THE FIRST TRAINING COURSE LASTED FOR  2 DAYS OF AUGUST 26-27, 2022 AT THE HCM CITY IN THE SOUTHERN PROVINCES OF VIETNAM

NEUROLOGICAL DISEASES PROGRAM

ELECTRODIAGNOSIS OF BRACHIAL PLEXOPATHY 

A/Prof T. Umapathi 

Senior Consultant, Department of Neurology 

National Neuroscience Institute, Singapore 

Table 1: Common causes of brachial plexopathy 

Pathologic categories	Specific causes
Inflammatory	Brachial Neuritis  (Parsonage –Turner syndrome)  Multifocal motor neuropathy  Radiation plexitis
Neoplastic	Metastatic breast carcinoma
Trauma	Motorcycle accidents  Fall from height  Backpack injuries  Obstetric Erb’s palsy  Post-CABG
Congenital/ hereditary	Hereditary neuropathy with liability for pressure palsies (HNPP)  Hereditary Neuralgic Amyotrophy  True neurogenic thoracic outlet  syndrome

There are four main aims to an electrodiagnostic study of the brachial plexus: 

1) Localise pathology to the brachial plexus 

2) Map accurately the parts of the plexus that have borne the brunt of the injury. This must be done in “two planes”, i.e. proximal (roots) vs. distal (cords/nerves); as well as upper, middle and lower sections of the brachial plexus. 

Objectives 1 & 2 require a good understanding of: 

• Functional anatomy of the brachial plexus 

• More importantly, the differential utility of various upper limb electrodiagnostic studies to help accurately delineate the lesion within the brachial plexus. 

3) Assess if pathology is predominantly demyelinating or axonal. 

This helps decide the etiology of the brachial plexopathy and prognosticate for neurological recovery. For instance, demyelination points to neuropraxic trauma or inflammatory causes like multifocal motor neuropathy. Conversely, axonopathy would indicate axontemesis or neurontemesis in traumatic plexopathies. 

4) Estimate severity of neural injury, and therefore again help 

prognosticate recovery. 

Aim 1: Localise pathology to the brachial plexus. 

Understaning the functional anatomy of the 

brachial plexus. 

Exercise 1 

C5 

C6 

C7 

C8 

T1 

Brachial plexus--- a simple approach to its anatomy 

C5, C6, C7, C8 T1 form the brachial plexus. 

C5, C6 make upper trunk 

C8, T1 make lower trunk 

C7 continues as the middle trunk 

Alltrunks must divide into anterior and posterior divisions. 

All 3 posterior divisions form the posterior cord which becomes the radial nerve after the axillary nerve exits. 

The anterior division of the lower trunk becomes the medial cord, which then becomes the ulnar nerve after the medial cutaneous nerve of the forearm and branch to median leave. 

The remaining anterior divisions of upper and middle trunks make lateral cord. The lateral cord leads to musculocutaneous nerve and gives a branch to median nerve. 

The musculocutaneous nerve becomes the lateral cutaneous nerve of the forearm after giving a branch to biceps. 

Finally add the suprascapular nerve to the upper trunk ---** 

Table 2: The path of individual nerves within the brachial plexus. 

Nerve	AHC/roots	Trunk	Division	Cord	Termination
Axillary	C5,6	Upper	Posterior	Posterior	Deltoid , teres minor
Musculo  Cutaneous	C5,6	Upper	Anterior	Lateral	Biceps, Lat cut nerve of  forearm (C6)
Radial	C6,  7,  8	Middle  Upper  Lower	Posterior	Posterior	EI, digit I  (C7,8)
Ulnar	C8,  T1	Lower	Anterior	Medial	ADM,  1st DIO,  digit V (C8)
Median	C6,  7,  8,T1	Upper	Anterior	Lateral	Digits I, II  PT, FCR
		Middle			Digits III, II  PT, FCR
		Lower		Medial	APB
Medial cut  nerve of the forearm	T1	Lower	Anterior	Medial	Medial cut  nerve of the  forearm
Digit I,  median	C6	Upper	Anterior	Lateral	Median
Digit III	C6 10%  C7 70%  C8 20%	Middle  70%  (LT 20%, UT 10%)	Anterior	Lateral  80%  (MC 20%)	Median
Digit V	C8	Lower	Anterior	Medial	Ulnar
Digit I,  radial	C6 60%,  C7 40%	UT 60%,  MT 40%	Posterior	Posterior	Radial

Exercise 2 

AIM 2: Map accurately the parts of the plexus that have borne the brunt of the injury. This must be done in “two planes”, i.e. proximal (roots) vs. distal (cords/nerves) as well as upper, middle or lower sections of the brachial plexus. 

Sequence of study. 

As in all electrodiagnostic studies, the initial part is a brief but focused clinical evaluation. Information to help decide on etiology, extent, severity and prognosis of plexopathy should be obtained. Attention should also be paid to the type and mechanism of trauma as it helps direct subsequent examinations. 

The nerve conduction and needle electrode survey is then planned. 

The first step is sensory nerve conduction studies. Depending on the findings from history and physical examination some or all of the sensory nerve studies listed in table 3 can be done. This is followed by the motor nerve conductions. Again, the studies chosen should be dictated by the earlier findings (table3). 

Needle electrode examination completes the examination. It is often quite detailed necessitating survey of a number of muscles (table3). 

Table 3: Nerve conduction and EMG abnormalities arising from pathology at different parts of the brachial plexus. 

Electro  Diagnostic  study	Upper trunk	Middle  trunk	Lower trunk	Lateral Cord	Posterior cord	Medial cord
Sensory	Lateral Cut. nerve of  the forearm.  Digit I (median)  Digit I (radial  60%)	Digit III  (median)  Digit I (radial 40%)	Digit V (ulnar) Medial cut.  nerve of the  forearm	Lateral cut.  nerve of the  forearm.  Digit I, II, III  (median)	Digit I (radial)	Digit V  (ulnar).  Medial cut.  nerve of the  forearm
Motor	Axillary nerve  (deltoid)  Musculocut.  nerve (biceps)	-	Ulnar (ADM)  Median (APB) Radial  (EI)	Musculocut.  nerve (biceps)	Axillary  (deltoid)  Radial (EI)	Ulnar (ADM) Median (APB)
EMG	Deltoid Biceps  Brachio- radialis  Infra- spinatus  Rhomboids  Serratus anterior Mid-Cx paraspinal	EDC  ECR  Brachio  radialis  Triceps  Latorsi d  Serratus  anterior Mid Cx  paraspinal	APB  1St DIO  EI  Lower Cx  paraspinal  (Horner’s)	Biceps  Pronator  teres FCR	EI EDC  ECR  Brachio  radialis  Triceps  Deltoid Lat  dorsi	APB  1St DIO  ADM  FCU  FDP (IV,V)

AIM 3 & 4: Assess pathology and severity. 

Proximal brachial plexus injury, as in avulsion injury to spinal roots, carries an extremely poor prognosis. Pre-ganglionic root-level localization is suggested by the presence of normal sensory potentials (SNAPs) in the areas of sensory loss. Needle electrode examination could confirm this by finding denervation in the paraspinal muscles of the same segment. 

In the acute period (at least more than a week after onset), the compound muscle action potential (CMAP) amplitude could give an idea of the severity of axon loss especially if compared with the normal contralateral side. However, this is not sensitive as up to 50% of axons may be lost before CMAP changes are noted. In chronic lesions collateral innervation from surviving axons would reduce further the utility of CMAP amplitude or area in estimating axon loss. 

The SNAP amplitude is a more sensitive index of axon loss but the changes take longer, up to ten days. 

At all stages, the interference pattern gives an accurate picture of lesion severity, although one has to be careful not to use this alone for prognostication. In demyelinating lesions conduction block would reduce recruitment of motor units, similar to axon loss in axonopathy. However, the prognosis for good neurological recovery is good in the former while guarded in the latter. Generally, the amount of spontaneous activity is not a good gauge of severity. 

At the end of the study, the electrodiagnostician would have been able to: 3) Localize pathology to brachial plexus 

4) Chart the lesion in “two planes” as elaborated above 

5) One would also have also been able to assess, from the sum of nerve conduction and EMG data, whether the lesion is predominantly demyelinating or axonal and therefore help the referring doctor in deciding on the etiology (table 1). Rarely the electrodiagnostician may be able to point the clinician towards a definite cause e.g. the presence of myokymia would suggest radiation plexitis rather than compressive brachial plexopathy from metastatic breast tumour. 

In summary, the key to the electro diagnostic evaluation of brachial plexus is a good understanding of its functional anatomy. The various nerve conduction and EMG examinations of the upper extremity are then utilised to accurately characterise the nature, extent and severity of the lesion. 

Nerve conduction studies (NCS) – The basics of Abnormal  Patterns. 

In this write–up the definition of common NCS abnormalities are  expanded and expounded upon. It would serve as a primer to the  practical sessions where these abnormalities would be  demonstrated on real patients. 

CMAP- Compound muscle action potential. 

A nerve trunk has thousands of axons; when stimulated extraneously  by current each individual axons will activate the muscle fibers that  constitutes its motor unit. The sum of the electrical activity of all the muscle fibers of a motor unit makes up its electrical potential  (MOTOR UNIT POTENTIAL). In turn, a summation of the electrical  activity of the many motor units within the muscles, when recorded  on the surface of the muscle belly, constitutes the bell-shape  electrical potential known as the COMPOUND MUSCLE ACTION  POTENTIAL (CMAP). In other words, the area of the CMAP curve is  made up of the sum off all the electrical potentials of individual  motor units. 

Some of the motor units are fast and are represented in the initial  part of the CMAP. The interval from the stimulus artifact to the point  of first electrical activity marks the DISTAL MOTOR LATENCY (DML).  Other motor units are slow and they are at the rear end of the CMAP.  The interval between the initial deflection to the point when the  CMAP returns to the baseline, reflects the spread of velocities among  the various motor units. This interval is the DURATION of CMAP.  

The majority of motor units hover around the 50th centile, and  summate to peak at this point. The voltage at this point defines the  AMPLITUDE of CMAP. 

Now what can go wrong? 

1) Axonopathy- less axons, therefore less motor units and: ∙ CMAP area decreases, 

∙ CMAP amplitude drops. 

Occasionally if the axon loss involves, by chance the fastest units, a  mild amount of slowing (not more than 20%) can occur.  

 2) Myelinopathy-all axons slow equally, therefore; ∙ CMAP DML prolongs 

3) Myelinopathy- various axons slow variably, then: 

∙ CMAP DML prolongs, 

∙ CMAP duration prolongs as the spread of velocity difference  between various motor units is increased. 

As a result of this spread there is a greater chance for the peak of one  motor unit potential to fall on the trough of another motor unit,  “phase-cancelling” each other so that they cannot contribute to the  CMAP. Therefore: 

∙ CMAP amplitude drops 

Conduction velocity-CV. 

By stimulating two points of the nerve, at a known distance, and  using the time interval between the onset of two recorded CMAPs,  CONDUCTION VELOCITY-CV can be calculated. 

Now what can go wrong? 

1) Axonopathy-less axons: 

∙ CV remains unchanged 

However, if the axon loss involves, by chance, the fastest units, a mild  amount of slowing (not more than 20%) can occur 

2) Myelinopathy-all axons slow equally: 

CV-decreases uniformly in all nerves and in all segments of the  nerves, distal and proximal. 

3) Myelinopathy- various axons slow variably, then: 

∙ CV-decreases but not uniformly. 

∙ CMAP amplitude decreases, because of the increase in phase  cancellation 

When recording over a longer distance of the nerve, the spread  between the velocities of various motor units is further increased.  This increases the phase cancellation and causes, TEMPORAL  DISPERSION (TD)- Abnormal TD is defined as reduction in proximal  CMAP amplitude with an increase in the duration by 30%. This  occurs when the variable slowing of many axons causes phase  

cancellation and a drop in CMAP amplitude; with a concomitant  increase in CMAP duration. The longer the segment of nerve studied  the more obvious the temporal dispersion becomes. As an analogy  imagine a cohort of runners with different speeds. When they are  made to run a longer, rather than a short, distance the varying  speeds of individual runners would “disperse” the cohort and  separate better the fastest from the slowest. 

Conduction block (CB) 

A reduction of the CMAP amplitude (or area) by >50% (without an  increase of CMAP duration of more than 30%) between proximal and&