Tips on how to examine a patient after an injury that may have damaged nerve function:



It is very strange that so many doctors loose their minds when faced with a nerve injury. Don’t be one of them.Nerve injury is like any other injury. We dont say “Ah yes it is ‘an owwey knee’ it will probably get better”. We might consider the history particularly the mechanism of injury, then examine the patient determining what is working and what is not. Then perhaps exclude various differentials and come to a short list. Then using tests perhaps to reach a final diagnosis; being ready to hone this with subsequent information.

Why then do we so often hear- “it is probably a nerve injury it will almost certainly get better”

: What features of the injury have led the clinician to this presumption? what features if present would have led him or her to a different diagnosis?

I suggest the clinician should approach his examination to answers three questions.
  1. Has there been a nerve injury?
  2. Where is that nerve injury?
  3. Is this a conduction block?  has there been a degenerative lesion of axons wwithin the nerve? If so is this there a favourable or non-favourable natural history if left alone?

To do this we should follow a standard clinical method.

The History & Examination

Mechanism of injury:

The history  is important: high speed collisions or open fracture or wounding indicate a serious lesion.   Nerve injuries caused by fractures or dislocations are usually more severe in the lower than in the upper limb because of higher energy transfer. It is important to seek for occult injuries to the head, the spine, the chest, the abdomen and pelvis in these patients before looking to treat the nerve lesion.

Examination :

  • Abnormal sensations.
  • Muscle paralysis.
  • Neuropathic pain
  • Sometimes the patient is aware of warming and dryness of all or part of an extremity. 

The signs of an acute nerve injury should be noted at a time when the patient may be the least able to co-operate in an examination; soon after injury when the patient may be in distress and when the general condition may be affected by loss of blood and other injuries or by drink and drugs.  When the lesion has been inflicted by a surgeon or anaesthetist, the patient’s response is likely to be distorted  by post operative pain, by the effects of recent general anaesthesia or by sedative or analgesic drugs. 

If there is a wound over the line of a major nerve and if there is any suggestion of loss of sensibility or impairment of motor function in the distribution of that nerve, it must be regarded as having been cut until and unless it is proved otherwise. 

Sensory loss is detected by the response  to light touch and pin prick comparing the injured and the uninjured limb.  The patient is asked: “does this feel the same or different?”  Many patients do not experience total loss of sensation in the first hours after injury even when a main nerve has been divided.  

Selected muscles: are examined.  The patient lying supine is usually able to demonstrate activity in serratus anterior by lifting the shoulders away from the couch, by “forward shrugging”. It is usually possible to observe the presence of flexion and abduction at the shoulder, flexion and extension of the elbow and wrist and flexion and extension of the fingers.  The radial, median and ulnar nerves are tested by asking the patient to form an “O” between the thumb and little finger, to give the “thumbs up”,  and to open and close the fingers like a fan.

Pain: should be treated first in any injured patient. You will not loose any ability to diagnose the injury by making our patient.  Neuropathic pain can be distinguished from the pain of fracture or dislocation by loss of sensation, by painful, spontaneous sensory symptoms, expressed throughout the territory of the nerve, and by ‘lancinating’ (shooting pain) radiating into the distribution of the nerve.  Constant crushing, bursting or burning pain in the otherwise undamaged hand or foot indicates serious and continuing injury to major trunk nerves more proximally.  Progression of  sensory loss with a deep bursting or crushing pain within the muscles of the limb signifies critical ischaemia.

Sympathetics: The palmar and plantar skin is scrutinised for changes in colour and in sweating.  The standard tendon reflexes are examined.

A more detailed examination is possible when the patient’s condition is stable, and when pain has been controlled.    Limb dominance, occupation, marital status, underlying disease or continuing medication are recorded.  Neuropathic pain is by now  easier to recognise, for it is less responsive to analgesics than is pain from skeletal injury.

Recognition of the  level and the depth of injury


A sound knowledge of  anatomy is essential here.

A wrist drop could of course be a radial lnerve injury but could also an injury be at any level to the posterior cord. Thus by examining teres major (lower subscapular nerve), Subscapularis (upper and lower subscap nerves), latissimus dorsi (thoraco dorsal nerve), and deltoid (circumflex nerve).  Triceps –The nerves to the medial head of triceps leave the main trunk before the spiral groove.  The nerve to brachioradialis consistently passes away from the trunk about three finger breadths above the lateral  epicondyle; the nerve to extensor carpi radialis longus comes off about a centimetre  more distally. One nerve to extensor carpi radialis brevis leaves the main nerve about one cm above the lateral epicondyle and another at the level of the branching into superficial radial and posterior interosseous nerves. 


Simple conduction block is likely to produce a patchy loss of sensibility and a patchy motor loss.  Further, it is likely to affect the large axons more than the small ones: vibration sense and sensibility to light touch are likely to be impaired, whereas pain sensibility may be unaffected. 

Degenerative nerve injury of a nerve with a cutaneous sensory component will lead to well-defined loss of sensibility and to complete motor, sudomotor and vasomotor paralysis in the distribution of the nerve.  One particularly reliable sign of a degenerative nerve injury (axonotmesis or neurotmesis) is the involvement of sympathetic fibres to the smooth muscle of blood vessels and sweat glands. The skin in the distribution of the affected nerve is  red, warm and dry.  This sign is almost always present within 24 hours of a deep injury to a nerve with a cutaneous distribution

Another way to test sympathetic dysfunction (particularly useful in kids) is  the “immersion test”. The involved digit is placed, for a few minutes, in warm water (or a wet gauze is applied under an occlusive dressing).  The skin of the denervated digits fails to wrinkle. Also notice here may be an abnormal posture of the denervated digits; The anaesthetic digit is ignored and held out of the way of the others.

Tinel’s sign

Percussion over a nerve in which axons have undergone a degenerative injury evokes sensations usually described as a wave or surge of pins and needles into the cutaneous distribution of that nerve.  This is Tinel’s sign and it is a most useful aid to diagnosis.  The sign can be elicited on the day of injury in most patients.  It indicates not only where the nerve has been injured but also the fact that at least some axons have been ruptured.   Tinel’s sign can be detected  over pure “motor” nerves, (such as the posterior interosseous nerve) in these nerves the sensory symptoms radiate  into the muscular territory rather than into the skin. It is more difficult to elicit the sign over deep seated nerves such as the Axillary nerve.

How to examine for a Tinel’s sign

The examiner’s finger percusses along the course of the each nerve from distal to proximal starting below the presumed level of lesion.  The patient is asked to say when the advancing finger elicits a wave or a surge of pins and needles or  abnormal sensations, which may be painful, into the distribution of the nerve which must be clearly indicated by the examiner. This sign is then documented (as a set distance from a bony landmark) it should then be examined again over time. A Tinel sign which remains static at the level of lesion strongly suggests rupture of the nerve or local conditions blocking regeneration.  An advancing Tinel sign indicates regeneration of axons so that it is usually possible to distinguish between a majority favourable or non favourable lesion in most nerves by between four and six weeks from the day of the injury.   It is particularly reassuring when the distal sign becomes the stronger of the two.   The sign at the level of the lesion disappears in uncomplicated cases of favourable prognosis nerve injury (majority axonotmesis).

Text adapted from Birch & Quick in Nerve Repair, Green’s Hand Surgery 7thEd. Elsevier