Thoracic radiculopathy

Ryan C. OConnor, DO
a,
*
, Michael T. Andary, MD
a
,
Randolph B. Russo, MD
b
, Mark DeLano, MD
c
a
Department of Physical Medicine and Rehabilitation, Michigan State University
College of Osteopathic Medicine, B401 West Fee Hall, East Lansing, MI 48824, USA
b
Orthopedic and Spine Specialists of West Michigan, Grand Rapids, MI 49525, USA
c
Department of Radiology, Michigan State University College of Human Medicine,
184 Radiology Building, East Lansing, MI 48824, USA
Thoracic radiculopathy represents an uncommon spinal disorder that is
frequently overlooked in the evaluation of spinal pain syndromes. Thoracic
disc disease and diabetes mellitus represent two of the most frequent etiol-
ogies for the development of thoracic radiculopathy. Advances in spinal
imaging techniques as well as electrodiagnostic medicine have led to
increased awareness of this disorder. Myelopathy often accompanies radi-
culopathy in the thoracic spine and is associated with increased morbidity,
necessitating prompt diagnosis and treatment. Percutaneous procedures
appear to have an increasing role in managing thoracic spinal pain syn-
dromes as well as radiculopathy. Despite recent advances in techniques,
thoracic disc surgery remains a complicated procedure reserved for patients
with unremitting symptoms or progressive neurologic compromise. This
article will discuss some of the causes and morbidities associated with thora-
cic radicular syndromes, as well as the anatomical properties of the thoracic
spine, which can make diagnosis and treatment of this disorder challenging.
Thoracic spinal unit
The thoracic spine has many unique properties that dierentiate it from
the cervical and lumbar spinal regions. The spinal curves and cervical and
lumbar lordosis, as well as thoracic kyphosis, begin to form shortly after
birth and continue to develop as an infant begins to raise his head, sit, crawl,
and come to a standing posture [1].
* Corresponding author.
E-mail address: dokroc@msn.com (R.C. OConnor).
1047-9651/02/$ see front matter 2002, Elsevier Science (USA). All rights reserved.
PII: S 1 0 4 7 - 9 6 5 1 ( 0 2 ) 0 0 0 1 8 - 9
Phys Med Rehabil Clin N Am
13 (2002) 623644
The upper 10 thoracic spinal vertebrae contain costal facets on the ante-
rolateral surfaces of the transverse processes to articulate with ribs. Unlike
the transverse processes of the cervical spine, the transverse processes of the
thoracic spine do not contain foramina. The spinous processes of the tho-
racic spine tend to point downward and overlap one another. The vertebral
bodies of the thoracic spine tend to be larger than the cervical spine yet
smaller than that of the lumbar spine. Transitional similarities are noted
between the T1 vertebral segment and that of the cervical spine, as well as
the T12 vertebral segment and the lumbar spine (Fig. 1) [2].
The vertebral canal of the thoracic spine is smaller and more rounded
than that of the cervical or lumbar spine. The minimal lateral clearance
between the spinal cord and bony spinal segments is approximately 9.2
mm in the thoracic spine compared with 11.3 mm in the cervical spine [3].
Fig. 1. Normal posteroanterior (A) and lateral (B) radiographs of the thoracic spine and
sagittal T2 weighted Mr imaging (C). Whereas alignment, osseous integrity, and degenerative
changes can be assessed on plain radiographs, sensitivity to disc disease, posterior osteophytes,
or fracture fragments impinging on neural structures is far greater with Mr imaging. Low signal
artifacts posterior to the spinal cord are caused by normal cerebrospinal uid ow pulsations.
624 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
The spinal cord/canal ratio is approximately 40% in the thoracic spine com-
pared with 25% in the cervical spine [4]. This theoretically places the spinal
cord and neural segments of the thoracic spine at increased risk of injury
from a space-occupying lesion (eg, herniated nucleus pulposus), vertebral
fracture, or trauma in this region. This narrowed canal is oset by other fac-
tors, however. The bony ribcage, which encases the rst 10 thoracic verte-
brae, oers additional protection against thoracic spinal injury. It also
enhances the stiness and limits the mobility of thoracic spinal segments.
The primary movements of the thoracic spine are rotation and lateral bend-
ing [5]. There are approximately 6 of lateral bending and 89 of rotation
present at each segment. The motions of exion and extension (F/E) increase
in degrees descending in the thoracic spine, with approximately 6 of F/E
present in the middle thoracic spine and 12 of F/E present in the lower,
transitional levels of the thoracic spine (T10T12) [4].
The intervertebral discs of the thoracic spine have the same chemical con-
sistency as that of the cervical and lumbar spine. The disc heights tend to be
smaller in the thoracic spine, however, and have less volume [6]. The outer
Fig. 1 (continued)
625 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
anular bers of the thoracic discs are primarily innervated by branches of
the sinovertebral nerve. Like the discs of the cervical and lumbar spine, the
inner nucleus is anneural.
There are 31 pairs of spinal nerves, which exit the spinal cord to innervate
the trunk and extremities. Twelve of these pairs exit from the thoracic spinal
column beneath their corresponding vertebrae. The posterior rami of cervi-
cal, thoracic, and lumbar spinal nerves exit the spinal column to innervate the
regional muscles of the back. But unlike the cervical or lumbar spine, the ven-
tral rami of the thoracic spine do not enter a plexus to innervate the skin and
muscles of an extremity. Instead, they run anterolaterally between the ribs
to innervate the chest and abdominal area. Therefore the radicular symp-
toms of spinal root injury or insult in the thoracic spine are often referred
in a band-like distribution to the anterior thorax, chest, or abdominal area.
Generators of thoracic pain syndromes
The causes of thoracic pain syndromes are numerous and encompass sev-
eral spinal and extraspinal conditions (Table 1). With such a large group of
dierential diagnostic possibilities, it is not surprising that thoracic radiculop-
athy is not discovered for months or years after symptoms arise. Dieren-
tiating other causes of pain from thoracic radiculopathy may be the most
important aspect of this problem. For example, left-sided chest pain related
to activity is most likely related to coronary artery disease until proven
otherwise. Many of the generators of thoracic pain listed in Table 1 may also
be involved in causing radiculopathy. As is the case with the lumbar and cer-
vical spine, degeneration of the posterior spinal elements of the thoracic
spine is an inherent source of axial back pain and radiculopathy. Osteopo-
rosis and compression fractures are common in the middle to lower thoracic
spine and can also cause thoracic radiculopathy. These are commonly
treated with orthotics and medications to strengthen bone density (eg,
alendronate, calcitonin) [7]. Newer treatments for vertebral compression
fractures and collapse deserve special mention and will be discussed below.
The thoracic spine may be involved in infection, with discitis, vertebral
osteomyelitis, and paraspinous abscess contributing to both radicular and
myelopathic symptoms (Fig. 2). Congenital or acquired lesions such as
arachnoid cysts (Fig. 3) or epidermoid inclusion tumors can also result
in both radicular and myelopathic symptoms. The lower thoracic and lum-
bar spine are common locations for metastatic cancer to spread. Radiation
treatment may help with this type of thoracic pain. Renal lithiasis and
hepatobiliary disease also may refer pain in the lower thoracic region. In the
middle to upper thoracic region, ischemic cardiac disease including myocar-
dial infarction can be referral sources of pain. Myofascial pain and tender
points of Fibromyalgia syndrome are common in the scapulothoracic region
and may respond to treatments consisting of modalities, manipulation, and
exercise. Costochondritis responds well to nonsteroidal anti-inammatory
626 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
Table 1
Generators of thoracic pain
Spinal
Infectious
Neoplastic
Primary
Metastatic
Degenerative
Spondylosis
Spinal stenosis
Facet syndrome
Disc disease/HNP
Metabolic
Osteoporosis
Osteomalacia
Deformity
Kyphosis
Scoliosis
Compression fracture
Somatic dysfunction
Neurogenic
Radiculopathy
Herpes Zoster
Arteriovenous malformation
Extraspinal
Intrathoracic
Cardiovascular
Pulmonary
Mediastinal
Intra-abdominal
Hepatobiliary
Gastrointestinal
Retroperitoneal/renal
Musculoskeletal
Post-thoracotomy syndrome
Polymyalgia rheumatica
Myofascial pain syndrome
Somatic dysfunction
Rib fractures
Costochondritis
Neurogenic
Intercostal neuralgia
Peripheral polyneuropathy
RSD/CRPS
Abbreviations: HNP, Herniated nucleus pulposus; RSD, reex sympathetic dystrophy;
CRPS, complex regional pain syndrome.
Data from Vanichkachorn JS, Vaccaro AR. Thoracic disk disease and treatment. J Am
Acad Orthop Surg 2000;8:15969.
627 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
medication. Ultimately, optimal treatment for thoracic pain syndromes is
dependent on determination of their underlying cause. Thoracic level back
pain may have a dierent and better natural history than cervical or lumbar
level back pain. One prospective study by Abenhhaim et al looked at the
recurrence rate of back pain over time in a sample of 2342 patients. The
patients were grouped by the predominant site of their symptoms and given
a designation as having cervical-, thoracic-, or lumbar spine-related back
pain. The recurrence of symptoms was signicantly lower in the thoracic
spine group compared with the cervical and lumbar groups [8].
Thoracic disc disease and radiculopathy
Thoracic disc disease and herniation is a common etiology for thoracic
radiculopathy (Fig. 4). Symptomatic cases of thoracic disc herniation have
Fig. 2. A 25-year-old Egyptian male patient presenting with both radicular and myelopathic
symptoms and fever. Tuberculous abscess was conrmed. T1-weighted sagittal (A) and axial
(B,C) images of the spine obtained after contrast. Bilateral posterior element and epidural
involvement results in cord compression and neural foraminal impingement.
628 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
been reported at almost all thoracic levels [9]. As in other spinal regions, Mr
imaging has all but replaced CT and myelography in the routine evaluation
of thoracic disc disease. The lower thoracic spine (T8T12 levels) is the most
frequent site of occurrence, with the T11T12 interspace accounting for 26
50% of all thoracic herniations [1012]. Degeneration is favored as the pre-
vailing cause for thoracic disc herniation, and the lower thoracic segments
are most at risk because of the increased motion present at these levels
[6]. Despite this degenerative etiology, thoracic disc disease is involved in
only 0.154% of symptomatic disc herniations of the spine, and they repre-
sent <2% of all spinal disc surgeries performed [13,14]. The incidence of
thoracic disc herniation is equal between men and women, and the age of
onset is generally between the third and sixth decades of life [15].
Signs and symptoms
The symptoms associated with thoracic disc herniation are variable and
usually include radicular symptoms such as variable pain, parasthesias,
Fig. 2 (continued)
629 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
dysesthesias, allodynia, and loss of sensation in a segmental distribution
across the anterior chest, thorax, and abdomen, depending on which nerve
root(s) are aected. For example, T4 radiculopathies usually radiate to the
nipple level; T6, the xiphoid; and T10, the umbilicus. First thoracic radicul-
opathy (T1) radiates into the median arm or ulnar aspect of the hand [9,16,
45], and for our purposes will be covered in the cervical radiculopathy
articles. Additionally, there may be localized axial pain at the level of spine
pathology and thoracic radiculopathy. Diagnosis of some patients who
report a deep aching-type pain is much more dicult because the pain can
mimic other thoracic or abdominal problems such as angina, dyspepsia, or
diverticular disease. It seems likely that some patients with atypical abdom-
inal and chest pain have undiagnosed thoracic radiculopathy; however, the
extent of this has never been adequately documented.
Physical examination is not a reliable way to diagnose thoracic radiculop-
athy. There may be localized spine and paraspinal tenderness, and sensory
changes in a dermatomal pattern, but this is not universal. Unlike cervical
or lumbosacral radiculopathies, there is no reliable way to test for muscle
Fig. 2 (continued)
630 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
weakness in a myotomal pattern. The muscles that are likely to be aected
(paraspinal, intercostal, and abdominal muscles) do not lend themselves to
isolated muscle testing. Physical examination is critical, however, to rule out
other causes of chest or abdominal pain and assess for myelopathy as dis-
cussed below.
There are also reports of thoracic disc herniations causing atypical symp-
toms. Two such cases involved patients with lower extremity leg pain mim-
icking that of lumbosacral disc disease and radiculopathy. The patients
symptoms did not subside until a thoracic herniated nucleus pulposus (HNP)
was identied and treated surgically at the involved T10 level [16,17].
Another case involved a patient with predominant shoulder pain and in-
complete paraplegia. After an acromioplasty procedure for impingement
syndrome failed to improve the patients shoulder symptoms, a large lower
thoracic disc herniation was identied via Mr imaging. Following surgical
removal of the thoracic disc, the patient reported complete resolution of his
shoulder pain symptoms and improvement in his paraplegia [18]. Thoracic
Fig. 3. A 42-year-old female patient with gait disturbance and back pain. Sagittal (A) and axial
(B) T2-weighted images at the level of the conus medullaris show cord compression from an
intraspinal arachnoid cyst.
631 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
discs generally herniate in a posterior-central or a posterior-lateral direction,
and true lateral herniations are rare [19]. The incidence of asymptomatic
thoracic disc herniation has been estimated at 37%, and the size of the her-
niation tends to uctuate over time in patients who remain without symp-
toms [20].
The most serious of symptoms related to thoracic disc herniation and
radiculopathy is the development of myelopathy. As in the cervical spine,
thoracic myelopathy can result in irreversible neurologic dysfunction and
threaten spinal cord tracts. It is often the result of spinal cord compression
of a large central thoracic disc, a calcied thoracic HNP, or an intradural
herniation [13,21]. Bladder dysfunction, a wide-based ataxic pattern of gait,
and upper motor neuron signs such as positive Babinski sign, ankle clonus,
and hyperreexia should be sought for in a patient with suspected myelop-
athy. Mild lower extremity paraparesis is the most common symptom asso-
ciated with thoracic disc herniation with myelopathy [22]. A thorough
neurologic examination should be performed on all patients with suspected
thoracic disc disease including tests usually reserved for patients with spinal
Fig. 3 (continued)
632 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
cord injury such as Beevors sign and the cremasteric reex. The coincidence
of thoracic degenerative disc disease in a patient with pre-existing myelop-
athy can present with particularly complex symptoms (Fig. 5).
Thoracic spinal stenosis represents another, less common cause of tho-
racic radiculopathy with myelopathy. It may be dened as the narrowing of
the anteroposterior (AP) diameter of the thoracic spinal canal to less than
<10 mm. Scheuermanns disease, achondroplasia, and epidural lipomatosis
have been considered conditions that can contribute to, or cause, thoracic
spinal stenosis. When present, thoracic spinal stenosis is highly associated
with coexisting lumbar spinal stenosis [23,46].
Diabetes and radiculopathy
Diabetes mellitus has been implicated in the development of peripheral
nerve disease at every imaginable level including root, plexus, and proximal
Fig. 4. A 55-year-old female patient with neck and upper chest pain and previous hardware
fusion in the cervical spine. Sagittal (A) and axial (B,C) T2 weighted Mr imaging of the thoracic
spine demonstrate a left paracentral disc herniation at the T78 level causing cord displacement
and deformity.
633 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
and distal nerve branches. As previously discussed, compressive radiculopa-
thies are less common in the thoracic spine compared with the cervical and
lumbar regions. Diabetic radiculopathy is a common cause for noncompres-
sive radicular symptoms in the thoracic spine [24]. The symptoms associated
with diabetic thoracic radiculopathy are similar to that of discogenic thora-
cic radiculopathy and may include burning pain and parasthesias in a
dermatomal distribution across the thoracic spine and radiating to the
anterior chest wall and abdominal regions. It can mimic the symptoms of
intrabdominal pathology and can lead to unnecessary exploratory abdomi-
nal surgery [25]. Symptoms can be unilateral or bilateral, with weakness in
abdominal musculature also described as a feature. Chaudhuri et al reported
six cases of diabetic thoracic radiculopathy, nding in four of the six cases
that patients presented with profound weight loss and generalized cachexia
in addition to radiculopathy. The resolution of radicular symptoms in these
patients included the regaining of lost weight [26]. Unlike the common distal
symmetrical sensorimotor peripheral neuropathy associated with diabetes,
diabetic thoracic radiculopathy is not associated with the length of time
one has had disease. It most typically occurs in older, noninsulin-dependent
diabetic men and runs a self-limiting course over approximately 618
months before symptoms resolve [26,27].
Fig. 4 (continued)
634 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
Electrodiagnostic evaluation of thoracic radiculopathy
The electrodiagnostic evaluation of suspected thoracic radiculopathy
should include needle EMGof thoracic paraspinal muscles. Associated inter-
costal and abdominal musculature may be additional muscles that can help in
the diagnosis. The rectus abdominis muscle can be localized by slowly insert-
ing the needle electrode perpendicular tothe skinwhile listening for insertional
activity from the preamplier. The amount of adipose tissue will vary greatly
between patients. In the unusual case where the abdominal muscle has no
active motor units; the needle may pass through the muscle and into the peri-
toneum, which may cause complications, especially if bowel is punctured.
When volitional motor units or insertional activity is found, the needle should
be redirected to sample various muscular segments [28]. The intercostal
muscles of associated thoracic segments can also be localized above underly-
ing ribs. Inadvertent pleural penetration can be avoided by placing ones n-
gers above and below the corresponding rib and inserting the needle between
the ngers soit makes contact withthe rib. The needle canthenbe redirectedto
Fig. 4 (continued)
635 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
sample the intercostal muscle segments. The authors do not routinely utilize
this technique and do not know of any evidence that the intercostal muscles
add to the diagnosis over the thoracic paraspinal muscles.
Positive sharp waves and brillation potentials found in the paraspinal
muscles with or without abnormalities in the abdominal or intercostal
muscle are most suggestive of a thoracic radicular process. The levels of
abnormality in the paraspinals can help to localize the level of the lesion
[29]. Positive ndings in thoracic segments should also prompt a search in
cervical and lumbar levels for widespread polyradicular disease.
In cases of suspected thoracic myelopathy, lower extremity somatosen-
sory evoked contentials (SEPs) can be performed to assess conduction in the
posterior columns and to look for possible spinal cord compression [30].
Fig. 5. A 46-year-old female patient with multiple sclerosis presenting with right-sided
midthoracic pain. T2-weighted sagittal (A) and axial (B,C) images of the cervical and thoracic
spine. C25 region cord lesions caused by demyelinating disease are seen. A small right
paracentral disc herniation is seen at the T89 level that was felt to be responsible for the
patients acute symptoms.
636 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
This is suggested by having normal tibial nerve SEP latencies to the L1
reference level, with delayed or absent latencies recorded at cortical levels.
Treatment of thoracic radiculopathy
The authors could not nd any randomized controlled trials that specif-
ically address the treatment of thoracic radiculopathy. Thus, treatment deci-
sions must be based on clinical experiences, case reports and series, and
other studies done on cervical and lumbosacral radiculopathies.
Conservative
Initial conservative management of thoracic radiculopathy is recom-
mended for patients with radicular symptoms that are the result of thoracic
Fig. 5 (continued)
637 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
HNP or disc disease, and for those who do not have symptoms of progressive
myelopathy or neuromuscular compromise [15]. Acute phase symptoms
of thoracic radiculopathy may be managed similarly to that of radiculop-
athy at the cervical or lumbosacral levels. This includes short-term bed rest,
nonsteroidal anti-inammatory medications and muscle relaxants. Physical
medicine modalities such as ice, heat, ultrasound, and electrical stimulation
may give short-termsymptomatic relief but will not alter the long-termcourse
of the problem[31]. Spinal extension exercises and orthotics may be utilized in
managing subacute and chronic symptoms [44]. Unlike the cervical or lumbar
spine, however, there are fewif any clinical studies that assess the eectiveness
of individual conservative treatment interventions specically for sympto-
matic thoracic radiculopathy or thoracic disc disease. Instead, natural history
studies utilizing a variety of conservative treatment interventions have shown
that the prognosis for symptomatic relief with nonsurgical management in
cases of thoracic disc disease without progressive myelopathy is quite good.
Fig. 5 (continued)
638 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
One such study by Brown et al looked at the conservative management of
40 patients with symptomatic thoracic disc disease. In this study, 77% of
the treated patients were able to return to their previous level of functional
activity [15].
Medications can also be of some help with symptomatic relief and neuro-
pathic pain. Antidepressants, anticonvulsants, non-steroidal antiinam-
matory drugs (NSAIDs), acetaminophen, opiates, muscle relaxants, and
sleep medications all have a role in symptomatic relief of thoracic radiculo-
pathies depending on the clinical situation.
Percutaneous procedures and spinal injections are becoming more fre-
quently used in the spine for diagnosis and treatment of spinal pain syn-
dromes. Few studies have assessed the ecacy of these procedures at the
thoracic level. Selective spinal nerve root and intercostal nerve blocks are
used to treat thoracic radiculopathy, discogenic pain, and postherpetic neu-
ralgia [32]. Epidural steroid injections (ESI) are also used, but patients are
far less likely to receive an ESI at the thoracic level for relief of radicular
symptoms than at the cervical or lumbar levels [33]. Radiofrequency neuro-
notomy of medial branches of the thoracic posterior primary rami may be
used for the treatment of pain mediated by thoracic zygapophyseal joints
[34]. In one study, Quinn et al performed 52 CT-guided nerve root blocks
and 27 CT-guided nerve root ablations in patients with pain associated
with malignant spine disease and evidence of equivocal disc herniation or
foraminal stenosis at a variety of spinal levels. The nerve root blockades
were done to determine the clinical signicance of disc herniation or fora-
minal stenosis at a particular level. A positive response to nerve root block-
ade was followed by a nerve root ablation procedure. Signicant relief of
pain was found in 90% (9 of 10) patients with nerve root ablation performed
at the thoracic level. Patients with pain poorly localized and at multiple seg-
mental levels did not respond as well to ablation. The authors concluded
that the procedure was most successful for patients with thoracic pain symp-
toms of no more than one or two segmental levels [35].
Percutaneous vertebroplasty
Vertebral body compression fractures have been treated with many non-
interventional management techniques, ie, external bracing, oral medica-
tions, physical therapy, instruction on protective measures for the spine,
and pain management. Surgical management is infrequently necessary and
used primarily for progressive neurologic decits or kyphotic collapse.
Percutaneous vertebroplasty, injection of acrylic cement polymethyl-
methacrylate (PMMA), was rst performed in 1984 in France by Deramond
et al [36]. Initially, it was performed on a vertebral body weakened by an
aggressive hemangioma. Over the subsequent several years, the procedure
was expanded to other weakened bone, including osteoporotic compression
fractures, vertebral myeloma, and metastatic vertebral lesions.
639 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
In 1994, Jensen et al rst began performing vertebroplasty in the United
States at the University of Virginia. Their series of 29 patients remains the
strongest scientic support for its use in treating continued pain following
a compression fracture [37]. To date, there are no randomized controlled
trials comparing the long-term outcomes of percutaneous vertebroplasty
with control therapy.
Alternate pain etiologies must be excluded prior to proceeding to verte-
broplasty, ie, herniated nucleus pulposus, spinal stenosis, and thoracic or
lumbar spondylosis. Diagnostic work-up should include plain radiographs,
and Mr imaging of the pathologic area. Utilization of a bone scan is left to
the physicians discretion. Vertebral bodies that do not demonstrate hyper-
intense signal on T2-weighted Mr imaging consistent with marrow edema
should be approached cautiously. These patients have demonstrated little
or no pain relief following vertebroplasty [38].
The following is a brief technique description of percutaneous vertebro-
plasty; specic details have been extensively described [3638]. The proce-
dure should be completed under high-quality uoroscopic equipment. A
biplane uoroscopic unit is preferable as it allows for rapid completion of
the procedure. Conscious sedation is utilized. The vertebral end plates of the
involved vertebra are positioned parallel under AP imaging. The image
intensier is then rotated to an oblique position in order to view the pedicle
in the center of the vertebral body (looking down the barrel of the pedicle).
A transpedicular approach is most often utilized for penetration into the
vertebral body. With the pedicle over the vertebral body, under uoroscopic
guidance, an 11-gauge trocar is advanced to the mid-portion of the pedicle.
Under AP and lateral imaging, the trocar is passed through the pedicle into
the vertebral body. Use of contrast is controversial but can assist in deter-
mining potential extravasation of the bone cement. PMMA opacied with
sterile barium sulfate is then injected into the vertebral body (Fig. 6). Con-
tinuous uoroscopic imaging is utilized during installation of the cement.
Needle placement must be reevaluated if extravasation is noted into the epi-
dural space, neuroforamen, out of the lateral portion of the vertebral body
or intravenous. Postprocedural care includes maintaining a recumbent posi-
tion for approximately 30 minutes, with 90% of hardening occurring within
the rst hour [13]. Complication rates are low and include the potential of
rib fractures, transient myelopathy, occasional persistent radiculopathy,
infection, and possible extravasation requiring neural decompression.
Vertebroplasty oers a promising treatment intervention for those indi-
viduals who suer from persistent pain after a compression fracture. The
existing published literature suggests benecial eects with its use, but wide-
spread utilization of interventional techniques must not be supported solely
by uncontrolled trials, anecdotal reports, and case series. Prior to expanding
its use, randomized controlled trials need to dene potential patient popu-
lations [39,40]. The standard of care for treatment of vertebral body
compression fractures remains a trial of noninterventional management.
640 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
Consideration for vertebroplasty in those patients who suer persistent dis-
comfort can be entertained as a nal option for pain reduction.
Surgical
Patients that present with unremitting thoracic radicular pain caused by
structural disease despite conservative treatments for 2 months, and/or pro-
gressive myelopathy as the result of structural disease, may be candidates
for surgical intervention. There are three general directions from which to
perform thoracic disc surgery. These include anterior (transternal and
transthoracic), posterior (pediculofacetectomy) and lateral (costotrans
versectomy and lateral extracavitary) approaches. Negotiating visceral anat-
omy and visualization diculties make thoracic disc surgery a challenging
procedure. There is little consensus in the literature as to the optimal surgi-
cal approach, and decisions are often made based on the type of herniation,
Fig. 6. Elderly female patient with osteoporotic compression fracture and back pain. Lateral
(A) and AP (B) views during and after the injection of polymethylmethacrylate opacied with
barium into a lower thoracic vertebral compression fracture.
641 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
symptoms, spinal level, general health of the patient, and experience of the
surgeon [22,41,42]. Unlike the lumbar spine, laminectomy procedure for disc
herniation in the thoracic spine has been disfavored because of high morbid-
ity among treated patients. In a retrospective review of 135 patients treated
with thoracic laminectomy for disc herniation, Acre and Dohrmann
reported that 58% were improved, 10% were unchanged, 28% were made
worse, and 4% had died following the procedure [14]. Stillerman et al
reported on their ndings in patients who underwent surgical management
for thoracic disc disease and found that myelopathic symptoms resolved in
95% of patients, and pain improved in 87%. Major complications were
found in 3.6% of their patients and compared well with complications found
in other reports, which averaged 6.1% [19]. Video assisted thoracic surgery is
a newer, minimally invasive thoracic disc surgical procedure that may ben-
et patients by minimizing postoperative pain and decreasing hospitaliza-
tion time. The procedure is technically demanding, however, and not
widely used by surgeons at this time [43]. Finally, proper patient selection
and the identication of symptomatic structural pathology are paramount
for the success of all thoracic spinal surgical procedures.
Fig. 6 (continued)
642 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
References
[1] Parke WW. Development of the spine. In: Rothman RH, Simeone FA, editors. The spine,
ed 2 (vol 1). Philadelphia: WB Saunders; 1982. pp. 117.
[2] Jenkins DB. The back. In: Hollinsheads functional anatomy of the limbs and back, ed 7.
Philadelphia: WB Saunders; 1998. pp. 20204.
[3] Depalma AF, Rothman RH. The intervertebral disc. Philadelphia: WB Saunders; 1970.
[4] Maiman DJ, Pintar FA. Anatomy and clinical biomechanics of the thoracic spine. Clin
Neurosurg 1992;38:296324.
[5] Parke WW. Biomechanics of the spine. In: Rothman RH, Simeone FA, editors. The spine,
ed 2 (vol 1). Philadelphia: WB Saunders; 1982. pp. 4749.
[6] Mcinerney J, Ball PA. The pathophysiology of thoracic disc disease. Neurosurg Focus
2000;9(4):18.
[7] Downs RW, Bell NH. Comparison of alendronate and intranasal calcitonin for treatment of
osteoporosis in postmenapausal women. Jour Clin Endicrinol Met 2000;05:85(5):178388.
[8] Abenhaim L, Suissa S, et al. Risk of recurrence of occupational back pain over three-year
follow up. Br J Int Med 1988;45:82933.
[9] Morgan H, Abood C. Disc herniation at T12. Report of four cases and a literature review.
J Neurosurg 1998;88(1):14850.
[10] Blumenkopf B. Thoracic intervertebral disc herniations: diagnostic value of magnetic
resonance imaging. Neurosurgery 1988;23:3640.
[11] Tahmouserie A. Herniated thoracic intervertebral disc, an unusual presentation. Case
report. Neurosurgery 1980;7:62325.
[12] Videman T, Battie MS, Gill K, et al. Magnetic resonance imaging ndings and their
relationships in the thoracic and lumbar spine. Spine 1995;20:92835.
[13] Alvarez O, Roque CT, Pampeti M. Multilevel thoracic disc herniations: CT and MR
studies. J Comp Assist Tomog 1988;12:649652.
[14] Acre CA, Dohrmann G. Thoracic disc herniation. Improved diagnosis with computed
tomographic scanning and a review of the literature. Surg Neurol 1985;23:35661.
[15] Brown CW, Deer Jr PA, et al. The natural history of thoracic disc herniation. Spine
1992;17(Suppl 6):S97102.
[16] Lyu RK, Chang HS. Thoracic disc herniation mimicking acute lumbar disc disease. Spine
1999;24(19):206667.
[17] Knoller SM, Haag M. Paralysis of the foot as the rst symptom of herniated thoracic disc.
Zentrabl Neurochir 1999;60(4):19195.
[18] Wilke A, Wolf U. Thoracic disc herniation: a diagnostic challenge. Man Therapy 2000;
5(3):18184.
[19] Stillerman CB, Chen TC, et al. Experience in the surgical management of 82 symptomatic
herniated thoracic discs and a review of the literature. J Neurosurg 1988;88:623633.
[20] Wood KB, Blair JM. The natural history of asymptomatic thoracic disc herniations. Spine
1997;22:52530.
[21] Epstein NE, Syrquin MS. Intradural disc herniations of the cervical, thoracic, and lumbar
spine: report of three cases and a review of the literature. J Spinal Disord 1990:12:396403.
[22] Vanichkachorn JS, Vaccaro AR. Thoracic disc disease: diagnosis and treatment. J Am
Acad Orthop Surg 2000;8:15969.
[23] Epstein NE, Schwall G. Thoracic spinal stenosis: diagnostic and treatment challenges.
J Spinal Disord 1994;7:25969.
[24] Bastron JA, Hames JE. Diabetic polyradiculopathy. Clinical and electromyographic
studies in 105 patients. Mayo Clinic Proc 1981;56:725732.
[25] Sellman MS, Mayer RF. Thoracoabdominal radiculopathy. South Med J 1988;81(2):
199201.
[26] Chaudhuri KR, Wren DR, et al. Unilateral abdominal muscle herniation with pain:
a distinct variant of diabetic radiculopathy. Diabet Med 1997;14:8037.
643 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644
[27] Asbury AK. Focal and multifocal neuropathies of diabetes. In: Asbury AK, editor. Diabetic
neuropathy. Philadelphia: WB Saunders; 1987. pp. 4755.
[28] Dumitru D. Thoracic radiculopathies. In: Dumitru D, editor. Electrodiagnostic medicine.
Philadelphia: Hanley & Belfus; 1995. pp. 558559.
[29] Haig AJ, Yamakawa K, Hudson DM. Paraspinal electromyography in high lumbar and
thoracic lesions. Am J Phys Med Rehabil 2000;79(4):33642.
[30] Dumitru D. Thoracic radiculopathies. In: Dumitru D, editor. Electrodiagnostic medicine.
Philadelphia: Hanley & Belfus; 1995. pp. 576577.
[31] Van Tulder MW, Waddell G. Conservative treatment of acute and subacute back pain.
In: Nachemson AL, Jonsson E: Neck and back pain: The scientic evidence of causes,
diagnosis, and treatment. Philadelphia: Lippincott Williams & Wilkens; 2000. pp. 24165.
[32] Woodward JL, Herring SA, Windsor RE. Epidural procedures in spine pain management.
In: Lenard TA. Pain procedures in clinical practice, ed 2. Philadelphia: Hanley & Belfus;
2000. pp. 34176.
[33] Fanciullo GJ, Hanscom B, et al. An observational study in the frequency and pattern use of
epidural steroid injection in 25,479 patients with spinal and radicular pain. Reg Anesth
Pain Med 2001;26(1):511.
[34] Dreyfuss P, Rogers CJ. Radiofrequency neuronotomy of the zygapophyseal and sacroiliac
joints. In: Lenard TA. Pain procedures in clinical practice, ed 2. Philadelphia: Hanley &
Belfus; 2000. pp. 395420.
[35] Quinn SF, Murtagh FR, et al. CT-guided nerve root block and ablation. Am J Roentgenol
1988;12:12136.
[36] Deramond H, Depriester C, Toussaint P, Galibert P. Percutaneous vertebroplasty. Sem
Muskuloskeletal Radiol 1997;1:28595.
[37] Jensen ME, Evans AJ, Mathis JM, Kallmes DF, Cloft HJ, Dion JE. Percutaneous
polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body
compression fractures; technical aspects. AJNR 1997;18:1897904.
[38] Mathis JM, Barr JD, Belko SM, Barr MS, Jensen ME, Deramond H. Percutaneous
vertebroplasty: a developing standard of care for vertebral compression fractures. AJNR
2001;22:37381.
[39] Jarvik JG, Dryo RA. Cementing the evidence: time for a randomized trial of
vertebroplasty. AJNR 2000;21:137374.
[40] Levine SA, Perin LA, et al. An evidence based evaluation of percutaneous vertebroplasty.
Manag Care 2000;9(3):5660, 63.
[41] Levi N, Gjerris F, Dons K. Thoracic disc herniation. Unilateral transepedicular approach
in 35 consecutive patients. J Neurosurg Sci 1999;43(1):3742.
[42] Currier BL, Eismont FJ, Green BA. Transthoracic disc excision and fusion for herniated
thoracic discs. Spine 1994;19:32328.
[43] Regan JJ, Mack MJ, et al. A technical report on video-assisted thoroscopy in thoracic
spinal surgery: preliminary discription. Spine 1995;20:83137.
[44] Fisher SV, Winter RB. Spinal orthoses in rehabilitation. In: Braddom RL, editor. Physical
medicine and rehabilitation. Philadelphia: WB Saunders; 1996. pp. 359.
[45] Levin KH. Neurologic manifestations of compressive radiculopathy of the rst thoracic
root. Neurology 1999;53(5):114951.
[46] Stoodley MA, Jones NR, Scott G. Cervical and thoracic juxtafacet cysts causing neurologic
decits. Spine 2000;25(8):97073.
644 R.C. OConnor et al / Phys Med Rehabil Clin N Am 13 (2002) 623644