3rournal ofNeurology, Neurosurgery, and Psychiatry 1995;59:531-533 531 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.5.531 on 1 November 1995. Downloaded from SHORT REPORT

Parietal kinetic without proprioceptive deficit

J Ghika, J Bogousslavsky, A Uske, F Regli

Abstract We have been able to study a patient pre- A patient with acute onset "classic" senting with classic kinetic of cerebellar ataxia of the right arm without the right arm, without clinically detectable clinically detectable deep sensory loss is deep sensory loss, and a minimal corti- reported, in relation to an acute poste- cospinal deficit, who was found to have a pos- rior parietal infarct. Wild back and forth terior parietal infarct. swaying of the arm, giving away, or worsening by suppression of vision were not seen. The lesion involved area 5, Patient history and study parts of area 7, the , the A 45 year old patient, with a history of recur- middle and posterior parieto-occipital rent transient ischaemic attacks (two hour gyri, and posterior parts of the superior right hemianopia in January 1992, transient and middle temporal gyri. The paracen- paraesthesia of the right hand in July 1992 tral lobule, commonly thought to be and on 1 March 1993), experienced pro- responsible for parietal ataxia, was nounced clumsiness of the right hand on 6 spared. Thus posterior parietal lesions March 1993 accompanied by a two minute can mimick cerebellar ataxia, possibly by feeling of tingling on the left lower hemiface severing specific projections to the ven- and a left temporal pulsating headache. trolateral thalamic nuclei. On the basis These had disappeared except for the clumsi- ofprevious studies in primates, the supe- ness when he consulted our emergency unit a rior parietal gyrus may play a major part few hours later. in the ataxia presented by this patient. On physical examination, a minimal slow , no weakness, but decreased (J Neurol Neurosurg Psychiatry 1995;59:531-533) fine motility and hypotonia were noted on the right upper limb. On the finger to nose test,

there was hypermetria with both undershoot- http://jnnp.bmj.com/ Keywords: parietal stroke; cerebellar ataxia ing and overshooting of the target index finger, asynergia and dyschronometria, Ataxic can be caused by lesions uncontrolled rebound, and dysdiadochokine- in the pons, internal capsule, corona radiata, sia. Rhythmic movements of the right hand thalamus, and frontal and parietal lobes.'-5 were grossly abnormal, and the patient was Pure hemiataxia has been described associ- unable to clap loudly using the right hand ated with lesions in the or its and left palm. All these tests were no worse pathways, in the thalamus,3 internal capsule with the eyes closed, and entirely normal on on September 29, 2021 by guest. Protected copyright. or corona radiata,' and .6 the left side. Slow distal motility with an Proprioceptive or sensory ataxia from periph- equivocal plantar response without ataxia eral nerve7 or posterior column involvement 8 were the only findings on the right lower may be difficult to distinguish clinically from limb. No static ataxia, ataxic gait, dysarthria, cerebellar ataxia, but it generally gets worse if or ataxic or abnormal eye movements were the visual control is suppressed. Parietal noted. On careful repetitive examinations, ataxia or "pseudocerebellar ataxia",69'0" has there was no abnormality in any epicritic, been considered as a particular type of protopathic, or discriminative sensory modal- Service de Neurologie proprioceptive ataxia, well described by ity, and no sensory extinction, neglect, or and Service de Radiologie, CHWV, Critchley" with "decomposition of move- allaesthesia on the right hemibody. Visual CH-1011 Lausanne, ment, hypometria and hypermetria, and fields on Goldmann perimetry showed mini- J Ghika intention ," "swaying movements and mal lower quadrantanopia. Sensory evoked J Bogousslavsky A Uske falling away of the outstretched hand"; on potentials from both upper and lower limbs F Regli attempting to touch an object the arm were normal on both sides. Neuro- Correspondence to: "swayed widely back and forth"; in finger to psychological examination showed only some Dr J Ghika, Service de nose was cerebellar in and decreased inci- Neurologie, CHWV, BH 13, testing, there "marked difficulty programming CH-1O1 1 Lausanne, ataxia", with the limb "rather hypotonic"; tation for speech. Switzerland. "rapidly alternating movements were per- On day 4, CT showed a corticosubcortical Received 2 May 1995 and in was lesion on the left side, hyperintense revised form 17 July 1995 formed badly", and there "considerable parietal Accepted 1 August 1995 ataxia on the heel-knee test". with contrast, and there was a left posterior 532 Ghika, Bogousslavsky, Uske, Regli J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.5.531 on 1 November 1995. Downloaded from Reconstruction of the MRI lesions showing R L involvement of the superior parietal gyrus (A,B,C,D,H,I), the angular gyrus (A, B, E, F), the parieto-occipital gyrus (D,E,F), posterior parts of the superior and medium temporal gyri (E,F,G), and the inferior parietalgyrus (E,F,G). The and the primary sensory areas in the are not involved. A B C

D E F http://jnnp.bmj.com/

G H I on September 29, 2021 by guest. Protected copyright. temporal arachnoid cyst. Brain MRI on day 6 Discussion showed an increased signal in parietal vascu- Parietal ataxia is generally considered to lar border zones involving most of the supe- result from the loss of proprioceptive feed- rior and parts of the inferior parietal gyri, the back inputs interfering with the smooth exe- angular supramarginal, anterior and posterior cution of motor functions. The clumsiness temporoparietal gyri, and the upper and pos- can be increased by suppression of vision, terior regions of the superior and medial tem- motions can be disrupted by wild, uncor- poral gyri and their underlying white matter; rected oscillations and giving way of the limb, the paracentral lobule and inferior parietal which makes a clearly recognisable clinical gyri were preserved (figure). MR angiography picture at bedside examination. and conventional angiography showed a 70% Here we describe an entirely different clini- stenosis of the right internal carotid artery at cal presentation; our patient showed all the the carotid syphon. No lesion or atrophy clinical features of an acute classic cerebellar could be seen in the cerebellum or its path- kinetic ataxia of the right upper limb, without ways in the brainstem, in the thalamic nuclei, deep sensory loss. This was associated with a or elsewhere in the white matter. Echo- posterior, probably watershed, parietal cardiography, ECG, and analysis of CSF infarct, involving the superior and parts of the were all normal. No follow up could be inferior parietal gyri, but preserving the para- obtained. central lobule supposedly responsible for Parietal kinetic ataxia without proprioceptive deficit 533 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.5.531 on 1 November 1995. Downloaded from parietal ataxia. No lesion was seen in the patient reported before ataxia, but primary cerebellum, brainstem, or in the sensory areas were not involved. in any reconstructions and thin slices of the In conclusion, patients with posterior pari- MRI. etal lesions can present with classic cerebellar This clinical picture hardly fits with ataxic kinetic ataxia without positional loss. Our hemiparesis, occasionally described with pari- case could be explained by the lesion of a spe- etal lesions, because the lower limb is gener- cific projection of the parietal lobe into the ally more severely involved and the motor cerebellothalamic pathways, probably from deficit is more prominent.' 2 The absence of area 5, as suspected in primates,'3 15 separated the typical axial and postural features and of from the proprioceptive elementary and com- any abnormal signal in the frontal lobes rules plex projection areas, with resulting cerebel- out frontal ataxia.'2 Proprioceptive ataxia78 lar-like ataxia without sensory loss. This cannot be considered as there was no posi- represents a new clinical picture. tional sense deficit detectable by detailed physical examination and sensory evoked 1 Fisher CM, Cole M. Homolateral ataxia and crural pare- potentials, and no worsening of the ataxia sis, a vascular syndrome. Jf Neurol Neurosurg Psychiatry, 1965;28:48-55. with the eyes closed. 2 Moulin T, Bogousslavsky J, Chopard JL, et al. Vascular We think that this unique case makes an ataxic hemiparesis: a re-evaluation. Jf Neurol Neurosurg important Psychiatry 1995;58:422-7. contribution to our understanding 3 Melo TP, Bogousslavsky J, Moulin T, Nader J, Regli F. of parietal sensorimotor integration, because Thalamic ataxia. J Neurol 1990;21:24-33. it points to a 4 Nicolesco J, Cretu V, Demetresco L. Syndrome de l'artere strategic location for ataxia inde- cerebrale anterieure. Monoplegie crurale droite avec pendently of postural loss in the parietal lobe. symptomatologie cerebelleuse preponderante. Bulletin de la Societe Midicale de Hopitaux di Bucarest 1920;10: In primates, the equivalent of area 5 of 247-50. humans is the main parietal area to project to 5 Yagnik PM, Dhaduk V, Huen L. Parietal ataxic hemipare- sis. Eur Neurol 1988;28:164-6. the ventrolateral nucleus of the thalamus, in 6 Gerebetzoff MA. Le probleme de la localisation et des the exact same region which receives fibres ataxies corticales comme conclusion a des recherches anatomo-experimentales. Journal Belge di Neurologie et from the cerebellum and the motor cor- Psychiatnie 1938;38: 108-32. tex.13-15 Moreover, through the pontine 7 Dalakas M. Chronic idiopathic ataxic neuropathy. Ann nuclei, Neurol 1986;19:545-54. a cerebellothalamoparietal pathway 8 Hainline B, Tuszynski MH, Posner JB. Ataxia in epidural has been described which could account for cord compression. Neurology 1992:42:2193-5. 9 Andre Thomas, Levy-Landry M. Monoplegie pure du the cerebellar ataxia presented by our membre superieur, motrice et sensitive dissociee. patient.'5 There was little involvement of the Distribution pseudo-radicualire des troubles de la sensi- inferior parietal bilite. Rev Neurol 1914;1:307-10. gyrus (area 7), supposedly 10 Claude H, Lhermitte J. Les paralysies cerebello-spasmod- responsible for visually guided movements, iques et ataxo-cerebello-spasmodiques consecutives aux lesions bilaterales des lobules paracentraux par projec- and there was no visuomotor ataxia.'6 The tile de guerre. Bulletin de la Societi Midicale de Paris paracentral lobule, considered as responsible 1916;40:798-804. 11 Critchley M. The parietal lobes. London: Macmillan, 1953: for the "pseudocerebellar ataxic parietal syn- 160-1. drome",9 1017-20 was clearly not involved in our 12 Bruns L. Uber Storungen der Gleichgewichtes bei Stirnhirntumoren. Dtsch Med Wochenschr 1892;18: patient. This shows that proprioceptive 138-40. deficits are not necessary for parietal ataxia, 13 Petras J. Connexions of the parietal lobe. J Psychiatr Res 1971;8:189-201. but when added, the motions take a more 14 Chow KL. A retrograde cell degeneration study of the uncontrolled and bizarre expression, typical cortical projection field of the pulvinar in the monkey. J Comp Neurol 1950;93:313-40. of the syndrome described by Critchley," 15 Wiesendanger RM, Wiesendanger M, Ruegg DG. An http://jnnp.bmj.com/ with "wild large oscillations", "falling" and anatomical investigation of the cortico-pontine projec- tion in the primate (Macaca fascicularis and Saimiri sci- "swaying away" and "back and forth" of the ureus) II: the projection from frontal and parietal outstretched arm, the position of which is association areas. Neuroscience 1979 4:747-65. 16 Pierrot-Deseilligny C, Gray F, Brunet P. Infarcts of both uncontrolled and sometimes even forgotten. inferior parietal lobules with impairment of visually These features could be perhaps specific for guided eye movements, peripheral visual inattention, and optic ataxia. Brain 1986;109:81-97. the paracentral lobule. Other findings 17 Besta C. Sulla funzione della regione parietale dell'uomo. encountered in patients with posterior pari- Rivista di Patologiea Nervosa e Mentali 1922;27:535-8. etal lesions, such as 18 Roussy G, Levy G. Troubles sensitivo-moteurs d'aspect on September 29, 2021 by guest. Protected copyright. complex sensory deficits, radiculaire et troubles d'aspect cerebelleux par lesion difficulty with precise grip, manipulation and corticale. Rev Neurol 1926;2:376-89. 19 Foix C, Thevenard A. Syndromes pseudo-cerebelleux exploration of objects, apraxia, difficulty in d'origine parietale, bilaterale de la region paracentrale copying meaningful and non-meaningful ges- posterieure. Rev Neurol 1922;29: 1502-4. tures of the hand, dystonia, or 20 Alajouanine T, Lemaire A. Tumeur de la region paracen- avoiding trale posterieure avec sympt6mes "pseudo-cerebelleux". responses were not seen.2' 22 The most ante- Rev Neurol 1925;1:71-5. rior lesion on 21 Pause M, Freund HY. Role of the parietal cortex for sen- MRI in our patient was in the sorimotor transformation. Evidence from clinical obser- anterior temporal gyrus, not far from the sen- vations. Brain Behav Evol 1989;33:136-40. sory representation of the which 22 Pause M, Kunesh E, Binkofski F, Freund HJ. Sensori- hand, may motor disturbances with lesions of the parietal cortex. explain the transient paraesthesia that the Brain 1989;112:1599-625.