Crossed Cerebellar Atrophy in Patients with Precocious Destructive Brain Insults

ORIGINAL CONTRIBUTION Crossed Cerebellar Atrophy in Patients With Precocious Destructive Brain Insults

Ricardo A. Teixeira, MD; Li M. Li, MD, PhD; Sergio L. M. Santos, MD; Veronica A. Zanardi, MD, PhD; Carlos A. M. Guerreiro, MD, PhD; Fernando Cendes, MD, PhD

Objective: To analyze the frequency and pathogenetic ciated with the extent of the supratentorial lesion (6 from factors of crossed cerebellar atrophy (CCA) in adult pa- group A, 1 from group B, and none from group C; tients with epilepsy secondary to destructive brain in- PϽ.001). Status epilepticus was present in 6 patients from sults of early development. group A and in none from the other groups. There was an association between the antecedent of status epilep- Methods: We studied 51 adult patients with epilepsy ticus and CCA (PϽ.001). All patients had atrophy of the and precocious destructive lesions. Patients were cerebral peduncle ipsilateral to the supratentorial lesion divided into 3 groups according to the topographic dis- and 4 had contralateral atrophy of the middle cerebellar tribution of their lesions on magnetic resonance imag- peduncle. The duration of epilepsy was not associated ing: group A, hemispheric (n=9); group B, main arterial with the presence of CCA (P=.20). territory (n=25); and group C, arterial border zone (n=17). We evaluated the presence of CCA visually and Conclusions: Our data suggest that in patients with epi- with cerebellar volumetric measurement, correlating it lepsy and destructive insults early in life, the extent of with the clinical data. Other features shown on mag- the supratentorial lesion as well as the antecedent of sta- netic resonance imaging, such as the thalamus, brain- tus epilepticus play a major role in the pathogenesis of stem, and middle cerebellar peduncle, were also care- CCA. Recurrent seizures do not seem to be relevant to fully analyzed. the development of CCA.

Results: Seven patients (13%) had CCA that was asso- Arch Neurol. 2002;59:843-847

TROPHY OF the cerebel- biological process. Damage to the corti- lum contralateral to a copontocerebellar pathway is the most ac- hemispheric supratento- cepted pathogenic mechanism in the de- rial lesion, or crossed cer- velopment of CCH or CCA.13-15 There is ebellar atrophy (CCA), has also a robust body of evidence on the de- beenA recognized by neuropathologists for structive effects of prolonged seizures in more than 100 years but the understand- vulnerable regions of the brain and on the ing of its pathogenesis is still incom- damage caused by partial status epilepti- plete.1-7 cus (SE) to the contralateral cerebel- In 1980, Baron et al8 described con- lum.16-20 tralateral cerebellar hypometabolism The role of the extension of the cere- (CCH) in positron emission tomo- bral lesion in CCH is not fully under- graphic (PET) images of adult patients with stood since it has been associated with supratentorial infarcts, calling it crossed the degree of CCH in some studies11,21 cerebellar diaschisis. Diaschisis is also an but not in others.22,23 Furthermore, the old concept, classically defined as a tran- role of recurrent seizures in the develop- sient impairment of functional activity in ment of CCH or CCA is not yet clear.5,8,24 an area remote from the site of a primary To further investigate the pathogenesis of lesion.9,10 However, the interpretation of CCA, we reviewed the results of magnetic CCH as a diaschisis is challenged since resonance imaging (MRI) in a series of From the Departments of there are several instances in which the patients with epilepsy and different types Neurology (Drs Teixeira, Li, 11,12 Guerreiro, and Cendes) and CCH lacks reversibility. Thus, a re- of destructive lesions of early develop- Radiology (Drs Santos and versible diaschisis and an irreversible at- ment to assess whether there is any par- Zanardi), University of rophy can hypothetically constitute the ex- ticular MRI or clinical feature related to Campinas, Campinas, Brazil. tremes of a continuum of the same CCA.

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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 METHODS (Rogue Research, Montreal, Quebec). This approach was very helpful for clear visualization of the extent of cortical involvement and allowed us to classify the patients into 3 We evaluated the MRI results of 51 consecutive adult pa- different groups according to the topographical distribu- tients with the diagnosis of epilepsy secondary to a de- tion of the lesion: group A, hemispheric lesions, defined structive brain lesion of early development, who were seen as a diffuse atrophy of an entire hemisphere without loss at our institution from March 1999 to April 2001 (median of tissue continuity (n=9); group B, lesions limited to a main age, 31.8 years; range, 15-55 years). Detailed histories of arterial territory, often constituting a cavity (n=25); and group prenatal, neonatal, and early childhood events were sys- C, lesions on the border zones between the main cerebral ar- tematically reviewed in the medical records, and direct in- terial territories (n=17)25,26 (Figure 1). Special attention was terviews with the patients and their relatives were con- also focussed on the morphology of the brainstem, thala- ducted. All patients had disease onset before the age of 5 mus, cerebellum, and middle cerebellar peduncle. years; we excluded all patients with evidence of adult- In addition, we performed volumetric measurements of onset disease. Informed consent was obtained from all sub- the cerebellums of all patients using a semiautomatic soft- jects. This study was approved by the ethics committee of ware program (NIH-Image; National Institute of Health, the faculty of medical sciences of University of Campinas Bethesda, Md). The cerebellum was manually outlined on (Campinas, Brazil). sagittal slices. To check right-left asymmetry, the measure- Magnetic resonance imaging was performed by a 2.0 T ments were distributed into right and left cerebellum accord- scanner (Elscint Prestige, Haifa, Israel). Our epilepsy pro- ing to the position of the cerebral aqueduct. When only 1 slice tocol consists of: (1) sagittal T1 spin-echo, 6 mm thick (rep- showed the cerebral aqueduct, half of its measurement was etition time [TR], 430; echo time [TR], 12) for optimal ori- computed to the right cerebellum and the other half to the entation of the subsequent images; (2) coronal T1 inversion left. More commonly, 2 slices showed the cerebral aque- recovery, 3 mm thick (tip angle, 200°; TR, 2700; TE, 14; TI, duct, and in these cases, each slice was computed to each hemi- 840; matrix, 130ϫ256; field of view [FOV], 16ϫ18 cm); cerebellum. The extracerebellar portion of the middle cer- (3) coronal T2-weighted fast spin-echo, 3 to 4 mm thick ebellar peduncle was not included and this limit was assumed (tip angle, 120°; TR, 4800; TE, 129; matrix, 252ϫ320; FOV, as the angle formed between the cerebellar hemisphere and 18ϫ18 cm); (4) axial images parallel to the long axis of the the middle cerebellar peduncle. hippocampus; T1 gradient echo, 3 mm thick (tip angle, 70°; The cerebellums of 12 healthy volunteers were mea- TR, 200; TE, 5; matrix, 180ϫ232; FOV, 22ϫ22 cm); (5) sured and constituted a control group. An asymmetry in- axial T2 fast spin-echo, 4 mm thick (tip angle, 120°; TR, 6800; dex (AI) was calculated for each subject by subtracting the TE, 129; matrix, 252ϫ328; FOV, 21ϫ23 cm); and (6) volu- right hemicerebellum volume from the left and then di- metric (3-dimensional) T1 gradient echo, acquired in the viding by the mean of the right and left. Values outside sagittal plane for multiplanar reconstruction, 1 to 1.5 mm 2 SDs (95% confidence interval) from the AI mean of the thick (tip angle, 35°; TR, 22; TE, 9; matrix, 256ϫ220; FOV, control group were considered abnormal. Cerebellar 23ϫ25 cm). volume was normalized to the total brain volume to check Visual analysis of MRI results was systematically per- for bilateral atrophy. formed by one of us (S.L.M.S.), blinded to the clinical data, We used the Pearson ␹2 test and Fisher exact test for in a workstation (Silicon Graphics O2; Silicon Graphics Com- comparisons between proportions. An analysis of vari- puter Systems, Mountain View, Calif) using Omnipro ance and the Tukey post hoc pairwise comparison were ap- software (Elscint Prestige). Curvilinear reconstruction of plied for comparison on continuous variables among the 3-dimensional MRI volumetric images was performed in 3 groups. We used the Pearson correlation test to assess all patients by a Power MacIntosh (Apple Computer correlation between duration of epilepsy and cerebellar vol- Inc, Cupertino, Calif) using the Brainsight software umes. The significance level was .05.

RESULTS ciated with a febrile illness was the first manifestation of their disease. Two patients had SE after experiencing un- Crossed cerebellar atrophy was visually identified in 6 complicated seizures, 1 of them since the neonatal period. patients. The volumetric studies confirmed the CCA in The single patient from group B did not experience any epi- these 6 patients and in a seventh patient whose visual sodes of SE and had the first seizure at age 27 years. This analysis did not definitively point to CCA. A visual di- patient had a right hemiparesis observed in the first year agnosis of bilateral cerebellar atrophy was made in 9 pa- of life without any potentially associated morbid event and tients, all of whom had long-term exposure to phe- had a large cystic infarct in the territory of the left middle nytoin. These patients showed thinner folia but had cerebral artery, pointing to a prenatal insult. Patients with preservation of the cerebellar contour dimension so that CCA exhibited the SE antecedent more commonly (6/7) while results of their volumetric studies tended to be ab- than those without CCA (2/44) (␹2 =22.49; PϽ.001). The normal, they did not reach significance. None of the pa- SE antecedent was by far more common in patients in group tients with cerebellar atrophy had clinical cerebellar signs. A (8/9) than in the other groups (group B, 1/25; group C, Six of the 7 patients with CCA belonged to group A 1/17) (␹2 =30.39; PϽ.001). (hemispheric) and 1 to group B (arterial territory) The duration of epilepsy and seizure frequency were (Figure 2). All 6 patients from group A had the anteced- similar between the groups and were not different in pa- ent of SE in the first 5 years of life, developing a perma- tients with CCA (PϾ.05). Recurrent generalized convul- nent hemiparesis just after the SE. In 4 patients, SE asso- sions throughout the course of epilepsy were more fre-

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Figure 2. A, A 40-year-old man who had the antecedent of status epilepticus, which led to a left motor deficit. Coronal inversion recovery (IR) T1-weighted image shows right hemiatrophy with left cerebellar atrophy. B B, A 51-year-old woman with a congenital right hemiparesis and epilepsy. Coronal IR T1-weighted image demonstrates a large cavity in the territory of the left middle cerebral artery and right cerebellar atrophy.

supratentorial lesion. The other 3 patients with CCA without atrophy of the cerebellar peduncle all exhibited the antecedent of SE. In contrast, patients without CCA did not exhibit atrophy of the middle cerebellar peduncle. Atrophy of the ipsilateral cerebral peduncle was more commonly observed in patients from groups A (8/9) and B (18/25) than from group C (4/13) (␹2 C =13.89; P=.001). All patients with CCA had ipsilateral cerebral peduncle atrophy and 2 of them also exhibited atrophy of the ipsilateral pons (Figure 3). Ipsilateral thalamus involvement was more frequent in patients from groups A and B (5/9 and 17/25, respectively) than in group C (2/15) (␹2 =13.16; P=.001). There was atrophy of the ipsilateral thalamus in all patients with CCA except one. Both thalamus and brainstem involvement were associated with the presence of CCA (Fisher exact test, PϽ.005).

Figure 1. Curvilinear reconstruction of 3-dimensional acquisitions and axial COMMENT images from different patients illustrating the 3 groups. A, Diffuse atrophy of the right cerebral hemisphere. B, Large cavity on the territory of the right middle In their classic article, Verhaart and Van Wieringen- cerebral artery (MCA). C, Bilateral atrophy on the border zone between the 3 2 main arterial territories, with a left predominance (black arrows) also shown on Rauws observed that CCA tends to be associated with the axial image. Discrete left parasagittal atrophy can be observed on the border long-standing, extensive unilateral lesions of the cere- zone between the anterior cerebral artery and the MCA (white arrow). bral hemisphere, usually originating in infancy or early childhood. Thirty years later, Baron et al8 described CCH quent among patients in group B (7/25) than groups A observed on PET scans of adult patients with supraten- (0/9) and C (1/17) but the difference was not statistically torial infarcts, suggesting that it represents the “early meta- significant (PϾ.05). The frequency of generalized convul- bolic correlate of the phenomenon of CCA.” Since then, sions was also not different between patients with CCA and it has been well accepted that CCH and CCA constitute those without (PϾ.05). Three patients from group A a spectrum of the same biological process but the fac- (33.3%), 6 patients from group B (24%), and none from tors that determine a reversible and functional phenom- group C exhibited hemiconvulsions as a habitual seizure enon (CCH) to become an irreversible structural change type (PϾ.05). Hemiconvulsions were equally frequent (CCA) are still not fully understood. among patients with CCA and those without CCA (PϾ.05). Tien and Ashdown12 were the first to report the pos- Ictal semiology exclusively of the temporal lobe was ob- sible connections between CCH and CCA, analyzing the served in 17 patients (33%) and it was more common among MRIs of patients with CCH observed on PET scan im- patients in group C (␹2 =11.41; P=.003). ages. They found that 8 of 26 patients with CCH also had Analysis of variance demonstrated that the AI was CCA. All 8 patients had long-standing unilateral hemi- different among the groups (F2,48=7.63; P=.001) and post spheric atrophy with intractable focal seizures. Con- hoc comparison showed that group A (mean, 3.83 ) was versely, most patients without CCA had cerebral tu- significantly different from groups B (0.99 ) and C (0.82). mors larger than 3 cm, and only 40% had seizures. Those Furthermore, no correlation was found between dura- patients were older and had shorter duration of symp- tion of epilepsy and AI (R2=1.11; P=.3). toms than the patients with CCA. This study suggests that Four of the 7 patients with CCA exhibited atrophy the differentiation of CCH from CCA depends on the na- of the middle cerebellar peduncle contralateral to the ture and extension of the lesion and the duration of symp-

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Figure 3. A 42-year-old woman with mental retardation and epilepsy, who had febrile status epilepticus followed by left hemiparesis at the age of 11 months. A, Coronal inversion recovery T1-weighted image shows right hemiatrophy and marked contralateral cerebellar atrophy. B, Axial T1-weighted image shows atrophy of the cerebral peduncle ipsilateral to the supratentorial lesion (arrow). C, Axial T1-weighted image exhibits atrophy of the middle cerebellar peduncle contralateral to the supratentorial lesion (arrow).

toms, as well as on the age of the patient at illness onset. a tumor. The patient died 6 days after a lateralized SE with Cautiously, the authors suggest that recurrent seizures predominant motor manifestations on the right hemi- can also play a role in CCA but unfortunately no men- body that culminated in multiorgan failure. The neuro- tion was made of the SE antecedent in these patients. pathologic findings included laminar cortical necrosis in In our study, all patients who had CCA had exten- the left hemisphere associated with a marked loss of Pur- sive unilateral hemispheric lesions. Most of the patients kinje cells in the right hemicerebellum. The presence of from group C (arterial border zone) had bilateral and small eosinophilic changes on many of the remaining Purkinje lesions, and none of them exhibited CCA. Of particular cells of the affected hemicerebellum pointed to recent dam- interest is the finding that CCA was almost exclusively age. In addition, MR diffusion-weighted images (2 days be- present among patients with hemiatrophy (group A). Only fore death) showed abnormal diffusion throughout the cor- 1 patient in group B (arterial territory) had CCA, al- tex of the left hemisphere and right hemicerebellum. though most of the patients in this group also had long- Other authors have suggested that repetitive sei- standing and extensive unilateral lesions with ipsilat- zures could be a main pathogenetic factor in CCA.5,8,24 eral atrophy of the brainstem. Some other factor in Our study does not support this concept since the du- addition to the extension of the lesion must have played ration of epilepsy and seizure frequency was similar be- a key role in the development of CCA in these patients. tween the groups and it was not different among the pa- Status epilepticus seems to have been a contributing fac- tients with CCA. In addition, the pattern of seizure tor, considering that it was much more frequent in group semiology did not seem to have an effect on CCA in our A than in the other groups. Since sequential MRI stud- series. Neither hemiconvulsions nor generalized convul- ies before and after SE are not available, it could be sions recurring long after the onset of epilepsy were dif- argued that SE is associated more with the extent of ce- ferent among the groups or between patients with CCA rebral injury rather than specifically with CCA. How- and those without. Patients with arterial border zone le- ever, there is major evidence that primary damage to a sions more commonly exhibited monomorphic seizure hemicerebellum is caused by a lateralized SE.14,15,20 semiology with a temporal lobe–like pattern (probably Strefling and Urich14 emphasized that severe epi- reflecting their less extensive lesions), and we cannot dis- leptic seizures are probably one of the most important card the possibility that this might be associated with the causes of CCA and proposed 2 main distinct patterns of absence of CCA in this group of patients. However, it CCA, one of them associated with transneuronal degen- seems unlikely that seizure semiology had a greater in- eration and the other with postictal damage. Tan and fluence on CCA compared with the extension and bilat- Urich15 described the necropsy findings of a patient who erality of the lesion in these patients. Given the few pa- died 2 days after a lateralized SE and compared them with tients with CCA, it is likely that the power of this study findings from 3 necropsies of patients who had exhib- is insufficient to conclude that there is a definite nega- ited the antecedent of SE months or years before death. tive relationship between habitual seizures and CCA. There was no difference in the extent or distribution of There is evidence that transneuronal degeneration neuronal necrosis between the acute and chronic cases, has a decisive role in the pathogenesis of CCA. Nec- suggesting that SE was sufficient to cause the pattern of ropsy studies of patients with CCA commonly show at- lesions observed in the chronic cases. All cases had uni- rophy of the middle cerebellar peduncle contralateral to lateral hemispheric necrosis with damage of the contra- the supratentorial lesion and in the nuclei of the ipsilat- lateral cerebellum.15 eral pons.14,15 A more recent work, using PET studies of Men et al20 described a patient who experienced 2 gen- patients with supratentorial tumors, showed a signifi- eralized uncomplicated seizures and was found to have a cant reduction in glucose metabolism in the ipsilateral small temporal lobe lesion on MRI that was suggestive of pons parallel to CCH.13 Patients with long-standing su-

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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 pratentorial damage but no history of seizures can occa- REFERENCES sionally develop CCA.27,28 Moreover, there is a report that describes a patient who developed CCA after a hemi- 1. Alpers BJ, Dear RB. Hemiatrophy of the brain. J Nerv Ment Dis. 1939;89:653- 29 spherectomy for seizure control. 671. Cerebral peduncle atrophy ipsilateral to the supra- 2. Verhaart WJC, Van Wieringen-Rauws GA. On cerebro-cerebellar atrophy. Folia tentorial lesion was significantly associated with CCA in Psychiat Neurol Neurochir Neerl. 1950;53:481-501. 3. Loiseau P, Vital C, de Boucaud P, et al. E´tude anatomo-clinique duń cas our study. This can be interpreted as a sign of wallerian d’he´miple´gie-e´pilepsie avec mouvements anormau: atrophie ce´re´belleuse croi- degeneration but can also represent the primary lesion. seé. Rev Neurol. 1968;118:77-82. 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Ann Neurol. des); critical revision of the manuscript for important in- 1984;15:425-434. tellectual content (Drs Teixeira, Li, Santos, Zanardi, 24. Duncan R, Patterson J, Bone I, Wyper DJ. Reversible cerebellar diaschisis in fo- Guerreiro, and Cendes); statistical expertise (Drs Teix- cal epilepsy. Lancet. 1987;2(8559):625-626. eira, Li, and Cendes); study supervision (Drs Li, Santos, 25. Kuzniecky RI, Jackson GD, eds. Magnetic Resonance in Epilepsy. New York, NY: Zanardi, Guerreiro, and Cendes). Raven Press; 1995:142-144. 26. Barkovich AJ. Pediatric Neuroimaging. 2nd ed. Philadelphia, Pa: Lippincott- Dr Teixeira was supported by scholarship grant 98/ Ravens; 1996. 13101-8 from FAPESP (Fundaçaõ de Amparo a` Pesquisa 27. Baudrimont M, Gray F, Meininger V, et al. Atrophie ce´re´belleuse croiseé apre´s do Estado de Saõ Paulo, Brazil). The study was supported le´sion he´misphe´rique survenue a`l’a´ge adulte. Rev Neurol. 1983;139:485-495. by grant 97/07584-3 from FAPESP (Dr Cendes). 28. Bouchareb M, Moulin T, Cattin F, et al. Wallerian degeneration of the descend- Corresponding author and reprints: Fernando Cen- ing tracts. J Neuroradiol. 1988;15:238-252. 29. Chiron C, Raynaud C, Jambaque I, et al. A serial study of regional cerebral blood des, MD, PhD, Department of Neurology, FCM- flow before and after hemispherectomy in a child. Epilepsy Res. 1991;8:232- UNICAMP, Campinas, SP, Brazil, CEP 13083-970 (e- 240. mail: [email protected]). 30. Chung HD. Retrograde crossed cerebellar atrophy. Brain. 1985;108:881-895.

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