Backache

An Important Issue
 One of the most common reasons for seeking medical
attention, second only to respiratory issues
 84% of adults will have low back pain at some point
 Wide variety of approaches for treatment
 Suggests that optimal approach is unsure
 Most episodes are self-limited
 Some suffer from chronic or recurrent courses, with
substantial impact on quality of life
Epidemiology

 Almost any structure in the back can cause pain,

including ligaments, joints, periosteum, musculature,
blood vessels, annulus fibrosus and nerves
 Intervertebral discs and facet joints most commonly affected
 85% of those with isolated low back pain do not have a clear
localization
 Usually called “strain” or “sprain”  no histopathology, no
anatomical location
 Men and women equally affected
 Age of onset 30-50 years
 Assessment of Back Pain

 History & Physical: Nocturnal exacerbation occurs w tumors or inf, w

benign causes like herniated disc pain improves w bed rest

 Limitation of spinal motion correlates with the presence of lower back

disability

 Palpation: Gentle & systemic palpation of the back, coccyx, sacrum, levator
ani, coccygeus, & piriformis ms, & associated ligament done

 Muscle spasm: has localized tenderness, & increase in ms tone

 Causes of back pain

 Pain sensitive structures are the supporting bone,

articulations, meninges, nerves, muscles, & aponeuroses
 Vertebral body despite being short is actually a long bone
with end plates of hard bone & a center of cancellous
bone
 It is innervated by dorsal roots
 Periosteum is pain sensitive as is facet joint which have a
capsule & meniscus richly innervated w nociceptors
 Muscular Pain

 Most back pains are

caused by sprain or strain
of the back muscles &
ligaments
 Pain will be in discrete
area & tender to touch
 It is of aching quality &
may involve muscle spasm
 Pain not involved
shooting pain
Spinal causes

 Osteoporosis
 Osteomylitis
 Herniated Disc
 Spondylolisthesis
 Spondylolysis
 Facet hypertrophy
 Ischemia of the spinal
cord
Natural History of LBP

 Acute LBP
 inflammatory or neuropathic injury
 resolves spontaneously with minimal treatment
 Intermittent, relapsing LBP
 more challenging diagnostic and treatment dilemma
 precipitates symptomatic care and more aggressive interventions
aimed at specific underlying pathology
 Unremitting, recurring chronic LBP
 structural, neurophysiological, and biopsychosocial pathology
 requires management at all these levels
 major public health problem
 Nociceptive vs Neuropathic LBP

Nociceptive Mixed Type Neuropathic

Pain Caused by a Pain
combination of both
Caused by activity in Initiated or caused by
primary injury and
neural pathways in primary lesion or
secondary effects
response to potentially dysfunction in the
tissue-damaging stimuli nervous system

Degenerative
Sports/exercise disc disease
injuries Sciatica
Facet joint
Postoperative
arthropathy
pain Medial branch
Internal disc HNP* without HNP* with neuropathy
disruption nerve root nerve root
compression compression

*Herniated nucleus pulposus.

Referred LBP Is Remote From Source of Pain
 LBP may radiate into
 groin
 buttocks
 upper thigh
areas that share an interconnecting nerve supply
 Source of somatic referred pain is a skeletal or
myofascial structure of the lumbar spine
 Source of visceral referred pain is within a body
organ
 ovarian cysts may refer pain to low back
 cancer of head of pancreas can present as low back pain
becoming excruciating at night
Radicular LBP Results From Irritation of Spinal Nerve or
Its Roots

 Damage to specific nerve root

 pain may radiate along the nerve down the lower extremity
 Lumbosacral radiculopathy often manifests as sciatica
LBP Patient Treatment Prototypes

 Chronic axial LBP

 pain does not extend beyond mid-buttock
 absence of radicular pain or sensory symptoms below the
knee
 Chronic axial LBP with radiation
 pain with radiation beyond mid-buttock
 absence of radicular pain or sensory symptoms below the
knee
 Chronic axial LBP with radicular component
 radicular pain or sensory symptoms below the knee
Considerations in the Clinical Assessment and Diagnosis
of Chronic LBP

Goals of Clinical Assessment

Medical History
General Pain Scales/Questionnaires

Neurologic Factors in the Elderly

Psychosocial

Physical Examination Diagnostic Studies

Neurologic Evaluation of the Elderly

Making the Diagnosis

Medical History

 Symptom onset/cause of LBP

 Duration, location, and character of LBP
(pain scales/questionnaires)
 Physical/functional impairment
 Factors that exacerbate or relieve LBP
 Associated features or secondary signs/symptoms
 Neurologic history
 Psychosocial history
 Red Flags
 Diagnostic tests indicated early on for
 current medical history: significant trauma, recent intervention, pain
unrelieved or worse with lying down, pain worse at night, progressive
neurological deficit
 past medical history: cancer, recent rapid weight loss, immunosuppression or
systemic steroids, IV drug use, recent bacterial infection, chills or fever, first
incident of back pain in older patient
 Patient offered appointment within 24 hours for
 fever lasting >48 h, new below-the-knee pain or numbness, new leg weakness,
loss of bladder or bowel control (retention or incontinence), progressive
neurologic deficit
 Psychosocial red flags
 suicidal ideation, social withdrawal, panic attacks, serious financial reversal,
homelessness: refer for psychiatric consultation or send to psychiatric crisis
center

Deyo RA, Weinstein JN. N Engl J Med. 2001;344:363-370.

Institute for Clinical Systems Improvement (ICSI). Adult low back pain. Bloomington, Minn: ICS;
September 2003:63.
Neurologic History
 Symptoms
 Onset
 Common etiologic factors
 leg pain (HNP with nerve root compression L4, L5, S1 )
 leg weakness (HNP, extrusion, fragment)
 groin pain (HNP with nerve root compression L2, L3)
 back pain with allodynia of skin (inflammatory recruitment of
non-nociceptors)
 non-dermatomal leg pain with weakness, mottling of skin,
temperature change, asymmetric hair growth, sweating, allodynia,
hyperalgesia (CRPS 1 or 2)

HNP=herniated nucleus pulposus;

CRPS=complex regional pain syndrome
 Musculoskeletal Examination
 Observation
 pain behaviors–groaning, position changes, grimacing, etc
 atrophy, swelling, asymmetry, color changes
 Palpation
 palpate area of pain for temperature, spasm, and pain
provocation
 point palpation for trigger points/tender points
 Range of motion
 active and passive
 flexion, extension, rotational, lateral bending
 leg raising
 Neurologic Exam Determines Presence/Absence and Level of
Radiculopathy and Myelopathy

The exam should include

 Motor elements  Autonomic elements
 muscle bulk/tone  limb temperature
 atrophy/flaccidity  sweating
 muscle strength  hair/nail growth
 coordination  skin color changes
 gait  Deep tendon reflexes
 Sensory elements
 sensory deficits, eg, touch,
position sense, temperature,
vibration
 allodynia: light touch
 hyperalgesia: single or
multiple pinpricks
 Medical Red Flags = Early Warning

Surgical emergency procedures scheduled

 Cauda equina syndrome  Spinal epidural
 LBP; sciatica hematoma/abscess
 saddle anesthesia  severe pain
 urinary  urinary/fecal incontinence
incontinence/hesitancy  focal neurologic findings
 fecal incontinence
 unilateral or bilateral lower
extremity motor and sensory
loss

Boukobza M, et al. Neuroradiology. 1994;36:456-459.

Gleave JR, Macfarlane R. Br J Neurosurg. 2002;16:325-328.
Thongtrangan I, et al. Neurosurg Focus. 2004;16(6):e6.
Physical Treatment Options

 Exercise (stabilization training)

 Neutral position
 Soft tissue mobilization
 Transcutaneous electrical nerve stimulation (TENS)
 Electrothermal therapy
 Complementary measures (acupuncture;
relaxation/hypnotic/biofeedback therapy)
 Spinal manipulative therapy
 Multidisciplinary treatment programs (back
schools/education/counseling/pain clinic)
 Treatment of cause of Chronic Back Pain

 Treat the cause like in osteomylitis, surgery with

antibiotics is used
 Vertebral metastasis will respond to high doses of
dexamethasone, definitive treatment with radiation &
surgery
 Osteoporosis treated with Biphosphonate, Robaxifene
 Muscle spasms may respond to ms relaxants
 Back Exercises

 Ankle pump
 Heel slides
 Abdominal contraction
 Wall squats
 Heel raises
 Straight leg raises
 Knee to chest stretch
 Hamstring stretch
 Exercises with swiss ball
 Epidural steroid injection

 Epidural space identified

w loss of resistance tech
or fluroscopy
 60-80 mg of triamcilone
with 0.25% bupivacaine
injected
Intradiscal electrothermic therapy

 IDET is done using fluoroscopy, a

hollow needle containing flexible
tube & heating element is inserted
into spinal disc
 The catheter placed in a circle in
the annular layer of disc & slowly
heated to 194 deg.
 The heat is meant to destroy the
nerve fibers & toughen the disc
tissue, sealing any small tear
 Vertebroplasty

 Under fluoroscopy, a
hollow needle is inserted
& a cement is injected to
restore the vertebra
 Kyphoplasty

 In kyphoplasty a ballon is
inserted through the
hollow needle into the
fractured bone to restore
the height & shape of the
vertebra.
 Once the ballon is
removed, the cement
mixture is injected.
Kyphoplasty / Vertebroplasty
Spondylolithesis
 Discectomy

 A scope is inserted
through a small cannula
to inspect disc surface
 Peri-annular fat is
removed & small
capillaries are cauterized
 Small nerves in the
annular fat can be
removed with peri-
annular tissue
 Treatment Strategies for LBP

Clinical Presentation Possible Cause of LBP Treatment Strategies

Intermittent unilateral leg Intermittent nerve • Short-acting opioids
pain, numbness, entrapment with nerve • NSAIDs
weakness radiating to root inflammation • Topical analgesics
foot

Constant burning, Permanent nerve damage • Opioids

stabbing, or deep aching • Tricyclic antidepressants
groin or leg pain • Anticonvulsants
• Topical analgesics

Moskowitz MH. Curr Pain Headache Rep. 2003;7:178-187.

 Treatment Strategies for LBP (cont’d)

Clinical Presentation Possible Cause of LBP Treatment Strategies

Axial, aching, throbbing Inflammation of • NSAIDs
and/or stabbing LBP with surrounding tissue or • Opioids
trigger points radiating to joint, myofascial • Topical analgesics
buttocks and anterior
thigh
Pain > expected from Sympathetically • Opioids
injury, burning, electrical, maintained pain • Tricyclic antidepressants
to one or both limbs, • Anticonvulsants
edema, mottling, nail,
skin, and hair changes, • Topical analgesics
temperature change,
allodynia, hyperalgesia

Moskowitz MH. Curr Pain Headache Rep. 2003;7:178-187.

Pharmacotherapy Options*

 Antidepressants
 Anticonvulsants
 Muscle relaxants
 Opioid analgesics
 Corticosteroids
 NSAIDs
 Topical analgesics

* Except for certain opioids, none of these agents are indicated for chronic LBP.
Where Can We Intervene?
 WHO Pain Ladder

 Step 1 Mild (pain rating 1-3)

Non opioid + co-analgesics
e.g. NSAID+TCA/membrane stabilizer/ms.relax.
 Step 2 Moderate (pain rating 4-6)
Opioid + Non opioid + co-analgesics
Lorcet + NSAID+TCA/memb. Stab./ms. Relax.
 Step 3 Severe ( pain rating 7-10)
Pure opioids + non-opioids + co-analgesics
e.g. Morphine SR + NSAID + above.
 Acetaminophen

 MoA: Cox-3 inhibter of PG in the CNS & peripheral pain

impulse
 Pain indication: Use alone for mild pain
 Do not exceed 4 gms / day
 Lorcet – 6 tabs/day= 60 mgs morphine
 Lortab- 8 tabs / day=40 mgs morphine
 Adverse effects:
-Lightheadedness, dizziness, hepatotoxicity
with high doses & chronic use
 NSAID’S

 Indications: anti-inflammatory, antipyretic, analgesic

 Acetylsalicylic acid ( ASA ) irreversibly inhibits platelet
 Side effects: Reversible antiplatelet effect, minimal
w/ non-acetylated salicylates ( eg Disalcid, Dolobid )
- GI ulceration, less w ibuprofen, etodolac, salsalate,
nabumentone
- Nephrotoxity – caution in CHF, dehydratation, elderly
- Hepatotoxicity: caution in elderly & alcoholics
- Avoid in asthmatics & nasal polyps
Mechanism of Action
 Phospholipids, released from cell membrane are cenverted to Arachidonic
acid by phospholipase A2

 Arachidonic acid is acted by lipo-oxygenase to be converted to Leukotrienes

 Cyclo-oxygenase acts on Arachidonic acid to form Prostaglandin
endoperoxides which are converted to Prostaglandin G & by isomerase into
Prostaglandin E2, Prostaglandin D2, & F2 alpha

 Prostaglandin H is formed from prostaglandin endoperoxides & converted by

Thromboxane to Thromboxane A2 & Thromboxane B2.

 Prostacyclin synthetase converts prostaglandin endoperoxides to Prostacyclin
( PGI )
Co-analgesic Pain Medications

 Antiepileptics  Alpha-2 agonists

 Antidepressants  Neuroleptics
 Muscle Relaxants  Antiarryhmics
 Anesthetics  Benzodiazepines
 Corticosteroids
 Psychostimulants
 Substance P inhibitors
 Antiepileptics

 MOA: Block Na+ & Ca+ channels>>inhibits release of glutamate>>

stabilizes neural memb.
 Uses: Trigeminal neuralgia, peripheral neuropathies, herpetic
neuralgia, phantom limb pain, migraines.
 Aniepileptics: Gabapentin, Carbamazepines, topiramate,
phenytoin, oxycarbamazepine, pregabalin
 Comared to TCA’s:
-equally efficacious in painful DN
-some AED may be more expensive
- differences in safty profile
- synergy with AED plus TCA
 Gabapentin (Neurontin)

 MOA: a 2-delta ca+ channel subunit modulator

 Uses: Peripheral neuropathic pain, phantom limb pain,
CRPS, post herptic & trigeminal neuralgia.
 Doses: adjust for elderly & renal failure
-range 300- 3600 mg /day divided in 3-4 doses
 Somnolance, dizziness, constipation, fatigue, peripheral
edema, difficulty concentrating
 Pregabalin (Lyrica)

 MoA: a 2 delta Ca+ channel subunit modulator

 Pain uses: Diabetic & post herpetic neuropathic pain at
doses 300-600 mgs/day divided 2-3 X.
 Other neuropathic pain conditions, fibromyalgia,
generalized anxiety disorder.
 Compared to gabapentin:
- Bioavailability remains 90% at all doses
- Time to effective dose (150-300mg/day) is 1-3days
- Class v schedules drug.
 Carbamazepine ( Tegretol)

 MoA: Na+ & Ca+ channel blockade

 Pain uses: trigeminal neuralgia, glossopharyngeal
neuralgia, DPN
 Dosing: 200-1000mg divided 2-3X (with food)
 Side effects: N & V, dizziness, sedation, transient
leukopenia, hepatic toxicity, thrombocytopenia, diplopia,
hyponatremia, rash, Steven-Johnsons syndrome.
Tricyclic antidepressants

 MoA: inhibits re-uptake of NE, SE, antihistamine

 Pain indications: Painful neuropathies, Phantom
limb pain, migraine prevention
 Dose: start low & adjust every 2- 3 days
 Drug interactions
- caution with other anticholinergics/serotonergics
- CYP2D6 substrate ( all TCA’s)
- CYP3A4 substrate ( Elavil )
 Choice of A TCA

 Amitriptyline ( Elavil)
- most widely studied
- more side effects- hang over effect.
 Doxepin ( Sinequan )
- similar to Elavil, but shorter duration of sedation
 Desipramine ( Norpramin ), Nortriptyline ( Pamelor)
- may cause insomnia
- less anticholinergic effect
- Desipramine may cause orthostatic hypotension
 TCA – Side Effects

Side effects  Desipramine

 Blurred vision
 Cognitine changes  Nortriptyline
 Constipation
 Dry mouth  Doxapin
 Orthostatic hypotention
 Sexual dysfunction  Amitriptyline
 Tachcardia
 Urinary retention
 Duloxetine ( Cymbalta )

 MoA : Dual reuptake inhibitor ( NE & SE )

 Indications : Neuropathic pain, depression
 Dosage : 30 mgs PO qd to 60 mgs PO bid
 Side effects : nausea, dry mouth, constipation decreased appetite,
dizziness, insomnia
 Drug interaction : CYPIA2 & 2D6 substrate –
SSRI’s , quinidine, cimetidine, quinolenes, may increase duloxitine
levels.
- mod. Inhibitor of CYP2D6 – increases TCA’s, phenothiazine, type
1C antiarrythmias
 Muscle Relaxants

 Heterogenous group of medications:

- Spasticity from upper motor neuron syndrome
- Muscular pain & / or spasm from peripheral musculoskeletal condition.
- Dose : may dose 6-8 hrs ATC or give more hs if daytime drowsiness does
not resolve ( e.g. Flexaril 10-30 mg po qhs )

Side effects:Drowsiness,dizziness,blurred vision

Drug interaction: Other CNS depressants

 Muscle Relaxants

 Spasticity:  Muscular pain & spasm

- Baclofen ( Lioresal ) - Methcarbamol (Robaxin)
- Tizanidine ( Zanaflex) - Cylobenzaprine(Flexaril)
- Dantrolene ( Dantrium ) - Carisoprodal ( Soma )
- Diazepam ( Valium ) - Baclofen ( Lioresal )
- Tizanidine ( Zanaflex )
Interventional Treatment Options
 Neural blockade
 selective nerve root blocks
 facet joint blocks, medial branch blocks
 Neurolytic techniques
 radiofrequency neurotomies
 pulse radio frequency
 Stimulatory techniques
 spinal cord stimulation
 peripheral nerve stimulation
 Intrathecal medication pumps
 delivery into spinal cord and brain via CSF
When to Refer for Surgical Consultation

 Motor weakness of one or both legs

 New bowel and urinary incontinence
 MRI HNP compressing nerve root
 MRI of grade 3 spondylolisthesis
 MRI/CT evidence of severe spinal stenosis with
correlative leg weakness and pain
 Standing flexion/extension films showing significant
movement
Surgery Options
 Primarily involve correction or stabilization of the underlying
pathological condition
 Principal reasons are to relieve pressure and nerve irritation
caused by a prolapsed lumbar disc or to stabilize spinal structures
 Techniques include:
 spinal fusion
 one or more vertebrae are fused to prevent motion
 decompression
 removal of bone or disc material to prevent pinching of the nerve
(neural impingement)
 Surgery may improve pain and lead to more effective nonsurgical
pain interventions
Summary

 Chronic LBP is a disease, not a symptom

 Progress is focused on targeting treatment at
the mechanisms that produce pain rather than
ameliorating the symptoms
 Biopsychosocial approach is critical for the successful
management of chronic LBP
 Promising treatments for chronic LBP include
 new agents
 new uses of agents
 new combinations of agents