The spinal cord contains motor, sensory, and autonomic fibers and nuclei in a tight spatial relationship with one another. Lesions of the spinal cord can cause a wide variety of neurological deficits, which can be combined with each other in many different ways.
The spinal cord, like the brain, is composed of gray matter and white matter. The white matter contains ascending and descending fiber tracts. The gray matter contains neurons of different kinds: the anterior horns contain mostly motor neurons, the lateral horns mostly autonomic neurons, and the posterior horns mostly somatosensory neurons participating in a number of different afferent pathways. In addition, the spinal cord contains an intrinsic neuronal apparatus consisting of interneurons, association neurons, and commissural neurons, whose processes ascend and descend in the fasciculus proprius.
The average length of the cord is 42 cm in women and 44.7 cm in men. In normal adults the cord ends between the twelfth thoracic vertebra (T12) and the lower third of the third lumbar vertebra (L3). The nerve roots, however, still exit from the spinal canal at the numerically corresponding levels. Spinal cord ends as the conus medullaris at the L1 or L2 level (rarely at L3). Below this level, the lumbar sac (theca) contains only nerve root filaments, the so-called cauda equina. The spinal cord has got the cervical and lumbar enlargements. The cervical enlargement contains the segments corresponding to the upper limbs (C4-T1), which form the brachial plexus; the lumbar enlargements contains the ones for the lower limbs (L2-S3), which form the lumbosacral plexus. Attached to the spinal cord are 31 pairs of nerves: 8 cervical (C), 12 thoracic (T), 5 lumbar (L), 5 sacral (S), and one or more (1-3) rudimentary coccygeal pairs. The spinal nerves are formed by the union of a dorsal and a ventral root.
The spinal cord is surrounded by pia mater, arachnoid, and dura mater. The pia mater is a delicate membrane that closely invests the spinal cord. The arachnoid is a transparent membrane that is close to the inner surface of the dura, but fine strands extend to the pia. The dura mater is a strong, fibrous membrane, penetrated by the nerve roots, which forms a firm, tubular sheath. It is separated from the wall of the vertebral canal by the epidural space, which contains areolar tissue and a plexus of veins. The subdural space is a potential space containing a small amount of fluid. The subarachnoid space, which extends to about the level of the second sacral vertebra, is a well-defined cavity containing cerebrospinal fluid. The dentate ligaments extend along the lateral surface of the spinal cord, between the anterior and posterior nerve roots, from the pia to the dura mater. They suspend the spinal cord in the vertebral canal.
On cross section (Fig. 4.1, 4.2) the spinal cord is seen to be divided into an H-shaped core of gray matter and a surrounding white matter. The superior limbs of the H are called the dorsal horns and the inferior, the ventral horns. This gray matter consists largely of neurons and glia, while the white matter consists of nerve fibers and glia. Within the center of the gray matter and running throughout the entire length of the cord is a minute remnant of the central canal consisting of a single layer of ependymal cells. The nerve fibers of the white matter of the cord group into definite tracts, most of which have a somatotopic arrangement. The origin and termination of the tracts is of critical importance clinically. Surrounding the gray matter are the so-called fasciculi proprii or ground bundles, consisting of many short and some long fibers linking the spinal segments into reflex patterns. The longer coursing tracts are located peripheral to these ground bundles. Most nerve fibers of the dorsal columns originate from the dorsal root ganglia. Many dorsal column axons ascend to the junction of the spinal cord with the medulla oblongata; there they synapse in the nuclei gracilis and cuneatus, leg fibers going to the nucleus gracilis and arm fibers to the nucleus cuneatus. These dorsal column fibers are primary; they are a direct extension of the entering dorsal root axons which form the dorsal columns without synapsing. From the nuclei gracilis and cuneatus, the sensory pathway decussates to travel to the thalamus and the cerebral cortex. The other sensory tracts of the spinal cord are composed of secondary or tertiary fibers, having one or more neurons interposed between the entering primary dorsal root axons and the cell of origin of the tract in the spinal cord. In addition to these intrinsic systems, the spinal cord contains many tracts originating from the brain. The essential tracts can be summarized briefly, according to whether they are motor or sensory.
Lesions of the spinal cord are characterized by sensory, motor, and autonomic changes. They occasionally affect only the white matter or only the gray matter (e. g., acute poliomyelitis), but more often affect both. The symptoms depend upon the location and extent of damage to various functional elements, and often upon the type of damage and the rapidity with which the lesion develops.
Syndrome of the dorsal root ganglion. Infection of one or more spinal ganglia by a neurotropic virus occurs most commonly in the thoracic region and causes painful erythema of the corresponding dermatomes, followed by the formation of a variable number of cutaneous vesicles. This clinical picture, called herpes zoster, is associated with very unpleasant, stabbing pain and paresthesiae in the appropriate area.
Posterior root syndrome. If two or more adjacent posterior roots are completely divided, sensation in the corresponding dermatomes is partially or totally lost. Incomplete posterior root lesions affect different sensory modalities to variable extents, with pain sensation usually being most strongly affected. Because the lesion interrupts the peripheral reflex arc, the sensory deficit is accompanied by hypotonia and hyporeflexia or areflexia in the muscles supplied by the affected roots. These typical deficits are produced only if multiple adjacent roots are affected.
Posterior column syndrome. Lesions of the posterior columns usually cause disturbances of position and vibration sense, discrimination, they also produce a positive Romberg sign, as well as gait ataxia that worsens significantly when the eyes are closed (unlike cerebellar ataxia, which does not). Posterior column lesions also often produce hypersensitivity to pain. Possible causes include vitamin B12 deficiency (“funicular myelosis”), AIDS-associated vascular myelopathy, and spinal cord compression (e. g., in cervical spinal stenosis).
Posterior horn syndrome can be a clinical manifestation of syringomyelia, hematomyelia, and some intramedullary spinal cord tumors. Like posterior root lesions, posterior horn lesions produce a segmental somatosensory deficit. Only pain and temperature sensation are lost in the corresponding ipsilateral segments, only second neuron of sensory pathway are in the posterior horn (whose axon ascends in the lateral spinothalamic tract). Loss of pain and temperature sensation with sparing of posterior column sense is called a dissociated somatosensory deficit.
Graymatter syndrome. Damage to the central gray matter of the spinal cord by syringomyelia, hematomyelia, intramedullary spinal cord tumors, or other processes interrupts all of the fiber pathways passing through the gray matter. The fibers which originate in posterior horn cells and conduct pressure, touch, pain, and temperature sensation; decussate in the central gray matter and then ascend in the anterior and lateral spinothalamic tracts. A lesion affecting them produces a bilateral dissociated sensory deficit in the cutaneous area supplied by the damaged fibers.
Anterior horn syndrome. Both acute poliomyelitis and spinal muscle atrophy of various types affect the anterior horn cells, particularly in the cervical and lumbar enlargements of the spinal cord. In poliomyelitis (a viral infection), a variable number of anterior horn cells are lost, mainly in the lumbar region, causing flaccid paresis of the muscles in the corresponding segments. Proximal muscles tend to be more strongly affected than distal ones. The muscles become atrophic and, in severe cases, may be completely replaced by connective tissue and fat.
Combined anterior horn and pyramidal tract syndrome (e.g. amyotrophic lateral sclerosis) is the result of degeneration of cortical and spinal motor neurons. The clinical picture is a combination of flaccid and spastic paresis.
The spinal cord hemisection syndrome (Brown-Sequard syndrome) is rare and usually incomplete. It’s usually caused by trauma and cervical disk herniation. Interruption of the descending motor pathways on one side of the spinal cord causes an initially flaccid, ipsilateral paresis below the level of the lesion (spinal shock), which later becomes spastic and is accompanied by hyperreflexia, Babinski signs, and vasomotor disturbances. At the same time, the interruption of the posterior columns on one side of the spinal cord causes ipsilateral loss of position sense, vibration sense, and tactile discrimination below the level of the lesion. The ataxia that would normally be caused by the posterior column lesion cannot be demonstrated because of the coexisting ipsilateral paresis. Pain and temperature sensation are spared on the side of the lesion, because the fibers subserving these modalities have already crossed to the other side to ascend in the lateral spinothalamic tract, but pain and temperature sensation are lost contralaterally below the level of the lesion, because the ipsilateral (crossed) spinothalamic tracts are interrupted.
