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Brachial plexus: root avulsion
(Brachial plexopathy, brachial plexus neuritis, radial neuritis)
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Introduction
  • Cause : trauma - usually RTA (HBC).
  • Most common cause of thoracic limb paralysis.
  • Signs : sudden onset neurological deficits in thoracic limb following trauma.
  • Diagnosis : thoracic limb paralysis.
  • Treatment : local wound treatment, physiotherapy/amputation.
  • Prognosis : guarded, very poor to fair.


Presenting signs
  • History of severe trauma, usually road traffic accident (hit-by-car).
  • Non-weightbearing lameness/altered gait after accident.
  • Neurogenic atrophy, seen 7-10 days after injury.
  • Limb mutilation or excoriation.


Age predisposition
  • Younger animals.


Special risks (e.g. anesthetic)
  • General anesthetic : if concurrent trauma to the chest Anesthesia: in chest trauma.
Pathogenesis Top

Etiology
  • Trauma, eg road traffic accident right_arrow traumatic traction of nerve roots at their origin inside dura mata.


Predisposing factors
General
  • Entire male.
  • (Pro) estrus female.
  • Dog lives on busy road or in city.
  • Dog allowed to exercise unsupervised.
  • Old or faulty extending lead.
  • Dog exercised off the lead.


Pathophysiology
  • Trauma can occur to a single nerve (misplaced injection into the sciatic nerve) or multiple nerves (brachial plexus avulsion).
  • The severity of involvement clinically will determine prognosis.
  • A neuropraxia (least severe injury) is an interruption in function and conduction in the nerve, usually associated with a lesion of the myelin without severe axonal involvement.
  • Axonotmesis suggests separation and damage of axons, where neurotmesis (most severe injury) is complete severance of all structures of the nerve.
  • The likelihood of regeneration is less with neurotmesis as compared to neuropraxia.
  • Brachial plexus avulsion occurs as a result of a trauma.
  • Clinical signs include LMN paresis/plegia in the affected thoracic limb.
  • Ipsilateral loss of the cutaneous trunci reflex (due to damage to the lateral thoracic nerve that exits the spinal cord at C8-T1 area) and/or Horner's syndrome (sympathetic nerves exit the spinal cord at T1-3) may be associated signs.
  • It is the nerve roots that are actually avulsed off of the spinal cord.
  • The innervation of regional nerves from the plexus varies in animals.
  • When regional nerves are formed by more cranial spinal rootlets than is usually seen, the plexus is said to be prefixed.
  • When the nerves originate from more caudal spinal cord segments than normal, the plexus is said to be post-fixed.
  • The relationship between prefixed, median, and post-fixed plexus types in the dog is 1:3:1.
  • Allam (1952) studied the nerves that form the brachial plexus in dogs and found the following percentages of dogs had the brachial plexus derived from the associated spinal segments:
    • 58.6 % were formed by C 6, 7, 8, and T1.
    • 20.7 % were formed by C 5, 6, 7, 8, and T1.
    • 17.24% were formed by C 6, 7, 8, T1, and T2.
    • 3.4% were formed by C 5, 6, 7, 8, T1, and T2.
  • Brachial plexus avulsion most commonly occurs in a single thoracic limb following automobile trauma.
  • (a) Pathologically, the nerve roots are contused or separated from the spinal cord.
  • (b) Diagnosis is based upon history and appropriate clinical signs.
  • (c) There is no currently available treatment.
  • (d) Prognosis depends upon the severity of nerve injury. Loss of pain sensation in the limb is a worse prognostic sign.
  • Limb forcibly abducted or rotated at its attachment to the body right_arrow traumatic traction on the spinal nerve roots at their origin inside the dura mater right_arrow disruption of the neural elements right_arrow interruption of spinal reflexes.
  • Skin desensitization and decreased muscle tone right_arrow neurogenic muscle atrophy right_arrow decreasing area of skin desensitization when nerves grow in from surrounding innervated areas.
  • Initial assessments should attempt to determine the extent of injury to the nerve:
    • Neuropraxia : a functional rather than anatomical interruption in peripheral nerve function.
    • Axonotmesis : more severe than neuropraxia. Actual axons within the nerve are separated, however, the nerve itself remains intact.
    • Neurotmesis : a complete severance of the nerve with anatomical separation of all axons.


Timecourse (incubation, duration)
  • Neurological deficits apparent immediately after injury.
  • Neurogenic muscle atrophy from 7-10 days after injury.

Diagnosis Top

Presenting problems
  • Thoracic limb paralysis/partial paralysis.
  • Thoracic limb lameness.


Client history
  • Paralysis of thoracic limb after accident.
  • In association with limb fractures.


Clinical signs
  • Neurological deficits in thoracic limb.
  • Muscle atrophy 7-10 days after accident.


Caudal avulsion
  • 55 % cases have partial Horner's syndrome on affected side:
    • Ipsilateral miosis.
    • Slight ptosis on same side as affected limb.
  • Neurological deficits:
    • Panniculus deficit on affected side.
    • Absence of panniculus reflex on the affected side of the body.
    • Sensory deficits variable.
    • Variable loss of sensation in distal thoracic limb.
  • Affected limb does not bear weight:
    • Limb carried with elbow and shoulder flexed.


Complete avulsion
  • Affected limb does not bear weight:
    • Dragging of dorsal paw, causing severe skin excoriation.
    • Complete absence of limb function.
    • Dropped elbow with carpal flexion.
    • Affected limb looks longer.
    • Occasionally brachium advanced when dog is walking.
  • Neourological deficits:
    • No spinal reflexes in affected limb.
    • Complete absence of sensation in distal limb.
    • Partial Horner's syndrome in 55% of cases.
    • Loss of panniculus reflex.


Cranial avulsion
  • Pain sensation intact despite severe motor dysfunction.
  • Weightbearing lameness:
    • Lack of elbow flexion.
    • Decreased protraction of the limb.
    • Atrophy of supra- and infraspinatus muscles.


Diagnostic investigation


Radiography
  • Lateral and dorsoventral views of humerus Radiography: humerus and thorax Radiography: thorax.
  • Rule out concurrent orthopedic injuries, which are rare.


Other
  • Electromyography (EMG) is helpful in determining evidence of denervation in muscle.
  • Electromyography will show evidence of denervation in muscles of the limb suggesting a neurogenic rather than orthopedic cause for the dysfunction.
  • EMG changes, however, may not be present for up to 5-7 days after the injury.
  • Nerve conduction velocities (NCV) assess the speed of impulse transmission.
  • Late potentials (H waves; F waves) are used to assess the integrity of the proximal peripheral nerve and nerve root.


Confirmation of diagnosis
Discriminatory diagnostic features
  • History.
  • Signs.

Definitive diagnostic features
  • Neurological signs.
  • EMG.


Gross autopsy findings
  • Hemorrhage is often noted in the intradural area around the nerve roots.


Histopathology findings
  • Severence of a nerve may result in Wallerian degeneration:
    • The neuronal cell enlarges, and nucleus become eccentrically positioned, and the Nissl substance usually comes together peripherally (central chromatolysis).
    • The distal segment of nerve below the severence will degenerate.
    • The proximal stump will enlarge and form collateral sprouts.


Differential diagnosis


Causes of partial paralysis of thoracic limb
  • Brachial plexus neoplasia Shoulder: brachial plexus neoplasia.
  • Brachial plexus neuritis Brachial plexus: neuropathy.
  • Brachial plexus neuritis is an idiopathic inflammation primarily involving the nerves of the brachial plexus.This uncommon disease may result in signs similar to a brachial plexus tumor or injury. In one dog, this disease was suspected to be due to an allergic reaction to ingestion of a horse meat diet.
  • Spinal cord diseases.
  • Lesions affecting single nerves.


Causes of thoracic limb lameness
  • Orthopedic problems.
  • Contracture of the infra or supraspinatus muscles Contracture of spinatus muscle 
  • Local infection.
  • Fractures.
  • Dislocations.
  • Neoplasia.

Treatment Top
Initial symptomatic treatment
  • Intravenous fluids Fluid therapy : if animal shocked.
  • Antibiotics Antimicrobial drug for skin wounds.
  • Non-steroidal anti-inflammatory drug Analgesia: overview : if pain.
  • Elizabethan collar Elizabethan collar : to prevent self-mutilation.
  • No treatment for the primary avulsion is successful.
  • Tendon transpositions and arthrodesis of the carpus may be salvage options in selected patients.
  • Nerve transpositions have been used in human beings, but have not been adequately evaluated in animals.
  • Local wound treatment.
  • Physiotherapy: to prevent contractures.


Standard treatment
  • Amputation Amputation: forelimb : if foot of affected limb is damaged by dragging or by self-mutilation.
  • Consider amputation if there is analgesia below the elbow, self-mutilation and no sign of improvement within 4 weeks.
  • Supportive treatment of local wounds and abrasions.
  • Prevent self-mutilation.
  • Prevent contractures.


Subsequent management

Treatment
  • Physiotherapy: continued to prevent muscle contractures.

Monitoring
  • Neurological re-examination :
    • Decreasing area of skin desensitization.
    • Improving reflexes.
    • Increasing muscle tone.
  • Electromyography :
    • Improving nerve function.
    • Increasing muscle innervation.

Prevention Top
Control
  • Measures to prevent dog involvement in road traffic accidents.

Sequelae Top
Prognosis
  • Depends on number of remaining nerve fibers and their ability to reinnervate denervated muscle.
  • Very poor if complete plexus avulsion.
  • Fair if deep pain sensation intact.


Expected response to treatment
  • Improvement in muscle tone, reflexes and skin sensitivity over 4-6 months.


Reasons for treatment failure
  • Lesion too severe.
  • Client non-compliance with management.
  • Client refusing amputation for economic or esthetic reasons.

Sources Top
Publications
Refereed papers
  • Braund K G (1991) Nerve and muscle biopsy techniques. Prog Vet Neurol 2 , 35-56.
  • Kline D G (1990) Surgical repair of peripheral nerve injury. Muscle and Nerve 13 , 843-852.
  • Gibson K L & Daniloff J K (1989) Peripheral nerve repair. Comp Cont Educ Pract Vet 11 , 938-944.
  • Allam M W, Lee D G, Nulsen F E & Fortune EA (1952) The anatomy of the brachial plexus of the dog. Anat Rec 114 , 173-180.

Other sources of information
  • Rodkey W G (1993) Peripheral Nerve Surgery. In: Textbook of Small Animal Surgery. 2nd edn. Slatter D(ed). Philadelphia: W B Saunders. pp 1135-1141.


Vetstream contributor(s)
  • H Scott BVSc CertSAD CertSAO MRCVS , 207 Daventry Road, Cheylesmore, Coventry, West Midlands CV3 5HH, UK.
  • Dr Rod Bagley DVM DipACVIM , Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, WA 99164-6610, USA.

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Amputation: forelimb
Analgesia: overview
Anesthesia: in chest trauma
Antimicrobial drug
Brachial plexus: avulsion
Brachial plexus: neuropathy
Contracture of spinatus muscle
Fluid therapy
Nerve sheath: neoplasia
Radiography: humerus
Radiography: thorax
Shoulder: brachial plexus neoplasia
Elizabethan collar Link Traumatic ulceration Link
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