This was a retrospective cohort study. Out of 1500 patient records with neuropathies, 270 (18%) patients diagnosed with ulnar neuropathies were recruited from the record database over a five-year period (2016–2021) from Clinical Physiology Lab of Department of Physiology, Chitwan Medical College, CMC, Nepal, and Arya Diagnostics, Bharatpur, Chitwan. The patient records having only ulnar mononeuropathy with mean age 39.92 ± 10.9 years of both sexes were included in the study, and the patients with neuropathies other than ulnar neuropathy and/or polyneuropathies and with comorbidities like diabetes and thyroid disorders causing neuropathy were excluded. The patients’ demographic data including age, sex, clinical features, known cause of lesion (etiology) and electro-diagnostic (EDx) findings were noted from the record. The following electro-diagnostic findings were noted: type of injury (demyelinating vs axonal), ulnar SNAP of the fifth finger, SNAP of dorsal ulnar cutaneous nerve, accompanying injury, CMAP of ulnar nerve, nerve conduction velocities across elbow and special Edx techniques, EMG findings with effects of ulnar nerve injury on corresponding muscles. All the Edx tests performed and the medical records were noted and diagnoses for neuropathy were made by the same investigator (Principal Author of this study) at both laboratories which avoided the discrepancy in observations and records. This study included the patient’s data following the standard protocol and laboratory conditions with room temperature maintained at 23 ± 2 °C during tests.
2.1 Ulnar sensory nerve conduction procedure
The ulnar sensory nerve conduction was recorded from fifth and fourth digits using ring electrodes by antidromic stimulation with placing the stimulating electrode 3 cm proximal to the distal crease at the wrist. The antidromic conduction of the dorsal branch of ulnar nerve was measured by stimulating the ulnar nerve 5–8 cm proximal to the ulnar styloid process between flexor carpi ulnaris and ulna. The active recording electrode was placed between fourth and fifth metacarpals and reference electrode at the base of fifth digit. The recommended filter setting for sensory conduction was set at 10 Hz to 2 kHz, sweep speed 2 ms/division and gain 5 mV/division. The signal enhancement with averaging was kept for 2000 times. Onset latency, SNAP amplitude, SNAP duration and sensory nerve conduction velocity (SNCV) were recorded for analysis.
2.2 Ulnar motor nerve conduction procedure and laboratory protocol for ulnar neuropathy at different sites
Ulnar nerve is relatively superficial along its course; therefore, motor nerve conduction velocity (MNCV) of various segments measured by stimulating Erb’s point, axilla, elbow, wrist and palm. Recording was made from central belly of ADM and FDI. For the electrophysiological evaluation of ulnar neuropathy at elbow, the ulnar MNCV was recorded from ADM and stimulation of the ulnar nerve at (1) wrist: 3 cm proximal to the distal crease; (2) below elbow: 3–4 cm distal to medial epicondyle; (3) above elbow: 5–8 cm proximal to the medial epicondyle; (4) axilla; and (5) Erb’s point. The onset latency and the base–to-peak amplitude of CMAP were measured. The limb position during stimulation and distance measurement was kept with 90º flexion of elbow and forearm was supinated with extended wrist. Ulnar NCV across the elbow segment if < 50 m/s was considered abnormal. Moreover, slowing of motor conduction by > 11 m/s across elbow compared to forearm segment considered significant. Further, secondary criteria for localization of ulnar neuropathy employed were reduction in CMAP amplitude across elbow. Fall in amplitude across elbow more than 50% or area reduction more than 40% with dispersion was considered UNE. A 20% fall in CMAP amplitude across elbow with stimulation at distance 10 cm difference was considered focal demyelination [10,11,12].
The inching method employed short segment of 1 or 2 cm showing a point of abrupt change in latency or amplitude for focal localization of the involved segment [12,13,14]. Similar to ulnar MNCV across elbow, antidromic ulnar sensory study was carried out from fifth digit by stimulating from different sites along nerve course and onset latency and SNAP amplitudes and SNCV were measured. SNCV below 50 m/s across elbow and reduction in base-to-peak amplitude by 43% or > 8 µV were considered abnormal [12, 15].
2.3 Muscles selected for electromyography (EMG)
EMG further aided in localization of ulnar neuropathy, chronicity, severity, degree of axonal degeneration and further differentiates from brachial plexopathy, C8-T1 radiculopathy and UNW. EMG included ADM, FDI, FCU, FDP and APB muscles. Mild lesions with sensory loss revealed normal EMG. Sharp waves and fibrillation along with clinically appreciated atrophy suggests axonal degeneration.
Ulnar neuropathy at distal forearm: In case of ulnar neuropathy at distal forearm, the patient usually complained of motor and sensory defect localized to ulnar distribution in hand. MNCV revealed normal to marginally affected but abnormal NCS to dorsal cutaneous branch of ulnar nerve. Short-segment inching technique from wrist to medial epicondyle (ME) demonstrated the conduction block at the site of lesion .
Ulnar neuropathy at wrist (UNW): UNW evaluated with electrodiagnostic findings along with clinical features. Shea and McClain classified ulnar compression syndromes of the wrist and hand into 3 types. In type I, the lesion is proximal to or within Guyon canal, involves both the superficial and deep branches and causes a mixed motor and sensory deficit, with weakness involving all the ulnar hand muscles.
In type II, the lesion is within Guyon canal or at the pisohamate hiatus, involves the deep branch and causes a pure motor deficit with a variable pattern of weakness depending on the precise site of compression.
A type III lesion is in Guyon canal or in the palmaris brevis, involves the superficial branch only and causes a purely sensory deficit. In the type I and III lesions, sensory loss should spare the dorsum of the hand, innervated by the DUC branch and should also largely spare the hypothenar eminence because its innervation is via the palmar cutaneous branch, which arises proximal to the wrist .
UNW evaluated from ulnar motor NCS recording from ADM and FDI, sensory conduction study from superficial and dorsal branch. Median motor and sensory conduction study were done to exclude the involvement of other nerves. Delayed distal motor latency usually more than 3.4 ms to ADM and 4.5 ms to FDI considered abnormal conduction across wrist. Similarly, normal CMAP amplitude for ADM and FDI was 5 mV and 6 mV, respectively. EMG of ADM, FDI and muscles of forearm (FCU, FDP) also put a clue to probable site of lesion .
The grading for the severity of ulnar neuropathy was based on the clinical features and electrodiagnostic findings. Patients with mild pain, paresthesia and abnormal ulnar sensory conduction parameters graded as mild neuropathy; pain, paresthesia, abnormal ulnar sensory and motor conduction parameters and neuropathic EMG of the related muscles graded as moderate; and paresthesia, muscle weakness, clawing/atrophy, complete absence or highly affected motor and sensory nerve conduction studies and chronic neuropathic EMG of the related muscles graded as severe neuropathy.
2.4 Ethical consideration
The data of the research have been employed from hospital records of patients who have signed and stated their consent for using their not-identifying data for the aim of research. This study was conducted according to the guidelines of the Declaration of Helsinki, and approval was taken by the Institutional Ethics Review Committee, Chitwan Medical College, CMC, Nepal.
2.5 Statistical analysis
The SPSS (version 21; IBM Corporation, Armonk, NY, USA) was used for data analysis. The descriptive tests were applied for all the study variables.