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 1,387 records · Page 77Linked to original sources
PubMed1990

Sensory ataxic hemiparesis in thalamic hemorrhage.

Ataxic hemiparesis with cerebellar-like features has been reported following infarction or hemorrhage of the thalamus. We describe five patients with incoordination and corticospinal tract signs in the limbs opposite a dorsolateral thalamic hemorrhage. In four patients the hemorrhage extended superiorly into the lateral ventricle, the adjacent paraventricular region, and the upper and medial parts of the posterior limb of the internal capsule. Instead of cerebellar dysfunction, these patients exhibited directional errors of movement that improved distinctly when performed under visual guidance. We explain the incoordination on the basis of conscious deep sensory loss in the involved limbs. Perception of light touch, painful pinprick, and temperature were preserved in all patients. We use the term "sensory ataxic hemiparesis" to distinguish these patients from those with "classic" ataxic hemiparesis and cerebellar-like features, a distinction that may be important when planning functional rehabilitation.

Adult↗
PubMed1990

Ataxic hemiparesis following thalamic infarction.

We describe a 73-year-old man with ataxic hemiparesis following infarction of the ventrolateral nucleus of the thalamus demonstrated by computed tomography and magnetic resonance imaging. Cerebellar ataxia was most likely due to interruption of the dentatorubrothalamocortical fibers at the level of the injured ventrolateral nucleus. Hemiparesis was probably caused by local edema compressing the corticospinal tract in the adjacent posterior limb of the internal capsule. We believe this to be the first reported case of classic ataxic hemiparesis following thalamic infarction.

Aged↗
PubMed1990

Wallerian degeneration of the pyramidal tract in capsular infarction studied by magnetic resonance imaging.

Using magnetic resonance imaging, we studied 24 patients with ischemic infarction of the internal capsule. Magnetic resonance imaging detected wallerian degeneration of the pyramidal tract below the capsular lesion in 11 patients (45.8%); all 11 had clinical evidence of pyramidal tract damage. In six additional patients magnetic resonance imaging findings, present only on axial slices, were considered to indicate possible wallerian degeneration. When motor deficit was associated with posterior limb lesions, magnetic resonance imaging detected wallerian degeneration of the pyramidal tract in 78.6% (11) of 14 patients.

Aged↗
PubMed1990

Clinical study of 227 patients with lacunar infarcts.

We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p less than 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p less than 0.005) or the internal capsule (p less than 0.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (21.1%), and severe disability was recorded in one case (0.4%). Lacunar infarcts are a clearly defined entity with characteristic clinical features and an excellent short-term prognosis. Magnetic resonance imaging is the current method of choice for demonstrating these small brain lesions.

Age Factors↗
PubMed1991

The anterior choroidal artery does not supply the corona radiata and lateral ventricular wall.

BACKGROUND AND PURPOSE: We sought first to characterize the clinical syndromes of patients found to have angiographic, computed tomographic, or magnetic resonance imaging scan indexes of anterior choroidal artery territory infarction and then to determine the frequency of involvement of the periventricular corona radiata in such patients. METHODS: Sixteen patients were selected based on angiographically, or surgically, documented occlusion of the anterior choroidal artery or based on infarcts whose minimal lesions included the anterior choroidal territory as defined by Kolisko and Beevor. We mapped the lesions using the templates of the Matsui and Hirano atlas and entered them into a computer using a program allowing overlapping diagrams of the cases. RESULTS: The anatomic distributions were fairly uniform, all involving the lower portion of the posterior limb of the internal capsule, the medial pallidum (75% of cases), cerebral peduncle in 44%, thalamus in 37%, and the medial temporal lobe in 38%. None extended outside these areas to include the upper corona radiata. The clinical picture corresponded to the well-established neurological syndrome featuring motor deficits with varying degrees of visual field and sensory impairments. Only two showed hypesthetic ataxic hemiparesis. CONCLUSIONS: Our findings indicate that the syndrome of anterior choroidal artery infarction is fairly uniform; ataxic hemiparesis occurs infrequently; and lesions in the lateral ventricular wall and the corona radiata are not part of the territory supplied by the anterior choroidal artery.

Adult↗
PubMed1991

Lacunar infarction as an embolic complication of cardiac and arch angiography.

BACKGROUND: Lacunar infarcts are small, deep cerebral infarcts resulting from occlusion of small, penetrating cerebral arteries. They are most commonly associated with hypertension. Cardiac sources of embolization are sometimes present in patients with lacunes, but direct proof of a causal relationship is lacking. This report attempts to support the contention that emboli can cause lacunar syndromes and lacunar infarction. CASE DESCRIPTIONS: We report two cases of pure motor hemiplegia, each of which developed while the patient was undergoing cardiac or aortic arch angiography. Neither patient had a history of previous transient ischemic attack or stroke. Initial computed tomography of the brain was normal in each. Repeat computed tomography in one confirmed a small, low-density lesion in the posterior limb of the internal capsule on the side appropriate to the patient's symptoms and remained normal in the second patient. CONCLUSIONS: These two cases offer evidence that the classic lacunar stroke syndrome of pure motor hemiplegia can occur on an embolic basis.

Aorta, Thoracic↗
PubMed1991

Clinical anatomic study of pure dysarthria.

Nine patients with pure dysarthria underwent computed tomography or magnetic resonance imaging. Eight patients had infarcts of lacunar or larger size in the internal capsule: four in the superior portion of the anterior limb or adjacent corona radiata and four in the superior portion of the genu or the adjacent corona radiata. In one patient, there was a small infarct in the bulbar motor cortex. Dysarthria was transient and characterized by poor articulation in all cases. Five patients also had contralateral facial weakness, and three patients with lesions in the genu had minimal and transient involvement of the contralateral fingers. These three cases appeared to be variants of the dysarthria-clumsy hand syndrome. We submit that this syndrome should sometimes be regarded as a stroke syndrome rather than always as a lacunar syndrome.

Aged↗
PubMed1992

Cheiro-oral syndrome due to lesions in the corona radiata.

BACKGROUND AND PURPOSE: We describe three patients with cheiro-oral syndrome caused by a small lesion in the corona radiata confirmed by high-resolution magnetic resonance imaging. CASE DESCRIPTIONS: Case 1: A 56-year-old hypertensive man who developed hypesthesia and paresthesia in the left perioral area and hand was found to have a small hematoma just lateral to the right internal capsule. Case 2: A 67-year-old man noticed hypesthesia around the left mouth angle and thumb and index finger. Magnetic resonance imaging revealed a lesion in the right corona radiata. Case 3: A 45-year-old hypertensive man developed numbness in his perioral region and left hand that later spread to his shoulder. Magnetic resonance imaging revealed a recent small infarct in the lower lateral aspect of the right corona radiata. CONCLUSIONS: A small lesion in the corona radiata can cause cheiro-oral syndrome, whose pathogenetic mechanism in such patients may be explained by the somatotopical location or by the differing vulnerability of the neuropils in the corona radiata.

Aged↗
PubMed1993

Apathy following cerebrovascular lesions.

BACKGROUND AND PURPOSE: Although apathy has been reported to constitute a frequent sequela of stroke lesions, there have been no prospective studies on the frequency and correlates of apathy after stroke lesions. In the present study, we examined the frequency and correlates of apathy in a consecutive series of 80 patients with cerebrovascular lesions. METHODS: We included patients within the first 10 days after a stroke lesion. Patients were examined with a comprehensive neuropsychiatric battery that included the Apathy Scale. RESULTS: Eighteen patients (22.5%) showed apathy, nine of whom were also depressed. On the other hand, 18 patients (22.5%) showed depression in the absence of apathy. Although depression and apathy may exist independent of one another, major depression (but not minor depression) was associated with an increased frequency of apathy. Apathy was also significantly associated with older age, cognitive impairments, and deficits in activities of daily living. Finally, apathy was significantly associated with lesions in the posterior limb of the internal capsule. CONCLUSIONS: These findings demonstrate that apathy is a frequent finding among patients with acute stroke lesions and may coexist with important emotional and cognitive poststroke disturbances.

Cerebral Hemorrhage↗
PubMed1994

Pure dysarthria, isolated facial paresis, or dysarthria-facial paresis syndrome.

BACKGROUND AND PURPOSE: Pure dysarthria, isolated supranuclear facial paresis, and their combination without somatic motor dysfunction are rarely encountered clinical syndromes and have not yet been clearly characterized. METHODS: Thirteen patients (9 men, 4 women; aged 33 to 72 [mean, 56] years) with unilateral strokes who developed dysarthria with or without facial paresis but without somatic motor dysfunction were reviewed in addition to case reports from previous literature. RESULTS: Computed tomographic scan and/or magnetic resonance imaging showed infarcts on the corona radiata in 4 patients, basal ganglia abutting the internal capsule in 3, basal ganglia-corona radiata in 1, pontine base in 3, and cortical-subcortical bulbar motor area in 2. The dysarthria and facial paresis were usually mild and transient, and either one was likely to be unnoticed. CONCLUSIONS: It is suggested that pure dysarthria or isolated facial paresis syndrome be considered as an extreme continuum of dysarthria-facial paresis syndrome, which is likely to be a variant of dysarthria-clumsy hand syndrome.

Adult↗
PubMed1994

Very early demonstration of secondary pyramidal tract degeneration by computed tomography.

BACKGROUND: While magnetic resonance imaging has revealed progressive changes in the pyramidal tract in accordance with histopathologic stages of wallerian degeneration secondary to a supratentorial lesion, computed tomography (CT) has only demonstrated a shrinkage of the pyramidal tract in the midbrain or pons during the chronic stage. We present a patient with frontoparietal subcortical hemorrhage in whom serial CT scans clearly demonstrated wallerian degeneration along the axis of the pyramidal tract early in the acute stage. CASE DESCRIPTION: A 63-year-old man with a history of hypertension suddenly developed a deterioration of consciousness, transcortical mixed aphasia, and dense hemiplegia on the right side. CT scans revealed a massive intracerebral hematoma in the frontoparietal subcortices of the left hemisphere. Although initial CT did not detect any hypodense areas along the left pyramidal tract below the hematoma, ill-defined areas of decreased density appeared in the posterior limb of the internal capsule, cerebral peduncle of the midbrain, and pontine base of the left side on day 13 after the stroke. These areas became well demarcated on day 22 and persisted thereafter. CONCLUSIONS: An extensive hematoma can interrupt the pyramidal tract fibers that arise not only from the motor cortex and caudal premotor cortex but also from the somatosensory and parietal cortices, allowing very early CT demonstration of wallerian degeneration of the pyramidal tract.

Cerebral Hemorrhage↗
PubMed1994

Cerebral blood flow in subcortical global aphasia. Perisylvian cortical hypoperfusion as a crucial role.

BACKGROUND AND PURPOSE: Global aphasia after subcortical stroke is very rare, and its pathophysiology remains unsolved. To clarify the mechanism underlying subcortical global aphasia, we investigated lesion sites and cerebral blood flow in patients with subcortical global aphasia and nonaphasic patients with subcortical stroke. METHODS: We examined four patients with global aphasia and four nonaphasic patients. Language testing was performed more than 4 weeks after the onset. Measurement of cerebral blood flow was done between 35 and 75 days after stroke by using single-photon emission computed tomography (SPECT) with N-isopropyl-p[123I]iodoamphetamine as a tracer and three-dimensional surface display generated from SPECT. RESULTS: All aphasic patients had subcortical lesions in the putamen, posterior internal capsule, temporal isthmus, and periventricular white matter in the left hemisphere. No cortical lesions were found on either magnetic resonance imaging or computed tomographic scanning. The nonaphasic patients had smaller periventricular white matter lesions and no temporal isthmus lesions. All aphasic patients showed cortical hypoperfusion mainly in the perisylvian areas, including Broca's and Wernicke's areas. In contrast, cortical cerebral blood flow of the nonaphasic patients was decreased in smaller areas and spared the perisylvian language areas. CONCLUSIONS: These results suggest that cortical hypoperfusion in the perisylvian language areas, presumably due to undercutting of the white matter, is crucial for the development of subcortical global aphasia.

Aged↗
PubMed1995

Impact of thalamic hematoma on six-month mortality and motor and cognitive functional outcome.

BACKGROUND AND PURPOSE: In this study we examined the functional outcome of thalamic hemorrhage after 6 months as it related to neurological and computed tomographic (CT) findings in 104 patients. METHODS: Level of consciousness was determined on admission. Extension and volume of hematoma were examined with CT within 3 days. After 6 months, motor function was evaluated using hemiplegic staging by the scale of Brunnström, and cognition was assessed by the Hasegawa dementia rating scale administered in Japanese. RESULTS: Twelve patients (12%) died from stroke after 6 +/- 6 days (mean +/- SD), which correlated with volume of hematomas (P < .001), levels of consciousness (P < .005), and miosis (P < .01). Six patients (6%) died from systemic complications after 23 +/- 18 days, which correlated with age (P < .05). Initially, 88 patients (85%) had hemiparesis; which persisted in 78 (75%) patients (18 deaths and 60 survivors). After 6 months, the Brunnström scale scores were lower in patients with hematomas extending to the internal capsule (P < .01) than in those with hematomas localized within the thalamus, and scores were lowest in patients with hematomas extending to the midbrain or putamen (P < .01). Motor function was well correlated with the extension and volume of hematomas (P < .001) and with the consciousness level (P < .001). Activities of daily living were correlated with hematoma extension and advanced age. Cognitive impairment was correlated with disturbance of consciousness (P < .01) and ventricular extension of the hematoma (P < .05) in 80 nonaphasic patients. CONCLUSIONS: The extension and volume of hematomas, indicating direct cerebral damage, are useful indicators of mortality from thalamic hemorrhage, motor functional outcome, and level of activities of daily living after 6 months. The disturbance of consciousness and ventricular extension of the hematoma, suggesting diffuse brain damage, could be predictors of cognitive function.

Activities of Daily Living↗
PubMed1995

Thalamic hemorrhage. A prospective study of 100 patients.

BACKGROUND AND PURPOSE: The clinical features of thalamic hemorrhage in terms of localization are of great interest in many studies. To better understand the relationship between the localization of thalamic hemorrhage and clinical features. we evaluated the characteristics of patients with four different topographic types of thalamic hemorrhage. METHODS: We prospectively studied 100 patients with thalamic hemorrhage who were admitted consecutively to our primary care unit. We divided them into two groups according to large (> 2 cm in diameter and/or > 4 mL in volume) and small thalamic hemorrhage. Four topographic subgroups (large and small) were compared to identify clinical syndromes associated with distinct lesion locations. RESULTS: All patients with posterolateral thalamic hemorrhage had severe sensorimotor deficit. Neuropsychological disturbances in patients with posterolateral thalamic hemorrhage were prominent, with primarily transcortical aphasia in those with left-sided lesions and hemineglect and anosognosia in those with right-sided lesions. Several variants of vertical gaze dysfunction, skew ocular deviation, gaze preference toward the site of the lesion, and miotic pupils were frequent in posterolateral thalamic hemorrhage, particularly in the large type. Patients with small and large anterolateral thalamic hemorrhage were characterized by severe motor and sensory deficits; language and oculomotor disturbances were also observed, although less frequently than in posterolateral hemorrhage. Sensorimotor deficits were observed in patients with medial thalamic hemorrhage (moderate in small hemorrhages and severe in large hemorrhages because of involvement of the adjacent internal capsule). Language disturbances in patients with left-sided lesions and neglect in patients with right-sided lesions were seen only in large medial thalamic hemorrhage. Dorsal thalamic hemorrhage was rare and characterized by mild and transient sensorimotor disturbances. Among patients with dorsal thalamic hemorrhages, only those with large lesions had oculomotor and neuropsychological disturbances. CONCLUSIONS: We concluded that despite clinical similarity among the four types of thalamic hemorrhage, there was some discrepancy in the clinical features of small and large thalamic hemorrhages. The most important predictors of death were initial consciousness, nuchal rigidity, maximum size, volume and ventricular extension of hemorrhage, and occurrence of hydrocephalus.

Adolescent↗
PubMed1995

Protective effect of cyclosporin A on white matter changes in the rat brain after chronic cerebral hypoperfusion.

BACKGROUND AND PURPOSE: Activation of glial cells and rarefaction of the white matter have been reported in rat brain after bilateral permanent occlusion of the common carotid arteries. Using this model, we investigated the effects of the immunosuppressant cyclosporin A on the activation of glial cells and the white matter rarefaction. METHODS: Both common carotid arteries were ligated bilaterally in 40 male Wistar rats. Twenty-two of these rats received an intraperitoneal injection of cyclosporin A, and the remaining 18 received a vehicle-solution injection. Microglia/macrophages were investigated with immunohistochemistry for the major histocompatibility complex class I and II antigens as well as for leukocyte common antigen. Astroglia were examined with glial fibrillary acidic protein as a marker. Activation of glial cells and white matter rarefaction were then investigated from 7 to 30 days after the ligation. RESULTS: In vehicle-treated animals, there was a persistent and extensive activation of both microglia/macrophages and astroglia in the white matter, including the optic nerve, optic tract, corpus callosum, internal capsule, and traversing fiber bundles of the caudoputamen. In cyclosporin A-treated rats, the number of activated microglia/macrophages was significantly reduced (P < .01) to approximately one fifth of that in vehicle-treated animals. Similarly, rarefaction of the white matter was much less intense in cyclosporin A-treated rats (P < .01). CONCLUSIONS: Cyclosporin A suppressed both glial activation and white matter changes after chronic cerebral hypoperfusion. These results suggest that immunologic reaction may play a role in the pathogenesis of the white matter changes and that the present model may be useful in investigating the pathophysiology of white matter changes induced by chronic cerebral hypoperfusion.

Animals↗
PubMed1996

Stroke in Williams syndrome.

BACKGROUND: Williams syndrome is a genetic disorder characterized by a high incidence of heart disease, arterial stenosis, and hypertension. Despite these features, cerebrovascular accidents have been described only recently and only in association with stenoses of the cerebral vasculature. CASE DESCRIPTION: A 19-year-old girl with Williams syndrome developed an acute-onset hemiparesis. MRI demonstrated an infarct involving the internal capsule and putamen. No stenotic areas were seen on angiography. CONCLUSIONS: Stroke should be considered as a possible consequence of Williams syndrome, even in the absence of stenoses of the cerebral vasculature. Comparison of this case with those previously reported in the literature emphasizes the multiplicity of features in Williams syndrome that can contribute to the risk of stroke.

Adult↗
PubMed1997

Early reperfusion in the anesthetized baboon reduces brain damage following middle cerebral artery occlusion: a quantitative analysis of infarction volume.

BACKGROUND AND PURPOSE: Because in humans the clinical benefits of reperfusion remain controversial, it is important to determine whether reperfusion per se reduces infarct volume. In the nonhuman primate, mostly semiquantitative assessments of infarction have been performed. When ischemic volumes have been calculated, it has been for the acute or subacute stages of experimental stroke and may thus not adequately reflect the total volume of consolidated infarction. METHODS: Anesthetized baboons were subjected to 6 hours of either reversible or permanent middle cerebral artery occlusion (MCAO). Approximately 4 weeks later, the brains were processed for neuropathological examination to allow assessment of the final infarct volume determined by the difference of healthy tissue between occluded and nonoccluded hemispheres. RESULTS: Reversible MCAO resulted in a small essentially subcortical infarction (mean+/-SD, 0.58+/-0.31 cm3) in 6 of 10 baboons: the infarct (pannecrosis) was restricted to the head of the caudate nucleus, internal capsule, and putamen; 4 of 10 baboons showed no evidence of macroscopic infarction. Permanent MCAO produced a larger subcortical infarct in all 7 baboons studied (2.37+/-1.32 cm3; P=.0006 by Wilcoxon-Mann-Whitney test); the lesion was more extensive and encompassed the external capsule and, in 2 baboons, the adjacent insular cortex. CONCLUSIONS: We conclude that under optimal experimental conditions, an ischemic episode of 6 hours in duration is well tolerated in the anesthetized adolescent baboon, with 4 animals showing no signs of macroscopic brain damage. Thus, early reestablishment of cerebral blood flow after a focal ischemic insult is not detrimental but indeed is beneficial in terms of the final infarct volume (both at the subcortical and cortical levels) produced by occlusion of a major cerebral artery. The data further suggest a feasible time window in which to initiate and continue therapeutic interventions.

Anesthesia↗
PubMed1997

Severe pathological crying after left anterior choroidal artery infarct. Reversibility with paroxetine treatment.

BACKGROUND: There is increasing evidence that serotonergic neurotransmission may be damaged in poststroke pathological crying. A correlation between the clinical severity of pathological crying and the size of stroke-induced serotonergic pathway lesions is commonly accepted. We present a case of severe pathological crying after a limited left anterior choroidal artery territory infarction. CASE DESCRIPTION: A right-handed 55-year-old man who was a heavy smoker was admitted to the hospital after a right hemiplegia of sudden onset. Clinical examination revealed a right global hemiplegia including the face and a right hemihypoesthesia. Cerebral CT scan and MRI showed an infarct in the retrolenticular part of the posterior limb of the left internal capsule extending upward into the posterior paraventricular corona radiata region. Transesophageal echocardiography revealed an atrial septal aneurysm of 15-mm excursion without associated patent foramen ovale. From the first day of admission, the patient exhibited very frequent and intense fits of pathological crying. Their persistence led to initiation of treatment with the selective serotonin reuptake inhibitor paroxetine on day 30. Complete and immediate resolution of pathological crying occurred 24 hours after onset of therapy. Follow-up examination at day 90 confirmed the absence of relapse of pathological crying. CONCLUSIONS: We conclude that poststroke pathological crying in our patient may have been due to unilateral disruption of the capsular ascending projections of the serotonergic brain stem raphe nuclei. A small left-sided capsular lesion may have led to severe pathological crying. This disabling condition may be reversible with selective serotonin reuptake inhibitor therapy.

Cerebral Arteries↗