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Neurologic Abnormalities in Children Presenting With Diskitis
Moshe Nussinovitch, MD;
Nir Sokolover, MD;
Benjamin Volovitz, MD;
Jacob Amir, MD
Arch Pediatr Adolesc Med. 2002;156:1052-1054.
ABSTRACT
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Background Neurologic impairment is not considered a clinical manifestation of
diskitis in children and has seldom been associated with it in the medical
literature.
Objective To describe neurologic findings and their implications in children with
diskitis.
Study Design Retrospective medical records review of children discharged with a diagnosis
of diskitis between January 1992 and December 2000. The study included children
in whom the diagnosis was based on the presence of clinical findings, laboratory
evidence of an inflammatory process, and findings on imaging studies compatible
with diskitis.
Results Neurologic findings of decreased muscle strength or hyporeflexia in
the lower extremities were found in 7 (41%) of 17 children who met the diagnostic
criteria for diskitis. Five of the 7 underwent magnetic resonance imaging,
2 of whom demonstrated intraspinal inflammatory involvement.
Conclusions Neurologic impairment does not exclude the diagnosis of diskitis and
may be a common manifestation of the disease in children. Nevertheless, when
neurologic findings are present, advanced imaging studies are needed to exclude
intraspinal involvement.
INTRODUCTION
DISKITIS, OR intervertebral disk inflammation, is an uncommon disease
occurring mostly in children. Its exact incidence is unknown, with most investigations
following a prolonged retrospective design.1
Although the disease is believed to be of infectious etiology, positive bacterial
cultures are rarely obtained, and some authors1-2
oppose the use of antibiotic treatment.
The onset of diskitis is usually subtle, and clinical manifestations
vary with age. Therefore, a high index of suspicion is required for diagnosis.
Diagnosis is established by narrowing of the intervertebral disk space on
radiography and irregularities of the adjacent vertebral bodies, or by increased
uptake of technetium Tc 99m in the disks on bone scan early in the course
of the disease.3
In our review of the relevant literature, we found only anecdotal descriptions
and little information about neurologic signs and symptoms associated with
diskitis.4-5 To determine the
incidence of neurologic impairment in children with diskitis and to discern
the implications, we conducted a retrospective study of all children discharged
from our department during 8 years with a diagnosis of diskitis.
METHODS
The medical records of all children discharged from the Schneider Children's
Medical Center of Israel between January 1992 (opening of the pediatrics department)
and December 2000 with a diagnosis of diskitis were reviewed. We included
only those children in whom the diagnosis was based on the presence of typical
clinical findings (limp, refusal to walk, or pain on changing position), laboratory
evidence of an inflammatory process (elevated erythrocyte sedimentation rate
or C-reactive protein level), and imaging study results compatible with diskitis
(narrowing of the intervertebral disk space on radiography or increased uptake
in that area on bone scan). The neurologic examinations were performed by
a neurologist. All children were initially treated with antibiotics for 3
to 4 weeks.
RESULTS
Seventeen children were discharged with a diagnosis of diskitis during
the study period. Neurologic findings of decreased muscle strength or hyporeflexia
in the lower extremities were found in 7 (41%) of them. Neurologic findings
and imaging results are found in Table 1. Nine of the children were male. The median age at presentation
was 16 months (range, 11-174 months). The median temperature on admission
was 38°C (range, 36.8-39.0°C). The median erythrocyte sedimentation
rate was 60 mm/h (range, 39-120 mm/h); the median white blood cell count was
11.7 x 103/µL (range, 6.5-18.5 x 103/µL).
Symptoms were present for a median duration of 14 days (range, 7-35 days).
Blood cultures were sterile in 15 (88%) of the 17 patients with diskitis.
Among patients who had positive blood culture results, Kingella kingae was isolated from 2. Penicillin G was given to patients
requiring intravenous therapy, and oxacillin sodium or a first-generation
cephalosporin (cefazolin) was given to those requiring oral therapy.
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Clinical Symptoms and Neurologic Signs Among Children With Diskitis*
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Neurologic findings on physical examination at admission revealed a
refusal to bear weight or move spontaneously in 7 of the 17 patients. Four
had a bilateral decrease in tendon reflexes (patients 1, 2, 5, and 17), 4
had a decrease in muscle tone (patients 5, 6, 11, and 17), and 4 had decreased
muscle power (4/5) (patients 2, 6, 8, and 11). Patient 8 had bilateral Babinski
sign, and patient 6 had a head lag that could not be explained by inflammatory
lesions. Five of these 7 children underwent magnetic resonance imaging; 2
patients improved before the imaging was done. Magnetic resonance imaging
demonstrated intraspinal inflammatory involvement in 2 of the 5. In patients
8 and 17, pressure on the spinal cord was demonstrated, and they were referred
to the Department of Neurosurgery at another hospital for treatment with laminectomy
and diskectomy. In patients 1 and 2, hyporeflexia and hypotonia were lateralized
and confined to the lower extremities, suggesting a localized injury, and
disappeared within 3 weeks. In all children, the neurologic findings and other
clinical manifestations of the disease resolved with antibiotic treatment
and bed rest. The mean time to diagnosis after onset of symptoms in patients
with neurologic signs was 20 days, compared with 17 days in patients without
neurologic findings.
COMMENT
Disk inflammation (pyogenic spondylitis) in children is believed to
result from an infection. Staphylococcus aureus and K kingae are the organisms most commonly isolated from
disk aspiration.1, 6
The differential diagnosis of neurologic impairment in the lower extremities
of children with low back pain generally includes spinal tumors, vertebral
osteomyelitis,1 or epidural abscess formation,6 but not a clinical presentation of diskitis.6-7 Our review of the literature revealed
only a few case reports and larger series4-5,8-11
describing neurologic involvement associated with diskitis.
Kelfer and Haller5 described a patient
with diskitis at the L4-5 intervertebral space who had Gowers sign as a notable
physical finding. Rocco and Eyring described "the meninges symptoms complex,"4(p449) which consists of meningeal irritation as manifested
by the presence of Kernig or Brudzinski signs. Hyperreflexia and clonus may
be present.
Crawford et al, in a review of 36 children with diskitis, suggested
that the protrusion of the disk and its contents into the spinal canal (as
seen on magnetic resonance imaging scan in only 1 patient among that group)
may explain the "occasional neurologic sign associated with diskitis."9(p78) Ring et al10 noted
neurologic involvement in the form of radicular pain with a mildly reduced
patellar reflex in the foot of 1 of 47 children with diskitis; the child developed
a paravertebral abscess.
In another review, Scoles and Quinn11
did not describe any neurologic impairment among 29 children with intervertebral
diskitis. Likewise, Ventura and colleagues12
described 12 children with diskitis, 1 of whom had exaggerated patellar reflexes.
Despite the presence of a paraspinal inflammation or a small collection of
hemorrhage in 36 patients with diskitis, Fernandez et al2
observed only 1 patient in whom adverse neurologic symptoms or signs were
noted.
In the present review of the medical records of 17 children treated
in our hospital for diskitis, we found signs of neurologic impairment in 7.
These signs could be explained by other causes, such as normal variation in
reflexes, tone, or pain. These reflex changes were present at initial evaluation
and evolved during the course of the illness. Although this small sample size
does not permit evaluation of the frequency of neurologic impairment in children
with diskitis, our findings suggest that it is not as rare as generally thought.
Furthermore, resolution of the neurologic impairment and other clinical manifestations
in 5 children after antibiotic treatment and in 2 children with neurosurgical
intervention points to an inflammatory pathogenesis. Therefore, neurologic
findings may serve as an indication for the follow-up and evaluation of the
progression of the disease.
The findings of decreased muscle tone, muscle weakness, and decreased
tendon reflexes in our patients are compatible with lower motor neuron injury.
This kind of injury is expected when pressure is applied on the spinal cord
or on the root of the nerves in the paravertebral region.
In summary, the spectrum of neurologic involvement associated with diskitis
in children ranges from no involvement to radicular pressure to intraspinal
pressure, depending on the extent of the inflammatory process that evolves
from the intervertebral disk. Because we define diskitis more heterogeneously
in terms of etiology and severity, the incidence of neurologic complications
in our series was higher than that among other surveys of diskitis in children.
We conclude that neurologic impairment does not exclude a diagnosis
of diskitis, as suggested in the past,2, 4-5,12
and may be a clinical manifestation of the disease. Nevertheless, when neurologic
findings are present, imaging studies are needed to exclude intraspinal involvement.
| What This Study Adds
Neurologic impairment is not considered a clinical manifestation of
diskitis in children and has rarely been referred to in the medical literature
in association with this disorder. The aim of this study was to describe neurologic
findings in children with diskitis and their implications. We conclude that
neurologic impairment does not exclude a diagnosis of diskitis, as was suggested
in the past, and may be a clinical manifestation of the disease. Nevertheless,
when neurologic findings are present, imaging studies are needed to exclude
intraspinal involvement.
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AUTHOR INFORMATION
Accepted for publication June 13, 2002.
We thank Gloria Ganzach and Phyllis Curchack Kornspan for their editorial
assistance.
Corresponding author and reprints: Jacob Amir, MD, Department of
Pediatrics "C", Schneider Children's Medical Center of Israel, Sackler School
of Medicine, Tel Aviv University, Petach Tikvah, 49202, Israel (e-mail: amirj{at}clalit.org.il).
From the Department of Pediatrics "C", Schneider Children's Medical
Center of Israel, Sackler School of Medicine, Tel Aviv University, Petach
Tikvah, Israel.
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