Developmental trajectory and sex differences in auditory processing in a PTEN-deletion model of autism spectrum disorders.

Autism Spectrum Disorders (ASD) encompass a wide array of debilitating symptoms, including severe sensory deficits and abnormal language development. Sensory deficits early in development may lead to broader symptomatology in adolescents and adults. The mechanistic links between ASD risk genes, sensory processing and language impairment are unclear. There is also a sex bias in ASD diagnosis and symptomatology. The current study aims to identify the developmental trajectory and genotype- and sex-dependent differences in auditory sensitivity and temporal processing in a Pten-deletion (phosphatase and tensin homolog missing on chromosome 10) mouse model of ASD. Auditory temporal processing is crucial for speech recognition and language development and deficits will cause language impairments. However, very little is known about the development of temporal processing in ASD animal models, and if there are sex differences. To address this major gap, we recorded epidural electroencephalography (EEG) signals from the frontal (FC) and auditory (AC) cortex in developing and adult Nse-cre PTEN mice, in which Pten is deleted in specific cortical layers (layers III-V) (PTEN conditional knock-out (cKO). We quantified resting EEG spectral power distribution, auditory event related potentials (ERP) and temporal processing from awake and freely moving male and female mice. Temporal processing is measured using a gap-in-noise-ASSR (auditory steady state response) stimulus paradigm. The experimental manipulation of gap duration and modulation depth allows us to measure cortical entrainment to rapid gaps in sounds. Temporal processing was quantified using inter-trial phase clustering (ITPC) values that account for phase consistency across trials. The results show genotype differences in resting power distribution in PTEN cKO mice throughout development. Male and female cKO mice have significantly increased beta power but decreased high frequency oscillations in the AC and FC. Both male and female PTEN cKO mice show diminished ITPC in their gap-ASSR responses in the AC and FC compared to control mice. Overall, deficits become more prominent in adult (p60) mice, with cKO mice having significantly increased sound evoked power and decreased ITPC compared to controls. While both male and female cKO mice demonstrated severe temporal processing deficits across development, female cKO mice showed increased hypersensitivity compared to males, reflected as increased N1 and P2 amplitudes. These data identify a number of novel sensory processing deficits in a PTEN-ASD mouse model that are present from an early age. Abnormal temporal processing and hypersensitive responses may contribute to abnormal development of language function in ASD.

Focused ultrasound and other lesioning in the treatment of tremor.

There has been a long history of lesioning procedures to treat tremor associated with both essential tremor (ET) and Parkinson's disease (PD). These include radiofrequency (RF) thalamotomy, gamma knife radiosurgical (GKRS) thalamotomy, and magnetic resonance-guided focused ultrasound (MRgFUS). In this review, we summarize the clinical studies of lesioning procedures for tremor focusing on these ablative therapies for ET and tremor-predominant PD (TDPD). We then consider clinical treatment variables that influence decision-making regarding ablative therapies versus consideration of deep brain stimulation (DBS) and conclude with ongoing and future studies. This article is part of the Special Issue "Tremor" edited by Daniel D. Truong, Mark Hallett, and Aasef Shaikh.

Regulation of NRG-1-ErbB4 signaling and neuroprotection by exogenous neuregulin-1 in a mouse model of epilepsy.

Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy. Dysregulation of glutamate transporters has been a common finding across animal models of epilepsy and in patients with TLE. In this study, we investigate NRG-1/ErbB4 signaling in epileptogenesis and the neuroprotective effects of NRG-1 treatment in a mouse model of temporal lobe epilepsy. Using immunohistochemistry, we report the first evidence for NRG-1/ErbB4-dependent selective upregulation of glutamate transporter EAAC1 and bihemispheric neuroprotection by exogeneous NRG-1 in the intrahippocampal kainic acid (IHKA) model of TLE. Our findings provide evidence that dysregulation of glutamate transporter EAAC1 contributes to the development of epilepsy and can be therapeutically targeted to reduce neuronal death following IHKA-induced status epilepticus (SE).

Astrocytes and Epilepsy.

Changes in astrocyte channels, transporters, and metabolism play a critical role in seizure generation and epilepsy. In particular, alterations in astrocyte potassium, glutamate, water and adenosine homeostasis and gap junctional coupling have all been associated with hyperexcitability and epileptogenesis (largely in temporal lobe epilepsy). Distinct astrocytic changes have also been identified in other types of epilepsy, such as tuberous sclerosis, tumor-associated epilepsy and post-traumatic epilepsy. Together, the emerging literature on astrocytes and epilepsy provides powerful rationale for distinct new therapeutic targets that are astrocyte-specific.

Astrocyte-Selective Volume Increase in Elevated Extracellular Potassium Conditions Is Mediated by the Na+/K+ ATPase and Occurs Independently of Aquaporin 4.

Astrocytes and neurons have been shown to swell across a variety of different conditions, including increases in extracellular potassium concentration (^[K+]o). The mechanisms involved in the coupling of K+ influx to water movement into cells leading to cell swelling are not well understood and remain controversial. Here, we set out to determine the effects of ^[K+]o on rapid volume responses of hippocampal CA1 pyramidal neurons and stratum radiatum astrocytes using real-time confocal volume imaging. First, we found that elevating [K+]o within a physiological range (to 6.5 mM and 10.5 mM from a baseline of 2.5 mM), and even up to pathological levels (26 mM), produced dose-dependent increases in astrocyte volume, with absolutely no effect on neuronal volume. In the absence of compensating for addition of KCl by removal of an equal amount of NaCl, neurons actually shrank in ^[K+]o, while astrocytes continued to exhibit rapid volume increases. Astrocyte swelling in ^[K+]o was not dependent on neuronal firing, aquaporin 4, the inwardly rectifying potassium channel Kir 4.1, the sodium bicarbonate cotransporter NBCe1, , or the electroneutral cotransporter, sodium-potassium-chloride cotransporter type 1 (NKCC1), but was significantly attenuated in 1 mM barium chloride (BaCl2) and by the Na+/K+ ATPase inhibitor ouabain. Effects of 1 mM BaCl2 and ouabain applied together were not additive and, together with reports that BaCl2 can inhibit the NKA at high concentrations, suggests a prominent role for the astrocyte NKA in rapid astrocyte volume increases occurring in ^[K+]o. These findings carry important implications for understanding mechanisms of cellular edema, regulation of the brain extracellular space, and brain tissue excitability.

Chronic Brain Imaging Across a Transparent Nanocrystalline Yttria-Stabilized-Zirconia Cranial Implant.

Repeated non-diffuse optical imaging of the brain is difficult. This is due to the fact that the cranial bone is highly scattering and thus a strong optical barrier. Repeated craniotomies increase the risk of complications and may disrupt the biological systems being imaged. We previously introduced a potential solution in the form of a transparent ceramic cranial implant called the Window to the Brain (WttB) implant. This implant is made of nanocrystalline Yttria-Stabilized Zirconia (nc-YSZ), which possesses the requisite mechanical strength to serve as a permanent optical access window in human patients. In this present study, we demonstrate repeated brain imaging of n = 5 mice using both OCT and LSI across the WttB implant over 4 weeks. The main objectives are to determine if the WttB implant allows for chronic OCT imaging, and to shed further light on the question of whether optical access provided by the WttB implant remains stable over this duration in the body. The Window to the Brain implant allowed for stable repeated imaging of the mouse brain with Optical Coherence Tomography over 28 days, without loss of signal intensity. Repeated Laser Speckle Imaging was also possible over this timeframe, but signal to noise ratio and the sharpness of vessels in the images decreased with time. This can be partially explained by elevated blood flow during the first imaging session in response to trauma from the surgery, which was also detected by OCT flow imaging. These results are promising for long-term optical access through the WttB implant, making feasible chronic in vivo studies in multiple neurological models of brain disease.

Optical Access to Arteriovenous Cerebral Microcirculation Through a Transparent Cranial Implant.

BACKGROUND AND OBJECTIVE: Microcirculation plays a critical role in physiologic processes and several disease states. Laser speckle imaging (LSI) is a full-field, real-time imaging technique capable of mapping microvessel networks and providing relative flow velocity within the vessels. In this study, we demonstrate that LSI combine with multispectral reflectance imaging (MSRI), which allows for distinction between veins and arteries in the vascular flow maps produced by LSI. We apply this combined technique to mouse cerebral vascular network in vivo, comparing imaging through the skull, to the dura mater and brain directly through a craniectomy, and through a transparent cranial "Window to the Brain" (WttB) implant. STUDY DESIGN/MATERIALS AND METHODS: The WttB implant used in this study is made of a nanocrystalline Yttria-Stabilized-Zirconia ceramic. MSRI was conducted using white-light illumination and filtering the reflected light for 560, 570, 580, 590, 600, and 610 nm. LSI was conducted using an 810 nm continuous wave near-infrared laser with incident power of 100 mW, and the reflected speckle pattern was captured by a complementary metal-oxide-semiconductor (CMOS) camera. RESULTS: Seven vessel branches were analyzed and comparison was made between imaging through the skull, craniectomy, and WttB implant. Through the skull, MSRI did not detect any vessels, and LSI could not image microvessels. Imaging through the WttB implant, MSRI was able to identify veins versus arteries, and LSI was able to image microvessels with only slightly higher signal-to-noise ratio and lower sharpness than imaging the brain through a craniectomy. CONCLUSIONS: This study demonstrates the ability to perform MSRI-LSI across a transparent cranial implant, to allow for cerebral vascular networks to be mapped, including microvessels. These images contain additional information such as vein-artery separation and relative blood flow velocities, information which is of value scientifically and medically. The WttB implant provides substantial improvements over imaging through the murine cranial bone, where microvessels are not visible and MSRI cannot be performed. Lasers Surg. Med. © 2019 Wiley Periodicals, Inc.

Chronic demyelination-induced seizures.

Multiple sclerosis (MS) patients are three to six times more likely to develop epilepsy compared to the rest of the population. Seizures are more common in patients with early onset or progressive forms of the disease and prognosticate rapid progression to disability and death. Gray matter atrophy, hippocampal lesions, interneuron loss, and elevated juxtacortical lesion burden have been identified in MS patients with seizures; however, translational studies aimed at elucidating the pathophysiological processes underlying MS epileptogenesis are limited. Here, we report that cuprizone-mediated chronically demyelinated (9-12weeks) mice exhibit marked changes to dorsal hippocampal electroencephalography (EEG) and evidence of overt seizure activity. Immunohistochemical (IHC) analyses within the hippocampal CA1 region revealed extensive demyelination, loss of parvalbumin (PV+) interneurons, widespread gliosis, and changes in aquaporin-4 (AQP4) expression. Our results suggest that chronically demyelinated mice are a valuable model with which we may begin to understand the mechanisms underlying demyelination-induced seizures.

GLT-1-Dependent Disruption of CNS Glutamate Homeostasis and Neuronal Function by the Protozoan Parasite Toxoplasma gondii.

The immune privileged nature of the CNS can make it vulnerable to chronic and latent infections. Little is known about the effects of lifelong brain infections, and thus inflammation, on the neurological health of the host. Toxoplasma gondii is a parasite that can infect any mammalian nucleated cell with average worldwide seroprevalence rates of 30%. Infection by Toxoplasma is characterized by the lifelong presence of parasitic cysts within neurons in the brain, requiring a competent immune system to prevent parasite reactivation and encephalitis. In the immunocompetent individual, Toxoplasma infection is largely asymptomatic, however many recent studies suggest a strong correlation with certain neurodegenerative and psychiatric disorders. Here, we demonstrate a significant reduction in the primary astrocytic glutamate transporter, GLT-1, following infection with Toxoplasma. Using microdialysis of the murine frontal cortex over the course of infection, a significant increase in extracellular concentrations of glutamate is observed. Consistent with glutamate dysregulation, analysis of neurons reveal changes in morphology including a reduction in dendritic spines, VGlut1 and NeuN immunoreactivity. Furthermore, behavioral testing and EEG recordings point to significant changes in neuronal output. Finally, these changes in neuronal connectivity are dependent on infection-induced downregulation of GLT-1 as treatment with the ß-lactam antibiotic ceftriaxone, rescues extracellular glutamate concentrations, neuronal pathology and function. Altogether, these data demonstrate that following an infection with T. gondii, the delicate regulation of glutamate by astrocytes is disrupted and accounts for a range of deficits observed in chronic infection.

Transparent nanocrystalline yttria-stabilized-zirconia calvarium prosthesis.

Laser-based diagnostics and therapeutics show promise for many neurological disorders. However, the poor transparency of cranial bone (calvaria) limits the spatial resolution and interaction depth that can be achieved, thus constraining opportunity in this regard. Herein, we report preliminary results from efforts seeking to address this limitation through use of novel transparent cranial implants made from nanocrystalline yttria-stabilized zirconia (nc-YSZ). Using optical coherence tomography (OCT) imaging of underlying brain in an acute murine model, we show that signal strength is improved when imaging through nc-YSZ implants relative to native cranium. As such, this provides initial evidence supporting the feasibility of nc-YSZ as a transparent cranial implant material. Furthermore, it represents a crucial first step towards realization of an innovative new concept we are developing, which seeks to eventually provide a clinically-viable means for optically accessing the brain, on-demand, over large areas, and on a chronically-recurring basis, without need for repeated craniectomies. FROM THE CLINICAL EDITOR: In this study, transparent nanocrystalline yttria-stabilized-zirconia is used as an experimental "cranium prosthesis" material, enabling the replacement of segments of cranial bone with a material that allows for optical access to the brain on a recurrent basis using optical imaging methods such as OCT.

Glial cell changes in epilepsy: overview of the clinical problem and therapeutic opportunities.

It is estimated that one in 26 people will develop epilepsy in their lifetime, amounting to almost 12 million people in the United States alone (Hesdorffer et al., 2011). Epilepsy is a group of conditions characterized by sporadic occurrence of seizures and unconsciousness. This severely limits the ability to perform everyday tasks and leads to increased difficulty with learning and memory, maintenance of steady employment, driving, and overall socioeconomic integration. A greater understanding of the cellular and molecular mechanisms underlying seizures and epilepsy is necessary, as it may lead to novel antiepileptic treatments. In this chapter, we will review the current literature surrounding the involvement of glial cells in epilepsy with particular emphasis on review of human tissue studies and some possible underlying mechanisms. Based on the current evidence and hypotheses of glial mechanisms in epilepsy, novel therapeutic opportunities for the treatment of epilepsy will also be presented.

Impact of aquaporin-4 channels on K+ buffering and gap junction coupling in the hippocampus.

Aquaporin-4 (AQP4) is the main water channel in the brain and primarily localized to astrocytes where the channels are thought to contribute to water and K(+) homeostasis. The close apposition of AQP4 and inward rectifier K(+) channels (Kir4.1) led to the hypothesis of direct functional interactions between both channels. We investigated the impact of AQP4 on stimulus-induced alterations of the extracellular K(+) concentration ([K(+)](o)) in murine hippocampal slices. Recordings with K(+)-selective microelectrodes combined with field potential analyses were compared in wild type (wt) and AQP4 knockout (AQP4(-/-)) mice. Astrocyte gap junction coupling was assessed with tracer filling during patch clamp recording. Antidromic fiber stimulation in the alveus evoked smaller increases and slower recovery of [K(+)](o) in the stratum pyramidale of AQP4(-/-) mice indicating reduced glial swelling and a larger extracellular space when compared with control tissue. Moreover, the data hint at an impairment of the glial Na(+)/K(+) ATPase in AQP4-deficient astrocytes. In a next step, we investigated the laminar profile of [K(+)](o) by moving the recording electrode from the stratum pyramidale toward the hippocampal fissure. At distances beyond 300 µm from the pyramidal layer, the stimulation-induced, normalized increases of [K(+)](o) in AQP4(-/-) mice exceeded the corresponding values of wt mice, indicating facilitated spatial buffering. Astrocytes in AQP4(-/-) mice also displayed enhanced tracer coupling, which might underlie the improved spatial re- distribution of [K(+)](o) in the hippocampus. These findings highlight the role of AQP4 channels in the regulation of K(+) homeostasis.

Deletion of aquaporin-4 renders retinal glial cells more susceptible to osmotic stress.

The glial water channel aquaporin-4 (AQP4) is implicated in the control of ion and osmohomeostasis in the sensory retina. Using retinal slices from AQP4-deficient and wild-type mice, we investigated whether AQP4 is involved in the regulation of glial cell volume under altered osmotic conditions. Superfusion of retinal slices with a hypoosmolar solution induced a rapid swelling of glial somata in tissues from AQP4 null mice but not from wild-type mice. The swelling was mediated by oxidative stress, inflammatory lipid mediators, and sodium influx into the cells and was prevented by activation of glutamatergic and purinergic receptors. Distinct inflammatory proteins, including interleukin-1 beta, interleukin-6, and inducible nitric oxide synthase, were up-regulated in the retina of AQP4 null mice compared with control, whereas cyclooxygenase-2 was down-regulated. The data suggest that water flux through AQP4 is involved in the rapid volume regulation of retinal glial (Müller) cells in response to osmotic stress and that deletion of AQP4 results in an inflammatory response of the retinal tissue. Possible implications of the data for understanding the pathophysiology of neuromyelitis optica, a human disease that has been suggested to involve serum antibodies to AQP4, are discussed.

Protective role of aquaporin-4 water channels after contusion spinal cord injury.

OBJECTIVE: Spinal cord injury (SCI) is accompanied by disruption of the blood-spinal cord barrier and subsequent extravasation of fluid and proteins, which results in edema (increased water content) at the site of injury. However, the mechanisms that control edema and the extent to which edema impacts outcome after SCI are not well elucidated. METHODS: Here, we examined the role of aquaporin-4 (AQP4) water channels after experimental contusion injury in mice, a clinically relevant animal model of SCI. RESULTS: Mice lacking AQP4 (AQP4(-/-) mice) exhibited significantly impaired locomotor function and prolonged bladder dysfunction compared with wild-type (WT) littermates after contusion SCI. Consistent with a greater extent of functional deterioration, AQP4(-/-) mice showed greater neuronal loss and demyelination, with prominent cyst formation, which is generally absent in mouse SCI. The extent of spinal cord edema, as expressed by percentage water content, was persistently increased above control levels in AQP4(-/-) mice but not WT mice at 14 and 28 days after injury. Immunohistochemical analysis indicated that blood vessels in the vicinity of the lesion core had incomplete barrier function because of sparse tight junctions. INTERPRETATION: These results suggest that AQP4 plays a protective role after contusion SCI by facilitating the clearance of excess water, and that targeting edema after SCI may be a novel therapeutic strategy.

Tumor-associated epilepsy.

Tumor-associated epilepsy is an important contributor to morbidity in patients with brain tumors. Proposed pathophysiological mechanisms to explain these effects range from neuronal and glial dysfunction to deranged vascular homeostasis, to ionic and pH changes. Perilesional tissue alterations play a vital role in the generation of tumor-associated seizures. Clinical studies have determined that tumor-associated seizures are usually focal with secondary generalization and often resistant to antiepileptic drugs. Tumor histopathological characteristics and location are independent factors that impact seizure burden. Further understanding of the mechanisms of tumor-associated epilepsy may lead to new types of treatments targeted at perilesional tissue alterations.

Isolated amygdala neurocysticercosis in a patient presenting with déjà vu and olfactory auras. Case report.

Neurocysticercosis is the most common parasitic infection in the CNS and a leading cause of epilepsy. Since it is a circumscribed lesional cause of epilepsy, specific locations of neurocysticercal lesions may lead to specific clinical presentations. The authors describe a 17-year-old Hispanic boy who had a single enhancing bilobar mass in the right amygdala. Initially, the patient presented with secondarily generalized tonic-clonic seizures, which resolved with antiepilepsy drug therapy. On further investigation, he was found to have persistent olfactory and déjà vu auras. A right amygdalectomy without hippocampectomy was performed, and both the seizures and auras immediately resolved. Pathological analysis revealed neurocysticercosis. To the authors' knowledge, this case is the first reported instance of 2 distinct mesial temporal aura semiologies associated with localized neurocysticercosis in the amygdala and successfully treated with resection. Uniquely, the case demonstrates that both olfactory and déjà vu auras can emanate from the amygdala.

Characteristics of auras in patients undergoing temporal lobectomy.

OBJECT: Prior studies suggest that aura semiology may have localizing value. However, temporal lobe aura characteristics and response to surgery have not been studied in large patient series. METHODS: The authors retrospectively analyzed the case records of 182 patients undergoing temporal lobectomy for medically intractable epilepsy at a single institution. They analyzed the frequency and type of auras and seizures preoperatively, and at 3 months and 1 year after temporal lobectomy. Auras were divided into medial semiology (rising epigastric, olfactory/gustatory, experiential, and fear) and lateral semiology (auditory, somatosensory, and visual), or other. RESULTS: Of 182 patients, 150 were included in this study. The preoperative prevalence of auras was 77%. Multiple types of auras were present in 20% of patients. The most common aura was rising epigastric (26% of all auras). Postoperatively, auras were eliminated in 63% of patients at 3 months and in 64% at 1 year. Seventy-seven patients (51%) were seizure-free and aura-free, 22 (15%) were seizure-free with auras, 26 (17%) had seizures but no auras, and 25 (17%) had seizures with auras. Despite having their auras eliminated, 6.7% of patients continued to have complex partial seizures. Lateral temporal auras were more than twice as likely as medial temporal auras to persist after surgery (p < 0.002). CONCLUSIONS: While the majority of patients in the authors' series became seizure- and aura-free, a significant minority still had persistent auras. Patients with lateral temporal auras appear to be at increased risk for having persistent postoperative auras. The discrepancy between aura and seizure outcomes results in a small group of patients having persistent seizures but losing their auras postoperatively.

Gamma Knife radiosurgery for brain metastases from primary breast cancer.

PURPOSE: The relative roles of stereotactic radiosurgery (SRS) vs. whole brain radiotherapy (WBRT) in the treatment of patients with brain metastases from breast cancer remain undefined. In this study, we reviewed our experience with these patients. MATERIALS AND METHODS: We retrospectively reviewed all patients treated between 1991 and 2005 with Gamma Knife SRS for brain metastases from breast cancer. The actuarial survival and freedom from progression endpoints were calculated using the Kaplan-Meier method. RESULTS: Between 1991 and 2005, 176 patients underwent SRS for brain metastases from breast cancer. The median survival time was 16.0 months for 95 newly diagnosed patients and 11.7 months for 81 patients with recurrent brain metastases. In the newly diagnosed patients, omission of upfront WBRT did not significantly affect the MST (p = .20), brain freedom from progression (p = .75), or freedom from new brain metastases (p = .83). Longer survival was associated with age <50 years, Karnofsky performance score >or=70, primary tumor control, estrogen receptor positivity, and Her2/neu overexpression. No association was found between the number of treated brain metastases and the survival time. CONCLUSION: We have described prognostic factors for breast cancer patients treated with SRS for newly diagnosed or recurrent brain metastases. Most patient subsets had a median survival time of >or=11 months. Unexpectedly, upfront WBRT did not appear to improve brain freedom from progression, and a larger number of brain metastases was not associated with a shorter survival time. Breast cancer might be distinct from other primary sites in terms of prognostic factors and the roles of WBRT and SRS for brain metastases.

Conquering the third ventricular chamber.

Surgery within the third ventricle was a special challenge early in the conception of the discipline of neurosurgery due to a lack of diagnostic methods and difficulty in reaching and removing lesions affecting this vital region. Walter Dandy and Harvey Cushing performed pioneering approaches of the third ventricular region. The authors have reviewed the previously undisclosed efforts of Cushing to approach the third ventricle through a direct review of his available patient records at the Cushing Brain Tumor Registry. The authors compare these efforts to those of Dandy published in Dandy's pioneering work Benign Tumors in the Third Ventricle of the Brain: Diagnosis and Treatment. Based on the review of these records, the authors attempt to examine the foundations of surgery within the third ventricle.

Surgical treatment of parietal lobe epilepsy.

OBJECT: Parietal lobe epilepsy (PLE) accounts for a small percentage of extratemporal epilepsies, and only a few and mostly smaller series have been reported. Preoperative findings, surgical strategies, pathological bases, and postoperative outcomes for PLE remain to be elucidated. METHODS: Patients with PLE were identified by screening a prospective epilepsy surgery database established in 1989 at the University of Bonn. Charts, preoperative imaging studies, surgical reports, and neuropathological findings were reviewed. Seizure outcome was classified according to Engel class (I-IV). RESULTS: Forty patients (23 females and 17 males) with PLE were identified and had a mean age of 25.0 years and a mean preoperative epilepsy duration of 13.7 years. Nine patients had a significant medical history (for example, trauma, meningitis/encephalitis, or perinatal hypoxia). Preoperative MR imaging abnormalities were identified in 38 (95%) of 40 patients; 26 patients (65%) underwent invasive electroencephalography evaluation. After lesionectomy of the dominant (in 20 patients) or nondominant (in 20 patients) parietal lobe and additional multiple subpial transections (in 11 patients), 2 patients suffered from surgical and 12 from neurological complications, including temporary partial Gerstmann syndrome. There were no deaths. Histopathological analysis revealed 16 low-grade tumors, 11 cortical dysplasias, 9 gliotic scars, 2 cavernous vascular malformations, and 1 granulomatous inflammation. In 1 case, no histopathological diagnosis could be made. After a mean follow-up of 45 months, 27 patients (67.5%) became seizure free or had rare seizures (57.5% Engel Class I; 10% Engel Class II; 27.5% Engel Class III; and 5% Engel Class IV). CONCLUSIONS: Parietal lobe epilepsy is an infrequent cause of extratemporal epilepsy. Satisfactory results (Engel Classes I and II) were obtained in 67.5% of patients in our series. A temporary partial hemisensory or Gerstmann syndrome occurs in a significant number of patients.