Recognition that paralysis resulted from injuries to the nervous system was described in the Hippocratic writings, but it was the work of three men Galen of Pergamon (130-200 ad), Andreas Vesalius (1514-1564), and Thomas Willis (1621-1675) that established the foundation of our current knowledge of the functional anatomy of weakness.1! Galen, who was also physician to the Roman emperor, Marcus Aurelius, was the first experimental physiologist. His vivisection studies on the brain established that cutting into the brain produced paralysis, but he gave undue attention to the ventricles as the source of the weakness rather than the substance of the hemispheres. Galen's experiments on the spinal cord were more definitive; he showed different levels of paralysis by sectioning different regions of the cord, including hemisections that caused paralysis on the same side of the body. Little more was added to our knowledge of the nervous system until the Renaissance anatomist Vesalius refined Galen's anatomical observations of the central nervous system (CNS) and corrected Galen's misconceptions about the function of muscles and the anatomy of nerves. Galen thought that muscles were mere protective flesh for the tendons, which produced movement when excited by the animal spirits flowing from the ventricle through hollow nerves. Vesalius recognized that Galen's "flesh" was the "particular organ of motion and not merely the stuffing and support of the fibers." He also recognized that nerves were solid, not hollow, and when ligated, produced paralysis according to which nerve was divided.
The English physician Thomas Willis recognized that weakness could result from lesions at all levels of the nervous system and that the distribution of the paralysis was determined by the site of the lesion. Charles Bell (1774-1842), and Brown-Sequard (1817-1894) further refined our understanding of the functional anatomy of paralysis, and Robert Bentley Todd (1809-1860) described epileptic hemiplegia. In more modern times, John Hughlings
Jackson contributed the concept of the hierarchical nature of the motor system, and Wilder Penfield refined the localization of motor function in the motor cortex by defining the now familiar motor homunculus by direct stimulation of the cortex in patients undergoing surgery for epilepsy.
Willis and Descartes introduced the notion of reflexes and reflex action, but until the latter half of the nineteenth century, tendon jerks and cutaneous reflexes were not appreciated as valuable aids in localizing lesions and diagnosing diseases of the nervous system. In his paper of 1875, Erb was the first to describe systematically the tendon reflexes and their exaggeration in patients with hemiplegia and paraplegia, although he acknowledged that his observations were not new to his neurological colleagues. Erb also described ankle clonus. A few years later, William Gowers noted that knee jerks were diminished or lost in diseases of the nerve roots or the muscle itself. Although the cutaneous flexor withdrawal reflex had already been described, Babinski pointed out in 1876 the diagnostic importance of the extensor response of the great toe when the sole of the foot is scratched. A few years later the brilliant English experimental neurophysiologist, Sir Charles Sherrington, defined the nature of reflex arcs and the importance of reciprocal inhibition in his landmark book, The Integrative Action of the Nervous System.y Other late nineteenth century neurologists also contributed important observations to help localize and diagnose diseases causing weakness. Charcot described the atrophy and fasciculations of muscle in amyotrophic lateral sclerosis, and Duchenne described the features of muscular dystrophy, including pseudohypertrophy.
Degrees and location of muscular weakness and changes in muscle tone are described by more or less precise terms. Paralysis refers to a complete loss of voluntary movement, whereas paresis is a reduced but not complete abolition of voluntary movement. Palsy is an older term that has been used interchangeably with either paralysis or paresis; currently, its use is confined to historical diagnoses that have been retained in conventional use such as Bell's palsy and cerebral palsy. The distribution of the paralysis or paresis is modified by the prefixes mono (for involvement of one limb), para (for involvement of both legs), hemi (for the limbs on one side of the body), and quadra or tetra (for all four limbs). A brachial paresis (or paralysis) refers to a monoparesis of an arm, and crural refers to involvement of one leg.
Changes in muscle tone that are elicited by passive movements of the limbs are described by the following terms. Flaccidity is the absence of normal muscle tone, while spasticity and rigidity are abnormal increases in muscle tone. Spasticity differs from rigidity in that it selectively increases the tone in the flexor muscles of the arm and the extensors of the leg, whereas rigidity affects flexors and extensors equally. The gegenhalten (German "hold against") phenomenon is felt as an increase in tone but is the result of resistance with an equal and opposite force by the patient to the examiner's attempt to move the limb passively.
The terms lower motor neuron and upper motor neuron are often used to differentiate two basic types of weakness: the first, due to a lesion of the motor neuron in the anterior spinal gray and its axon coursing to the muscle through the spinal roots and peripheral nerves and the second, due to a lesion that interrupts the descending motor pathways from supraspinal neurons that converge on the lower motor neuron pool. These very useful terms in clinical neurology derive from the concept that pools of upper motor neurons exist in a hierarchical order in the brain stem and motor cortex and converge via several different pathways on the lower motor neuron pool consisting of alpha and gamma motor neurons.
The neuromuscular junction is the specialized anatomical connection between the motor nerve endings and the skeletal muscle. The muscles that convert the electrical impulse into the force that produces movement is striated muscle, which is often referred to as skeletal muscle; this muscle type contrasts with smooth muscle, which responds to activation of the autonomic nervous system.
The term fatigability is used in a general sense to describe the feeling of being tired and not being able to put out full effort. It is also used more precisely to define a change in force-generating capacity of the neuromuscular apparatus brought about by muscular activity. Normal fatigue results from intense muscular contraction. When one or more muscles used in a specific task become weaker and weaker with repetitive but normal use, the phenomenon is referred to as fatigability and implies dysfunction at the neuromuscular junction.
Finally, weakness should be differentiated from dyspraxia (see Chapter.4 ). Weakness is an inability to carry out a desired movement with normal force because of a reduction in strength of the muscles necessary to carry out the movement. In dyspraxia, strength is normal, and the inability to perform a movement results from a failure in the motor centers in the cortex that plan and provide the proper commands to execute the movement.
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