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Navigating menopause involves traversing a complex terrain of hormonal changes that extend far beyond reproductive consequences. Menopausal transition is characterized by a decrease in estradiol-17ß (E2), and the impact of menopause resonates not only in the reproductive system but also through the central nervous system, musculoskeletal, and gastrointestinal domains. As women undergo menopausal transition, they become more susceptible to frailty, amplifying the risk and severity of injuries, including traumatic brain injury (TBI). Menopause triggers a cascade of changes leading to a decline in muscle mass, accompanied by diminished tone and excitability, thereby restricting the availability of irisin, a crucial hormone derived from muscles. Concurrently, bone mass undergoes reduction, culminating in the onset of osteoporosis and altering the dynamics of osteocalcin, a hormone originating from bones. The diminishing levels of E2 during menopause extend their influence on the gut microbiota, resulting in a reduction in the availability of tyrosine, tryptophan, and serotonin metabolites, affecting neurotransmitter synthesis and function. Understanding the interplay between menopause, frailty, E2 decline, and the intricate metabolisms of bone, gut, and muscle is imperative when unraveling the nuances of TBI after menopause. The current review underscores the significance of accounting for menopause-associated frailty in the incidence and consequences of TBI. The review also explores potential mechanisms to enhance gut, bone, and muscle health in menopausal women, aiming to mitigate frailty and improve TBI outcomes.
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Lesões Encefálicas Traumáticas , Fragilidade , Menopausa , Humanos , Lesões Encefálicas Traumáticas/metabolismo , Lesões Encefálicas Traumáticas/fisiopatologia , Feminino , Menopausa/metabolismo , Menopausa/fisiologia , Fragilidade/metabolismo , Estradiol/metabolismoRESUMO
BACKGROUND: Nicotine-containing electronic cigarette (EC) vaping has become popular worldwide, and our understanding of the effects of vaping on stroke outcomes is elusive. Using a rat model of transient middle cerebral artery occlusion, the current exploratory study aims to evaluate the sex-dependent effects of EC exposure on brain energy metabolism and stroke outcomes. METHODS: Adult Sprague-Dawley rats of both sexes were randomly assigned to air/EC vapor (5% nicotine Juul pods) exposure for 16 nights, followed by randomization into 3 cohorts. The first cohort underwent exposure to air/EC preceding randomization to transient middle cerebral artery occlusion (90 minutes) or sham surgery, followed by survival for 21 days. During the survival period, rats underwent sensorimotor and Morris water maze testing. Subsequently, brains were collected for histopathology. A second cohort was exposed to air/EC after which brains were collected for unbiased metabolomics analysis. The third cohort of animals was exposed to air/EC and received transient middle cerebral artery occlusion/sham surgery, and brain tissue was collected 24 hours later for biochemical analysis. RESULTS: In females, EC significantly increased (P<0.05) infarct volumes by 94% as compared with air-exposed rats, 165±50 mm3 in EC-exposed rats, and 85±29 mm3 in air-exposed rats, respectively, while in males such a difference was not apparent. Morris water maze data showed significant deficits in spatial learning and working memory in the EC sham or transient middle cerebral artery occlusion groups compared with the respective air groups in rats of both sexes (P<0.05). Thirty-two metabolites of carbohydrate, glycolysis, tricarboxylic acid cycle, and lipid metabolism were significantly altered (P≤0.05) due to EC, 23 of which were specific for females. Steady-state protein levels of hexokinase significantly decreased (P<0.05) in EC-exposed females; however, these changes were not seen in males. CONCLUSIONS: Even brief EC exposure over 2 weeks impacts brain energy metabolism, exacerbates infarction, and worsens poststroke cognitive deficits in working memory more in female than male rats.
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Sistemas Eletrônicos de Liberação de Nicotina , Vaping , Humanos , Adulto , Ratos , Masculino , Feminino , Animais , Ratos Sprague-Dawley , Nicotina/efeitos adversos , Infarto da Artéria Cerebral Média/metabolismoRESUMO
Naturally occurring life stages in women are associated with changes in the milieu of endogenous ovarian hormones. Women of childbearing age may be exposed to exogenous ovarian hormone(s) because of their use of varying combinations of estrogen and progesterone hormones-containing oral contraceptives (OC; also known as "the pill"). If women have central nervous system (CNS) injury such as spinal cord injury (SCI) and traumatic brain injury (TBI) during their childbearing age, they are likely to retain their reproductive capabilities and may use OC. Many deleterious side effects of long-term OC use have been reported, such as aberrant blood clotting and endothelial dysfunction that consequently increase the risk of myocardial infarction, venous thromboembolism, and ischemic brain injury. Although controversial, studies have suggested that OC use is associated with neuropsychiatric ramifications, including uncontrollable mood swings and poorer cognitive performance. Our understanding about how the combination of endogenous hormones and OC-conferred exogenous hormones affect outcomes after CNS injuries remains limited. Therefore, understanding the impact of OC use on CNS injury outcomes needs further investigation to reveal underlying mechanisms, promote reporting in clinical or epidemiological studies, and raise awareness of possible compounded consequences. The goal of the current review is to discuss the impacts of CNS injury on endogenous ovarian hormones and vice-versa, as well as the putative consequences of exogenous ovarian hormones (OC) on the CNS to identify potential gaps in our knowledge to consider for future laboratory, epidemiological, and clinical studies.
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Lesões Encefálicas Traumáticas , Traumatismos do Sistema Nervoso , Feminino , Humanos , Contracepção Hormonal , Sistema Nervoso Central , EstrogêniosRESUMO
BACKGROUND: Cholinergic cells originating from the nuclei of the basal forebrain (BF) are critical for supporting various memory processes, yet BF cholinergic cell viability has not been explored in the context of focal cerebral ischemia. In the present study, we examined cell survival within several BF nuclei in rodents following transient middle cerebral artery occlusion. We tested the hypothesis that a previously established neuroprotective therapy-resveratrol preconditioning-would rescue BF cell loss, deficits in cholinergic-related memory performance, and hippocampal synaptic dysfunction after focal cerebral ischemia. METHODS: Adult (2-3-month old) male Sprague-Dawley rats or wild-type C57Bl/6J mice were injected intraperitoneally with a single dose of resveratrol or vehicle and subjected to transient middle cerebral artery occlusion using the intraluminal suture method 2 days later. Histopathological, behavioral, and electrophysiological outcomes were measured 1-week post-reperfusion. Animals with reduction in cerebral blood flow <30% of baseline were excluded. RESULTS: Cholinergic cell loss was observed in the medial septal nucleus and diagonal band of Broca following transient middle cerebral artery occlusion. This effect was prevented by resveratrol preconditioning, which also ameliorated transient middle cerebral artery occlusion-induced deficits in cognitive performance and hippocampal long-term potentiation. CONCLUSIONS: We demonstrate for the first time that focal cerebral ischemia induces cholinergic cell death within memory-relevant nuclei of the BF. The preservation of cholinergic cell viability may provide a mechanism by which resveratrol preconditioning improves memory performance and preserves functionality of memory-processing brain structures after focal cerebral ischemia.
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Infarto da Artéria Cerebral Média , Transtornos da Memória , Fármacos Neuroprotetores , Resveratrol , Animais , Camundongos , Ratos , Isquemia Encefálica , Morte Celular/efeitos dos fármacos , Resveratrol/farmacologia , CogniçãoRESUMO
Women have a higher risk of having an ischemic stroke and increased cognitive decline after stroke as compared to men. The female sex hormone 17ß-estradiol (E2) is a potent neuro- and cognitive-protective agent. Periodic E2 or estrogen receptor subtype-beta (ER-ß) agonist pre-treatments every 48 h before an ischemic episode ameliorated ischemic brain damage in young ovariectomized or reproductively senescent (RS) aged female rats. The current study aims to investigate the efficacy of post-stroke ER-ß agonist treatments in reducing ischemic brain damage and cognitive deficits in RS female rats. Retired breeder (9-10 months) Sprague-Dawley female rats were considered RS after remaining in constant diestrus phase for more than a month. The RS rats were exposed to transient middle cerebral artery occlusion (tMCAO) for 90 min and treated with either ER-ß agonist (beta 2, 3-bis(4-hydroxyphenyl) propionitrile; DPN; 1 mg/kg; s.c.) or DMSO vehicle at 4.5 h after induction of tMCAO. Subsequently, rats were treated with either ER-ß agonist or DMSO vehicle every 48 h for ten injections. Forty-eight hours after the last treatment, animals were tested for contextual fear conditioning to measure post-stroke cognitive outcome. Neurobehavioral testing, infarct volume quantification, and hippocampal neuronal survival were employed to determine severity of stroke. Periodic post-stroke ER-ß agonist treatment reduced infarct volume, improved recovery of cognitive capacity by increasing freezing in contextual fear conditioning, and decreased hippocampal neuronal death in RS female rats. These data suggest that periodic post-stroke ER-ß agonist treatment to reduce stroke severity and improve post-stroke cognitive outcome in menopausal women has potential for future clinical investigation.
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Receptores de Estrogênio , Acidente Vascular Cerebral , Ratos , Feminino , Animais , Ratos Sprague-Dawley , Receptor beta de Estrogênio , Dimetil Sulfóxido , Estrogênios/farmacologia , Estradiol/farmacologia , Estradiol/uso terapêutico , Acidente Vascular Cerebral/tratamento farmacológico , Cognição , Infarto/tratamento farmacológico , Receptor alfa de Estrogênio/agonistasRESUMO
Spontaneous intracerebral hemorrhage (sICH) is a disabling stroke sub-type, and tobacco use is a prominent risk factor for sICH. We showed that chronic nicotine exposure enhances bleeding post-sICH. Reduction of hematoma growth is a promising effective therapy for sICH in smoking subjects. Red-blood-cell-derived microparticles (RMPs) are hemostatic agents that limit hematoma expansion following sICH in naïve rats. Considering the importance of testing the efficacy of experimental drugs in animal models with a risk factor for a disease, we tested RMP efficacy and the therapeutic time window in limiting hematoma growth post-sICH in rats exposed to nicotine. Young rats were chronically treated with nicotine using osmotic pumps. sICH was induced in rats using an injection of collagenase in the right striatum. Vehicle/RMPs were administered intravenously. Hematoma volume and neurological impairment were quantified ≈24 h after sICH. Hematoma volumes in male and female nicotine-exposed rats that were treated with RMPs at 2 h post-sICH were significantly lower by 26 and 31% when compared to their respective control groups. RMP therapy was able to limit hematoma volume when administered up to 4.5 h post-sICH in animals of both sexes. Therefore, RMPs may limit hematoma growth in sICH patients exposed to tobacco use.
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Micropartículas Derivadas de Células , Nicotina , Masculino , Feminino , Ratos , Animais , Nicotina/efeitos adversos , Resultado do Tratamento , Hemorragia Cerebral/terapia , Hematoma/etiologiaRESUMO
Smoking-derived nicotine (N) and oral contraceptive (OC) synergistically exacerbate ischemic brain damage in females, and the underlying mechanisms remain elusive. In a previous study, we showed that N + OC exposure altered brain glucose metabolism in females. Since lipid metabolism complements glycolysis, the current study aims to examine the metabolic fingerprint of fatty acids in the brain of female rats exposed to N+/-OC. Adolescent and adult Sprague-Dawley female rats were randomly (n = 8 per group) exposed to either saline or N (4.5 mg/kg) +/-OC (combined OC or placebo delivered via oral gavage) for 16-21 days. Following exposure, brain tissue was harvested for unbiased metabolomic analysis (performed by Metabolon Inc., Morrisville, NC, USA) and the metabolomic profile changes were complemented with Western blot analysis of key enzymes in the lipid pathway. Metabolomic data showed significant accumulation of fatty acids and phosphatidylcholine (PC) metabolites in the brain. Adolescent, more so than adult females, exposed to N + OC showed significant increases in carnitine-conjugated fatty acid metabolites compared to saline control animals. These changes in fatty acyl carnitines were accompanied by an increase in a subset of free fatty acids, suggesting elevated fatty acid ß-oxidation in the mitochondria to meet energy demand. In support, ß-hydroxybutyrate was significantly lower in N + OC exposure groups in adolescent animals, implying a complete shunting of acetyl CoA for energy production via the TCA cycle. The reported changes in fatty acids and PC metabolism due to N + OC could inhibit post-translational palmitoylation of membrane proteins and synaptic vesicle formation, respectively, thus exacerbating ischemic brain damage in female rats.
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Anticoncepcionais Orais , Nicotina , Humanos , Ratos , Feminino , Animais , Ratos Sprague-Dawley , Ácidos Graxos/metabolismo , Encéfalo/metabolismo , Metabolismo dos Lipídeos , OxirreduçãoRESUMO
Low-frequency whole-body vibration (WBV; 40 Hz), a low impact form of exercise, intervention for a month following moderate transient middle-cerebral artery occlusion (tMCAO) reduces infarct volume and improves motor function in reproductively senescent, middle-aged female rats. Since post-stroke cognitive decline remains a significant problem, the current study aims to investigate the efficacy of WBV in ameliorating post-tMCAO cognitive deficits and to determine the underlying putative mechanism(s) conferring benefits of WBV in middle-aged rats. Middle-aged rats of both sexes were randomly assigned to tMCAO (90 min) or sham surgery followed by exposure to either WBV (twice a day for 15 min each for 5 days a week over a month) or no WBV treatment groups. Following the last WBV treatment, rats were tested for hippocampus-dependent learning and memory using a water maze followed by harvesting brain and blood samples for histopathological and inflammatory marker analyses, respectively. Results show that post-tMCAO WBV significantly lessens cognitive deficits in rats of both sexes. Post-tMCAO WBV significantly decreased circulating pro-inflammatory cytokines and increased serum levels of irisin, a muscle-derived hormone that may play a role in brain metabolism and inflammation regulation, which suggests putative beneficial mechanisms of WBV.
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Incidents of strokes are increased in young women relative to young men, suggesting that oral contraceptive (OC) use is one of the causes of stroke among young women. Long-term exposures to the varying combinations of estrogen and progestogen found in OCs affect blood clotting, lipid and lipoprotein metabolism, endothelial function, and de novo synthesis of neurosteroids, especially brain-derived 17ß-estradiol. The latter is essential for neuroprotection, memory, sexual differentiation, synaptic transmission, and behavior. Deleterious effects of OCs may be exacerbated due to comorbidities like polycystic ovary syndrome, sickle cell anemia, COVID-19, exposures to endocrine disrupting chemicals, and conventional or electronic cigarette smoking. The goal of the current review is to revisit the available literature regarding the impact of OC use on stroke, to explain possible underlying mechanisms, and to identify gaps in our understanding to promote future research to reduce and cure stroke in OC users.
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COVID-19 , Sistemas Eletrônicos de Liberação de Nicotina , Acidente Vascular Cerebral , Masculino , Feminino , Humanos , Anticoncepcionais Orais/farmacologia , Amigos , Acidente Vascular Cerebral/etiologiaRESUMO
Spontaneous intracerebral hemorrhage (sICH) is a deadly stroke subtype, and tobacco use increases sICH risk. However epidemiological studies show that, there are no confirmatory studies showing the effect of tobacco use on sICH outcome. Therefore, we evaluated the effect of chronic nicotine exposure (as a surrogate for tobacco use) on outcomes following sICH. Young male and female rats were randomly assigned to either nicotine (4.5 mg/kg b.w. per day) or vehicle (saline) treatment (2-3 weeks) groups. sICH was induced by injecting collagenase into the right striatum. Neurological score and hematoma volume were determined 24 h post-sICH. The hematoma volumes in nicotine-treated male and female rats were significantly higher by 42% and 48% when compared to vehicle-treated male and female rats, respectively. Neurological deficits measured in terms of neurological score for the nicotine-treated male and female groups were significantly higher when compared to the respective vehicle-treated male and female groups. Our results show that chronic nicotine exposure increases hematoma volume post-sICH in rats of both sexes. Identifying the mechanism of nicotine-dependent increase in hematoma growth post-sICH will be crucial to understanding the detrimental effect of tobacco use on the severity of bleeding following intracerebral hemorrhage.
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Nicotina , Acidente Vascular Cerebral , Animais , Hemorragia Cerebral/induzido quimicamente , Hemorragia Cerebral/terapia , Colagenases , Feminino , Hematoma/induzido quimicamente , Masculino , Nicotina/toxicidade , RatosRESUMO
Electronic cigarettes (ECs) are battery-powered nicotine delivery devices that have rapidly gained popularity and attention globally. ECs work by heating a liquid to produce an aerosol that usually contains nicotine, flavoring compounds, and other chemicals, which are inhaled during vaping. EC aerosols are depicted to contain a lower number and overall quantity of harmful toxicants than conventional cigarettes (CCs). However, emerging research indicates that EC aerosols contain harmful ingredients including ultrafine particles, volatile organic compounds, and heavy metals. One common ingredient found in both CCs and ECs is nicotine, which has been shown to be both highly addictive and toxic. Particularly relevant to our current review, there is an enormous amount of literature that shows that smoking-derived nicotine exacerbates ischemic brain damage. Therefore, the question arises: will EC use impact the outcome of stroke? ECs are highly popular and relatively new in the market; thus, our understanding about the long-term effects of EC use on brain are lacking. The current review strives to extrapolate the existing understanding of the nicotine-induced effects of conventional smoking on the brain to the possible effects that ECs may have on the brain, which may ultimately have a potential for adverse stroke risk or severity.
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Isquemia Encefálica , Sistemas Eletrônicos de Liberação de Nicotina , Acidente Vascular Cerebral , Vaping , Humanos , Vaping/efeitos adversos , Nicotina/efeitos adversos , Aerossóis/efeitos adversos , Isquemia Encefálica/etiologiaRESUMO
Traumatic brain injury (TBI) is a leading cause of death and disability and a global public health challenge. Every year more than 50 million people suffer a TBI, and it is estimated that 50% of the global population will experience at least one TBI in their lifetime. TBI affects both men and women of all ages, however there is a male bias in TBI research as women have frequently been left out of the literature despite irrefutable evidence of male and female dimorphism in several posttraumatic measures. Women uniquely experience distinct life stages marked by levels of endogenous circulating sex hormones, as well as by physiological changes that are nonexistent in men. In addition to generalized sex-specific differences, a woman's susceptibility, neurological outcomes, and treatment success may vary considerably depending upon when in her lifespan she incurred a traumatic insult. How women impacted by TBI might differ from other women as a factor of age and physiology is not well understood. Furthermore, there is a gap in the knowledge of what happens when TBI occurs in the presence of certain sex-specific and sex-nonspecific variables, such as during pregnancy, with oral contraceptive use, in athletics, in cases of addiction and nicotine consumption, during perimenopause, postmenopause, in frailty, among others. Parsing out how hormone-dependent and hormone-independent lifespan variables may influence physiological, neurodegenerative, and functional outcomes will greatly contribute to future investigative studies and direct therapeutic strategies. The goal of this review is to aggregate the knowledge of prevalence, prognosis, comorbid risk, and response of women incurring TBI at differing phases of lifespan. We strive to illuminate commonalities and disparities among female populations, and to pose important questions to highlight gaps in the field in order to further the endeavor of targeted treatment interventions in a patient-specific manner.
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Lesões Encefálicas Traumáticas/epidemiologia , Longevidade , Fatores Etários , Feminino , Humanos , Gravidez , PrognósticoRESUMO
Xenoestrogens, foreign synthetic chemicals mimicking estrogens, are lurking in our surroundings. Climate change may alter their toxicity and bioavailability. Since xenoestrogens have extremely high lipid solubility and are structurally similar to natural endogenous estrogens, they can bind to estrogen receptors (ERs) -alpha (ER-α) and -beta (ER-ß). Scientific evidence accumulated over the past decades have suggested that natural 17ß-estradiol (E2; a potent estrogen), via activation of its receptors, plays a pivotal role in regulation of brain development, differentiation, metabolism, synaptic plasticity, neuroprotection, cognition, anxiety, body temperature, feeding and sexual behavior. In the brain, ER-ß is predominantly expressed in the various regions, including cerebral cortex and hippocampus, that have been shown to play a key role in cognition. Therefore, disturbances in function of ER-ß mediated E2 signaling by xenoestrogens can lead to deleterious effects that potentiate a variety of neurological diseases starting from prenatal to post-menopause in women. The goal of this review is to identify the possible neurological effects of xenoestrogens that can alter estrogen receptor-mediated signaling in the brain during different stages of the female lifespan.
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Encéfalo/efeitos dos fármacos , Disruptores Endócrinos/toxicidade , Exposição Ambiental/efeitos adversos , Doenças do Sistema Nervoso/induzido quimicamente , Receptores de Estrogênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Encéfalo/metabolismo , Feminino , Humanos , Doenças do Sistema Nervoso/metabolismoRESUMO
We analyzed early brain metabolic adaptations in response to mitochondrial dysfunction in a mouse model of mitochondrial encephalopathy with complex IV deficiency [neuron-specific COX10 knockout (KO)]. In this mouse model, the onset of the mitochondrial defect did not coincide with immediate cell death, suggesting early adaptive metabolic responses to compensate for the energetic deficit. Metabolomic analysis in the KO mice revealed increased levels of glycolytic and pentose phosphate pathway intermediates, amino acids and lysolipids. Glycolysis was modulated by enhanced activity of glycolytic enzymes, and not by their overexpression, suggesting the importance of post-translational modifications in the adaptive response. Glycogen synthase kinase 3 inactivation was the most upstream regulation identified, implying that it is a key event in this adaptive mechanism. Because neurons are thought not to rely on glycolysis for adenosine triphosphate production in normal conditions, our results indicate that neurons still maintain their ability to upregulate this pathway when under mitochondrial respiration stress.
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Alquil e Aril Transferases , Quinase 3 da Glicogênio Sintase , Alquil e Aril Transferases/metabolismo , Animais , Encéfalo/metabolismo , Quinase 3 da Glicogênio Sintase/metabolismo , Glicólise/genética , Proteínas de Membrana/metabolismo , Camundongos , Mitocôndrias/genética , Mitocôndrias/metabolismo , Neurônios/metabolismoRESUMO
Irisin, a newly discovered protein hormone that is secreted in response to low frequency whole body vibration (LFV), could be a promising post-stroke rehabilitation therapy for patients who are frail and cannot comply with regular rehabilitation therapy. Irisin is generated from a membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5). Aside from being highly expressed in muscle, FNDC5 is highly expressed in the brain. The cleaved form of FNDC5 was found in the cerebrospinal fluid as well as in various regions of the brain. Numerous studies suggest that irisin plays a key role in brain metabolism and inflammation regulation. Both the metabolism and inflammation govern stroke outcome, and in a published study, we demonstrated that LFV therapy following middle cerebral artery occlusion significantly reduced innate immune response, improved motor function and infarct volume in reproductively senescent female rats. The observed effect of LFV therapy could be working via irisin, therefore, the current review focuses to understand various aspects of irisin including its mechanism of action on the brain.
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Fibronectinas , Acidente Vascular Cerebral , Animais , Encéfalo/metabolismo , Feminino , Fibronectinas/metabolismo , Humanos , Infarto da Artéria Cerebral Média , Inflamação , RatosRESUMO
The past decade has brought tremendous progress in diagnostic and therapeutic options for cerebrovascular diseases as exemplified by the advent of thrombectomy in ischemic stroke, benefitting a steeply increasing number of stroke patients and potentially paving the way for a renaissance of neuroprotectants. Progress in basic science has been equally impressive. Based on a deeper understanding of pathomechanisms underlying cerebrovascular diseases, new therapeutic targets have been identified and novel treatment strategies such as pre- and post-conditioning methods were developed. Moreover, translationally relevant aspects are increasingly recognized in basic science studies, which is believed to increase their predictive value and the relevance of obtained findings for clinical application.This review reports key results from some of the most remarkable and encouraging achievements in neurovascular research that have been reported at the 10th International Symposium on Neuroprotection and Neurorepair. Basic science topics discussed herein focus on aspects such as neuroinflammation, extracellular vesicles, and the role of sex and age on stroke recovery. Translational reports highlighted endovascular techniques and targeted delivery methods, neurorehabilitation, advanced functional testing approaches for experimental studies, pre-and post-conditioning approaches as well as novel imaging and treatment strategies. Beyond ischemic stroke, particular emphasis was given on activities in the fields of traumatic brain injury and cerebral hemorrhage in which promising preclinical and clinical results have been reported. Although the number of neutral outcomes in clinical trials is still remarkably high when targeting cerebrovascular diseases, we begin to evidence stepwise but continuous progress towards novel treatment options. Advances in preclinical and translational research as reported herein are believed to have formed a solid foundation for this progress.
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INTRODUCTION: White matter tracts can be observed using tractograms generated from diffusion tensor imaging (DTI). However, the dependence of these white matter tract images on subjective variables, including how seed points are placed and the preferred level of fractional anisotropy, introduces interobserver inconsistency and potential lack of reliability. We propose that color-coded maps (CCM) generated from DTI can be a preferred method for the visualization of important white matter tracts, circumventing bias in preoperative brain tumor resection planning. METHODS: DTI was acquired retrospectively in 25 patients with brain tumors. Lesions included 15 tumors of glial origin, 9 metastatic tumors, 2 meningiomas, and 1 cavernous angioma. Tractograms of the pyramidal tract and/or optic radiations, based on tumor location, were created by marking seed regions of interest using known anatomical locations. We compared the degree of tract involvement and white matter alteration between CCMs and tractograms. Neurological outcomes were obtained from chart reviews. RESULTS: The pyramidal tract was evaluated in 20/25 patients, the visual tracts were evaluated in 10/25, and both tracts were evaluated in 5/25. In 19/25 studies, the same patterns of white matter alternations were found between the CCMs and tractograms. In the 6 patients where patterns differed, 2 tractograms were not useful in determining pattern alteration; in the remaining 4/6, no practical difference was seen in comparing the studies. Two patients were lost to follow-up. Thirteen patients were neurologically improved or remained intact after intervention. In these, 10 of the 13 patients showed tumor-induced white matter tract displacement on CCM. Twelve patients had no improvement of their preoperative deficit. In 9 of these 12 patients, CCM showed white matter disruption. CONCLUSION: CCMs provide a convenient, practical, and objective method of visualizing white matter tracts, obviating the need for potentially subjective and time-consuming tractography. CCMs are at least as reliable as tractograms in predicting neurological outcomes after neurosurgical intervention.