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Fornicotomy has been used to treat intractable temporal lobe epilepsy with mixed success historically; however, modern advances in stereotactic, neurosurgical, and imaging techniques offer new opportunities to target the fornix with greater precision and safety. In this review, we discuss the historical uses and quantify the outcomes of fornicotomy for the treatment of temporal lobe epilepsy, highlight the potential mechanisms of benefit, and address what is known about the side effects of the procedure. We find that fornicotomy, with or without anterior commissurotomy, resulted in 61% (83/136) of patients having some seizure control benefit. We discuss the potential operative approaches for targeting the fornix, including laser ablation and the use of focused ultrasound ablation. More work is needed to address the true efficacy of fornicotomy in the modern surgical setting. This review is intended to serve as a framework for developing this approach.

INTRODUCTION: Rett syndrome is a neurodevelopmental genetic disorder, characterized by developmental delay, hand stereotypies, abnormal gait, and acquired microcephaly. Epilepsy is very common in Rett syndrome and can be medically intractable. It remains uncertain if a patient with epileptic drop attacks associated with this genetic disease can benefit from corpus callosotomy. CASE REPORT: We report an 8-year-old girl with Rett syndrome and medically intractable epileptic drop attacks who underwent endoscopic total corpus callosotomy without any complications that led to the successful elimination of her seizures. CONCLUSION: Total corpus callosotomy is a feasible treatment option for medically intractable epileptic drop attacks in Rett syndrome and should not be considered as a contraindication in this condition. This is the first reported case of corpus callosotomy in Rett syndrome.

Herein, we report the case of a 35-year-old female with a trapped right lung secondary to catamenial haemothorax. Following surgical decortication, re-expansion of the lung was not observed until postoperative day 81. This delay represents a heretofore unencountered complication that should be considered in the surgical management of catamenial haemothorax due to thoracic endometriosis syndrome.

The balance between glutamate (cortex and thalamus) and dopamine (substantia nigra) inputs on striatal neurons is of vital importance. Dopamine deficiency, which breaks this balance and leads to the domination of cortical glutamatergic inputs, plays an important role in Parkinson's disease (PD). However, the exact impact on striatal neurons has not been fully clarified. Thus, the present study aimed to characterize the influence of corticostriatal glutamatergic inputs on striatal neurons after decortication due to dopamine depletion in rats. 6‑Hydroxydopamine was injected into the right medial forebrain bundle to induce dopamine depletion, and/or ibotenic acid into the primary motor cortex to induce decortication. Subsequently, the grip strength test and Morris water maze task indicated that decortication significantly shortened the hang time and the latency that had been increased in the rats subjected to dopamine depletion. Golgi staining and electron microscopy analysis showed that the total dendritic length and dendritic spine density of the striatal neurons were decreased in the dopamine‑depleted rats, whereas decortication alleviated this damage. Immunohistochemistry analysis demonstrated that decortication decreased the number of caspase‑3‑positive neurons in the dopamine‑depleted rats. Moreover, reverse transcription‑quantitative PCR and western blot analyses showed that decortication offset the upregulation of caspase‑3 at both the protein and mRNA levels in the dopamine‑depleted rats. In conclusion, the present study demonstrated that a relative excess of cortical glutamate inputs had a substantial impact on the pathological processes of striatal neuron lesions in PD.

Epilepsy surgery revealed dramatically improved seizure outcomes over medical therapy in drug-resistant epilepsy patients. Children with epilepsy, however, have multiple epileptic focuses which require multilobar resection for better seizure outcome. Multilobar resection has not only the several severe surgical complications, such as hydrocephalus and shunt-related craniosynostosis, due to intracranial volume reduction. Isolation method (disconnection surgery) was progressively studied over epileptic focus removal (resective surgery) for seizure control. This concept was first introduced for functional hemispherotomy, and its primary principle is to preserve the vital vascularized brain that is functionally disconnected from the contralateral healthy brain. Currently in most epilepsy centers, the predominant disconnection surgical methods, including functional hemispherotomy, are continually being refined and are showing excellent results. They allow the functional isolation of the hemisphere or multi-lobe, affected by severe epilepsy. This review describes recent findings concerning the indication, surgical technique, seizure outcome and complications in several disconnection surgeries including the functional hemispherotomy for refractory pediatric epilepsy.

One of the potential disadvantages of conventional pleurectomy/decortication for malignant pleural mesothelioma is the need for opening the pleural sac, which might worsen survival. In this study, we have introduced non-incisional pleurectomy/decortication as an alternative technique that does not require the opening of the pleural sac.

Background An extensive frontal resection is a frequently performed neurosurgical procedure, especially for treating brain tumor and refractory epilepsy. However, there is a paucity of reports available regarding its surgical anatomy and technique. Objectives We sought to present the anatomic landmarks and surgical technique of the frontal lobe decortication (FLD) in epilepsy. The goals were to maximize the gray matter removal, spare primary and supplementary motor areas, and preserve the frontal horn. Material and Methods The anatomic study was based on dissections performed in 15 formalin-fixed adult cadaveric heads. The clinical experience with 15 patients is summarized. Result FLD consists of 5 steps: 1) coagulation and section of arterial branches of lateral surface; 2) paramedian subpial resection 3 cm ahead of the precentral sulcus to reach the genu of corpus callosum; 3) resection of gray matter of lateral surface, preserving the frontal horn; 4) removal of gray matter of basal surface preserving olfactory tract; 5) removal of gray matter of the medial surface under the rostrum of corpus callosum. The frontal horn was preserved in all 15 patients; 12 patients (80%) had no complications; 2 patients presented temporary hemiparesis; and 1 Rasmussen syndrome patient developed postoperative fever. The best seizure control was in cases with focal magnetic resonance imaging abnormalities limited to the frontal lobe. Conclusion FLD is an anatomy-based surgical technique for extensive frontal lobe resection. It presents reliable anatomic landmarks, selective gray matter removal, preservation of frontal horn, and low complication rate in our series. It can be an alternative option to the classical frontal lobectomy.

The current decerebration procedures discard the role of the thalamus in the motor control and decortication only rules out the brain cortex part, leaving a gap between the brain cortex and the subthalamic motor regions. In here we define a new preparation denominated Brain Cortex-Ablated Cat (BCAC), in which the frontal and parietal brain cortices as well as the central white matter beneath them were removed, this decerebration process may be considered as suprathalamic, since the thalamus remained intact. To characterize this preparation cat hindlimb electromyograms (EMG), kinematics and cutaneous reflexes (CR) produced by electrical stimulation of sural (SU) or saphenous (SAPH) nerves were analyzed during locomotion in intact and in BCAC. In cortex-ablated cats compared to intact cats, the hindlimb EMG amplitude was increased in the flexors, whereas in most extensors the amplitude was decreased. Bifunctional muscle EMGs presented complex and speed-dependent amplitude changes. In intact cats CR produced an inhibition of extensors, as well as excitation and inhibition of flexors, and a complex pattern of withdrawal responses in bifunctional muscles. The same stimuli applied to BCAC produced no detectable responses, but in some cats cutaneous reflexes produced by electrical stimulation of saphenous nerve reappeared when the locomotion speed increased. In BCAC, EMG and kinematic changes, as well as the absence of CR, imply that for this cat preparation there is a partial compensation due to the subcortical locomotor apparatus generating close to normal locomotion.

Following brain damage, especially in juvenile animals, large-scale reorganization is known to occur in the remaining brain structures to compensate for functional deficits. In rats with neonatal hemidecortication, corticospinal fibers originating from the undamaged side of the sensorimotor cortex issue collateral sprouts to the ipsilateral spinal gray matter that mediate cortical excitation to ipsilateral forelimb motoneurons and compensate for the deficit in forelimb movements. The present study was designed to investigate the origins of the ipsilateral corticospinal projection in neonatally hemidecorticated rats. Corticospinal neurons (CSNs) were labeled in adults by injecting retrograde neural tracers, cholera toxin subunit B with different fluorescent probes, into either side of the cervical spinal gray matter. In the undamaged cortex, double-labeled neurons were rarely found. CSNs with contralateral projections (contra-CSNs) and those with ipsilateral projections (ipsi-CSNs) were distributed both in the rostral forelimb motor area (RFA) and the caudal forelimb motor area (CFA). However, there was a difference in the distributions of the ipsi-CSNs between the two forelimb areas. Whereas the distribution of the ipsi-CSNs largely overlapped with that of the contra-CSNs in the RFA, the ipsi-CSNs tended to be segregated from the contra-CSNs in the CFA. The results suggested that the RFA and the CFA contribute to the compensatory process in different ways.

To examine the compensatory mechanisms in rats that underwent left decortication at postnatal day 7 (P7), we injected the retrograde tracers fluorescein isothiocyanate-cholera toxin B subunit (FITC-CTB) and Fast Blue (FB) into the right and left upper cervical spinal cord, respectively, at postoperative weeks 2, 3, 4, and 5 and counted the number of retrogradely labeled corticospinal neurons in the right cerebral cortex compared with that in normally developed rats. Significantly more ipsilaterally projecting neurons were labeled with FITC-CTB in the decorticated rats compared with normal rats at all time points examined. The number of labeled neurons was similar to that at P7 in normal rats. There were also some FITC-CTB and FB double-labeled neurons in both decorticated and normal rats. The number of double-labeled neurons in the decorticated rats increased each week and was significantly greater than that in normal rats at postoperative weeks 4 and 5. The present results suggest that the elimination of ipsilaterally projecting axons observed in normal rats was prevented in the decorticated rats, so that the cerebral cortex neurons on the unlesioned side projected corticospinal tracts to the ipsilateral spinal cord. Furthermore, the collaterals of the corticospinal tracts originating from the cerebral cortex on the unlesioned side also project to the ipsilateral spinal cord. These compensatory mechanisms might underlie the acquisition of motor function in these animals.

Neonatally hemidecorticated rats show fairly normal reaching and grasping behaviors of the forelimb contralateral to the lesion at the adult stage. Previous experiments using an anterograde tracer showed that the corticospinal fibers originating from the sensorimotor cortex of the intact side projected aberrant collaterals to the spinal gray matter on the ipsilateral side. The present study used electrophysiological methods to investigate whether the aberrant projections of the corticospinal tract mediated the pyramidal excitation to the ipsilateral forelimb motoneurons and, if so, which pathways mediate the effect in the hemidecorticated rats. Electrical stimulation to the intact medullary pyramid elicited bilateral negative field potentials in the dorsal horn of the spinal cord. In intracellular recordings of forelimb motoneurons, oligosynaptic pyramidal excitation was detected on both sides of the spinal cord in the hemidecorticated rats, whereas pyramidal excitation of motoneurons on the side ipsilateral to the stimulation was much smaller in normal rats. By lesioning the dorsal funiculus at the upper cervical level, we clarified that the excitation was transmitted to the ipsilateral motoneurons by at least two pathways: one via the corticospinal tract and spinal interneurons and the other via the cortico-reticulo-spinal pathways. These results suggested that in the neonatally hemidecorticated rats, the forelimb movements on the side contralateral to the lesion were modulated by motor commands through the indirect ipsilateral descending pathways from the sensorimotor cortex of the intact side either via the spinal interneurons or reticulospinal neurons.

A best evidence topic in thoracic surgery was written according to a structured protocol. The question addressed was whether video-assisted thoracoscopic surgical decortication (VATSD) might be superior to open decortication (OD) (or chest tube drainage) for the management of adults with primary empyema? Altogether 68 papers were found using the reported search, of which 14 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. We conclude that VATSD has superior outcomes for the treatment of persistent pleural collections in terms of postoperative morbidity, complications and length of hospital stay, and gives equivalent resolution when compared with OD. One study comparing VATSD and chest tube drainage of fibrinopurulent empyema found video-assisted thoracoscopic surgery (VATS) had higher treatment success (91% vs. 44%; P0.05), lower chest tube duration (5.8+/-1.1 vs. 9.8+/-1.3 days; P=0.03), and lower number of total hospital days (8.7+/-0.9 vs. 12.8+/-1.1 days; P=0.009). Eight studies comparing early and late empyema report conversion rates to OD of 0-3.5% in early, 7.1-46% in late stage and significant reductions in length of stay with VATSD compared with OD both postoperatively (5 vs. 8 days; P=0.001) and in total stay (15 vs. 21; P=0.03). Additionally VATS resulted in reduced postoperative pain (P0.0001) and complications including atelectasis (P=0.006), prolonged air-leak (P=0.0003), sepsis (P=0.03) and 30-day mortality (P=0.02). Five studies considered only chronic persistent empyema of which two directly compared VATSD to tube thoracostomy (TT). VATS resolved 88% of cases and had mortality rates of 1.3% compared with 62% and 11%, respectively, for TT. Moreover, conversion to OD was 10.5-17.1% with VATS and 18-37% with TT (P0.05). In agreement with mixed stage empyema, hospital stay was reduced both postoperatively (8.3 vs. 12.8 days; P0.05) and in total (14+/-1 vs. 17+/-1 days; P0.05), and when compared with OD (one study), pain (P0.0001), postoperative air-leak (P=0.004), hospital stay (P=0.020) and time to return to work (P0.0001) were all reduced with VATS. Additionally, re-operation (4.8% vs. 1%; P=0.09) and mortality (4/123% vs. 0%) were lower in VATS vs. OD.

The orbitofrontal cortex (OFC) has been implicated in reinforcement-guided decision making, error monitoring, and the reversal of behavior in response to changing circumstances. The anterior cingulate cortex sulcus (ACCS), however, has also been implicated in similar aspects of behavior. Dissociating the unique functions of these areas would improve our understanding of the decision-making process. The effect of selective OFC lesions on how monkeys used the history of reinforcement to guide choices of either particular actions or particular stimuli was studied and compared with the effects of ACCSlesions. Both lesions disrupted decision making, but their effects were differentially modulated by the dependence on action– or stimulus–value contingencies. OFC lesions caused a deficit in stimulus but not action selection, whereas ACCSlesions had the opposite effect, disrupting action but not stimulus selection. Furthermore, OFC lesions that have previously been found to impair decision making when deterministic stimulus–reward contingencies are switched were found to cause a more general learning impairment in more naturalistic situations in which reward was stochastic. Both OFC and ACCSare essential for reinforcement-guided decision making rather than just error monitoring or behavioral reversal. The OFC and ACCSare both, however, more concerned with learning and making decisions, but their roles in selecting between stimulus and action values are distinct.

In the brain after infarction or trauma, the tissue eventually becomes pannecrotic and forms a cavity. In such situations, a scaffold is necessary for the implanted or migrated cells to produce new tissue. In this present study, therefore, we attempted to restore brain tissue using a novel biomaterial, polydimethylsiloxane-tetraethoxysilane (PDMS-TEOS) hybrid with or without vascular endothelial growth factor (VEGF), which is crucial for new vessel formation. When PDMS-TEOS scaffold was implanted into the artificial brain defect, it remained at the implanted site and kept the integrity of the brain shape. At 30 days after the implantation, the marginal territory of PDMS-TEOS scaffold became occupied by newly formed tissue. Immunohistochemical analysis revealed that the new tissue was constituted by astrocytes and endothelial cells. Addition of VEGF increased the newly produced tissue volume, and the immunohistochemical analysis showed that the numbers of astrocytes and endothelial cells were increased. Double staining with proliferation maker Ki67 demonstrated that VEGF significantly increased newly formed astrocytes and endothelial cells, indicating that addition of VEGF accelerated tissue restoration and angiogenesis. These findings show that implantation of PDMS-TEOS scaffold with VEGF might be effective for treating old brain infarction or trauma.

We describe a new test of vibrissae-elicited forelimb placing ability that allows testing of sensorimotor integration across the midline. Rats were given unilateral brain lesions using one of three methods: (1) middle cerebral artery occlusion (MCAo) causing significant damage to the cortex and striatum, (2) aspiration lesions to remove tissue from the sensorimotor cortex, and (3) infusions of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle, producing a parkinsonian syndrome. Application of the new test to these animals revealed that with some lesion types, the ability of vibrissae on the unimpaired side of the body to trigger placing in the functionally impaired forelimb recovers before vibrissae on the impaired side can elicit placing. This occurs despite the lack of any apparent vibrissae sensory deficit, since the contralesional vibrissae maintained the ability to trigger placing in the unimpaired forelimb in all lesions studied. Chronically, MCAo-lesioned rats do not place the impaired forelimb upon stimulation of the impaired-side vibrissae, but do place if the vibrissae on the good side are stimulated (i.e., when the placing is triggered "across the midline"). This is in contrast to 6-OHDA-lesioned rats which, consistent with parkinsonian akinesia, cannot place the impaired limb regardless of sensory trigger. Also, differences in the pattern of recovery between MCAo- and aspiration-lesioned rats suggest a possible anatomical substrate for cross-midline placing ability and its recovery. Unlike other tests, cross-midline placing methods can readily distinguish between severe stroke and severe parkinsonism in rats.

Cross-correlation functions were used to study the time delay (a measure of synchronization) in the appearance of epileptic discharges in distant areas of the cortex in the intact cortex and in neuronally isolated cortical strips in Wistar rats. Experiments were performed at different stages of axon sprouting 30 and 90 days after isolation of cortical areas and in intact cortex. Significant increases in the number of synapses in layer V of isolated cortical strips at 30 days correlated with significant decreases in the time delay, while decreases in the number of synapses at 90 days correlated with a significant increase in the time delay. This is evidence that newly formed synapses increase the extent of synchronization and thus affect epileptogenesis. The data obtained here suggest that large pyramidal cells in layer V of the rat neocortex form a neural network in pathological conditions, this supporting intracortical synchronization of epileptic discharges.

The hippocampus and the amygdala are involved in avoidance learning in mammals. The medial and lateral pallia of actinopterygian fish have been proposed as homologous to the mammalian pallial amygdala and hippocampus, respectively, on the basis of neuroanatomical findings. This work was aimed at studying the effects of ablation of the medial telencephalic pallia (MP) and lateral telencephalic pallia (LP) in goldfish on the retention of a conditioned avoidance response previously acquired in two experimental conditions. In the first experiment, fish were trained in nontrace avoidance conditioning. In the second experiment, fish were trained in trace avoidance conditioning in which temporal cues were crucial for the learning process. An MP lesion affected the retention of the avoidance response in both procedures; in contrast, an LP lesion impaired the retention only in the trace-conditioning procedure. These data support the presence of two different systems of memory in fish, based on discrete telencephalic areas: the MP, involved in an emotional memory system; and the LP, involved in a spatial, relational, or temporal memory system. Moreover, these differential effects were similar to those produced by amygdalar and hippocampal lesions in mammals. We conclude that these specialized systems of memory could have appeared early during phylogenesis and could have been conserved throughout vertebrate evolution. Ministerio de Ciencia y Tecnología BF-I2001-3178 Ministerio de Ciencia y Tecnología I2000-0315 Ministerio de Ciencia y Tecnología I2003-0029 Ministerio de Ciencia y Tecnología PB-96-1334 Junta de Andalucía CVI-242

This experiment tested the effect of cortical spreading depression on the sympathetic and thermogenic effects induced by orexin A. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures and heart rate were monitored in urethane-anesthetized male Sprague-Dawley rats before and 5 h after an injection of orexin A (1.5 nmol) into the lateral cerebral ventricle. The same variables were monitored in rats with cortical spreading depression, induced by an application of cotton pellets soaked with 2 M KCl to the frontal cortex. The results show that orexin A increases the sympathetic firing rate, IBAT and colonic temperatures and heart rate. The increases in firing rate, IBAT and colonic temperatures are blocked by cortical spreading depression, while the increase in heart rate is not affected by cortical spreading depression. These findings suggest that the cerebral cortex is involved in the control of the orexin A-induced hyperthermia. Furthermore, we suggested the name "hyperthermine A," as additional denomination of "orexin A." (C) 2003 IBRO. Published by Elsevier Ltd. All rights reserved.

Lesions of primary sensory cortex produce impairments in brain function as an outcome of the direct tissue damage. In addition, indirect lesion effects have been described that consist of functional deficits in areas sharing neural connections with the damaged area. The present study characterizes interhemispheric deficits produced as a result of unilateral lesions of the entire vibrissa representation of S-I barrel field cortex (BFC) in adult rats using single-neuron recording under urethane anesthesia. After unilateral lesions of adult BFC, responses of neurons in the contralateral homotopic BFC are severely depressed. Background (spontaneous) activity is reduced by approximately 80%, responses to test stimuli applied to the whiskers are reduced by approximately 50%, and onset of synaptic plasticity induced by trimming all but two whiskers ("whisker-pairing plasticity") is delayed over sevenfold compared with sham-lesion control animals. These deficits persist with only slight improvement for at least 4 months after lesion. Both fast-spiking and regular-spiking neuron responses are diminished contralateral to the lesion, as are cells above, below, and within the cortical barrels. Enriched environment experience increased the magnitude of responses and accelerated the rate of synaptic plasticity but did not restore response magnitude to control levels. Deficiencies in evoked responses and synaptic plasticity are primarily restricted to areas that share direct axonal connections with the lesioned cortex, because equivalently sized lesions of visual cortex produce minimal deficits in contralateral BFC function. These results indicate that interhemispheric deficits consist of remarkable and persistent decrements in sensory processing at the single-neuron level and support the idea that the deficits are somehow linked to the shared neural connections with the area of brain damage.

Many studies have confirmed the time-limited involvement of the hippocampus in mnemonic processes and suggested that there is reorganization of the responsible brain circuitry during memory consolidation. To clarify such reorganization, we chose trace classical eyeblink conditioning, in which hippocampal ablation produces temporally graded retrograde amnesia. Here, we extended the temporal characterization of retrograde amnesia to other regions that are involved in acquisition during this task: the medial prefrontal cortex (mPFC) and the cerebellum. At a various time interval after establishing the trace conditioned response (CR), rats received an aspiration of one of the three regions. After recovery, the animals were tested for their CR retention. When ablated 1 d after the learning, both the hippocampal lesion and the cerebellar lesion group of rats exhibited a severe impairment in retention of the CR, whereas the mPFC lesion group showed only a slight decline. With an increase in interval between the lesion and the learning, the effect of the hippocampal lesion diminished and that of the mPFC lesion increased. When ablated 4 weeks after the learning, the hippocampal lesion group exhibited as robust CRs as its corresponding control group. In contrast, the mPFC lesion and the cerebellar lesion groups failed to retain the CRs. These results indicate that the hippocampus and the cerebellum, but only marginally the mPFC, constitute a brain circuitry that mediates recently acquired memory. As time elapses, the circuitry is reorganized to use mainly the mPFC and the cerebellum, but not the hippocampus, for remotely acquired memory.

We previously reported anatomical plasticity in the adult motor cortex after a unilateral sensorimotor cortex (SMC) lesion and treatment with monoclonal antibody (mAb) IN-1, which permits neurite outgrowth from the intact, opposite cortex into deafferented subcortical targets. This study was designed to investigate whether treatment with the mAb IN-1 after SMC lesion in the adult leads to functional reorganization of the intact, opposite motor cortex. Adult rats underwent unilateral SMC aspiration lesion and treatment with either mAb IN-1 or control antibody, or no treatment. After a 6 week survival period, the intact, opposite forelimb motor cortex was explored using intracortical microstimulation to evoke forelimb movements. A dramatic increase in ipsilateral movements of the lesion-impaired forelimb was found in animals treated with mAb IN-1 compared with control animals. These results resembled our previous findings of cortical reorganization in the spared hemisphere after neonatal cortical lesion and without any additional treatment. These results show that, after adult cortical lesion, treatment with mAb IN-1 induces a functional reorganization of the intact, opposite motor cortex.

Cytogenesis in the adult brain can result from the recruitment of circulating precursors, but the proposal that some such cells transdifferentiate into neural elements is controversial. We have reinvestigated this issue by following the phenotypic fate of bone marrow cells expressing the green fluorescent protein transplanted into the systemic circulation of irradiated mice. Thousands of donor-derived cells were detected throughout brains of recipients killed 1–12 months after transplantation, but none displayed neuronal, macroglial, or endothelial characteristics, even after injury. Among those that crossed the endothelium of the cerebral cortex, >99.7% were identified as perivascular macrophages. Newly formed parenchymal microglia were found in significant numbers only in the cerebellum and at injury sites. Therefore, bone marrow does supply the mature brain with new specialized cells; however, mesenchymal precursors neither adopt neural phenotypes nor contribute to cerebral vascular remodeling. This continuous traffic of macrophages across the blood–brain barrier provides a vehicle to introduce therapeutic genes into the nervous system.

International audience; Fetal neurons (embryonic age E16) of occipital origin grafted in the visual cortex of albino rats at increasing postnatal stages (P0, P7, P15, P30, P60, P120) can be activated by photic stimulation. Inputs originate from five major areas of the brain ipsilateral to the graft, namely, the claustrum, the periallocortex/proisocortex, the isocortex, the visual thalamus, and some unspecific subthalamic and hypothalamic nuclei. All inputs decrease in number with the age at which grafting was performed. Isocortical afferents exhibit furthermore a progressive laminar shaping. In neonates, layer II-III and layer V-VI neurons contribute equally to the graft input. In adults, grafts receive prominent input (approximately 70-80%) from layer VI neurons whereas layer II-III neurons account for less than 10%. Proportions of layer IV (approximately 2-4%) and layer V (approximately 15-20%) neurons innervating the graft remain stable, irrespective of the age of the recipient. The adult pattern of connectivity between the host brain and the graft establishes in frontal and temporal areas 1 week earlier than in occipital areas. It is nearly completed in postnatal day 15 (P15) grafted recipients. Supragranular neurons would be thus unable to innervate and to make stable synapses at the graft level beyond P15, i.e., when eyes open. Some infragranular neurons (supposedly remnants of the earliest generated cortical cell population) still have this capacity in adults.

Disruption of corticostriatal glutamate input in the striatum decreased significantly extracellular striatal glutamate and dopamine levels. Local administration of 300 microM concentration of excitatory receptor agonist kainic acid increased significantly extracellular striatal dopamine in intact freely moving rats. These findings support the hypothesis that glutamate exerts a tonic facilitatory effect on striatal dopamine release. The effect of kainic acid on extracellular striatal glutamate concentration in intact rats was a biphasic increase. The first glutamate increase can be explained by stimulation of presynaptic kainate receptors present on corticostriatal glutamatergic nerve terminals; the second increase is probably the result of a continuous interaction of the different striatal neurotransmitters after disturbance of their balance. Release of dopamine and glutamate was modulated differently in the intact striatum and in the striatum deprived of corticostriatal input. Dopamine release in the denervated striatum after kainate receptor stimulation was significantly lower than in intact striatum, confirming the so-called cooperativity between glutamate and kainic acid. Loss of presynaptic kainate receptors on the glutamatergic nerve terminals after decortication resulted in a loss of effect of kainic acid on glutamate release in denervated striatum. Aspartate showed no significant changes in this study.

Oxidative stress and excitotoxicity have been implicated in selective striatal vulnerability caused by the mitochondrial toxin, 3-nitropropionic acid (3-NP), which may simulate Huntington's disease in animals and humans. The detailed mechanism of the role of superoxide in striatal vulnerability induced by 3-NP is still unknown. The authors investigated oxidative cellular injury and DNA fragmentation after systemic 3-NP injection in wild-type (Wt) mice and mutant mice with a deficiency in manganese superoxide dismutase (MnSOD; Sod2 −/+). Furthermore, they investigated the effects of decortication after 3-NP treatment in Sod2 −/+ mice, and copper/zinc SOD (CuZnSOD) treatment in recently developed Sod2 −/+ mice that overexpress CuZnSOD (SOD1 +/− / Sod2 −/+ mice). Oxidized hydroethidine, 8-hydroxyguanosine immunoreactivity, and nitrotyrosine immunoreactivity were increased in the Sod2 −/+ mice compared with the Wt mice after 3-NP treatment ( P < 0.001). Decortication completely abolished oxidative striatal damage after 3-NP treatment in the Sod2 −/+ mice. Increased CuZnSOD attenuated DNA fragmentation and striatal lesion volume after 3-NP treatment in the Sod2 −/+ mice ( P < 0.001). These data suggest that production of superoxide may be a critical step to excitotoxicity and subsequent DNA fragmentation in selective striatal vulnerability after 3-NP treatment.

In brain cortex‐ablated cats (BCAC), hind limb motoneurons activity patterns were studied during fictive locomotion (FL) or fictive scratching (FS) induced by pinna stimulation. In order to study motoneurons excitability: heteronymous monosynaptic reflex (HeMR), intracellular recording, and individual Ia afferent fiber antidromic activity (AA) were analyzed. The intraspinal cord microinjections of serotonin or glutamic acid effects were made to study their influence in FL or FS. During FS, HeMR amplitude in extensor and bifunctional motoneurons increased prior to or during the respective electroneurogram (ENG). In soleus (SOL) motoneurons were reduced during the scratch cycle (SC). AA in medial gastrocnemius (MG) Ia afferent individual fibers of L6‐L7 dorsal roots did not occur during FS. Flexor digitorum longus (FDL) and MG motoneurons fired with doublets during the FS bursting activity, motoneuron membrane potential from some posterior biceps (PB) motoneurons exhibits a depolarization in relation to the PB (ENG). It changed to a locomotor drive potential in relation to one of the double ENG, PB bursts. In FDL and semitendinosus (ST) motoneurons, the membrane potential was depolarized during FS, but it did not change during FL. Glutamic acid injected in the L3‐L4 spinal cord segment favored the transition from FS to FL. During FL, glutamic acid produces a duration increase of extensors ENGs. Serotonin increases the ENG amplitude in extensor motoneurons, as well as the duration of scratching episodes. It did not change the SC duration. Segregation and motoneurons excitability could be regulated by the rhythmic generator and the pattern generator of the central pattern generator.

Juvenile animal brains are highly plastic and thus often achieve better functional recovery after injury compared with adult brains. Recently, Umeda et al. (Umeda T, Takahashi M, Isa K, Isa T. J Neurophysiol 104: 1707–1716, 2010) have shown that the remodeling of both corticospinal and extra-pyramidal pathways can contribute to the recovery of grasping and reaching ability in hemidecorticated juvenile rats. They have further unveiled the strengthening of the cortico-reticulo-spinal pathway after injury, that mediates the fast excitation of ipsilateral motoneurons for functional recovery.

Charles Bonnet syndrome is a condition characterized by visual hallucinations. These simple or complex visual hallucinations are more common in elderly individuals with impaired peripheral vision. The current report describes a case of transient Charles Bonnet syndrome appearing after the removal of a meningioma. The patient was a 61-year-old man who already had impaired visual acuity due to diabetic retinopathy. Brain MRI revealed a cystic tumor severely compressing the right occipital lobe. Starting on day 2 postoperatively, the patient was troubled by recurring visual hallucinations involving people, flowers, pictures, and familiar settings(the train and a coffee shop). These continued for 3.5 months. This period roughly coincided with the time for the occipital lobe to recover from the compression caused by the tumor, a fact that was confirmed by several MRI scans. ¹²³I-IMP SPECT performed 1 month after the surgical operation showed an area of hypoperfusion in the right parieto-occipital lobe. Based on the patient's clinical course and MRI findings, the mechanism of onset of visual hallucinations in this patient was put forward. The release of pressure in the brain by tumor removal and subsequent recovery changed the blood flow to the brain. This triggered visual hallucinations in the patient, who was already predisposed to developing Charles Bonnet syndrome because of diabetic retinopathy. This case is interesting since it indicates that central neurological factors, as well as visual deficits, may induce the appearance of visual hallucinations in Charles Bonnet syndrome.

Sinonasal neuroendocrine carcinomas (NECs) are rare tumors. We present a rare case of intracranial invasion of sinonasal small-cell NEC. A 61-year-old woman with nasal obstruction and bleeding was referred to our hospital. Computed tomography showed a polyp-like tumor occupying her left nasal cavity and extending to the paranasal sinuses and anterior cranial fossa. The tumor was removed using a transfacial approach by otolaryngologists and a bifrontal cranial approach by neurosurgeons. In histopathological analyses, we found that the tumor presented with both an epithelial and neuroendocrine nature, and was diagnosed as a small-cell NEC. Post-surgery, she received localized radiation therapy and chemotherapy, and is alive, 18 months after diagnosis. In cases where it is difficult to perform a differential diagnosis of tumors arising from the frontal cranial base and extending to the nasal and cranial sides, NEC should be considered as a possibility.

Extracellularly recorded field potentials, evoked by stimulation of cortico-nucleus accumbens border, were recorded in the nucleus accumbens (NAcc) in horizontal slices of rat ventral forebrain. The field excitatory postsynaptic potential (EPSP) event (N2) was calcium dependent, blocked by tetrodotoxin (1 microM), and reduced by over 70% by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), the antagonist of AMPA-type glutamate receptors. The EPSP amplitude was enhanced by either of the GABA(A) receptor antagonists, picrotoxin (10 microM; by 252+/-33%, n=18) and bicuculline methiodide (20 microM; by 216+/-34%, n=4). Additionally, picrotoxin (3-50 microM) and bicuculline methiodide (20 microM) promoted epileptiform activity within the NAcc, manifest as the emergence of additional late components, N3, N4 and N5, in the evoked synaptic waveform. In slices with the frontal cortex removed, picrotoxin (10-50 microM) and bicuculline methiodide (20 microM) were unable to promote epileptiform activity within the NAcc, although a smaller increase in the peak amplitude of the field EPSP (163+/-18%, n=6) was observed at the highest concentrations of picrotoxin (50 microM). Histological examination of the slice demonstrated that in such decorticated slices, the piriform cortex (PC) had been removed. We propose that stimulation of the cortico-NAcc border not only evokes an orthodromic EPSP in the NAcc, but also causes antidromic activation of cortical tissue. Disinhibition by GABA(A) antagonists of circuits intrinsic to the cortex, possibly the piriform cortex, is the principal cause of the facilitation of the EPSP and of regenerative epileptiform activity in NAcc evoked by stimulation of cortical input.

Leukocyte infiltration in the CNS after trauma or inflammation is triggered in part by upregulation of the chemokine, monocyte chemoattractant protein-1 (MCP-1), in astrocytes. However the signals that induce the upregulation of MCP-1 in astrocytes are unknown. We have investigated the roles for ATP P2X7 receptor activation because ATP is an intercellular signaling transmitter that is released in both trauma and inflammation and P2X7 receptors are involved in immune system signaling. Astrocytes in primary cell culture and acutely isolated from the hippocampus were immunopositive for P2X7 receptors. In astrocyte cultures, application of the selective P2X7 agonist, benzoyl-benzoyl ATP (Bz-ATP), activated MAP kinases extracellular signal receptor-activated kinase 1 (ERK1), ERK2, and p38. Purinergic antagonists depressed this activation with a profile suggesting P2X7 receptors. Bz-ATP also increased MCP-1 expression in cultured astrocytes, and again P2X7 antagonists prevented this increase. Blocking either the ERK1/ERK2 or the p38 pathway (with PD98059 or SB203580, respectively) significantly inhibited Bz-ATP-induced MCP-1 expression. Coapplication of both antagonists caused a greater depression. We also tested the roles for ATP receptor activation in inducing MCP-1 upregulation in corticectomy, an in vivo model of trauma. This model of cortical trauma was previously shown to increase MCP-1 expression in vivo principally in astrocytes. Suramin, a wide-spectrum purinergic receptor antagonist, significantly depressed the rapid (3 hr) trauma-induced increase in MCP-1 mRNA. These data indicate that purinergic transmitter receptors in astrocytes are important in regulating chemokine synthesis. The regulation of MCP-1 in astrocytes by ATP may be important in mediating communication with hematopoietic inflammatory cells.

We have examined a hemispherectomized patient who complained of touch-evoked pricking and burning pain in her paretic hand, especially when the hand was cold. Psychophysical examination showed that for the paretic side she confused cool and warm temperatures, and confirmed that she had a robust allodynia to brush stroking that was enhanced at a cold ambient temperature. Functional magnetic resonance imaging (fMRI) showed that during brush-evoked allodynia, brain structures implicated in normal pain processing (viz. posterior part of the anterior cingulate cortex, secondary somatosensory cortex, and prefrontal cortices) were activated. The fMRI findings thus indicate that the central pain in this patient was served by brain structures implicated in normal pain processing. Possible pathophysiological mechanisms include plasticity as well as thalamic disinhibition.

Extraocular muscles are characterized by their faster rates of contraction and their higher resistance to fatigue relative to limb skeletal muscles. Another often reported characteristic of extraocular muscles is that they generate lower specific forces ( sP o, force per muscle cross-sectional area, kN/m2) than limb skeletal muscles. To investigate this perplexing issue, the isometric contractile properties of the levator palpebrae superioris (levator) and superior rectus muscles of the rat were examined in situ with nerve and blood supply intact. The extraocular muscles were attached to a force transducer, and the cranial nerves exposed for direct stimulation. After determination of optimal muscle length ( L o) and stimulation voltage, a full frequency-force relationship was established for each muscle. Maximum isometric tetanic force ( P o) for the levator and superior rectus muscles was 177 ± 13 and 280 ± 10 mN (mean ± SE), respectively. For the calculation of specific force, a number of rat levator and superior rectus muscles were stored in a 20% nitric acid-based solution to isolate individual muscle fibers. Muscle fiber lengths ( L f) were expressed as a percentage of overall muscle length, allowing a mean L f to L o ratio to be used in the estimation of muscle cross-sectional area. Mean L f: L owas determined to be 0.38 for the levator muscle and 0.45 for the superior rectus muscle. The sP o for the rat levator and superior rectus muscles measured in situ was 275 and 280 kN/m2, respectively. These values are within the range of sP o values commonly reported for rat skeletal muscles. Furthermore P o and sP o for the rat levator and superior rectus muscles measured in situ were significantly higher ( P < 0.001) than P oand sP o for these muscles measured in vitro. The results indicate that the force output of intact extraocular muscles differs greatly depending on the mode of testing. Although in vitro evaluation of extraocular muscle contractility will continue to reveal important information about this group of understudied muscles, the lower sP o values of these preparations should be recognized as being significantly less than their true potential. We conclude that extraocular muscles are not intrinsically weaker than skeletal muscles.

Using the monkey as a model for human hemispherectomy, the effects of early removal of a whole cerebral hemisphere on the cytoarchitecture and cytochrome oxidase histochemistry of the superior colliculus (SC) were evaluated. Results show that the SC ipsilateral to the cortical lesion suffers a 29.9% average volume reduction and a 32.7% total loss of neurons compared to the contralateral SC. Neuronal densities and metabolic activity are similar in normal and hemispherectomized monkeys. Furthermore, the ipsi- and contralesional SC receive retinal inputs as revealed with intraocular injections of tritiated proline. These data suggest that the superior colliculus retains functional capabilities following hemispherectomy in monkey.

Excitotoxic lesions of the striatum are mediated by the combined activity of N-methyl-d-aspartate (NMDA) receptors and metabotropic glutamate receptors (mGluRs). Intrastriatal injection of the NMDA receptor agonists NMDA or quinolinic acid creates large lesions, but in rats that have been decorticated to remove endogenous glutamatergic input, NMDA and quinolinic acid are no longer toxic. We report that NMDA toxicity can be restored in decorticated animals by coinjection of the group I mGluR agonists t-ACPD, t-ADA, or CHPG. In addition, injections of two group I mGluR antagonists, AIDA and (S)-4C3HPG, can protect against striatal lesions produced by quinolinic acid or NMDA injections in normal rats by blocking activation of group I mGluRs. The group II mGluR agonist APDC fails to protect against quinolinic acid or NMDA toxicity in intact animals or to restore NMDA toxicity in decorticated animals, suggesting that the role of group II receptors in this excitotoxic model is minimal. These observations confirm the important role of group I mGluRs in excitotoxicity and identify these receptors as promising targets for therapeutic intervention in neurodegenerative disease processes.

The reorganisation of primary somatosensory cortex that occurs after lesioning the corresponding cortex of the contralateral hemisphere in rat has been termed, 'transhemispheric cortical reorganisation'. Cholinergic and noradrenergic innervations are hypothesized to be involved in cortical plasticity. The present study investigated the change in responses of somatosensory neurones in the hindpaw representation area to muscarinic cholinoceptor and beta-adrenoceptor receptor stimulation, by iontophoretic application of acetylcholine, noradrenaline, propranolol and atropine, during the process of transhemispheric cortical reorganization at 3-4 days and at 20-21 days after lesioning the corresponding area in the contralateral hemisphere. Most neurones in control rats showed excitatory atropine-sensitive responses to acetylcholine, and inhibitory propranolol-sensitive responses to noradrenaline. A marked reduction in neurones exhibiting muscarinic responses (from 69% to 22%) and beta-noradrenoceptor-mediated responses (from 62% to 24%) were seen in rats 3-4 days post lesion. The proportion of neurones responding had recovered by 3 weeks but the direction of the responses had changed with muscarinic response becoming predominantly inhibitory and beta-noradrenoceptor responses predominantly excitatory. It is concluded that transhemispheric cortical reorganization involves both receptor types and that the reciprocal changes at different stages after injury maintain cortical plasticity.

Children who have suffered extensive unilateral brain injury early in life may show a remarkable degree of residual sensorimotor function. It is generally believed that this reflects the high capacity of the immature brain for cerebral reorganization. In this study, we investigated 17 patients who had undergone hemispherectomy for relief from seizures; eight of the patients had congenital brain damage and nine had sustained their initial insult at the age of 1 year or older. Sensorimotor functions of the hand were investigated using functional MRI (fMRI) during a passive movement task, somatosensory evoked potentials (SEPs) arising from electrical and vibration stimulation, and behavioural tests including grip strength, double simultaneous stimulation and joint position sense. On fMRI, two of the eight patients studied with this technique (one with congenital damage and one with damage acquired at the age of 3 years) showed activation in the sensorimotor cortex of the remaining hemisphere with passive movement of the hemiplegic hand. The location of the ipsilateral brain activation was similar to that found on movement of the normal contralateral hand, although the latter was greater in spatial extent. In one of these patients, a greater role was demonstrated for the ipsilateral secondary sensorimotor area (compared with the ipsilateral primary sensorimotor area) for movement of the hemiplegic hand than for movement of the normal hand. Median nerve stimulation of the hemiplegic hand showed reproducible early-latency ipsilateral SEP components in the remaining sensorimotor cortex in 10 of the 17 patients (five with congenital and five with acquired disease). Five of the patients who demonstrated ipsilateral electrical SEPs also showed ipsilateral vibration SEPs (two with congenital and three with acquired disease). The behavioural tests revealed residual sensorimotor function in 14 of the patients; however, not all of the patients who exhibited ipsilateral SEP or fMRI responses had residual sensorimotor function in the hemiplegic hand. Ipsilateral sensorimotor responses were demonstrated both in patients with congenital disease and those with acquired disease, suggesting that factors additional to aetiology and age at injury may influence the degree of residual sensorimotor function and cerebral reorganization.

To identify cortical structures that subserve residual motor and sensory function in patients with congenital hemiparesis due to a porencephalic cyst, we examined, using [(15)O]H2O, PET and somatosensory evoked potentials (SEPs) in three patients with left-sided hemiparesis who had undergone hemispherectomy. Motor stimulation of the affected hand produced ipsilateral activation in the premotor area in all patients, the SMA in two patients, and SII in two patients. Vibrotactile stimulation resulted in activation of the ipsilateral SII in all subjects. Median nerve stimulation of the affected hand produced ipsilateral long-latency SEPs in fronto-centro-parietal areas, whereas stimulation of the non-affected hand produced normal early cortical potentials in the contralateral hemisphere. Our results suggest that residual function in the paretic hand is warranted through non-primary motor and sensory areas, and higher order associative areas in the intact hemisphere.

Intraocular injections of tritiated proline were used to test the hypothesis that unilateral removal of all visual cortical areas results in increased distribution of retinal terminals in the pregeniculate nucleus (PGN) of the thalamus in monkeys. Following hemispherectomy, retinal input to the ipsilateral PGN was reduced by an average of 18.5% when compared to its contralateral homologue, which corresponded to the reduction in nuclear volume (19.3%). Our results show that removal of cortical afferents to the external layer of the PGN does not induce invasion of retinal projections into this region of the nucleus.

We evaluated motor cortical excitability of the unaffected hemisphere in three patients with intractable epilepsy who underwent hemispherectomy, using transcranial magnetic stimulation (TMS) and PET. TMS of the unaffected hemisphere evoked motor responses not only in the contralateral muscles but also in the ipsilateral ones in all the patients. A PET study in one patient showed activation of the unaffected motor cortex by movement of either arm. All of these responses were enhanced after the hemispherectomy, probably due to motor cortical disinhibition by transection of the corpus callosum. The PET study also showed postoperative activation of the premotor area of the unaffected hemisphere. These phenomena indicate posthemispherectomy neuroplastic reorganization leading to preservation of the motor function after the operation.

Recent intracellular and local field potential recordings from thalamic reticular (RE) neurons in vivo as well as computational modeling of the isolated RE nucleus suggest that, at relatively hyperpolarized levels of membrane potentials, the inhibitory postsynaptic potentials (IPSPs) between RE cells can be reversed and γ-aminobutyric acid-A (GABAA) -mediated depolarization can generate persistent spatio-temporal patterns in the RE nucleus. Here we investigate how this activity affects the spatio-temporal properties of spindle oscillations with computer models of interacting RE and thalamocortical (TC) cells. In a one-dimensional network of RE and TC cells, sequences of spindle oscillations alternated with localized patterns of spike-burst activity propagating inside the RE network. New sequences of spindle oscillations were initiated after removal of I h-mediated depolarization of the TC cells. The length of the interspindle lulls depended on the intrinsic and synaptic properties of RE and TC cells and was in the range of 3–20 s. In a two-dimensional model, GABAA-mediated 2–3 Hz oscillations persisted in the RE nucleus during interspindle lulls and initiated spindle sequences at many foci within the RE-TC network simultaneously. This model predicts that the intrinsic properties of the reticular thalamus may contribute to the synchrony of spindle oscillations observed in vivo.

We have reviewed a battery of useful tests for evaluating sensorimotor function and plasticity acutely and chronically in unilateral rat models of central nervous system injury. These tests include forelimb use for weight shifting during vertical exploration in a cylindrical enclosure, an adhesive removal test of sensory function, and forelimb placing. These tests monitor recovery of sensorimotor function independent of the extent of test experience. Data are presented for four models, including permanent focal ischemia, focal injury to the forelimb area of sensorimotor cortex, dopaminergic neurodegeneration of the nigrostriatal system, and cervical spinal cord injury. The effect of the dendrite growth promoting factor, Osteogenic Protein-1 (OP-1) on outcome following permanent middle cerebral artery (MCA) occlusion was used as an example to illustrate how the tests can be applied preclinically. OP-1 showed a beneficial effect on limb use asymmetry in the cylinder test.

Damage to the motor cortex of the rat (Rattus norvegicus) impairs skilled movements used in reaching for food with the contralateral forepaw. Nevertheless, there is substantial recovery in success over a two-week postsurgical period. The profile of behavioral recovery is believed to reflect the eventual normalization of behavior, but this idea has not been explicitly examined. The present experiments examined postsurgical reaching success and reaching movements as a function of (1) lesion type, (2) lesion size, (3) lesion location, (4) depletion of forebrain noradrenaline, and (4) presurgical and postsurgical experience. The results show that at least two separate processes contribute to recovery in postsurgical performance. The early postsurgical period was characterized by extreme difficulties in making reaching movements. The experiments suggest that this initial impairment was due to the loss of the innate cortical engram that supports the action patterns used for skilled movements. Subsequent recovery in reaching success was not due to the reacquisition of normal movements, but was due rather to the use of compensatory movements. The results are discussed in relation to the idea that true recovery from motor cortex injury will require that damaged neurons and their connections be rescued or replaced.

The size of cortical removal was varied in rats that were given medial frontal lesions on postnatal day 2. In adulthood, the animals were trained on the Morris water task and Whishaw reaching task following which the brains were harvested and dendritic arborization and spine density was examined in the layer III pyramidal cells in Zilles' area Par1. There was a small relationship between lesion size and behavioral outcome as smaller lesions produced somewhat smaller deficits. In contrast, both small and large lesions produced large reductions in brain weight, dendritic arborization, and spine density. The cortex of newborn rats appears to be especially vulnerable to even restricted injury. This contrasts to the effects of similar injury a week later when animals show extensive functional recovery and anatomical compensation.

The purpose of this study is to investigate the level of disability of children who are either candidates for or have undergone a hemidecorticectomy. The Activity Scales for Kids and the Pediatric Evaluation Disability Inventory were demonstrated to be useful measurement tools yielding comparative results between subgroups. Overall, children with congenital disease seemed less autonomous postoperatively than were preoperative patients or children with acquired disease. Age at surgery and the interval between seizure onset and surgery are potentially important predictors of disability. This could reflect the importance of timing of surgery, development, environment, and possibly brain plasticity processes in this population. (J Child Neurol 2000;15:7-14).

Unilateral temporal lobectomy to treat seizure disorders in humans often results in cognitive impairment after the surgery. To determine the potential utility of a rodent model of unilaterally induced cognitive deficits, the present experiment evaluated spatial cognition in adult rats after either left or right hemisphere lesioning of temporal neocortex and underlying hippocampal regions. Evaluation of performance in the eight arm radial maze revealed that both lesioned groups committed more reference memory errors than did nonoperated controls. Working memory errors did not differ statistically between groups. The production of a spatial learning deficit by unilateral damage suggests that this rodent model could serve to test potential improvements in interventional strategies aimed at attenuating cognitive effects of the surgical treatment.

A best evidence topic in thoracic surgery was written according to a structured protocol. The question addressed was: Does video-assisted thoracoscopic (VATS) decortication in advanced malignant mesothelioma improve prognosis? Altogether more than 25 papers were found using the reported search, of which five represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. We conclude that VATS decortication is useful as a palliative measure in advanced malignant mesothelioma. VATS provides a diagnostic tool, yielding tissue for histological diagnosis. Secondly, drainage of effusion and pleurectomy/decortication improves the quality of life and may increase survival as well.

The present study was designed to measure cerebral glucose and oxidative metabolisms and to assess relationships with previously identified morphological changes in adult cats with a unilateral, restricted neocortical lesion sustained either during fetal life or neonatally. Local cerebral metabolic rates for glucose (LCMRglc) were measured using the [ 14 C ]2-deoxy- d -glucose (2 DG) autoradiography method and oxidative capacity was determined using cytochrome oxidase histochemistry (C.O.). Only glucose metabolism in the fetal-lesioned cats was affected substantially. There was a global decrease (31.0% relative to controls) of the LCMRglc for both cerebral hemispheres while focal decreases were seen mainly in thalamic and neostriatal nuclei (and reaching declines of over 50%). Cats with a neonatal lesion showed only a tendency to such declines (19.5% and 22.0% for the right and left hemispheres, respectively). C.O. values were not affected significantly either globally or locally in any of the age-at-lesion groups. In previous work using fetal animals with similar lesions, morphological evidence of subcortical neuropile degeneration was not observed; instead, a marked decrease in size of the ipsilateral remaining neocortex and a pronounced distortion of gyri and sulci patterns bilaterally were found. In this context, we propose that in the fetal-lesioned cats, there was a widespread lesion-induced decrease in corticofugal (and transcortical) synaptic inputs which was responsible for a decline in functional (synaptic) activities, and that this, in turn, caused a downturn in glucose utilization. In the neonatal cats minor degeneration, coupled with lack of reinnervation, would account for the tendency to 2 DG declines. These results indicate that the long-term metabolic response of the fetal brain to injury is also less adaptive than that of the neonatal brain. Since standard methods are available to measure cerebral metabolism in humans, our studies in animal models may help understanding the long term physiological consequences of developmental focal brain damage in patients as well as to predict the relationships between cerebral metabolism and the underlying long-term morphological effects of such lesions.

Summary: Purpose: We have developed an intraoperative optical tracking-based navigational system that allows localization in the operative space. Using three-dimensional reconstruction, this system has provided precise spatial information for intraoperative cortical mapping in patients with intractable epilepsy in whom the lesion lies close to eloquent cortex. Methods: A 23-year-old man with intractable complex partial seizures (CPS) presented to our institution. Proton-density magnetic resonance imaging (MRI) showed a 3-cm lesion which lay 2 cm beneath the left frontal operculum. A three dimensional model of the patient was reconstructed using MR modalities. Intraoperatively, subdural grid and strips were placed over the lesion and their electrodes were registered to the three-dimensional model, which was displayed on a monitor. The navigational system was used to localize each electrode on the three-dimensional model. By the second operation, the sites of seizure activity were established and recorded on the three-dimensional model. A bipolar stimulator was also used to determine the speech area. Results: The lesion, which proved to be cortical dysplasia, was removed completely and the cortical speech area was avoided. During the postoperative period, the patient had no neurological symptoms and no seizure activity. Conclusions: The localization of a lesion and its correlation with epileptogenic foci is important in optimizing treatment in patients with cortical dysplasia. Our navigational system provided accurate localization of the lesion and correlation with the epileptogenic focus and related eloquent cortex. We believe that the safe removal of the lesion was facilitated by this system.