(e) Universal spasms, tonic, clonic, or mixed, occur in numerous diseased states—in hysteria, epilepsy, chorea, tetanus, toxic conditions, etc. A universal tonic spasm may last long enough (tetanus, epilepsy) to kill by apnœa.
(f) Localized spasms, not monoplegic, are observed. For example, the orbicularis palpebrarum may be the seat of clonic spasm, or the masseters of tonic spasm for long periods of time; the œsophagus or urethra may be temporarily closed by constriction; chorea may affect a small muscular group. A rhythmic spasm limited to a single muscle is termed myoclonus; the use of this term should not lead one to forget the nervous origin of the spasm. A localized tonic arterial spasm may be so severe and prolonged as to produce great ischæmia, even gangrene of the affected part.
(g) Fibrillary contractions, non-rhythmic contractions of fasciculi in muscles, spontaneous or provoked by direct mechanical excitation, may be considered as hyperkinesis. Subjectively, fibrillary contractions are felt as a quivering or as if a worm moved under the skin; objectively, they appear not unlike the rising and falling of a cord under the cutaneous covering. They unquestionably occur frequently in muscles which are undergoing degenerative or atrophic changes (progressive muscular atrophy), but they are also met with in cases of lead paralysis, neurasthenia, etc.
INCO-ORDINATION, or DYSKINESIS, is the condition in which volitional movements are not performed with normal precision and steadiness. Several varieties are recognized.
(a) Ataxic tremor is distinguished from common or spasmodic tremor by the fact that it is developed during the performance of a volitional act in parts which are quiet when not used. Thus, tremor appears in speaking, putting out the fingers, using the hands, etc. in the muscles actively employed, and occasionally also in others at the same time. This form of tremor is well seen in dementia paralytica, where in certain cases the patient's muscles are still until we induce him to make voluntary movements or provoke expression movements. In cases of disseminated sclerosis the same phenomenon is a characteristic symptom, a coarse tremulous ataxia or oscillatory trembling appearing whenever volitional acts are attempted. In looking, there appears nystagmus, a rhythmic ataxic tremor of some of the ocular muscles; in speaking, an irregular, jerky, slow, or syllabic speech is heard; and when the hand is carried to a given object or pointed the extremity exhibits oscillatory trembling. Common and ataxic tremors may coincide, as in some cases of dementia paralytica and in alcoholism.
(b) Ataxia is a symptom of the utmost importance, and its strict definition should be maintained. It is that form of inco-ordination in which there is want of harmony in the action of the various muscular groups employed in the voluntary performance of a given act. The simplest movement of an extremity (and more complicated ones a fortiori) is made up of simultaneous contractions of flexor and extensor muscles, often also of adductors and abductors in due proportion, so as to produce a steady position and movement of the parts. This is not accomplished by the will acting directly on the different muscles themselves, but through the medium of a co-ordinating mechanism which is strictly spinal (including the intracranial expansion of the cord as far frontad as the third ventricle), and which is educated or trained from the first days of life. We will the action and set the co-ordinating mechanism going, so that the movement is in a certain sense indirectly accomplished. Yet volition does interfere directly to a certain extent by estimating through the muscular sense, and by exerting the proper amount of force required, and by guiding the movement in a general way. The most striking peculiarity about ataxic movements is the defect in the harmonious action of the various (antagonistic) muscles employed, resulting in jerky, oscillatory, but non-rhythmic movements, constantly made worse by greater tension of the will. In simple tremor volition may for a few moments stop the movements (as best shown in paralysis agitans), while in ataxia the more the patient tries to achieve the act, the greater becomes the disorder. The anatomical fault is mostly in the spinal co-ordinating mechanism; the long-established motor and sensori-motor associations are interrupted or confused, and in some cases besides the muscular sense is impaired.5 The idea that ataxia results from faulty centripetal impressions due to various degrees of anæsthesia is certainly erroneous and misleading. In the first place, there are cases recorded in which typical ataxia of the extremities occurred without the slightest impairment of sensibility; and, secondly, neither in animals (section of posterior roots of spinal nerves) nor in man does ataxia appear as a result of anæsthesia. In this condition there is inco-ordination, to be sure, but not ataxia in the strict meaning of the term. Ataxia is nearly always a symptom of organic disease of the spinal cord, more especially posterior spinal sclerosis and diphtheritic myelitis. It may also occur from disease of the oblongata, pons, and crura cerebri. In certain cases of lesion in caudo-lateral part of the thalamus involving the caudal part of the internal capsule (irritation or partial destruction), we observe various forms of irregular movements which have been designated by Weir Mitchell as post-paralytic chorea. We long ago became satisfied that this term included quite a number of forms of inco-ordination, some cases showing choreiform and trembling movements, others ataxic tremor, true ataxia, and athetoid movements (also the true athetosis of Hammond?). It seems probable that diseases of the cerebellum, by exerting pressure on or by irritating subjacent parts, may sometimes cause pure ataxia of the extremities on the side opposite the lesion. That a strictly localized cortical lesion can give rise to ataxia we are not now prepared to admit.
5 Ataxia is greatly aggravated by closing the eyes.
(c) Uncertainty in voluntary movements is sufficiently defined by the term employed and by the absence of ataxia. This is well illustrated in those rare cases in which the muscular sense is impaired or lost: in such a case volitional movements, such as placing the fore finger on an object or fastening a button, are fairly well done with the aid of sight, but without it the hand and fingers grope almost or quite hopelessly about the object. It is important to note that persistent trying to do the act does not aggravate the disorder, but that, on the other hand, success is often achieved after feeling about. In certain cases of blindness irregular movements of the eyeball are observed, due to semi-voluntary efforts to look or to direct the eyeballs in the direction of a person or object. In states of cutaneous anæsthesia when the eyes are closed the same disorder appears in muscular movements. Claude Bernard many years ago showed that section of the posterior roots of spinal nerves in an animal was followed, not by ataxia, but by vague inco-ordination and staggering. In human cases we find that where the sensibility of one hand is lost or greatly impaired, without paralysis, there is extreme awkwardness and uncertainty in delicate muscular movements, but no ataxia. The staggering exhibited by patients having plantar anæsthesia is largely of this type: they stand fairly well while their eyes are open, but oscillate or fall when they are closed. This variety of inco-ordination may result from toxic conditions (alcohol), peripheral, neural, or central nervous disease. A few cases are on record which would seem to show that there is a centre for muscular sense in the cortex of the brain, in a part intermediate between the caudal sensory area and the central motor one—viz. in the inferior parietal lobule, supramarginal gyrus (and angular gyrus?). It has also been shown (by Spitzka and others) that there is a conduction tract for muscular sense, dorsad of the pyramidal tract in the pons and oblongata (in the stratum intermedium and interolivary tract), lesions of which produce inco-ordination (ataxia?) without marked paralysis or anæsthesia.
(d) Titubation, or staggering, is the inability to stand erect or walk straight because of impaired equilibrium. There is neither tremor nor ataxia present, and paralysis and anæsthesia are not necessary factors. It is distinguished from vertigo and dizziness by absence of subjective sensations of movement. Staggering may show itself in a general way or in the shape of latero-, retro-, or propulsion (disease of the internal ear, paralysis agitans). A well-defined variety of staggering is the wrongly-termed cerebellar ataxia. In this the patient, having disease of the cerebellum involving its vermis superior, stands with feet widely separated to increase his base of support; the body is bent somewhat forward, and the arms and hands are used as balancing-rods to maintain a sort of equipoise. In walking, this attitude is exaggerated, and if the feet be bare it will be seen that the toes are unconsciously clutching the floor for support; there is no outward jerk of the leg or stamp of the heel as in the ataxic gait, and closing the eyes does not aggravate the attitude or walk. Besides, if the extremities be separately tested, it is found that with closed eyes the patient can perfectly well place his fore-finger on his nose or one heel on the opposite patella (lying down). The proper term for the disorder is cerebellar titubation. Yet it must be remembered that titubation also occurs from disease of the oblongata and pons, from lesions of the base of the brain in general, and from alcoholic, etc. intoxication. In many cases titubation occurs in connection with vertigo or dizziness.
(e) Inco-ordination more or less of the ataxic form often affects the muscles of articulation, phonation, and deglutition, giving to the symptoms dysarthria, dysphonia, and dysphagia. Dysarthria and dysphagia are probably often caused by lesions of the insula and subjacent white substance, as well as by those affecting the oblongata. There are two recent autopsies which would indicate that there may be a cerebral cortical centre for phonation laryngeal movements: in the ventral extremity of the right third frontal gyrus—a part homologous to the speech centre on the left side of the brain. In some cases, however, dysphonia and aphonia indicate a lesion of the laryngeal nerves or of the oblongata (nucleus of NN. x. and xi.).