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. [Footnote 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 {49} 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.