Athirty-year-old man presented with a one-month history of pain in
the lumbar region, difficulty walking for one week, and urinary hesitancy for
two days. There was weakness of the ankle plantar flexors (grade-2 of 5
strength) and dorsiflexors (grade-2 of 5 strength), and both ankle reflexes
were absent. Hypoesthesia in the fourth lumbar to fifth sacral dermatomes (the
right side was greater than the left) was noted. There was no deformity, but
tenderness was elicited over the spinous processes of the third and fourth
lumbar vertebrae. Radiographs of the lumbosacral spine revealed a loss of
sharpness of the margins of the laminae of the fourth lumbar vertebra
(Fig. 1).
Magnetic resonance imaging of the lumbosacral spine (Figs.
2 and
3) showed altered signal
intensity (a hyperintense signal in the T2-weighted image and a hypointense
signal in the T1-weighted image) in the posterior elements of the third lumbar
to the first sacral vertebra and in the posterior portions of the fourth and
fifth lumbar vertebral bodies, with a large multiloculated fluid collection in
the right paraspinal region. This epidural fluid collection caused marked
extradural compression of the thecal sac and the cauda equina from the third
lumbar to the first sacral vertebra and was suggestive of the diagnosis of
tuberculosis. Antitubercular drug therapy (isoniazid, rifampin, pyrazinamide,
and ethambutol) was started, and surgical exploration of the lumbosacral spine
(the second lumbar to first sacral vertebrae) through a posterior midline
approach was done. The laminae of the third and fourth lumbar vertebrae had
roughened surfaces. Portions of these laminae were soft to the touch; however,
no discontinuity was found. The diseased laminae of the third and fourth
lumbar vertebrae were removed, and greenish-yellow pus was drained. The cauda
equina was found ensheathed in what appeared to be an inflammatory membrane.
Following careful removal of this membrane, the dural sheath was found to be
intact and dural pulsations were present. A culture of the pus was sterile,
and a biopsy specimen from the inflammatory membrane and resected osseous
tissue showed a typical tubercular granuloma
(Fig. 4) with Langhans giant
cells, epithelioid cells, and round cells, confirming the diagnosis of
tuberculosis.
The patient was continued on the four-drug antitubercular therapy
(isoniazid, rifampin, pyrazinamide, and ethambutol) and bed rest. The surgical
decompression and multidrug therapy resulted in rapid improvement in the
neurological signs and a satisfactory recovery. Within twelve weeks, the
patient had no motor weakness, sensory deficit, or bladder or bowel symptoms.
The medical therapy was changed to two drugs (isoniazid and rifampin) at three
months and was continued for a total of eighteen months. The patient was able
to walk without any support six months after surgery. Normal alignment of the
lumbosacral spine was maintained, and the patient was free of symptoms at the
last follow-up examination at twenty-four months after surgery.
Tuberculosis of the lumbosacral spine is uncommon, representing 3%
of the cases in a series of 600 patients with spinal
tuberculosis2. Pain
in the lumbosacral region is the most frequent symptom, and neurological
involvement in this region of the spine is rare, as the vertebral canal is
relatively large and contains the cauda equina rather than the spinal
cord4.
Isolated involvement of vertebral laminae and/or posterior spinous
processes is rare, and the prevalence has varied; however, it represented
<2% of the 600 patients described by
Tuli2, 0.2% of the
>2000 patients reported on by Adendorff et
al.5, and 10% of the
228 patients in the study by Babhulkar et
al.3. Since
tuberculosis of the posterior vertebral elements (the pedicles, transverse
processes, laminae, and spinous process) alone is rare, there is often a delay
in the diagnosis and irreversible neurological sequelae may occur. However,
with magnetic resonance imaging, the disease process can be seen in the very
early stage of reactive bone-marrow edema, before osseous destruction has
occurred, and the diagnosis can be established along with the clinical
findings. Treatment started during this stage may prevent morbidity, spinal
deformity, or even cord compression due to vertebral collapse. Anterior or
anterolateral decompression is the appropriate surgical approach for operative
management of the classic paradiscal form of
tuberculosis3,
whereas we believe that laminectomy is required in such atypical cases of
neural arch
tuberculosis3,6.
Extrapulmonary tuberculosis is spread hematogenously. The typical
paradiscal involvement in tuberculosis is explained by arterial
spread2. The
uncommon involvement of the posterior element is better explained by venous
spread. The posterior external venous plexus of vertebral veins is located on
the posterior surfaces of the laminae and around the spinous, transverse, and
articular
processes7. They
anastomose freely with the other vertebral venous plexuses and constitute the
final pathway for the infection to reach the neural
arch6.
Such uncommon presentations are diagnosed on clinical suspicion, and
appropriate diagnostic studies need to be obtained early. Once the diagnosis
of tuberculosis of the posterior vertebral elements was established in our
patient, the functional results following treatment were dramatic. ?