Contents
7.1 The Basics in Neurophysiological Testing 173 7.1.1 Aim of Nerve Conduction Testing 173 7.1.2 Terminology 173
7.1.3 Measuring Nerve Conduction Velocity 173 7.1.4 Key Concept 1 173
7.1.5 Key Concept 2 174 7.1.6 The H (Hoffman) Reflex 174 7.1.7 The F Wave 174
7.1.8 Deductions from Compound Muscle Action Potential 174 7.1.9 Generation of MAP 174
7.1.10 Use of MUP in the Differential Diagnosis of Neuromuscular Disorders 175 7.1.11 EMG at Rest 175
7.1.12 Selection of Needles 175 7.1.13 Insertional Activity 175
7.1.14 After Voluntary Contraction and Recruitment 175 7.1.15 Factors Affecting Measurement 176
7.2 Some Clinical Applications 176 7.2.1 Nerve Injuries 176
7.2.1.1 Nerve Anatomy 176
7.2.1.2 What Happens After Nerve Injury? 176 7.2.1.3 What Happens After Injury – Microscopic? 176 7.2.1.4 Outcome 177
7.2.1.5 Seddon Classes of Nerve Injury 177 7.2.1.6 Sunderland Classification 177
7.2.1.7 Feature of the Sunderland Classification 177 7.2.1.8 Assessment After a Nerve Injury 177 7.2.1.9 Autonomic Changes After Nerve Injury 178 7.2.1.10 Checking for and the Importance of Tinel’s Sign 178 7.2.1.11 Motor and Sensory Charting 178
7.2.1.12 Investigations 179
7.2.1.13 Timing of NCT in Nerve Injuries 179
7.2.1.14 What Happens to the Muscle After Denervation? 179 7.2.1.15 Key Concept 179
7.2.1.16 What are Fibrillation Potentials? 179
7.2.1.17 Summary of EMG Changes After Acute Nerve Injury 179
Neurophysiological Testing
and Intraoperative Monitoring
7
7.2.1.18 EMG Changes in the Face of Chronic Denervation 179 7.2.2 Entrapment Neuropathy 180
7.2.2.1 Pathophysiology of Entrapment 180 7.2.2.2 More on Pathophysiology 180
7.2.2.3 Other Possible Contributing Factors Besides Compression 180 7.2.2.4 Physical Assessment 180
7.2.2.5 Typical NCT Findings 180
7.2.2.6 CMAP Changes in Demyelination 180 7.2.2.7 CMAP Changes from Axonal Loss 181 7.2.2.8 Prognosis 181
7.2.3 Neuropathy, Myopathy and Neuromuscular Junction Disorders 181 7.2.3.1 Neuropathy 181
7.2.3.2 Myopathy 181
7.2.3.3 Possible Faults at the Level of NMJ 181
7.2.3.4 Differential Diagnosis of NMJ Disorder – Repetitive Nerve Stimulation 182 7.3 Intraoperative Neural Monitoring 182
7.3.1 Indications of Intraoperative Neural Monitoring 182 7.3.2 Main Goals of Intraoperative Neural Monitoring 182 7.3.3 General Categories of Methods 183
7.3.4 Wake-Up Testing 183
7.3.5 Stimulation and Recipient sites for SSEP 184 7.3.5.1 Pros and Cons of SSEP 184
7.3.5.2 Interpretation of SSEP 184
7.3.6 Stimulation and Recipient Sites for MEP 184
7.3.7 False-Positive and False-Negative for Nerve Monitoring 185 7.3.8 Pre-Requisites for Proper Intraoperative Neural Monitoring 185 7.3.9 Selecting the Ideal Method 185
7.3.10 Key Observations to Look for Intraoperatively 186
7.3.11 Typical Changes in Compression, Ischaemic and Traction Injuries 186 7.3.12 Advantages of Spinal Cord Monitoring 186
7.3.13 Disadvantage of Spinal Cord Monitoring 186 7.3.14 Current Trend and the Future 186
General Bibliography 187
Selected Bibliography of Journal Articles 187
7.1 The Basics in Neurophysiological Testing 7.1.1 Aim of Nerve Conduction Testing
n Aim:
– Check motor/sensory responses of peripheral nerves – Check conduction velocity
– Locate site(s) of compression or injury
– Together with electromyography (EMG), may differentially diagnose denervation from myopathy
– Other related studies, e.g. f-wave studies, etc.
– Sometimes as base-line study for documentation before operative intervention and in medico-legal cases
7.1.2 Terminology
n Latency – time between stimulus onset and response
n Amplitude – size of response
n Velocity (V) – calculated by distance over time
n Motor response – elicited by neural stimulation over motor point after placement of ground electrode, point of stimulation is where the nerve is more superficial. Stimulator administered until CMAP (com- pound motor action potential) is obtained, later maximise potential
n Sensory response – the sensory nerve action potential (SNAP) has lower amplitude than motor potential, can either be anti- or ortho- dromic
n SSEP – refers to somatosensory evoked potential, elicited via stimula- tion of peripheral sensory nerves and recording on the scalp
7.1.3 Measuring Nerve Conduction Velocity
n Measures the time taken for the impulse to travel along the axon be- tween the two sites of stimulation
n Velocity = distance between the two sites divided by the difference in latencies between the two sites of stimulation
7.1.4 Key Concept 1
n The measured conduction velocity represents the velocity of the fast- est nerve fibres
n Hence, in order for velocity to diminish, almost all of the nerve fibres need to be affected
a 7.1 The Basics in Neurophysiological Testing 173
7.1.5 Key Concept 2
n Nerve conduction velocity can remain normal even in the face of only a few intact nerve fibres left
7.1.6 The H (Hoffman) Reflex
n Measured by stimulating the posterior tibial nerve, and checking the latency to complete the monosynaptic reflex arc from the Ia afferents to thea motor fibres of the S1 root
n Increased latency in the H reflex of the gastrocnemius-soleus muscle group can occur in S1 radiculopathy or peripheral neuropathy
n Can be absent in the elderly 7.1.7 The F Wave
n Elicited usually via a supramaximal stimulus during motor stimula- tion – via possible antidromic transmission of a handful of the stimu- lated motor fibres
n Latency may be increased in lesions at the proximal nerve fibres; f waves have been described most commonly for tibial nerve, peroneal nerve, ulna nerve, and median nerve
n It is not a reflex
7.1.8 Deductions from Compound Muscle Action Potential
n Compound muscle action potential (CMAP) amplitude: depends on the number of nerve fibres that are activated, decreased amplitude oc- curs in the face of axonal loss. The most significant end of the spec- trum is conduction block (as occurs sometimes in segmental demyeli- nation)
n CMAP duration: depends on the synchrony of conduction of individu- al nerve fibres throughout the nerve. Thus, increased dispersion or multiphase may be detected in the face of some fibres with much re- duced conduction
n Both conduction block and dispersion can occur in demyelination 7.1.9 Generation of MAP
n Upon arrival of the action potential, an end-plate potential (EPP) is generated
n When EPP reaches the necessary threshold, a muscle action potential (MAP) will be generated, detectable by EMG as MUP
n MUP as detected by our needle in EMG studies does not include the activity of all the fibres in the motor unit, but only the sum of the ac- tivity of muscle fibres in the neighbourhood of the needle electrode 7.1.10 Use of MUP in the Differential Diagnosis
of Neuromuscular Disorders
n Differential diagnosis is via MAP:
– At rest and during insertion
– During minimal voluntary contraction – By assessing the pattern of recruitment 7.1.11 EMG at Rest
n In normal situations, should be silent at rest, though can be punctu- ated by miniature end plate potentials or end plate spikes
7.1.12 Selection of Needles
n Concentric needles have the advantages of obviating the need for a reference electrode and less electrical noise. But have the disadvan- tages of less patient comfort and sensitivity for recording of sponta- neous electrical activity
n Monopolar electrodes therefore tend to be more popular 7.1.13 Insertional Activity
n Some transient insertional activity is expected in normal individuals, duration < 300 ms
n Differential diagnosis of decreased insertional activity: myopathy, mus- cle fibrosis, paralysis
n Differential diagnosis abnormal increase in insertional activity (> 300–500 ms): can be seen in denervations, or myopathies, or nor- mal variant
7.1.14 After Voluntary Contraction and Recruitment
n Normally, the more voluntary contraction, the more motor units will be recruited
n In muscles affected by axonal degeneration, the recruitment may be- come abnormal, for there may be very few motor units left
a 7.1 The Basics in Neurophysiological Testing 175
7.1.15 Factors Affecting Measurement
n Age: conduction velocity decreases at extremes of age. Adult value of nerve conduction velocity occurs at age 4, conduction velocity starts to decline > 60
n Temperature: velocity increases with increase in temperature and de- creases in a cold environment. Reporting and performance of NCT should be done in a room shielded electrically from interference and with measured skin temperatures. Conversely, cool limbs need to be warmed before proper NCT measurements can be obtained
n Method of measuring the distance, such as proper positioning of body parts during measurement
7.2 Some Clinical Applications
7.2.1 Nerve Injuries 7.2.1.1 Nerve Anatomy
n Discussion of details of nerve anatomy is beyond the scope of this book, the reader is referred to standard neuroanatomy texts
7.2.1.2 What Happens After Nerve Injury?
n Retraction
n Inflammation + factors secreted to attempt to stimulate neurites
n Degeneration
7.2.1.3 What Happens After Injury – Microscopic?
n Distal part of severed nerve – Wallerian degeneration (according to Waller who first described the phenomenon) survival of nerve fibres occurs only if still remaining connected to nerve cell body – starts on day 3
n Proximal part of severed nerve – cell body becomes basophilic (chro- matolysis), nucleus move to periphery, swollen (changes in proximal seg- ment only as far as the next Ranvier’s node)
n Activation of Schwann cells close to injured site – takes few weeks to clear debris + axonal sprouts start as early as day 1 (nerve growth fac- tors help this process if the perineurium is disrupted)
n Self repair does not occur with gaps of > 2 mm
7.2.1.4 Outcome
n Sprouts make distal connection then nerve fibre matures, (increased axon and myelin thickness)
n Neurites that fail to make distal connection die back and lost ? if the perineurium not disrupted, then the axons will be guided along the original path at 1 mm/day
7.2.1.5 Seddon Classes of Nerve Injury
n Neuropraxia – most are compressive in aetiology? local conduction block/demyelination – heal by repair of demyelination, especially of the thick myelin nerves
n Axonotmesis – mostly traction and/or severe compression cases, ? Wallerian degeneration, prognosis not bad since will regenerate and not miswiring (sensory recovers better since sensory receptors live longer, especially more proximal injuries)
n Neurotmesis – complete cut, no recovery unless repaired – yet can miswire and hence reduced mass of innervation
7.2.1.6 Sunderland Classification
n Neuropraxia – no Tinel’s sign
n Axon – both epi- and perineurium intact, Tinel’s sign + progresses distally
n Axon – only epineurium injured, Tinel’s sign + progresses distally
n Axon – perineurium injured, Tinel’s sign + but Tinel’s sign not pro- gressing distally
n Neurotmesis
n Neuroma in continuity (i.e. partly cut nerve, the remainder can be 1st/2nd/3rd/4th degree of injury)
7.2.1.7 Feature of the Sunderland Classification
n Accounts for injuries between axonotmesis and neurotmesis – based on involvement of perineurium
7.2.1.8 Assessment After a Nerve Injury
n Motor – assess power + differential diagnosis level of injury
n Sensory – mapping and pattern recognition
n Autonomic – e.g. wrinkle test (RSD in 3%, featuring swelling, porosis, sweating, pain, etc.) Tinel’s sign may be presen
a 7.2 Some Clinical Applications 177
n Reflexes – not good guide to injury severity? of course lost if affer- ent or efferent limb affected, but sometimes absent in partial injuries as well
7.2.1.9 Autonomic Changes After Nerve Injury
n Three major losses – vasomotor, sweat, “pilomotor”
– Test pilomotor – loss of wrinkle of denervated skin when im- mersed in water
– Test sweating – rub smooth pen against side of finger/ninhydrin test – due to diminished sweating
– Vasomotor – observation: initial 2/52 pink, then pale and mottled skin 7.2.1.10 Checking for and the Importance of Tinel’s Sign
n Start distally, proceed to proximal percussion when you test for Tinel’s sign
– Positive Tinel’s sign = regenerating axonal sprouts that have not completed myelinisation
– Distally advancing Tinel’s sign = seen in Sunderland 2 and 3, good sign but does not indicate complete recovery alone
(Note: Type 1 Sunderland with no Tinel’s sign, types 4 and 5 Sun- derland no Tinel’s unless repaired)
7.2.1.11 Motor and Sensory Charting
n Motor
– Grade 0 – NIL – Grade 1 – flicker
– Grade 2 – not against gravity, can contract – Grade 3 – against gravity
– Grade 4 – some resistance – Grade 5 – normal
(Motor end plate lasts only 12 months after denervation)
n Sensory – S0 – nil
– S1 – pain recovers
– S2 – pain and touch returning
– S3 – pain and touch throughout autonomy zone – S4 – as S3 + 2-point discrimination returning – S5 – normal
7.2.1.12 Investigations
n Role of NCT/EMG in differential diagnosis of neurapraxia and axo- notmesis
n Presence or absence of a progressing Tinel’s sign 7.2.1.13 Timing of NCT in Nerve Injuries
n Ideal time after nerve injury = 2 weeks
n Reason: needs 7–10 days to have absence of sensory conduction, (and 3–7 days to get an absent distal motor potential, or in other words, the distal motor response may still initially be intact in the immediate few days after nerve injury)
n As from 2/52, usually can differentially diagnose axonotmesis from neurotmesis
7.2.1.14 What Happens to the Muscle After Denervation?
n Increased excitability to Ach starts within 2 weeks
n Increased response of the muscle to even smaller quanta of Ach 7.2.1.15 Key Concept
n Excitability of nerves becomes abnormal around 72 h after a signifi- cant nerve injury
7.2.1.16 What are Fibrillation Potentials?
n These represent the depolarisation of single muscle fibres 7.2.1.17 Summary of EMG Changes After Acute Nerve Injury
n What changes do we expect after nerve cut?
n Answer: at first normal then, positive sharp waves as from days 5–14;
later, at 2 weeks, spontaneous denervation fibrillation
n Implication: good sign if no denervation fibrillation at 2 weeks
n Another important use of EMG: differential diagnosis of neuropathic muscle atrophy from myopathy
7.2.1.18 EMG Changes in the Face of Chronic Denervation
n Expect to see long duration and high amplitude MUPs, since surviv- ing muscle fibres in chronic denervation will increase fibre density and motor unit territory
a 7.2 Some Clinical Applications 179
7.2.2 Entrapment Neuropathy 7.2.2.1 Pathophysiology of Entrapment
n Mild – ionic block (recovers in hours)
n Moderate – myelin back-flow/myelin intussusception (recovers in
£3 months usually), severe cases can have segmental demyelination
n Severe – axonotmesis (with Waller degeneration) takes longer to recover.
Recovery related to distance between site of injury and motor end organs 7.2.2.2 More on Pathophysiology
n The more central fibres spared till late in compression process
n Proximal fusiform swelling of the nerve
n The only case of neurotmesis is that associated with fractures 7.2.2.3 Other Possible Contributing Factors Besides Compression
n Traction
n Excursion
n Tethering
n Scarring
n Ischaemia
(Do not forget the “Double Crush” syndrome) 7.2.2.4 Physical Assessment
n Sensory symptoms sometimes not well localised and can be confusing
n Use provocative test to reproduce clinical symptoms if possible
n Accurate motor testing
n Refer to the indications for NCT (nerve conduction testing) 7.2.2.5 Typical NCT Findings
n Focal conduction block at the segment of entrapment with demyelination
n Evidence of axonal loss reflected more in the lowering of the amplitude.
7.2.2.6 CMAP Changes in Demyelination
n In general, both conduction block (or marked slowing of conduction velocity) and CMAP dispersion (with needling technique) can occur in demyelination
n In entrapment neuropathy, only focal demyelination occurs, unlike the more diffuse demyelinating neuropathies
7.2.2.7 CMAP Changes from Axonal Loss
n Here, conduction velocity is normal or slightly slowed, and reduced amplitude are the hallmarks of axonal loss
n The amplitude is most affected by axonal loss 7.2.2.8 Prognosis
n Age – worse in the elderly
n Chronicity
n Completeness of paresis – complete and > 15 month much less likely to recover
n Underlying pathology
n If there is dissociated loss of motor or sensory function, prognosis sometimes better
7.2.3 Neuropathy, Myopathy
and Neuromuscular Junction Disorders 7.2.3.1 Neuropathy
n Here, sensory fibres are usually affected earlier than motor fibres
n For this reason, the sensory nerve conduction changes are usually de- tected prior to motor nerve conduction changes
n The changes expected of demyelination have already been discussed.
The loss of conduction velocity commences initially in the distal por- tion of the nerves (glove and stocking distribution)
n Assessing both UL and LL peripheral nerves are needed if polyneuro- pathy is suspected
7.2.3.2 Myopathy
n Here, the MUPs are of short duration and small amplitude as there is decreased fibre density and motor unit territory from degeneration of the muscle fibres
n In myotonia, there are high frequency discharges that wax and wane 7.2.3.3 Possible Faults at the Level of NMJ
n Presynaptic, e.g. botulinum toxin (see Chap. 11 on CP), and Eaton- Lambert syndrome – decreased presynaptic Ach release from anti- body against calcium channel
n Postsynaptic: myasthenia – antibody binding to Ach receptor
a 7.2 Some Clinical Applications 181
7.2.3.4 Differential Diagnosis of NMJ Disorder – Repetitive Nerve Stimulation
n Pre- and post-synaptic disorders differential diagnosis by high rate stimulation at 10–50 Hz
7.3 Intraoperative Neural Monitoring
7.3.1 Indications of Intraoperative Neural Monitoring
n Real-time monitoring of function of neural structures (Figs. 7.1, 7.2)
n Help reduce intraoperative neural complications especially, e.g. at the time of deformity correction in spine surgery
n May aid in intraoperative identification of neural structures, e.g.
brachial plexus surgery
n Adjunct in other advanced procedures like deep brain stimulation
n Also used in research
7.3.2 Main Goals of Intraoperative Neural Monitoring
n Detection of changes in neural function from say ischaemia and stretching
n And diagnose such changes early, before they become irreversible
Fig. 7.1. A typical ma- chine used for intra-op- erative neural monitor- ing commonly used in spinal operations. Pic- ture shows the com- mercially used popular Axon System
n This requires knowledge of the possible changes in neural function, particularly early changes
7.3.3 General Categories of Methods
n Non-electronic methods: wake-up testing; ankle-clonus test (less used, observed during induction of anaesthesia and these findings com- pared with the patient who is partially awake intraoperatively or post- operatively)
n Electronic monitoring, e.g. SSEP/MEP 7.3.4 Wake-Up Testing
n Advantage:
– Safe when done properly
– Excellent back-up test when comprehensive electrophysiological methods are unreliable or unavailable
– Low cost
(Procedure: the anaesthetised patient is awakened to a level that they can respond to verbal commands to move the hands. Once this has been performed, the patient is asked to move their foot and ankle)
n Disadvantage:
– The results are difficult to interpret in the context of global neuro- logic function
– Delay in detecting adverse event
a 7.3 Intraoperative Neural Monitoring 183
Fig. 7.2. Close-up film of the monitor screen of the system shown in Fig. 7.1
– Neurologic injury may have occurred hours before, especially if there is a delay in waking up after corrective manoeuvre. Best op- portunity for timely intervention may be lost
7.3.5 Stimulation and Recipient sites for SSEP
n Stimulus:
– Peripheral nerve
– Skin dermatome – unreliable – Nerve root
– Spinal cord
n Recording site:
– Cranium scalp – Spine
– Erb’s point
7.3.5.1 Pros and Cons of SSEP
n Disadvantage:
– Only indirect information of motor tract integrity – Crude global cord integrity
– Not measure motor function
– Owen (Spine 1991) documented SSEP alone detects 70% of spinal cord injuries, and motor loss can occur without SEP changes
n Advantage: sensitive to dorsal medial tracts of SC 7.3.5.2 Interpretation of SSEP
n Amplitude: depends on number of axons and synchrony; warning cri- teria – decrease in 50%
n Latency: depends on neuron conduction velocity. Changes early in compression; late in ischaemic warning criteria: > 10% prolonged (but natural degradation only up to 5% when under anaesthesia)
7.3.6 Stimulation and Recipient Sites for MEP
n Site of stimulus: motor cortex, sometimes at cord
n Transcranial MEP more specific for cortico-spinal tract function
n Stimulus: electrical (magnetic not yet FDA approved)
n Advantage of electrical stimulus – less sensitive to anaesthesia, practi- cal usefulness during operation
n Recording area:
– SC (spinal cord evoked potential)
– Muscle-myogenic: specific muscle function, useful for specific mus- cle group, e.g. polio surgery. More useful if already partial neurol- ogy preoperatively
– Nerve-neurogenic, reflects global function of spinal cord and ex- tremity, the waveform is mainly a backfire antidromic sensory po- tential, not a substitute for myogenic MEP
7.3.7 False-Positive and False-Negative for Nerve Monitoring
n False-positive: test abnormal, but wake-up/postoperatively normal
n False-negative: new neurology not detected intraoperatively by test;
causes include inappropriate criteria, inappropriate test selected, equip- ment/personnel faults; notice SSEP cannot reliably detect motor func- tion
7.3.8 Pre-Requisites for Proper Intraoperative Neural Monitoring
n Select the appropriate monitoring method
n Minimise interference
n Proper and secure positioning of electrodes
n Maximise quality of signals, e.g. in performing far-field SSEP, tech- niques like signal averaging and filtering are useful
n Trained personnel to run the monitoring devices, most having certifi- cation from ABNM (American Board for Neurophysiological Monitor- ing)
n Surgeon knowledgeable of basic neurophysiology and willing to take heed of intraoperative warnings voiced by the technicians
7.3.9 Selecting the Ideal Method
n Consider the anatomy at risk:
– Spinal cord – Nerve roots – Level
– Select appropriate procedure, e.g. SC at risk – MEP with stimula- tion at motor strip of cerebral cortex, SC, transcranial MEP (Or mixed nerve SEP with stimulation at median, ulna, posterior tibial, peroneal, femoral nerves)
a 7.3 Intraoperative Neural Monitoring 185
7.3.10 Key Observations to Look for Intraoperatively
n Looking out for sudden changes (e.g. decrease in amplitude) in the neurophysiologic potentials rather than their absolute values
n The neurophysiologist must be able to diagnose quickly whether the change is likely to be genuine or represents interference
7.3.11 Typical Changes in Compression, Ischaemic and Traction Injuries
n Compression: less amplitude (fewer axons respond), increase latency (early)
n Distraction: less amplitude, increase in latency to as great as compres- sion
n Ischaemic: less amplitude (fewer axons), change in latency occurs late
n Association with correction of deformity – slow deterioration multiple levels
7.3.12 Advantages of Spinal Cord Monitoring
n Easy to use
n Reliable
n Minimise significant changes in anaesthesia
n Not interfere with surgery
n Monitor continuously – not only during critical manoeuvre (P.S. isch- aemic injury due to spinal distraction takes a while to become evident) 7.3.13 Disadvantage of Spinal Cord Monitoring
n False positives can occur: test abnormal, but wake-up/postoperatively normal
n False negatives can occur: neurological deficit not detected intraoper- atively by test; causes include inappropriate criteria for what consti- tutes normality, inappropriate test selected, equipment/personnel faults; notice also SSEP cannot detect motor function. Owen (Spine 1991) documented that SSEP alone detects 70% of spinal cord injuries 7.3.14 Current Trend and the Future
n Simultaneous measure of various neurophysiological procedures since each with its own pros and cons
n Multiple recording sites – consider multiple permutation of stimulus and recording sites; multiple electro-physiological procedures
General Bibliography
Echternach JL (2003) Electromyography and nerve conduction testing, Slack, New Jersey
Selected Bibliography of Journal Articles
1. Lehman RM (2004) A review of neurophysiological testing. Neurosurg Focus 16(4):ECP1
2. Owen JH, Bridwell KH et al. (1991) The clinical application of neurogenic motor evoked potentials to monitor spinal cord function during surgery. Spine 16(8):
S385–S390
a Selected Bibliography of Journal Articles 187
