Cerebrocerebellar structural covariance in temporal lobe epilepsy with hippocampal sclerosis.

PURPOSE: The purpose of the study was to evaluate cerebral morphological changes in temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) and their relationship to the cerebellum. METHODS: The study cohort included 21 patients with intractable TLE-HS (14 left-sided, 7 right-sided) and 38 healthy controls (HC). All patients later underwent anteromedial temporal lobe resection. All subjects were examined using a 1.5-T magnetic resonance imaging (MRI). Volumes of distinct cerebral and cerebellar structures were measured using voxel-based morphometry. The structural covariance of temporal lobe structures, insula, and thalamus with cerebellar substructures was examined using partial least squares regression. RESULTS: Morphological changes were more significant in the group with left TLE-HS when comparing left-sided with right-sided structures as well as when comparing patients with controls. The gray matter volume (GMV) of the temporal lobe structures was smaller ipsilaterally to the seizure onset side in most cases. There was a significant amygdala enlargement contralateral to the side of hippocampal sclerosis in both patients with right and left TLE-HS as compared with controls. Selected vermian structures in patients with left but not right TLE-HS had significantly larger GMV than the identical substructures in controls. The structural covariance differed significantly between patients with left and right TLE-HS as compared with HC. The analysis revealed significant negative covariance between anterior vermis and mesial temporal structures in the group with left TLE-HS. No significance was observed for the group with right TLE-HS. CONCLUSION: There is significant asymmetry in the GMV of cerebral and cerebellar structures in patients with TLE-HS. Morphological changes are distinctly more pronounced in patients with left TLE-HS. The observed structural covariance between the cerebellum and supratentorial structures in TLE-HS suggests associations beyond the mesial temporal lobe structures and thalamus.

Morphological changes of cerebellar substructures in temporal lobe epilepsy: A complex phenomenon, not mere atrophy.

PURPOSE: To evaluate cerebellar volume changes in temporal lobe epilepsy (TLE) patients in greater detail. We aimed to determine which discrete substructures significantly differ in patients with TLE compared to controls and the nature of this difference. Correlations with age at epilepsy onset, epilepsy duration, seizure frequency, and total number of antiepileptic drugs (AED) in the patient's history were studied. We analyzed the potential association between cerebellar atrophy and epilepsy surgery outcome. METHODS: Study participants were 36 TLE patients; 22 hippocampal sclerosis (HS) only and 38 healthy controls. All patients later underwent temporal lobe resection. All subjects were examined using 1.5T MRI. Cerebellar volume was adjusted for total intracranial volume, age, and gender, and measured using voxel-based morphometry. Cerebellar substructures were defined using the AAL atlas. Data processing was performed automatically. Separate analyses for HS only subset were performed. RESULTS: Total cerebellar gray matter volume (GMV) appeared non-significantly smaller in epilepsy patients. Within the substructures, the GMV of the selected vermian segments were significantly larger in patients. The GMV of the whole cerebellum and of all individual cerebellar substructures non-significantly decreased with increasing complex partial seizure frequency and total number of AEDs in the patient's history. Total cerebellar GMV was significantly smaller in patients with persistent seizures after epilepsy surgery than in seizure-free patients. CONCLUSION: Cerebellar atrophy is a complex phenomenon, the character of changes differs significantly within the cerebellar substructures. Total cerebellar GMV reduction is associated with worse outcome of temporal lobe resection.

Interrater variability for CT angiography evaluation between neurologists and neuroradiologist in acute stroke patients.

OBJECTIVE: The diagnosis of arterial occlusion has a considerable impact on the indication of mechanical thrombectomy, and CT angiography (CTA) is recommended in the management of acute stroke. The goal of the present study is to assess the interrater agreement in the diagnosis of occlusion of intracranial arteries on CTA between a neuroradiologist and neurologists. METHODS: CTA images of 75 acute stroke patients were evaluated for occlusion of intracranial arteries by an experienced interventional neuroradiologist, and stroke and general neurologists. RESULTS: 75 patients who were treated by intravenous thrombolysis were enrolled in the study. CTA images were available for all 75 patients (34 females; mean age ± SD, 72 ± 14 years; National Institutes of Health Stroke Scale 10; median 8-14; and Alberta Stroke Program Early CT mean 9.7). The agreement between the neuroradiologist and neurologists in evaluation of intracranial artery occlusion was as follows: occlusion of the middle cerebral artery segment M1: observer agreement 77%, kappa (κ) = 0.61 and middle cerebral artery M2: observer agreement 77%, κ 0.48; internal carotid artery: observer agreement 92%, κ 0.84; T occlusion: observer agreement 90.0%, κ 0.33; posterior cerebral artery segments P1 and P2: observer agreement 98%, κ 0.97; basilar artery: observer agreement 96%, κ 0.92; and vertebral artery segment V4: observer agreement 88%, κ 0.48. CONCLUSION: Interrater agreement of CTA evaluation of occlusion between the neurologists and the neuroradiologist was very strong. The ability of the trained neurologists to read an intracranial large vessel occlusion correctly may improve the door-to-needle times in acute stroke. Advances in knowledge: In this study, the neurologists were able to recognize occlusion of intracranial arteries. This could accelerate the management of acute stroke care.

Cerebellar Dysfunction and Ataxia in Patients with Epilepsy: Coincidence, Consequence, or Cause?

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.

Claustrum damage and refractory status epilepticus following febrile illness.

OBJECTIVE: To characterize the clinical, EEG, and brain imaging findings in an adult case series of patients with de novo refractory status epilepticus (SE) occurring after a febrile illness. METHODS: A retrospective study (2010-2013) was undertaken with the following inclusion criteria: (1) previously healthy adults with refractory SE; (2) seizure onset 0-21 days after a febrile illness; (3) lacking evidence of infectious agents in CSF; (4) no history of seizures (febrile or afebrile) or previous or concomitant neurologic disorder. RESULTS: Among 155 refractory SE cases observed in the study period, 6 patients (17-35 years old) fulfilled the inclusion criteria. Confusion and stupor were the most common symptoms at disease onset, followed after a few days by acute repeated seizures that were uncountable in all but one. Seizures consisted of focal motor/myoclonic phenomena with subsequent generalization. Antiepileptic drugs failed in every patient to control seizures, with all participants requiring intensive care unit admission. Barbiturate coma with burst-suppression pattern was applied in 4 out of 6 patients for 5-14 days. One participant died in the acute phase. In each patient, we observed a reversible bilateral claustrum MRI hyperintensity on T2-weighted sequences, without restricted diffusion, time-related with SE. All patients had negative multiple neural antibodies testing. Four out of 5 surviving patients developed chronic epilepsy. CONCLUSIONS: This is a hypothesis-generating study of a preliminary nature supporting the role of the claustrum in postfebrile de novo SE; future prospective studies are needed to delineate the specificity of this condition, its pathogenesis, and the etiology.