Transmuscular tubular (s. Minimally invasive) diskectomy 14
Spinal Stabilization 14
Intraoperative Complications 15
Postoperative Complications 15
Prevention of recurrence 17
anterior and posterior longitudinal ligaments blend with and strengthen annulus fibrosis.
in early childhood, nucleus pulposus is gelatinous, containing hydrophilic polysaccharides (water content > 80%).
annulus fibrosus is composed of concentric collagenous layers that are attached to adjacent vertebrae; fibers are directed obliquely (at ≈ 55° degrees to horizontal plane) between vertebrae in successive layers that are perpendicular to each other.
N.B.disk elasticity is provided in large measure by annulus fibrosus!
Disk degeneration (acceleration of aging effects):
internal layers of annulus fibrosus progressively grow into nucleus pulposus → disk becomes amorphous, sometimes discolored, and increasingly fibrotic → more compressible, less elastic disk - more prone to tear and rupture.
wear & tear (accumulation of axial loading, motion trauma effects) → cracks in inner layers of annulus fibrosus.
N.B. disc degeneration is universal accompaniment of aging! (degeneration is identifiable in virtually everyone over age 60 years)
propensity to develop degeneration is correlated with ↑mobility of spinal segments:
cervical region, L4-S1, upper lumbar and lower thoracic spine;
- decreased capacity for shock absorption in degenerated discs → greater forces are transmitted directly onto adjacent vertebral bodies:
Type I - edema: ↓signal on T1-MRI, ↑signal on T2-MRI; differentiate from edema seen in infectious discitis/osteomyelitis (with infection, disc is abnormally bright on T2-MRI, whereas degenerated discs are dark).
Type II - end-plate infiltration by fat; marrow is brighter on T1-MRI and dark on T2-MRI; represents burned-out type I.
Type III - degenerative discogenic sclerosis of end-plate: ↓signal on both T1- and T2-MRI.
Possible further changes:
invasion of cancellous spaces by fibrovascular reactive tissue continuous with that of disc.
end-plate fracture and displacement into vertebral body.
Bulge - circumferential extension of disc margin beyond vertebral body margins.
identified in 50% asymptomatic persons.
annulus normally may bulge diffusely little (< 2-3 mm) beyond vertebral margins, esp. in children.
Herniation - focal displacement of disc material (nucleus pulposus and/or annulus) beyond margins of disc space; can occur in any direction (most clinically significant – posterolaterally).
protrusion (hard disc protrusion, spondylosis) – hardened nucleus bulges beneath attenuated annulus; associated osteophytes add to mass effect;
identified in 25% asymptomatic persons.
extrusion (herniation, soft disc protrusion, disc rupture) – soft nucleus extrudes through tear in annulus;
identified in < 1% asymptomatic persons.
sequestered fragment - extruded disc fragment separates entirely from its disc of origin, and may migrate within epidural space (occasionally, penetrates dura and can be seen intrathecally – can simulate neurinoma).
Schmorl node – nucleus pulposus herniation through cartilaginous end plateinto vertebral body; usually incidental radiographic or postmortem finding (prevalence in general population ≈ 20%).
seen most frequently in lower thoracic and upper lumbar spine.
occur through defects of end-plate (e.g. gaps in chondrification formed by vessels arising from vertebral body).
may be consequence of trauma.
reactive sclerosis forms around herniated cartilage nodule and it becomes easily visible radiographically.
thinning of disc space may or may not accompany herniation (caused not so much by actual herniation of disc material but by disc desiccation).
N.B. term “herniation” should be reserved for situations in which more precise classification cannot be made!
Disc degeneration + Traumatization is prime cause of disc herniation.
genetic predisposition in many cases!
commonly trauma is trivial.
major trauma is usually cause in children and young adults.
development of radial fissure through inner* concentric rings of anulus fibrosus; nucleus pulposus may begin to extend into this fissure; patient may experience low back pain and perhaps some referred pain into buttock or hip.
*outer layers of anulus fibrosus are tightly bound to adjacent vertebral end-plates
nucleus protrusion causing bulging of outer layers of anulus and of posterior longitudinal ligament (sufficient to pinch adjacent nerve root between protruding disc and lamina or intervertebral facet).
free disc fragment is completely extruded and becomes wedged anterior to nerve root.
Disc displacement causes symptoms by several mechanisms:
N.B. intervertebral disks (at least, nucleus pulposus) are not pain-sensitive!
exposed disc material has direct toxic effect → local inflammatory response.
regional muscle spasm.
Radiculopathy / myelopathy – due to compression by mass of disc material:
herniation into lateral recess or neural foramen (posterolateral herniation) → spinal root compression.
herniation into spinal canal (central herniation) → spinal cord compression (in cervical ÷ thoracic region) or cauda equina compression (in lumbosacral region).
N.B. spinal stenosis & spondylosis are major contributors to compression syndromes of cord and cauda equina! (even bulges and small protruding discs may compress neural structures).
disc extrusion is more likely to be source of symptoms than is disc protrusion (protrusions and annular bulges do cause symptoms, but this depends on additional anatomic factors - proximity of disc material to roots, caliber of bony spinal canal).
mechanisms by which compression causes neurological dysfunction: mechanical alteration of axonal membranes, impaired axonal flow, ischemia, eventual demyelination.
bending and lifting involved in child rearing → cervical herniation.
Signs & symptoms relate to geometry:
size and strategic location of disc fragments
size and configuration of spinal canal (incl. foramina).
Local pain (s. axial pain) – may be absent, or may precede herniation for weeks or months.
radiculopathy see p. PN1 >>
N.B. radicular pain may radiate into extremity episodically, extending further down extremity with each episode.
myelopathy (may be preceded by spinal shock) - paresis, with loss of pain and temperature sensations below level of lesion; vibration and position sensations are frequently retained (posterior location of dorsal columns). see p. Spin1 >>
onset of symptoms:
follows trauma (e.g. sudden rotation of head)
begins with stiff neck (reactive splinting of erector capital muscles), discomfort at medial border of scapula.
local neck pain (axial pain) radiates to interscapular region, shoulders, arms (radicular pain).
palpation of brachial plexus and supraclavicular fossa is often painful.
symptoms are worsened by:
stretching dependent arm
neck movements (esp. extension, lateral flexion to side of herniation – i.e. lateral flexion toward painful side*).
*vs. in trivial muscle spasm – pain on lateral flexion to opposite side (i.e. during stretch of painful muscle)!
vs. cervical spondylosis - exacerbated by any neck movements!
Source of picture: Barbara Bates “A Guide to Physical Examination”, 3rd ed. (1983); J.B. Lippincott Company; ISBN-13: 978-0397543991 >>
for relief patient adopts recumbent position with arm elevated and flexed behind head (vs. shoulder disease - patient maintains arm in dependent position, avoiding elevation or abduction at shoulder joint).
axial loading test, Spurling test (support diagnosis of cervical root disease) → see p. D1 >>
N.B. do not omit motor and sensory examination in lower extremities - to detect cord compression!
bouts of nonspecific low back pain (usually remittent) already begin in twenties.
in majority, there is no history of antecedent trauma - herniation follows lifting* / twisting injuries (or may result from accumulated low-level trauma); sneeze, cough, or trivial movement may also be trigger.
N.B. in many cases, inciting event cannot be identified!
*increasing intra-abdominal pressure during heavy lifting even adds to compressive load on vertebrae but otherwise stabilizes spinal column and may prevent twisting injury
patient appears uncomfortable.
symptoms are often episodic (remissions are characteristic).
pain may be restricted to parasacral area or may radiate to buttocks, thigh, leg, foot.
sciatica – L5 or S1 *radicular pain.
*any of L4-S3 roots (take part in ischiadic nerve) may produce sciatica to varying degree
paresthesias are common.
pain is aggravated by: see p. PN1 >>
heavy lifting from bent position
back movement (extension or twisting).
provocative root stretch maneuver:
passive straight-leg rising s. Lasègue sign (for roots L5 and S1);
femoral stretch test (for root L4).
pain is characteristically relievedpromptly when patient lies down* (no matter how severe pain is when patient is erect!; vs. spinal tumor - pain is not relieved or even worsens!) on one side with hips and knees flexed.
*some patients are more comfortable standing and some can find no comfortable position
patient may not be able to stand erect because paraspinal muscles contract so vigorously, yet pain may be relieved as soon as patient lies down, only to return again on any attempt to stand.
most uncomfortable position is sitting - causes increased intervertebral pressure!
later, short walks can bring relief, but long walks or extended sitting (especially driving) can aggravate pain.
protective splinting of paraspinal muscles:
asymmetric prominence of long erector muscles.
loss of lumbar lordosis (flattening of lumbar spine), lumbar scoliosis.
elevated one iliac crest (list or tilt) – “longer leg on one side” (erroneous assignment of back pain to leg length asymmetry) – often causes patient to raise heel on shoe of “short” leg to level pelvis).
muscle atrophy and weakness (fasciculation is rare). see p. PN1 >>
e.g. wasted gluteus - one gluteal fold hangs down and shows added skin creases when patient is erect.
sciatic tenderness on direct pressure at some point along nerve (e.g. popliteal).
with sacral roots involvement, disturbances of bladder & bowel function are common.
- herniations are uncommon! (suspect other underlying lesions – tumor, abscess, etc).
motion trauma (wear and tear) plays no role (vs. cervical, lumbosacral disc degenerations) - thoracic vertebrae are designed for stability rather than excursion, and heavy rib cage contributes to rigidity of this structure.
small capacity of thoracic canal → spinal cord compression is more frequent and more critical than root compression - early recognition is important! (to avoid irreversible myelopathy)
thoracic disc disease may result from Scheuermann disease with later trauma.
N.B. asymptomatic patients have high incidence of anatomical lesions – try to establish closest possible clinical correlation with anatomical findings!
infections, recent fever
bleeding disorders, anticoagulant medications
Immediately establish major deficits that demand rapid diagnosis & surgical treatment (see below – clear indications for surgery).
Findings consistent with ruptured disc + no ÷ moderate deficit → plain X-ray of affected area → no unexpected lesions → conservative therapy.
this approach is justified by good prognosis for spontaneous recovery of acute radiculopathy with up to moderate deficits.
if clinical examination leaves doubt about lesion localization (root vs. peripheral nerve or plexus) → EMG, nerve conduction studies (more sensitive if delayed until at least 10-14 days after onset of new deficit).
if surgery is considered necessary, it should be preceded by MRI or CT myelography.
Indirect diagnostic information (radiographs cannot show neural tissues or disc itself!):
isolated loss of disc space height
normal cervical ÷ thoracic discs are almost equal in height.
normal lumbar discs progressively increase in height from T12-L1 through L4-5; L5-S1 disc has variable height because of its transitional status.
other degenerative changes: osteophytes, end-plate sclerosis, malalignment (scoliosis, retrolisthesis, anterolisthesis).
Degenerative changes do not mean patient has “arthritis” as many asymptomatic patients (esp. young females) have some changes!
gas may be visible within degenerated discs (nitrogen drawn from blood by negative pressure generated during spine extension within airtight disc fissures).
severe degenerative disc disease may progress to spontaneous fusion between adjacent vertebrae.
Screen for unexpected infection, tumor, bony deformity.
many disc syndromes are genetic - abnormal skeletal features should be sought throughout spine (spinal stenosis, spondylolisthesis, widespread disc disease, Marfan disease, etc).