The spinal cord and its associated spinal nerves are of immense functional importance. These structures act to:
receive afferent fibres from sensory receptors of the trunk and limbs
control movements of the trunk and limbs
provide autonomic innervation for most of the viscera.
The internal organisation of the cord permits many functions to operate in an automatic or reflex fashion. In addition, extensive connections with the brain, through ascending and descending nerve fibre tracts, both convey afferent information to higher centres and mediate their controlling influence over spinal mechanisms.
External features of the spinal cord
The spinal cord occupies the vertebral (or spinal) canal within the vertebral column, which provides support and protection (Figs 8.1, 8.2). Rostrally, the cord is continuous with the medulla oblongata of the brain stem.
Figure 8.1 Transverse section through the thoracic region. The diagram shows the relationship between the spinal cord, spinal nerves and vertebral column.
Figure 8.2 MR image of the vertebral column and spinal cord in the living subject.
(Courtesy of Professor A Jackson, Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK.)
The spinal cord is essentially a segmental structure; from rostral to caudal, it consists of 8 cervical (C), 12 thoracic (T), 5 lumbar (L), 5 sacral (S) and 1 coccygeal segments (Fig. 8.3). The cord is approximately cylindrical in shape but its diameter varies considerably at different levels. It bears two enlargements, cervical and lumbar. The cervical enlargement consists of cord segments C4–T1 and provides innervation for the upper limb via the brachial plexus (see Fig. 3.11). The lumbar enlargement is made up of segments L1–S3 and is associated with innervation of the lower limb via the lumbosacral plexus (see Fig. 3.13). Caudal to the lumbar enlargement, the cord tapers abruptly to form a conical termination, the conus medullaris. From the tip of the conus, a strand of connective tissue, the filum terminale (Fig. 8.4), extends caudally and is attached to the dorsal surface of the first coccygeal vertebra.
Figure 8.3 The relationships between spinal cord segments, spinal nerves and vertebral column.
Figure 8.4 Dorsal aspect of the spinal cord caudal to T9–T10. The dura/arachnoid mater have been cut longitudinally and reflected to reveal the spinal cord and nerve roots within the subarachnoid space.
Until the third month of fetal life, the spinal cord occupies the entire length of the vertebral canal. Thereafter, the rate of elongation of the vertebral column exceeds that of the spinal cord; as a result, at birth the cord terminates at the level of the third lumbar vertebra (L3) and in adult life, it terminates at the level of the intervertebral disc between L1 and L2 (Figs 8.3, 8.4).
The spinal cord provides sensory, motor and autonomic innervation for the trunk and limbs.
The cord possesses two enlargements: cervical (C4–T1), associated with innervation of the upper limbs, and lumbar (L1–S3), innervating the lower limbs.
The cord terminates at vertebral level L1–L2 in the adult.
The approximate location of spinal cord segments relative to the bony vertebrae may be identified in the living subject by reference to the posterior spinous processes of the vertebrae. As a rule-of-thumb, cervical cord segments lie approximately one spine higher than their corresponding vertebrae (e.g. C7 cord segment lies adjacent to C6 vertebra), thoracic segments lie approximately two spines higher, and lumbar segments three to four spines higher than their corresponding vertebrae (Fig. 8.3).
The spinal cord bears 31 bilaterally paired spinal nerves, each pair being associated with its corresponding cord segment. The spinal nerves originate as two linear series of nerve fascicles, or rootlets, attached to the dorsolateral and ventrolateral aspects of the cord (Fig. 8.5). The groups of six to eight contiguous fascicles that are attached to each cord segment coalesce to form dorsal and ventral nerve roots. The dorsal and ventral roots of each cord segment then pass to their corresponding intervertebral foramen (Fig. 8.6), in or near which they join to form the spinal nerve proper. While the spinal nerves are mixed nerves, containing both afferent and efferent neurones, the dorsal and ventral roots are functionally distinct. The dorsal roots contain primary afferent neurones, running from peripheral sensory receptors to the spinal cord and brain stem. The nerve cell bodies of these neurones are located in dorsal root ganglia (Fig. 8.5; see also Figs 1.8, 1.16), which appear as small enlargements on the dorsal roots near their convergence with the ventral roots at the entrance to the intervertebral foramina. The ventral roots of the spinal nerves carry efferent neurones, the cell bodies of which are located in the spinal grey matter. These are comprised of motor neurones, which innervate skeletal muscle, and preganglionic neurones of the autonomic nervous system.
Figure 8.5 Ventral aspect of the spinal cord, showing relationships of the spinal nerve roots and the meninges.
Figure 8.6 Lateral aspect of the spinal column in the lumbar region, illustrating the intervertebral foramina and the emerging spinal nerves.
The C1–C7 spinal nerves exit from the vertebral canal above the first seven cervical vertebrae; C8 spinal nerve exits below the seventh cervical vertebra and the remainder leave below their corresponding vertebrae (Fig. 8.3). Because of the different lengths of the spinal cord and the vertebral canal, only in the cervical region do the spinal cord segments lie adjacent to their corresponding vertebral bodies. Below this level, successive spinal nerve roots follow an increasingly oblique downwards course to reach their respective intervertebral foramina. This is most marked for the lumbar and sacral roots, which descend below the termination of the cord in a leash-like arrangement, the cauda equina (Figs 8.3, 8.4).
Immediately after leaving the intervertebral foramina, spinal nerves divide to produce a thin dorsal (posterior) ramus and a much larger ventral (anterior) ramus (Fig. 8.1). The dorsal ramus supplies the muscles and skin of the back region. The ventral ramus supplies the muscles and skin of the front of the body and also the limbs.
The peripheral distribution of spinal nerves, including their pattern of cutaneous innervation (dermatomes) and innervation of muscle groups (myotomes) is described in Chapter 3.
The spinal cord, like the brain, is invested by three concentric meningeal coverings: the pia mater, arachnoid mater and dura mater (Figs 8.4, 8.5).
The innermost covering, the pia mater, is a delicate, vascular membrane that is closely applied to the surface of the cord and nerve roots. Along a line midway between the dorsal and ventral roots of the spinal nerves is attached a flat, membranous continuation of the pia, called the denticulate ligament. The ligament has a free lateral border for much of its length but, intermittently, lateral projections tether the spinal cord to the arachnoid, and through it to the dura.
Lumbar puncture and epidural anaesthesia
The lowest part of the spinal canal does not contain the spinal cord; consequently, hollow needles can be safely inserted into the subarachnoid space in order to remove CSF for diagnostic purposes (lumbar puncture) or to inject radio-opaque substances for the radiological delineation of the spinal canal and its contents (myelography). Similarly, anaesthetics may be introduced into the epidural space in surgical procedures (epidural block).
Spinal nerve injury
The spinal nerve roots are vulnerable to compression by degenerative changes in the joints of the spinal column (spondylosis) and by prolapse of intervertebral discs. Prolapsed intervertebral discs in the cervical spine cause pain in the neck radiating to the arm and hand, accompanied by tingling sensations (paraesthesiae), weakness and wasting of the muscles corresponding to the radicular distribution, and numbness of the skin corresponding to the dermatomal distribution, together with loss of the tendon reflexes subserved by the particular root (Fig. 8.7). Similarly, lumbar prolapsed intervertebral discs lead to back pain and radiation of pain into the legs, known as sciatica. A large lumbosacral prolapsed disc may cause paralysis of the bladder and incontinence, demanding urgent neurosurgery.
Figure 8.7 Spinal nerve root lesion at the level of C5.
The arachnoid mater lies between the pia and dura. It is a translucent membrane that invests the cord like a loose-fitting bag. Between the pia and arachnoid lies the subarachnoid space. This contains CSF, which is produced in the cerebral ventricular system (Ch. 6).
The outer covering of the cord, the dura mater, is a tough, fibrous membrane. It envelops the cord loosely, as does the arachnoid with which it is in contact, though separated by a theoretical plane, the subdural space. The dura is separated from the bony wall of the vertebral canal by the epidural space.
Although the spinal cord terminates at vertebral level L1–L2, the arachnoid and dural sheaths and, therefore, the subarachnoid space, continue caudally to S2. As the spinal nerve roots pass towards their intervertebral foramina they evaginate the arachnoid and dura, forming meningeal root sleeves that extend as far as the fusion of dorsal and ventral roots. Thereafter, the arachnoid and dura become continuous with the epineurium ensheathing the spinal nerve.
Spinal nerves and meninges
The 31 pairs of spinal nerves attach to the spinal cord as dorsal and ventral roots, carrying afferent and efferent nerve fibres, respectively.
The cell bodies of afferent neurones are located in dorsal root ganglia. The cell bodies of efferent neurones reside in the spinal grey matter.
Spinal nerves exit the vertebral canal via intervertebral foramina.
Below the termination of the cord, spinal nerve roots descend as the cauda equina.
The cord and nerve roots are susceptible to traumatic injury, e.g. prolapsed intervertebral disc, cervical spondylosis, spinal dislocation.
The cord is invested by three meninges (pia, arachnoid and dura mater).
The subarachnoid space contains CSF.
CSF may be removed by lumbar puncture at L2–L3 or L3–L4.
Epidural anaesthesia of lumbar and sacral spinal nerves is possible at the same level.
Internal structure of the spinal cord
The spinal cord is incompletely divided into two symmetrical halves by a dorsal median sulcus and a ventral median fissure (Fig. 8.8). In the centre of the cord is the small central canal, which is continuous rostrally with the cerebral ventricular system. Surrounding the central canal is the spinal grey matter, consisting of nerve cell bodies, their dendrites and synaptic contacts. The outer part of the cord consists of white matter, which contains ascending and descending nerve fibres. Some of these serve to join neighbouring and distant cord segments for the integration of their functions, while others run between the cord and the brain. Many of the fibres that share a common origin, course and termination are grouped together in fascicles, forming the long tracts of the spinal cord.
Figure 8.8 Transverse section through the spinal cord showing the general disposition of grey and white matter.
The lower motor neurones of the spinal cord may be selectively affected by two diseases.
Poliomyelitis is an acute viral infection of the neurones leading to rapid paralysis and wasting of the limb and respiratory muscles. The disability is often asymmetrical and frequently affects the legs. Recovery occurs but may be incomplete.
Motor neurone disease is a chronic degenerative disorder that affects both lower motor neurones and the descending tracts to the spinal cord (upper motor neurones). Degeneration of ventral horn cells causes weakness, wasting, hypotonia and fasciculation of the limb muscles (progressive muscular atrophy). Degeneration of descending pathways leads to weakness and spasticity of the limb muscles (amyotrophic lateral sclerosis).
Different cord levels vary in the relative amounts and configuration of grey and white matter (Fig. 8.9). Higher levels contain greater amounts of white matter. This is because ascending tracts gain fibres at each successive level, whereas the opposite is true of descending tracts.
Figure 8.9 Transverse sections through the spinal cord at (A) cervical, (B) thoracic, (C) lumbar and (D) sacral levels. The histological method employed (Weigert–Pal) stains white matter (myelinated nerve fibres), leaving grey matter (nerve cell bodies) relatively unstained.
Grey matter of the spinal cord
The grey matter is approximately H-shaped, or butterfly-shaped, with four protrusions, the dorsal (posterior) and ventral (anterior) horns, extending dorso- and ventrolaterally towards the attachment zones of the dorsal and ventral root fascicles, respectively. The size and shape of the dorsal and ventral horns varies according to the level (Fig. 8.9). Many afferent nerve fibres entering in the dorsal roots terminate in the dorsal horn, while the ventral horn contains the cell bodies of motor neurones that exit through the ventral nerve roots and innervate skeletal muscle. Both dorsal and ventral horns are, therefore, particularly well developed at cervical and lumbar levels in association with innervation of the upper and lower limbs. Thoracic and upper lumbar segments additionally possess a small lateral or intermediolateral horn, located between the dorsal and ventral horns, which contains the cell bodies of preganglionic sympathetic neurones (Figs 8.8, 8.9B).
The grey matter of the spinal cord may be divided, on the basis of its cytoarchitecture, into ten zones, known as Rexed’s laminae, which are numbered sequentially from dorsal to ventral (Fig. 8.10). Some of these laminae are equated with cell groupings of particular functional types.
Figure 8.10 Lamination of spinal grey matter (Rexed’s laminae).
Afferent fibres entering through the dorsal roots divide into ascending and descending branches. They mostly terminate near their point of entry but may travel for varying distances in either direction, running in the dorsolateral fasciculus or Lissauer’s tract, which is located superficial to the tip of the dorsal horn (see Fig. 8.14). Dorsal root afferents may, therefore, establish synaptic contacts over several segments of spinal grey matter. Dorsal root fibres terminate extensively within the grey matter but most densely in the dorsal horn. Cutaneous afferents tend to terminate in superficial (dorsal) laminae, while proprioceptive and muscle afferents project mostly to deeper laminae.
The tip of the dorsal horn, approximating to Rexed’s laminae I–III, is also known as the substantia gelatinosa. This region receives collaterals of the smallest-diameter myelinated (group A delta) and unmyelinated (group C) afferents that are associated with nociception. These neurones are excitatory and use glutamic acid and the peptide substance P as neurotransmitters. In the substantia gelatinosa, complex interactions occur with other types of afferent terminal, interneurones, and with descending pathways from the brain, which control the transmission of pain information to ascending spinothalamic and spinoreticular tract neurones distributed throughout the dorsal horn. For example, input from large-diameter afferents carrying tactile information inhibits transmission of nociceptive impulses to ascending tract neurones, which explains why rubbing a sore spot can relieve pain.
The substantia gelatinosa contains high levels of the endogenous opioid peptide enkephalin, which is thought to act as a transmitter of some dorsal horn interneurones. These establish presynaptic contacts with the terminals of primary afferent neurones that possess opiate receptors. Occupation of these receptors decreases the release of substance P. The analgesic properties of opiates such as morphine are partly a result of their action at this site. The complex interactions between afferent nerve terminals, spinal interneurones and descending pathways, that together regulate the transmission of nociceptive information to ascending spinothalamic and spinoreticular tract fibres, constitute what is referred to as the ‘gate control theory’ of pain.
Deeper in the dorsal horn, lamina VII contains a number of important cell groups. At cord levels C8–L3 lie the cells of Clarke’s column (thoracic nucleus, nucleus dorsalis), which are the origin of ascending fibres of the dorsal spinocerebellar tract. The cells of Clarke’s column receive afferent input from muscle spindles, Golgi tendon organs, tactile and pressure receptors. At thoracic and upper lumbar levels, the lateral part of lamina VII also contains preganglionic sympathetic neurones that constitute the lateral horn, while at sacral levels (S2–S4) it contains preganglionic parasympathetic neurones.
In the ventral horn, lamina IX corresponds to groups of motor neurones that innervate skeletal muscle. These are of two types:
1. Alpha motor neurones, which innervate extrafusal muscle fibres
2. Gamma motor neurones, which innervate intrafusal muscle fibres (within muscle spindles).
The ventral horn is particularly well developed in the cervical and lumbar enlargements owing to the presence of motor neurones innervating the upper and lower limbs. Generally speaking, neurones innervating axial musculature (neck and trunk) tend to be located medially, while those innervating limb muscles are positioned more laterally. In the ventral horn of cord segments C3–C5 is located the phrenic nucleus, a group of motor neurones that innervate the diaphragm via the phrenic nerve and are, thus, essential for breathing. Cells in the ventral horn receive direct input from certain dorsal root afferents (e.g. from muscle spindles for mediation of the stretch reflex). Importantly, they also receive input from pathways descending from higher centres concerned with motor control.
Grey matter of the spinal cord
Internally, the spinal cord consists of a central core of grey matter (cell bodies) and an outer mantle of white matter (nerve fibres).
Within the grey matter, the dorsal horn is the main site of termination of primary afferent fibres. It includes the substantia gelatinosa, which is important in transmission of nociceptive impulses to the brain.
The lateral horn contains preganglionic sympathetic neurones.
The ventral horn contains alpha and gamma motor neurones, also known as lower motor neurones.
A reflex is an involuntary, stereotyped pattern of response brought about by a sensory stimulus. Although the qualitative nature of an established reflex response is constant, it may vary considerably in a quantitative sense (e.g. in delay, duration and extent) as a result of intersegmental and supraspinal influences.
Anatomically, the pathways mediating reflex actions consist of afferent neurones conveying impulses from sensory receptors to the CNS (spinal cord or brain stem) and efferent neurones running from the CNS to the effector organ (muscle or gland). In all but the simplest reflexes, interneurones within the CNS are interposed between the afferent and efferent components. The internal organisation of the spinal cord (and brain stem) thus subserves a number of more or less complex reflex functions, some of which are both relatively well understood and clinically important.
If a muscle is stretched, it responds by contracting, and this is known as the stretch or myotatic reflex. Anatomically, this is the simplest of reflexes and is mediated by a monosynaptic reflex arc (Fig. 8.11). It consists of afferent neurones that convey impulses from muscle stretch receptors to the CNS and motor neurones that convey impulses back to the stretched muscle.
Figure 8.11 The stretch reflex and reciprocal innervation. (A) The quadriceps stretch reflex is illustrated, whereby striking the patellar tendon elicits extension of the knee; (B) Reciprocal innervation. While stretching of the quadriceps muscle causes its reflex contraction, the motor neurones of antagonistic muscles (knee flexors) are inhibited by interneuronal connection within the spinal cord.
Stretch receptors within muscles consist of sensory nerve endings that attach to the central, non-contractile region of specialised muscle cells called intrafusal muscle fibres (see also Ch. 3). Intrafusal muscle fibres are oriented parallel to the long axis of the main muscle and occur in groups called muscle spindles. Stretch applied to the muscle in which they lie stimulates the sensory endings. Their afferent fibres carry impulses to the CNS, where they make monosynaptic excitatory contact with alpha motor neurones that innervate the bulk of the muscle (extrafusal muscle fibres) and make it contract.
There are two types of intrafusal muscle fibre: nuclear bag and nuclear chain fibres. These bear two types of sensory ending:
1. Primary or annulospiral endings, associated with group Ia afferent fibres,
2. Secondary or flower-spray endings, associated with group II afferents.
When a muscle is stretched, these endings are stimulated. Primary endings have both velocity and length sensitivity, while secondary endings have essentially only length sensitivity. Group Ia afferents from a particular muscle make excitatory monosynaptic contact with alpha motor neurones innervating the same muscle and, thus, mediate the myotatic reflex.
Stretch reflexes are important in the control of skeletal muscle tone, which refers to the degree of resistance to passive movement and is determined by the proportion of motor units that are active at any one time. When the upper motor neurones are damaged, muscle tone is increased during initial muscle stretch (spasticity). Since stretch reflexes operate to maintain muscles at a constant length in opposition to imposed stretch, they are important in the control of posture. By their action, activity is maintained in neck, trunk and lower limb extensor muscles (anti-gravity muscles) that support an upright body posture against the force of gravity and are stretched when these body parts become flexed.
Deep tendon reflexes, or tendon jerks, are monosynaptic stretch reflexes elicited during clinical examination by percussion of the tendon of the muscle by a tendon hammer. Each tendon reflex is subserved by certain spinal cord segments:
Biceps reflex (biceps jerk)
Brachioradialis reflex (supinator jerk)
Triceps reflex (triceps jerk)
Quadriceps reflex (knee jerk)
Achilles tendon reflex (ankle jerk)
In addition to alpha motor neurones, which innervate extrafusal muscle fibres, the ventral horn of the spinal cord (and motor cranial nerve nuclei) contain gamma motor neurones, which innervate the polar, contractile elements of intrafusal muscle fibres (Fig. 8.12). When gamma motor neurones are activated, the resultant contraction of the intrafusal muscle fibre applies tension to the sensory endings. This lowers the threshold of the stretch receptors to externally applied stretch and, thus, increases the sensitivity of the stretch reflex (the gamma reflex loop, Fig. 8.12).
Figure 8.12 Gamma reflex loop.
Like alpha motor neurones, gamma motor neurones are under the influence of descending pathways from the brain. Abnormalities in the activity of these pathways, therefore, which occur in many pathological conditions, induce changes in the sensitivity of stretch reflexes. This is evidenced by abnormalities in muscle tone.
When a stretch reflex is elicited (e.g. the quadriceps reflex, by tapping the patellar tendon), primary afferent fibres from the muscle spindle excite not only the alpha motor neurones of the stretched muscle but also interneurones that inhibit the alpha motor neurones of antagonistic muscles (e.g. the knee flexors, Fig. 8.11). This illustrates the general principle of reciprocal innervation of agonist and antagonist muscle groups.
Noxious cutaneous stimulation of the limbs causes withdrawal from the offending stimulus. This is mediated by a polysynaptic reflex in which one or more interneurones are interposed between afferent and efferent neurones. Primary afferent fibres activate interneurones within the spinal grey matter, which in turn excite alpha motor neurones innervating the limb flexor muscles (Fig. 8.13). Flexion of a limb about several joints requires the coordinated action of more than one spinal segment and this is achieved by collateralisation of primary afferents and interneurones.
Figure 8.13 Flexor reflex and crossed extensor reflex.
All forms of cutaneous stimulation have the potential to elicit the flexor reflex, but this is normally prevented by descending pathways from the brain unless the stimulus is painful. In certain pathological conditions, the descending inhibitory influence is lost and even innocuous cutaneous stimulation can cause limb withdrawal. The extensor plantar response (Babinski reflex) is characterised by extension (dorsiflexion) of the great toe and splaying of the other toes in response to stimulation of the sole of the foot. Physiologically, it is a flexor reflex and is present in infants before myelination of the corticospinal tract has taken place. Thereafter, the reflex is absent, being suppressed by descending corticospinal influences (stimulation of the sole of the foot then causing a flexor plantar response, with curling of the toes). When the descending influence is lost (e.g. following a stroke in the internal capsule) the extensor plantar reflex re-emerges. It is regarded as pathonomic of damage to the corticospinal tract.
Activation of the flexor reflex in a weight-bearing limb (e.g. by standing on a pin) simultaneously causes reflex extension of the contralateral limb to take the weight of the body. This is called the crossed extensor reflex (Fig. 8.13). It is mediated by axon collaterals which cross the midline of the cord and excite the alpha motor neurones of contralateral limb extensor muscles.
The internal organisation of the cord subserves a number of important reflex functions.
The monosynaptic stretch reflex mediates muscle contraction in response to stretch of muscle spindles.
The sensitivity of the stretch reflex is regulated by gamma motor neurones, which provide motor innervation to the spindle fibres.
The stretch reflex is responsible for maintenance of muscle tone and is clinically tested as the deep tendon reflexes.
The polysynaptic flexor reflex mediates limb withdrawal from noxious stimuli.
White matter of the spinal cord
The grey matter of the spinal cord is completely surrounded by white matter, which consists of ascending and descending nerve fibres. The white matter is sometimes considered to be divided into dorsal, lateral and ventral columns or funiculi (Fig. 8.8). Nerve fibres sharing common origins, terminations and functions are organised into tracts or fasciculi (Latin for small bundles). Some fibres interconnect adjacent or distant cord segments and permit intersegmental coordination, while other fibres are longer and serve to join the spinal cord with the brain. The intersegmental, or propriospinal, fibres occupy a narrow band immediately peripheral to the grey matter. This is known as the fasciculus proprius (Fig. 8.14). Nerve fibres running between the spinal cord and the brain constitute the ascending and descending tracts of the spinal cord (Figs 8.14-8.20).
Figure 8.14 Ascending and descending tracts of the spinal cord. All ascending and descending tracts are present bilaterally. In this figure, ascending tracts are emphasised on the left side and descending tracts are emphasised on the right side. In addition, the location of Lissauer’s tract and the fasciculus proprius (which contain both ascending and descending fibres) are shown.
Figure 8.15 The dorsal columns. The central pathways carrying conscious proprioception and discriminative touch are illustrated.
Figure 8.16 The spinothalamic tract. The central pathways for pain, temperature, touch and pressure are illustrated.
Figure 8.17 Corticospinal tracts.
Figure 8.18 Rubrospinal tract.
Figure 8.19 Tectospinal tract.
Figure 8.20 Vestibulospinal tracts.
Ascending spinal tracts
Ascending tracts carry impulses from pain, thermal, tactile, muscle and joint receptors to the brain. Some of this information eventually reaches a conscious level (the cerebral cortex), while some is destined for subconscious centres (e.g. the cerebellum).
Pathways that carry information to a conscious level share certain common characteristics.
There is a sequence of three neurones between the peripheral receptor and the cerebral cortex.
The first neurone (first-order neurone or primary afferent neurone) enters the spinal cord through the dorsal root of a spinal nerve and its cell body lies in the dorsal root ganglion. The central process may collateralise extensively and make synaptic connections that mediate spinal reflexes and intersegmental coordination. The main fibre remains on the ipsilateral side of the cord and terminates in synaptic contact with the second neurone either in the spinal grey matter or in the medulla oblongata of the brain stem, depending on the modality.
The second neurone (second-order neurone) has its cell body in the cord or medulla oblongata. Its axon crosses over (decussates) to the opposite side of the CNS and ascends to the thalamus, where it terminates upon the third neurone.
The third neurone (third-order neurone) has its cell body in the thalamus. Its axon passes to the somatosensory cortex in the parietal lobe of the ipsilateral cerebral hemisphere.
Two main tract systems in the spinal cord fit into this pattern: the dorsal (posterior) columns and the spinothalamic tracts.
The dorsal columns are located between the dorsal median sulcus and the dorsal horn. Two tracts are recognised: the fasciculus gracilis, situated medially and the fasciculus cuneatus, situated laterally. The tracts carry impulses concerned with proprioception (movement and joint position sense) and discriminative (fine) touch.
The dorsal columns contain the axons of primary afferent neurones that have entered the cord through the dorsal roots of spinal nerves (Fig. 8.15). The fasciculus gracilis consists of fibres that join the cord at sacral, lumbar and lower thoracic levels and, thus, includes those from the lower limb. Fibres of the fasciculus cuneatus enter via the upper thoracic and cervical dorsal roots and, thus, include those from the upper limb. Since the dorsal columns contain primary afferent neurones, they carry information relating to the ipsilateral side of the body. Fibres ascend without interruption to the medulla oblongata where they terminate upon second-order neurones, the cell bodies of which are located in the nucleus gracilis and nucleus cuneatus (see also p. 92).
The axons of the second-order neurones decussate in the medulla as internal arcuate fibres and, thereafter, ascend through the brain stem as the medial lemniscus. The medial lemniscus terminates in the ventral posterior (VP) nucleus of the thalamus upon third-order thalamocortical neurones. These in turn project to the somatosensory cortex, located in the postcentral gyrus of the parietal lobe.
Lesions of the dorsal columns
Tabes dorsalis is a late manifestation of syphilitic infection of the CNS. It chiefly affects the lumbosacral dorsal spinal roots and the dorsal columns of the spinal cord. The loss of proprioception leads to a high steppage and unsteady gait (sensory ataxia), which is exacerbated when the eyes are closed (Romberg’s sign).
Subacute combined degeneration of the spinal cord is a systemic disease resulting from a deficiency of vitamin B12 (cyanocobalamin), which also causes pernicious anaemia. The degeneration of the dorsal columns produces sensory ataxia. The lateral columns of the spinal cord are also involved (combined), causing weakness and spasticity of the limbs. The disorder, although uncommon, is an important one since proper treatment with vitamin B12 can lead to complete recovery.
In multiple sclerosis, an immune disease, specific damage to the fasciculus cuneatus of the cervical spinal cord leads to loss of proprioception in the hands and fingers, causing profound loss of dexterity and inability to identify the shape and nature of objects by touch alone (astereognosis).
The spinothalamic tract lies lateral and ventral to the ventral horn of the spinal grey matter. It carries information related to pain and thermal sensations and also non-discriminative (course) touch and pressure. Some authorities identify distinct lateral and ventral spinothalamic tracts conveying pain and temperature or touch and pressure, respectively, but fibres carrying these modalities are probably intermingled to some extent.
The spinothalamic tract contains second-order neurones, the cell bodies of which lie in the contralateral dorsal horn and receive input from primary afferent fibres that terminate in this region (Fig. 8.16). After leaving the parent cell bodies, spinothalamic axons decussate to the opposite side of the cord by passing through the ventral white commissure, which lies ventral to the central canal of the cord, and, thus, enter the contralateral spinothalamic tract. Axons carrying pain and temperature decussate promptly within one segment of their origin, while those carrying touch and pressure may ascend for several segments before crossing.
In the brain stem, the spinothalamic fibres run in close proximity to the medial lemniscus and are known as the spinal lemniscus. The majority of fibres terminate in the ventral posterior nucleus of the thalamus, contacting third-order thalamocortical neurones that project to the somatosensory cortex.
The spinothalamic tract is sometimes referred to as the neospinothalamic system. It is highly organised somatotopically; consequently, the origin of sensory stimuli can be accurately localised. It is thought to be the route via which sharp, pricking pain (sometimes called ‘fast’ pain) is conducted.
Spinothalamic tract lesions
The spinothalamic tracts can be selectively damaged in syringomyelia, in which the central canal becomes enlarged to form a cavity compressing adjacent nerve fibres. The second-order neurones subserving pain and temperature are damaged as they decussate in the ventral white commissure, close to the central canal, causing a selective loss of pain and temperature awareness in the upper limbs. This is termed a dissociated sensory loss, since light touch and proprioceptive sensation are retained. The patient injures and burns the hands painlessly, and the joints of the limbs become disorganised without discomfort (Charcot’s joints).
Selective surgical destruction of the spinothalamic tracts (cordotomy or tractotomy) is sometimes performed for the neurosurgical relief of intractable pain from a variety of causes.
The spinoreticulothalamic system represents an additional, phylogenetically older, route by which nociceptive sensory impulses ascend to higher centres. Some second-order neurones arising from the dorsal horn ascend in the ventrolateral region of the cord and then terminate in the brain stem reticular formation, particularly within the medulla. Reticulothalamic fibres then ascend to the intralaminar thalamic nuclei, which in turn activate the cerebral cortex. The spinoreticulothalamic system is poorly organised somatotopically and is thought to be the route via which dull, aching pain (sometimes called ‘slow’ pain) is transmitted to a conscious level. Activation of spinothalamic and spinoreticular fibres, which may ultimately be perceived as unpleasant or painful, can be modulated by descending pathways from the brain.
Ascending pathways that carry impulses to a subconscious level are represented principally by the spinocerebellar tracts.
Fibres of the ascending spinocerebellar tracts form dorsal and ventral tracts that are located near the dorsolateral and ventrolateral surfaces of the cord, respectively. Both tracts carry information derived from muscle spindles, Golgi tendon organs and tactile receptors to the cerebellum for the control of posture and coordination of movement.
The spinocerebellar system consists of a sequence of only two neurones. Both spinocerebellar tracts contain second-order neurones whose cell bodies of origin lie in the base of the dorsal horn; they receive input from primary afferent fibres terminating in this region. The tract neurones terminate directly in the cerebellar cortex, predominantly within the vermis. Fibres of the dorsal spinocerebellar tract originate from a prominent group of cells known as Clarke’s column. The axons ascend ipsilaterally to enter the cerebellum through the inferior cerebellar peduncle. Fibres of the ventral spinocerebellar tract decussate, ascend on the contralateral side of the cord and enter the cerebellum via the superior cerebellar peduncle. Some axons then re-cross within the cerebellar white matter.
Friedreich’s ataxia is an inherited degenerative disease in which the spinocerebellar tracts are particularly disordered, leading to profound incoordination of the arms (intention tremor) and a wide-based, reeling gait (ataxia). The disorder begins in childhood and the patient is wheelchair-bound by 20 years of age.
White matter of the spinal cord: principal ascending tracts
Ascending tracts carry afferent information to conscious and subconscious levels. Pathways to a conscious level follow a basic plan of three neurones in a chain from peripheral receptor to cerebral cortex.
Dorsal columns (fasciculus gracilis and cuneatus) carry proprioception and discriminative touch. They convey first-order neurones ipsilaterally to the nuclei gracilis and cuneatus of the medulla. Second-order neurones decussate and pass to the thalamus. Third-order neurones project to the somatosensory cortex. Lesions (e.g. tabes dorsalis, vitamin B12 deficiency) lead to ataxia and loss of discriminative touch.
Spinothalamic tract carries pain, temperature, touch and pressure. The tract contains second-order neurones with cell bodies in the dorsal horn. Axons decussate and pass to the thalamus. Third-order neurones project to the somatosensory cortex. Lesions (e.g. syringomyelia) lead to impairment of pain, temperature, touch and pressure sensitivity on the contralateral side.
Dorsal and ventral spinocerebellar tracts contain second-order neurones carrying muscle, joint and tactile information involved in motor control. Lesions lead to ataxia (e.g. Friedreich’s ataxia).
Descending spinal tracts
Descending tracts of the spinal cord (Fig. 8.14) originate from the cerebral cortex and brain stem. They are concerned with the control of movement, muscle tone, spinal reflexes, spinal autonomic functions and the modulation of sensory transmission to higher centres.
The corticospinal tracts (Fig. 8.17) are particularly concerned with the control of voluntary, discrete, skilled movements, especially those of the distal parts of the limbs. Such movements are sometimes referred to as ‘fractionated’ movements. Corticospinal tract neurones arise from cell bodies in the cerebral cortex. The cells of origin are widely distributed in the motor and sensory cortices, including the precentral gyrus or primary motor cortex, where the large Betz cells give rise to the largest diameter corticospinal axons. Corticospinal axons leave the cerebral hemispheres by passing through the massive subcortical fibre systems of the corona radiata and internal capsule to enter the crus cerebri of the midbrain.
Having passed through the ventral portion of the pons, corticospinal fibres reach the medulla oblongata, where they form two prominent columns on the ventral surface. These are called the pyramids and for this reason the term pyramidal tract is used as an alternative name for the corticospinal tract. In the caudal medulla, the fibres of the pyramids undergo subtotal decussation. About 75–90% of fibres decussate and enter the contralateral lateral corticospinal tract, which is located in the lateral part of the spinal white matter, deep to the dorsal spinocerebellar tract; 10–25% of pyramidal fibres remain ipsilateral and enter the ventral corticospinal tract located lateral to the ventral median fissure. They also decussate near to their termination; as a result, the fibres of the pyramidal tract effectively innervate the contralateral side of the spinal cord.
Hereditary spastic paraparesis
Hereditary spastic paraparesis is an inherited degenerative disorder (autosomal dominant) in which progressive weakness affects the legs, leading to marked stiffness of gait. Degeneration of the lateral columns, including the lateral corticospinal tract, chiefly affects the thoracic spinal cord, causing a spastic paraparesis with hyperreflexia and extensor plantar responses, but with sparing of sensation and bladder function.
Approximately 55% of corticospinal neurones terminate at cervical levels, 20% at thoracic and 25% at lumbosacral levels. Fibres terminate extensively in the spinal grey matter. Many of those fibres that originate from the motor cortex terminate in the ventral horn, some making monosynaptic contact with motor neurones.
The rubrospinal tract originates from the red nucleus of the midbrain tegmentum (Fig. 8.18). It exerts control over the tone of limb flexor muscles, being excitatory to the motor neurones of these muscles. Axons leaving the cells of the red nucleus course ventromedially and cross in the ventral tegmental decussation, after which they descend to the spinal cord where they lie ventrolateral to, and partly intermingled with, the lateral corticospinal tract.
The red nucleus receives afferent fibres from the motor cortex and from the cerebellum. The rubrospinal tract, therefore, represents a non-pyramidal route by which the motor cortex and cerebellum can influence spinal motor activity.
Tectospinal fibres arise from the superior colliculus of the midbrain (Fig. 8.19). Axons pass ventromedially around the periaqueductal grey matter and cross in the dorsal tegmental decussation. In the spinal cord, descending tectospinal fibres lie near the ventral median fissure and terminate predominantly in cervical segments. The superior colliculus receives visual input and the tectospinal tract is thought to mediate reflex movements in response to visual stimuli.
Vestibulospinal fibres arise from the vestibular nuclei situated in the pons and medulla, in and near the floor of the fourth ventricle (Fig. 8.20). The vestibular nuclei receive input from the labyrinthine system by way of the vestibular nerve and from the cerebellum.
Axons from cells of the lateral vestibular nucleus (Deiters’ nucleus) descend ipsilaterally as the lateral vestibulospinal tract, which is located in the ventral funiculus. Lateral vestibulospinal tract fibres mediate excitatory influences upon extensor motor neurones. They serve to control extensor muscle tone in the anti-gravity maintenance of posture.
The medial vestibular nucleus contributes descending fibres to the ipsilateral medial longitudinal fasciculus, also known as the medial vestibulospinal tract, which is located adjacent to the ventral median fissure.
The reticular formation of the pons and medulla gives rise to reticulospinal fibres. Axons arising from the pontine reticular formation descend ipsilaterally as the medial (or pontine) reticulospinal tract. Axons from the medulla descend bilaterally in the lateral (or medullary) reticulospinal tracts. Both tracts are located in the ventral funiculus.
Reticulospinal fibres influence voluntary movement, reflex activity and muscle tone by controlling the activity of both alpha and gamma motor neurones. They also mediate pressor and depressor effects upon the circulatory system and are involved in the control of breathing.
White matter of the spinal cord: principal descending tracts
Corticospinal tract controls discrete, skilled movements, particularly of the distal extremities. It originates from motor and sensory cortices. Fibres descend through the internal capsule, crus cerebri and ventral pons to reach the medullary pyramid. Most fibres (75–90%) decussate to form the lateral corticospinal tract, the remainder forming the ventral corticospinal tract.
Rubrospinal tract controls limb flexor muscles and originates from the red nucleus of the midbrain. Fibres cross in the ventral tegmental decussation.
Tectospinal tract is involved in reflex responses to visual input. It originates from the contralateral superior colliculus and fibres cross in the dorsal tegmental decussation.
Vestibulospinal tracts descend from the vestibular nuclei. The lateral tract originates from the ipsilateral lateral vestibular nucleus and mediates excitation of limb extensor muscles.
Reticulospinal tracts descend from the pons and medulla. They are involved in the control of reflex activities, muscle tone and vital functions.
Lesions of the spinal cord
Focal lesions of the spinal cord and the nerve roots produce clinical manifestations in two ways:
1. The lesion destroys function at the segmental level.
2. The lesion interrupts descending motor and ascending sensory tracts.
Damage to different parts of the spinal cord, therefore, is accompanied by distinctive clinical syndromes (Fig. 8.21).
Figure 8.21 (A) Upper cervical cord lesion. A high cervical cord lesion causes spastic tetraplegia with hyperreflexia, extensor plantar responses (upper motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. (B) Lower cervical cord lesion. A lower cervical cord lesion causes weakness, wasting and fasciculation of muscles, and areflexia of the upper limbs (lower motor neurone lesion). In addition, there is spastic paraparesis, hyperreflexia and extensor plantar responses (upper motor neurone lesion) in the lower limbs, incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. (C) Thoracic cord lesion. A thoracic cord lesion causes a spastic paraparesis, hyperreflexia and extensor plantar responses (upper motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. (D) Lumbar cord lesion. A lumbar cord lesion causes weakness, wasting and fasciculation of muscles, areflexia of the lower limbs (lower motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. (E) Hemisection of the cord gives rise to the Brown–Séquard syndrome. This is characterised by ipsilateral loss of proprioception and upper motor neurone signs (hemiplegia/monoplegia) plus contralateral loss of pain and temperature sensation.