Comparing the risks of frameless stereotactic biopsy in eloquent and noneloquent regions of the brain: a retrospective review of 284 cases

2009 ◽  
Vol 111 (4) ◽  
pp. 820-824 ◽  
Author(s):  
Ellen L. Air ◽  
James L. Leach ◽  
Ronald E. Warnick ◽  
Christopher M. McPherson

Object Frameless stereotactic biopsy has been shown in multiple studies to be a safe and effective tool for the diagnosis of brain lesions. However, no study has directly evaluated its safety in lesions located in eloquent regions in comparison with noneloquent locations. In this study, the authors determine whether an increased risk of neurological decline is associated with biopsy of lesions in eloquent regions of the brain. Methods Medical records, including imaging studies, were reviewed for 284 cases in which frameless stereotactic biopsy procedures were performed by 19 neurosurgeons at 7 institutions between January 2000 and December 2006. Lesion location was classified as eloquent or noneloquent in each patient. The incidence of neurological decline was calculated for each group. Results During the study period, 160 of the 284 biopsies predominately involved eloquent regions of the brain. In evaluation of the complication rate with respect to biopsy site, neurological decline occurred in 9 (5.6%) of 160 biopsies in eloquent brain areas and 10 (8.1%) of 124 biopsies in noneloquent regions; this difference was not statistically significant (p = 0.416). A higher number of needle passes was associated with the presence of a postoperative hemorrhage at the biopsy site, although not with a change in the result of neurological examination. Conclusions Frameless stereotactic biopsy of lesions located in eloquent brain regions is as safe and effective as biopsy of lesions in noneloquent regions. Therefore, with careful planning, frameless stereotactic biopsy remains a valuable and safe tool for diagnosis of brain lesions, independent of lesion location.

2021 ◽  
Vol 12 ◽  
Author(s):  
João Castelhano ◽  
Gisela Lima ◽  
Marta Teixeira ◽  
Carla Soares ◽  
Marta Pais ◽  
...  

There is an increasing interest in the neural effects of psychoactive drugs, in particular tryptamine psychedelics, which has been incremented by the proposal that they have potential therapeutic benefits, based on their molecular mimicry of serotonin. It is widely believed that they act mainly through 5HT2A receptors but their effects on neural activation of distinct brain systems are not fully understood. We performed a quantitative meta-analysis of brain imaging studies to investigate the effects of substances within this class (e.g., LSD, Psilocybin, DMT, Ayahuasca) in the brain from a molecular and functional point of view. We investigated the question whether the changes in activation patterns and connectivity map into regions with larger 5HT1A/5HT2A receptor binding, as expected from indolaemine hallucinogens (in spite of the often reported emphasis only on 5HT2AR). We did indeed find that regions with changed connectivity and/or activation patterns match regions with high density of 5HT2A receptors, namely visual BA19, visual fusiform regions in BA37, dorsal anterior and posterior cingulate cortex, medial prefrontal cortex, and regions involved in theory of mind such as the surpramarginal gyrus, and temporal cortex (rich in 5HT1A receptors). However, we also found relevant patterns in other brain regions such as dorsolateral prefrontal cortex. Moreover, many of the above-mentioned regions also have a significant density of both 5HT1A/5HT2A receptors, and available PET studies on the effects of psychedelics on receptor occupancy are still quite scarce, precluding a metanalytic approach. Finally, we found a robust neuromodulatory effect in the right amygdala. In sum, the available evidence points towards strong neuromodulatory effects of tryptamine psychedelics in key brain regions involved in mental imagery, theory of mind and affective regulation, pointing to potential therapeutic applications of this class of substances.


2014 ◽  
Vol 75 (S 02) ◽  
Author(s):  
J. Zhang ◽  
Y. Wang ◽  
X. Yu ◽  
R. Hui ◽  
R. Liu ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lani Cupo ◽  
Eric Plitman ◽  
Elisa Guma ◽  
M. Mallar Chakravarty

AbstractAcute exposure to cannabis has been associated with an array of cognitive alterations, increased risk for neuropsychiatric illness, and other neuropsychiatric sequelae including the emergence of acute psychotic symptoms. However, the brain alterations associating cannabis use and these behavioral and clinical phenotypes remains disputed. To this end, neuroimaging can be a powerful technique to non-invasively study the impact of cannabis exposure on brain structure and function in both humans and animal models. While chronic exposure studies provide insight into how use may be related to long-term outcomes, acute exposure may reveal interesting information regarding the immediate impact of use and abuse on brain circuits. Understanding these alterations could reveal the connection with symptom dimensions in neuropsychiatric disorders and, more specifically with psychosis. The purpose of the present review is to: 1) provide an update on the findings of pharmacological neuroimaging studies examining the effects of administered cannabinoids and 2) focus the discussion on studies that examine the sensitive window for the emergence of psychosis. Current literature indicates that cannabis exposure has varied effects on the brain, with the principal compounds in cannabis (delta-9-tetrahydrocannabinol and cannabidiol) altering activity across different brain regions. Importantly, we also discovered critical gaps in the literature, particularly regarding sex-dependent responses and long-term effects of chronic exposure. Certain networks often characterized as dysregulated in psychosis, like the default mode network and limbic system, were also impacted by THC exposure, identifying areas of particular interest for future work investigating the potential relationship between the two.


2017 ◽  
Author(s):  
Kyle Stanley Burger

Advances in neuroimaging techniques have provided insight into the role of the brain in the regulation of food intake and weight. Growing evidence demonstrate that energy dense, palatable foods elicit similar responses in reward-related brain regions that mimic those of addictive substances. Currently, various models of obesity’s relation to reward from food have been theorized. There is evidence to support a theory of hypo-responsivity of reward regions to food, where individuals consume excess amounts to overcome this reward deficit. There is also data to support a theory of hyper-responsivity of reward regions, where individuals who experience greater reward from food intake are at risk for overeating. However, these seemingly discordant theories are static in nature and do not account for the possible effects of repeated overeating on brain responsivity to food and initial vulnerability factors. Here we review data that support these theories and propose a dynamic vulnerability model of obesity that appears to offer a parsimonious theory that accommodates extant findings.


2020 ◽  
pp. 5821-5830
Author(s):  
Peter J. Nestor

Clinicopathological and imaging studies indicate strong associations between particular disorders of cognition and focal disease in the brain, but not all focal lesions induce specific loss of higher functions. Neuropsychological research has deepened our understanding by suggesting organizational frameworks for human cognitive faculties. Modern scientific study of higher cerebral function began in the late 19th century with the case studies of Broca and Wernicke. Their observations of language disorders associated with damage to the left hemisphere gave rise to the notion that specific mental faculties could be dissociated from each other and localized to specific regions within the cerebral hemisphere. Since that time clinicopathological and, more recently, imaging studies have established associations between specific cognitive disorders and focal brain lesions; these studies also show that some lesions do not give rise to highly specific deficits.


2020 ◽  
Vol 267 (S1) ◽  
pp. 126-135 ◽  
Author(s):  
Björn Machner ◽  
Jin Hee Choi ◽  
Peter Trillenberg ◽  
Wolfgang Heide ◽  
Christoph Helmchen

AbstractThe usefulness of brain imaging studies in dizzy patients presenting to the emergency department (ED) is controversial. We aimed to assess the ‘real-world’ probability of ischemic stroke and other acute brain lesions (ABLs) in these patients to create an algorithm that helps decision-making on whether which and when brain imaging is needed. By reviewing medical records, we identified 610 patients presenting with dizziness, vertigo or imbalance to our university hospital’s ED and receiving neurological workup. We collected timing/triggers of symptoms, ABCD2 score, focal neurological abnormalities, HINTS (head impulse, nystagmus, test-of-skew) and other central oculomotor signs. ABLs were extracted from CT/MRI reports. Uni-/multivariate logistic regression analyses investigated associations between clinical parameters and ABLs. Finally, the likelihood of ABLs was assessed for different clinically defined subgroups (‘dizziness syndromes’). Early CT (day 1) was performed in 539 (88%) and delayed MR imaging (median: day 4) in 299 (49%) patients. ABLs (89% ischemic stroke) were revealed in 75 (24%) of 318 patients with adequate imaging (MRI or lesion-positive CT). The risk for ABLs increased with the presence of central oculomotor signs (odds ratio 2.8, 95% confidence interval 1.5–5.2) or focal abnormalities (OR 3.3, 95% CI 1.8–6.2). The likelihood of ABLs differed between dizziness syndromes, e.g., HINTS-negative acute vestibular syndrome: 0%, acute imbalance syndrome with ABCD2-score ≥ 4: 50%. We propose a clinical pathway, according to which patients with HINTS-negative acute vestibular syndrome should not receive brain imaging, whereas imaging is suggested in dizzy patients with acute imbalance, central oculomotor signs or focal abnormalities.


2012 ◽  
Vol 24 (6) ◽  
pp. 1275-1285 ◽  
Author(s):  
Caterina Gratton ◽  
Emi M. Nomura ◽  
Fernando Pérez ◽  
Mark D'Esposito

Although it is generally assumed that brain damage predominantly affects only the function of the damaged region, here we show that focal damage to critical locations causes disruption of network organization throughout the brain. Using resting state fMRI, we assessed whole-brain network structure in patients with focal brain lesions. Only damage to those brain regions important for communication between subnetworks (e.g., “connectors”)—but not to those brain regions important for communication within sub-networks (e.g., “hubs”)—led to decreases in modularity, a measure of the integrity of network organization. Critically, this network dysfunction extended into the structurally intact hemisphere. Thus, focal brain damage can have a widespread, nonlocal impact on brain network organization when there is damage to regions important for the communication between networks. These findings fundamentally revise our understanding of the remote effects of focal brain damage and may explain numerous puzzling cases of functional deficits that are observed following brain injury.


CNS Spectrums ◽  
1999 ◽  
Vol 4 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Mark S. George ◽  
Charlotte C. Teneback ◽  
Courtnay W. Bloomer ◽  
Michael D. Horner ◽  
Raymond F. Anton

AbstractSome of the profound effects alcohol has on the brain were discovered years ago through pathological studies at autopsy. However, the recent development of new tools for structural and functional brain imaging has enabled researchers to expand upon this earlier knowledge. For example, some imaging studies have revealed that chronic alcohol consumption causes cortical loss, some of which is reversible with abstinence. Other studies have found that alcohol acts as a global central nervous system depressant, with chronic use resulting in reduced activity that can take a month or more to recover. Finally, imaging tools are also beginning to shed light on which brain regions are active when an alcoholic has the urge to drink.


2005 ◽  
Vol 17 (6) ◽  
pp. 969-980 ◽  
Author(s):  
Kim M. Dalton ◽  
Ned H. Kalin ◽  
Thomas M. Grist ◽  
Richard J. Davidson

Anxiety is a debilitating symptom of many psychiatric disorders including generalized anxiety disorder, mood disorders, schizophrenia, and autism. Anxiety involves changes in both central and peripheral biology, yet extant functional imaging studies have focused exclusively on the brain. Here we show, using functional brain and cardiac imaging in sequential brain and cardiac magnetic resonance imaging (MRI) sessions in response to cues that predict either threat (a possible shock) or safety (no possibility of shock), that MR signal change in the amygdala and the prefrontal and insula cortices predicts cardiac contractility to the threat of shock. Participants with greater MR signal change in these regions show increased cardiac contractility to the threat versus safety condition, a measure of the sympathetic nervous system contribution to the myocardium. These findings demonstrate robust neural-cardiac coupling during induced anxiety and indicate that individuals with greater activation in brain regions identified with aversive emotion show larger magnitude cardiac contractility increases to threat.


Author(s):  
Ian Q. Whishaw ◽  
Megan Okuma

A brain lesion is an area of damage, injury, or abnormal change to a part of the brain. Brain lesions may be caused by head injury, disease, surgery, or congenital disorders, and they are classified by the cause, extent, and locus of injury. Lesions cause many behavioral symptoms. Symptom severity generally corresponds to the region and extent of damaged brain. Thus, behavior is often a reliable indicator of the type and extent of a lesion. Observations of patients suffering brain lesions were first recorded in detail in the 18th century, and lesion studies continue to shape modern neuroscience and to give insight into the functions of brain regions. Recovery, defined as any return of lost behavioral or cognitive function, depends on the age, sex, genetics, and lifestyle of patients, and recovery may be predicted by the cause of injury. Most recovery occurs within the first 6 to 9 months after injury and likely involves a combination of compensatory behaviors and physiological changes in the brain. Children often recover some function after brain lesions better than adults, though both children and adults experience residual deficits. Brain lesion survival rates are improved by better diagnostic tools and treatments. Therapeutic interventions and treatments for brain lesions include surgery, pharmaceuticals, transplants, and temperature regulation, each with varying degrees of success. Research in treating brain lesions is progressing, but in principle a cure will only be complete when brain lesions are replaced with healthy tissue.


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