| Autor: |
Marcián V; First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic; Medical Faculty of Masaryk University, Brno, Czech Republic.; First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic; Medical Faculty of Masaryk University, Brno, Czech Republic; Behavioral and Social Neuroscience Research Group, CEITEC (Central European Institute of Technology), Masaryk University, Brno, Czech Republic; Department of Neurology, School of Medicine, University of Minnesota, Minneapolis, MN, USA., Filip P; First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic; Medical Faculty of Masaryk University, Brno, Czech Republic., Bareš M; First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic; Medical Faculty of Masaryk University, Brno, Czech Republic; Behavioral and Social Neuroscience Research Group, CEITEC (Central European Institute of Technology), Masaryk University, Brno, Czech Republic; Department of Neurology, School of Medicine, University of Minnesota, Minneapolis, MN, USA., Brázdil M; First Department of Neurology, St. Anne's University Hospital, Brno, Czech Republic; Medical Faculty of Masaryk University, Brno, Czech Republic; Behavioral and Social Neuroscience Research Group, CEITEC (Central European Institute of Technology), Masaryk University, Brno, Czech Republic. |
| Abstrakt: |
Basic epilepsy teachings assert that seizures arise from the cerebral cortex, glossing over infratentorial structures such as the cerebellum that are believed to modulate rather than generate seizures. Nonetheless, ataxia and other clinical findings in epileptic patients are slowly but inevitably drawing attention to this neural node. Tracing the evolution of this line of inquiry from the observed coincidence of cerebellar atrophy and cerebellar dysfunction (most apparently manifested as ataxia) in epilepsy to their close association, this review considers converging clinical, physiological, histological, and neuroimaging evidence that support incorporating the cerebellum into epilepsy pathology. We examine reports of still controversial cerebellar epilepsy, studies of cerebellar stimulation alleviating paroxysmal epileptic activity, studies and case reports of cerebellar lesions directly associated with seizures, and conditions in which ataxia is accompanied by epileptic seizures. Finally, the review substantiates the role of this complex brain structure in epilepsy whether by coincidence, as a consequence of deleterious cortical epileptic activity or antiepileptic drugs, or the very cause of the disease. |
