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Antiganglioside GQ1b antibodies mediate a continuum of disorders with overlapping features, fostering the concept of anti-GQ1b antibody syndrome. We present a patient whose palatal insufficiency was the only clinical sign of postinfectious GQ1b antibody syndrome. Cerebral magnetic resonance imaging confirmed involvement of the glossopharyngeal nerve and vagus nerve bilaterally, revealing gadolinium enhancement of both nerves bilaterally and thickening of the left nervus vagus. Magnetic resonance imaging may help in diagnosing postinfectious GQ1b antibody syndrome, especially at early stages and in monosymptomatic patients. Early diagnosis may lead to early therapy, resulting in a milder disease course by preventing further deterioration leading to the ataxia and ophthalmoplegia usually observed in patients with postinfectious GQ1b antibody syndrome., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Encephalitis is characterized clinically by fever, seizure, and an altered level of consciousness. Mycoplasma pneumoniae, a common respiratory pathogen, has been implicated as an etiology of encephalitis. The present study was designed to analyze status epilepticus associated with M. pneumoniae encephalitis in a series of children through retrospective review of cases between January 2002 and January 2008. Systematic clinical data were evaluated. Nine patients were identified: five girls and four boys, aged 4 years to 10 years. All were positive for M. pneumoniae by serology. Six of the nine children (67%) developed refractory status epilepticus. The major clinical symptoms included fever (100%) and upper respiratory symptoms (78%). The most common seizure type was primary focal with secondary generalized seizure (44%). The time of follow-up for this study ranged from 18 months to 86 months. At the end of the study period, two patients had died, seven had developed epilepsy or neurologic deficits, and none had returned to baseline. These data indicate that children with status epilepticus associated with M. pneumoniae encephalitis have high mortality and morbidity. Clinicians should be aware of the potential role of M. pneumoniae in status epilepticus.

We report on the first published case of a Mycoplasma pneumoniae-associated transverse myelitis appearing in childhood and leading to persistent paraplegia and bowel and bladder dysfunctions. Magnetic resonance imaging of the spinal cord indicated extensive transverse myelitis extending from T(5)-T(12). A repeated scan established spinal cord atrophy in the affected area. Various therapies (methylprednisolone pulse therapy, plasmapheresis, and roxythromycine) produced no clinical effect.

In a case of Mycoplasma pneumoniae encephalopathy in a 7-year-old girl, the microorganism was identified by serologic and pharyngeal-swab polymerase chain reaction methods. Failure to detect or isolate the pathogen in the cerebrospinal fluid and the significant rapid clinical recovery of the patient after intravenous immunoglobulin administration suggest an immune-mediated mechanism. In critically ill patients with M. pneumoniae encephalopathy, prompt intravenous immunoglobulin treatment may be beneficial and can be considered as a primary or alternative therapeutic approach, especially when use of corticosteroids is insecure.

Mycoplasma pneumoniae sometimes causes central nervous system manifestations, which may involve the host immune response, as the organism does not directly damage neural cells, or release toxins. Therefore we measured the levels of interleukin-6, interleukin-8, interleukin-18, interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta1 in serum and cerebrospinal fluid samples from patients who manifested central nervous system manifestations during acute M. pneumoniae infection. The subjects were nine patients with early-onset encephalitis (central nervous system disease onset within 7 days from the onset of fever), four with late-onset encephalitis (onset at 8 days or later), three with encephalitis but without fever, and three with aseptic meningitis. Intrathecal elevations of interleukin-6 and interleukin-8 in all four types of central nervous system manifestations, and of interleukin-18 in late-onset encephalitis were observed. None of the cerebrospinal fluid samples contained detectable levels of interferon-gamma, tumor necrosis factor-alpha, or transforming growth factor-beta1. In conclusion, interleukin-6, interleukin-8, and interleukin-18 might be involved in the inflammatory process leading to the central nervous system manifestations caused by M. pneumoniae.

A 4-year-old male presented with acute disseminated encephalomyelitis with seizures and transient amaurosis after initial symptoms of a flulike febrile infection 1 week earlier. Immunoglobulin M type antibody titers against Mycoplasma pneumoniae were significantly increased in serum and cerebrospinal fluid. The patient improved appreciably on immunosuppressive therapy with immunoglobulin. This patient exemplifies a rare case of acute disseminated encephalomyelitis presenting with bilateral transient amaurosis as a complication of M. pneumoniae infection. Aydin A, Atasever S, Cakmakci H. Acute disseminated encephalomyelitis presenting with bilateral transient amaurosis.

We report three new cases of acute central nervous system disease occurring shortly after Mycoplasma pneumoniae infection. The clinical phenotypes were characterized by encephalopathy (n = 2), optic neuritis (n = 1), transverse myelitis (n = 1), and seizures (n = 1). Although there was strong supportive evidence of preceding M. pneumoniae infection, cerebrospinal fluid polymerase chain reaction for M. pneumoniae was negative in all three patients. We propose that these cases resulted from a para-infectious immune-mediated process rather than parenchymal invasion by the microorganism. The two patients treated with steroids improved rapidly, and all three patients have made a full recovery. We review the literature regarding M. pneumoniae central nervous system complications and discuss the proposed pathologic mechanisms; para-infectious immune-mediated disease and parenchymal invasion of the central nervous system. Systematic investigation to discriminate between these two processes will be essential to select appropriate antibiotic and immunomodulatory therapies.

Group A beta-hemolytic streptococcal infections have been reported to cause neuropsychiatric symptoms, such as chorea, tics, and obsessive-compulsive disorder, presumably through autoimmune damage to basal ganglia. Mycoplasma pneumoniae infections have also been reported to cause damage to the basal ganglia. Restless legs syndrome is a movement disorder with focal restlessness, an irresistible desire to move, and exacerbation by long periods of sitting or lying. We present three children with transient restless legs syndrome-like symptoms possibly associated with group A beta-hemolytic streptococcal infection or Mycoplasma pneumoniae infection. One of three patients had persistently elevated enzyme-linked immunosorbent optical density values against human caudate and putamen.

We report on an 8-year-old male with bilateral striatal necrosis secondary to Mycoplasma pneumoniae respiratory infection. This patient has been remarkable for persistent severe dystonia that has been difficult to treat. We share our experience of beneficial responses to multimodal treatment, including moderate doses of trihexyphenidyl, botulinum toxin, and intrathecal baclofen.

Central nervous system manifestations are a common extrapulmonary complication of Mycoplasma pneumoniae infection, of which encephalitis is a well-recognized abnormality in children. In this report the first description of M. pneumoniae infection simultaneously complicated by meningoencephalitis and hemophagocytosis is presented.

Mycoplasma pneumoniae encephalitis is a recognized cause of reversible coma in children. As an etiology of infectious encephalitis, it yields a relatively poorer prognosis than most other causes of infectious encephalopathies. Encephalitis is generally diagnosed by a constellation of clinical symptoms and confirmed by a cerebrospinal fluid (CSF) examination revealing cell pleocytosis and elevated protein. That Mycoplasma pneumoniae encephalopathy can occur in the presence of a normal CSF examination is less well appreciated. The authors report two children who presented with coma and normal CSF findings in whom a diagnosis of acute Mycoplasma pneumoniae infection was made. The two children both had rapid and complete recovery over several days. These cases exemplify that coma can result from acute infection with Mycoplasma pneumoniae in the absence of an inflammatory CSF response and that a normal CSF may herald a more favorable prognosis.

A male patient with acute meningoencephalitis and cerebellitis associated with Mycoplasma pneumoniae infection is described. T2-weighted MRI demonstrated a high-intensity lesion involving the deep white matter of the right cerebellar hemisphere, which was not enhanced on injection of gadolinium. Brain perfusion scintigraphy revealed hypoperfusion in the bilateral cerebellar hemisphere. Polymerase chain reaction analysis using M. pneumoniae-specific primers failed to reveal the existence of the M. pneumoniae genome in cerebrospinal fluid. Conversely, serum antibodies to gangliosides (GM1, GM2, and GT1b) were detected, suggesting a mycoplasma-related neurologic disorder mediated by an immunologic mechanism. These findings support the hypothesis that vasculopathy and demyelination caused by an immunologic mechanism play an important role in the pathogeneses of neurologic disorders associated with M. pneumoniae infection.

Benign acquired isolated abducens nerve palsy in children is a rare condition. The palsy may be due to a postinfectious process; Epstein-Barr virus and cytomegalovirus have been documented etiologies. This is a case report of a boy 26 months of age with benign acquired isolated bilateral abducens nerve palsy. It may be the first report of Mycoplasma pneumoniae as the cause of benign isolated abducens nerve palsy in children.

A transient expressive aphasia associated with focal slowing in the electroencephalogram, is described in a patient with documented Mycoplasma infection. The hypothesis that ischemia is a mechanism for the transient clinical findings is considered in relation to animal studies.

We report a 9-year-old girl with leukoencephalopathy who demonstrated serologic evidence of a Mycoplasma pneumoniae infection. She had a mild upper respiratory tract illness 10 days prior to admission and developed walking difficulty and somnolence. The neurologic symptoms progressed to semicoma and spastic paraplegia over a few days but began to improve on the fourth day. Cranial computed tomography on the eleventh day revealed an area of diffuse low density in the white matter. Cerebrospinal fluid examination was normal. The patient recovered with minimal motor deficits. Cranial computed tomography was normal. She was diagnosed as having leukoencephalopathy complicated by a Mycoplasma pneumoniae infection. The pathogenesis of this infection is believed to be an allergic reaction to Mycoplasma pneumonia of the central nervous system as well as an acute disseminated encephalomyelitis.