Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Internal Capsule”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1995

Peri-insular hemispherotomy: surgical principles and anatomy.

THE NATURE OF functional hemispherectomy continues to be misunderstood despite its 20-year history. Recently, we introduced the concept of peri-insular hemispherotomy, a functional hemispherectomy with minimal brain removal (9, 21). To avoid additional confusion, a detailed neuroanatomic account of this operation, which has been performed in 11 patients, is presented. The name of the operative variant presented derives from the central importance of the exposure of the insula as the first surgical landmark. Incising along the circular sulcus that surrounds the insula not only allows access to the dilated ventricular system but also disrupts the entire internal capsule. A parasagittal callosotomy is performed from within the lateral ventricle by incising the medial ventricular roof. Projections through the anterior commissure are disrupted at the time of radical amygdalar resection. The posterior hippocampus need not be radically removed, because its posterior transsection disconnects it. Overall, peri-insular hemispherotomy can be viewed as a radical hemispheric tractotomy, resulting in a completely disconnected hemisphere. Advantages include shorter operative times, a less stormy postoperative course, and better anatomic preservation of the operated hemisphere, thus presumably reducing long-term complications.

Adolescent↗
PubMed2003

Long-term electrical capsular stimulation in patients with obsessive-compulsive disorder.

OBJECTIVE: Because of the irreversibility of lesioning procedures and their possible side effects, we studied the efficacy of replacing bilateral anterior capsulotomy with chronic electrical capsular stimulation in patients with severe, long-standing, treatment-resistant obsessive-compulsive disorder. METHODS: We stereotactically implanted quadripolar electrodes in both anterior limbs of the internal capsules into six patients with severe obsessive-compulsive disorder. Psychiatrists and psychologists performed a double-blind clinical assessment. A blinded random crossover design was used to assess four of those patients, who underwent continuous stimulation thereafter. RESULTS: The psychiatrist-rated Yale-Brown Obsessive Compulsive Scale score was lower in the stimulation-on condition (mean, 19.8 +/- 8.0) than in the postoperative stimulator-off condition (mean, 32.3 +/- 3.9), and this stimulation-induced effect was maintained for at least 21 months after surgery. The Clinical Global Severity score decreased from 5 (severe; standard deviation, 0) in the stimulation-off condition to 3.3 (moderate to moderate-severe; standard deviation, 0.96) in the stimulation-on condition. The Clinical Global Improvement scores were unchanged in one patient and much improved in the other three during stimulation. During the stimulation-off period, symptom severity approached baseline levels in the four patients. Bilateral stimulation led to increased signal on functional magnetic resonance imaging studies, especially in the pons. Digital subtraction analysis of preoperative [(18)F]2-fluoro-2-deoxy-d-glucose positron emission tomographic scans and positron emission tomographic scans obtained after 3 months of stimulation showed decreased frontal metabolism during stimulation. CONCLUSION: These observations indicate that capsular stimulation reduces core symptoms 21 months after surgery in patients with severe, long-standing, treatment-refractory obsessive-compulsive disorder. The stimulation elicited changes in regional brain activity as measured by functional magnetic resonance imaging and positron emission tomography.

Adult↗
PubMed2003

Image-guided transsylvian, transinsular approach for insular cavernous angiomas.

OBJECTIVE: Surgical treatment of cavernomas arising in the insula is especially challenging because of the proximity to the internal capsule and lenticulostriate arteries. We present our technique of image guidance for operations on insular cavernomas and assess its clinical usefulness. METHODS: Between 1997 and 2003, with the guidance of a frameless stereotactic system (BrainLab AG, Munich, Germany), we operated on eight patients who harbored an insular cavernoma. Neuronavigation was used for 1) accurate planning of the craniotomy, 2) identification of the distal sylvian fissure, and, finally, 3) finding the exact site for insular corticotomy. Postoperative clinical and neuroradiological evaluations were performed in each patient. RESULTS: The navigation system worked properly in all eight neurosurgical patients. Exact planning of the approach and determination of the ideal trajectory of dissection toward the cavernoma was possible in every patient. All cavernomas were readily identified and completely removed by use of microsurgical techniques. No surgical complications occurred, and the postoperative course was uneventful in all patients. CONCLUSION: Image guidance during surgery for insular cavernomas provides high accuracy for lesion targeting and permits excellent anatomic orientation. Accordingly, safe exposure can be obtained because of a tailored dissection of the sylvian fissure and minimal insular corticotomy.

Adult↗
PubMed2002

Pax6 is required for the normal development of the forebrain axonal connections.

The transcription factor PAX6 has been implicated in forebrain patterning, cerebral cortical arealization and in development of thalamocortical connections. Using a Pax6/lacZ knockout mouse, in which the endogenous Pax6 expression is reflected by beta-galactosidase activity, we have studied the consequences of the loss of Pax6 function on thalamocortical (TCA) and corticofugal axon (CFA) pathfinding during the period of embryonic day (E) 14.5 to E18.5. Carbocyanine dye tracing in Pax6 heterozygotes (Pax6(+/-)) and Pax6 wild-type (Pax6(+/+)) brains revealed that CFAs and TCAs temporarily arrested their growth at E14.5 at the border of the beta-galactosidase-positive region at the pallial/subpallial boundary (PSPB), before they continued towards their targets. However, in Pax6 homozygous (Pax6(-/-)) embryos, CFAs and TCAs were unable to encounter each other at the PSPB and reach their final targets. Instead of crossing the PSPB, they had the tendency to descend into the ventral pallium in large aberrant fascicles. In addition, cells with a presumptive guide-post function, which are normally situated in the ventral thalamus, internal capsule and hypothalamus, were more dispersed in the hypothalamus and ventral pallium. These pathfinding defects were confirmed by immunohistochemistry for L1 and TAG1, markers of the early axonal connections. The aberrant development of axonal connections in absence of Pax6 function appear to be related to ultrastructural defects of cells along the PSPB, as well as to a failure of axonal guidance molecule expression, including Sema3c and Sema5a.

Animals↗
PubMed1993

[Pharmacological studies on human urinary kallidinogenase (SK-827): cerebral protective effects].

We investigated the cerebral protective effects of human urinary kallidinogenase (SK-827) in rabbits. The following results were obtained: 1) At a dose of 5.0 x 10(-3) to 1.25 x 10(-2) PNA U/kg, SK-827 significantly inhibited the decrease of focal cerebral blood flow and the impairment of electrocorticogram (ECoG) activity in infarcted rabbits. 2) SK-827 at a dose of 2.5 x 10(-3) PNA U/kg inhibited the development of infarction area induced by internal carotid arterial injection of glass beads. 3) SK-827 at a dose of 2.5 x 10(-3) to 5.0 x 10(-3) PNA U/kg inhibited the decrease of cerebral cortical pO2 induced by 5% oxygen inhalation. 4) On subacute phase 7 days after the destruction of internal capsule, SK-827 at a dose of 1.25 x 10(-2) PNA U/kg improved the abnormality of spontaneous ECoG. These findings suggest that SK-827 minimizes the reduction of cerebral function induced by ischemia.

Animals↗
PubMed1984

[Effect of nizofenone on pyramidal response, electrocorticogram and regional cerebral blood flow following recirculation after complete global brain ischemia in cats].

Effect of nizofenone on pyramidal response (PR), electrocorticogram (ECoG) and regional cerebral blood flow (rCBF) following recirculation after complete global brain ischemia was compared with that of pentobarbital in gallamine-immobilized cats. The basilar artery and the branches of both carotid arteries (superior thyroid artery, dorsal muscular branch, internal carotid artery, occipital artery and ascending pharyngeal artery) were all ligated. The cats were subjected to complete brain ischemia by occluding both common carotid arteries for 45 min, followed by 180 min recirculation. rCBF of the cortex (suprasylvian gyrus) and the internal capsule was monitored by the hydrogen clearance method. Blood gases were regulated within a range determined previously in freely-moving cats throughout the experiment. Nizofenone (1 mg/kg, i.v.) facilitated the recovery of PR and ECoG, and it inhibited the phenomenon of secondary suppression evidenced by interruption and reversion of the recovery process. rCBF showed good recovery throughout the recirculation period. Pentobarbital (20 mg/kg, i.v.) facilitated the recovery of PR during the early period of recirculation, but secondary suppression of PR, associated with the decline of rCBF, was evident. These results suggest that the ameliorative effect of nizofenone on the recovery of neuronal functions is due to its ability to protect neurons against ischemic anoxia and to prevent interruption of postischemic circulation, and also the good recovery of rCBF is due to its ability to protect vasculature against ischemic anoxia.

Animals↗
PubMed1987

[Effects of buflomedil on survival rate, local cerebral blood flow and glucose utilization after cerebral ischemia in spontaneously hypertensive rats].

Cerebral protective effects of oral Buflomedil administration for 7 days were studied in spontaneously hypertensive rats (SHR). After permanent bilateral carotid artery occlusion (BCAO), the survival rates at 24 hr were 38% and 44% in groups treated with Buflomedil at the doses of 30 mg/kg (n = 16) and 90 mg/kg (n = 15), respectively, which were significantly higher than that in the control group (orally given saline for 7 days), 6%. In rats that survived and given Buflomedil, carbon filling of the brain after BCAO was extended to the territories of the internal carotid artery, while it was restricted to the brainstem and cerebellum in rats died within 3 hr and given either saline or Buflomedil. Local cerebral blood flow (LCBF), monitored by [14C]-Iodoantipyrine autoradiography, was determined at 3 hr after the start of BCAO or at 2 hr after reperfusion in rats orally given either saline or Buflomedil 30 mg/kg for 7 days. Local cerebral glucose utilization (LCGU), monitored by [14C]-Deoxyglucose autoradiography, was determined at 2 hr after reperfusion. At 3 hr after the start of BCAO, the LCBF in the Buflomedil group was higher by 71-128% in the cerebral cortex, 61-150% in the amygdala, caudate-putamen, nucleous accumbens and globus pallidus, and 82% in the internal capsule. At 2 hr after reperfusion, LCBF did not differ between groups, but LCGU in the Buflomedil group was significantly higher by 26-49% in the cerebral cortex, cochlear nuclei and vestibular nuclei than that in the control group. From these results, it is concluded that Buflomedil improved survival rate after permanent BCAO and have beneficial effect on local cerebral blood flow distribution after BCAO in SHR.

Animals↗
PubMed2006

Enhanced visualization and quantification of magnetic resonance diffusion tensor imaging using the p:q tensor decomposition.

Many scalar measures have been proposed to quantify magnetic resonance diffusion tensor imaging (MR DTI) data in the brain. However, only two parameters are commonly used in the literature: mean diffusion (D) and fractional anisotropy (FA). We introduce a visualization technique which permits the simultaneous analysis of an additional five scalar measures. This enhanced diversity is important, as it is not known a priori which of these measures best describes pathological changes for brain tissue. The proposed technique is based on a tensor transformation, which decomposes the diffusion tensor into its isotropic (p) and anisotropic (q) components. To illustrate the use of this technique, diffusion tensor imaging was performed on a healthy volunteer, a sequential study in a patient with recent stroke, a patient with hydrocephalus and a patient with an intracranial tumour. Our results demonstrate a clear distinction between different anatomical regions in the normal volunteer and the evolution of the pathology in the patients. In the normal volunteer, the brain parenchyma values for p and q fell into a narrow band with 0.976<p<1.063 x 10(-3) mm2 s(-1) and 0.15<q<1.08 x 10(-3) mm2 s(-1). The noise appeared as a compact cluster with (p,q) components (0.011, 0.141) x 10(-3) mm2 s(-1), while the cerebrospinal fluid was (3.320, 0.330) x 10(-3) mm2 s(-1). In the stroke patient, the ischaemic area demonstrated a trajectory composed of acute, sub-acute and chronic phases. The components of the lesion were (0.824, 0.420), (0.884, 0.254), (2.624, 0.325) at 37 h, 1 week and 1 month, respectively. The internal capsule of the hydrocephalus patient demonstrated a larger dispersion in the p:q plane suggesting disruption. Finally, there was clear white matter tissue destruction in the tumour patient. In summary, the p:q decomposition enhances the visualization and quantification of MR DTI data in both normal and pathological conditions.

Algorithms↗
PubMed1997

[Measurement of regional cerebral blood flow and glucose utilization in rat brain under chronic hypoperfusion conditions following bilateral carotid artery occlusion. Analyzed by autoradiographical methods].

OBJECTIVE: Although the pathology of chronic hypoperfusion in rat following bilateral carotid artery occlusion has been documented, long term changes in cerebral blood flow and metabolism have not been reported. In this study regional cerebral blood flow (rCBF) and regional glucose utilization (rCGU) were analyzed by autoradiographical methods, pathological observation of the brains was also conducted. METHODS: Male Wistar rats aged 12 weeks were anesthetized and the bilateral carotid arteries were occluded. Physiological parameters, ABG, MABP, and rectal temperature were measured before and through occlusion. After 2 days, 1, 4, and 8 weeks and controls of rCBF (Sakurada) and rCGU. (Sokoloff) were measured (n = 6). Evaluated regions included frontal cortex (Fcor), parietal cortex (Pcor), temporal cortex (Tcor), occipital cortex (Ocor), genu corpus callosum (gCC), corpus callosum (CC), splenium corpus callosum (sCC), caudate putamen (CPu), globus pallidus (GP), internal capsule (IC), thalamus (Thal), hippocampus CA 1 (CA 1), hypothalamus (HypoTh), amygdal (Amygd), and substantia nigra (SNR). In separate animals (n = 3) tissue sections were stained using Klüver-Barrera (KB) and Hematoxylin-Eosin (HE), and pathological changes were observed. RESULTS: After 2 days the rCBF values were significantly reduced to 33-58% of control values in the Fcor. Pcor, Tcor, Ocor, gCC, CC, sCC, CPu, GP, JC, and Amygd. The reductions were observed from the 2nd day to the 1st week. From the 1st week to the 4th week values began to recover to control levels. However, after 4 weeks they were still significantly reduced in the Ocor, gCC, CC, sCC, GP, IC, and SNR (51-63%). After 8 weeks, the rCBF values in the areas except white matter, CPu, GP, and Ocor, etc., recovered to approximately 90% of control levels. However, in the Ocor, gCC, CC, sCC, CPu, GP, and IC, they were still 70-89% of control levels. After 2 days the rCGU values were reduced to 56-95% (except Amygd) in the measured regions, although not as reduced as the rCBF levels. From the 2nd day to the 1st week, the rCGU values were reduced further and after 1 week the rCGU values were significantly reduced to 39-69% in the Fcor, Pcor, Tcor, Ocor, gCC, CC, sCC, CPu, GP, IC (Lt), Thal (Rt), Amygd, and SNR From the 1st week to the 4th week, the values began to recover to control levels. After 4 weeks, rCGU improved to approximately 90-100% of controls, and remained at that level through 8 weeks occlusion. Rarefaction of the myelinated fibers was observed in the white matter from the 1st week to the 4th week in the KB stained sections, while little change in cortex was observed throughout 1st to 8th week. CONCLUSION: In this chronic hypoperfusion model rCBF remained depressed after 8 weeks in the Ocor, white matter, and basal ganglia, and rarefaction of the white matter was observed. These results indicate that this model is suitable for the study of chronic cerebral hypoperfusion.

Animals↗
PubMed2001

Periventricular changes associated with spontaneous canine hydrocephalus.

Causes of canine juvenile hydrocephalus have been well documented. However, the effects of hydrocephalus on periventricular white matter have been only partially described. The present report shows that hydrocephalus-associated lesions of the periventricular white matter, i.e., formation of diverticula, clefts, and tears, are prevalent. Marked hydrocephalus was identified at necropsy in 20 juvenile dogs between 1990 and 1999. The severity grade was based upon a ratio of lateral ventricular dimensions to cortical thickness. All animals exhibited ependymal lesions consisting of attenuation, with or without abortive attempts of ependymal regeneration, and ulceration. In 10 dogs (50%), unilateral or bilateral periventricular diverticula and cleft formation in the region of the caudate nucleus were observed. The diverticula were formed at the caudal pole of the caudate nucleus, communicated with the ventricular lumen, and were associated with ependymal denudation. Loss of the ependymal lining probably contributes to a bulk shift of cerebrospinal fluid from the ventricular lumen to the periventricular white matter, leading to diverticulum formation. Clefts were observed within the parenchyma at the border of the internal capsule and putamen, consistent with an ischemic insult. Occasionally tearing with separation of the caudate nucleus from the subcortical white matter was found, representing unification of expanding clefts and diverticula. In one of the few clinically well-documented cases, tearing was correlated with a sudden decline in neurologic function, culminating in euthanasia. However, tears and clefts may exhibit a chronicity of several days, as indicated by the presence of astroglial scars along the lesion margins.

Animals↗
PubMed2005

Frameless stereotactic aspiration and thrombolysis of deep intracerebral hemorrhage is associated with reduction of hemorrhage volume and neurological improvement.

INTRODUCTION: This is a phase-2 safety trial to demonstrate the ability of frameless stereotactic aspiration and thrombolysis of ICH to safely remove blood. METHODS: Patients with ICH in the deep basal ganglia and internal capsule of > 5 cc volume were consented to undergo computed tomographic imaging for frameless stereotactic guidance registration. Using the frameless stereotactic (CT) guidance, a 4-mm diameter catheter was inserted into the body of the hematoma using a frontal burr hole approach. The catheter was aspirated and then flushed with saline and aspirated to remove unclotted blood. After a confirmatory CT scan to localize the catheter, 1 mg of recombinant tissue plasminogen activator (t-PA) was infused into the clot, permitted to bathe the clot for 30 minutes, and then drained into a closed circuit collection system. t-PA was infused every 8 hours for 48 hours. A follow up CT scan was obtained at 48 hours. RESULTS: 28 patients with ICH (mean age 67.1) were admitted and underwent the procedure. Mean initial ICH volume was 54.6 cc +/-6 37.8. Mean time from onset to aspiration was 44 hours (range 7-180). Mean initial NIH Stroke scale (NIHSS) score was 24 (range 15-33). Compared with initial CT scan, there was a mean reduction of ICH volume by 77 +/-6 13% on final CT scan (p < 0.0002). Compared with initial NIHSS, the discharge mean NIHSS (16 +/- 6) was significantly improved (p < 0.001). There were no infectious, hemodynamic or neurologic complications. There were no episodes of symptomatic hemorrhagic enlargement and one case of asymptomatic bleeding along the catheter tract. CONCLUSION: Frameless stereotactic aspiration and thrombolysis (FAST) of deep spontaneous intracerebral hemorrhage is a safe therapy that is associated with reduction in ICH volume, early improvement in NIHSS and potentially could be used to improve outcome.

Adult↗
PubMed2000

Transient structures of the human fetal brain: subplate, thalamic reticular complex, ganglionic eminence.

Morphological features of the subplate, the thalamic reticular complex and the ganglionic eminence, which represent three major transient structures of the human fetal forebrain, are summarized with special reference to their functional roles. The subplate harboring various neuronal types is an outstandingly wide zone subjacent to the cortical plate in the human fetal brain. Within the subplate various cortical afferents establish synaptic contacts for a prolonged period before entering the cortical plate. Therefore, the subplate is regarded as a "waiting compartment" which is required for the formation of mature cortical connections. Next to the thalamic reticular nucleus, within the fibers of internal capsule, the perireticular nucleus is located which has been established as a distinct entity during development. Its various neuronal types express a number of different neuroactive substances. Perinatally, the perireticular nucleus is drastically reduced in size. It is involved in the guidance of corticofugal and thalamocortical fibers. The ganglionic eminence is a conspicuous proliferative area that persists throughout nearly the entire fetal period. In the human fetal brain it extends medially upon the dorsal thalamic nuclei which receive precursor cells from the ganglionic eminence. Postmitotic cells in the marginal zone of the ganglionic eminence serve as an intermediate target for growing axons. On the whole, all three structures establish transient neural circuitries that may be essential for the formation of adult projections. The characteristics of the three transient structures are particularly relevant for developmental neuropathology as these structures may be damaged in disorders that preferentially occur in preterm infants.

Animals↗
PubMedDate not supplied

Hypoparathyroidism with extensive intracerebral calcification in patients with beta-thalassemia major.

We report marked intracerebral calcification in eight thalassemic patients with hypoparathyroidism, followed regularly at the Haematology Research Center, Department of Pediatrics, Shiraz, Iran. Their mean age was 16.8 years (range 12-21 years). Six of the eight patients with thalassemia were females. The daily dose of calcitriol was between 0.01 and 0.1 microg/kg b. wt. Calcium-phosphate metabolic control was good or satisfactory in all patients. Three patients had at least one episode of generalized convulsions caused by hypocalcemia, before and during treatment. One patient complained of chronic headache and another patient had a low intelligence quotient. All were on treatment with calcitriol and oral calcium supplementation. The mean serum ferritin concentration was 3225 microg/l (range 2000-6000 microg/l). Calcification was present in the cerebral hemispheres, thalamic nuclei, basal ganglia, the internal capsule, part of the caudate nuclei and the posterior fossa. There was no history of birth asphyxia, head trauma, infections or metabolic diseases in any of the patients. No relationship was observed between the degree of cerebral calcification and the severity of hypoparathyroidism at diagnosis. Our observations stress the importance of a periodic assessment of calcium metabolism, prompt treatment of the endocrinopathy and strict control of calcium metabolism.

Adolescent↗
PubMed2005

Activity-dependent synaptic plasticity in the central nucleus of the amygdala.

Much evidence indicates that fear conditioning involves potentiation of some thalamic inputs to the lateral amygdala (LA). In turn, the LA would excite more neurons in the central nucleus (CE), leading to the generation of fear responses via their brainstem and hypothalamic projections. However, the posterior thalamus not only projects to LA but also to the medial sector of CE (CEm), suggesting that CEm might also be a site of plasticity. To test whether CEm also exhibits activity-dependent synaptic plasticity, we performed whole-cell recordings of CEm neurons in amygdala slices and stimulated thalamic axons coursing through the internal capsule and, as a control, the basolateral (BL) nucleus. High-frequency stimulation of thalamic inputs led to a long-lasting potentiation of thalamic responses, whereas BL-evoked responses remained unchanged. This thalamic long-term potentiation (LTP) developed even when slices were prepared with a cut severing the connections between the LA and CEm but was greatly reduced when an NMDA receptor antagonist was added to the perfusate shortly before and during LTP induction. Yet, intracellular dialysis with the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate did not prevent induction of the thalamic LTP, suggesting that presynaptic NMDA receptors are required for its induction. Consistent with this, the thalamic LTP also developed when the cells were dialyzed with a calcium chelator or kept hyperpolarized during induction. Finally, this thalamic LTP was associated with reduced amounts of paired-pulse facilitation, suggesting that it is expressed presynaptically. These results are consistent with the idea that the CEm plays an active role in fear conditioning.

2-Amino-5-phosphonovalerate↗
PubMed2006

Activity-dependent bidirectional modification of inhibitory synaptic transmission in rat subthalamic neurons.

Rebound burst activity can be generated in neurons in the subthalamic nucleus (STN) by strong GABAergic inhibitory inputs from the globus pallidus externa (GPe) that is reciprocally connected with the STN. It has been proposed that the rebound burst activity in STN neurons is a key event for generating synchronized rhythmic burst activity in the GPe-STN loop, which may be relevant to the resting tremor in Parkinson's disease. Here we report that rebound burst firing of STN neurons induces long-lasting bidirectional modifications of GABAergic synaptic transmission in STN neurons themselves. Using the gramicidin perforated-patch clamp technique in the brain slice preparation, we recorded IPSPs from STN neurons during electrical stimulation of the internal capsule. Rebound spikes triggered by hyperpolarizing current pulses were used to induce modification of inhibitory synaptic transmission. We found that long-lasting potentiation of IPSPs could be induced in the neurons exhibiting three or more rebound spikes that had interspike intervals shorter than half of those during base spontaneous activity, whereas long-lasting depression or no change of IPSP amplitude was likely to be observed in neurons that had no rebound burst or two rebound spikes within a burst. The potentiation or depression of IPSPs was associated with a negative or positive shift of reversal potential of IPSPs (E(IPSP)). The modifications of IPSPs were dependent on activation of postsynaptic voltage-gated calcium channels. This study is the first demonstration that activity-dependent bidirectional modifications of inhibitory synaptic transmission are attributable to bidirectional shifts of E(IPSP).

Action Potentials↗
PubMed2005

Developmental changes in diffusion anisotropy coincide with immature oligodendrocyte progression and maturation of compound action potential.

Disruption of oligodendrocyte lineage progression is implicated in the white-matter injury that occurs in cerebral palsy. We have previously published a model in rabbits consistent with cerebral palsy. Little is known of normal white-matter development in perinatal rabbits. Using a multidimensional approach, we defined the relationship of oligodendrocyte lineage progression and functional maturation of axons to structural development of selected cerebral white-matter tracts as determined by diffusion tensor imaging (DTI). Immunohistochemical studies showed that late oligodendrocyte progenitors appear at gestational age 22 [embryonic day 22 (E22)], whereas immature oligodendrocytes appear at E25, and both increase rapidly with time (approximately 13 cells/mm2/d) until the onset of myelination. Myelination began at postnatal day 5 (P5) (E36) in the internal capsule (IC) and at P11 in the medial corpus callosum (CC), as determined by localization of sodium channels and myelin basic protein. DTI of the CC and IC showed that fractional anisotropy (FA) increased rapidly between E25 and P1 (E32) (11% per day) and plateaued (<5% per day) after the onset of myelination. Postnatal maturation of the compound action potential (CAP) showed a developmental pattern similar to FA, with a rapid rise between E29 and P5 (in the CC, 18% per day) and a slower rise from P5 to P11 (in the CC, <5% per day). The development of immature oligodendrocytes after E29 coincides with changes in FA and CAP area in both the CC and IC. These findings suggest that developmental expansion of immature oligodendrocytes during the premyelination period may be important in defining structural and functional maturation of the white matter.

Action Potentials↗
PubMed1995

[Brain deformation caused by hyperplasia molar teeth (macrodonts) in the Japanese field vole (Microtus montebelli)].

Protrusion of hyperplastic upper molar teeth (macrodonts) into the cranial cavity was observed in the Japanese field vole. Protrusions of the upper molars occurred on both sides, but were large on the left than on the right. The teeth invaded the cranial cavity and brain parenchyma. Large concavities on the ventral side of the brain were interposed between the lateral olfactory tract and the optic tract. Invation by one macrodont reached the basal nuclei, hypothalamic and thalamic nuclei. The brain was deformed bilaterally, and nearly the entire olfactory bulb, globus pallidus, internal capsule, and lateral preoptic nucleus, and a portion of the hypothalamus, thalamus and anterior commissure were absent on the left side.

Animals↗
PubMed1999

Early prognostic indicators of outcome in infants with neonatal cerebral infarction: a clinical, electroencephalogram, and magnetic resonance imaging study.

OBJECTIVE: The aim of this study was to identify prognostic factors in newborns with cerebral infarction. DESIGN: Antenatal and perinatal factors and early clinical, electroencephalogram (EEG), and magnetic resonance imaging (MRI) findings were compared with neurodevelopmental outcome in 24 children with evidence of cerebral infarction on neonatal MRI. RESULTS: Out of 24 infants, 19 had an infarction in the territory of a major cerebral vessel and 5 in the borderzone between cerebral arteries. Neuromotor outcome was normal in 17 and abnormal in 7 infants. Of these 7 infants, 5 infants showed a definite hemiplegia, whereas the other 2 showed some asymmetry of tone or function but no definite hemiplegia. None of the adverse antenatal or perinatal factors was significantly associated with abnormal outcome. Neonatal clinical examination was also not always predictive of the outcome. The extent of the lesion on MRI was a better predictor. In particular, it was the concomitant involvement of hemisphere, internal capsule and basal ganglia that was always associated with an abnormal outcome whereas the involvement of only one or two of the three tended to be associated with a normal outcome. EEG was also very helpful. Abnormal background activity either unilateral or bilateral was found in 6 infants and 5 out of 6 developed hemiplegia. In contrast, the presence of seizure activity in presence of a normal background was not related to abnormal outcome. CONCLUSIONS: Early MRI and EEG can help to identify the infants with cerebral infarction who are likely to develop hemiplegia.

Cerebral Infarction↗