Cerebellar Degeneration in Epilepsy: A Systematic Review

Ibdali, Manar; Hadjivassiliou, Marios; Grünewald, Richard A.; Shanmugarajah, Priya

doi:10.3390/ijerph18020473

Cited by 22 publications

(19 citation statements)

References 89 publications

(67 reference statements)

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“…Hagemann et al 20 found a significant association between cerebellar atrophy and epilepsy with generalized tonic‐clonic seizures. Overall, our study confirms the conclusions drawn by Ibdali et al, 32 in their systematic review, that focal (in the majority temporal lobe) epilepsy, poor seizure control, and phenytoin drug therapy are predictors of cerebellar deterioration in patients with epilepsy.…”

Section: Discussionsupporting

confidence: 92%

Differences in brain changes between adults with childhood‐onset epilepsy and controls: A prospective population‐based study

Sillanpää

Hermann

Rinne

et al. 2021

Acta Neuro Scandinavica

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Section: Discussionsupporting

confidence: 92%

Differences in brain changes between adults with childhood‐onset epilepsy and controls: A prospective population‐based study

Sillanpää

Hermann

Rinne

et al. 2021

Acta Neuro Scandinavica

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“…Firstly, this pattern of cerebellar atrophy may be a consequence of epileptic discharges, as it has been shown in other epileptic conditions, especially chronic temporal lobe epilepsy. 26 , 27 In our study, the influence of recurrent seizures on bilateral cerebellar atrophy is supported by the stronger atrophy observed in chronically affected patients. Of interest, anterior and posterior lobes were oppositely affected in acute and chronic patients, with the anterior lobe being spared in the chronic subsample.…”

Section: Discussionsupporting

confidence: 71%

“…Second, adverse effects of antiseizure medications, particularly phenytoin, may have resulted in bilateral, symmetric cerebellar atrophy. 27 However, only 12 of 57 patients received phenytoin in our cohort. Thus, the influence of this drug on measured atrophy is negligible.…”

Section: Discussionmentioning

confidence: 88%

Infratentorial MRI Findings in Rasmussen Encephalitis Suggest Primary Cerebellar Involvement

Reiter

David

Enders

et al. 2021

Neurol Neuroimmunol Neuroinflamm

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Background and ObjectiveRasmussen encephalitis (RE) is characterized by its unilateral cerebral involvement. However, both ipsi- and contralesional cerebellar atrophy have been anecdotally reported raising questions about the nature and extent of infratentorial findings. Using MRI, we morphometrically investigated the cerebellum and hypothesized abnormalities beyond the effects of secondary atrophy, implicating a primary involvement of the cerebellum by RE.MethodsVoxel-based morphometry of the cerebellum and brainstem was conducted in 57 patients with RE and in 57 matched controls. Furthermore, patient-specific asymmetry indices (AIs) of cerebellar morphometry and fluid-attenuated inversion recovery (FLAIR) intensity were calculated. Using diffusion tensor imaging, the integrity of the cortico-ponto-cerebellar (CPC) tract was assessed. Finally, a spatial independent component analysis (ICA) was used to compare atrophy patterns between groups.ResultsPatients with RE showed bilateral cerebellar and predominantly ipsilesional mesencephalic atrophy (p < 0.01). Morphometric AIs revealed ipsilesional < contralesional asymmetry in 27 and ipsilesional > contralesional asymmetry in 30 patients. In patients with predominant ipsilesional atrophy, morphometric AIs strongly correlated with FLAIR intensity AIs (r = 0.86, p < 0.0001). Fractional anisotropy was lower for ipsilesional-to-contralesional CPC tracts than opposite tracts (T = 2.30, p < 0.05). ICA revealed bilateral and strictly ipsi- and contralesional atrophy components in patients with RE (p < 0.05).DiscussionWe demonstrated atrophy of the ipsilesional-to-contralesional CPC pathway and, consequently, interpret the loss of contralesional gray matter as secondary crossed cerebellar atrophy. The ipsilesional cerebellar atrophy, however, defies this explanation. Based on FLAIR hyperintensities, we interpret ipsilesional atrophy to be due to inflammation in the scope of a primary involvement of the cerebellum by RE.

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“…This is because both epilepsy and carbamazepine are known to cause cerebellar degeneration. 16 , 17 In patients with epilepsy treated with carbamazepine, it may be impossible to determine if the cerebellar degeneration is due to one or the other. All NS cases in this study had recurrent seizures and were treated with carbamazepine.…”

Section: Discussionmentioning

confidence: 99%

The spectrum of disease and tau pathology of nodding syndrome in Uganda

Pollanen

Onzivua

McKeever

et al. 2022

Brain

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Nodding syndrome is an enigmatic recurrent epidemic neurologic disease that affects children in East Africa. The illness begins with vertical nodding of the head and can progress to grand mal seizures and death after several years. The most recent outbreak of nodding syndrome occurred in northern Uganda. We now describe the clinicopathologic spectrum of nodding syndrome in northern Uganda. The neuropathologic findings of 16 children or young adults with fatal nodding syndrome were correlated with the onset, duration and progression of their neurological illness. The affected individuals ranged in age from 14 to 25 years at the time of death with a duration of illness ranging from 6–15 years. All 16 cases had chronic seizures. In ten cases, detailed clinical histories were available and showed that three individuals had a clinical course that was predominantly characterized by epilepsy whereas the other seven individuals had progressive cognitive, behavioural and motor decline, in addition to epilepsy. The main neuropathologic findings included: tau pathology (16/16 cases), cerebellar degeneration (11/16 cases), and white matter degeneration (7/16 cases). The tau pathology was characterized by filamentous tau-positive deposits in the form of neurofibrillary tangles, pre-tangles, and dot-like grains and threads in the neuropil. All cases showed some degree of tau pathology in the neocortex and in the locus coeruleus with frequent involvement of the substantia nigra and tegmental nuclei and lesser involvement of other grey matter sites, but there was a lack of glial tau pathology. The tau pathology in the neocortex showed a multifocal superficial laminar pattern. We conclude that nodding syndrome is a clinicopathological entity associated consistently with tau pathology, but our observations did not establish the cause of the disease, or an explanation for the tau pathology.

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Cerebellar Degeneration in Epilepsy: A Systematic Review

Cited by 22 publications

References 89 publications

Differences in brain changes between adults with childhood‐onset epilepsy and controls: A prospective population‐based study

Differences in brain changes between adults with childhood‐onset epilepsy and controls: A prospective population‐based study

Infratentorial MRI Findings in Rasmussen Encephalitis Suggest Primary Cerebellar Involvement

The spectrum of disease and tau pathology of nodding syndrome in Uganda

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