(b) Exaggeration of reflex actions. This is due, theoretically, to any condition which increases the excitability of the reflex arc, but practically and usually the cause of the increase is more or less complete removal of the inhibitory supraspinal or cerebral influence. The reflex arc itself remains structurally sound, but its function is abnormally active. Thus, we meet with the most exquisite exhibition of exaggerated reflexes in the paralyzed part after a transverse lesion of the dorsal part of the cord. The lesion cuts off all communication between the lumbar enlargement and the brain; no sensations pass to consciousness, and no volitional influence can be exerted upon the legs; yet the legs are abnormally active, the least touch on or pricking of the skin, tapping a tendon, handling a joint, the pressure of feces in the rectum, etc., produce more or less violent spasmodic movements of mixed clonic and tonic forms (spinal epilepsy). Increased knee-jerk, foot-clonus, and epileptoid trepidation are also present. Other proofs that removal of the inhibitory cerebral influences is the chief cause of increase of spinal reflexes are given by the history of various cerebral diseases. Thus, in hemiplegia with secondary contracture the cutaneous and tendinous reflexes on the paralyzed side are much exaggerated; in dementia paralytica, as a rule, the patellar reflex is increased on both sides; and in cerebral neurasthenia all reflexes are often extremely great.
A variety of increased tendon reflex is known as clonus—a series of rhythmic clonic muscular contractions set up by stretching the body and tendon of a muscle. This is best studied at the ankle. By holding the patient's leg nearly extended upon our left hand, and rather suddenly forcing back the foot (dorsal flexion) by pressing under the ball of the foot with our right hand, a series of oscillations or to-and-fro movements of the ankle-joint are produced for a few moments (ankle- or foot-clonus). Sometimes the same rhythmic clonic contractions may be produced in the quadriceps by quickly pulling down the patella with the leg semi-extended.
In some instances, together with great increase of tendon reflex, we observe a transfer of the centrifugal impulse to other nerves of the same extremity, or across the spinal cord to nerves and muscles of the homologous limb.
Another interesting manifestation of morbid reflex movements is the defensive tonic spasm of muscles about a diseased joint (of the hip-muscles in coxitis, of vertebral muscles in Potts' disease). This constitutes a valuable symptom for the differential diagnosis between articular and neural diseases in certain cases.
Clinically, increase of reflex action is not as valuable an indication as its absence, many healthy persons having high reflexes. Still, when studied comparatively as to topography (comparing the two sides of the body) and as to variations at different times in a given case, the symptom is of considerable assistance.
IV. Trophic Symptoms.
Our present knowledge of this great group of symptoms of nervous disease is in a somewhat chaotic state; and although we possess a large accumulation of facts of this category, their classification is incomplete and their explanation is for the most part theoretical and unsatisfactory. The following subdivisions may be made to include all the phenomena, and is sufficient for clinical purposes:
1. DEGENERATIVE ATROPHY, as distinguished from the simple atrophy of insufficient nutrition, of disuse of the parts, and of retarded growth, includes all those trophic symptoms in which, under the influence of nervous disease, the solid tissues exhibit histological and chemical alterations as well as reduction of volume. The principal factor of this group is—
(a) Muscular atrophy due to lesions of some part of the nervous apparatus (thus excluding directly traumatic or inflammatory atrophy), as seen in the course of progressive muscular atrophy, of various forms of poliomyelitis, of lead paralysis, of neuritis, and injuries of nerves. These muscular atrophies are characterized by reduction in the size of the affected muscles, by altered electrical reactions, and by histological changes. Reduction in size may affect one muscle or a muscular group shortly after paralysis (as in poliomyelitis, lead paralysis, affections of nerve-trunks), or without evident paralysis it may involve only small fasciculi of a muscle at a time (as in progressive muscular atrophy); so that we speak of diffused and fascicular atrophy, of secondary (post-paralytic) and primary atrophy. In some cases the wasting proceeds to such a degree that apparently no muscular tissue remains, and the skin seems to rest directly on the bones; in others the reduction in bulk is moderate, and is compensated by increase in the intra- and extra-muscular fat (thus in stout children the atrophy of severe poliomyelitis may be quite masked to the eye); in still another category the increase in connective tissue with fatty accumulation overbalances the muscular wasting, and we have the pseudo-hypertrophic condition. Alterations in electro-muscular contractility are most important signs of impaired muscular innervation and nutrition. They present numerous and somewhat complicated variations of value for diagnosis and prognosis, but which cannot here be noticed at length. The general principle underlying these variations is this: that a muscle deprived of its normal innervation (centrifugal or motor) soon loses its capacity to respond to the induced (faradic) current, and reacts in an abnormal way to the galvanic current. This constitutes the reaction of degeneration of Erb.6 The chief abnormality in the galvanic reaction of a paralyzed and diffusely atrophied muscle is its slow or wave-like contraction, which on a graphic, or even to the observer's eye, presents a striking contrast to the sharp, jerking, complete contraction of a healthy muscle. Besides, the reactions to the two poles become equal, or even reversed, so that we may obtain in testing by the polar method such formulas as CaCC = AnCC, or CaCC < AnCC. With reference to the failure of atrophied muscles to respond to the induced or faradic current, this qualification must be added: If the poles are applied on the moistened skin, as usual in testing or treating cases, no reaction occurs even with most intense currents; but if a needle be made one pole of the battery and inserted into the affected muscle, slight and limited contractions may be obtained with a moderate current for many months. Of this we have repeatedly satisfied ourselves in cases of poliomyelitis, lead paralysis, and traumatic peripheral paralysis. In the later stages of diffused paralytic atrophy, after an uncertain number of years, no reaction can be obtained with either electrical current. In fascicular non-paralytic muscular atrophy (as in progressive muscular atrophy) the loss of faradic contractility is only demonstrable in the affected fasciculi, good contractions being obtained in adjacent healthy fasciculi of the same muscle. The amount or extent of contraction varies pari passu with the progress of the atrophy. The galvanic reactions of this form of muscular atrophy are not yet well established. Muscles and muscular groups in a condition of impaired nutrition exhibit at an early period an interesting condition—viz. that they no longer contract by reflex excitation. Thus in a case of infantile poliomyelitis with paralysis of the muscles of the leg, these muscles no longer contract when the sole of the foot is tickled, and if the thigh-muscles are affected even so slightly as to appear of normal size and consistence, the patellar reflex is found wanting. In these and in traumatic cases the reflex act is prevented by lesion of the centrifugal motor nervous apparatus, and perhaps also by the associated muscular trophic alterations.
6 Conveniently expressed by the symbol De R.