Unilateral Cortical Infarction Research Articles

Isolated Complete Tongue Paralysis as a Manifestation of Focal Cortical Infarction

Although isolated contralateral tongue deviation following unilateral cortical infarction was occasionally reported, the unilateral lesion usually produces no significant deficit of tongue motility considering bilateral supranuclear innervation of the hypoglossal nerve. We observed a patient with obvious tongue paralysis, including intrinsic muscles, caused by ischemic stroke involving the motor area of the tongue in the primary motor cortex.

P13.8 Functional brain networks during motor imagery after stroke

In the present study, we propose a methodological approach to assess the functional brain functional network organization underlying motor imagery after stroke. Functional brain connectvity was estimated from high density EEG recorded during motor imagery of hand movements performed with the affected and unaffected hand by a patient affected by unilateral cortical infarction. stroke. The use of a graph theoretical approach allowed the characterizatio of the connectivity pattrens and revealed that a different topological orgainization exists between the affected and unaffected movement imagination. These preliminary findings are promising for the investigation of network plasticiy during post-stroke rehabilitation.

Remodeling the Brain With Behavioral Experience After Stroke

Behavioral experience can drive brain plasticity, but we lack sufficient knowledge to optimize its therapeutic use after stroke. We outline recent findings from rodent models of cortical stroke of how experiences interact with postinjury events to influence synaptic connectivity and functional outcome. We focus on upper extremity function. After unilateral cortical infarcts, behavioral experiences shape neuronal structure and activity in both hemispheres. Experiences that matter include interventions such as skill training and constraint-like therapy as well as unguided behaviors such as learned nonuse and behavioral compensation. Lateralized behaviors have bihemispheric influences. Ischemic injury can alter the sensitivity of remaining neocortical neurons to behavioral change and this can have positive and negative functional effects. Because experience is ongoing in stroke survivors, a better understanding of its interaction with brain reorganization is needed so that it can be manipulated to improve function and prevent its worsening.

Dissociable effects in reaction time performance after unilateral cerebral infarction: A comparison between the left and right frontal cortices in rats

Reaction time performance reflects the speed of information processing, both in humans and lower vertebrates like the rat. The present study compared reaction time performance in rats following unilateral infarction to the frontal cortex. The objective was to model cognitive impairment as it is seen in humans after stroke. Rats were trained in a reaction time paradigm, after which unilateral cortical infarction was induced photochemically. Reaction time performance was differentially affected after unilateral infarction to either the left or right frontal cortex, whereas sham operation did not result in a significant alteration in reactivity. An overall increase in reaction time of about 10% was present at 4 weeks after frontal infarction. In addition, a lateralized reaction time deficit occurred very early after right frontal infarction as an increase of 10–15% in trials directed towards the contralesional side. Additional analyses showed that these reaction time deficits can be explained differently: the former as a gradual and general decrease in the speed of information processing, whereas the latter shows specific impairment to initiate a contralateral motor response. The former matches well with the mental slowing observed in stroke patients, whereas the latter resembles a neglect phenomenon. We conclude that measuring reaction time performance after frontal cortical infarction in rats could offer a useful tool to model particular human cognitive impairments following cerebral infarction.

Motor improvements after focal cortical ischemia in adult rats are mediated by compensatory mechanisms

Initial functional impairments after cerebral ischemia often improve considerably during the early period after the insult. Although pathological changes associated with post-lesion improvements have been widely investigated, it has not been resolved whether behavioral improvement represents true restoration of function (recovery) or development of new strategies (compensation). This study investigated whether early motor improvements after focal cerebral ischemia reflect recovery or compensation. Adult female Wistar rats were trained to retrieve food pellets in a skilled reaching task prior to receiving a unilateral cortical infarction induced by photothrombosis in forelimb motor cortex. Animals were continuously tested in the reaching task up to 3 weeks after lesion. The end point measures revealed that reaching success rates remained at pre-lesion levels, however, qualitative analysis of reaching movements indicated permanent changes in forelimb movement patterns. Similar observations were made in a skilled walking task and a test for forelimb asymmetry. These data indicate that lesion animals adopted alternative movement strategies in order to successfully perform the tasks. The changes in postoperative performance were compared to anatomical data in individual animals. The finding that reaching success was not related to lesion size supports the idea that the degree of adaptive behavior after cortical ischemia depends on plastic properties of the remaining intact tissue.

Crossed cerebellar diaschisis in patients with cortical infarction: logistic regression analysis to control for confounding effects.

Crossed cerebellar diaschisis (CCD) refers to reduced metabolism and blood flow in the cerebellar hemisphere contralateral to a cerebral lesion. Many cortical areas have been reported to cause CCD without consideration of confounding factors. We performed single-photon emission computed tomography (SPECT) in patients with cortical infarction to identify regions independently related to CCD, controlling for possible confounding effects. Patients with unilateral cortical infarction (n=113; 75 male, 38 female; mean+/-SD age, 66+/-13 years) underwent SPECT of the brain with N-isopropyl-p-[(123)I]iodoamphetamine ((123)I-IMP). Regional cerebral blood flow was measured autoradiographically. Asymmetry indices (AIs) were calculated on the basis of ratios representing symmetrical regional cerebral blood flow in the cerebellum and 16 cerebral regions. CCD was defined as AI for cerebellum >0.1. AIs for 16 cortical regions were considered for both dichotomous and continuous variables for analysis of CCD occurrence by means of backward logistic regression. For dichotomized variables, hypoperfusion of postcentral (odds ratio [OR]=7.607; 95% CI, 2.299 to 25.174) and supramarginal (OR=3.916; 95% CI, 1.394 to 11.003) regions independently influenced CCD. For continuous variables, hypoperfusion of postcentral (OR=1.044; 95% CI, 1.019 to 1.068) and supramarginal (OR=1.021; 95% CI, 1.001 to 1.041) regions (and, as a negative factor, medial occipital regions; OR=0.942; 95% CI, 0.895 to 0.991) independently influenced CCD. Many cortical areas apparently do not contribute to CCD. Correspondence of CCD between dichotomized and continuous analyses suggests that location of a lesion, not severity, is the main determinant of CCD.

Induction of bilateral plasticity in sensory cortical maps by small unilateral cortical infarcts in rats.

Behavioural impairments caused by brain lesions show a considerable, though often incomplete, recovery. It is hypothesized that cortical and subcortical plasticity of sensory representations contribute to this recovery. In the hindpaw representation of somatosensory cortex of adult rats we investigated the effects of focal unilateral cortical lesions on remote areas. Cortical lesions with a diameter of approximately 2 mm were induced in the parietal cortex by photothrombosis with the photosensitive dye Rose Bengal. Subsequently, animals were kept in standard cages for 7 days. On day seven, animals were anaesthetized and cutaneous receptive fields in the cortical hindpaw representations ipsi- and contralateral to the lesion were constructed from extracellular recordings of neurons in layer IV using glass microelectrodes. Receptive fields in the lesioned animals were compared to receptive fields measured in nonlesioned animals serving as controls. Quantitative analysis of receptive fields revealed a significant increase in size in the lesioned animals. This doubling in receptive field size was observed equally in the hemispheres ipsi- and contralateral to the lesion. The results indicate that the functional consequences of restricted cortical lesions are not limited to the area surrounding the lesion, but affect the cortical maps on the contralateral, nonlesioned hemisphere.

Inosine induces axonal rewiring and improves behavioral outcome after stroke.

Cerebral infarct (stroke) often causes devastating and irreversible losses of function, in part because of the brain's limited capacity for anatomical reorganization. The purine nucleoside inosine has previously been shown to induce neurons to express a set of growth-associated proteins and to extend axons in culture and in vivo. We show here that in adult rats with unilateral cortical infarcts, inosine stimulated neurons on the undamaged side of the brain to extend new projections to denervated areas of the midbrain and spinal cord. This growth was paralleled by improved performance on several behavioral measures.

Altered Food Preference after Cortical Infarction: Korean Style

Background: Altered food preference or preoccupation with certain food after stroke has been rarely described in the literature. Methods: We report four Korean patients who developed altered food preference secondary to unilateral cortical infarction. Results: Two patients showed preoccupation with meat such as Pulgogi or Kalbi (roast beef flavored with ingredients), which had not been their preference prior to the occurrence of stroke. All the patients became intolerant to the smell and taste of mackerel, and two disfavored hot Kimchi (cabbage salted with hot pepper). Quantitative taste assessment done in the patients revealed decreased taste perception in a variable pattern along with dysgeusia. Imaging studies showed that the region commonly involved was the frontal opercular area corresponding to the taste cortex. Conclusion: It is suggested that strokes involving the taste cortex may produce altered food preference associated with decreased taste sensation.

Masticatory force and function in patients with hemispheric brain infarction and hemiplegia.

Recent functional animal studies have reported that the motor control of masticatory muscle function is bilaterally guided by both hemispheres, which may fundamentally differ from the cortical control of limb muscle function. In this study, we investigated whether unilateral cortical brain infarction induces different impairments in masticatory and upper limb motor performance. Evidence of the importance of both hemispheres in controlling masticatory movements would be greater if the masticatory function were shown to be unimpaired in patients with severe hemiplegia. The masticatory function of 16 patients with severe hemiparesis caused by brain infarction in the region of the middle cerebral artery was studied by means of interview, clinical examination, and bite-force measurements. Finger-thumb grip-force measurements and clinical examination of the upper limbs were also performed for evaluation of the effect of infarction on upper limb motor function. Localization of the infarction was confirmed with computer tomography and magnetic resonance imaging. The Scandinavian Stroke Scale demonstrated that each patient had a major unilateral cortical infarction which had caused a marked handicap with a serious impairment of upper limb function on the contralateral side. The clinical examination revealed no major signs of temporomandibular disorders, and the masticatory muscles, when examined by palpation, contracted symmetrically. None of the patients with unilateral brain infarction showed any differences in bite forces between the healthy and paralyzed sides. These results indicate that, in hemiparetic patients, great differences may exist between the motor performances of the masticatory and upper limb muscles. The present investigation clinically illustrates the importance of both hemispheres in the control of masticatory function and movements.

Acidic FGF induces NGF and its mRNA in the injured neocortex of adult animals.

Recently we reported that human recombinant acidic fibroblast growth factor (aFGF) is capable of preventing degeneration of nucleus basalis magnocellularis neurons in vivo and inducing growth of astrocytes in vitro. In the present study, the effects of aFGF on the concentration of nerve growth factor (NGF) and its messenger RNA were investigated in the rat cerebral cortex following unilateral cortical infarction. Lesioned animals exhibited a significant increase of NGF in the remaining cortex ipsilateral to the lesion. After combining cortical lesion with intracerebroventricular application of aFGF (12 micrograms/day for 7 days), we observed an 8-fold increase in the NGF concentration and a marked increase in the level of steady state NGF mRNA relative to controls ipsilaterally, and a less pronounced aFGF effect in the contralateral cerebral cortex. These results support the hypothesis that the neurotrophic effects previously shown for aFGF and basic FGF (bFGF) in neurotrophin-sensitive neurons is mediated by inducing increased production of NGF within the injured central nervous system (CNS) of adult animals.

Multi-focal metabolic disturbances in human brain after cerebral infarction studied with 18FDG and positron emission tomography.

We measured cerebral metabolic rates for glucose (CMRGlc) in the remote brain areas of 7 patients, who were affected by unilateral cortical infarction, at a chronic stage using 2[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography. There were significant decreases of CMRGlc compared with each control value (p < 0.01), not only in the cerebral cortex directly damaged by the ischaemic insult, but also in the ipsilateral thalamus and in the contralateral cerebellum, areas in which no lesions had been detected by MRI or CT scan. The present study indicates that different mechanisms may be responsible for multi-focal metabolic disturbances in the remote areas after stroke. We suggest that these multi-focal brain dysfunctions may exacerbate clinical symptoms at a chronic stage of stroke.

T2- and diffusion-weighted magnetic resonance imaging of a focal ischemic lesion in rat brain.

We sought to evaluate the application of T2-weighted and diffusion-weighted magnetic resonance imaging techniques in the study of a focal ischemic lesion in the rat brain. Unilateral cortical infarcts were induced using the photosensitive dye rose bengal and 560 nm light irradiation. Magnetic resonance images were recorded from a total of 11 rats at selected intervals from 1.5 hours to several days after induction of the lesion. Parallel experiments were performed in which Evans blue dye was injected into the lesioned animals either immediately after lesion induction (n = 11) or 1 hour before the animals were killed (n = 11). The second procedure was designed to show regions of blood-brain barrier permeability to plasma proteins at the time of sacrifice, whereas the first procedure showed the accumulation and subsequent dispersion of plasma protein following disruption of the blood-brain barrier. Regions of the cortex highlighted by the T2-weighted images corresponded well to the pattern of dye staining seen from the first procedure while the diffusion-weighted images showed visual correspondence with the staining pattern obtained using the second procedure. These results illustrate the complementary use of T2-weighted and diffusion-weighted magnetic resonance imaging in discerning the pathophysiology of developing lesions.

Macrophage and Astrocyte Populations in Relation to [3H]PK 11195 Binding in Rat Cerebral Cortex following a Local Ischaemic Lesion

PK 11195 is a selective and specific ligand for the peripheral-type benzodiazepine binding site. Its potential for in vivo visualisation of lesioned human brain using positron emission tomography (PET) is currently being assessed. The present study examines the relationship between the temporal development of a local ischaemic lesion with its associated cell populations and the binding of [3H]PK 11195 in rat brain. Unilateral cortical infarcts were induced using the photosensitive dye Rose Bengal. At time intervals from 1 to 7 days after lesioning, the localisation of [3H]PK 11195 binding was determined using in vivo and in vitro autoradiography. Sections adjacent to those used for autoradiography were processed for immunohistochemistry using glial fibrillary acidic protein for astrocytes and ED-1 for macrophages. The results show that the binding of [3H]PK 11195 correlates in both time and spatial localisation with the appearance of macrophages around the lesion. Reactive astrocytes, although present, occupy a separate region in the tissue surrounding the lesion and lie outside the region defined by the [3H]PK 11195 binding. We conclude that the [3H]PK 11195 signal associated with this ischaemic lesion originates primarily from binding to macrophages and that [11C]PK 11195 could be used for imaging acute inflammatory response in human brain using PET.

Selective cortical infarction reduces [3H]sulpiride binding in rat caudate-putamen: autoradiographic evidence for presynaptic D2 receptors on corticostriate terminals.

Although the existence of presynaptic D2 dopamine receptors on corticostriate terminals has been supported by numerous receptor-binding studies, recent autoradiographic data has failed to demonstrate loss of striatal D2 receptors following cortical lesions. In the present study, Long-Evans rats were subjected to unilateral middle cerebral artery (MCA) infarction in order to produce reproducible lesions of the neocortex without damaging subcortical structures. Animals were sacrificed 2 and 4 wk following lesion and brains were prepared for receptor autoradiography. D2 receptors were studied using the selective ligand [3H]sulpiride, while D1 dopamine receptors were examined using [3H]SCH 23390. Sodium-dependent, high-affinity choline uptake sites were labeled with [3H]hemicholinium-3, thereby providing a quantitative measure of cholinergic neuronal integrity. Unilateral cortical infarction resulted in approximately a 20% reduction in [3H]sulpiride binding in several discrete regions of the ipsilateral caudate-putamen (CPu), but not in the nucleus accumbens. D2 receptor binding was also reduced significantly in some areas of the contralateral CPu when compared with [3H]sulpiride binding in sham-operated, control animals. In contrast, D1 receptors (as identified by [3H]SCH 23390 and high-affinity choline uptake sites (labeled with [3H]-HC-3) were not affected by the cortical lesion. The results provide autoradiographic confirmation of the existence of presynaptic D2 receptors on corticostriate terminals.

A quantitative analysis of responses of direction-sensitive neurons in somatosensory cortex of awake monkeys.

A quantitative analysis of responses of direction-sensitive neurons in somatosensory cortex of awake monkeys.

Reconstruction of population response to a vibratory stimulus in quickly adapting mechanoreceptive afferent fiber population innervating glabrous skin of the monkey.

Reconstruction of population response to a vibratory stimulus in quickly adapting mechanoreceptive afferent fiber population innervating glabrous skin of the monkey.