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BRIEF COMMUNICATIONS: M. Vokaer, J. C. Bier, S. Elincx, T. Claes, P. Paquier, S. Goldman, E. J. Bartholomé, and M. Pandolfo The cerebellum may be directly involved in cognitive functions Neurology 2002; 58: 967-970 [Abstract] [Full text] [PDF]

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The cerebellum may be directly involved in cognitive functions

M Gomez Beldarrain   (3 May 2002)

The cerebellum may be directly involved in cognitive functions

Louis R Caplan   (3 May 2002)

Reply to both Letters to the Editor

Jean-Christophe Bier, Mathieu Vokaer, Emmanuel J Bartholome and Massimo Pandolfo   (3 May 2002)

The cerebellum may be directly involved in cognitive functions 3 May 2002
M Gomez Beldarrain Hospital de Galdacano Send Correspondence to journal: Re: The cerebellum may be directly involved in cognitive functions mgomezab{at}sarenet.es M Gomez Beldarrain	We read with interest the article by Vokaer et al. [1], who describe one patient with bilateral anterior ponto-cerebellar ischemic lesions associated with some cognitive deficits (impaired verbal learning, fluency and naming, and perseverative errors on the r-WCST). Since no perfusion defects were observed on PET and SPECT in the cerebral cortex the authors suggest that the cerebellum may be directly responsible for the cognitive impairment. This interesting report adds to the controversy of the cognitive role of the cerebellum. However, we believe that large series, rather than individual patients, are needed to clarify this issue. In this particular patient, we wonder whether anxiety or depression -perhaps related to having a stroke and being hospitalized- could have accounted, at least in part, for his neuropsychological (NPS) defects. Also, the results of the NPS studies of this patient, who was a heavy smoker and drinker, could hardly be compared with healthy population. In this regard, we have studied two series (the first with 14 patients and the second with 26 patients), with cerebellar stroke and compared them with healthy controls [2. 3] and found no impairments in a extensive battery of well-known NPS tests; only differences in motor control and procedural learning of motor sequences were detected. Vokaer et al. mention that the absence of diaschisis points to the cerebellum and not to the deactivation of other cortical areas as the cause of the cognitive impairment after cerebellar damage. In our series, 13 of 19 patients, who underwent SPECT one month after the stroke, exhibited diaschisis. While this phenomenon was persistent, none of the patients showed evidence of NPS impairment other than that previously mentioned. Regarding the scarcity of data about the cognitive role of the anterior portion of the cerebellum, it should be mentioned that Schmahmann et al. [4] reported a series of 20 patients with cognitive impairment and diverse cerebellar lesions and found that patients with anterior lobe lesions had only minor changes in executive and visuo-spatial functions. Elucidating the role of cerebellum in cognition, an area of utmost interest in neuroscience, will require additional studies of large series of patients. A few steps, however, have already been taken. References: 1. Vokaer M, Bier J.C, Elincx S, et al. The cerebellum may be directly involved in cognitive functions. Neurology 2002;58:967-970. 2. Gómez-Beldarrain M, García-Moncó J.C, Rubio, B, Pascual-leone A. Effect of cerebellar lesions on procedural learning on the serial reaction time task. Exp Brain Res 1998;120:25-30. 3. Gómez Beldarrain M, García-Moncó J.C, Quintana J et al. Diaschisis and neuropsychological performance after cerebellar stroke. Eur Neurol 1997;37:8-89. 4. Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998; 121:561-579.
The cerebellum may be directly involved in cognitive functions 3 May 2002
Louis R Caplan Beth Israel Deaconess Medical Center Boston MA Send Correspondence to journal: Re: The cerebellum may be directly involved in cognitive functions lcaplan{at}caregroup.harvard.edu Louis R Caplan	Vokaer et al. [1] posit a direct role for the cerebellum in causing neuropsychological deficits during acute stroke. This hypothesis is based on a single patient whose MRI showed bilateral brachium pontis and left cerebellar infarcts. No vascular image is shown, described, discussed, or considered relevant. The usual vascular lesion in patients such as that described by Vokaer et al. [1] is an occlusive lesion within the basilar artery located at the origins of the anterior inferior cerebellar arteries (AICAs). The AICAs supply the brachium pontis and the region of the cerebellar infarct shown on the published MRIs. An occlusive lesion at this site within the basilar artery can diminish blood supply to the thalamus, a region recognized to affect cognition and behavior. Decreased blood flow without infarction would not be seen on the MRIs, PET or SPECT scans performed a month or more after stroke onset. Furthermore, recognizing the vascular etiology would be very important in managing this patient. It is impossible to interpret clinico-anatomical correlations in patients with acute stroke from a brain image alone. The nature, location, and severity of the causative vascular lesion is also critical in understanding brain regions that have diminished blood flow but are not yet infarcted. It is incomprehensible to me that the authors would have performed PET and SPECT scans without performing an image of the intracranial posterior circulation arteries. If they did perform an MRA, it is incomprehensible that they would not have described it and would not have seen that it was important enough to mention and discuss. The Neurology Journal and other medical journals should not publish this or other articles purporting clinico-anatomical correlations in acute stroke patients without vascular data. Reference: 1) Vokaer M, Bier JC, Elincx S et al. The cerebellum may be directly involved in cognitive functions. Neurology 2002;58:967-970.
Reply to both Letters to the Editor 3 May 2002
Jean-Christophe Bier Hopital Erasme Bruxelles Belgium, Mathieu Vokaer, Emmanuel J Bartholome and Massimo Pandolfo Send Correspondence to journal: Re: Reply to both Letters to the Editor Jean-Christophe.Bier{at}ulb.ac.be Jean-Christophe Bier, et al.	We thank Prof. Caplan for his interest in our article [1] and for his observations. Prof. Caplan points out that the nature, location and severity of causative vascular lesion is critical in understanding brain regions that have been affected, especially in the acute phase. MRA performed thirteen days after onset on our patient showed irregular basilar artery. There was no basilar artery occlusive lesion but both AICA were not visualized. Furthermore, atherosclerotic disease was found on ultrasonographical carotid examination. We thus confirm the atherosclerotic etiology of the bilateral AICA occlusion. [2, 3] The absence of basilar occlusion in our case does not support Prof. Caplan's hypothesis of thalamic hypoperfusion. The main interest of our description is the peculiarity of cognitive dysfunctions remaining after the acute phase of ponto-cerebellar stroke without any supratentorial involvement. [1] When similar cognitive deficits have been described in case of thalamic lesion, hypometabolism was not isolated to the thalamus. [4, 5] Moreover, this is clearly not the presentation of our patient who had no occlusive lesion on basilar artery and any thalamic lesion, hypoperfusion or hypometabolism even when major cognitive deficits were still present. [1] We also thank Gomez-Beldarrain et al. for their comments on our article. [1] The sudden onset of the patient's deficits, as well as the pattern and evolution of his neuropsychological impairment without any antidepressive treatment strongly argue against an alcoholic or anxiodepressive etiology. [1] We agree with the necessity of further studies including functional imaging to define how lesions in different portions of the cerebellum may alter functional connectivity between brain regions involved in cognitive tasks. [1] However, the efficacy of larger series may be precluded by the heterogeneity of cerebellar stroke presentation. As already discussed, the absence or paucity of neuropsychological deficits observed in previous descriptions of anterior cerebellar lesions may be due to a threshold effect, if, as we think, bilateral anterior lesions are required to produce significant cognitive abnormalities. [1, 6, 7, 8] References: 1. Vokaer M, Bier JC, Elincx S, Claes T, Paquier P, Goldman S, Bartholome EJ, Pandolfo M. The cerebellum may be directly involved in cognitive functions. Neurology 2002; 58: 967-970. 2. Chang HM, Linn FH, Caplan LR. Bilateral anterior inferior cerebellar artery territory infarcts. J Neuroimaging 1998; 8: 42-44. 3. Amarenco P, Rosengart A, De Witt LD, Pessin MS, Caplan LR. Anterior inferior cerebellar artery territory infarcts. Mechanisms and clinical features. Arch Neurol 1993; 50: 154-161. 4. Pepin EP, Auray-Pepin L. Selective dorsolateral frontal lobe dysfunction associated with diencephalic amnesia. Neurology 1993; 43: 733- 41. 5. Van Der Werf YD, Weerts JG, Jolles J, Witter MP, Lindeboom J, Scheltens P. Neuropsychological correlates of a right unilateral lacunar thalamic infarction. J Neurol Neurosurg Psychiatry 1999; 66: 36-42. 6. Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998; 121: 561-579. 7. Daum I, Ackermann H. Neuropsychological abnormalities in cerebellar syndromes - fact or fiction? International Review of Neurobiology, Vol. 41. San Diego: Academic Press 1997;455-471. 8. Neau JP, Arroyo-Anllo E, Bonnaud V, Ingrand P, Gil R. Neuropsychological disturbances in cerebellar infarcts. Acta Neurol. Scand. 2000;102:363-370.