sample chapter handbook of pain medicine 2e by dureja to order call sms at 91 8527622422

S E C T I O N I

GENERAL PRINCIPLES OF PAIN

MANAGEMENT1 Evaluation of the Pain Patient 3

2 Pain Measurement and Assessment 193 Radiography and Imaging in Pain Medicine 43

4 Ultrasonography in Pain Medicine 615 Pharmacotherapeutics (Drugs) in Pain Management 69

6 Neurolytic Agents 977 How to Set Up a Pain Clinic? 105

8 Acute Pain Management: Practical Guidelines 113

3

A perceptual phenomenon, like pain, is not accessible to objective vali-dation. The subjective experience of pain is universal and one of the most common reasons that a patient seeks a clinician's help. Patients are referred to pain clinics by other hospital departments wishing to have help in man-aging their patients in pain. The referring physicians, however, may have widely varying opinions about what they expect the patients in the pain clinic to achieve, which they in turn convey to them.

As the saying goes, ‘Healing begins with the history.’ Clinicians should be able to put the patient at ease and should then ask open-ended ques-tions that will give the patient an opportunity to describe the pain in their own terms. A good way to start may be ‘Tell me all about your pain.’ This generally will allow the patient to describe what he or she believes is important. This is indeed therapeutic in itself.

TAKING HISTORY OF A PAIN PATIENT

Obtaining history is a skill. The cornerstone of accurate pain diag-nosis is the medical history. In this age of superfast technology, a large amount of time and energy is often given to investigations at the expense of time spent with the patient in collecting a coherent and relevant history.

Enquiries about the nature of the pain have three main purposes.

1. The patient's description of symptoms may be helpful in diagnosing the cause of the pain.

2. A description of the type of pain may be important in choosing the most appropriate treatment for that symptom.

3. It may give the pain clinician an idea of the patient's reaction to the pain, and the effects that it has on his or her life.

C H A P T E R

1 Evaluation of the Pain

Patient

1. EVALUATION OF THE PAIN PATIENT4

I . GENERAL PRINCIPLES OF PAIN MANAGEMENT

Common Questions in the Pain Targeted History

1. The pain clinician finds out if the pain was followed by any physical or psychological events or trauma in the patient's life.

2. Is there a history of trauma, surgery or other medical illnesses? 3. Has the pain been continuously present, or are there pain-free

periods? Are there any obvious factors that might account for these fluctuations?

4. Is the pain constant, getting worse or better with time or are there diurnal variations?

5. How does the patient describe his pain? Visceral pains are usually described as dull aching, sickening pain, which is difficult to localize. Neuralgic pain is generally described as stabbing, shooting, lancinating or lightning-like in some areas. Associated with pain may be other sensory disturbances such as tenderness, paraesthesias, hyperalgesia, hyperpathia or anaesthesia. Myofascial pain may be described as dull, diffuse aching pain with some tender areas. There may also be associated paraesthesias, and pain on combing the hair or putting a hat.

6. Has the pain been investigated previously; if so, how and what were the findings? What was the patient told previously about the pain? What operations, drugs, physical treatments, and so on have been applied, and what were the results of such treatments?

7. It is also important to enquire about any other major areas of the patient's medical, psychiatric, social and employment histories.

Summing up all the above points, the targeted history in a pain patient includes the following:

1. Mode of onset 2. Chronicity and duration 3. Site of pain 4. Tempo (duration and frequency) 5. Character and severity 6. Associated factors a. Premonitory symptoms and aura b. Precipitating factors c. Environmental factors d. Family history e. Age at onset f. Pregnancy and menstruation g. Gender h. Past medical and surgical histories i. Socioeconomic considerations j. Psychiatric history k. Medications, drug and alcohol use

TAKING HISTORY OF A PAIN PATIENT 5

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

Psychosocial History

The algologist or the pain clinician will find it useful to know about patient's previous pain experiences and the reaction to them. The anxiet-ies associated with pain can lead to phobic and avoidance behaviours, such as kinesiophobia (fear of movement), which must be identified to be treated and which often persists long after the original conditioning stim-ulus has become a history. Psychosocial problems, which could be sup-pressed or managed prior to the onset of pain syndrome, become terrible barriers to progress and success unless specifically identified as problems. Such problems are often ignored by insurance adjusters in the mistaken belief that the physical domain is their only responsibility and the psycho-logical aspect somehow is the patient's own responsibility. Therefore, it is important to

• Consider the role of formal or informal psychometric testing • Know about contributions of family, friends, employers, culture and

others to the pain syndrome • Estimate the degree of pain augmentation • Quantify the degree of pain suffering • Obtain an adequate sexual history • Ask for any professional or financial problems • Look for internal versus external locus of pain control

General Aspects

Some valuable aids to enhance the interview output

• The patient should be appropriately gowned and be sitting upright and at eye level with the interviewer, if possible.

• Old records, investigations and scans are obtained before the consultation.

• The pain physician pays full attention, listens patiently and does not interrupt the patient or allow outside interruptions.

• Physician remains nonjudgemental; her/his own moral, religious and political beliefs are irrelevant to this process.

• The physician is honest and open with the patient. • Both the patient and the physician can trust the confidentiality of both

the consultations and the medical records.

Physical Examination

Physical examination is an extension of the history providing objec-tive support if performed efficiently and methodically. The very physical aspect of examining the patient imparts a reassuring sense of personal caring to the entire consultation. Patients want to be examined, expect to



be examined and ultimately derive benefit from the process. As Goethe said ‘We see only what we know.’ The faculty with which we examine patients is ultimately a function of our knowledge, experience and will-ingness to learn.

A Quick Guide to Pain Examination

General physical examination

• Height/weight and vital signs. • Entire body for skin lesions, haemangiomas, café au lait spots, surgical

or injury scars, etc. • Needle marks, skin ulcerations, etc. • Overall assessment of multiple joints can be done for deformities,

arthritic change, trauma or prior surgery. • Scan room for assistive devices brought by the patient.

Pain-Related Behaviours

Note facial expression, colour and grimacing. Speech patterns suggest emotional factors as well as intoxication with alcohol or prescription or nonprescription drugs. Some patients attempt to convince the practitioner how much pain they are suffering by augmenting their verbal presenta-tion with grunting, moaning, twitching, grabbing the painful area, exag-gerating the antalgic gait or posture or tightening muscle groups.

Systemic Examination

A quick but thorough systemic examination of the cardiorespiratory system always helps to point towards the diagnosis and the physician should be aware of it while prescribing drugs or formulating other treat-ment options.

Neurological Examination

Table 1.1 highlights the efficient approach to the clinical evaluation of cranial nerves. Specific attention should be given to this portion of the examination when headache and facial pain are the complaints. The key concern again is to develop a routine that with practice becomes thorough.

Motor system examination begins with observation of muscle bulk and tone with a note on hypertrophy and atrophy. Muscle strength is tested in upper and lower extremities ( Table 1.2 ). Further knowledge can be gath-ered by testing deep tendon reflexes ( Fig. 1.1 ), clonus and pathological reflexes such as Babinski ( Table 1.3 ).



TABLE 1.1 Clinical Evaluation of Cranial Nerve Function

Cranial nerve(s) Evaluation procedure(s)

Number Name

I Olfactory Test ability to identify familiar aromatic odours, one naris at a time with eyes closed (not routinely tested).

II Optic Test vision with Snellen chart or Rosenbaum near-vision chart. Perform opthalmoscopic examination of fundi. Be able to recognize papilloedema. Test fields of vision using confrontation and double simultaneous stimulation. Inspect eyelids for drooping (ptosis).

III, IV, VI Oculomotor, trochlear, abducens

Inspect pupil size for equality (direct and consensual response). Check for nystagmus. Assess basic fields of gaze. Note asymmetric extraocular movements.

V Trigeminal Palpate jaw muscles for tone and strength while patient clenches teeth. Test superficial pain and touch sensation in each branch: V 1 , V 2 , V 3 .

VII Facial Test corneal reflex. Inspect symmetry of facial features. Have patient smile, frown, puffed cheeks, wrinkled forehead. Watch for spasmodic, jerking movements of face.

VIII Acoustic Test sense of hearing with watch or tuning fork. Compare bone and air conduction of sound.

IX Glossopharyngeal Test gag reflex and ability to swallow. X Vagus Inspect palate and uvula for symmetry with gag

reflex. Observe for swallowing difficulty. Have patient take small sip of water. Watch for nasal or hoarse quality of speech.

XI Spinal accessory Test trapezius strength (have patient shrug shoulders against resistance). Test sternocleidomastoid muscle strength (have patient turn head to each side against resistance).

XII Hypoglossal Inspect tongue in mouth and while protruded for symmetry, fasciculations and atrophy. Test tongue strength with index fingers when tongue is pressed against cheek.



TABLE 1.2 Grading of Muscle Strength

Clinical fi nding Grade Normal response (%)

No evidence of contractility 0 0 Slight contractility, no movement 1 10 Full range of motion, gravity eliminated 2 25 Full range of motion, with gravity 3 50 Full range of motion against gravity, some resistance 4 75 Full range of motion against gravity, full resistance 5 100

Triceps

Biceps

Patellar L2

Achilles S1

FIGURE 1.1 A deep tendon reflex examination.

TABLE 1.3 Deep Tendon Refl ex Scale

Grade Deep tendon refl ex response

0+ No response 1+ Sluggish 2+ Active or normal 3+ More brisk than expected, slightly hyperactive 4+ Abnormally hyperactive, with intermittent clonus

The sensory examination should be kept simple and guided by clues obtained through history. Figure 1.2 shows the difference between skin areas innervated by dermatomes and the corresponding peripheral nerve cutaneous distribution. Boxes 1.1 and 1.2 summarize the localization of cervical and lumbar radicular nerves. For pain syndromes of upper

BOX 1.1

C L I N I C A L D I F F E R E N T I AT I O N O F C E RV I C A L R O O T S V E R S U S N E RV E

L E S I O N S I N T H E U P P E R E X T R E M I T Y

Root lesions C5 Sensory supply — Lateral border upper arm Refl ex affected — Biceps Motor loss — Deltoid, infra- and supraspinatus, rhomboids C6 Sensory supply — Lateral forearm, including first finger Refl ex affected — None Motor loss — Biceps, brachialis, brachioradialis C7 Sensory supply — Over triceps, midforearm, and third finger Refl ex affected — Triceps Motor loss — Latissimus dorsi, pectoralis major, triceps, wrist

extensors and flexors C8 Sensory supply — Medial forearm to fifth finger Refl ex affected — None Motor loss — Finger extensors and flexors; flexor carpi ulnaris T1 Sensory supply — Axilla to elbow Refl ex affected — None Motor loss — Intrinsic hand muscles (in some cases, thenar muscle

through C8)

Nerve lesions Axillary Sensory supply — Over deltoid (C5, C6) Refl ex affected — None Motor loss — Deltoid C5, C6 Sensory supply — Lateral forearm to wrist Refl ex affected — Biceps Motor loss — Biceps and brachialis Radial (C5 – C8)

Sensory supply — Lateral dorsal forearm, back of thumb and second finger

Refl ex affected — Triceps Motor loss — Brachioradialis; forearm supinator; finger,

triceps and wrist extensors Median (C6 – C8, T1)

Sensory supply — Lateral palm and fingers first, second, third and half of fourth

Refl ex affected — None Motor loss — Abductor pollicis brevis; long flexors of first,

second & third fingers; pronators of forearm; wrist flexors Ulnar (C8, T1)

Sensory supply — Medial palm, fifth finger and medial half of fourth finger

Refl ex affected — None Motor loss — Intrinsic hand muscles, flexor carpi ulnaris,

flexors of fourth and fifth fingers

Abbreviations : C, cervical root; T, thoracic root.



(a)

TrigeminalOphthalmic division

Maxillary divisionMandibular division

Great auricular, C2, C3

Cervical plexus,superficial branches

Intercostalnerves

T2–T11

Lateral cutaneous br.

Anterior cutaneous br.Axillary

IntercostobrachialMedial cutaneous

Musculocutaneous

Radial

Posteriorcutaneous

Superficial branch

Brachialplexus

MedianUlnar

Lumbarplexus

IlioinguinalGenitofemoral

Lateral cutaneousAnterior

cutaneousramiFemoral

Saphenous

Sacralplexus

Sciatic

Lateral cutaneousnerve of calf

Superficial and deep peroneal

Sural

Medial plantar

SuralLateral plantar

TibialLateral plantarSaphenousMedial cutaneous

Lateralplantar

Medialplantar

Anterior aspect

vC2C3C4

C5

C6

C7C8

T5

T3T6T7T8T9T10T11T12

T1

T2

S1

Obturator

L1

L2

L3

L4

L5

S2, S3

�

��

��

�

FIGURE 1.2 Comparison of spinal segmental and peripheral nerve cutaneous sensory supply v: Fifth (trigeminal) nerve, br: Branch .



TrigeminalOphthalmic divisionMaxillary divisionMandibular divisionMastoid branch, C2, C3Great auricular branch, C2, C3

Occipital, C5–C8

Dorsal branches

Occipital, C2Occipital, C3Occipital, C4

Superficialcervical plexus

Supraclavicular, C3, C4

Dorsal rami of thoracic nerves

Cutaneous branch of axillaryLateral cutaneous branchesof intercostal nerves

Medial and lateral cutaneous br. of radialMedial cutaneousIntercostobrachial

Musculocutaneous

Anterior branch of radial

Median

Dorsal cutaneous branch of ulnarGluteal branch of 12th intercostalLateral cutaneous br. of iliohypogastricLateral branches of dorsal rami of lumbar and sacral

Medial branches of dorsal rami, L1–S6Perforating branch ofposterior cutaneous Pudendal plexus

Lateral cutaneousObturatorMedial cutaneous

FemoralLumbar plexus

SaphenousPosterior cutaneousSuperficial peroneal Common

peronealSacral plexusSural

TibialLateral plantar

Posterior aspect

L4

L5

L5

S1

S1

C2C2C3C4

C5

T1

T2

T3

T4

T5T6T7

T8T9T10T11T12

L1

L2

L3

C6

C8

C7

L4

L5

L3

S2

S3

Dermatomes

�

�

��

�

�

� �

�

�

�

(b)

FIGURE 1.2, cont’d



BOX 1.2

C L I N I C A L D I F F E R E N T I AT I O N O F L U M B A R / S A C R A L R O O T S V E R S U S

N E RV E L E S I O N S I N T H E L O W E R E X T R E M I T Y

Root lesions L2 Sensory supply — Across upper thigh Refl ex affected — None Motor loss — Hip flexion L3 Sensory supply — Across lower thigh Refl ex affected — None Motor loss — Knee extension L4 Sensory supply — Across knee to medial malleolus Refl ex affected — Patellar Motor loss — Inversion of foot L5 Sensory supply — Side of leg to dorsum Refl ex affected — None Motor loss — Dorsiflexion of toes and foot S1 Sensory supply — Behind lateral malleolus to lateral foot Refl ex affected — Achilles Motor loss — Plantar flexion and eversion of foot

Nerve lesions Obturator Sensory supply — Medial thigh (L2 – L4) Refl ex affected — None Motor loss — Adduction of thigh Femoral (L2 – L4) Sensory supply — Anterior thigh to medial

malleolus Refl ex affected — Patellar Motor loss — Knee extension Peroneal division of sciatic nerve

Sensory supply — Anterior leg to dorsum of foot

(L4, L5, S1 – S3) Refl ex affected — None Motor loss — Dorsiflexion, inversion, and

eversion of foot Tibial division of sciatic nerve

Sensory supply — Posterior leg to sole and lateral aspect of foot

(L4, L5, S1 – S3) Refl ex affected — Achilles Motor loss — Plantar flexion and inversion of

foot

Abbreviations : L, lumbar root; S, sacral root.

SPECIFIC TESTS 13


extremity, the examiner should be able to differentiate sensory involve-ment of the radial, median and ulnar nerves from specific roots. Similarly, for lower extremities one should be able to differentiate the peroneal and tibial nerve sensory distribution from that of the L4, L5, S1 roots; such distinctions elucidate most of the common problems.

Sensation

Sensation to light touch, pinprick, hot and cold stimuli is tested. Tactile sensation can be evaluated quantitatively with cotton. The sharp end of a broken sterile wooden tip is convenient way for testing pinprick.

Examination of the Musculoskeletal System

This includes inspection of gait and posture. Deformities and devia-tions from symmetry are observed. Testing active movement will deter-mine range, muscle strength and willingness of the patient to cooperate. Passive movements, on the other hand, when performed properly, test for pain, range and end-feel. Palpation of soft tissues, bony structures and stationary or moving joints may reveal temperature differences, presence of oedema, fluid collections, gaps, crepitus, clicks or tenderness. For a patient with back pain, the suggested sequence of examinations is testing range of motion of cervical, thoracic and lumbosacral spine, sacroiliac and hip joints, and SLRT.

SPECIFIC TESTS

SLRT or Lasègue Sign

Tension on the sciatic nerve begins with 15 – 30° of elevation in the supine position. This puts traction on the nerve roots from L4 to S2 and on the dura. The end of the range is normally restricted by hamstring muscle tension at 60 – 120°. More than 60° of elevation causes movement in the sacroiliac joint and therefore may be painful in sacroiliac joint disorders.

Basic Sacroiliac Tests

Sacroiliac tests are performed to determine when pain occurs in the buttock.

1. Push the ilia outwards and downwards in the supine position with the examiner's arms crossed. If gluteal pain results, the test is repeated



with patient's forearm placed under the lumbar spine to stabilize the lumbar joints.

2. Forcibly compress the ilia to the midline with the patient lying on the painless side. This stretches posterior sacroiliac ligaments.

3. Exert forward pressure on the centre of the sacrum with the patient prone.

4. Patrick's or ‘FABER'S’ test – flex, abduct and externally rotate femur while holding down contralateral anterior superior iliac spine. This stretches anterior sacroiliac ligament and reveals pain caused by ligamentous strain.

5. Force lateral rotation of the hip joint with knee held in 90° of flexion and the patient in the supine position.

Spinal Flexibility

Spinal flexion, extension, and rotation and lateral bending may be lim-ited or painful, leading to a diagnosis of zygapophyseal joint, discogenic, muscular, or ligamentous pain.

Tinel Test

The Tinel test involves percussion of the carpal tunnel. When it is posi-tive, it gives rise to distal paraesthesias. It can be performed at other loca-tions (e.g. the cubital or tarsal tunnel), where it might be suggestive of nerve entrapment.

Phalen Test

The Phalen test is positive for carpal tunnel syndrome when a passive flexion in the wrist for 1 min, followed by sudden extension, results in sensation of paraesthesias.

Adson Test

Adson test has been advocated for diagnosis of thoracic outlet syn-drome. The examiner evaluates the change of radial artery pulsation in a standing patient with arms resting at the side. Ipsilateral head rotation during inspiration may cause vascular compression by the anterior scalene muscle. In modified Adson test, the patient's head is rotated to the contralateral side. Pulse change suggests compression by the middle scalene muscle. Both tests are regarded unreliable by some clinicians, as the results are found positive in about 50% of the normal population.

CONCLUSION 15


Fallacies in the History and Examination of the Pain Patient

The frequently quoted Waddell nonorganic signs may raise suspicion in patients with low back pain. The Waddell nonorganic signs are grouped into five categories:

1. Tenderness a. Widespread superficial sensitivity to light touch over lumbar spine b. Bone tenderness over a large lumbar area 2. Simulation a. Axial loading, during which light pressure is applied to the skull in

the upright position b. Simulated rotation of lumbar spine with the shoulders and pelvis

remaining in the same plane 3. Distraction a. Greater than 40° difference in sitting versus supine straight leg

raising 4. Regional disturbance a. Motor: generalized giving way or cogwheeling resistance in

manual muscle testing of lower extremities b. Sensory: nondermatomal loss of sensation to pinprick in lower

extremities 5. Overreaction a. Disproportionate pain response to testing (pain behaviour with

assisted movement using cane or walker, rigid or slow movement, rubbing or grasping the affected area for more than 3 s, grimacing, sighing with shoulders rising and falling).

CONCLUSION

’Like an alarm bell stuck in “on” position such is chronic benign pain’ – Bruce Smoller and Brian Schullman.

It is evidently impossible to transmit the impression of pain by teach-ing, since it is only known to those who have experienced it. Moreover, we are ignorant of each type of pain before we have felt it. The history and physical examination are the foundation of pain evaluation and treatment. Finally, your brilliant ideas conceived after completion of the above steps and the patient's informed consent equals a good manage-ment plan.

We can conclude by saying ‘The clinical assessment is the base of the treat-ment statue.’ If it is narrow, the statue may crash down. If it is broad and well made, the statue will be stable and reliable.



ALL INDIA INSTITUTE OF MEDICAL SCIENCES (AIIMS) PAIN CLINIC

PAIN ASSESSMENT FORM

Date Regd. no. Referred by Patient's name Address and phone no. Weight/age/sex Occupation Present complaints

Description of pain and findings

1. Duration of pain 2. Site of pain (please shade the affected area) 3. Type of pain a. Sharp b. Dull aching c. Burning d. Spasmodic e. Pricking f. Freezing g. Any other words (patient's words) 4. Onset/variations/rhythms 5. Pain continuous/intermittent/momentary 6. Does pain disturb night and daily activities 7. Aggravating or relieving factors 8. Effects of pain 9. Other comments

Right Right RightLeft Left Right

Right

RightRight

Left

Left

LeftLeft

R RL LLeft

Relevant past history/associated diseases Any drug allergy General physical examination

ALL INDIA INSTITUTE OF MEDICAL SCIENCES (AIIMS) 17


Chest Musculoskeletal

Cardiovascular system

Central nervous system

Investigations Laboratory tests X-ray CT scan MRI Diagnosis Present treatment for pain • NSAID • Narcotics • Sedatives/anxiolytics • Antidepressants/

Anticonvulsants

• Nerve blocks/Transforaminal Epidural Injection

• Any other – Advanced Intervention/acupuncture/TENS /laser

Treatment

DateModality of treatment

Response (visual analog scale readings)

Any other treatment modality details

Treatment-related side effects Results Excellent (75% relief in

symptoms)

Good (50–75% relief in symptoms)

Fair (25–50% relief) Poor (25% relief) No relief

Remarks Clinical studies carried out if any Visual analog scale

No pain

0 1 2 3 4 5 6 7 8 9 10

Mild Discomforting Distressing Horrible Excruciating

Signature of Pain Physician

143

Headache is the most common medical complaint encountered in clinical practice. Patients with refractory headaches unresponsive to drug treatment are often referred to a pain clinic. Headache is broadly classified into chronic and episodic types. Headache presenting for more than 15 days per month and lasting more than 4 h per day is classified as chronic daily headache. About 5% of the general population is affected by chronic daily headache and the incidence is significantly higher in women. Headaches occurring at irregular intervals are episodic headaches; the most common being cluster headaches. Occasionally, tension-type headaches may also be episodic in nature.

MECHANISMS OF HEADACHES

The mechanisms of head pain include

1. Traction on intracranial structures, i.e. intracranial mass, postlumbar puncture headache

2. Dilatation of cranial arteries (it is felt that both tension-type and migraine or vascular headaches have a central brainstem pacemaker that affects structures in the trigeminal nerve selectively)

a. Intracranial: cluster headaches, anoxia, CO 2 intoxication, pheochromocytoma

b. Extracranial: migraine or cluster 3. Inflammation a. Intracranial: meningitis b. Extracranial: temporal arteritis 4. Contraction of the striated muscles of the head or neck, i.e. contraction

headache (this concept has been questioned by the recent discovery of central-type pacemaker on positron emission tomography scan)

5. Cranial neuralgias 6. Diseases of the eyes, nose, sinus, ears or teeth

C H A P T E R

10 Headache

10. HEADACHE144

II. CHRONIC PAIN SYNDROMES

CLASSIFICATION OF TYPES OF HEADACHES

The major categories of headache disorders are given in Box 10.1 ( Fig. 10.1 ).

HEADACHE EVALUATION: HISTORY

The headache evaluation consists of a detailed history, pertinent infor-mation from the physical examination and pertinent diagnostic studies. Of these, the most important element is the headache history. ‘If you have thirty minutes to see a patient, spend twenty-nine on history, one on the examination’ (Sahs, 1987 ). Evaluation of a patient with headache requires the following:

1. Detailed history 2. Pertinent information from physical examination 3. Pertinent diagnostic laboratory, neurophysiologic and radiographic

studies

In the headache evaluation, factors that cause concern are

1. Headaches associated with neurologic dysfunction 2. Exertional headache 3. Headaches that peak rapidly 4. Nocturnal headaches 5. Headaches associated with systemic symptoms 6. Focal headaches 7. Recent headaches 8. A recent change in headache

Before evaluating in detail, a simple questionnaire (MIDAS Question-naire) is administered to grade the disability level of patients with chronic intractable headache ( Box 10.2 ).

The following are important questions that should always be asked to a patient with headache.

1. What is the character and location? 2. What is the onset to peak time? 3. What is the usual time of day it occurs and the total duration? 4. Are there any associated and/or residual neurological phenomena or

sequelae? 5. Is there an aura? 6. What makes the headache worse? 7. What makes the headache better? 8. Is there a family history? 9. Were there headaches in childhood?

HEADACHE EVALUATION: HISTORY 145


BOX 10.1

C L A S S I F I C AT I O N O F H E A D A C H E S

Primary headache disorders

1. Migraine Migraine with aura Migraine without aura

2. Tension-type headache Episodic tension-type headache Chronic tension-type headache Cluster headache and chronic paroxysmal hemicrania

3. Cluster headache Episodic cluster headache Chronic cluster headache

4. Miscellaneous headaches unassociated with structural lesion Idiopathic stabbing headache External compression headache Cold stimulus headache Benign cough headache

Secondary headache disorders

5. Headache associated with head trauma Acute posttraumatic headache Chronic posttraumatic headache

6. Headache associated with vascular disorders Acute ischaemic cerebrovascular disease Intracranial haematoma Subarachnoid haemorrhage Venous thrombosis Arterial hypertension

7. Headache associated with nonvascular intracranial disorder High/low cerebrospinal fluid pressure Intracranial infection Headache related to intrathecal injections Intracranial neoplasm

8. Headache associated with substance withdrawal 9. Headache associated with noncephalic infections 10. Headache associated with metabolic disorders 11. Headache or focal pain associated with disorder of cranium, neck,

eyes, nose, sinuses, teeth, mouth or other facial or cranial structures 12. Cranial neuralgias, nerve trunk pain and deafferentation pain

10. HEADACHE146


10. Was there motion sickness, cyclical vomiting, dizziness, or unexplained fever in childhood?

11. Were there any prior diagnostic tests? 12. What were the results of prior medication? 13. Are there any other medical illnesses? 14. Are there any psychiatric illnesses, history of alcohol or substance

abuse and what is the quality of the individual's life?

EVALUATING A PATIENT WITH HEADACHE: EXAMINATION

A headache patient will commonly show no abnormalities on exami-nation if he or she has a chronic benign type of headache. Incidental abnormalities may be encountered that are not germane to the patient's situation. However, in all patients, a careful general physical and neu-rological examination should be carried out. In addition to the general examination, the skull and spine should be examined. The patient should have a complete examination of the head, eyes, ears, nose and throat for sinus disease, temporomandibular joint disease and even dental disease. Often, pain referred to the head will come from the tooth.

In the general examination, attention should be paid to the possible existence of cafe au lait spots or other stigmata of the phakomatoses. Examination of the range of motion of the neck as well as a complete neurovascular examination should be carried out. In the elderly with any suspicion of temporal arteritis, examination of the joints of the body plus the temporal arteries is mandatory.

Sinus:pain is usually

behind the foreheadand/or cheekbones

Cluster:pain is in

and aroundone eye

Tension:pain is like

a band squeezingthe head

Migraine:pain, nausea

and visual changesare typical ofclassic form

FIGURE 10.1 Common Types of Headaches .

EVALUATING A PATIENT WITH HEADACHE: EXAMINATION 147


BOX 10.2

M I D A S H E A D A C H E Q U E S T I O N N A I R E Instructions: Please answer the following questions about all the head-aches you have had over the last 3 months. Write your answer in the box next to each question. Write zero if you did not do the activity in the last 3 months.

1. On how many days in the last 3 months did you miss work or school because of your headaches?

days

2. How many days in the last 3 months was your productivity at work reduced by half or more (do not include days counted in question (1))?

days

3. On how many days in the last 3 months did you not do household work because of your head-aches?

days

4. How many days in the last 3 months was your productivity in household work reduced by half or more because of your headaches? (Do not include days you counted in question (3) where you did not do household work.)

days

5. On how many days in the last 3 months did you miss family, social or leisure activities because of your headaches?

days

Total days a. On how many days in the last 3 months did you

have a headache? (If a headache lasted more than 1 day, count each day.)

days

b. On a scale of 0 – 10, on average, how painful were these headaches (where 0 = no pain at all and 10 = pain as bad as it can be)?

days

Grading system for the MIDAS Questionnaire

Grade Defi nition Score I Minimal or infrequent disability 0 – 5 II Mild or infrequent disability 6 – 10 III Moderate disability 11–20 IV Severe disability 21+

10. HEADACHE148


The general configuration of the body especially a short neck or a low hair line may suggest congenital anomalies that may lead to headaches. Obesity should be considered as a risk factor for the development of pseu-dotumor cerebri.

The steps to examination of a patient with headache are

1. Check the patient's gait, noting his arm swing. Check tandem walking and walking on heels or toes. Remove any high-heeled shoes. It gives a general idea as to whether or not there is any hemiparesis, any limp, any postural abnormalities, and will quickly reveal any extrapyramidal or cerebellar signs.

2. Check the patient's posture with feet together and then have the patient close the eyes (Romberg test).

3. Have the patient step up and down alternatively with either leg onto a stool. This is a gross test of the strength of the lower extremity plus the patient's balance.

4. Test the motor power of the patient, fine finger movements and alternating hand movements. This is a test for both upper and lower motor neuron disease.

5. Check the reflexes starting with the jaw jerk, and for the presence of a snout reflex. Check the biceps , triceps, brachioradialis reflexes, knee and ankle jerk, and check the foot for possible Babinski respose. Also, check the abdominal reflexes.

6. Check sensation starting with the face, first with a wisp of cotton, then with a pin. Use a cotton pledget to test corneal reflexes. Check vibration and position sense in both upper and lower extremities as well as the pin prick sensation in both upper and lower extremities.

7. Check cranial nerves. The first cranial nerve can be checked with common substances such as coffee, perfume, etc. Check the second cranial nerve by the pupillary light response, optic fundus and field by confrontation. With eye movements in all directions check the third, fourth and sixth cranial nerves. The sensory part of the fifth nerve has already been checked under sensation, so the strength of the temporalis and masseter muscles should be checked and also whether the jaw is protruded in the midline.

The seventh cranial nerve is conveniently checked by having the patient close the eyes tightly and bare his or her teeth. The patient can also elevate the eyebrows and flare the nostrils. At this point, tongue movements can be checked including whether or not the tongue is protruded in the midline. The tongue then should push the examiner's finger away in each cheek. The eighth cranial nerve has been checked already when the vibration is checked during the sensory examination. The ninth and tenth cranial nerves should be checked by observing the palate, the palatal movements and touching the back of the throat on either side with a cotton swab. The eleventh cranial nerve is checked by resistance of the patient to attempts to

HEADACHE: FACTORS THAT CAUSE CONCERN 149


turn his head from right to left and left to right. At this point, the strength of anterior flexion and extension of the neck should be checked. Finally, shoulder shrugging should be checked.

This entire scheme of the neurological exam should not take more than 5 – 7 min in a healthy, normal adult.

HEADACHE: FACTORS THAT CAUSE CONCERN

Clues to headaches that are life threatening and that cause concern come from the history, the physical examination and the diagnostic tests that are ordered. Four key factors distinguishing physiological (primary) from secondary (organic) headaches are

1. Abruptness of onset 2. Progression of the headache pattern 3. The presence of abnormal neurological and physical findings 4. The nature of the provoking and alleviating factors

Danger Signs in Headache

‘Danger signs’ in headache patients that suggest the need for immedi-ate attention are

1. Headache is a new symptom for the individual in the past 3 months, or the nature of the headache has changed markedly in the past 3 months.

2. Presence of any sensory or motor deficits preceding or accompanying the headache other than the typical visual prodromata of migraine with aura. Examples include hands or feet, aphasia or slurred speech.

3. Headache is one sided and has always been on the same side of the head.

4. Headache is due to trauma, especially if it follows a period of unconsciousness (even if only momentary).

5. Headache is constant and unremitting. 6. For a patient reporting tension-type headache-like symptoms: a. Pain intensity has been steadily increasing over a period of weeks

to months with little or no relief. b. Headache is worse in the morning and becomes less severe during

the day. c. Headache is accompanied by vomiting. 7. Patient has been treated for any kind of cancer and now has a

complaint of headache (to this may be added any patient who is immunosuppressed).

8. Patient or significant others report a noticeable change in personality or behaviour, or a notable decrease in memory or other intellectual functioning.

10. HEADACHE150


9. The patient is over 60 years of age, and the headache is a new complaint.

10. Pain onset is sudden and occurs during conditions of exertion (such as lifting objects, sexual intercourse or ‘heated’ interpersonal situation).

11. Patient's family has a history of cerebral aneurysm, other vascular anomalies or polycystic kidneys.

DIAGNOSTIC TESTING IN A PATIENT WITH HEADACHE

1. Laboratory testing: complete blood count, erythrocyte sedimentation rate, blood sugar, renal functions, thyroid functions

2. Radiographic testing: plain skull radiograph 3. Computed tomography of head 4. Magnetic resonance imaging head/cervical spine 5. Electroencephalogram and somatosensory evoked potential testing 6. Arteriography/digital subtraction angiography 7. Electromyography of cranial nerves

MANAGEMENT OF HEADACHES

Primary headaches (migraine, tension-type headache, cluster head-ache, chronic daily headache) can be very debilitating for the individual. Unfortunately, there is no ‘magic bullet’ to treat these conditions and as a pain clinician it will be a challenging task to provide optimal relief to the sufferer. While a cure for headaches is not currently possible, ade-quate control can be achieved for the majority of sufferers. The manage-ment strategies are primarily pharmacological, although few patients do require nonpharmacological therapies including interventional manage-ment. Overuse of drugs should be avoided and analgesic intake should be restricted.

Migraine

Clinical Presentation Episodic attacks characterized by pulsating and throbbing headache in

association with nausea, photophobia and phonophobia.

Treatment of Acute Attacks Acute attack of migraine is generally aborted by drugs such as aspi-

rin, paracetamol (650 mg), NSAIDs such as oral or parenteral diclofenac

MANAGEMENT OF HEADACHES 151


75 mg, opioids such as tramadol 50 – 100 mg IM or butorphanol 1 – 2 mg IM. Specific antimigraine drugs such as ergotamine, DHE and the trip-tans are also effective in aborting the acute attack. Antiemetics such as metoclopramide may also be useful. All the oral triptans appear to be equally effective. Sumatriptan by nasal spray or by subcutaneous injec-tion may be faster acting. DHE appears to be less effective. Tramadol, although frequently used, is not particularly effective. Combinations such as acetaminophen, aspirin, and caffeine may be useful in mild cases. Opiate analgesics including nasal butorphanol appear to be more effec-tive than oral opiates. Corticosteroids IV plus antiemetics are reasonably effective.

Doses 1. DHE 1 mg IM to be repeated after every 1 h (maximum up to 3 mg).

Nasal spray of DHE (maximum up to 2 mg). 2. Triptans – Drugs of choice due to their safety profile. Sumatripan

is available as injection, tablets and nasal sprays (50 – 100 mg orally) zolmitriptan nasal spray (2.5 – 5 mg).

Preventive Treatment of Migraine Prophylactic drugs are indicated when patients have three or more

severe migraine attacks a month and symptomatic medication alone is not satisfactory. Preventive treatment is taken on daily basis, whether or not the patient is having an attack of migraine. The response to preventive treatment is unpredictable. Nonpharmacological treatments such as acu-puncture, relaxation training and biofeedback have also been found to be effective in select group of patients with migraine. The six main classes of drugs that may be used as prophylactics are as shown in Box 10.3 .

Tension-Type Headache

It is characterized by pain that is mild to moderate in severity, bilat-eral in distribution, pressing or tightening in quality and not accompanied with any neurological sign. There is evidence of sustained contraction of pericranial muscles in majority of patients with tension-type headaches. Treatment strategies are aimed at treating an acute episode as well as pro-phylaxis of chronic headache ( Box 10.4 ).

Cluster Headache

Cluster headache is a well-defined neurovascular entity occurring in both episodic and chronic varieties. The attacks are extremely intense and of short duration, occur unilaterally and are accompanied by signs of autonomic dysfunction.

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BOX 10.3

C L A S S E S O F D R U G S U S E D I N T H E P R E V E N T I V E T R E AT M E N T O F

M I G R A I N E

Class/Substance Adverse events Beta-adrenoceptor antagonists

Propranolol: 80–160 mg/day Bradycardia Metoprolol: 100–200 mg/day Hypotension Atenolol: 50–100 mg/day Sleep disturbance

Calcium channel antagonists

Flunarizine: 5 – 10 mg/day Sedation Weight gain Bradycardia

5-Hydroxytryptamine antagonists

Cyproheptadine: 4 mg tablet × 2 – 4 per day

Nausea Sleep disturbance Peripheral Vasoconstriction

Methysergide: 1–2 mg × 1 – 3 per day

Antiepileptics

Sodium valproate: 300–600 mg × 1 – 3 per day

Nausea, vomiting Tremor Weight gain/loss

Divalproex sodium 250–1000 mg/day

Topiramate 25–100 mg/day Hepatotoxicity Thrombocytopenia

Tricyclics

Amitriptyline: 10–100 mg/day (bedtime) Sedation Dry mouth Constipation Urinary retention Postural hypotension

NSAIDs

Naproxen: 250–500 mg × 1 – 2 per day Abdominal pain Nausea Headache Tinnitus



The medical treatment includes both acute therapy and prophylactic therapy ( Box 10.5 ).

Chronic Daily Headache

Many of these patients are rebound-type patients. When treated with amitriptyline, there is a 30% improvement, but with the withdrawal of analgesics, 72% improvement. When not treated with amitriptyline and analgesics were continued, there was an 18% improvement, with analgesics withdrawn at 43% improvement.

Botulinum Toxin in the Treatment of Headaches Recently, botulinum toxin has been under intensive clinical investiga-

tion for the treatment of migraine and other types of headaches. Pain relief conferred by botulinum toxin is probably due to actions beyond those on neuromuscular transmission, which may help to explain its effectiveness in headache.

BOX 10.4

A C U T E A N D P R E V E N T I V E T R E AT M E N T A LT E R N AT I V E S I N T E N S I O N - T Y P E

H E A D A C H E

Attack treatment: First-line alternatives

Analgesics Aspirin: Effervescent tablet 500 – 1000 mg × 1 – 4 per day Acetaminophen: Effervescent tablet/supp. 500 – 1000 mg × 1 – 4 per day

NSAIDs Naproxen: Tablet/supp. 250 – 750 mg × 1 – 2 per day Diclofenac-K: Tablet/supp. 50 – 100 mg × 1 – 2 per day Ibuprofen: Tablet 400 – 800 × 1 – 2 per day

Combinations Acetaminophen + codeine: Tablet/supp. 500 – 1000 mg + 30 – 60 mg × 1 – 4 per day Aspirin + caffeine: Tablet 500 – 1000 mg + 50 – 100 mg × 1 – 4 per day

Preventive therapy: First-line alternative

Amitriptyline: Tablet 10 – 75 mg × 1 per day

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Dose: 100 – 150 units of botulinum toxin are injected at multiple fixed symmetrical pericranial sites (frontalis, temporalis, corrugator and pro-cerus muscles) ( Fig. 10.2 ). The headache severity, headache frequency and acute medication usage is significantly reduced within 2 weeks of inject-ing the toxin. Botulinum toxin has an extremely favourable toxicity and safety profile ( Box 10.6 ).

BOX 10.5

AT TA C K A N D P R E V E N T I V E T R E AT M E N T A LT E R N AT I V E S I N

C L U S T E R H E A D A C H E

Attack treatment

1. First-line alternatives Sumatriptan: Injection 6 mg × 1 – 3 alternatively Oxygen (100% O 2 ) inhalation through a facemask, 6 – 8 L/min for 10 – 15 min

2. Second-line alternatives (optional for convenience but less effective) Sumatriptan: Nasal spray 20 mg × 1 – 3 alternatively Zolmitriptan: Tablet 5 – 10 mg × 1 – 3 or nasal spray 5 mg × 1 – 3 or Lidocaine: Spray 10 mg/dose alternatively Ergotamine: Tablet 1 – 2 mg × 1 – 2

Preventive therapy

1. First-line alternative Verapamil: Tablet 360 – 720 mg/day Short-term prophylaxis Prednisolone: Tablet 45 – 80 mg/day during 3 days, gradually tapered by 10 – 20 mg/week. Ergotamine: Tablet 3 – 4 mg/day Long-term prophylaxis Lithium sulfate: Tablet 42 mg × 2 – 3 per day (Therapeutic plasma concentration 0.3 – 0.8 mmol/L)

2. Second-line alternatives (optional) Methysergide: Tablet 3 – 6 mg/day alternatively Sodium valproate: Tablet 500 – 1500 mg/day alternatively Melatonin: Tablet 6 – 12 mg at bedtime



Frontalismuscle

Procerusmuscle

Corrugatormuscle

FIGURE 10.2 Botulinum toxin injection sites in headache.

BOX 10.6

S E L E C T I O N O F PAT I E N T S F O R B O T U L I N U M T O X I N T Y P E A T H E R A P Y

F O R H E A D A C H E • Patients with disabling primary headaches • Patients who have failed to respond adequately to conventional

treatments • Patients with unacceptable side effects (from existing treatment) • Patients in whom standard preventive treatments are contraindicated • Patients in special populations or situations (the elderly, those at risk

of unacceptable side effects from trial drugs or traditional treatments, aeroplane pilots, students studying and preparing for examinations)

• Patients misusing, abusing or overusing medications • Patients with coexistent jaw, head or neck muscle spasm • Patients with disabling primary headaches • Patients who have failed to respond adequately to conventional

treatments

165

Back pain is an extremely common medical entity and the most com-mon cause of disability in population younger than 45 years. Studies have shown that about 80% of the population will suffer low backache of moderate to severe intensity at some part during their lifetime. It is a major cause of work absenteeism with significant emotional, physical and economic ramifications. Fortunately, majority of cases of backache resolve in 6 weeks with or without treatment. Up to 85% of patients cannot be given a definite diagnosis because back pain is a symptom rather than a disease.

The differential diagnosis of back pain is extensive, physical findings may vary from one examination to the next and investigations are incon-clusive quite often. It has been surmised that musculoskeletal structures of the back are rarely the sole cause of back pain; therefore, a thorough and systematic examination is always indicated.

The goal of pain management therapy in back pain is to reduce the pain to the extent that the patient is able to cooperate with corrective/restorative therapy.

COMMON CAUSES OF THORACOLUMBAR PAIN

1. Myofascial lower back pain 2. HNP of lumbar spine 3. HNP of thoracic spine 4. Spinal canal stenosis 5. Lumbar spondylolysis 6. Spondylolisthesis 7. Facet syndrome 8. Adult kyphosis and scoliosis 9. Infective pathology of spine, e.g. tuberculosis and osteomyelitis 10. Primary neoplasms of the neural tissues and multiple myeloma 11. Metastatic disease of spine

C H A P T E R

12 Back Pain

12. BACK PAIN166


12. Rheumatic conditions, e.g. ankylosing spondylitis and fibromyalgia 13. Metabolic causes of back pain 14. FBSS

The salient clinical symptoms and signs in some of the common condi-tions enumerated above are as follows:

1. Myofascial lower back pain a. Nonradiating back pain b. No clear aetiology c. Pain referred in a nondermatomal pattern d. Examination reveals localized tenderness and limitation of

movement (due to pain) e. Responds to physical therapy f. No positive diagnostic tests

2. HNP of the lumbar spine a. Displacement of central area of the disc (nucleus) resulting in

impingement of a nerve root b. Most commonly involves L 4–5 disc (L 5 nerve root) c. Symptoms of radicular leg pain present; may or may not have back

pain d. Signs of motor weakness – L 4 – tibialis anterior weakness – L 5 – EHL weakness e. Asymmetric reflexes – Knee jerk (L 4 ) – Ankle jerk (S 1 ) f. Patient presents with pain along nerve root distribution (see Fig. 12.1 )

FIGURE 12.1 Straight leg raising test.

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g. Signs of nerve root impingement (tension signs) are positive – SLRT – Lasègue manoeuvre – Crossed leg raise test – Bowstring signs – Femoral stretch test h. Diagnostic tests – MRI – EMG – Nerve conduction studies – Epidurography (as part of advanced pain management

techniques)

3. HNP of thoracic spine a. Less common than lumbar b. Mostly involves lower thoracic discs c. Patient presents with thoracic back pain with or without

circumferential radiating pain around thorax d. Pain exacerbated by sneezing or coughing e. Sensory distribution in trapped dermatomal area f. Diagnostic tests same as for lumbar HNP

4. Spinal canal stenosis a. Involves narrowing of the spinal canal (central stenosis) or neural

(intervertebral) foramen b. Congenital/acquired (narrowing of the spinal canal from facet joint

hypertrophy or hypertrophy of supporting soft tissues) c. Presents with insidious pain and paresthesias d. Diagnosis based on symptoms of neurogenic claudication and CT

and MRI findings e. Lateral recess stenosis (intervertebral foramen stenosis) – Commonly due to bony spurs (osteophytes) – Presents with feature of HNP – May not respond to conservative management f. Farout syndrome – Extraforaminal lateral root compression of L 5 root between L 5

transverse process and sacral ala

5. Spondylolysis a. Represents a defect in the pars interarticularis b. Common cause of back pain in adolescents c. Precipitated by repeated hyperextension activities (e.g. gymnasts) d. Diagnosed by X-rays and bone scan e. CT scan that shows a ‘collar’, i.e. break in the neck of the ‘Scottie dog’ f. Responds to activity restriction, stretching, exercise and bracing

12. BACK PAIN168


6. Spondylolisthesis a. Forward displacement of one vertebra over the other b. Severity of slip – Grade I: 0 – 25% – Grade II: 25 – 50% – Grade III: 50 – 75% – Grade IV: 75 – 100% – Grade V: >100%

7. Facet syndrome a. Inflammation/degeneration of facet joints on MRI b. Lower back pain becomes worse with extension c. May have referred pain to buttock and posterior thigh

8. Adult scoliosis and kyphosis a. Presents with progressively increasing back pain and deformity b. May respond to symptomatic treatment initially c. May need surgical correction later for cosmetic purpose and

intractable pain due to mechanical compression

THORACOLUMBAR SPINE: ANATOMICAL CONSIDERATIONS

In normal posture, the anterior vertebral column carries most of the weight of the low back, and the discs absorb shocks and allow flexion yet limit motion. The discs comprise one-third of the height of the lumbar vertebral column and one-fifth in the thoracic region. These discs are composed of viscous gel-like centre of mucopolysaccharides surrounded by a tough annulus fibrosis. The thinnest part of the annulus is posterior, which may explain herniation in that direction with sudden uneven loads on the spine. Also, with increasing age, discs become less resilient and lose the ability to distribute mechanical forces evenly. The posterior longitudinal ligament narrows from L 2 to L 3 and is thus a poor barrier to prevent posterolateral disc herniation. It is thus not surprising that maximum disc herniations occur in L 4 – L 5 or L 5 – S 1 regions.

In the cervical region, nerve roots exit the foramina above the corre-sponding vertebra; the thoracic lumbar and sacral nerve roots exit below the corresponding vertebra. Therefore, when the L 4 – L 5 disc herniates, it compresses the S 1 nerve root. It is important to remember that only 1 – 2% of the patients with back pain have herniated discs.

The posterior structures of the spine include lamina, pedicles, and facet joints, which together encircle and protect the spinal cord and the emerging nerve roots.

The posterior elements restrict the range of movements and anchor mus-cles, ligaments, and tendons. The intervertebral foramina are formed by ped-icles and apposing articular surfaces of the facet joints. The nerve roots fill

THORACOLUMBAR SPINE: ANATOMICAL CONSIDERATIONS 169


35 – 50% of the foramina. The facet joint is innervated by articular filaments from the medial branch of the posterior primary division of the spinal nerve at and from the level above the joint (may occasionally be from three levels).

Differential Diagnosis of Back Pain

Differential diagnosis of common thoracolumbar spine complaints

1. Back pain with no radiation of pain a. Musculoskeletal lower back pain b. Spondylolysis c. Facet syndrome d. Adult scoliosis e. Adult kyphosis f. Spondylolisthesis g. Infections h. Tumours i. Fractures j. Dislocations k. Arthritis l. Rheumatologic conditions m. Referred pain from viscera

2. Back pain with radicular lower extremity pain or weakness a. HNP b. Spinal stenosis c. Fractures d. Dislocation e. Cauda equina syndrome

Examination of a Patient with Back Pain

• Observation • Skin • Redness, skin markings, unusual stain and patches • Posture • Curves of the spine

• Palpation • Spinous processes • Coccyx • Sacral promontory • Iliac crest • Posterior superior iliac spine • Ischial tuberosities

• Soft tissue • Paraspinal muscle spasm

12. BACK PAIN170


• Sciatic nerve (tenderness along its route) • Psoas muscle

• Movements of the spine • Flexion (normal – can bend over to touch the toes) • Extension (normal – 30 – 40°) • Lateral bending (normal – 30° to each side) • Rotation (symmetric)

• Reflexes • L 4 – knee jerk • S 1 – ankle jerk • S 2 – 4 – bulbocavernosus reflex

• Motor power • Iliopsoas – hip flexion (T 12 – L 3 ) • Quadriceps – knee extension hip adduction (L 2 – L 4 ) • Tibialis anterior – ankle dorsiflexion and inversion (L 4 ) • Extensor hallucis longus – great toe extension (L 5 ) • Gluteus maximus – hip abduction (L 5 ) • Bowel/bladder – (S 2 – S 4 )

• Tests for nerve compression • SLRT – Passive lifting of leg reproduces radicular symptoms especially

of lower lumbar nerve roots L 4 , L 5 , and S 1 – A positive SLR is defined as one that reproduces sciatica between

30 and 70° of leg elevation • Lasègue test dorsiflexion of foot during straight leg raising worsens

the symptoms ( Fig. 12.2 ) • Crossed SLR (Fajersztajn test)

1

2

FIGURE 12.2 Lasègue test.

THORACOLUMBAR SPINE: ANATOMICAL CONSIDERATIONS 171


Raising the contralateral leg can cause symptoms in affected leg when there is central disc herniation. This test is highly specific for indicating symptomatic disc herniation.

• Femoral stretch test

This is useful for testing the entrapment of upper lumbar nerve roots (mostly L 2 and L 3 ). With the patient in a complete prone position, with the hip off the table the knees are flexed as the legs are stretched towards buttocks. Pain on the front thigh may indicate a femoral nerve problem.

• Kernig test: With the patient in a supine position, the thigh is flexed to 90° and the knee is flexed 90° to the thigh. A positive Kernig test causes leg pain as a result of nerve root irritation

Tests for Sacroiliac Joint Evaluation

Pathology of the SI joint is relatively uncommon. Tenderness on palpa-tion of the SI joint does not necessarily signify SI joint dysfunction. The tests for SI joint disease should be interpreted with care, as their sensitivi-ties are moderate at best.

Pelvic Rock Test

With the patient lying supine on the table, the examiner should place both hands on the superior anterior iliac spine and compress the pelvis towards the midline. Pain can be produced in the SI joint if there is local-ized pathology.

Gaenslen Test

The patient is supine with the left leg beyond the edge of the table. The examiner flexes the patient's right knee and hip and presses downwards over the left thigh to hyperextend the left hip. Pain is present on the left SI joint in the presence of SI joint dysfunction. The manoeuvre is repeated on the right side with the right leg by hanging over the edge on the table.

Patrick Test

The patient lies supine on the table and places the foot of the painful side on the opposite knee. The examiner can stress the SI joint by plac-ing one hand on the flexed knee joint and the other hand on the anterior superior iliac spine of the opposite side. This test is also called the FABER test, as it designates flexion, abduction, and external rotation of involved SI joint or hip. This test is used to detect pathology in the SI joint as well as in the hip.

12. BACK PAIN172


Extension Test

The patient is prone and the examiner places one hand under the thigh above the knee on the affected side. With the other hand, the examiner presses downwards over the crest of the ileum to elicit the pain in the SI joint.

Investigations

1. X-ray of the thoracolumbosacral spine 2. CT scan 3. MRI 4. Discography (provocative) 5. Epidurography 6. Triphasic bone scan 7. Nerve conduction velocity (NCV) 8. EMG 9. Human leucocyte antigen typing, where indicated 10. Appropriate blood investigations for underlying medical conditions

enumerated above

TREATMENT PLAN FOR THORACOLUMBAR BACKACHE

When a patient reports with an acute attack of back pain he or she should be evaluated thoroughly both systemic and locoregional for specific joint or disc pathology, and appropriate investigations ordered (blood and radiology).

In the acute phase, bed rest with analgesics, muscle relaxants and sedatives is advised for a period of 7 days. Pain becomes chronic when it lasts for more than 4 weeks. Treatment goals for chronic pain are different from those for acute pain. There may be structural reasons such as soft-tissue scarring, nerve root fibrosis, or bony derangement, which do not allow complete recovery.

Therefore, realistic goals for chronic pain management include the following.

1. Decrease the frequency and intensity of pain (with medications, nerve blocks, surgery, stimulation techniques).

2. Improve coping mechanisms to tackle residual pain (psychological strategies).

3. Optimize functional capacity of the patient.

PHARMACOLOGICAL THERAPY

Pharmacotherapy forms an important part of the multimodal therapy that is essential for tackling chronic low backache. Detailed pharmacology with

PHARMACOLOGICAL THERAPY 173


respect to appropriate drugs is discussed in the relevant section. Here, we will only outline the pharmacotherapeutic protocol for chronic low backache.

If the pain is predominantly of inflammatory origin in the musculo-skeletal system, then NSAIDs are advocated. They should be combined with indirect acting muscle relaxants (cyclobenzaprine, methocarbamol, tizanidine and baclofen) for short periods. One should be aware of their sedative effects, which may become additive when used with drugs hav-ing similar side effects.

Oral narcotics such as tramadol and codeine should be used in the set-ting of moderate to severe pain unresponsive to NSAIDs.

TCAs and anticonvulsants are useful adjuncts to pharmacotherapy where neuralgic symptoms are predominant.

Epidural Steroids

Mechanism of Action of Epidural Steroids Steroids relieve pain by reducing inflammation and by blocking trans-

mission of nociceptive C fibre input. They decrease inflammation by inhibiting the action of phospholipase A 2 (released from the injured disc), which induces membrane injury and oedema by release of arachadonic acid. This is the rate-limiting step in the production of prostaglandins and leukotrienes, which sensitize small neurons and enhance pain generation.

Steroids also produce analgesia by blocking transmission of nociceptive output. They also prevent the development of ectopic neural discharge foci.

Effectiveness of Epidural Steroid Injections in Different Causes of Back Pain

Causes of back pain Effect of epidural steroid injection

1. Anulus tear Hastens recovery 2. Chronic lumbar degenerative disc

diseaseTransient relief

3. HNP without neurological deficit Transient relief 4. HNP with nerve root irritation Therapeutic 5. HNP with nerve root compression Therapeutic 6. Spondylolisthesis Therapeutic if there is nerve root irritation 7. Facet arthropathy Injections into the joint are therapeutic 8. Scoliosis Relief if nerve entrapment is present 9. Ankylosing spondylitis Ineffective

10. Spinal stenosis Transient relief 11. Functional low backache Ineffective

Success Rate of Epidural Steroids in Relation to Duration of Symptoms

Duration of symptoms (months) Success rate (%)

<3 83–100 3–6 67–81 6–12 44 – 69 >12 46 – 58

12. BACK PAIN174


Controversies Regarding Epidural Steroids

1. Methyl prednisolone or triamcinolone? There has been no study to directly compare the two drugs and they

both seem to be equally effective. Toxicity of polyethylene glycol (preser-vative in methyl prednisolone) has been noted at concentrations beyond 40% in experimental models. Most commercial preparations contain only 2 – 3% polyethylene glycol.

2. How soon do you get a positive response? Most patients take several days to respond (2 – 7 days). It is therefore

advisable to wait for 1 week before planning further injections.

3. Where does one ideally site the epidural injection and do large volumes help? Although there have been studies indicating that both epidural and

caudal routes to deposit the steroid are equally efficacious, it is recom-mended to select the interspace corresponding to the radicular symp-toms. A volume of 8 – 10 mL is recommended; however, larger volumes are needed if the caudal route is chosen.

4. Is it normal to have discomfort after an epidural injection? Symptoms may vary from mild heaviness to an exacerbation of symp-

toms for 2 – 3 days.

5. What is the ideal number for therapeutic epidural injections? There has been little evidence in the literature to indicate that more than

three injections improve the clinical benefit of this therapy. A minimum of three injections at intervals of 3 – 4 weeks is recommended for a better overall success rate.

6. Can you add local anaesthetic to the steroid solution? No clinical advantage has been reported by adding local anaesthetic

to epidural injection, although in dural sleeve foraminal injections local anaesthetic can be used to diagnose correct needle placement.

7. Is fluoroscopic guidance a must for this procedure? As far as possible, the procedure must be carried out under fluoro-

scopic guidance. Various studies have reported only 30 – 75% correct needle placement in blind techniques. Adhesions, especially in the ‘failed backs’, make it imperative that the procedure be done under fluoroscopy for optimal results.

Injection Technique and Protocol

Get the standard armamentarium for epidural injection ready. It should include 18 or 20 gauge Touhy needle, a well-lubricated glass

PHARMACOLOGICAL THERAPY 175


syringe or a commercially available LOR syringe, local anaesthetic for the skin wheal, noniodinated contrast, 80 mg methyl prednisolone or 60 mg triamcinolone, 1500 units of hyalase and 20 mL saline for injection.

The patient is placed in a prone position with a pillow under the hips to minimize the lumbar curve. The appropriate space is selected by the ‘no touch technique’ fluoroscopically – the point of entry should correspond to a point just distal to the spinous process of the upper vertebra of the selected interspace. After a skin wheal, the Touhy needle is advanced perpendicular to the skin till the typical LOR of the epidural space is appreciated. Then, 2 – 5 mL of contrast is injected to confirm the space and for a diagnostic epi-durography ( Photograph 12.1 ). Epidurography would give us information about the degree of bilateral spread and the presence of adhesions (appear as filling defects).

Once the space is confirmed, the steroid with hyalase is deposited. In the presence of adhesions, special spring-loaded catheters (Racz catheters Epimed Inc USA ) are threaded to negotiate the adhesions and percuta-neous saline adhesionolysis is done. If an epiduroscope is available, the patient can be posted for epiduroscopic removal of adhesion bands.

Our institutional protocol for epidural steroids is as follows:

1. First appointment Epidurography performed; interspace selected according to clinical

presentation coupled with MRI findings a. Note the epidurography findings – pattern of spread of the dye b. About 80 mg methyl prednisolone + 1500 units hyalase deposited

epidurally (10 mL volume, saline diluent) after negative aspiration for blood and CSF

c. If foraminal block is detected, combine transforaminal injection at the appropriate level in the same sitting ( Photograph 12.2 )

PHOTOGRAPH 12.1 Epidurogram showing good bilateral spread of contrast.

12. BACK PAIN176


d. If adhesions are detected, insert epidural catheter for percutaneous saline neuroplasty

2. Review in OPD (Outpatient department) after a week. Continue with oral medications prescribed; avoid rigorous exercise

a. If the patient is a responder, i.e. has at least 20% relief in symptoms, post for a second injection between 2 and 4 weeks and a third after 8 – 12 weeks from the first injection.

b. If the patient is not a responder, i.e. no relief, reassess, consider a repeat injection at the earliest; if the patient still does not respond, consider other modalities

Complications 1. Unintentional dural puncture and its consequences 2. Epidural haematoma 3. Neurotoxicity of methyl prednisolone is a theoretical possibility 4. Steroid-induced arachnoiditis 5. Aseptic meningitis 6. Epidural abscess 7. Systemic effects of steroids – iatrogenic Cushing syndrome and adrenal

suppression. Difficulty in controlling blood sugar of diabetic patients

PHOTOGRAPH 12.2 Transforaminal injection showing delineation of the nerve root.

FAILED BACK SURGERY SYNDROME 177


SI Joint Pain and Injection Techniques

The SI joint is a synovial joint that is more mobile in youth than in later life. The upper two-thirds of the joint becomes fibrotic in adulthood. Liga-ments and muscle attachments help maintain stability of the pelvic ring. Further motion is limited by the irregular shape of joint articulation, in which the ridges and grooves increase resistance friction. Prolonged load-ing (standing or sitting for long periods) and alterations of sacral base (leg asymmetry or ligamentous injury) are associated with joint hypermobility and resultant low backache.

SI joint is also commonly involved with tubercular infections and this must be ruled out in any patient with history of fever, local tenderness and loss of appetite. Joint effusion and pain is also commonly seen in rheuma-tological conditions such as ankylosing spondylitis. Relevant laboratory investigations can clinch the diagnosis.

Treatment of nonspecific inflammatory conditions of SI joint causing pain includes physical therapy, stabilization of joint, local heat or ultrason-ics and anti-inflammatory medications.

The SI joint is densely innervated by several levels of spinal nerves (L 3 – S 1 ) and may produce lumbar disc-like symptoms when stimulated.

SI pain is usually located in the gluteus and referred to the groin, hip, anterior thigh and calf. The pain is more intense in the morning and remits during the day. Pressure on the joint elicits pain. Specific tests for the SI have been described earlier in the text.

SI Joint Injection Procedure

The patient lies prone. The fluoroscope is started in the PA view and rotated towards the oblique view till a clear view of the SI joint is obtained. The image must show the entire joint for needle entry at the most inferior aspect. The scope is angled in such a way that the anterior and posterior aspects of the joint appear to overlap. Injection of contrast spreads the dye throughout the joint in an inferior to superior fashion ( Photograph 12.3 ).

Once needle position is confirmed, 40 mg of methyl prednisolone + 500 units of hyalase is injected twice weekly for five sittings.

SI joint RF denervation can also be done. Multiple lesions along the entire posterior joint line must be attempted for good results. The facets and dorsal root ganglia of S 1 – 3 must be lesioned to complete the therapy.

FAILED BACK SURGERY SYNDROME

FBSS refers to persistent or recurrent chronic pain after one or more sur-gical procedures on the lumbosacral spine. FBSS refers to both persistence

12. BACK PAIN178


of back pain and occurrence of a different type of pain following surgery. It does not necessarily imply failure of treatment or surgery but only a functional failure of the back. In terms of time duration, it would be rea-sonable to describe this syndrome if the pain persists or occurs 8 – 12 weeks following the surgical procedure. The prevalence of FBSS is in a range of 10 – 40% of lumbar spine operations.

Aetiology of FBSS

1. Nerve injury causing neuropathic pain 2. Unrecognized lateral recess stenosis or lateral disc herniation 3. Inappropriate patient selection 4. Postsurgical arachnoid fibrosis or arachnoiditis 5. Extensive fusion causing abnormal position and pain 6. Segmental instability due to generous laminectomy

CT and MRI may reveal the causative factor, although few patients may require detailed neurological evaluation including EMG, NCV, etc. Epi-durography and CT myelography is helpful in refractory FBSS patients.

Treatment Options in FBSS

FBSS patients are commonly referred to a pain clinic for detailed evalu-ation and treatment. The pain clinician has to treat these patients skillfully and with compassion. FBSS can be a difficult and frustrating condition to treat. Multiple treatments and interventions result in psychosocial prob-lems thus aggravating pain and suffering. The treatment modalities include

PHOTOGRAPH 12.3 Sacroiliac joint injection.

PERCUTANEOUS EPIDURAL ADHESIONOLYSIS 179


1. Rehabilitation and medical management 2. Anticonvulsants such as gabapentin in patients with neuropathic pain 3. Antidepressant drugs such as serotonin-specific reuptake inhibitor

(fluoxetine) and TCA (amitriptyline) 4. Percutaneous fluoroscopic procedures such as epidural adhesionolysis 5. RF denervation of facet joints, DRG lesioning 6. Neuromodulatory techniques such as spinal cord stimulation and

intrathecal morphine delivery systems

PERCUTANEOUS EPIDURAL ADHESIONOLYSIS

The most common cause of FBSS is epidural fibrosis and adhesions. Postsurgical bleeding and the associated healing process frequently pro-duce scarring. Epidural adhesions alone do not cause pain. The associated irritation or inducement of epidural venous engorgement may contrib-ute to pain production. Whether by the direct mechanical encasement of nerve roots within scar tissue or the secondary process of epidural venous congestion with increasing nerve root oedema, pain is produced by move-ment of the swollen inflamed nerve root.

MRI can be used to detect epidural fibrosis, but it is not a perfect test. It has been documented that myelography, CT, and MRI have been unsuccessful.

Technique of epidural adhesionolysis: The ideal epidural catheter used for adhesionolysis is a stainless steel, fluoropolymer-coated, spiral-tipped catheter. Such a catheter is passed through the needle into the scar tissue by the caudal epidural route. The bevel of the needle should face the ven-trolateral aspect of the caudal canal on the affected side. This facilitates passage of the catheter to the desired side and decreases the chance of shearing the catheter. Because scar formation is usually uneven, multiple passes may be necessary to place the catheter into the scarred area. For this reason, it is best to use a 16 gauge epidural needle, which has been specially designed to allow multiple passes of the catheter. To facilitate steering of the catheter into the desired location, a 15° bend is placed at its distal end. After final placement of the catheter and negative aspira-tion, 5 – 10 mL of contrast medium is injected through the catheter. This dye should spread into the area of the previous filling defect and out-line the targeted nerve root. Then, 1500 units of hyaluronidase in 10 mL of preservative-free saline is injected rapidly. After negative aspiration, 10 mL of 0.125% bupivacaine and 40 mg of triamcinolone/methyl prednisolone are injected through the 0.2 micron bacteriostatic filter; the steroid must be injected before the in-line filter is installed.

When the procedure is completed, the catheter should be secured to the skin with 2-0 nylon on a cutting needle. Caution must be exercised to

12. BACK PAIN180


avoid puncturing the catheter with the needle or cutting the catheter coating while wrapping it.

The catheter is left in place for 3 days. On the second and third days, it is injected once a day with 10 mL of 0.125% bupivacaine with low dose of methyl prednisolone after negative aspiration from the catheter. Fifteen minutes later, 10 mL of 10% saline is infused over 20 min.

The procedure is usually followed by significant improvement in pain and motor function. As pain is relieved, it is important to initiate aggres-sive physical therapy to improve muscle strength and tone, which are usually reduced by disease secondary to pain. Often, it is not possible to lyse existing epidural adhesions completely because of the extensive scar tissue. If necessary, we repeat the procedure after 6 – 8 weeks. Because of the steroids, a 1- to 2- month delay between procedures is necessary, dur-ing which time the patient should be encouraged to continue intensive physical therapy.

Clearly, lysis of adhesions in the epidural space is a procedure that must be used after simpler procedures, such as rest, nonsteroidal anti-inflammatory medications, muscle relaxants, physical therapy, activity programs, two or three single shots of epidural steroid, and transcutane-ous electrical nerve stimulation. Better informed patients will opt for pro-cedures such as lysis of adhesions rather than surgery. The results clearly show a dramatic decline in the need for complete avoidance of surgical intervention in appropriately selected patients with clearly documented herniated discs and nerve root compression.

The technique described above overcomes the obstacle of being able to get the medication to a lesion-specific site by placing the tip of a soft spring catheter within the scar and letting the injected fluid under pressure find the path of least resistance within the scar and open up the perineural space. Thus, steroid can reach the inflamed, angry nerve root and produce its anti-inflammatory effect.

The addition of hyaluronidase has resulted in threefold reduction of outright failures in our patients, and this needs to be investigated further to determine whether we are looking at a volume or if the addition of hyaluronidase really makes the difference.

239

CRPS is a challenging neuropathic pain states quite difficult to com-prehend and treat. Although not yet fully understood, advances are being made in the knowledge of the mechanisms and treatment involved with CRPS. CRPS was earlier known as causalgia, RSD, shoulder-hand syn-drome, Sudeck dystrophy and a variety of other terminologies. The term RSD was introduced by Evans in as early as 1946. Some of the earliest and most interesting descriptions of causalgia came from the American Civil War by Silas Weir Mitchell (1916).

CRPS is the term introduced in 1994 by International Association for the Study of Pain and is defined as a ‘painful syndrome that develops after an initiating noxious event such as trauma’. Ongoing pain is often associ-ated with hyperalgesia to cutaneous stimuli.

TYPES OF CRPS

CRPS type 1 (formerly RSD): A syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportionate to the inciting event. It is associated at some point with evidence of oedema, changes in skin blood flow, abnormal sudomotor activity in the region of the pain, and allodynia or hyperalgesia.

CRPS type 2 (formerly causalgia): A syndrome of sustained burning pain, allodynia and hyperpathia after a traumatic nerve lesion, often con-tinued with vasomotor dysfunction and later trophic changes.

C H A P T E R

19 Complex Regional Pain

Syndrome

19. COMPLEX REGIONAL PAIN SYNDROME240


DIAGNOSTIC FEATURES OF CRPS

1. Continuing pain that is disproportionate to any inciting agent. 2. Must report at least one symptom in each of the following four

categories: a. Sensory: Reports of hyperaesthesia. b. Vasomotor: Reports of temperature asymmetry and/or skin colour

changes and/or skin colour asymmetry. c. Sudomotor/oedema: Reports of oedema and/or changes and/or

sweating asymmetry. d. Motor/trophic: Reports of decreased range of motion and/or motor

dysfunction (weakness, tremor, and dystonia) and/or trophic changes (hair, nail, and skin).

3. Must display at least one sign in two or more of the following categories: a. Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia

(to light touch). b. Vasomotor: Evidence of temperature asymmetry and/or skin

colour changes and/or asymmetry. c. Sudomotor/oedema: Evidence of oedema and/or sweating

changes and/or sweating asymmetry. d. Motor/trophic: Evidence of decreased range of motion and/

or motor dysfunction (weakness, tremor, and dystonia) and/or trophic changes (hair, nail, and skin).

Diagnosis of CRPS would be precluded by the existence of any known pathology that would otherwise account for symptoms and signs present in the distal parts of an extremity but outside the territory of an injured nerve.

The term CRPS was chosen for the following reasons:

• Complex signifies the varied clinical features found in these conditions. • Regional emphasizes that in the majority of cases it involves a region

of the body, usually an extremity, but may occur on another part of the body or spread to different areas of the body.

• Pain is considered essential to the diagnosis of CRPS and includes pain that is spontaneous or evoked such as allodynia or hyperalgesia. In rare cases otherwise resembling CRPS, pain may be minimal or absent.

The cardinal symptoms and signs that constitute CRPS are as follows:

1. Pain a. Follows a known initiating noxious event, seems to be physically

quite minor. b. Disproportionate in duration, severity and distribution. c. Noxious event may occur peripherally, in the CNS, or in the viscera.

DIAGNOSTIC FEATURES OF CRPS 241


d. May be spontaneous, deep and aching in quality aggravated by orthostasis and touch.

e. May be associated with allodynia or hyperalgesia.

2. Vasomotor and sudomotor abnormalities Tend to be more obvious early in the course of the disorder.

a. Swelling of affected joints and other soft tissues. b. Temperature differences that may be either colder or warmer than

the contralateral extremity. c. Associated with changes in skin colour – red, dusky, and blue.

3. Trophic changes These are generally described as occurring late in the disorder.

a. Skin, nail and hair growth changes.

4. Motor changes a. Weakness b. Tremor c. Reduced movement d. Dystonia.

Three clinical stages of CRPS type 1 are classified as follows:

1. Acute stage (hyperaemic) 2. Dystrophic stage (ischaemic) 3. Atrophic stage.

Acute stage

• Commences at the time of injury. • Characterized by constant moderate burning pain. • Localized to the area of injury. • Associated with hyperpathia, allodynia and hyperalgesia. • Skin – red and warm. • Evidence of localized oedema, muscle spasm and tenderness. • Stage can be completely reversed by sympathetic blockade. • If untreated, can progress to the second dystrophic stage.

Dystrophic Stage

The dystrophic stage is characterized by

• spreading of oedema; • increasing stiffness of the joints and muscular wasting; • pain which is usually spontaneous and burning in nature and may

radiate proximally or distally from the site of injury; • pronounced hyperpathia and allodynia; • moist, cyanotic and cold skin;



• coarse hair. • sympathetic blocks may still be effective in reversing the process

though a larger series of blocks or a prolonged sympathetic blockade may be necessary to afford permanent relief;

• if not treated, it progresses to the third atrophic stage.

Atrophic Stage

The atrophic stage is characterized by

• smooth, glossy, tight, pale or cyanotic skin; • loss of hair; • lowering of local temperature; • extreme weakness and limitation of motion at virtually all of the

involved joints; • contracture of flexor tendons; • advanced osteoporosis; • aggravated by weight bearing, movement and frequently by exposure

to cold; • in the atrophic stage, syndrome becomes irreversible. Although

sympathetic blockade may still provide the temporary relief, it is no longer effective in terminating the process permanently.

AETIOLOGY AND PATHOPHYSIOLOGY

Understanding of pathophysiology of CRPS has significantly improved over 2001 – 10. It has been established that in certain patients with CRPS, pain depends on continued sympathetic activity in affected areas. Roberts introduced the term ‘SMP’ to describe the aspect of pain which is relieved by blockade of efferent sympathetic nervous system.

Certain models have been proposed to explain how CRPS produces disproportionate pain in duration as well as in severity, in response to noxious stimuli. The model ( Fig. 19.1 ) which could help in understanding the role of SMP in CRPS is as follows:

1. Afferent sensitization, in which afferent nociceptive fibres are sensitized by chemical compounds – i.e. prostaglandins – released from sympathetic terminals, resulting in aberrant activity in response to mechanical, thermal and chemical stimulation.

2. Ephaptic activity of abnormal synaptic connections between efferent sympathetic and afferent sensory nerves resulting in aberrant impulses.

3. Increased density of adrenergic receptors on the plasma membrane of nociceptive afferents leads to chemical coupling of sympathetic sensory system, leading to excessive painful signal transmission.

AETIOLOGY AND PATHOPHYSIOLOGY 243


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This altered physiological state keeps the CNS in a sensitized state and any minor noxious stimulus in the affected area is interpreted as severe pain, in terms of intensity as well as duration, by CNS.

MANAGEMENT OF CRPS

Management of CRPS involves multidisciplinary co-ordinated approach to function restoration built around a treatment algorithm, and attempts to normalize functions should guide therapy, keeping in mind that each patient needs to have treatment plans tailored to his individual problems.

Comprehensive diagnostic evaluation and early and aggressive ther-apeutic interventions are imperative to prevent onset of the irreversible stage III. While progress is being made in treating patients with CRPS, it is important to remember that the goals of care in CRPS are to

1. perform a comprehensive diagnostic evaluation; 2. be prompt and aggressive in treatment interventions; 3. assess and reassess the patient's clinical and psychological status; 4. be consistently supportive; 5. strive for the maximal pain relief and functional improvement.

The therapeutic approach often calls for a combination of treatments. Antiepileptics, opioids, antidepressants, vasodilators and topical agents along with regional sympathetic blocks and a rehabilitation program can help several patients suffering from these disorders. However, the main-stay for therapy of CRPS is sympathetic efferent blockade, primarily by sympathetic chain/ganglion blockade at various anatomical sites by injecting local anaesthetic or neurolytic agent or RF ablation depending upon the region affected.

TREATMENT PROTOCOL OF CRPS

When a patient with CRPS reports in a pain clinic, a detailed history and a comprehensive physical examination are undertaken and are docu-mented. The patient is assessed for the following clinical parameters and the same parameters are assessed for clinical evidence of recovery during treatment period.

• Pain (on visual analogue scale 1 – 10) • Neuropathic pain scale • Hyperalgesia/allodynia/hyperaesthesia • Skin colour/temperature • Oedemas • Range of motion

TREATMENT PROTOCOL OF CRPS 245


CRPS of Upper Extremity: Mild to Moderate Pain

• Intermittent SGB at C6 level by classical anterior paratracheal approach.

• Injection of bupivacaine 0.25% (10 mL) at each sitting. • A series of 10 – 15 blocks is administered on alternate days to each

patient.

Effectiveness of block at each sitting is assessed by the following methods:

1. Presence of Horner syndrome 2. Feeling of warmth in limb 3. Rise in temperature of limb (by telethermometry) 4. Improvement in pulse oximeter graph/saturation (by pulse oximeter).

CRPS of Upper Extremity: Moderate to Severe Pain

Continuous SGB Continuous SGB through ambulatory infusion pump using mixture of

bupivacaine and morphine was first described in a case report by Owen Flakenberg et al. (1992) and they concluded that continuous infusion with a mixture of bupivacaine and morphine provided prolonged relief from symptoms in RSD compared to single-shot injections. Continuous SGB has been found useful when (1) conservative treatment with physical ther-apy, mild analgesics and other drugs has failed; (2) conservative therapy and intermittent SGB have failed; and (3) patients show limited and short-lived response to intermittent SGB.

Advantages of continuous SGB 1. Prolonged sympathetic block provides faster relief from

sympathetically mediated pain. 2. Multiple injections are avoided. 3. Incidence of accidental vascular injection is significantly reduced. 4. Provides continuous relief from associated symptoms.

Contraindications: In spite of SGB being very effective and treatment of choice in CRPS of upper extremity, there are certain circumstances where this block is contraindicated, which are as follows:

1. Absolute contraindication a. Patient on anticoagulant therapy b. Patient having pneumothorax or pneumonectomy on the

contralateral side c. Recent cardiac infarction.

2. Relative contraindications



a. Glaucoma b. Marked impairment of cardiac conduction system

(e.g. atrioventricular heart block).

Technique: After careful and detailed evacuation, the patient is selected for block. Informed consent must be obtained. Potential risks, complica-tions, and possible side effects should be explained in detail. The patient should share the responsibility for decision making and must understand the risks and the fact that complications do occur. All standard resuscita-tive gadgets need to be readily accessible.

The patient is made to lie supine with the head resting flat on the table without a pillow; the C 6 tubercle (Chassaignac's) is usually located 2.5 cm lateral and cephaloid to midsternal notch at the cricoid level. At the point of entry, the index finger of left hand is insinuated in the groove between the trachea and medial border of the sternocleidomastoid muscle and the common carotid artery is well felt and retraced laterally. A 20 gauge IV cannula is then attached to a 10 mL saline-filled syringe, which is inserted perpendicular to the skin medial to index finger till it hits the C 6 tuber-cle ( Photograph 19.1 ). Aspiration test is done to rule out the presence of blood and cerebrospinal fluid. The stylet is then taken out and cannula is firmly secured to skin with sutures and connected to the ambulatory elas-tomeric infusion pump filled with the local anaesthetic agent bupivacaine 0.125% to deliver a fixed flow of 2 mL/h for 7 – 10 days; during the infusion

(a) (b)

(c) (d)

PHOTOGRAPH 19.1 Continuous stellate ganglion block. (a) Identifying the land-marks. (b) Insertion of cannula. (c) Injection of drug. (d) Cannula in place.



period, patient is assessed continuously for clinical evidence of recovery ( Photograph 19.2 ).

Complications and side effects: A proper technique is used and due attention is given to safety measures while giving SGB although it is a sim-ple, safe, minimally invasive and an effective procedure. Most unpleasant side effects result from Horner syndrome, e.g. ptosis, miosis and nasal congestion. Common complications result from diffusion of local anaes-thetic into nearby nervous structures. These include the recurrent laryn-geal nerve with complaints of hoarseness, feeling of a lump in the throat, and sometimes a subjective shortness of breath. Partial brachial plexus block can also occur. The two most feared complications are intraspinal and intravascular injections of local anaesthetic. Respiratory embarrass-ment and need for mechanical ventilation can result from injection into

(a)

(b)

PHOTOGRAPH 19.2 (a) Fixation of cannula. (b) Ambulatory patient with continuous stellate ganglion block.



intrathecal space. Sinus arrest syndrome, haematoma formation, severe hypotension, migraine headache, delayed subdural block and pneumo-thorax have been reported following SGB.

CRPS of Lower Extremity: Mild Disease

Medications and adjuvants.

CRPS of Lower Extremity: Moderate to Severe Disease

Percutaneous lumbar sympathectomy by either RF ablation or chemi-cal neurolysis by phenol or alcohol.

Lumbar Sympathectomy by RF Ablation The procedure is performed under mild sedation in prone position.

The RF cannula is introduced 5 cm lateral to spinous process of L 2 , L 3 , L 4 , and vertebral bodies (L 3 , L 4 and L 5 if the foot is involved). The area is made aseptic and a disposable, sterile top-pole needle (23 gauge, 150 mm long) is inserted through the wheal under the guidance of C-arm with image intensifier. The needle is directed to the junction of the middle and lower thirds of vertebral body at L 2 and at the junction of the middle and upper thirds at L 3 according to lateral fluoroscopy. The midvertebral body is targeted at L 4 . If the foot is involved, L 5 vertebral body is targeted as well. The position of needle tip is checked by X-ray in PA and lateral views. In lateral view, the needle tip should barely reach anterior border of vertebral body. The sympathetic chain was then identified by administering injection of 0.5 – 1 mL of omnipaque, which is checked in lateral and PA views. After noting the spread of contrast material behind facet joint line on PA view and after negative aspiration for blood, 1 – 2 mL of 1.0% lignocaine solution is injected through the needle. This is taken as the test block. The test block is done at L 2 , L 3 , and L 4 levels if the foot is not involved or at L 3 , L 4 and L 5 levels if the foot is involved. After 2 min, skin temperature at great toe, heel and foot is checked. If skin temperature change of at least 1°C is obtained, it is taken as a positive sympathetic block. If any sensory or motor dysfunc-tion is noted after test block, the results are considered invalid and the test block is repeated.

After 5 min, the RF electrode is introduced inside the RF cannula and is kept in position for a total of 90 s at a temperature of 80°C. The can-nula is then advanced anteriorly by 5 mm and a second lesioning is made. Lesioning sites are at L 2 , L 3 , and L 4 levels or L 3 , L 4 , and L 5 levels (if the foot is involved). Each time, the temperature as well as colour change of the foot is observed. When a satisfactory effect is achieved, the RF cannula is removed.



Patients are continuously followed up in the pain clinic for clinical evi-dence of recovery. Patients who have inadequate recovery or who need frequent repeated sympatholysis are also prescribed medication.

Advantages of RF ablation in CRPS • Low morbidity and no mortality • Least possibility of neuroma formation • No radiculopathy • Minimally invasive • Outpatient procedure.

Chemical neurolysis by injecting 2 – 3 mL of 6% phenol at each site is also used for sympathetic neurolysis.

Drug Therapy in CRPS

Two basic classes of drugs are used: Class A: drugs used for prophylaxis to manage pain in CRPS and other

symptoms (daily drugs). Class B: abortive drugs for crisis management (rescue agents).

Class A TRICYCLIC ANTIDEPRESSANTS

Patients with CRPS have usually visited multiple physicians and have continuously suffered for prolonged period and are therefore very anxious, depressed and suspicious about the outcome of treatment modalities. In these patients, TCA are very effective. Amitriptyline is the most com-monly used drug with a dosage of 12.5 – 50 mg hs; nortriptyline is given at a dosage of 10 – 20 mg hs.

Side effects: Dryness of mouth, constipation, epigastric distress, urinary retention, blurred vision, palpitation, sedation, and fine tremors.

Cautions: Used with caution in patients of hyperthyroidism, ischaemic heart disease, renal and hepatic diseases.

ANTIEPILEPTIC DRUGS

Gabapentin works primarily by enhancing natural GABA systems in pain modulation but may also have some impact in suppressing excit-atory amino acids such as glutamate. Gabapentin is frequently adminis-tered to CRPS patients at a dosage to start with 300 mg once a day and gradually increased to 300 mg thrice a day to four times a day. Dizziness and fatigue are the major side effects frequently encountered and can be taken care of by increasing the dosage gradually. Oxcarbazepine and car-bamazepine are another group of drugs frequently administered; sedation with oxcarbazepine is much less than carbamazepine. Oxcarbazepine is



started with a dosage of 300 mg once a day and is gradually increased to 900 – 1200 mg daily.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

They are particularly useful in cases where there is considerable inflam-mation. Aspirin and ibuprofen are frequently prescribed. However, gas-tric irritation remains a main concern, and so these drugs are usually combined with drugs like ranitidine and pantoprazole . They are used with caution in patients having coexisting renal disease. Cox-2 inhibitors like etoricoxib and valdecoxib are not found to be very effective though supposed to have minimal gastric irritation properties and should be used with caution in patients with cardiovascular diseases.

PERIPHERAL VASODILATORS

Patients having intense vasoconstriction, supposedly due to overactiv-ity of sympathetic nervous system, are frequently administered drugs like nifedipine 5 – 20 mg twice or thrice a day, pentoxifylline 400 mg thrice a day, and xanthinol nicotinate 500 mg twice a day. Flushing of skin can be troublesome in some patients. Oral nifedipine has been found to show persistent and promising results.

Patients with severe burning sensation, allodynia, hyperalgesia or hyperaesthesia are advised to apply lidocaine jelly 2% or eutectic mixture of local anaesthetics cream. It is effective in some patients for short dura-tion and repeated application is required.

Class B STEROIDS

Steroids are used for a short period (5 – 7 days) only when severe inflam-mation resulting in intractable pain is present. Prednisolone 20 mg twice a day to thrice a day is usually prescribed. Dexamethasone 2 – 4 mg twice a day is another alternative steroid used frequently.

OPIOIDS

Patients complaining of severe pain and who have already received NSAIDs are administered opioids for a short duration in early phase. Usu-ally tramadol at a dosage of 50 – 100 mg three times a day is prescribed, which is withdrawn gradually as other treatment modalities become effective.

When all the above modalities fail, the following are considered:

• IVRA In patient's refractory to conventional treatment modalities, intravenous regional sympathetic blockade is achieved by using bretylium 0.5 mg/kg body weight with lidocaine 0.5%, 40 mL for upper extremity and 60 mL for lower extremity. The results are equivocal.



• Programmable implantable devices Spinal cord stimulation: spinal cord stimulator is effective and relieves pain by modulating spinal pain signalling neurons and resetting altered spinal physiological state.

Continuous intrathecal morphine with clonidine and/or midazolam infusion by programmable implantable drug delivery system may also be used as a last resort in patients where both pharmacological and interven-tional therapies fail. • Physiotherapy • The principle of functional restoration is based on a steady pro-

gression from very gentle movements on an active basis to gentle weight bearing.

• Manage oedema, optimize range of motion and encourage general aerobic activity throughout.

• Gradual desensitization to increasing sensory stimulus goes along with increased function. Desensitization techniques are rubbing with silk, cotton and then towelling or contrast baths.

• Gradually increasing the strength and flexibility with ultimate return to normal use is the goal, and this is accomplished by a series of exercises and devices (e.g. foam rubber balls progressing to spring grip strengtheners) and mat exercises.

• The physiotherapist is also actively involved in gait training and postural correction.

• CRPS of upper extremity: weight-loading part of the treatment starts with small objects carried in the hand, and soon progresses to a handled bag, which can later be loaded with heavier weights.

• CRPS of lower extremity: partial weight-bearing with gait training. • Vocational rehabilitation • Patients are advised to continue in their job or go back to job as

early as possible. • Employers are advised to make required adjustments in nature of

work as and when necessary. • Recreational therapy • Recreational therapy helps in rebuilding their confidence in

themselves and in developing positive outlook towards life. • Patients are encouraged to take part in recreational activities, retain/

revive their hobbies, and participate in dance, drama and music. • Cognitive behavioural therapy • Patients who continue to have depression and/or anxiety, avoiding

gainful employment or taking undue advantage of the disease are managed with the help of clinical psychologists.

Cognitive behavioural psychotherapy is the mainstay of treatment in the atrophic stage of CRPS and those with intractable pain.



CONCLUSION

CRPS presents with varied clinical features, pain being the most domi-nant one. Better understanding of pathophysiological mechanisms of CRPS and/with role of overactivity of sympathetic nervous system and technological advancement in treatment modalities has helped pain cli-nicians to diagnose the entity more accurately, controlling signs and symptoms in majority of patients and preventing them progressing to irreversible atrophic stage. However, continued research is needed to con-vert the symptom-oriented treatment approach into mechanism- targeted treatment approach to tailor treatment plan according to individual patient's requirement.

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