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| Year : 2001 | Volume
: 49
| Issue : 1 | Page : 67-70 |
Ulnar nerve palsy due to axillary crutch.
Veerendrakumar M, Taly AB, Nagaraja D
Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore - 560029, India.
Correspondence Address:
Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore - 560029, India.
A young lady with residual polio, using axillary crutch since early childhood, presented with tingling, numbness and weakness in ulnar nerve distribution of five months duration. Ulnar motor conduction study revealed proximal conduction block near the axilla, at the point of pressure by the crutch while walking. Distal ulnar sensory conduction studies were normal but proximal ulnar sensory conduction studies showed absence of Erb's point potential. These findings suggested the presence of conduction block in sensory fibers as well. Proper use and change of axillary crutch resulted in clinical recovery and resolution of motor and sensory conduction block.
How to cite this article:
Veerendrakumar M, Taly A B, Nagaraja D. Ulnar nerve palsy due to axillary crutch. Neurol India 2001;49:67-70 |
Ulnar mononeuropathy most often results from a lesion across the elbow and less frequently from a lesion at the wrist or hand.[1] Rarely, it is due to lesions across the axilla.[2],[3] Hitherto, use of axillary crutch has been reported to cause radial, axillary and digital sensory neuropathy.[1] We report a young girl with crutch-related high ulnar neuropathy with conduction block in motor and sensory fibers.
Five months prior to consultation, this 22 year old lady developed tingling sensation along the medial border of right palm and little finger. Over the next three weeks, she developed numbness along the medial border of hand and little finger, and right grip weakness. She had 'polio-like' illness at the age of 11 months, with severe residual weakness of right lower limb and moderate proximal muscle weakness of right upper limb. Because of this, she had been using indigenous axillary crutch on the right side since the age of seven years. There was no history of neck pain, hypopigmented patches or symptoms suggestive of vasculitis.
Apart from sequelae of old 'polio-like' illness,examination showed mild wasting of first dorsal interosseous (FDI), mild weakness of flexor digitorum profundus (digits IV and V), no palpable contraction of flexor carpi ulnaris (FCU) and moderate weakness of ulnar innervated small muscles of hand in right upper limb. Touch and pain sensations were severely impaired over dorsal and palmar aspects of ulnar border of right hand and digits IV and V. Kinesthetic sense was impaired in digit V.
Electrophysiological Observations : Right ulnar, median, radial, common peroneal motor conduction studies and bilateral ulnar, right median (orthodromic), radial, sural (antidromic) sensory conduction studies were performed using standard techniques.[4] Ulnar dorsal cutaneous branch sensory conduction studies were carried out using Jabre's technique.[5]
Results of ulnar motor and sensory conduction studies are shown in [Table I]. Right ulnar motor conduction study with stimulation at wrist, below and above elbow, and ulnar sensory conduction study from digit V and dorsal cutaneous branch were normal. However, ulnar F wave latency was prolonged (43 ms at wrist). Hence, ulnar motor conduction study was repeated with stimulation at Erb's point. It failed to evoke motor response. The site of conduction block could be localised to a point high up in the arm near axilla by an inching technique [Figure 1a]. The CMAP, 2 cm distal to this point was normal. Proximal ulnar sensory conduction study showed normal potentials on the left side whereas, on the right side, there was a low amplitude potential above elbow and absent potential at Erb's point [Figure 2a]. Right median and radial motor conduction studies were normal, except that the usual high amplitude volume conducted CMAPs were not recorded with stimulation at axilla or Erb's point. Right median sensory conduction study (stimulation at digit II) showed normal potentials at wrist and at Erb's point. Right radial, sural and left ulnar sensory (digit V and dorsal cutaneous branch) conduction studies were normal. Right common peroneal nerve was inexcitable.
Concentric needle electromyography showed changes of mild denervation in right digiti minimi, FDI and FCU muscles. Right FCU muscle also showed long duration motor unit potentials, suggestive of reinnervation. Electromyography of right abdutor pollicis brevis muscle was normal.
Subsequent to electrophysiological studies, the patient was re-examined. She reported pain and worsening of tingling sensation in right upper limb while walking with the crutch. She was bearing her entire weight over the crutch due to shortening and severe weakness of right lower limb. The crutch pressed against the medial aspect of right arm near axilla. Tinel's sign was present at the point of pressure by the crutch. These features suggested a possibility of crutch related high ulnar neuropathy.
She was changed over to a light aluminum crutch and was trained to use it properly, so that, the crutch inclined against her ribs and not against the apex of the axilla. Two weeks later, the sensory loss had resolved completely; after another one month, her weakness of ulnar innervated muscles in right hand had recovered almost fully. Repeat electrophysiological evaluation, two months after the first study, showed resolution of motor conduction block [Figure 1b]. Proximal ulnar sensory conduction study still showed absence of potential at Erb's point. Subsequently, she was lost to follow up. Two and half years later, though the conduction block was absent, ulnar motor conduction studies still showed slowing in the arm segment. Proximal ulnar sensory
conduction study showed normal potentials above elbow and at Erb's point [Figure 2b].
Our subject presented with history and findings suggestive of right ulnar neuropathy above elbow. Ulnar motor conduction studies showed conduction block high up in the arm, near axilla. The site of motor conduction block corresponded to the site of pressure by the axillary crutch while walking. She made clinical and electrophysiological recovery subsequent to the change and proper use of axillary crutch. These observations confirm that, the high ulnar neuropathy in our subject was secondary to the improper use of axillary crutch. Axillary crutch is known to cause radial, axillary and median digital branch neuropathy.[1] To the best of our knowledge, axillary crutch has not been reported to cause isolated ulnar neuropathy. Further, the ulnar neuropathy was predominantly demyelinating in nature as evidenced by the presence of conduction block and rapid improvement of muscle weakness.
Normal distal ulnar sensory nerve action potential (SNAP) in the presence of significant sensory loss, five months after the onset of the symptoms, suggested that the lesion was pre-ganglionic.[6],[7],[8],[9] However, proximal ulnar sensory conduction study showed low amplitude potential above elbow and absent potential at Erb's point. These findings suggested presence of conduction block in sensory fibers as well, in the above elbow-Erb's point segment. The absence of Erb's point potential was not merely due to increased temporal dispersion and phase cancellation as they would not account for the significant sensory loss seen in our subject. The presence of conduction block in sensory fibers was also corroborated by the rapid resolution of the sensory loss following the change of axillary crutch.
Conduction block in sensory fibers is sparsely reported. Trojaborg[10] described two patients with brachial plexopathy who had conduction block in musculocutaneous and radial sensory fibers. Krarup et al[2] reported another patient with neuralgic amyotrophy and conduction block in ulnar sensory fibers. All these three patients had normal distal SNAPs in the presence of variable sensory loss.
Following the landmark paper by Bonney and Gilliatt,[6] normal SNAP in the presence of dense sensory loss is regarded as the hallmark of preganglionic lesion.[6],[7],[8],[9] In the evaluation of entrapment neuropathies, sensory conduction studies are sometimes done first,[11] as sensory fibers being more sensitive to pressure, show abnormalities earlier. Our case suggests that when the proximal postganglionic lesion is demyelinating in nature, distal axon and the SNAP remain normal and mimic preganglionic lesion. If proximal stimulation studies are not performed because of normal distal SNAP/sensory conduction studies, post-ganglionic demyelinating lesions may be missed.
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