scholarly journals Multimodal Approach to the Surgical Removal of Gliomas in Eloquent Brain Regions

10.5772/24446 ◽  
2011 ◽  
Author(s):  
Giannantonio Spena ◽  
Antonio Pepoli ◽  
Marcella Bruno ◽  
Federico DAgata ◽  
Franco Cauda ◽  
...  
Keyword(s):  
Brain Regions ◽  
Surgical Removal ◽  
Multimodal Approach

scholarly journals Electrocorticography-guided resection of temporal cavernoma: is electrocorticography warranted and does it alter the surgical approach?

2009 ◽  
Vol 110 (6) ◽  
pp. 1179-1185 ◽  
Author(s):  
Jamie J. Van Gompel ◽  
Jesus Rubio ◽  
Gregory D. Cascino ◽  
Gregory A. Worrell ◽  
Fredric B. Meyer
Keyword(s):  
Temporal Lobe ◽  
Surgical Approach ◽  
Brain Regions ◽  
Surgical Removal ◽  
Seizure Outcome ◽  
Surgical Decision ◽  
Cavernous Hemangiomas ◽  
Study Support ◽  
Surgical Decision Making

Object Cavernous hemangiomas associated with epilepsy present an interesting surgical dilemma in terms of whether one should perform a pure lesionectomy or tailored resection, especially in the temporal lobe given the potential for cognitive damage. This decision is often guided by electrocorticography (ECoG), despite the lack of data regarding its value in cavernoma surgery. The purpose of the present study was several-fold: first, to determine the epilepsy outcome following resection of cavernomas in all brain regions; second, to evaluate the usefulness of ECoG in guiding surgical decision making; and third, to determine the optimum surgical approach for temporal lobe cavernomas. Methods The authors identified from their surgical database 173 patients who had undergone resection of cavernomas. One hundred two of these patients presented with epilepsy, and 61 harbored temporal lobe cavernomas. Preoperatively, all patients were initially evaluated by an epileptologist. The mean follow-up was 37 months. Results Regardless of the cavernoma location, surgery resulted in an excellent seizure control rate: Engel Class I outcome in 88% of patients at 2 years postoperatively. Of 61 patients with temporal lobe cavernomas, the mesial structures were involved in 35. Among the patients with temporal lobe cavernomas, those who underwent ECoG typically had a more extensive parenchymal resection rather than a lesionectomy (p < 0.0001). The use of ECoG in cases of temporal lobe cavernomas resulted in a superior seizure-free outcome: 79% (29 patients) versus 91% (23 patients) of patients at 6 months postresection, 77% (22 patients) versus 90% (20 patients) at 1 year, and 79% (14 patients) versus 83% (18 patients) at 2 years without ECoG versus with ECoG, respectively. Conclusions The surgical removal of cavernomas most often leads to an excellent epilepsy outcome. In cases of temporal lobe cavernomas, the more extensive the ECoG-guided resection, the better the seizure outcome. In addition to upholding the concept of kindling, the data in this study support the use of ECoG in temporal lobe cavernoma surgery in patients presenting with epilepsy.

Astroglial Scarring and Seizures

2016 ◽  
Vol 23 (2) ◽  
pp. 152-168 ◽  
Author(s):  
Stefanie Robel
Keyword(s):  
Central Nervous System ◽  
Neurological Diseases ◽  
The United States ◽  
Brain Regions ◽  
Surgical Removal ◽  
Drug Resistant ◽  
Neuronal Function ◽  
Network Function ◽  
Drug Resistant Epilepsy ◽  
The Brain

Epilepsy is among the most prevalent chronic neurological diseases and affects an estimated 2.2 million people in the United States alone. About one third of patients are resistant to currently available antiepileptic drugs, which are exclusively targeting neuronal function. Yet, reactive astrocytes have emerged as potential contributors to neuronal hyperexcitability and seizures. Astrocytes react to any kind of CNS insult with a range of cellular adjustments to form a scar and protect uninjured brain regions. This process changes astrocyte physiology and can affect neuronal network function in various ways. Traumatic brain injury and stroke, both conditions that trigger astroglial scar formation, are leading causes of acquired epilepsies and surgical removal of this glial scar in patients with drug-resistant epilepsy can alleviate the seizures. This review will summarize the currently available evidence suggesting that epilepsy is not a disease of neurons alone, but that astrocytes, glial cells in the brain, can be major contributors to the disease, especially when they adopt a reactive state in response to central nervous system insult.

scholarly journals Physiological Ripples Associated With Sleep Spindles Can Be Identified in Patients With Refractory Epilepsy Beyond Mesio-Temporal Structures

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonas C. Bruder ◽  
Christoph Schmelzeisen ◽  
Daniel Lachner-Piza ◽  
Peter Reinacher ◽  
Andreas Schulze-Bonhage ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Outcome Prediction ◽  
Group Analysis ◽  
Brain Regions ◽  
Surgical Removal ◽  
Sleep Spindles ◽  
Seizure Outcome ◽  
Individual Patient Level ◽  
Temporal Structures ◽  
Rate Ratios

Introduction: High frequency oscillations (HFO) are promising biomarkers of epileptic tissue. While group analysis suggested a correlation between surgical removal of HFO generating tissue and seizure free outcome, HFO could not predict seizure outcome on an individual patient level. One possible explanation is the lack of differentiation between physiological and epileptic HFO. In the mesio-temporal lobe, a proportion of physiological ripples can be identified by their association with scalp sleep spindles. Spike associated ripples in contrast can be considered epileptic. This study investigated whether categorizing ripples by the co-occurrence with sleep spindles or spikes improves outcome prediction after surgery. Additionally, it aimed to investigate whether spindle-ripple association is limited to the mesio-temporal lobe structures or visible across the whole brain.Methods: We retrospectively analyzed EEG of 31 patients with chronic intracranial EEG. Sleep spindles in scalp EEG and ripples and epileptic spikes in iEEG were automatically detected. Three ripple subtypes were obtained: SpindleR, Non-SpindleR, and SpikeR. Rate ratios between removed and non-removed brain areas were calculated. We compared the distinct ripple subtypes and their rates in different brain regions, inside and outside seizure onset areas and between patients with good and poor seizure outcome.Results: SpindleR were found across all brain regions. SpikeR had significantly higher rates in the SOZ than in Non-SOZ channels. A significant positive correlation between removal of ripple-events and good outcome was found for the mixed ripple group (rs = 0.43, p = 0.017) and for ripples not associated with spindles (rs=0.40, p = 0.044). Also, a significantly high proportion of spikes associated with ripples were removed in seizure free patients (p = 0.036).Discussion: SpindleR are found in mesio-temporal and neocortical structures, indicating that ripple-spindle-coupling might have functional importance beyond mesio-temporal structures. Overall, the proportion of SpindleR was low and separating spindle and spike associated ripples did not improve outcome prediction in our patient group. SpindleR analysis therefore can be a tool to identify physiological events but needs to be used in combination with other methods to have clinical relevance.

Synaptic organization of the gustatory NST

1994 ◽  
Vol 52 ◽  
pp. 150-151
Author(s):  
M. C. Whitehead
Keyword(s):  
Central Nervous System ◽  
Dendritic Spines ◽  
Fundamental Problem ◽  
Cell Types ◽  
Brain Regions ◽  
Excitatory Synapses ◽  
Solitary Tract ◽  
Synaptic Organization ◽  
Synaptic Junctions ◽  
Afferent Terminals

A fundamental problem in taste research is to determine how gustatory signals are processed and disseminated in the mammalian central nervous system. An important first step toward understanding information processing is the identification of cell types in the nucleus of the solitary tract (NST) and their synaptic relationships with oral primary afferent terminals. Facial and glossopharyngeal (LIX) terminals in the hamster were labelled with HRP, examined with EM, and characterized as containing moderate concentrations of medium-sized round vesicles, and engaging in asymmetrical synaptic junctions. Ultrastructurally the endings resemble excitatory synapses in other brain regions.Labelled facial afferent endings in the RC subdivision synapse almost exclusively with distal dendrites and dendritic spines of NST cells. Most synaptic relationships between the facial synapses and the dendrites are simple. However, 40% of facial endings engage in complex synaptic relationships within glomeruli containing unlabelled axon endings particularly ones termed "SP" endings. SP endings are densely packed with small, pleomorphic vesicles and synapse with both the facial endings and their postsynaptic dendrites by means of nearly symmetrical junctions.

A Phonomotor Approach to Apraxia of Speech Treatment

2020 ◽  
Vol 29 (4) ◽  
pp. 2109-2130
Author(s):  
Lauren Bislick
Keyword(s):  
Phase I ◽  
Treatment Effects ◽  
Single Case ◽  
Motor Planning ◽  
The Other ◽  
Multimodal Approach ◽  
Apraxia Of Speech ◽  
Duration Of Treatment ◽  
Treatment Gains ◽  
Future Work

Purpose This study continued Phase I investigation of a modified Phonomotor Treatment (PMT) Program on motor planning in two individuals with apraxia of speech (AOS) and aphasia and, with support from prior work, refined Phase I methodology for treatment intensity and duration, a measure of communicative participation, and the use of effect size benchmarks specific to AOS. Method A single-case experimental design with multiple baselines across behaviors and participants was used to examine acquisition, generalization, and maintenance of treatment effects 8–10 weeks posttreatment. Treatment was distributed 3 days a week, and duration of treatment was specific to each participant (criterion based). Experimental stimuli consisted of target sounds or clusters embedded nonwords and real words, specific to each participants' deficit. Results Findings show improved repetition accuracy for targets in trained nonwords, generalization to targets in untrained nonwords and real words, and maintenance of treatment effects at 10 weeks posttreatment for one participant and more variable outcomes for the other participant. Conclusions Results indicate that a modified version of PMT can promote generalization and maintenance of treatment gains for trained speech targets via a multimodal approach emphasizing repeated exposure and practice. While these results are promising, the frequent co-occurrence of AOS and aphasia warrants a treatment that addresses both motor planning and linguistic deficits. Thus, the application of traditional PMT with participant-specific modifications for AOS embedded into the treatment program may be a more effective approach. Future work will continue to examine and maximize improvements in motor planning, while also treating anomia in aphasia.

Musical Anhedonia

2020 ◽  
Vol 31 (2) ◽  
pp. 62-68
Author(s):  
Sara E. Holm ◽  
Alexander Schmidt ◽  
Christoph J. Ploner
Keyword(s):  
Quality Of Life ◽  
Nucleus Accumbens ◽  
Brain Damage ◽  
Parietal Cortex ◽  
Neurological Disorders ◽  
Brain Regions ◽  
Precise Information ◽  
Exact Localization ◽  
High Prevalence

Abstract. Some people, although they are perfectly healthy and happy, cannot enjoy music. These individuals have musical anhedonia, a condition which can be congenital or may occur after focal brain damage. To date, only a few cases of acquired musical anhedonia have been reported in the literature with lesions of the temporo-parietal cortex being particularly important. Even less literature exists on congenital musical anhedonia, in which impaired connectivity of temporal brain regions with the Nucleus accumbens is implicated. Nonetheless, there is no precise information on the prevalence, causes or exact localization of both congenital and acquired musical anhedonia. However, the frequent involvement of temporo-parietal brain regions in neurological disorders such as stroke suggest the possibility of a high prevalence of this disorder, which leads to a considerable reduction in the quality of life.

Serotonergic Genes and Suicidality

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 54-60 ◽  
Author(s):  
Lisheng Du ◽  
Gabor Faludi ◽  
Miklos Palkovits ◽  
David Bakish ◽  
Pavel D. Hrdina
Keyword(s):  
Suicidal Ideation ◽  
Suicidal Behavior ◽  
Tryptophan Hydroxylase ◽  
Association Studies ◽  
Receptor Gene ◽  
Brain Regions ◽  
Depressive Illness ◽  
Control Group ◽  
Serotonergic Activity ◽  
Completed Suicide

Summary: Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of depressive illness and suicidal behavior. Studies have shown that the number of brain and platelet serotonin transporter binding sites are reduced in patients with depression and in suicide victims, and that the density of 5-HT2A receptors is increased in brain regions of depressed in suicide victims and in platelets of depressed suicidal patients. Genes that code for proteins, such as tryptophan hydroxylase, 5-HT transporter, and 5-HT2A receptor, involved in regulating serotonergic neurotransmission, have thus been major candidate genes for association studies of suicide and suicidal behavior. Recent studies by our group and by others have shown that genetic variations in the serotonin-system-related genes might be associated with suicidal ideation and completed suicide. We have shown that the 102 C allele in 5-HT2A receptor gene was significantly associated with suicidal ideation (χ2 = 8.5, p < .005) in depressed patients. Patients with a 102 C/C genotype had a significantly higher mean HAMD item #3 score (indication of suicidal ideation) than T/C or T/T genotype patients. Our results suggest that the 102T/C polymorphism in 5-HT2A receptor gene is primarily associated with suicidal ideation in patients with major depression and not with depression itself. We also found that the 5-HT transporter gene S/L polymorphism was significantly associated with completed suicide. The frequency of the L/L genotype in depressed suicide victims was almost double of that found in control group (48.6% vs. 26.2%). The odds ratio for the L allele was 2.1 (95% CI 1.2-3.7). The association between polymorphism in serotonergic genes and suicidality supports the hypothesis that genetic factors can modulate suicide risk by influencing serotonergic activity.

Inefficient Encoding as an Explanation for Age-Related Deficits in Recollection-Based Processing

2014 ◽  
Vol 28 (3) ◽  
pp. 148-161 ◽  
Author(s):  
David Friedman ◽  
Ray Johnson
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Cognitive Processes ◽  
Brain Activity ◽  
Memory Performance ◽  
Brain Regions ◽  
Semantic Retrieval ◽  
Age Related ◽  
The Face ◽  
Episodic Memories

A cardinal feature of aging is a decline in episodic memory (EM). Nevertheless, there is evidence that some older adults may be able to “compensate” for failures in recollection-based processing by recruiting brain regions and cognitive processes not normally recruited by the young. We review the evidence suggesting that age-related declines in EM performance and recollection-related brain activity (left-parietal EM effect; LPEM) are due to altered processing at encoding. We describe results from our laboratory on differences in encoding- and retrieval-related activity between young and older adults. We then show that, relative to the young, in older adults brain activity at encoding is reduced over a brain region believed to be crucial for successful semantic elaboration in a 400–1,400-ms interval (left inferior prefrontal cortex, LIPFC; Johnson, Nessler, & Friedman, 2013 ; Nessler, Friedman, Johnson, & Bersick, 2007 ; Nessler, Johnson, Bersick, & Friedman, 2006 ). This reduced brain activity is associated with diminished subsequent recognition-memory performance and the LPEM at retrieval. We provide evidence for this premise by demonstrating that disrupting encoding-related processes during this 400–1,400-ms interval in young adults affords causal support for the hypothesis that the reduction over LIPFC during encoding produces the hallmarks of an age-related EM deficit: normal semantic retrieval at encoding, reduced subsequent episodic recognition accuracy, free recall, and the LPEM. Finally, we show that the reduced LPEM in young adults is associated with “additional” brain activity over similar brain areas as those activated when older adults show deficient retrieval. Hence, rather than supporting the compensation hypothesis, these data are more consistent with the scaffolding hypothesis, in which the recruitment of additional cognitive processes is an adaptive response across the life span in the face of momentary increases in task demand due to poorly-encoded episodic memories.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

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