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A coronal image taken along a straight line between the front edge of the medulla and the deepest point of the interpeduncular cistern clearly displayed wallerian degeneration of the segment of the pyramidal tract between the internal capsule and the pons, the medulla, or the decussation. This visualization was verified in 21 patients with moderate or severe hemiparesis following a stroke episode.
PURPOSE: The purpose was to obtain normal values of the apparent diffusion coefficient (ADC) in the infant brain and to compare ADC maps with T1- and T2-weighted images. METHOD: Diffusion was measured in nine infants with an ECG-gated SE sequence compensated for first-order motion. One axial slice at the basal ganglia level was investigated with the diffusion-encoding gradients in the slice-selection direction. RESULTS: On ADC maps, the corpus callosum and the optic radiations appeared dark before the onset of myelination, and the crus posterior of the internal capsule could be visualized before it appeared on T1- or T2-weighted images. In gray and white matter, the mean ADC ranged from 0.95 x 10(-9) to 1.76 x 10(-9) m2/s. In the frontal and occipital white matter, in the genu corporis callosi, and in the lentiform nucleus, the ADC decreased with increasing age. The cortex/white matter ratio of the ADC increased with age and approached 1 at the age of 30 weeks. CONCLUSION: ADC maps add information to the T1 and T2 images about the size and course of unmyelinated as well as myelinated tracts in the immature brain.
PURPOSE: This study was designed to examine the use of quantitative magnetization transfer imaging (MTI) in naturally occurring globoid cell leukodystrophy (GLD) in the Cairn terrier. METHOD: A model of GLD was established via a breeding colony, and a total of seven animals were studied with MTI, including two dogs with GLD, one of which underwent whole-body irradiation (725 cGy) and bone marrow transplantation from a genotypically normal littermate. The remaining dogs served as untreated, irradiated, and unirradiated controls. RESULTS: Region-of-interest (ROI) analysis of the MTI showed a decrease in MT ratio (MTR) in the internal capsule of the untreated/affected dog compared with age-matched controls but revealed similar results in the two other study animals. On MT contour plotting, inside-to-out gradients of MTR mimicked the demyelination pathology of the disease in the untreated/affected dog. CONCLUSION: MT contour plotting demonstrated patterns of MT abnormality in the untreated/affected dog that were consistent with histopathology, establishing a clear relationship between pathology-proven demyelination and MTR as well as a striking contrast to the patterns of radiation damage.
PURPOSE: As MR scanner hardware has improved, allowing for increased gradient strengths, we are able to generate higher b values for diffusion-weighted (DW) imaging. Our purpose was to evaluate the appearance of the normal brain on DW MR images as the diffusion gradient strength ("b value") is increased from 1,000 to 3,000 s/mm2. METHOD: Three sets of echo planar images were acquired at 1.5 T in 25 normal subjects (mean age 61 years) using progressively increasing strengths of a diffusion-sensitizing gradient (corresponding to b values of 0, 1,000, and 3,000 s/mm2). All other imaging parameters remained constant. Qualitative assessments of trace images were performed by two neuroradiologists, supplemented by quantitative measures of MR signal and noise in eight different anatomic regions. RESULTS: As gradient strength increased from b = 1,000 to 3,000, both gray and white matter structures diminished in signal as expected based on their relative diffusion coefficients [calculated average apparent diffusion coefficient (ADC) values: gray matter = 8.5 x 10(-4) mm2/s, white matter = 7.5 x 10(-4) mm2/s]. The signal-to-noise ratios for the b = 1,000 images were approximately 2.2 times higher than for the b = 3,000 images (p < 0.0001). As the strength of the diffusion-sensitizing gradient increased, white matter became progressively hyperintense to gray matter. Relative to the thalamus, for example, the average MR signal intensity of white matter structures increased by an average of 27.5%, with the densely packed white matter tracts (e.g., middle cerebellar peduncle, tegmentum, and internal capsule) increasing the most. CONCLUSION: Brain DW images obtained at b = 3,000 appear significantly different from those obtained at b = 1,000, reflecting expected loss of signal from all areas of brain in proportion to their ADC values. Consequently, when all other imaging parameters are held constant, b = 3,000 DW images appear significantly noisier than b = 1,000 images, and white matter tracts are significantly more hyperintense than gray matter structures.
We present conventional magnetic resonance (MR) imaging with diffusion-weighted and diffusion-tensor imaging findings in a 10-day-old neonate with maple syrup urine disease (MSUD). On conventional MR imaging, signal abnormalities were noted in the affected white matter of cerebellum, dorsal brainstem, thalami, posterior limbs of internal capsules, and the corona radiata. These regions showed marked hyperintensity on diffusion-weighted images with decreased apparent diffusion coefficient values (average 68% reduction). Diffusion-tensor imaging showed decreased anisotropy (average 57% reduction) in the corresponding areas. Both diffusion-weighted and diffusion-tensor imaging are valuable in the diagnosis and understanding of the pathogenesis of MSUD, with findings that suggest cytotoxic edema and damaged oligodendro-axonal units within the affected white matter.
The concept of the presence of mucopolysaccharides forming an interstitial ground substance in central nervous tissues is revived. The biochemical reports of both neutral and acid mucopolysaccharides in both gray and white matter of the normal brain are reviewed. The earlier histochemical reports and the histochemical studies in this laboratory are appraised and are thought to demonstrate the presence of neutral mucopolysaccharides in both gray and white matter, more evident in the former. These mucopolysaccharides are thought somewhat greater in the arcuate white matter than in the deeper white matter and greater in the striae of white matter coursing through the corpus striatum than in the internal capsule. The presence of acid mucopolysaccharides in normal brain substance is not clearly demonstrated histochemically, though they have been noted in some oligodendrogliomas and in rare well differentiated astrocytomas. The possibility is suggested that acid mucopolysaccharides are present, as the biochemical studies indicate, but that their acid groups are normally blocked or otherwise rendered non-reactive, preventing their histochemical disclosure in normal tissues but serving as a source of those seen in pathologic conditions. The concept of a ground substance has important implications for the understanding of the distribution of excellular fluid in brain tissues in both the normal state and in edema.
Decreased density of neurons was found throughout the head of the caudate nucleus in Huntington's disease (HD), with the most severe neuronal loss early in the disease in the medial region. The density of reactive astrocytes is inversely proportional to the neuronal loss. In cases of mild Huntington's disease which had no identifiable abnormality on conventional neuropathologic evaluation (grade 0), there is a reduction in neuron density without an accompanying reactive astrocytosis. The pattern for decrease in neurons and accompanying astrocytosis suggests that the earliest changes occur in the most medial portion of the head of the caudate nucleus and subsequently sweep laterally across the caudate nucleus to the internal capsule. An increased density of oligodendrocytes is observed in the head of the caudate nucleus for the lower grades (0, 1 and 2). The decreased neuronal and increased oligodendroglial densities may be of significance in understanding the pathogenesis of HD. These altered densities, observed in the absence of reactive astrocytosis, suggest that these changes may not represent recent effects of disease, but rather that HD gene expression may influence brain cell densities from early in the life of the gene carrier.
Brains of 19 AIDS patients with HIV encephalitis were examined by immunohistochemistry and in situ hybridization using antisense HIV DNA and RNA probes. Double immunohistochemical labeling, using antibodies against viral and cell-type specific antigens, was utilized to study lesions in some brains. Other combined studies included use of in situ hybridization and immunohistochemical labeling of the same section, using antibodies against either viral or cell-type specific antigens. Hybridization signals were abundant and were concentrated mainly in the white matter. Heavy labeling was found in the subcortical white matter, the corpus callosum, the internal capsule, and white matter regions of the brainstem and cerebellum. Deeper cortical layers often contained cells with hybridized probe when the subcortical white matter was intensely labeled. HIV nucleic acid sequences were found almost exclusively in macrophages. Counts showed that 16-25% of macrophages contained viral antigens and exhibited hybridized HIV probe. Almost all of these macrophages contained proviral DNA, viral RNA and viral proteins; i.e. they were actively replicating HIV. We also examined brains from three AIDS cases without clinical or pathological evidence of HIV encephalitis; no HIV sequences or immunoreactive proteins were detected.
We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n = 6) or high (8 psi, n = 6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p < 0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI-32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.
C6 tumor cells (10(6] were grafted as suspensions into freshly made implantation pockets in rat host cerebral cortex. Specimens were prepared for transmission and scanning electron microscopy 1 to 7 days postimplantation (DPI). By 3 DPI vacuolated C6 cells had migrated on or invaded the host brain. C6 cells were observed on the glia limitans on the surface of the brain, in the corpus callosum, subependymal space, and perivascular space and had invaded the cortex under the implantation pocket. In addition to the tumor mass that was observed under the implantation pocket, by 7 DPI individual C6 cells had migrated into the corpus callosum and internal capsule. Migrated C6 cells were observed in a perineuronal position in the hippocampus and other gray matter structures inferior to the corpus callosum. Micropockets were found around each C6 cell and the processes of these cells had replaced host parenchyma. The preferred routes of migration were on basal lamina and parallel and intersecting nerve fiber bundles. Invasion occurred through gray and white matter. The movement of homografted C6 cells in the brain suggests that these cells actively migrate as individual cells in addition to invading as a mass.
Changes in blood-brain (BBB) permeability and local cerebral blood flow after intracarotid administration of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) were examined quantitatively in rats with double-tracer autoradiography using [14C]alpha-amino-isobutyric acid and [18F]fluoroantipyrine. Forty-eight female Wistar rats were divided into four groups. The control group (Group 1) received 1 ml of 5% dextrose. The other three groups received three different doses of BCNU dissolved in 5% dextrose: Group II rats received 1 mg, Group III 3 mg, and Group IV 10 mg. The tracer study was performed on Day 1 or Days 4 to 12 after intracarotid administration of BCNU. In 11 rats in Group II, there were no changes of BBB permeability. Transient BBB permeability changes were seen in the striatum or hippocampus in 3 of the 5 rats (60%) in Group III within 24 hours. In 8 of 9 rats (89%) in the same group, late BBB permeability changes were observed in the hypothalamus with or without histological changes. BBB permeability changes were seen in all rats of Group IV. Focal increase of local cerebral blood flow on the infused side compared with the non-infused side of the brain was observed, although not at a significant level, in 5 of 25 rats examined with [18F]fluoroantipyrine. The results of BBB permeability and histological examinations and study of heterogenous distribution by [18F]fluorodeoxyglucose indicated that the ipsilateral subcortical structures such as the hypothalamus, amygdala, internal capsule, and caudate putamen have the highest incidence of neurotoxicity, which are closely related to histopathological damage seen in human BCNU leucoencephalopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Although the application of stereotactic radiosurgery for the management of functional brain disorders began in 1951, almost 50 years elapsed before it received appropriate attention. Radiosurgical techniques are used to create image-guided, physiological inactivity or focally destructive brain lesions without neurophysiological guidance. The lack of neurophysiological guidance remains the greatest argument against the use of radiosurgery for selected disorders. Current anatomic targets include the trigeminal nerve (for trigeminal neuralgia), the thalamus (for tremor or pain), the cingulate gyrus or anterior internal capsule (for pain or psychiatric illness), the globus pallidus (for symptoms of Parkinson's disease), and the hippocampus (for epilepsy). The use of radiosurgery as a "lesion generator" is based on extensive animal studies that defined the dose, volume, and temporal response of the irradiated tissue. The usefulness of radiosurgery has been compared with that of microsurgical, percutaneous, and electrode-based techniques used for functional neurological disorders. At present, the long-term results after functional radiosurgery procedures remain to be documented. The current indications and expected outcomes after radiosurgery are discussed.
OBJECTIVE AND IMPORTANCE: We describe two patients with symptomatic septum pellucidum cysts managed by endoscopic fenestration. In each case, tissue from the cyst wall was studied to define the origin of the cyst wall and fluid. CLINICAL PRESENTATION: The patients, a 6-year-old boy and a 42-year-old man, each presented with headaches and a syncopal episode. Imaging studies demonstrated large septum pellucidum cysts with obstruction of the foramina of Monro. INTERVENTION: The patients underwent endoscopic transventricular cyst fenestration with a 4-mm steerable fiberscope. The fenestrations were created to allow communication with the right and left lateral ventricles. In one patient, adhesions between the cyst wall and the foramen of Monro were lysed with endoscopic monopolar cautery. Tissue from the cyst walls was removed for examination by electron microscopy. Postoperatively, the headaches and syncopal episodes resolved in both patients. CONCLUSION: Endoscopic fenestration of symptomatic septum pellucidum cysts produces immediate relief of the mass effect of the cyst and resolution of associated symptoms. Cannulation of the lateral ventricle before cyst fenestration prevents inadvertent injury to the fornices, thalamus, internal capsule, caudate nucleus, and septal and thalamostriate veins. The endoscopic approach allows the surgeon to ensure communication within the ventricular system, thus avoiding placement of a shunt. Preliminary ultrastructural analysis indicates that the cyst walls derive from the septum pellucidum rather than the choroid plexus or arachnoid. The cellular machinery necessary for fluid secretion was identified in some specimens.
OBJECTIVE AND IMPORTANCE: Central nervous system lymphomas exhibit angiotropic characteristics. Nevertheless, direct association with an intracranial aneurysm is very rarely reported. We present a case of a giant aneurysm infiltrated with a large cell non-Hodgkin's lymphoma. The incidence of primary central nervous system lymphoma is increasing, and similar cases may become more frequent in the future. CLINICAL PRESENTATION: A 65-year-old man had presented with a giant anterior cerebral artery aneurysm, new onset of seizures, aphasia, and hemiparesis. The aneurysm was treated with Guglielmi detachable coils. Six months later, the patient exhibited fever and neurological deterioration. Magnetic resonance images suggested an enhancing lesion posterior to the neck of the aneurysm. Antibiotic treatment given elsewhere was unsuccessful. INTERVENTION: A craniotomy for a suspected abscess was performed, with removal of the aneurysm and clipping of the neck. The aneurysm sac appeared to be filled with thrombus and pus. The results of aerobic, anaerobic, and fungal cultures were negative. Postoperative magnetic resonance images demonstrated a residual mass, posterior to the aneurysm within the striatum and the internal capsule. Histological examination of the aneurysm wall revealed a large B-cell lymphoma. The diagnosis was confirmed by a stereotactic biopsy. Radiation therapy resulted in a transient decrease in the size of the lesion. CONCLUSION: Although the tumor was not apparent on the initial imaging studies, it may have been the cause of the patient's presenting symptoms. Infiltration of the aneurysm wall by the lymphoma also raises the possibility of a causal relationship. As the incidence of primary central nervous system lymphoma is reported to be on the increase, awareness this uncommon association of an aneurysm and malignant lymphoma is of value.
It is possible to reconstruct a breast mound of almost any size by utilizing tissue expansion. In order to produce a pendulous breast which is also ptotic, the tissue-expansion technique has been combined with two other procedures. A new technique is being introduced. It is that of elevating the lower third of the mature breast capsule surrounding the tissue expander at the time the permanent prosthesis is to be exchanged for the expander. The established techniques of inframammary fold reconstruction of Pennisi and Ryan are used to provide pedicle skin coverage for the undersurface of the breast and the bed of the elevated capsule. Internal and external surgical approaches are described, and two examples of each are illustrated. Breasts reconstructed in this manner have remained pendulous structures. Some loss of the initial degree of ptosis has been noted in some cases.
PURPOSE: A 28-year-old hypertensive professional football player suffered a lacunar stroke. Given the rarity of stroke at this young age, the contributory roles of hypertension and competitive athletics merit consideration. CASE SUMMARY: A 28-year-old defensive lineman, with long-standing, albeit recently well-controlled hypertension, experienced slurred speech and veering to his right after a game. Computerized tomography revealed a small internal capsule infarct. Diagnostic investigation, including coagulation profiling, sickle screen, antiphospholipid antibody, carotid imaging, and echocardiography did not reveal a cause. The patient recovered within days with no residual impairment. DISCUSSION: Despite the extreme blood pressure elevation associated with isometric straining in young athletes, stroke almost never occurs. Vascular changes resulting from chronic hypertension and/or marked volume depletion, and hemoconcentration resulting from restricted salt intake, diuretic use, and heavy sweating, offer the only explanations for this stroke. RELEVANCE: The case suggests physicians should exercise caution in using diuretics and salt-restricted diets to treat hypertensive athletes. Guidelines for treatment are discussed.
Ischemia/reperfusion injury to the developing brain is a major cause of neurologic abnormalities in preterm infants. To investigate the underlying mechanisms, we modified a previously described rat model of unilateral uterine-artery ligation on the 17th embryonic day (E17). Growth retardation was taken as an index of in utero ischemia, and pups born with a birth weight more than 2 standard deviations below that of controls were compared with the same-litter, normal-growth control pups born from the nonligated horn. Prenatal ischemia probably associated with hypoxia and followed by reperfusion at birth induced white matter damage at a developmental stage corresponding to extreme prematurity in humans. On P0 (day of birth), growth-retarded pups exhibited lesions in the cingular white matter and internal capsule with increased counts of activated microglial cells for 2 weeks compared with controls. Astrogliosis was detected in the injured white matter. On P3, increased apoptotic cell death was seen in O4-positive preoligodendrocytes, which were abnormally scarce on P7. Defective myelination, as assessed by myelin-binding-protein labeling, was detected until adulthood. The diffuse white matter damage in growth-retarded rats replicated the main features of white matter damage in human preterm infants.
We present two pediatric cases demonstrating that diffusion tensor imaging is more efficient at revealing microstructural abnormalities of the brain than conventional magnetic resonance imaging because it enables measurements of the directionality and integrity of white matter fiber tracts. One patient suffered from left hemiparesis, and the other had right hemiparesis. However, whereas conventional magnetic resonance imaging showed only the findings of traumatic contusional hemorrhages in the left temporal and parietal lobes of the first patient and focal encephalomalacia in the left anterior thalamus of the second patient, diffusion tensor imaging successfully disclosed microstructural abnormalities in the right cerebral peduncle of the midbrain of the first patient and in the posterior limb of the left internal capsule of the second. Theses two cases demonstrate that diffusion tensor imaging is more capable than magnetic resonance imaging at detecting the microstructural pathologic lesions that are responsible for clinical motor weakness, especially when conventional magnetic resonance imaging has failed to detect subtle structural abnormalities.