For pain medication, see Analgesics, page 44.
Major types of pain:
1. nociceptive
A. somatic: well localized. Described as sharp, stabbing, aching or cramping. Results from tissue injury or inflammation, or from nerve or plexus compression. Responds to treating the underlying pathology or by interrupting the nociceptive pathway
B. visceral: poorly localized. Poor response to primary pain medications
2. deafferentation: poorly localized. Described as crushing, tearing, tingling or numbness. Also causes burning dysesthesia numbness often with lancinating pain, and hyperpathia. Unaffected by ablative procedures
3. “sympathetically maintained” pain and the likes (e.g. causalgia): see page 576
20.1. Neuropathic pain syndromes
Definition: Neuropathic pain: pain caused by a lesion of the peripheral and/or central nervous system manifesting with sensory symptoms and signsA.
A. Backonja1 modified from the International Association for the Study of Pain2
Neuropathic pain syndromes (NPS) are typified by painful diabetic neuropathy (PDN) and postherpetic neuralgia (PHN). Common chronic NPSs are shown in Table 20-13, divided into central or peripheral nervous system origin of the pain. The pain of PDN and PHN is typically burning and aching, and is continuous. and is characteristically refractory to medical and surgical treatment.
Table 20-1 Common neuropathic pain syndromes
|
Peripheral neuropathic pain |
|
acute & chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) alcoholic polyneuropathy chemotherapy induced polyneuropathy complex regional pain syndrome (CRPS) entrapment neuropathies HIV sensory neuropathy iatrogenic neuralgias (e.g. postthoracotomy pain) idiopathic sensory neuropathy neoplastic nerve compression or infiltration nutritional-deficiency neuropathies painful diabetic neuropathy (PDN) phantom limb pain postherpetic neuralgia (PHN) postradiation plexopathy radiculopathy toxic exposure-related neuropathies trigeminal neuralgia posttraumatic neuralgias |
|
Central neuropathic pain |
|
cervical spondylotic myelopathy HIV myelopathy multiple sclerosis-related pain Parkinson disease-related pain postischemic myelopathy postradiation myelopathy poststroke pain posttraumatic spinal cord injury pain syringomyelia |
MEDICAL TREATMENT OF NEUROPATHIC PAIN
Treatment traditionally includes narcotic analgesics4, and tricyclic antidepressants (see below). For further details and other treatment measures, see page 796 for PDN, and page 565 for PHN.
Tricyclic antidepressants: Use is often limited by anticholinergic and central effects and by limited pain relief5, 6. Possibly because serotonin potentiates the analgesic effect of endorphins and elevates pain thresholds, serotonin re-uptake blockers are more effective than norepinephrine re-uptake blockers, e.g. tranzodone (Desyrel®) blocks only serotonin. Also useful: amitriptyline (Elavil®) 75 mg daily; desipramine (Norpramin®) 10-25 mg/d; doxepin (Sinequan®) 75-150 mg/d. Some benefit may also derive from the fact that many patients with chronic pain are depressed. SIDE EFFECTS: anticholinergic effects and orthostatic hypotension, especially in the elderly. ✖ Not recommended for use in patients with ischemic heart disease.
Gabapentin: Effective in postherpetic neuralgia (PHN) (see page 566) and painful diabetic neuropathy. Benefit also reported in pain associated with: trigeminal neuralgia, cancer7, multiples sclerosis, HIV-related sensory neuropathy, CRPS, spinal cord injury, post-operative state8, migraine9 (a number of these studies may have been sponsored by the manufacturer10). See page 416 for side effects, dosing & availability…
Lidocaine patch (Lidoderm®): may be effective3. Rx: apply patch for up to 12 hrs/day up to a maximum of 3 patches at a time to the intact skin over the most painful area (may trim patch to appropriate size). SUPPLIED: 5% lidocaine (see page 566).
Tramadol (Ultram®): A centrally acting analgesic3 (see page 47).
20.2. Craniofacial pain syndromes
Possible pathways for facial pain include: trigeminal nerve (portio major as well as portio minor (motor root)), facial nerve (usually deep facial pain), and eighth nerve11. Etiologies (adapted12 (p 2328), 13).
1. cephalic neuralgias
A. trigeminal neuralgia (see below)
1. vascular compression of V at root entry zone: the most common cause
2. MS: plaque within V nerve
B. glossopharyngeal neuralgia: pain usually in base of tongue and adjacent pharynx (see page 563)
C. geniculate neuralgia: otalgia and deep prosopalgia (see page 563)
D. tic convulsif: geniculate neuralgia with hemifacial spasm (see page 564)
E. occipital neuralgia: see page 804
F. superior laryngeal neuralgia: a branch of the vagus, results primarily in laryngeal pain and occasionally pain on the auricle
G. sphenopalatine neuralgia
H. herpes zoster: pain is continuous (not paroxysmal). Characteristic vesicles and crusting usually follow pain, most often in distribution of V1 (isolated V1 TGN is rare). In rare cases without vesicles, diagnosis may be difficult
I. postherpetic neuralgia (Ramsay-Hunt syndrome): see page 564
J. supraorbital neuralgia (SON) (see page 562)
K. trigeminal neuropathic pain (AKA trigeminal deafferentation pain)13: may follow injuries from sinus or dental surgery, head trauma
L. trigeminal deafferentation pain: follows trigeminal denervation including therapeutic measures to treat trigeminal neuralgia13
M. short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)14: rare. Usually affects males 23-77 years old. Brief (< 2 minutes) pain (burning, stabbing or shock-like) usually near the eye, occurring multiple times per day. Associated autonomic findings (the “hallmark of SUNCT”): ptosis, conjunctival injection, lacrimationA, rhinorrhea, hyperemia. May be due to CPA AVM. Microvascular decompression or trigeminal rhizotomy may be effective in some cases refractory to medical treatment with AEDs or corticosteroids
2. ophthalmic pain
A. Tolosa-Hunt syndrome (page 837): painful ophthalmoplegia
B. (Raeder’s) paratrigeminal neuralgia (page 838): unilateral Horner’s syndrome + trigeminal neuralgia
C. orbital pseudotumor (page 837): proptosis, pain, and EOM dysfunction
D. diabetic (oculomotor) neuritis
E. optic neuritis
F. iritis
G. glaucoma
H. anterior uveitis
3. otalgia (see below)
4. masticatory disorders
A. dental or periodontal disease
B. nerve injury (inferior and/or superior alveolar nerves)
C. temporo-mandibular joint (TMJ) dysfunction
D. elongated styloid process
E. temporal & masseter myositis
5. vascular pain syndromes
A. migraine headaches: see Migraine, page 57
1. simple migraine
a. classic
b. common
2. complicated migraine
a. hemiplegic
b. ophthalmoplegic
B. cluster H/A (subtypes: episodic, chronic, chronic paroxysmal hemicrania) (see page 58)
C. giant cell arteritis (temporal arteritis): see page 74. Tenderness over STA
D. toxic or metabolic vascular H/A (fever, hypercapnia, EtOH, nitrites, hypoxia, hypoglycemia, caffeine withdrawal)
E. hypertensive H/A
F. aneurysm or AVM (due either to mass effect or hemorrhage)
G. carotidynia: e.g. with carotid dissection (see page 1162)
H. basilar dolichoectasia with fifth n. compression or indentation of the pons
6. sinusitis (maximally, frontal, ethmoidal, sphenoidal)
7. dental disease
8. neoplasm: may cause referred pain or fifth nerve compression
A. extracranial
B. intracranial tumor: primarily posterior fossa lesions, neoplastic compression of trigeminal nerve usually causes sensory deficit (see Tumors and trigeminal neuralgia, page 552)
9. atypical facial pain (AFP) (prosopalgia): traditionally a “wastebasket” category used for many things. It has been proposed13 to reserve this term for a psychogenic disorder. May be suspected by
10. primary (nonvascular) H/A: including
A. tension (muscle contraction) H/A
B. post-traumatic H/A
A. lacrimation (the most common) or other autonomic signs may occur in V1 trigeminal neuralgia but are usually mild, and appear only in the later stages of the condition and with long lasting attacks15. Dramatic lacrimation and conjunctival injection from the onset of symptoms with SUNCT are the best characteristics to distinguish this from trigeminal neuralgia16. May also occur in cluster headache (see page 58)
OTALGIA
Because of redundant innervation of the region of the ear, primary otalgia may have its source in the 5th, 7th, 9th, or 10th cranial nerves or the occipital nerves17. As a result, sectioning of the 5th, 9th or 10th nerve or a component of the 7th (nervus intermedius, chorda tympani, geniculate ganglion) has been performed with varying results18. Also, microvascular decompression (MVD) of the corresponding nerve may also be done19.
Work-up includes: neurotologic evaluation to rule out causes of secondary otalgia (otitis media or externa, temporal bone neoplasms…). CT or MRI should be done in any case where no cause is found.
Primary otalgia
Primary otalgia is unilateral in most (≈ 80%). Trigger mechanisms are identified in slightly more than half, with cold air or water being the most common18. About 75% have associated aural symptoms: hearing loss, tinnitus, vertigo. Pain relief upon cocainization or nerve block of the pharyngeal tonsils suggests glossopharyngeal neuralgia (see page 563), however, the overlap of innervation limits the certainty.
An initial trial with medications used in trigeminal neuralgia (carbamazepine, phenytoin, baclofen…, see page 552) is the first line of defense. In intractable cases not responding to pharyngeal anesthesia, suboccipital exploration of the 7th (nervus intermedius) and lower cranial nerves may be indicated. If significant vascular compression is found, one may consider MVD alone. If MVD fails, or if no significant vessels are found, Rupa et al. recommend sectioning the nervus intermedius, the 9th and upper 2 fibers of 10th nerve, and a geniculate ganglionectomy (or, if glossopharyngeal neuralgia is strongly suspected, just 9th and upper 2 fibers of 10th)18.
20.2.1. Trigeminal neuralgia
Key concepts:
• sharp. electric shock-like paroxysmal lancinating pain in the distribution of one or more branches of the trigeminal nerve on one side
• characterized by periods of remission and initial response to carbamazepine
• neurologic exam must be intact (only exception: mild sensory loss)
• 80-90% of cases are caused by compression of the trigeminal nerve at the root entry zone by the superior cerebellar artery (SCA). In MS patients, may be due to MS plaque (MS patients are usually less responsive to procedures)
• 75% will ultimately fail medical therapy and require a procedure (main options: microvascular decompression, percutaneous rhizotomy or radiosurgery). Choice of modality depends on patient age, location of symptoms, prior treatment…
Trigeminal neuralgia (TGN) (AKA tic douloureux): paroxysmal lancinating electric-like pain lasting a few seconds, often triggered by sensory stimuli, confined to the distribution of one or more branches of the trigeminal nerve (see Figure 20-1) on one side of the face, with no neurologic deficit. The term “atypical facial pain” (AFP) is sometimes used to describe any other type of facial pain.
Rarely, TGN manifests as status trigeminus, a rapid succession of tic-like spasms triggered by seemingly any stimulus. IV carbamazepine (where available) or phenytoin may be effective for this.
Figure 20-1 Pain/temperature innervation of the head*
* KEY: V1 = ophthalmic nerve; V2 = maxillary nerve; V3 = mandibular nerve; IX = glossopharyngeal nerve; X = vagus
EPIDEMIOLOGY
See Table 20-2. Annual incidence 4/100,000. There is no correlation with herpes simplex infection20. There is a tendency for spontaneous remission with pain free intervals of weeks or months being characteristic, regardless of treatment. 2% of patients with MS have TGN21, whereas ≈ 18% of patients with bilateral trigeminal neuralgia have MS22.
PATHOPHYSIOLOGY
Probably due to ephaptic transmission in trigeminal nerve from large-diameter partially demyelinated A fibers to thinly myelinated A-delta and C (nociceptive) fibers. Pathogenesis may be due to:
1. vascular compression of the trigeminal nerve at the root entry zone (NB: compression may be seen in up to 50% of autopsies in patients without TGN25):
A. most commonly (80%) by the SCA (see Neurovascular compression syndromes, page 542 for more details)
B. persistent primitive trigeminal artery26 (see page 107)
C. dolichoectatic basilar artery27 (p 1108)
2. posterior fossa tumor (see Tumors and trigeminal neuralgia below)
3. in MS, plaque within brainstem may cause TGN that is often poorly responsive to microvascular decompression
In addition to the sensory division of the trigeminal nerve, other possible pain path-ways include11: the motor branch of the 5th nerve (portio minor), or the 7th or 8th nerve.
EVALUATION
MRI is often used to evaluate these patients for possible intracranial tumors or MS plaques, especially in cases with atypical features. The yield in typical cases is low.
Table 20-2 Epidemiology of trigeminal neuralgia23, 24
|
age (years) |
typically > 50 (average 63) |
|
female:male |
1.8:1 |
|
Laterality |
|
|
right |
60% |
|
left |
39% |
|
both |
1% |
|
Division involved |
|
|
V1 only |
2% |
|
V2 only |
20% |
|
V3 only |
17% |
|
V1 & V2 |
14% |
|
V2 & V3 |
42% |
|
all three |
5% |
Differential diagnosis
See Craniofacial pain syndromes on page 549.
History and physical (in addition to routine)
• history
A. accurate description of pain localization to determine which divisions of trigeminal nerve need to be treated
B. determine time of onset of TGN, trigger mechanisms
C. ascertain presence and length of pain-free intervals (lack of any pain-free interval is atypical for TGN)
D. determine duration, side-effects, dosages, and responses to medications tried
E. inquire about symptoms that may indicate the presence of conditions other than TGN: e.g. history of herpetic vesicles, excessive tearing of the eye (may indicate SUNCT (page 549)), facial twitching (tic convulsif), tongue pain (glossopharyngeal neuralgia), sensory loss (tumor…), progressive relentless pain (tumor, herpes…), symptoms that suggest MS
• physical exam: the exam should be normal in TGN, any neurologic deficit (except very mild sensory loss) in previously unoperated patient should prompt search for structural cause, e.g. tumor (see below). This exam also serves as a baseline for post-op comparison
A. assess sensation in all 3 divisions of trigeminal nerve bilaterally (include corneal reflexes)
B. assess masseter function (bite) and pterygoid function (on opening mouth, chin deviates to weak side)
C. assess EOM function
TUMORS AND TRIGEMINAL NEURALGIA
In > 2000 patients with facial pain seen over 10 yrs, only 16 harbored tumor (< 0.8% incidence)28. 3 tumors outside cranial vault included nasal carcinoma and skull base mets; all had hypalgesia and AFP. 6 middle fossa tumors included 2 meningiomas, 2 schwannomas (1 primary tumor of Gasserian ganglion), and 1 pituitary adenoma. Posterior fossa tumors are the most likely to cause symptoms that most closely resemble true TGN; of these, vestibular schwannoma (VS) is most common. 2 of 7 VSs had tumors contralateral to the neuralgia (presumably due to brainstem shift). Patients with true TGN initially responded to carbamazepine, none with AFP did.
When facial pain is caused by tumor, especially with peripheral tumors, the pain is frequently atypical (usually constant), neurologic abnormalities are often present (usually sensory loss, although some are neurologically normal at first), and the age is often younger than typical TGN.
MEDICAL THERAPY FOR TRIGEMINAL NEURALGIA
carbamazepine (Tegretol®)DRUG INFO
Complete or acceptable relief in 69% (if 600-800 mg/d are tolerated and give no relief, diagnosis of TGN is suspect21). SIDE EFFECTS: Drowsiness. Rash in 5-10%. Possible Stevens-Johnson syndrome. Relative leukopenia is common (usually does not require discontinuing drug). See precautions under carbamazepine (CBZ) (Tegretol®) on page 411.
Rx 100 mg PO BID, increase by 200 mg/d up to maximum of 1200 mg/d divided TID. SUPPLIED: see page 411.
oxcarbazepine (Trileptal®)DRUG INFO
Rapidly metabolized to carbamazepine, similar efficacy, often tolerated at higher doses than carbamazepine. SIDE EFFECTS: symptomatic hyponatremia.
Rx for trigeminal neuralgia: 300 mg PO BID, increase by 600 mg/d q week. Usual dose: 450-1200 mg. Maximum of 2400 mg/d. SUPPLIED: 150, 300, 600 mg tablets; 500 mg/5-ml suspension.
baclofen (Lioresal®)DRUG INFO
2nd DOC (not as effective as carbamazepine, but fewer side-effects). Caution: teratogenic in rats. Avoid abrupt withdrawal (can cause hallucinations and seizures). May be more effective if used in conjunction with low dose carbamazepine.
Rx Start low, 5 mg PO TID, increase q 3 d by 5 mg/dose; not to exceed 20 mg QID (80 mg/d); use smallest effective dose.
gabapentin (Neurontin®)DRUG INFO
An anticonvulsant (see page 416), may act synergistically with carbamazepine and baclofen. SIDE EFFECTS: include ataxia, sedation and rash.
Rx start with 100mg po BID, titrate to 5-7mg/kg/day (3600 mg/d max).
MISCELLANEOUS DRUGS
Also possibly effective:
1. phenytoin (Dilantin®): may be useful IV in patients in too much pain to open their mouths to take carbamazepine orally (see page 409 for dosages)
2. capsaicin (Zostrix®): 1 gm applied TID for several days resulted in remission of symptoms in 10 of 12 patients (4 relapsed in < 4 mos, but remained pain free for 1 yr after 2nd course)29
3. clonazepam (Klonopin®): works in 25% (see page 415)
4. lamotrigine (Lamictal®)
5. amitriptyline (Elavil®): more commonly used for atypical facial pain
6. botulinum toxin (Botox®): reduces transmission of CGRP producing a direct effect on the sensory nerve fibers
SURGICAL THERAPY FOR TRIGEMINAL NEURALGIA
Reserved for cases refractory to medical management, or when side effects of medications exceed risks and drawbacks of surgery.
SURGICAL OPTIONS
1. peripheral trigeminal nerve branch procedures to block or ablate the division involved with pain, or can be used to block the trigger30:
A. means of blocking
1. local blocks (phenol, alcohol) s
2. neurectomy of trigeminal branch involved
B. nerve branches:
1. V1 (ophthalmic division) at the supraorbital, supratrochlear, or infraorbital nerves
2. V2 (maxillary division) at the foramen rotundum
3. V3 (mandibular division) block at the foramen ovale, or neurectomy of inferior dental nerve
2. blocking the trigger: either via percutaneous rhizotomy or alcohol block
3. percutaneous trigeminal rhizotomy (PTR): AKA percutaneous (stereotactic) rhizotomy (PSR) of trigeminal (Gasserian) ganglion (see below) (not truly a stereotactic procedure in the current sense of the word, therefore the term percutaneous trigeminal rhizotomy is preferred). Objective is to selectively destroy A-delta and C fibers (nociceptive) while preserving A-alpha and beta fibers (touch). Ideally, a retrogasserian lesion (not a ganglionic lesion). May also be used to block trigger. Lesioning techniques include (see below for comparison of techniques):
A. radiofrequency rhizotomy (RFR) (originated by Sweet and Wespic31). Uses radiofrequency energy to thermocoagulate the pain fibers. Requires the patient to be awake at intervals during the procedure
B. glycerol injection into Meckel’s cave32, 33: possibly lower incidence of sensory loss and anesthesia dolorosa than with radiofrequency lesion34. Water soluble contrast cisternography was recommended in original description, may not be essential35
C. mechanotrauma (percutaneous microcompression (PMC) rhizolysis): via inflation of No. 4 Fogarty catheter balloon36-38. Does not require the patient to be awake
D. injection of sterile boiling water
4. intradural retrogasserian trigeminal nerve section (sensory portion ± motor root, see below): may be performed during MVD if no vascular compression is identified
5. cutting descending trigeminal tract in lower medulla (99.5% success): rarely used
6. microvascular decompression (MVD)39: (see below) microsurgical exploration of root entry zone, usually via posterior fossa craniectomy, and displacement of vessel impinging on nerve (if such a vessel is found). Usually with the placement of a non-absorbable “insulator” (Ivalon® sponge or shredded Teflon felt - see page 543 for relative merits of Ivalon® vs. Teflon felt)
7. complete section of the nerve proximal to the ganglion via a p-fossa crani
8. stereotactic radiosurgery: see below
9. motor cortex stimulation40: (somewhat analogous to spinal cord stimulation for spinal or extremity pain). Better for neuropathic trigeminal pain (as distinct from trigeminal neuralgia)
SELECTION OF SURGICAL OPTION
Some pearls that influence treatment option choices (expert opinion41):
1. V3 neuralgia: RF. Can selectively treat V3 without involving other divisions
2. V1 or V2: balloon compression. Causes numbness in all 3 divisions, but unlike RF the corneal numbness is better tolerated and the corneal reflex is often preserved
3. bilateral pain: glycerol. It has the shortest duration of effect, which is an advantage if you think you may need to treat the other side at some point
4. SRS: due to latency until pain relief, suboptimal for patients who need immediate pain relief
Peripheral nerve ablation and neurectomies
Limited to pain or trigger points in territory of supraorbital/supratrochlear, infraorbital, or inferior dental nerves. Neurectomy may be a consideration especially for elderly patients who are not candidates for MVD (neurectomy may be done under local anesthesia) with pain in the forehead (to avoid anesthesia of the eye, as could occur with RFR). Disadvantages include sensory loss in the distribution of the nerve and a high rate of pain recurrence due to nerve regeneration (usually in 18-36 months) which often responds to repeat neurectomy42. May also be used following PTR.
Supraorbital and supratrochlear nerve: For information on supraorbital neuralgia (SON) or supratrochelar neuralgia (STN), see page 562. SON may be treated with rhizotomy (e.g. with alcohol or radiofrequency) or with neurectomy. Alcohol injection is used with caution for STN because of risk of injury to the superior oblique muscle. For neurectomy, these nerves are exposed through a 2 cm incision parallel to and just above the medial portion of the eyebrow (never through the eyebrow as this can create an unsightly “bi-brow”; shaving the eyebrow is also discouraged since it occasionally does not grow back). The incision is carried down to the bone and the periosteum is elevated caudally towards the supraorbital foramen or notch. The nerves will be visible on the undersurface of the periosteal flap. The supraorbital nerve is freed in its foramen/notch, and is then avulsed by grasping it with a mosquito hemostat and twisting the clamp. The nerve avulses “like pulling a worm out of a hole”. The distal portion of the nerve should be located at the site were the periosteum was incised and it, too, should be avulsed. The process can be repeated for the more medially situated supratrochlear nerve.
Other nerves: Not covered here, other nerve branches that may be cut or avulsed include: infratrochlear, lacrimal (the branch of V1 at the lateral edge of the orbit), infraorbital nerve, inferior alveolar, lingual and mental nerves43 (p 290).
Percutaneous trigeminal rhizotomy (PTR)
Recommended for patients who: are poor risk for general anesthesia (elderly or those with increased risk for general anesthesia), wish to avoid “major” surgery, have unresectable intracranial tumors, have MS, have impaired hearing on the other side, or have limited life expectancy (< 5 yrs)34. For “atypical facial pain”, denervating the painful region of the face benefits < 20% of patients, and worsens 20%44. Recurrences are easily treated by repeat procedures. May be used to treat failures of peripheral nerve ablation.
Choice of lesion technique:
Recurrence rates and incidence of dysesthesias are comparable among the various lesioning techniques. Incidence of intraoperative hypertension is less with PMC than with radiofrequency rhizotomy (RFR)lesion38 (no reports of intracerebral hemorrhage). Bradycardia occurs regularly with PMC which may not be harmful (some prophylax with atropine45). RFR requires a patient who is able to cooperate; PMC can be done with the patient asleep. Paralysis of ipsilateral trigeminal motor root (e.g. pterygoids) is more common after PMC (usually temporary) than RFR, and so PMC should not be done if there is already contralateral paralysis from a previous procedure. See page 556 for technique.
Microvascular decompression (MVD)
(For more details, see page 559).
Recommended for patients with inadequate medical control of pain with > 5 years anticipated survival and able to tolerate a small craniotomy34 (surgical morbidity increases with age). Relief is often long lived, persevering 10 yrs in 70%. Incidence of facial anesthesia is much less than with PTR, and anesthesia dolorosa does not occur. Mortality: < 1%. Incidence of aseptic meningitis (AKA hemogenic meningitis): 20%. 1-10% major neurologic morbidity. Failure rate: 20-25%.
1-2% of patients with MS will have a demyelinating plaque at the root entry zone, this usually does not respond to MVD, and one should attempt a PTR.
Stereotactic radiosurgery (SRS)
The first use of SRS by Leksell was for the treatment of TGN. Initially, this was reserved for refractory cases following multiple operations46, now becoming more widely practiced. The least invasive procedure. Generally recommended for patients with comorbidities, high-risk medical illness, pain refractory to prior surgical procedures, or those on anticoagulants (anticoagulation does not have to be reversed to have SRS).
Treatment plan: 4 -5 mm isocenter in the trigeminal nerve root entry zone identified on MRI. Use 70-80 Gy at the center, keeping the 80% isodose curve outside of the brainstem.
Results: Significant pain reduction after initial SRS: 80-96%47-50, but only ≈ 65% become pain free. Median latency to pain relief: 3 months (range: 1 d-13 months)51. Recurrent pain occurs within three years in 10-25%. Patients with TN and multiple sclerosis are less likely to respond to SRS than those without MS. SRS can be repeated, but only after four months following the original procedure.
Favorable prognosticators: higher radiation doses, previously unoperated patient, absence of atypical pain component, normal pretreatment sensory function52.
Side effects: Hypesthesia occurred in 20% after initial SRS, and in 32% of those requiring repeat treatment51 (higher rates associated with higher radiation doses48).
MANAGEMENT OF TREATMENT FAILURES
90% of recurrences are in distribution of previously involved divisions; 10% are in new division and may represent progression of the underlying process. Some treatment failures are not persistent TN, but rather represent trigeminal neuropathic pain (AKA trigeminal deafferentation pain).
PTR may be repeated in patients who have a recurrence with some preservation of facial sensation. Attempted repeat PTR is often productive, and failures can be managed as below.
MVD may be performed in patients failing PTR, but the success rate may be reduced53 (91% for patients undergoing MVD first, vs. 43% for those having MVD following PTRA). Repeat MVD may also be performed, with attention given to possible slippage of the insulating sponge, or the fact that the true offending vessel may be “artificially” moved away from the nerve secondary to the surgical positioning.
A. 91% may be an unrealistically high success rate, and taking patients that fail PTR may select for a more difficult subgroup
SRS can be repeated, using the same dose, with reported significant reduction in pain in 89%, and complete relief in 58%51.
Intradural retrogasserian trigeminal nerve section
May be used as a measure of last resort in patients who have recurrent TGN following one or more PTRs in the presence of total facial anesthesia, or in patients undergoing posterior-fossa craniectomy for the purpose of MVD when no impinging vessel can be identified. In the latter case, a partial rhizotomy is performed by sectioning 2/3 of nerve, with resulting partial anesthesia. In the case of patients with facial anesthesia pre-op, consideration should be given to sectioning the motor division (portio minor) as an alternate pain pathway11.
PERCUTANEOUS TRIGEMINAL RHIZOTOMY (PTR)
Due to concerns about hemorrhage, check coagulation profile (PT/PTT, consider bleeding time), and discontinue ASA and NSAIDs, preferably 10 days pre-op. Procedure may be performed in OR with fluoro, or in angiography suite in x-ray department.
BOOKING THE CASE - PERCUTANEOUS TRIGEMINAL RHIZOTOMY
(For any of the percutaneous methods: balloon, glycerol, RFR)
Also see defaults & disclaimers (page v) and pre-op orders (see below).
1. position: supine
2. anesthesia: MAC with sedation
3. equipment:
A. lesion generator and needle kit for radiofrequency rhizotomy
B. C-arm fluoroscopy (2 C-arms for balloon compression)
C. calibrated inflatable balloons (as in kyphoplasty) for balloon rhizotomy
4. consent (in lay terms for the patient - not all-inclusive):
A. procedure: put a needle into the cheek to numb the nerve to the face
B. alternatives: medical treatment, surgery through the back of the skull (microvascular decompression), radiation (stereotactic radiosurgery)
C. complications: facial numbness is anticipated, rarely: stroke, bleeding, blindness
PRE-OP ORDERS (RFR)
1. NPO after MN except meds
2. continue Tegretol® & other meds PO with sips of water
3. AM of procedure: IV NS @ KVO in arm contralateral to neuralgia
4. atropine 0.4 mg IM PRN (✖ contraindications include rapid a-fib)
5. non-disposable LP tray to accompany patient
TECHNIQUE PERCUTANEOUS TRIGEMINAL RADIOFREQUENCY RHIZOTOMY (RFR)
Adapted technique54. NB: needle insertion and/or lesioning may cause HTN, consider monitoring BP. Use either a straight electrode (bare 5 mm for 1 division, 7.5 mm for 2 divisions, or 10 mm for total lesions) or a curved electrode55.
Electrode insertion
1. attach ground electrode to patient’s upper arm
2. prep the cheek on the involved side with Betadine
3. entry point: under short-acting anesthetic agent (e.g. propofol (Diprivan® - see page 24) or methohexital (Brevitol® - see page 24), insert electrode-needle 2.5-3 cm lateral to oral commissure
4. trajectory:
A. palpate the buccal mucosa with a gloved finger inside the mouth (lateral to the teeth) and with the other hand pass the electrode medial to the coronoid process of the mandible (keeping the needle deep to the oral mucosa, i.e. outside the oral cavity) initially aiming towards the plane intersecting a point 3 cm anterior to EAM and the medial aspect of the pupil when the eye is directed forward. Be careful not to contaminate the field with the hand that was in the patient’s mouth
B. as insertion progresses, use fluoroscopy to direct the tip towards the intersection of the top of the petrous bone with the clivus (5-10 mm below floor of sella along clivus)
C. upon entering foramen ovale the masseter often contracts, causing the jaw to briefly close. Remove the stylet, look for CSF to verify location (may not occur in re-do cases), and insert electrode through needle
In difficult cases, intraoperative fluoroscopy may assist in localizing the needle to Meckel’s cave and to R/O e.g. entry into superior orbital fissure (which can cause blindness after lesioning), or entry into foramen spinosum (middle meningeal artery). If necessary to visualize (e.g. when there is difficulty entering), the foramen ovale is optimally seen on a submental x-ray by hyperextending neck 20° and rotating head 15-20° away from side of pain56.
Impedance measurements: from the tip of the electrode when available may help indicate location of needle tip. Impedance: CSF (or any fluid) low (≈ 40-120 Ω); connective tissue, muscle, or nerve is usually 200-300 Ω (may be up to 400 Ω); if > 400 Ω this likely indicates electrode is contacting periosteum or bone. After starting the lesion, impedance often goes down by 30 Ω transiently, and then as the lesioning continues it gradually returns to baseline or ≈ 20 Ω above it. If char develops on the electrode tip, the impedance will read higher than where it started.
Stimulation and repositioning
Once the foramen ovale is entered, the needle is positioned with the following guidelines: for V3 division lesion the curved electrode should be just short of the clivus and pointing down, for V2 it is at the clivus and directed up, for V1 it is 5 mm beyond clivus and pointing up. ✖ At no time should the needle tip extend > 8 mm beyond clival line (to avoid Cr. N. III or VI complications).
The patient is allowed to wake up and is stimulated through the electrode with the following settings: frequency = 50-75 Hz, 1 mS duration, start at 0.1 V amplitude and slowly increase (usually 0.2-0.5 V is adequate, higher voltages may indicate that the needle is not near the target and that stimulation is due to far-field currents, however, in previously lesioned patients up to 4 V may sometimes be necessary). If stimulation does not reproduce pain in the distribution of the patient’s TGN, then the amplitude is returned to 0, the electrode is repositioned (straight electrode: advance needle < 5 mm at a time, until the tip is in the vicinity of the clival line; curved tip electrode: advance and/or rotate) and then slowly elevate the voltage again from 0 and repeat the repositioning-stimulating process until stimulation reproduces the distribution of tic pain. If previous lesions have produced analgesia and the patient cannot feel the stimulating current, one may stimulate at 2 Hz. and watch for masseter twitch (requires preserved motor root).
Lesioning
When stimulation produces pain in the involved distribution of the TGN, perform the first lesion under short-acting anesthesia at 60-70° C x 90 sec. A facial flush may be noted56. After every lesion, perform a post-lesion assessment (see below). The goal is analgesia (but not anesthesia) in the areas of tic pain and hypalgesia in areas of trigger points. An average of three lesions are necessary at the first sitting, each ≈ 5° C higher than the previous for 90 seconds. Anesthetic may not be needed after the first lesion if moderate analgesia has been produced by previous lesions.
Post-lesion assessment
After each lesion and at completion of procedure, assess:
1. sensitivity to pinprick and light touch in all three divisions of trigeminal nerve (grading: normal, hypalgesic, analgesic, anesthetic)
2. corneal reflex bilaterally
3. EOM function
4. masseter muscle strength (patient clenches teeth, palpate cheeks for contraction)
5. pterygoid muscle strength (ask patient to open mouth, chin deviates towards side of pterygoid weakness)
POST-OP CARE (PTR)
Include in post-op orders:
1. ice pack to face on side of procedure for 4 hrs
2. soft diet
3. routine activity when alert
4. avoid narcotics (usually not necessary)
5. if corneal reflex impaired: risk of neuroparalytic keratitis. Natural tears 2 gtt q 2 hrs while awake to eye on affected side. Lacrilube® to eye & tape eye shut q hs
Prior to discharge from hospital, repeat post-lesion assessment (see above). Patients are then weaned off of carbamazepine as tolerated.
PERCUTANEOUS MICROCOMPRESSION RHIZOLYSIS BALLOON (PMC)
Via inflation of No. 4 Fogarty catheter balloon.
Technique
1. the needle is placed as with RFR (see page 556).
2. aim for balloon placement in the medial foramen ovale (to avoid entering the middle fossa). After placing the balloon, insert the stylet to visualize where the balloon will go. Use Omnipaque 240 to fill the balloon
3. inflate to 1.4 atmospheres of pressure
COMPLICATIONSA
1. mortality: only 17 deaths in over 22,000 procedures (includes lesser experienced neurosurgeons and patients often considered poor surgical risks)21
2. dysesthesias24 (sometimes called “annoying paresthesias”): higher rate in more complete lesions
A. minor: 9%
B. major (requiring medical treatment): 2%
C. anesthesia dolorosa (severe, constant, burning aching pain that is refractory to all treatment): 0.2-4%
3. meningitis23: 0.3%
4. alterations in salivation57: 20% (increased in 17%, decreased in 3%)
9. intracranial hemorrhage: personal report of 7 cases (6 fatal) in > 14,000 procedures, probably due to transient HTN (SBP up to 300 torr)
10. alterations in lacrimation57: 20% (increased in 17%, decreased in 3%)
11. herpes simplex eruption: prescribe antiherpetic drug if patient develops symptoms (e.g. Acyclovir® - see page 360)
12. bradycardia and hypotension: 1% with RFR, up to 15% with glycerol injection
13. rare58, 59:
A. temporal lobe abscess
B. intracerebral abscess: 0.1%
C. aseptic meningitis
D. trigeminal trophic syndrome (TTS)60: triad of unilateral crescentic nasal alar ulceration with anesthesia and paresthesia of the trigeminal dermatome (may present with severe pruritus and self-induced skin lesions from scratching). A result of trigeminal nerve injury. Treatment has included: carbamazepine, diazepam, amitriptyline, chlorpromazine, clonazepam or pimozide61
E. complications related to needle placement62:
1. carotid cavernous fistula (CCF): may occur with any percutaneous technique63 (including balloon microcompression64)
2. injury to other cranial nerves: II, III, IV, VI65
3. blindness: from penetration of inferior orbital fissure66
F. subarachnoid hemorrhage
G. seizures
A. NB: some “numbness” is actually expected in most successful PTRs and occurs in 98% of cases24, and is not considered a complication here
RESULTS (PTR)
Results of various PTR techniques compared to microvascular decompression (MVD) are shown in Table 20-3. Recurrence rate is higher in patients with multiple sclerosis (50% at 3 yrs mean F/U)67.
MICROVASCULAR DECOMPRESSION (MVD) FOR TRIGEMINAL NEURALGIA
Indications:
1. patients unable to achieve adequate medical control of trigeminal neuralgia with ≥ 5 yrs anticipated survival, without significant medical or surgical risk factors34 (although a small p-fossa exploration is usually well tolerated, surgical morbidity increases with age)
2. may be used in patients who do not fit the above criteria, but have intractable pain and fail PTR
3. patient with tic involving V1 for whom the risk of exposure keratitis due to corneal anesthesia would be unacceptable (e.g. already blind in contralateral eye) or patient wishing to avoid facial anesthesia for any reason
✖ patients with MS are usually not considered candidates for MVD due to low response rate
BOOKING THE CASE - MICROVASCULAR DECOMPRESSION
Also see defaults & disclaimers (page v) and pre-op preparation (see below).
1. position: park bench
2. equipment: microscope
3. implants: Ivalon sponge or shredded Teflon
4. intra-op monitoring: (optional) BAER, possible nervus intermedius
5. consent (in lay terms for the patient - not all-inclusive):
A. procedure: surgery behind the ear to move a blood vessel from the sensory nerve of the face, if no offending vessel can be identified then possible partial sectioning of the appropriate part of the trigeminal nerve with associated numbness)
B. alternatives: needle procedures through the cheek (percutaneous rhizotomy), radiation (stereotactic radiosurgery)
C. complications: (in addition to usual craniotomy complications), CSF leak, hearing loss, facial numbness, pain near incision (occipital neuralgia or lesser occipital neuralgia), rarely: diplopia, facial paralysis, failure of the procedure
TECHNIQUE
Also see Paramedian suboccipital craniectomy, page 154 for important pointers, including use of armored endotracheal tube.
Preoperative preparation
An MRI is recommended to rule-out mass lesion or vascular abnormality. Baseline BAER are performed by some68 (see below for intra-op monitoring).
O.R. setup
Setup for lateral oblique suboccipital (posterior-fossa) craniotomy (see page 154). Microscope: observer’s eyepiece is placed on the side opposite to that of the tic.
Positioning69
• lateral oblique position (see page 154), symptomatic side up, axillary roll
• thorax elevated 10-15° to reduce venous pressure
• 3-pin skull fixation. Head position:
head rotation: head rotated just slightly away from the affected side
lateral head tilt
• for trigeminal neuralgia or VIII nerve approach: the head is parallel to the floor (if it is lower, nerves VII & VIII will obscure view of V)
• for VII nerve or lower, the vertex is tilted 15° down from the horizontal
flex neck: leave 2 fingerbreadths room between the chin and the sternum
• upper shoulder retracted caudally with adhesive tape
• option: lumbar spinal drain. Drain 20-30 cc during craniotomy, then drain off small amounts from time-to-time during the case to keep the field mostly dry, but occasionally letting CSF build up to bathe cranial nerves
Intra-operative monitoring
Option: intraoperative monitoring of facial EMG and BAER (assesses acoustic nerve)68.
Approach
1. skin incision69: vertical incision 3-5 cm in length, 5 mm medial to mastoid notch (a small “5-6-4” incision - see page 155) (in thick or short-necked patients, a slightly longer incision that angles inferomedially is used). 75% of the incision is inferior to the transverse sinus, 25% superior
2. burr hole:
A. 1 cm inferior and 1 cm medial to the asterion70 pp 60
B. if the asterion is not easily identified or if there are concerns about the reliability of the asterion as a landmark for the junction of the transverse and sigmoid sinuses71, place the burr hole directly over the mastoid emissary vein which drains superolaterally into the sigmoid sinus
3. craniotomy: top of bone opening as close as possible to transverse sinus. The position of the transverse sinus can be approximated by a line drawn from the posterior base of the zygomatic process to the inion, or roughly ≈ 2 finger-breadths above the upper end of the mastoid notch. Lateral limit of bone opening is sigmoid sinus. A triangular bony opening with a leg along each sinus works well. Craniectomy diameter needs to be only ≈ 3 cm. Apply bone wax liberally (blocks off any possible opening into the mastoid air cells)
4. dural opening: either a curvilinear with each end at a sinus and the convexity away from the junction (Jannetta) or an inverted “T” (with one incision towards each sinus and the third towards junction of sinuses)
Technique
• minimal or no retraction of cerebellum is usually required
• allow CSF to drain before proceeding: this may require gentle advancement of a cottonoid in the CPA. A lumbar drain should be placed if CSF cannot be drained
• follow the junction of tentorium with temporal bone deep. Place a retractor that both medially displaces the cerebellum and slightly “lifts” the cerebellum towards the surgeon (medial displacement alone is not as effective)
• petrosal vein: coagulate and divide the petrosal vein complex (usually 2-3 veins connecting to the tentorial dura). If the vein is torn, the dural side is tamponaded (sometimes up to 30 minutes is needed) while the free end is coagulated
• V is deeper than the VII/VIII complex, which should not even be seen with this approach. If VII/VIII are seen, move the retractor superiorly as even gentle traction may cause hearing loss (see Figure 5-8, page 90). There is often a hillock of bone just posterior to Meckel’s cave obscuring the site where the fifth nerve enters the cave
• arachnoid overlying the fifth nerve is sharply divided (caution re Cranial Nerve IV which follows the tentorial opening in the arachnoid rostral to the fifth nerve). Intra-op changes in BAER are often attributed to retraction of arachnoid that is tethered to the VII/VIII complex
• the fifth nerve may be markedly atrophic if previous PTRs have been done
• identify the smaller motor root (portio minor) of the fifth nerve
• arteries and/or veins compressing V should be dissected off the nerve. NB: vessels located proximally are the most likely offenders, however, the dorsal root entry zone (which is the sensitive part of the nerve) may be variable in location and peripheral vessels may be culpable. The nerve should be inspected and freed of vessels from its origin at the brainstem all the way to its entrance into Meckel’s cave69. Veins may be coagulated and then should be divided (to prevent recanalization)
• the most common cause of compression is the superior cerebellar artery (SCA)
• check the nerve at the junction with brainstem for any residual compression prior to the next step
• insulating material is interposed between nerve and vessel to prevent re-compression. Options include:
e.g. Ivalon®, (polyvinyl formyl alcohol) sponge (Ivalon Surgical Products, 1040 OCL Parkway, Eudora, KS, 66025, U.S.A. distributed by Fabco in the U.S.A. (860) 536-8499, toll free: (888) 813-8214, http://www.fabcousa.net) cut in a saddle shape. Note: if an Ivalon block is used instead of pre-packaged sterile pads, it must be rinsed thoroughly to remove formalin, then autoclaved. Ivalon should be hydrated in NS for 10 minutes prior to cutting it
shredded Teflon felt (see page 543 for merits of Ivalon® vs. Teflon or muscle)
• Wilson recommends performing a partial sensory rhizotomy of the inferior one-half to two-thirds of the portio major for the following: cases where no vascular contact with the nerve or no deformity of the nerve is identified, in most cases of patients undergoing a repeat MVD, or for cases with duration of symptoms > 8-9 yrs as this latter group tends to have a lower success rate with MVD alone72
• if the procedure is for a failed MVD and it is desired to partially divide the nerve, the nerve is organized somatotopically with V1 fibers superiorly, and V3 inferiorly. If the goal is total elimination of pain pathways and there is concern about pain conduction through ancillary pathways, consider also dividing the motor root (portio minor)
Closure
• bone wax should be applied liberally to the exposed lateral bone edges (to paraphrase Dr. Jannetta69 and Mr. Miyagi73, “Wax in, wax out.”)
• irrigate gently with warm saline (avoid “jet” irrigation which can damage the VIII nerve)
• intra-op BAER decline may occur on dural closure and should prompt reopening of the dura and checking for tension on the VIII nerve from a vessel or Telfa
• perform several Valsalva maneuvers to ensure watertight closure of dura
• the bone defect should be covered e.g. with burr hole cover to reduce chance of pain associated with uncovered craniectomy
• after fascial closure, Valsalva maneuver is performed again to ensure watertight closure
• use 4-0 running locked nylon to approximate skin in watertight fashion (avoid excessive tension)
POST-OP CARE FOLLOWING MVD
Include in post-op orders
1. admit to ICU
2. arterial-line for continuous BP monitoring
3. analgesics (e.g. codeine 30-60 mg IM q 3 hrs)
4. anti-emetics (e.g. ondansetron 4 mg IV q 6 hrs)
5. medication to aggressively treat HTN (viz. SBP > 160 mm Hg)
Post-op H/A, nausea and pain
Patients routinely have H/A and nausea for 2-3 days (there tends to be less intracranial air and less “pneumoencephalogram sickness” if the park-bench position is used instead of the sitting position). However, severe H/A should prompt a STAT CT to R/O bleeding. If the CT is negative, severe H/A may be due to transient elevation of CSF pressure that occurs in some, and which usually responds to 1, or at most 2, LPs to halve the pressure. Aseptic meningitis usually responds to steroids. Some patients have continued but lessened tic douloureux pain for several days post-op, this usually subsides69.
COMPLICATIONS
The short list:
1. cerebellar injury
2. hearing loss
3. CSF leak
The long list:
1. mortality: 0.22-2% in experienced hands (> 900 procedures)74, 75
2. meningitis
A. aseptic meningitis (AKA hemogenic meningitis): H/A, meningismus, mild fever, culture negative CSF, pleocytosis. Incidence: ≈ 2% (up to 20% has been reported). Usually occurs 3-7 days post-op. Responds to LP + steroids
B. bacterial meningitis: 0.9%
3. major neurologic morbidity: 1-10% (higher rates with less experienced surgeons), including:
A. deafness: 1%
B. vestibular nerve dysfunction
C. facial nerve dysfunction
4. mild facial sensory loss: 25%
5. cranial nerve palsies76:
A. fourth nerve (diplopia): 4.3% (only ≈ 0.1% are permanent)
B. facial nerve: 1.6% (most are transient)
C. eighth nerve (hearing loss): 3%
6. postoperative hemorrhage77: subdural, intracerebral (1%24), subarachnoid
7. seizures: including status epilepticus77
8. infarction77: including posterior cerebral artery distribution, brain stem
9. CSF leak: resolves with lumbar drainage in most cases
10. pneumonia: 0.6%
OUTCOME
1. success rateA: 75-80%; good but not total relief in an additional ≈ 10%
2. recurrence rate in large series is difficult to ascertain from literature; in a series of 40 patients followed 8.5 yrs mean75:
A. major recurrence (recurrent tic not controlled by medications) rate: 31%
B. minor recurrence (mild or controlled by medications) rate: 17%
C. using Kaplan-Meier curve, expect 70% to be either pain free or have minor recurrence by 8.5 years (or ≈ 80% at 5 years)
the risk for a major recurrence after MVD is 3.5% annually
the risk for a minor recurrence after MVD is 1.5% annually
D. major recurrence rate is lower for patients having major arterial cross-compression of the nerve discovered at the time of surgery (patients with venous compression had much higher rate)
E. this study found no correlation between previous destructive surgery and major recurrence rate (in 11 patients)
A. rates may be lower in patients having prior destructive procedure, see Management of treatment failures, page 555
Some feel that the longer one waits before performing a MVD, the lower the success rate.
20.2.2. Supraorbital and supratrochlear neuralgia
Anatomy
The supraorbital and supratrochlear nerves arise from the frontal nerve and are 2 of the 5 branches of V1 (ophthalmic division of the trigeminal nerve). The supraorbital nerve is the largest branch. It exits the orbit through the supraorbital notch or foramen, usually within the medial third of the orbital roof (mean distance from exit to medial angle of orbit: 20 mm (range: 5-47)78). The supratrochlear nerve exits the orbit without a foramen or notch 3-38 mm medial to the supraorbital nerve (mean: 15.3 mm)78), the most medial branch varies from 8-30 mm lateral to the patient’s midline78.
Supraorbital neuralgia characteristics
Trigeminal neuralgia (TGN) may present with pain in the distribution of the supraorbital nerve, however, the supraorbital nerve may be involved in supraorbital neuralgia (SON), a distinct syndrome with different clinical characteristics. SON is a rare condition slightly more common in women, with onset typically 40-50 years of age79. Characteristics80: 1) unilateral pain in the distribution of the supraorbital nerve (see Figure 7-2, page 151), 2) tenderness in the region of the supraorbital notch or along the distribution of the nerve, and 3) temporary relief with nerve block.
The pain is usually chronic-continuous or remitting-intermittent79.
SON may be:
1. primary (no identifiable etiology): these cases lack any sensory loss
2. secondary (e.g. due to trauma to the area, or resulting from chronic pressure such as with wearing swim goggles): more common than primary SON. Most cases remit within one year79 with elimination of the offending pressure
Supratrochlear neuralgia
Cases of pain isolated to the supratrochlear nerve appear to exist. Supratrochlear neuralgia (STN) may be differentiated from SON by restriction of pain in the more medial forehead, and with relief on blockade of the supratrochlear nerve alone.
Differential diagnosis
1. migraine: suggested by nausea, vomiting and photophobia
2. associated autonomic activity is rare with SON, and should prompt consideration of cluster H/A (see page 58) or SUNCT (page 549)
3. TGN: typical TGN features lacking in SON include characteristic triggers and pain consisting exclusively of paroxysmal/ultra-brief electric shock-like pain
4. hemicrania continua: continuous unilateral pain that tends to be located more posteriorly and is absolutely responsive to indomethacin80
5. trochleitis: inflammation of the trochlea/superior-oblique muscle complex, may mimic supratrochlear neuralgia with pain of the medial upper orbit extending a short distance to the forehead81. The pain is typically exacerbated by supraduction of the eye and to palpation of the trochlea, and is relieved with injection of local anesthetic or, by the usually definitive treatment of infiltration of corticosteroids close to the trochlea. Diplopia is rare and minimal
6. numular (coin-like) H/A82: round or oval 2-6 cm diameter area of pressure-like continuous head pain without underlying structural abnormality. In 13 patients, 9 (70%) the area was located at the parieto-occipital junction. 9 (70%) demonstrated hypoesthesia and touch provoked paresthesias in the affected area
Treatment
Gabapentin (800-2400 mg/d) or pregabalin (150 mg/d) is helpful for some83.
Topical capsaicin applied to the symptomatic area may help (see page 553).
Refractory cases may respond to rhizotomy with alcohol (providing an average of 8.5 months relief84) or with radiofrequency ablation.
Persistent cases may require exploration and decompression of the nerve by lysing bands overlying the supraorbital notch85, or, ultimately, to neurectomy (see page 554) which provides an average of 33.2 months relief86.
20.2.3. Glossopharyngeal neuralgia
Incidence: 1 case for every 70 of trigeminal neuralgia87 (p 3604-5).
CLINICAL
Severe, lancinating pain in the distribution of the glossopharyngeal and vagus nerves (throat & base of tongue most commonly involved, radiates to ear (otalgia), occasionally to neck), occasionally with salivation and coughing. Rarely: hypotension88, syncope89, cardiac arrest and convulsions may accompany. May be triggered by swallowing, talking, chewing. Trigger zones are rare.
TREATMENT
Pain may be reduced by cocainization of tonsillar pillars and fossa. Usually, the persistence and severity of pain requires surgical intervention. One may either perform microvascular decompression, or nerve division via extra- or intracranial approach (latter may be required for permanent relief).
Intracranial approach: Section of preganglionic glossopharyngeal nerve (IX) and upper one third or two fibers (whichever is larger) of vagus (X). IX is readily identified at it’s dural exit zone where it is separated from X by a dural septum. The upper third of X is usually composed of a single rootlet, or less commonly, multiple small rootlets. Initial post-op dysphagia usually resolves. Cardiovascular complications following vagal section have been reported, warrants close monitoring x 24 hrs.
20.2.4. Geniculate neuralgia
Geniculate neuralgia (GeN) AKA Hunt’s neuralgia AKA nervus intermedius neuralgia: a very rare neuralgia affecting the nervus intermedius (the somatic sensory branch of the facial nerve primarily innervating mechanoreceptors of the hair follicles on the inner surface of the pinna and deep mechanoreceptors of nasal and buccal cavities and chemoreceptors in the taste buds on the anterior 2/3 of the tongue).
Symptoms: unilateral paroxysmal otalgia (lancinating pain experienced deep within the ear, often described as an “ice pick in the ear”) radiating to the auricle, with occasional burning sensations around the ipsilateral eye and cheek, and prosopalgia (pain referred to deep facial structures, including orbit, posterior nasal and palatal regions). During pain attacks, some patients have: salivation, bitter taste, tinnitus, or vertigo.
GeN occasionally has cutaneous trigger points in the anterior EAC and tragus, and pain may also be triggered by cold, noise, or swallowing.
Work-up includes neuro-otologic evaluation with audiometry and ENG. Some patients may require imaging (MRI or high-resolution CT) and angio (to R/O aneurysm).
Variants
Tic convulsif (AKA convulsive tic): GeN combined with hemifacial spasm, usually due to neurovascular compression of both the sensory and motor roots of the facial nerve17, most often by AICA. First described by Cushing in 1920.
GeN may be associated with herpetic infections of the geniculate ganglion (AKA herpetic ganglionitis, AKA Ramsay Hunt syndrome (RHS)) in which case herpetic lesions appear on pinna, in EAC, and possibly on TM. May include facial palsy, decreased auditory acuity, tinnitus or vertigo. Unlike idiopathic GeN, RHS is more chronic and less paroxysmal, tends to remit with time, and is usually refractory to carbamazepine. Idiopathic GeN tends to be more painful than RHS, and does not remit spontaneously.
Treatment
1. medical therapy
A. mild cases may respond to carbamazepine, sometimes in combination with phenytoin
B. may respond to valproate (Depakote®) 250 mg PO BID
C. topical antibiotics for secondary infections of herpetic lesions
D. local anesthetic to EAC
2. surgery: for severe cases where medical treatment fails or is not tolerated
A. microvascular decompression together with division of the nervus intermedius (nerve of Wrisberg)90). Operating under local anesthesia allows verification by stimulating nerve
B. geniculate ganglion section91
20.3. Postherpetic neuralgia
Herpes zoster (HZ) (Greek: zoster - girdle) (shingles in lay terms): painful vesicular cutaneous eruptions caused by the herpes varicella zoster virus (VZV) (the etiologic agent of chickenpox, a herpesvirus distinct from herpes simplex virus). It occurs in a dermatomal distribution over one side of the thorax in ≈ 65% of cases (rarely, infections occur without vesicles, called zoster sine herpete). In 20% of cases it involves the trigeminal nerve (with a predilection for the ophthalmic division, called herpes zoster ophthalmicus). Pain usually resolves after 2-4 weeks. When the pain persists > 1 month after the vesicular eruption has healed, this pain syndrome is known as postherpetic neuralgia (PHN). PHN can follow a herpes varicella infection in any site and is difficult to treat by any means (medical or surgical). It can occasionally be seen in a limb, and follows a dermatomal distribution (not a peripheral nerve distribution). PHN may remit spontaneously, but if it hasn’t done so by 6 mos this is unlikely.
EPIDEMIOLOGY
Incidence of herpes zoster is ≈ 125/100,000/year in the general population, or about 850,000 cases per year in the U.S.92. Both sexes are equally affected. There is no seasonal variance. HZ is also more common in those with reduced immunity and in those with a coexistent malignancy (especially lympho-proliferative)93, 94. PHN occurs in ≈ 10% of cases of HZ92. Both HZ and PHN are more common in older patients (PHN is rare in age < 40 yrs, and usually occurs in age > 60) and in those with diabetes mellitus. PHN is more likely after ophthalmic HZ than after spinal segmental involvement.
ETIOLOGY
It is postulated that the VZV lies dormant in the sensory ganglia (dorsal root ganglia of the spine, trigeminal (semilunar) ganglion for facial involvement) until such time that the patient’s immune system is weakened and then the virus erupts. Inflammatory changes within the nerve are present early and are later replaced by fibrosis.
CLINICAL
PHN is usually described as a constant burning and aching. There may be superimposed shocks or jabs. It rarely produces throbbing or cramping pain. Pain may be spontaneous, or may be triggered by light cutaneous stimulation (allodynia) (e.g. by clothing), and may be relieved by constant pressure. The pain is present to some degree at all times with no pain-free intervals. Scars and pigmentary changes from the acute vesicular eruption are usually visible. It is not known if PHN can follow zoster sine herpete. The involved area may demonstrate hypesthesia, hypalgesia, paresthesias and dysesthesias.
Table 20-4 Medical treatments for PHN*
|
Treatment |
Efficacy |
|
PHN treatments that appear effective |
|
|
tricyclic antidepressants |
widely used(see text) |
|
lidocaine patch (Lidoderm®) 95 |
effective, few side effects (see page 566) |
|
intrathecal steroids + lidocaine (see text) |
appears very effective, larger studies & long-term follow-up needed |
|
gabapentin |
proven efficacy (see text) |
|
oxycodone CR 10 mg PO BID4 |
proven efficacy |
|
Treatments of questionable efficacy |
|
|
SSRIs† |
may be effective |
|
SNRIs |
may be effective |
|
tramadol |
may be effective |
|
topical capsaicin |
controversial (see text) |
|
iontophoresis |
insufficient evidence |
|
nonsteroidal creams |
questionable |
|
aspirin suspended in acetone, ether or chloroform |
questionable |
|
EMLA cream |
questionable |
|
Treatments that are not useful |
|
|
dextromethorphan, benzodiazepines, acyclovir, acupuncture |
no benefit96 |
|
ketamine (NMDA receptor antagonist) |
may be beneficial, but hepatotoxic |
|
Preventative treatment |
|
|
oral antiherpetic drugs given during HZ infection |
shortens length of HZ, may reduce incidence of PHN |
|
varicella vaccination of older patients |
trials of this strategy are in progress92 |
* modified with permission from Rubin M, Relief for postherpetic neuralgia, Neurology Alert, 6: 33-4, 2001
† abbreviations: oxycodone CR = controlled release (Oxycontint®); HZ = herpes zoster; PHN = postherpetic neuralgia; SNRIs = serotonin-norepinephrine reuptake inhibitor; SSRIs = selective serotonin reuptake inhibitors (e.g. Prosac®),
MEDICAL TREATMENT
Varicella vaccination of older individuals can increase immunity to herpes zoster, but it will be several years before it can be determined if this will reduce PHN92.
FOR HERPES ZOSTER
Treatment for the pain of the acute attack of herpes zoster may be accomplished with epidural or paravertebral somatic (intercostal) nerve block97 (p 4018).
Oral antiherpetic drugs: Also effective (they shorten the duration of pain) and also reduce the incidence of PHN. They may cause thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) when used in severely immunocompromised patients at high doses. These drugs include:
Acyclovir (Zovirax®): poorly absorbed from the GI tract (15-30% bioavailability). Rx 800 mg PO q 4 hrs 5 times/d x 7 d.
Valacyclovir (Valtrex®)98 is a pro-drug of acyclovir and is more completely absorbed and should be equally as effective with fewer daily doses. Rx 1,000 mg PO TID starting within 72 hrs of onset of the rash x 7 days.
Famciclovir (Famvir®): Rx 500 mg PO TID x 7 d.
FOR POST-HERPETIC NEURALGIA
Most drugs useful for trigeminal neuralgia (see page 552) are less effective for PHN. Some treatment alternatives for PHN are summarized in Table 20-4. Details of some drugs follows. It is suggested to initiate therapy with lidocaine skin patches (see page 566) since this modality has the lowest potential for serious side effects92.
Antiepileptic drugs
gabapentin (Neurontin®)DRUG INFO
FDA approved only for partial seizures and postherpetic neuralgia (PHN).
SIDE EFFECTS: dizziness and somnolence (usually during titration, often diminish with time). Ataxia, fatigue, peripheral edema, confusion and depression may occur.
Rx For PHN, start with 300 mg on Day 1, 300 mg BID on Day 2, and 300 mg TID on Day 3. Dose may be titrated up to 1800 mg/d divided TID. To limit daytime drowsiness, patients may need to start with 100 mg at hs and increase slowly over 3-8. Although doses up to 3600 mg/day (the antiseizure dose) were studied99 there was no significant benefit for PHN over 1800 mg/d. Lower doses are required for renal insufficiency. SUPPLIED: 100, 300 & 400 mg capsules; 600 & 800 mg scored tabs. 50 mg/ml suspension.
oxcarbazepine (Trileptal®)DRUG INFO
Rx 150 mg PO BID.
zonisamide (Zonegran®)DRUG INFO
Rx Initiate therapy with 100 mg PO q PM x 2 wks, then increase dose by 100 mg/d q 2 wks up to 400 mg/d. Bioavailability is not affected by food. Steady state is achieved within 14 days of dosage changes. SUPPLIED: 100 mg capsules.
Tricyclic antidepressants (TCA):
For side effects see page 797.
amitriptyline (Elavil®)DRUG INFO
Helpful in ≈ 66% of patients at a mean dose of 75 mg/d even without antidepressant effect5. SIDE EFFECTS: (see Amitriptyline, side effectspage 797), minimized by starting low and slowly incrementing dose.
Rx Start with 12.5-25 mg PO q hs, and increase q 2-5 days to a max of 150 mg/d.
nortriptyline (Pamelor®)DRUG INFO
Fewer side effects than amitriptyline.
Rx Start with 10-20 mg PO q hs, and increase gradually to a max of 150 mg/d.
Topical treatment:
capsaicin (Zostrix®)DRUG INFO
A vanillyl alkaloid derived from hot peppers, available without prescription for topical treatment of the pain of herpes zoster and diabetic neuropathy. Beneficial in some patients with either of these conditions (response rate at 8 weeks was 90% for PHN, 71% for diabetic neuropathy, vs. 50% with placebo in either group), although the high placebo response rate is disturbing and many authorities are skeptical100. Expensive. SIDE EFFECTS: include burning and erythema at the application site (usually subsides by 2-4 weeks).
Rx Manufacturer recommends massaging the medication into the affected area of the skin TID-QID (apply a very thin coat). Some authorities recommend q 2 hr application. Avoid contact with eyes or damaged skin. Supplied as Zostrix® (0.25% capsaicin) or Zostrix-HP® (0.75%).
lidocaine patch 5% (Lidoderm®)DRUG INFO
Often better tolerated by elderly patients than TCAs (due to pre-existing cognitive impairments, cardiac disease, or systemic illness).
Rx Apply up to 3 patches of 5% lidocaine (to cover a maximum of 420 cm2) to intact skin q 12 hrs to cover as much of the area of greatest pain as possible95.
Intrathecal steroids
Over 90% of patients receiving intrathecal methylprednisolone (60 mg) + 3% lidocaine (3 ml) given once per week for up to 4 weeks, reported good to excellent pain relief for up to 2 years101. This technique was not studied for use in PHN involving the trigeminal nerve. Further clinical trials are needed to verify the efficacy and safety92 (potential long-term side effects include adhesive arachnoiditis).
SURGICAL TREATMENT
There is no operation that is uniformly successful in treating PHN. Numerous operations have been shown to work occasionally. Procedures that have been tried include:
1. nerve blocks: once PHN is established, nerve blocks provide only temporary relief102
2. cordotomy: although percutaneous cordotomy (see page 568) may work when the level of PHN is at least 3-4 segments below the cordotomy, this procedure is not recommended for pain of benign etiology because of possible complications and the high likelihood of pain recurrence
3. rhizotomy: including retrogasserian for facial involvement
4. neurectomies
5. sympathectomy
6. DREZ103: often offers good early relief, but recurrence rate is high (see page 575).
7. acupuncture104
8. TENS
9. spinal cord stimulation: see page 572
10. undermining the skin
11. motor cortex stimulation: for facial PHN
20.4. Pain procedures
Medical therapy must be maximized before a patient is a candidate for a pain procedure. Usually this requires escalating the dose of oral narcotic pain medications until the point that the pain is relieved or the side effects (usually somnolence or hallucinations) are intolerable (e.g. up to 300-400 mg/day of MS Contin may sometimes be necessary).
Choice of pain procedure: Table 20-5 shows some pain procedures that may be used for various indications. In general, nonablative procedures are exhausted before resorting to ablative procedures.
Types of pain procedures
For pain procedures particular to trigeminal neuralgia, see page 553. Techniques for other conditions include:
1. electrical stimulation
A. deep brain stimulation105: targets include thalamus and periaqueductal or periventricular gray matter (see page 574)
B. spinal cord stimulation: see page 572
2. direct drug administration into the CNS:
A. different routes: spinal (see page 570) epidural or intrathecal, intraventricular (see page 572)
B. different agents: local anesthetics, narcotics (without motor, sensory, or sympathetic impairment seen with local anesthetics) see page 570
3. intracranial ablative procedures:
A. cingulotomy: theoretically reduces the unpleasant affect of pain without eliminating the pain. Must be done bilaterally, recently with MRI. Intolerable pain usually recurs after ≈ 3 mos. 10-30% develop flattened affect
B. medial thalamotomy: controversial. May be useful for some for nociceptive cancer pain. Performed stereotactically, see page 575
C. stereotactic mesencephalotomy 106: for unilateral head, neck, face and/or UE pain. Use MRI to create lesion 5 mm lateral to sylvian aqueduct at the level of the inferior colliculus. Unlike spinal cordotomy, the lesion is not near any motor tracts. Main complication is diplopia due to interference with vertical eye movement, often transient
4. spinal ablative surgical procedures
A. cordotomy: see below
1. open
2. percutaneous
B. cordectomy
C. commissural myelotomy: for bilateral pain (see page 570)
D. punctate midline myelotomy: for relief of visceral cancer pain
E. dorsal root entry zone lesion: see page 575
F. dorsal rhizotomy: not useful for large areas of involvement
G. dorsal root ganglionectomy (an extraspinal procedure)
H. sacral cordotomy: for patients with pelvic pain who have colostomy and ileostomy. A ligature is tied around the dural sac below S1 nerve roots
5. sympathectomy: possibly for causalgia major (see Sympathectomy, page 545 and Complex regional pain syndrome (CRPS) on page 576)
6. peripheral nerve procedures
A. nerve block107:
1. neurolytic: injection neurodestructive agents (e.g. phenol or absolute alcohol) on or near the target nerve
2. nonneurolytic: using local anesthetics, sometimes in combination with corticosteroids
B. neurectomy: (e.g. intercostal neurectomy for pain due to infiltration of chest wall by malignancy). Performed open or percutaneously with radiofrequency lesion. May sacrifice motor function with mixed nerves
C. peripheral nerve stimulators: rarely discussed
20.4.1. Cordotomy
Interruption of the lateral spinothalamic tract fibers in the spinal cord. Cordotomy is the procedure of choice for unilateral pain below the C5 dermatomal level (≈ nipple)A, in a terminally ill patient. Better for aching pain, poor for central pain, dysesthesias, causalgia (deafferentation pain) midline visceral pain. May be performed as an open procedure, but is more easily performed percutaneously at the C1-2 interspace (which limits the procedure to the cervical region). If there is any contralateral pain, it will tend to be magnified following the procedure and often leads to dissatisfaction with cordotomy. If there is any bladder dysfunction, it will usually be worse following cordotomy. Bilateral cervical cordotomies carries a risk of the loss of automaticity of breathing108 (one form of sleep apnea, so-called Ondine’s curse109). Therefore, if bilateral cordotomies are desired, the second should be staged after normal respiratory function and CO2 responsiveness are verified following the first procedure, or the second stage may be done as an open procedure in the thoracic region.
A. occasionally pain as high up as the mandible may be treated
Review the cross sectional spinal cord anatomy for relationships of the critical tracts (spinothalamic and corticospinal) to the dentate ligament, the anterior spinal artery, respiratory (see Figure 5-12, page 93), and bladder areas (see Figure 5-29, page 117).
PRE-OP EVALUATION
Spirometric measurement of minute volume before and after breathing a mixture of 5% CO2 and 95% O2 for 5 minutes. If the MV decreases, these patients are at increased risk of having sleep apnea (usually transient), no increased risk if MV increases or stays the same. Also, patients with < 50% of predicted values on PFTs are not candidates.
In patients with pulmonary cancer contralateral to the planned side of cordotomy, check that the contralateral diaphragm is functioning with fluoroscopy, otherwise if the ipsilateral diaphragm is lost due to cordotomy, the patient may be hypopneic.
PERCUTANEOUS CORDOTOMY
Indicated for unilateral pain below ≈ C4-5 in a terminally ill patient. Radiofrequency current is used to lesion the lateral spinothalamic tract.
TECHNIQUE
Patient does not need to be NPO. Usual pain medications should be given. The patient must be awake and cooperative (any movement with the needle in the cord may lacerate the cord), however one may give e.g. hydroxyzine (Vistaril®) 50 mg IM on call to procedure for relaxation.
The procedure is performed in the x-ray department with either fluoroscopic or CT guidance. For fluoroscopy, the head is placed in a Rosomoff headholder with the height adjusted to keep the mastoid process in the same horizontal plane as the acromioclavicular joint. Working on the side contralateral to the pain, local anesthetic without epinephrine is infiltrated 1 cm caudal to the mastoid tip. An 18 gauge lumbar puncture needle is inserted perfectly horizontal aiming halfway between the posterior margin of the body of C2 and the anterior portion of the C2 spinous process. Stay rostral to the C2 lamina to avoid the nerve (which is painful).
The dura will be penetrated at about the time that the tip of the needle is approximately even with the midline of the odontoid process on AP fluoro. A few ml of CSF are aspirated and shaken in a syringe together with a few ml of Pantopaque®A, and several ml of the mixture are injected into the subarachnoid space under lateral fluoro guidance. Some dye will layer on the anterior cord, some on the dentate ligament, and most in the posterior thecal space. The dye will only stay momentarily on the dentate ligament, thus be ready to immediately advance the needle just barely anterior to this while monitoring the tip impedance which will jump from ≈ 300-500 Ω (ohms) in the CSF to ≈ 1200-1500 Ω as the spinal cord is penetrated.
A. Pantopaque is no longer available, and water soluble agents are less effective. A needle endoscopic technique may be able to localize the spinal cord anterior to the dentate ligaments
Stimulation at 100 Hz. should produce contralateral tingling at a threshold of ≤ 1 volt. No motor response should be elicited with 100 Hz. in the spinothalamic tract, and if muscle tetany occurs, lesioning must not be performed. If tingling is in the arm, lesioning will usually render from the arm and below analgesic. If tingling is in the lower extremity it will render only that limb analgesic. Stimulation at 2 Hz. should produce ipsilateral twitching of the arm or neck at ≈ 1-3 volts.
Radiofrequency lesioning is performed for 30 seconds while the patient sustains contraction of the ipsilateral hand and the voltage is gradually increased from zero. Any twitching of the hand is indication to back down on the voltage. A second lesion is performed in the same region and is usually less painful. The appropriate body area is then checked for analgesia to pinprick.
If the procedure is performed satisfactorily, an ipsilateral Horner’s syndrome usually occurs.
COMPLICATIONS
For complications, see Table 20-6.
OUTCOME
In experienced hands, 94% will achieve at least significant pain relief at the time of hospital discharge. The level of analgesia falls with time. At 1 year 60% will be pain free, and at 2 years this will be only 40%. ab
POST-PROCEDURE MANAGEMENT
CSF leakage will cease spontaneously. Patient is kept supine for 24 hrs to prevent “spinal” (post-LP) headache. Pain medication appropriate to post-operative management is prescribed. If successful, one can rapidly stop the narcotics for the primary pain, withdrawal syndromes occur only rarely.
Table 20-6 Post-cordotomy complications
|
Complication |
Frequency |
|
ataxia |
20% |
|
ipsilateral paresis |
5% total 3% permanent |
|
bladder dysfunction |
10% total |
|
postcordotomy dysesthesia |
8% |
|
sleep induced apnea |
0.3% unilateral cordotomy |
|
death (respiratory failure) |
0.3% unilateral cordotomy |
OPEN CERVICAL CORDOTOMY (SCHWARTZ TECHNIQUE)
A relatively quick method for open cervical cordotomy110. Can theoretically be done under local for patients who cannot tolerate general anesthesia.
TECHNIQUE
Position: prone; face carefully placed on padded horseshoe headrest, neck slightly flexed to open the interlaminar spaces and to lower the head to prevent accumulation of intracranial air.
Skin incision: midline from occiput to C3. Working only on the side contralateral to the pain, muscles are stripped off the posterior lip of the foramen magnum, and from the lamina of C1 and C2. A Schwartz or Gelpi retractor is engaged between the occiput and C2. To increase exposure, the inferior half of C1 and superior half of C2 lamina are removed with a punch.
Dural incision: the ligamentum flavum is thin between C1-2, and can usually be opened with the dura in a linear incision from the lamina of C1 to C2 placed in the lateral third of the exposure, taking care to avoid bleeding from epidural veins. An angle is cut in the incision at either end to allow increased dural retraction. Tack-up sutures are placed in the dura, the arachnoid is opened, the dentate ligament is located and is gripped with a hemostat and divided between the hemostat and the dura.
Cordotomy: the dentate ligament is used to slightly rotate the spinal cord. A cordotomy knife (or 11 blade) with bone wax placed at 5 mm, is inserted into the cord in an avascular area just anterior to the dentate ligament, sharp side down. The anterolateral quadrant of the cord is cut with the following caveats:
• do not go posterior to the dentate ligament (to avoid corticospinal tract)
• do not cross the midline of the spinal cord
• do not injure the anterior spinal artery
• for patients with lower extremity pain, be sure to start exactly at the dentate ligament (to avoid missing lumbar and sacral fibers)
20.4.2. Commissural myelotomy
AKA mediolongitudinal myelotomy. Interrupts pain fibers crossing in the anterior commissure on their way to the lateral spinothalamic tract.
Indications: Bilateral or midline pain, primarily below the thoracic levels (including abdomen, pelvis, perineum and lower extremities).
Technique: Laminectomy must extend at least 3 levels above the highest dermatome involved in pain. The dura is opened longitudinally and the operating microscope is then used to identify the midline sulcus (this is usually very difficult to see, and is then estimated as being halfway between where the dorsal roots enter the cord). Veins in the mid-line are sacrificed for the length of the proposed incision. A number 11 scalpel blade is then placed in a hemostat with 6-7 mm of the tip exposed. The blade is inserted in the midline at the upper end of the desired incision and is then passed caudally for the length of the planned incision (usually 3-4 cm).
Outcome: 60% of patients have complete pain relief, 28% have partial, and 8% have none.
Complications: Weakness in the lower extremities occurs in ≈ 8% (usually lower motor neuron, presumably due to injury to anterior horn motor neurons). Dysesthesias occur in almost all patients, but persists > a few days in ≈ 16% (these patients also have impaired joint position sense, all of which are presumably due to posterior column injury). Bladder dysfunction is seen in ≈ 12%. Sexual dysfunction may also occur. There is a risk of injury to the anterior spinal artery (rare).
20.4.3. Punctate midline myelotomy
Indications: Pelvic and visceral pain refractory to other therapies111.
Technique: Interruption of a midline posterior column pathway.
20.4.4. CNS narcotic administration
INTRASPINAL NARCOTICS
Spinal narcotics may be administered epidurally or intrathecally for pain relief. Satisfactory pain control can usually be achieved for pain below the neck, although for pain above the diaphragm/umbilicus some recommend intraventricular morphine112 (see page 572). May also be performed on a “one-time” basis e.g. injection into epidural space following a lumbar laminectomy. Or, it may be given on a short term continuous basis, via an external epidural or intrathecal catheter. It may also be performed on an intermediateterm basis (< 60 days) with the use of a subcutaneous reservoir113 or on a long-term basis with an implantable drug infusion pump114 (e.g. Infusaid® or Medtronic® pump). Advantages over systemic narcotics include less sedation and/or confusion, less interference with GI motility (constipation), and possibly less N/V. The effectiveness is usually limited to ≈ 1 year and is thus not indicated for chronic benign pain. With time, increased doses are required because of the development of tolerance and/or progression of disease115 with the concomitant development of the usual narcotic side effects.
SPINAL NARCOTICS
Must be preservative-free (for either intrathecal or epidural use). This may be prepared by a pharmacist (e.g. add enough preservative free 0.9% saline to 1 or 3 gm morphine sulfate powder to yield a total of 100 ml produces 10 or 30 mg/ml solution respectively, and then filter this through a 0.22 μm filter116). Alternatively, commercially available preparations include Duramorph® (available as 0.5 or 1 mg/ml) and Infumorph® (available in 20 ml ampules of 10 or 25 mg/ml), any of which may be diluted to a lower strength with preservative free diluent (normal saline). Cross tolerance to systemic narcotics does occur, and spinal narcotics are more effective in patients who have not been on continuous high dose IV opiates (patients on high-dose IV narcotics need higher initial intraspinal narcotic doses).
SIDE EFFECTS: include pruritus (often diffuse, and may be experienced most intensely in the nose), respiratory depression (the respiratory depression with spinal narcotics is usually very gradual, and is often easily detected by monitoring respiratory rate q 1 hr and taking action if the rate decreases), urinary retention, and N/V.
Trial injection
Before implanting a permanent delivery system a test injection should be performed to verify pain relief and tolerance for medication. Administered via percutaneously inserted epidural or intrathecal catheter connected to an external pump. Doses required for intrathecal catheters are usually ≈ 5-10 times lower than those for epidural catheters.
Sample post-injection orders after a one-time injection:
1. use no other narcotics for ≈ 24 hrs (with a continuous infusion additional narcotics should be withheld until the effect of the spinal narcotics has been determined)
2. 2 ampules (0.4 mg each) of naloxone (Narcan®) and syringe taped to patients bed (for the first 24 hrs after a single injection; at all times with continuous infusion)
3. head of bed elevated ≥ 10° for 24 hrs
4. record respiratory rate q1 hr for 24 hrs; if asleep and respiratory rate < 10 breaths/min, awaken patient. If unable to awaken, administer naloxone 0.4 mg IV and notify physician. Repeat naloxone 0.4 mg IV q 2 min PRN
• optional: pulse oximeter for 24 hrs
5. diphenhydramine (Benadryl®) 25 mg IV q 1 hr PRN itching
6. droperidol (Inapsine®) 0.625 mg (which is 0.25 ml of the 2.5 mg/ml standard concentration available) IV q 30-60 mins PRN nausea
7. PRN supplemental pain medication:
A. narcotic agonist/antagonist: e.g. nalbuphine (Nubain®) 1-4 mg IV q 3 hrs
OR
B. ketorolac tromethamine (Toradol®) 15 mg IV or IM or 30 mg IM q 6 hrs (use lower dose for weight < 50 kg, age > 65 yrs, or reduced renal function)
IMPLANTABLE DRUG DELIVERY PUMPS
Although satisfactory pain control can be achieved with either epidural or intrathecal narcotics (morphine diffuses easily through the dura to the CSF where it gains access to pain receptors), epidural catheters commonly develop problems with scarring and may become less effective sooner than intrathecal catheters. Pumps should only be implanted if patients have successful pain control with test injection of spinal epidural (5-10 mg) or intrathecal (0.5-2 mg) morphine. A life expectancy of > 3 months is recommended for implantable pumps (if shorter longevity is anticipated, an external pump may be used).
One such series of commonly used implantable drug delivery pumps is manufactured by Infusaid [Infusaid, Inc., 1400 Providence Highway, Norwood, MA 02062, Phone: 1-800-451-1050]. The only needle that should be used with their devices are special 22 gauge Huber (non-coring) needles. Delivery rates increase with body temperature 10-13% per °C above 37° C, they decrease by the same amount for every °C below 37°C, and also they become inaccurate at ≤ 4 ml of reservoir fluid. These pumps should never be allowed to run until empty, as this may permanently affect accuracy and reliability of drug delivery. In addition to the pump reservoir port, most models have one or more side “bolus” ports that delivers injected fluid directly to the outlet tubing. One should not aspirate when accessing either port.
Medtronic produces a programmable pump.
Surgical insertion
Similar to the insertion of a lumbar-peritoneal shunt (see page 213). The patient is placed in the lateral position, such as on a bean-bag device. The pump is inserted into a subcutaneous pocket, created with a slightly curved 8-10 cm skin incision. The pump may be sutured to the fascia of the abdomen (in obese patients, it may be sutured to the subcutaneous tissue). Excess tubing should be coiled underneath the pump to prevent inadvertent puncture when accessing either reservoir.
The spinal catheter is inserted through a Tuohy needle inserted between lumbar spinous processes either percutaneously or via a small incision 2-3 mm lateral to the spinous processes. Alternatively, it may be inserted directly via a hemilaminectomy. Fluoroscopy may be used intraoperatively to verify rostral placement of the catheter (radiographic visualization of the catheter may be aided by filling it with iodinated contrast, e.g Omnipaque-300, see page 122). All bends in the tubing should be very gradual to avoid kinking.
Post-op pain management:
Although the pump will be infusing when the patient leaves the operating room, unless they have been on intraspinal narcotics up until the time of surgery, it will usually take several days for the drug to reach equilibrium in the CSF before the level of pain control will be adequate. This can be mitigated by a bolus infusion (3-4 mg morphine for epidural catheters, or 0.2-0.4 mg for intrathecal catheters).
Complications
Meningitis and respiratory failure are rare complications. CSF fistula and spinal H/A may occur. Disconnection or dislodgment of catheter tip may result in failure to control pain, but can usually be surgically corrected.
Outcome
Cancer pain is significantly improved in up to 90%. Success rate for neuropathic pain (e.g. postherpetic neuralgia, painful diabetic sensory neuropathy): 25-50%.
INTRAVENTRICULAR NARCOTICS
Indications
May be used for cancer pain (especially head and neck)117 unresponsive to other methods in patients with a life expectancy < 6 mos.
Technique
An intraventricular catheter is connected to a ventricular access device (see page 211). 0.5-1 mg of intrathecal morphine is injected via the VAD and usually provides ≈ 24 hrs of analgesia.
Complications
SIDE EFFECTS: common ones include dizziness, N/V. The risk of respiratory depression is minimized by using correct dosing. Complications in a series of 52 patients117: bacterial colonization of reservoir (4%), dislodged catheter (2%), blocked catheter (6%), postoperative meningitis (2%).
Outcome
Pain is successfully controlled in 70% at 2 mos, but thereafter the effectiveness diminishes as a result of tolerance to the narcotics.
20.4.5. Spinal cord stimulation (SCS)
Originally developed as dorsal column stimulation (DCS), it has since been determined that pain relief also occurs with ventral stimulation (without stimulation induced paresthesias seen with DCS). Pain relief in humans persists beyond the stimulation time, and is not reversed by naloxone. The exact mechanism of action is un-determined, but probably involves some combination of neurohumoral (i.e. endorphin), antidromic stimulation of a spinal pain “gate”, and supraspinal center stimulation. GABA and serotonin levels have been shown to be increased with SCS.
Indications
1. pain118: postlaminectomy pain syndrome (the most common indication, especially if LE pain > back pain (see below)), complex regional pain syndrome (CRPS) (see page 574), postthoracotomy pain (intercostal neuralgia), multiple sclerosis, diabetic neuropathy (see page 574) and sometimes postherpetic neuralgia
✖ generally not used for cancer pain or for patients with limited life expectant
2. refractory angina pectoris: see page 574
3. painful limb ischemia from inoperable peripheral vascular disease: see page 574
4. functional: spastic hemiparesis, dystonia, bladder dysfunction
Technique
In order for SCS to be effective, it is necessary for the patient to feel the stimulation in the areas of pain119. Two techniques are used to place electrodes in the epidural space:
1. plate-like electrodes placed via hemilaminectomy
2. wire-like electrodes placed percutaneously with a Tuohy needle
Following electrode placement, a trial with an external generator over several days determines if SCS is effective. The electrodes are removed unless clear improvement occurs, in which case an implantable pulse generator is placed subcutaneously.
Complications
With plate electrodes, there is a 3.5% incidence of infection which respond to electrode removal and IV antibiotics. Less common complications: electrode migration (usually seen with first few weeks), lead breakage (less common with present systems), CSF leak, radicular pain, intermittent interference with cardiac pacemakers, and weakness.
Outcome
Success rate in pain control is ≈ 50% improvement in 50% of patients in experienced hands at specialized centers where multidisciplinary approach is available119. In a retrospective long-term follow-up study (ave = 96 months) of 410 patients that had SCS implantation due to numerous indications, success rate was 74%120.
Prognosticators of a poor response to SCS include: pain resulting from spinal cord injury, from lesions proximal to the ganglion (e.g. root avulsion), failed back syndrome with back pain > LE pain and multiple previous operations (see below), psychological factors such as litigation, workers compensation, familial/marital discord or drug seeking behavior121.
SPECIFIC SYNDROMES TREATED
Failed back surgery syndrome
|
Σ |
The addition of SCS improves pain control over either PT or medical management alone for failed back surgery syndrome. At 24 months, SCS is as effective as reoperation in treating radicular pain, with no difference in ADLs or work status. |
In the PROCESS trial122 (Prospective Randomized Controlled Multicenter Trial of the Effectiveness of Spinal Cord Stimulation), 100 patients with failed back surgery syndrome were randomized to SCS placement plus conventional medical management (52 patients) vs. conventional medical management alone (48 patients). The health-related quality of life, measured using EuroQol-5D questionnaire, was greater in the SCS group despite a higher total health care cost at 6 months.
In long-term follow-up at 24 months, the primary outcome (>50% relief in leg pain) is achieved in 37% of patients that were randomized to SCS plus conventional medical management and 2% of patients that were randomized to conventional medical management only. Patients were allowed to cross-over. After cross-over, the primary outcome is achieved in 47% of patients (34 of 72) who had SCS plus medical management as final treatment versus 7% of patients (1 of 15) in the other group (P=0.02)123.
In another randomized prospective study, patients with persistent or recurrent radicular pain after lumbosacral surgery were randomized to reoperation vs. SCS. On an average of 3-year follow-up, the SCS group required less opiate analgesics. 9 of 19 patients in the SCS group compared to only 3 of 26 patients reoperated had self reported pain relief and satisfaction (P < 0.01), and there was no difference in ADLs and work status. Patients in the SCS group were less likely to crossover to undergo reoperation (5 of 24 patients from the SCS group versus 14 of 26 patients in the reoperation group, P = 0.02)124.
Complex regional pain syndrome
|
Σ |
SCS may be effective for treating CRPS during the first couple of years, however no significant benefit was evident at 5-year follow-up. |
CRPS is a chronic pain condition marked by continuous disabling intense aching or burning pain. Type I has no known nerve injury, Type II follows a nerve injury (see page 576). In a randomized clinical trial125, patients with CRPS Type I were randomized to receive SCS plus physical therapy (PT) (36 patients) or PT alone (18 patients). 24 of 36 patients had successful SCS trial and underwent implantation. At 6 months, in the group that received SCS plus PT, pain intensity reduced by 2.4 cm on the visual-analogue scale as opposed to an increase of 0.2 cm in the PT only group (P<0.001). In addition, 39% of patients in the SCS group, had “much improved” globally perceived effect vs. 6% (P=0.01). The health-related quality of life only improved in the SCS group. At 2-year follow-up, pain intensity in the SCS group reduced by 2.1 vs. 0.0 cm in the PT group compared to baseline (P < 0.001) and global perceived effect were “much improved” in 43% vs. 6% (P = 0.001)126. However, these benefits were no longer significant in 5 years127.
Peripheral vascular disease
|
Σ |
SCS does help with pain due to inoperable limb ischemia. It may or may not improve healing of pressure ulcers |
In a retrospective, non-control study of 38 patients, ≈ 94% experienced pain relief and ≈ 50% experienced healing of ischemic ulcers128.
In a recent review129 of six controlled studies of nearly 450 patients, SCS + medical treatment was compared to medical treatment alone. Although there was no significant difference in ulcer healing, the use of analgesics was less and limb salvage after 12 months was significantly higher in the SCS group (relative risk = 0.71).
Angina pectoris
|
Σ |
SCS was as effective as CABG in controlling refractory angina and protecting against MIs. SCS improves exercise capacity by an unknown mechanism |
SCS reduces anginal pain and improves exercise capacity by an unknown mechanism, which may be related to decrease in myocardial oxygen consumption130 or altering myocardial blood flow131 rather than just masking symptoms
In a multicenter, randomized, prospective clinical trial, comparing SCS to CABG in selected patient132, there was no significant difference in decreasing anginal attack and nitrates consumption between the groups. 5-year follow-up from this trial found that both CABG and SCS offered similar protection from angina pectoris and myocardial infarction133.
In a prospective study of 104 patients who underwent SCS placement for refractory angina pectoris (average follow-up ≈ 13 months), 73% had > 50% reduction of weekly anginal episodes compared to baseline134.
Diabetic Neuropathy
|
Σ |
Available data is limited, but SCS may be a viable modality for refractory pain from diabetic neuropathy. Further study is needed |
No good clinical data are available. A few studies with small numbers of patients suggest SCS can provide significant pain relieve in most patients with diabetic neuropathy that failed conservative management135-137.
A small prospective, open-label study reported 9 of 11 patients with diabetic neuropathy that failed conservative treatment had significant pain relieved after SCS implantation at 6 months. Pain score on visual analogue scale decreased from 77 to 34. Microcirculatory perfusion did not change significantly from baseline137.
20.4.6. Deep brain stimulation (DBS)
Deafferentation pain syndromes (anesthesia dolorosa, pain from spinal cord injury, or thalamic pain syndromes) may benefit from stimulation of sensory thalamus (ventral posteromedial (VPM) or ventral posterolateral (VPL)). DBS for chronic neuropathic pain produces a 40-50% reduction in pain in about 25-60% of patients138.
Nociceptive pain syndromes are more likely to benefit from stimulation of periventricular gray matter (PVG) or periaqueductal gray matter (PAG) although PAG stimulation is rarely used because it often produces unpleasant side effects. Still, response rate has been only ≈ 20%139 resulting in failure of the FDA to approve these devices for pain.
Cluster headaches: may respond to hypothalamic stimulation, but larger trials with longer follow-up are needed138.
20.4.7. Dorsal root entry zone (DREZ) lesions
Although use has been reported for a variety of indications, DREZ lesions appear to be most effective in treating the following:
1. deafferentation pain resulting from nerve root avulsion140-142. This most commonly occurs in motorcycle accidents
2. spinal cord injuries (SCI) with pain around the lowest spared dermatome with caudal extension of pain restricted to a few dermatomes (SCI with diffuse pain involving the entire body and limbs below the injury is less responsive)
3. post herpetic neuralgia (see page 564): usually good initial response, but early recurrence in ≤ few months is common, and only 25% have long-term relief of pain
4. postamputation phantom limb pain: there is some support for this in the literature, but others feel this is not a good indication68
5. ✖ generally not used for cancer pain
Technique: A laminectomy is performed over the involved segment(s) using radiographic localization. The dura is opened, and the DREZ is identified under microscope magnification using intact posterior rootlets above or below for orientation (contralateral rootlets may also be used to estimate the mirror-image location). Lesions are created ipsilateral to the avulsed nerve roots by radiofrequency current (approximately 50-60 lesions are required for several segments, each lesion is done at 75° for ≈ 15 seconds) or selective incisions extending from the last completely normal rootlet at the rostral end to the first normal rootlet caudally. The lesioning needle or knife blade is angled 30-45° medially and inserted to a depth of 2-3 mm. DREZ lesions may be combined with a cordectomy at the level of anatomic cord disruption in paraplegic patients68.
Post-op management: Bed rest for 3 days may reduce the risk of CSF leakage. Analgesics appropriate for a multilevel laminectomy are administered.
Complications: Ipsilateral weakness (related to corticospinal tract) or loss of proprioception (dorsal columns) occurs in 10% of patients, and is permanent in ≈ half (i.e. 5%).
Outcome: In pain related to brachial plexus avulsion, 80-90% long-term significant improvement can be expected. Paraplegics with pain limited to the region of injury have an 80% rate of improvement, compared to 30% for those with pain involving the entire body below the lesion.
20.4.8. Thalamotomy
Controversial & rarely used. Not a routine treatment for pain. May be useful for some nociceptive cancer pain, especially of head, neck and face. Neuropathic pain syndromes respond infrequently. The target is the medial thalamus which exhibits high-frequency bursts associated with deafferentation pain.
Pre-op preparation: CT and/or MRI is used to rule-out mass lesion and to establish target coordinates. Platelet count and coagulation studies must be within normal limits. NSAIDs should be discontinued 10 d pre-op. HTN must be avoided during surgery.
TECHNIQUE
A stereotactic frame is applied parallel to the orbitomeatal line. MRI shows the anterior (AC) and posterior commissure (PC) to better advantage than CT, but suffers from some geometric inaccuracies (shift and distortion). A burr hole is placed 2 cm lateral to the midline just anterior to the coronal suture. A radiofrequency probe is inserted to the medial thalamus and then electrophysiologic localization of the target is performed. Following the procedure, a CT scan is done to rule-out hemorrhage.
COMPLICATIONS
Mortality: < 1%. Morbidities: significant hemorrhage: 0.5%, subdural hematoma: 0.5%, hemiparesis: 1%, cognitive impairment: 20-70%. Aphasia occurs infrequently.
OUTCOME
Significant pain control occurs in ≈ 50% of those with cancer pain, but recurrence of pain is common and is seen in 60% at 6 months. Only ≈ 20% of cases of neuropathic pain respond.
20.5. Complex regional pain syndrome (CRPS)
The terminology is confusing. Formerly also called causalgia (reflex sympathetic dystrophy). The term causalgia (Greek: kausis - burning, algos - pain) was introduced by Weir Mitchell in 1864. It was used to describe a rare syndrome that followed a minority of partial peripheral nerve injuries in the American civil war. Triad: burning pain, autonomic dysfunction and trophic changes.
CRPS Type II (AKA major causalgia) follows nerve injury (originally described after high velocity missile injuries). CRPS Type I (AKA reflex sympathetic dystrophy or causalgia minor) denoted less severe forms, and has been described after non-penetrating trauma143. Shoulder-hand syndrome and Sudek’s atrophy are other variant designations. In 1916, the autonomic nervous system was implicated by René Leriche, and the term reflex sympathetic dystrophy (RSD) later came into use144 (but RSD may be distinct from causalgia145).
Post-op CRPS has been described following carpal tunnel surgery as well as surgery on the lumbar146 (see page 450) and cervical spine.
At best, CRPS must be regarded as a symptom complex, and not as a discrete syndrome nor medical entity (see the essay by Ochoa147). Patients exhibiting CRPS phenomenology are not a homogeneous group, and include148:
1. actual CRPS (for these, Mailis proposes the term “physiogenic RSD”): a complex set of neuropathic phenomena that may occur with or without nerve injury
2. medical conditions distinct from CRPS but with signs and symptoms that mimic CRPS: vascular, inflammatory, neurologic…
3. the product of mere immobilization: as in severe pain avoidance behavior, or at times psychiatric disorders
4. part of a factitious disorder with either a psychological basis (e.g. Munchausen’s syndrome) or for secondary gain (financial, drug seeking…) i.e. malingering
Pathogenesis
Early theories invoked ephaptic transmission between sympathetics and afferent pain fibers. This theory is rarely cited currently. Another more recent postulate involves nor-epinephrine released at sympathetic terminals together with hypersensitivity secondary to denervation or sprouting. Many modern hypotheses do not even embrace involvement of the autonomic nervous system in all cases144, 145, 148.
Thus, many of the alterations seen in CRPS may simply be epiphenomena rather than part of the etiopathogenetic mechanism.
CLINICAL
CRPS may be described as a phenomenology, i.e. a variable complex of signs and symptoms due to multiple etiologies included in this nonhomogeneous group148. No diagnostic criteria for the condition have been established, and various investigators select different factors to include or exclude patients from their studies.
Symptoms
Pain: affecting a limb, usually burning, and prominent in the hand or foot. Onset in the majority is within 24 hrs of injury (unless injury causes anesthesia, then hrs or days may intervene); however, CRPS may take days to weeks to develop. Median, ulnar and sciatic nerves are the most commonly cited involved nerves. However, it is not always possible to identify a specific nerve that has been injured. Almost any sensory stimulus worsens the pain (allodynia is pain induced by a nonnoxious stimulus).
Signs
The physical exam is often difficult due to pain.
Vascular changes: either vasodilator (warm and pink) or vasoconstrictor (cold, mottled blue). Trophic changes (may be partly or wholly due to immobility): dry/scaly skin, stiff joints, tapering fingers, ridged uncut nails, either long/course hair or loss of hair, sweating alterations (varies from anhidrosis to hyperhidrosis).
DIAGNOSTIC AIDS
In the absence of an agreed upon etiology or pathophysiology, there can be no basis for specific tests, and the lack of a “gold-standard” diagnostic criteria makes it impossible to verify the authenticity of any diagnostic marker. Numerous tests have been presented as aids to the diagnosis of CRPS, and essentially all have eventually been refuted. Candidates have included:
1. thermography: discredited in clinical practice
2. three-phase bone scan: typical CRPS changes also occur after sympathectomy149, which has traditionally been considered curative of CRPS
3. osteoporosis on x-ray150, particularly periarticular demineralization: nonspecific
4. response to sympathetic block (once thought to be the sine qua non for causalgia major and minor, the response sought was relief (complete or significant) with sympathetic block of appropriate trunk (stellate for UE, lumbar for LE)): has failed to hold up once stringent placebo-controlled trials were executed
5. various autonomic tests151: resting sweat output, resting skin temperature, quantitative sudomotor axon reflex test
TREATMENT
In the absence of a delineated pathophysiology, treatment is judged purely by subjective impression of improvement. CRPS treatment studies have had an unusually high placebo response rate152. Medical therapy is usually ineffective. Proposed treatments include:
1. tricyclic antidepressants
2. 18-25% have satisfactory long-lasting relief after a series of sympathetic blocks (see Stellate ganglion block and Lumbar sympathetic block starting on page 215), although one report found no long-lasting benefit in any of 30 patients153
3. intravenous regional sympathetic block, particularly for UE CRPS: agents used include guanethedine154 20 mg, reserpine, bretylium…, injected IV with arterial tourniquet (sphygmomanometer cuff) inflated for 10 min. If no relief, repeat in 3-4 wks. No better than placebo in several trials155, 156
4. surgical sympathectomy (see page 545): some purport that this relieves pain in > 90% of patients (with a few retaining some tenderness or hyperpathia). Others opine that there is no rational reason to consider sympathectomy since sympathetic blocks have been shown to be no more effective than placebo144
5. spinal cord stimulation: some success has been reported
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