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Pediatric stroke among Hong Kong Chinese subjects.

BACKGROUND: The incidence of pediatric stroke was estimated to be 2.5 to 2.7 cases per 100,000 children per year in North America and 13 cases per 100,000 children per year in France. Stroke is among the top 10 causes of death among children in the United States, with the highest incidence in the first 1 year of life. The annual mortality rate was 0.34 deaths per 100,000 person-years, with an average of 244 deaths per year. Interethnic differences have been demonstrated to be important in pediatric stroke. However, most population-based studies on pediatric stroke were from Europe or North America, and there was a lack of data on the incidence of stroke among Chinese or Asian children. Whether the etiologic patterns and risk factors for death and morbidity among Chinese children with stroke were similar to those described for other ethnic groups was unknown. OBJECTIVES: To calculate the incidence of stroke among Chinese children in Hong Kong and to examine the clinical spectrum, causes, patterns, risk factors, and outcomes of pediatric stroke among Chinese subjects. METHODS: The population of Hong Kong was 6.7 million in 2001, and >98% of our population is Chinese in origin. In Hong Kong, public hospitals under the Hospital Authority provide >95% of the hospital service for the region. We identified children (>1 month to <15 years of age) who were admitted and given a discharge diagnosis of stroke from the Clinical Data Analysis and Reporting System, which is a centralized computerized database for all public hospitals. The discharge coding of stroke used codes from the International Classification of Diseases, 9th Revision, Clinical Modification. Only first admissions during the study period were included. We excluded any subsequent admissions by using multiple demographic characteristics of the patients. The incidence of pediatric stroke was estimated as the number of first hospitalizations divided by the person-years at risk. Since 1991, we had been collecting a database on pediatric stroke (ages of 1 month to 16 years) from a single center (the university-affiliated pediatric unit). The clinical presentation, causes, risk factors, and outcomes for those in the Hong Kong Children's Stroke Registry with follow-up data for > or =2 years were analyzed. Data on outcomes, in terms of survival and neurologic deficits, were studied. For survivors, neurologic deficits were defined as short-term if they resolved within 3 months and long-term if they persisted for >3 months. The severity of deficits was defined as mild when function was minimally affected and the patient remained independent in activities of daily living, moderate when the patient required supervision or partial assistance in activities of daily living or when the deficit caused delay in developmental milestones, and severe when the patient required total or near-total care in activities of daily living. Potential risk factors for death and poor neurologic outcomes, including gender, age at the time of stroke, clinical presentation, causes, and neuroimaging findings, were analyzed. RESULTS: Using projections from census data in 2001, the number of children <15 years of age in Hong Kong from 1998 to 2001 was estimated to be 1,104100 to 1,158800, resulting in 4,545300 person-years. During the same period, 94 children with discharge coding of stroke were identified. Therefore, the estimated incidence of pediatric stroke between 1998 and 2001 was 2.1 cases per 100,000 children-years. The average number of new cases treated annually was 4.5 (0-15 cases/year). Fifty children (28 boys and 22 girls; male/female ratio: 1.27:1) were identified in the 11-year period. The mean age at presentation was 5.6 +/- 4.9 years. Thirty-six strokes (72%) were ischemic and 14 (28%) were hemorrhagic. Despite evaluation for possible underlying causes, 12% (6 cases) remained idiopathic. Eighteen patients with ischemic strokes had cerebral thrombosis, whereas 15 had cerebral embolism. We did not observe any case of sinovenous thrombosis. The 36 cases of ischemic stroke were subtyped according to vascular territories. Eleven cases had infarction involving the middle cerebral artery territory; 2 were limited to the cortical region, 3 were limited to subcortical structures such as the basal ganglia or internal capsule or both, and 6 had complete middle cerebral artery involvement, with cortical and subcortical stroke. Involvement of the anterior cerebral artery occurred in 2 cases, with involvement of cerebellar/basilar artery territories in another 2 cases. The remaining 15 cases had multiple sites of infarction. Three patients experienced secondary hemorrhagic transformation after the initial thrombotic event. Of the 14 patients with hemorrhagic strokes, only 1 had subarachnoid hemorrhage. All others had intracerebral bleeding, at single (N = 9) or multiple (N = 4) loci. Important causes included complications related to congenital heart diseases (N = 15, 30%), vascular diseases (N = 13, 26%), and hematologic diseases (N = 14, 28%). Six cases had no determined causes. One case involved mitochondrial encephalopathy with lactic acidosis and stroke-like episodes and constituted the only case with a metabolic cause. For the 7 patients for whom prothrombotic screening was performed, findings were negative. Seizures (52%) and hemiplegia (34%) were the most common presenting features. Other presenting clinical features included headaches (22%), decreased consciousness (30%), visual field defects (12%), dysphasia (10%), and lethargy (8%). Only 1 patient, with moyamoya disease, had a family history of stroke. The median follow-up time was 8.7 years (range: 2-12.4 years). Nine patients (18%) died, 5 with ischemic stroke and 4 with hemorrhagic stroke. Among the 5 cases of death with ischemic stroke, 3 involved hemorrhagic transformation before death. Seven patients (77%) died within 31 days (range: 2-31 days), whereas the other 2 died 6 months and 2.5 years after the episode. Recurrence occurred in 5 cases (10%). Long-term neurologic deficits occurred among 41% of survivors, including mental retardation (N = 11), epilepsy (N = 7), and hemiplegia (N = 10). The functional deficits were classified as severe in 7 cases, moderate in 3 cases, and mild in 7 cases, for patients with long-term neurologic deficits. Decreased levels of consciousness, hematologic causes, and hemorrhagic transformation (applicable only in ischemic stroke) were significant risk factors associated with high mortality rates. For the 41 patients who survived, the only significant risk factor for long-term neurologic deficits was seizures at the initial presentation. Other factors, such as gender, age, other clinical features, stroke type, vascular territory, other causes, and recurrence of stroke, were all insignificant for both death and long-term deficits. The 3 risk factors identified for death were analyzed in multivariate logistic regression analyses, with adjustment for the confounding variables, and only decreased levels of consciousness remained significant (odds ratio = 15.6). CONCLUSIONS: The incidence of stroke among Chinese children was slightly lower than that in Europe or North America. The etiologic pattern was different in our cohort, and there was no sickle cell anemia, thrombophilia, or sinovenous thrombosis. Despite these differences, however, mortality and long-term neurologic deficit rates were similar.

Adolescent↗

Magnetic resonance image correlates of hemiparesis after neonatal and childhood middle cerebral artery stroke.

OBJECTIVE: Motor impairment after neonatal and childhood-onset ischemic stroke (IS) is common, although the prevalence and type of hemiparesis differs between the 2 age groups. Lesion topography is an important predictor of hemiparesis after neonatal IS, but it is not known if the same topographic predictors of adverse motor outcome apply to childhood-onset IS. We used a consistent approach to define lesion topography and evaluate motor outcome in both age groups to (1) investigate whether early topographic predictors of hemiparesis after unilateral middle cerebral artery-territory stroke are the same in neonates and older children and (2) compare the prevalence of dystonia and loss of independent finger movements between the 2 age groups. DESIGN: Twenty-eight patients with neonatal-onset IS (Hammersmith Hospital, London, United Kingdom) were studied together with 43 patients with childhood-onset IS (Great Ormond Street Hospital, London, United Kingdom). All patients had exclusive unilateral middle cerebral artery-territory IS. Lesion topography was studied by using the first magnetic resonance image acquired after the onset of symptoms and was coded for involvement of cerebral cortex (CC), posterior limb of the internal capsule (PLIC), basal ganglia (BG), and white matter. The primary outcome was hemiparesis, and secondary outcomes were dystonia and loss of age-appropriate independent finger movements. RESULTS: Hemiparesis was more common after childhood-onset IS (56%) than neonatal-onset IS (24%). In neonatal-onset IS, concomitant involvement of BG, CC, and PLIC predicts the development of hemiparesis (odds ratio: 99; 95% confidence interval: 5.2-1883.8), and no child with 1 or 2 of these structures involved developed hemiparesis. In contrast, in childhood-onset IS, concomitant BG, CC, and PLIC lesions tended to be associated with hemiparesis (9 of 11), but this adverse outcome was seen also among patients with 1- or 2-site involvement. However, hemiparesis was less likely if the infarction involved BG only (odds ratio: 0.162; 95% confidence interval: 0.036-0.729). Dystonia was present in 15 of 24 in the childhood-onset group with hemiparesis but was not seen after neonatal-onset IS. In both age groups upper-limb impairment was more severe than lower-limb impairment, with frequent loss of independent hand function among hemiparetic patients. CONCLUSIONS: In neonatal and childhood-onset IS, early magnetic resonance imaging provides useful prognostic information about subsequent motor outcome. There are differences in the functional response of the neuromotor system to injury between the 2 age groups that cannot be attributed to methodological differences alone.

Adolescent↗

Use of 2-channel bedside electroencephalogram monitoring in term-born encephalopathic infants related to cerebral injury defined by magnetic resonance imaging.

OBJECTIVE: Single-channel amplitude-integrated electroencephalography has been shown to be predictive of neurodevelopmental outcome in term infants with hypoxic-ischemic encephalopathy. We describe the relationship of quantifiable electroencephalogram (EEG) measures, obtained using a 2-channel digital bedside EEG monitor from term newborn infants with encephalopathy and/or seizures, to cerebral injury defined qualitatively by MRI. METHODS: Median values of minimum, mean, and maximum EEG amplitude were obtained from term-born encephalopathic infants during a 2-hour seizure-free period obtained within 72 hours of admission. Infants underwent MRI with images qualitatively scored for abnormalities of cortex, white matter, deep nuclear gray matter, and posterior limb of the internal capsule. Eighty-six infants had EEG measures related to qualitative MRI outcomes. RESULTS: The most common diagnosis was hypoxic ischemic encephalopathy (n = 40). For all infants there was a negative relationship between EEG amplitude measures and MRI abnormality scores assessed on a scale from 4 to 15, with a higher score indicating more abnormalities. This relationship was strongest for the minimum amplitude measures in both hemispheres; that is, for every unit increase in score there was a mean drop of 0.41 microV for the left cerebral hemisphere, with 35% of variance explained. This relationship persisted on sub-group analyses for infants with hypoxic-ischemic encephalopathy, infants with other diagnoses and infants monitored after the first 24 hours of life. Using an MRI abnormality score cutoff of 8 or worse for cerebral injury in infants with hypoxic-ischemic encephalopathy, a minimum amplitude of 4 microV showed a higher specificity (80%: left hemisphere), whereas a minimum amplitude of 6 muV showed a higher sensitivity (92%: left hemisphere). CONCLUSIONS: Bedside EEG measures in term-born encephalopathic infants are related to the severity of cerebral injury as defined by qualitative MRI. A minimum amplitude of <4 microV appears useful in predicting outcome.

Cerebral Cortex↗

Biocompatibility studies of the Anaconda stent-graft and observations of nitinol corrosion resistance.

PURPOSE: To validate the deployment, in vivo performance, biostability, and healing capacity of the Anaconda self-expanding endoprosthesis in a canine aortic aneurysm model. METHODS: Aneurysms were surgically created in 12 dogs by sewing a woven polyester patch onto the anterior side of the thoracic or abdominal aorta. Anaconda prostheses were implanted transfemorally for prescheduled periods (1 or 3 months). Aneurysm exclusion and stent-graft patency were monitored angiographically. Healing was assessed with histological analysis and scanning electron microscopy (SEM). Textile analysis determined the physical and chemical stability of the woven polyester material, while the biostability of the nitinol wires was evaluated with SEM and spectroscopy. RESULTS: All prostheses were intact at explantation. After 1 month, endothelial-like cells were migrating in a discontinuous manner both proximally and distally over the internal collagenous pannus at the device-host boundary. After 3 months, endothelialization had reached the midsections of the devices, with a thicker collagenous internal capsule. Patches of endothelial-like cells were sharing the luminal surface with thrombotic deposits. However, the wall of the device at the level of the aneurysm was generally poorly healed, with multiple thrombi scattered irregularly over the luminal surface. The polyester fabric was intact except for some filaments that were ruptured adjacent to the sutures and some abrasion caused by the nitinol wires. No evidence of corrosion was found on the nitinol stents. CONCLUSIONS: This Anaconda stent-graft has demonstrated its ability to exclude arterial aneurysms. The device used in this study was an experimental prototype, and the manufacturer has incorporated new immobilization features into the model for clinical use. The constituent materials appear to be suitable in terms of biocompatibility, biofunctionality, and short-term durability.

Alloys↗

[Striatocapsular infarction in childhood. Report of 4 cases].

The authors present the study of four children that manifested asymmetric hemiparesis with sudden onset, without consciousness loss. The diagnosis of striatocapsular infarction was confirmed by computed tomography (CT) and magnetic resonance imaging (MRI). The clinical and neurological examination, and laboratorial results are discussed. Familial history of migraine was found in two of the patients. Migraine was diagnosed in two, mild head trauma, viral miocarditis and mitral valve prolapse in one. Left hemiparesis, with brachiofacial features in three, and brachial in one. CT showed lenticular nucleus and internal capsule lesions in all of them, head of caudate nucleus in three, and white substance in two. MRI was done in two and confirmed CT findings. Electroencephalogram, at the acute phase in three, showed abnormalities in all patients.

Adolescent↗

Isolated intracranial fibromuscular dysplasia presents as stroke in a 19-year-old female.

Isolated intracranial fibromuscular dysplasia is rare and may present with cerebrovascular events. It should be considered as etiology of stroke in otherwise healthy young patients. Though diagnosis is often challenging, characteristic morphologies may be revealed on magnetic resonance and catheter angiography. Cephalocervical fibromuscular dysplasia typically involves the extracranial portion of the internal carotid artery (nearly 95%). This rare case demonstrates isolated intracranial fibromuscular dysplasia in a 19-year-old female with left caudate and genu of internal capsule stroke.

Adult↗

[Microsurgical anatomy of the human basal anterior perforated substance].

The anterior perforated substance (APS) is a landmark in the basal forebrain. It has a basal face located above the carotid bifurcation in the subarachnoid space, and an interhemispheric one. It is the site of passage of the arteries to the caudate nucleus, putamen, internal capsule, adjacent areas of the globus pallidus and thalamus. Fifty hemispheres from twenty-five adult cadavers were obtained. The arteries were perfused with colored latex, Batsons resin and gelatin colored with carmine. Using a surgical microscope we have determined the origin, local and number of origin from the parent vessel. The sites of penetration in the mediolateral and anteroposterior direction were also recorded. The anterior communicating artery contribution to the basal APS was reviewed. Significant vascular variations and anastomoses were encountered mainly involving middle cerebral and anterior choroidal arteries. The precise understanding of these vessels has surgical and clinical implications in the management of vascular and tumoral maladies related to the anterior perforated substance.

Adolescent↗

Arrest reaction in man: motor arrest response by electrical stimulation of the deep structure of the cerebrum.

In spite of many reports of arrest reaction in animals, there are very few reports in man. During a therapeutic stereotactic operation we observed peculiar phenomena caused by electrical stimulation to the deep structure of the cerebrum. The electrical stimulation caused an interruption of counting and other motor actions, which could be resumed following release of stimuli. In almost all cases psychic confusion of memory disturbances were not observed. The head of the caudate nucleus and its adjacent white matter cause arrest reaction with the lowest threshold of 5 V; on the other hand, substantia medullaris lobi frontalis, radiatio corporis callosi and nucl. reticularis oralis of the thalamus caused arrest reaction with the highest threshold of 10--15 V. The arrest reaction that we observed is thought to be due to a direct effect on the head of the caudate nucleus, not due to secondary effects on the internal capsule and the motor fiber in the vicinity of the caudate nucleus. However, the possibility that the current spread to the motor fiber cannot be definitely ruled out.

Adult↗

Vascular dementia.

Vascular dementia is almost always associated with organic brain lesions due to ischemia, not with arteriosclerosis alone. In Japan, more than 50% of dementia in population older than 65 years are of vascular origin. Vascular dementia occurs with diffuse vascular lesions in the cerebral white matter or circumscribed lesions in particular areas such as the thalamus, anterior limb of the internal capsule, and cingulate gyrus, all of which constitute the ascending activating system or the limbic system. Vascular dementia is clinically characterized by stepwise progression, fluctuating course and predominant deterioration of intelligence with relative preservation of personality. Reversibility, disproportionate impairment of intelligence and personality, and dementia caused by a focal lesion observed in vascular dementia pose problems with regard to the classical concept of dementia. The similarity and difference between remitting dementia and disturbance of consciousness remain to be scrutinized.

Adult↗

Thrombotic stroke in a child with diarrhea-associated hemolytic-uremic syndrome with a good recovery.

A boy aged 3.5 years with post-diarrheal hemolytic-uremic syndrome (HUS) was referred to our hospital because of convulsion and stupor. He had been admitted to a regional hospital with a 3-day history of bloody diarrhea, colic abdominal pain and fever. Two days later, he had complained of generalized seizures and oliguria. On admission, he developed anuria, and serum blood nitrogen and creatinine increased to 56 mg/100 ml and 2.8 mg/100 ml, respectively. Platelets decreased to 42,000/microl. Under the diagnosis of HUS, a continuous hemodiafiltration treatment had to be instituted. Computed tomography of his head at hospital day 5 revealed abnormal low density area of infarction with edema in both the basal ganglia involving with the posterior limb of internal capsule. Serum titer of IgM antibody to Escherichia coli O157 showed positive value. Although his anuria and stupor persisted over 10 days, he recovered without serious complications. These clinical observations may indicate that patients with similar lesions do not necessarily have serious morbidity.

Child↗

Regional changes of fractional anisotropy with normal aging using statistical parametric mapping (SPM).

OBJECTIVE: There has been reports on the usefulness of diffusion tensor imaging (DTI) about age-or disease-related degradation. DTI is generally evaluated by the region of interest (ROI) methodology. In this study, we applied a statistical way using Statistical Parametric Mapping (SPM) to assess normal aging by DTI and compared results of these two methods. METHODS: Ten young and ten senior normal volunteers were examined. On SPM, tensor images were changed into normalized tensor images. They were compared between the two groups by t-test. RESULTS: In the senior group, fractional anisotropy (FA) values were higher on the basal ganglia, cingulated gyrus and other cortical gray matter, lower in the corona radiata, internal capsule, centrum semiovale and corpus callosum by using SPM. In the ROI method, the results were almost compatible except in the brain periphery. CONCLUSIONS: Aging changes on water diffusion anisotropy was clearly shown by SPM method which would be useful to evaluate change of water diffusion anisotropy without operator bias even in clinical setting instead of ROI measurement.

Adult↗

Hypertensive brainstem encephalopathy.

A 45-year-old man developed severe arterial hypertension associated with unusual hyperintensity in the brainstem, around the right internal capsule and in the deep white matter around the bilateral anterior horn of the lateral ventricle on T2-weighted and fluid-attenuated inversion-recovery images. The characteristic clinical findings were mild left hepiparesis and altered mental status which corresponded to the lesions of MR imagings. The lesions improved gradually with improvements in hypertension, which suggested that edema could be the principal cause of the unusual hyperintensity on MR images.

Brain Edema↗

[Clinical analysis of 24 cases of caudate hemorrhage].

Twenty-four patients with caudate hemorrhage, in whom such definite organic lesions as arteriovenous malformations or ruptured cerebral aneurysms could not be proved, were analyzed. These cases comprise 2.0% of 1202 cases of hypertensive intracerebral hemorrhage diagnosed by computed tomography and experienced from 1976 through 1987. Thirteen patients were male and 11 were female. Their average age was 61 years. Headache (67%) and nausea and vomiting (50%), which were often the initial symptoms, were similar to those of subarachnoid hemorrhage. The main clinical symptoms were signs of meningeal irritation. Ten patients (42%) had transient disturbance of consciousness, and nine (38%) of these were somnolent; only one patient, who had a massive hematoma, was stuporous. When the hematoma extended to the internal capsule, the patient showed motor disturbance (38%). Two patients (8%) had Horner's sign, five (21%) exhibited diminished activity, and one (4%) suffered anosognosia. The volume of the intracerebral hematoma averaged 4.7 ml and was less than 5 ml in 17 patients (71%). In 20 patients (83%), the hematoma was confined to the head of the caudate nucleus. The hemorrhage tended to rupture into the anterior horn of the lateral ventricle, and in nearly all cases (96%), intraventricular hematoma was observed. Seventeen patients (71%) underwent cerebral angiography. There were no instances of dilation of the recurrent artery of Heubner. Twenty patients (83%) were treated conservatively. Continuous ventricular drainage was employed in four patients (17%), and ventriculoperitoneal shunting in three (13%). However, it was judged retrospectively that continuous ventricular drainage had been necessary in only two cases in which disturbance of consciousness was progressed due to acute hydrocephalus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Paramedian thalamic infarction following blunt head injury--case report.

A 19-year-old male was admitted following a blow to the face. Computed tomographic (CT) scans 1 hour after injury revealed low-density areas in the bilateral thalami and midbrain, which were enhanced postcontrast except for the core 3 hours later. CT scans 2 days after injury revealed that the size of the low-density areas had increased. CT scans and magnetic resonance images 3 weeks after injury disclosed only small infarcted lesions in the bilateral thalami, the right side of the midbrain, and the left internal capsule. These findings suggest that the injury initially caused thrombus on the basilar arterial wall, leading to occlusion of the perforators, but almost all affected perforators were recanalized. Bilateral thalamic infarction resulting from head injury is unusual, as is the transient nature of the infarction in this case.

Adult↗

Clinical application of diffusion-weighted magnetic resonance imaging to intracranial disorders.

Diffusion-weighted magnetic resonance imaging was performed to determine the changes in water diffusion and to investigate the detectability of diffusion anisotropy in patients with intracranial disorders. Diffusion maps of the apparent diffusion coefficient (ADC) were created of 19 patients with cerebral infarction, five with intracerebral hematoma, four with glioma, four with meningioma, four with hydrocephalus, and five with subdural hematoma. ADC was increased in chronic cerebral infarction and glioma, and decreased in acute cerebral infarction, meningioma, and the marginal area of glioma compared with the ADC of the normal gray matter. There was a significant difference in ADC between the marginal and internal areas of glioma. Increased ADC may be due to increased vasogenic edema in infarction and a lack of significant restriction of diffusion within glioma. Decreased ADC can be attributed to restricted diffusion caused by cytotoxic edema in infarction and the underlying histological pattern of densely packed tumor cells in glioma. Diffusion anisotropy of the internal capsule was less detectable in pathological than normal hemispheres. Diffusion anisotropy was less detectable in patients with hydrocephalus and subdural hematoma. Intracranial lesions were thought to have influenced the compression of the brain structures and cells, resulting in decreased diffusion. The measurement of ADC by diffusion-weighted magnetic resonance imaging has the potential for greater understanding of the biophysical changes in various intracranial disorders, including correct diagnosis of cerebral infraction, and histological diagnosis of brain tumor.

Adolescent↗

Radiation-induced diffuse brain injury in the neonatal rat model--radiation-induced apoptosis of oligodendrocytes.

The mechanism of radiation-induced diffuse brain injury was investigated using a model of delayed myelination in the irradiated neonatal rat brain in which the number of oligodendrocytes decreases without associated necrosis of the cerebral white matter. Immunohistochemical analysis using antibody against the large myelin-associated glycoprotein, a specific marker of oligodendrocytes at an early stage of development, showed that the number of the oligodendrocytes associated with myelination decreased in the irradiated hemisphere 1 day after irradiation and remained low until 5 days after irradiation. In situ terminal deoxynucleotidyl transferase-mediated nick end-labeling assay revealed that apoptosis mainly occurred in the cerebral white matter of the irradiated hemisphere. Three hours after irradiation, apoptotic cells were found in the subcortical white matter and the periventricular white matter. Six hours after irradiation, apoptotic cells were found in the internal capsule, and the numbers of apoptotic cells in the periventricular white matter and subcortical white matter increased. One day after irradiation, the number of apoptotic cells in the periventricular white matter decreased. Three days after irradiation, apoptotic cells were not observed in the cerebral white matter. These results suggest that the oligodendrocytes associated with myelination may be damaged via radiation-induced apoptosis, and depletion of the oligodendrocytes may cause delay of myelination.

Animals↗

MRI of brain iron.

A prominently decreased signal intensity in the globus pallidum, reticular substantia nigra, red nucleus, and dentate nucleus was routinely noted in 150 consecutive individuals on T2-weighted images (SE 2000/100) using a high field strength (1.5 T)MR system. This MR finding correlated closely with the decreased estimated T2 relaxation times and the sites of preferential accumulation of ferric iron using the Perls staining method on normal postmortem brains. The decreased signal intensity on T2-weighted images thus provides an accurate in vivo map of the normal distribution of brain iron. Perls stain and MR studies in normal brain also confirm an intermediate level of iron distribution in the striatum, and still lower levels in the cerebral gray and white matter. In the white matter, iron concentration is (a) absent in the most posterior portion of the internal capsule and optic radiations, (b) higher in the frontal than occipital regions, and (c) prominent in the subcortical "U" fibers, particularly in the temporal lobe. There is no iron in the brain at birth; it increases progressively with aging. Knowledge of the distribution of brain iron should assist in elucidating normal anatomic structures and in understanding neurodegenerative, demyelinating, and cerebrovascular disorders.

Adolescent↗

Radiation effects on cerebral white matter: MR evaluation.

The purpose of this study was to evaluate the white-matter changes associated with cranial radiation by MR imaging. The MR scans of 95 patients receiving conventional external beam radiation for a wide variety of central nervous system tumors were reviewed. Moderately T2-weighted spin-echo images with a 2000-msec repetition time and 56-msec-echo time were analyzed for white-matter abnormalities without knowledge of the patient's history. These were correlated with radiation dose, port, and time interval since completion of therapy, and then compared with an age-matched control group of 180 patients with nonirradiated, space-occupying, intracranial lesions. Radiation-related lesions were characterized as symmetric, high-signal foci in the periventricular white matter. Relative sparing of the posterior fossa, basal ganglia, and internal capsules was noted. In patients older than 20 years, these changes paralleled those seen in ischemia but were more prevalent (p less than .005). In 25 patients with sequential MR scans, these findings remained stable. In those patients with limited treatment fields, for example, pituitary adenomas, no statistical differences were seen between radiation-treated and nontreated groups. Cerebral white-matter changes that mimic deep white-matter infarction are frequently seen in response to therapeutic radiation. There is a variable incidence of radiation effects, becoming more marked in older patients. MR interpretation must consider the neuropathologic consequences of therapeutic radiation, which include demyelination, microvascular occlusion, and blood-brain barrier breakdown.

Adult↗