Acute flaccid paraplegia: a rare complication of meningococcal meningitis

Rathore, Farooq Azam; Gill, Zaheer Ahmed; Malik, A A; Farooq, Fareeha

doi:10.1038/sj.sc.3102120

Cited by 8 publications

(8 citation statements)

References 7 publications

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“…Focal cerebral signs (principally hemiparesis, dysphasia, visual field defects, and gaze preference) occur in a considerable number of patients. Spinal cord dysfunction is a very rare complication of bacterial meningitis and its occurrence is limited to case reports only (2–5). Reported mechanisms for spinal cord dysfunction include infarction due to vasculitis, direct infection of the cord with abscess formation, and immune-mediated inflammatory myelopathy (myelitis) (2–6).…”

Section: Discussionmentioning

confidence: 99%

“…Spinal cord dysfunction is a very rare complication of bacterial meningitis and its occurrence is limited to case reports only (2–5). Reported mechanisms for spinal cord dysfunction include infarction due to vasculitis, direct infection of the cord with abscess formation, and immune-mediated inflammatory myelopathy (myelitis) (2–6). Among bacteria causing meningitis, N. meningitidis and Streptococcus pneumoniae are the most frequent bacterial pathogens associated with spinal cord involvement (4, 7).…”

Section: Discussionmentioning

confidence: 99%

“…Myelitis during bacterial meningitis has been rarely reported and seems to have unfavorable prognosis with persistence of paresis, and bladder and bowel incontinence (4). Most of the cases of spinal cord dysfunction associated with bacterial meningitis occur during treatment or as a late complication of bacterial meningitis (2, 4). In our case, spinal cord dysfunction as the initial and sole manifestation of meningococcal meningitis (in absence of fever, neck stiffness, and other manifestations of meningitis) makes it an unusual and unique case.…”

Section: Discussionmentioning

confidence: 99%

“…Well-known neurological complications of meningococcal meningitis include brain edema, obstructive hydrocephalus, cranial nerve palsies, and septic shock (1, 2). Acute myelopathy with sudden paraplegia is a very rare complication of N. meningitidis infection with only a few cases reported in the literature (2, 3). Most of the previously reported cases of acute myelopathy complicating meningococcal meningitis develop during or following treatment for meningitis.…”

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confidence: 99%

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Acute myelopathy with sudden paraplegia as the sole manifestation of meningococcal meningitis

Ibrahim

Elalamy

Doiphode

et al. 2010

Libyan Journal of Medicine

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Acute myelopathy with sudden paraplegia is a very rare manifestation of meningococcal meningitis, with only a few cases reported in the literature. In almost all previously reported cases, other clinical manifestations of meningitis, such as fever, headache, and neck stiffness preceded acute myelopathy. In this paper, we report a case of acute myelopathy with sudden paraplegia as the sole manifestation of meningococcal meningitis, in the absence of other clinical manifestations of meningitis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Acute myelopathy with sudden paraplegia as the sole manifestation of meningococcal meningitis

Ibrahim

Elalamy

Doiphode

et al. 2010

Libyan Journal of Medicine

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“…[2][3][4][5][6]8 Myelitis, an inflammation of the spinal cord, is a rare complication of meningococcal meningitis that usually occurs during treatment or as a late complication. [2][3][4][5][6][7][8] The thoracic cord and conus medullaris are most commonly affected. 4 Symptoms may evolve over hours or days, with lower extremity flaccidity, bowel and bladder dysfunction, and a reduced sensory level.…”

Section: Commentmentioning

confidence: 99%

Diffuse Bacterial Meningitis and Myelitis Secondary to a Diplococcus Organism

Wiebe

Fanella

Wrogemann

et al. 2015

Can. J. Neurol. Sci.

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A 16-year-old, previously healthy, female presented with a 1-week history of sore throat, fever, vomiting, and occipital headache. She also complained of generalized myalgia and lower limb weakness. There was no medication or substance use. Her immunizations were up to date, and she had no recent travel history or contact with persons from overseas. Examination in emergency revealed an unwell girl with nuchal rigidity and generalized hyperesthesia. Muscle strength in the lower extremities was graded 3−/5. In the upper extremities, strength was graded 4+/5 except distally on the right side, which was graded 4−/5 with scooping fingers and difficulty with extension of fingers, along with weak wrist flexion. Sitting was noted to be difficult. Reflexes were decreased in the lower limbs; brisk reflexes were found in the upper limbs.Initial magnetic resonance imaging (MRI) showed extensive T2 signal changes throughout the spinal cord ( Figure 1A,B). MRI of the brain did not reveal any significant intracranial abnormality. Initial differential diagnosis included demyelinating myelitis from an infectious, postinfectious, or inflammatory process. Infarction and neoplastic infiltration of the spinal cord were also considered. Her cerebrospinal fluid (CSF) had increased protein (2.29 g/L), lactate (4.2 mmol/L), cell count 840 × 10 6 /L (neutrophils, 39; lymphocytes, 53; monocytes/macrophages, 8) and normal glucose (2.5 mmol/L). A CSF Gram stain revealed gram-negative diplococci versus coccobacilli (orientation of organism unclear). Blood and CSF cultures were obtained before treatment with intravenous cefotaxime and vancomycin at meningitic doses and dexamethasone (7.5 mg every 6 hours).Overnight, she developed progressive flaccid paralysis of extremities; cefotaxime was switched to ceftriaxone and dexamethasone was switched to daily methylprednisone (1 g for 5 days) followed by oral prednisone (1 g/kg) in tapering doses over 20 days. She demonstrated gradual improvement of her extremity weakness. Repeat MRI showed minimal interval improvement (Figure 2). CSF and blood cultures yielded negative results, as did CFS analysis using 16S RNA PCR. 1 CFS, stool, and nasopharyngeal secretion viral cultures (including polio virus) revealed no causative organism. She was treated with 14 days of antibiotics for presumed bacterial meningitis resulting from either Neisseria meningitidis or Haemophilus influenzae, based on the initial CSF Gram stain. Follow-up MRI 1 month after presentation revealed improvements, with minor residual inflammation/demyelination seen within the cervical/thoracic spinal cord (Figure 3). Two months after her presentation, she was ambulating with cane assistance. A repeat MRI 9 months after presentation showed resolution of abnormal findings. Follow-up 11 months after presentation showed almost complete neurological recovery, with only mild residual bowel and bladder dysfunction.

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