The key to anatomic localization is a thorough understanding of the anatomy of the cervical spinal cord, the nerve roots, and peripheral nerves. The cervical spinal cord consists of eight cervical segments that are surrounded by seven cervical vertebrae. The first cervical root emerges between the atlas and the occiput, and the second to seventh roots leave the spinal canal above the corresponding vertebrae, whereas the eighth root emerges between the intervertebral foramina of C7 and T1. There is a cervical enlargement in the lower four segments of the cervical cord and the first segment of the thoracic cord due to the innervation of the upper limbs. The cervical cord contains the largest number of fibers in the white matter because the descending fibers for the lower limbs have not yet left the cord, and the ascending fibers contain both upper and lower limb fibers (5,6). The gray matter is also larger because of innervation of the upper limbs. A cross section of the cervical cord consists of an H-shaped gray matter surrounded by white matter. The gray matter is divided into a dorsal, ventral, and intermediate zone. The white matter can be divided into three funiculi or columns: dorsal, lateral, and ventral.

The dorsal funiculus carries ipsilateral ascending axons from neurons in the dorsal root ganglion and dorsal horn. It is bound by the dorsal horn and dorsal septum and consists of a medial fasciculus gracilis and a lateral fasciculus cuneatus. The dorsal columns contain axons, which are traditionally thought to subserve functions of discriminative touch, vibration, and position sense. However, the functional importance of the dorsal columns is far more complex because surgical lesioning can only produce minimal persistent sensory deficits. Furthermore, other studies have shown that proprioceptive signals from the lower limbs are carried only in the dorsal columns as far as the thoracic cord and then synapse with the dorsal nucleus of Clarke; the pathway then continues rostrally by way of the dorsal spinocerebellar tract in the lateral funiculus. However, clinically, loss of the posterior columns secondary to disease states such as subacute combined degeneration or neurosyphilis still results in loss of position sense with unsteadiness of gait. These columns are also arranged somatotopically as the medial fasciculus gracilis carries impulses from more caudal regions, whereas the lateral cuneatus has the more rostral fibers. There are also other descending axons within the dorsal columns, which have little clinical importance.

The lateral white matter tracts are composed of a multitude of ascending and descending tracts. Of these, only the most clinically important tracts are briefly discussed. The lateral spinothalamic tract carries innervation concerning pain and temperature sensation. The axons originate from laminae I and V of the dorsal horn and initially cross within one or two spinal segments ventral to the central canal in the ventral white commissure and then continue in the spinothalamic tract. The tract is somatotopically arranged with fibers corresponding to the rostral region medially and the caudal regions more laterally.
Other ascending tracts include the ventral spinocerebellar tract and the previously described dorsal spinocerebellar tract. The lateral corticospinal tract is also located in the lateral funiculus. This tract consists of axons from the premotor and motor cortex of the contralateral frontal lobe and is responsible for voluntary, discreet, and skilled movements. Similar to other tracts previously described, this tract also has a somatotopic organization with the arrangement with cervical fibers more medial than the lumbar and sacral fibers. Other descending tracts include the rubrospinal tract and the medullary reticulospinal tract.

In the ventral funiculus, there is a ventral corticospinal tract composed of fibers that did not cross the midline at the pyramidal decussation. The anterior spinothalamic tract also runs in the ventral funiculus and carries fibers conveying “light touch” sensation. The vestibulospinal tract is a third tract that is in the ventral funiculus and is responsible for mediating equilibratory reflexes.

The gray matter in the cervical spinal cord, as compared with the other regions of the spinal cord, is similarly divided into the dorsal and ventral horns and the intermediate zone. The dorsal horn contains neurons, which synapse with axons from the dorsal root ganglion and therefore mainly subserve a sensory function. The spinal trigeminal nucleus and tract also descend into the first two to four segments of the cervical cord terminating in the substantia gelatinosa of the dorsal horn and the dorsolateral tract of Lissauer, respectively. The ventral horn contains large motor neurons whose axons leave the spinal cord to synapse on skeletal spinal muscle fibers.

Cervical injury is not difficult to diagnose, but care must still be taken when patients are examined so as not to miss devastating injuries. Patients who on cursory examination appear to have nothing more than neck pain and radicular symptoms can in reality have compression of the cord secondary to an extrinsic mass. The key to distinguishing these and other pathology is to have a systematic approach to the patient, which must be used each time. The first step to localization is to distinguish between disease in the central nervous system and that in the peripheral nervous system. Disease in the peripheral nervous system can then be further subdivided into processes that involve the nerve roots, nerve plexuses, or peripheral nerves. This distinction is obviously important because it allows for the proper treatment of these conditions. Sensory symptoms secondary to nerve root pathology normally involve numbness or pain in the specific dermatome distribution, although overlap of adjacent nerve roots prevents complete anesthesia of the dermatome. The pain is usually sharp in nature and is often aggravated by changes in head position or neck motion. The Spurling sign (rotation and lateral bending of the head to the symptomatic side) can be elicited with nerve root pathology secondary to disk herniation (7). Increases in intrathoracic pressure, such as straining or coughing, can also exacerbate the pain. Pain is often a more prominent feature of nerve root pathology than sensory deficits. The area of pain involved may also be more extensive than the nerve root dermatome it sometimes extends to the muscle groups subserved by the root. A C5 nerve root lesion can cause pain from the rhomboids to the biceps. Paresthesias may also occur as a result of nerve root irritation. Of the above sensory symptoms, pain is usually the most obvious from nerve root compression. Peripheral nerve lesions result in a more definitive area of numbness than root lesions, and the area involved is no longer dermatomal in distribution but follows the particular nerve involved. Similarly, nerve root dysfunction affects a different set of muscles when compared with peripheral nerve injury. Injury to a single nerve root may only cause paresis to a group of muscles because of compensation by adjacent roots, whereas complete muscle paralysis may mean multiple nerve roots or peripheral nerve injury. Muscular atrophy may also be masked with single nerve root lesions.

Spinal cord lesions differ from peripheral lesions in that they can present with root symptoms and signs, but they have more generalized effects as well. Cord lesions can cause motor and sensory deficits below the level of injury. In terms of motor deficits, there can be paresis to paralysis of muscle groups below the lesion, which do not occur with peripheral nervous system injuries. Chronically, the affected muscles become spastic in tone with accompanying hyperreflexia. Similarly, sensory deficits due to spinal cord lesions can vary from mild to complete sensory loss of all modalities. The sensory impairment may be subtle, presenting with clumsiness of gait or grasp due to involvement of proprioceptive tracts. Electrical shock-like sensations can radiate up and down the spine, usually as a result of flexion of the neck (Lhermitte sign), and can indicate spinal cord pathology (8), although the causes can vary from multiple sclerosis to central disk herniation. Pain from cord lesions can be different from radicular pain because it is more diffuse and ill defined. Cord lesions also affect the autonomic nervous system, causing loss of bowel and bladder function and loss of regulation of vascular tone. A more complete description of the effects of spinal cord lesions is given later in this chapter.

Once the pathology has been identified as being localized to the roots, peripheral nerves, brachial plexus, or spinal cord, then other more specific signs and symptoms may point to the exact root, nerve, or cord level involved.

Cervical radiculopathy at different levels can often be distinguished by specific signs and symptoms. Each cervical nerve root innervates a specific dermatome and muscle group (Figs. 13.1 and 13.2). C1 and C2 radiculopathies are extremely rare. The C1 nerve root subserves no sensory dermatome, and the C2 dermatome includes the dorsal aspect of the head behind the ears. C1 and C2 have no specific motor innervation but can contribute to the motor innervation of cranial nerve 11 and the ansa cervicalis. C3 nerve root dysfunction is also quite rare (9). The C3 dermatomal pattern involves the ventral and dorsal aspect of the neck. Again, there is no specific motor function
with the C3 root, although diaphragmatic paresis may be noted. Patients with C2 or C3 radiculopathy may complain of headache. C4 radiculopathy involves pain over the base of the neck above the clavicle and medial shoulder. Diaphragmatic and shoulder muscle paresis can occur with C4 involvement. Radiculopathy of the C5 nerve root is still uncommon but less so than the above nerve roots. The sensory innervation ranges from the top of the shoulder to the lateral aspects of the arm. A complete examination of shoulder motion is necessary to differentiate from shoulder pathology. The deltoid muscle is mainly innervated by this root, and there may be profound weakness in abduction of the shoulder. This may mimic a rotator cuff tear, but unlike the rotator cuff tear, there should be minimal tenderness over the shoulder itself. There may also be weakness in internal and external rotation (supraspinatus and infraspinatus) of the shoulder. These muscle groups are less consistently affected. The biceps brachii muscle can also be weakened, along with a diminution of the biceps reflex. C6 radiculopathy is quite common and often presents with pain radiating from the base of the neck, along the biceps, and down the lateral aspect of the forearm to involve the thumb and pointer finger. There may also be numbness in the first two digits. There may be paresis of the biceps, the brachioradialis, and the wrist extensors. The biceps reflex is often abnormal. C7 radiculopathy is just as common as C6 if not more so. Pain or numbness involving the middle finger is the usual sensory disturbance with possible overlap to the surrounding fingers. The pain may radiate from the dorsal shoulder, along the triceps, to the middle finger. The main muscle weakness that is seen with C7 nerve root dysfunction is that of the triceps. Patients can sometimes compensate by internal rotation, and this must be looked for and avoided during the physical examination. The triceps reflex is affected with C7 radiculopathy. Other muscle groups involved include the pronators, finger extensors, latissimus dorsi, and wrist flexors. The C8 nerve root mediates sensation from the ulnar side of the hand, mainly the
ring and pinkie fingers; therefore, pain and numbness are mostly in that region. C8 primarily supplies both the digitorum flexor superficialis and profundus and therefore controls finger flexion. There may also be paresis of finger adduction and abduction because C8 and T1 innervate the interossei muscles of the hand. The patient may complain of difficulties grasping objects such as cups. Innervation of the upper limb muscle by the cervical nerve roots is summarized in Figure 13.2.