Back ground: The pathophysiology of idiopathic neuralgic amyotrophy (INA) has been presumed to be localized inflammatory immune process in brachial plexus. Persistent pain and weakness remain in about 20% of INA patients without treatment. Up to now, high dose oral corticosteroid therapy is conventionally used for the treatment of INA. This would help control systemic inflammation, but about 20% of patients has experienced systemic side effects. Therefore, we intended to modulate therapeutic approach to be locally active by performing ultrasound-guided brachial plexus and cervical root block with reduced the dose of steroid. The purpose of this therapy is to improve functional recovery with effective pain control and reduce systemic side effects of steroid.
Case: One month ago, a 41-year old right handed female has got common cold and this has gradually got better. Two weeks later, she felt acute pain and sudden weakness on left upper arm without trauma and sensory loss. Her history was negative for hereditary or metabolic neuropathies. On physical examination, she had proximal muscle weakness of left upper limb without atrophy; shoulder flexion and abduction (MRC score 2/5), elbow flexion (MRC 4/5). A laboratory study showed no evidence of abnormalities. We performed nerve conduction study and needle electromyography at 2 weeks after onset, suggesting of C5 radiculopathy. However, we suspected brachial plexus lesion regarding her history and physical examination clinically. We have finally diagnosed an INA by brachial plexus MRI, it showed the brachial plexopathy involving divisions and lateral, posterior cord with mild swelling on C5 nerve root, suggesting C5 radiculopathy (Fig. 1).
We started low dose oral steroid therapy (0.5 mg/kg for 3 days, 0.4mg/kg for 3 days, 0.2mg/kg for maintaining dose, totally 4 weeks course) about 2 weeks after onset. Concurrently, 2 weeks interval, 3 times ultrasound-guided brachial plexus injection (dexamethasone 5mg, 2 times on C5 root and triamcinolone 40mg, 1 time on division level of brachial plexus) were performed (Fig. 2). We used MRC grades of the following 3 muscle pairs comprising the MRC sum score; shoulder flexor, abductor and elbow flexor. These muscles grade in MRC sum score (total score:15) were increased from 8 to 13 in one month, and further improved up to 15 in 2nd months. The pain scale (NRS) was graded from 5 to 2 and finally 0 in the same periods.
Conclusion: Although the precise pathophysiology of INA is unknown, it is thought to be associated with localized inflammatory-immune attack. In comparison with previous studies, this case report showed ultrasound-guided steroid injection with low dose steroid therapy could induce successful functional recovery and effective pain control without the systemic complications of steroid. Therefore, localized ultrasound-guided brachial plexus injection would be a recommendable approach to treat INA.
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Fig 1. a Sagittal T2 water excited image shows mild high signal intensity at left supraspinatous, infraspinatous muscle, suggesting denervation change related to suprascapular nerve b Axial T2 image shows left C5 nerve root compression with mild swelling(red arrow) c Coronal T2 water excited image shows swelling and high signal intensity left divisions and lateral, posterior cord(red arrows)
Fig 2. Ultrasound guided injection on left brachial plexus at the level of division (short arrow); Needle path (long arrow)
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