Interventional Spine

Susan M Renner, PhD,
Avinash G Patwardhan, PhD, Non ASSR Member
Chris Carson, MS, Non ASSR Member
Braden McIntosh, BS, Non ASSR Member
Robert M Havey, BS, Non ASSR Member
Anastasios Dimitriadis, MD, Non ASSR Member

Scientific Paper

Mentor Award: No

Institution where work was conducted

Edward Hines Jr. VA Hospital

Affiliation and Department

Musculoskeletal Biomechanics Laboratory, Edward Hines Jr. VA Hospital

Address

5000 South 5th Ave
Bldg1 RmA201
Hines, Illinois
60141
Phone: 312-420-9722, Fax: 708-202-7938
Email: susan.renner@va.gov

Purpose

Recent studies suggest endplate fracture incurred during vertebral compression fracture (VCF) alters intervertebral disc mechanics at the adjacent levels [1]. The deformity created by the endplate fracture leads to increased nucleus volume, which does not allow the nucleus to pressurize, and thus alters disc behavior. This altered disc behavior has recently been theorized to increase fracture risk adjacent to an endplate deformity. This study tested the hypothesis that reduction of endplate deformity after both endplate fracture and subsequent vertebral compression fracture will restore disc mechanics.

Methods & Materials

Six thoraco-lumbar spine segments (T10-L2, T12-L4, or L1-L5 age:72.2±6.4yrs) were tested. A void was created under the upper endplate of the middle vertebra. The specimen was compressed via follower load until the weakened endplate fractured and a notable endplate deformity was observed on digital fluoroscopy. The specimen was then compressed further to create a vertebral compression fracture. The compression fracture was corrected, as observed radiographically, taking special care to correct the endplate deformity as much as possible using the StaXx® FX Structural Kyphoplasty device (Spine Wave, Inc., Shelton, CT). Specimens were tested in flexion-extension (±6Nm) under 400N preload before and after endplate and vertebral fractures and after endplate deformity reduction. Lateral radiographs were taken in neutral posture under 400N preload to measure maximum endplate deformity. Intradiscal-pressure (IDP) in flexion-extension was recorded in the discs above and below the fractured body and normalized so pressure in neutral position was taken to zero.

Results

Vertebral height after endplate and vertebral fracture was significantly less than intact (73.3±9.1% and 67.7±6.0% of intact respectively, p<0.001) (Figure 1A-B). Vertebral height was significantly increased after endplate fracture reduction (p<0.001), but remained significantly less than intact (89.0±9.3% of intact, p=0.014) (Figure 1C).
Intact IDP increased 0.12±0.13MPa during flexion under 400N preload. After endplate and vertebral fractures the disc with endplate fracture developed significantly less IDP at maximum flexion in the disc with endplate fracture than intact (32±19% and 34±7.8% of intact respectively, p<0.004). After endplate fracture reduction IDP during flexion was restored to 73±47% of intact (p=0.162), and was significantly improved compared to after endplate and vertebral fractures (p<0.03) (Figure 2A). The IDP during flexion was not significantly affected in the disc below the fractured vertebra, where the endplates remained intact throughout testing (Figure 2B).

Conclusion

The inability of the disc with a damaged endplate to develop normal intradiscal pressure during flexion was previously shown to increase loading of the anterior cortex of the adjacent vertebra and may increase the risk of subsequent fracture. Although reduction of the endplate fracture with StaXx FX did not fully restore the endplate to its intact condition, enough correction of the endplate deformity was achieved to improve the disc’s load sharing ability. Further studies are needed to investigate whether the reduction of endplate fracture will alleviate the risk of adjacent fractures.

References

1. Tzermiadianos, MN, Renner, SM, Phillips, FM, Hadjipavlou, AG, Zindrick, MR, Havey, RM, Voronov, M, Patwardhan, AG. Altered disc pressure profile after an osteoporotic vertebral fracture is a risk for adjacent vertebral body fracture. Eur Spine J. 2008; Sept. 16. (EPub ahead of print).

Financial Disclosures: Chirs Carson-Employee of Spine Wave, Inc. Avinash G. Patwardhan institutional research grant Department of Veterans Affairs and Spine Wave, Inc.

This abstract has not been previously presented.

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Interventional Spine

Wayne J Olan, MD,

Scientific Paper

Mentor Award: No

Institution where work was conducted

Suburban Hospital

Affiliation and Department

Director of Neuroradiology / MRI

Address

8600 Old Georgetown Rd
Bethesda, Maryland
20814
Phone: (301) 896-3202
Email: wjo39@aol.com

Purpose

A new implantable device now allows the physician greater in situ management during kyphoplasty procedures. Using an innovative PEEK wafer stack, structural kyphoplasty permits directional control for vertical reduction of the vertebral body while still providing fracture stabilization and pain relief. The purpose of this retrospective review is to determine the safety and efficacy of the StaXx® FX Structural Kyphoplasty System in the treatment of vertebral compression fractures.

Methods & Materials

Using fluoroscopic guidance, the vertebral body was accessed through a peri-pedicular approach. PEEK StaXx® FX wafers were inserted via instrumentation in 1 mm increments. A small amount of cement was then inserted anterior to the stack for stabilization. Surgical data, pain relief and initial outcome information were retrospectively analyzed on an initial series of structural kyphoplasty cases at a single center. Determination of the subsequent fracture rate was assessed via patient interviews over a 14 month period.

Results

Twenty-six osteoporotic VCFs (T11-L4) in 25 patients were percutaneously treated for fracture repair. A mean of 2.0 cc of cement was injected anteriorly to the wafer stack. Average follow-up was eight months. Post-operative VAS pain score was significantly decreased (p<0.001) from 9 to and initial 1.6 and 1.5 at follow-up. No neurological complications as a result of the device or the procedure have been reported. No cement extravasation was noted. No post-operative subsequent fractures have been report in this series of patients.

Conclusion

Controlled vertebral augmentation, not possible with balloon kyphoplasty, is now possible when the StaXx® FX Structural Kyphoplasty System. Structural kyphoplasty appears to be a safe and effective procedure that relieves pain, and uses less cement volume than vertebroplasty and balloon kyphoplasty. No procedure related complications have occurred. Refracture rates appear to be as low as if not lower than traditional VCF fracture fixation methods, and no adjacent level fractures have occurred.

References

Author is a consultant for Spine Wave.

General Spine

Uei Pua, MBBS, MMed, FRCR, FAMS,
Arun Thomas, MBBS, FRCR, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

Tan Tock Seng Hospital

Affiliation and Department

Diagnostic Radiology

Address

11 Jalan Tan Tock Seng
Singapore, Alabama
308433
Phone: 97547525
Email: druei@yahoo.com

Excerpta

A 38 year old man with achondroplasia, presented with exacerbation of chronic low back pain, with radiation to both lower limbs. Apart from external features of achondroplasia, physical examination including neurological examination of the lower limbs was essentially unremarkable. Frontal and lateral radiographs of the lumbar spine demonstrate typical features of achondroplasia: decreased lumbar interpedicular distance, posterior vertebral scalloping, short pedicles with narrow spinal canal and hyperlordosis with a horizontal sacrum. In addition, anterior wedging of the L1 vertebral body with mild thoracolumbar kyphosis was noted (Fig. 1a, 1b). MR of the lumbar spine confirmed multilevel lumbar degenerate disc disease (Fig. 2a, b, c), worst at L1/2 with loss of disc height and disc dessication. In addition, multilevel severe spinal canal stenosis and compression of the thecal sac is seen. Crowding of the nerve roots within the thecal sac with narrowing of the lateral recesses and the neural foramina at all levels from L1-L2 to L5-S1 is also present. Interestingly, anterior wedging of the L1 vertebral body with areas of T2 signal prolongation was noted (Figure 2a, b, c), the latter consistent with bone edema.

The working diagnosis was spinal canal stenosis as the cause for the low back pain. However, as there were no previous images for comparison and with the bone edema being confined to a single wedged vertebral level, an acute fracture involving either a congenitally wedged L1 vertebra or less likely an acute wedge compression fracture were considered possibilities. The patient elected conservative management and was treated with oral analgesia.

Eighteen months later, a repeat MR was performed to assess the progression of spinal canal stenosis when he re-presented with recurrent back pain. Although the changes related to degenerate disc disease (DDD) and spinal canal stenosis were stable. New signal changes were noted at the L1 vertebral body, notably, the anterior wedged L1 vertebral body showed signal changes consistent with Modic type 2 end-plate changes, in the same morphology as the areas of bone edema seen in the earlier study (Fig. 3a, b, c). In retrospect, the changes in the early MR were related to Modic type 1 changes within a congenitally wedged vertebral body, rather than an acute fracture.

DISCUSSION

Achondroplasia is a non-lethal form of chondrodysplasia with an autosomal-dominant pattern of inheritance. The skeletal changes in achondroplasia reflect retarded endochondral bone formation with normal appositional growth, resulting in abnormally short and wide long bones. The length of the vertebral column is however preserved, giving rise to the familiar phenotypic appearance of a “short-limb” dwarf [1, 2].

Spinal complications in achondroplastic dwarfism causing neurologic disturbance are well-described [1] and many are related to the narrowed spinal canal. Neurological deficits can range from nerve root compression syndromes to transverse myelopathy [1, 2]. Stenosis of the spinal canal is secondary to abnormalities of endochondral ossification with premature synostosis of the ossification centers of the vertebral body and the posterior arch. This results in thickening of the laminae, shortening of the pedicles, and a reduction in the height of the vertebral bodies; with resultant decrease in dorsoventral space within the spinal canal. Additionally, prolapsed intervertebral disks and premature hypertrophic osteoarthritis is not uncommon, causing further narrowing and nerve root impingement at the lateral recesses or foraminal level. [1, 2, 3]

Despite having a vertebral column with normal length, vertebral deformities (e.g. flattening of the vertebral bodies) and kyphoscoliosis are relatively common. Thoracolumbar kyphosis further compound spinal canal stenosis and is usually first noticed in infancy. It is not a congenital fixed deformity but arise as result of mechanical factors, specifically the general muscular hypotonia of achondroplastic children [4, 5]. In some cases, kyphosis is accompanied by anterior wedging of the vertebral bodies, which begins as a result of the physiological anterior compression of the vertebral growth areas. Progressive fixed thoracolumbar kyphosis results from the disruption of the vertebral epiphyseal ring, which begins in childhood. There is a resultant decrease in growth of the anterior column and subsequently the formation of a fixed thoracolumbar kyphotic deformity [6] with anterior wedged vertebral bodies. In adult achondroplasts, one or more anterior wedged vertebral bodies are common and can occur anywhere from T11 to L2 vertebral level, sometimes in the absence of significant kyphosis. [3, 4]

Low back pain in adult achondroplasts represents a diagnostic challenge with protean etiologies. Differentiating acute from chronic causes can often be difficult based on history and physical examination. Similarly, imaging can be equally challenging as acute changes can exist amidst congenital deformities and chronic degenerative changes [7].

Conventional radiography being readily available is most commonly ultilized, however, MR has certain distinct advantages. MR can detect bone edema and is therefore highly sensitive in demonstrating early or occult fractures [8]. This is particularly so in dysplastic vertebral bodies [7], where assessment with conventional radiography is difficult. Furthermore, MR allows multiplanar assessment of the posterior elements and spinal canal necessary for surgical planning, and has the ability to image soft tissues enabling visualization of ligaments, intervertebral discs prolapses and areas of nerve root conflicts.

Modic changes and its association with degenerative disc disease is well-described [9]. Briefly, Modic type 1 change is postulated be due to bone edema and represent the acute inflammatory stage of degenerative disc disease with background biomechanical instability [9, 10], while Modic type 2 changes represent the more chronic and biomechanically more stable state [9] with conversion of normal red hemopoietic marrow into yellow fatty marrow as a result of marrow ischemia [3, 4, 9]. Lastly, Modic type 3 changes reflect the final and sclerotic stage. The respective MR changes therefore mirrors bone edema in Modic type 1 (Figure 2), marrow fat replacement in Modic type 2 (Figure 3) and bone marrow sclerosis in Modic type 3. In our case, the conclusive diagnosis of Modic type change in L1 vertebral body was made by observing progression of MR signal changes from the “acute” (Modic type 1) to the more “chronic” (Modic type 2) state over an 18 month period (Figures 2 and 3).

In the present case, the pattern of Modic change being confined to a single vertebral level (L1) with sparing of the rest of the lumbar vertebral levels is interesting and has not been previous described in an adult achondroplast. In normal individuals, the thoracolumbar junction is subjected to many different vectorial forces (e.g. axial loading, rotational) and as a result acute traumatic fractures in the region are not uncommon [11]. This single vertebral level bone edema with its location at L1, made exclusion of an acute fracture is difficult (Fig. 2); especially in the absence of old studies for comparison and single level Modic change would be a remote consideration at the time of interpretation of the patient’s first MR study.

Nevertheless, in retrospect, the single level of Modic change would not be surprising. Besides the normal vectorial forces experienced at the thoracolumbar junction, the fixed thoracolumbar kyphosis together with lumbar hyperlordosis in achondroplasts results in altered biomechanics and further augments the stress in this region. The congenitally wedged L1 vertebral body is further compounding. As a result, early and perhaps accelerated DDD with its associated Modic changes in the region can therefore be expected. The associated dessicated disc with loss of height of the adjacent L1/2 intervertebral disc is supportive of this postulate.

This case highlights a few points. Firstly, the typical “end-plate” distribution of Modic change related signal changes can be difficult to appreciate in dysplastic vertebral bodieS. Furthermore, single vertebral level or atypical distribution of Modic change can be expected in patients with a dysplastic spine due to altered biomechanics and stress distribution, and the Modic change reflects the region of increased stress and the related DDD. Lastly, while acute fracture is a common cause for MR signal change of bone edema, such signal change needs to be interpreted with caution in patients with a dysplastic spine. This is particularly relevant in this current era where more aggressive options for treatment of vertebral fractures such as vertebroplasty [12] and kyphoplasty are gaining popularity. Therefore, trial of conservative treatment with follow-up imaging is probably prudent in equivocal cases.

To conclude, this case illustrates the continuing challenge in the evaluation of back pain in an adult achondroplast with a dysplastic spine, and highlights the need to consider Modic change when single level bone edema is encountered.

References

REFERENCES:

1. Galanski M, Herrmann R, Knoche U. Neurological complications and myelographic features of achondroplasia. Neuroradiology. 1978 Nov 24; 17(1):59-63.

2. Lutter LD, Langer LO. Neurological symptoms in achondroplastic dwarfs – surgical treatment. J Bone Joint Surg Am. 1977; 59:87-92

3. Hamamci N, Hawran S, Biering-Sorensen F. Achondroplasia and spinal cord lesion. Three case reports. Paraplegia. Jun 1993; 31(6):375-9.

4. O’Brien JP, Mehdian H: Relevant principles in the management of spinal disorders in achondroplasia. Basic Life Sci 48: 293–298, 1988

5. Pauli RM, Breed A, Horton VK, et al: Prevention of fixed, angular kyphosis in achondroplasia. J Pediatr Orthop 17: 726–733, 1997

6. SN Misra, Howard W Morgan: Thoracolumbar spinal deformity in achondroplasia. Neurosurg Focus 14 (1): Article 4, 2003

7. Harrop JS, Jeyamohan S, Sharan A, Ratliff J, Flanders A, Maltenfort M, Falowski S, Vaccaro A. Acute cervical fracture or congenital spinal deformity? J Spinal Cord Med. 2008; 31(1):83-7.

8. Ito Z, Harada A, Matsui Y, Takemura M, Wakao N, Suzuki T, Nihashi T, Kawatsu S, Shimokata H, Ishiguro N. Can you diagnose for vertebral fracture correctly by plain X-ray? Osteoporos Int. 2006; 17(11):1584-91. Epub 2006 Aug 18.

9. R. Rahme, R. Moussa: The Modic Vertebral Endplate and Marrow Changes: Pathologic Significance and Relation to Low Back Pain and Segmental Instability of the Lumbar Spine. AJNR Am J Neuroradiol 29:838–42 _ May 2008

10. Kokkonen SM, Kurunlahti M, Tervonen O, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine: correlation with pain provocation and disc changes observed on computed tomography diskography. Spine 2002; 27: 2274–78.

11. Saboe LA, Reid DC, Davis LA, Warren SA, Grace MG. Spine trauma and associated injuries. J Trauma. 1991 Jan; 31(1):43-8

12. Gray DT, Hollingworth W, Onwudiwe N, Deyo RA, Jarvik JG. Thoracic and lumbar vertebroplasties performed in US Medicare enrollees, 2001-2005. JAMA 2007 Oct 17; 298 (15):1760-2.

No financial disclosures.

Images

General Spine

L E Pack, MD MPH,
Joshua M Ng, MD, Non ASSR Member
Cathyrn M Christensen, MD, Non ASSR Member
Karen J Bos, MD, Non ASSR Member
Stephen R Baker, MD, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

University of Medicine and Dentistry of New Jersey, New Jersey Medical School University Hospital /

Affiliation and Department

UMDNJ NJMS, Dept. of Radiology

Address

150 Bergen St
C320, Dept of Radiology
Newark, New Jersey
7103
Phone: 973-769-3813
Email: ellie.pack@gmail.com

Excerpta

We report a case of a 24 year old Brazilian immigrant who presented to the emergency department of Cambridge Hospital, in Cambridge, Massachusetts with the rapid development of weakness and pain in his legs, progressing to numbness below the knees. An MR examination of the thoracolumbar spine revealed a discrete spinal cord tumefaction expanding the conus medullaris. After a serum serology test was positive for Schistosoma mansoni he was successfully treated with Praziquantal and Dexamethasone and experienced a full resolution of symptoms over several weeks.

Schistosoma myeloradiculopathy can simulate a spinal cord neoplasm by both physical examination and imaging studies. It is a well recorded complication of Schistosoma infestation in enzootic regions of eastern Brazil. With increasing migration to the United States from Brazil and the expansion of domestic and foreign tourism to affected areas in that country, Schistosoma myeloradiculopathy will be encountered with increasing frequency in North America where its manifestations as an acute or sub acute paraparesis if not frank paraplegia, will likely occasion initial presentation to an emergency facility.

Images

General Spine

Kunal I Nanavati, MD,
M Judith Don Post, MD, Non ASSR Member
Kunal I Nanavati, MD, Non ASSR Member
Natalya Nagornaya, MD, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

University of Miami / Jackson Memorial Hosptial

Affiliation and Department

Jackson Memorial Hospital, Radiology Department

Address

1611 NW 12th Avenue
Rm 279
miami, Florida
33136
Phone: 786 547 0091
Email: knanavati@med.miami.edu

Excerpta

Due to the paucity of literature dealing with MR findings in Herpes zoster myelitis and radiculitis, we illustrate the MR features in two such unusual cases. Our purpose is to emphasize the importance of early recognition by MR of this clinically elusive infection in HIV positive patients, an infection which if diagnosed early is potentially treatable but if left unrecognized can cause fulminating infection and death (1,2). Due to the accelerated clinical course of Herpes zoster infection in the CNS in individuals who are HIV positive, and due to atypical clinical presentations including absence of skin rash, knowledge of the MR characteristics of this infection in the spine is critical to early diagnosis and early treatment (3). Additionally, knowledge of MR findings in the spine and brain in HIV positive patients with recurrent Herpes zoster infection who present with neurological symptoms can also lead to earlier and efficacious medical therapy. Also it becomes imperative to follow these patients with MRI while on treatment as acyclovir resistance is a known possibility in neurologically complicated herpes zoster patients (4).
First patient was a 37 year old female, with history of treated T7 dermatomal shingles six weeks prior to presentation with bilateral lower extremity tingling and numbness with weakness on left side. MRI of the spine was consistent with myelitis and showed diffuse high signal intensities extending over multiple segments ( T2 through T11) within the expanded thoracic spinal cord on fast spin echo T2 weighted images(Image 1).On gadolinum enhanced T1 weighted images there was peripheral enhancement located more posteriorly and was patchy and ill-defined extending over multiple segments within the substance of cord along with leptomeningeal enhancement (Image 2 and 3). No high signal on T1 weighted images was noted. Her absolute CD4 count was 140 cells/microlitre, and CSF PCR test for Herpes zoster DNA was positive. Unfortunately she progressed to paraplegia and right upper extremity weakness due to vasculitis with involvement of brain.

Second patient, was 51 year old female, who was recently diagnosed to be HIV positive after presenting with generalized tonic-clonic seizure and shingles on left L5-S1 dermatome. Her absolute CD4 count was 283 cells/microlitre, MRI of the spine was consistent with radiculitis and showed dramatic isolated enhancement of ventral and dorsal nerve roots of L5 and S1 dermatome with prominence of dorsal root ganglia on left side(Image 4). While our second patient did have a typical vesicular skin rash with L5-S1 dermatome distribution, the MR findings in this patient serve as an illustration of spectrum of spine abnormalities in Herpes zoster and it can serve as a baseline to track spread of infection(5).

In summary, acute onset with rapid progression of neurological symptoms and MRI findings in HIV positive patients with findings of cord expansion, patchy multisegment cord enhancement, leptomeningeal enhancement or nerve root enhancement should alert us to include Herpes zoster infection in the differential diagnosis, so that appropriate CSF laboratory investigations can be performed and appropriate medical treatment can be instituted.

References

1. Gilden DH, Kleinschmidt-DeMasters B K, LaGuardia JJ, et.al. Neurologic complications of reactivation of varicella-zzoster virus. NEJM 2000; 342: 635-645
2. de Silva SM, Mark AS, Gilden DH, et al. Zoster myelitis: improvement
with antiviral therapy in two cases. Neurology 1996;47:929-31.
3. Gilden DH, Dueland AN, Devlin ME, Mahalingham R, Cohrs
R. Varicella-zoster virus reactivation without rash. J Infect Dis
1992; 166 (Suppl 1): S30–4.

4. Snoeck R, Ge´rard M, Sadzot-Delvaux C, et al. Meningoradiculoneuritis
due to acyclovir-resistant varicella-zoster virus in an acquired immune deficiency syndrome patient. J Med Virol 1994;42:338–47.
5. R. Toledano, J. Lo´pez-Sendo´n, F. Gilo et. al. Posterior horn varicella-zoster virus myelitis. J Neurol (2007) 254:400–401

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General Spine

Micheal L Gilbert, D.C.,
Celia Maguire, D.C., Non ASSR Member
Jean-Nicolas Poirier, D.C., Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

Parker College of Chiropractic

Affiliation and Department

Diagnostic Imaging Section, Department of Clinical Sciences

Address

2500 Walnut Hill Lane
Suite E200
Dallas, Texas
75229
Phone: 214-902-2459, Fax: 214-902-2448
Email: mgilbert@parkercc.edu

Excerpta

Introduction
Gorham-Stout disease (GSD) represents a rare, idiopathic pathology of the musculoskeletal system, characterized by angiomatous invasion of bone, resulting in osteolysis with subsequent replacement by vascular fibrous tissue. It commonly affects the pelvic and shoulder girdles of young adults, but may be seen at any age. There is no gender preference. Prognostically, the disease is unpredictable. An effective treatment is not known; however, surgery and radiation have become most widely used. The natural history of the disease is one of relentless progression. Involvement of visceral and spinal structures may occur, resulting in increased morbidity and mortality. Early, accurate diagnosis can be made with a high index of suspicion clinically combined with characteristic radiographic and histopathological findings.

Clinical Features and Outcome
A 38-year-old male power-lifter with a history of trauma to his low back about 20 years prior presented to a chiropractor complaining of bilateral sacroiliac pain. Physical examination revealed absence of the normal palpatory bony prominence of the spinous processes of the third and fourth lumbar segments. Findings consistent with osteolysis characterized by dissolution of neural arch components of the L3 and L4 segments were seen on conventional radiography and computerized tomography (CT). Magnetic resonance imaging (MRI) demonstrated abnormal signal alterations in the posterior body of the third and fourth lumbar vertebra with extension into the pedicles, laminae and spinous processes. These alterations were characterized by low signal intensity (SI) on T1-weighted images and increased, heterogeneous SI on short tau inversion recovery (STIR) and proton density (PD) sequences. T1-weighted images further revealed high SI of the third and fourth lumbar vertebral bodies, consistent with fatty marrow conversion. Inhomogeneous enhancement was observed following the administration of gadolinium. There was no evidence of osseous expansion or paraspinal or epidural masses. Technetium 99m methylene diphosphonate (99mTc MDP) bone scan revealed focal photopenia at the involved levels. Laboratory studies were normal. Biopsy showed exuberant vessel proliferation with endothelial hyperplasia and fatty marrow conversion with minimal residual trabecular bone. No cellular atypia or mitotic figures were noted. A watchful waiting protocol was advocated by the oncologist with periodic re-examination. At last report the patient remains asymptomatic.

Conclusions
The diagnosis of GSD is supported by associated imaging findings, lack of clinical lab abnormalities, and biopsy results. In fact, a set of diagnostic criteria has been suggested by Heffez and colleagues. This criterion includes: 1) negative hereditary etiology and a progressive bone resorption without evidence of osteoblastic response; 2) normal laboratory values, ruling out the presence of metabolic, neoplastic, infectious or immunological processes; and 3) no dystrophic calcification or visceral involvement and angiomatous tissue demonstrating no cellular atypia on histopathological sample. The disease is potentially life-threatening, complicated by neural and visceral involvement. Imaging findings consistent with osteolysis are common and may mimic aggressive neoplastic etiologies. Practitioners should be cognizant of this potential differential diagnosis.

References

References
1. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone): its relation to hemangiomatosis. J Bone Joint Surg [Am] 1955; 37-A:985-1004.
2. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). J Bone Joint Surg [Br] 1999; 81-B:501-6.
3. Yoo SY, Hong SH, Chung HW, Choi JA, Kim CJ, Kang HS. MRI of Gorham’s disease: findings in two cases. Skeletal Radiol 2002; 31:301-6.
4. Duffy BM, Manon R, Patel RR, Welsh JS. A Case of Gorham’s Disease with Chylothorax Treated Curatively with Radiation Therapy. Clin Med Res 2005; 2:83-86.
5. Patel DV. Gorham’s Disease or Massive Osteolysis. Clin Med Res 2005; 2:65-74.
6. Chung C, Yu JS, Resnick D, Vaughan LM, Haghighi P. Gorham syndrome of the thorax and cervical spine: CT and MRI findings. Skeletal Radiol 1997; 26:55-9.
7. Heffez L, Doku HC, Carter BL, Feeney JE. Perspectives on massive osteolysis: report of a case and review of the literature. Oral Surg Oral Med Oral Pathol 1983: 55:331-343.

Images

General Spine

Roshan B Pai, MD,
Anant Krishnan, MD, Non ASSR Member
Philip Estrellas, MD, Non ASSR Member
Anindya K Roy, MD, Non ASSR Member
William J Romano, MD, Non ASSR Member
Paul G Bove, MD, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: Yes

Institution where work was conducted

William Beaumont Hospital

Affiliation and Department

Radiology

Address

1067 Emmons Avenue
Birmingham, Michigan
48009
Phone: 248-891-8491
Email: roshan.pai@beaumont.edu

Excerpta

We report and present a rapidly progressive osteolytic lesion in the lumbar spine of a 73 year old gentleman. The lesion was biopsied under CT guidance revealing an angiosarcoma. Concurrently, the patient’s known abdominal aortic aneurysm previously followed for several years had increased in size. Biopsy of the surface of the abdominal aorta confirmed an identical histological diagnosis to that of the osteolytic lesion. The unusual nature of the diagnosis as determined by the imaging findings in this patient including CT and MRI together with the histology are presented and discussed. While uncommon, such a condition may be considered when faced with a rapidly progressive spinal lesion in patients with abdominal aortic aneurysms.

Images

General Spine

Christopher P Petrie, DC,
Farshid Marzban, PhD, DC, Non ASSR Member
Afsar Sokhansanj, MS, DC, Non ASSR Member
Concetta Tofan, , Non ASSR Member
Kenneth Garrett, DC, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

Parker College of Chiropractic

Affiliation and Department

Department of Clinical Sciences

Address

2500 Walnut Hill Lane
Suite E200
Dallas, Texas
75229
Phone: 940-367-0840, Fax: 214-902-2448
Email: cpetrie@parkercc.edu

Excerpta

INTRODUCTION

Infectious spondylitis represents up to 4 percent of all cases of osteomyelitis. Cases have been reported in all age groups, but it is most frequent in the fifth and sixth decades. The most frequent site of involvement is the lumbar spine followed in order by the thoracic spine, cervical spine and sacrum. It classically affects the anterior elements of the spine, starting in the vertebral body and extending to involve the adjacent disc(s). Persistent vascularity to the disc in children provides a hematogenous route to the disc resulting in initial involvement of the disc (discitis) with spread to the adjacent vertebral bodies. Staphylococcus aureus is the most frequently implicated etiological agent representing 50 to 90 percent of cases. Patients typically present with a history of recent primary infection frequently involving the urinary tract or skin or a recent interventional procedure such as catheterization or surgery. The case presented here is distinctly unusual, both for its location of involvement (thoracic disc and adjacent bodies) and the infective agent involved (salmonella).

CLINICAL AND IMAGING PRESENTATION

The patient is a male, 15 years of age, that presented with thoracic spine pain. The pain began the same day as lifting furniture and was aggravated during football practice the following day. The patient began a course of conservative management that included chiropractic manipulative therapy and acupuncture. Five days after the onset of pain, a mild fever was noted that intensified and then remitted over the next four days. The patient’s symptoms failed to improve with care and he was referred to an orthopedic specialist for consultation and evaluation. Physical examination and radiographic studies of the thoracic spine were performed eleven days after the initial symptoms began. The radiographs showed Schmorl’s nodes and endplate irregularities in the lower thoracic region. No evidence of a destructive pathology was visualized. Conservative management was continued. Twenty-six days after the initial onset of symptoms, the pain intensified and a fever returned. The patient was subsequently referred for a magnetic resonance (MR) imaging exam of the thoracic spine.

Non-contrast MR examination of the thoracic spine (performed 31 days after the initial symptoms) showed diffuse signal hypointensity in the T9 and T10 vertebral bodies on T1-weighted imaging (T1WI) with signal hyperintensity on T2-weighted imaging (T2WI). The anterior cortical margin of the vertebral bodies and endplates was poorly defined. Mild anterior displacement of the prevertebral soft tissue structures by a sessile-shaped mass was seen anterior to T9-T10. The mass demonstrated signal hypointensity on T1WI and heterogeneous signal hyperintensity on T2WI. On T2WI an area of conspicuous signal hyperintensity was seen centered at the anterior portion of the T9/10 disc. The clinical and radiographic findings suggested a diagnosis of infection and the patient was referred for evaluation and management by an infectious disease specialist and a spine surgeon.

INTERVENTION AND OUTCOME

The patient was admitted to the hospital and antibiotic therapy was initiated immediately. A computed tomography exam of the thoracic spine was performed and demonstrated fragmentation of the anterior portion of the vertebral bodies of T9 and T10. Additionally, a hypodense para- and perivertebral soft tissue mass was visualized at the T9/T10 level. CT-guided needle-aspiration of the prevertebral soft tissue mass yielded group E/G salmonella bacteria upon culturing. Laboratory values demonstrated an elevated erythrocyte sedimentation rate (ESR) and increased concentration of C-reactive protein (CRP). Complete blood count (CBC) values were within normal limits.

Follow-up MR seven days after admission demonstrated mild expansion of the paravertebral abscess. There was no evidence of spinal cord edema or abscess within the spinal canal. Continued antibiotic therapy resulted in steadily decreasing lab values for ESR and CRP. The patient was discharged after twelve days and continued antibiotic therapy at home for a total of 87 days. At 5 weeks post-admission, follow-up MR showed a mild decrease in the size of the paravertebral abscess. A focal kyphotic angulation could be seen at the T9-T10 level. Clinical evaluation at one year revealed markedly reduced pain at the site of involvement. The patient has resumed normal activities and continues to improve. Further imaging followup to evaluate for paravertebral mass resolution and late sequelae are pending.

CONCLUSION

Infection of the spine is an infrequent, but clinically important condition that can affect patients of all ages. A lack of early radiographic findings highlights the importance of recognizing the clinical findings suggestive of infection. Advanced imaging, especially MR and gallium nuclear imaging, can detect early involvement and suggest the diagnosis. MR imaging with fat-suppression techniques, such as STIR, or intravenous gadolinium injection may provide additional insight in cases where age-related marrow changes may obscure the findings. Primary differential consideration should be given to advanced degenerative changes and neoplastic involvement. In most cases, the combined clinical and radiographic pictures will strongly suggest an infectious process. Prompt treatment with appropriate antibiotic therapy reduces long-term complications that can include ankylosis, spinal deformity, neurological impairment and rarely, para- or quadriplegia.

References

Berant M, Shrem M. Vertebral osteomyelitis in a young infant. Clin.Pediatr.(Phila) 1974;13:677-9.

Bolivar R, Kohl S, Pickering LK. Vertebral osteomyelitis in children: report of four cases. Pediatrics 1978;62:549-53.

Bremner AE, Neligan GA. Benign form of acute osteitis of the spine in young children. Br.Med J 1953;1:856-60.

Cahill DW, Love LC, Rechtine GR. Pyogenic osteomyelitis of the spine in the elderly. J Neurosurg. 1991;74:878-86.

Coventry MB, Ghormley RK, Kernohan JW. The intervertebral disc: Its microscopic anatomy and pathology. J Bone Joint Surg Am 1945;27:105.

Garcia A, Jr., Grantham SA. Hematogenous pyogenic vertebral osteomyelitis. J Bone Joint Surg Am 1960;42-A:429-36.

Goldman AB, Freiberger RH. Localized infectious and neuropathic diseases. Semin.Roentgenol. 1979;14:19-32.

Griffiths HE, Jones DM. Pyogenic infection of the spine. A review of twenty-eight cases. J Bone Joint Surg Br. 1971;53:383-91.

Kulowski JACO. Pyogenic Osteomyelitis of the Spine: An Analysis and Discussion of 102 Cases. J Bone Joint Surg Am 1936;18:343-64.

Resnick D. Diagnosis of Bone and Joint Disorders. 4th ed. Philadelphia: Saunders, 2002:2481-2520.

Wilensky AO. Osteomyelitis of the Vertebrae. Ann.Surg. 1929;89:561-70.

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General Spine

Zahir K Javeri, MD,
Evelyn Sklar, MD, Non ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

University of Miami/Jackson Memorial Hospital

Affiliation and Department

University of Miami/Jackson Memorial Hospital

Address

1611 NW 12 Avenue WW-279
Miami, Florida
33136
Phone: 214-454-4788
Email: zjaveri@hotmail.com

Excerpta

Purpose: To report a rare case of intradural renal cell metastasis to a nerve root which mimicked a benign lesion.

Case Report: The patient is a 50 year old male with past medical history of metastatic renal cell carcinoma status post right nephrectomy and right middle and lower lobectomies of the lung in November 2003. The patient also developed a duodenal recurrence and underwent a Whipple procedure in February 2008.
In November 2005, the patient developed mild left back pain and sciatica. Physical exam revealed a left S1 radiculopathy which worsened over time. Subsequent MRI and PET CT were performed and the mass was eventually resected. Pathological analysis revealed metastatic clear cell renal carcinoma to the left S1 nerve root.

Imaging Findings: Initial MRI exam showed enlargement and enhancement of the left S1 nerve root believed to represent either a schwannoma or neuroma and less likely metastatic disease. There was surrounding remodeling and expansion of the neural foramen consistent with a slow growing lesion without bony destruction/infiltration or paraspinal mass component. A subsequent MRI 3 months later showed no change. A concurrent PET-CT showed new metastatic disease in the duodenum which was hypermetabolic on PET. The left SI nerve root lesion however showed no abnormal increased metabolic activity and was therefore favored to represent a schwannoma. Due to worsening left back and leg pain, a follow up MRI 15 months later showed the noninfiltrating, well circumscribed mass with new areas of cystic degeneration, mild increase in size of the lesion and further bony remodeling without osseous destruction.

Discussion: The mass had characteristics of a benign slow growing process such as a schwannoma with remodeling and expansion of the neural foramen. Also, the lesion was nonhypermetabolic on a PET scan, although a recurrence of the duodenum noted on the same PET scan showed increased metabolic activity.
CT, MRI and ultrasound have roles in diagnosing, staging and assessing renal cell metastases; however, the role of FDG-PET has yet to be defined given its relatively low sensitivity. This case illustrates that a lesion with all of the characteristics of a benign slow growing process including a negative PET scan may represent a metastatic lesion considering the low sensitivity of PET with renal cell carcinoma.
Intradural metastasis to a nerve root is a rare entity. Previous reports of metastasis to a nerve root have described aggressive features including pedicle erosion, pathological fractures, and paraspinal soft tissue component, none of which were present in this case. Our case shows that even if a nerve root lesion possesses benign characteristics, metastatic disease should be considered in the differential diagnosis in the appropriate clinical setting.

References

1. Mak, K., Kwok, J. Intradural spinal metastasis from renal cell carcinoma: A case report. Journal of Orthopaedic Surgery 2001, 9(2):57-61.
2. Kang, D., White,R.,Zuger,J.,Sasser,H.,Teigland,C. Clinical Use of Fluorodeoxyglucose F18 Positron Emission Tomography for Detection of Renal Cell Carcinoma. Journal of Urology.Vol 171 1806-1809 May 2004.

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General Spine

Edward C Fourgas, M.D.,
Suresh C Patel, M.D., ASSR Member

Excerpta Extraordinaire

Mentor Award: No

Institution where work was conducted

Henry Ford Hospital

Affiliation and Department

Resident Physician, Radiology

Address

21520 Francis
St Clair Shores, Michigan
48082
Phone: 586-212-7105
Email: furxhi@hotmail.com

Excerpta

A 83 year old male with a history of gout and chronic renal failure secondary to glomerular nephrosclerosis presented with a long history of chronic back pain which had worsened over the past three years. He denied lower extremity focal weakness, bowel or bladder dysfunction. Physical examination did not reveal any focal neurological deficits. He had no appendicular manifestation of gout.

Serum uric acid remained elevated for the past seven years. Patient did not receive any medications for gout.

CT images of the lumbar spine dated 6/22/2005 showed normal osseous structures.

CT images of the lumbar spine dated 4/5/2008 showed multiple lucent lesions involving the articular processes of the bilateral facet joints at the level of L1 which extend into the lamina on the left. Additionally there were bilateral lobular periarticular lesions at this level which are slightly hyperdense to muscle. Significant disk space narrowing and end plate erosions were noted at L3-L4 and L4-L5. Axial computed tomographic images at the level of L5-S1 demonstrated interval disk space narrowing, well marginated erosions, and lobulated soft tissue densities surrounding the posterior elements.

MRI imaging of the lumbar spine showed hyperintense T2 signal in the L3-L4 and L5-S1 discs without focal fluid collections to suggest epidural or paravertebral abcess. End plate erosions and disk space narrowing corresponding to abnormalities noted on the CT images.

Diagnostic considerations included gout, diskitis/osteomyelitis complex and amyloid arthropathy. Gouty arthropathy was the favored diagnosis.

There are few reports describing the involvement of spine by gouty arthritis. These studies demonstrate that involvement of the spine entails a spectrum of clinical presentation from the rare asymptomatic patient to the more common patient with pain and neurological signs. Our patient had constant back pain and no evidence for focal neurological deficits.

It is unclear why the urate crystals accumulate in the spine as opposed to the appendicular skeleton. It has been suggested that irrespective of the tissue which is affected a previous injury or tissue necrosis is a prerequisite for urate deposition. Most cases of gout that involve the spine occur at the lumbar and sacral levels where degenerative disease also predominates, and hence may be a predisposing factor.

The classic findings of gout in the spine are lobular juxta-articular masses with an attenuation density greater that that of the surrounding muscle, well defined end plate erosions with reactive vertebral sclerosis and normal bone density. Although in classic gout the disk space is preserved, often times, this entity occurs in the setting of degenerative disk disease and disc space narrowing is noted. The differential diagnosis when the disk and the adjacent vertebral body are involved by tophaceous gout must include pyogenic spondylitis/diskitis and amyloid deposition. In our patient infection was suspected in the initial CT study of the lumbar spine but the follow up MRI study excluded this diagnosis by showing lack of edema in T2 weighed images. Furthermore well defined erosions are less likely associated with infection. Although our patient had long standing renal failure, he was not on dialysis, so amyloid arthropathy is less likely.

The diagnosis of gout is more likely in our patient given the tophaceous involvement of upper lumbar vertebrae and the clean margins of the erosions in L1-2. Although the arthropathy caused by gout is characteristic radiographically, it is not commonly seen since to takes several years for gout to cause radiographically evident disease. In our patient tophus formation at the L1-2 level developed over a course of 3 years. The patient had elevated serum uric acid levels for over 7 years.

Unlike peripheral gouty arthritis the lack of readily available synovial fluid or biopsy material for demonstration of urate crystals renders the diagnosis of spinal gout more difficult. The lumbar spine lesions in our patient were not biopsied. Hence this case demonstrates the importance of including gout in the differential diagnosis when periarticular tophaceuos lesions and well marginated erosions are seen.

This case of a 83 year-old male with erosive tophaceous gout of the lumbar spine is an excellent illustration of recognizing the classic radiographic features of gout arthropathy in an anatomic location that is not commonly involved by this entity.

Purpose

To describe the radiographic features of gouty arthropathy of the lumbar spine.

Methods & Materials

CT and MR images of a patient with presumed erosive tophaceous gout of the lumbar spine are presented.

Results

Axial CT images of the lumbar spine dated 6/12/2005 show normal osseous structures while those obtained three years later showed multiple erosive changes and disk space narrowing at multiple levels of the lumbar spine but especially at L1-L2 and L5-S1. Periarticular soft tissue masses were also seen surrounding the facets of L1-L2 and the spinous process of L5 vertebrae.

T2 weighed MRI images of the lumbar spine showed hyperintensities near the endplates at L3-L4 and L5-S1. Hyperintense soft tissue masses surrounding the facets of L1 vertebrae and posterior elements of L5 vertebrae were seen. Disk space narrowing and erosions as seen in the computed tomography images were noted.

Conclusion

Although rare, gouty arthropathy of the lumbar spine should be considered in patients with periarticular tophi and well marginated erosions in the setting of known or suspected gout.

References

1. Bonaldi VM, Duong H, Starr MR, et. al. Tophaceous gout of the lumbar spine mimicking an epidural abcess: MR features. American J Neuroradiology 1996;17:1949-1952.

2. Fenton P, Young S, Prutis K. Gout of the spine. Two case reports and a review of the literature. J Bone and Joint Surg Am. 1995:77:767-771.

3. Kuo YJ, Chiang CJ, Tsuang YH. Gouty arthropathy of the cervical spine in a young adult. J Chin Med Assoc 2007:70(4): 180-182.

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