75 neurosurgery for chronic - hindawi publishing...

Neurosurgery for chronicneuropathic pain

Jung Y Park MD PhD1,2, Andres M Lozano MD PhD FRCSC1,2

Chronic pain has been defined as pain that lasts longerthan three to six months or, as proposed by the Interna-

tional Association for the Study of Pain. It is pain that out-lasts the period of normal healing of an acute abnormality(1). Any acute pain has the potential to become chronic, andthis conversion can follow different temporal courses for dif-ferent problems. Pain of primarily neural origin is termedneuropathic pain.

Common features of chronic neuropathic pain include

spontaneous burning, paroxysmal jabbing or shocking pain,

hyperpathia, hyperalgesia, and allodynia or touch-evoked

pain. These features may occur alone or in combination.

Causes of neuropathic pain include injuries to the nervous

system, whether by trauma, ischemia or metabolic dysfunc-

tion. Neuropathic pain is idiosyncratic; not every patient who

suffers neural injury develops this type of pain. The inci-

dence of neuropathic pain may also vary according to the site

of neural injury. It is classified as ‘peripheral type’ when it re-

sults from neural injury or dysfunction from peripheral

sources or as ‘central type’, when it arises from dysfunction

in the brain and spinal cord. Neuropathic pain, in contrast to

somatic or nociceptive pain, usually occurs without ongoing

physiological activation of nociceptors. However, neuro-

pathic and nociceptive pain may have overlapping features,

and both types may at times be complicated by psychological

and psychosocial factors. Table 1 lists the broad range of

causes of peripheral and central neuropathic pain.

Only patients with chronic neuropathic pain that fails to

respond to medical treatment are considered potential candi-

dates for surgical treatment. Hence, neurosurgeons are called

upon to treat these often difficult pain syndromes. The goal

here is to describe neurosurgical treatments for the chronic,

intractable neuropathic pain states and to provide a brief out-

line of current neurosurgical approaches in these settings.

Pain Res Manage Vol 5 No 1 Spring 2000 101

JY Park, AM Lozano.Neurosurgery for chronic neuropathic pain.Pain Res Manage 2000;5(1):101-106.

Neurosurgery can play a role in the management of patients withrefractory chronic neuropathic pain. However, selecting patientsas candidates for surgery and choosing the most appropriate surgi-cal procedure is challenging, and surgical interventions often havelimited efficacy. When considering surgery, neuroaugmentative orneuromodulative procedures (eg, peripheral, spinal, motor cortexor deep brain stimulation) are generally preferred over ablativeprocedures as initial modalities. With better understanding of spe-cific pain mechanisms, surgery will have more to offer patientswith chronic neuropathic pain.

Key Words: Chronic neuropathic pain; Surgery

La neurochirurgie pour la douleurneuropathique chroniqueRÉSUMÉ : La neurochirurgie peut jouer un rôle dans la prise encharge des patients souffrant d’une douleur neuropathique chroniqueréfractaire. Cependant, la sélection des patients comme candidats à lachirurgie et le choix de l’intervention chirurgicale la mieux appropriéerestent un défi, et les interventions chirurgicales ont souvent uneefficacité limitée. Si l’on envisage une chirurgie, les interventions quiont un effet neuromodulateur ou neuroamplificateur (par exemple, unestimulation cérébrale profonde, ou celle du cortex moteur ou unestimulation spinale ou bien périphérique) sont généralementpréférables à des méthodes ablatives comme méthodes de premierchoix. Avec une meilleure compréhension des mécanismes de ladouleur, la chirurgie aura plus à offrir aux patients atteints d’unedouleur neuropathique chronique.

Toronto Western Hospital, University of Toronto, Toronto, Ontario

Correspondence and reprints: Dr Andres M Lozano, 1The Toronto Hospital, Western Division, McLaughlin Pavilion 2-433, 399 Bathurst Street,

Toronto, Ontario M5T 2S8. Telephone 416-603-6200, fax 416-603-5298, e-mail [email protected]

NEUROLOGY AND CHRONIC PAIN

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Detailed review is not intended, but rather an attempt is made

to establish a framework within which the practising clini-

cian can add insights when providing care to these patients.

SURGICAL TREATMENT OF CHRONICNEUROPATHIC PAIN

Before considering any surgical measure to treat patientswith chronic neuropathic pain, appropriate medical thera-peutic approaches should be thoroughly investigated andexhausted. Generally, when neurosurgical therapy is consid-ered, neuroaugmentative or neuromodulative procedures arepreferred over ablative approaches as the initial surgical mo-dality. This is because of their reversibility and low incidenceof significant side effects. These approaches are only un-dertaken after the primary and causative disturbances, forexample compression, tumours, infections and ongoing me-chanical injury, etc, have been addressed.

Pain associated with peripheral nerve abnormalities that is

located primarily in the distribution of a single peripheral

nerve may be treated with peripheral nerve stimulation

(PNS) (2). The mechanism of action of PNS may be central

or peripheral. As with other pain control operations, there

must be a clear cut etiology for the pain, and a correctable pa-

thology (eg, nerve entrapment syndrome) should be ex-

cluded. The surgery is usually done in two phases. Usually, a

site proximal to the injury site is selected for electrode place-

ment. After a skin incision and dissection to free 5 to 6 cm of

nerve, the electrode is placed directly under the nerve and su-

tured in place. The electrode lead is then externalized

through a small stab wound and connected to a temporary

electrical stimulator. The effects of stimulation through the

implanted electrode are evaluated over this trial phase, which

can last two to three days. The settings of the temporary

stimulator are considered satisfactory when the patient re-

ports a fine tingling sensation in the nerve distribution. There

are two potential outcomes of this trial. In patients where

stimulation does not help the pain, the device is removed. On

the other hand, patients who derive substantial pain relief,

usually greater than 50% on a pain visual analogue scale, go

on to permanent implantation in which the stimulating elec-

trode is connected to a battery powered, pacemaker-like, im-

planted pulse generator. Results from a large series (3)

indicated good to excellent pain relief in 70% to 80% of pa-

tients. These devices, like all stimulation implants, are sub-

ject to displacement, infection, breakage of leads and loss of

battery power over time.

Peripheral nerve pain from multiple sources, including

neuropathic pain secondary to neural injury as a consequence

of degenerative disc disease, postamputation pain (eg, phan-

tom limb pain, stump pain), reflex sympathetic dystrophy

(now replaced with the term ‘complex regional pain syn-

drome’ [CRPS] type 1), or causalgia (CRPS type 2), may be

relieved by spinal cord stimulation (SCS) (4,5) (Figure 1). A

relevant animal model of chronic neuropathic pain, showing

apparent relief by SCS, has been developed recently (6). Its

exact mechanism of action of SCS is not fully understood but

may at least partly be mediated via GABAergic and

adenosine-dependent mechanisms, or modulated by influ-

encing the transmission of A fibres and not of c fibres. Some

effects of SCS may be mediated by the sympathetic nervous

102 Pain Res Manage Vol 5 No 1 Spring 2000

Park and Lozano

TABLE 1Various types of peripheral and central neuropathic pain

Peripheral neuropathic pain Central neuropathic pain

Peripheral nerve injury with orwithout sympatheticallymaintained pain

Complex regional painsyndromes (reflexsympathetic dystrophy orcausalgia)

Carpal tunnel syndrome

Meralgia paresthetica

Diabetic neuropathy

Failed back surgery syndrome orpostlaminectomy syndrome

Trigeminal neuralgia ortrigeminal neuropathic pain

Glossopharyngeal neuralgia

Postherpetic neuralgia

Occipital neuralgia

Brachial plexus neuropathy oravulsion

Incisional neuralgia

Phantom pain

Pain of spinal cord origin

Trauma

Inflammation (eg, myelitis)

Tumour

Vascular pain (eg, Wallenberg’ssyndrome)

Iatrogenic pain (postcordotomydysesthesia)

Other (eg, syringomyelia)

Pain of brain stem origin

Syringobulbia

Multiple sclerosis (symptomatictrigeminal neuralgia)

Thalamus (ventroposteriorthalamus)

Stroke, tumour, abscess

Cortical or subcortical pain

Stroke, tumour

Figure 1) Postoperative thoracolumbar spine x-ray showing spinal cordstimulation electrode with four contacts on T10-11 epidural space. Re-produced with permission from Medtronic Inc, Minneapolis

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system. The development of percutaneous placement of elec-

trode arrays and of improved programmable implanted elec-

tronics have been major technical advances in the application

of SCS in patients with intractable neuropathic pain.

A temporary, percutaneous electrode is first placed in the

patient under local anesthesia and connected to a temporary

stimulation device either in a fluoroscopy suite or operating

room. A permanent implant with pulse generator may be in-

troduced to the patient if satisfactory pain results are ob-

tained during the trial period. Both percutaneous and

laminectomy designs for SCS electrodes are available. The

success rates reported in the literature on SCS have varied

widely, but recent long term follow-up studies based on third

party evaluations indicate 52% to 66% good to excellent re-

sults (7,8). As with PNS, SCS has the inherent advantage of a

low morbidity trial or test phase that is used as a predictor of

the long term effect.

Although intraspinal analgesic therapy is considered to be

more effective for nociceptive than for neuropathic pain, if

PNS or SCS is unsuccessful or inappropriate, a trial of in-

traspinal analgesic therapy may be warranted. The role of in-

traspinal (ie, intrathecal or epidural) infusion therapy in cases

of intractable neuropathic pain is not fully established, but up

to 50% of patients with neuropathic pain may be improved

by intrathecal or epidural analgesic substances (9,10). De-

spite the relative insensitivity of these pain states to systemic

narcotics, significant relief has been observed in some pa-

tients by using intraspinal narcotics. Moreover, the risk of

becoming dependent or addicted to these agents from long

term use seldom exists. Other drugs such as clonidine and

adenosine in intraspinal use are also reported to be effective

in refractory cases (11-13). However, these agents and other

newly introduced drugs are still considered investigational

for this application.

Deep brain stimulation (DBS) (Figure 2) may be appro-

priate for some patients with intractable neuropathic pain,

especially when other neuroaugmentation therapies fail.

Theoretically, pain may be modulated by stimulation or

lesioning of any of the following structures or regions of

brain related to ascending or descending pain pathways:

periaqueductal grey (PAG)/periventricular grey (PVG)

region, thalamus, internal capsule and medial lemniscus. Al-

though the mechanisms underlying the effects of DBS are

not established, possible mechanisms may involve opiate

mediation and activation of descending inhibitory pathways

for PVG/PAG stimulation (14), and inhibition of spinotha-

lamic neurons in dorsal horn or blockage of disrupted activ-

ity in various thalamic nuclei (15,16). DBS has the potential

to treat chronic pain of any etiology, in any location.

However, its success rate varies according to the nature of

pain, the site of stimulation and the criteria used to define

success. The range of success is typically from 30% to 70%

(17,18). This technique is not widely available, and as with

other surgically implanted pain therapies it remains expen-

sive. Recommended brain targets for DBS electrode implan-

tation to treat central pains related to deafferentation or

neuropathic pain (eg, anesthesia dolorosa, postcordotomy

dysesthesia, thalamic syndrome, brachial plexus avulsion,

postherpetic neuralgia, and spinal and peripheral nerve inju-

ries) are thalamic sensory relay nuclei, ventral posterior lat-

eral or ventral posterior medial, and the medial lemniscus or

internal capsule (19). However, implantation of electrodes on

the PVG region may be more suitable for patients with no-

ciceptive pain when other measures fail.

Electrodes are implanted stereotactically when the patient

is under local anesthesia supplemented as necessary by in-

travenous midazolam and/or fentanyl. Electrodes are

introduced according to anatomical targets, based on pre-

operatively obtained anterior commissure and posterior com-


Surgery for chronic neuropathic pain

Figure 2) Configuration of implanted brain electrode and connections toremainder of deep brain stimulation equipment (top) and magnetic reso-nance imaging after implantation of a thalamic deep brain stimulationelectrode (bottom). Reproduced with permission from Medtronic Inc,Minneapolis, Minnesota

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missure coordinates from stereotactic magnetic resonance

images. Intraoperative physiological studies such as single

unit microelectrode recording, and micro- and macrostimu-

lation techniques greatly enhance the correct targeting before

implantation of the electrode. A trial stimulation period of

two to seven days is carried out. If significant pain relief en-

sues, the electrode is connected either to a radiofrequency re-

ceiver or to a fully implanted pulse generator for chronic

stimulation. The internalization procedure, which is done un-

der short general anesthesia, involves connecting the elec-

trode to a pulse generator subcutaneously, usually in the sub-

clavicular area. Although nociceptive pain is known to

respond better to DBS, about 30% to 60% of patients with

neuropathic pain are expected to have long term pain relief

from DBS (8,17). However, DBS is among the most invasive

techniques available and is associated with substantial mor-

bidity. The incidence of minor complications (electrode dis-

lodgement, breakage, skin erosion infection) is approxi-

mately 10%, while the incidence of serious neurological

complications including intracerebral hemorrhage leading to

permanent neurological deficit is 2% to 3% with these proce-

dures.

Other areas of the brain have been studied for

stimulation-induced analgesia and pain relief for neuropathic

pain. In particular, chronic stimulation of the motor cortex

(Figure 3) has recently gained attention. Favourable results

have been reported for intractable central and neuropathic

pain of peripheral origin including thalamic pain, trigeminal

neuropathic pain, postherpetic neuralgia pain, bulbar pain of

Wallenberg syndrome, and pain from peripheral nerve or spi-

nal cord injuries (20-24). Again, the therapeutic mechanism

underlying motor cortex stimulation is unclear, but it has

been proposed that precentral stimulation activates non-

nociceptive neurons in the sensory cortex, which may then

act to inhibit presumed hyperactive nociceptive cortical neu-

rons (24). The surgical procedure is similar to that of DBS,

except that mapping of the motor cortex is necessary by in-

traoperative somatosensory-evoked potentials. Although this

technique is not widely investigated, it appears to be a new

and promising possibility of pain treatment, especially in

cases with chronic, refractory neuropathic pain.

Ablative procedures in the spinal cord such as cordotomy

have been used in some patients with intractable nonmalig-

nant pain but are known to be more effective in nociceptive

pain than in neuropathic pain conditions. Cordotomy is sel-

dom used to treat disorders, except malignant diseases, be-

cause of concern about the development of postcordotomy

dysesthesia or fading of the level of pain relief with time.

Dorsal root entry zone (DREZ) lesions, however, can be

uniquely effective in select cases of intractable neuropathic

pain, including roots or plexus avulsions and postparaplegic

pain, with long term success rates often greater than 50%.

The segmental, end zone pain of spinal cord injury may also

respond to DREZ lesions; the more diffuse, distal pain fol-

lowing spinal cord injury tends to be refractory. Also, it is not

as successful for the treatment of postamputation stump pain

(25). DREZ destroys the dorsal horn (including substantia

gelatinosa), Lissauer’s tract, and the adjacent portion of the

posterior and lateral funiculi, thus inhibiting incoming no-

ciceptive inputs and modulating signals descending via the

Raphe spinal, reticulospinal and cortical spinal tracts. After

laminectomy and dural opening at appropriate levels have

been achieved under general anesthesia, the electrode is in-

troduced to a depth of 2 mm, and the lesion is generally made

by heating the radio frequency (RF) electrode tip to 75°C and

holding the temperature for 15 s. Successive lesions are

spaced 2 mm apart, and spinal cord function is monitored by

using somatosensory- and motor-evoked potential during the

operation. In summary, pain recalcitrant to conventional

therapy, in cases of neuropathic pain due to brachial plexus

injury, is seen in about one-third of patients and causes sig-

nificant disability. DREZ lesions mitigate this pain in ap-

proximately 60% of patients (26). In addition, although up to

50% of patients experience some neurological deficits fol-

lowing surgery, this occasionally results in worsening of

functional impairment.

Intracranial ablative procedures, including medial thala-

motomy, mesencephalic tractotomy, anterior capsulotomy,

hypophysectomy and cingulotomy, have been used primarily

in terminally ill patients with cancer-related pain. However,

these procedures have often been associated with recurrence

or worsening of pain after the procedure. Cingulotomy le-

sions neurons and interrupts the Papez circuit of the limbic

system; its target is the anterior cingulated gyrus, caudal por-

tion, area 24. The recommended target for thalamotomy is

the medial thalamus, involving the central lateral or parafas-

cicular nucleus (27). The results, however, do not seem to be

as good as those of DBS and are usually short lived. Overall,

these procedures have limited indications, are used infre-

quently and are not generally applicable to patients with

chronic neuropathic pain. However, with improved stereo-

tactic techniques guided by better imaging systems, refined

microelectrode recordings and stimulation techniques; rela-


Park and Lozano

Figure 3) Postoperative skull x-ray showing electrodes placed on motorcortex for chronic stimulation

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tively low morbidity; lower cost than that of augmentative

procedures; and lack of need for general anesthesia, they may

be suitable in certain circumstances.

Generally, patients with trigeminal neuralgia are managed

by medical treatment. However, up to 30% of patients will

ultimately require more aggressive therapy. There are two

common mainstays of surgical therapy for these patients (ie,

percutaneous trigeminal gangliolysis and microvascular

decompression), both with similar high success rates (70%

to 90%) of long lasting or even permanent pain relief (28-30).

Recently, radiosurgery with gamma knife for chronic pain

has been used by several investigators with some promising

results (31-34). The role of radiosurgery in disorders such as

trigeminal neuralgia is being studied (35,36). Although it is a

noninvasive procedure to the brain, it may produce unpre-

dictably large lesions, and until well-designed, long term

follow-up studies are available, this technique remains

speculative.

CONCLUSIONSThe main challenge facing the treatment of neuropathic painis the incomplete understanding of its pathogenesis andconsequently the limited success of its treatment. The selec-tion of patients who are likely to respond to surgery and the

choice of the surgical procedure should be carefully decidedbased on diligent evaluation.

Some surgical interventions have substantial potential

morbidity, and this must be considered before deciding to op-

erate. Also, no one neurosurgical procedure can relieve the

pain complaints of all patients, and surgery performed be-

cause there is ‘nothing left to try’ is most likely to fail.

Whichever procedure is chosen or intended, treating neuro-

surgeons should have the necessary neuroscience background

and surgical skills to be an important member of the team car-

ing for these multifaceted, chronically ill patients.

Neurosurgical strategies will be more diverse, and neuro-

surgery will likely offer better and more options for the man-

agement of chronic neuropathic pain syndromes in the future.

These strategies will be driven by a better understanding of

basic pathophysiological mechanisms underlying neuropathic

pain. Animal models of chronic neuropathic pain are available

to test novel strategies. Further, the available surgical proce-

dures (eg, SCS, DBS and chronic cortical stimulation) are be-

ing refined and will be more widely available. Other

promising modes of therapies (eg, transplantation, gene ther-

apy) are also being intensely investigated. Advances in these

surgical and pharmacological strategies will make a signifi-

cant impact on the treatment of pain of neural origin.

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