Podcasts about meningeal

Ever wondered how your brain takes out the trash?

In this week's podcast, Neurology Today's editor-in-chief highlights articles on the safety of middle meningeal artery embolization for chronic subdural hematoma, the processed red meat and risk for dementia, and editors' picks for the best advances of 2024.

Emily takes Clara on a trip down memory lane to her first job in the field of biology... chopping up deer. In this week's episode, we learn the relationship between a meningeal nematode, moose, deer, and gastropods in mainland Nova Scotia. Trigger Warning for some discussion of dissections.LOW-DOSE MENINGEAL WORM (PARELAPHOSTRONGYLUS TENUIS) INFECTIONS IN MOOSE (ALCES ALCES) : https://meridian.allenpress.com/jwd/article/38/4/789/122782/LOW-DOSE-MENINGEAL-WORM-PARELAPHOSTRONGYLUS-TENUISThe ecological relationships of meningeal worm and north American cervids: https://meridian.allenpress.com/jwd/article/8/4/304/126681/THE-ECOLOGICAL-RELATIONSHIPS-OF-MENINGEAL-WORM-ANDUNDERSTANDING THE IMPACT OF MENINGEAL WORM, PARELAPHOSTRONGYLUS TENUIS, ON MOOSE POPULATIONS: https://shorturl.at/wAKU1Parelaphostrongylus tenuis in New Brunswick: The Parasite in Terrestrial Gastropods: https://meridian.allenpress.com/jwd/article/22/4/582/119580/Parelaphostrongylus-tenuis-in-New-Brunswick-ThePneumostrongylus tenuis in Deer in Minnesota and Implications for Moose: https://www.jstor.org/stable/3798320?casa_token=eT7dPrmjEmoAAAAA%3AG8VWzU0eh3CvsbgAFsVGUg2Z1pXoYwcR4sfW0_QBf_OYBAtiQt0UZq_P0I1_qs0yfHi9vDzEyfjcoYQ379sxampO7IGjo5OBfN8eiu5Gzba8DKQVB8vjGw&seq=1Nova Scotia Department of resources and renewables: https://novascotia.ca/natr/wildlife/sustainable/mmoosefaq.aspContinuing environmental change: an example from Nova scotia: https://www.canadianfieldnaturalist.ca/cfn/index.php/cfn/article/view/880/881Parelaphostrongylus tenuis (FRYADKO AND BOEV) IN THE MOOSE AND WHITE-TAILED DEER OF NOVA SCOTIA : https://scholar.acadiau.ca/islandora/object/theses:3327/datastream/PDF/file.pdfUNDERSTANDING THE IMPACT OF MENINGEAL WORM, PARELAPHOSTRONGYLUS TENUIS, ON MOOSE POPULATIONS: https://alcesjournal.org/index.php/alces/article/view/59Parasites of Caribou: https://www.gov.nl.ca/ffa/files/agrifoods-animals-health-pdf-ds-08-007.pdfBiology and diseases of ruminants: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/parelaphostrongylus-tenuis

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.31.549838v1?rss=1 Authors: Blaeser, A. S., Zhao, J., Sugden, A. U., Carneiro-Nascimento, S., Andermann, M. L., Levy, D. Abstract: Migraine headache is thought to involve the activation and sensitization of trigeminal sensory afferents that innervate the cranial meninges. However, this notion is based mainly on preclinical studies in anesthetized animals with surgically exposed meninges. Here, we used two photon calcium imaging via a closed cranial window in awake, behaving mice to investigate the responses of meningeal afferents that might lead to migraine pain using a preclinical model of migraine involving cortical spreading depolarization (CSD). A single CSD episode caused a second-slong wave of calcium activation that propagated across afferents and along the length of individual afferents. Surprisingly, few afferents exhibited prolonged activation or suppression following CSD. However, a specific subset of afferents - those sensitive to acute meningeal deformation - exhibited stronger activation during locomotion bouts. Moreover, following CSD, a subset of previously silent afferents developed sensitivity to locomotion-related meningeal deformation. Our data point to acute calcium signaling in meningeal afferents as a potentially critical nociceptive factor contributing to migraine pain and support the notion that enhanced responsiveness of meningeal afferents to local mechanical deformation of the meninges is the neural substrate underlying the worsening of migraine headache pain during physical activity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Following the Meninges podcast, this soundbite is dedicated to the anatomy of bleeds inside the skull.  Terms covered this week include the cerebral arteries & subarachnoid haemorrhages. Cerebral bridging veins & subdural haemorrhages. Meningeal arteries & extra/epidural haemorrhages.   

May 2023 Journal Club Podcast Title: Onyx versus Particles for Middle Meningeal Artery Embolization in Chronic Subdural Hematoma To read journal article: https://journals.lww.com/neurosurgery/Fulltext/2023/05000/Onyx_Versus_Particles_for_Middle_Meningeal_Artery.10.aspx Author: Pascal Jabbour Guest Faculty: Phillipp Taussky Resident Planner: Alexander Suarez Moderator: Kimberly Hoang

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526853v1?rss=1 Authors: Zhao, J., Levy, D. Abstract: Cortical spreading depolarization (CSD) is a key pathophysiological event that underlies visual and sensory auras in migraine. CSD further drives the headache phase in migraine by promoting the activation and sensitization of trigeminal meningeal sensory afferents. The factors responsible for this meningeal nociceptive response in the wake of CSD remain poorly understood, but potentially involve the local release of algesic, proinflammatory mediators, including ATP. Here, we used an in vivo extracellular single-unit recording of meningeal afferent activity in combination with topical administration of pharmacological agents in a rat model to explore the role of ATP-P2X receptor signaling in mediating CSD-evoked meningeal afferent activation and sensitization. We found that broad-spectrum inhibition of P2X receptors, P2X7 receptor antagonist, and blockade of the related pannexin1 channel suppressed CSD-evoked afferent mechanical sensitization, but did not affect afferent activation. Pharmacological inhibition of the pronociceptive P2X2,3 ATP receptor did not affect meningeal nociception post-CSD. Finally, we provide evidence supporting the notion that the anti-nociceptive effect mediated by P2X7 is localized to the meningeal and not the cerebral cortex. We propose that meningeal P2X7 and Panx1 signaling, potentially in meningeal macrophages or neutrophils mediates the mechanical sensitization of meningeal afferents, and contributes to migraine pain by exacerbating the headache during normally innocuous physical activities. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode, we chat with Dr. Guillermo Oliver.  Guillermo Oliver is a Uruguayan-American research scientist. He is currently the Thomas D. Spies Professor of Lymphatic Metabolism at Northwestern University, and director of the Center for Vascular and Developmental Biology at the Feinberg Cardiovascular Research Institute. Oliver is an elected member of both the American Association for the Advancement of Science and the Academia de Ciencias de América Latina. One of Oliver's research focuses has been the lymphatic vasculature, and his laboratory demonstrated that Prox1 activity was required for the differentiation of lymphatic endothelial cells and the formation of the entire lymphatic vasculature.[9][10] They later showed the role of lymphatic vasculature on obesity.[11][12] His laboratory also identified Six2 as a critical gene in the process of generation of nephron progenitors[13] and demonstrated that Six3 activity was required for the formation of the mammalian forebrain and neuroretina in mice.[14][15] He expanded those results using embryonic stem cells and induced pluripotent stem cells to generate eye organoids that mimic early eye development.[8] In 2020, he published his research on the role of the Reelin protein promotes cardiac regeneration and repair by reducing cell death after heart injury in the journal Nature.[16][1 (Bio reference: Wikipedia) Highlights of this podcast include: What is Lymphatics Removal of toxins Immune response Lymphedema Weight gain and lymphatics Obesity and lymphatics Meningeal lymphatics Cardiac repair Lymphatics and organ growth Comorbidity Diet and lymphatics Crohns, IBS and lymphatics Lipedema And so much more... To learn more about Guillermo Oliver, visit @NU_Lymphatics on Twitter or on the Northwestern Medicine website and bio.  Reference: The Lymphatic Vasculature in the 21st Century: Novel Functional Roles in Homeostasis and Disease. 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.05.506398v1?rss=1 Authors: Santisteban, M. M., Faraco, G., Brea Lopez, D., Wang, G., Sobanko, M. J., Sciortino, R., Racchumi, G., Waisman, A., Anrather, J., Iadecola, C. Abstract: Hypertension, a disease afflicting over one billion individuals worldwide, is a leading cause of cognitive impairment, the mechanisms of which remain poorly understood. In a mouse model of hypertension involving brain angiotensin signaling, we found that the neurovascular and cognitive dysfunction depends on IL-17, a cytokine elevated in the circulation of hypertensive individuals. However, neither circulating IL-17 or brain angiotensin signaling could account in full for the dysfunction. Rather, IL-17 produced by meningeal T-cells was the major culprit by activating IL-17 receptors on brain associated macrophages. Accordingly, depleting brain macrophages or suppressing meningeal T cells completely rescued cognitive function without attenuating blood pressure elevation, circulating IL-17 or brain angiotensin signaling. The data unveil a critical role of meningeal T-cells and macrophage IL-17 signaling in the neurovascular and cognitive dysfunction of hypertension and suggest novel therapies to counteract the devastating effects of hypertension on cognitive health. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

TWiN describes how neurotropic viruses leave the brain via meningeal lymphatic vessels located dorsally and basally beneath the skull. Hosts: Vincent Racaniello, Ori Lieberman, Jason Shepherd, and Timothy Cheung Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Links for this episode Meningeal lymph vessels and viral exit from brain (Nature Neuroscience) Clearing mouse brain video (YouTube) Timestamps by Jolene. Thanks! Music is by Ronald Jenkees Send your neuroscience questions and comments to twin@microbe.tv

In this episode, we chat with Jonathan Kipnis, Ph.D. - BJC Investigator. Jonathan Kipnis is a neuroscientist, immunologist, and professor of pathology and immunology at the Washington University School of Medicine. His lab studies interactions between the immune system and nervous system. He is best known for his lab's discovery of meningeal lymphatic vessels in humans and mice, which has impacted research on neurodegenerative diseases such as Alzheimer's disease and multiple sclerosis, neuropsychiatric disorders, such as anxiety, and neurodevelopmental disorders such as autism and Rett syndrome. Kipnis is credited with the 2014 discovery of meningeal lymphatic vessels, a recently discovered network of conventional lymphatic vessels located parallel to the dural sinuses and meningeal arteries of the mammalian central nervous system (CNS). As a part of the lymphatic system, meningeal lymphatics are responsible for draining immune cells, small molecules, and excess fluid from the CNS and into the deep cervical lymph nodes. While it was initially believed that both the brain and meninges were devoid of lymphatic vasculature, the landmark Nature paper by Jonathan Kipnis and his postdoctoral fellow Antoine Louveau was published in 2015. By 2016, this paper was cited nearly 200 times. His discovery of meningeal lymphatic vessels was included in Scientific American's "Top 10 Science Stories of 2015", Science Magazine's "Breakthrough of the Year", Huffington Post's "Eight Fascinating Things We Learned About the Mind in 2015" and the National Institutes of Health's director Francis Collins year-end review. Other research has included the 2015 discovery that the immune system directly affects social behavior and that IFN-gamma is necessary for social development. This expands upon his work as a graduate student when he discovered that mice lacking T-cells had cognitive impairments.  (Biography reference - Wikipedia)  Highlights of this podcast include: Menigineal immunity and functions Functions of the glymphatics and meningeal lymphatics Neuroimmune system  Meningeal lymphatics draining the CNS Immune system affects on the brain  Pia, arachnoid, and dura mater Difference between the Lymphatic system and the Glymphatic system Aging and glymphatics Brain tumors  Sleep and glymphatic draining Alzheimers Immuno-therapies and combination therapies And So Much More! To learn more about Jonathan Kipnis PhD., please visit kipnislab.wustl.edu This episode is brought to you by Therasage. Use code: STOPCHASINGPAIN at checkout.   

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September 2021 Journal Club Podcast Middle Meningeal Artery Embolization Versus Conventional Treatment of Chronic Subdural Hematomas To read the journal article: https://academic.oup.com/neurosurgery/article/89/3/486/6309701?login=true Moderator: Rimal H. Dossani, MD Author: Ajith J. Thomas, MD Faculty: Jonathan A. Grossberg, MD and Aqueel H. Pabaney, MD

Meningeal worm, also known as deer worm, is a worm that is normally found in white tail deer, but goats can become infected. In this episode Dr. Tatiana Stanton, a goat and sheep specialist with Cornell University Extension, is talking about how deer worm is different than intestinal worms that goats have, symptoms of an infection, and treatment. Although deer worm is not nearly as common as intestinal worms, they can be much more deadly. While a goat can walk around with thousands of roundworms in its digestive tract, a single deer worm in the spinal column or brain stem can paralyze a goat and even kill it, if it is not treated. Getting treatment started as quickly as possible also plays a big role in a successful outcome.For more information:Deer Worm Factsheet for goat and sheep producers, Cornell UniversityDeer Worm Treatment Protocols, Small Ruminant Parasite Research, Cornell UniversityMeningeal Worm (Deer, Brain Worm) by Dr. Mary Smith, DVM, and Dr. Tatiana Stanton (PowerPoint presentation)

DeLa isA husband A father A musician A brain tumor survivor and A believer!He is the saxophonist for the band slightly stoopid and also leads his own band Dela & steady rock easy. 0:00:00 Bringing awareness to others0:05:08 Symptoms preceding diagnosis0:09:25 Tunnel vision0:13:15 Tumor doubles in size0:16:13 Tumor responds to the threat0:17:39 Brief synopsis of Bert’s cancer journey0:24:18 Scott Palmer0:29:54 When it all hit home0:33:35 Full frontal bilateral craniotomy0:39:37 Anesthesia or local anesthetic0:42: 31 Dela wakes up completely blind0:45:46 From the O.R. to the Stage0:50:13 Radiation therapy0:58:20 The power of music1:03:19 Nurses our heroes1:13:21 Dela’s eyesight returns 1:16:08 The blessing of it all1:21:21 Living fully/On Kilimanjaro1:28:42 We go it alone1:37:29 Radiation breakdown1:43:40 Ringing the bell1:48:33 Post-treatment follow-up https://delasaxmusic.comhttps://www.slightlystoopid.comSocials @delasaxmusic

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.03.281543v1?rss=1 Authors: van Olst, L., Rodriguez-Mogeda, C., Picon-Munoz, C., Kiljan, S., James, R. E., Kamermans, A., van der Pol, S. M. A., Knoop, L., Drost, E., Franssen, M., Schenk, G., Geurts, J. J. G., Amor, S., Mazarakis, N. D., van Horssen, J., de Vries, H. E., Reynolds, R., Witte, M. E. Abstract: Meningeal inflammation strongly associates with demyelination and neuronal loss in the underlying cortex of progressive MS patients, contributing to clinical disability. However, the pathological mechanisms of meningeal inflammation-induced cortical pathology are still largely elusive. Using extensive analysis of human post-mortem tissue, we identified two distinct microglial phenotypes, termed MS1 and MS2, in the cortex of progressive MS patients. These phenotypes differed in morphology and protein expression, but both associated with inflammation of the overlying meninges. We could replicate the MS-specific microglial phenotypes in a novel in vivo rat model for progressive MS-like meningeal inflammation, with microglia present at 1 month post-induction resembling MS1 microglia whereas those at 2 months acquired an MS2-like phenotype. Interestingly, MS1 microglia were involved in presynaptic displacement and phagocytosis and associated with a relative sparing of neurons in the MS and animal cortex. In contrast, the presence of MS2 microglia coincided with substantial neuronal loss. Taken together, we uncovered that in response to meningeal inflammation, microglia acquire two distinct phenotypes that differentially associate with neurodegeneration in the progressive MS cortex. Our data suggests that these phenotypes occur sequentially and that microglia may lose their protective properties over time, contributing to neuronal loss. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.26.268250v1?rss=1 Authors: Bhargava, P., Kim, S., Reyes, A. A., Grenningloh, R., Boshcert, U., Absinta, M., Pardo-Villamizar, C., Van Zijl, P., Zhang, J., Calabresi, P. Abstract: Leptomeningeal inflammation in multiple sclerosis is associated with worse clinical outcomes and greater cortical pathology. Despite progress in identification of this process in multiple sclerosis patients using post-contrast FLAIR imaging, early trials attempting to target meningeal inflammation have been unsuccessful. There is a lack of appropriate model systems to screen potential therapeutic agents targeting meningeal inflammation. We utilized ultra-high field (11.7 Tesla) MRI to perform post-contrast FLAIR imaging in SJL/J mice with experimental autoimmune encephalomyelitis induced using immunization with proteolipid protein peptide (PLP139-151) and complete Freund's adjuvant. Imaging was performed in both a cross-sectional and longitudinal fashion at time-points ranging from 2 to 14 weeks post-immunization. Following imaging, we euthanized animals and collected tissue for pathological evaluation, which identified dense cellular infiltrates corresponding to areas of contrast-enhancement involving the leptomeninges. These areas of meningeal inflammation contained B cells (B220+), T cells (CD3+) and myeloid cells (Mac2+). We also noted features consistent with tertiary lymphoid tissue within these areas - presence of peripheral node addressin (PNAd) positive structures, CXCL13 producing cells and FDC-M1+ follicular dendritic cells. In the cortex adjacent to areas of meningeal inflammation we identified astrocytosis, microgliosis, demyelination and evidence of axonal stress/damage. Since areas of meningeal contrast enhancement persisted over several weeks in longitudinal experiments, we utilized this model to test the effects of a therapeutic intervention on established meningeal inflammation. We randomized mice with evidence of meningeal contrast enhancement on MRI scans performed at 6 weeks post-immunization, to treatment with either vehicle or evobrutinib (a Bruton's tyrosine kinase inhibitor) for a period of 4 weeks. These mice underwent serial imaging and we examined the effect of treatment on the areas of meningeal contrast enhancement and noted a significant reduction in the evobrutinib group compared to vehicle (30% reduction versus 5% increase; P = 0.003). We utilized ultra-high field MRI imaging to identify areas of meningeal inflammation and to track them over time in SJL/J mice with experimental autoimmune encephalomyelitis and then utilized this model to identify Bruton's tyrosine kinase inhibition as a novel therapeutic approach to target meningeal inflammation. The results of this study provide support for future studies in multiple sclerosis patients with imaging evidence of meningeal inflammation. Copy rights belong to original authors. Visit the link for more info

Prof Madhi has recently co-authored a number of articles about South Africa’s route out of lock down. So we chatted about how this might look. He emphasised the need for people to observe distancing protocols in order to slow the rate of corona virus infection. We chatted about the changing understanding of how corona virus acts on people. We also discussed the reasons behind the lock down and how some of these reason are no longer valid according to Shabir. Another issue we touched on  is  the spread of corona virus via asymptomatic carriers. Shabir is also concerned that many decisions taken by government have not been based on science.  We also discussed the global bun-fight around developing a vaccine. It is clear that we will have to live with corona virus as best we can until a vaccine is available and this process might take years. Read Shabir's latest article about South Africa's COVID-19 strategy here (https://theconversation.com/south-africas-covid-19-strategy-needs-updating-heres-why-and-how-138368) .

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.01.072611v1?rss=1 Authors: Hsu, S.-J., Zhang, C., Jeong, J., Lee, S.-i., McConnell, M., Utsumi, T., Iwakiri, Y. Abstract: Background and aims: Hepatic encephalopathy (HE) is a serious neurological complication in patients with liver cirrhosis. Nothing is known about the role of the meningeal lymphatic system in HE. We tested our hypothesis that enhancement of meningeal lymphatic drainage could decrease neuroinflammation and ameliorate HE. Methods: A 4-week bile duct ligation (BDL) model was used to develop cirrhosis with HE in rats. Brain inflammation in patients with HE was evaluated using archived GSE41919. Motor function of rats was assessed by the rotarod test. AAV8-VEGF-C was injected into the cisterna magna of BDL rats one day after surgery to induce meningeal lymphangiogenesis. Results: Cirrhotic rats with HE showed significantly increased microglia activation in the middle region of the cortex (p

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.25.060939v1?rss=1 Authors: Mikhailov, N., Koroleva, K., Abdollahzadeh, A., Giniatullina, R., Gafurov, O., Malm, T., Sierra Lopez, A., Tohka, J., Noe, F. M., Giniatullin, R. Abstract: Background: A system of lymphatic vessels has been recently characterized in the meninges, with a postulated role in cleaning of the brain via cerebro-spinal fluid drainage. As meninges are an important tissue involved in the origin of migraine pain, we hypothesized that malfunctioning of a cleaning lymphatic system should affect the functional properties of meningeal nociception. To test this hypothesis, we studied migraine-related nociceptive and inflammatory mechanisms in the meninges, in a mouse model of primary lymphedema (K14-VEGFR3-Ig mice) characterized by the lack of functional meningeal lymphatic system. Methods: To study the migraine-related nociceptive and inflammatory mechanisms we recorded spiking activity from meningeal fibers of the trigeminal nerve, estimated the local mast cells infiltration, calcitonin gene-related peptide (CGRP) and cytokine levels (basal and under stimulating conditions), as well as the dura mater innervation in freshly-isolated hemiskull preparations from K14-VEGFR3-Ig (K14) or wild type C57BL/6 mice (WT). Results: We found that the level of CGRP and the production of TNF , which both are implicated in migraine, were reduced in meninges of K14 mice. There was a trend of having a larger number of dural mast cells, consistent with the increased level of the mast cell activator MCP-1 found in these animals. In addition, we found an increased spontaneous and ATP-induced nociceptive firing in the meningeal afferents of mice lacking meningeal lymphatic system. However, the patterns of trigeminal innervation in meninges remained unchanged. Conclusions: In summary, the lack of meningeal lymphatic system leads to a new balance between pro- and anti-inflammatory mechanisms implicated in peripheral nociception, affecting key cellular and humoral factors implicated in migraine. Copy rights belong to original authors. Visit the link for more info

Brain worm!Parelaphostrongylus tenuis aka meningeal worm aka brain worm is a problem for small ruminants, camelids and cervids in areas where there is a white tailed deer population. These weird worms do not have negative effects on their normal definitive hosts, white tailed deer, but when they get lost trying to complete their lifecycles in other species, they cause issues.In this episode, I talk about what P teuis does, why it causes issues, what the issues look like, how I tend to treat clinical cases, and what can be done for prevention. See acast.com/privacy for privacy and opt-out information.

Chronic pain, tightness and less flexibility may be caused by the life force being blocked within the spine and meningeal system (sheath that surrounds the spinal cord). This is caused by not recovering from emotional, mental, chemical, and physical stress. Dr Larry helps us understand (with a bit of humor) this process and what we can do about it. Krista Poulton, Medical Herbalist, is back for a very informative check in on TEAS. Larry Zaleski, D.C. is a chiropractor with over 30 years experience in practice. He graduated from Sherman College of Chiropractic in South Carolina in 1981. Larry provided chiropractic care in his successful chiropractic practice in Delaware from 1983-2000. In 1987, Larry became a national instructor of Network Chiropractic which involved training chiropractors from around the world about the philosophy and technique of freeing the spine of interference (subluxations). After passing the licensing examinations and relocating to British Columbia, Dr. Larry opened his chiropractic practice at the Hand & Soul Wellness Center in Silverton, BC. He practices in Silverton, Nakusp and Winlaw BC. Here is the Amazon link to the book Dr. Larry was talking about, The Presence Process by Michael Brown The Presence Process Here is the Link to Dr. Larry's Website The exercises that Dr. Larry spoke of are from the book 3 Minutes to a Pain Free Life by by Joseph Weisberg and Heidi Shink the exercises start on page 132.Download.

Chronic pain, tightness and less flexibility may be caused by the life force being blocked within the spine and meningeal system (sheath that surrounds the spinal cord). This is caused by not recovering from emotional, mental, chemical, and physical stress. Dr Larry helps us understand (with a bit of humor) this process and what we can do about it. Krista Poulton, Medical Herbalist, is back for a very informative check in on TEAS. Larry Zaleski, D.C. is a chiropractor with over 30 years experience in practice. He graduated from Sherman College of Chiropractic in South Carolina in 1981. Larry provided chiropractic care in his successful chiropractic practice in Delaware from 1983-2000. In 1987, Larry became a national instructor of Network Chiropractic which involved training chiropractors from around the world about the philosophy and technique of freeing the spine of interference (subluxations). After passing the licensing examinations and relocating to British Columbia, Dr. Larry opened his chiropractic practice at the Hand & Soul Wellness Center in Silverton, BC. He practices in Silverton, Nakusp and Winlaw BC. Here is the Amazon link to the book Dr. Larry was talking about, The Presence Process by Michael Brown The Presence Process Here is the Link to Dr. Larry's Website The exercises that Dr. Larry spoke of are from the book 3 Minutes to a Pain Free Life by by Joseph Weisberg and Heidi Shink the exercises start on page 132.Download.

Dr. Taofeek Owonikoko reviews why we often see brain metastases develop as a first or only site of progression in patients with NSCLC and a driver mutation.

Dr. Taofeek Owonikoko reviews why we often see brain metastases develop as a first or only site of progression in patients with NSCLC and a driver mutation.

Dr. Taofeek Owonikoko reviews why we often see brain metastases develop as a first or only site of progression in patients with NSCLC and a driver mutation.

Question and answer session with Dr. Minesh Mehta, Professor of Radiation Oncology at Northwestern University, on topics related to treatments for brain metastases and related complications, especially in the setting of lung cancer.

Question and answer session with Dr. Minesh Mehta, Professor of Radiation Oncology at Northwestern University, on topics related to treatments for brain metastases and related complications, especially in the setting of lung cancer.

In neurology, paroxysmal syndromes are well-known, eg, as manifestations of multiple sclerosis. We report a patient with meningeal carcinomatosis, who presented with therapyrefractory nausea and vomiting. The clinical suspicion of a paroxysmal syndrome prompted a trial of carbamazepine, which resulted in complete cessation of the symptoms. In cancer patients with central nervous system (CNS) involvement and therapy-refractory symptoms with sudden onset, carbamazepine treatment should be considered.