarre´ syndrome (GBS) and optic neuritis (ON) [2–5]. This is the first report of a child developing GBS and ON following M. pneumoniae infection. 2. Case report A previously healthy 12-year-old girl was admitted to a local hospital with fever and cough. Based on clinical ⇑ Corresponding author at: Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. E-mail address: [email protected] (Y. Kodama).
symptoms, she was diagnosed with M. pneumoniae infection and treated successfully with a short course of minocycline. Fourteen days after this diagnosis, she noticed tingling in the palms and fingertips of both hands. She was diagnosed with a straight neck on both cervical computed tomography and magnetic resonance imaging (MRI), and her symptoms improved slightly after taking vitamin supplements. About 30 days after the diagnosis of M. pneumoniae infection, she experienced sudden bilateral vision loss and was admitted to our hospital. On admission, a general clinical examination revealed no abnormality. Neurological symptoms revealed severe loss of visual acuity in both eyes (20/1000, right; 20/50, left) and numbness in both ulnar palms and the first to third right toes. She had no motor weakness, walking disturbance, or paresis after admission. Her level of con-
https://doi.org/10.1016/j.braindev.2018.01.007 0387-7604/Ó 2018 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
2
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx
sciousness, muscle strength, sensitivity, and deep tendon reflexes were normal. Laboratory testing showed normal peripheral blood and biochemical studies. Her M. pneumoniae particle agglutination titers were elevated (1:1280 on admission). Her cerebrospinal fluid revealed a protein concentration of 90.7 mg/dL, cell count of 6/mL, and no oligoclonal band. Plain head MRI showed swelling in both optic nerves (Fig. 1). Plain spinal MRI results were normal. We diagnosed her with bilateral ON associated with M. pneumoniae infection based on imaging findings, examination, and clinical course. She was treated with methylprednisolone pulse therapy (MPT) (1000 mg/day for 3 days) for her ON. At the end of MPT (day 3 of admission), her right eyesight recovered to 20/200. On day 4 after the commencement of MPT, a nerve conduction study showed prolonged duration of proximal and distal compound muscle action potential (CMAP) and delayed F-wave latency in several nerves, and as well as reduced motor nerve conduction velocity, reduced CMAP, and reduced sensory nerve action potential in the ulnar nerve (Table 1),
consistent with demyelinating polyneuropathy. We diagnosed the tingling of the hands and foot as GBS. These findings suggested that the GBS and ON were associated with the M. pneumoniae infection. Antigalactocerebroside (Anti-Gal-C) IgM antibody was detected, but not IgG. Anti-aquaporin-4 antibody results were negative. We observed that the tingling improved after beginning MPT. On day 10, the tingling disappeared completely and her eyesight recovered completely. Plain head MRI showed improvement, except for some abnormal signals in the optic nerves. She was discharged on day 11. She continued taking prednisolone (PSL) and the dose was gradually tapered off. One month after PSL cessation, she was symptomfree, and nerve conduction studies showed that her peripheral nerve was normal. 3. Discussion Our patient experienced GBS and ON following M. pneumoniae infection. Four adults with GBS and ON after M. pneumoniae infection have been reported in
Fig. 1. T2 magnetic resonance image showing swelling in both optic nerves pre-treatment (A) and reduced swelling post-treatment (B).
Table 1 Nerve conduction study. Motor Nerve
Right Median
Left Median
Right Ulnar
Left Ulnar
Right Peroneal
Right Tibial
DML (ms) dDur (ms) dCMAP (mV) pDur (ms) pCMAP (mV) NCV (m/s) F-wave latency Sensory Nerve SNAP (uV) NCV (m/s)
3.5 13.6 3.4 13.9 3.2 55.6 29.8 Right Median 9.6 52.0
3.6 12.1 4.7 NE NE NE NE
3.2 11.2 3.6 14.9 2.8 35.3 35.8 Right Ulnar 5.8 51.9
3.0 8.1 5.6 NE NE NE NE
6.3 9.6 3.6 10.1 3.7 48.3 46.5 Right Sural 21.6 46.1
3.6 6.5 14.3 7.1 12 51.1 43.2
Skin temperature: upper extremity: 32.5 °C, lower extremity: 32.1 °C, underline; abnormal value DML; distal motor latency, CMAP; compound muscle action potential, dCMAP; distal CMAP, pCMAP; proximal CMAP, NCV; nerve conduction velocity, dDur; Duration of distal CMAP, pDur; Duration of proximal CMAP, SNAP; sensory nerve action potential, NE; not examined.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx
3
Table 2 Characteristics in patients with ON and GBS following M. pneumonia infection. Ref
Age
Gender
The duration between infect and neurol symptoms (days)
The order of onset
Treatment
Outcome
J neurol 2004 Eur J Neurol 2002 Aus Nz J Med 1998 Neurol 1993 Our patient
69 53 22 28 12
M M M F F
10 12 8 14 14
ON, GBS ON, GBS GBS, ON GBS, ON GBS, ON
mPSL, IVIg (sep) PE, PSL (con) IVIg, MPT (sep) PE, MPT (sep) MPT
Cure Cure Cure Cure Cure
ON, optic neuritis; GBS, Guillaine-Barre´ syndrome; M. pneumonia, Mycoplasma pneumonia; mPSL, methylprednisolone; IVIg intravenous immuneglobuline; PE, plasma exchange; MPT, methylprednisolone pulse therapy; sep, separately; con, concurrently.
the English literature [2–5] (Table 2). To the best of our knowledge, this is the first pediatric case. In all reported patients, neurological symptoms occurred 8–14 days after the infectious symptoms, similar to our patient’s clinical course, whose extremity tingling occurred 14 days after the diagnosis of M. pneumoniae infection. The order of onset in neurological disease, including GBS and ON, is likely to vary; 2 patients had GBS following ON, and the remaining 3, including ours, experienced ON following GBS. In those reports, even for patients experiencing GBS and ON simultaneously, plasma exchange (PE) or intravenous immunoglobulin (IVIg) was used to treat GBS, while PSL or MPT was used to treat ON. Treatments were performed concurrently or separately depending on the appearance of each symptom. We used only MPT to treat ON. The patient’s tingling and visual acuity improved dramatically following MPT. Although the standard treatment for GBS is IVIg and PE, MPT might have been effective for our patient’s neurological symptoms, including GBS, although it is also possible that her GBS followed a natural clinical course. Gal-C is a major glycolipid in the myelin of both the central and peripheral nervous systems. Anti-Gal-C antibodies have been demonstrated to cross-react with M. pneumoniae antigens and cause demyelination in spinal ganglia, roots, cauda equina, and, less frequently, in peripheral nerves in rabbits immunized with Gal-C. Anti-Gal-C antibody has been detected in patients with GBS and central nervous system diseases, including acute encephalitis and acute disseminated encephalomyelitis. Additionally, in a rat model, ON was induced by injecting anti-Gal-C antibody to the optic nerve [7]. Anti-Gal-C IgM antibodies were detected in our patient. Recently, Kuwahara et al. found that anti-Gal-C IgM antibodies were detected more often in younger patients with CNS diseases, which they speculated could be attributed to a relatively undeveloped blood-brain barrier in children [6]. Based on this paper and our result, the ON in our patient might be related to the anti-Gal-C IgM antibody. By contrast, our patient also had GBS following M. pneumoniae infection. Meyer Sauteur et al. suggested that the anti-
Gal-C IgM antibody was not associated with GBS because there was no difference in the detection of anti-Gal-C IgM antibodies between M. pneumoniae infection with and without GBS [8]. By contrast, they demonstrated that anti-Gal-C IgG was exclusively detected in patients with GBS [8]. However, there have been some reports of patients with GBS with antiganglioside IgM, like our patient [9,10]. A class switch from IgM to IgG might contribute to the pathogenesis of GBS, although anti-Gal-C IgG was not detected in our patient. In conclusion, the combination of GBS and ON following M. pneumoniae infection was observed for the first time in a pediatric patient. Further basic and clinical studies to clarify the role of anti-Gal-C IgM in GBS and ON following M. pneumoniae are warranted. Acknowledgement The authors thank Professor Susumu Kusunoki (Department of Neurology, Kinki University School of Medicine) for examination of serum anti-Gal-C IgG and IgM antibodies. References [1] Tsiodras S, Kelesidis I, Kelesidis T, Stamboulis E, Giamarellou H. Central nervous system manifestations of Mycoplasma pneumoniae infections. J Infect 2005;51:343–54. [2] Ginestal RC, Plaza JF, Callejo JM, Rodrı´guez-Espinosa N, Ferna´ndez-Ruiz LC, Masjua´n J. Bilateral optic neuritis and Guillain-Barre´ syndrome following an acute Mycoplasma pneumoniae infection. J Neurol 2004;251:767–8. [3] Pfausler B, Engelhardt K, Kampfl A, Spiss H, Taferner E, Schmutzhard E. Post-infectious central and peripheral nervous system diseases complicating Mycoplasma pneumoniae infection. Report of three cases and review of the literature. Eur J Neurol 2002;9:93–6. [4] Henderson RD, Ohlrich GD, Pender MP. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Aust N Z J Med 1998;28:481–2. [5] Nadkarni N, Lisak RP. Guillain-Barre´ syndrome (GBS) with bilateral optic neuritis and central white matter disease. Neurology 1993;43:842–3. [6] Kuwahara M, Samukawa M, Ikeda T, Morikawa M, Ueno R, Hamada Y, et al. Characterization of the neurological diseases
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
4
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx associated with Mycoplasma pneumoniae infection and antiglycolipid antibodies. J Neurol 2017;264:467–75. [7] Zhu B, Moore GR, Zwimpfer TJ, Kastrukoff LF, Dyer JK, Steeves JD, et al. Axonal cytoskeleton changes in experimental optic neuritis. Brain Res 1999;824:204–17. [8] Meyer Sauteur PM, Huizinga R, Tio-Gillen AP, Roodbol J, Hoogenboezem T, Jacobs E, et al. Mycoplasma pneumoniae triggering the Guillain-Barre´ syndrome: a case-control study. Ann Neurol 2016;80:566–80.
[9] Koga M, Takahashi M, Yokoyama K, Kanda T. Ambiguous value of anti-ganglioside IgM autoantibodies in Guillain-Barre´ syndrome and its variants. J Neurol 2015;262:1954–60. [10] Furiya Y, Hirano M, Kusunoki S, Ueda M, Sugie K, Nishiwaki T, et al. Complete recovery of an aged patient with Guillain-Barre´ syndrome associated with multiple IgM anti-ganglioside antibodies. Muscle Nerve 2008;38:1630–3.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
Case Report
Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection Manaka Matsunaga a, Yuichi Kodama a,⇑, Shinsuke Maruyama a, Akinori Miyazono a, Shunji Seki a, Takayuki Tanabe a, Michiyoshi Yoshimura b, Junichiro Nishi c, Yoshifumi Kawano a b
a Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan c Department of Microbiology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
Received 3 April 2017; received in revised form 9 January 2018; accepted 19 January 2018
Abstract We report the case of a 12-year-old girl who developed Guillain-Barre´ syndrome (GBS) and optic neuritis (ON) following Mycoplasma pneumoniae infection. Her symptoms, including bilateral vision impairment and tingling in her hands and right foot, were resolved after methylprednisolone pulse therapy. Serum anti-galactocerebroside (Gal-C) IgM antibodies were detected in our patient. This is the first report of a child with GBS and ON associated with M. pneumoniae infection. Ó 2018 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Keywords: Mycoplasma pneumoniae; Optic neuritis; Guillain-Barre´ syndrome, anti-Gal-C
1. Introduction Neurological manifestations have been reported to occur in 1–10% of Mycoplasma pneumoniae infections [1]. Some adults have reportedly developed GuillainBarre´ syndrome (GBS) and optic neuritis (ON) [2–5]. This is the first report of a child developing GBS and ON following M. pneumoniae infection. 2. Case report A previously healthy 12-year-old girl was admitted to a local hospital with fever and cough. Based on clinical ⇑ Corresponding author at: Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. E-mail address: [email protected] (Y. Kodama).
symptoms, she was diagnosed with M. pneumoniae infection and treated successfully with a short course of minocycline. Fourteen days after this diagnosis, she noticed tingling in the palms and fingertips of both hands. She was diagnosed with a straight neck on both cervical computed tomography and magnetic resonance imaging (MRI), and her symptoms improved slightly after taking vitamin supplements. About 30 days after the diagnosis of M. pneumoniae infection, she experienced sudden bilateral vision loss and was admitted to our hospital. On admission, a general clinical examination revealed no abnormality. Neurological symptoms revealed severe loss of visual acuity in both eyes (20/1000, right; 20/50, left) and numbness in both ulnar palms and the first to third right toes. She had no motor weakness, walking disturbance, or paresis after admission. Her level of con-
https://doi.org/10.1016/j.braindev.2018.01.007 0387-7604/Ó 2018 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
2
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx
sciousness, muscle strength, sensitivity, and deep tendon reflexes were normal. Laboratory testing showed normal peripheral blood and biochemical studies. Her M. pneumoniae particle agglutination titers were elevated (1:1280 on admission). Her cerebrospinal fluid revealed a protein concentration of 90.7 mg/dL, cell count of 6/mL, and no oligoclonal band. Plain head MRI showed swelling in both optic nerves (Fig. 1). Plain spinal MRI results were normal. We diagnosed her with bilateral ON associated with M. pneumoniae infection based on imaging findings, examination, and clinical course. She was treated with methylprednisolone pulse therapy (MPT) (1000 mg/day for 3 days) for her ON. At the end of MPT (day 3 of admission), her right eyesight recovered to 20/200. On day 4 after the commencement of MPT, a nerve conduction study showed prolonged duration of proximal and distal compound muscle action potential (CMAP) and delayed F-wave latency in several nerves, and as well as reduced motor nerve conduction velocity, reduced CMAP, and reduced sensory nerve action potential in the ulnar nerve (Table 1),
consistent with demyelinating polyneuropathy. We diagnosed the tingling of the hands and foot as GBS. These findings suggested that the GBS and ON were associated with the M. pneumoniae infection. Antigalactocerebroside (Anti-Gal-C) IgM antibody was detected, but not IgG. Anti-aquaporin-4 antibody results were negative. We observed that the tingling improved after beginning MPT. On day 10, the tingling disappeared completely and her eyesight recovered completely. Plain head MRI showed improvement, except for some abnormal signals in the optic nerves. She was discharged on day 11. She continued taking prednisolone (PSL) and the dose was gradually tapered off. One month after PSL cessation, she was symptomfree, and nerve conduction studies showed that her peripheral nerve was normal. 3. Discussion Our patient experienced GBS and ON following M. pneumoniae infection. Four adults with GBS and ON after M. pneumoniae infection have been reported in
Fig. 1. T2 magnetic resonance image showing swelling in both optic nerves pre-treatment (A) and reduced swelling post-treatment (B).
Table 1 Nerve conduction study. Motor Nerve
Right Median
Left Median
Right Ulnar
Left Ulnar
Right Peroneal
Right Tibial
DML (ms) dDur (ms) dCMAP (mV) pDur (ms) pCMAP (mV) NCV (m/s) F-wave latency Sensory Nerve SNAP (uV) NCV (m/s)
3.5 13.6 3.4 13.9 3.2 55.6 29.8 Right Median 9.6 52.0
3.6 12.1 4.7 NE NE NE NE
3.2 11.2 3.6 14.9 2.8 35.3 35.8 Right Ulnar 5.8 51.9
3.0 8.1 5.6 NE NE NE NE
6.3 9.6 3.6 10.1 3.7 48.3 46.5 Right Sural 21.6 46.1
3.6 6.5 14.3 7.1 12 51.1 43.2
Skin temperature: upper extremity: 32.5 °C, lower extremity: 32.1 °C, underline; abnormal value DML; distal motor latency, CMAP; compound muscle action potential, dCMAP; distal CMAP, pCMAP; proximal CMAP, NCV; nerve conduction velocity, dDur; Duration of distal CMAP, pDur; Duration of proximal CMAP, SNAP; sensory nerve action potential, NE; not examined.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx
3
Table 2 Characteristics in patients with ON and GBS following M. pneumonia infection. Ref
Age
Gender
The duration between infect and neurol symptoms (days)
The order of onset
Treatment
Outcome
J neurol 2004 Eur J Neurol 2002 Aus Nz J Med 1998 Neurol 1993 Our patient
69 53 22 28 12
M M M F F
10 12 8 14 14
ON, GBS ON, GBS GBS, ON GBS, ON GBS, ON
mPSL, IVIg (sep) PE, PSL (con) IVIg, MPT (sep) PE, MPT (sep) MPT
Cure Cure Cure Cure Cure
ON, optic neuritis; GBS, Guillaine-Barre´ syndrome; M. pneumonia, Mycoplasma pneumonia; mPSL, methylprednisolone; IVIg intravenous immuneglobuline; PE, plasma exchange; MPT, methylprednisolone pulse therapy; sep, separately; con, concurrently.
the English literature [2–5] (Table 2). To the best of our knowledge, this is the first pediatric case. In all reported patients, neurological symptoms occurred 8–14 days after the infectious symptoms, similar to our patient’s clinical course, whose extremity tingling occurred 14 days after the diagnosis of M. pneumoniae infection. The order of onset in neurological disease, including GBS and ON, is likely to vary; 2 patients had GBS following ON, and the remaining 3, including ours, experienced ON following GBS. In those reports, even for patients experiencing GBS and ON simultaneously, plasma exchange (PE) or intravenous immunoglobulin (IVIg) was used to treat GBS, while PSL or MPT was used to treat ON. Treatments were performed concurrently or separately depending on the appearance of each symptom. We used only MPT to treat ON. The patient’s tingling and visual acuity improved dramatically following MPT. Although the standard treatment for GBS is IVIg and PE, MPT might have been effective for our patient’s neurological symptoms, including GBS, although it is also possible that her GBS followed a natural clinical course. Gal-C is a major glycolipid in the myelin of both the central and peripheral nervous systems. Anti-Gal-C antibodies have been demonstrated to cross-react with M. pneumoniae antigens and cause demyelination in spinal ganglia, roots, cauda equina, and, less frequently, in peripheral nerves in rabbits immunized with Gal-C. Anti-Gal-C antibody has been detected in patients with GBS and central nervous system diseases, including acute encephalitis and acute disseminated encephalomyelitis. Additionally, in a rat model, ON was induced by injecting anti-Gal-C antibody to the optic nerve [7]. Anti-Gal-C IgM antibodies were detected in our patient. Recently, Kuwahara et al. found that anti-Gal-C IgM antibodies were detected more often in younger patients with CNS diseases, which they speculated could be attributed to a relatively undeveloped blood-brain barrier in children [6]. Based on this paper and our result, the ON in our patient might be related to the anti-Gal-C IgM antibody. By contrast, our patient also had GBS following M. pneumoniae infection. Meyer Sauteur et al. suggested that the anti-
Gal-C IgM antibody was not associated with GBS because there was no difference in the detection of anti-Gal-C IgM antibodies between M. pneumoniae infection with and without GBS [8]. By contrast, they demonstrated that anti-Gal-C IgG was exclusively detected in patients with GBS [8]. However, there have been some reports of patients with GBS with antiganglioside IgM, like our patient [9,10]. A class switch from IgM to IgG might contribute to the pathogenesis of GBS, although anti-Gal-C IgG was not detected in our patient. In conclusion, the combination of GBS and ON following M. pneumoniae infection was observed for the first time in a pediatric patient. Further basic and clinical studies to clarify the role of anti-Gal-C IgM in GBS and ON following M. pneumoniae are warranted. Acknowledgement The authors thank Professor Susumu Kusunoki (Department of Neurology, Kinki University School of Medicine) for examination of serum anti-Gal-C IgG and IgM antibodies. References [1] Tsiodras S, Kelesidis I, Kelesidis T, Stamboulis E, Giamarellou H. Central nervous system manifestations of Mycoplasma pneumoniae infections. J Infect 2005;51:343–54. [2] Ginestal RC, Plaza JF, Callejo JM, Rodrı´guez-Espinosa N, Ferna´ndez-Ruiz LC, Masjua´n J. Bilateral optic neuritis and Guillain-Barre´ syndrome following an acute Mycoplasma pneumoniae infection. J Neurol 2004;251:767–8. [3] Pfausler B, Engelhardt K, Kampfl A, Spiss H, Taferner E, Schmutzhard E. Post-infectious central and peripheral nervous system diseases complicating Mycoplasma pneumoniae infection. Report of three cases and review of the literature. Eur J Neurol 2002;9:93–6. [4] Henderson RD, Ohlrich GD, Pender MP. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Aust N Z J Med 1998;28:481–2. [5] Nadkarni N, Lisak RP. Guillain-Barre´ syndrome (GBS) with bilateral optic neuritis and central white matter disease. Neurology 1993;43:842–3. [6] Kuwahara M, Samukawa M, Ikeda T, Morikawa M, Ueno R, Hamada Y, et al. Characterization of the neurological diseases
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007
4
M. Matsunaga et al. / Brain & Development xxx (2018) xxx–xxx associated with Mycoplasma pneumoniae infection and antiglycolipid antibodies. J Neurol 2017;264:467–75. [7] Zhu B, Moore GR, Zwimpfer TJ, Kastrukoff LF, Dyer JK, Steeves JD, et al. Axonal cytoskeleton changes in experimental optic neuritis. Brain Res 1999;824:204–17. [8] Meyer Sauteur PM, Huizinga R, Tio-Gillen AP, Roodbol J, Hoogenboezem T, Jacobs E, et al. Mycoplasma pneumoniae triggering the Guillain-Barre´ syndrome: a case-control study. Ann Neurol 2016;80:566–80.
[9] Koga M, Takahashi M, Yokoyama K, Kanda T. Ambiguous value of anti-ganglioside IgM autoantibodies in Guillain-Barre´ syndrome and its variants. J Neurol 2015;262:1954–60. [10] Furiya Y, Hirano M, Kusunoki S, Ueda M, Sugie K, Nishiwaki T, et al. Complete recovery of an aged patient with Guillain-Barre´ syndrome associated with multiple IgM anti-ganglioside antibodies. Muscle Nerve 2008;38:1630–3.
Please cite this article in press as: Matsunaga M et al. Guillain-Barre´ syndrome and optic neuritis after Mycoplasma pneumoniae infection. Brain Dev (2018), https://doi.org/10.1016/j.braindev.2018.01.007