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#3 Surg > 46 - Entrapment Neuropathies > Flashcards

46 - Entrapment Neuropathies Flashcards

1
Q

Peripheral nerve anatomy

A
  • A nerve is a very complex structure – not going to test this
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2
Q

Dermatomes

A
  • L4, L5, S1 are the main dermatomes you will be seeing in the lower extremity
  • Consults for peripheral neuropathy are very common in podiatry
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3
Q

Management of peripheral neuropathy

A
  • Peripheral neuropathy is a manifestation of a systemic disease (idiopathic, diabetes, chemotherapy, alcoholism, etc.)
  • He used to try to manage these patients, but now he will send them to family practice, neuropathy, or even back to their oncologist
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4
Q

Nerve entrapment

A
  • Impingement of a peripheral nerve trunk by neighboring anatomic structures.
  • Most often occurs where nerve traverses a fibro-osseous tunnel
  • Tarsal tunnel – located posterior to medial malleolus, tunnel composed of medial malleolus, wall of calcaneus, retinacula – a lot of structures run through this small area
  • Each structure has a small osseous-fibrous tunnel and it doesn’t take too much to impinge that nerve, typically a space-occupying lesion (engorged vein is common)
  • “A region of localized injury and inflammation in a peripheral nerve caused by mechanical irritation from some impinging neighboring anatomical structure.”
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5
Q

Seddon’s classification of nerve entrapment

A

o Published in 1942 in British Medical Journal
o H.J. Seddon – Professor of Orthopaedic Surgery at University of Oxford
o Described 3 types of nerve injury based on study of 460 cases

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6
Q

3 types of nerve injury due to Seddon

A
  • Neurotmesis (Nerve Division)
  • Axonotmesis (Lesion in continuity)
  • Neuropraxia (Transient block)
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7
Q

Neurotmesis

A

Nerve division
o Most devastating nerve injury
o Implies complete disruption of a nerve as well as associated connective tissue, typically caused by lacerations, gunshots, fractures, severe traction, etc.
o Budding neurites unable to bridge defect (neurites that do bridge often do so in malalignment resulting in poor reinnervation)
o Requires surgical intervention – resect necrotic tissue, realign fasciculi, nerve fiber regeneration occurs at approximately 1mm/day

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8
Q

Axonotmesis

A

Lesion in continuity
o Axonal disruption
o Supportive connective tissue is maintained
o Typical causes: prolonged compression, traction, ischemia, toxins
o Distally: Wallerian degeneration, distal axon degradation
o Proximally: Axon and nerve cell body convert from neurotransmitter production to axonal regeneration
o Affects myelinated and unmyelinated fibers
o In general; due to maintenance of supportive structures new axons are able to regenerate and grow down corresponding endoneural tube
o Functional recovery is dependent on proximity of lesion:
- Proximal lesions have wider distribution
- * As distance from site of lesion to end organ increases, functional recovery diminishes – This means that the further away the lesion is from the structure it is innervating, the chance of a functional recovery decreases*

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9
Q

Neuropraxia

A

Transient block
o Disruption of the myelin sheath
o Susceptible nerves: thickly myelinated, large diameter, rapidly conducting
o Physiologic conduction blockade (blunt trauma, compression)
o People do very well recovering from a neuropraxia, short lived paralysis may develop
o Repair can occur in days to months
o Patients usually fully recover as injury involves only the myelin sheath

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10
Q

Sunderland’s classification

A

o Don’t need to worry about class/degree of an injury – this is more for a historical review
o Expansion of Seddon’s classification (1951) with 5 degrees (3 classes of injury)

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11
Q

First Degree (Class I)

A

o Conduction deficit without axonal interruption, equivalent to Seddon’s Neuropraxia

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12
Q

Second Degree (Class II)

A

o Axon severed without breaching the endoneurium
o Breakdown of myelin and wallerian degeneration, EMG changes of denervation occur
o Regeneration follows pattern of axonal regrowth, equivalent to Seddon’s axonotmesis

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13
Q

Third Degree (Class II)

A

o Nerve fiber disruption – lesion in endoneurium ONLY (epi/perineurieum remain intact)
o Recovery is possible but may require surgery
o Regeneration is irregular, residual defects common, unpredictable with poor outcomes

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14
Q

Fourth Degree (Class II)

A

o Only epineurium remains intact, injury requires surgical repair

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15
Q

Fifth Degree (Class III)

A

o Complete transection of the nerve, requires surgical repair

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16
Q

Common sites of peripheral nerve entrapment

A

o Tarsal Tunnel (tibial nerve)
o Intermetatarsal spaces (common and proper digital nerves – also occurs plantar to intermetatarsal ligament)
o Adductor canal (Saphenous Nerve)
o Fibular head (Common Peroneal Nerve)
o Deep fascia proximal to ankle (Superficial Peroneal Nerve)
o Lateral Malleolus (Sural Nerve)
- **This is why anatomy is important **
o If you know your anatomy, all of this will make sense – this is what he will ask in the OR

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17
Q

Evaluation and treatment of nerve entrapment

A
  • Tarsal Tunnel Syndrome

- Morton’s neuroma

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18
Q

Tarsal tunnel syndrome

A
  • Entrapment neuropathy involving the Tibial nerve
  • First described by Kopell & Thompson in N Engl J Med in 1960
  • Involves entrapment of the Tibial (or one of its terminal branches)
  • Often compared/likened to carpal tunnel syndrome – need to keep this in mind because these patients may take longer to treat, may not respond to treatment, may need to do a release
19
Q

Anatomy of tarsal tunnel

A
  • Fibro-osseous canal
  • Posterior to medial malleolus

Borders:
o Anterior – Tibia
o Lateral – Talus (posterior process) & calcaneus
o Medial – Flexor retinaculum (Lacinate ligament)

20
Q

Tibial nerve

A
  • Enters proximally

Branches within tunnel into 3 terminal branches:
o Medial Plantar Nerve
o Lateral Plantar Nerve
o Medial Calcaneal Nerve

21
Q

Common symptoms of entrapment neuropathies

A
  • Patient’s present with various symptoms
  • Commonly complain of diffuse plantar pain and/or medial ankle pain (Burning, Stabbing, Shooting, “Electrical,” Numbing, Tingling)

Pain aggravated by standing and relieved with rest
o Some patients report pain worse at night and better throughout the day after walking/activity.
o Many patients will report pain radiating proximal into the calf

22
Q

When evaluating for entrapment neuropathies, look for other systemic disease

A

Diabetes, rheumatologic, obesity, radiculopathy

23
Q

More common causes of entrapment neuropathies

A

o Space occupying lesion(s): ganglion, lipoma, varicosities, neurilemoma
o Exostosis or fracture fragments
o Hindfoot varus or valgus
o Talo-calcaneal coalition
o Accessory muscle within canal: accessory soleus, accessory FDL

24
Q

When evaluating for entrapment neuropathy, carefully review and identify patient’s activities

A

o High performance athletes - sprinters, jumpers, martial arts
o Anything that puts a heavy load on the ankle

25
Q

When evaluating for entrapment neuropathy, carefully examine patient in NWB and WB

A

o Varus or Valgus alignment

o Decreases volume within tarsal tunnel – increase pressure on tibial nerve

26
Q

When evaluating for entrapment neuropathy, test stability of the hindfoot

A

o Instability of plantar fascia
o Instability of PTT
o Instability of supportive structures leads to increased traction on Tibial nerve

27
Q

When evaluating for entrapment neuropathy, palpate entire course of the nerve

A

o Space occupying lesions

o Palpable osseous ridges/fragments

28
Q

When evaluating for entrapment neuropathy, percuss over the tarsal tunnel

A

o Percussion over area of entrapment may elicit radiating pain along course of the nerve
o Tinel sign – Pain radiating distal: most common, patients will feel shooting pain along the course of the MPN and LPN
o Villeix sign – Pain radiating proximal
o TD = touch down, Tarsal tunnel is distal
o VP = vice president, Vileix sign is proximal

29
Q

Diagnostic studies for entrapment neuropathy

A
  • X-ray
  • MRI
  • Ultrasound
  • Electrodiagnostic
30
Q

X-ray

A

o Fractures

o Degenerative Joint Disease

31
Q

MRI

A

o Space-occupying lesion
o 1993 – Frey & Kerr: MRI studies revealed pathology in 88% of patients with Tarsal Tunnel Syndrome, confirmed intra-operatively in 90% of patients
o MRI is a pretty reliable – ALWAYS get a pre-op MRI to prepare/plan for surgery

32
Q

Ultrasound

A

o Technician dependent – He does not use it for anything, except PT

33
Q

Electrodiagnostic studies

A 
o	Nerve conduction velocity (NCV)
o	Electromyography (EMG)
34
Q

Diagnostic criteria

KNOW THIS ***

A

Three criteria
o History of neuritic symptoms
o Positive Tinel sign
o Supporting NCV studies

Diagnosis guidelines
o If none of above criteria is met then diagnosis should be excluded **
o If one of above criteria is met then other diagnosis should be considered *
o If all 3 criteria are met, symptoms are reproducible, then diagnosis is considered

35
Q

Non-surgical treatment (if you know there is no space occupying lesion)

A 
o	NSAIDs
o	Oral vitamin B6
o	Gabapentin
o	Lyrica
o	Immobilization
o	Corticosteroid injections
o	Stabilization of hindfoot with orthotics
36
Q

Indications for surgical treatment

A
  • Space occupying lesions

- Failed conservative treatment

37
Q

Tarsal tunnel syndrome surgery

A
  • Does not repair the retinaculum because they will scar, just throws 1-2 stitches
  • Then implements immobilization
38
Q

Morton’s neuroma history

A
  • 1845 – Neuritic pain between the 3rd and 4th metatarsals was first described
  • 1876 – Neuroma/hypertrophy of the common plantar digital nerve was hypothesized by Morton as etiology of intermetatarsal pain
39
Q

Morton’s neuroma definition

A
  • Entrapment of the common plantar digital nerve occupying the 3rd inner space
40
Q

Morton’s neuroma causative factors

A

Many causative factors presumed – He thinks it is a COMBINATION of all of them ***

Transverse metatarsal ligament
o Narrower inner space between 3rd and 4th metatarsals
o Increased mobility between 3rd and 4th rays
o Tethering of nerve beneath metatarsal heads during dorsiflexion when ambulating

ALL VERY PLAUSABLE THEORIES

41
Q

Physical exam for Morton’s neuroma

A
  • Medial-Lateral squeeze and focal tenderness to deep palpation
  • Positive Mulder’s click (not usually audible, but can feel it on larger neuromas)
  • Complaints of anesthesia to neighboring toes
42
Q

Non-surgical treatment of Morton’s neuroma

A
  • Padding, orthoses
  • Corticosteroid injections
  • NSAIDs, ultrasound, icing
  • Alcohol sclerosis injections (need to do 6 weeks of injections 1x/week)
43
Q

Surgical treatment of Morton’s neuroma

A
  • External neurolysis
  • Excision of involved nerve

Plantar and dorsal approaches described – he goes in dorsally
o Assistant pushes up on the interspace, cut intermetatarsal ligament
o If it is big enough neuroma, he cuts it out by taking out the entire digital nerves then resect the common back as far as he can
o If it isn’t that big, he just resects it

#3 Surg (12 decks)

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