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PubMed1998

Intracerebral hemorrhage in the rat: effects of hematoma aspiration.

BACKGROUND AND PURPOSE: Deep intracerebral hemorrhage is associated with considerable mortality and morbidity, but the value of surgical therapy is debatable. The purpose of this study was to evaluate whether aspiration of the hematoma in a rodent model of intracerebral hemorrhage could improve final neurological outcome. METHODS: Intracerebral hemorrhage was induced in 2 groups of rats by injection of bacterial collagenase into the caudate nucleus. In 1 group of rats, streptokinase was used to lyse the hematoma 4 hours after hemorrhage induction, and the clot was then aspirated. Behavioral function was evaluated repeatedly until the rats were killed 7 weeks after collagenase injection. Histology was used to assess neuronal loss, astroglial proliferation, and overall brain morphology. In a second experiment, brain water was measured at 24 hours. RESULTS: The treated rats performed significantly better than controls on a motor-behavior evaluation on days 1, 2, and 28 after aspiration. Skilled forelimb testing performed for 3 weeks after the global behavior evaluations showed a significant deficit of contralateral forelimb function in both groups, but there was no significant difference between the 2 groups. Neuronal loss in the perihematoma striatum was significantly greater in untreated compared with treated rats. In most rats, structural damage extended into the internal capsule and thalamus. CONCLUSIONS: Aspiration of the hematoma after collagenase-induced hemorrhage slightly improved acute functional outcome and reduced neuronal loss from the striatum. Further studies are required to delineate the mechanism of the effect.

Animals↗
PubMed1999

Acute caudate vascular lesions.

BACKGROUND AND PURPOSE: We sought to evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate lesion, either with infarct or with hemorrhage involving the caudate nucleus. METHODS: We studied all patients with acute caudate stroke confirmed by CT or MRI who were admitted to our stroke unit over a 5-year period. A database containing risk factors, clinical features, type and mechanism of stroke, and caudate vascular territories was analyzed. RESULTS: Thirty-one patients had acute caudate stroke (24 men and 7 women; mean age, 62.3 years). Caudate infarct was present in 25 patients and caudate hemorrhage in 6. The main risk factors for caudate infarct were hypertension (64%), hypercholesterolemia (32%), diabetes mellitus (28%), and previous myocardial infarct (20%). Hypertension was present in 4 patients (67%) with caudate hemorrhage, and arteriovenous malformation was present in 1 patient (17%). Small-artery disease was diagnosed in 14 patients (59%), cardiac embolism in 5 patients (20%), and large-artery disease in 2 patients (8%), and 2 patients (8%) had mixed etiology. The most frequent neurological abnormalities were abulia and psychic akinesia (48%), frontal system abnormalities (26%), speech deficits in patients with left-sided lesions (23%), and neglect syndromes in those with right-sided lesions (10%). Fifteen patients with caudate infarct (60%) and 3 patients with hemorrhage (50%) were able to return to normal daily life. Patients with infarct in the territory of the lateral lenticulostriate arteries extending to neighboring structures showed more frequent motor and neuropsychological deficits than those with infarct in the territory of the anterior lenticulostriate arteries. CONCLUSIONS: The clinical presentation of patients with caudate hemorrhage mimicked subarachnoid hemorrhage with or without motor and neuropsychological signs. Caudate vascular lesions with concomitant neighboring structure involvement represent a specific stroke syndrome, usually caused by small-artery disease and in one fifth of the patients caused by cardiac embolism. The behavioral abnormalities were mostly due to medial, lateral, and ventral caudate subnuclei damage and coexisting lesion of the anterior limb of the internal capsule.

Acute Disease↗
PubMed1999

Diffusion-weighted MRI in acute lacunar syndromes. A clinical-radiological correlation study.

BACKGROUND AND PURPOSE: Clinical-radiological correlation studies in lacunar syndromes have been handicapped by the low sensitivity of CT and standard MRI for acute small-vessel infarction and their difficulty in differentiating between acute and chronic lesions. METHODS: We prospectively studied 43 patients presenting with a classic lacunar syndrome using diffusion-weighted MRI, a technique with a high sensitivity and specificity for acute small-vessel infarction. RESULTS: All patients were scanned within 6 days of stroke onset. An acute infarction was identified in all patients. Pure motor stroke was associated with lesions in the posterior limb of the internal capsule (PLIC), pons, corona radiata, and medial medulla; ataxic hemipareses with lesions in the PLIC, corona radiata, pons, and insular cortex; sensorimotor stroke with lesions in the PLIC and lateral medulla; dysarthria-clumsy hand syndrome with lesions in the PLIC and caudate nucleus; and pure sensory stroke with a lesion in the thalamus. Supratentorial lesions extended into neighboring anatomic structures in 48% of the patients. CONCLUSIONS: Lacunar syndromes can be caused by lesions in a variety of locations, and specific locations can cause a variety of lacunar syndromes. Extension of lesions into neighboring structures in patients with lacunar syndromes appears to be more frequent than previously described in studies using CT and standard MRI.

Acute Disease↗
PubMed1999

Experimental model of small deep infarcts involving the hypothalamus in rats: changes in body temperature and postural reflex.

BACKGROUND AND PURPOSE: Intraluminal middle cerebral artery (MCA) occlusion in rats has been reported to cause hyperthermia assumed to be caused by hypothalamic damage. To clarify the effects of hypothalamic ischemia on body temperature and to obtain a model simulating lacunar infarction, we attempted to produce small infarcts in deep structures (including the hypothalamus). METHODS: A surgical suture was advanced to occlude the origin of the hypothalamic (HTA) and/or anterior choroidal arteries (AChA) without compromise of the anterior or middle cerebral artery origins. After treatment, rectal temperature and postural reflex were examined repeatedly for 3 days under nonanesthetic conditions. The AChA and HTA and their link with small deep infarction were then confirmed by TTC, hematoxylin and eosin, and TUNEL stains and by microsurgical dissection after colored silicone perfusion into the cerebral arteries. RESULTS: Advancement of the suture near to but not occluding the MCA origin (0.5 to 1.9 mm proximal) produced small, deep, nonneocortical strokes in 25 of 36 animals without producing MCA ischemic changes. These infarctions mainly affected the hypothalamus in 13 animals (HTA area: infarct volume 6+/-1 mm(3)) and involved both the internal capsule and hypothalamus in 12 animals (HTA+AChA area infarct volume 48+/-10 mm(3)). Rats with HTA infarction alone exhibited persistent hyperthermia for 72 hours; some also had transient mild postural abnormality. The AChA+HTA infarct group showed a transient elevation of body temperature for 24 hours and definitive postural abnormality. In the remaining 11 animals, the suture was inadvertently advanced across the MCA origin, producing a large infarct that affected both the neocortex (MCA territory) and nonneocortical structures (volume 381+/-30 mm(3), n=11). The MCA infarct group displayed a transient hyperthermia and severe postural abnormality. CONCLUSIONS: When properly positioned, the intraluminal suture method permits selective AChA and/or HTA obstruction without inducing MCA territory ischemia. This model confirms that selective hypothalamic infarction produces significant and sustained temperature regulation abnormalities. The model also may be useful in investigating the pathophysiology of small, deep, end-vessel infarction.

Animals↗
PubMed2001

Effect of lesion location on upper limb motor recovery after stroke.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the effects of stroke involvement of primary and secondary hemispheric motor systems and corticofugal tracts on arm and hand recovery. METHODS: Forty-one patients participating in an inpatient stroke rehabilitation database, admitted 17+/-2 (SEM) days after initial unilateral hemispheric ischemic stroke, with neuroimaging studies performed >48 hours after stroke and with minimal upper limb (UL) movement (admission Fugl-Meyer UL motor scores </=9; normal score, 58) were studied. Patients were divided into 3 groups according to their UL discharge Fugl-Meyer score: 0 to 9, no/poor recovery; 10 to 18, well-defined flexion-extension synergies; and >18, synergies+isolated movements. Lesions affecting the following structures were recorded: primary motor cortex, premotor area, supplementary motor area, anterior half of the middle third of corona radiata (secondary motor efferents), posterior half of the middle third of corona radiata (primary motor efferents), genu, anterior and posterior limbs of the internal capsule (PLIC), basal ganglia, and thalamus. chi(2) Analysis and ANOVA were used to study the significance of stroke location on UL motor recovery. RESULTS: The effect of involvement of primary, premotor, or supplementary motor areas on motor recovery did not reach statistical significance. Patients with purely cortical stroke were likely to recover UL isolated movement (3 of 4) compared with purely subcortical (1 of 17) or mixed cortical-subcortical stroke location (2 of 20) (P:=0.009). Of those with cortical, subcortical, or mixed cortical plus subcortical lesions sparing the PLIC, 5 of 13 recovered isolated UL movement (P:=0.01). Only 1 of 28 patients with involvement of the PLIC plus adjacent corona radiata, basal ganglia, or thalamus recovered isolated UL movement (P:=0.01). Patients with small lacunar strokes affecting only the PLIC did not have sufficient motor deficits 2 weeks after stroke to meet inclusion criteria. CONCLUSIONS: The probability of recovery of isolated UL movement decreases progressively with lesion location as follows: cortex, corona radiata, and PLIC. This is consistent with our current understanding of redundant cortical motor representation and convergence of corticofugal motor efferents as they pass through the corona radiata to the PLIC.

Activities of Daily Living↗
PubMed2001

Hypertensive caudate hemorrhage prognostic predictor, outcome, and role of external ventricular drainage.

BACKGROUND AND PURPOSE: The purpose of the present study was to analyze the outcome and outcome predictors of caudate hemorrhage and role of external ventricular drainage in acute hydrocephalus. METHODS: Clinical data from 36 consecutive patients with hypertensive caudate hemorrhage was used in the present study. Age, gender, volume of parenchymal hematoma, hematoma in the internal capsule, initial Glasgow Coma Scale (GCS), hydrocephalus, severity of intraventricular hemorrhage, and hemorrhagic dilatation of the fourth ventricle were analyzed for effect on outcome. Effect of external ventricle drainage for hydrocephalus was evaluated by comparing preoperative and postoperative GCS scores. RESULTS: By univariate analyses, poor outcome was associated with a poor initial GCS score (P=0.016), hydrocephalus (P<0.001), intraventricular hemorrhage severity (P<0.01), and hemorrhagic dilatation of the fourth ventricle (P=0.02). By multivariate analysis, stepwise logistic regression revealed that hydrocephalus was the only independent prognostic factor for poor outcome (P<0.001). Postoperative 48-hour GCS score was better than the preoperative score by use of paired-sample t test (P<0.001). CONCLUSIONS: Hydrocephalus is the most important predictor of poor outcome. External ventricular drainage response for hydrocephalus was good in the present study, whereas an early decision should be made regarding preoperative neurological condition.

Basal Ganglia Hemorrhage↗
PubMedDate not supplied

Immediate effects of cerebral ischemia: evolution and resolution of neurological deficits after experimental occlusion of one middle cerebral artery in conscious cats.

Acute occlusion of the left middle cerebral artery (MCA) was accomplished without anesthesia and inside an intact cranium containing cerebrospinal fluid (CSF) in ten cats five to nine days after implantation of an occlusive device through the orbit. Immediate neurological deficits included forced ambuxlation, circling, and tonic deviation of the head and neck toward the side of the occluded artery; weakness of the opposite limbs; and an apathetic or akinetic state. Two cats died within 24 hours. The other eight cats improved but secondary deficits developed in two, causing death. In two of the remaining six cats no deficits were apparent seven days later. The cerbral infarcts regularly involved the basal ganglia, internal capsule, and cortical regions, and were larger and less variable than those produced by MCA occlusion through and open optic foramen or craniectomy with cranial decompression by drainage of CSF. This model of acute focal cerebral ischemia may be of value for studies of physiological and biochemical factors uninfluenced by sedatives, anesthesia, or recent surgical procedures.

Animals↗
PubMedDate not supplied

Surgical treatment of primary intracerebral hemorrhage- Part 1: new angiographical classification.

A new angiographical classification of primary intracerebral hemorrhage is presented. We have clarified the predilection sites of intracerebral hemorrhage and the advancing direction of the hematoma by studying autopsy cases. Furthermore, we tried to detect the presence or absence of destruction of the internal capsule and ventricular rupture by means of angiography. Our classification, introducing the idea of dynamic changes of hematoma advancement from localized to advanced type, can be applied to clinical practice. This classification, along with the patient's level of consciousness, it felt to be the most important indication for operation.

Cerebral Angiography↗
PubMed2005

White matter abnormalities in first-episode schizophrenia or schizoaffective disorder: a diffusion tensor imaging study.

OBJECTIVE: The goal of this study was to investigate brain white matter abnormalities by using diffusion tensor imaging in patients with schizophrenia or schizoaffective disorder close to illness onset. METHOD: Ten patients experiencing a first episode of schizophrenia or schizoaffective disorder and 13 healthy volunteers received diffusion tensor imaging and structural magnetic resonance imaging examinations. Voxel-wise analysis was used to compare fractional anisotropy maps in the white matter of the two groups following intersubject registration to Talairach space. RESULTS: Compared with healthy volunteers, patients demonstrated lower fractional anisotropy in the left internal capsule and left-hemisphere white matter of the middle frontal gyrus and posterior superior temporal gyrus. There were no areas of significantly higher fractional anisotropy in patients compared with healthy volunteers. CONCLUSIONS: These findings suggest that white matter pathology is present early in the course of schizophrenia and may be less pronounced than has been found in previous diffusion tensor imaging studies of patients with chronic illness. Further, these data are consistent with hypotheses regarding frontotemporal dysfunction and the failure of left-hemisphere lateralization in the pathophysiology of schizophrenia.

Adult↗
PubMed1995

Vertebral artery injury presenting with signs of middle cerebral artery occlusion. A case report.

Therapeutic manipulation of the neck has been shown to produced injury to the vertebral artery. The clinical syndromes produced by this arterial insufficiency generally reflect dysfunction of the brainstem or cerebellum. The authors present a case of such injury that presented with clinical findings, namely, hemiparesis and aphasia, suggestive of involvement of the dominant middle cerebral artery. These findings may have been the result of disruption of flow through the posterior cerebral artery to the thalamus, internal capsule, and cerebral peduncles.

Adult↗
PubMed1996

Serial changes in blood pressure and neurohormone levels after the onset of lacunar stroke.

To assess serial changes in blood pressure and its circadian variation following a lacunar stroke, the authors studied 7 patients who developed a single lacunar infarction in either the internal capsule or the corona radiata. Blood pressure and pulse rate were monitored noninvasively for twenty-four hours by an ambulatory blood pressure monitoring device in the acute, subacute, and chronic phases of the strokes. In the acute and chronic phases, the authors also measured urinary excretion of catecholamines every 6 hr, and serum cortisol concentration at 9:00, 17:00, and 21:00 hr. The patients were free from antihypertensive agents during the study. The twenty-four-hour averages of both systolic and diastolic blood pressure in the chronic phase were lower than those in the acute phase (P < 0.05). A nighttime fall in blood pressure was observed in the subacute and chronic phases (P < 0.05), but not in the acute phase. Urinary excretion of epinephrine at night in the acute phase was significantly higher than that in the chronic phase (P < 0.05). Serum levels of cortisol at 17:00 and 21:00 hr in the acute phase also exceeded those in the chronic phase (P < 0.05 and P < 0.01, respectively). The authors conclude that an increased secretion of epinephrine and cortisol might, at least in part, contribute to a high blood pressure and a lack of circadian variation in blood pressure in the acute phase of lacunar stroke.

Acute Disease↗
PubMed2002

Immunohistochemical localization of the nucleosome-binding protein HMGN3 in mouse brain.

HMGN3 (Trip7) is a member of the high-mobility group N (HMGN) nucleosome-binding protein family, which binds specifically to nucleosomes, reduces the compactness of the chromatin fiber, and enhances transcription from chromatin templates. By Western blotting and Northern blotting analysis, we showed that HMGN3 is expressed in a tissue-specific manner, with the strongest expression in mouse brain. Here we analyzed the expression of HMGN3 in various regions of the mouse brain by histological techniques. Enhanced expression of HMGN3 was observed in the lateral olfactory tract, anterior commissure, corpus callosum, internal capsule, fornix, stria medullans, optic tract, and axon bundles. The expression patterns of HMGN3 in the mouse brain was significantly different from that of the related protein HMGN2 and was very similar to that of the glial fibrillary acidic protein (GFAP). We suggest that HMGN3 might play a role in astrocyte function.

Animals↗
PubMed2002

Diffuse magnetic resonance imaging white-matter changes in a 15-year-old boy with mitochondrial encephalomyopathy.

We report a 15-year-old boy who presented with recurrent headaches associated with numbness, confusion, and speech difficulty. Brain magnetic resonance imaging (MRI) revealed diffuse bilateral white-matter hyperintensity on fluid-attenuated inversion-recovery and T2-weighted images in the internal capsule, periventricular and subcortical white matter, base of the pons, and middle cerebellar peduncles. Lesions were isointense on T1-weighted images and nonenhancing. Muscle biopsy showed changes consistent with a mitochondrial myopathy. Mitochondrial respiratory chain enzyme activity analysis revealed a significant reduction in complex II activity. Genetic testing was negative. We conclude that mitochondrial encephalomyopathy may present with unusual diffuse supratentorial and infratentorial white-matter changes on MRI.

Adolescent↗
PubMed2005

Magnetic resonance imaging findings and novel mutations in GM1 gangliosidosis.

Two unrelated children and their siblings of Arab origin were diagnosed as having GM1 gangliosidosis on the basis of clinical features and markedly low levels of beta-galactosidase. The T2-weighted magnetic resonance images of the brain revealed certain characteristic features, including delayed myelination and abnormal appearance of the subcortical white matter, internal capsule, and basal ganglia. Their mutation analysis showed two novel mutations, which have not been described in an Arabic population.

Arabs↗
PubMed2005

Aphasia owing to subcortical brain infarcts in childhood.

The aim of this study was to further define the clinical features of subcortical aphasia in children with deep brain infarcts and to define the sequelae associated with childhood strokes. We retrospectively studied nine children with left subcortical brain infarcts who presented with acquired language disorder and underwent language investigations based on standardized tests. Stroke in these patients involved the left internal capsule, lenticular or thalamic nuclei, or a combination of these. Early aphasic manifestations following the deep cerebral infarcts affected language expression. These included mutism, nonfluent speech, word finding difficulties, and phonemic and semantic paraphasia. Speech comprehension was generally more preserved. All patients subsequently improved, although variably; sequelae such as dysfluency, word finding difficulties, and written language learning impairment could be detected through standardized tests in six of them (all younger than 6 years at the time of the infarct). Two of the three remaining patients (both older than 6 years at the time of the infarct) had a full recovery. Our study confirms the concept of childhood subcortical aphasia, depicts the linguistic profile in these patients, and sustains the indication of systematic formal language assessment during the follow-up of all children with subcortical infarct involving the dominant hemisphere.

Adolescent↗
PubMed2006

Acute childhood hemiplegia associated with chickenpox and elevated anticardiolipin antibody.

Chickenpox is a common infection of childhood. Central nervous system complications, such as cerebellar ataxia and meningoencephalitis, are estimated to occur in less than 1% of cases of chickenpox. Although transverse myelitis and hemiplegia have also, although rarely, been reported, hemiplegia associated with chickenpox and elevated anticardiolipin antibody has not been reported in the literature. We report the case of a 2.5-year-old boy who developed a right hemiplegia 3 weeks after the onset of a primary varicella infection. The serum level of anticardiolipin antibody IgG was markedly elevated. Brain magnetic resonance imaging (MRI) revealed an infarction involving the left globus pallidus, caudate nucleus, and posterior leg of the internal capsule. Laboratory studies ruled out all known causes of stroke. Neurologic signs and symptoms slowly improved with supportive treatment. Varicella infection should be considered one of the possible causes of acute ischemic strokes in children. Usually, two or more risk factors are detected in children with ischemic strokes, and we suggest that all possible causes of strokes be investigated in children with ischemic strokes.

Antibodies↗
PubMed1992

Congenital muscular dystrophy with abnormal radiographic myelin pattern.

We report 11 children with a homogeneous clinical syndrome affecting both sexes, characterized by weakness at birth, slowly improving course, weakness of all muscle groups, arreflexia, elevated blood creatine kinase, normal nerve conduction velocity, dystrophic changes on muscle biopsy, and diffuse periventricular cortical white-matter abnormalities with sparing of corpus callosum, internal capsule, and brain stem. We compare them to 48 other previously reported similar cases and designate them as altered myelin radiographic pattern congenital muscular dystrophy (CMD), which is the same as occidental CMD. We compare them to the other presently accepted phenotypes: progressive Fukuyama CMD, Walker-Warburg or cerebral-ocular CMD, and Santavuori or muscle-eye-brain CMD. We suggest that the different phenotypes are alleles of the same gene, which regulates or expresses a structural protein required for muscle integrity, myelination, and formation of the cortex. Such phenotypic diversity has been established for mutations of Xp21 in X-linked muscular dystrophies.

Biopsy↗
PubMed1998

Transient cerebral arteriopathy: a disorder recognized by serial angiograms in children with stroke.

Repeated clinical evaluation and cerebral arteriography during the evolution of ischemic strokes of idiopathic origin allowed us to characterize a transient cerebral arteriopathy. We retrospectively studied the clinical characteristics, course, and neuroimaging features of this disorder in nine children. Of 34 children with ischemic strokes seen consecutively between 1984 and 1995, 9 (26%) were diagnosed as having transient attack of the cerebral arterial wall, termed transient cerebral arteriopathy. All of these patients had previously been in good health. The mean age at the time of the first stroke was 6 years (range, 2 9/12 years to 13 4/12 years). All children presented with acute hemiplegia. A recurrence of the stroke took place 3 months at the latest after the initial infarct in three children (mean clinical follow-up 2 7/12 years). Cerebral imaging in all the patients showed small subcortical infarcts located in basal ganglia or internal capsule. Arteriography revealed multifocal lesions of the arterial wall (focal stenosis or segmental narrowing), mostly located in the initial parts of basal arteries of the carotid system. Longitudinal arteriographic follow-up showed initial worsening of these arterial lesions (n = 5) for a maximum duration of 7 months followed by complete regression (n = 2), improvement (n = 5), or stabilization of the lesions (n = 2). Five patients had a complete clinical recovery. Further studies are necessary to confirm a presumed inflammatory cause of this arteriopathy.

Acute Disease↗