2021Progress in Rehabilitation MedicineOpen access

Clinical Features of Ulnar Tunnel Syndrome and the Diagnostic Value of Nerve Conduction Measurements

Shingo Nobuta, Hiroshi Okuno, Taku Hatta, Ryo Sato, Eiji Itoi

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Abstract

OBJECTIVES: The purposes of this study were to assess the clinical features of ulnar tunnel syndrome (UTS) and to investigate the diagnostic value of nerve conduction measurements for UTS. METHODS: Eighteen patients with UTS were reviewed retrospectively. Fifteen patients had intrinsic muscle atrophy and motor weakness, and 15 had numbness with hypesthesia. The compound muscle action potentials (CMAPs) from the first dorsal interosseous (FDI) muscle and the abductor digiti minimi (ADM) muscle and the sensory nerve action potential (SNAP) from the little finger were recorded and analyzed. All patients underwent ulnar tunnel release surgery and neurolysis. Static two-point discrimination test results and pinch strengths were assessed before and after surgery. RESULTS: Before surgery, FDI-CMAP was recorded in 17 patients, and ADM-CMAP in 16, and all showed delayed latency and/or low amplitude. SNAP was recorded in eight patients and two showed delayed latency. The causes of ulnar nerve lesions were ganglion in five patients, traumatic adhesion in four, ulnar artery aberrancy in four, pisohamate arch in three, anomalous muscle in one, and ulnar vein varix in one. The sites of the lesions were in zone 1 of the ulnar tunnel anatomy in 12 patients, in zone 2 in 2, and in zones 1 and 2 in 4. After surgery, all patients obtained recovery of motor function and sensation; however, postoperative FDI-CMAP and ADM-CMAP did not improve to the normal range. CONCLUSIONS: The causes of UTS were ganglion, traumatic adhesion, ulnar artery aberrancy, and pisohamate arch. Both FDI-CMAP and ADM-CMAP were valuable for electrophysiological diagnosis of UTS.

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OBJECTIVES: The purposes of this study were to assess the clinical features of ulnar tunnel syndrome (UTS) and to investigate the diagnostic value of nerve conduction measurements for UTS. METHODS: Eighteen patients with UTS were reviewed retrospectively. Fifteen patients had intrinsic muscle atrophy and motor weakness, and 15 had numbness with hypesthesia. The compound muscle action potentials (CMAPs) from the first dorsal interosseous (FDI) muscle and the abductor digiti minimi (ADM) muscle and the sensory nerve action potential (SNAP) from the little finger were recorded and analyzed. All patients underwent ulnar tunnel release surgery and neurolysis. Static two-point discrimination test results and pinch strengths were assessed before and after surgery. RESULTS: Before surgery, FDI-CMAP was recorded in 17 patients, and ADM-CMAP in 16, and all showed delayed latency and/or low amplitude. SNAP was recorded in eight patients and two showed delayed latency. The causes of ulnar nerve lesions were ganglion in five patients, traumatic adhesion in four, ulnar artery aberrancy in four, pisohamate arch in three, anomalous muscle in one, and ulnar vein varix in one. The sites of the lesions were in zone 1 of the ulnar tunnel anatomy in 12 patients, in zone 2 in 2, and in zones 1 and 2 in 4. After surgery, all patients obtained recovery of motor function and sensation; however, postoperative FDI-CMAP and ADM-CMAP did not improve to the normal range. CONCLUSIONS: The causes of UTS were ganglion, traumatic adhesion, ulnar artery aberrancy, and pisohamate arch. Both FDI-CMAP and ADM-CMAP were valuable for electrophysiological diagnosis of UTS.

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Available abstract

OBJECTIVES: The purposes of this study were to assess the clinical features of ulnar tunnel syndrome (UTS) and to investigate the diagnostic value of nerve conduction measurements for UTS. METHODS: Eighteen patients with UTS were reviewed retrospectively. Fifteen patients had intrinsic muscle atrophy and motor weakness, and 15 had numbness with hypesthesia. The compound muscle action potentials (CMAPs) from the first dorsal interosseous (FDI) muscle and the abductor digiti minimi (ADM) muscle and the sensory nerve action potential (SNAP) from the little finger were recorded and analyzed. All patients underwent ulnar tunnel release surgery and neurolysis. Static two-point discrimination test results and pinch strengths were assessed before and after surgery. RESULTS: Before surgery, FDI-CMAP was recorded in 17 patients, and ADM-CMAP in 16, and all showed delayed latency and/or low amplitude. SNAP was recorded in eight patients and two showed delayed latency. The causes of ulnar nerve lesions were ganglion in five patients, traumatic adhesion in four, ulnar artery aberrancy in four, pisohamate arch in three, anomalous muscle in one, and ulnar vein varix in one. The sites of the lesions were in zone 1 of the ulnar tunnel anatomy in 12 patients, in zone 2 in 2, and in zones 1 and 2 in 4. After surgery, all patients obtained recovery of motor function and sensation; however, postoperative FDI-CMAP and ADM-CMAP did not improve to the normal range. CONCLUSIONS: The causes of UTS were ganglion, traumatic adhesion, ulnar artery aberrancy, and pisohamate arch. Both FDI-CMAP and ADM-CMAP were valuable for electrophysiological diagnosis of UTS.

Key concepts: Ulnar nerve, Compound muscle action potential, Medicine, Ulnar neuropathy, Cubital tunnel, Anatomy, Nerve conduction velocity, Surgery

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