Locognosia, the ability to localise touch, is one aspect of tactile spatial discrimination which relies on the integrity of peripheral end-organs as well as the somatosensory representation of the surface of the body in the brain. The test presented here is a standardised assessment which uses a protocol for testing locognosia in the zones of the hand supplied by the median and/or ulnar nerves. The test-retest reliability and discriminant validity were investigated in 39 patients with injuries to the median or ulnar nerve. Intraclass correlation coefficients were used to calculate the test-retest reliability. Discriminant validity was assessed by comparing the injured with the unaffected hand. Excellent test-retest reliability was demonstrated for the injuries to the median (intraclass correlation coefficient 0.924, 95% confidence interval 0.848 to 1.00) and the ulnar nerves (intraclass correlation coefficient 0.859, 95% confidence interval 0.693 to 1.00). The magnitude of the difference in scores between affected and unaffected hands showed good discriminant validity. For injuries to the median nerve the mean difference was 11.1 points (1 to 33; . sd. 7.4), which was statistically significant (p < 0.0001, paired t-test) and for those of the ulnar nerve it was 4.75 points (1 to 13.5; . sd. 3.16), which was also statistically significant (paired t-test, p < 0.0001). The locognosia test has excellent test-retest reliability, is a valid test of tactile spatial discrimination and should be included in the evaluation of outcome after injury to peripheral nerves

We prospectively studied 26 consecutive patients with clinically documented sensory or motor deficiency of a peripheral nerve due to trauma or entrapment using ultrasound, and in 19 cases surgical exploration of the nerves was undertaken. The ultrasonographic diagnoses were correlated with neurological examination and the surgical findings. Reliable visualisation of injured nerves on ultrasonography was achieved in all patients. Axonal swelling and hypoechogenity of the nerve was diagnosed in 15 cases, loss of continuity of a nerve bundle in 17, the formation of a neuroma of a stump in six, and partial laceration of a nerve with loss of the normal fascicular pattern in five. The ultrasonographic findings were confirmed at operation in those who had surgery.

Ultrasound may be used for the evaluation of peripheral nerve injuries in the upper limb. High-resolution ultrasound can show the exact location, extent and type of lesion, yielding important information that might not be obtainable by other diagnostic aids.

We describe two patients with claw hand as a result of a bee sting. It is likely that this was caused by the apamin in the sting which has an effect on the upper limb, at the spinal cord and on the peripheral nerves. It is important to recognise that the claw hand is not owing to compartment syndrome. Both patients were treated conservatively with full resolution within 48 hours, without any lasting effects

We describe 20 patients, aged between 43 and 88 years, with delayed nerve palsy or deepening of an initial palsy caused by arterial injury from low-energy injuries to the shoulder. The onset of palsy ranged from immediately after the injury to four months later. There was progression in all the patients with an initial partial nerve palsy. Pain was severe in 18 patients, in 16 of whom it presented as neurostenalgia and in two as causalgia. Dislocation of the shoulder or fracture of the proximal humerus occurred in 16 patients. There was soft-tissue crushing in two and prolonged unconsciousness from alcoholic intoxication in another two.

Decompression of the plexus and repair of the arterial injury brought swift relief from pain in all the patients. Nerve recovery was generally good, but less so in neglected cases. The interval from injury to the repair of the vessels ranged from immediately afterwards to 120 days.

Delayed onset of nerve palsy or deepening of a nerve lesion is caused by bleeding and/or impending critical ischaemia and is an overwhelming indication for urgent surgery. There is almost always severe neuropathic pain.

We reviewed 101 patients with injuries of the terminal branches of the infraclavicular brachial plexus sustained between 1997 and 2009. Four patterns of injury were identified: 1) anterior glenohumeral dislocation (n = 55), in which the axillary and ulnar nerves were most commonly injured, but the axillary nerve was ruptured in only two patients (3.6%); 2) axillary nerve injury, with or without injury to other nerves, in the absence of dislocation of the shoulder (n = 20): these had a similar pattern of nerve involvement to those with a known dislocation, but the axillary nerve was ruptured in 14 patients (70%); 3) displaced proximal humeral fracture (n = 15), in which nerve injury resulted from medial displacement of the humeral shaft: the fracture was surgically reduced in 13 patients; and 4) hyperextension of the arm (n = 11): these were characterised by disruption of the musculocutaneous nerve. There was variable involvement of the median and radial nerves with the ulnar nerve being least affected.

Surgical intervention is not needed in most cases of infraclavicular injury associated with dislocation of the shoulder. Early exploration of the nerves should be considered in patients with an axillary nerve palsy without dislocation of the shoulder and for musculocutaneous nerve palsy with median and/or radial nerve palsy. Urgent operation is needed in cases of nerve injury resulting from fracture of the humeral neck to relieve pressure on nerves.

We evaluated 56 patients for neurological deficit after enucleation of a histopathologically confirmed schwannoma of the upper limb. Immediately after the operation, 41 patients (73.2%) had developed a new neurological deficit: ten of these had a major deficit such as severe motor or sensory loss, or intolerable neuropathic pain. The mean tumour size had been significantly larger in patients with a major neurological deficit than in those with a minor or no deficit. After a mean 25.4 months (12 to 85), 39 patients (70%) had no residual neurological deficit, and the other 17 (30%) had only hypoaesthesia, paraesthesiae or mild motor weakness.

This study suggests that a schwannoma in the upper limb can be removed with an acceptable risk of injury to the nerve, although a transient neurological deficit occurs regularly after the operation. Biopsy is not advised. Patients should be informed pre-operatively about the possibility of damage to the nerve: meticulous dissection is required to minimise this.

Ulnar nerve function, during and after open reduction and internal fixation of fractures of the distal humerus with subperiosteal elevation of the nerve, was assessed by intra-operative neurophysiological monitoring. Intermittent recording of the compound muscle action potentials was taken from the hypothenar muscles in 18 neurologically asymptomatic patients.

The mean amplitude of the compound muscle action potential after surgery was 98.1% (sd 17.6; −37% to +25%). The amplitude improved in six patients following surgery. Despite unremarkable recordings one patient had progressive paresis. Motor impairment is unlikely if the compound muscle action potential is continuously preserved and not reduced by more than 40% at the end of surgery. Temporary decreases in amplitude by up to 70% were tolerated without clinical consequences. However, repeated clinical examination is obligatory to recognise and treat early post-operative palsy.