Journal of Neurological Sciences 155 (1998) 204–207 Optic ataxia following unilateral stroke N. Nagaratnam*, D. Grice, H. Kalouche Department of Medicine ( Geriatrics) Blacktown, Mt Druitt Health, NSW 2148, Australia Received 25 June 1997; accepted 29 August 1997 Abstract Five patients with optic ataxia together with tactile apraxia are described. They also demonstrated difficulty in finger movements under visual guidance. The CT scan showed lesions in the posterior parietal region in three and in two they were located anteriorly. It is well recognised that lesions in the posterior parietal area may cause disruption of visual guided movements. On the basis of the two cases it is postulated that the same phenomenon could occur with lesions located more anteriorly. The assumption is that optic ataxia may occur either following damage to the parieto-occipital region or to disruption of its occipitofrontal connections.  1998 Elsevier Science B.V. Keywords: Optic ataxia; Tactile apraxia; Astereognosis; Posterior watershed infarction 1. Introduction Ataxia could be due to impaired proprioception (sensory ataxia), damage to the cerebellum (cerebellar ataxia) or of the corticopontine fibres (ataxic hemiparesis) or to motor incoordination due to muscle weakness. Balint (1909) an opthalmologist used the term optische ataxie to describe a condition where there was difficulty in directing the eyes and hands to targets. Visuomotor ataxia (Rondot et al., 1977) or visuomotor apraxia (Freund, 1987) are other terms used for optic ataxia. According to Damasio and Benton (1979) it is rare as an isolated sign or may be a prominent sign in the cerebrovascular syndrome or be submerged in other abnormalities or may be missed because of lack of awareness. The diagnosis of optic ataxia requires that there is an isolated inability to point accurately to a target under visual guidance, whereas patients had no difficulty pointing to targets in their own body or garments (somatosensory guidance). They may also demonstrate difficulty in fine finger movements under visual guidance (Damasio and Benton, 1979). We wish to report *Corresponding author. Tel.: 161 2 98308000; fax: 161 2 98308020. 0022-510X / 98 / $19.00  1998 Elsevier Science B.V. All rights reserved. PII S0022-510X( 97 )00301-8 five patients with optic ataxia following a unilateral stroke and describe one in detail and discuss the pathophysiology. 2. Case reports 2.1. Case 1 JC an 80 year old previously independent and active Maltese man with background of hypertension, ischaemic heart disease, non-insulin-dependent diabetes mellitus and gout presented following a fall with inability to communicate. On presentation, he was alert, had expressive dysphasia limited to ‘no’ but was able to obey simple commands inconsistently. He was also noted to have rightsided visual inattention. He had a right sided facial droop with frontalis sparing and a weak gag reflex. He was moving all limbs with subtle right arm weakness. His reflexes were normal, symmetrical and plantar reflexes were downgoing. His pulse was 70 bpm and blood pressure was 200 / 110 mmHg. CT scan on admission showed a hypodense area in the left anterior parietal cortex (Fig. 1). ECG showed a sinus rhythm with left axis deviation, left bundle branch block and poor R wave N. Nagaratnam et al. / Journal of Neurological Sciences 155 (1998) 204 – 207 Fig. 1. CT scan of case 1 showing hypodense area in the anterior parietal region. 205 progression. Electrolytes and full blood count were unremarkable. Carotid doppler showed 34% stenosis of the left internal carotid, 48% stenosis of right internal carotid. Three days after admission, the expressive dysphasia remained, but he was able to follow commands and repetition was possible. Six days after admission, he was able to stand from a sitting position with help from one person, although he continued to neglect his right side. He could only say his first name and could reasonably consistently reply yes / no. An orthoptist review demonstrated good vision and no visual field defects. Five-finger movements were not possible and sequencing was poor and visual aided movements such as for instance touching the crossing points of several Xs were not possible bilaterally, the right more than the left. Palpatory movements were not possible. Twenty seven days after admission, monosyllable communication was possible with normal comprehension and repetition. Language dysfunction was that of transcortical motor aphasia. He had no cutaneous sensory impairment but a subtle right-sided weakness remained. Thirty days after admission repetitive movements in both hands remained clumsy, the right worse than the left and reciprocal coordination was not possible. Paper crumpling was possible with the left hand but not with the right. Buttoning was possible only with the left hand. One finger tapping was slower on the right. There was finger agnosia on the right and the patient continued to exhibit optic ataxia. Thirty four days after Table 1 Summarises the clinical and neurological findings in patients with optic ataxia JC 1) 2) 3) 4) 5) 6) 7) Age (years) / Sex Laterality Motor function Power (MRC) Sensory function Cutaneous Discriminative –Jointsense –Topographical localisation –Direct simultaneous stimulation –Stereognosis Movement of hand and fingers Alternate repetitive Purposive Paper crumpling finger tapping Explorative pattern Object bound hand movement with visual guidance (optic ataxia) Communication Speech Language 1, present or possible. 2, absent or not possible. ND, not done. N, normal. Case 1 JS Case 2 JJ Case 3 TC Case 4 SK Case 5 80 / M Left 68 / M Right 59 / M Left 56 / M Right 68 / F Right 4/5 4/5 4/5 4/5 3–4 / 5 1 1/2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 ND 2 2 2 2 2 2 2 2 2 2 2 2 2 2 N Dysphasia N N N N N N N N 206 N. Nagaratnam et al. / Journal of Neurological Sciences 155 (1998) 204 – 207 admission there was no demonstrable finger agnosia. Complex movements were not possible with the right hand, and there was poor eye / finger coordination. Tests for apraxia-transitive limb and intrasitive limb gestures, facial and complex movements (serial acts) to command and immitation were possible. 2.2. Cases 2 – 5 Table 1 summarizes the clinical and neurological findings and Fig. 2 the topography of the infarcts as revealed by computed topography. All of them could not coordinate hand and eye movements and pointed erratically at objects. They were unable to trace a hand drawing with either hand. They had minimal or no weakness or cutaneous sensory impairment but exhibited dysfunction of discriminative sensation with several disturbances of purposive behaviour of the hand during explorative finger movements and in the handling of objects. 3. Discussion Fig. 2. Diagrams of topography of infarcts revealed by computed tomography. We have described five patients with deranged reaching movements (optic ataxia) together with pronounced loss of purposive movements of the hands and fingers (tactile apraxia). Motor and cutaneous sensory deficits in all of them were none or minimal and visual fields were normal. The most obvious abnormality with optic ataxia is the difficulty in reaching target objects but patients may also exhibit impairment of executive fine finger movements under visual guidance which may involve one or both hands (Damasio and Benton, 1979) as in the case of our patient. The loss of purposive movements was traditionally called apraxia (Freund, 1987), Delay (1935) coined the term tactile apraxia for these deficits. In case 1 the optic ataxia was bilateral and more prominent on the contralateral side of the cerebral lesion, so were the purposive movements of the hands. It is well known that lesions in the parieto-occipital regions could give rise to uncoordinated volitional movements with normal visual fields (Rondot et al., 1977; Damasio and Benton, 1979). In three patients (cases 2, 4 and 5) the lesions were in the parieto-occipital regions and in the remaining two (cases 1 and 3) they were anatomically further forwards. Rondot et al. (1977) described a patient with left sided optic ataxia following surgical damage to the right occipital lobe. The impairment was seen in both hands but in the left visual field and the causative lesion was unilateral as in case 1. In the case of Damasio and Benton (1979) optic ataxia was the prominent sign following bilateral infarctions in the posterior watershed territory. Boller et al. (1975) describe a case with bilateral but asymmetric lesions, one in the left occipital region, the other in right premotor and a third in the splenium of the corpus callosum. Unilateral lesions N. Nagaratnam et al. / Journal of Neurological Sciences 155 (1998) 204 – 207 following parieto-occipital leucotomy in experimental animal studies, resulting in dissociation of the visual association areas from the premotor regions and information crossing the corpus callosum gave rise to impaired reading and hand movements (Haaxma and Kuypers, 1975). The lesions for optic ataxia could probably be located in the parieto-occipital border zones (Rondot et al., 1977; Damasio and Benton, 1979) and according to Freund (1987) tactile apraxia and optic ataxia are due to deficits of sensory guided motor behaviour due to lesions of the posterior cerebral cortex rather than to unimodal deafferentation or disconnection syndromes. However, experimental lesions in the premotor regions have produced optic ataxia in the monkey (Moll and Kuypers, 1975). In cases 1 and 3 the lesions were far forward in the parietal region. It is now believed that the supplementary motor area (SMA) contributes to the programming and initiation of movements (Roland et al., 1980) and its anatomical and physiological properties are similar to the motor cortex. Simple and repetitive movements in the hands in all our patients were slow and clumsy so was reciprocal coordination. Laplane et al. (1977) reported that the only sequel to unilateral ablation of the SMA in man was impairment of alternating hand movements especially reciprocal coordination. Although there were no direct involvement of the SMA in any of our patients, the disturbance could have resulted from interruption of the connections to the SMA. Optic ataxia and tactile apraxia could thus be attributed not only to damage to the parieto-occipital region but also to disruption of the occipito-parieto-frontal bundle. Case 1 exhibited bihemispheric dysfunction and this could be explained by possible: (1) slight mass effect on 207 the contralateral SMA; (2) existence of bilateral integration; (3) to a conjoined action of both SMA when direct unilateral limb movement is initiated (Meador et al., 1986); or (4) diaschisis effect. References ¨ ¨ Balint, R., 1909. Seelenlahmung des Schaunens, optische ataxie, raum¨ liche storung der Aufmerkasamkeit. Monatsschr. Psychiatr. Neurol. 25, 51–81. 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