26.1. Dizziness and vertigo
Differential diagnosis of dizziness:
1. near syncope: some overlap with syncope (see Syncope and apoplexy, page 1199)
A. orthostatic hypotension
B. cardiogenic hypotension
1. arrhythmia
2. valvular disease
C. vasovagal episode
D. hypersensitive carotid sinus: (see Syncope and apoplexy, page 1199)
2. dysequilibrium
A. multiple sensory deficits: e.g. peripheral neuropathy, visual impairment
B. cerebellar degeneration
3. vertigo: sensation of movement (usually spinning)
A. inner ear dysfunction
1. labyrinthitis
2. Meniere’s disease (see below)
3. trauma: endolymphatic leak
4. drugs: especially aminoglycosides
5. benign (paroxysmal) positional vertigo 1: AKA cupulolithiasis. Attacks of severe vertigo when the head is turned to certain positions (usually in bed). Due to calcium concretions in the semicircular canals. Self limited (most cases do not last > 1 year). No hearing loss
6. syphilis
7. vertebrobasilar insufficiency: see page 1158
B. vestibular nerve dysfunction
1. vestibular neuronitis: sudden onset of vertigo, gradual improvement
2. compression:
a. meningioma
b. vestibular schwannoma: usually slowly progressive ataxia instead of severe vertigo. BAER latencies usually abnormal. CT or MRI usually abnormal
C. disabling positional vertigo: as described by Jannetta et al.2, constant disabling positional vertigo or dysequilibrium, causing ≈ constant nausea, no vestibular dysfunction nor hearing loss (tinnitus may be present). One possible cause is vascular compression of the vestibular nerve which may respond to microvascular decompression
D. brainstem dysfunction
1. vascular disease (see Vertebrobasilar insufficiency, page 1158): less distinct vestibular symptoms, prominent nonvestibular symptoms
2. migraine: especially basilar artery migraine
3. demyelinating disease: e.g. multiple sclerosis
4. drugs: anticonvulsants, alcohol, sedatives/hypnotics, salicylates
E. dysfunction of cervical proprioceptors: as in cervical osteoarthritis
4. poorly defined light-headedness: mostly psychiatric. May also include:
A. hyperventilation
B. hypoglycemia
C. anxiety neurosis
D. hysterical
VESTIBULAR NEURECTOMY
Complete loss of vestibular function from one side is thought to produce transient vertigo due to the mismatch of vestibular input from the two ears. Theoretically, a central compensatory mechanism (the “cerebellar clamp”) results in the amelioration of symptoms. In cases of unilateral fluctuating vestibular dysfunction, this compensatory mechanism may be impaired. Unilateral selective vestibular neurectomy (SVN) may convert the fluctuating or partial loss to a complete cessation of input and facilitate compensation. Bilateral SVN is often complicated by oscillopsia (see page 839, AKA Dandy’s syndrome, with difficulty in maintaining balance in the dark due to loss of the vestibulo-ocular reflex) and is to be avoided.
Indications
The two conditions for which SVN is most commonly employed are Meniere’s disease (see below) and partial vestibular injury (viral or traumatic). SVN may be indicated in disabling cases refractory to medical or non-destructive surgical treatment when vestibular studies demonstrate continued or progressive uncompensated vestibular dysfunction3.
SVN preserves hearing and in Meniere’s disease is > 90% effective in eliminating episodic vertiginous spells (≈ 80% success rate in non-Meniere’s cases), but is unlikely to improve stability with rapid head movement.
Surgical approaches for SVN
1. retrolabyrinthine, AKA postauricular approach: anterior to sigmoid sinus. Primary choice in patients with Meniere’s disease who have not had previous endolymphatic sac (ELS) procedures since it permits simultaneous SVN and decompression of the endolymphatic sac. Requires mastoidectomy with skeletonization of the semicircular canals and ELS. The dural opening is bounded anteriorly by the posterior semicircular canal, posteriorly by the sigmoid sinus. Water-tight dural closure is difficult
2. retrosigmoid, AKA posterior fossa, AKA suboccipital approach: posterior to sigmoid sinus. The original approach plied by Dandy in pre-microsurgical era, usually sacrificed hearing, and occasionally facial nerve function. Better results today with microscopic techniques. Indicated for cases other than Meniere’s disease where there is no need for identification of the ELS. Also the best approach for positive identification of eighth nerve
3. middle fossa (extradural) approach: the fibers of the vestibular division may be more segregated from the cochlear fibers in the IAC than in the CPA, thus permitting more complete section of the vestibular nerve. May be appropriate for failed response to SVN by the above approaches. Disadvantages: requires temporal lobe retraction, does not allow exposure of ELS, and higher morbidity and risk of damage to facial nerve4 than retrolabyrinthine approach
Surgical considerations for selective vestibular neurectomy
(Also see Figure 5-7, page 90)
• the vestibular nerve is in the superior half of the eighth nerve complex, and is slightly more gray in color than the cochlear division (due to less myelin5). They may be separated by a small vessel or by an indentation in the bundle
• facial (VII) nerve:
whiter than the VIII nerve complex
lies anterior and superiorly to the VIII nerve
EMG monitoring of the facial nerve is recommended
direct stimulation confirms the identification
• any vessels present on eighth nerve bundle must be preserved to save hearing (primarily, the artery of the auditory canal must be preserved)
• if no plane of cleavage can be defined between vestibular & cochlear divisions, the superior half of the nerve bundle is divided
• the endolymphatic sac lies ≈ midway between the posterior edge of the internal auditory meatus and the sigmoid sinus
26.2. Meniere’s disease
Key concepts:
• increased endolymphatic pressure
• clinical triad: vertigo, tinnitus & fluctuating hearing loss
• surgical options for failure of medical management include endolymphatic shunt or selective vestibular neurectomy
Probably due to a derangement of endolymphatic fluid regulation (a consistent finding is endolymphatic hydrops: increased endolymphatic volume and pressure with dilatation of endolymph spaces), with resultant fistulization into the perilymphatic spaces.
CLINICAL
Clinical triad
• attacks of violent vertigo (due to vestibular nerve dysfunction): usually the earliest and the most disabling symptom. Nausea, vomiting, and diaphoresis are frequent concomitants. Severe attacks may cause prostration. Vertigo may persist even after complete deafness. Balance is normal between attacks
• tinnitus: often described as resembling the sound of escaping steam, not a true “ringing”
• fluctuating low frequency hearing loss: may fluctuate for a periods of weeks to years, and may progress to permanent deafness if untreated (a sensation of fullness in the ear is commonly described6, however, this is nonspecific and may occur with hearing loss for any reason)
Drop attacks (“otolithic crises of Tumarkin”) occasionally occur.
Attack duration: ≈ 5-30 minutes (some say 2-6 hours), with a “post-ictal” period of fatigue lasting several hrs.
Frequency: varies from one or two attacks a year to several times per week.
Two subtypes differ from classical form: vestibular Meniere’s (episodic vertigo with normal hearing) and cochlear Meniere’s (few vestibular symptoms).
Natural course of syndrome is characterized by periods of remission. Eventually the vertiginous attacks either progress in severity, or “burn out” (being replaced by constant unsteadiness6).
EPIDEMIOLOGY
Incidence ≈ 1 per 100,000 population7. Most cases have onset between 30-60 years of age, rarely in youth or in the elderly. May become bilateral in 20%.
DIFFERENTIAL DIAGNOSIS
(Also see Differential diagnosis: Dizziness and vertigo on page 840 for more details)
1. benign (paroxysmal) positional vertigo: AKA cupulolithiasis. Self limited (most cases last < 1 year). No hearing loss
2. disabling positional vertigo: constant disabling positional vertigo or dysequilibrium, ≈ constant nausea, no vestibular dysfunction nor hearing loss (tinnitus may be present)
3. vestibular schwannoma: usually slowly progressive ataxia instead of episodic severe vertigo. BAER latencies usually abnormal. CT or MRI usually positive
4. vestibular neuronitis: sudden onset of vertigo with gradual improvement
5. vertebrobasilar insufficiency (VBI): less distinct vestibular symptoms, and prominence of nonvestibular symptoms (see page 1158)
DIAGNOSTIC STUDIES
1. electronystagmography (ENG) with bithermal caloric stimulation usually abnormal, may show blunted thermal responses
2. audiogram: low frequency hearing loss, fairly good preservation of discrimination and loudness recruitment, negative tone decay on impedance testing
3. BAER usually shows normal latencies
4. radiographic imaging (CT, MRI, etc.): no findings in Meniere’s disease
5. in bilateral cases, a VDRL should be checked to R/O luetic disease
TREATMENT
MEDICAL TREATMENT
1. reduced intake of salt (strict salt restriction is as effective as any medication) and caffeine
2. diuretics: taken daily until ear fullness abates, then PRN ear pressure (usually once or twice weekly suffices)
A. acetazolamide: Rx Diamox® sequels 500 mg p.o. q d x 1 week, increase to BID if symptoms persist. D/C if paresthesias develop. Do not use during 1st rimester of pregnancy
3. vestibular suppressants
A. diazepam (Valium®): probably the most effective
B. meclizine HCl (Antivert®): Rx Adult dose for vertigo associated with the vestibular system (during attacks): 25-100 mg/day PO divided. Dose for motion sickness: 25-50 mg PO one hr prior to stimulus. Supplied: 12.5, 25 & 50 mg tabs. SIDE EFFECTS: drowsiness
4. vasodilators: postulated to be mediated by increased cochlear blood flow: inhalation of 5-10% CO2 works well, but relief is short lived
SURGICAL TREATMENT
Reserved for incapacitating cases refractory to medical management. When functional hearing exists, procedures that spare hearing are preferred because of high incidence of bilateral involvement. Procedures include:
1. endolymphatic shunting procedures: to mastoid cavity (Arenberg shunt) or to subarachnoid space. Reserved for cases with serviceable hearing. ≈ 65% success rate (see below). If symptoms are relieved ≥ 1 year, then a recurrence would be treated by shunt revision, if < 1 year then vestibular neurectomy
2. direct application of corticosteroids to the inner ear
3. nonselective vestibular ablation (in cases with nonserviceable hearing on the side of involvement)
A. surgical labyrinthectomy
B. middle ear perfusion with gentamicin
C. translabyrinthine section of the 8th nerve
4. selective vestibular neurectomy (in cases with serviceable hearing): see page 840
OUTCOME
ENDOLYMPH SHUNTING PROCEDURES
Outcomes from 112 endolymphatic shunting procedures are shown in Table 26-1.
NEURECTOMY PROCEDURES
Vestibulocochlear nerve section (based on early posterior fossa surgery by Dandy; entire eighth nerve bundle was sectioned in 587 patients; all were deaf post-op): 90% relieved of vertigo, 5% unchanged and 5% worse; 9% incidence of facial paralysis (3% incidence of permanent paralysis).
Selective vestibular nerve section (sparing cochlear portion, 95 patients from Dandy): 10% had improved hearing, 28% unchanged, 48% worse, 14% deaf.
Retrolabyrinthine approach: in 32 patients with Meniere’s syndrome (25 failed endolymph shunt) responding to survey, 85% had complete relief of vertigo, 6% improved, 9% no relief (one of whom responded to middle fossa neurectomy)5.
Complications and untoward effects
Patients with little vestibular nerve function pre-op (determined by ENG) usually have little difficulty immediately following vestibular neurectomy; patients with more function may have a transient worsening post-op until they accommodate.
Among 42 patients undergoing retrolabyrinthine approach: none lost hearing as a result of surgery, no facial weakness, one CSF rhinorrhea requiring re-operation, and one meningitis with good outcome5.
In post-op failures, check ENG. If any vestibular nerve function is demonstrated on operated side, then the nerve section was incomplete; consider re-operating.
26.3. Facial nerve palsy
Severity of facial palsy is graded with the House and Brackmann scale (see Table 21-27, page 622).
LOCALIZING SITE OF LESION
Central facial palsy (AKA supranuclear facial palsy)
The cortical representation for facial movement occurs in the motor strip along the lateral aspect (just above the most inferior opercular portion of the precentral gyrus). The keys to differentiating central paralysis (due to supranuclear lesions) from peripheral facial palsy are that central palsies:
1. are confined primarily to the lower face due to some bilateral cortical representation of upper facial movement
2. may spare emotional facial expression8 (e.g. smiling at a joke)
Nuclear facial palsy
The motor nucleus of the seventh nerve is located at the pontomedullary junction. Nuclear VII palsy results in paralysis of all VII nerve motor function. In nuclear facial palsies, other neurologic findings also often occur from involvement of adjacent neural structures by the underlying process (stroke, tumor…), e.g. in Millard-Gubler syndrome, there is ipsilateral abducens palsy + contralateral limb weakness (see page 114). Tumors invading the floor of the 4th ventricle (e.g. medulloblastoma) may also cause nuclear facial palsy (from involvement of facial colliculus in the floor of 4th ventricle).
Facial nerve lesion
Motor fibers ascend within the pons and form a sharp bend (“internal genu”) around the sixth nerve (abducens) nucleus, forming a visible bump in the floor of the 4th ventricle (facial colliculus). The seventh nerve exits from the brain stem at the pontomedullary junction (see Figure 5-20, page 102) where it may be involved in CPA tumors. It enters the supero-anterior portion of the internal auditory canal (see Figure 5-7, page 90). The geniculate ganglion (“external genu”) is located within the temporal bone. The first branch from the ganglion is the greater superficial petrosal nerve (GSPN) which passes to the pterygopalatine ganglion and innervates the nasal and palatine mucosa and the lacrimal gland of the eye; lesions proximal to this point produce a dry eye. The next branch is the branch to the stapedius muscle; lesions proximal to this point produce hyperacusis. Next, the chorda tympani joins the facial nerve bringing taste sensation from the anterior two thirds of the tongue. Basal skull fractures may injure the nerve just proximal to this point. Travelling with the chorda tympani are fibers to the submandibular and sublingual glands. The facial nerve exits the skull at the stylomastoid foramen. It then enters the parotid gland, where it splits into the following branches to the facial muscles (cranial to caudal): temporal, zygomatic, buccal, mandibular, and cervical. Lesions within the parotid gland (e.g. parotid tumors) may involve some branches but spare others.
ETIOLOGIES
These etiologies produce primarily facial nerve palsy, also see Multiple cranial nerve palsies (cranial neuropathies), page 1202.
1. Bell’s palsy: see below } 90-95% of all cases of facial palsy9
2. herpes zoster oticus (auris): see page 846 } 90-95% of all cases of facial palsy9
3. trauma: basal skull fracture } 90-95% of all cases of facial palsy9
4. birth:
A. congenital
1. *bilateral facial palsy (facial diplegia) of Möbius syndrome: unique in that it affects upper face more than lower face (see page 1202)
2. *congenital facial diplegia may be part of facioscapulohumeral or myotonic muscular dystrophy
B. traumatic
5. otitis media: with acute otitis media, facial palsy usually improves with antibiotics. With chronic suppurative otitis surgical intervention is required
6. central facial paralysis and nuclear facial paralysis: see Localizing site of lesion above
7. neoplasm: usually causes hearing loss, and (unlike Bell’s palsy) slowly progressive facial paralysis
A. most are either benign schwannomas of the facial or auditory nerve, or malignancies metastatic to the temporal bone. Facial neuromas account for ≈ 5% of peripheral facial nerve palsies10; the paralysis tends to be slowly progressive (see page 1210)
B. parotid tumors may involve some branches but spare others
C. Masson’s vegetant intravascular hemangioendothelioma (see page 716)
8. *neurosarcoidosis: VII is the most commonly affected cranial nerve (see page 71)
9. diabetes: 17% of patients > 40 yrs old with peripheral facial palsy (PFP) have abnormal glucose tolerance tests. Diabetics have 4.5 times the relative risk of developing PFP than nondiabetics11
10. *stage II Lyme disease12 (see page 368): facial diplegia is a hallmark
11. *Guillain-Barré syndrome: facial diplegia occurs in ≈ 50% of fatal cases
12. occasionally seen in Klippel-Feil syndrome
13. *isolated 4th ventricle (see page 309): compression at the facial colliculus
* items with an asterisk are often associated with facial diplegia (i.e. bilateral facial palsy), for multiple cranial neuropathies see page 1202
BELL’S PALSY
Bell’s palsy (BP), AKA idiopathic peripheral facial palsy (PFP), is the most common cause of facial paralysis (50-80% of PFPs). Incidence: 150-200/1-million/yr.
Etiology: by definition, PFP is called Bell’s palsy when it is not due to known causes of PFP (e.g. infection, tumor or trauma) and there are no other neurological (e.g. involvement of other cranial nerves) or systemic manifestations (e.g. fever, diabetes, possibly hypertension13)14. Thus, true BP is idiopathic, and is a diagnosis of exclusion. Most cases probably represent a viral inflammatory demyelinating polyneuritis15 usually due to the herpes simplex virus16. Facial palsy due to Lyme disease can usually be recognized on clinical grounds17. Severity may be graded on the House & Brackmann grading scale (see Table 21-27, page 622).
PRESENTATION
A viral prodrome is frequent: URI, myalgia, hypesthesia or dysesthesia of the trigeminal nerve, N/V, diarrhea… Paralysis may be incomplete and remain so (Type I); it is complete at onset in 50% (Type II), the remainder progress to completion in 1 week. Usually exhibits distal to proximal progression: motor branches, then chorda tympani (loss of taste and decreased salivation), then stapedial branch (hyperacusis), then geniculate ganglion (decreased tearing). Associated symptoms are shown in Table 26-2, and are usually, but not always, ipsilateral. Herpes zoster vesicles develop in 4% of patients 2-4 days after onset of paralysis; and in 30% of patients 4-8 days after onset. During the recovery phase excessive lacrimation may occur (aberrant nerve regeneration).
Table 26-2 Associated symptoms with Bell’s palsy
|
Symptom |
% |
|
facial & retroauricular pain |
60% |
|
dysgeusia |
57% |
|
hyperacusis |
30% |
|
reduced tearing |
17% |
PROGNOSIS
All cases show some recovery (if none by 6 mos, other etiologies should be sought). Extent of recovery: 75-80% of cases recover completely, 10% partial, remainder poor. If recovery begins by 10-21 d, tends to be complete; if not until 3-8 wks → fair, if not until 2-4 mos → poor recovery. If paralysis is complete at onset, 50% will have incomplete recovery. Cases of incomplete paralysis at onset that do not progress to complete paralysis → complete recovery; incomplete paralysis at onset that progresses to complete → incomplete recovery in 75%. A worse prognosis is associated with: more proximal involvement, hyperacusis, decreased tearing, age > 60 yrs, diabetes, HTN, psychoneuroses, and aural, facial or radicular pain.
MANAGEMENT
Patients with PFP should be examined at an early stage to optimize outcome.
Electrodiagnostics: EMG may detect re-innervation potentials, aids prognostication. Nerve conduction study: electrical stimulation of the facial nerve near the stylomastoid foramen while recording EMG in facial muscles (a facial nerve may continue to conduct for up to ≈ 1 week even after complete transection).
Eye protection: protection of the eye is critical. Artificial tears during the day, eye ointment at night, avoid bright light (using dark glasses during the day).
Steroids: prednisolone 25 mg p.o. BID x 10 days, started within 72 hours of onset of symptoms, improves the chances of complete recovery at 3 & 9 months.
Acyclovir: does not help (alone or in combination with prednisolone)18.
Surgical decompression: controversial. The definitive study has not been done. Rarely utilized. Indications may include:
1. complete facial nerve degeneration without response to nerve stimulation (although this absence is also used as an argument against surgery9)
2. progressively deteriorating response to nerve stimulation
3. no clinical nor objective (nerve testing) improvement after 8 wks (however, in cases where the diagnosis of Bell’s palsy is felt to be certain, the active disease will have abated by ≈ 14 days after onset9)
HERPES ZOSTER OTICUS FACIAL PARALYSIS
Symptoms are more severe than Bell’s palsy, herpetic vesicles are usually present, and antibody titers to varicella-zoster virus rise. These patients have a higher risk of facial nerve degeneration.
SURGICAL TREATMENT OF FACIAL PALSY
For cases with focal injury to the facial nerve (e.g. trauma, injury during surgery for CPA tumor…), dynamic reconstruction by nerve anastomoses are usually considered superior to static methods19. For nonfocal causes, e.g. Bell’s palsy, only “static” methods may be applicable. A functional neural repair is not possible if the facial muscles have atrophied or fibrosed.
Surgical treatment options include:
1. for intracranial injury to facial nerve (e.g. during CPA tumor surgery): intracranial reapproximation (with or without graft) offers the best hope for the most normal facial reanimation
A. timing
1. at time of tumor removal (for a divided facial nerve during removal of vestibular schwannoma20-22): the best result that can be achieved with this is House-Brackmann Grade III. The operation fails to produce good results in ≈ 33% of cases22
2. in delayed fashion, especially if the nerve was left in anatomic continuity
B. techniques
1. direct reanastomosis: difficult due to the frail nature of the VII nerve (especially when it has been stretched by a tumor)
2. cable graft: e.g. using greater auricular nerve23 or sural nerve
2. extracranial facial nerve anastomosis
A. hypoglossal nerve (Cr. N. XII)-facial nerve anastomosis: (see below)
B. spinal accessory nerve (Cr. N. XI)-facial nerve anastomosis: (see below)
C. phrenic nerve-facial nerve anastomosis
D. glossopharyngeal (Cr. N. IX)-facial nerve anastomosis
E. crossface grafting (VII-VII): results have not been very good
3. “mechanical” or “static” means
A. facial suspension: e.g. with polypropylene (Marlex®) mesh24
B. eye closure techniques (protects the eye from exposure and reduced tearing)
1. tarsorrhaphy: partial or complete
2. gold weights in eyelid
3. stainless-steel spring in eyelid
Timing of surgery
If the facial nerve is known to be interrupted (e.g. transected during removal of vestibular schwannoma) then early surgical treatment is indicated. When the status of the nerve is unknown or if in continuity but not functioning, then several months of observation and electrical testing should be allowed for spontaneous recovery. Very late attempts at anastomosis have less chance for recovery due to facial muscle atrophy.
HYPOGLOSSAL NERVE-FACIAL NERVE (XII-VII) ANASTOMOSIS
Cannot be used bilateral in patients with facial diplegia or in those with other lower cranial nerve deficits (or potential for same). In spite of some suggestions to the contrary, sacrificing the XII nerve does create some morbidity (tongue atrophy with difficulty speaking, mastication and swallowing in ≈ 25% of cases, exacerbated when the facial muscles do not function on that side; aspiration may occur if vagus (Cr. N. X) dysfunction coexists with loss of XII).
Not as effective as it would theoretically seem possible. The resultant facial reanimation is often less than ideal (may permit mass movement). To avoid severe disappointment, the patient should thoroughly understand the likely side effects and that the facial movement will probably be much less than normal, often with poor voluntary control.
Usually performed in conjunction with anastomosis of the descendens hypoglossi to the distal hypoglossal nerve to try and reduce hemiatrophy of the tongue. Atrophy may also be reduced by using a “jump graft” without completely interrupting XII25.
Technique
Position: supine, head turned slightly to the opposite side. Skin incision: 6-8 cm incision from just above the mastoid process obliquely downward across the neck to 2 cm below the angle of the jaw. The platysma is opened, and the tip of the mastoid is exposed by incising the insertion of the SCM and using a periosteal elevator. Incise the deep fascia; avoid the parotid gland, which is retracted superiorly. Rongeur the anterior third of the mastoid process (wax any exposed air cells) and identify the facial nerve as it exits the stylomastoid foramen between the mastoid process and the styloid process. Retract the posterior belly of the digastric inferiorly to aid the exposure.
The SCM is retracted laterally until the carotid sheath is identified, revealing the hypoglossal nerve. It loops around the occipital artery at this level (where it gives off the descendens hypoglossi) to pass between the carotid artery and jugular vein. The nerve is freed proximally to the point where it enters the carotid sheath and distally to the submandibular triangle where it is sharply divided.
The facial nerve is divided at the stylomastoid foramen and is approximated to the proximal hypoglossal nerve. The descendens hypoglossi is divided as far distally as possible and is then anastomosed to the distal stump of the hypoglossal nerve.
Variations:
1. interposition jump grafts: spares function in the XII nerve (to minimize glottic denervation, the incision of XII should be distal to the descendens hypoglossi25)
A. using cutaneous nerve jump graft25
B. using muscle interposition jump graft26
2. mobilizing the infratemporal portion of VII out of the fallopian canal (as previously described27) and then anastomosing it using a bevelled cuts to a partially incised XII28
Outcome
Results are better if performed early, although good results can occur up to 18 mos after injury. In 22 cases, 64% had good results, 14% fair, 18% poor, and 1 patient had no evidence of reinnervation. In 59% of cases, evidence of reinnervation was seen by 3-6 mos, in the remaining patients with reinnervation improvement was noted by 8 mos29. Recovery of forehead movement occurs in only ≈ 30%. Return of tone precedes movement by ≈ 3 months.
SPINAL ACCESSORY NERVE-FACIAL NERVE (XI-VII) ANASTOMOSIS
First described in 1895 by Sir Charles Ballance30. Sacrifices some shoulder movement rather than use of tongue. Initial concerns about significant shoulder disability and pain resulted in the technique of using only the SCM branch of XI31, however these problems have not occurred in the majority of patients even with use of the major division32.
Technique32
Skin incision: curves across the mastoid tip along the anterior margin of the SCM. Strip and remove the anterior third of the mastoid process (wax any exposed air cells), identify the facial nerve and divide it as close to its exit from the stylomastoid foramen as possible. Locate the XI nerve 3-4 cm below the mastoid tip, and divide it distal to the SCM division. Mobilize the free end and anastamose it to the distal stump of VII. Results in loss of trapezius function, which may not cause deficit even if done bilaterally. Alternatively, the SCM branch of XI may be used, sparing the trapezius function, however the shorter length may be difficult to work with and in some individuals there may only be multiple small branches to the SCM.
26.4. Hearing loss
Two anatomic types: conductive and sensorineural.
1. conductive hearing loss
A. patients tend to speak with normal or low volume voice
B. etiologies: anything that interferes with ossicular movement, including: otitis media with middle ear effusion, otosclerosis
C. clinical findings with unilateral hearing loss (see Table 26-3):
1. Weber testA will lateralize to side of hearing loss
2. Rinne testB will be abnormal (BC > AC) on the side of hearing loss, called a negative Rinne
D. middle ear impedance measurements are abnormal
2. sensorineural hearing loss (SNHL)
A. patients tend to speak with loud voice
B. clinical findings with unilateral hearing loss (see Table 26-3):
1. Weber testA will lateralize to side of better hearing
2. Rinne testB will be normal (AC > BC), called a positive Rinne
C. further divided into sensory or neural. Distinguished by otoacoustic emissions (only produced by a cochlea with functioning hair cells) or BSAERs
1. sensory: loss of outer hair cells in the cochlea. Etiologies: cochlear damage (usually causes high-frequency hearing loss) from noise exposure, ototoxic drugs (e.g. aminoglycosides), senile cochlear degeneration, viral labyrinthitis. Speech discrimination may be relatively preserved
2. neural: due to compression of the 8th cranial nerve. Etiologies: CP angle tumor (e.g. vestibular schwannoma). Typically loss of word discrimination out of proportion to pure tone audiogram abnormalities
• Sensory and neural hearing loss may be distinguished by otoacoustic emissions (only produced by a cochlea with functioning hair cells) or BSAERs. An elevated stapedial reflex threshold out of proportion to PTA abnormalities is also highly diagnostic of a retrocochlear (neural) lesion
Table 26-3 Interpretation of Weber and Rinne test results
|
Weber |
Rinne |
Interpretation |
|
nonlateralizing |
AC > BC bilat |
normal* |
|
lateralizes to side A |
normal bilaterally (AC > BC) |
sensorineural hearing loss (SNHL) side B |
|
lateralizes to side A |
abnormal in side A (BC > AC) |
conductive hearing loss side A |
|
lateralizes to side A |
abnormal in side B (BC > AC) |
combined conductive + SNHL side B |
* normal, or symmetric hearing loss
A. Weber test: place a vibrating 256 or 512 Hz tuning fork on the center of the forehead. The sound will lateralize (sound louder) on the side of conductive hearing loss, or opposite to the side of SNHL
B. Rinne test: place a vibrating 256 or 512 Hz tuning fork on the mastoid process, when sound is no longer heard, move the fork to just outside the ear to see if air conduction (AC) is > bone conduction (BC)
26.5. References
1. Brandt T, Daroff R B: The multisensory physiological and pathological vertigo syndromes. Ann Neurol 7: 195-203, 1980.
2. Jannetta P J, Moller M B, Moller A R: Disabling positional vertigo. N Engl J Med 310: 1700-5, 1984.
3. Arriaga M A, Chen D A: Vestibular nerve section in the treatment of vertigo. Contemp Neurosurg 19 (14): 1-6, 1997.
4. McElveen J T, House J W, Hitselberger W E, et al.: Retrolabyrinthine vestibular nerve section: A viable alternative to the middle fossa approach. Otolaryngol Head Neck Surg 92: 136-40, 1984.
5. House J W, Hitelsberger W E, McElveen J, et al.: Retrolabyrinthine section of the vestibular nerve. Otolaryngol Head Neck Surg 92: 212-5, 1984.
6. Glassock M E, Miller G W, Drake F D, et al.: Surgical management of Meniere’s disease with the endolymphatic subarachnoid shunt. Laryngoscope 87: 1668-75, 1977.
7. Tarlov E C: Microsurgical vestibular nerve section for intractable Meniere’s disease. Clin Neurosurg 33: 667-84, 1985.
8. Shambaugh G E: Facial nerve decompression and repair. In Surgery of the ear. W. B. Saunders, Philadelphia, 1959: pp 543-71.
9. Adour K K: Diagnosis and management of facial paralysis. N Engl J Med 307: 348-51, 1982.
10. Shambaugh G E, Clemis J D: Facial nerve paralysis. In Otolaryngology, Paparella M M and Schumrick D A, (eds.). W. B. Saunders, Philadelphia, 1973, Vol. 2: pp 275.
11. Adour K K, Wingerd J, Doty H E: Prevalence of concurrent diabetes mellitus and idiopathic facial paralysis (Bell’s palsy). Diabetes 24: 449-51, 1975.
12. Treatment of Lyme disease. Med Letter 30: 65-6, 1988.
13. Abraham-Inpijn L, Devriese P P, Hart A A M: Pre-disposing factors in Bell’s palsy: A clinical study with reference to diabetes mellitus, hypertension, clotting mechanism and lipid disturbance. Clin Otolaryngol 7: 99-105, 1982.
14. Devriese P P, Schumacher T, Scheide A, et al.: Incidence, prognosis and recovery of Bell’s palsy: A survey of about 1000 patients (1974-1983). Clin Otolaryngol 15: 15-27, 1990.
15. Adour K K, Byl F M, Hilsinger R L, et al.: The true nature of Bell’s palsy: Analysis of 1000 consecutive patients. Laryngoscope 88: 787-801, 1978.
16. Adour K K, Bell D N, Hilsinger R L: Herpes simplex virus in idiopathic facial paralysis (bell palsy). JAMA 233: 527-30, 1975.
17. Kuiper H, Devriese P P, de Jongh B M, et al.: Absence of Lyme borreliosis among patients with presumed Bell’s palsy. Arch Neurol 49: 940-3, 1992.
18. Sullivan F M, Swan I R, Donnan P T, et al.: Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med 357 (16): 1598-607, 2007.
19. Conley J, Baker D C: Hypoglossal-facial nerve anastamosis for reinnervation of the paralyzed face. Plast Reconstr Surg 63: 63-72, 1979.
20. Pluchino F, Fornari M, Luccarelli G: Intracranial repair of interrupted facial nerve in course of operation for acoustic neuroma by microsurgical technique. Acta Neurochir 79: 87-93, 1986.
21. Stephanian E, Sekhar L N, Janecka I P, et al.: Facial nerve repair by interposition nerve graft: Results in 22 patients. Neurosurgery 31: 73-7, 1992.
22. King T T, Sparrow O C, Arias J M, et al.: Repair of facial nerve after removal of cerebellopontine angle tumors: A comparative study. J Neurosurg 78: 720-5, 1993.
23. Alberti P W R M: The greater auricular nerve. Donor for facial nerve grafts: A note on its topographical anatomy. Arch Otolaryngol 76: 422-4, 1962.
24. Strelzow V V, Friedman W H, Katsantonis G P: Reconstruction of the paralyzed face with the polypropylene mesh template. Arch Otolaryngol 109: 140-4, 1983.
25. May M, Sobol S M, Mester S J: Hypoglossal-facial nerve interpositional-jump graft for facial reanimation without tongue atrophy. Otolaryngol Head Neck Surg 104: 818-25, 1991.
26. Drew S J, Fullarton A C, Glasby M A, et al.: Reinnervation of facial nerve territory using a composite hypoglossal nerve-muscle autograft-facial nerve bridge. An experimental model in sheep. Clin Otolaryngol 20: 109-17, 1995.
27. Hitselberger W E: Hypoglossal-facial anastamosis. In Acoustic tumors: Management, House W F and Luetje C M, (eds.). University Park Press, Baltimore, 1979, Vol. II: pp 97-103.
28. Atlas M D, Lowinger D S G: A new technique for hypoglossal-facial nerve repair. Laryngoscope 107: 984-91, 1997.
29. Pitty L F, Tator C H: Hypoglossal-facial nerve anastamosis for facial nerve palsy following surgery for cerebellopontine angle tumors. J Neurosurg 77: 724-31, 1992.
30. Duel A B: Advanced methods in the surgical treatment of facial paralysis. Ann Otol Rhinol Laryngol 43: 76-88, 1934.
31. Poe D S, Scher N, Panje W R: Facial reanimation by xi-VII anastamosis without shoulder paralysis. Laryngoscope 99: 1040-7, 1989.
32. Ebersold M J, Quast L M: Long-term results of spinal accessory nerve-facial nerve anastamosis. J Neurosurg 77: 51-4, 1992.