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146
12 Spinal Rehabilitation and Disability Evaluation
(2) An occupational disorder aggravated by a supervening other
occupational condition arising out of or in the course of employment
by the same employer.
(3) An occupational disorder aggravated by a supervening other
occupational condition arising in the course of employm ent by a
di erent employer.
(4) An occupational disorder aggravated by a preexisting
nonoccupational condition.
(5) An occupational disorder aggravating a preexisting nonoccupational
condition.
3. Determine end of healing:
a. Often an arbitrary period based on the individual clinician’s practice,
patient population, local culture, and experience (Maximum Medical
Im p r ove m en t ).
4. Assign impairment rating.
a. May be temporary or permanent.
b. Encompasses both residual symptoms as well as permanent restrictions.
c. Ultim ately should be based on an objective assessment of the patient’s
ability to perform certain functional tasks, such as sitting, lifting,
gripping, and pushing.
d. Formal evaluation methods are evolving.
(1) None are yet proven to be more objective or reliable than the treating
physician’s completion of the work capacity evaluation form based
on his or her estimation of the patient’s current abilities.
III. Sp in al im p air m e n t rat in g.
A. Th e r e a re m an y r at in g s yst e m s a va ila b le , in clu d in g o n es d evelo p e d b y t h e
Am e r ic a n M e d ica l As so cia t io n a n d t h e Am e r ica n Aca d e m y o f Or t h op a e d ic
Su r ge o n s.
B. Ele m e n t s fo r d et er m in in g im p air m e n t in clu d e t h e fo ll o w in g:
1. Range of motion.
a. Measured with goniometer or inclinometer.
2. Neurological impairment.
a. Includes sensory changes, loss of re ex, and loss of motor function
(weakness to paralysis).
3. Speci c diagnosis or surgical intervention.
4. Psychosocial impairment.
a. Includes such items as activities of daily living, social functioning,
concentration, and coping.
C. Th e clin icia n w i ll b e n e t fr o m n d in g o n e r at in g s y s t e m a n d u sin g it
consisten tly so as to becom e m ost pro cient.
D. Treat ing p hysicia n s m u st n ot view im pair m en t rat in gs as re ect ion s of
treatment failure.
12 Spinal Rehabilit ation and Disability Evaluat ion 147
Sugg este d Reading
Dau b s MD, Nor vell DC, McGu ir e R, et al. Fusion versu s n o n op e rat ive care for ch ron ic
low back pain: do psychological factors a ect outcom es? Spine 2011;36(21, Suppl):
S96 – S10 9
Fu r l a n JC, No o n a n V, Si n g h A, Fe h lin gs M G. As s e s sm e n t o f d is a b ilit y in p a t ie n t s w i t h a cu t e
traumatic spinal cord injury: a systematic review of the literature. J Neurotrauma
2011;28(8):1413–1430
Ro n d in e lli RD. Ch a n ge s fo r t h e n e w AM A Gu id e s t o im p a ir m e n t r a t i n g s , 6 t h Ed it io n : im p l i -
cations and applications for physician disability evaluations. PM R 2009;1(7):643–656
Ro n d in e lli RD, Ge n o ve se E, Br ig h am CR, e d s. Gu id e s t o t h e Ev a lu a t io n o f Pe r m a n e n t Im -
pairm ent . Ch icago, IL: American Medical Associat ion ; 200 8
Sin ik a llio S, Aa lt o T, Air a k s in e n O, Leh t o SM, Kr ö ge r H, Vi i n a m ä ki H . De p re s sio n is a ss oci-
ated w ith a poorer outcome of lum bar spinal stenosis surgery: a two-year prospective
follow -up st u d y. Spin e 201 1;3 6(8):677–68 2
13 Biochemical Aspects of
In t e rv e rt e b ra l Dis k De g e n e ra t i o n
13.1 General Considerations
I. In t er ver tebr a l d isk.
A. Ce lls .
1. Notochordal cells:
a. Present embryologically and disappear by adult life.
2. Chondrocyte-like cells.
3. Likely originate from chondrocytes in the cartilaginous end plate.
4. No signi cant cell turnover.
5. These cells undergo apoptosis with aging and disk degeneration.
B. Gr os s s t r u c t u re s (fr om p er ip h er al t o ce n t ra l) (Fig. 13.1).
1. Outer brous annulus brosus.
a. Primarily collagen brils that are aligned in oblique layers.
b. Limited vascular and nerve supply.
c. Sinuvertebral nerve runs posteriorly.
d. Sympathetic bers run anteriorly.
2. Inner annulus brosus.
a. Fibrocartilaginous tissue.
(1) Gradually blends with the nucleus pulposus.
(2) Posterolaterally the annulus is thinner and has more disorganized
collagen an d a greater proportion of vertical bers.
(a) Weakest part of annulus.
(b) Contributes to a greater propor t ion of disk herniat ion s.
3. Transition zone.
a. Thin zone of brous tissue between the inner annulus and the nucleus
pulposus.
148
Fi g . 1 3 . 1 Ba s ic a n a t o m i ca l s t r u c t u r e s o f t h e
disk in relat ionship to the ne ural elem ents.
13 Bioche m ical Aspect s of Intervert ebral Disk Dege neration 149
4. Nucleus pulposus.
C. M at r ice s (Table 13.1).
1. Collagens.
D. Disk degen e rat ion .
1. Collagen synthesis and content increase in the nucleus.
2. Decreased concentration of cross-linking in the annulus.
3. Decreased water content.
E. Pr o t eoglyca n s (PGs ).
1. PG aggregates’ constituents.
a. Central hyaluronan lament.
b. Link proteins attach multiple glycosaminoglycan molecules.
c. Large PGs.
(1) Aggrecan.
(a) Similar to articular cartilage.
(b) Half the size of PGs found in cartilage.
(c) Higher keratin sulfate:chondroitin sulfate ratio.
(d) Higher molecular weights of keratin sulfate.
(e) Increased hyaluronan content.
(f) Im por tant in w at e r reten t ion.
(g) Provides compressive st rength.
d. Small PGs.
(1) Biglycan, decorin, lum ican, brom odulin.
(2) Involved in organization of collagen and brillin form ation.
(3) PG content and synthesis vary depending on age, region, and
degeneration.
(a) PG activit y in a norm al adult annulus is approximately one-third
lower th an in a young nucleus.
(b) Syn thetic activity is greatest in the inner annulus.
Ta b l e 1 3 . 1 Co m p o n en t s o f t he in t e rve r t eb ra l d isk
An n u l u s ( 7 0 %)
1. Predominantly type I
2. Type I, II, III, V, VI, IX, XI
3. Predominantly type II
4. Type II, VI, IX, and XI provide tensile strength
Co lla ge n c ro ss-lin kin g b y co va le nt b on d s via m o d i c at io n o f lysin e / hyd roxylys in e re sid ue s
High e st co nce nt rat ion of cro ss-linking in nucleus
Nu cle us (20 %)
1. Predominantly type II
2. Type II, VI, IX, and XI
150
13 Bioche m ical Aspect s of Intervertebral Disk Dege neration
F. Ag i n g a n d d e g e n e r a t i o n (Fig. 13.2).
1. The keratin sulfate:chondroitin sulfate ratio increases with age.
2. Nonaggregating PGs or PGs that cannot bind to hyaluronic acid increase.
G. Ho m eo st a sis of in ter ve rt eb r a l d isk m et abolism .
1. Anabolic enzymes, growth factors, and cytokines.
a. Growth factors.
(1) Transform ing grow th factor-b (TGF-b), b broblast grow th factor
(FGF), insulin-like grow th factor-1 (IGF-1), platelet-derived grow th
factor (PDGF), bon e m or p hogen e t ic p rotein -2 (BMP-2), BMP-4, BMP- 7 .
(2) IGF-1, epiderm al grow th factor (EGF), FGF, and TGF-b stim ulate
matrix synthesis.
(3) FGF prom otes proliferation of chondrocytes in degenerative disks.
(4) IGF-1 stim ulates proteoglycan synthesis in the nucleus.
(5) BMPs, such as BMP-2, BMP-7, and latent mem brane protein (LMP)-1,
have been shown to upregulate PG synthesis in vitro and in vivo.
2. Catabolic enzymes and cytokines.
a. Enzymatic degradation of the matrix:
(1) Matrix metalloproteinases (MMPs):
(a) Collagenase, gelatinase, strom elysin.
(2) Proin am matory cytokines and free radicals increase in degenerative
disks.
(a) Nitric oxide, prostaglandin E2 (PGE2), and interleukin (IL)-6 are
increased in degenerated disks.
(b) Ph osph olipase A2, tum or necrosis factor alph a (TNF-a), and IL-1
are increased in herniated disks and radiculopathy.
b. Cytokine blockers such as IL-1, TNF blockers, and tissue inhibitors of
metalloproteinase can upregulate PG synthesis by blocking catabolic
processes.
H. Nutrition by di usion th rough the end plates (Fig. 13.3).
1. Blood supply to the end plates and outer annulus decreases with aging.
a. Lactate concentration increases.
b. pH decreases.
c. Cellular metabolism is a ected with decreased nutrition (Fig. 13.4).
I. Biologic st r a t egies fo r in te r ve rt e b ra l d isk (IVD) d e gen erat io n re p air or
regeneration.
1. Growth factors.
a. BMPs.
b. Blocking cytokine pathways.
2. Therapeutic gene transfer.
a. Viral.
b. Nonviral.
3. Cell transplantation.
a. IVD cells.
b. Chondrocytes.
c. Mesenchym al stem cells.
13 Bioche m ical Aspect s of Intervert ebral Disk Dege neration 151
ab
Fi g . 1 3 . 2 Varying st ages of disk degenerat ion (I–V) cat egorized via the Thom pson grading scale. (a)
Cadave ric sp e cim ens a n d co rre sp on d ing (b) m ag net ic reso nance im a g e s. Gra d e I re prese n t s a healt hy
disk, and grade V represents a disk with osteophytic end plate changes, loss of disk height, and loss
of water content.
152
13 Bioche m ical Aspect s of Intervertebral Disk Dege neration
Fig . 1 3 . 3 Diagra m dem o n st rating the
di usion of nutrients into the intervertebral disk space.
Fi g . 1 3 . 4 Therapeut ic approach for repair of intervertebral disk degeneration.
13 Bioche m ical Aspect s of Intervert ebral Disk Dege neration 153
4. Cells and matrix transplantation.
5. Molecules (peptides or other compounds) that upregulate the anabolic
pathway and downregulate in ammatory or pain pathways.
J. Bio lo gi c d is k r e ge n e r a t io n .
1. Increases the synthesis and content of PG and collagen.
2. May improve biomechanical properties of the disk or the motion segment in
early stages of disk degeneration.
a. May not be e ective if disk degeneration is severe and the posterior
structures are comprom ised.
b. Use of growth factor stim ulation to restore nucleus height and metabolic
funct ion.
3. May not address pain perception.
K. Po t e n t ia l l i m it a t io n s o r u n a n s w e r e d q u e s t io n s o f g r ow t h fa c t or fo r IVD r e p a i r .
1. Duration of therapeutic e ect in vivo.
2. Optimal dosage.
3. Optimal delivery system.
a. Injection.
b. Prolonged delivery systems.
c. Carriers.
d. Multiple proteins.
4. E ect of biomechanical stresses on disk metabolism and in uence of growth
fact o r s o n cells .
5. E cacy of nonsurgical pain-relieving procedures.
a. Chemonucleolysis.
(1) Minim ally invasive procedure involving the injection of an enzyme
from papayas called chym opap ain.
(2) The enzym e metabolizes disk material that has bulged to reduce
nerve root compression.
(3) In 2003, the Food and Drug Adm inistration discontinued the sale of
chym opapain du e to grow ing rep or ts of hem or rh age, p ain, p aralysis,
allergic reactions, fatal anaphylactic shock, and transverse myelitis.
Sugg este d Reading
Co lo m b in i A, Lo m b a r d i G, Co r s i M M, Ba n G. Pa t h o p h ys i olo gy o f t h e h u m a n i n t e r ve r t e b r a l
disc. Int J Bioch em Cell Biol 2 008 ;40 (5):837–842
Raj PP. In te r ve r t e b r a l d is c: a n at o m y- p h ysio log y - p at h o p h ys io log y- t re at m e n t. Pa in Pr a ct
2008;8(1):18–44
Sin gh V, M an ch ik a n t i L, Ca lo d n ey AK, e t a l. Pe r cu t a n eo u s l u m b a r la se r d is c d e co m p r e ss i o n :
an update of current evidence. Pain Physician 2013;16(2, Suppl):SE229–SE260
Wardlaw D, Rithchie IK, Sabboubeh AF, Vavdha M, Eastm ond CJ. Prospective random -
ized trial of ch em onucleolysis com pared w ith su rger y for soft disc her n iation w ith
1-year, intermediate, and long-term outcome: part I: the clinical outcome. Spine
2013;38(17):E1051–E1057
14 Degenerative Cervical Spine Disorders
14.1 Cervical Degenerative Disease
I. Clin ical cat e go r ies.
A. Diskoge n ic a x ia l p ain w it h o r w it h o u t r e fe r re d p ain .
B. Disk h e r n ia t io n .
1. Myelopathy.
2. Radiculopathy.
C. Ce r vic a l sp on dylo s is (Table 14.1).
1. Radiculopathy (foraminal stenosis).
2. Myelopathy (spinal cord compression).
II. Hist or y an d exam in at ion .
A. Ce r v ical r a d icu lo p at h y.
1. Dermatomal pain distribution (Fig. 14.1).
a. Spurling’s sign.
(1) Pain exacerbated by neck extension and rotation toward the
symptomatic side.
b. Shoulder abduction relief sign.
(1) Pain ameliorated by shoulder abduction (more often present with
soft disk herniations).
2. Neurological ndings (nerve root distribution).
a. Numbness.
b. Paresthesias.
Ta b l e 1 4 . 1 Dem ogra p h ics o f ce r vica l spine d ise ase
Ce r v i c a l s p o n d y l o s i s D i s k h e rn i a t i o n
Ag e > 5 0 < 5 0
Se x Male > fe m a le Male = fe m ale
Onset Insidious Acute
Lo c a t i o n o f p a i n N e c k a n d a r m A r m
154
Neck st i n ess Ye s N o
Weakne ss Yes Yes o r n o
Mye lo p a t hy Mo re co m m o n Le ss co m m o n
Derm atom al dist ribut ion Multiple Sing le
14 Dege nerative Ce rvical Spine Disorders 155
Fi g . 1 4 . 1 De rm at om al d ist ribution o f cervica l and t hora cic n e r ve root s.
c. Weakness.
d. Hypore exia.
B. Ce r vic a l m y e lo p a t h y.
1. Pain is usually absent.
a. Discomfort varies from a dull ache to sharp pain.
2. Symptoms:
a. Wide, ataxic gait pattern.
b. Poor hand dexterity.
(1) Buttoning shirt.
(2) Writing.
(3) Holding onto a co ee mug.
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