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Figure 13.22 The Flexor and Crossed Extensor Reflexes. The pain stimulus triggers a withdrawal reflex, which results in contraction of flexor muscles of the injured limb. At the same time, a crossed extensor reflex results in contraction of extensor muscles of the opposite limb. The latter reflex aids in balance when the injured limb is raised. Note that for each limb, while the agonist contracts, the a motor neuron to its antagonist is inhibited, as indicated by the red minus signs in the spinal cord.

Would you expect this reflex arc to show more synaptic delay, or less, than the ones in figure 13.15? Why?

Saladin: Anatomy & I 13. The Spinal Cord, Spinal I Text

Physiology: The Unity of Nerves, and Somatic

Form and Function, Third Reflexes Edition

508 Part Three Integration and Control extended leg. To a large extent, the coordination of all these muscles and maintenance of equilibrium is mediated by the cerebellum and cerebral cortex.

The flexor reflex employs an ipsilateral reflex arc— one in which the sensory input and motor output are on the same sides of the spinal cord. The crossed extensor reflex employs a contralateral reflex arc, in which the input and output are on opposite sides. An intersegmen-tal reflex arc is one in which the input and output occur at different levels (segments) of the spinal cord—for example, when pain to the foot causes contractions of abdominal and hip muscles higher up the body. Note that all of these reflex arcs can function simultaneously to produce a coordinated protective response to pain.

The Golgi Tendon Reflex

Golgi tendon organs are proprioceptors located in a tendon near its junction with a muscle (fig. 13.23). A tendon organ is about 1 mm long and consists of an encapsulated tangle of knobby nerve endings entwined in the collagen fibers of the tendon. As long as the tendon is slack, its collagen fibers are slightly spread and they put little pressure on the nerve endings woven among them. When muscle contraction pulls on the tendon, the collagen fibers come together like the two sides of a stretched rubber band and squeeze the nerve endings between them. The nerve fiber sends signals to the spinal cord that provide the CNS with feedback on the degree of muscle tension at the joint.

The Golgi tendon reflex is a response to excessive tension on the tendon. It inhibits a motor neurons to the muscle so the muscle does not contract as strongly. This serves to moderate muscle contraction before it tears a tendon or pulls it loose from the muscle or bone. Nevertheless, strong muscles and quick movements sometimes damage a tendon before the reflex can occur, causing such athletic injuries as a ruptured calcaneal tendon.

The Golgi tendon reflex also functions when some parts of a muscle contract more than others. It inhibits the fibers connected with overstimulated tendon organs so that their contraction is more comparable to the contraction of the rest of the muscle. This reflex spreads the workload more evenly over the entire muscle, which is beneficial in such actions as maintaining a steady grip on a tool.

Table 13.7 and insight 13.5 describe some injuries and other disorders of the spinal cord and spinal nerves.

Insight 13.5 Clinical Application

Spinal Cord Trauma

Each year in the United States, 10,000 to 12,000 people become paralyzed by spinal cord trauma, usually as a result of vertebral fractures. The group at greatest risk is males from 16 to 30 years old, because of

Golgi Tendon Organ What
Figure 13.23 A Golgi Tendon Organ.

their high-risk behaviors. Fifty-five percent of their injuries are from automobile and motorcycle accidents, 18% from sports, and 15% from gunshot and stab wounds. Elderly people are also at above-average risk because of falls, and in times of war, battlefield injuries account for many cases.

Effects of Injury

Complete transection (severance) of the spinal cord causes immediate loss of motor control at and below the level of the injury. Transection superior to segment C4 presents a threat of respiratory failure. Victims also lose all sensation from the level of injury and below, although some patients temporarily feel burning pain within one or two dermatomes of the level of the lesion.

In the early stage, victims exhibit a syndrome (a suite of signs and symptoms) called spinal shock. The muscles below the level of injury exhibit flaccid paralysis and an absence of reflexes because of the lack of stimulation from higher levels of the CNS. For 8 days to 8 weeks after the accident, the patient typically lacks bladder and bowel reflexes and thus retains urine and feces. Lacking sympathetic stimulation to the blood vessels, a patient may exhibit neurogenic shock in which the vessels dilate and blood pressure drops dangerously low. Fever may occur because the hypothalamus cannot induce sweating to

Saladin: Anatomy & I 13. The Spinal Cord, Spinal I Text I © The McGraw-Hill

Physiology: The Unity of Nerves, and Somatic Companies, 2003

Form and Function, Third Reflexes Edition

Chapter 13 The Spinal Cord, Spinal Nerves, and Somatic Reflexes 509

Table 13.7 Some Disorders of the Spinal Cord and Spinal Nerves

Guillain-Barre syndrome

An acute demyelinating nerve disorder often triggered by viral infection, resulting in muscle weakness, elevated heart rate, unstable blood pressure, shortness of breath, and sometimes death from respiratory paralysis


General term for nerve pain, often caused by pressure on spinal nerves from herniated intervertebral discs or other causes


Abnormal sensations of prickling, burning, numbness, or tingling; a symptom of nerve trauma or other peripheral nerve disorders

Peripheral neuropathy

Any loss of sensory or motor function due to nerve injury; also called nerve palsy

Rabies (hydrophobia)

A disease usually contracted from animal bites, involving viral infection that spreads via somatic motor nerve fibers to the CNS and then autonomic nerve fibers, leading to seizures, coma, and death; invariably fatal if not treated before CNS symptoms appear

Spinal meningitis

Inflammation of the spinal meninges due to viral, bacterial, or other infection

Disorders described elsewhere

Amyotrophic lateral sclerosis p. 490 Leprosy p. 589 Sciatica p. 494

Carpal tunnel syndrome p. 365

Multiple sclerosis p. 453 Shingles p. 493

Crutch paralysis p. 494

Poliomyelitis p. 490 Spina bifida p. 484

Diabetic neuropathy p. 670

Paraplegia p. 509 Spinal cord trauma p. 508

Hemiplegia p. 509

Quadriplegia p. 509

cool the body. Spinal shock can last from a few days to 3 months, but typically lasts 7 to 20 days.

As spinal shock subsides, somatic reflexes begin to reappear, at first in the toes and progressing to the feet and legs. Autonomic reflexes also reappear. Contrary to the earlier urinary and fecal retention, a patient now has the opposite problem, incontinence, as the rectum and bladder empty reflexively in response to stretch. Both the somatic and autonomic nervous systems typically exhibit exaggerated reflexes, a state called hyperreflexia or the mass reflex reaction. Stimuli such as a full bladder or cutaneous touch can trigger an extreme cardiovascular reaction. The systolic blood pressure, normally about 120 mmHg, jumps to as high as 300 mmHg. This causes intense headaches and sometimes a stroke. Pressure receptors in the major arteries sense this rise in blood pressure and activate a reflex that slows the heart, sometimes to a rate as low as 30 or 40 beats/minute (bradycardia), compared to a normal rate of 70 to 80. The patient may also experience profuse sweating and blurred vision. Men at first lose the capacity for erection and ejaculation. They may recover these functions later and become capable of climaxing and fathering children, but without sexual sensation. In females, menstruation may become irregular or cease.

The most serious permanent effect of spinal cord trauma is paralysis. The flaccid paralysis of spinal shock later changes to spastic paralysis as spinal reflexes are regained, but lack inhibitory control from the brain. Spastic paralysis typically starts with chronic flexion of the hips and knees (flexor spasms) and progresses to a state in which the limbs become straight and rigid (extensor spasms). Three forms of muscle paralysis are paraplegia, a paralysis of both lower limbs resulting from spinal cord lesions at levels T1 to L1; quadriple-gia, the paralysis of all four limbs resulting from lesions above level C5; and hemiplegia, paralysis of one side of the body, resulting not from spinal cord injuries but usually from a stroke or other brain lesion. Spinal cord lesions from C5 to C7 can produce a state of partial quadriplegia—total paralysis of the lower limbs and partial paralysis (paresis, or weakness) of the upper limbs.


Spinal cord trauma produces two stages of tissue destruction. The first is instantaneous—the destruction of cells by the traumatic event itself. The second wave of destruction, involving tissue death by necrosis and apoptosis, begins in minutes and lasts for days. It is far more destructive than the initial injury, typically converting a lesion in one spinal cord segment to a lesion that spans four or five segments, two above and two below the original site.

Microscopic hemorrhages appear in the gray matter and pia mater within minutes and grow larger over the next 2 hours. The white matter becomes edematous (swollen). This hemorrhaging and edema spread to adjacent segments of the cord, and can fatally affect respiration or brainstem function when it occurs in the cervical region. Ischemia (iss-KEE-me-uh), the lack of blood, quickly leads to tissue necrosis. The white matter regains circulation in about 24 hours, but the gray matter remains ischemic. Inflammatory cells (leukocytes and macrophages) infiltrate the lesion as the circulation recovers, and while they clean up necrotic tissue, they also contribute to the damage by releasing destructive free radicals and other toxic chemicals. The necrosis worsens, and is accompanied by another form of cell death, apoptosis (see chapter 5). Apoptosis of the spinal oligodendrocytes, the myelinating glial cells of the CNS, results in demyelination of spinal nerve fibers, followed by death of the neurons.

In as little as 4 hours, this second wave of destruction, called posttraumatic infarction, consumes about 40% of the cross-sectional area of the spinal cord; within 24 hours, it destroys 70%. As many as five segments of the cord become transformed into a fluid-filled cavity, which is replaced with collagenous scar tissue over the next 3 to 4 weeks. This scar is one of the obstacles to the regeneration of lost nerve fibers.


The first priority in treating a spinal injury patient is to immobilize the spine to prevent further injury to the cord. Respiratory or other life support may also be required. Methylprednisolone, a steroid, dramatically

Saladin: Anatomy & I 13. The Spinal Cord, Spinal I Text I © The McGraw-Hill

Physiology: The Unity of Nerves, and Somatic Companies, 2003

Form and Function, Third Reflexes Edition

510 Part Three Integration and Control improves recovery. Given within 3 hours of the trauma, it reduces injury to cell membranes and inhibits inflammation and apoptosis.

After these immediate requirements are met, reduction (repair) of the fracture is important. If a CT or MRI scan indicates spinal cord compression by the vertebral canal, a decompression laminectomy may be performed, in which the vertebral arch is removed from the affected region. CT and MRI have helped a great deal in recent decades for assessing vertebral and spinal cord damage, guiding surgical treatment, and improving recovery. Physical therapy is important for maintaining muscle and joint function as well as promoting the patient's psychological recovery.

Treatment of spinal cord injuries is a lively area of medical research today. Some current interests are the use of antioxidants to reduce free radical damage, and the implantation of embryonic stem cells, which has produced significant (but not perfect) recovery from spinal cord lesions in rats.

Before You Go On

Answer the following questions to test your understanding of the preceding section:

  1. Name five structural components of a typical somatic reflex arc. Which of these is absent from a monosynaptic arc?
  2. State the function of each of the following in a muscle spindle: intrafusal fiber, annulospiral ending, and y motor neuron.
  3. Explain how nerve fibers in a tendon sense the degree of tension in a muscle.
  4. Why must the withdrawal reflex, but not the stretch reflex, involve a polysynaptic reflex arc?
  5. Explain why the crossed extensor reflex must accompany a withdrawal reflex of the leg.

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