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Spinal Cord Anatomy

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Below the brainstem is the elongated, segmented spinal cord and its associated dorsal and ventral roots which merge to form spinal nerves. Some disorders are confined to the spinal cord while others may include its roots; injuries to these structures produce a number of distinctive syndromes. The features of spinal cord disorders reflect its anatomy and physiology, i.e., ascending sensory tracts, descending motor systems, sensory afferent fibers and the nuclei receiving incoming sensory information, nuclei giving rise to exiting motor fibers, and the reflexes which result from the interaction of all these elements. A. Anatomy: 1) Dorsal roots feed a variety of sensory fibers carrying information to synapse in the dorsal gray horn nuclei and form the ascending pathways, e.g., nucleus proprius and Clarke's column; some fibers ascend without synapsing: ascending pathways include: a) the posterior white column - conscious proprioception, discriminative touch and vibratory sense - fibers ascend uncrossed without synapsing. b) the anterior and lateral spinothalamic tracts - after synapsing in the nuclei of the dorsal gray horn, pain, temperature and light touch fibers cross in the anterior white commissure to ascend. c) the posterior spinocerebellar tract - "unconscious" proprioception from the lower extremity, incoming fibers synapse in Clarke's column of the dorsal gray horn and ascend without crossing; upper extremity fibers ascend uncrossed without synapsing, in the posterior white column, to finally synapse in the ipsilateral accessory cuneate nucleus of the medulla. 2) Ventral roots from all spinal cord segments carry fibers from anterior horn cells to control voluntary muscle. Ventral roots from thoracolumbar and sacral regions also carry preganglionic autonomic fibers from cells of the intermediate gray for control of the viscera. a) the lateral corticospinal tract (along with the lateral reticulospinal tract) helps control the anterior horn cells for skeletal muscle volitional motor activity. b) the lateral vestibulospinal tract (along with the medial reticulospinal tract) helps control the anterior horn cells and are especially important in the reflex control of skeletal muscle. c) descending autonomic fibers descend (mixed with the lateral corticospinal tract) for the control of the preganglionic autonomics responsible for visceral functions.

1) HEMISECTION OF THE SPINAL CORD (BROWN-SEQUARD SYNDROME) Pure hemisection of the cord rarely occurs but it is among the best cases for illustrating the features of spinal cord injury. Briefly stated, symptoms include: spastic paralysis, loss of position sense, discriminative touch and vibratory sense on the side of the lesion - this represents involvement of the lateral corticospinal tract and the posterior white column on the side of the lesion. On the side opposite the lesion there is a loss of pain and temperature due to involvement of the lateral spinothalamic tract. At times, it is possible to also demonstrate a bilateral sensory deficit and flaccid paralysis at the level of the lesion. A Sample Case: A young woman complained of pain in her left breast and progressive weakness of her left lower limb for a period of many months before finally visiting her physician. The neurologic evaluation revealed weakness in the left lower limb. This was associated with spasticity (increased tone), hyperreflexia (increased deep tendon reflexes) at the knee and ankle, which also demonstrated clonus. On the left side there was loss of two-point touch, vibratory sense and proprioception at levels below the hip. The right side showed a loss of pain and temperature sensation below dermatome T-7. The patient was determined to have an extramedullary tumor expanding from the dorsal roots at spinal cord levels T-5,6. Explanation Ipsilateral paralysis below the lesion. Paralysis is the "Upper Motor Neuron" or spastic type; there is spasticity, slow (disuse) muscle atrophy, hypertonia, ankle clonus and a positive Babinski sign. Superficial reflexes, e.g., the abdominal and cremasteric are lost. Spastic paralysis is attributed to interruption of the lateral corticospinal tract and the accompanying lateral reticulospinal tract. Loss of these upper motor neurons deprives the anterior horn cells, i.e., lower motor neurons, of the impulses which generate contraction of skeletal muscle, hence, weakness (paresis) or paralysis. Hypertonia and hyperreflexia appear to result from loss of the inhibitory effects of these two descending motor pathways on the stretch reflexes, leaving them hyperexcitable to segmental muscle afferents . It may be possible to also demonstrate a "Lower Motor Neuron Syndrome" or flaccid paralysis ipsilaterally at the level of the lesion. If the anterior horn cells supplying the skeletal muscles are injured at the level of the lesion then these muscles are denervated. This paralysis is of the flaccid type; muscles undergo rapid atrophy due to loss of the trophic influence of the nerves as well as disuse. Tone and tendon reflexes are diminished since they are reflex responses and the injured lower motor neurons are the "final common pathway" to the muscle in the stretch reflex, hence, there is no reflex. Loss of conscious proprioception, two-point discrimination and vibratory sense ipsilaterally is due to interruption of the posterior white columns (fasciculus gracilis/cuneatus). This is frequently accompanied by a Romberg sign. A normal individual, standing erect with heels together and eyes closed, sways only slightly. Stable posture is achieve by 1) a sense of position from the vestibular system, 2) awareness of the position and status of muscles and joints by conscious proprioception and 3) visual input regarding our position. Closing the eyes has only slight effect on the normal individual's stance since the vestibular and conscious proprioception systems are sufficient. In a patient with an impaired posterior column conscious proprioception is diminished; when the eyes are closed loss of both systems renders the patient unstable and they are likely to sway or fall to the side. Pain and temperature sensation is lost below the lesion, on the opposite side beginning about one dermatomal segment below the level of the lesion. These sensations are carried by

the lateral spinothalamic tract whose fibers originated on the sideopposite the lesion but which crossed in the anterior white commissure. Dorsal root afferents carrying pain and temperature synapse in the dorsal gray; the second order neuron crosses in the anterior white commissure along an ascending path for a distance of about one spinal segment. Because of the oblique ascent of the crossing fibers in the anterior white commissure, injury of the spinothalamic tract is not likely to be carrying sensation from that level. A careful sensory evaluation may reveal that at the dermatomal level of the lesion there is a bilateral loss of pain and temperature sensation. Since the second order neurons from both sides cross in the midline below the central canal, a hemisection of the cord may interrupt the crossing fibers from both sides and produce this limited bilateral deficit. The pain in the left breast was the result of the pressure of the tumor on the dorsal root.

2) TRANSECTION OF THE CORD Transection most frequently results from trauma but it can be associated with vascular infarction or hemorrhage, compression, demyelinating or inflammatory lesions. Shearing or compressing the cord produces destruction of the gray and white matter. Pathologic changes are maximal at the level of the lesion but injury extends above and below the lesion for a segment or two. The final clinical outcome is a result of the irreversible structural damage and functional disorders created. A Sample Case: A healthy man of 50 years of age was thrown from his horse. He was immediately rendered quadriplegic (paralyzed in all four extremities) and described a numb feeling from the neck on down. He never lost consciousness. The immediate neurologic exam revealed flaccid paralysis of all four extremities and no deep tendon reflexes could be demonstrated. All sensation was absent bilaterally from his arms on down. Some weeks after the accident the limbs showed signs of spastic paralysis with markedly increased deep tendon reflexes but there was no return of sensory function. Bowel and bladder control were lost. X-ray examination showed severe fractures and displacement of the C5,6 vertebrae. Explanation "Spinal shock". As a result of a rapid and complete transection there is complete loss of voluntary movement and sensation from levels below the cord lesion and loss of all reflexes in the isolated cord segments. This is called "spinal shock" and its duration can vary, 1 to 6 weeks is common. As this phenomenon fades it may be replaced by heightened flexor reflex activity in which exaggerated deep tendon reflexes occur in response to noxious or even trivial stimuli. A mass reflex may develop in which slight stimuli elicit severe bilateral flexor spasms of the arms and legs accompanied by evacuation of the bowel and bladder, profuse sweating and even priapism (a sustained reflexogenic erection). Reflex emptying of the bowel and bladder may also begin at this time. Autonomic reflex activity is also heightened and

so filling of the bladder or rectum may result in increased sweating, flushing of the face, piloerection, shivering, slowing of the pulse, elevation of blood pressure, etc. After 6 -12 months many of the exaggerated reflex responses wane. The mechanisms underlying all of the phenomena of spinal shock are not completely understood. In general, the initial loss of all reflexes is thought to be due to the effect of the sudden withdrawal of all supraspinal influences on the segments of the cord below the lesion. After a period of time the segmental reflex arcs reappear and become supersensitive to segmental sensory information, the effects of which easily spread to adjacent cord levels. The reflex responses are now operating without the usual controls imparted by the now absent descending pathways. Spastic paralysis follows the period of spinal shock. At first only a positive Babinski sign occurs; later the other signs appear, e.g., increased muscle tone, heightened deep tendon reflexes, disuse (slow) atrophy of muscle, and loss of superficial (abdominal and cremasteric) reflexes below the level of the lesion. There is loss of all sensation bilaterally below the level of the lesion: loss of proprioception, vibratory sense, tactile discrimination, pain, temperature, light touch, and visceral sensibility. All sensory tracts are immediately severed and if the lesion is in fact complete there is no recovery. Autonomic disturbances include bowel and bladder functions. Initially, there is retention of urine and feces, which are no longer under voluntary control. Since ascending sensory pathways are interrupted there is no awareness of bowel or bladder fullness. After several weeks hypertrophy of the smooth muscle overcomes sphincter resistance so emptying occurs when eventually those organs become overfilled (overflow incontinence). Even if there was an awareness, the absence of the descending tracts would preclude volitional control. Eventually, the bowel and bladder empty on a segmental automatic basis reflexly, when they become full. Cutaneous blood vessels in the areas below the lesion do not respond to hot or cold stimuli. Horner's syndrome (ptosis, miosis, anhydrosis) also is likely, due to the loss of the descending autonomics which are scattered among the lateral corticospinal tract fibers in the cord. A careful sensory evaluation may reveal that at the dermatomal level of the lesion there is a bilateral loss of pain and temperature sensation. Since the second order neurons from both sides cross in the midline below the central canal, a hemisection of the cord may interrupt the crossing fibers from both sides and produce this limited bilateral deficit.
3) SYRINGOMYELIA Syringomyelia refers to a cavitation of the cord characteristically originating in the central canal. The condition is frequently of congenital origin, however, it may result from defects in the vasculature, neoplasms, trauma, etc. Degeneration often occurs in the central canal of the cervical cord and progresses peripherally in an irregular fashion. Generally, the cavitation first affects the crossing spinothalamic fibers in the anterior white commissure producing segmental loss of pain and temperature sensation. As the cavitation extends it may involve

varied structures depending on the direction of the expansion. It may expand to involve the anterior horn with segmental signs of lower motor neuron disease; if the intermediolateral cell column is involved there may localized autonomic effects. When syrinx proceeds dorsally it may affect the posterior white columns leading to loss of discriminatory touch and proprioception below the level of the cavity. A Sample Case: A 30 year old man noticed a weakness of his right hand which was progressing and causing him problems serious enough to seek medical attention. On examination he demonstrated bilateral weakness, atrophy, and fasciculations of the intrinsic muscles of his hands and shoulders. Upper motor neuron syndrome signs, i.e., weakness, hypertonia, hyperreflexia, positive Babinski, were evident in both lower extremities. Dermatomes C-2 through T-6 demonstrated bilateral loss of pain and temperature sensation. There was bilateral impairment of position and vibratory sense below the hips. MRI investigation showed a central cavitation at C-2 through T-7 which expanded symmetrically in all directions. It involved the anterior white commissure (spinothalamic fibers) and included portions of the posterior white columns, lateral white funiculus, and anterior gray horns. Explanation Weakness in the right hand was the major complaint but the neurologic exam demonstrated weakness, atrophy and fasciculation indicative of lower motor neuron disease, i.e., anterior horn cells, in both hands. Though the patient had not noticed loss of pain sensation in his hands the loss could be demonstrated upon testing; apparently there was enough sparing of the crossing fibers of the spinothalamic tracts to make the effect less noticeable. Though the patient did not complain of weakness of the lower extremity, there were upper motor neuron syndrome symptoms, e.g., hyperreflexia and Babinski sign, indicating some involvement of the lateral white funiculus containing the lateral corticospinal and lateral reticulospinal tracts. The unrecognized loss of vibratory sensation from the lower extremity indicates some impact on the fasciculus gracilis. 4) VASCULAR DISEASES - ANTERIOR SPINAL ARTERY SYNDROME The spinal cord is not as susceptible to vascular disorders as the brain but infarction and hemorrhage do occur. Damage from such lesions reflects the pattern of the blood supply where a) posterior spinal arteries supply the dorsal part of the cord, 2) anterior spinal arteries supply the anterior 2/3rds of cord, and 3) the arterial vasocorona in the pial plexus supplies the periphery of the anterolateral cord. A Sample Case: A sudden bilateral weakness of the legs occurred in a young woman causing her to seek medical attention. The neurologic exam revealed bilateral loss of pain and temperature sensation in the legs without loss of discriminative touch or vibratory sense. At first the lower limb paralysis was flaccid and areflexic but after several weeks spasticity, hyperreflexia, and Babinski signs appeared. After an initial period of incontinence bowel and bladder control was regained. Explanation -

Spinal shock - An infarction of the anterior spinal artery usually involves the gray and white matter (less frequently only the gray) of the anterolateral cord. The suddenness of the lesion leads to "spinal shock" and hence the voluntary and involuntary paralyses and areflexia. With recovery from spinal shock you might expect to see evidence of lower motor neuron signs at the level of the lesion with upper motor neurons signs below. Recovery of bowel and bladder function indicates some sparing of the descending autonomic fibers which are in the lateral white funiculus, perhaps due to vessels of the pial plexus. The sensory signs, i.e, bilateral loss of pain and temperature sense, are indicative of injury to the spinothalamic tracts in the lateral white funiculi with sparing of the posterior white columns which are supplied by the posterior spinal arteries. 5) DEGENERATIVE DISEASES - POLIOMYELITIS Such diseases include a spectrum of disorders in which lesions may be widely disseminated or may more specifically affect certain tracts or cell groups. Examples include: poliomyelitis (viral) which attacks anterior horn cells; amyotrophic lateral sclerosis (etiology unknown) in which anterior horn cells as well as the corticospinal tracts are involved; tabes dorsalis (syphilis due to a spirochete infection) where there is involvement of the posterior white columns and the dorsal roots; posterolateral sclerosis (a nutritional deficiency disease associated with pernicious anemia) involving the corticospinal tracts and posterior white columns; Friedreich's ataxia (an hereditary disorder) shows degenerative changes of the posterior columns, spinocerebellar tracts, lateral white funiculus and cerebellum. A Sample Case: In the days before the polio vaccine, a 9 year old boy developed fever, headache, malaise, stiff neck, and increasing weakness of the left arm. He was admitted to the hospital where examination revealed nuchal rigidity, a flaccid paresis with muscle fasciculation, hypotonia and hyporeflexia of the left upper extremity which was most pronounced in the biceps and deltoid muscles. Clinical diagnosis was poliomyelitis with involvement limited to the anterior horn cells on the left side, principally in the C-5,6 segments of the cord. Explanation Flu-like symptoms of increased temperature, muscle ache, headache, sore throat, etc., may accompany the initial phase of the viral infection. After subsiding, these initial signs may recur along with the CNS symptoms. Stiffness of the neck on forward flexion (nuchal rigidity) indicates inflammation of the meninges. These preparalytic signs may resolve without further incident. However, muscle weakness may occur during the fever stage; the weakness may be limited to the spinal cord as in this case or also involve the brainstem. Lower motor neuron signs, e.g., coarse fasciculations are seen as the muscles weaken; atrophy and hypotonia are detectable within 3 weeks of onset due to the killing of anterior horn cells. 5) DEGENERATIVE DISEASES - AMYOTROPHIC LATERAL SCLEROSIS A Sample Case: A 30 year old man noticed that he was having trouble buttoning his shirt and began to drop items from either hand during a period of several months. A neurologic exam demonstrated weakness in all tests of motor strength in both of his hands. In addition, there was atrophy of the intrinsic muscles of the hand and fasciculations could be seen. There were hyperactive deep tendon reflexes upon testing of the biceps, patellar, and ankle reflexes. Explanation Typically, this disease first manifests itself as uselessness of the hand and awkwardness of fine finger movements. Slight atrophy of the hand usually accompanies this clumsiness along

with fasciculations in the hand and arm. These are all signs of irritation and death of anterior horn cells. Increasing spasticity and hyperreflexia of the arms and then the legs indicate involvement of the tracts of the lateral white funiculus, e.g., lateral corticospinal tract. In time, the symptoms of atrophy spread to include the muscles of the neck, tongue, pharynx, larynx and trunk. Usually control over the sphincters is maintained.

5) DEGENERATIVE DISEASES - SYPHILIS (TABES DORSALIS) A Sample Case: A 60 year old female complained of "shooting" pains in the legs and enlargement of the knee joints for about 2 years. Her physician said that she had severe arthritis. The patient began to experience difficulty walking in the dark and urinary incontinence and sought other medical advice. The neurologic exam demonstrated Argyll Robertson pupils and radiographs of the knees were consistent with arthritic "Charcot type" joints. The patellar and ankle reflexes were absent and there was loss of vibratory and position sense in the lower extremity. The patient's ataxia was evident as she walked with a broad-based gait. She was very nervous when asked to walk or stand with her eyes closed and demonstrated the Romberg sign. Explanation Syphilis is caused by the spirochete Treponema pallidum which may invade the CNS 3 - 18 months after infection. Even when clinical symptoms are referable to only one part of the nervous system post-mortem examination reveals diffuse changes in both the brain and spinal cord. In its most severe form there is progressive mental and physical deterioration. The neurologic symptoms of tabes dorsalis usually develops 15 - 20 years after infection. Ataxic gait and hyporeflexia are caused by purely sensory deficits due to irritation and destruction of the sensory afferents in the lumbosacral dorsal roots, affecting the incoming heavily myelinated proprioceptive fibers (later seen as demyelination in the posterior white columns). Dorsal root inflammation produces bouts of shooting pains, most common in the legs but they "roam" over the body from the feet to the face. Other paresthesias are described and are associated with impairment of pain, temperature and touch sensation; there is also sensory impairment from the bowel and bladder (S-2,3) accounting for the incontinence. "Charcot joints" is a neuropathic arthritis, a severe form of osteoarthritis. The arthritic knee joints result from the relative insensitivity of the joints, due to destruction of the dorsal root fibers, and the resultant repeated injury; remaining pain fibers however were still sufficient to permit pain to occur. Charcot joints occur in less than 10 percent of tabes patients. About 90 percent of the patients exhibit the Argyll Robertson pupils in which the pupils fail to constrict in reaction to light but constrict during convergence when the focus moves from a far to a near object. The cause of this response is unknown but there are usually additional signs of ophthalmoplegia and optic atrophy. 5) DEGENERATIVE DISEASES - POSTEROLATERAL SCLEROSIS A Sample Case: A 43 year old woman complained of increasing weakness of the legs and difficulty walking which developed over a period of 9 months. She felt numbness and tingling (paresthesia) in her hands and feet. The neurologic exam revealed loss of position and vibratory sense in both lower extremities. The patient stood and walked clumsily on a wide base and demonstrated the Romberg sign. There was paresis in the lower extremities, with hypertonia, hyperreflexia, and positive Babinski signs. Obvious motor signs in the upper limb were not demonstrated.

Lab studies indicated anemia and a blood smear showed large RBCs (macrocytes). Studies of stomach contents showed a small volume of gastric secretions and a higher than normal pH. The Schilling test, measuring absorption of vitamin B12, showed a decrease. Explanation Neurologic findings of faulty proprioception and paresthesia indicate involvement of the posterior white columns; motor findings indicating upper motor neuron disease implicate the corticospinal tract. The pathology is diffuse, usually symmetrical, and sometimes involves the legs before the arms. There is degeneration of myelin sheaths followed by death of the axons. These changes are scattered irregularly and usually begin in the cervical and upper thoracic segments and then spread up and down the cord. Laboratory findings of megaloblastic anemia suggest the disease of pernicious anemia. This is usually caused by an atrophic gastric mucosa which fails to secrete intrinsic factor resulting in failure to absorb sufficient quantities of vitamin B12 as required for effective erythropoiesis. B12 is also an important co-factor in synthesis of fatty acids, important building blocks of cell membranes and hence myelin; this may be the basis of the neurologic findings. 5) DEGENERATIVE DISEASES - FRIEDREICH'S ATAXIA A Sample Case: A 15 year old boy was referred to a neurologist when he complained of difficulty in running and developed a staggering gait, poor articulation in speech and clumsiness in the hands during an 8 month period. These symptoms were recalled to be like that of his uncle who became similarly disabled in his early 20's and confined to a wheelchair before finally becoming bedridden. The physical examination revealed an unsteady, broad-based stance and sudden lurching when walking which was accompanied by a "slapping" sound made by the feet. Loss of vibratory and position sense was observed bilaterally in all extremities. There was a tremor of the upper extremity as the patient reached for objects. Speech was slurred, slow and with an uneven pattern. Hyporeflexia was present but there was only a slight indication of muscle atrophy though there were bilateral Babinski signs. Explanation The findings of the exam indicate an ataxia of the sensory as well as cerebellar type; there are also indications of corticospinal tract disease. The broad-based, unsteady stance and gait are consistent with posterior white column disease as well as cerebellar disease. Slapping of the feet, to auditorily supplement sensory feedback, is consistent with patients deprived of conscious proprioception. Decreased or abolished tendon reflexes is usual with sensory deprivation due to degeneration of the dorsal roots, as occurs with posterior white column degeneration. Intention tremor and slurred speech is characteristic of patients with cerebellar disease. Positive Babinski signs indicate involvement of the corticospinal tracts. In this disorder there is usually a foot deformity called pes cavus in which there is hypertonia resulting in a high plantar arch with retraction of the toes at the metatarsal-phalangeal joints. Pathologic examination of the cord in Friedreich's ataxia indicate a small cord with degeneration in the posterior white columns, corticospinal and posterior spinocerebellar tracts. The motor cortex and cerebellum also show loss of cells. This is a hereditary progressive ataxia. About half the cases appear before the age of 10 and within 5 years of onset walking is no longer possible. There are two patterns of inheritance, one dominant the other recessive. Males are somewhat more susceptible.

5) DEGENERATIVE DISEASES - INFANTILE MUSCULAR ATROPHY (WERDNIGHOFFMAN'S DISEASE) A Sample Case: A woman with two prior pregnancies reported that the fetal movements of her third baby were less vigorous than previous fetuses. At birth the baby was weak and limp, the cry and sucking movements feeble, and respiratory movements ineffective. The baby died at 6 months. Neurologic examination showed the baby was hypotonic and weak. Muscle fasciculations were present but not visible, except for those of the tongue, because of the covering adipose tissue. Tendon reflexes were absent but normal sensory responses to pain, temperature, and touch were present. Explanation The anterior horn cells in the spinal cord and major motor nuclei of the brainstem are degenerative, dying, and reduced in number. Other systems of neurons are not affected. This is a form of infantile, hereditary, progressive, non-myopathic muscular atrophy due to death of the anterior horn cells. An adult form of this hereditary muscular atrophy, which simulates muscular dystrophy but is due to death of anterior horn cells, is the KugelbergWelander syndrome.