Search Results

You are looking at 1 - 6 of 6 items for

  • Author or Editor: Frederic B. Meyer x
Clear All Modify Search
Restricted access

Aaron A. Cohen-Gadol, Jeffrey W. Britton, Frederic P. Collignon, Lisa M. Bates, Gregory D. Cascino and Fredric B. Meyer

Object. Surgical treatment options for intractable seizures caused by a nonlesional epileptogenic focus located in the central sulcus region are limited. The authors describe an alternative surgical approach for treating medically refractory nonlesional perirolandic epilepsy.

Methods. Five consecutive patients who were treated between 1996 and 2000 for nonlesional partial epilepsy that had originated in the central lobule were studied. The patients' ages ranged from 16 to 56 years (mean 28.6 years; there were four men and one woman). The duration of their epilepsy ranged from 8 to 39 years (mean 20.2 years), with a mean seizure frequency of 19 partial seizures per week. Preoperative assessment included video electroencephalography (EEG) and subtracted ictal—interictal single-photon emission computerized tomography coregistered with magnetic resonance imaging (SISCOM). Patients underwent an awake craniotomy stereotactically guided by the ictal EEG and SISCOM studies. Cortical stimulation was used to identify the sensorimotor cortex and to reproduce the patient's aura. A subdural grid was then implanted based on these results. Subsequent postoperative ictal electrocorticographic recordings and cortical stimulation further delineated the site of seizure onset and functional anatomy. During a second awake craniotomy, a limited resection of the epileptogenic central lobule region was performed while function was continuously monitored intraoperatively. One resection was limited to the precentral gyrus, two to the postcentral gyrus, and in two the excisions involved regions of both the pre- and postcentral gyri.

In three patients a hemiparesis occurred postsurgery but later resolved. In the four patients whose resection involved the postcentral gyrus, transient cortical sensory loss and apraxia occurred, which completely resolved in three. Two patients are completely seizure free, two have experienced occasional nondisabling seizures, and one patient has benefited from a more than 75% reduction in seizure frequency. The follow-up period ranged from 2 to 5.5 years (mean 3.5 years).

Conclusions. A limited resection of the sensorimotor cortex may be performed with acceptable neurological morbidity in patients with medically refractory perirolandic epilepsy. This procedure is an alternative to multiple subpial transections in the surgical management of intractable nonlesional epilepsy originating from the sensorimotor cortex.

Restricted access

Aaron A. Cohen-Gadol, Brian G. Wilhelmi, Frederic Collignon, J. Bradley White, Jeffrey W. Britton, Denise M. Cambier, Teresa J. H. Christianson, W. Richard Marsh, Fredric B. Meyer and Gregory D. Cascino


The authors reviewed the long-term outcome of focal resection in a large group of patients who had intractable partial nonlesional epilepsy, including mesial temporal lobe sclerosis (MTS), and who were treated consecutively at a single institution. The goal of this study was to evaluate the long-term efficacy of epilepsy surgery and the preoperative factors associated with seizure outcome.


This retrospective analysis included 399 consecutive patients who underwent epilepsy surgery at Mayo Clinic in Rochester, Minnesota, between 1988 and 1996. The mean age of the patients at surgery was 32 ± 12 years (range 3–69 years), and the mean age at seizure onset was 12 ± 11 years (range 0–55 years). There were 214 female (54%) and 185 male (46%) patients. The mean duration of epilepsy was 20 ±12 years (range 1–56 years). The preceding values are given as the mean ± standard deviation.

Of the 399 patients, 237 (59%) had a history of complex partial seizures, 119 (30%) had generalized seizures, 26 (6%) had simple partial seizures, and 17 (4%) had experienced a combination of these. Preoperative evaluation included a routine and video-electroencephalography recordings, magnetic resonance imaging of the head according to the seizure protocol, neuropsychological testing, and a sodium amobarbital study. Patients with an undefined epileptogenic focus and discordant preoperative studies underwent an intracranial study. The mean duration of follow up was 6.2 ± 4.5 years (range 0.6–15.7 years). Seizure outcome was categorized based on the modified Engel classification. Time-to-event analysis was performed using Kaplan–Meier curves and Cox regression models to evaluate the risk factors associated with outcomes.

Among these patients, 372 (93%) underwent temporal and 27 (7%) had extratemporal resection of their epileptogenic focus. Histopathological examination of the resected specimens revealed MTS in 113 patients (28%), gliosis in 237 (59%), and normal findings in 49 (12%). Based on the Kaplan–Meier analysis, the probability of an Engel Class I outcome (seizure free, auras, or seizures related only to medication withdrawal) for the overall patient group was 81% (95% confidence interval [CI] 77–85%) at 6 months, 78% (CI 74–82%) at 1 year, 76% (CI 72–80%) at 2 years, 74% (CI 69–78%) at 5 years, and 72% (CI 67–77%) at 10 years postoperatively. The rate of Class I outcomes remained 72% for 73 patients with more than 10 years of follow up. If a patient was in Class I at 1 year postoperatively, the probability of seizure remission at 10 years postoperatively was 92% (95% CI 89–96%); almost all seizures occurred during the 1st year after surgery. Factors predictive of poor outcome from surgery were normal pathological findings in resected tissue (p = 0.038), male sex (p = 0.035), previous surgery (p < 0.001), and an extratemporal origin of seizures (p < 0.001).


The response to epilepsy surgery during the 1st follow-up year is a reliable indicator of the long-term Engel Class I postoperative outcome. This finding may have important implications for patient counseling and postoperative discontinuation of anticonvulsant medications.

Restricted access

Ross C. Puffer, Luz M. Cumba Garcia, Benjamin T. Himes, Mi-Yeon Jung, Frederic B. Meyer, David O. Okonkwo and Ian F. Parney


The objective of this study was to isolate extracellular vesicles (EVs) from plasma in a cohort of patients with traumatic brain injury (TBI) and analyze their contents for novel biomarkers that could prove useful for rapid diagnosis and classification of brain injury during initial evaluation.


Plasma EVs were isolated by serial ultracentrifugation from patients with TBI (n = 15) and healthy controls (n = 5). Samples were obtained from the TRACK-TBI biorepository (2010–present). Size and concentration were determined by nanoparticle tracking. Glial fibrillary acidic protein (GFAP) concentration was determined in EV protein. EV RNA was isolated and deep sequencing of short noncoding RNA was performed.


Plasma EVs are physically similar but contained approximately 10 times more GFAP in TBI patients with altered consciousness than patients and controls with normal consciousness. Eleven highly differentially expressed microRNAs (miRNAs) were identified between these groups. Genes targeted by these miRNAs are highly associated with biologically relevant cellular pathways, including organismal injury, cellular development, and organismal development. Multiple additional coding and noncoding RNA species with potential biomarker utility were identified.


Isolating plasma EVs in patients with TBI is feasible. Increased GFAP concentration—a validated plasma TBI marker—in EVs from TBI patients with altered consciousness, along with differential expression of multiple miRNAs targeting TBI-relevant pathways, suggests that EVs may be a useful source of TBI biomarkers. Additional evaluation in larger patient cohorts is indicated.

Restricted access

Frederic Collignon, Nicholas M. Wetjen, Aaron A. Cohen-Gadol, Gregory D. Cascino, Joseph Parisi, Fredric B. Meyer, W. Richard Marsh, Patrick Roche and Stephen D. Weigand


The causes of epileptic events remain unclear. Much in vitro and in vivo experimental evidence suggests that gap junctions formed by connexins (Cxs) between neurons and/or astrocytes contribute to the generation and maintenance of seizures; however, few experiments have been conducted in humans, and those completed have shown controversial data. The authors designed a study to compare the level of expression of Cxs in hippocampi from epileptic and nonepileptic patients to assess whether an alteration of gap junction expression in epileptic tissue plays a role in seizure origin and propagation.


The expression of Cxs32, -36, and -43 was studied in 47 consecutive samples of hippocampi obtained from epileptic patients who had undergone an amygdalohippocampectomy for the treatment of intractable seizure. These expression levels were compared with those in hippocampi obtained in nonepileptic patients during postmortem dissection. Immunostaining was performed to create one slide for each of the three Cxs. Each slide demonstrated multiple cells from each of six regions (CA1, CA2, CA3, CA4, dentate gyrus, and subiculum). Two independent reviewers rated each Cx–region combination according to an immunoreactive score.

Across all three measures—that is, staining intensity, percentage of positively stained cells, and immunoreactive score—Cx32 appeared to be expressed at a significantly lower level in the epileptic patients compared with controls (p < 0.001 for each measure), whereas Cx43 appeared to be expressed more among the epileptic patients (p < 0.001 for each measure). There was no evidence of any differential expression of Cx36. There was, however, regional variation within each Cx subtype. For Cx36, the staining intensity was higher in the CA2 region in the epilepsy group.


The increase in Cx43, decrease in Cx32, and preservation of Cx36 expression in hippocampi from epileptic persons could play a role in the development of seizures in patients with temporal sclerosis. Additional studies must be completed to understand this mechanism better.