The term cerebellar seizures refers to any clinical paroxysmal event believed or proven to be due to pathological, massive, and repetitive cortical cerebellar neuronal depolarization. Cerebellar seizures are characterized by hemifacial contraction (click on clip), head and eye deviation, nystagmus and autonomic dysfunction; consciousness is usually not affected. They occur with cerebellar tumors.
Facial spasms due to cerebellar seizures may be very subtle. Ipsilateral arm contraction is often present (click on clip).
Figure 57.1.— [A] Sagittal MRI of the brain demonstrating a large posterior fossa tumor (contrast) and dilatation of the third ventricle. [B] Hematoxylin-eosin stain of tumor tissue demonstrating a solid proliferation of large balloon cells with abundant glassy to finely granular or foamy eosinophilic cytoplasm with frequent eccentric uniformly regular nuclei with bland chromatin and a distinct nucleoli. The histology was consistent with a subependymal giant cell astrocytomas.
Antiepileptic drugs and etiological treatment stop seizures by preventing massive repetitive and synchronous neuronal depolarization. During depolarization, the voltage-dependent sodium channels open and sodium enters the cell driven by its concentration (there is more sodium outside the cell than inside the cell) and electrical gradients (there are more negative charges than positive charges adjacent to the inner surface of the membrane). When the inner side of the membrane is flooded with enough positive ions to decrease its normal negativity above the threshold of the voltage-dependent sodium channels, these channels will open. Medications that maintain the inner membrane surface and prevent it from reaching the threshold of the voltage-dependent sodium channel prevent seizures.