- NERVE INJURIES
- NEUROMAS
- Nerve Conduction Studies
- Electromyography (EMG) - shows progress of re-innervation
- Spine Monitoring
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- Numerical classification:
- Type 1 (myelinated) = proprioception and Motor
- Type 2 (myelinated) = touch and pressure
- Type 3 (myelinated) = fast pain
- Type 4 (unmyelinated) = slow pain and heat [implicated in radial tunnel syndrome where pain precedes neurological deficit]
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- Resting potential of -70mV due to high concentration of K+ and low concentration of Na+ and Cl- in cell
- Opposite in extracellular
- Maintained by lipid membrane and active Na/K pump, Donnan equilibrium (large organic ion in cell)
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- Threshold stimulus leads to depolarization when it reaches about -50mV
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- Electric potential falls below -70mV due to delayed closure of K+ channels
- Absolute refractory period begins when membrane potential crosses the threshold and depolarization begins.
- Relative refractory period = after the overshoot while active Na/K pump restores resting potential. "Relative" because a stronger depolarizing current is needed to initiate an action potential.
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- Via saltatory conduction across nodes of Ranvier
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- Consists of sensory dorsal root and motor ventral root
- Sensory DORSAL root (posterior)
- Cell body in dorsal root ganglion
- Afferent (retrograde) impulses from mechanoreceptors, thermoreceptors, nociceptors
- Motor VENTRAL root
- Cell body in spinal cord
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- Pre-ganglionic myelinated efferent axons from grey matter of T1 to L2
- Goes into ventral spinal root (with motor nerve) ➔ White ramus into sympathetic ganglia ➔ 3 possible exits after synapsing with postganglionic axons (white in, grey out)
- Pass directly to viscera and blood vessels
- Pass via grey ramus to accompany motor nerve to tissue
- Pass along sympathetic trunk to another level
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- Arises from CN 3,7,9,10,11 and S2-4 spinal nerves
- Goes directly to synapse close to target organs
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- Cell body, dendrites, axon, nodes of Ranvier, Schwann cells and myelin sheath
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- Nerve cells (neurons)
- Glial cells - supportive cells, not involved in signaling
- Microglia - phagocytes
- Macroglia
- Schwann cells - produce myelin sheath in PNS
- Oligodendrocytes - produce myelin sheath in CNS
- Astrocytes - form blood-brain barrier
NERVE INJURIES
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- By Seddon or Sunderland classification
- Seddon classification (3 stages)
- Neuropraxia (Sunderland 1)
- Axonotmesis (Sunderland grades 2/3/4)
- Neurotmesis (Sunderland 5)
- Sunderland classification (5 stages)
- Grade 1: Myelin sheath damage (demyelination)
- Grade 2: + axon damage
- Grade 3: + endoneurium damage
- Grade 4: + perineurium damage
- Grade 5: + epineurium damage
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- Intermittent impairment of intraneural microcirculation — occurs when tissue pressure exceeds epineural vessel microcirculation pressure
- Impairment of axonal transport +/- loss of myelin sheath
- Axonal loss leading to Wallerian degeneration
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- It occurs in Axonotmesis and Neurotmesis injuries (Seddon types 2 and 3) in 4 stages:
- Hematoma formation — Distal myelin sheath degenerates while macrophages remove axonal debris
- Proliferation — Schwann cells proliferate and migrate, forming Bands of Büngner
- Growth Cones — Proximal axon forms multiple axonal sprouts with growth cone at each sprout
- Axonal growth occurs via 3 mechanisms:
- Filopodia — contact guidance
- Neurotropism — end organ guidance
- Neurotrophism — growth factors
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- Progressive Tinel's sign advancing at 1mm/day (check distal to proximal)
- Order of recovery: pain → temperature → touch → proprioception → motor function
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- Direct repair:
- Group fascicular repair — repairing the perineurium
- Epineural repair
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- Autograft options: sural nerve (up to 20cm!), LABCN, MABCN, saphenous nerve, distal PIN (supplies wrist joint capsule), vein conduits
- Allografts — collagen conduits (can be very long). (Aymeric: synthetic materials rarely used now due to poor results)
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- In brachial plexus cases, can be intra- or extra-plexal
- Intra-plexal options:
- Oberlin Transfer — Ulnar nerve (branch to FCU) to MCN
- C7 spinal nerve (minimal functional loss due to redundancy; possible mild triceps weakness) — can be ipsi- or contralateral
- Extra-plexal options:
- Spinal Accessory N. (CN XI) to MCN, Suprascapular N.
- Spinal nerves C3/C4
- Intercostal N. → MCN, phrenic
- Hypoglossal nerve (CN XII)
- Tendon transfers
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- Early repair
- Match fascicles to maximize regeneration
- Tension-free repair - can shorten bone to achieve this
- Do not over-mobilize (to avoid devascularization)
- Minimize scarring by using minimal sutures
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- Epineural repair - oldest and most widely accepted technique
- Fascicular repair - repairing the perineurium that covers each fascicle
- Interfascicular repair - bundling groups of fascicles together
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- According to Levinthal et al. (1977) study on dog peroneal nerves, epineural and fascicular repairs showed similar outcomes, while interfascicular repair had poorer results
levinthal1977.pdf2565.8KB
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- They act as a conduit, providing a scaffold for nerve regeneration across the defect
- Prevents mechanical block e.g. fat, blood clot from being interposed between the two ends
- Allows nutrient exchange and accessibility of neurotrophic factors for axonal growth, creating a biologically enhanced microenvironment that minimizes fibrosis and scar tissue ingrowth
- This reduces axonal escape or misdirection and improves regeneration into distal nerves
- Nerve autografts provide additional Schwann cells to aid nerve regeneration
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- Limited by degeneration of motor end plates
- End plates degenerate by 9-12 months
- Must plan procedure to allow nerve regeneration (1mm/day) to complete within 9-12 months
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- There are at least 5 methods
- Align epineural features such as the vas nervorum
- Cross sectional appearance (fascicular size and position)
- Funicular charts
- Intraoperative electrical stimulation
- Staining
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- Patient factors - age and comorbidities
- Nerve factors - mechanism (sharp cuts heal better than crush/avulsion), injury level (distal injuries heal better), size of gap
- Repair factors - repair type (end-to-end better than graft), tension-free repair, tissue quality (vascularity), timing (early repair better), presence of infection, quality of repair (suture only epineurium without passing needle through fascicles)
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- Paraesthesia - spontaneous abnormal sensation
- Dysaesthesia - unpleasant abnormal sensation, which includes allodynia and hyperalgesia
- Allodynia - pain from stimulation that normally does not cause pain
- Hyperalgesia - increased response to stimuli that are not normally painful
NEUROMAS
- SRN neuroma post op
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- A terminal neuroma occurs when nerve growth cone regeneration fails to reach its peripheral target
- Presents with sharp, burning, or tingling pain
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- Neuroma in continuity — some sensation remains intact, with Tinel's sign distally
- Neuroma not in continuity — complete anesthesia with autonomic dysfunction
- Note: The type only affects presentation. Management depends on function and whether repair/reconstruction is worthwhile
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- Cut neuroma proximally and bury the nerve end
- If distal function is required, perform nerve reconstruction or tendon transfer
Nerve Conduction Studies
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- A measurement of sensory SNAP (sensory nerve action potential) or motor CMAP (compound motor action potential) using supramaximal stimulation of the nerves.
- Measured through 3 parameters: amplitude, latency (time taken), and velocity (calculated using known distance)
- For Motor CMAP, the process is more complex (may not apply to CTS):
- It involves neuromuscular transmission time, muscle membrane depolarization, and contraction
- Nerve velocity between two points is calculated using an additional proximal stimulation point and subtracting the values
- Set up requires 4 electrodes: stimulating, receiving, grounding, and reference.
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- Neuropraxia: increased latency, lower velocity, normal amplitude
- Partial Axonotmesis: normal latency and velocity, reduced amplitude
- Neurotmesis: no conduction at all
- Note: Mixed patterns can occur
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- When stimulating nerves electrically, it is important to ensure that all nerve fibers are fully stimulated to their maximum response. Inaccurate readings occur if this isn't achieved.
- This common source of operator error can lead to reduced amplitudes and prolonged latencies.
- Stimulus intensity is incrementally increased until reaching maximal amplitude, then increased by another 20–30% for confirmation. Typical intensities range from 30–40 milliamps.
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- SNAPs help distinguish between post-ganglionic lesions (reduced SNAPs in peripheral neuropathy) and preganglionic lesions (normal SNAPs in radiculopathy, polio, motor neuron disease, and certain neuropathic disorders).
- This occurs because NCS tests nerve circuitry up to the cell body. Since the dorsal root ganglion (DRG), which contains peripheral nerve cell bodies, lies outside the intervertebral foramina, it often escapes radicular compression even when dorsal roots are compressed. This explains why SNAPs remain normal despite numbness.
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- Used for assessing proximal nerves
- F-response: detected in nerve root injuries; works by identifying "echoes." A prolonged F-response indicates injury
- H-reflex: similar to a deep tendon reflex; absent in polyneuropathy/radiculopathy (i.e., lower motor neuron lesion)
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- When electrical stimulation of a peripheral nerve causes depolarization in both directions (orthodromic and antidromic), the antidromic current travels to the anterior horn cells and stimulates a small percentage of them. This triggers a secondary orthodromic response to the muscles. These small responses, approximately 10% of the motor amplitude, are called F-waves (first described in feet but also present in hands).
- F-waves are not a reflex as they travel only in the α motor fibers and do not involve any sensory fibers.
- Use:
- (1) Evaluation of proximal (nerve root/plexus/proximal segment) lesions of peripheral nerves.
- (2) Early loss of these in Guillain–Barré Syndrome where demyelination often begins in the nerve roots.
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- Named after Hoffmann (who worked for Erb).
- A true reflex where selective stimulation of the 1a muscle spindle sensory afferent fibers triggers a monosynaptic spinal cord reflex, causing muscle contraction. This requires submaximal stimulation of the mixed nerve.
- It is the neurophysiological equivalent of an ankle jerk and is typically studied in the tibial nerve innervated soleus muscle.
- Uses:
- (1) In unilateral sciatica, it helps differentiate S1 (unilateral abnormality of soleus H reflex) from L5 radiculopathy.
- (2) In evaluation of demyelinating neuropathies (early loss in Guillain–Barré Syndrome).
- (3) Demonstrating that reflexes are intact when clinically difficult to elicit, particularly in elderly patients.
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- Measuring SNAP and CMAP
- Sensory setup - antidromic [usually antidromic]
- Stimulating proximal to wrist
- Receiver at the fingers
- Stimulate nerve and measure at the finger
- Motor setup
- Stimulating at forearm
- Receiver over abductor pollicis bulk
- Stimulate and measure muscle contraction
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- Normal reference values (Rule of 5): amplitude 5mV, latency 5ms, velocity > 50m/s
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- For a 40-year-old, minimal SNAP amplitudes are 5, 10, and 15 microvolts for ulnar, median, and radial responses
- 5 and 10 microvolts for superficial peroneal and sural SNAPs
- Values double for 20-year-olds and halve for 80-year-olds
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- Nerve conduction velocities are sensitive to temperature, with cooling causing slower velocities.
- Therefore, testing should be performed at temperatures above 32°C
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- Orthodromic potentials follow the natural physiological route—sensory potentials travel toward the spinal cord, and motor potentials travel away from it.
- Antidromic studies measure potentials traveling opposite to the physiological direction and can be used for sensory testing.
- In the UK, orthodromic responses are preferred for hand testing as they provide more accurate take-off latencies, crucial for carpal tunnel evaluation.
- For the feet, antidromic studies are preferred as they provide more accurate amplitudes, essential for peripheral neuropathy assessment.
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Electromyography (EMG) - shows progress of re-innervation
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- Assessment of muscle activity using electrodes, measuring two key aspects:
- 1. Spontaneous activity - normally absent
- 2. Motor Unit Action Potential (MUAP) - amplitude proportional to number of muscle fibers (measured during muscle contraction)
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- Spontaneous activities:
- Normal = no spontaneous activity
- Acute denervation = Positive sharp waves
- Chronic denervation = fasciculations - spontaneously arising action potentials
- Motor Unit Action Potential (MUAP):
- Reinnervation = polyphasic MUAP
- Early reinnervation = reduced amplitude
- Late reinnervation = larger, more consistent amplitude
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- Very acute setting (first 2–3 weeks) of complete axonal loss:
- Spontaneous - none or positive sharp waves
- MUAP - absent
- Thereafter:
- Spontaneous - fasciculations appear due to Chronic denervation
- MUAP - permanently absent due to lack of muscle conduction
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- Acute stage (first 2 weeks):
- Spontaneous - none or positive sharp waves
- MUAP - present, as remaining axons distal to injury can recruit muscle fibers
- After 2 weeks - nerve regeneration:
- Spontaneous - none or positive sharp waves
- MUAP:
- Reinnervation produces polyphasic MUAP, followed by increasing amplitude
- As reinnervation progresses, MUAP amplitude continues to increase
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- In myopathies, the muscle fibres shrink (atrophy), resulting in small-amplitude MUAPs.
- Spontaneous activity is typically absent as there is no denervation
- However, fibrillations, positive sharp waves, or complex repetitive discharges may indicate active inflammation (myositis)
Spine Monitoring
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- 3 types: SSEP, MEP, and EMG
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- Monitoring of DCML (more posterior)
- Involves continuous peripheral nerve stimulation while monitoring somatosensory cortex response
- Electrodes are placed on lower extremity, stimulating the posterior tibial nerve behind ankle and ulnar nerve in upper extremity
- Control areas (supraclavicular area for cervical op C4, popliteal fossa for lumbar spine op S2) help exclude technical errors
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- Monitoring of the corticospinal tract (more anterior)
- Involves cortical stimulation with peripheral reception, e.g., EHL or soleus for lumbar spine
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- Both have distinct advantages and limitations
- SSEP - Less affected by anaesthesia but unreliable for detecting ischemic injury
- MEP - Effectively detects ischemic injury (especially loss of anterior spinal artery in anterior two-thirds of cord)
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- Anaesthetist factors - Muscle relaxants affect MEP, inhalational agents affect SSEP. Use TIVA (Total intravenous anaesthesia); monitor depth of anaesthesia, BP, and oxygenation
- Surgeon factors - Large deformity correction, positioning, and retractor placement
- System factors - Quality of electrode placement
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- Surgeon – stop manipulation, release traction, apply warm saline, check for implant malposition
- Anaesthetist – review recent medications, lighten anesthesia, increase blood pressure, check electrolytes
- Neurophysiologist – repeat MEP trials, increase stimulus strength
- OTT – reduce noise and electrical interference
- If no improvement → consider Stagnara Wake Up test or abort surgery
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- Tests nerve root, particularly useful for lumbar spine surgery below the spinal cord terminus
- 2 Types of EMG
- Free running EMG (spontaneous)
- Records depolarization induced by nerve root microtrauma
- Can be triggered by mechanical stimulation from instruments
- Triggered EMG
- Based on the principle that bone poorly conducts electricity
- Surgeon stimulates the screw; detected depolarization indicates bone breach
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