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Section IV • Neuroscience

In A Nutshell

Motor end plate of skeletal muscles

UMN, upper motoneuron; LMN, lower motoneuron

Intermediate Zone

Theintermediate zone ofthe spinal cord from Tl to L2 contains preganglionic sym­ pathetic neuron cell bodies and Clarke nucleus, which sends unconscious proprio­ ception to the cerebellum.

NEURAL SYSTEMS

There are 3 major neural systems in the spinal cord that use neurons in the gray matter and tracts or fasciculi of axons in the white matter. These neural systems have components that can be found at all levels of the CNS from the cerebral cortex to the tip ofthe spinal cord. An understanding of these 3 neural systems is essential to understanding the effects oflesions in the spinal cord and brain stem, and at higher levels of the CNS.

Motor System

Voluntaryinnervation ofskeletal muscle

Upper and Lower Motoneurons

Two motoneurons, an upper motoneuron and a lower motoneuron, together form the basic neural circuit involved in the voluntary contraction of skeletal muscle everywhere in the body. The lower motoneurons are found in the ven­ tral horn ofthe spinal cord and in cranial nervenuclei in thebrain stem. Ax­ ons of lower motoneurons of spinal nerves exit in a ventral root, then join the spinal nerve to course in one of its branches to reach and synapse directly at a neuromuscular junction in skeletal muscle. Axons of lower motoneurons in the brain stem exit in a cranial nerve.

To initiate a voluntary contraction of skeletal muscle, a lower motoneuron must be innervated by an upper motoneuron (Figure IV-4-3). The cell bodies ofupper motoneurons are found in the brain stem and cerebral cortex, and their axons descend into the spinal cord in a tract to reach and synapse on lower motoneurons, or on interneurons, which then synapse on lower motoneurons. At a minimum, therefore, to initiate a voluntary contraction of skeletal muscle, 2 motoneurons, an upper and a lower, must be involved. The upper motoneuron innervates the lower motoneuron, and the lower motoneuron innervates the skeletal muscle.

The cell bodies of upper motoneurons are found in the red nucleus, reticular for­ mation, and lateral vestibular nuclei of the brain stem, but the most important

location ofupper motoneurons is in thecerebralcortex. Axons of these cortical neurons course in the corticospinal tract.

Both ends ofthe muscle spindle are connected in parallel with the extrafusal fibers, so these receptors monitor the length and rate of change in length of extrafusal fibers. Muscles involved with fine movements contain a greater density of spindles than those used in coarse movements.

Commonlytested muscle stretch reflex.es

The deep tendon (stretch, myotatic) reflex is monosynaptic and ipsilateral. The afferent limb consists of a muscle spindle, Ia sensory neuron, and efferent limb

(lower motor neuron). These reflexes are useful in the clinical exam.

Muscle stretch (myotatic) reflex

1be muscle stretch (myotatic) reflex is the stereotyped contraction of a muscle in response to stretch of that muscle. The stretch reflex is a basic reflexthat oc­ curs in allmuscles and is the primary mechanism for regulating muscle tone.

Muscle tone is the tension present in all resting muscle. Tension is controlled by the stretch reflexes.

The best example of a muscle stretch or deep tendon reflex is the knee-jerk re­ flex. Tapping the patellar ligament stretches the quadriceps muscle and its muscle spindles. Stretch of the spindles activates sensory endings (Ia afferents), and af­ ferent impulses are transmitted to the cord. Some impulses from stretch recep­ tors carried by Ia fibers monosynaptically stimulate the alpha motoneurons that supply the quadriceps. This causes contraction ofthe muscle and a sudden exten­ sion of the leg at the knee. Afferent impulses simultaneously inhibit antagonist muscles through interneurons (in this case, hamstrings).

Inverse muscle stretch reflex

The inverse muscle stretch reflex monitors muscle tension. This reflex uses Golgi tendon organs (GTOs). These are encapsulated groups of nerve endings that ter­ minate between collagenous tendon fibers at the junction of muscle and tendon. GTOs are oriented in series with the extrafusal fibers and respond to increases in force or tension generated in that muscle. Increases in force in a muscle increase the firing rate of lb afferent neurons that innervate the GTOs, which, in turn, polysynaptically facilitate antagonists and inhibit agonist muscles.

Muscle tone and reflex activity can be influenced by gamma motoneurons and by upper motoneurons. Gamma motoneurons directly innervate the muscle spindles and regulate their sensitivity to stretch. Upper motoneurons innervate gamma motoneurons and also influence the sensitivity of muscle spindles to stretch. Stimulation of gamma motoneurons causes intrafusal muscle fibers lo­ cated at the pole of each muscle spindle to contract, which activates alpha moto­ neurons, causing an increase in muscle tone.

Chapter It • The Spinal Cord

MEDICAL 365

Section IV • Neuroscience

Clinical Correlate

Tabes patients present with paresthesias (pins-and-needles sensations), pain, polyuria, Romberg sign.

Clinical Correlate

Spastic bladder results from lesions of the spinal cord above the sacral spinal cord levels. There is a loss of inhibition of the parasympathetic nerve fibers that innervate the detrusor muscle during the filling stage. Thus, the detrusor muscle responds to a minimum amount of stretch, causing urge incontinence.

Clinical Correlate

Atonic bladder results from lesions to the sacral spinal cord segments or the sacral spinal nerve roots. Loss of pelvic splanchnic motor innervation

with loss of contraction of the detrusor muscle results in a full bladder with a continuous dribble of urine from the bladder.

378 MEDICAL

Brown-Sequardsyndrome

Hemisection of the cord results in a lesion of each of the 3 main neural systems: the principal upper motoneuron pathway of the corticospinal tract, one or both dorsal columns, and the spinothalamic tract. The hallmark of a lesion to these 3 long tracts is that the patient presents with 2 ipsilateral signs and one contralat­ eral sign. Lesion of the corticospinal tract results in an ipsilateral spastic paresis below the level of the injury. Lesion to the fasciculus gracilis or cuneatus results in an ipsilateral loss ofjoint position sense, tactile discrimination, and vibratory sensations below the lesion. Lesion ofthe spinothalamic tract results in a contra­ lateral loss of pain and temperature sensation starting one or 2 segments below the level of the lesion. At the level of the lesion, there willbe an ipsilateral loss of allsensation, including touch modalities as well as pain and temperature, and an ipsilateral flaccid paralysis in muscles supplied by the injured spinal cord seg­ ments (Figure IV-4-15).

Polio

a.Flaccid paralysis

b.Muscle atrophy

c.Fasciculations

d.Areflexia

e.Common at lumbar levels

Tabes Dorsalis

a."Paresthesias, pain, polyuria"

b.Associated with late-stage syphilis, sensory ataxia, positive Romberg sign: sways with eyes closed, Argyll Robertson pupils, suppressed reflexes

c.Common at lumbar cord levels

Amyotrophic Lateral Sclerosis (ALS)

a.Progressive spinal muscular atrophy (ventral horn)

b.Primary lateral sclerosis (corticospinal tract)

•Spastic paralysis in lower limbs

•Increased tone and reflexes

•Flaccid paralysis in upper limbs

c.Common in ceNical enlargement

Anterior Spinal Artery (ASA) Occlusion

a.DC spared

b.All else bilateral signs

c.Common at mid thoracic levels

d.Spastic bladder

Figure IV-4-1 8. Lesions of the Spinal Cord I

Subacute Combined Degeneration

a.Vitamin 812, pernicious anemia

b.Demyelination of the:

•Dorsal columns (central and peripheral myelin)

•Spinocerebellar tracts

•Corticospinal tracts (CST)

c.Upper thoracic or lower cervical cord

Syringomyelia

a. Cavitation of the cord (usually cervical) b. Bilateral loss of pain and temperature at

the level of the lesion

c.As the disease progresses, there is muscle weakness; eventuallyflaccid paralysis and atrophy of the upper limb muscles due to destruction of ventral horn cells

Hemisection: Brown-Sequard Syndrome (cervical)

Figure IV-4-1 9. Lesions of the Spinal Cord II

Poliomyelitis

Poliomyelitis results from a relatively selective destruction oflower motoneurons in the ventral horn by the poliovirus. The disease causes a flaccid paralysis of muscles with the accompanying hyporeflexia and hypotonicity. Some patients may recover most function, whereas others progress to muscle atrophy and per­ manent disability (Figure IV-4-18).

Amyotrophic lateralsclerosis

Amyotrophic lateral sclerosis (ALS, Lou Gehrig disease) is a relatively pure mo­ tor system disease that affects both upper and lower motoneurons. The disease typically begins at cervical levels of the cord and progresses either up or down the cord. Patients present with bilateral flaccid weakness of the upper limbs and bilateral spastic weakness of the lower limbs. Lower motoneurons in the brainstem nuclei may be involved later (Figure IV-4- 18).

Chapter 4 • The Spinal Cord

Clinical Correlate

Subacute combined degeneration patients present paresthesias, bilateral spastic weakness, Babinski signs, and antibodies to intrinsic factor.

Clinical Correlate

Syringomyelia may present with hydrocephalus and Arnold-Chiari II malformation.

Note

Syringomyelia results in a "belt-like" or "cape-like" loss of pain and temperature.