Presentation
Acute is usually pain in the shoulder or upper arm
Insidious may be progressive pain, evolving numbness, weakness of muscles, or a combination
Painful plexopathies can make it difficult to determine true 'weakness' from reduced effort due to pain
Sensory loss is commonly in the axially nerve distribution
Differentiating between CRPS and brachial plexus injuries can be difficult however autonomic symptoms of CRPS is uncommon. Also the severely heightened sensitivity of the limb is more common in CRPS.
C5 lesions --> Shoulder pain
C6 lesions --> Thumb and index finger
C7,C8,T1 - difficult to localise from elbow to hand
Pain often worsens with climate changes and improves during recreation/social activity
Epidemiology
Brachial plexus syndromes are rare (e.g. 0.4% of cancer patients, 2-5% of radiation pts)
Patients experiencing neuropathic pain after brachial injury range from 67-95% (1)
From cervical root avulsion - neuropathic pain occurs in 80-90% of patients with up to 30% saying pain is severe and intense
Neuropathic pain may develop immediately, or up to months after the injury. Intensity often worsens with time (due to sympathetic system plasticity mechanisms)
Severe pain immediately, particularly burning, indicates deafferentation (the interruption or destruction of the afferent connections of nerve cells, performed especially in animal experiments to demonstrate the spontaneity of locomotor movement.) pain secondary to avulsion of multiple routes. Pain is typically constant burning and crushing sensation associated with paroxysmal electrical shocks and throbbing in the affected limb
Some pain is usually felt in the hand no matter which root is affected
Pathophysiology
- Injury to the brachial plexus can take many different forms:
Compression (rare because protected by bony structures)
Transection (Major trauma to neck and shoulder causes down traction on shoulder)
Ischaemia (occlusion of small vessels)
Inflammation (uncertain)
Metabolic (Diabetic plexopathies)
Neoplastic (local pressure from cancer mass)
Radiation treatment (direct injury to axons or the vasa nervorum with ischaemic changes)
Neuropathic pain from POST ganglionic lesions can be from abnormal nerve regeneration, painful neuroma formation, and compression from fibrous tissues
Neuropathic pain from PRE ganglionic lesions depends more upon how many axons are affected
Postganglionic brachial plexus lesions are characterised by persistent connection between the dorsal ganglia and the CNS. Increased permanent neuronal activity is likely due to ectopic ganglionic action potentials. Spontaneous discharges of Adelta fibres likely causes paraesthesias and dysaesthesias, whereas disturbed C fibres produces burning and shooting pain.
Increased sodium channels in the damaged nerve fibres also upsets neural transmission and promoted pathologic connections between regenerating axons - called 'Ephaptic coupling' - causing short circuiting of nociceptive neurons.
Root avulsion has the strongest association with CNS plasticity changes. Sudden disconnection causes primary changes in the affected segment due to neuronal death, and secondary alterations due to a reactive inflammatory response and glial activation. These alter the substantial gelatinous and Lissauer tract which are the first point of integration for input from primary sensory afferents.
A dorsal root entry zone (DREZ) lesioning procedure is where a spinal surgeon enters the spinal cord to silence damaged areas of pain signalling nerve cells - useful at time for patients with root avulsions.
Cortical changes after peripheral nerve lesions such as loss of effector input to sensorimotor cortex and loss of normal sensory and motor cortices. Some patients then experience phantom limb sensations/movements.
Examination
Investigations
Nerve conduction studies can be used particularly for alternative diagnoses such as entrapment syndromes
Sensory nerve testing is more sensitive to axonal loss than motor nerve studies
Needle electromyography (EMG) - is most sensitive test for showing axonal loss
Plain films of the area are useful for bony impingement/pathological lesions
CT myelography is useful for detecting root avulsions
MRI can also be utilised
Treatment
Medications: The usuals (TCA, SNRIs, calcium channel ligands etc)
Topical: Capsaicin or lignocaine can be of assistance
Non-pharm: Psychologist, TENS. OT, acupuncture, Physio, hypnosis etc.
Surgery:
Decompression, reconstruction, ablation and modulation
DREZ lesioning can be very affective for brachial plexus root avulsions which don't repond to medications or primary repair. Effective in 70-90% of patients for the paroxysmal component of avulsion pain
However, post procedure the pain gradually reappears often. 50-70% get longer term benefit
Peripheral nerve stim:
Success between 70-80% however 10-15% get some form of complication
Spinal cord stim:
Less helpful - likely due to fact that these nerves are somewhat degenerative anyway in complete root avulsion. More helpful perhaps in incomplete or non-avulsilve brachial plexus injuries
Prognosis
Golden pearls
References / Articles / Resources
Lovaglio, A. C., Socolovsky, M., Di Masi, G., & Bonilla, G. (2019). Treatment of neuropathic pain after peripheral nerve and brachial plexus traumatic injury. Neurology India, 67(7), 32.
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