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 1,441 records · Page 80Linked to original sources
PubMed1982

Local cerebral glucose utilization in the symptomatic thiamine-deficient rat: increases in fornix and pyramidal tract.

Local cerebral glucose utilization (LCGU) was measured in asymptomatic rats on a thiamine (B1)-deficient diet for 70 days and in symptomatic rats on a B1-deficient diet for 98 days. LCGU increased in postcommissural fornix (F), pyramidal tracts (P), and inferior internal capsule (CAI) of symptomatic, compared with asymptomatic B1-deficient rats but decreased in thalamic nuclei, auditory structures, and lesioned vestibular nuclei. B1 administration to symptomatic rats improved symptoms; decreased LCGU in F. P, and CAI; increased LCGU in the lesioned vestibular nuclei; but decreased LCGU in mammillary nuclei, anteroventral nucleus of thalamus, and medial raphe. The results indicate that B1 deficiency symptoms correlate with LCGU changes in F and P and vestibular nuclei.

Animals↗
PubMed1983

Improvement of ataxic hemiparesis with trihexyphenidyl.

In a patient with the syndrome of crural paresis and homolateral ataxia, administration of trihexyphenidyl resulted in improvement of disabling unilateral ataxia and gross intention tremor. Symptoms returned when drug therapy was interrupted. CT showed a radiolucent lesion deep in the parietal white matter close to the internal capsule.

Adult↗
PubMed1983

Capsular stroke as a cause of hemiplegia in infancy.

Small, deep lesions of the internal capsule are an uncommon cause of infantile hemiplegia. We report the clinical and radiographic findings of three children with hemiplegia with capsular lesions. Although the etiology of capsular stroke in these children remains uncertain, neither hypertension, coagulopathy, nor vascular malformation was an important factor.

Cerebrovascular Disorders↗
PubMed1984

Anatomic basis of transcortical motor aphasia.

Analysis of language profiles and CT anatomy in transcortical motor aphasia (TCMA) suggests that the essential lesion is disruption of connections at sites between the supplementary motor area and the frontal perisylvian speech zone. If the lesion is extended, there may also be poor articulation (lesion deep to motor strip for face), impaired auditory comprehension (lesion in anterior head of caudate, anterior limb internal capsule, anterior putamen, and anterior portion of external capsule, claustrum, extreme capsule, and insula), or stuttering (lesion in pars opercularis and lower third of premotor region). This concept unifies disparate anatomic and psychophysiologic observations about three syndromes: classical TCMA, aphasia after left medial frontal infarction, and TCMA during recovery from Broca's aphasia.

Adult↗
PubMed1985

Locked-in syndrome due to tentorial herniation.

A 28-year-old man had a chronic locked-in syndrome following tentorial herniation caused by an epidural hematoma. Postmortem examination revealed bilateral corticospinal tract degeneration caudal to the midbrain, with infarction of the right internal capsule just rostral to the cerebral peduncle and pressure necrosis of the pyramidal portion of the left cerebral peduncle.

Adult↗
PubMed1985

Comparison of glucose metabolism, x-ray CT, and postmortem data in a patient with multiple cerebral infarcts.

We studied a 69-year-old man with multiple brain infarcts who died 8 days after being studied with positron emission tomography and (F-18)-fluorodeoxyglucose. Metabolic abnormalities were greater than structural changes in size and extent. They were found in areas with no gross pathologic abnormalities. Remote metabolic effects were attributed both to degeneration of fiber tracts with disconnection of remote structures, as demonstrated by hypometabolism in the left frontal cortex associated with an infarct in the genu of the left internal capsule, and to microscopic infarcts not apparent on gross examination but manifested as hypometabolic regions.

Aged↗
PubMed1986

Consciousness and amnesia after penetrating head injury: neurology and anatomy.

Among 342 men who survived severe penetrating brain wounds, only 15% had prolonged unconsciousness and 53% had no or momentary unconsciousness after injury, emphasizing the focal nature of these wounds. The left (or language-dominant) hemisphere was dominant for the "wakefulness" component of consciousness. The areas most associated with unconsciousness included the posterior limb of the left internal capsule, left basal forebrain, midbrain, and hypothalamus. Left dominance was not seen for posttraumatic amnesia after elimination of the wakefulness variable, suggesting that wakefulness may be linked to the role of the left hemisphere in verbal memory.

Amnesia↗
PubMed1987

Cerebellar glucose metabolism in chronic aphasia.

(18F)-Fluorodeoxyglucose PET was used to compare left/right cerebellar hemispheric glucose metabolism in 37 aphasic patients with left hemisphere lesions and 22 age-matched controls. Sixteen aphasic subjects showed cerebellar symmetry. Twenty-one aphasic subjects were found to have cerebellar metabolic asymmetry, which (1) resulted from an absolute reduction in local cerebral metabolic rates of glucose in the right cerebellar hemisphere; (2) was associated with left less than right glucose metabolic asymmetry in the frontal, parietal, caudate, and thalamic regions; (3) was associated with Broca's region and deep hemisphere structural damage to the internal capsule and basal ganglia; (4) related to reduced functional motor performance, spontaneous speech, naming, reading, and writing; and (5) included all Broca's aphasia subjects.

Aphasia↗
PubMed1987

Subcortical neglect: quantitation, anatomy, and recovery.

Fifteen patients with right hemispheric subcortical infarcts localized by CT or MRI were evaluated with a neglect testing battery. Trimodal extinction was present in one case, visual extinction in three, tactile in three, and auditory in six. Although frequent (10 cases), hemispatial neglect was rarely severe (3 cases). Three cases recovered completely. Large posterior internal capsule lesions were associated with more frequent impairment on a cancellation test. The probable mechanism of hemispatial neglect was attentional in one case and intentional in six. Visual and auditory extinction is explained by striatonigral mechanisms. Although subcortical structures participate in attentional and intentional behavior, cortical structures can substitute for their functions.

Attention↗
PubMed1989

Traumatic basal ganglia hemorrhage: clinicopathologic features and outcome.

Traumatic basal ganglia hemorrhage (TBGH) is probably secondary to rupture of lenticulostriate or anterior choroidal arteries. We evaluated 6 consecutive cases of this entity to define its clinical and pathologic dimensions. Relative frequency of TBGH was 3% (3 left, 3 right) in this acute rehabilitation population. Lesion size and associated pathology varied. Contralateral hemiparesis, present in all, recovered to varying extents, apparently related to lesion location (posterior limb, internal capsule, or midperiventricular white matter), not size. Prolonged muteness occurred in 4 of 6; these 4 patients also had severe diffuse axonal injury. Clinical findings corresponded with previously recognized subcortical hemisphere profiles. All achieved a moderate disability or good recovery rating on the Glasgow Outcome Scale. Rather than any features of the TBGH itself, duration of coma and/or associated temporal herniation predicted slower recovery and worse outcome. In conclusion, TBGH is a rare entity compatible with a favorable recovery, especially when occurring in isolation. The hemorrhage itself determines clinical signs related to particular subcortical structures involved and the side of the lesion. Overall cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.

Adolescent↗
PubMed1990

Cerebral hemispheric localization of smooth pursuit asymmetry.

We recorded horizontal smooth pursuit in 23 patients with discrete unilateral cerebral hemispheric lesions and in 12 normal subjects. Most patients had bidirectional reduction of smooth pursuit gain, indicating that each cerebral hemisphere participates in smooth pursuit in both directions. Pursuit gain fell proportionately more with increasing target acceleration in patients than in normals. A normal phase relationship between eye and target motion in patients indicated an intact predictor mechanism for smooth pursuit. Ten patients had pursuit asymmetry with lower gain when tracking toward the side of cerebral damage; none had lower gain when tracking away. Two patients with lower ipsilateral gain had frontal lobe lesions. Areas of anatomic overlap of lesions associated with asymmetric pursuit in 8 patients provide evidence for a pursuit pathway that originates from Brodmann areas 19 and 39 and descends to the brainstem through the posterior limb of the internal capsule.

Adolescent↗
PubMed1990

Congenital absence of the corticospinal fibers: pathologic and clinical observations.

We describe 2 patients with primary absence of corticospinal tracts. Both presented with delayed motor development, head lag, and spasticity of the limbs. We could not identify precentral cortex, and there were no corticospinal fibers below the internal capsules. We postulate that the fibers were displaced or interrupted early in their development.

Brain↗
PubMed1991

Conjugate eye deviation: side, site, and size of the hemispheric lesion.

Conjugate eye deviation (CED) is a well-known sign that occurs rather frequently in stroke patients. To study the lateralizing and localizing value of this sign, we investigated prospectively 78 consecutive patients presenting with CED due to a hemispheric lesion. CED occurred more frequently after right-sided hemispheral damage (64%). The lesions in the right hemisphere were located predominantly in the subcortical (fronto-) parietal region and the internal capsule; the lesions in the left hemisphere were larger, covering the entire fronto-temporo-parietal area. In the majority of patients there was no direct involvement of the frontal eye fields on either side. The results indicate that a lesion at different sites within the circuit between the inferior parietal lobule and frontal eye fields, and their projections to the superior colliculus or paramedian pontine reticular formation, can be responsible for CED. The right-left asymmetry is probably related to cerebral asymmetry for directed spatial attention.

Adult↗
PubMed1992

Symptomatic retrochiasmal lesions in multiple sclerosis: clinical features, visual evoked potentials, and magnetic resonance imaging.

We have studied 18 patients with relapsing-remitting multiple sclerosis (MS) who had symptomatic visual field defects due to retrochiasmal lesions. In 17, the lesion responsible was identified by magnetic resonance imaging (MRI), computed x-ray tomography (CT), or both. The lesion responsible involved the posterior optic radiations in eight cases, the optic tract and lateral geniculate nucleus in six, and the posterior limb of the internal capsule in three. The prognosis for recovery of the field defect was good; complete recovery occurred in 14 patients, and only two showed no recovery at all. The striking characteristic of the lesions was that most were unusually large; indeed, many were detectable on CT as well as MRI. Half-field asymmetries of either amplitude or latency of the visual evoked potentials (VEPs), consistent with a postchiasmal lesion, were present in only five out of 13 patients acutely. In only three of these did the abnormality persist at follow-up. We conclude that only large postchiasmal lesions are likely to cause symptomatic homonymous field defects in MS, usually characterized by rapid recovery. Hemifield VEPs have a low sensitivity for the detection of postchiasmal as compared with prechiasmal abnormalities.

Adult↗
PubMed1992

Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome?

We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."

Aged↗
PubMed1992

Type and extent of hemispheric brain infarctions and clinical outcome in early and delayed middle cerebral artery recanalization.

We evaluated the influence of time of recanalization or degree of initial leptomeningeal collateral blood flow in cardioembolic or arterio-arterial middle cerebral artery (MCA) occlusion on infarct size and clinical outcome in a series of 34 consecutive acute stroke patients with main stem (N = 31) or major branch (N = 3) occlusions using CT, initial cerebral arteriography (N = 21), repetitive close-meshed transcranial Doppler ultrasonography, and a neurologic stroke scale. We treated 15 patients with tissue plasminogen activator intravenously within the first 6 hours. The type and size of infarction depended on the location of the occluding lesions within the MCA trunk. Proximal MCA occlusion always led to infarction involving the striatum and internal capsule. Sixty-five percent of patients showed recanalization of the occluded MCA within 1 week. Following MCA recanalization, hyperperfusion was present in 38 to 44% of cases. There was a marginally significant relation between size of infarction on CT and recanalization time within the first 24 hours. The more rapidly recanalization occurred, the smaller the size of the infarct. When recanalization time was greater than 8 hours, the lesions always extended to the cortex. An additional good leptomeningeal collateral blood flow significantly reduced the size of the infarct and improved clinical outcome after 17 days and after 10 months. Early recanalization of embolic MCA occlusions within up to 8 hours, in conjunction with good transcortical collateralization, has a favorable impact on infarct size and outcome and may constitute the therapeutic window of opportunity.

Aged↗
PubMed1993

Cheiro-oral topography of sensory disturbances due to lesions of thalamocortical projections.

Sensory disturbance in the unilateral hand and ipsilateral mouth region, the cheiro-oral syndrome, may be due to cortical, thalamic, or brainstem lesions. We report five patients with this syndrome due to infarction at the border of the posterior limb of the internal capsule and the corona radiata. The sensory fibers from the mouth area and hand probably travel to the cortical sensory areas in close proximity after leaving the posterior ventral thalamic nucleus.

Adult↗