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Neurosurgery has traditionally been overtly focused on the study of anatomy and functions of cortical areas with microsurgical techniques aimed at preserving eloquent cortices. In the last two decades, there has been ever-increasing data emerging from advances in neuroimaging (principally diffusion tensor imaging) and clinical studies (principally from awake surgeries) that point to the important contribution of white matter tracts (WMT) that influence neurological function as part of a brain network. Major scientific consortiums worldwide, currently working on this human brain connectome, are providing evidence that is dramatically altering the manner in which we view neurosurgical procedures. The development of the telencephalic flexure, a major landmark during the human embryogenesis of the central nervous system (CNS), severely affects the cortical/subcortical anatomy in and around the sylvian fissure and thus the different interacting brain networks. Indeed, the telencephalic flexure modifies the anatomy of the human brain with the more posterior areas becoming ventral and lateral and associative fibers connecting the anterior areas with the previous posterior ones follow the flexure, thus becoming semicircular. In these areas, the projection, association, and commissural fibers intermingle with some WMT remaining curved and others longitudinal. Essentially the ultimate shape and location of these tracts are determined by the development of the telencephalic flexure. Five adult human brains were dissected (medial to lateral and lateral to medial) with a view to describing this intricate anatomy. To better understand the 3D orientation of the WMT of the region we have correlated the cadaveric data with the anatomy presented in the literature of the flexure during human neuro-embryogenesis in addition to cross-species comparisons of the flexure. The precise definition of the connectome of the telencephalic flexure is primordial during glioma surgery and for disconnective epilepsy surgery in this region.

OBJECTIVE Anterior quadrant disconnection represents a safe surgical option in well-selected pediatric patients with a large frontal lobe lesion anterior to the motor cortex. The understanding of the anatomy of the white matter tracts connecting the frontal lobe with the rest of the cerebrum forms the basis of a safe and successful disconnective surgery. The authors explored and illustrated the relevant white matter tracts sectioned during each surgical step using fiber dissection techniques. METHODS Five human cadaveric hemispheres were dissected to illustrate the frontal connections in the 3 planes. The dissections were performed from lateral to medial, medial to lateral, and ventral to dorsal to describe the various tracts sectioned during the 4 steps of this surgery, namely the anterior suprainsular window, intrafrontal disconnection, anterior callosotomy, and frontobasal disconnection. RESULTS At the beginning of each surgical step, the U fibers were cut. During the anterior suprainsular window, the superior longitudinal fasciculus (SLF), the uncinate fasciculus, and the inferior fronto-occipital fasciculus (IFOF) were visualized and sectioned, followed by sectioning of the anterior limb of the internal capsule. During the intrafrontal disconnection, the SLF was cut, along with the corona radiata. At the medial surface the cingulum was sectioned. The anterior callosotomy disconnected the anterior third of the body of the callosum, the genu, and the rostrum. The frontobasal disconnection addressed the last remaining fibers connecting the frontal lobe with the rest of the hemisphere, namely the anterior limb of the anterior commissure. CONCLUSIONS The anterior peri insular quadrantotomy aims at effectively treating children with large lesions of the frontal lobe anterior to the motor cortex. A precise understanding of the gyral anatomy of this lobe along with the several white matter connections is crucial to avoid motor complications and to ensure complete disconnection.

OBJECTIVE Surgery for frontal lobe epilepsy remains a challenge because of the variable seizure outcomes after surgery. Disconnective procedures are increasingly applied to isolate the epileptogenic focus and avoid complications related to extensive brain resection. Previously, the authors described the anterior quadrant disconnection procedure to treat large frontal lobe lesions extending up to but not involving the primary motor cortex. In this article, they describe a surgical technique for unilateral disconnection of the prefrontal cortex, while providing an accurate description of the surgical and functional anatomy of this disconnective procedure. METHODS The authors report the surgical treatment of a 5-month-old boy who presented with refractory epilepsy due to extensive cortical dysplasia of the left prefrontal lobe. In addition, with the aim of both describing the subcortical intrinsic anatomy and illustrating the different connections between the prefrontal lobe and the rest of the brain, the authors dissected six human cadaveric brain hemispheres. These dissections were performed from lateral to medial and from medial to lateral to reveal the various tracts sectioned during the three different steps in the surgery, namely the intrafrontal disconnection, anterior callosotomy, and frontobasal disconnection. RESULTS The first step of the dissection involves cutting the U-fibers. During the anterior intrafrontal disconnection, the superior longitudinal fasciculus in the depth of the middle frontal gyrus, the uncinate fasciculus, and the inferior frontooccipital fasciculus in the depth of the inferior frontal gyrus at the level of the anterior insular point are visualized and sectioned, followed by sectioning of the anterior limb of the internal capsule. Once the frontal horn is reached, the anterior callosotomy can be performed to disconnect the genu and the rostrum of the corpus callosum. The intrafrontal disconnection is deepened toward the falx, and at the medial surface, the cingulum is sectioned. The frontobasal disconnection involves cutting the anterior limb of the anterior commissure. CONCLUSIONS This technique allows selective isolation of the epileptogenic focus located in the prefrontal lobe to avoid secondary propagation. Understanding the surface and white matter fiber anatomy is essential to safely perform the procedure and obtain a favorable seizure outcome.

The effects of noradrenaline (NA) on synaptic responses in layer II of the entorhinal cortex (EC) were studied in normal and spontaneously epileptic mutant mice tottering using intracellular recording in a slice preparation. Neither the membrane properties of neurones nor the responses to NA differed between normal and tottering mice. NA (50 microM) hyperpolarized most (29/54) of the neurones via alpha 2 adrenergic receptors. Synaptic responses of EC neurones were complex. NA (10-100 microM) reduced all the components of the synaptic response in a concentration-dependent and reversible manner. The pharmacological properties of the inhibitory effect of NA were characterised and quantified on one component of the complex synaptic response, the fast excitatory postsynaptic potential. The effect of NA was mimicked by the alpha 2 agonist UK 14,304 and blocked by the alpha 2 antagonist yohimbine. It is concluded that NA can inhibit via an alpha 2 receptor-mediated action synaptic responses in the superficial layers of the EC.

The entorhinal cortex is a gateway to the hippocampus; it receives inputs from several cortical associative areas as well as subcortical areas. Since there is evidence showing that noradrenaline reduces the epileptic activity generated in the entorhinal cortex, we have examined the action of noradrenaline in the superficial layer of the entorhinal cortex, which is the main source of afferents to the hippocampus. In a previous study we showed that noradrenaline hyperpolarized layer II entorhinal cortex neurons and reduced global synaptic transmission via alpha 2-adrenoreceptors. Here we present a detailed analysis of the effect of noradrenaline on membrane resistance and on the pharmacologically isolated postsynaptic potentials in layer II entorhinal cortex neurons of mice. Noradrenaline (50 microM) hyperpolarized most layer II entorhinal cortex neurons. This hyperpolarization corresponded to an outward current with a reversal potential following the Nernst equilibrium potential for potassium. The hyperpolarizing effect of noradrenaline was blocked by 10 microM yohimbine. These observations suggest that noradrenaline activates a potassium conductance via an alpha 2-adrenoreceptor. Noradrenaline (10-50 microM) reversibly reduced the amplitude of the pharmacologically isolated excitatory potentials mediated by both NMDA and alpha-amino-3-hydroxy-5-methyl-isoxazole-propionic acid (AMPA) receptors, the former being more strongly affected. Again this effect was blocked by 10 microM yohimbine. In contrast, GABAA-mediated synaptic transmission was virtually unaffected by noradrenaline. Thus, noradrenaline appears to strongly inhibit the glutamate-mediated synaptic transmission in the entorhinal cortex without affecting inhibitory post-synaptic potentials. These observations suggest that alpha 2-adrenergic receptor agonists may exert a beneficial effect in the control of hyperexcitability in temporal lobe epilepsy.

The entorhinal cortex and the amygdala are interconnected structures of the limbic system in which paroxysmal activity occurs during temporal lobe epilepsy. Conflicting evidence shows that noradrenaline (i) inhibits the spreading to other parts of the limbic system of paroxysmal activity generated in the amygdala or the entorhinal cortex, but also (ii) increases glutamatergic transmission in the basolateral amygdala. Given our previous work on the inhibitory effect of noradrenaline on entorhinal cortex neurons, we developed an in vitro slice preparation to study the synaptic transmission in the basolateral amygdala and its modulation by noradrenaline. Noradrenaline reduced the fast excitatory postsynaptic potential (EPSP) by approximately 40% at 100 microM and the slow EPSP by approximately 50% at 50 microM. A similar effect was obtained with the alpha2-agonist UK 14304 at 100 and 50 microM respectively. In contrast, the beta-agonist isoproterenol increased the fast EPSP by approximately 40% at 100 microM and the slow EPSP by approximately 20% at 50 microM. Accordingly, the effect of noradrenaline on the EPSPs was blocked by the alpha2-antagonist yohimbine (10 microM) but not by the alpha1-antagonist prazosine (10 microM) and the beta-antagonist propranolol (10 microM). Noradrenaline (50-100 microM) was ineffective on most (14/16) of the isolated inhibitory postsynaptic potentials (IPSPs). These experiments provide evidence that noradrenaline inhibits the excitatory synaptic response of basolateral amygdala neurons. A pharmacological analysis revealed that the noradrenergic modulation of the excitatory transmission in the basolateral amygdala can be dissected into a predominant alpha2-adrenoreceptor-mediated inhibition and a beta-adrenoreceptor-mediated excitation.