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11. PERIPHERAL NERVE Robert J. Spinner eripheral nerve is an important and historical part of neurosurgery. It also has been a major focus of both the written and oral examinations administered by the American Board of Neurological Surgeons. Candidates typically have considerable fears and concerns about their preparedness in this field because they have not had broad exposure during their neurosurgery training and practice. The Oral Board Examination candidate must be prepared for receiving one to several questions on some of the com mon disorders of the peripheral nervous system. In this chapter, an approach to peripheral nerve prob lems is presented. Common areas that might be examined include tumors, injuries, inflammatory conditions, entrap ments, and neuropathic pain. Five cases are illustrated, and “pearls” are provided. SYSTEMA TIC APPROACH TO PA TIENTS WITH PERIPHERAL NER v E PROBLEMS • History • Ask about three things: motor, sensory, and pain. An important question is, Where does the pain start? • Physical examination • Examine for three things: motor, sensory, and pain. Motor testing includes an examination of strength (Medical Research Council grading 0 to 5/ 5), atrophy, and tone. Sensory testing can include pinprick, light touch, and two- point discrimination. Pain can be assessed by a provocative test (such as the presence of Phalen’s sign, or a positive elbow flexion test or a thoracic outlet maneuver); the presence of percussion tenderness (a so- called Tinel’s sign) can help localize the site of a peripheral nerve lesion. The major differential diagnosis is often peripheral versus spinal. For peripheral nerve lesions, one would typically find a positive sign in the periphery and a negative one at the spine level (e.g., Spurling’s test, straight- leg raise test). For spinal sources, one would typically not find a provocative sign in the periphery but would find one at the spine level. • Electrodiagnostic studies • Electromyography (EMG) • Nerve conduction study (NCS) • Imaging: ultrasound (US) or magnetic resonance imaging (MRI) and nerve blocks where applicable • Image nerves at unusual sites of compression (localized clinically, such as with percussion tenderness) to rule out an undiagnosed mass lesion with high- resolution US or MRI. • Nerve blocks may be done for diagnostic purposes (local agents) and may provide transient relief of pain. They do not define the exact site of the problem but may block the pathway. Therapeutic blocks (with steroids) can also be considered. An analogy would be the four legs of a table– the more legs (i.e., “positives” of the four parts of the evaluation), the more stable the table. CASE 1 HISTORY A 45- year- old woman presents with a 6- month history of right calf pain with dysesthesias radiating into the plantar aspect of the right foot. She has no low back pain and no weakness. She is otherwise healthy.

ore legs (i.e., “positives” of the four parts of the evaluation), the more stable the table. CASE 1 HISTORY A 45- year- old woman presents with a 6- month history of right calf pain with dysesthesias radiating into the plantar aspect of the right foot. She has no low back pain and no weakness. She is otherwise healthy. 120 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW PHYSICAL EXAMINA TION The patient has normal strength in the lower limb. She has normal sensation in the leg and foot. She has a negative SLR test. DIFFERENTIAL DIAGNOSIS The differential diagnosis is tibial neuropathy versus S1 radiculopathy. ADDITIONAL INFORMA TION Physical examination would reveal pain on percussion in the proximal posterior leg, which would reproduce her symptoms. No mass there could be appreciated. ADDITIONAL TESTING An EMG/ NCS was normal. Outside MRI of the lumbar spine also was unrevealing. Because the proximal leg is an unusual site of nerve compression, MRI (or US) of the proximal leg should be considered. This would reveal a mass lesion within the tibial nerve (Figure 11.1). T2- weighted imaging shows an approximately 2- cm hyperintense well- encapsulated round lesion with a speckled appearance (target sign). HOW SHOULD THIS CASE BE MANAGED? The clinical and radiologic features would be consistent with a benign nerve sheath tumor (contrast those of a malignant peripheral nerve sheath tumor [MPNST]). Further ques tioning would reveal no history or family history suggestive of multiple nerve sheath tumors (such as schwannomatosis or neurofibromatosis). Surgical resection is generally safe. For a schwannoma (the most common benign nerve sheath tumor found in a nonsyndromic patient), the mass can typically be removed at a fascicular level (Figure 11.2). In this case, the lesion, although relatively small, is sufficiently symptomatic to warrant surgical resection. Alternatively, this could be observed with clinical and radiologic follow- up. At operation, a posterior approach to the proximal leg is performed with the patient in the prone position. Preoperative localization could be done using US. The nerve is accessed through a longitudinal incision from the popliteal crease distally, centered on the region of pain. The interval between the two heads of the gastrocnemius muscles is opened. Proximal and distal control of the tibial nerve is obtained (Figure 11.3A). The nerve tumor is seen. Major branches to the gastrocnemius and soleus muscles are protected. Mapping of the tumor can be performed using a portable electrical stimulator. Nerve stimulation allows one to determine that the fascicle of origin is nonmotor. T ypical stimulation parameters are 1 to 2 mA. A longitudinal inci sion is made in the bare area on the top surface of this image, and the fascicles are swept away. A single entering fascicle and two exiting fascicles are identified (Figure  11.3B). Stimulation of these fascicles does not produce any mus cle contraction (or nerve action potentials [NAPs] if this technique was used). The lesion is resected (Figure 11.3C). Histologically, it is a schwannoma. One of the critical aspects of any Oral Board Examination case involving a peripheral tumor is to ensure before surgery that it does not represent a malignant lesion such as an MPNST. Clinical factors that favor this diagnosis are a history of neurofibromatosis type 1 (NF- 1), rapid growth over weeks or months, increased refractory pain, large size, and most important, significant motor deficits at presentation. Most benign tumors present like the current case with paresthesias and pain that is less severe. Radiologic features that may support the diagnosis of an MPNST would include irregular borders, irregular enhancement, Figure 11.1 A mass lesion (arrow) within the tibial nerve.

, significant motor deficits at presentation. Most benign tumors present like the current case with paresthesias and pain that is less severe. Radiologic features that may support the diagnosis of an MPNST would include irregular borders, irregular enhancement, Figure 11.1 A mass lesion (arrow) within the tibial nerve. T2- weighted magnetic resonance image shows an approximately 2- cm hyperintense, wellencapsulated round lesion with a speckled appearance (target sign).

, significant motor deficits at presentation. Most benign tumors present like the current case with paresthesias and pain that is less severe. Radiologic features that may support the diagnosis of an MPNST would include irregular borders, irregular enhancement, Figure 11.1 A mass lesion (arrow) within the tibial nerve. T2- weighted magnetic resonance image shows an approximately 2- cm hyperintense, wellencapsulated round lesion with a speckled appearance (target sign). PERIPHERAL  NER v E • 121 necrosis on MRI, and increased avidity on positron emis sion tomography. COMPLICA TIONS One hour after surgery, while the patient is in the recov ery room, you get a call that the she is experiencing severe calf pain that has been refractory to medical treatment. Plantarflexion and toe flexion are quite weak (and painful). She is numb on the plantar aspect of the foot. The history and the presence of a new ( evolving) neurologic deficit would be diagnostic with a tibial neuropa thy likely from an expanding hematoma (rather than nerve injury from the surgical manipulation). Removal of the dressing would reveal a large hematoma in the posterior calf. This should be evacuated emergently. Benign Nerve Sheath T umors Benign nerve sheath tumors may include the following: • Schwannoma • Neurofibroma (may rarely transform into malignancy) • Most solitary and conventional globular masses • if multiple, suspect syndromes (know features and genetics) • NF- 1 (neurofibromas in periphery); NF- 2 and schwannomatosis (schwannomas in periphery) • Resect symptomatic or large conventional lesions. T ypically, tumors can be resected at the fascicular level, sparing most of the nerve with good to excellent outcomes 80% to 90% of the time in skilled hands. • T reat plexiform lesions (especially those with NF- 1 and NF- 2) with respect (observe in most cases; perform subtotal debulking of the predominant nodule on occasion for worsening symptoms, growth, or concern about malignant transformation). Other Benign Lesions • Intrinsic mass— intraneural ganglion cyst (cyst within the epineurium) This typically occurs within in the common peroneal nerve near the fibular neck. It produces a predominant deep peroneal nerve palsy (foot and toe drop and strong eversion). EMG scan help localize the mass. Imaging reveals a cystic lesion. Cyst is derived from a neighboring joint (for com mon peroneal nerve, the origin is from the anterior aspect of the superior tibiofibular joint). Intraneural ganglion cyst is formed by propagation along the articular branch with extension into the parent nerve (common peroneal nerve). Nerve Nerve fascicles Schwannoma Figure 11.2 A schwannoma being removed at the fascicular level. (Used with permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

glion cyst is formed by propagation along the articular branch with extension into the parent nerve (common peroneal nerve). Nerve Nerve fascicles Schwannoma Figure 11.2 A schwannoma being removed at the fascicular level. (Used with permission of Mayo Foundation for Medical Education and Research. All rights reserved.) 122 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW The main goal of surgery is to disconnect the articular branch connection and decompress the cyst. • Extrinsic mass— may compress neighboring nerve by mass effect Protect the nerves first, then remove the tumor. Examples include extraneural ganglion cysts and lipomas. Malignant Peripheral Nerve Sheath T umor An MPNST may form spontaneously, occur after radiotherapy, or appear in patients with neurofibromas and NF- 1. If a lesion were suspicious for malignancy based on clinical and radiologic features (see case discussion), then percutaneous (image-guided) or limited open biopsy and staging would be performed. Most surgeons prefer wide nerve tumor resection after a definitive diagnosis has been made. This approach is often combined with radiotherapy. The 5- year survival rate is about 50%. Do not perform aggressive resection based on intraoperative histology because the frozen section may be incorrect. CASE 2 HISTORY An 18- year- old female high school senior presented with persistent paralysis of her left dominant upper limb affecting shoulder motion and elbow flexion. She was in a rollover bus accident 6 months previously. There were no other injuries at the time, and she was discharged from the hospital on the same day. She has not noted any improvement in her condition. PHYSICAL EXAMINA TION The patient has no active shoulder abduction. She has no elbow flexion. There is no muscular contraction of shoulder abductors or elbow flexors. She has normal trapezius func tion. She has strong elbow extension as well as wrist and finger flexion and extension. She has decreased sensation in the proximal posterior arm and in the volar forearm and thumb. A Tinel’s sign was demonstrated in the supraclavicular fossa. TESTING EMG demonstrates no activation and 3+ fibrillations in the biceps, deltoid, and infraspinatus muscles; the rhomboid and cervical paraspinal muscles are normal. Lateral ante brachial nerve conduction is absent on the left compared with a normal right- sided response. Chest radiograph is normal. Computed tomographic (CT) myelogram (or high- resolution brachial plexus MRI) shows no evidence of pseudomeningoceles. DIAGNOSIS The diagnosis is upper trunk (C5- C6) brachial plexopathy, posttraumatic (postganglionic). HOW SHOULD THIS CASE BE MANAGED? Surgical exploration would be indicated because there is no evidence of clinical or electrical improvement at an appro priate time— i.e., 6 months after injury. A supraclavicular approach would be done (know the basics). Either a transverse incision several fingerbreadths above the clavicle in the posterior triangle or a zigzag approach along the posterior border of the sternocleidomastoid and clavicle could be used. The external jugular vein is mobilized. The omohyoid is typically divided. The fat pad is reflected laterally. The phrenic nerve is seen on the ante rior scalene and can be traced to the C5 nerve. The upper trunk and the rest of the brachial plexus are found in the interscalene triangle. The trunks are lateral to the anterior scalene. The spinal nerves are beneath the anterior scalene, AB C Figure 11.3 Open interval between the gastrocnemius muscles. A: Proximal (P) and distal (D) control of the tibial nerve is obtained with nerve tumor (arrow) shown. B: A single entering fascicle and two exiting fascicles are identified. C: Resected schwannoma.

ne. The spinal nerves are beneath the anterior scalene, AB C Figure 11.3 Open interval between the gastrocnemius muscles. A: Proximal (P) and distal (D) control of the tibial nerve is obtained with nerve tumor (arrow) shown. B: A single entering fascicle and two exiting fascicles are identified. C: Resected schwannoma. PERIPHERAL  NER v E • 123 which can be divided to improve proximal exposure. The subclavian artery is caudad by the lower trunk. A neuroma- in- continuity of the upper trunk is found. WHA T SHOULD BE DONE NEXT? After external neurolysis, NAPs across the upper trunk lesion are recorded (Figure 11.4). No further surgical reconstruction would be necessary. The finding of preserved NAPs in this situation is an excellent prognosticator. Neurolysis alone yields an approxi mately 90% good or better recovery over 2 years. Recovery of proximal targets (shoulder and elbow) is better than that of more distal targets (below the elbow). Nerve grafting or nerve transfers could have been con sidered if NAPs were not present in this postganglionic lesion. Details of nerve grafting or nerve transfer options are provided later in the discussion of preganglionic injury. FOLLOW- UP The patient made an excellent recovery over the following 2 years. There was mild atrophy of the deltoid and biceps, but the patient was able to return to full activity. WHA T IF A PREGANGLIONIC INJURY WERE FOUND? If a preganglionic C5- C6 lesion were presented instead, rhomboid and midcervical paraspinal muscles would typi cally have fibrillations on EMG, and the myelogram would have shown abnormalities involving the cervical roots at that level (absence or asymmetry compared with the other side) or pseudomeningoceles. Intraoperative electrophysiologic testing would reveal a preganglionic (rapid) NAP and absent evoked potentials. Nerve transfers would be performed to reconstruct shoulder function and elbow flexion (see later discussion). Neurolysis and nerve grafting would not be appropriate. TIMING OF RECONSTRUCTION: RULE OF 3S + 1 • Less than 3 days— sharp injury, presumed laceration or transection (e.g., stab wound). If the patient presents later, then operate at the time of initial evaluation. • At 3 weeks— blunt or jagged transection, rupture (e.g., propeller blade). This is controversial. Some surgeons prefer tagging nerve ends on tension (operation 1— immediately after injury) so that they do not retract, and then reexploring and reconstructing the injured nerve subacutely about 3 weeks later (operation 2) when the zone of injury is better delineated. Others prefer performing the definitive operation immediately after injury and making a decision about the extent of injury based on the initial intraoperative appearance. • At 3 to 6 months— closed injury, stretch, and gunshot wounds (note that most gunshot wounds do not transect nerve). If there is no clinical or electrophysiologic improvement, explore and perform NAP recordings (see later). • At 1 year— secondary surgery and reconstruction (e.g., other procedures, such as tendon transfers or joint fusions). Nerve (primary) surgery has the best results when performed by 6 months, but it typically does not work well after 9 months and especially after 1 year. OPTIONS FOR NERVE SURGERY Neurolysis Circumferential dissection of nerve is done as the first part of the procedure. If an NAP is obtained across a neuromain- continuity, neurolysis alone is performed. In this situa tion, about 90% of patients obtain favorable outcomes at long- term follow- up. Nerve Repair Direct repair is performed to approximate nerve ends after transection or after a focal neuroma- in- continuity is resected (in the setting of an absent NAP).

neuromain- continuity, neurolysis alone is performed. In this situa tion, about 90% of patients obtain favorable outcomes at long- term follow- up. Nerve Repair Direct repair is performed to approximate nerve ends after transection or after a focal neuroma- in- continuity is resected (in the setting of an absent NAP). Mobilize stumps Figure 11.4 Nerve action potentials (NAPs) across the upper trunk (UT) lesion (arrow) present after external neurolysis. AD, anterior division of upper trunk; PD, posterior division of upper trunk; SSN, suprascapular nerve; 3 prong, stimulator; 2 prong, recorder).

neuromain- continuity, neurolysis alone is performed. In this situa tion, about 90% of patients obtain favorable outcomes at long- term follow- up. Nerve Repair Direct repair is performed to approximate nerve ends after transection or after a focal neuroma- in- continuity is resected (in the setting of an absent NAP). Mobilize stumps Figure 11.4 Nerve action potentials (NAPs) across the upper trunk (UT) lesion (arrow) present after external neurolysis. AD, anterior division of upper trunk; PD, posterior division of upper trunk; SSN, suprascapular nerve; 3 prong, stimulator; 2 prong, recorder). 124 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW to obtain end- to- end repair if possible without tension. T echniques to shorten the nerve gap include mobilization of nerve ends by freeing them up proximally and distally; transposition of nerve to make a straighter line (such as for ulnar or radial nerves) when feasible; and gentle flexion of the joint and immobilization postoperatively in that posi tion if necessary for several weeks. Early repair facilitates direct repair. Align fascicles as best as possible. Several fas cicular or epineurial sutures are applied using microsurgical technique and 8- 0 to 10- 0 suture material. Immobilize for 3 weeks postoperatively to protect the integrity of the suture line. Results with nerve repair (one suture line) are better than with nerve grafting (two suture lines). Nerve Grafting If a gap exists after nerve stump retraction (following delay in treatment of transection or rupture) or after resection of a more lengthy neuroma- in- continuity (absent NAP), resect the neuroma back to normal nerve ends and good fascicular structure as gauged by visual inspection after sectioning or determined microscopically at frozen section. Estimate the gap between stumps and the number of cable grafts needed to fill the face of the nerves. Harvest an appropriate length of sural nerve from the leg. Be generous with the nerve harvest— err on taking more because nerve shrinks during surgery. Avoid tension in the repair. Sometimes, you will need or want an extra cable graft. Make an incision in the posterolateral leg obliquely from the ankle to popliteal fossa as necessary. The sural nerve is identified midway between the lateral malleolus and lateral edge of the Achilles tendon next to the lesser saphenous vein. Y ou can obtain 30 to 40 cm of sural nerve from each leg if necessary. Donor morbidity includes an expected sensory loss in the dorsolateral foot and the possibility for neuropathic pain after harvest. T echniques Option 1: Suture each graft individually both proximally and distally. Option 2: Use fibrin glue to form a cable of grouped grafts. Freshen up ends with a sharp knife. Suture cabled grafts as one unit. Following either method, immobilize the limb for 3 weeks. Nerve T ransfer T ransfer of an expendable or redundant nerve, nerve branch, or fascicle may be done for preganglionic (avulsion) injury when standard nerve grafting techniques can not be performed. An example in a patient with a severe brachial plexus injury would include intercostal nerve transfers used to obtain elbow flexion in brachial plexus reconstruction (usually three intercostal nerves from T3 to T5 are transferred from chest to the musculocutaneous nerve in the axilla). Because of encouraging results with nerve transfers, these techniques are being employed by some surgeons in patients with postganglionic injury as a substitute for nerve grafts (which could also be done). A new approach to an upper trunk (C5- C6) brachial plexus injury would be to transfer the distal portion of the spi nal accessory nerve to the suprascapular nerve to try to regain some shoulder stability (abduction and external rotation), along with a branch of the triceps to the axil lary nerve (for deltoid function— additional abduction), and transfer a fascicle of the ulnar nerve in the proximal arm directly to the biceps branch of the musculocutane ous nerve (Oberlin procedure) to try to regain elbow flex ion.

lity (abduction and external rotation), along with a branch of the triceps to the axil lary nerve (for deltoid function— additional abduction), and transfer a fascicle of the ulnar nerve in the proximal arm directly to the biceps branch of the musculocutane ous nerve (Oberlin procedure) to try to regain elbow flex ion. These types of nerve transfers are done closer to the muscle end organs, and they speed up and often improve recover y. CASE 3 HISTORY A 35- year- old man presents with difficulty raising his right arm above his head for 6 months. He had received a teta nus shot into his right arm a few days before the onset of his shoulder symptoms. He had experienced severe right periscapular pain, which lasted for 10 days. The pain then resolved, and the weakness became apparent and has persisted. PHYSICAL EXAMINA TION The patient is only able to abduct and forward- flex 90 degrees. He has strong deltoid and supraspinatus muscles. There is no sensory abnormality. He has prominent winging of the right scapula (Figure 11.5). DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS The clinical scenario would be quite typical for Parsonage- T urner syndrome (idiopathic brachial plexopathy). Here the trigger was provided. If it is not obvious, ask about known immune or infectious- type associations (e.g., flu, flu shots or immunizations, recent surgery or trauma). Parsonage- T urner syndrome is well known to affect the

would be quite typical for Parsonage- T urner syndrome (idiopathic brachial plexopathy). Here the trigger was provided. If it is not obvious, ask about known immune or infectious- type associations (e.g., flu, flu shots or immunizations, recent surgery or trauma). Parsonage- T urner syndrome is well known to affect the PERIPHERAL  NER v E • 125 long thoracic nerve by causing winged scapula (differentiate other causes of winged scapula from a spinal accessory nerve lesion— i.e., following posterior triangle of the neck opera tions, the trapezius is affected but not the sternomastoid, or after dorsal scapular nerve injury, which is rare). Long tho racic neuropathy may also occur in combination with other nerves (e.g., suprascapular, axillary, and anterior and pos terior interosseous nerves, which may have a predilection) as part of Parsonage- T urner syndrome, producing a more diffuse patchy neurological process (know how to differentiate this condition from a several- level spinal localization). The serratus anterior is innervated by C5- 7 spinal nerves; a spinal level localization would not produce isolated serratus anterior paralysis; other C5- 7 innervated muscles (e.g., deltoid, spinati, rhomboids, biceps, brachioradialis, brachialis, triceps, etc) would also have to be affected. Nerve injury could follow directly from a needlestick or indirectly from a hematoma and might be considered. However, the clinical picture and the timing of the neuro logical deficit would differ from this case. ADDITIONAL TESTING Electrophysiologic testing would confirm an isolated long thoracic neuropathy In this case, fibrillations were present (indicative of denervation)along with several nascent units (indicative of reinnervation). Note that standard EMG examination would not ordinarily include needling the serratus anterior muscle. Cervical MRI would be norrmal but might show subtle pathology, such as mild central or foraminal stenosis at several levels of the cervical spine. Do not be fooled in to suggesting a multilevel anterior cervical discectomy and fusion for example. Brachial plexus MRI could be considered and might show some subtle T2- weighted hyperintensity (i.e., nonspecific inflammatory) changes diffusely in the brachial plexus. HOW SHOULD THIS CASE BE MANAGED? Given the fact that there was some evidence of EMG recovery at 6 months, the patient would be treated with physical therapy. Pain management may be necessary. In general, the natural history is favorable; approximately 80% of patients make a good (although incomplete) recovery of function; rarely do patients have persistent problematic pain. Some surgeons have described decompression of the long thoracic nerve at the level of the middle scalene (supraclavicular) in suspected cases of entrapment, but this is controversial. There is no proven benefit of medications or even steroids, although frequently a short course may be tried empiri cally. Surgical decompression in my opinion was not rec ommended here given the early recovery. Maximal recovery may take up to 2½ years (note the long time for reinnerva tion, especially given the anatomic course of the long tho racic nerve). Patients should be counseled about the small risk for having a second attack or having a family member affected with an inflammatory neuropathy. FOLLOW- UP The patient noted slow improvement in shoulder active range of motion over the next 18  months. Mild scapu lar winging persisted at long- term follow- up but was asymptomatic. A tendon transfer could be considered at approximately 2 years to stabilize the winged scapula for persistent symp toms (i.e., periscapular pain or loss of motion) or cosmetic concerns. CASE 4 HISTORY A 38- year- old man presents with a 3- year history of burning lateral thigh pain.

erm follow- up but was asymptomatic. A tendon transfer could be considered at approximately 2 years to stabilize the winged scapula for persistent symp toms (i.e., periscapular pain or loss of motion) or cosmetic concerns. CASE 4 HISTORY A 38- year- old man presents with a 3- year history of burning lateral thigh pain. He is unable to wear long pants due to hypersensitivity. He has no weakness in the lower limb and Figure 11.5 Prominent winging of the right scapula (arrow).

erm follow- up but was asymptomatic. A tendon transfer could be considered at approximately 2 years to stabilize the winged scapula for persistent symp toms (i.e., periscapular pain or loss of motion) or cosmetic concerns. CASE 4 HISTORY A 38- year- old man presents with a 3- year history of burning lateral thigh pain. He is unable to wear long pants due to hypersensitivity. He has no weakness in the lower limb and Figure 11.5 Prominent winging of the right scapula (arrow). 126 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW no history of back pain. He is taking multiple medications for pain control. PHYSICAL EXAMINA TION The patient is an obese man. He is numb and has allodynia in the lateral thigh. He has normal strength in the lower limb, including the quadriceps. His deep tendon reflex at the knee is normal. He has a negative straight leg raise. ADDITIONAL TESTS AND DIFFERENTIAL DIAGNOSIS Percussion (over the lateral femoral cutaneous nerve) just medial to the anterior superior iliac spine over the inguinal ligament would be painful and produce radiating paresthesias in the lateral thigh (Figure 11.6A). Blood tests (such as glucose or hemoglobin A 1C) would be normal and would be a good consideration for a diabetic neuropathy. Routine electrophysiologic testing would be normal and would differentiate a lumbar radiculopathy. Specifically, NCS of the lateral femoral cutaneous nerve (not ordinarily done) can show an asymmetrical or absent response com pared with the opposite limb. However, technical issues, especially with an obese patient, might limit the utility. Multiple imaging studies had been done. The patient presented with stacks of lumbar MRI results that were repeatedly normal. US or high- resolution MRI of the lateral femoral cutaneous nerve could show a subtle nerve abnormality. The major differential diagnosis is a lumbar radiculopathy. Pain would start in the back and radiate distally to the lower limb. For upper lumbar radiculopathies, pain may radiate to the groin. L3 radiates to the anterior thigh. L4 goes below the knee. Physical examination, including pro vocative maneuvers, would also differ for a spine rather than a peripheral origin (see earlier discussion of the systematic approach to patients with peripheral nerve problems). US- guided diagnostic (local) block could be considered and would produce transient block and pain relief. A local A B Figure 11.6 A: Percussion (x) over the lateral femoral cutaneous nerve just medial to the anterior superior iliac spine over the inguinal ligament (IL). B: The lateral femoral cutaneous nerve found beneath the fascia overlying the sartorius muscle just distal to the inguinal ligament (IL). C: The nerve is compressed at the leading edge of the inguinal ligament (arrow). The ligament is released laterally. D: Lateral femoral cutaneous nerve resected with neuroma (arrow).

B: The lateral femoral cutaneous nerve found beneath the fascia overlying the sartorius muscle just distal to the inguinal ligament (IL). C: The nerve is compressed at the leading edge of the inguinal ligament (arrow). The ligament is released laterally. D: Lateral femoral cutaneous nerve resected with neuroma (arrow). PERIPHERAL  NER v E • 127 block also would afford the patient the opportunity to experience the expected numbness if a neurectomy is being considered. HOW SHOULD THIS CASE BE MANAGED? W eight reduction was recommended without benefit. The patient avoided compressive objects (e.g., tight belts). In my experience, an US- guided therapeutic block (using ste roids) does not often produce lasting results. Pain manage ment was unsuccessful. Surgery was offered. A transverse incision was made in one of Langer’s lines just medial to the anterior superior iliac spine. (This is preferred over a longitudinal incision, which has more wound- related problems in the groin.) The lateral femoral cutaneous nerve (Figure 11.6B) is a relatively large cutaneous nerve that is found beneath the fascia overlying the sartorius muscle just distal to the inguinal ligament. The nerve can be difficult to locate, and some surgeons favor using US to assist. The nerve is compressed at the leading edge of the inguinal ligament; a pseudoneuroma is frequently identified. The ligament is released laterally (to avoid a postoperative hernia) (Figure  11.6C). Some sur geons favor neurectomy (Figure 11.6D) rather than decompression and allow the proximal stump to retract into the pelvis. FOLLOW- UP This patient underwent neurectomy and noted instan taneous improvement. The hypersensitivity was gone in the recovery room. He resumed wearing long pants and stopped pain medications (Figure 11.7). At last evaluation, 5 years after surgery, he had complete relief. CASE 5 HISTORY A 57- year- old man underwent open carpal tunnel release 2 months ago. He had nocturnal paresthesias in the thumb, index, middle and radial side of the ring finger that were relieved by shaking his hands. Symptoms were exacerbated by driving and wrist position. EMG and NCS confirmed mild CTS. The patient presents with severe pain and dense numbness in the radial 3½ digits and new weakness in the thumb, which he noted immediately after the surgery. EXAMINA TION The patient had a healed wrist- level incision (Figure 11.8). He has paralysis of the abductor pollicis brevis muscle. Other finger, thumb, and wrist flexors are of normal strength. He has severe loss of sensation to light touch and no two- point discrimination in the thumb, index, middle, and radial side of the ring fingers. TESTS Electrodiagnostic Studies Electrodiagnostic studies showed a severe complete median neuropathy at the level of the wrist. EMG revealed fibril lations and no motor units in the abductor pollicis brevis. There was no motor or sensory conduction in the median nerve across the wrist. The preoperative study was compared with the postoperative study. The neurologist confirmed the original diagnosis and localization but documented a new, severe lesion after surgery. Imaging Studies Either MRI or US could be considered to determine a possible structural or anatomic cause for the postoperative worsening. MRI (Figure 11.9) showed a severely flattened and hyperintense median nerve at the distal site of the carpal tunnel by the incompletely divided transverse carpal liga ment. The nerve was compressed but in- continuity. The benefit of imaging in this case is that it excluded the possibility of an iatrogenic transected nerve. DIAGNOSIS The diagnosis in this patient is severe compression of the median nerve at the distal edge of the carpal tunnel, presumably due to incomplete release of the transverse carpal tunnel.

but in- continuity. The benefit of imaging in this case is that it excluded the possibility of an iatrogenic transected nerve. DIAGNOSIS The diagnosis in this patient is severe compression of the median nerve at the distal edge of the carpal tunnel, presumably due to incomplete release of the transverse carpal tunnel. The entire median nerve at the level of the wrist is affected. Motor loss of thenar muscles is present, although more proximal innervated muscles (wrist, finger, and thumb flexors) are spared. Sensory loss in the radial 3 ½ fingers is present, but sensation in the palmar cutaneous nerve distribution is normal. HOW SHOULD THIS CASE BE MANAGED? Surgical exploration would be indicated because this is a new (iatrogenic) and complete lesion. 128 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW The prior incision would be lengthened to facilitate iden tifying the median nerve in the normal proximal zone. The incision would also be lengthened distally into the palm. Note that the original skin incision may not have been optimum to allow full visualization of the median nerve in the region of the carpal tunnel, At the revision surgery, the median nerve would be cir cumferentially mobilized through the area, ensuring com plete decompression. Under tourniquet control, the median nerve was iden tified in the distal forearm and traced through the palm (Figure 11.10A). The transverse carpal ligament had not been completely released. The distal edge of it was com pressing the median nerve (see Figure 11.10A). When the edge was divided, an abnormal indentation of the nerve was seen (Figure 11.10B). The median nerve was mobilized to the level of the digital nerves (note the recurrent motor branch). The median nerve appeared well decompressed. When the tourniquet was released (Figure 11.10C and D), abnormal vascular markings were seen in that area of compression. Figure 11.7 Happy patient who underwent lateral femoral cutaneous neurectomy and was able to resume wearing long pants and stopped pain medications. Figure 11.8 Healed carpal tunnel incision above wrist crease. Figure 11.9 Magnetic resonance image of a sagittal view of compressed median nerve. The T2-weighted image shows a severely flattened and hyperintense median nerve (MN) at the distal site of the carpal tunnel by the incompletely divided transverse carpal ligament (arrow). R, radius.

l tunnel incision above wrist crease. Figure 11.9 Magnetic resonance image of a sagittal view of compressed median nerve. The T2-weighted image shows a severely flattened and hyperintense median nerve (MN) at the distal site of the carpal tunnel by the incompletely divided transverse carpal ligament (arrow). R, radius. PERIPHERAL  NER v E • 129 If imaging had not been done preoperatively, one would have needed to be prepared for the possibility of finding a transected nerve and performing nerve grafting (see information on nerve grafting in earlier discussion of nerve injury). FOLLOW- UP When in the recovery room, the patient noted improve ment in his pain and resolution of the hypersensitivity in the radial 3½ digits. At the first postoperative visit, his wound had healed (Figure  11.11A shows the healed incision, which now extends to the palm). He had regained some degree of opposition already (Figure  11.11B). He made steady and full recovery over 9 months. COMMON NERVE ENTRAPMENT SYNDROMES Carpal T unnel Syndrome In CTS, pain radiates from the wrist to the radial 3 ½ digits and sometimes proximal into the forearm and arm. Symptoms worsen with wrist flexion and extension. Classical provocative features include symptoms that occur with driving or sleeping but that are improved with shak ing hands. Atrophy in the thenar eminence is a late finding. Palmar sensation is normal. Tinel’s sign (percussion tenderness) is noted when tapping over the wrist crease; Phalen’s and reverse Phalen’s signs and compression test are also positive. EMG and NCS confirm the diagnosis of CTS. Beware of false- positive results; false- negative results also occur on occasion. In these cases, US or MRI can support the clinical diagnosis. Know how to distinguish CTS from other, more proximal median nerve compression syndromes (commonly tested on Oral Board Examinations); these include ante rior interosseous nerve (AIN) syndrome (discussed later); entrapment by a supracondylar spur or process, which can be palpated or identified on imaging (found in 0.5% of the normal population, 6 cm above the elbow; the bony spur is found in association with the ligament of Struthers, cre ating a “tunnel, ” in which the median nerve and brachial artery might be compressed); and cervical radiculopathies (e.g., C6 or C7). Figure 11.10 A: Median nerve (MN) identified in the distal forearm and traced through the palm, with the distal edge of the transverse carpal ligament not completely released and compressing the MN (arrow). B: Abnormal indentation of the nerve seen when the edge was divided (arrow). C, D: Abnormal vascular markings seen in area of compression (arrow) when the tourniquet was released.

and traced through the palm, with the distal edge of the transverse carpal ligament not completely released and compressing the MN (arrow). B: Abnormal indentation of the nerve seen when the edge was divided (arrow). C, D: Abnormal vascular markings seen in area of compression (arrow) when the tourniquet was released. 130 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW Surgery Surgery is performed in patients with persistent symptoms of CTS after nonoperative trial (avoidance of exacerbating activities, splinting with the wrist in relatively neutral position) or steroid injection and in those with severe findings. Know the anatomic landmarks for incisions. Most neuro surgeons perform open release through a standard palmar incision: one needs to release the ligament so that the sur geon sees fat distally and decompresses the nerve proximal to the distal wrist crease). Some use endoscopic techniques (one vs. two portals). Open and endoscopic techniques have similar results after 3 months. The endoscopic tech nique may have slight advantage in the initial 3 months after surgery in terms of return to work and grip strengths; results at longer follow- up after open and endoscopic techniques are comparable. Meta- analyses have shown a slight increased neurological risk with the endoscopic technique. Note, as a practical point, that there is a learning curve to the endoscopic technique. Ulnar Nerve Entrapment at the Elbow (Cubital T unnel Syndrome) In cubital tunnel syndrome, elbow pain radiates into the ulnar two digits of the hand. Symptoms often worsen with elbow flexion. Sensory abnormality occurs on the palmar (ulnar 1½ digits) and dorsoulnar aspects of the hand (dor sal cutaneous branch arises 6 cm above the wrist); weak ness occurs in extrinsic (forearm) and intrinsic (hand) ulnar- innervated muscles. Tinel’s sign is found at the elbow, and the elbow flexion test is positive, Spurling’s sign is negative, and thoracic outlet maneuvers are nega tive. EMG and NCS confirm the diagnosis. MRI or US of the elbow also can confirm the diagnosis but are not routinely done. Surgery Surgery is performed in patients with persistent symptoms after nonoperative trial (avoidance of exacerbating activi ties such as elbow flexion, splinting with the elbow mildly flexed) and in those with severe findings. Surgical options include in situ decompression and transposition (subcuta neous, intramuscular, or submuscular). Few neurosurgeons perform a medial epicondylectomy. Recently published studies show no significant differences in outcomes for primary cases between various surgical options; transpo sition has higher complications (infection, hematoma). Submuscular transposition is generally performed for secondary cases. Peroneal Nerve Palsy Peroneal nerve compression may occur at the level of the fibular tunnel by a fibrous band beneath the peroneus longus. Know how to distinguish L5 radiculopathy and pero neal nerve palsy, which are the most common causes of footdrop. If the posterior tibialis is abnormal, then the footdrop is not from peroneal nerve palsy. T o test the posterior tibialis, have patient position the foot down and in (innervated by L5, tibial nerve). EMG can help localize peroneal nerve lesions. The short head of the biceps is the only peroneal- innervated muscle above the fibular head and neck region. Fibrillations in the short head of the biceps on EMG confirm a more proximal lesion (such as in the peroneal division of the sciatic nerve in the thigh or buttock). The footdrop differential diagnosis is broad and can also occur from upper motor neuron causes (brain or spine) or from other lower motor neuron causes (sciatic neuropathy or lumbosacral plexopathy). Figure 11.11 A: Healed incision that extends to the palm (arrow).

ivision of the sciatic nerve in the thigh or buttock). The footdrop differential diagnosis is broad and can also occur from upper motor neuron causes (brain or spine) or from other lower motor neuron causes (sciatic neuropathy or lumbosacral plexopathy). Figure 11.11 A: Healed incision that extends to the palm (arrow). B: Some degree of opposition regained.

ivision of the sciatic nerve in the thigh or buttock). The footdrop differential diagnosis is broad and can also occur from upper motor neuron causes (brain or spine) or from other lower motor neuron causes (sciatic neuropathy or lumbosacral plexopathy). Figure 11.11 A: Healed incision that extends to the palm (arrow). B: Some degree of opposition regained. PERIPHERAL  NER v E • 131 UNUSUAL ENTRAPMENT SYNDROMES Ulnar Nerve Entrapment at the W rist (Guyon’s Canal Syndrome) In Guyon’s canal syndrome, wrist pain radiates into the ulnar digits of the hand. Symptoms worsen with wrist flexion (often seen in cyclists and mechanics, for example) and may affect the deep branch only, producing isolated motor findings. (An important differential diagnosis would be amyotrophic lateral sclerosis [ALS], so you should know about ALS, i.e., features of an upper and lower motor neu ron lesion, tongue fasciculations, etc.) Guyon’s canal syn drome also may after superficial branch only, producing sensory symptoms only, or the parent ulnar nerve, produc ing motor and sensory symptoms. Sensory abnormalities occur only on palmar side, not dorsally. Extrinsic muscles (flexor carpi ulnaris and flexor digitorum profundus to the little and ring fingers) are normal clinically and elec trophysiologically. EMG is helpful in localizing and rul ing out other pathology. MRI may reveal a mass lesion. In general, ulnar nerve entrapment at the wrist accounts for only 1% of all cases of ulnar nerve entrapment— other cases are nearly all at the cubital tunnel (see earlier discus sion of common nerve entrapment syndromes). Neurogenic TOS One must be able to distinguish ulnar nerve pathology from thoracic outlet syndrome (TOS) (symptomatic and neurogenic forms) as well as plexopathy from a Pancoast’s tumor or a C8 or T1 radiculopathy. In neurogenic TOS, patients may have clinical and electrophysiologic findings of a lower trunk plexopathy. In neurogenic TOS, the hand would have both thenar (median- innervated) and hypothenar (ulnarinnervated) motor weakness producing a Gilliatt- Sumner hand. EMG would show changes in muscles of C8 and T1 (beyond ulnar nerve distribution). A chest radiograph could show a cervical rib or an elongated transverse process for neurogenic TOS, or an apical lung mass lesion (in which case, additional imaging with MRI or CT scans would be done). In cases with neurogenic TOS, MRI (or US) of the brachial plexus could help localize the lesion. MRI of the spine would rule out a C8 or T1 radiculopathy. Surgery on neurogenic TOS could be done supraclavicularly or by the transaxillary route; most surgeons would perform scalenectomy (and removal of the cervical rib or elongated process); some would also perform first rib resection. Pathology usually affects C8 and T1 or the lower trunk near the foramina. Four unusual entrapments must be distinguished from Parsonage- T urner syndrome, or brachial plexitis (anterior interosseous nerve syndrome, posterior interosseous nerve syndrome, suprascapular nerve entrapment and long tho racic neuropathy (previously discussed in Case 3). Anterior Interosseous Nerve Syndrome In AIN syndrome, the flexor pollicis longus, flexor digito rum profundus (index and middle fingers), and pronator quadratus are weak. There is no cutaneous innervation by the anterior interosseous nerve. The patient cannot make an “O” sign, which results in a “square pinch.” Posterior Interosseous Nerve Syndrome In the posterior interosseous nerve syndrome, the wrist can dorsiflex strongly in radial deviation, but cannot dorsiflex in neutral position because of the lack of extensor carpi ulnaris. The patient has finger drop, but no sensory loss.

“O” sign, which results in a “square pinch.” Posterior Interosseous Nerve Syndrome In the posterior interosseous nerve syndrome, the wrist can dorsiflex strongly in radial deviation, but cannot dorsiflex in neutral position because of the lack of extensor carpi ulnaris. The patient has finger drop, but no sensory loss. ( Contrast PIN palsy at the arcade of Frohse in the proximal forearm with wrist and finger drop characteristic of a radial nerve palsy from Saturday night palsy, which occurs at the spiral groove at the midarm level and is usually due to compression on the arm, such as occurs from nonphysiologic sleeping, e.g., owing to coma, drug, or alcohol use. In typical radial nerve palsy, the patient has normal triceps strength.) Fortunately, most patients with so- called Saturday night palsy recover quickly (within days or weeks) because of neurapraxia (conduction block); those patients with a history of Saturday night palsy who do not show the expected recovery should have baseline EMG and NCS testing at 3 to 6 weeks. Suprascapular Nerve Entrapment Suprascapular nerve entrapment presents with weakness of the supraspinatus (shoulder abduction) and infraspinatus (external rotation) muscles. It typically occurs at the trans verse scapular ligament. MRI may show a ganglion cyst from the shoulder joint. The differential diagnosis includes C5 radiculopathy and rotator cuff pathology. NINE PHOTOGRAPHS YOU NEED TO KNOW f OR THE BOARDS Figure 11.12 displays nine photographs that you will need to be familiar with when taking the Oral Board Examination.

capular ligament. MRI may show a ganglion cyst from the shoulder joint. The differential diagnosis includes C5 radiculopathy and rotator cuff pathology. NINE PHOTOGRAPHS YOU NEED TO KNOW f OR THE BOARDS Figure 11.12 displays nine photographs that you will need to be familiar with when taking the Oral Board Examination. 132 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW A. THENAR A TROPHY In thenar atrophy, median nerve loss causes intrinsic muscle weakness, such of the as abductor pollicis brevis or oppo nens policis. This patient had severe CTS (proximal median innervated muscles, such as wrist, finger, and thumb flexors, would be normal). B. ANTERIOR INTEROSSEOUS NERVE PALSY The patient is trying to make an “O” (the OK sign) but is unable because of paralysis of the terminal phalanges in the thumb (flexor pollicis longus) and index finger (flexor digitorum profundus). Note that the flexion at the proxi mal interphalangeal joint of the index finger is functioning AB C DE F GH I Figure 11.12 Nine hands to know for the Oral Board Examination. A: Thenar atrophy. B: Anterior interosseous nerve (AIN) palsy. C: High median nerve palsy. D: W asting of first dorsal interosseous muscle. E: Ulnar nerve clawing. F: Radial nerve palsy. G: Posterior interosseous nerve (PIN) palsy. H: Right suprascapular nerve palsy. I: W aiter’s tip posture.

he Oral Board Examination. A: Thenar atrophy. B: Anterior interosseous nerve (AIN) palsy. C: High median nerve palsy. D: W asting of first dorsal interosseous muscle. E: Ulnar nerve clawing. F: Radial nerve palsy. G: Posterior interosseous nerve (PIN) palsy. H: Right suprascapular nerve palsy. I: W aiter’s tip posture. PERIPHERAL  NER v E • 133 because it is supplied more proximally from a branch of the median nerve (not the AIN). C. HIGH MEDIAN NERVE PALSY The patient is attempting to make a fist but is unable to because of paralysis of the finger flexors. Contrast with the patient who has AIN palsy in B. Note the paralysis of the flexor digitorum superficialis, which is supplied by the median nerve proximal to the AIN. The middle, ring, and little fingers flex through the ulnar- innervated flexor digitorum profundi. This person would also have paralysis of the pronator teres, flexor carpi radialis, palmaris longus, and abductor pollicis brevis as well as sensory loss in the median nerve distrubtion. D. W ASTING OF FIRST DORSAL INTEROSSEOUS MUSCLE This photograph shows severe atrophy of ulnar- innervated hand muscles. This can be seen with a low or high ulnar nerve lesion. With ulnar nerve lesions, the patient would typically have sensory loss as well. If there is no sensory abnormality, you should consider a lesion affecting the deep branch (motor) of the ulnar nerve or ALS. E. ULNAR NERVE CLA WING This patient has hyperextension at metacarpophalangeal joints of the little and ring fingers. The patient is trying to extend the fingers but is unable to because of imbalance and weakness in ulnar- innervated intrinsics. F. RADIAL NERVE PALSY This patient has wrist and finger drop. The triceps muscle has normal strength. Sensory loss would be present in the posterior forearm (shown) and dorsum of wrist. The lesion is in the mid or distal arm (in this case, “X” marks site of entrapment and percussion tenderness). G. POSTERIOR INTEROSSEOUS NERVE PALSY In this patient with PIN palsy, the wrist is in dorsiflexion and is strong but radially deviated. It is unable to be dor siflexed in neutral position. The patient has finger drop at the metacarpophalangeal joints. Cutaneous sensation is normal. The lesion is in the proximal forearm just below the elbow. Contrast with the patient who has radial nerve palsy in F . H. RIGHT SUPRASCAPULAR NERVE PALSY Atrophy of the supraspinatus and infraspinatus is seen. The right scapular spine is more prominent because of the associated muscle loss. Right- side abduction is mildly affected in this muscular patient because of compensation of the well- functioning deltoid muscle. External rota tion would be weak, and there would not be any sensory abnormality. I. W AITER’S TIP POSTURE This would be the expected appearance of an infant with a birth- related upper trunk (C5, C6) palsy. There is no shoulder abduction because of loss of C5 function (no deltoid or supraspinatus). There is no elbow flexion from C6. The arm is internally rotated because of overpull of the lower portion of the functioning pectoralis major muscle (C7- T1) and paralysis of the infraspinatus muscle (C5). W rist and hand function is typically preserved.