For functional neurosurgery related to pain, see Pain procedures, page 567.
19.1. Deep brain stimulation
This section covers issues related to deep brain stimulation (DBS) in general. For specific conditions, refer to that section. A variety of conditions may be treated including:
1. movement disorders
A. Parkinson’s disease: STN stimulation may be superior to best medical management1, 2 because of similar efficacy to levodopa with fewer side effects (primarily dyskinesias) (see below)
B. dystonia: see page 536
C. tremor: see page 545
2. epilepsy: see page 422
3. pain: response is variable, typically only 25-60% respond (see page 574)
4. potential uses
A. psychiatric disorders: mainly
1. Tourette syndrome: thalamic & pallidal DBS (case reports3, 4)
2. obsessive compulsive disorders: anterior capsule and STN stimulation5 and, recently, targets more posterior and rostral6
3. depression: subgenual cingulate gyrus7 and anterior capsule stimulation8
B. obesity9
C. drug addiction10
D. hypertension (case report of lowering BP in a patient who was being treated for pain11)
Typical targets used in functional brain surgery
Figure 19-1 depicts relationships of typical targets to other structures and effects of DBS (or lesioning). This figure is intended for illustrative purposes only, and is not presented for purposes of performing surgical procedures.
19.2. Surgical treatment of Parkinson’s disease
HISTORICAL BACKGROUND
An early procedure was ligation of the anterior choroidal artery. Due to variability in distribution, destruction often extended beyond the desired confines of the pallidum and the results were too unpredictable (see page 1028). Anterodorsal pallidotomy became an accepted procedure in the 1950’s, but long-term improvement was mainly in rigidity, while tremor and bradykinesia did not improve12. The ventrolateral thalamus subsequently became the preferred target. Lesions there were most effective in diminishing tremor. In actuality, the tremor was often not the most debilitating symptom, particularly since it is a resting tremor at first (it may become more pervasive later). Bradykinesia and rigidity were frequently more problematic. Furthermore, the procedure only reduces tremor in the contralateral half of the body, and bilateral thalamotomies were not recommended due to an unacceptably high risk of post-op dysarthria and gait disturbance. Use of thalamotomy fell off dramatically in the late 1960’s with the introduction of Ldopa13.
Figure 19-1 Illustration of some targets for functional brain surgery Abbreviations: AC = anterior commissure, GPi = globus pallidus interna, H1 = Forel’s H1 field, MCP = midcommissural point (halfway between AC & PC), PC = posterior commissure, STN = subthalamic nucleus, subst.nigr = substantia nigra, z.i = zona incerta
However, at some point most patients will experience problematic side effects and/or resistance to treatment with antiparkinsonian drugs. Tissue transplantation (e.g. with adrenal medullary tissue) appears to have only modest benefits (see below). Lesioning or stimulation techniques have therefore gained in popularity with renewed interest in the posteroventral pallidum as the target.
19.2.1. Tissue transplantation
Tissue transplantation for Parkinson’s disease is generally limited to research centers. The present status of implantation of fetal dopaminergic brain cells into Parkinson’s disease patients is that it may reduce the severity of the illness and increase the effectiveness of levodopa14. For ethical reasons, this procedure is rarely performed in the U.S.
Other transplanted tissues include cells from the patients own adrenal medulla. After initial enthusiastic results15, later studies failed to corroborate the dramatic outcomes, and benefits appear to be modest16-18.
A double-blinded, randomized, placebo-controlled trial19 of 34 subjects with severe PD noted initial improvement at 6 and 9 months, but found no efficacy 2 years after fetal mesencephalic cell transplantation. Of note: immunosuppression was only used for six months. Further research is ongoing20.
19.2.2. Ablative surgery & electrical stimulation
Ablative surgery is giving way to less destructive beep brain stimulation.
PALLIDOTOMY21,22
Pallidotomy may work by one of the following mechanisms: directly destroying portions of the internal segment of the globus pallidus internus (GPi), interrupting pallid-ofugal pathways, or diminishing inputs to the medial pallidum (especially from the subthalamic nucleus) (see Pathophysiology, page 59). Although early methodologies included stereotactic radiosurgery23, modern techniques (excluding very select cases) rely primarily on radiofrequency or cryoprobe lesioning after confirming target location by electrical stimulation.
Electrical stimulation: Deep brain stimulation (DBS) in the area of the GPi24 and subthalamic nucleus (STN) can also relieve parkinsonian symptoms25 without irreversibly destroying tissue. A randomized study showed similar efficacy between thalamotomy and DBS, but fewer side-effects with DBS26. A more recent target of interest for DBS is the pedunculopontine nucleus (PPN).
Indications
1. patients refractory to medical therapy (including multiple agents). However, some investigators feel the response to surgery might be better if done early
2. primary indication (based on an opinion survey27): patients with levodopa-induced dyskinesias (especially those with associated painful muscle spasms). Initial results indicate that these are very responsive to pallidotomy
3. gait and postural instability28 as well as falls and freezingA29 may respond to DBS of the pedunculopontine nucleus (PPN)
4. patients primarily with rigidity or bradykinesia (unilateral or bilateral), on-off fluctuations or dystonia. Tremor may be present, but if it is the predominant symptom, then using the ventralis intermedius (VIM) nucleus of the thalamus as the target (for ablation (thalamotomy) or stimulation)30 is a better procedure. VIM stimulation is also used to treat essential tremor31
A. non-human primate data
Contraindications
1. patients with significant dementia: further cognitive impairment has been noted primarily in patients with cognitive deficits prior to treatment
2. patients with risk of intracerebral hemorrhage: those with coagulopathy, poorly controlled hypertension, those on anti-platelet drugs that cannot be withheld (may consider stereotactic radiosurgery lesions for these rare patients)
3. patients with ipsilateral hemianopsia: due to the risk of post-op contralateral hemianopsia from optic tract injury which would make the patient blind
4. age ≥ 85 yrs
5. patients with secondary Parkinsonism (see page 60 for more details) i.e. not idiopathic Parkinson’s disease: respond poorly, presumably due to different patho-physiology. Look for:
A. signs of autonomic nervous system dysfunction (suggests Shy-Drager)
B. EOM abnormalities (may occur in progressive supranuclear palsy (PSNP))
C. long-tract signs
D. cerebellar findings (as in olivo-ponto-cerebellar atrophy (OPCA))
E. failure to improve with levodopa
F. MRI: lacunar infarcts in basal ganglia (as in arteriosclerotic Parkinsonism), or tumor in region of substantia nigra
G. PET scanning (if available): decreased striatal metabolism detected by deoxyglucose PET scan (suggests striato-nigral degeneration (SND))
TECHNIQUE
Antiparkinsonian medications are withheld the morning of the procedure to bring out symptoms. A stereotactic frame is applied under local anesthetic parallel to the orbitomeatal line (which aligns with the anterior-posterior commissural (AC-PC) line).
Radiologic target localization
May utilize: MRI, CT, and/or ventriculography. MRI is the most common imaging modality, and may best demonstrate the desired anatomy, but is susceptible to geometric distortion. Therefore many centers also utilize CT and/or ventriculography to supplement MRI. T1WI images are commonly employed, however some feel that optimal MRI imaging may be performed with gadolinium-enhanced axial and coronal projections using 1 mm slice intervals and a STIR or spoiled GRASS volume acquisition protocol.
The posterior commissure is the white-matter band at the level of the pineal that crosses at the posterior third ventricle.
The typical initial target27 is shown in Table 19-1. Avoid encroachment on internal capsule (medial to GPi) and optic tract (inferior to GPi). Lesions of the subthalamic nucleus are associated with hemiballismus. An entry site is chosen from imaging studies, and is usually just anterior to the coronal suture and 15-20 mm lateral to the midline. A 4 mm twist drill hole is used. The trajectory should avoid midline venous structures, arterioles within sulci (therefore enter through a gyrus), and passage through the lateral ventricle.
Table 19-1 Target for pallidotomy
|
1. 1-3 mm anterior to the mid-point of the AC-PC line |
MEDIAN |
|
2 mm |
|
|
2. 18-23 mm lateral* |
21 mm |
|
3. 2-6 mm inferior |
5 mm |
* may be decreased in women (start at ≈ 19 mm), or increased when the 3rd ventricle is dilated
Electrophysiologic target localization
Stimulation:
The patient must be awake for the procedure. For patients with dyskinesias that occur only following a dose of medication, their normal dose of medicine is given after imaging to bring out the symptoms for the procedure. Stimulation is required to verify the neurophysiologic target which varies between individuals. Macroelectrode stimulation may be done with the lesioning electrode. Impedance typically drops when a white matter tract is encountered. The impedance of the desired target is usually > 600 Ω. Stimulate with square wave at 1, 5, 50 and 100 Hz with voltage range of 0.5-3 volts (NB: above ≈ 2 V you may be seeing wide-field stimulation). Pallidum stimulation usually increases (but occasionally decreases) contralateral muscle tone. Also look for reduction of tremor or dyskinesia. Contralateral weakness or hypotonia indicates proximity to the internal capsule. Visual scotomata suggests stimulation of the optic tract.
Micro-electrode recording:
About half the institutions surveyed perform microelectrode recording, and half the remaining centers were considering starting it.
Lesioning
Kondziolka et al.22 use a 1.1 mm diameter probe with a 3 mm exposed tip. A small lesion is made at 45°C for 30 seconds, before making the definitive lesion at 70-80°C for 60 seconds. The probe is withdrawn 3-4 mm and a second lesion is made. Lesions with cryoprobes may be associated with a higher incidence of intracerebral hemorrhage.
For the very rare patient in whom insertion of an electrode is contraindicated (e.g. refractory coagulopathy), lesioning may be done with stereotactic radiosurgery, however, this eliminates the critical ability to verify the site of the planned lesion electrophysio-logically before a permanent lesion is made.
Unilateral pallidotomy produces primarily contralateral effects, although some ipsilateral changes occur. Bilateral procedures are usually staged separately with a 3-12 hiatus between sides. Although they can been done in one sitting, bilateral pallidotomies may carry an increased risk of speech difficulties and cognitive decline.
RESULTS
At present, the major focus of therapy has been on improvement of motor symptoms. Although 97% of patients showed at least some improvement (some poor results may derive from inclusion of some patients with secondary Parkinsonism), in 17% the degree of improvement was graded as mild.
Significant reduction of levodopa induced dyskinesias occurred in 90%. Bradykinesia improved in 85%, rigidity in 75%, and tremor in 57%. Other areas of improvement include: speech, gait, posture, and reduction of on-off phenomenon and freezing. Although symptoms may be ameliorated, overall functional improvement may not be remarkable32.
Although dosages of antiparkinsonian medication are often reduced, continued medical therapy is usually required, and no change is made for at least 2 months following pallidotomy.
Indications are that beneficial surgical effects can last ≥ 5 years, with early failures possibly due to production of too small of a lesion, and late failures possibly due to progression of the disease.
Ongoing studies are investigating longer term results, microelectrode recording, alternate lesioning targets, the role of early surgery… Until more information is available, one cannot make any statements about the optimal target, localizing method, etc.
COMPLICATIONS
Visual field deficit occurs in 2.5% due to proximity of the optic tract to the globus pallidus. Hemiparesis may occur due to the nearby passage of the internal capsule. Intracerebral hemorrhage may also occur. Dysarthria occurs in ≈ 8%, but is usually temporary. Speech difficulties and also cognitive decline may be more risky when bilateral pallidotomies are performed at the same sitting.
THALAMIC LESIONS
Lesioning the thalamic ventralis intermedius nucleus (VIM) nucleus reduces Parkinsonian tremor in > 85%. It can also be useful in the treatment of rigidity and drug induced dyskinesias by extending the lesioning anteriorly to include the ventral oralis. However thalamotomy does not improve symptoms of akinesia or bradykinesia and can result in worsening of gait symptoms or speech problems.
SUBTHALAMOTOMY
Lesioning the subthalamic nucleus (STN) is classically associated with intractable hemiballism. There are few studies as a result, but the limited data suggests that selective lesioning in this region provides relief on par with pallidotomy. Postoperative hemichorea is a known complication but is generally transitory and mild33. DBS in this region may be a better option (see page 532).
19.3. Dystonia
Pallidal stimulation is the primary surgical treatment for dystonia34. Response is better for primary dystonias, e.g. tardive dystonias than for secondary dystonias such as postanoxic, postencephalitic, perinatal and poststroke dystonias34 (other targets need to be assessed).
For primary dystonias, the globus pallidus internus (GPi) is the most common primary target (see Figure 19-1, page 533). Good results have also been reported with STN DBS.
19.4. Spasticity
Results from lesions in upper motor neuron pathway, causing absence of inhibitory influence on alpha motor-neurons (αMN) (alpha spasticity) as well as on gamma motor neurons (intrafusal fibers) (gamma spasticity). Causes uninhibited reflex arc between αMN and Ia afferents from muscle spindles resulting in a hypertonic state of muscles with clonus, and sometimes with involuntary movements. Etiologies include: injury to cerebrum (e.g. stroke) or spinal cord (spasticity is an expected sequelae of spinal cord injury rostral to the conus medullaris), multiple sclerosis, and congenital abnormalities (e.g. cerebral palsy, spinal dysraphism).
CLINICAL
Increased resistance to passive movement, hyperactive muscle stretch reflexes, simultaneous activation of antagonistic muscle groups, may occur spontaneously or in response to minimal stimuli. Characteristic postures include scissoring of legs or hyperflexion of thighs. May be painful, or may disrupt patient’s ability to sit in wheel-chair, lay in bed, drive modified vehicles, sleep, etc. May also promote development of decubitus ulcers. A spastic bladder will have low capacity and will empty spontaneously.
Spasticity is often exacerbated by same type of stimuli that aggravate autonomic hyperreflexia (see Autonomic hyperreflexia, page 1000).
The onset of spasticity following spinal cord injury may be delayed for several days to months (the latency period is attributed to “spinal shock”, during which time there is decreased tone and reflexes)35 (see page 930). Onset of spasticity following spinal shock starts with increasing flexor synergistic activity over 3-6 mos, with more gradual increases of extensor synergy which ultimately predominates in most cases.
Some “beneficial” aspects of mild spasticity:
1. maintains muscle tone and therefore bulk: provides support for patient when sitting in wheelchair, helps prevent decubitus ulcers over bony prominences
2. muscle contractions may help prevent DVTs
3. may be useful in bracing
Grading spasticity
Assessment should be performed with patient supine and relaxed. The Ashworth scale (see Table 19-2) is commonly used for the clinical grading of the severity of spasticity. Many attempts have been made to quantitate spasticity electrodiagnostically, the most reliable has been H-reflex measurement.
Table 19-2 Ashworth scores36
|
Ashworth score |
Degree of muscle tone |
|
1 |
no increase in tone (normal) |
|
2 |
slight increase, a “catch” with flexion or extension |
|
3 |
more marked increase, passive movements easy |
|
4 |
considerable increase, passive movements difficult |
|
5 |
affected part rigid in flexion or extension |
TREATMENT
Depends on extent of useful function (or potential for same) present in areas at and below the level where spasticity starts (complete spinal cord injuries usually have little function, whereas patients with MS may have significant function).
MEDICAL TREATMENT
1. “prevention”: measures to decrease inciting stimuli (physical therapy to prevent joint damage, good skin & bladder care… see Autonomic hyperreflexia, page 1000)
2. prolonged stretching (more than just range of motion): not only prevents joint and muscle contractures, but modulates spasticity
3. oral medications37 (see Surgical treatment below for intrathecal medications): few drugs are effective without significant undesirable side effects
A. diazepam (Valium®): activates GABAA receptors, increases pre-synaptic inhibition of αMN. Most useful in patients with complete spinal cord injuries. Rx start with 2 mg PO BID-TID, increase by 2 mg per day q 3 days up to a max of 20 mg TID.
SIDE EFFECTS: may cause sedation, weakness, decreased stamina (most of which may be minimized by gradual increases in dosage). Abrupt discontinuation may cause depression, seizures, withdrawal syndrome
B. baclofen (Lioresal®): activates presynaptic GABAB receptors of Ia muscle spindle afferents, causes pre-synaptic inhibition of αMN and decreases nociception. May be most useful in patients with spinal cord lesions (complete or incomplete).
Rx start with 5 mg PO BID-TID, increase in 5 mg increments q 3 days up to max of 20 mg QID. SIDE EFFECTS: sedation, lowers seizure threshold. Must be tapered to discontinue (abrupt discontinuation may result in seizures, rebound hyperspasticity or hallucinations).
C. dantrolene (Dantrium®): reduces depolarization induced Ca++ influx into sarcoplasmic reticulum of skeletal muscle; acts on all skeletal muscle (with no preferential effect on spasmogenic reflex arc).
Rx start with 25 mg PO q d, increase q 4-7 days to BID, TID, then QID, then by 25 mg per day up to max of ≈ 100 mg QID (may take 1 week at new steady state to see effect); SIDE EFFECTS: muscle weakness (may make ambulation impossible), sedation, idiosyncratic hepatitis (may be fatal; more common in patients on > 300 mg/d x > 2 mos) that is often preceded by anorexia, abdominal pain, N/V; D/C if no benefit is seen by ≈ 45 days; follow LFTs (SGPT or SGOT)
D. progabide: activates both GABAA and GABAB receptors. Useful for patients with severe flexor spasms
E. theoretical benefits may be derived from other agents, but they have not been used for some practical reason in each case 35 (e.g. phenothiazines reduce gamma spasticity, but only at high PO doses or parenterally; clonidine; Darvon; tetrahydrocannabinal…)
SURGICAL TREATMENT
Reserved for spasticity refractory to medical treatment, or where side effects of medications are intolerable. Generally either orthopedic (e.g. tendon release operations (tenotomies) of heel cord or hamstrings, iliopsoas myotomies, etc.) or neurosurgical (e.g. nerve blocks, neurectomies, myelotomy, etc.).
1. nonablative procedures
A. intrathecal (IT) baclofen (see below)
B. intrathecal morphine (tolerance and dependence may develop)
C. electrical stimulation via percutaneously placed epidural electrodes38
2. ablative procedures, with preservation of potential for ambulation
A. motor point block35 (intramuscular phenol neurolysis): preserves sensation and existing voluntary function. Especially useful in patients with incomplete myelopathies; time consuming
B. phenol nerve block: similar to motor point block, but used when spasticity more severe and complete block of muscle desired. Open phenol block used instead of percutaneous when nerve is mixed and sensory preservation is desired (also reduces post-block dysesthesias)39
C. selective neurectomies35
1. sciatic neurectomy (may be done with RF lesion)40
2. obturator neurectomy: useful if strong hip adductor spasticity that causes scissoring and wasted energy expenditure in ambulating
3. pudendal neurectomy: useful if excessive detrusor dyssynergy interferes with bladder retraining
D. percutaneous radiofrequency foraminal rhizotomy: small unmyelinated sensory fibers are more sensitive to RF lesions than larger myelinated A-alpha fibers of motor units.
Technique: start at S1 on one side, and work up to T12, then repeat on other side. At each level: verify needle position by stimulating with 0.1-0.5 V and watch for movement in appropriate myotome (tip should be extradural, avoid subarachnoid placement), ablate with 70-80° C x 2 mins for S1, and 70° C x 2 mins for L5 to T12 (to preserve motor function). If symptoms recur, may repeat with lesions at 90° C x 2 mins
E. myelotomies41
1. Bischof’s myelotomy: divides anterior and posterior horns via laterally placed incision, disrupts reflex arc. No effect on α–spasticity
2. midline “T” myelotomy: interrupts reflex arc from sensory to motor units without disrupting connections from corticospinal tract to anterior motor neurons. Slightly higher risk of losing motor function. Technique: laminectomy from T11 to L1. Mobilize midline dorsal longitudinal vein and incise cord in midline from T12 at a depth of 3 mm to S1 at a depth of 4 mm (preserving S2-S4 maintains bladder reflex pathways. Unilateral extension up to conus medullaris reduces bladder spasticity and increases capacity before reflex emptying occurs)
F. selective dorsal rhizotomy42, 43: uses intraoperative EMG and electrophysio-logical stimulation to eliminate sensory rootlets involved in “handicapping spasticity” (leaves rootlets subserving “useful spasticity” intact). Interrupts the afferent limb of pathologic reflex arc. May be temporary, but seems to persist at least ≈ 5 yrs. No effect on α–spasticity. Ambulatory children with cerebral palsy have improved gait, nonambulatory children are improved but are still not able to ambulate afterwards
G. stereotactic thalamotomy or dentatotomy: may be useful in cerebral palsy44. Useful for unilateral dystonia, but cannot be used for bilateral dystonia as bilateral lesions would be required which jeopardizes speech. Effective only for dystonia distal to shoulders or hips, and should not be used if the condition is rapidly progressive
3. ablative procedures, with sacrifice of potential for ambulation (in complete cord injuries, nonablative procedures are not indicated because there is no motor function to recover). Used after failure of percutaneous rhizotomy (see above) and “T” myelotomy (see above)
A. intrathecal injection of 6 ml of 10% phenol (by weight) in glycerin mixed with 4 ml of iohexol (Omnipaque® 300) (see page 122) for a final concentration of 6% phenol and ≈ 120 mg iodine/ml. Administered via LP at L2-3 interspace with patient in lateral decubitus position (most symptomatic side down) under fluoro until T12-S1 nerve root sleeves are filled (sparing S2-4 for bladder function). Patient is maintained in this position x 20-30 mins and then kept sitting upright x 4 hrs45 (absolute alcohol provides more permanent blocks, but is hypobaric and more difficult to control)
B. selective anterior rhizotomy: results in flaccid paralysis with denervation atrophy of muscles
C. neurectomies, often combined with tenotomies40
D. intramuscular neurolysis by phenol injection40
E. cordectomy 46: most drastic measure, reserved for patients who do not respond to any other measure. Results in total flaccidity with loss of benefits from mild spasticity. Converts bladder from UMN to LMN control. Works well for progressive deficit from syringomyelia and for spasticity, but poor for “phantom” leg pain47
F. cordotomy: rarely used
INTRATHECAL BACLOFEN48-51
Selection criteria used in one study50 are shown in Table 19-3. Other indications include: CVA52, cerebral palsy, TBI, dystonia, stiff-man syndrome.
Test doses: Incremental test doses of 50, 75, and then 100 mcg intrathecal baclofen (ITB) via lumbar puncture or temporary catheter were used50, randomly alternated with placebo, with dose escalation halted if a response to active drug occurred. The following parameters were evaluated at 0.5, 1, 2, 4, 8 & 24 hrs post injection: pulse and respiratory rate, BP, hypertonia (Ashworth score, see Table 19-2, page 537), reflexes, spasm score, voluntary muscle movement, and adverse effects (if any, including seizures). Pump implantation was offered if there was a 2 point reduction in the Ashworth score and muscle spasm score for ≥ 4 hrs after bolus injection of active drug without intolerable side effects. Usual daily dose for ITB is twice the test dose, typically 200 micrograms/d.
Alternatively, give 25 mcg IT in the O.R., and if the patient improves, insert subcutaneous pump37.
Table 19-3 Selection criteria for baclofen pump
|
• age 18-65 yrs (older patients treated on compassionate use basis) • able to give informed consent • severe, chronic spasticity (≥ 12 mos duration) due to spinal cord lesion or MS • spasticity refractory to oral drugs (including baclofen), or unacceptable side effects • no CSF block (e.g. on myelography) • positive response to IT baclofen at test dose ≤ 100 μg and no response to placebo • no implanted programmable device such as cardiac pacemaker* • females of childbearing potential: not pregnant & using adequate contraception • no hypersensitivity (allergy) to baclofen • no history of stroke, impaired renal function, or severe hepatic or GI disease |
* this study used a programmable IT pump
Pump systems: Available programmable systems include N’Vision, manufactured by Medtronic, Inc., Minneapolis, MN.
Insertion technique: IT catheter is typically inserted ≈ L2-3, and is threaded rostrally ≈ 3 levels, but should be no higher than T10 (risk of rostral progression of hypotonia).
Post-op orders: Guidelines for post-operative orders following baclofen pump insertion
1. admit PACU, transfer to:
A. floor if insertion follows test dosing or if patient has just been transitioned from stable PO dose
B. ICU if there has been a hiatus in baclofen therapy
2. neuro checks q 2 hrs for 1st 24 hours
3. baclofen:
A. for patients on oral or IV baclofen: continue baclofen at the previous dose via the same route (oral or IV) until the ITB takes effect (usually 2-4 hrs, full effect is delayed up to 24 hrs). The IV/PO drug is then tapered
B. if there has been a hiatus in baclofen therapy: baclofen 20 mg PO QID
4. have 2 vials of IV physostigmine available and labeled “FOR EMERGENCY USE ONLY” for possible baclofen overdose
Baclofen overdose:
1. ABCs (airway/breathing/circulation). Intubate if necessary
2. empty pump reservoir to stop drug flow (record amount withdrawn)
3. administer physostigmine if not contraindicated:
A. Rx adult: 0.5-1.0 mg IM or IV @ rate ≤ 1 mg/min (may repeat q 10-30 minutes PRN)
B. Rx peds: 0.02 mg/kg IM or IV @ rate ≤ 0.5 mg/min (may repeat q 5-10 min up to 2 mg max)
4. withdraw 30-40 ml CSF either via LP or through catheter access port
5. notify the pump manufacturer
Complications: Device-related complications are shown in Table 19-4. The frequency of most is ≈ 1%, except catheter-related problems which had a rate of ≈ 30% 50.
Complications related to the drug therapy itself include: overdosage problems (rostral progression of hypotonia, respiratory depression, coma, and seizures.
Table 19-4 ITB pump complications*
|
• mechanical problems • pump underinfusion • catheter problems: occlusion, kink, dislodgment, cut, break or disconnection • wound complications • pocket erosion • incisional pain • infection • seroma (may require aspiration) • CSF collection |
* device-related complications requiring a secondary invasive procedure
Intrathecal baclofen withdrawal: Interruption of ITB therapy may occur as a result of: empty pump reservoir, pump battery failure, catheter migration/breakage/kinking/disconnection/occlusion, programming error. Steps in assessing the infusion system are shown in Table 19-5.
The severity of withdrawal syndrome depends on dose of drug used (increased with higher dose) and duration of therapy (increased with longer therapy).
Syndromes: with abrupt discontinuation of ITB
• mild withdrawal symptoms: return of spasticity and rigidity, tachycardia, piloerection (goosebumps) & pruritus
• more significant withdrawal symptoms: seizures & hallucinations
• severe withdrawal symptoms (estimated incidence: 3-5%)Coffey, 2002 #5531]: increased rebound spasticity, rigidity, fever, labile BP, and reduced level of consciousness (resembling but distinct from malignant hyperthermia (see page 5) or neuroleptic malignant syndrome). If untreated, the severe syndrome can progress over 24-72 hours to rhabdomyolysis (with elevated creatine kinase (CK) and transaminase), hepatic and renal failure, DIC, and occasionally death
Table 19-5 Assessing ITB infusion systems
|
• interrogate the pump (with device programmer) • refill reservoir with drug if empty (by experienced ITB practitioner) • obtain AP & lateral x-rays to assess location of catheter tip and to look for breaks, kinks or migration |
Management of abrupt ITB withdrawal syndrome53:
1. ABCs (airway/breathing/circulation). Intubate if necessary
2. primary goal is to reestablish ITB therapy at the same dose as soon as possible
3. assess pump/system as outlined in Table 19-5
4. early use of high-dose oral/enteral baclofen: ≥ 120 mg/d in 6-8 divided doses if the patient’s condition permits (NB: PO baclofen is not reliable as the lone treatment for ITB withdrawal, and safety not established for age < 12 yrs)
5. attempt to restore ITB therapy at or near pre-withdrawal dosage by experienced physician by one of the following:
A. using a programmed bolus through the pump
B. via the catheter access port
C. via LP
D. via new externalized catheter
6. if restoration of ITB therapy is delayed and if symptoms persist
A. move pt. to ICU if not already there
B. parenteral benzodiazepine infusion: diazepam or midazolam. Titrate dose to reduce muscle rigidity, hyperthermia, BP lability, seizures
C. cyproheptadine54: a serotonin antagonist. Start with 4 mg po q 6 hrs
D. diphenhydramine 50 mg PO or IM, may repeat q 6 hrs for pruritus
E. dantrolene may not be as effective as it is for malignant hyperthermia
If it is necessary to electively (or semi-electively) remove a pump system, the optimal scenario is to gradually taper the drug by reprogramming the pump and/or by filling the reservoir with solution of decreased baclofen concentration.
19.5. Torticollis
AKA wry neck. A form of dystonia resulting in a failure to control head position (if shoulders or trunk are also involved, dystonia is a more proper label).
A symptom of diverse causes. Differential diagnosis includes:
1. congenital torticollis (may be the initial presentation of dystonia musculorum deformans)
2. spasmodic torticollis, AKA wry neck: a specific subtype of torticollis that is idiopathic by definition. The shortened sternocleidomastoid (SCM) muscle is usually in spasm
3. extrapyramidal lesions (including degenerative): often alleviated by lying down; EMG shows abnormal grouped activity
4. psychogenic (often mentioned, seldom verified)
5. torticollis from atlantoaxial rotatory subluxation: (see page 955) the elongated SCM may be in spasm (opposite of that in spasmodic torticollis)
6. neurovascular compression of the 11th nerve (see below)
7. hemorrhage into sternocleidomastoid muscle (with subsequent contracture)
8. infection of the cervical spine
9. cervical adenitis
10. syringomyelia
11. cerebellar tumors in children
12. bulbar palsies
13. “pseudotorticollis” may develop as an unconscious correction to reduce diplopia that occurs with imbalance of extraocular eye musculature
Non-surgical treatment of torticollis
Should be attempted first, and includes:
1. relaxation training, including biofeedback
2. thorough neuropsychiatric evaluation
3. trans-epidermal neuro-stimulation (TENS) to the neck
Surgical procedures
Reserved for disabling, refractory cases. Includes:
1. dorsal cord stimulation
2. local injection of botulinum toxin: may work for retrocollis, is poor for lateral torticollis (must inject posterior cervicals and both SCM, and may cause temporary pharyngeal muscle dysfunction resulting in dysphagia), and is totally ineffective for anterocollis
3. selective rhizotomy and spinal accessory nerve section
Other treatments for torticollis include
1. stereotactic electrocoagulation of Forel’s H1 field
TORTICOLLIS OF 11TH NERVE ORIGIN
1. usually a horizontal type (manifests as horizontal head movement) which may be exacerbated when supine (unlike extrapyramidal torticollis)
2. contraction of SCM is usually accompanied by activity in contralateral agonist muscles
3. may be treated surgically. Procedures include
A. sectioning of the anastomotic branches between the 11th nerve and the upper cervical posterior root (C1 anastomotic branch is sensory only)
B. microvascular decompression of the 11th nerve (most cases caused by vertebral artery, but PICA compression is also described55). Relief takes several weeks post-op
19.6. Neurovascular compression syndromes
Syndromes due to compression of cranial nerves at the root entry zone (REZ) (or in the case of motor nerves, root exit zone). The REZ (AKA Obersteiner-Redlich zone) is the point where central myelin (from oligodendroglial cells) changes to peripheral myelin (from Schwann cells).
Syndromes include:
1. trigeminal neuralgia (see Trigeminal neuralgia, page 551)
2. hemifacial spasm: see below
3. disabling positional vertigo
4. some forms of torticollis of 11th nerve origin (see Torticollis above)
19.6.1. Hemifacial spasm
Key concepts:
• intermittent unilateral painless contractions of facial muscles
• typically caused by compression of VII nerve by AICA
• along with palatal myoclonus: the only movement disorder that persists in sleep
• responds well to microvascular decompression, but risk of hearing loss is ≈ 20%
Hemifacial spasm (HFS) is a condition of intermittent, painless, involuntary, spasmodic contractions of muscles innervated by the facial nerve in one side of the face only. May be limited to the upper or lower half of the face only, and excess lacrimation may be present. HFS usually begins with rare contractions of the orbicularis oculi, and slowly progresses to involve the entire half of the face and increases in frequency until the ability to see out of the affected eye is impaired.
HFS may be associated with trigeminal neuralgia, geniculate neuralgia (see Tic convulsifpage 564), or vestibular and/or cochlear56 nerve dysfunction.
HFS is more common in women, is seen more often on the left, and usually presents after the teenages. Auditory function testing reveals abnormal acoustic middle ear reflex in almost half of patients, indicating some degree of VIII compromise56.
Meige’s syndrome: hemifacial spasm with oral movements.
HFS and palatal myoclonus are the only involuntary movement disorders that persist during sleep57.
ETIOLOGIES
1. vascular compression syndrome (see below): the most common etiology (much more common than with trigeminal neuralgia)
2. idiopathic
3. tumor compressing the nerve
4. can follow some cases of Bell’s palsy
5. conditions that can mimic HFS
A. blepharospasm (bilateral spasmodic closure of the orbicularis oculi muscles) which is more common in the elderly, and may be associated with organic brain syndrome. Blepharospasm is notorious for disappearing when the patient presents for medical evaluation (an effect of alerting), but may be elicited by asking patient to gently close the eyes and then rapidly open them, following which a blepharospasm may occur. HFS usually involves more than the ocular muscles
B. facial myokymia: continuous facial spasm which may be a manifestation of an intrinsic brainstem glioma or of multiple sclerosis. Often associated with other findings
Vascular compression
HFS is usually caused by compression of the facial nerve at the root exit zone (REZ) by a vessel, which is most often an artery (most commonly AICA58 (either pre- or postmeatal59), but other vascular possibilities include an elongated PICA, SCA, a tortuous VA, the cochlear artery, a dolichoectatic basilar artery, AICA branches…), aneurysm, a vascular malformation, and rarely, veins have been implicated. In typical HFS (onset in the orbicularis oculi, and progressing downward over the face), the vessel impinges on the antero-caudal aspect of the VII/VIII nerve complex, in atypical HFS (beginning in the buccal muscles and progressing upward over the face) the compression is rostral or posterior to VII60.
Vessels contacting the REZ of the vestibular nerve may cause vertigo, whereas tinnitus or hearing loss may result from cochlear nerve REZ compression.
Infrequently, benign tumors or a cyst in the cerebellopontine angle, multiple sclerosis, adhesions, or osseous skull deformities will be the cause of HFS.
Evidence indicates that there is not cross (ephaptic) conduction at the compressed REZ, but that the facial motonucleus is involved secondarily as a result of the REZ compression, via a phenomenon similar to kindling61. In addition to the spasm, a 2nd electro-physiological phenomenon associated with HFS is synkinesis, where stimulation of one branch of the facial nerve results in delayed discharges through another branch (average latency: 11 mSec62).
EVALUATION
In typical cases of HFS, the diagnostic work-up is negative.
Most patients should have MRI of the posterior fossa (CT scan is less sensitive here) to R/O tumors or AVMs.
Vertebral angiography is usually not performed if imaging is normal. The neurovascular compression responsible for HFS usually cannot be identified on angiography.
TREATMENT
MEDICAL MANAGEMENT
HFS is generally a surgical condition. Early, mild cases may be managed expectantly. Carbamazepine and phenytoin are generally ineffective, unlike the situation with the causally similar condition of trigeminal neuralgia. Local injection of botulinum toxin (Oculinum®) may be effective in treating HFS and/or blepharospasm63, 64. Baclofen has been advocated but is not very effective.
SURGICAL MANAGEMENT
Many ablative procedures are effective for HFS (including sectioning of divisions of the facial nerve), however, this leaves the patient with some degree of facial paresis. The current procedure of choice for HFS is microvascular decompression (MVD) wherein the offending vessel is physically moved off of the nerve, and a sponge (e.g. Ivalon®, polyvinyl formyl alcohol foam) is interposed as a cushion. Other cushions may not prove to be as satisfactory (muscle may disappear, and Teflon felt may thin65).
Most often, the offending vessel approaches the nerve at a right angle, and causes grooving in the nerve. Compression must occur at the root exit zone; decompression of vessels impinging distal to this area is usually ineffective.
Operative risks: see below.
Post-operatively, there may be episodes of mild HFS, however they usually begin to diminish 2-3 days following MVD. Severe spasm that does not abate suggests failure to achieve adequate decompression, and reoperation should be considered.
Surgical results of MVD depends on the duration of symptoms (shorter duration has better prognosis) as well as on the age of the patient (elderly patients do less well). Complete resolution of HFS occurred in 44 (81%) of 54 patients undergoing MVD, however, 6 of these patients had relapse66. 5 patients (9%) had partial improvement, and 5 (9%) had no relief.
Technique of MVD
Intraoperative brainstem auditory evoked potential (BAER)67, or more applicable, direct VIII nerve monitoring68 may help prevent hearing loss during MVD for 7th or 8th nerve dysfunction. Furthermore, monitoring for the disappearance of the (delayed) syn-kinetic response may aid in determining when adequate decompression has been achieved (generally reserved for teaching institutions)61.
For a diagram of the normal anatomy of the CPA, see Figure 5-8, page 90. The facial nerve should not be manipulated, and one should avoid dissection around the VII and VIII nerves near the IAC69. Vessels must be preserved, especially the cochlear artery and small perforators.
Place gentle medial traction on the cerebellum (< 1 cm is recommended69), and incise the arachnoid membrane between the flocculus and the eighth nerve (to avoid tension on nerves that could cause post-op deficit). The IX nerve may be followed medially from the jugular foramen to locate the origin of the VII nerve (the origin of VII is 4 mm cephalad and 2 mm anterior to that of the IX nerve70).
SURGICAL RESULTS
Complete resolution of spasm occurs in ≈ 85-93%65, 71-74. Spasm is diminished in 9%, and unchanged in 6%74. Of 29 patients with complete relief, 25 (86%) had immediate post-op resolution, and the remaining 4 patients took from 3 mos to 3 yrs to attain quiescence.
Recurrence
Return of symptoms after a period of complete resolution of HFS occurs in up to 10% of patients, 86% of recurrences happen within 2 yrs of surgery, and the risk of developing recurrence after 2 yrs of post-op relief is only ≈ 1%74.
Surgical complications
1. ipsilateral hearing loss: may occur from traction injury or a vasospasm
A. total hearing loss occurs in ≈ 13% (range: 1.6-15%) (2.8% in one series56, 15% in another series66)
B. partial hearing loss: 6%
2. facial weakness
A. transient: 18%
B. permanent facial weakness: 6%72
3. ataxia in 1-6%
4. other complications that are minor or temporary include:
A. aseptic meningitis (AKA hemogenic meningitis) in 8.2%
B. hoarseness or dysphagia in 14%
C. CSF rhinorrhea in 0.3%
D. perioral herpes in 3%69
19.7. Hyperhidrosis
Either essential (primary, or idiopathic) or secondary (etiologies include: hyperthyroidism, diabetes mellitus, pheochromocytoma, acromegaly, parkinsonism, CNS trauma, syringomyelia, hypothalamic tumors, menopause)75.
Due to overactivity of eccrine sweat glands (found over entire body, highest concentration in palms and soles of feet). They produce a hypotonic secretion with saline as the primary constituent. These glands are under control of the sympathetic nervous system, however, the neurotransmitter is paradoxically acetylcholine (i.e. they are cholinergic, unlike most sympathetic end organs which are adrenergic). Most eccrine sweat glands serve a thermoregulatory function, however, those on the palms and soles respond primarily to emotional stress75.
Essential hyperhidrosis is a generalized condition that usually manifests mostly in the palms. The incidence is unknown, although it was ≈ 1% in an Israeli study (probably high).
Treatment
Mild cases are treated medically with:
1. topical agents: astringents (potassium permanganate, tannic acid…) or antiperspirants (contact dermatitis usually limits use of these agents)
2. or systemically with anticholinergics: including atropine, probantheline bromide… (side effects of dry mouth and blurred vision usually limits use of these)
3. tap water iontophoresis: may produce keratinization of palmar epithelium
Severe cases refractory to medical therapy may be candidates for surgical sympathectomy (see below).
19.8. Tremor
Thalamotomy or thalamic stimulation may be useful for tremors that are refractory to medical treatment (including parkinsonian (see page 534), essential76, 77, cerebellar and post-traumatic)30.
19.9. Sympathectomy
Cardiac sympathectomy
With the advances in percutaneous coronary artery techniques, cardiovascular surgery and drugs, cardiac sympathectomy for angina pectoris has found less application. However, it may still be useful in patients who have no further treatment options. Bilateral sympathectomy from the stellate ganglion through the T7 ganglia is required. Newer thoracoscopic techniques may revive some interest in this.
UPPER EXTREMITY SYMPATHECTOMY
Various pathologies that may be indications for upper extremity sympathectomy are shown in Table 19-6.
Removal of the only second thoracic ganglion is probably adequate, and avoids a Horner’s syndrome in most. Techniques used include: anterior transthoracic, thoracic endoscopic78, percutaneous radiofrequency, and supraclavicular. An approach via a midline posterior incision with a T3 costotransversectomy allows bilateral access75, 79. The risk of significant complications is ≈ 5% and include pneumothorax, intercostal neuralgia, spinal cord injury, and Horner’s syndrome.
Table 19-6 Indications for UE sympathectomy
|
• essential hyperhidrosis • primary Raynaud’s disease • shoulder-hand syndrome • intractable angina • ± causalgia major (see page 576) |
UPPER THORACIC SYMPATHECTOMY
Approaches include:
1. posterior paravertebral approach
2. axillary thoracotomy with transthoracic exposure of the sympathetic chain
3. supraclavicular, retropleural exposure
4. percutaneous radiofrequency technique80, 81
5. video endoscopic approach82
LUMBAR SYMPATHECTOMY
Primary indication is for causalgia major of the lower extremity. Preoperative lumbar sympathetic blocks may be utilized to evaluate patient for response.
Removal of the L2 and L3 sympathetic ganglion is usually adequate to remove sym-pathetic tone from the lower extremities (occasionally L1 and sometimes T12 are also removed for causalgia of the thigh).
The most common approach is a retroperitoneal approach through a flank incision. The patient is placed in a lateral oblique position, and the skin incision is made from the anterior superior iliac spine to the tip of the 12th rib. The peritoneum is dissected from the muscular wall and is retracted anteriorly. The kidney and ureter are retracted anteriorly; injury to the ureter being a major risk of the operation. The sympathetic chain is identified on the lateral aspect of the vertebral bodies. The vena cava makes a right-sided approach more difficult as the aorta is easier to deal with on left-sided approaches.
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