1. Fibular nerve palsy after hip replacement: Not only surgeon responsibility. Hereditary neuropathy with liability to pressure palsies (HNPP) a rare cause of nerve liability.
Logroscino G, Del Tedesco F, Cambise C, Coraci D, Donati F, Santilli V, Padua L. Orthop Traumatol Surg Res. 2016 Jun;102(4):529-31
Logroscino et al. report an interesting case of 66-year-old man presenting severe weakness at inferior limb muscles after hip prosthesis revision. In this case, the authors documented a severe right fibular nerve damage in NCS, while marked enlargement of the same nerve, associated with focal enlargements in other nerves was found in US studies. The diagnosis of hereditary neuropathy with liability to pressure palsies was suspected and confirmed by genetic test.
This report highlights the possible diagnostic role of nerve ultrasound in detecting structural changes at sites where no impairment is expected on pure clinical and electrophysiological grounds. The ultrasound detection of generalised focal enlargements in various peripheral nerves led to the correct suspicion and final diagnosis of a HNPP.
2. Neuroimaging of classic neuralgic amyotrophy
Lieba-Samal D, Jengojan S, Kasprian G, Wöber C, Bodner G. Muscle Nerve. 2016 Apr 13. doi: 10.1002/mus.25147
Liebe-Samal et al. reported on the possible diagnostic role of MRI and high-resolution ultrasound (HRUS) in 6 cases with classic neuralgic amyotrophy.
The authors reported that HRUS showed segmental swelling of all clinically affected nerves/trunks in all cases with neuralgic amyotrophy, while atrophy of muscles was detected in those assessed >1 month after onset. On the other hand, MRI showed T2-weighted hyperintensity in all clinically affected nerves, except for the long thoracic nerve, and denervation edema of muscles.
This study highlights that both HRUS and MRI are valuable diagnostic tools in assessing and quantifying both primary (neural) and secondary (muscular) structural changes in patients with neuralgic amyotrophy
3. High-Resolution Ultrasonography of the Superficial Peroneal Motor and Sural Sensory Nerves May Be a Non-invasive Approach to the Diagnosis of Vasculitic Neuropathy.
Uceyler et al. evaluated the use of HRUS of sensory nerves of the lower extremities as a non-invasive tool to differentiate vasculitic neuropathy from polyneuropathies of different etiologies.
Overall 26 patients with different PNP underwent clinical, laboratory, electrophysiological assessment, while a diagnostic sural nerve biopsy as part of the routine work-up. The authors reported that patients with vasculitic neuropathy showed significantly larger superficial peroneal nerves LD (P < 0.001) and larger sural nerve cross-sectional areas when compared with disease controls (P < 0.001).
The main highlight of this study is that this is the first report of possible ultrasound biomarkers in order to differentiate non-invasively vasculitic from other PNPs.
4. Nerve ultrasound protocol in differentiating chronic immune-mediated neuropathies
Kerasnoudis A, Pitarokoili K, Haghikia A, Gold R, Yoon MS. Muscle Nerve. 2016 Apr 7. doi: 10.1002/mus.25138
Kerasnoudis et al. reported on the possible diagnostic role of a new nerve ultrasound protocol (NUP) in differentiating chronic immune-mediated neuropathies.
The NUP was evaluated overall in 110 patients with clinical presentations of chronic immune-mediated neuropathies. All patients were evaluated clinically and electrophysiologically and were divided into 4 groups: a) symmetric demyelinating, b) symmetric axonal, c) asymmetric demyelinating; and d) asymmetric axonal polyneuropathy.
The NUP led overall to correct classification in 42 of 49 (85.7%) patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 13 of 15 (86.9%) with multifocal motor neuropathy (MMN), and 5 of 5 (100%) with multifocal acquired demyelinating sensory and motor neuropathy (MADSAM). The NUP had > 80% sensitivity and specificity in distinguishing CIDP, MMN, and MADSAM in all 4 study groups.
The main take-home message of this study is that the new NUS may contribute to the correct etiological classification of chronic immune-mediated neuropathies, even in cases with atypical clinical and electrophysiological presentation.