Sensory Examination

The sensory examination should include assessment of both pain perception and proprioception as these two modalities travel through distinct anatomic tracts in the spinal cord (spinothalamic tracts and posterior columns, respectively). Appreciation of noxious stimulus requires a dermatome-by-dermatome assessment from the highest cervical to the lower sacral levels (Figure 101.1).

The lower cervical and upper thoracic dermatomes (C5-T2) are not represented on the anterior torso. The upper cervical dermatomes (C3-4) extend to the supramammary region, immediately superior to the T3-4 dermatome. Examination of the torso alone results in a sensory assessment that makes the transition from the C4 to the T4 levels, not directly testing the intervening dermatomes. For this reason, a detailed examination must be carried out in the arms and hands to assess these areas. Otherwise, a patient with a low cervical injury can be misdiagnosed as having an upper thoracic injury by a sensory assessment limited to the torso.

The upper extremity sensory assessment must include all six dermatomes represented on the arm for adequate localization of a deficit. Individual leg dermatomes should also be assessed, although disparity in sensory function in a dermatomal pattern after a spinal cord injury is less common in the legs (see Figure 101.1).

The sacral dermatomes, located within the perineal region, should also be tested (see Figure 101.1). The presence of perineal sensation alone (“sacral sparing”) in a patient who otherwise has no demonstrable neurologic function represents an incomplete spinal cord injury, which may have a better prognosis for recovery of spinal cord function than can be expected in a patient with a complete injury.

The assessment of posterior column function involves position and vibration sense testing. Because pain and proprioceptive fibers travel within the same peripheral sensory nerves, posterior column testing can involve the distal aspects of the upper and lower extremities alone, after the detailed noxious stimulus assessment. A disparity in the results of sensory assessments between proprioceptive and pain appreciation occurs only in a patient with a partial cord injury affecting either the posterior or anterior aspects of the cord alone. Transverse injury, or an injury involving a peripheral nerve, should affect spinothalamic and posterior tracts with equal severity.

Motor Examination

Like the sensory examination, the motor examination must be meticulously performed, assessing individual myotomes of the upper and lower extremities. Proximal arm and forearm motion observed by a cursory examination can obscure the presence of a lower cervical injury involving the triceps and intrinsic hand functions. In the lower extremities, thoracic spinal cord compression can manifest itself as proximal motor weakness in the legs with sparing of distal muscle groups.

Reflex Examination

The reflex examination includes deep and superficial reflex assessments. The deep tendon reflexes are tested in the arms and legs. The significance of abnormal reflexes depends on the location and time course of the injury.

In the presence of an acute complete spinal cord injury, the deep tendon reflexes below the level of the lesion are hypoactive. In some instances, normal reflex activity may be seen in the hyperacute state. Hyperactive reflexes develop in the subacute phase (4 to 6 weeks) after an injury because of the loss of inhibition from descending corticospinal pathways. The Babinski reflexes follow the time course of the deep tendon reflexes. In the acute phase of an injury to the spinal cord, they remain unreactive, or a flexor response is occasionally identified. Extensor plantar response develops from chronic compression of the spinal cord or in the subacute phase of an injury.

In acute trauma, the differential diagnosis of hypoactive reflexes includes nerve root injury, plexus injury, and spinal shock. The underlying cause of hyporeflexia is determined by the pattern of the patient’s neurologic symptoms and associated motor and sensory deficits. In addition, hypoactive reflexes may be due to a preexisting condition such as peripheral neuropathy or chemotherapy use, or they may be a normal variant.

Focal hypoactive reflexes in the upper extremities are often the result of a nerve root or brachial plexus abnormality. If the motor and sensory deficits correspond to multiple, adjacent motor or sensory root levels, a plexus injury is likely the underlying cause. Contusions or abrasions of the skin, or underlying fractures involving the shoulder girdle structures, pelvis, or transverse processes, can be associated with these deficits, and their presence should be sought to confirm the diagnosis.

Spinal shock is a phenomenon that is present after a complete spinal cord injury. The patient has absence of all volitional and reflex neurologic activity below the level of the lesion. In contrast, neurogenic shock is a hemodynamic phenomenon. After spinal cord injury at or above the T5 vertebral level, patients may become hypotensive. Characteristically, patients have a relative bradycardia in the presence of low blood pressure. The shock results from the loss of sympathetic outflow. This causes peripheral vasodilation and pooling of blood, which, in turn, impairs venous return to the heart. Loss of sympathetic outflow also has negative inotropic and chronotropic effects on the heart.

Superficial reflexes are diminished in the presence of a spinal cord injury. Nerves from T6-9 and T10-12 subserve the upper and lower superficial abdominal reflexes, respectively. The absence of both upper and lower superficial abdominal reflexes indicates that the lesion is above T6. The absence of lower and preservation of upper superficial abdominal reflexes indicates that the lesion is below T9. Likewise, the L1-2 segmental nerves mediate the cremasteric reflex, and loss of this reflex is pathologic.

The tone of the anal sphincter should also be assessed as part of a full neurologic workup. It is usually diminished or absent in the presence of a complete acute spinal cord injury.