Capsular Infarct Research Articles

Acute isolated capsular strokeA clinical study of 148 cases

The objectives of the study were to assess differential features between capsular stroke of ischemic and hemorrhagic origin, and to compare capsular strokes with all other (non-capsular) strokes. Data of 148 patients with isolated capsular stroke were collected from a prospective hospital-based stroke registry in which 2000 consecutive acute stroke patients were included. Isolated capsular stroke accounted for 8.4% of strokes included in the registry (8.4% of ischemic strokes and 10.5% of intracerebral hemorrhages). Capsular stroke of hemorrhagic origin (n=24) was more severe than ischemic capsular stroke (n=124) as determined by a significantly higher in-hospital mortality, length of stay, and lower number of patients free of functional deficit at discharge. After multivariate analysis, limb weakness, sudden onset, and sensory symptoms were independently associated with capsular hemorrhage, whereas pure motor hemiparesis appeared to be associated with capsular infarction. In summary, one of each 12 patients with acute ischemic stroke and one of each 10 patients with acute intracerebral hemorrhage had an isolated capsular stroke. Lacunar syndrome was the most frequent clinical presentation being more common (particularly pure motor hemiparesis) in ischemic than in hemorrhagic capsular stroke. Capsular hemorrhage and capsular infarction showed identical risk factor profiles suggesting the same underlying vascular pathology for both conditions.

Acute isolated capsular stroke: A clinical study of 148 cases

The objectives of the study were to assess differential features between capsular stroke of ischemic and hemorrhagic origin, and to compare capsular strokes with all other (non-capsular) strokes. Data of 148 patients with isolated capsular stroke were collected from a prospective hospital-based stroke registry in which 2000 consecutive acute stroke patients were included. Isolated capsular stroke accounted for 8.4% of strokes included in the registry (8.4% of ischemic strokes and 10.5% of intracerebral hemorrhages). Capsular stroke of hemorrhagic origin ( n=24) was more severe than ischemic capsular stroke ( n=124) as determined by a significantly higher in-hospital mortality, length of stay, and lower number of patients free of functional deficit at discharge. After multivariate analysis, limb weakness, sudden onset, and sensory symptoms were independently associated with capsular hemorrhage, whereas pure motor hemiparesis appeared to be associated with capsular infarction. In summary, one of each 12 patients with acute ischemic stroke and one of each 10 patients with acute intracerebral hemorrhage had an isolated capsular stroke. Lacunar syndrome was the most frequent clinical presentation being more common (particularly pure motor hemiparesis) in ischemic than in hemorrhagic capsular stroke. Capsular hemorrhage and capsular infarction showed identical risk factor profiles suggesting the same underlying vascular pathology for both conditions.

“Fou rire prodromique” associated with simultaneous bilateral capsular genu infarction

Pathological laughter is exaggerated, uncontrollable, and inappropriate laughter usually unrelated to a true emotion or a congruent mood. “Fou rire prodromique” is a rare form of prodromal pathological laughter of uncertain pathophysiology that heralds an ischaemic neurologic deficit. We report a case of prodromal pathological laughter marking the onset of bilateral capsular genu infarction. T2-weighted cranial magnetic resonance imaging (MRI) showed bilateral capsular genu infarction. There was also a diffusion defect in the same areas on diffusion-weighted imaging (DWI). Although it is known that bilateral subcortical lesions can cause pathological laughter, this is the first demonstration of simultaneous associated bilateral capsular genu infarction on cranial DWI MRI.

Recurrent Small-Artery Disease in Hyperhomocysteinemia: Widowers' Stroke Syndrome?

Hyperhomocysteinemia is thought to cause ischemic strokes. We report two middle-aged widowers with frequent recurrences of small-artery strokes, two capsular infarcts and a thalamic hemorrhage in one patient, and two thalamic and pontine infarcts in the other. Blood tests following the final stroke showed hyperhomocysteinemia and methylenetetrahydrofolate reductase C677T gene mutation, with low concentration of vitamin B6. Multivitamin supplementation normalized plasma homocysteine levels in both patients. Hyperhomocysteinemia is treatable; therefore, serum homocysteine should be measured as a potential risk factor for stroke recurrence in relatively young patients with recurrent small-artery infarctions or hemorrhage, especially those with insufficient lifestyle factors.

Akinetic Mutism Following Unilateral Anterior Cerebral Artery Occlusion

Akinetic Mutism Following Unilateral Anterior Cerebral Artery Occlusion

Reorganization of Speech Production at the Motor Cortex and Cerebellum following Capsular Infarction: a Follow-up Functional Magnetic Resonance Imaging Study

Reorganization of Speech Production at the Motor Cortex and Cerebellum following Capsular Infarction: a Follow-up Functional Magnetic Resonance Imaging Study

Reorganization of speech production at the motor cortex and cerebellum following capsular infarction: a follow-up functional magnetic resonance imaging study

Reorganization of speech production at the motor cortex and cerebellum following capsular infarction: a follow-up functional magnetic resonance imaging study

Reorganization of Speech Production at the Motor Cortex and Cerebellum following Capsular Infarction: a Follow-up Functional Magnetic Resonance Imaging Study

Based on clinical data, Geschwind assumed left hemisphere dominance of speech production to extend to the cortical representation of articulatory and phonatory functions at the motor cortex. This author suggested, furthermore, that the clinical observation of rapid recovery from articulatory impairments after damage to the left-sided corticobulbar tracts reflects compensatory activation of an alternative pathway involving the contralateral pre-central gyrus and its efferent projections. In order to test this hypothesis, functional magnetic resonance imaging (fMRI) was performed 4 and 35 days after stroke in a 38-year-old man who had experienced sudden speech deterioration (‘dysarthric speech’) concomitant with weakness of the right upper limb and the right side of the face. Computerized tomography demonstrated an ischaemic infarction within the left internal capsule. The patient fully recovered from dysarthria within 9 days. Activation of the right hemisphere analogues of Broca and Wernicke areas has been assumed to contribute to recovery from aphasia. As a further aspect of the reorganization of speech function, the present case study demonstrates for the first time by means of fMRI a selective ‘shift’ of the cortical representation of speech motor control to the right Rolandic cortex and the left cerebellum during restitution of articulation in a case of transient dysarthria following infarction of the left internal capsule.

Extensive metabolic and neuropsychological abnormalities associated with discrete infarction of the genu of the internal capsule

OBJECTIVEThe clinical presentation of capsular genu infarct varies. Prominent faciolingual weakness and subcortical dementia are the rule, but symptoms depend on the precise location and extension of the lesion beyond...

Patients with capsular infarct and Wallerian degeneration show persistent regional premotor cortex activation on functional magnetic resonance imaging

Background and Purpose: By using neurorehabilitation outcome measures and functional magnetic resonance imaging (fMRI), we attempted to elucidate the effect of Wallerian degeneration (WD) in the pyramidal tract distal to a posterior capsular stroke on functional recovery. Methods: In 18 patients with pure motor hemiparesis caused by capsular infarct, we identified the presence of WD and then tested whether it affected the rate of motor improvement and the final motor outcome. The discharge T2-weighted MRI (139 ± 5 days on average after stroke) showed WD in 10 of 18 patients (WD-positive, n = 10; WD-negative, n = 8). All patients performed mass grasping of paretic fingers before and after inpatient neurorehabilitation for the fMRI. Results: Demographic characteristics, rate of disability change, final motor status, and volume of lesion were comparable between the groups. On the first fMRI, patterns of fMRI activation in the sensorimotor cortex, premotor cortex (PMC), and supplementary motor area were comparable. However, on the second fMRI, considerably more patients in the WD-positive group (8 out of 10) exhibited persistent contralateral activation in PMC than in the WD-negative group (1 out of 8; P =.0044, chi-square test). Ipsilateral PMC was also more frequently activated (P =.04) in WD-positive patients than in WD-negative patients. Conclusions: Persistent WD had no effect on the impairment or disability outcome; however, it was associated with novel regional activation on repeat fMRI after recovery. To determine whether persistent PMC activation resulted from effort or represents a general effect of WD on motor recovery will require a longer follow-up time and more precise control of functional measurement during imaging. Copyright © 2001 by National Stroke Association

Subcortical Anarthria: A Case Report

A 56-year-old right-handed male with a history of hypertension and diabetes presented two episodes of stroke: The first affected territory was the left anterior coroidal artery (capsular and paracapsular infarcts at the level of the genu and posterior arm of the internal capsule) and the second was the right thalamus, due to a hematoma. Following the first stroke, the patient developed severe dysarthria and after the second stroke remained anarthric. The pathophysiology of the disorder is discussed, and the role of the left and right thalamus as far as speech is concerned is reviewed.

Role of Varicella-Zoster Virus in Pediatric Stroke Syndromes

Infectious Diseases| October 01 2000 Role of Varicella-Zoster Virus in Pediatric Stroke Syndromes AAP Grand Rounds (2000) 4 (4): 34–35. https://doi.org/10.1542/gr.4-4-34-a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Role of Varicella-Zoster Virus in Pediatric Stroke Syndromes. AAP Grand Rounds October 2000; 4 (4): 34–35. https://doi.org/10.1542/gr.4-4-34-a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search nav search search input Search input auto suggest search filter All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: cerebrovascular accident in children, human herpesvirus 3 Sources: (1) Moriuchi H, Rodriguez W. Role of varicella-zoster virus in stroke syndromes. Pediatr Infect Dis J. 2000;19:648–653. (2) Berger TM, Caduff JH, Gebbers JO. Fatal varicella-zoster virus antigen-positive giant cell arteritis of the central nervous system. Pediatr Infect Dis J. 2000;19:653–656. Moriuchi and Rodriguez report the case of a previously healthy 12-year-old girl who developed acute right facial weakness and left hemiparesis and was admitted to the Children’s National Medical Center, Washington, DC. MRI of her brain on admission showed edema within the right putamen and right caudate and a beaded irregularity of the first segment of the right middle cerebral artery. Gradual improvement in motor function occurred without therapy, until no neurologic deficit remained. Her past history was unremarkable except for an episode of right herpes zoster ophthalmicus 9 months earlier. Primary varicella occurred at 9 months. The clinical diagnosis of a herpes zoster related vasculitis of the right middle cerebral artery was confirmed when polymerase chain reaction (PCR) for VZV-specific DNA in CSF was positive. A review of the literature yielded 28 cases of stroke associated with varicella, almost always in normal children aged 8 months to 16 years, who developed hemiplegia or other stroke manifestation a few weeks or months after primary varicella (median interval 2 months) and who had basal ganglia and/or capsular infarct(s) due to vasculopathy of the middle cerebral artery. The neurologic outcome without treatment has been generally good. In the above patient a related entity occurred, stroke syndrome associated with contralateral herpes zoster ophthalmicus. This is usually seen in adults, but 5 children (all immunocompetent) have been reported with an interval of 4 weeks to 9 months between the herpes zoster ophthalmicus and stroke; recovery had been complete in only some of these patients. In the companion article, Berger et al report a case from Lucerne, Switzerland, of a previously healthy 4-year-old girl with an acute right hemiparesis and aphasia who had had a similar episode lasting several hours seven months earlier, and another 15-minute episode one week earlier. Imaging studies confirmed a left middle cerebral artery infarct, and the child died within 48 hours of presentation. Autopsy revealed a left cerebral infarct and an active giant cell granulomatous arteritis involving the wall of the left middle cerebral artery, with occlusion by fresh thrombus. Immunohistochemical staining for varicella zoster virus was positive in the smooth muscle of the vessel wall. This child had acute varicella 13 months earlier. These reports, in addition to over 30 prior ones demonstrate that varicella infection plays a substantial role in pediatric ischemic stroke syndromes1,2 and highlight the value of molecular-based diagnostic techniques. PCR detected the presence of specific DNA in the CSF of Moriuchi’s patient by repeated amplification cycles to expand the number of molecules present in CSF to a number that could be detected. Stroke has not been reported following varicella vaccine and it seems quite likely that immunization with the highly attenuated... You do not currently have access to this content.

Respuesta electromiográfica asociada en ictus capsular

Lesions of the pyramidal system are characterized by their effects on qualitative aspects of movement. One of the features of pyramidal defects is the presence of associated movements or synkinesis. We present a case with residual associated electromyographic (EMG) response in a patient who had had a capsular stroke 11 months previously. The patient presented with acute onset of a syndrome of purely motor right hemiparesis (PMH) which improved satisfactorily with complete functional recovery three months later. Eleven months after the acute episode, there was good functional recovery and neurophysiological examination showed the presence of EMG responses associated with the unaffected limb (left hand) when voluntary movements were made with the right hand. The appearance of qualitative alterations of movement associated with pyramidal syndromes and particularly the presence of associated EMG responses in the case of capsular infarct described, may reflect the different processes of reinnervation and functional reorganization which occur following the lesion and which are involved in recovery of motor function.

Somatosensory evoked potential studies in internal capsule and corona radiata infarction.

To document the somatosensory evoked potential (SEP) changes in capsular and corona radiata infarction and correlate these with clinical and radiological findings, 15 patients with corona radiata and 16 with internal capsular infarction were studied. The mean age of the patients was 55 years (range 26-80), and 6 of them were female. In the patients with corona radiata infarction, median N9-N20 conduction time was abnormal in 4 cases, which correlated with sensory abnormalities in 1. In 3 of these patients, infarction was located in the anterior two-thirds and in 1 there was total corona radiata infarction. The amplitude of N20 potential on the affected side was reduced in 1 patient. In the capsular infarction group, N9-N20 conduction time was abnormal in 1 patient only who had total involvement of the posterior limb of the internal capsule. The amplitude of N20 was reduced in another patient. There were 4 patients who had abnormal sensory findings, but their SEPs were normal. At 3 months, the SEP changes remained stable in all of the patients who were followed up. The SEP changes did not correlate with changes in sensation or 3-month outcome as assessed by the Barthel index score. The lack of clinicoradiological and SEP correlation may be owing to variation on the organisation of sensory pathways in the corona radiata and internal capsule.

Central motor conduction studies in internal capsule and corona radiata infarction

Clinical and evoked-potential studies in internal capsule and corona radiata infarction are lacking. We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction. Patients's outcome was defined at the end of 3 months on the basis of the Barthel Index score. Four patients with type A capsular infarction (middle third of posterior limb of internal capsule) all had severe weakness, while 2 also had persistently unrecordable CMCT and poor outcome. Twelve patients with type B internal capsular infarction (genu, anterior limb, anterior or posterior third of posterior limb) had a milder degree of weakness, and CMCT was recordable in 9. At 3 months' follow-up, however, CMCT was recordable in all 12 patients. All of these patients had a partial (n = 4) or complete (n = 5) recovery. Thirteen patients with type A corona radiata infarction (middle third of corona radiata) had more pronounced weakness, and CMCT was unrecordable in all of these patients except 1 on initial examination. Follow-up after 3 months was possible in 8 patients, and CMCT became recordable in 3. One of these patients had complete, 3 partial, and 4 poor recovery. In type B corona radiata infarction (anterior or posterior third of corona radiata), the clinical signs and CMCT did not follow a regular pattern. Clinical and CMCT abnormalities in internal capsular infarction followed a more predictable pattern compared with those in corona radiata infarction. A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule.

Abulia from unilateral capsular genu infarction: Report of two cases

We report two cases of capsular genu infarction in patients showing pure abulia without motor weakness. One case is left-sided infarction, and another is right-sided. Single photon emission computed tomography (SPECT) examination in both disclosed hypoperfusion in the ipsilateral frontal cortex at the infarction. In one case, reversion of frontal hypoperfusion was observed later. We considered that the frontal hypoperfusion was due to trans-synaptic hypofunction of thalamo-frontal projections from the deep-seated capsular genu lesion and that it resulted in the pure abulia without neurological deficits.

Acute hemiplegia syndrome in childhood

Three types of clinical features at the onset are well known to be characteristic of acute hemiplegia syndrome (AHS). Type 1 comprises status epilepticus of hemiconvulsions with fever. Representative diseases of this type are the infectious diseases of the central nervous system, acute encephalopathy and cerebral vascular diseases. Type 2 comprises status epilepticus of hemiconvulsions without fever. Cerebral vascular diseases and epilepsy are the major ones of this type. Type 3 comprises hemiplegia or hemiparesis of sudden onset without fever or convulsions. Most patients with this type had cerebral vascular diseases, about half of which were moyamoya disease in Japan. Recent progress in neuroimaging studies has allowed considerable elucidation of the etiology of AHS. Gadolinium-enhanced MRI showed minimal lesions such as capsular infarction more clearly than plain MRI. Acetazolamide test 99mTc-HMPAO SPECT imaging is one of the useful assisted diagnostic techniques for moyamoya disease, because it reveals the reserve capacity of the collaterals. [ 123I]IMP SPECT is useful for the diagnosis and follow-up of acute disseminated encephalomyelitis (ADEM), as the images of the lesions coincide well with the MRI ones. 99mTc-HMPAO SPECT in a case with alternating hemiplegia revealed normoperfusion in the ictal periods. Four cases of AHS are reported here.

Lacunar Infarcts: A 1-Year Clinical and MRI Follow-Up Study

There are only a few reports on long-term prognosis and functional outcome after lacunar infarction, and little is known about the evolution of MRI abnormalities with time in this subtype of stroke. To address these issues, we performed a 1-year clinical and MRI follow-up study in 81 patients with presumed lacunar infarction. AT 1 year after stroke onset 1 patient had died, whereas 5 patients (6.2%) had had recurrent strokes. Based on the Oxford Handicap Scale, 63 (79%) of the surviving patients were functionally independent at the time of follow-up. MRI at 1 year revealed new, clinically silent infarcts in 8 patients (10%), and wallerian degeneration of the pyramidal tract in 8 (24%) of the 34 patients with posterior capsular or putamenal infarcts on initial MRI. Our data suggest that new, clinically silent infarcts may be at least as common as recurrent strokes in patients with lacunar infarctions.

Cerebral infarction due to painless thoracic aortic and common carotid artery dissections.

Aortic arch dissection is usually lethal unless emergency surgery is performed. The dissection rarely may have a benign outcome or may occur without pain and be revealed by cerebral infarction. It is then likely to be seen primarily by a neurologist. In such cases, the value of new noninvasive diagnostic testing has not been reported. A 51-year-old man had a sudden left-sided hemiplegia due to hemorrhagic capsular and caudate infarcts on the right side. Cervical ultrasound examination with color flow imaging showed a bilateral common carotid artery dissection extending up to the bifurcation. Transesophageal echocardiography showed an aortic arch dissection, involving the innominate and left common carotid artery origins, which was confirmed by magnetic resonance imaging and aortography. The patient spontaneously fully recovered and is still alive 24 months after the stroke onset. This case emphasizes the usefulness of new noninvasive techniques such as transesophageal echocardiography and color-coded Doppler echocardiography in the diagnosis and follow-up of painless dissection of aortic and common carotid arteries. This cause of stroke may be underestimated.

Capsular infarct with occlusion of the internal carotid artery: Report of two cases

Small infarction in the deep brain is well known by the term lacunar infarct. Among these infarcts, the relatively larger ones localized in the internal capsule and adjacent basal ganglia are designated as capsular infarct or striatocapsular infarction. Their pathogenesis has been mainly attributed to the occlusive lesion of a single penetrating artery as well as the usual lacunae. The authors recently encountered 2 cases of capsular infarct, in whom complete occlusion of the internal carotid artery was angiographically demonstrated. These cases suggest that the extracranial carotid occlusion may also be implicated in the pathogenesis of capsular infarct. The authors present these 2 cases in this communication with possible explanations for the mechanism by which carotid occlusive disease causes capsular infarct.