Cerebellar seizures

2009

Patients with cerebellar lesions rarely present with seizures. There is only limited data about seizure types and electroencephalographic findings in patients with cerebellar lesions. We present here three children with cerebellar lesions whose first clinical presentations were seizures. One of these children (cerebellar dysplasia) was operated and his seizures stopped after the surgery. Two other children are followed with periodic cranial magnetic resonance imaging every 6 months. Their seizures have been controlled with antiepileptic medications. Seizures can develop in children with cerebellar lesions. The coexistence of a cerebellar lesion with seizures should raise the possibility of cerebellar epileptic seizures and prompt a thorough investigation of the presence of subcortical epilepsy.

Epilepsia, 2002

The cerebellum is known to have an inhibitory effect on seizures. Nevertheless, cerebellar dysplastic lesions can be epileptogenic. A 4-month-old infant had paroxysmal facial contractions; tachypnea and nystagmoid eyeball and tremulous movements were occasionally combined. These evolved to stereotypic clinical patterns and frequencies, which increased despite administration of antiepileptic drugs (AEDs). Magnetic resonance imaging (MRI) demonstrated a mass arising from the superior cerebellar peduncle, although video-scalp EEG monitoring revealed no abnormal findings. Positron emission tomography with [ 18 F]fluorodeoxyglucose revealed focal

Child's Nervous System, 2007

Objective The role of the cerebellum in the pathogenesis of seizures remains controversial. Cerebellar origin of seizures, albeit rare, has been described in the literature in association with intrinsic lesions of the cerebellum. We present a unique case of a patient with medically intractable, secondary generalized epilepsy, associated with a superior cerebellar quadrigeminal arachnoid cyst. Clinical presentation A 9-year-old child presented with medically refractory secondary generalized epilepsy associated with recurrent headaches since 6 months of age. The child also had moderate intellectual impairment and autism. On the magnetic resonance imaging (MRI) of the head, he was noticed to have a small superior cerebellar arachnoid cyst in the quadrigeminal area that had increased in size slightly. Interictal electroencephalograph (EEG) was unable to localize the site of the epilepsy. Neurological examination was unremarkable. Intervention A suboccipital craniotomy and supracerebellar infratentorial approach to the cyst was performed at 9 years of age. Intraoperative electrocorticography (ECOG) demonstrated epileptic activity from the cerebellar tissue adjacent to the cyst. The cyst was fenestrated, and the cyst wall was sent for histology. Seizure control improved dramatically after fenestration of the cyst. Conclusion This case provides strong evidence that, albeit rare, the cerebellum may be a source of epileptic activity due to compression by a lesion in the posterior fossa. Hence, in cases with intractable epilepsy of unknown supratentorial source, the differential diagnosis should include a posterior fossa lesion. The finding of a posterior fossa lesion in such cases, even if it is small and appears benign, should precipitate a discussion about the possible relationship between the posterior fossa lesion and the epilepsy.

Epilepsy Research, 2013

Please cite this article in press as: Lascano, A.M., et al., Tracking the source of cerebellar epilepsy: Hemifacial seizures associated with cerebellar cortical dysplasia. Epilepsy Res. (2013), http://dx.Summary Traditionally, subcortical structures such as the cerebellum are supposed to exert a modulatory effect on epileptic seizures, rather than being the primary seizure generator. We report a 14-month old girl presenting, since birth, with seizures symptomatic of a right cerebellar dysplasia, manifested as paroxystic contralateral hemifacial spasm and ipsilateral facial weakness. Multimodal imaging was used to investigate both anatomical landmarks related to the cerebellar lesion and mechanisms underlying seizure generation. Electric source imaging (ESI) supported the hypothesis of a right cerebellar epileptogenic generator in concordance with nuclear imaging findings; subsequently validated by intra-operative intralesional recordings. Diffusion spectrum imaging-related tractography (DSI) showed severe cerebellar structural abnormalities confirmed by histological examination. We suggest that hemispheric cerebellar lesions in cases like this are likely to cause epilepsy via an effect on the facial nuclei through ipsilateral and contralateral aberrant connections.

2020

ABSTRACTThe new aggregate data analyses revealed the earlier missing role played by the cerebellum long-term electrical stimulation in the absence epilepsy. Neurophysiologic data gained by authors favor that cerebellar serial deep brain stimulation (DBS) (100 Hz) causes the transformation of penicillin-induced cortical focal discharges into prolonged 3,5-3,75 sec oscillations resembling spike-wave discharges (SWD) in cats. Such SWDs were not organized in the form of bursts and persisted continuously after stimulation. Therefore the appearance of prolonged periods of SWD is regarded as a tonic cerebellar influence upon pacemaker of SWD and might be caused by the long-lasting DBS-induced increase of GABA-ergic extrasynaptic inhibition in forebrain networks. At the same time, cerebellar DBS high-frequency (100 Hz) suppressed bursts of SWD observed during the phase of stimulation. Different types of cerebellar DBS upon epileptic activity emphasized the absence seizure facilitation discu...

Brain and Development, 2010

We present a male infant with hemifacial seizures refractory to antiepileptic medication. Hemifacial spasms around the left eye were frequent during wakefulness and sleep since birth. He also had mild psychomotor retardation. Magnetic resonance imaging (MRI) revealed a large tumor in the left middle cerebellar peduncle. Ictal single photon emission computed tomography (SPECT) and ictal 18 F-fluorodeoxyglucose [ 18 F-FDG] positron emission tomography (PET) revealed hyperperfusion and hyper glucose metabolism at the tumor. Total removal of the tumor resulted in complete disappearance of hemifacial seizures and improved psychomotor development, indicating that the cerebellar tumor caused hemifacial seizures. A histopathological study confirmed that the tumor was a ganglioglioma. This case and the literature on similar cases indicated that this was a new epileptic syndrome originating in the cerebellum. Early diagnosis and early complete removal of the epileptogenic lesion should be recommended for this syndrome.

Epilepsia, 2000

To determine the incidence of cerebellar atrophy (CA) in patients with intractable temporal lobe epilepsy, whether any clinical factors are significantly associated with CA, whether CA is unilateral or asymmetric and whether this feature has any relationship to the side of epileptogenicity, and whether the presence of CA is related to epilepsy surgery outcome. Methods: We developed a magnetic resonance imaging method of measuring the presurgical volumes of the cerebellar hemispheres of 185 patients who underwent temporal lobectomy for intractable epilepsy and of 80 control subjects. In addition, cerebellar volumes were normalized to the total brain volumes. CA was determined as being present when the measured volume was smaller than two standard deviations from the mean value found in control subjects. Results: Both absolute and normalized cerebellar volumes were found to be significantly reduced in the epilepsy patients compared with the control subjects. Without normalization of Cerebellar atrophy (CA) is a common finding among patients with longstanding partial epilepsy (1-5). The cause, frequency, and degree of atrophy are largely unknown. Several hypotheses have been proposed to explain this phenomenon: excitotoxicity in patients with a long duration of intractable epilepsy (1,6,7), hypoxia during secondarily generalized tonic-clonic seizures (8), toxicity from antiepileptic drugs (AEDs), particularly phenytoin (4,9,10),-and preexisting brain injury resulting from the initial epileptogenic insult (4). Also, although there has been experimental and clinical evidence to support the role of the cerebellum in the inhibition of partial seizures (1 1-17), the exact role of the cerebellum in seizures is unclear. Cerebrocerebellar diaschisis has been thought to be responsible for the CA seen in patients with partial seizures (1 8). Diaschisis is a disturbance of function in one

Journal of Neurosurgery, 2002

HERE seems to be no epileptic seizure that results from a lesion of the cerebellar cortex." This statement by Penfield and Erickson 38 exemplifies the classic teaching of Hughlings-Jackson that epileptic seizures arise only in the cerebral cortex. Epileptic seizures are defined as paroxysmal, excessive, and/or hypersynchronous discharges of neurons that may be associated with clinical manifestations and EEG changes. In 1886, Hughlings-Jackson 26 proposed that such activity had its origin in discharging lesions in the cerebral cortex. Over the last 120 years, the understanding of the fundamental role of the cerebrum in epilepsy has evolved, such that modern definitions of epilepsy in humans rely on cerebrocortical origins (that is, temporal compared with extratemporal). Subcortical structures, such as the brainstem and cerebellum, are thought to have only modulatory effects on cerebral epileptiform discharges; 17,19,33 thus, they are presumed to be indirectly involved in epileptic seizures. 6,11 Although subcortical epilepsy has been demonstrated in animal models, 22,23 and may be seen in conjunction with hypothalamic hamartomas, 5,30,37,45 only one case of focal motor seizures arising in the cerebellum has been reported in humans; 24 generalized seizures

Epilepsia, 1998

To determine the frequency and patterns of periictal cerebellar hyperperfusion, whether it is associated with increased cerebellar atrophy, and whether cerebellar hyperperfusion and cerebellar atrophy are associated with predisposing clinical factors or with the outcome of epilepsy surgery. Methods: Periictal and interictal SPECT scans and volumetric brain magnetic resonance imaging (MRI) were quantitatively analyzed in 54 consecutive patients with medically refractory partial epilepsy. Their histories were reviewed and their postsurgical outcomes assessed. Results: Significant periictal cerebellar hyperperfusion was found in 26 (48.1%) patients, of whom 18 had CCH, two had homolateral cerebellar hyperperfusion (HCH), and six had symmetrical bilateral hyperperfusion (BCH). No relation found between the site of the SPECT seizure localization and the presence or type of cerebellar hyperperfusion. CCH was more common when the injected seizure involved unilateral clonic motor activity (p < 0.05). A smaller MRI relative cerebellar volume (cerebellar volume/cerebral volume) was correlated with a greater seizure frequency (R, =-0.30; p < 0.05) but not with the duration of epilepsy. There was no difference in the cerebellar volumes between the different patterns of cerebellar perfusion (p > 0.05). However, patients without a focal structural MRI lesion had significantly smaller cerebellar volumes (p < 0.05). In patients who underwent epilepsy surgery (n = 31), there was a trend for those without excellent outcomes to have smaller relative cerebellar volumes than did those with excellent outcome (10.6 vs. 11.8%; p = 0.08). Conclusions: Periictal changes in cerebellar perfusion, particularly CCH, are common in patients with intractable partial epilepsy. However, periictal hyperperfusion does not appear to be a major contributor to the development of cerebellar atrophy.

Annals of Neurology, 1996

We investigated a 6-month-old infant with daily episodes of left hemifacial contraction, head and eye deviation to the right, nystagmoid jerks to the right, autonomic dysfunction, and retained consciousness. The episodes began on day 1 of life and were unresponsive to antiepileptic medication. Interictal and ictal scalp electroencephalographic (EEG) recordings were unremarkable. Magnetic resonance imaging revealed a mass in the left cerebellar hemisphere and peduncle. Ictal single-photon emission computed tomography revealed focal hyperperfusion in the region of the cerebellar mass. Ictal EEG recordings with implanted cerebellar electrodes demonstrated focal seizure discharges in the region of the mass. Resection of the mass resulted in remission of seizures and histopathology revealed ganglioglioma. Six previously reported infants with similar semiology (described as "hemifacial spasm"), imaging findings, and histopathology are reviewed. We believe the previously reported infants and our patient constitute a rare but important clinicopathological syndrome of infancy characterized by epileptic seizures of cerebellar origin. Harvey AS, Jayakar P, Duchowny M, Resnick T, Prats A, Altman N, Renfroe JB. Hemifacial seizures and cerebellar ganglioglioma: an epilepsy syndrome of infancy with seizures of cerebellar origin. Ann Neurol 1996;40:91-98