Muscular Sclerosis

Autonomic dysfunction

(bladder, bowel, circulatory system genital organs, sweating)

Babinski sign

(pyramidal tract lesion)

Segmental muscular atrophy

(anterior horn

Lhermitte's sign

Lesions Pyramidal Tract
Sites of spinal lesions

Localization of lesions

(left, dermatomes; right, segment-indicating muscles)

Signs

Paralysis of peripheral origin can be caused by lesions of the anterior horn (lower motor neuron, LMN), nerve root, peripheral nerve, or motor end plate and must be distinguished from weakness due to disease of the muscle itself (myopathy). Apparent weakness can also be produced by tendon rupture or injury to bones and joints.

Paralysis. Paralysis is accompanied by diminution of muscle tone (flaccidity). The extent of weakness depends on the type, severity, and distribution of LMN or myopathic involvement. Reflex abnormalities. The intrinsic muscle ren flexes are diminished or absent to a degree that .O may be disproportionate to the degree of weak-u ness: in LMN-type paralysis, loss of reflexes is § independent from the loss of strength; in my-^ opathy, it parallels the weakness. Extrinsic re-,2 flexes are unaffected unless the effector muscle S is atrophic. Pathological reflexes are absent.

Muscle atrophy. Muscle atrophy due to an LMN lesion may be disproportionate to the degree of weakness (either greater or less). Progressive atrophy of paralyzed muscles begins ca. 3 weeks after a peripheral nerve injury. The distribution and severity of muscle atrophy in myopathy depends on the etiology.

Spontaneous movements. Spontaneous movements are seen in affected muscles. Fascicula-tions are involuntary, nonrhythmic contractions of motor units in a relaxed muscle. They are not exclusively caused by anterior horn lesions. Myokymia is rhythmic contraction of muscle fibers; if the affected muscle is superficial (e. g., the orbicularis oculi), waves of muscle contraction are visible under the skin.

Lower Motor Neuron (LMN) Lesions

Anterior horn. Loss of motor neurons in the spinal cord paralyzes the motor units to which they belong. The flaccid segmental weakness may begin asymmetrically and is accompanied by severe muscle atrophy. There is no sensory deficit. The intrinsic reflexes of the affected muscles are lost at an early stage. The weakness may be 50 mainly proximal (tongue, pharynx, trunk muscles) or distal (hands, calf muscles) depending on the etiology of anterior horn disease.

Radicular syndrome. A lesion of a single ventral nerve root (caused, for example, by a herniated intervertebral disk) produces weakness in the associated myotome. Muscles supplied by multiple nerve roots are only slightly weakened, if at all, but those supplied by a single root may be frankly paralyzed and atrophic (segment-indicating muscles, cf. Table 2, p. 357). Involvement of the dorsal root produces pain and paresthesia in the associated dermatome, which may be triggered by straining (sneezing, coughing), movement (walking), or local percussion. Au-tonomic deficits are rare. Peripheral nerve. Paralysis may be caused by plexus lesions (plexopathy) or by lesions of one or more peripheral nerves (mononeuropathy, polyneuropathy). Depending on the particular segment(s) of nerve(s) affected, the deficit may be purely motor, purely sensory, or mixed, with a variable degree of autonomic dysfunction. Motor end plate. Disorders of neuromuscular transmission are typified by exercise-induced muscle fatigue and weakness. The degree of involvement of specific muscle groups (eyes, pharyngeal muscles, trunk muscles) depends on the type and severity of the underlying disease. There is no associated sensory deficit. Hy-poreflexia characteristically occurs in Lambert-Eaton syndrome and is found in myasthenia gravis to an extent that parallels weakness. Au-tonomic dysfunction occurs in Lambert-Eaton syndrome and botulism. Myopathy (see p. 52) and musculoskeletal lesions of the tendons, ligaments, joints, and bones may cause real or apparent weakness and thus enter into the differential diagnosis of LMN lesions. They cause no sensory deficit. Musculoskeletal lesions may restrict movement, particularly when they cause pain, sometimes to the extent that the muscle becomes atrophic from disuse. Severe autonomic dysfunction may also occur (p. 110).

> Purely sensory nerve

Muscle

End plate region

> Purely sensory nerve

Muscle

Radicular pain

(here due to lumbar disk herniation)

Muscle Paresis

End plate region

Radicular pain

(here due to lumbar disk herniation)

Paresis of finger extensors

(supinator syndrome in right hand)

Distal muscular atrophy Distal muscular atrophy

(here lesion of deep branch of (here polyneuropathy)

ulnar nerve)

Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

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