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Brachial plexus disordersDr Dinesh Khandelwal, DMAssociate ProfessorDepartment of NeurologySMS Medical College, Jaipur
Shoulder pain-frozen shoulder, cervical spondylosis, fibromyalgia, brachial plexopathy, parkinsonism Weakness of shoulder muscles-brachial plexopathy, cervical spondylosis, stroke, muscular dystrophyAtrophy-sequelae of brachial plexopathy, MND, muscular dystrophyPresenting to a neurologist
Brachial plexus anatomyDisordersidiopathic injuryothersApproach-clinicalelectrophysiologicalManagement Brachial plexopathy
Anatomy of brachial plexus
InjuryIdiopathic plexitisThoracic outlet syndromeMetastatic brachial plexopathyRadiation plexopathyBrachial plexus nerve involvementDisorders of brachial plexus
Unknown etiology, with unilateral/asymmetric involvement of the brachial plexus.It occurs in all age groups but is more common between the third and seventh decadeMen are affected more often than womenAntecedent events occurring days or weeks prior to the onset have been reported in 28-83% of the cases in various series-Upper respiratory infection, flu-like illness, immunization, surgery and emotional stress have been the common triggersNo triggers can be found in half of the casesIdiopathic brachial neuritis (IBN)
Beginning as an ache/deep burning around shoulderRapidly intense with burning severe pain for few days-rapid development of shoulder weakness-pain subsideSerratus anterior, deltoid, biceps, or triceps-totally or almost paralyzedDistal muscles can also be involvedBrachial plexitis
No fever/leucocytosis/ESROccasionally mild pleocytosis in CSFRecovery-usually complete in few months to 12 monthsRecurrence is rare (except in familial)EPS-early only f wave and motor axonal after a week Brachial plexitis..
Highly restricted form-one or two nerve of brachial plexusMost common-isolated serratus anteriorOther-suprascapular, axillary, posterior interosseus or phrenic nerve (dyspnea/elevated one dome of diaphragm on CXR)The pathophysiology of IBN is not fully elucidated but is believed to be an immune-mediated disorder.
Atrophy of muscle if any or twitchingsMuscle power testing at each joint and individual muscle testing at involved jointSensory testing in each dermatome and each sensory nerveConclusion drawn from clinical testing before proceeding for EPS (extension of clinical examination)Clinical examination
Clinical courseMovements are not painfulNumbness more distally, weakness is mild, exacerbation with neck movementEPS-CMAP, SNAP, EMGMRI-root avulsions, intrinsic and extrinsic masses of the brachial plexus, pseudomeningoceles, post-traumatic neuromas, hematomas, fibrosis, and inflammatory plexitis such as infectious, immune mediated, radiation induced, or idiopathicDifferentiating form radiculopathy
Routine nerve conduction study-median, ulnar and radial motor sensory studyErbs stimulation-axillary, triceps (radial), biceps (musculocutaneous)Medial antecubital nerve of forearmF wave, SEP Compared with other limbEMG-selecting muscles from each myotome and each nerve, paraspinal (C5 to T1)Electrophysiology
It range from normal to mild thickening of the plexus and hyperintensity on T2WI with or without enhancement. Fat deposition and denervation signal-intensity changes appear in the muscles of the shoulder girdle and chest in the subacute and chronic phases of brachial plexitisMRI brachial plexus
Figure 2 MRI of the chest showing the enhanced signal intensity of the left brachial plexus (arrows).
R.H. Chabot, and P.W. Wirtz Neurology 2011;76:e76Copyright 2011 by AAN Enterprises, Inc.
MRI of the chest showing the enhanced signal intensity of the left brachial plexus (arrows)
Corticosteroids-limited data are available to support its useA study by van Eijket al, indicates that oral prednisolone may be an effective pain treatment for brachial neuritis.A retrospective case series of 50 treated patients compared with 203 untreated cases.Median time-for initial pain relief was 12.5 days in the treated group compared with 20.5 days in the untreated patients.18% of the prednisolone patients recovered strength within the first month of treatment, with only 6.3% of the control group12% of the patients in the prednisolone group attained a full recovery within 1 year, while only 1% of the untreated groupThe authors recommended that oral prednisolone be used during the acute phase of brachial neuritis; but, they also advised that a prospective, randomized trial be conducted to verify their results.Physiotherapy Treatment
Hereditary neuralgic amyotrophy (HNA) is an autosomal-dominant disorder characterized by repeated episodes of paralysis and sensory disturbances in an affected limb preceded by severe pain. HNA is genetically linked to chromosome 17q25, where mutations in the septin-9 (SEPT9) gene have been foundClinical course is same as that of idiopathic except recurrent attacksHereditary Neuralgic Amyotrophy
Symptoms-Pain, paresthesias (ulnar aspect) or weakness in the upper extremity. Severity-increase after certain activities, and worsens at the end of the day or during sleep.Advanced cases of nTOS are characterized by objective signs of weakness of the hand, loss of dexterity of the fingers, and atrophy of the affected muscles (thenar>hypothenar).It is commonly seen in womenOften, bilateral cervical rib or enlarged down-curving C7 transverse processes, fibrous band across the cervical rib and scalene tubercle of the first cervical rib are noted in these casesX-rays of the chest should be performed to rule out the possibility of an infiltrative process or space-occupying mass (e.g., Pancoast tumor) compressing the brachial plexus.MRI, especially sagittal T1WI through neurovascular bundles as well as MR angiography and MR venogram of the subclavian vessels in both neutral and abduction positions, aid in depiction of neurovascular compression, stenosis, thrombosis, and aneurysmsNeurogenic Thoracic Outlet Syndrome
Sensory : Absent or reduced amplitude ( clawhand
Clinical examination-bulk and power of muscles, sensation testingEPS-SNAP starts dropping in amplitude by day 7 post-injury and reaches its lowest value by day 10 or 11-distal stump degeneration timeEarly-SNAP-normal-misdiagnosis of preganglionicThe SNAP is not useful for predicting recovery in brachial plexus lesions as once absent, it does not return to normal, even with regeneration
Clinical and EPS
Amplitude of the distal CMAP starts to drop by day 3 following the injury, and it reaches its lowest valve by day 7Severity-judged by day 7Well-preserved CMAP amplitude from a clinically weak muscle at least 7 days after the injury suggests a neurapraxic lesionAmplitude of the CMAP correlates well with the severity of the lesion (till re-innervation has occurred), and it can be judged by comparing the CMAP from the affected limb with that of the unaffected limb
formula U-A/U X 100= % of axon loss, where U = CMAP amplitude of unaffected side, A = CMAP amplitude of affected side. 50-75% indicates a moderate axon loss, >75% a severe axon loss and absent CMAP indicates no viable axons at the time of the study
If there is no response, then regeneration has to occur by proximo-distal nerve growth as there are no surviving axons for collateral innervation. If the denervated muscle lies more than 24 inches from the site of a complete nerve injury, recovery is not possible as by the time the nerve (if at all) would reach the muscle, it would have been replaced by fibrous or fatty tissue
Nerve growth rate is about one inch a monthA progressive increase in the amplitude from a muscle on serial studies would signify re-innervation of that muscleNeedle Electromyography (EMG) examination is required to document and record the axon loss, its proximal extent, and the completeness of the lesion, especially for proximal muscles where CMAP recording is not possible
Needle EMG also documents the earliest sign of recovery in the form of nascent units and unstable polyphasic units.Axon loss is objectively confirmed by the presence of fibrillation potentials, which develop about 3 weeks after the injury (in the most distal musclesOn voluntarily activating the muscle, if motor units are seen, it indicates that there are surviving axons and the lesion is partial. In such cases, the regeneration will take place by co-lateral sprouting.
If there are no motor units and no recordable CMAP from the muscle, it indicates a functionally complete lesion, and re-innervation would happen only by nerve growth from the proximal stump, provided the nerve is in anatomical continuityAfter adequate time is allowed, regeneration is detected on needle EMG by the presence of unstable polyphasic units, which suggest ongoing re-innervation
Upper limb somatosensory-evoked potentials are useful for documenting a complete pre-ganglionic avulsion of the sensory roots
MRI findings of asymmetric thickening, T2 hyperintensity, and diffuse contrast enhancement of the injured plexus are observed.The MRI in pre-ganglionic injuries may show root avulsion, pseudomeningocele (a tear in the meningeal sheath around the nerve roots with extravasation of the CSF in the neighboring tissue), enhancement of the root exit zone, signal-intensity changes in the spinal cord at the level of root avulsion and/or paraspinal muscles and avulsion of the spinal cord.In post-ganglionic lesions, enhancing nodular thickening (neuroma) and hematoma in the vicinity of the plexus are common imaging findingsMRI of brachial plexus injury
More common in the elderly patientsL