Removal Of Cortex Research Articles

Innervation of the caudate nucleus, thalamus and red nucleus by the remaining sensorimotor cortex in cats with fetal or neonatal unilateral frontal cortex removal

We studied the projections to the caudate nuclei, thalami and red nuclei from the remaining sensorimotor cortex in adult cats that had sustained a unilateral frontal cortex resection prenatally or neonatally. Four cats had the lesion at age E 50–55 and six animals sustained the ablation at age P 8–14 (seven cats were intact controls). All cats grew to young adulthood and then received injections of tritiated leucine-proline in the remaining sensorimotor cortex. Injection sites and axon terminal fields were reconstructed using autoradiography-processed tissue. In all cats the label filled a similar extent of the right pericruciate cortex. Terminal field densities in the subcortical nuclei were estimated using computer-based video software. Three medial-lateral sectors at five coronal levels were examined in the caudate nucleus. Three nuclear groups were analyzed in the thalamus (intralaminary, ventralis lateralis and ventrobasal complex). For the red nucleus, the four quadrants were examined at four coronal levels. The main goal of the study was to assess possible changes in the cortical innervation of the nuclei ipsilateral to the lesion. Therefore, the mean particle counts per nucleus (and per area or sector of nuclei) and per animal group were used to calculate percentage values for the decussated (crossed, or contralateral to the injection site) as a function of the non-decussated (uncrossed, or ipsilateral to the injection site) innervation. The percentage values for the crossed projections were: (a) for the entire caudate nucleus, 61.3% for the intact, 56.7% for the fetal-lesioned and 42.7% for the neonatal-lesioned cats, with no statistical differences between groups; (b) for the thalamus the proportion of crossed projections was minimal fluctuating between a low 0.06–0.16% for the nucleus ventralis lateralis and a high of 2.01–3.46% for the intralaminary nuclei, with the highest values belonging to the lesioned groups but with no significant differences between groups; (c) for the entire red nucleus, 1.98%, 12.74% ( P < 0.05) and 6.76% for the intact, fetal- and neonatal-lesioned cats respectively. In the lesioned cats, the topography of the distribution of the axon terminals was bilaterally the same as in the controls. In conclusion, only the red nucleus of the frontal-lesioned cats showed an increased crossed innervation from the remaining sensorimotor cortex but this was relatively weak and statistically significant only for the fetal-lesioned animals. These results as well as the literature suggest that: (a) the crossed corticorubral projections in fetal cats may represent true reinnervation (i.e., newly originated, no preexisting terminals); (b) the relative paucity of the crossed projections in the present cats as compared to the extensive reorganization of subcortical terminals seen after cerebral hemispherectomy (our original postnatal lesion model) may be due to the much smaller size of the present cortical lesion which presumably induced only a limited amount of subcortical nuclear deafferentation.

Inhibitory effect of norepinephrine on the heat response of cutaneous nociceptors in normal rats

The locations and receptive fields of thalamic neurons projecting to the motor cortex were examined and the following results were obtained.(1)Neurons located at the border area between nucleus ventralis lateralis (VL) and nucleus ventralis posterolateralis (VPL) could be activated antidromically from the motor cortex.(2)These neurons received topographically organized somesthetic inputs arising from skin and deep receptors.(3)The receptive fields of neurons in the small area of the motor cortex where these thalamic neurons projected could be examined in 8 instances. In 6 instances, the cortical neurons and the thalamic projection neurons were activated by exactly the same stimuli in the periphery.(4)Removal of the sensory cortex did not significantly change the characteristics of afferent inputs from the periphery to the motor cortex.(5)It is concluded that the motor cortex receives somesthetic inputs directly from the thalamus. The functional role of these inputs was discussed in relation to the known cortical reflexes.

Complications in the removal of the posterior vitreous cortex.

Complications in the removal of the posterior vitreous cortex.

Epileptic afterdischarge in the hippocampal–entorhinal system: current source density and unit studies

The contribution of the various hippocampal regions to the maintenance of epileptic activity, induced by stimulation of the perforant path or commissural system, was examined in the awake rat. Combination of multiple-site recordings with silicon probes, current source density analysis and unit recordings allowed for a high spatial resolution of the field events. Following perforant path stimulation, seizures began in the dentate gyrus, followed by events in the CA3–CA1 regions. After commissural stimulation, rhythmic bursts in the CA3–CA1 circuitry preceded the activation of the dentate gyrus. Correlation of events in the different subregions indicated that the sustained rhythmic afterdischarge (2–6Hz) could not be explained by a cycle-by-cycle excitation of principal cell populations in the hippocampal–entorhinal loop. The primary afterdischarge always terminated in the CA1 region, followed by the dentate gyrus, CA3 region and the entorhinal cortex. The duration and pattern of the hippocampal afterdischarge was essentially unaffected by removal of the entorhinal cortex. The emergence of large population spike bursts coincided with a decreased discharge of interneurons in both CA1 and hilar regions. The majority of hilar interneurons displayed a strong amplitude decrement prior to the onset of population spike phase of the afterdischarge.These findings suggest that (i) afterdischarges can independently arise in the CA3–CA1 and entorhinal–dentate gyrus circuitries, (ii) reverberation of excitation in the hippocampal–entorhinal loop is not critical for the maintenance of afterdischarges and (iii) decreased activity of the interneuronal network may release population bursting of principal cells.

Transsulcal approach to mesiotemporal lesions. Anatomy, technique, and report of three cases.

Surgical resection of mesiotemporal lesions, particularly those in the dominant hemisphere, is often challenging. Standard approaches require excessive brain retraction, removal of normal cortex, or manipulation of the middle cerebral artery branches. This report describes a transsulcal temporal approach to mesiotemporal lesions and its application in three patients. Gross-total resection of the lesion was accomplished in all cases. An anatomical cadaveric study was also performed to delineate the microsurgical anatomy of this approach. Precise knowledge of temporal intraventricular landmarks allows navigation to the lesion without the need for a navigational system. This approach is helpful for neurologically intact patients with mesiotemporal lesions.

Bimanual irrigation/aspiration

A bimanual irrigation/aspiration (I/A) device was developed to allow safer, easier removal of the lens cortex after phacoemulsification. The device can be used in cases of subincisional cortex, small pupils, flat anterior chambers, subluxated lenses, or previous damaged anterior segments. It can also minimize vitreous complications in cases of a posterior capsule rupture.

Prevention and management of posterior capsule rupture.

To present the means and technique used in our Department for prevention and management of posterior capsule rupture during planned extracapsular cataract extraction. Prospective analysis of 550 extracapsular cataract operations from October 1993 to March 1994. Our technique (a slight modification of Blumenthal's technique) included a triplanar watertight small scleral incision, a relatively large continuous curvilinear capsulorhexis, or can-opener capsulotomy, nucleus hydrodissection and hydroexpression, use of an anterior chamber maintainer and residual cortex removal through a 10 o'clock side-port corneal incision. Best corrected postoperative visual acuity ranged from 7-10/10 in 93.45% of our cases. Posterior capsule rupture with or without vitreous loss occurred in 1.63% and 2.72% of the cases, respectively. These rates are much lower than those, observed, when we used the sclerocorneal incision and nucleus extraction with external pressure. The combination of a triplanar watertight small scleral incision. A relatively large continuous curvilinear capsulorhexis, an anterior chamber maintainer and residual cortex aspiration through the 10 o'clock side-port corneal incision greatly reduced the posterior capsule rupture rate.

Age dependent modification of cytochrome oxidase activity in the cat dorsal lateral geniculate nucleus following removal of primary visual cortex.

The purpose of the present study was to assess changes in the levels of cytochrome oxidase (CO) activity in the dorsal lateral geniculate nucleus (dLGN) of the adult cat following removal of primary visual cortical areas 17 and 18 on the day of birth (PI), P28, or in adulthood (> or = 6 months). Cytochrome oxidase activity was measured in histological sections 9 or more months after the cortical ablation. Control measures obtained from intact cats show that CO activity is normally highest in the A-laminae of dLGN, and slightly lower in the C-complex. Following visual cortex ablations incurred at any age, CO activity levels are reduced in the A-laminae. This reduction is most profound following ablations incurred on P28 or in adulthood. In contrast, CO activity in the C-complex of dLGN is at nearly normal levels following ablations on P1 or P28, but not in adulthood. These findings contribute to our understanding of the role played by the dLGN in the transfer of visual signals along retino-geniculo-extrastriate pathways that expand following early removal of areas 17 and 18. Moreover, they have implications for our understanding of spared behavioral functions attributed to the extrastriate cortex in cats which incurred early damage of areas 17 and 18.

The effect of dark-rearing, strobe-rearing and acute visual cortex removal on the visual responses in the superficial superior colliculus of the guinea-pig

The effect of dark-rearing, strobe-rearing and acute visual cortex removal on the visual responses in the superficial superior colliculus of the guinea-pig

Postembedding immunocytochemistry demonstrates directly that both retinal and cortical terminals in the cat superior colliculus are glutamate immunoreactive.

Although the excitatory neurotransmitter glutamate is known to be present in the cat superior colliculus (SC), the types of synapses that contain glutamate have not been examined. We, therefore, studied the ultrastructure of synaptic profiles labeled by a glutamate antibody by using electron microscopic postembedding immunocytochemistry. In addition, unilateral aspiration lesions of areas 17-18 were made at 5-28 days before death in order to determine whether degenerating terminals from visual cortex were glutamate immunoreactive (Glu-ir). Three types of axon terminal were glu-ir: 1) those containing large, round synaptic vesicles and pale mitochondria, characteristic of retinal terminals (RT profiles); 2) those containing small, round synaptic vesicles and dark mitochondria (RSD profiles); and 3) those containing large, round synaptic vesicles and dark mitochondria (RLD profiles). Measures of mean gold particle density revealed that RT, RSD, and RLD profiles had similar average grain densities (11.3-12.7 particles/unit area). Other labeled profile types included cell bodies, large-calibre dendrites, and myelinated axons. Axon terminals containing flattened synaptic vesicles and vesicle-containing presynaptic dendrites, both of which contain gamma-aminobutyric acid (GABA), had many fewer gold particles (3.6 and 4.8 mean particles/unit area, respectively). Following unilateral removal of visual cortex, normal RSD terminals were observed infrequently in the SC ipsilateral to the lesion. Synaptic terminals in the initial stages of degeneration were heavily labeled by the glutamate antibody, as were axon terminals and myelinated axons undergoing hypertrophied or neurofilamentous degeneration. These results show that both major sensory afferents to the superficial layers of cat SC contain glutamate--RT terminals from the retina and RSD terminals from visual cortex. The origin of RLD terminals is unknown.

Postembedding immunocytochemistry demonstrates directly that both retinal and cortical terminals in the cat superior colliculus are glutamate immunoreactive

Although the excitatory neurotransmitter glutamate is known to be present in the cat superior colliculus (SC), the types of synapses that contain glutamate have not been examined. We, therefore, studied the ultrastructure of synaptic profiles labeled by a glutamate antibody by using electron microscopic postembedding immunocytochemistry. In addition, unilateral aspiration lesions of areas 17–18 were made at 5–28 days before death in order to determine whether degenerating terminals from visual cortex were glutamate immunoreactive (Glu-ir). Three types of axon terminal were glu-ir: 1) those containing large, round synaptic vesicles and pale mitochondria, characteristic of retinal terminals (RT profiles); 2) those containing small, round synaptic vesicles and dark mitochondria (RSD profiles); and 3) those containing large, round synaptic vesicles and dark mitochondria (RLD profiles). Measures of mean gold particle density revealed that RT, RSD, and RLD profiles had similar average grain densities (11.3–12.7 particles/unit area). Other labeled profile types included cell bodies, large-calibre dendrites, and myelinated axons. Axon terminals containing flattened synaptic vesicles and vesicle-containing presynaptic dendrites, both of which contain γ-aminobutyric acid (GABA), had many fewer gold particles (3.6 and 4.8 mean particles/unit area, respectively). Following unilateral removal of visual cortex, normal RSD terminals were observed infrequently in the SC ipsilateral to the lesion. Synaptic terminals in the initial stages of degeneration were heavily labeled by the glutamate antibody, as were axon terminals and myelinated axons undergoing hypertrophied or neurofilamentous degeneration. These results show that both major sensory afferents to the superficial layers of cat SC contain glutamate—RT terminals from the retina and RSD terminals from visual cortex. The origin of RLD terminals is unknown. © 1996 Wiley-Liss, Inc.

The effect of dark-rearing, strobe-rearing and acute visual cortex removal on the visual responses in the superficial superior colliculus of the guinea-pig

Extracellular multi-unit responses to visual stimuli were recorded in the cells of the superficial layers of the superior collliculus (SC) in four groups of adult guinea-pigs: a control group, a strobe-reared group, a dark-reared group and a group with the ipsilateral visual cortex removed acutely. Single unit visual responses were also recorded in a control and a dark-reared group. When guinea-pigs were either strobe or dark-reared from birth, the number of directionally selective responses in the superficial SC decreased significantly. Acute removal of the visual cortex had no affect on the number of directionally selective cells recorded in the SC. The correlation between azimuthal visual receptive field and rostrocaudal position of the recording electrode in the SC was not significantly different from the control group following strobe, dark-rearing or acute visual cortex removal. These data imply that, during early development, visual information is necessary for directional selectivity of the visual responses in the superficial SC. However, the map of visual azimuthal space is essentially unperturbed by visual restriction (in the form of dark or strobe-rearing) or acute visual cortex removal.

Cortical target depletion and the developing lateral geniculate nucleus: implications for trophic dependence.

The dependence of the developing dorsal lateral geniculate nucleus (LGd) on visual cortex for survival has been well documented. Complete removal of visual cortex during early postnatal development results in degeneration of the LGd. To further explore the nature of this trophic relationship, we depleted variable proportions of the principal targets of geniculocortical axons, layer IV neurons, and also variable proportions of the supragranular neurons by intraperitoneal injections of different dosages of a mitotic inhibitor MAM (methylazoxymethanol acetate) into pregnant hamsters at the time when these neurons were being generated in the ventricular zone. We demonstrate that after more than 75% loss of layer IV there is no reduction in cell number in the LGd. HRP (horseradish peroxidase) injections into the LGd in adult animals reveal an essentially normal pattern of termination without evidence of rerouting of geniculocortical axons to other cortical areas, nor compensatory increase in arborization in layer VI and VIb (subplate). Geniculocortical axons terminate principally in the middle stratum of the depleted cortex above layer V, with obvious reduction in both the extent and density of arborization. After higher dosages of MAM treatment resulting in more severe cell loss in layers II-IV with the apparent loss of layer IV, the extent and density of geniculocortical arborization are further reduced. Reduction in size as well as total number of geniculate neurons become detectable. Above depletions of 75% of layer IV neurons, the number of surviving LGd neurons is linearly related to the total number of remaining layer II-IV neurons in the cortex. These findings are discussed in light of the possible trophic mechanisms that match cell populations in number during development.

Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors.

There is little axonal growth after central nervous system (CNS) injury in adult mammals. The administration of antibodies (IN-1) to neutralize the myelin-associated neurite growth inhibitory proteins leads to long-distance regrowth of a proportion of CNS axons after injury. Our aim was: to determine if spinal cord lesion in adult rats, followed by treatment with antibodies to neurite growth inhibitors, can lead to regeneration and anatomical plasticity of other spinally projecting pathways; to determine if the anatomical projections persist at long survival intervals; and to determine whether this fibre growth is associated with recovery of function. We report here that brain stem-spinal as well as corticospinal axons undergo regeneration and anatomical plasticity after application of IN-1 antibodies. There is a recovery of specific reflex and locomotor functions after spinal cord injury in these adult rats. Removal of the sensorimotor cortex in IN-1-treated rats 2-3 months later abolished the recovered contact-placing responses, suggesting that the recovery was dependent upon the regrowth of these pathways.

The entorhinal cortex entrains fast CA1 hippocampal oscillations in the anaesthetized guinea-pig: role of the monosynaptic component of the perforant path.

Entorhinal inputs reach the hippocampal CA1 field through a trisynaptic circuit involving dentate granule cells and CA3 pyramidal neurons, as well as through a monosynaptic path ending on the distal apical dendrites of CA1 pyramidal cells. The influence of monosynaptic entorhinal inputs onto CA1 operations is poorly understood. In this study, we characterized the involvement of the monosynaptic pathway in the generation of the fast CA1 oscillation bursts (30-60 Hz) that occur in the dorsal hippocampus of anaesthetized guinea-pigs after partial cortex removal. Using multiple-site extracellular and intracellular recording, we found that in this particular preparation, devoid of theta rhythm, fast oscillations are temporally coherent over a large portion of the CA1 region along the hippocampal septotemporal axis. Current source density analysis revealed that fast CA1 oscillations involve two dipoles reflecting synchronous synaptic activities in the stratum lacunosum-moleculare of the hippocampus proper and in the stratum moleculare of the dentate gyrus. These layers constitute the two major termination zones of entorhinal afferents, suggesting that the entorhinal cortex entrains fast CA1 oscillations. This hypothesis was corroborated by the concomitant occurrence of fast oscillation bursts in the entorhinal cortex and CA1 region. Furthermore, fast CA1 oscillations were abolished by lidocaine or tetrodotoxin injections in the entorhinal cortex. Finally, acute interruption of the hippocampal trisynaptic loop did not affect the stratum lacunosum-moleculare dipole recorded extracellularly, but also intracellularly, as high-frequency postsynaptic potentials in CA1 pyramidal cells. These results indicate that the monosynaptic pathway is involved in the genesis of fast CA1 oscillations.

Induction of opioid receptor-mediated macrophage chemotactic activity after neonatal brain injury.

Macrophages have a prominent role in the injury response of the brain, yet the molecular mechanisms that control their invasion to the site of neuronal degeneration is unknown. After removal of the posterior cortex at birth, there is massive and specific targeting of nonresident macrophages to axotomized neurons in the lateral thalamus. The present study has identified an injury-induced, brain-derived chemotactic factor (BDCF) capable of eliciting chemotactic responses from resident peritoneal macrophages and brain macrophages. Conditioned media collected from tissue slices containing the axotomized central nervous system neurons exhibit BDCF activity. Initial experiments indicated that BDCF is a small peptide and, thus, we used specific pharmacologic reagents to characterize further BDCF activity. Naloxone, a pan opioid receptor antagonist, completely blocks BDCF activity. Although both kappa and mu opioid receptor antagonists failed to modify BDCF-induced macrophage chemotaxis, two specific delta receptor antagonists blocked BDCF. Analysis of BDCF by reverse phase HPLC and RIA revealed peak chemotactic activity in fractions consistent with the presence of an opioid peptide. The results suggest that cells in the brain respond to neuronal injury by producing and releasing opioids that can initiate a specific macrophage response.

Use of intravitreal autologous blood to identify posterior cortical vitreous in macular hole surgery.

Surgical management of macular holes involves removal of tractional prefovial vitreous cortex. Accurately identifying this adherent tissue can potentially decrease intraoperative complications. A new, effective technique using autologous whole blood can be used to identify and facilitate separation of the posterior cortical vitreous.

Dentate EEG spikes and associated interneuronal population bursts in the hippocampal hilar region of the rat.

1. This paper describes two novel population patterns in the dentate gyrus of the awake rat, termed type 1 and type 2 dentate spikes (DS1, DS2). Their cellular generation and spatial distribution were examined by simultaneous recording of field potentials and unit activity using multiple-site silicon probes and wire electrode arrays. 2. Dentate spikes were large amplitude (2-4 mV), short duration (< 30 ms) field potentials that occurred sparsely during behavioral immobility and slow-wave sleep. Current-source density analysis revealed large sinks in the outer (DS1) and middle (DS2) thirds of the dentate molecular layer, respectively. DS1 and DS2 had similar longitudinal, lateral, and interhemispheric synchrony. 3. Dentate spikes invariably were coupled to synchronous population bursts of putative hilar interneurons. CA3 pyramidal cells, on the other hand were suppressed during dentate spikes. 4. After bilateral removal of the entorhinal cortex, dentate spikes disappeared, whereas sharp wave-associated bursts, reflecting synchronous discharge of the CA3-CA1 network, increased several fold. 5. These physiological characteristics of the dentate spikes suggest that they are triggered by a population burst of layer II stellate cells of the lateral (DS1) and medial (DS2) entorhinal cortex. 6. We suggest that dentate spike-associated synchronized bursts of hilar-region interneurons provide a suppressive effect on the excitability of the CA3-CA1 network in the intact brain.

Hemispherical Deafferentation

An alternative technique for so-called functional hemispherectomy has been developed to be used for the classical indications of hemispherectomy or the various modifications of functional hemispherectomy. The technique entails a smaller trepanation, less operation time, and less blood loss, and it leaves more brain tissue in place as compared with other functional hemispherectomy techniques. It starts with either hippocampectomy alone or with hippocampectomy and anterior temporal lobectomy. After this, deafferentation of the white matter of the temporal, occipital, parietal, and frontal lobe, using either a transcortical transventricular approach along the outline of the lateral ventricle or a sylvian key hole approach, is performed. The technique includes a transventricular callosotomy, and it leaves in place only a small portion of the suprainsular cortex and the insular cortex. However, as one modification, removal of the insular cortex can easily be performed, if necessary, and, as a second modification, the entire transventricular deafferentation can be performed through a sylvian key hole. In this report, the technique is described and the surgical experience for the first 13 patients is outlined. The immediate seizure relief with an average follow-up of 12 months was similar to that for patients with functional hemispherectomy, but the follow-up period for these 13 patients is not long enough to allow definite conclusions concerning long-term control of seizures and long-term complications

Frontal Sinus Obliteration

The controversies concerning obliteration of the frontal sinus in response to trauma, infection, or tumor growth are long-standing (1913 to the present) and related to the field of training of the surgeon. Successful frontal sinus obliteration requires (1) meticulous removal of the frontal sinus mucosa, (2) removal of the inner cortex of the sinus wall, and (3) permanent occlusion of the nasofrontal duct. It is significant to note that most of the clinical literature relates to management of infected sinuses (sinusitis) and most experimental studies are done on uninfected, unfractured feline models. Therefore, no direct reference can be made to the management of the fractured frontal sinus. The techniques in current use are autologous implantation of fat, bone, and muscle, along with the technique of spontaneous osteogenesis. These techniques are all effective when the preceding guidelines are followed, with the only real advantage being that the spontaneous osteogenesis avoids the problem of donor-site morbidity, which has been as high as 5 percent. This factor makes the osteogenesis technique the method of choice for frontal sinus obliteration. This literature review provides the surgeon with the objective data available for optimal frontal sinus obliteration.