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Introduction: Acute Leriche syndrome is a rare but potentially life-threatening condition. Pain, pallor, and coldness of the lower extremities serve as clues for suspecting Leriche syndrome. However, the absence of these findings may pose a diagnostic challenge. Case Presentation: An 83-year-old man presented at our emergency department with a complaint of sudden-onset paraparesis. Initially, spinal cord infarction was suspected due to clinical course and neurological findings, but thoracolumbar MRI showed normal findings. On admission, symptoms associated with aortoiliac occlusion were not present, except for muscle atrophy in the thigh. CT angiography revealed aortoiliac occlusion, leading to a diagnosis of Leriche syndrome. Conclusion: Leriche syndrome should be considered as a potential differential diagnosis in patients with acute paraparesis. Muscle atrophy of the lower limbs disproportionate to the clinical course may be the clue for suspecting acute Leriche syndrome with symptoms related to atherosclerotic occlusion which are inconspicuous.

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Objective: To establish the utility of the additional evaluation of the P15 potential generated at the greater sciatic foramen in the tibial nerve somatosensory evoked potentials (SEPs) in diagnosing lumbar spinal stenosis (LSS). Methods: We retrospectively reviewed tibial nerve SEP findings in patients having MRI-confirmed LSS at the cauda equina or conus/epiconus region. P15 and N21 potentials were recorded and the following findings were defined as localizing abnormalities: 1) normal P15 latency either with prolonged P15-N21 interval or with absent N21; 2) decreased ratio of the N21 amplitude to P15 amplitude. As non-localizing abnormalities, N21 and P38 latencies were also evaluated. Tibial nerve F-wave findings were also investigated. Results: According to the entry criteria, 18 patients were included, 15 with cauda equina lesions and 3 with conus/epiconus lesions. Localizing abnormalities in SEPs were found in 67% of patients, achieving significantly higher sensitivity than delayed P38 latency (28%), and higher sensitivity than N21 abnormalities (39%), though this was not significant. Localizing abnormalities were observed even in 6 out of 11 patients lacking both sensory symptoms and signs. Tibial nerve F-wave was abnormal in 36% of 14 patients with F-wave examinations, whereas the localizing abnormalities in SEPs were found in 64% of the same patient population. P15 amplitude was depressed in 4 patients (22%), which may indicate the involvement of the dorsal root ganglion in LSS, although its latency was normal even for these patients. Conclusions: Tibial nerve SEPs with the recording of P15 and N21 potentials achieved sufficiently high sensitivity in diagnosing LSS. They have the advantage over F-wave in that they can localize the lesion at the cauda equina or conus/epiconus level. Significance: Tibial nerve SEPs are promising in evaluating LSS, especially in documenting sensory tract involvement in cases lacking sensory symptoms/signs.

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INTRODUCTION: In chronic inflammatory demyelinating polyneuropathy (CIDP), exclusion of secondary axonal degeneration is challenging with conventional methods such as nerve conduction study (NCS), needle electromyography, and nerve biopsy. Increased echo intensity (EI) and decreased muscle thickness (MT) identified on muscle ultrasound (MUS) examination represent muscle denervation due to axonal degeneration in neurogenic disorders, suggesting MUS as a new tool to detect secondary axonal degeneration in patients with CIDP. METHODS: EI and MT of abductor pollicis brevis, abductor digiti minimi, and first dorsal interosseous muscles were measured in 16 CIDP patients. Raw values were converted into z-scores using data from 60 normal controls (NCs). RESULTS: Six of 45 muscles showed abnormally high EI and low MT, suggesting denervation following secondary axonal degeneration. These six muscles belonged to two patients with long disease history, unresponsiveness to treatment, and long interval from onset to initial therapy. There were no significant differences in EI and MT (p = .23 and .67, respectively) between the CIDP and NC groups, although NCS results revealed obvious demyelinating abnormalities in all CIDP patients, suggesting the fact that muscle structures will be preserved, and EI and MT will not change unless secondary axonal degeneration occurs in CIDP. CONCLUSION: MUS is a promising tool for evaluating secondary axonal degeneration in patients with CIDP.

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