Signs and Symptoms From a Cerebral Lesion That Suggest Cerebellar Dysfunction Erwin B. Montgomery, Jr, MD \s=b\ Lesions of the cerebral hemispheres produce signs and symptoms very similar to those produced by cerebellar lesions. I studied a case that demonstrated the signs of dysmetria and intention tremor; it resulted from an infarct of areas 5, 7, and, to a lesser extent, 40, of the contralateral cerebral hemisphere. (Arch Neurol 1983;40:422-423) can Qigns and symptoms usually associ- ated with cerebellar lesions but resulting from lesions of the cerebral hemispheres are not widely appreci¬" ated, despite previous case reports.1 In addition to the potential for misdiagnosis, this phenomenon has inter¬ esting implications for current hy¬ potheses of the central control of movement. The following case report describes symptoms appropriate for a cerebellar lesion resulting from an infarction restricted to areas 5, 7, and, to a lesser extent, 40. REPORT OF A CASE An 83-year-old, right-handed man noted the sudden onset of weakness in the left upper extremity, clumsiness, and a sensa¬ tion he described as feeling as though the left upper extremity did not belong to him. The weakness disappeared within hours but the clumsiness and unusual feeling persisted. Eighteen years earlier he had experienced two episodes of right-sided weakness without speech impairment. Recovery was complete except for a slight impairment of the right hand during piano playing. He was also told at the time that he had a myocardial infarction. He has since been in atrial fibrillation. Examination showed normal speech, full visual fields, and normal cranial nerve function. Strength and muscle tone were normal but there were decreased speed and Accepted for publication Oct 15, 1982. From the Department of Neurology and Neurological Surgery, Washington University School of Medicine, St Louis. Reprint requests to Department of Neurology and Neurological Surgery, Washington University School of Medicine, 660 S Euclid Ave, Box 8111, St Louis, MO 63110 (Dr Montgomery). Fig 1.—Composite drawings taken from motion pictures. Top, With eyes open, patient performs finger-to-nose-to-finger test. Closed circles represent index finger position at approximately 0.06-s intervals. Bottom, Patient traces square in air by following examiner's fingertip with his own. Open circles represent position of examiner's finger at 0.3-s intervals; closed circles, patient's finger at same intervals (only first side of square is shown). Downloaded From: http://archneur.jamanetwork.com/ by a Western University User on 06/07/2015 Fig 2.—Left, Computed tomographic scan of patient after injection of contrast material showing area of recent infarction (arrows). Right, Corresponding level showing that lesion involves predominantly areas 5, 7, and 40 (not shown) (from Gado et al5). dexterity of fine finger movements of the right hand. Right-sided deep-tendon reflexes were increased but the plantar responses were flexor bilaterally. Pinprick, light-touch, and vibratory sensations were intact. Joint position sense, topesthesia, and stereognosis were markedly reduced on the left side. Performance of the fingerto-nose-to-finger test with the left hand was abnormal (Fig 1, top), as was tracing a square in the air (Fig 1, bottom). Both tests, performed with eyes open, showed dysmetria and intention tremor. These signs were considered by several neurolo¬ gists to be indistinguishable from deficits usually associated with cerebellar lesions. The patient improved within a few weeks, but these signs and symptoms were still that produce signs and symptoms similar to those produced by cerebel¬ lar lesions have been known for some time." There have been many case reports of suboccipital explorations performed for what were subsequent¬ ly found to be supratentorial lesions involving frontal and parietal lobes.1·3 There has been controversy as to whether the ataxia from frontal lobe tumors is limited to a disturbance of gait more appropriately described as a A computed tomographic scan following injection of contrast material, performed nine days following the onset of the symp¬ the case reports, there have been instances cited of cerebellar signs and symptoms due to lesions of the cere¬ bral hemispheres not associated with increased intracranial pressure," as in this case. Lesions in the parieto-occip¬ ital region have long been known to result in inaccurate and uncoordi¬ nated volitional movements without significant visual field loss.6'8 Experimental lesions of the sensory association cortex in laboratory ani¬ mals can result in inaccurate and uncoordinated volitional movement.910 The authors suggest that these defi¬ cits are due to the failure of cortico- present on examination 13 months later. toms, showed a restricted pattern of enhancement in the region of the right superior parietal lobule consistent with a recent infarct (Fig 2, left). Comparison with the atlas of Gado et als (Fig 2, right) showed that the lesion involved predomi¬ nantly areas 5, 7, and, to a lesser extent, 40. A small infarct was also seen in the left internal capsule consistent with the strokes experienced 18 years earlier. No lesions were found in the cerebellum. COMMENT Lesions of the cerebral hemispheres gait apraxia. However, subsequent reviews of frontal lobe tumor signs have demonstrated dyssynergia, dysdiadochokinesia, and dysmetria.5 Al¬ though instances of tumors dominate cortical transmission of important information to the motor areas. How¬ ever, it is possible that subcortical structures are also involved. Jones and Powell11 have shown in monkeys that the primary somatosensory areas project to areas 4 and 5. Though area 5 projects to areas 6 and 7, area 7 does not project to area 4 or 6. Stein10 has shown that cooling area 7 in monkeys was more effective in producing inac¬ curate and uncoordinated movement than was cooling area 5. This suggests that loss of direct sensory input to motor areas of the cortex is not the most significant cause of the motor deficits, but that loss of information processed in area 7 sent to other areas involved in motor programming may be important. One such area may be the lateral cerebellum (made up of the cerebellar hemispheres and dentate nucleus). This is suggested by the striking similarity of the ataxia pro¬ duced by cerebral lesions to that expected from lesions of the lateral cerebellum, although similar symp¬ toms do not necessarily imply the same mechanisms. The similarity of the ataxia due to lesions of the somatosensory associa¬ tion cortex to that expected from a lateral cerebellar lesion is consistent with recent hypotheses of lateral cere¬ bellar function.12·13 The lateral cerebel¬ lum is described as interposing between the associational cerebral cortex and the motor cortex, function¬ ing to integrate information into a motor program to be executed by the motor cortex. Lesions of the lateral cerebellum would then result in loss of adequate motor programs with result¬ ing ataxia. These motor programs could also become inadequate if the lateral cerebellum is deprived of nec¬ essary information, as might occur with lesions of the cerebral part of the cortex that provides information to the lateral cerebellum. In either case, the symptoms might be expected to be very similar, as shown in the case presented. References 1. Grant FC: Cerebellar symptoms produced by supratentorial tumors. Arch Neurol 1928; 20:292-308. 2. Frazier CH: Tumor involving the frontal lobe alone: A symptomatic survey of 105 verified cases. Arch Neurol 1936;35:525-571. 3. Critchley M: The Parietal Lobes. New York, Hafner Publishing Co, 1953, p 161. 4. Gracin R: The ataxias, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. Amsterdam, North-Holland Publishing Co, 1969, vol 1: Disturbances of Nervous Function, pp 309-355. 5. Gado M, Hanaway J, Frank R: Functional anatomy of the cerebral cortex by computed tomography. J Comput Assist Tomogr 1979;3:1\x=req-\ 19. 6. Rondot P, DeRecondo J, Ribadeau Dumas JL: Visumotor ataxia. Brain 1977;100:355-376. 7. Levine DN, Kaufman KJ, Mohr JP: Inaccurate reaching associated with a superior parietal tumor. Neurology 1978;28:556-561. 8. Damasio AR, Benton AL: Impairment of hand movements under visual guidance. Neurol- ogy 1979;29:170-178. 9. Haaxma R, Kuypers HGJM: Intra-hemispheric cortical connexions and visual guidance of hand and finger movements in the rhesus monkey. Brain 1975;98:239-260. 10. Stein J: Effects of parietal lobe cooling on Downloaded From: http://archneur.jamanetwork.com/ by a Western University User on 06/07/2015 manipulative behavior in the conscious monkey, in Gordon G (ed): Active Touch. Oxford, England, Pergamon Press, 1978, pp 79-90. 11. Jones EG, Powell TPS: An anatomical study of converging sensory pathways within the cerebral cortex of the monkey. Brain 1970;93:793\x=req-\ 820. 12. Evarts EV, Thach WT: Motor mechanisms of the CNS: Cerebrocerebellar interrelations. Ann Rev Physiol 1969;31:451-498. 13. Allen GI, Tuskahara N: Cerebro cerebellar communication systems. Physiol Rev 1974; 54:957-1006.