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Fig. 44.5 Three options

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of surgical approach: ① posterolateral, ② lateral, and ③ anterior approaches (Case 3, 60-year-old male with T11–12 TDH)

Y. K awagu chi

Fig. 44.6 Posterolateral approach with posterior fusion. This patient had T8–L1 posterior fusion with transpedicular screws because the patient had diffuse idiopathic skeletal hyperostosis (Case 1; Chap. 54)

condition is acceptable. With this approach, however, fusion carries a risk of injury to the major vessels, lungs, and diaphragm. Fusion surgery is usually performed in most of patients with TDH, but fusion is not required in cases where a single-level

44 Thoracic Disk Herniation

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265

thoracic discectomy is treated with MIS.Neuromonitoring is performed by motorevoked potentials and/or somatosensory-evoked potentials. There is no consensus about whether intraoperative neuromonitoring is useful for preventing spinal cord damage because neuromonitoring does not always prevent spinal cord dysfunction after surgery.

44.7 Expected Outcomes

The surgical outcome is considered satisfactory when the TDH is removed and adequate decompression of the spinal cord is achieved at an early stage. Factors such as age and preoperative severity of the spinal cord dysfunction affect the surgical outcome. There can be postoperative neurological deterioration after surgery. The pathogenesis of this deterioration is unknown, but spinal shock, medullary contusion, and vascular impairment might be considered as causes.

44.8 Potential Complications

Neurological deterioration can be a major complication. Dural tears are encountered during surgery in about 40% of patients who had a massive calcied TDH and a thoracoscopic resection. Lung-related complications can occur in both anterior and posterior approaches. In addition, injury to the intercostal nerve might cause postoperative pain syndrome and neuralgia.

44.9 What Should Patient andFamily Know?

The incidence of TDH is rare, compared to herniation in the cervical and lumbar disks. TDH has the potential to cause the severe neurological decits, including paraplegia. The prognosis after any of the treatments for TDH can be favorable, but the surgical procedures have a risk of complications, including neurological deterioration.

Further Readings

Bouthors C, et al. Surgical treatment of thoracic disc herniation: an overview. Int Orthop.

2019;43:807–16.

Robinson WA, etal. Thoracic disc herniation, avoidance, and management of the surgical compli-

cations. Int Orthop. 2019;43:817–23.

Sharma SB, etal. A review of minimally invasive surgical techniques for the management of tho-

racic disc herniation. Neurospine. 2019;16:24–33.

Lumbar Degenerative Disc Disease

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andLumbar Disc Herniation

JamesE.Dowdell III andToddJ.Albert

45.1 Definition

Low back pain (LBP; Chap. 41) can have a variety of generators including degenerative disc disease (DDD) and lumbar disc herniation (LDH; Chap. 46). DDD can be dened as an age accelerated structural failure of the intervertebral disc (IVD), and thus disc degeneration does not necessarily equal DDD.To make a diagnosis of DDD, the clinical picture must be evaluated in addition to the radiographic presence of disc degeneration. LDH can occur in both degenerated and non-degenerated disc segments. LDH occurs when the nucleus pulposus is able to herniate through the annulus brosis. LDH can cause back pain, radicular pain, and sensory/motor disturbances.

45.2 Natural History

LBP is the most common cause of disability in young adults with an indirect loss of >100 billion dollars per year in decreased productivity. Over 80% of young adults will experience an episode of back pain in their lifetime, and an additional 2% to 3% of these patients will get radiculopathy as well. Typically, patients with DDD will

Supplementary Information The online version contains supplementary material available at [https://doi.org/10.1007/978- 3- 030- 80356- 8_45].

J. E. Dowdell III (*) · T. J. Albert Hospital for Special Surgery, Department of Orthopaedic Surgery, Weill Cornell Medical College, New York, NY, USA e-mail: dowdellj@HSS.EDU

https://doi.org/10.1007/978-3-030-80356-8_45

267

268

Inner Annulus

Outer Annulus

Cartilaginous endplate

Bony Endplate

Cancellous bone

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J. E. Dowdell III and T. J. Albert

Pain recepotors

Disc

Fig. 45.1 Nutrition of the IVD

Nucleus

Vascular loops and channels in bony endplate

Fluid

Artery

have a self-limited course of back pain, with 95% experiencing a recovery in 3 months with appropriate nonoperative treatment modalities. However, chronic back pain is a possibility for these patients. The pathway that leads to DDD is a complex interplay between nutritional, environmental, and genetic factors. Decreased nutritional supply limits the IVD from responding to load (Fig. 45.1), while genetic polymorphisms can affect genes that contribute to IVD structure and upregulate pro- inammatory pathways (Fig. 45.2). Environmental factors that contribute to DDD include obesity and cigarette smoking. Understanding the degenerative cascade is important for the development of future treatment modalities. For LDH, the vast majority of patients (~75%) will experience relief at 1 year. However, in patients who remain symptomatic beyond 6 weeks, there is a small but statistically signicant benet to undergoing a direct decompression of the affected nerve root.

45.3 Physical Examination

Observation of behavior, gait, and muscle atrophy is important when evaluating patients with DDD and LDH.Observation of Waddell’s signs is important for this patient population as well. Patients with a large LDH may be very uncomfortable and

45 Lumbar Degenerative Disc Disease andLumbar Disc Herniation

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Fig. 45.2 Inammatory pathways in DDD

Collagen

Degradation

269

Loss of structural integrity

Degradation

IL1, IL6

Increased

Inflammation

Proteoglycan

PAIN

Loss of hydrostatic pressure

MMP’s

be unable to sit down. Patients with DDD will present most commonly with back pain. Midline spinous process tenderness is very common. The range of motion will be limited secondary to pain (Appendix N). Pain that worsens with extension is likely facet- oriented, while worsening of pain with lumbar exion suggests a discogenic mediator of pain. Radicular pain is very common with disc herniation. There are commonly motor, sensory, and reex decits along the affected nerve root as well (Video

45.4). The straight leg raise test can reproduce radicular limb pain. A positive contralateral leg raise test usually indicates a massive or extruded disc fragment.

45.4 Imaging

Radiographs of the lumbar spine should include anteroposterior (AP) and lateral radiographs of the affected area (Fig.45.3). The AP view may show arthritic changes in the facets or osseous bridging between the disc spaces. The lateral view can show a variety of pathology including loss of disc height, spondylolisthesis, and vacuum disc (Fig. 45.4). Computed tomography (CT) scan will clearly show arthritic changes throughout the spine including in the facet joints, end plate sclerosis, and calcied disc herniation. However, a CT scan is not always required for these patients unless it is to address a specic question or if the patient is unable to obtain magnetic resonance imaging (MRI).

MRI is indicated for patients who fail to recover after 6–12 weeks of proper

nonoperative management and for those with any neurological decit (sensory/

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J. E. Dowdell III and T. J. Albert

Fig. 45.3 Normal lumbar radiographs (normal disc height, no vacuum phenomenon in the disc, no arthritic changes)

motor) in a radicular pattern. Patients with DDD will typically have a loss of signal within the nucleus pulposus and disc space collapse on MRI (Fig.45.5). Annular tears can be appreciated as high-intensity zones in the posterior annulus on T2-weighted imaging. Some MRI classications include the Modic system and the Prrmann classication (Fig. 45.6; Tables 45.1 and 45.2). The clinical utility of these classication systems is uncertain, but there is evidence to suggest a higher failure of nonoperative treatment in those with Modic changes on MRI.

45.5 Differential Diagnosis

There is a broad differential diagnosis for DDD and LDH (Tab le 45.3). Potential pain sources could be viscerogenic (renal/abdominal causes), neoplastic (primary or metastatic bone tumors; Chap. 63), neurogenic (spinal cord tumors/cysts), inammatory disease (ankylosing spondylitis; Chap. 54), infectious (discitis, osteomyelitis; Chap. 65), psychogenic, and spondylogenic (muscle strains, spinal stenosis, disc disease, facet arthropathy; Chap. 41; Chap. 46). Radiculopathy is most commonly

45 Lumbar Degenerative Disc Disease andLumbar Disc Herniation

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Fig. 45.4 Lumbar lateral radiograph showing vacuum disc phenomenon with accumulation of air in the disc space (black arrows)

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caused by a disc herniation but may be mimicked from peripheral nerve compression (e.g., piriformis syndrome) or intraneural pathology (e.g., peripheral nerve sheath tumor).

45.6 Treatment Options

The vast majority of patients undergo nonoperative care for DDD.Physical therapy is a mainstay of treatment, along with lifestyle modication (smoking cessations/ weight loss/core strengthening/back education). Anti-inammatory medications are very effective for treating pain related to DDD and LDH. Steroid medications are useful for radiculopathy. Cognitive behavioral therapy is effective at treating back pain in patients with chronic pain. Alternative therapies are frequently attempted as well, including yoga, CBT, chiropractor, CBD oil, and oral CBD with varying success. In patients with radiculopathy, transforaminal epidural injections can be effective in reducing the chemical/inammatory component of the radiculopathy but do not change the natural history of the disc herniation.

272

Modic 1

Modic 2 Modic 3

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Fig. 45.5 T2 lumbar MRI showing degenerative disc at L4-5, L5-S1 (loss of hydration, disc collapse), no Modic changes

J. E. Dowdell III and T. J. Albert

Fig. 45.6 Modic changes (Reproduced from Jones etal.)

45 Lumbar Degenerative Disc Disease andLumbar Disc Herniation

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Tab le 45.1 Modic changes as illustrated

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Type I Hypointense Hyperintense II Hyperintense Iso or hyperintense III Hypointense Hypointense

Reproduced

Tab le 45.2 Prrmann grades as illustrated

Structure

Grade I White, homogenous Clear Isointense to

II Inhomogeneous,

with banding

III Gray,

inhomogeneous

IV Gray to black

inhomogenous

V Black inhomogenous No distinction Hypointense Collapsed

Reproduced

Tab le 45.3 Differential diagnosis of low back pain

Type Differential Viscerogenic Abdominal and renal Neoplastic Primary and metastatic bone tumors Neurogenic Spinal cord tumors or cysts Inammatory

diseases Infectious Diskitis, osteomyelitis, psoas abscess Spondylogenic Myofascial syndromes

Ankylosing spondylitis, Reiter’s syndrome, inammatory bowel diseases, and psoriatic arthritis (sacroiliitis)

Iliolumbar syndrome, piriformis syndrome, quadratus Lumborum syndrome, and brositis (trigger point syndrome) Motion segment disorders Disk disease, facet syndrome, spinal stenosis Bony problems Fractures, including osteoporotic compression fractures Spondylolisthesis Sacral lesions, coccyx pain Psychogenic

T1 MRI signal intensity

Distinction (nucleus and annuals) T2 MRI signal intensity

cerebrospinal uid (hyperintense)

Clear Isointense to

cerebrospinal uid (hyperintense)

Unclear Intermediate Normal to

No distinction Intermediate to

hypointense

T2 MRI signal intensity

Disc space height

Normal

decreased Normal to

decreased

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J. E. Dowdell III and T. J. Albert

For LDH, in patients who fail conservative treatment for at least 6 weeks, surgical intervention can lead to improved outcomes. For any patient with a progressive neurological decit or neurological ndings (radicular pain/straight leg raise positive), operative management is appropriate (Video 45.4). Any method of lumbar decompression and stabilization is appropriate (open or minimally invasive) for these patients if a direct nerve decompression can be achieved (Video 45.3).

45.7 Expected Outcomes

The majority of patients recover very well from disc herniation. Patients with DDD can have a more variable clinical course due to the complexity of treating LBP.Nonoperative modalities of treatment can provide signicant relief for these patients, but for those with chronic unrelenting pain, surgical treatment without any accompanying neurological symptom is very controversial with no guarantee it will relieve pain.

45.8 Potential Complications

The major complication risk prole for lumbar decompression surgery is continued symptoms, nerve root injury, dural tear, re-herniation, and infection. However, the complication of nonoperative care for an LDH in a patient with neurological compromise is chronic pain and permanent loss of muscle function.

45.9 What Should Patient andFamily Know?

DDD is a lifelong condition that will require signicant efforts in lifestyle modications and physical therapy for the best chance of a good outcome. Patients with LDH with symptoms lasting longer than 6 weeks or with neurological compromise have better outcomes with surgery. These patients have a great chance for a full functional recovery.