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 » Clinical Evaluation
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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 6  |  Page : 918-925

Management of brachial plexus injuries in adults: Clinical evaluation and diagnosis

1 Department of Neurosurgery, Jai Prakash Narayan Apex Trauma Centre, All Institute of Medical Sciences, New Delhi, India
2 Department of Neurosurgery, Nizam's Institute of Medical Sciences, Hyderabad, Telengana, India
3 Department of Clinical Neurosciences, University of Calgary, Calgarye, Alberta, Canada

Date of Web Publication20-Nov-2015

Correspondence Address:
Sumit Sinha
Room 307, 3rd  Floor, Jai Prakash Narayan Apex Trauma Centre, All India Institutes of Medical Sciences, New  Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.170114

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 » Abstract 

Brachial plexus injuries are devastating injuries that usually affect the younger population. The usual modes of injuries are roadside accidents, falls, and assaults. The affected individuals are crippled and may suffer from excruciating peripheral or central deafferentation pain for rest of their lives. The loss of functional capacity accounts for a significant number of man-hours lost at the workplace and consequent financial burden on the family. The results of brachial plexus reconstructive surgery have generally been unsatisfactory in the past. However, in recent decades, the efficacy of surgery has been proven beyond doubt, and there have been various published series in literature that have reported a good outcome after surgical management of these injuries. This has been made possible by the use of operating microscopes, better microsuture techniques for nerve graft and nerve or tendon transfer repair, and advanced perioperative electrophysiological techniques. The key to successful management lies in the proper clinical evaluation, supplemented with electrophysiology, preoperative imaging studies, and planning of surgical strategy. The partial injuries have a better outcome as compared with global palsies, and early referral should be emphasized. Selective combinations of nerve graft and transfers provide a moderate shoulder and elbow control. However, a multispecialty approach involving hand surgeons, plastic surgeons, and physiotherapists is required.

Keywords: Brachial plexus lesions; clinical evaluation; management

How to cite this article:
Sinha S, Pemmaiah D, Midha R. Management of brachial plexus injuries in adults: Clinical evaluation and diagnosis. Neurol India 2015;63:918-25

How to cite this URL:
Sinha S, Pemmaiah D, Midha R. Management of brachial plexus injuries in adults: Clinical evaluation and diagnosis. Neurol India [serial online] 2015 [cited 2022 Aug 16];63:918-25. Available from: https://www.neurologyindia.com/text.asp?2015/63/6/918/170114

 » Introduction Top

Brachial plexus injuries are the most severe nerve injuries of the upper extremity, often resulting in marked functional impairment. Young to middle-aged men are most frequently affected, and road traffic accidents are the most common cause.[1],[2] In addition to the severe motor impairment, brachial plexus injuries take a heavy toll on economical and psychosocial aspects, rendering previously healthy individuals physically and socio-economically handicapped.[3],[4]

Although the surgical management of such injuries dates back to early 20th century, it was not widely practised because of consistently poor results.[5] The advent of operating microscope and the development of refinements in the microneurosurgical techniques in the latter half of the past century created a resurgence of interest in these injuries. A more aggressive approach toward management of these cases was popularized and maintained after good results were reported by Millesi and Narakas.[6],[7] Since then, various studies have documented the utility of surgery.[8],[9]

Surgery is indicated in the patients not showing any signs of regeneration even after 3 months of injury. Various surgical modalities of treatment have been described, which include neurolysis and neurotization (nerve transfer) with or without nerve grafting.[10] Although many such studies have focussed on the motor outcome of these patients, very few studies have also concentrated on the functional and psychosocial aspects of these injuries.[11],[12],[13]

The key to successful management of these injuries lies in the proper clinical evaluation, supplemented with electrophysiology, preoperative imaging studies, and planning of surgical strategy. This article focuses on diagnosing and localizing these lesions by a detailed and thorough clinical evaluation, on performing proper preoperative imaging studies and also on examining the role of electrophysiology in the management of brachial plexus injuries.

 » Clinical Evaluation Top

Clinical evaluation carries the greatest value in the presurgical assessment of these patients, perhaps even more than electrophysiology and imaging, which are mere supporting ancillary diagnostic methods. A proper and detailed systematic examination is the key to localizing the lesion, and a sound knowledge of the functional anatomy of the plexus is mandatory to accomplish this [Figure 1].
Figure 1: Schematic illustration of a left-sided brachial plexus showing roots, trunks, divisions and cords with important peripheral branches

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The muscles should be evaluated in a systematic manner proximally to distally. The aims of the clinical examination are to identify: i) the nerve involved, ii) the level of injury, and iii) the severity of injury—incomplete or complete. The injury can be at pre- or postganglionic level and can involve the roots, trunks, divisions, cords, or individual peripheral nerves, either alone or in various combinations. The most important issue is to determine is whether the injury is pre- or postganglionic, as former injuries are associated with a worse prognosis and necessitate an earlier surgical management.

Motor function

The examination begins with a thorough inspection of the affected limb. The posture of the limb gives an idea about the plexal elements involved. An adducted, pronated limb (waiter's tip hand) in Erb's palsy involves the upper plexus; and, the predominant hand involvement in Klumpke's palsy is due to affliction of the lower plexus. Some characteristic upper-extremity postures are illustrative. The "pointing index" or "Benedict's finger" is characteristic of median nerve injury [Figure 2]; claw hand, combined ulnar and median nerve injury [Figure 3]; wrist drop, radial nerve injury [Figure 4]; and "winging scapula," serratus anterior palsy [Figure 5]. Asymmetry is noted in the affected limb due to the muscle wasting. For example, the classic "groove sign" between the acromion process and the head of the humerus suggests deltoid palsy [Figure 6].
Figure 2: Pointing index or Benedict's sign suggesting paralysis of the median nerve—inability to flex the median innervated fingers

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Figure 3: Clawing of the fourth and the fifth digit in ulnar nerve palsy

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Figure 4: Wrist drop

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Figure 5: Winging of the scapula on the right side indicating involvement of nerve to the serratus anterior muscle

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Figure 6: Groove sign: Space between the acromion and the humeral head due to deltoid muscle wasting and atrophy suggests deltoid paralysis

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The spinati muscle atrophy may be appreciated at the back of the scapula in cases of suprascapular nerve involvement. The atrophy of the intrinsic hand muscles is seen in lower trunk injuries.

The branches to the rhomboids, serratus anterior, and paravertebral muscles leave the roots very close to the neural foramen. Hence, the injury to these roots is suspected due to the involvement of these muscles. The suprascapular nerve palsy (atrophy and paralysis of the supraspinatus and infraspinatus muscles) indicates the involvement of the upper trunk. The musculocutaneous nerve involvement (paralysis of elbow flexors) indicates upper trunk or lateral cord injury. The loss of sensation in the median nerve distribution indicates C5–C6, upper trunk, or lateral cord injury. The median nerve motor function is supplied by C8–T1. The total loss of pectoralis major muscle indicates involvement of all the roots; upper, middle, and lower trunks; or lateral and medial cord. The latissimus dorsi can be assessed by palpating the muscle between the thumb and the index finger. The intact muscle will contract involuntarily when the patient is asked to cough. The myotomal pattern quickly suggests which roots are involved, and there are certain pointer myotomes indicating injury to specific spinal roots: C5, shoulder abduction; C6, elbow flexion; C7, elbow extension; and C8–T1, hand intrinsic muscles. However, triceps function may be preserved even with avulsion of C7 root, owing to contributions from C6 and C8.

The presence of Bernard–Horner sign with ptosis and miotic pupil on the affected side, is highly indicative of a very proximal C8 and T1 root damage [Figure 7]. False negatives are more common than false positives, and the sign may not be present during the first 48 hours after injury.
Figure 7: Horner's sign on the left side indicating preganglionic injury of the C8–T1 nerve roots and involvement of the sympathetic trunk

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Paralysis of the phrenic nerve points to a very proximal injury to the C5–C7 roots. The presence of phrenic nerve damage may be assessed by tidal percussion of the back in the sitting position on inspiration and expiration and noting that the level of resonance fails to move on inspiration.

The presence of severe deafferentation pain suggests C8–T1 root avulsion. This may also occur with C5–C7 avulsions; however, it is less problematic. The worst deafferentation pain is seen in the setting of pan plexus injury with multiple root avulsions.

Paralysis of brachioradialis and teres major along with spinati, deltoid, biceps, and teres minor points toward an upper trunk lesion. However, if brachioradialis and teres major are intact, a more peripheral injury is likely. The presence of normal spinati muscles rules out the involvement of C5 root in a normal fixed plexus. As a practical consideration, it should be determined that the most distal portion of the peripheral nerve is functioning before excluding a lesion of a peripheral nerve. The presence of a strong wrist extension does not preclude an injury to the posterior interosseous nerve, which innervates the finger and the thumb extensors after some extensors of the wrist have received branches. The "cone test" is a rapid and simple means to assess the distal-most function of the ulnar, radial, and median nerves [Figure 8]. The patient is asked to make a five-fingered cone with the tips of the fingers and then to open and extend his fingers. The fingers and the thumb are brought together by the opponens pollicis (median nerve) and opponens digiti minimi (ulnar nerve) and the finger flexors (median and ulnar nerves). The fingers are then opened up and extended by the radial innervated extensor muscles.
Figure 8: Cone test: A rapid and straightforward test for assessing distal function of the median, radial, and ulnar nerves. The fingers and the thumb are brought together by opponens pollicis (median nerve) and opponens digiti minimi (ulnar nerve). The fingers are then opened up by finger extensors (radial nerve)

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The abductor digiti minimi is supplied by the ulnar nerve branches arising in the Guyon's canal, whereas the flexor digitorum profundus (flexors of the terminal phalanx) is supplied by branches arising from the ulnar nerve in the proximal forearm. Therefore, these two muscles are important for localizing the level of injury in the ulnar nerve. Similarly, the triceps is supplied by the radial nerve branches in the axilla. Hence, injury to the radial nerve at the lateral humeral level is not accompanied by triceps weakness. The adductor of the thumb is supplied by the ulnar nerve (adductor pollicis). The patient is asked to maintain the thumb in adducted position and prevent the card from being pulled by the examiners hand. In case of ulnar palsy, as the adductor pollicis is weak, the patient tries to hold the card by using the median innervated flexor pollicis longus (Froment's sign) [Figure 9].
Figure 9: Froment's sign: The thumb adductor (adductor pollicis) is supplied by the ulnar nerve. In ulnar palsy, the patient compensates and prevents the card from slipping by flexing the thumb owing to median nerve innervated flexors (Flexor pollicis longus)

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The examiner needs to be aware of the subtleties of movements at a joint and which muscles are involved. The biceps muscle is supplied by the upper trunk, anterior division, lateral cord, and musculocutaneous nerve and flexes the elbow in full supination. The brachioradialis muscle is supplied by the upper trunk, posterior division, posterior cord, and radial nerve and is a flexor of the elbow in the midpronated position. The brachioradialis muscle hypertrophies in cases of biceps palsy and makes elbow flexion stronger.

The muscles in the noninjured nerve distribution can sometimes substitute for the affected muscles and make the paralysis appear partial or nonexistent. In patients with deltoid palsy, enough shoulder abduction can be achieved by the supraspinatus and the long head of the biceps; and, due to scapular rotation and elevation by the trapezius and the levator scapulae muscles. This can be prevented by stabilizing the shoulder and asking the patient to abduct his arm without elevating the shoulder. The ulnar nerve-supplied abduction of the fingers can be mistaken for radial innervated finger extension. This can be best avoided by examining for the finger abduction with the wrist extended, thereby nullifying any possibility for the radial innervated extensors to mimic abduction of the fingers. The reverse can be true for ulnar palsy where extension of the fingers by the intact extensor communis muscle may provide some abduction.

Autonomic function

The moisture of the skin may give useful information about the level of the lesion. The presence of a dry skin in an anesthetic area suggests a postganglionic lesion, whereas normal sweating suggests a preganglionic lesion. The loss of sweating in the sensory distribution of a peripheral nerve indicates an injury to that nerve. This can be demonstrated by magnification provided by an ophthalmoscope, which shows sweat as individual droplets as they appear at the mouth of sweat ducts of the fingers. Other methods of testing sweating are Minor's starch iodine method or the use of paper impregnated with iron solution that changes color with moisture. The palpation of the denervated area reveals a characteristic dry sensation giving least resistance to the examiner's fingers while gliding over the affected skin. The presence of sweating in the autonomous zones of the median and ulnar nerves indicates that there cannot be a complete lesion of these nerves. The return of sweating may precede sensory or motor recovery by weeks or months. The presence or absence of the autonomic function can also be tested by O'Rian wrinkle test. The patient is asked to immerse the fingers in tepid water for 5–10 minutes. With denervation, the affected fingers will no longer wrinkle.

Sensory function

The dermatomal pattern for the upper limb is shown in the [Figure 10]a. The sensation of the affected limb should be compared to that of the uninvolved limb. The testing for the sensory function should be made in the autonomous zones where the likelihood of overlapping is minimal [Figure 10]b. The sensory return in the nonautonomous areas usually antedates the motor return and that in the autonomous zones follows the earliest motor return. A normal two-point discrimination in a normal adult finger pad should be 3–5 mm, while that on the dorsal surface of the hand is 7–12 mm. However, this modality testing is of lesser significance than a relative decrease in response to touch and pinprick.
Figure 10: (a) Dermatomal map of the upper limb. A dermatome is an area of skin supplied by a spinal nerve. The pointer dermatomes are shown encircled separately (b). The areas of sensory loss in the hand in median (dark circles on the lateral aspect of the hand) and ulnar nerve injury (dark circles on the medial aspect). The triangles shown here are the areas of autonomous innervation where the loss can be only due to the respective nerve injuries

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Tinel's sign

The presence of paresthesias after distal to proximal nerve percussion, especially with the response moving distally with time, provides some evidence of the continuity of axons from the point percussed through the lesion to the cell body. The absence of a Tinel's sign in the neck points toward a total plexal avulsion. The expected rate of progression is 1 mm/day distally in accordance with the growing axon. A nonadvancing Tinel's sign indicates the likelihood of poor recovery. The nerve is not percussed over the site of the lesion, but rather distal to the injury to detect an advancing Tinel's sign. A positive Tinel's sign only implies fine fiber regeneration but does not provide any information regarding the quality and the number of axons regenerating. An absent Tinel's sign distal to the injury after appropriate time has elapsed (4–6 weeks) implies total neural interruption and poor axonal growth.

Lesion localization

The localization of the level of the lesion in brachial plexus injuries is straightforward and necessitates a thorough knowledge of the clinical examination. The examiner should make an effort towards identifying the most proximal level of involvement on the basis of the group of muscles and sensory dermatomes involved and whether the lesion involves the roots, trunks, divisions, cords, or peripheral branches of the plexus. The distinction between pre- and postganglionic injuries is absolutely essential because the preganglionic injuries do not recover spontaneously; hence, they should be identified and managed early. The diagnosis of preganglionic root avulsion is based on i) Horner's syndrome, ii) injury to proximal nerves such as long thoracic, phrenic, and dorsal scapular nerve, iii) denervation of cervical paraspinal musculature on EMG, iv) normal sensory nerve conduction in anesthetic areas, v) absence of Tinel's sign in the supraclavicular fossa, and vi) severe deafferentation pain.

 » Electrophysiological Testing Top

The electrical testing is useful in the initial workup of the patient in localizing the site of the lesion; and, also in documenting the recovery in a patient with brachial plexus injury.


The response to nerve stimulation persists for sometime after the injury because  Wallerian degeneration More Details takes time to develop along the nerve. The affected muscle will show electrical changes suggestive of denervation by approximately 2–3 weeks. The baseline EMG is therefore planned at 3 weeks after injury, and this is repeated every 1–2 months for lesions showing serial improvement. There are three phases of activity while performing an EMG. The first phase is a brief period of insertional activity, which occurs in response to a needle being placed into the affected muscle. The second phase occurs with the needle inside the muscle and with the muscle at rest. The third phase occurs with the contraction of the muscle. There are distinct patterns of EMG recordings with a normal muscle, denervation, and early recovery [Figure 11].
Figure 11: Three phases of activity on EMG recording from a muscle with a needle, in normally innervated muscle, denervated muscle, and early recovery

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Nerve conduction studies

The nerve conduction studies are performed by stimulating the peripheral nerve and recording the response at some distance.[14] The action potential can be generated by the depolarization of the muscle (motor nerve conduction study), also called the compound muscle action potential (CMAP), or by the nerve itself (sensory nerve conduction study), which is called as sensory nerve action potential (SNAP). The action potentials are analyzed for (i) amplitude (milli- or microvolts) and (ii) latency (time between the stimulus and the potential, in milliseconds). The conduction velocities can then be measured by dividing the distance from the latency.[15] As a general rule, the velocities should be more than 50 m/s in the upper limbs and more than 40 m/s in the lower limbs. The amplitude of CMAP and SNAP are variable; however, side to side differences of up to 50% can be considered normal.[15]

The traumatic axonal neuropathies are characterized by reduced amplitudes with near-normal conduction velocities. Another pattern seen is conduction block, which correlates with neuropraxia. The CMAP amplitude evoked by distal stimulation is normal, but the stimulation of the nerve above the lesion site shows more than 50% reduction. In brachial plexus lesions, where proximal stimulation above the lesion is not possible, the presence of normal CMAP in a very weak muscle suggests conduction block.

The SNAP can differentiate preganglionic from postganglionic injuries. The lesions at preganglionic region between the dorsal root ganglion and the spinal cord are associated with a distal sensory loss, but preserved distal sensory conduction and hence a normal SNAP. However, if both pre- and postganglionic lesions coexist, there will be a flat trace or negative SNAP. Hence, a negative study is not as helpful as a positive one in excluding a preganglionic injury.

 » Radiological Studies Top


The plain X-rays have been often underutilized for the diagnosis of brachial plexus injury; however, they may indicate the site and the severity of the injury. The fractures of long bones may be associated with nerve injuries, such as axillary nerve injury in fracture of the surgical neck of the humerus, radial nerve injury in fracture of mid-shaft, and combined median and ulnar nerve injury in comminuted ulnar or radial fractures. Shoulder dislocation or fracture can be associated with neural injury. The fracture of the first rib is associated with brachial plexus injury. The fractures of the cervical spine transverse process may be associated with severe proximal stretch injuries to the roots of the plexus. Chest X- ray done after inspiration and expiration might demonstrate the presence of hemidiaphragmatic palsy. The finding of an elevated diaphragm on the side of the injury points toward a proximal injury to the C3–C5 spinal nerve. The fracture of a rib may indicate injury to the intercostal nerves.

CT myelography

CT myelography (CTM) is helpful in defining the level of root injury by assessing the emergence of the spinal nerves from the spinal cord.[16],[17] The traction injury to the roots of the brachial plexus may pull them from the spinal cord, tearing the arachnoidal sleeve of the roots. The contrast material fills the sleeves, giving rise to characteristic traumatic pseudomeningoceles (TM), which are highly suggestive, though not absolutely specific, of root avulsion. The presence of an intact ventral and dorsal rootlet without a TM rules out a root avulsion. The presence of root avulsion is likely if the TM extends outside the foramen. In addition, a severe intradural injury is suspected when there is deformation or displacement of the spinal cord.

CTM should be obtained at least 1 month after the injury to allow the blood clots to resolve and for the TM to develop fully. It has a false positive and false negative rate of 5%–10%.


Although CTM is still considered by many as the "gold standard" for imaging root lesions, recent developments in MRI technology have obtained images with an even greater resolution, such that MRI can now match the diagnostic accuracy of CTM.[16],[18]

MRI has become the imaging modality of choice for overall characterization of lesions within the brachial plexus. The basic sequences performed include a combination of T1-weighted imaging (WI) for defining anatomy, T2WI with fat suppression for identifying lesions that are hyperintense compared with normal structures, T2WI acquired with fast spin-echo or short T1 inversion recovery (STIR) sequence and fat-suppressed T1WI to characterize lesions after contrast administration [Figure 12].
Figure 12: Normal intradural nerve roots (shown by arrows)

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The injured peripheral nerve shows an increased signal on T2WI and STIR sequences owing to endoneurial or perineural edema. The atrophic changes in the muscle develop over a period of several months after denervation, appearing as high-intensity signal compared with normal muscles on T1WI [Figure 13]. The typical MR findings, as seen on T2WI and STIR images, vary with the grade and the severity of the injury.[19] In a neuropraxic injury, there is a focal increase in the nerve signal intensity, whereas in an axonotmetic injury, there is a transient increase in the nerve signal intensity distal to the site of injury, followed by normalization with axonal regeneration. In a neurotmetic injury, there is an increased signal intensity disappearing very late and associated with muscle denervation changes and reduction of the muscle mass and fatty atrophy of the nerves.[19]
Figure 13: Hyperintensity of paraspinal muscles suggesting a postganglionic injury

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The presence of traumatic pseudomeningoceles on MR strongly indicates the presence of a spinal root avulsion [Figure 14]. However, they can occur without root avulsion or avulsion may happen without meningoceles. A strong association exists between the presence of root avulsions and pseudomeningoceles.[20],[21]
Figure 14: (a) Nonvisualization/absence of nerve root on the left in the absence of pseudomeningocele (shown by arrow). (b) Post-traumatic pseudomeningocele due to C8 root injury (shown by arrow)

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CTM and MR myelography have the same sensitivity (92.9%) for detecting root avulsions.[18],[20]

MR myelography

MR myelography is a noninvasive and relatively quick investigation modality requiring no contrast medium and providing imaging in multiple projections. This is comparable in diagnostic ability to the more invasive and time-consuming techniques of conventional myelography and CTM.[22],[23],[24]

MR neurography

MR neurography (MRN) is the direct imaging of the nerves in the body that is performed by optimizing selectivity for unique MRI water properties of the nerves. It is a modification of MRI. This technique yields a detailed image of a nerve from the resonance signal that arises from the nerve itself rather than from the surrounding tissues or from the fat in the nerve lining [25],[26] [Figure 15].
Figure 15: MR neurography showing postganglionic injury with involvement of the upper trunk in the right-sided plexus

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 » Conclusions Top

The brachial plexus injuries are devastating lesions, mainly affecting the young to middle-aged population. The results of treatment of these injuries have considerably improved over the recent years owing to the technological advancements. The main aim of the clinical examination is to localize the lesion along the brachial plexus and to estimate the severity of the injury. A thorough clinical examination has to be supplemented with electrophysiological and radiological evaluation. The preganglionic injuries have to be identified early and managed surgically, as they do not recover spontaneously.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Flores LP. Epidemiological study of traumatic brachial plexus injuries in adults. Arq Neuropsiquiatr 2006;64:88-94.  Back to cited text no. 1
Midha R. Epidemiology of brachial plexus injuries in a multitrauma population. Neurosurgery 1997;40:1182-9.  Back to cited text no. 2
Goldie BS, Coates CJ. Brachial plexus injury: A survey of incidence and referral pattern. J Hand Surg Br 1992;17:86-8.  Back to cited text no. 3
Solagberu BA, Ofoegbu CK, Nasir AA, Ogundipe OK, Adekanye AO, Abdur-Rahman LO. Motorcycle injuries in a developing country and the vulnerability of riders, passengers, and pedestrians. Inj Prev 2006;12:266-8.  Back to cited text no. 4
Narakas AO. The treatment of brachial plexus injuries. Int Orthop 1985;9:29-36.  Back to cited text no. 5
Narakas AO, Hentz VR. Neurotization in brachial plexus injuries. Indication and results. Clin Orthop Relat Res 1988;237:43-56.  Back to cited text no. 6
Kim DH, Cho YJ, Tiel RL, Kline DG. Outcomes of surgery in 1019 brachial plexus lesions treated at Louisiana State University Health Sciences Center. J Neurosurg 2003;98:1005-16.  Back to cited text no. 7
Terzis JK, Verkis MD, Soucacos PN. Outcomes of brachial plexus reconstruction in 204 patients with devastating paralysis. Plast Reconstr Surg 1999;104:1221-40.  Back to cited text no. 8
Prasad L, Sinha S, Kale SS, Nehra A, Mahapatra AK, Sharma BS. Traumatic brachial plexopathies—Analysis of postsurgical functional and psychosocial outcome. Indian J Neurotrauma 2013;10:72-9.  Back to cited text no. 9
Dubuisson AS, Kline DG. Brachial plexus injury: A survey of 100 consecutive cases from a single service. Neurosurgery 2002;51:673-83.  Back to cited text no. 10
Kitajima I, Doi K, Hattori Y, Takka S, Estrella E. Evaluation of quality of life in brachial plexus injury patients after reconstructive surgery. Hand Surg 2006;11:103-7.  Back to cited text no. 11
Choi PD, Novak CB, Mackinnon SE, Kline DG. Quality of life and functional outcome following brachial plexus injury. J Hand Surg Am 1997;22:605-12.  Back to cited text no. 12
Bonnard C, Narakas AO. Supraclavicular traction injuries in adults. In: Boome RB, editor. The Hand and Upper Extremity: The Brachial Plexus. Edinburgh, New York: Churchill Livingstone; 1997. p. 71-8.  Back to cited text no. 13
Mallik A, Weir AI. Nerve conduction studies: Essentials and pitfalls in practice. J Neurol Neurosurg Psychiatry 2005;76(Suppl 2):ii23-31.  Back to cited text no. 14
Wilbourn AJ. Nerve conduction studies: Types, components, abnormalities, and value in localization. Neurol Clin 2002;20:305-38, v.  Back to cited text no. 15
Carvalho GA, Nikkhah G, Matthies C, Penkert G, Samii M. Diagnosis of root avulsions in traumatic brachial plexus injuries: Value of computerized tomography myelography and magnetic resonance imaging. J Neurosurg 1997;86:69-76.  Back to cited text no. 16
Walker AT, Chaloupka JC, de Lotbiniere AC, Wolfe SW, Goldman R, Kier EL. Detection of nerve rootlet avulsion on CT myelography in patients with birth palsy and brachial plexus injury after trauma. AJR Am J Roentgenol 1996;167:1283-7.  Back to cited text no. 17
Doi K, Otsuka K, Okamoto Y, Fujii H, Hattori Y, Baliarsing AS. Cervical nerve root avulsion in brachial plexus injuries: Magnetic resonance imaging classification and comparison with myelography and computerized tomography myelography. J Neurosurg 2002;96(Suppl):277-84.  Back to cited text no. 18
Andreisek G, Crook DW, Burg D, Marincek B, Weishaupt D. Peripheral neuropathies of the median, radial, and ulnar nerves: MR imaging features. Radiographics 2006;26:1267-87.  Back to cited text no. 19
Bowen BC, Pattany PM, Saraf-Lavi E, Maravilla KR. The brachial plexus: Normal anatomy, pathology, and MR imaging. Neuroimaging Clin N Am 2004;14:59-85, vii-viii.  Back to cited text no. 20
Grant GA, Goodkin R, Maravilla KR, Kilot M. MR neurography: Diagnostic utility in the surgical treatment of peripheral nerve disorders. Neuroimag Clin N Am 2004;14:115-33.  Back to cited text no. 21
Yeoman PM. Cervical myelography in traction injuries of the brachial plexus. J Bone Joint Surg Br 1968;50:253-60.  Back to cited text no. 22
Nakamura T, Yabe Y, Horiuchi Y, Takayama S. Magnetic resonance myelography in brachial plexus injury. J Bone Joint Surg Br 1997; 79:764-9.  Back to cited text no. 23
Filler AG, Howe FA, Hayes CE, Kliot M, Winn HR, Bell BA, et al. Magnetic resonance neurography. Lancet 1993;341:659-61.  Back to cited text no. 24
Du R, Auguste KI, Chin CT, Engstrom JW, Weinstein PR. Magnetic resonance neurography for the evaluation of peripheral nerve, brachial plexus, and nerve root disorders. J Neurosurg 2009;112:362-71.  Back to cited text no. 25
Zhou L, Yousem DM, Chaudhry V. Role of magnetic resonance neurography in brachial plexus lesions. Muscle Nerve 2004;30:305-9.  Back to cited text no. 26


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15]

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Journal of Medical Case Reports. 2017; 11(1)
[Pubmed] | [DOI]


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