Orthopedic and Neurologic Procedures in Chiropractic

Orthopedic and Neurologic Procedures in Chiropractic

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We would all like to thank Dr. Richard C. Schafer, DC, PhD, FICC for his lifetime commitment to the profession. In the future we will continue to add materials from RC’s copyrighted books for your use.

This is Chapter 3 from RC’s best-selling book:
“Basic Chiropractic Procedural Manual”

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Chapter 3: Orthopedic and Neurologic Procedures in Chiropractic

This chapter presents the general diagnostic methods currently used in differential diagnosis of selected orthopedic and neurologic conditions.

SELECTED NEUROLOGIC PROBLEMS

Overview

The typical patient presents the challenge of differential diagnosis of a number of neurologic conditions. These range from a variety of peripheral neuritides that may be completely reversible to serious degenerations of the central nervous system.

The tendency of the geriatric patient to develop neurologic problems is often related to the aging process: loss of tissue elasticity, particularly that of the musculoskeletal system. This is manifested by greater rigidity of the spinal column with the appearance of fixation subluxations. These, together with dehydration and subsequent thinning of the intervertebral discs, predispose to radiculitis, neuritis, and vasomotor disturbances and metabolic effects on the cord and brain. The neurologic disturbances can be superimposed on already degenerating arteriosclerotic vessels and alter metabolism of the gastrointestinal and other systems, which may cause serious problems unless recognized early and prompt corrective measures are administered.

Types of Neuritides

Peripheral Neuritis

Peripheral neuritis is a general peripheral neuritis such as that which may be present in such disorders as diabetes, anemia, and vitamin deficiency. Diminution of all sensation will be noted, with proprioception affected most. A stocking distribution with an ill-defined border is commonly witnessed. Glove distribution may appear later, along with paresthesias in the distal areas of sensory distribution. The clinical picture does not conform to either dermatome or nerve patterns of distribution. The cause for this is unknown.

Local Neuritis

Acute.   Pain and hyperalgesia are witnessed in the area of nerve distribution, along with tenderness on palpation of the nerve trunk and muscles supplied by the nerve. One or more trigger points may be found. Reflexes are either unaffected or possibly increased.

Chronic.   Paresthesias are reported over the area of nerve distribution, along with tenderness over nerve fibers and muscles supplied by the involved nerve. Hypoesthesia and hypoalgesia are usually present. Diminished reflexes and motor weakness of muscles supplied by affected nerve are typical.

Radiculitis.   Paresthesia and sensory changes are witnessed similar to those present in neuritis, but the area affected corresponds to the dermatome, myotome, or sclerotome of affected roots. Coughing, straining, jugular compression, and other causes of increased cerebral spinal fluid pressure increase symptoms. In chronic cases, there may be paresis of muscles partly supplied by the affected root but not overt paralysis.

Disassociated Anesthesias in Cord Lesions

Unilateral partial loss of sensation requires complete sensory evaluation of the area of complaint and contralateral side. For example, loss of proprioception in one leg with retention of pain, temperature, and light touch sensation in the same leg, but loss of pain, temperature, and light touch sensation with retention of proprioception in the opposite leg can only occur with an unilateral cord lesion. A classic example is seen in the Brown-Sequard syndrome of hemisection of the cord. This is the result of interruption of the gracilis pathway that runs ipsilateral in the cord and interruption of the spinothalamic tract that lies contralateral in the cord. Other patterns of disassociated anesthesias from cord lesions include:

Syringomyelia.   The typical signs are a shawl loss of pain, temperature, and epicritic sense.

Subacute combined degeneration of the cord.   Bilateral reduction of proprioception and decrease of pain, temperature, and epicritic sense, particularly in the feet and hands are typical, as is a bilateral increase in myotactic reflexes.

Tabes dorsalis.   Bilateral loss of proprioception manifested by locomotor ataxia, and loss of position and vibratory senses with retention of pain, temperature, and light touch are typical.

Cervical Lesions and Cerebral Vasomotor Disturbances

The course of the vertebral arteries through the foramen transversarium and over the arch of the atlas and their frequent inequality of size predispose them to compression and vasomotor disturbances when cervical subluxation exists. Manifestation of cerebral vasomotor disturbances is presented chiefly as alterations of motor function.

The Pyramidal System

The pyramidal system is composed of upper motor neurons that extend from the motor area of the cerebral cortex through the internal capsule, the basilar parts of the mesencephalon and pons, the pyramid of the medulla where the majority of the fibers decussate to the opposite side, and the posterior portion of the lateral funiculus of the cord. Lesions anywhere along this pathway result in symptoms of an upper motor neuron lesion. These include:

Spastic Paralysis.   The affected part is in firm contraction and efforts to move it are greatly resisted.

Hyperactive Myotactic Reflexes.   These refer to the tendon stretch reflexes in the affected area. The biceps, triceps, quadriceps, or Achilles reflexes are exaggerated when compared with the unaffected side or with the normal when both sides are involved.

Pathologic Reflexes.   These responses appear only with a pyramidal tract lesion. The classical response is the Babinski reflex where the great toe dorsiflexes and the remaining toes fan in abduction when the bottom of the foot is firmly stroked from the heel to the base of the great toe. Similar responses may be elicited by squeezing the Achilles tendon (Schaeffer’s sign), by squeezing the calf muscles (Gordon’s sign), by stroking near the lateral maleolus (Chaddock’s sign), or by stroking downward on the tibia (Oppenheim’s sign). In contrast, lower motor neuron lesions show flaccid paralysis, decreased or absent reflexes, muscle atrophy, and reaction of degeneration appearing in 10–14 days.

The Extrapyramidal System

Basal ganglia lesions are characterized by hypertonic muscles, rigidity, uncontrolled and involuntary movements, resting tremor, an attitude of flexion, and a festination gait. The rigidity is of the “lead pipe” type where passive movement is resisted but can be achieved. In moving the part, there is a “cog-wheel” effect; and clonus can be demonstrated at the ankle, patella, or wrist, depending on the site of the lesion.

Cerebellar Lesions

These lesions are characterized by a lack of coordination, an intention tremor, disturbances of equilibrium, and nystagmus. In contrast to most lesions of the brain, cerebellar symptoms are ipsilateral with the lesion. Tests for cerebellar function include Romberg’s, finger-to-finger, finger-to-nose, and heel-to-shin tests, along with rapid pronation and supination of hands, attempting to drum rhythmically on a desk top, and the ability to quickly stop a movement as in Holmes’ rebound phenomenon. Nystagmus, when present, shows the fast component when looking toward the side of the lesion.

Localizing Symptoms and Signs of Intracranial Lesions