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PubMed1978

The quest for an image of brain: a brief historical and technical review of brain imaging techniques.

Each of the brain imaging techniques in common clinical use (skull radiography, midline ultrasonography, isotope scan, pneumoencephalography, angiography and computerized tomography) depicts some structural or functional characteristic of the brain. Each produces a correspondingly restricted concept of the status of the brain. Computerized tomography, which defines the radiodensity of head tissues, has a fundamental advantage over the other techniques in that it defines with quite good resolution a characteristic of brain tissue itself (radiodensity), rather than visualizing some anatomic compartment other than brain parenchyma. It provides an explicit image of the brain quite analogous to gross sections of the brain seen at autopsy. Computerized tomography has already substantially reshaped the practice of neurology wherever it has become available and probably will come to play a role as pivotal in clinical neurology as does bone radiography in orthopedics.

Brain↗
PubMed1988

Dynamic axial brain stem distortion as a mechanism in the production of brain stem hemorrhages: role of the carotid arteries.

Dynamic axial distortion of the brain stem has long been recognized as occurring in the presence of supratentorial mass lesions. Although brain stem hemorrhages occur under these circumstances, the pathophysiology of these hemorrhages is still a matter of controversy. In the present study, the role of the carotid arteries in tethering the brain stem was evaluated during dynamic axial distortion of the neuraxis of the dog. Brain stem hemorrhages occurred in 32 of 48 dogs in which the carotid arteries were left intact (67%) and in only 9 of 46 animals in which the carotid arteries were sectioned (20%). The difference between the two groups is statistically significant (chi 2 = 19.3; P less than 0.001). In this study, we can eliminate intracranial pressure as the primary cause of the lesions because a single variable is present in one series and absent in the other, whereas intracranial pressure and its duration are kept constant. It is concluded that the tethering effect of the carotid arteries is a significant factor in the production of brain stem hemorrhages in the dog by dynamic axial distortion of the brain stem. A selective review of the literature on production of brain stem lesions is provided to support these findings.

Animals↗
PubMed2001

Brain hypothermia relieves severe brain swelling following acute major cerebral artery occlusion.

Seven patients were treated with brain hypothermia following acute major cerebral artery occlusion to utilize the suppressive effect against brain swelling. Five patients had internal carotid and two had proximal middle cerebral artery occlusion. Except for the first two cases, hypothermia was introduced early and the temperature reached 35.0 degrees C within 6 hours after the onset. The core temperature finally stabilized between 32 degrees C to 34 degrees C. Hypothermia had a suppressive effect against brain swelling and the temperature showed a significant correlation to intracranial pressure. Recurrence of brain swelling was observed during the rewarming process, but two patients became independent and three patients were moderately disabled in wheelchairs. Only two patients died. Brain hypothermia is an effective treatment for acute major cerebral artery occlusion through the relief of brain swelling. The overall outcome may be improved by combining brain hypothermia with other conventional therapies such as osmotherapy and external decompression implemented with an extended period of rewarming.

Acute Disease↗
PubMed2003

[Expression of brain-derived neurotrophic factor at acute inflammatory injury of the brain].

OBJECTIVE: To investigate the expression of brain-derived neurotrophic factor (BDNF) mRNA and immunoreactivity in experimental acute inflammatory brain injury. METHODS: Ten rats were inoculated with pneumococcus to establish the model of bacterial inflammatory brain injury and other 6 rats were used as normal controls. At 24 h after inoculating, the expression of BDNF mRNA and BDNF protein in brain tissue was detected by in situ hybridization and immunohistochemical methods, respectively. RESULT: The necrosis of neuron in cerebral cortex and hippocampus was observed after infection. The increase of BDNF mRNA expression in the cerebral cortex and hippocampus of experimental animals was demonstrated at 24 h after inoculation: (0.1194 +/- 0.02941 compared with 0.0662 +/- 0.01176)A and (0.1608 +/-0.01854 compared with 0.0680 +/- 0.00946)A (P<0.01), respectively. Compared with controls the expression of BDNF protein in the cerebral cortex and hippocampus was enhanced at 24 h of inoculation:(177.04+/-43.66 compared with 79.79+/-7.23)mm(2) (P<0.01) and (81.78 +/-37.47 compared with 42.98 +/-20.44)mm(2) (P<0.01), respectively. Strong positive hybridization and immunoreactivity were observed in the infiltrated inflammatory cell in leptomeninges, subarachnoid cavity, ventricles and brain parenchyma in the brain from the experimental rats. CONCLUSION: The expression of BDNF mRNA and BDNF protein increases following brain inflammatory injury, which supports the hypothesis that BDNF may constitute intrinsic neuroprotective mechanism as a part of the inflammatory response.

Acute Disease↗
PubMed2001

Decrease in Ca2+-ATPase activity in the brain plasma membrane of rats with increasing age: involvement of brain calcium accumulation.

The alteration in Ca(2+)-ATPase activity in the brain plasma membrane of rats with increasing age was investigated. Calcium content in the brain tissues was significantly raised in aged rats (50 weeks old) as compared with that of young rats (5 weeks old). Increasing age caused a significant decrease in Ca(2+)-ATPase activity in the brain plasma membranes. The presence of N-ethylmaleimide (2.5 or 5 mM), a modifying reagent of thiol (SH)-groups, in the reaction mixture caused a significant decrease in the brain plasma membrane Ca(2+)-ATPase activity of young and aged rats, while dithiothreitol (2.5 or 5 mM), a protecting reagent of SH-groups, produced a significant increase in the enzyme activity, indicating that the SH-group is an active site of Ca(2+)-ATPase. The active site of Ca(2+)-ATPase may not be impaired by ageing. The brain plasma membrane Ca(2+)-ATPase activity of young rats was significantly reduced in the presence of dibutyryl cyclic AMP (10(-7)-10(-5) M) or inositol 1, 4, 5-trisphosphate (10(-7)-10(-5) M) in the reaction mixture. Such an decrease was not seen in aged rats. The responsibility for signaling factors seemed to be weakened by ageing. Calmodulin (2.5 and 5 microg/ml) or regucalcin (10(-8) and 10(-7) M), a Ca(2+)-regulating protein, did not have an effect on Ca(2+)-ATPase activity. This study demonstrates that ageing induces a decrease in Ca(2+)-ATPase activity in the brain plasma membranes. This finding suggests a cellular mechanism by which ageing causes calcium accumulation in brain.

Aging↗
PubMed1978

Identification of endogenous gamma-hydroxybutyrate in human and bovine brain and its regional distribution in human, guinea pig and rhesus monkey brain.

Gamma-Hydroxybutyric acid (GHB), a compound that has interesting neuropharmacological actions when administered systemically, was shown by means of gas chromatography-mass spectrometry to be present in postmortem samples of human brain in concentrations ranging from 2 to 20 nmol/g. Tissue samples from the basal ganglia contained 2 to 3 times as much GHB as tissue samples from cortical regions. The regional brain distribution of GHB was examined in the guinea pig and rhesus monkey and found to parallel the distribution observed in human brain. The levels of GHB found in the regional areas of human and monkey brain investigated were higher than the levels found in similar regions of guinea-pig brain. Additional studies demonstrated that there is a slow postmortem increase (about 2-fold) in the endogenous levels of GHB in bovine caudate and guinea-pig brain which is maximal about 6 hr postmortem. This postmortem increase could in part explain the higher levels of GHB found in human brain. However, postmortem changes could not account for the large differences observed in the levels of GHB found in bovine caudate and those found in guinea-pig, monkey and human caudate. Only traces of GHB could be detected in human blood and cerebrospinal fluid.

Animals↗
PubMed2005

Cultured human embryonic neocortical cells survive and grow in infarcted cavities of adult rat brains and interconnect with host brain.

BACKGROUND: There are no reports on exnografting cultured human fetal neocortical cells in this infracted cavities of adult rat brains. This study was undertaken to observe whether cultured human cortical neurons and astrocytes can survive and grow in the infarcted cavities of adult rat brains and whether they interconnect with host brains. METHODS: The right middle cerebral artery was ligated distal to the striatal branches in 16 adult stroke-prone renovascular hypertensive rats. One week later, cultured cells from human embryonic cerebral cortexes were stereotaxically transferred to the infarcted cavity of 11 rats. The other 5 rats receiving sham transplants served as controls. For immunosuppression, all transplanted rats received intraperitoneal injection of cyclosporine A daily starting on the day of grafting. Immunohistochemistry for glial fibrillary acidic protein (GFAP), synaptophysin, neurofilament, and microtubule associated protein-2 (MAP-2) was performed on brain sections perfused in situ 8 weeks after transplantation. RESULTS: Grafts in the infarcted cavities of 6 of 10 surviving rats consisted of bands of neurons with an immature appearance, bundles of fibers, and GFAP-immunopositive astrocytes, which were unevenly distributed. The grafts were rich in synaptophysin, neurofilament, and MAP2-positive neurons with long processes. The graft/host border was diffuse with dendrites apparently bridging over to the host brain, into which neurofilament immunopositive fibers protruded. CONCLUSION: Cultured human fetal brain cells can survive and grow in the infarcted cavities of immunodepressed rats and integrate with the host brain.

Animals↗
PubMed1990

[The distribution of toluene in the brain and its effects on the brain catecholamines in acute toluene poisoning].

The regional distribution of toluene in the brain and its effects on the brain catecholamine levels in rats is reported. Separate sets of rats were exposed to the toluene via inhalation, at 1,500 ppm and at 10,000 ppm respectively, and via an ingestion (400 mg/kg). Given these three exposure conditions, the values of brain/blood toluene ratios were found to be the highest in the brain stem areas (2.85-3.22) such as the pons and medulla oblongata, in the middle range in the midbrain, the thalamus, the caudate-putamen, the hypothalamus and the cerebellum (1.77-2.12), and in the lowest ranges in the olfactory bulb, the hippocampus and the cerebral cortex (1.22-1.64). The values of the partition coefficient of toluene in the brain regions and in the blood of rats examined in vitro were also the highest in the brain stem and the lowest in the cerebral cortex. The highest values of brain/blood toluene and partition coefficients of toluene in the brain regions and blood were obtained in the lipid-rich regions. These results suggest that toluene, which has a high lipid solubility and no protein binding capability, distributes according to lipid contents of the brain. The inhalation of toluene (1,500 ppm and 10,000 ppm) caused decreases in the noradrenaline (NA) levels in the dorsal part of rat pons, rich in locus coeruleus, and in the dopamine (DA) levels in the hypothalamus and ventral part of the rat midbrain, rich in substantia nigra.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1983

Identification of tissue kallikrein in brain and in the cell-free translation product encoded by brain mRNA.

A monoclonal antibody against purified rat urinary kallikrein was coupled to agarose and used to isolate kallikrein from rat brain. The purified enzyme has N alpha-tosyl-L-arginine methyl esterase activity with a pH optimum at 9.0, kinin-releasing activity from a purified low molecular weight kininogen, and a parallelism with standard curves of rat urinary kallikrein in a direct radioimmunoassay. Brain kallikrein is inhibited by a series of tissue kallikrein inhibitors with IC50 values similar to those for urinary kallikrein. The purified brain enzyme was labeled with [14C]diisopropylphosphorofluoridate and visualized by fluorography on a sodium dodecyl sulfate-polyacrylamide gel. Electrophoretic mobility of the enzyme was closely similar to that of urinary kallikrein with estimated Mr of approximately 38,000. With Western blot analyses using a rabbit anti-kallikrein antibody, both brain and urinary kallikrein were visualized at identical positions by immunoperoxidase staining and by autoradiography with 125I-protein A binding. Brain mRNA was used to direct cell-free protein synthesis in wheat germ and rabbit reticulocyte lysate systems. [35S]Methionine-labeled kallikrein was identified by fluorography of sodium dodecyl sulfate-polyacrylamide gels after the translation products were subject to immunoprecipitation with affinity-purified kallikrein antibody. Collectively, the data show that tissue kallikrein exists in brain and can be synthesized by brain mRNA.

Animals↗
PubMed1980

Analysis of brain weight. II. Adult brain weight in relation to body height, weight, and surface area.

Analysis of 1,261 adult subjects, ages 25 to 80 years, showed that there is a positive relationship between the brain weight and the body dimensions. The brain weight, however, increases at a slower rate than the body dimensions. There is indication that only a small portion of the brain varies with variation in the body dimensions. Among parameters, the brain weight correlates best with the body surface area, followed by the body height and body weight. The brain weight is related to the body weight partly because it increases with increasing height. When adjusted to body dimensions, the brain weight is greater for white men than for black men and for white women than for black men. Our study also shows that the loss of brain mass proceeds at a slightly faster rate than loss of body mass.

Adult↗
PubMed1995

Brain temperature before and after brain death.

Although there has been renewed interest in human brain temperature, very little information is available on the association between brain temperature and cerebral perfusion pressure. In this study, we measured brain, tympanic, and rectal temperatures, arterial blood pressure and intracranial pressure in a case of massive hemorrhage deteriorating to brain death, and showed for the first time that when cerebral perfusion pressure began to decrease markedly brain temperature fell rapidly. Rectal and tympanic temperatures were higher than brain temperatures during the period of very low cerebral perfusion pressure. Circadian change in temperature (high at day, low at night) was preserved during the period of brain death.

Body Temperature Regulation↗
PubMed1996

Evaluation of brain perfusion with high resolution single photon emission tomography in the diagnosis of brain death.

Nuclear Medicine studies performed with tomographic acquisition and tracers such as Technetium-99m hexamethyl-propyleneamine oxime (99mTc-HMPAO) are able to assess cerebral blood flow. A case is reported of a patient with a large intracranial tumor, of possible pituitary origin, with a clinical and electroencephalographic suspicion of brain death. The patient had endocrinous-metabolic impairments for a history of impotence, since 18 months, and diabetes insipidus with a urine output of 350 ml/hr in the first 24 hours from the clinical suspicion of brain death. Due to the endocrinous-metabolic impairments, according to Italian law, it was necessary to confirm the diagnosis of brain death by performing a study able to assess cerebral blood flow. A single Photon Emission Tomography (SPET) scan was performed after the intravenous administration of 99mTc-HMPAO using a high resolution, brain dedicated device. No tracer uptake was evident in cerebral, cerebellar and brain stem structures. The cerebral blood flow study by SPET confirmed the diagnosis of brain death and made the organ transplant possible in a short period of time. High resolution SPET studies are useful to confirm the diagnosis of brain death when there are factors that can influence clinical and electroencephalographic signs, reducing time to authorise the organ explant.

Adult↗
PubMed1997

Differential muscarinic receptor binding of acetylcholinesterase inhibitors in rat brain, human brain and Chinese hamster ovary cells expressing human receptors.

Displacement of muscarinic radioligands by the cholinesterase inhibitors parathion, paraoxon, physostigmine and phenyl saligenin cyclic phosphate was examined in rat cortex and brain stem, human cortex and brain stem, and in Chinese hamster ovary (CHO) cells expressing human M2 or M4 muscarinic acetylcholine receptors. None of the cholinesterase inhibitors tested significantly affected binding of the antagonist [3H]quinuclinidyl benzilate. However, the agonist [3H]oxotremorine-methiodide (3H]oxo-M) was displaced by all compounds tested in a differential manner. Parathion only marginally displaced [H]oxo-M binding with pKi values < 5 in all tissue or cell types. In rat brain paraoxon, physostigmine and phenyl saligenin cyclic phosphate displaced [3H]oxo-M with pKi values of 7.5, 7.0 and 6.1, respectively. The cholinesterase inhibitors displaced [3H]oxo-M in human brain at 15- to 250-fold higher concentrations, that is with pKi values of 6.3, 4.6 and 4.2, respectively. Maximal displacement of [3H]oxo-M varied between 25% and 95%, depending on the species and the compound. Human receptors in brain and in CHO cells were equally sensitive to displacement of [3H]oxo-M by parathion, physostigmine and phenyl saligenin cyclic phosphate. However, paraoxon displaced [3H]oxo-M at > or = 35-fold lower concentrations from human receptors in brain than in CHO cells. In conclusion, the data show that cholinesterase inhibitors interfere with agonist binding to muscarinic acetylcholine receptors. The species-selectivity of the displacement appears to result from differences between rat and human muscarinic acetylcholine receptors. In addition, for paraoxon marked differences exist between the sensitivity of human muscarinic acetylcholine receptors in brain tissue and of those expressed in clonal CHO cells.

Adult↗
PubMed1998

Assessment of anandamide interaction with the cannabinoid brain receptor: SR 141716A antagonism studies in mice and autoradiographic analysis of receptor binding in rat brain.

Anandamide is the newly discovered endogenous cannabinoid ligand that binds to brain cannabinoid receptors and shares most, but not all, of the pharmacological properties of delta 9-THC. Therefore, this study was undertaken to determine whether its interaction with the CB1 receptor in brain was identical to that of delta 9-THC. Anandamide depressed spontaneous activity and produced hypothermia, antinociception and immobility in mice after i.v. administration. However, none of these effects was blocked by pretreatment with the selective CB1 antagonist, SR 141716A. However, the metabolically stable analog 2-methyl-2'-fluoroethylanandamide produced reductions in motor activity and antinociception in mice, effects that were blocked by the antagonist. To determine whether anandamide's receptor binding mimicked that of other cannabinoids, an autoradiographic comparison of anandamide, SR 141716A and CP 55,940 competition for [3H]CP55,940 binding was conducted throughout rat brain. The receptor affinities for all three compounds did not change according to brain area. As expected, Bmax values differed dramatically among differ brain areas. However, the Bmax values for each brain area were similar regardless of the compound used for displacement. These data suggest that anandamide, SR 141716A and CP 55,940 compete for the same cannabinoid receptor throughout brain despite SR 141716A's failure to block anandamide's pharmacological effects. Although there is no question that anandamide binds to the cannabinoid receptor, failure of SR 141716A to block its pharmacological effects in mice poses a dilemma. The results presented herein raise the possibility that anandamide may not be producing all of its effects by a direct interaction with the CB1 receptor.

Animals↗
PubMed1998

[The control of brain tissue temperature and stimulation of dopamine-immune system to the severe brain injury patients].

The recovery of injured neurons in primely brain damage, neuroprotection to the secondary brain damage (such as brain edema, brain ischemia, free radicals, neuroexcitation and ICP elevation), activation of gene-tropic regeneration, and prevention of apobiosis are major targets on the management of severe brain injury. However, excess release of catecholamines (catecholamine surge) make a very difficult to control of cerebral hypoxia by changes of systemic blood circulations. Mild cerebral hypothermia is only one method to prevent of these catecholamines surge. We developed new technique, cerebral hypothermia that control brain tissue temperature at 32-34 degrees C with more than 800 ml/min. oxygen delivery at acute stage. Combination therapy with these cerebral hypothermia and replacement of cerebral dopamine-pituitary hormone-estrogen was very successful to prevent of vegetation after severe brain injury.

Brain Injuries↗
PubMed2006

Cognitive and magnetic resonance imaging brain morphometric correlates of brain-derived neurotrophic factor Val66Met gene polymorphism in patients with schizophrenia and healthy volunteers.

CONTEXT: Relatively little is known about genetic determinants of cognitive dysfunction in schizophrenia. Recent studies suggest that a brain-derived neurotrophic factor (BDNF) prodomain single nucleotide polymorphism resulting in a valine (Val)-to-methionine (Met) substitution is associated with impaired declarative memory in healthy volunteers and patients with schizophrenia. These studies indicate that the BDNF(Met) variant may mediate hippocampal cognitive functions by modulating intracellular trafficking and activity-dependent BDNF release. To our knowledge, the way in which this functional single nucleotide polymorphism affects other neurocognitive measures has not been examined. Its role in determining cognitive deficits in schizophrenia has also not been systematically studied. OBJECTIVES: To characterize the neurocognitive and brain morphometric phenotypic correlates of the BDNF Val66Met polymorphism and to test the specificity of the BDNF(Met) variant on cognitive dysfunction in schizophrenia. DESIGN, SETTING, AND PARTICIPANTS: A comprehensive battery of standardized neuropsychological tests was administered to 144 healthy volunteers and 293 patients with schizophrenia spectrum disorder at a tertiary care university hospital. Approximately two thirds of the sample also underwent high-resolution magnetic resonance imaging brain scans. MAIN OUTCOME MEASURES: Genotype effects (in Met allele carriers vs Val homozygotes) on 5 cognitive domain z scores and magnetic resonance imaging gray matter brain volume measures (Talairach atlas-based cerebral lobes and optimized voxel-based morphometry) were examined using general linear models. RESULTS: On verbal memory, there was a significant genotype effect but no genotype x diagnosis effects. In both patients with schizophrenia and healthy volunteers, Met allele carriers had poorer verbal memory performance than their Val-homozygous counterparts. On visuospatial abilities, there were significant genotype and genotype x diagnosis effects. Met allele-associated visuospatial impairment was specific to patients with schizophrenia but not healthy volunteers. There were significant genotype effects on gray matter volumes within brain regions known to subserve these 2 cognitive domains, with Met allele carriers having smaller temporal and occipital lobar gray matter volumes. Optimized voxel-based morphometry further suggests that parietal heteromodal cortical gray matter deficits may underlie visuospatial impairment in patients with schizophrenia carrying the Met allele. CONCLUSIONS: We replicated the association between the BDNF(Met) variant and poor medial temporal lobe-related memory performance. The consonance of our cognitive and brain morphology findings further suggests that the BDNF(Met) variant may have a specific role in conferring visuospatial dysfunction in schizophrenia.

Adult↗
PubMed2002

Comparison of functional brain PET images and intraoperative brain-mapping data using image-guided surgery.

OBJECTIVE: Knowledge about the spatial localization of eloquent brain areas is essential for resecting lesions in the vicinity of these areas. The classical approach is to perform surgery on the awake patient under local anesthesia using brain-mapping techniques. As an alternative, the location of eloquent areas can be visualized by preoperative functional brain-imaging techniques, for example, positron emission tomography (PET), functional magnetic resonance imaging (fMRI), or magnetoencephalography (MEG). Using functional activation PET, both methods were combined by integration into a frameless navigation system (BrainLAB) and used to map speech-eloquent areas. PATIENTS AND METHODS: Speech-eloquent areas were localized preoperatively in seven patients with a left-sided glioma using 2-[(18)F]-2-desoxy-D-glucose PET. Patients were scanned under silence conditions (i.e., with the patient remaining silent in a sound-proof cabin), and speech was activated using a verb-generation paradigm. The PET data were transferred to the neuronavigation workstation and matched with a preoperative 3D-MRI using an automatic image-fusion algorithm. Intraoperative speech localization was performed using brain-mapping techniques under local anesthesia with bipolar cortical stimulation. The stimulator position was mapped into the MRI/PET data set by neuronavigational tracking of the instrument. RESULTS: Functional PET images were integrated into the MRI-based neuronavigational system and could be transferred exactly to the operative field. By the additional integration of cortical stimulation, intraoperative electrophysiological findings can be directly compared with preoperative functional images. Seven patients with left-sided glioma were operated on using this protocol, confirming the technical feasibility. In three of seven patients, preoperative PET findings were not supported by intraoperative mapping. CONCLUSIONS: This matching and mapping technique is suitable for monitoring eloquent speech areas during surgical resection of extensive left-sided low-grade gliomas, allowing a direct comparison between intraoperative electrophysiological brain mapping and preoperative functional brain-imaging findings. The sensitivity and specificity of functional imaging techniques can now be evaluated by reconciling the data with the intraoperative stimulation results.

Adult↗
PubMed1981

Ultracytochemical evidence for endothelial channel-lysosome connections in mouse brain following blood-brain barrier changes.

An investigation designed to define relationships between endothelial channels and lysosomes was conducted in the mammalian brain microvasculature. Microvessels from normal and mechanically injured mouse brains were studied ultracytochemically for: (1) transport of horseradish peroxidase (HRP) protein tracer through endothelial channels, and (2) for acid phosphatase (AcP) activity as an enzymatic marker of lysosomes. Following traumatic brain injury for 1 week with 2 h circulation of intravenously injected HRP, selected brain slices were processed for ultrastructural localization of either HRP, AcP, or for both reactions together within the same tissue slices. One week after blood-brain barrier (BBB) damage, the presence of HRP reaction product (RP) was observed within endothelial channels and vesicles of capillaries and arterioles with concomitant increase in lysosomal enzymatic activity of the endothelial cells bordering regions of brain damage. Lysosomes were observed to be directly connected to the endothelial channels. Our observations present cytochemical evidence for endothelial channel-lysosome connections which may suggest intralysosomal modification of blood-born materials before entering the neuropil. Such modification could have important immunological and/or metabolic significance.

Acid Phosphatase↗