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Acute Severe Spinal Cord Dysfunction in Bacterial Meningitis in Adults
MRI Findings Suggest Extensive Myelitis
Stefan Kastenbauer, MD;
Frank Winkler, MD;
Gunther Fesl, MD;
Xaver Schiel, MD;
Helmut Ostermann, MD, PhD;
Tarek A. Yousry, MD, PhD;
Hans Walter Pfister, MD, PhD
Arch Neurol. 2001;58:806-810.
ABSTRACT
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Background Bacterial meningitis is rarely complicated by acute spinal cord involvement
(eg, myelitis, ischemic infarction, spinal abscess, or epidural hemorrhage).
In spinal cord dysfunction, magnetic resonance imaging (MRI) is the imaging
modality of choice. Still, MRI findings of myelitis due to bacterial meningitis
in adults have not been reported.
Methods Spinal MRIs were obtained during the acute stage of meningitis and on
follow-up in 3 adults with bacterial meningitis that was complicated by paraparesis
or tetraparesis and bowel and bladder incontinence. The causative pathogens
were Streptococcus pneumoniae and Neisseria meningitidis; in 1 patient, the pathogen was not identified.
Results In all cases, spinal MRI ruled out a compression of the cord by an extramedullary
mass but demonstrated hyperintensities on T2-weighted images that predominantly
involved the gray matter and extended from the cervical to the lumbar cord.
Leptomeningeal and discrete nodular intramedullary enhancement on T1-weighted
images was detected only in 1 patient. Follow-up examinations revealed that
hyperintensities resolved completely in 1 patient, while a central cavitation
developed in the cervical spinal cord of another, and the MRI findings were
progressive during the first 4 weeks in the third patient. In all cases, severe
paresis and bowel and bladder incontinence persisted.
Conclusion We demonstrate for the first time the MRI findings of adults with acute
spinal cord involvement during bacterial meningitis. Magnetic resonance imaging
showed central intramedullary hyperintensities on T2-weighted images that
extended from the cervical to the lumbar cord, indicating myelitis. Clinical
follow-up examinations suggest that myelitis during bacterial meningitis has
an unfavorable prognosis.
INTRODUCTION
BACTERIAL MENINGITIS is frequently accompanied by intracranial complications,
such as cerebrovascular involvement, brain edema, hydrocephalus, or hearing
impairment, as well as systemic complications, such as septic shock, adult
respiratory distress syndrome, or disseminated intravascular coagulation.1, 2, 3 Spinal cord involvement
is a rare complication of bacterial meningitis.4
Besides cord compression by a spinal abscess or epidural hemorrhage following
lumbar puncture, the cord can be affected by ischemia due to vasculitis, shock,
herniation, or arachnoiditis, and by myelitis.4
Spinal magnetic resonance imaging (MRI) during the acute stage of spinal cord
dysfunction has been reported in only 2 children: no abnormalities were detected
in one child,4 and enhancement of the cauda
equina and lumbosacral nerve roots was seen in the other.5
We describe 3 patients who developed severe spinal cord dysfunction
during the acute stage of bacterial meningitis and their MRI findings during
this condition.
REPORT OF CASES
CASE 1
A 36-year-old woman was admitted to a local hospital with a 4-day history
of fever, back pain, and weakness of both legs. Three years previously, she
had undergone splenectomy for idiopathic thrombocytopenic purpura, and 3 months
prior to admission, she had received her last pneumococcal vaccination. On
admission, the patient was febrile, agitated, and confused. Neurologic examination
revealed neck stiffness, an incomplete bilateral sixth nerve palsy, and a
tetraparesis (muscle power grade, 4/5 in the arms and 2/5 in the legs). Muscle
tone and tendon reflexes were decreased in the legs compared with the arms.
The plantar response of the left foot was extensor. Blood cultures were positive
for Streptococcus pneumoniae. Intravenous benzylpenicillin
and ceftriaxone were administered, and the patient was transferred to our
hospital. The cerebrospinal fluid (CSF) contained 792 cells/µL (94%
granulocytes), the protein level was 6.3 g/L, and the CSF glucose level was
less than 10% of the serum glucose level. Gram-positive diplococci were present
in the CSF, and the latex agglutination test result was positive for pneumococcal
antigen; however, CSF cultures remained sterile. Because myelitis was suspected,
the patient was given intravenous dexamethasone (24 mg/d) for 4 days. The
clinical course was further complicated by ischemic infarction in the right
frontal lobe due to cerebral vasculitis. Three months after the onset of disease,
the patient had a spastic tetraparesis (muscle power grade, 4/5 in the arms
and 2/5 in the legs). Sensibility was intact, but bladder and bowel control
were still absent.
CASE 2
A 33-year-old man who had been hospitalized because of bronchitis and
mild graft-vs-host disease of the liver following allogeneic bone marrow transplantation
for chronic myeloid leukemia 6 months previously developed fever and headache
despite oral antibiotic therapy (amoxicillin, ciprofloxacin, and fluconazole).
Within 24 hours of admission, weakness of both legs and bowel and bladder
incontinence appeared. Examination revealed discrete neck stiffness, spastic
paraplegia, and a sensory level at C1. The CSF contained 2976 cells/µL
(94% granulocytes, no malignant cells), the protein level was 1.07 g/L, and
the CSF glucose level was less than 40% of the serum glucose level. There
were no findings on Gram stain of CSF, and cultures of blood and CSF were
sterile. Transcranial Doppler sonography and cranial MRI were normal. Nosocomial
bacterial meningitis was suspected, and the patient was treated with intravenous
vancomycin, meropenem, metronidazole, and a 4-day regimen of oral dexamethasone,
24 mg/d. Six weeks after onset of meningitis, follow-up examination showed
a motor level at C8, with a power grade of 4/5 in the small muscles of the
hand and 2/5 in the legs. No clear sensory level could be determined, but
sensibility and vibratory sense were decreased in both legs. Bowel and bladder
incontinence were still present.
CASE 3
A previously healthy 17-year-old boy was admitted to a local hospital
with a 1-day history of fever, nausea, and headache. Examination revealed
no focal neurologic deficit, but a discrete neck stiffness and a petechial
rash on the trunk and extremities. Shortly after admission, he had a respiratory
arrest, at which time no blood pressure could be detected. The patient required
mechanical ventilator support, sedation, and treatment with vasopressors.
Intravenous treatment with ceftriaxone was started. His CSF contained 300
cells/µL (71% granulocytes), the protein level was 1.66 g/L, and the
CSF glucose level was less than 40% of the serum glucose level. There were
no findings on Gram stain and cultures from CSF and blood, but DNA from Neisseria meningitidis was detected in the CSF and blood
by polymerase chain reaction. When sedation and ventilator support were discontinued
5 days after admission, flaccid paraplegia and a sensory level at T8 were
noted. The patient was given intravenous prednisolone (150 mg/d for 3 days,
then 75 mg/d) for suspected myelitis. Seventeen days after onset, the patient
was transferred to our department. Despite repeated corticosteroid treatment,
the spinal cord dysfunction was progressive until 4 weeks after onset. Seven
weeks after onset, the patient still had a flaccid tetraparesis (muscle power
grade, 4/5 in the arms and 0/5 in the legs) and a sensory level at T6. Furthermore,
bowel and bladder incontinence were present.
METHODS
In all patients, MRI was performed on a 1.5-T MRI scanner (Magnetom
Vision; Siemens, Munich, Germany). Detailed information on the sequences is
given in the figure legends.
RESULTS
For all 3 patients, T2-weighted images showed intramedullary hyperintensities
during the acute stage of spinal cord dysfunction (day 5 of meningitis/day
5 of spinal cord dysfunction in patient 1; day 2 of meningitis/day 2 of spinal
cord dysfunction in patient 2; day 6 of meningitis/after day 1 of spinal cord
dysfunction in patient 3), which appeared to be most pronounced in the gray
matter. The signal abnormalities extended from the cervical to the lumbar
cord in patients 1 and 2 and from the cervical to the thoracic cord in patient
3 (Figure 1 and Figure 2). While swelling of the spinal cord was clearly evident
in patient 3, it was not observed in the other patients. Intense leptomeningeal
and discrete nodular intramedullary gadolinium enhancement was observed in
patient 1 but not in patients 2 and 3 (Figure
1A). On native T1-weighted images, the central spinal cord lesion
appeared hypointense in patient 1 and isointense in patients 2 and 3. In none
of the patients did we detect an intramedullary abscess or compression of
the cord by a mass, such as an epidural hemorrhage, extramedullary abscess,
or subdural empyema.
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Figure 1. Patient 1 on day 5 of meningitis
due to Streptococcus pneumoniae. A, Sagittal postcontrast
T1-weighted image (repetition time [TR], 587 milliseconds; echo time [TE],
12 milliseconds) shows intense leptomeningeal enhancement and discrete intramedullary
enhancement. Sagittal (B) (TR = 3894 ms, TE = 112 ms) and axial (C) T2-weighted
images at the level of T8 (TR, 5700 milliseconds; TE, 120 milliseconds) show
central intramedullary hyperintensities in the cervical, thoracic, and lumbar
cord that predominantly involve the gray matter.
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Figure 2. Patient 3 on day 17 of meningitis
due to Neisseria meningitidis. Sagittal T2-weighted
image (repetition time, 3894 milliseconds; echo time, 112 milliseconds) shows
swelling of the cervical cord and central intramedullary hyperintensities
in thoracic and cervical cord extending up to C4.
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On follow-up, the intramedullary signal abnormalities had completely
resolved in patient 2. In patient 1, the extensive hyperintensities had almost
completely resolved by day 17 after onset of meningitis, but on day 24, a
central hyperintense lesion was detected in the cervical spinal cord at the
level of C6. This lesion was interpreted to be a newly formed syrinx. In patient
3, the T2 signal abnormalities that initially involved only the thoracic cord
extended to C4 by day 17 (Figure 2)
and to C3 by day 29. Furthermore, the high intensity of the T2 signal was
substantially unchanged in the thoracic and cervical cord compared with day
17 after onset of meningitis.
COMMENT
Acute spinal cord dysfunction is a rare complication of bacterial meningitis;
since 1971, 29 cases have been reported.4, 5, 6, 7
Of these 29 patients, 4 were adults and 25 children. Causative pathogens were N meningitidis (n = 10), S pneumoniae (n = 6), Escherichia coli (n = 5), Haemophilus influenzae (n = 4), Streptococcus
agalactiae (n = 2), Klebsiella pneumoniae
(n = 1), and Corynebacterium jeikeium (n = 1). The
most frequent initial symptom was quadriplegia or paraplegia. Spinal cord
symptoms became evident from the time of diagnosis of meningitis until 4 days
after the initiation of therapy. Six patients died, and only 3 of the 23 survivors
had a complete neurological recovery. The most common residual deficits were
spasticity and weakness, walking difficulties, and bowel and bladder dysfunction.
Possible causes of spinal cord dysfunction in acute bacterial meningitis
are mass effect, ie, cord compression, vascular compromise, or myelitis. Compression
of the spinal cord was ruled out in all of the above-mentioned cases examined
by myelogram (10 patients) or MRI (5 patients). Magnetic resonance imaging
of the spinal cord during the acute illness was performed in 2 children. While
spinal MRI was reported to be normal in one child,4
it showed enhancement of the cauda equina and lumbosacral nerve roots in the
other,5 which was interpreted to be lumbosacral
polyradiculopathy. Three patients were examined only later. Five weeks after
the acute illness, cystic dilatation of the upper thoracic cord was present
in one case,7 which was believed to be due
to vasculitis. Seven weeks after onset of meningitis, atrophy of the cervical
spinal cord was detected in another patient,8
and 1 year after meningitis, spinal MRI was reported to be normal in one patient.9 We first performed spinal MRI in our patients during
the first days of meningitis and spinal cord involvement. The dominant finding—in
addition to the exclusion of cord compression—was the high T2 signal
in the central spinal cord, which appeared to predominantly involve the gray
matter. A low intramedullary signal on T1-weighted images and discrete nodular
contrast enhancement of the cord were present only in patient 1. In view of
the MRI findings and the exclusion of spinal cord compression, the differential
diagnoses for our patients were venous congestion, ischemic infarction, and
myelitis, alone or in combination.
Cerebral septic venous thrombosis is a well-recognized complication
of purulent meningitis,10 and compromised venous
drainage of the spinal cord due to septic venous thrombosis or adhesive arachnoiditis
is also conceivable in meningitis. High T2 signals in the central spinal cord
are a common finding in venous congestion, eg, because of spinal dural arteriovenous
fistulas.11 However, there is no pathological
report of spinal venous thrombosis in bacterial meningitis in the absence
of myelitis. Nevertheless, it may have contributed to the spinal cord damage
in our patients.
Ischemic infarction of the cord during bacterial meningitis can be caused
by vasculitis, systemic hypotension due to shock, or arachnoiditis with secondary
vasculitis.4 Severe hypotension or shock, which
may have contributed to vascular compromise of the cord, preceded manifestation
of spinal symptoms in 12 of the above-mentioned cases and in 1 of the patients
presented herein (patient 3). However, the respiratory arrest and hypotension
in this patient were probably not the only cause of spinal cord dysfunction
because MRI signal abnormalities were progressive for 4 weeks after the event.
Adhesive arachnoiditis with constriction of the spinal cord and putative interference
with the blood supply has been reported to occur from 10 days to several years
after acute bacterial meningitis.12, 13
However, adhesive arachnoiditis seems unlikely in our patients, since spinal
cord symptoms developed during the first days of meningitis. Furthermore,
the resolution of the extensive intramedullar signal abnormalities in patients
1 and 2 at follow-up makes ischemia unlikely.
Myelitis during purulent meningitis has been rarely demonstrated on
postmortem examination. In particular, edema, focal hemorrhages, perivascular
inflammation in the subarachnoid space, capillary thrombosis, dilatation and
thrombosis of the anterior spinal artery, and myelomalacia have been reported.6, 12, 14, 15, 16
In 3 patients, myelomalacia primarily affected the gray matter and spared
the white matter.6, 14 In our patients,
the high T2 signal possibly reflected edema due to inflammation, while discrete
nodular contrast enhancement was seen only in patient 1. Enhancement was not
observed in the other 2 patients, possibly because of early antibiotic and
anti-inflammatory (steroid) therapy.
On follow-up, signal abnormalities resolved in patient 2. In patient
1, a small syrinx had developed in the cervical cord (a known late complication
of purulent meningitis17). In patient 3, neurologic
deficits and MRI alterations were progressive for 4 weeks. All 3 patients
had persisting tetraparesis and bowel and bladder incontinence, although MRI
signal alterations of the cord had resolved in 2 of them. In at least these
2 cases, the neurologic deficits must be attributed to diffuse damage to the
spinal cord, which cannot be discerned on MRI.
In conclusion, we have demonstrated for the first time the MRI findings
of adults with spinal cord involvement during bacterial meningitis. The observed
extensive central intramedullary hyperintensities and the follow-up MRIs (signal
abnormalities resolved completely in one patient, left a small syrinx in the
cervical cord of another patient, and even progressed in the third patient)
are consistent with myelitis. Findings of clinical follow-up examinations
suggest that myelitis during bacterial meningitis has an unfavorable prognosis.
AUTHOR INFORMATION
Accepted for publication September 9, 2000.
We thank Claudio Padovan, MD; Werner Scheuerer, MD; Chrostoph Siebold,
MD; Manfred Wick, MD; Beatrice Grabein, MD; Hans-Jochem Kolb, MD, PhD; Maximilian
Reiser, MD, PhD; Matthias Frosch, MD, PhD; and Hanns Lohner, MD, for their
clinical cooperation. We also thank J. Benson for copyediting the manuscript.
From the Departments of Neurology (Drs Kastenbauer, Winkler, and Pfister),
Neuroradiology (Drs Fesl and Yousry), and Internal Medicine (Drs Schiel and
Ostermann), Klinikum Großhadern, Ludwig-Maximilians University, Munich,
Germany.
Corresponding author and reprints: Hans Walter Pfister, MD, Department
of Neurology, Ludwig-Maximilians University, Marchioninistrasse 15, 81377
Munich, Germany (e-mail: Pfister{at}nefo.med.uni-muenchen.de).
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