Electrodiagnostic Studies in Compression Neuropathy

Each peripheral nerve has a unique clinical anatomic signature vis-à-vis motor and sensory deficits when these nerves are compromised. This is illustrated by the seemingly complicated cutaneous sensory distribution of the median, radial, and ulnar nerves in the hand. With this knowledge, clinicians are often able to outline characteristic clinical features of a specific pattern of compromised function appropriate to a mononeuropathy. Frequently, symptoms of a mononeuropathy are stereotyped and sometimes evanescent, such as with the carpal tunnel syndrome.

Occasionally, underlying systemic illnesses predispose to the occurrence of more than one acute mononeuropathy, that is, mononeuritis multiplex. A sudden footdrop secondary to a fibular (peroneal) nerve lesion is followed in days to weeks by another mononeuropathy, such as a wristdrop from an acute radial nerve lesion, and soon thereafter another nerve becomes acutely compromised. Systemic vasculitides, such as occurs in polyarteritis nodosa, are often responsible. Hereditary neuropathies with liability to pressure palsies (HNPP) lead to recurrent multiple neuropathies in a chronic setting (see Plate 5-22). Sometimes symptoms of a possible mononeuropathy actually represent an initial sign of a plexus, nerve root, spinal cord, or brain lesion.

Patients with recurrent hand numbness or weakness require consideration for transient cerebral ischemic attacks or, rarely, an intracranial tumor such as a meningioma. Parasagittal cerebral lesions may occasionally manifest primarily with foot weakness. Individuals presenting with hand weakness but no sensory loss or pain may have a deep ulnar motor lesion within their medial palm or even motor neuron disease.

Neck or low back pain usually indicates a protruded or herniated disk (nucleus pulposus) affecting one specific nerve root. Often this discomfort radiates into an arm or a leg and is associated with tingling and numbness (paresthesias), and sometimes weakness is confined to the distribution of a nerve root. However, this clinical picture is not always straightforward enough to allow for simple clinical judgment to make a diagnosis based on history alone. For example, in the common setting of a footdrop, the clinician needs to examine carefully the leg muscles to define whether the affected muscles have only a peroneal nerve distribution with weakness confined to dorsiflexors (tibialis anterior) and evertors (peroneus longus). In contrast, the affected muscles may have an L5 nerve root derivation, that is, tibialis anterior primarily, but also a subtle inability to invert the foot because of weakness of the tibialis posterior. These muscles are innervated by two different peripheral nerves, fibular and tibial, and the weakness is thus compatible with a specific L5 radiculopathy. This distinction is sometimes difficult to make initially, and thus electromyography (EMG) is the first study of choice.

Often, the degree of weakness is more profound in a mononeuropathy than a nerve root lesion because the affected muscles are solely dependent on that nerve, whereas a nerve root lesion does not affect all fibers going to the affected muscles. For example, with a wristdrop where there is concomitant C6 and C7 root supply, if just the C7 root is affected, the muscles continue to have partial innervation from the C6 root, and thus there is not a total paralysis of the wrist and finger extensors. In contrast, if the radial nerve is damaged, there is no overlapping safety feature of multiple innervations as in nerve root disorders. Here the deficit’s severity is directly related to how significant the damage is within that nerve itself. Often, total paralysis occurs with acute radial nerve damage. Muscle atrophy develops when there is significant peripheral denervation.

Measuring extremity circumference may document significant side-to-side asymmetries representative of muscle atrophy and, by inference, anterior horn cell, nerve root, or peripheral nerve damage. Patients with brachial or lumbosacral plexus lesions are less likely to have neck or back pain but, rather, pain within the affected extremity. Here the numbness may be more diffuse, and muscles are weakened within the distribution of multiple peripheral nerves/nerve roots.

Numbness rather than pain is much more common with early mononeuropathies. The symptom onset and progression can help in diagnosis. Because sensory examination is the most subjective part of the neurologic examination, occasionally this is difficult to define clearly. Sometimes the patient can provide the most accurate assessment by roughly outlining the area in question using a finger to demonstrate the area of diminished sensation; this is best demonstrated with meralgia paresthetica (see Plates 5-15 and 5-16), where the patient outlines an elliptic loss of sensation on the lateral thigh. These assessments often clarify whether the pattern of sensory loss is specific to one peripheral nerve or nerve root dermatome. Meralgia paresthetica best illustrates this with lateral thigh sensory loss secondary to a lateral femoral cutaneous nerve lesion. Often, it is easier for the patient to outline the precise deficit than the clinician.

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