Infarction In Cortex Research Articles

Prepro-thyrotropin-releasing hormone 178-199 exerts partial protection against cerebral ischemia in adult rats.

We examined in the present study the effects of the centrally administered prepro-thyrotropin-releasing-hormone 178-199 (prepro-TRH 178-199) on cerebral ischemia induced by ligation of the middle cerebral artery (MCA) in adult Sprague-Dawley rats. Animals were intracerebrally injected with prepro-TRH 178-199 (6 microg/kg or 200 microg/kg) or saline 1-2 h before ligation of MCA. Ischemic animals that received prepro-TRH 178-199, regardless of dosage, displayed some amelioration (20%) of motor asymmetry associated with MCA ligation, while ischemic animals that received saline continued to exhibit significant asymmetrical behaviors. Interestingly, triphenyltetrazolium chloride staining (a marker for tissue metabolic activity) revealed that four of five ischemic animals that received 200 microg/kg prepro-TRH 178-199 showed a marked reduction (90-100%) in the infarction of the frontal cortex, although the posterior sections of the cortex remained infarcted. In contrast, ischemic animals that received 6 microg/kg prepro-TRH 178-199 demonstrated infarction that did not differ in size and extent from those that received saline. Post hoc examination revealed that ischemic animals treated with 200 microg/kg prepro-TRH 178-199 had significantly lower corticosterone (CORT) levels (115+/-23 ng/ml) than ischemic animals treated with 6 microg/kg prepro-TRH 178-199 or saline (288+/-51 ng/ml). The present observation provides the first evidence that prepro-TRH 178-199 can promote neuroprotection against cerebral ischemia.

Pure wod deafness after bilateral primary auditory cortex infarcts

Pure wod deafness after bilateral primary auditory cortex infarcts

Application of endovascular suture occlusion of middle cerebral artery in gerbils to obtain consistent infarction

Middle cerebral artery occlusion (MCAO) by endovascular suture has gained increasing acceptance because it is relatively non-invasive and allows reperfusion. However, Its application in rats has resulted In inconsistent infarction volumes which involve only the subcortex or subcortex plus some cortex. In order to eliminate this drawback, we applied the intraluminal suture occlusion of MCA to gerbils that have an incomplete Circle of Willis. MCAO was induced by inserting an endovascular 5-0 nylon suture with a blunted tip into the Circle of Willis. Animals were divided into two groups: permanent MCAO for 24 h fn = 8) and transient MCAO for 3 h with 21 h reperfusion fn = 8). The corrected infarction volume in the permanent MCAO group was 232 ± 37 mm3 whereas it was 230 ± 45 mm3 in the transient MCAO group. All animals in both groups had infarction in both cortex and subcortex. Results of this study show that endovascular suture occlusion of MCA can be easily applied in gerbils to obtain consistent infarction. This would allow both transient and permanent focal ischemia to be tested in the same model of ischemia. [Neurol Res 1999; 21: 574–578]

Intracisternal antisense oligonucleotide to growth associated protein-43 blocks the recovery-promoting effects of basic fibroblast growth factor after focal stroke.

Focal infarction (stroke) of the lateral cerebral cortex of rats (including the sensorimotor cortex) produces deficits in sensorimotor function of the contralateral limbs that recover partially over time. In previous studies, we found that the intracisternal injection of basic fibroblast growth factor (bFGF), a potent neurotrophic growth factor, starting at 1 day after stroke, significantly enhanced recovery of sensorimotor function of the contralateral forelimb and hindlimb. Moreover, immunoreactivity (IR) for growth-associated protein-43 (GAP-43), a molecular marker of new axonal growth, was increased in the intact contralateral sensorimotor cortex following bFGF treatment. In the current study, we found that the intracisternal administration of antisense, but not missense, oligonucleotide to GAP-43 blocked the recovery-enhancing effects of bFGF and blocked the increase in GAP-43 IR in the contralateral cortex. These results suggest that upregulation of GAP-43 expression and consequent enhanced axonal sprouting in intact uninjured parts of the brain are likely mechanisms for the recovery-promoting effects of bFGF.

Vestibulo-ocular dysfunction induced by cortical damage in man:: a case report

We studied the rare case of a patient presenting with vestibulo-ocular dysfunction and clinical vestibular symptoms after right temporo-parietal cortex infarction. The vestibulo-ocular reflex (VOR) was elicited in the dark, by sinusoidal (0.02; 0.05 and 0.1 Hz) and by step velocity rotation (100°/s 2) in clockwise and counterclockwise directions. Horizontal and vertical eye movements were recorded by DC electro-oculography (EOG). When compared to a control group of 8 healthy subjects, this patient presented VOR asymmetry with (1) a significant VOR velocity bias toward the lesioned side revealed as a vestibulo-ocular offset that occurred only under dynamic conditions (2) a significant reduction of the VOR time constant when rotation was directed to the lesioned side. VOR gain was normal. We suggest that the parieto-temporal cortex is implicated in the regulation of vestibulo-ocular symmetry in man. This cortical processing of vestibular integration might involve a multidimensional velocity storage integrator that subserves the maintenance of spatial coordinates along the spatial vertical axis.

Pure motor monoparesis of a lower limb due to a small infarction in the contralateral motor cortex

Pure motor monoparesis (PMM) is a rare condition characterized by weakness limited to one limb without sensory disturbance. We report a 42-year-old woman with PMM of the right lower limb caused by a small infarction in the contralateral motor cortex that could be detected by the magnetic resonance imaging of the brain. This case suggests that small lesions, missed by carelessly performed scans, could be a potential cause of PMM. This is especially true in the case of lower limb PMM, because the lesion may be located in the top of the frontal lobe cortex, an area that can be easily missed by routine scans. Therefore, we should pay careful attention to the opposite side of the motor cortex in examining neuroimages of PMM cases.

Specific Behavioral Effects Related to Age and Cerebral Ischemia in Rats

Rats at 4, 14, and 20 months of age were subjected to permanent occlusion of the left middle cerebral artery (MCAO) and the effects of age and ischemia assessed in tests for spatial learning (Morris’ water maze), social behavior, olfactory learning, exploratory behavior, and motor function. Furthermore, the extent of ischemic damage to the brain of rats of 5 and 19 months of age was studied. An age-related decline in water-maze performance was observed, and aged rats were less agile, less explorative, and less frequently engaged in social interactions than young rats. After ischemia, mild memory impairment was observed in old rats, while changes in some exploratory behaviors were observed in young rats. Neuropathological analyses revealed a variable and limited degree of infarction in the piriform cortex and the insular cortex with no difference between age groups. In conclusion, the present study confirmed and extended current data on behavioral differences between young and old rats. MCAO had limited influence on the tested behaviors.

Neurogenic ST depression in stroke

Background: Stroke is occasionally associated with ECG repolarization changes including ST depression. Recent evidence suggests a neurogenic contribution to these abnormalities in stroke patients. Animal studies implicate the insular cortex in cardiovascular control. We describe a patient with a left insular infarct and without cardiac or coronary artery disease, who developed ST depression indicating a neurogenic etiology. Case description: A 48 year-old female, with no risk factors for stroke, developed sudden expressive aphasia. MRI brain showed an infarct in the left insular cortex. Twenty-four hour Holter monitoring on the third day revealed transient ST depression more than 1.5 mm, which was not reproducible on subsequent monitoring. Transesophageal echo-cardiography (TEE) was normal. She had no cardiac symptoms and serial ECGs, cardiac enzymes (CKMB) and adenosine–thallium scan were normal. To-date, there had been no cardiac events like congestive heart failure or myocardial ischemia. Conclusion: These findings suggest neurogenic ST depression is related to the left insular infarct in view of the normal adenosine–thallium scan, non-reproducibility and evanescence of the ST segment changes and lack of associated cardiac symptoms. When neurogenic ST depression is combined with underlying coronary artery disease, it may adversely influence cardiac outcome after stroke.

Headache with neurological deficits and CSF lymphocytosis: A transient ischemic attack mimic

Headache with neurological deficits and cerebrospinal fluid (CSF) lymphocytosis (HaNDL) is a benign condition with a transient ischemic attack (TIA)-like presentation. It is a disease of young adults that is characterized by headache, transient focal neurological symptoms, and lymphocytic pleocytosis. The onset of neurological symptoms after cerebral angiography in patients with this disease has occasionally been reported. The authors present the case of a 28-year-old man with episodes of left-sided numbness and weakness associated with headache. He underwent cerebral angiography as part of his evaluation, after which he experienced an episode of right hemiplegia and aphasia. A subsequent magnetic resonance image (MRI) revealed two small new infarcts in the left parietal cortex. A diagnosis of HaNDL was made based mainly on clinical symptoms and CSF analysis. The symptoms resolved with conservative therapy. HaNDL is a benign condition that can present with symptoms similar to a TIA. Although HaNDL remains a diagnosis of exclusion, caution is required when considering cerebral angiography in the evaluation of patients with a HaNDL-like syndrome, because these patients seem prone to developing neurological symptoms after angiography.

Increased long-term potentiation in the surround of experimentally induced focal cortical infarction.

Functional recovery after stroke is partly due to cortical reorganization on a structural as well as a functional level. Recent investigations have shown that the excitability of brain areas surrounding cortical ischemic lesions is increased, probably due to a down-regulation of gamma-aminobutyric acid-receptor activity. There is some evidence that these changes might increase the susceptibility of the lesioned brain for adaptive changes and recovery. Here, we investigated the propensity for the induction of long-term potentiation (LTP) in the surround of experimentally induced focal cortical infarcts in rat somatosensory cortex in vitro. By using standard paradigms, LTP induction was found to be facilitated ipsilaterally in slices of lesioned animals 1 week after lesion induction. In homotopic contralateral areas, LTP was not different from control values. As LTP is commonly associated with plasticity and learning, the results provide further evidence for the lesion-induced amplification of network plasticity, as it is required for the reshaping of cortical circuits by timely training procedures.

Auditory evoked neuromagnetic response in cerebrovascular diseases: a preliminary study

OBJECTIVESMagnetoencephalography (MEG) measures aspects of the function of the auditory cortex of the human brain with high spatial resolution. The objective was to determine whether MEG also accurately identifies the...

Visual-imitative dissociation apraxia

Liepmann posited that, in right handers, the left parietal lobe contains movement formulas or representations. Therefore, performance failures may be induced by degraded representations, a failure of these representations to influence motor systems or a failure of stimuli to fully access these representations. Imitation may help the performance of subjects with degraded representations. However, patients who have impaired visual access to movement representations may perform more poorly with imitation than to verbal command. Trajectories of repetitive ‘slicing’ gestures made by a previously reported subject (Raymer et al.) with an infarction in the left visual association cortex (left occipital and inferior temporal lobe) that spared the parietal lobe were contrasted with those of three apraxic subjects with lesions that included the left parietal lobe and four non-brain-damaged control subjects. All subjects were asked to produce the gesture to verbal command and to imitation. Movements of the left hand, wrist, elbow and shoulder were digitized from neighboring views, reconstructed in three dimensions, and analysed graphically and numerically. The apraxic subjects with left parietal damage were unable to maintain the proper linearity and spatiotemporal attributes of their wrist motions and showed interjoint coordination deficits. Their deficits were most pronounced to verbal command, with their movements improving though remaining poorly performed when they imitated. The subject with the left occipital and inferior temporal lesion that spared parietal cortex, however, showed an opposite pattern. This subject exhibited close to normal performance when producing the movement to verbal command, but significant deficits when imitating.

Degeneration of the ipsilateral substantia nigra after striatal infarction: evaluation with MR imaging.

To evaluate the degeneration of the ipsilateral substantia nigra after striatal infarction by using magnetic resonance (MR) imaging. Twenty-five adult patients with embolic cerebral infarction of the middle cerebral artery distribution underwent MR imaging 0-4, 5-9, 12-15, and 27-29 days after the stroke. Sixteen of them also underwent follow-up MR imaging 2-12 months after the stroke. Ten patients had an infarct in the striatum with or without a cortical infarct (striatal infarction group); the other 15 patients had an infarct in the cerebral cortex of the middle cerebral artery distribution without a striatal infarct (cortical infarction group). In all 10 patients with striatal infarction, a hyperintense spot appeared in the ipsilateral substantia nigra on T2-weighted fast spin-echo images 7-12 days after the onset. This area became less intense and smaller 3 months later. In the cortical infarction group, no hyperintense spot in the ipsilateral substantia nigra was observed at any time. Degeneration of the substantia nigra ipsilateral to the striatal infarction was clearly demonstrated at MR imaging. This finding should not be mistaken for further cerebral infarction.

Inhibition of ischemia-induced fodrin breakdown by a novel phenylpyrimidine derivative NS-7: an implication for its neuroprotective action in rats with middle cerebral artery occlusion.

The effect of a novel neuroprotective compound, NS-7 [4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy)pyrimidine hydrochloride], on ischemia-induced fodrin breakdown was examined both in vitro and in vivo. The fodrin breakdown was measured by western blot followed by a densitometric analysis. In slices of the rat cerebral cortex, a pronounced fodrin breakdown was observed under hypoxic and hypoglycemic conditions. The enhancement of fodrin breakdown was completely blocked by omission of extracellular Ca2+ and significantly inhibited by calpain inhibitors such as E-64 and calpain inhibitor-I, thereby suggesting that the fodrin breakdown induced by hypoxia/hypoglycemia is due to the activation of Ca2+-stimulated neutral protease calpain. NS-7 (1-30 microM) produced a concentration-dependent inhibition of hypoxia/hypoglycemia-induced fodrin breakdown. In rats with unilateral middle cerebral artery occlusion (MCAO), a pronounced fodrin breakdown was observed in the cerebral cortex and striatum, although the time course for the development of the fodrin breakdown was much slower in the cerebral cortex than in the striatum. NS-7 (0.5 mg/kg i.v.), when injected immediately after MCAO, suppressed not only the fodrin breakdown but also the infarction in the cerebral cortex. From these results it is suggested that inhibition of calpain activation is implicated in the neuroprotective action of NS-7.

Phagocytic response in photochemically induced infarction of rat cerebral cortex. The role of resident microglia.

In this study we assessed the relative extent to which resident microglia and blood-borne macrophages contribute to the population of phagocytes after focal infarction of the rat cortex. Focal cerebral infarction was induced in rats by photothrombosis after hematogenous macrophages were depleted by means of liposomes containing dichloromethylene diphosphonate. The phagocytic activation of microglia and macrophages was monitored by immunocytochemistry with the antibody ED1. In both macrophage-depleted rats and controls, ED1+ phagocytes bordered the infarct to the same extent at day 3 after photothrombosis. By contrast, at day 6 after photothrombosis ED1+ phagocytes in control rats greatly outnumbered those in macrophage-depleted rats. With the use of the antibody Ox42 directed against the CR3 receptor on the surface of microglia, it was possible to selectively document the transition of resident microglia into stellate and ameboid phagocytic microglia during the first 6 days after photothrombosis in the absence of bloodborne macrophages. The initial phagocytic response after focal brain ischemia is an intrinsic property of the nervous system mainly performed by resident microglia. The majority of hematogenous macrophages are recruited secondarily to participate in the removal of necrotic tissue.

両側感音難聴にて発症した一側皮質性難聴例

A patient with bilateral sensorineural hearing loss on a pure tone audiogram (PTA), associated with unilateral (right side) cerebral infarction in the auditory cortex is described. The PTA on the left (contralateral) side initially showed a “scale out”. The PTA threshold improved rapidly, and finally returned to almost normal levels within 2 months. The PTA on the right side initially showed mild sensorineural hearing loss. The PTA threshold gradually returned to normal levels within 2-3 months. In contrast to the rapid recovery of the PTA threshold, the maximum speech perception ability on the left side showed a very low score during the follow-up period of 2 years, and showed little improvement. The maximum speech perception ability on the right side maintained a high score from the time of first examination. All of the objective auditory examinations, including the auditory brainstem response (ABR), oto-acoustic emission (OAE), electrocochleogram (ECoG), middle latency response (MLR), and slow vertex response (SVR), indicated that hearing loss on the left (contralateral) side was closely associated with unilateral (right side) cerebral infarction of the auditory cortex. These results suggest that sensorinueral hearing loss on the PTA could be detected at the early stages of onset, even after unilateral damage to the auditory cortex.

Brain edema associated with progressive selective neuronal death or impending infarction in the cerebral cortex.

This study examined the temporal profile of brain edema in the cerebral cortex associated with selective neuronal death or focal infarction after repeated ischemia at an intensity of ischemic insult just under and above the threshold level to induce infarction. The left carotid artery of adult gerbils was twice occluded for 10 min each time with a 5-hr interval between the blockages. In this model, focal infarction developed in coronal sections examined at the chiasmatic level (face A), whereas only selective neuronal death without infarction was found in the coronal section observed at the infundibular level (face B). In each animal, Evans blue (2%) was intravenously injected 1 hr prior to sacrifice as an indicator of blood-brain barrier (BBB) disruption. Brain edema was assessed by gravimetry in samples taken from both faces at 15 min, 5 hr, 12 hr, 24 hr, and 48 hr after the 2nd 10-min ischemia. Evans blue extravasated only in face A, corresponding to focal infarction at 24 and 48 hr after the 2nd 10-min ischemia. The specific gravities of the ischemic cortex of both faces decreased significantly from control at 15 min (P < 0.05) and had recovered by 5 hr after ischemia. By 12 hr, the specific gravities of both faces had again decreased significantly from the control values (P < 0.05), but did not differ significantly from each other. At 24 and 48 hr, the specific gravities of both faces were significantly lower than the control values (P < 0.01), and the specific gravity of face A was markedly lower than that of face B (P < 0.01). We concluded that in face B, where only selective neuronal death without infarction occurred only cytotoxic edema develops, whereas in face A, where infarction progresses, vasogenic edema develops in addition to cytotoxic edema.

“Semantic” Conduction Aphasia from a Posterior Insular Cortex Infarction

A unique infarction limited to the posterior insula and intrasylvian parietal opercular cortex produced a subtype of conduction aphasia, characterized by a predominance of semantic paraphasias. Temporal lobe hypoperfusion seen on hexamethylpropyleneamineoxime single-photon emission computed tomography in the absence of any signs of ischemia suggested that cortical diaschisis played a role in the emergence of this syndrome.

Acquired dysfluencies following infarction of the left mesiofrontal cortex

Abstract The present study describes the acquired dysfluencies observed in a patient with transcortical motor aphasia (TCMA) following ischaemic infarction of the mesiofrontal cortex due to occlusion of the anterior cerebral artery. Prolongation of labial plosives and labiodental fricatives as well as hesitations concomitant with a few repetitions of syllables and sounds, respectively, were noted. The dorsolateral aspects of the frontal lobe of the dominant hemisphere have been considered the relevant site of lesion in instances of acquired stuttering concomitant with TCMA. The present case demonstrates that dysfluencies May-June be present with mesiofrontal lesions as well. The patient's stuttering was confined to production of complex sentences. Since transcortical motor aphasia is characterized by paucity of speech, consisting mostly in one- to two-word utterances, the dysfluencies of patients with this kind of disorder often might be masked. The observed stuttering-like behaviour differed in two respects from other reports on this disorder: the dysfluencies, first, were restricted to word-initial sounds and, secondly, did not occur during repetition tasks and reading aloud. Thus, acquired stuttering due to mesiofrontal lesions might represent a specific constellation of dysfluencies.

Cyclic Decrease in Mixed Venous Oxygen Saturation for the Early Diagnosis of Seizure Complications After Cardiac Surgery

Cyclic Decrease in Mixed Venous Oxygen Saturation for the Early Diagnosis of Seizure Complications After Cardiac Surgery