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The computed tomographic findings in seven boys and two girls with infarction of the internal capsule are reported. Ages at the time of examination ranged from 8 months to 14 years. The etiology was head injury (concussion) in six and unknown in three. Cerebral angiography carried out in four cases showed narrowing of main arteries in two patients.
Localization of the corticofugal projection in the corona radiata (CR) and internal capsule (IC) can assist in evaluating a patient's residual motor capacity following subtotal brain damage and predicting their potential for functional restitution. To advance our understanding of the organization of the corticofugal projection in this critical brain region, we studied the trajectories of the projection arising from six different cortical arm representations in rhesus monkeys. They included the arm representation of the primary (M1), ventral lateral pre- (LPMCv), dorsolateral pre- (LPMCd), supplementary (M2), rostral cingulate (M3) and caudal cingulate (M4) motor cortices. In the CR, each pathway was segregated as medial motor area fibres arched over the caudate and lateral motor area fibres arched over the putamen. In the IC, the individual corticofugal pathways were found to be widespread, topographically organized and partially overlapping. At superior levels of the IC, the corticofugal projection from the arm representation of M3 coursed through the middle and posterior portion of the anterior limb (ICa). The projection from M2 passed through the posterior portion of the ICa and the genu (ICg). The projection from LPMCv travelled through the genu and anterior portion of the posterior limb (ICp). The projection from LPMCd occupied the anterior portion of the ICp. The projection from M4 descended through the mid-portion of the ICp. Fibres from M1 also travelled in the ICp, positioned immediately posterior to the M4 projection. As each fibre system progressed inferiorly within the IC, all fibres shifted posteriorly to occupy the ICp. Within the ICp, the projections from M3, M2, LPMCv, LPMCd, M4 and M1 maintained their anterior to posterior orientation, respectively. M2, LPMCd and LPMCv fibres overlapped extensively, as did fibres from M4 and M1. Our data suggest that CR and superior capsular lesions may correlate with more favourable levels of functional recovery due to the widespread nature of arm representation. In contrast, the extensive overlap and comparatively condensed organization of arm representation at inferior capsular levels suggest that lesions seated inferiorly are likely to correlate with poorer levels of recovery of upper limb movement. Based on the relative density of corticospinal neurones associated with the motor areas studied, our findings also suggest that motor deficit severity is likely to increase as a lesion occupies progressively more posterior regions of the IC.
OBJECTIVE: Predicting long-term outcome in infants with hypoxic-ischemic encephalopathy (HIE) is a difficult task. Magnetic resonance imaging, particularly diffusion imaging, holds promise in this regard as it is more sensitive to brain injury than any other available imaging modality. Previous studies have suggested that abnormal signal intensity in the posterior limb of the internal capsule (PLIC), detectable on inversion-recovery T1-weighted imaging, is a strong predictor of outcome. The aim of this study was to assess the relationship between apparent diffusion coefficient (ADC) values from the PLIC, measured by diffusion imaging, and neuromotor outcome in term infants with HIE. METHODS: Twenty-eight term infants with a clinical diagnosis of HIE underwent magnetic resonance imaging as soon as practicable after birth (mean age: 5.6 days), including diffusion-weighted imaging, from which ADC values in the PLIC were measured. Motor outcome was assessed in 12 of 16 survivors. RESULTS: The ADC value in the PLIC was significantly associated with survival in term infants with HIE. For survivors, the mean ADC value in the PLIC was 0.89 +/- 0.17 microm2/ms, whereas the mean ADC value for nonsurvivors was 0.75 +/- 0.17 microm2/ms (t = 2.25). Among survivors, the ADC value in the PLIC was also associated with neuromotor outcome (F = 5.60). CONCLUSION: The ADC value in the PLIC is an indicator of ischemic injury and may be of use as an objective prognostic marker for infants with HIE.
OBJECTIVE: Radiosurgery is accepted as the first option for treating deep arteriovenous malformations (AVMs), although the clinical outcome in this subgroup of brain AVMs is not well studied. The objective of this study is to review our experience with radiosurgical treatment for these AVMs. METHODS: Between October 1989 and December 2000, 45 patients with deep AVMs (including basal ganglia, internal capsule, and thalamus) underwent stereotactic radiosurgery. Three patients were lost to follow-up and therefore were excluded from this study. Patient characteristics and outcomes were collected and analyzed. The obliteration prediction index and the radiosurgery-based AVM score were calculated and tested. RESULTS: Forty-two patients were followed up for a median of 39 months (range, 25-90 mo; mean, 45.8 mo). The median maximum AVM diameter during the radiosurgery was 1.8 cm (range, 0.9-4.0 cm; mean, 2.07 cm), and the median AVM volume was 2.8 cm(3) (range, 0.2-18.3 cm(3); mean, 4.74 cm(3)). The mean marginal dose was 16.2 Gy (median, 15 Gy), and the median maximum dose was 22.4 Gy (range, 16.6-30 Gy). The AVM cure rate after the first radiosurgical treatment, using angiography- and magnetic resonance imaging-confirmed obliteration, was 61.9%. The predicted obliteration using the obliteration prediction index was 60%. Eight patients developed radiation-induced complications (19%). The deficit was transient in three patients (7.1%) and permanent in five patients (11.9%). The risk of postradiosurgical hemorrhage in this cohort was 9.5% for the first year, 4.7% for the second year, and 0% thereafter. Excellent outcome (obliteration plus no new deficit) was achieved in 70% of the patients in the group with radiosurgery-based AVM score less than 1.5 compared with 40.9% in the group with radiosurgery-based AVM score greater than 1.5% (P = 0.059). CONCLUSION: Radiosurgery for deep AVMs has a satisfactory obliteration rate and acceptable morbidity, considering the risk of hemorrhage without treatment and the risk of morbidity associated with other treatment modalities.
OBJECTIVE: The 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 the genu. The aim was to characterise the radiographic, electroencephalographic, and neuropsychometric abnormalities in a woman who had a history of recurrent transient memory loss. METHOD: Case report. RESULTS: Magnetic resonance imaging showed an infarct in the genu of the left internal capsule. Positron emission tomography scan demonstrated decreased metabolic activity in the ipsilateral temporal, occipitotemporal, and contralateral cerebellar hemispheres. Electroencephalography showed intermittent rhythmic delta activity in the left frontotemporal region, and findings on neuropsychometric evaluation were consistent with cognitive impairment. Follow up evaluation 7 months after the stroke showed improvement in some areas of the cognitive domain, but residual neuropsychometric and neurophysiological abnormalities persisted. CONCLUSION: This case illustrates that cerebral and cerebellar diaschisis may contribute to the symptomatic presentation and recovery from capsular genu infarct, although its precise role remains elusive.
Therapy for neurodegenerative lysosomal Tay-Sachs (TS) disease requires active hexosaminidase (Hex) A production in the central nervous system and an efficient therapeutic approach that can act faster than human disease progression. We combined the efficacy of a non-replicating Herpes simplex vector encoding for the Hex A alpha-subunit (HSV-T0alphaHex) and the anatomic structure of the brain internal capsule to distribute the missing enzyme optimally. With this gene transfer strategy, for the first time, we re-established the Hex A activity and totally removed the GM2 ganglioside storage in both injected and controlateral hemispheres, in the cerebellum and spinal cord of TS animal model in the span of one month's treatment. In our studies, no adverse effects were observed due to the viral vector, injection site or gene expression and on the basis of these results, we feel confident that the same approach could be applied to similar diseases involving an enzyme defect.
A patient was presented with an outstanding symptom of abulia due to cerebral infarcts in the bilateral genua of internal capsules. A 53-year-old woman, generally in good health and active, had no contributory medical history except for hypertension. She was well until August 20, 1988, when she was noted to have become taciturn and absent-minded. In the morning, she got up and went to work as usual. Although she worked without trouble, she hardly talked with her colleagues. After getting home from work, she would lie down without doing any housework, and this was continued on the following day. However, she had no physical problems. She was thus admitted to a hospital on August 22. Lethargy and urinary incontinence were apparent for a few days. Thereafter she became awakeful and could take care of herself. She sat on her bed all the time, and could talk normally with her daughter. She was referred subsequently to the Department of Neurology, Hyogo Prefectural Tsukaguchi Hospital on August 30. On examination, the patient was alert, polite and cooperative with no physical abnormalities except for high blood pressure. Neurological examination indicated the patient to be attentive and well-oriented. Cranial nerves and eye movements were normal except for slight anisocoria and sluggish pupils. There were no muscle weakness, extrapyramidal signs, or cerebellar signs. Deep tendon reflexes were normal. Babinski signs and forced grasping were not noted. A neuropsychological study showed the patient not to be demented, aphasic, or apraxic.(ABSTRACT TRUNCATED AT 250 WORDS)
A 68-year-old right handed man with treated hypertension presented with acute-onset somnolence without hemiparesis, dysarthria or sensory disturbance. Although he became laconic and his verbal responses were only in short terms, his replies were accurate and judgmental. A cranial MRI in axial, coronal, and sagittal section revealed small hemorrhagic infarcts essentially limited to the bilateral capsular genua without involvement of the inferior thalamic peduncles. A 123I-IMP single photon emission CT disclosed remarkable hypoperfusion in the bilateral frontal cortex. After a week of somnolence, he gradually became wakeful, but was still abulic. Neuropsychological examinations revealed no memory disturbance. We consider that disconnection of the thalamo-frontal projection at the genua of the internal capsules caused somnolence, apathy, and abulia in our case. The hitherto reported cases of the genu infarcts that showed memory disturbance had the lesion involving both the inferior thalamic peduncle and its nearby mamillothalamic tract. In contrast, our case without memory disturbance had infarcts confined to the genua apparently sparing the two tracts, implicating that memory function may be preserved when such structures are intact.
Animal experiments suggest that astrocytic glycogen may act as an energy source for axons especially during heightened activity. In this model astrocytic glycogen breaks down to lactate that is shuttled to axons where it is metabolized oxidatively to generate ATP. The aim of this study was to investigate whether (1)H-magnetic resonance spectroscopy could be used to detect a rise in lactate levels in human white matter during enhanced axonal activation. Six healthy volunteers (four women and two men; age range 21-38 years) participated in the study. We were unable to detect any significant MR spectral change, i.e. neither in the peak areas of inositol, choline, creatine, glutamate and N-acetylaspartate nor in the lactate level, in the contralateral posterior limb of the internal capsule during intense motor activation of the hand (four successive episodes of squeezing a soft ball for 7 min followed by 7 min rest). Possible explanations are that the technique is not sensitive enough to detect a small rise in lactate, or lactate turnover is too fast to be detected, or that another monocarboxylate different from lactate may be involved in axonal energy metabolism.
Epidemiologic and experimental findings implicate maternal infection in the etiology of injury to brain white matter, which may lead to cerebral palsy in preterm newborns. In the present study, inflammation and brain damage in 1- and 7-d-old rats were investigated after maternal inflammation. Intraperitoneal injection of 300 microg/kg of Escherichia coli lipopolysaccharide was administered to pregnant Wistar rats at d 19 and 20 of gestation (LPS group). Control females received a saline injection. Proinflammatory cytokines IL-1beta, tumor necrosis factor-alpha, and IL-6 expression in the fetal brain were determined by reverse transcription quantitative polymerase chain reaction. Brain injury was examined in 16-mum coronal brain sections by GFAP, MBP, caspase-3 immunohistochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. Expression of IL-1beta was significantly increased 3 d after maternal administration (P1). A significant increase in cell death occurred at P1 and P7 in specific brain areas, i.e. in the subventricular striatal zone at P1, and in 1) the periventricular striatum, 2) the periventricular white matter, and 3) the germinative ventricular zone at P7. We also observed typical astrogliosis and strong hypomyelination in the external and internal capsule in the LPS group at P7. These results demonstrate that maternal LPS treatment induces persistent fetal inflammatory reactions associated with significant white matter injury in progeny at P1 and P7. This model should be relevant for the study of the pathophysiological mechanisms involved in cerebral white matter damage in preterm human newborns and in the development of therapeutic strategies.
A persistent hemispatial neglect developed in a patient following a small infarction of the posterior limb of the right internal capsule. This defect was restricted to tasks requiring spontaneous motor performance on the contralateral hemispace, especially when carried out under visual control. It was not associated with an extinction phenomenon. Verbal cues improved exploratory behavior, suggesting that hemispatial akinesia in this case was due to an intentional disorder. A pulvinar-parietal disconnection, depriving the right parietal cortex from relevant visuospatial information from the contralateral hemispace, was probably the anatomic basis of hemispatial neglect in this case.
A posttraumatic patient was tetraplegic and mute (locked-in), but he retained consciousness and communicated by eye movements. CT showed bilateral internal capsule (IC) infarcts involving the posterior limb and caudal part of the genu, sparing the ventral brainstem. This is the first report of the locked-in state caused by infarcts in both IC.
A patient with a right internal capsule and thalamic hemorrhage showed ipsilateral hemiplegia. MRI at 10 months after the cerebral hemorrhage demonstrated Wallerian degeneration, which could be traced to the ipsilateral anterior funiculus at the cervical level. The findings of motor evoked potentials and somatosensory evoked potentials indicate a predominantly ipsilateral innervation of motor and sensory systems in this particular patient.
A patient developed hemilateral tonic spasms associated with a relapse of multiple sclerosis. An area of demyelination in the right internal capsule was observed on a magnetic resonance imaging scan. This lesion was not detectable on a second magnetic resonance imaging scan 10 months after the spasms had ceased. Paroxysmal symptoms in multiple sclerosis may represent transient phenomena related to inflammation in acute plaques.
We studied three right-handed patients with small, lacunar infarcts localized by CT to the posterior and lateral putamen and the posterior limb of the internal capsule. All had moderate or severe right hemiparesis and mild aphasia that was not characteristic of any traditional aphasia syndrome. Two had mild dysarthria. Aphasic abnormalities included mild, nonfluent, telegraphic speech and mild, fluent aphasia with impaired repetition, naming, and comprehension. All three had severely impaired writing. Unlike previously reported patients with subcortical infarcts, these cases indicate that small lesions limited to the posterior capsuloputaminal area can cause aphasia and agraphia as well as dysarthria.
OBJECTIVE: The aim of this study was to establish whether abnormal signal intensity in the posterior limb of the internal capsule (PLIC) on magnetic resonance imaging is an accurate predictor of neurodevelopmental outcome at 1 year of age in infants with hypoxic-ischemic encephalopathy (HIE). METHODS: We have examined 73 term neonates with HIE between 1 and 17 days after birth with cranial magnetic resonance imaging and related the magnetic resonance imaging findings to neurodevelopmental outcome at 1 year of age. RESULTS: All infants with an abnormal signal intensity in the PLIC developed neurodevelopmental impairment although in 4 infants with very early scans the abnormal signal was not apparent until up to 4 days after birth. A normal signal intensity was associated with a normal outcome in all but 4 cases; 3 of these infants had minor impairments and all had persistent imaging changes within the white matter. The 4th infant with a normal signal intensity on day 2 died before a further image could be obtained. The absence of normal signal predicted abnormal outcome in term infants with HIE with a sensitivity of 0.90, a specificity of 1.0, a positive predictive value of 1.0, and a negative predictive value of 0.87. The test correctly predicted outcome in 93% of infants with grade II HIE, according to the Sarnat system. Applying a Bayesian approach, the predictive probability of the test (the probability that the test would predict an outcome correctly) was distributed with a mean of 0.94 and 95% confidence limits of 0.89 to 1.0. CONCLUSION: Abnormal signal intensity in the PLIC is an accurate predictor of neurodevelopmental outcome in term infants suffering HIE.
A sixty-nine year old hypertensive man had left motor neglect following an infarct of the anterior limb of the right internal capsule. He also had left auditory extinction on verbal dichotic listening and a sligh constructional apraxia. Regional cerebral blood flow (CBF) was measured at rest with Xenon 133 inhalation and was found to be slightly decreased in a diffuse fashion. Motor activation of the right hand resulted in an increase of CBF in the contralateral superior rolandic area, whereas no such increase was found during motor activation of the left hand. This lack of cortical CBF increase on contralateral motor activation is interpreted as a consequence of the failure of some corticosubcortical connexions involved in motor arousal. The specifically dynamic appearance of regional CBF abnormalities, i.e. during selective activation as opposed to rest measurements, is consistent with the functional character of neglect.
Coronal sonograms in infants obtained with 3.5 and 5.0 MHz sector and linear-array transducers now depict the anterior limb, genu, posterior limb, and sublenticular parts of internal capsule; the caudate nucleus; the putamen; the lateral and medial nuclei of globus pallidus; the lateral and medial medullary laminae of the lenticular nucleus; the nucleus accumbens septi; and some of the thalamic nuclei. Correlation of sonograms obtained in vivo with gross and myelin-stained sections of human brain illustrates the configurations of these structures and the interrelations among them. Physicians familiar with this anatomy may now use sonography to localize focal lesions more accurately than has been possible previously.