Posts tagged neurology
Articles and news from the latest research reports.
Low Diastolic Blood Pressure May Be Associated With Brain Atrophy
Low baseline diastolic blood pressure (DBP) appears to be associated with brain atrophy in patients with arterial disease, whenever declining levels of blood pressure (BP) over time among patients who had a higher baseline BP were associated with less progression of atrophy, according to a report published Online First by JAMA Neurology, a JAMA Network publication.
(Image: Wikimedia Commons)
“Studies have shown that both high and low blood pressure (BP) may play a role in the etiology of brain atrophy. High BP in midlife has been associated with more brain atrophy later in life, whereas studies in older populations have shown a relation between low BP and more brain atrophy. Yet, prospective evidence is limited, and the relation remains unclear in patients with manifest arterial disease,” according to the study.
Hadassa M. Jochemsen, M.D., of University Medical Center Utrecht, the Netherlands, and colleagues examined the association of baseline BP and change in BP over time with the progression of brain atrophy in 663 patients (average age 57 years; 81 percent male). The patients had coronary artery disease, cerebrovascular disease, peripheral artery disease or abdominal aortic aneurysm.
According to the results, patients with lower baseline DBP or mean arterial pressure (MAP) had more progression of subcortical (the area beneath the cortex of the brain) atrophy. In patients with higher BP (DBP, MAP or systolic BP), those with declining BP levels over time had less progression of subcortical atrophy compared with those with rising BP levels.
“This could imply that BP lowering is beneficial in patients with higher BP levels, but one should be cautious with further BP lowering in patients who already have low BP,” the study authors conclude.
(Source: media.jamanetwork.com)
Study Expands Concerns About Anesthesia’s Impact on the Brain
As pediatric specialists become increasingly aware that surgical anesthesia may have lasting effects on the developing brains of young children, new research suggests the threat may also apply to adult brains.
Researchers from Cincinnati Children’s Hospital Medical Center report June 5 the Annals of Neurology that testing in laboratory mice shows anesthesia’s neurotoxic effects depend on the age of brain neurons – not the age of the animal undergoing anesthesia, as once thought.
Although more research is needed to confirm the study’s relevance to humans, the study suggests possible health implications for millions of children and adults who undergo surgical anesthesia annually, according to Andreas Loepke, MD, PhD, a physician and researcher in the Department of Anesthesiology.
“We demonstrate that anesthesia-induced cell death in neurons is not limited to the immature brain, as previously believed,” said Loepke. “Instead, vulnerability seems to target neurons of a certain age and maturational stage. This finding brings us a step closer to understanding the phenomenon’s underlying mechanism”.
New neurons are generated abundantly in most regions of the very young brain, explaining why previous research has focused on that developmental stage. In a mature brain, neuron formation slows considerably, but extends into later life in dentate gyrus and olfactory bulb.
The dentate gyrus, which helps control learning and memory, is the region Loepke and his research colleagues paid particular attention to in their study. Also collaborating were researchers from the University of Cincinnati College of Medicine and the Children’s Hospital of Fudan University, Shanghai, China.
Researchers exposed newborn, juvenile and young adult mice to a widely used anesthetic called isoflurane in doses approximating those used in surgical practice. Newborn mice exhibited widespread neuronal loss in forebrain structures – confirming previous research – with no significant impact on the dentate gyrus. However, the effect in juvenile mice was reversed, with minimal neuronal impact in the forebrain regions and significant cell death in the dentate gyrus.
The team then performed extensive studies to discover that age and maturational stage of the affected neurons were the defining characteristics for vulnerability to anesthesia-induced neuronal cell death. The researchers observed similar results in young adult mice as well.
Research over the past 10 years has made it increasingly clear that commonly used anesthetics increase brain cell death in developing animals, raising concerns from the Food and Drug Administration, clinicians, neuroscientists and the public. As well, several follow-up studies in children and adults who have undergone surgical anesthesia show a link to learning and memory impairment.
Cautioning against immediate application of the current study’s findings to children and adults undergoing anesthesia, Loepke said his research team is trying to learn enough about anesthesia’s impact on brain chemistry to develop protective therapeutic strategies, in case they are needed. To this end, their next step is to identify specific molecular processes triggered by anesthesia that lead to brain cell death.
“Surgery is often vital to save lives or maintain quality of life and usually cannot be performed without general anesthesia,” Loepke said. “Physicians should carefully discuss with patients, parents and caretakers the risks and benefits of procedures requiring anesthetics, as well as the known risks of not treating certain conditions.”
Loepke is also collaborating with researchers from the Pediatric Neuroimaging Research Consortium at Cincinnati Children’s Hospital Medical Center to examine anesthesia’s impact on children’s brain using non-invasive magnetic resonance imaging (MRI) technology.
Study identifies new approach to improving treatment for MS and other conditions
Working with lab mice models of multiple sclerosis (MS), UC Davis scientists have detected a novel molecular target for the design of drugs that could be safer and more effective than current FDA-approved medications against MS.
The findings of the research study, published online today in the journal EMBO Molecular Medicine could have therapeutic applications for MS as well as cerebral palsy and leukodystrophies, all disorders associated with loss of white matter, which is the brain tissue that carries information between nerve cells in the brain and the spinal cord.
The target, a protein referred to as mitochondrial translocator protein (TSPO), had been previously identified but not linked to MS, an autoimmune disease that strips the protective fatty coating off nerve fibers of the brain and spinal cord. The mitrochronical TSPO is located on the outer surface of mitochondria, cellular structures that supply energy to the cells. Damage to the fatty coating, or myelin, slows the transmission of the nerve signals that enable body movement as well as sensory and cognitive functioning.
The scientists identified mitochondrial TSPO as a potential therapeutic target when mice that had symptoms of MS improved after being treated with the anti-anxiety drug etifoxine, which interacts with mitochondrial TSPO. When etifoxine, a drug clinically available in Europe, was administered to the MS mice before they had clinical signs of disease, the severity of the disease was reduced when compared to the untreated lab animals. When treated at the peak of disease severity, the animals’ MS symptoms improved.
“Etifoxine has a novel protective effect against the loss of the sheath that insulates the nerve fibers that transmit the signals from brain cells,” said Wenbin Deng, principal investigator of the study and associate professor of biochemistry and molecular medicine at UC Davis.
“Our discovery of etifoxine’s effects on an MS animal model suggests that mitochondrial TSPO represents a potential therapeutic target for MS drug development,” said Deng.
“Drugs designed to more precisely bind to mitochondrial TSPO may help repair the myelin sheath of MS patients and thereby even help restore the transmission of signals in the central nervous system that enable normal motor, sensory and cognitive functions,” he said.
Deng added that better treatments for MS and other demyelinating diseases are needed, especially since current FDA-approved therapies do not repair the damage of immune attacks on the myelin sheath.
The UC Davis research team hopes to further investigate the therapeutic applications of mitochondrial TSPO in drug development for MS and other autoimmune diseases. To identify more efficacious and safer drug candidates, they plan to pursue research grants that will enable them to test a variety of pharmacological compounds that bind to mitochondrial TSPO and other molecular targets in experimental models of MS and other myelin diseases.
(Source: ucdmc.ucdavis.edu)
Man’s chronic runny nose was actually brain fluid leaking
Arizona had one of the worst allergy seasons in recent memory this year. Even people who normally don’t suffer found themselves with itchy eyes and runny noses.
Thankfully it’s only a couple months out of the year, but for one valley man, he had year-round allergy symptoms. A runny nose all the time.
He was shocked to find out after years of suffering, his runny nose was really a leaking brain.
Joe Nagy first noticed it when he sat up to get out of bed.
"Brooop! This clear liquid dribbled out of my nose like tears out of your eyes. I go what is this?"
A runny nose that got worse.
"Once or twice a week. Then pretty soon it was all the time."
He started taking allergy medicine, but the runny nose didn’t stop.
"I got to the point where I had tissues all the time. in my pocket full of tissues always had them all folded up."
He still remembers the embarrassing moments when he couldn’t get to the tissues in time, like when he was picking up blueprints for his model airplanes.
"It was about a teaspoon full. Splashed all over the top sheet… I said, these damn allergies. I was embarrassed as hell."
Fed up with the runny nose, Joe went to a specialist to test that fluid dripping out of his nose and found out it wasn’t a runny nose. It was leaking brain fluid.
"I was scared to death if you want to know the truth."
The membrane surrounding Joe’s brain had a hole in it and his brain fluid was leaking out.
"You don’t really think about it, but our brains are really just above our noses all of the time," says Barrow Neurological Institute neurosurgeon Peter Nakaji.
"This is one of the more common conditions to be missed for a long time… because so many people have runny noses."
Joe was ready to have brain surgery to fix the leak. When he got a near-deadly case of meningitis, that brain fluid became infected.
"Some people come in with meningitis and at first they have to be treated to stop the infection itself. Then as soon as the infection is under control we repair the leak."
You might wonder how Joe could have brain fluid leaking out of his nose for a year and a half. Wouldn’t the brain dry out?
Each day our bodies produce about 12 ounces of brain fluid, give or take. Producing enough to keep the brain bathed in liquid.
"These leaks can be very very tiny, a little like a puncture on a bicycle tire, that sometimes you have trouble even finding where it is."
Dr. Nakaji eventually found the leak.
"If you look right here you can see a little tiny hole. You see a little bit of what looks like running water."
Dr. Nakaji showed us how this problem is fixed with surgery.
"Nowadays we do quite a bit of surgery on the brain and base of brain through the nose. We never have to cut up into the brain. We’re getting a needle up into the space to check it out, and then to put a little bit of glue. This is just a bit of cartilage from the nose that we can get to repair over it and then the body will seal it up."
Joe wasn’t convinced it would work. After all, he’d been dealing with the problem for so long. But days after the surgery, they removed the gauze from his nose.
"I was waiting for the dribble. This leaking cause I was so used to it every day. I got my hankie. Nothing. It’s never come back."
What has come back is his desire to work on the hobbies he loves, like his model airplanes. And bigger projects.
"Now I’m going to build a sailboat and the sailboat I’m building is called a Great Pelican."
And after all he’s been through, Joe feels pretty confident this boat won’t leak.
Before you call a brain surgeon about your runny nose, Dr. Nakaji says it most likely is just a runny nose. Brain fluid, it’s different than a runny nose caused by allergies in that the liquid is very, very clear.
So if you have a chronic runny nose, start with an allergist or an ear, nose and throat specialist. They can perform a simple test to determine if it’s a typical runny nose or something more serious.
The causes of this type of leak can be numerous. Sometimes a past head injury can lead to brain fluid leaking, or it can be caused from complications of a spinal tap or surgery.
Cancer Drug Prevents Build-up of Toxic Brain Protein
Researchers at Georgetown University Medical Center have used tiny doses of a leukemia drug to halt accumulation of toxic proteins linked to Parkinson’s disease in the brains of mice. This finding provides the basis to plan a clinical trial in humans to study the effects.
They say their study, published online May 10 in Human Molecular Genetics, offers a unique and exciting strategy to treat neurodegenerative diseases that feature abnormal buildup of proteins in Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), frontotemporal dementia, Huntington disease and Lewy body dementia, among others.
“This drug, in very low doses, turns on the garbage disposal machinery inside neurons to clear toxic proteins from the cell. By clearing intracellular proteins, the drug prevents their accumulation in pathological inclusions called Lewy bodies and/or tangles, and also prevents amyloid secretion into the extracellular space between neurons, so proteins do not form toxic clumps or plaques in the brain,” says the study’s senior investigator, neuroscientist Charbel E-H Moussa, MB, PhD. Moussa heads the laboratory of dementia and Parkinsonism at Georgetown.
When the drug, nilotinib, is used to treat chronic myelogenous leukemia (CML), it forces cancer cells into autophagy — a biological process that leads to death of tumor cells in cancer.
“The doses used to treat CML are high enough that the drug pushes cells to chew up their own internal organelles, causing self-cannibalization and cell death,” Moussa says. “We reasoned that small doses — for these mice, an equivalent to one percent of the dose used in humans — would turn on just enough autophagy in neurons that the cells would clear malfunctioning proteins, and nothing else.”
Moussa, who has long sought a way to force neurons to clean up their garbage, came up with the idea of using cancer drugs that push autophagy in tumors to help diseased brains. “No one has tried anything like this before,” he says.
Moussa, and his two co-authors — graduate student Michaeline Hebron and Irina Lonskaya, PhD, a postdoctoral researcher in Moussa’s lab — searched for cancer drugs that can cross the blood-brain barrier. They discovered two candidates — nilotinib and bosutinib, which is also approved to treat CML. This study discusses experiments with nilotinib, but Moussa says that use of bosutinib is also beneficial.
The mice used in this study over-express alpha-Synuclein, the protein that builds up in Lewy bodies in Parkinson’s disease and dementia patients and which is found in many other neurodegenerative diseases. The animals were given one milligram of nilotinib every two days. (By contrast, the FDA approved use of up to 1,000 milligrams of nilotinib once a day for CML patients.)
“We successfully tested this for several diseases models that have an accumulation of intracellular protein,” Moussa says. “It gets rid of alpha synuclein and tau in a number of movement disorders, such as Parkinson’s disease as well as Lewy body dementia.”
The team also showed that movement and functionality in the treated mice was greatly improved, compared with untreated mice.
In order for such a therapy to be as successful as possible in patients, the agent would need to be used early in neurodegenerative diseases, Moussa hypothesizes. Later use might retard further extracellular plaque formation and accumulation of intracellular proteins in inclusions such as Lewy bodies.
Moussa is planning a phase II clinical trial in participants who have been diagnosed with disorders that feature build-up of alpha Synuclein, including Lewy body dementia, Parkinson’s disease, progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).
(Source: explore.georgetown.edu)
Fainting May Run in Families While Triggers May Not
New research suggests that fainting may be genetic and, in some families, only one gene may be responsible. However, a predisposition to certain triggers, such as emotional distress or the sight of blood, may not be inherited. The study is published in the April 16, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology. Fainting, also called vasovagal syncope, is a brief loss of consciousness when your body reacts to certain triggers. It affects at least one out of four people.
“Our study strengthens the evidence that fainting may be commonly genetic,” said study author Samuel F. Berkovic, MD, FRS, with the University of Melbourne in Victoria, Australia, and a member of the American Academy of Neurology. “Our hope is to uncover the mystery of this phenomenon so that we can recognize the risk or reduce the occurrence in people as fainting may be a safety issue.”
Researchers interviewed 44 families with a history of fainting and reviewed their medical records. Of those, six families had a large number of affected people, suggesting that a single gene was running through the family. The first family consisted of 30 affected people over three generations with an average fainting onset of eight to nine years. The other families were made up of four to 14 affected family members. Affected family members reported typical triggers, such as the sight of blood, injury, medical procedures, prolonged standing, pain and frightening thoughts. However, the triggers varied greatly within the families.
Genotyping of the largest family showed significant linkage to a specific region on chromosome 15, known as 15q26. Linkage to this region was excluded in two medium-sized families but not in the two smaller families.
(Image: Fotolia)
Tapeworm-Linked Seizures May Be Rising in U.S.
Tapeworm infection in the brain that can trigger seizures is a growing health concern, doctors say.
But the infection, which leads to swelling in the brain, is usually treatable with medication, according to a leading association of neurologists.
Estimated cases of neurocysticercosis, as the tapeworm infection is called, range from 40,000 to 160,000 each year in the United States, said Dr. Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston. “It’s been around a long time, affecting people living in severe poverty, but the disease is not well-studied or understood,” Hotez said.
Texas is one area of the country with many cases. “The disease has now become a leading cause of epilepsy in Houston,” Hotez said. “Every [week], we have patients come into our tropical medicine clinic with it.”
Concerns about an apparent increase of neurocysticercosis within the United States led the American Academy of Neurology to issue treatment guidelines for doctors and patients in the April 9 issue of the journal Neurology.
The recommendations are based on a review of 10 studies published between 1980 and 2010 that evaluated so-called cysticidal drugs for treatment of tapeworm infections. The infection involves infestation of the brain with the larvae of the Taenia solium tapeworm. In severe cases, it can cause death.
Tapeworm infection is common in Third World countries because of inadequate sanitation and hygiene, and an estimated 2 million people worldwide have epilepsy as a result. The good news is that good hygiene and food preparation can prevent it.
People develop the tapeworm infection when they consume improperly cooked meat, such as pork, or any food or drink that contains the tapeworm eggs or larvae (also known as cysts). Touching the fecal matter of an infected person is another means of transmission. The larvae then transform into full-sized tapeworms, which can grow to several feet, Hotez said.
In pigs, tapeworm larvae travel to the brain and await transmission to another animal (a human, for instance) when the pigs are eaten, he said. The parasites do the same thing in humans, but there’s nowhere to go from the human brain. Ultimately, the larvae die, and that’s when the trouble begins.
As the larvae die, they lose the ability to hide from the body’s immune system. The immune system responds by causing inflammation, which leads to epileptic seizures and brain swelling, Hotez said.
The guidelines for children and adults recommend using the medication albendazole to kill the cysts if they’re alive and treating brain swelling with corticosteroid drugs that dampen the immune system. The study found that albendazole (Albenza), used with or without the corticosteroids, reduced seizure frequency and the number of brain lesions seen in imaging scans. Not enough data was available to evaluate another drug, praziquantel, the researchers said.
Only limited evidence exists to support specific treatment approaches, however, and the treatments may produce side effects, such as abdominal complaints, according to the guidelines. It’s also unclear whether anti-epileptic medications may help prevent the seizures caused by the inflammation.
For now, the key is physician awareness, said Dr. Karen Roos, a professor of neurology at the Indiana University School of Medicine and lead author of the guidelines. “Physicians from areas of the world where this infection is endemic are very knowledgeable about this infection,” she said. “They know more than U.S. physicians.”
Infection with the tapeworm is preventable through proper sanitation, good hygiene and thorough cooking of meat.
(Source: nlm.nih.gov)
New minimally invasive, MRI-guided laser treatment for brain tumor found to be promising in study
The first-in-human study of the NeuroBlate™ Thermal Therapy System finds that it appears to provide a new, safe and minimally invasive procedure for treating recurrent glioblastoma (GBM), a malignant type of brain tumor. The study, which appears April 5 in the Journal of Neurosurgery online, was written by lead author Andrew Sloan, MD, Director of Brain Tumor and Neuro-Oncology Center at University Hospitals (UH) Case Medical Center and Case Comprehensive Cancer Center, who also served as co-Principal Investigator, as well as Principal Investigator Gene Barnett, MD, Director of the Brain Tumor and Neuro-Oncology Center at Cleveland Clinic and Case Comprehensive Cancer Center, and colleagues from UH, Cleveland Clinic, Cleveland Clinic Florida, University of Manitoba and Case Western Reserve University.
NeuroBlate™ is a device that “cooks” brain tumors in a controlled fashion to destroy them. It uses a minimally invasive, MRI-guided laser system to coagulate, or heat and kill, brain tumors. The procedure is conducted in an MRI machine, enabling surgeons to plan, steer and see in real-time the device, the heat map of the area treated by the laser and the tumor tissue that has been coagulated.
"This technology is unique in that it allows the surgeon not only to precisely control where the treatment is delivered, but the ability to visualize the actual effect on the tissue as it is happening," said Dr. Sloan. "This enables the surgeon to adjust the treatment continuously as it is delivered, which increases precision in treating the cancer and avoiding surrounding healthy brain tissue."
The study was a Phase I clinical trial investigating the safety and performance of NeuroBlate™ (formerly known as AutoLITT™), a specially-designed laser probe system. The FDA gave the system’s developer Monteris Medical and the Case Comprehensive Cancer Center, (comprised of the UH Case Medical Center, Cleveland Clinic, and Case Western Reserve University School of Medicine), an investigatory device exemption (IDE) to study the system in patients with GBMs. The device has recently been cleared by the FDA due, in part, to the results of the study.
The paper describes the treatment of the first 10 patients with this technology. These patients, who had a median age of 55, had tumors which were diagnosed to be inoperable or “high risk” for open surgical resection because of their location close to vital areas in the brain, or difficult to access with conventional surgery.
"Overall the NeuroBlate™ procedure was well-tolerated," said Dr. Sloan. "All 10 patients were alert and responsive within one to two hours post-operatively and nine out of the 10 patients were ambulatory within hours. Response and survival was also nearly 10 ½ months, better than expected for patients with such advanced disease."
"Previous attempts using less invasive approaches such as brachytherapy and stereotactic radiosurgery have proven ineffective in recent meta-analysis and randomized trials," said Dr. Barnett. "However, unlike therapies using ionizing radiation, NeuroBlate™ therapy results in tumor death at the time of the procedure. A larger national study will be developed, as a result of this initial success."
Experts Call for Research on Prevalence of Delayed Neurological Dysfunction After Head Injury
One of the most controversial topics in neurology today is the prevalence of serious permanent brain damage after traumatic brain injury (TBI). Long-term studies and a search for genetic risk factors are required in order to predict an individual’s risk for serious permanent brain damage, according to a review article published by Sam Gandy, MD, PhD, from the Icahn School of Medicine at Mount Sinai in a special issue of Nature Reviews Neurology dedicated to TBI.
About one percent of the population in the developed world has experienced TBI, which can cause serious long-term complications such as Alzheimer’s disease (AD) or chronic traumatic encephalopathy (CTE), which is marked by neuropsychiatric features such as dementia, Parkinson’s disease, depression, and aggression. Patients may be normal for decades after the TBI event before they develop AD or CTE. Although first described in boxers in the 1920s, the association of CTE with battlefield exposure and sports, such as football and hockey, has only recently begun to attract public attention.
"Athletes such as David Duerson and Junior Seau have brought to light the need for preventive measures and early diagnosis of CTE, but it remains highly controversial because hard data are not available that enable prediction of the prevalence, incidence, and individual risk for CTE," said Dr. Gandy, who is Professor of Neurology and Psychiatry and Director of the Center for Cognitive Health at Mount Sinai. "We need much more in the way of hard facts before we can advise the public of the proper level of concern."
Led by Dr. Gandy, the authors evaluated the pathological impact of single-incident TBI, such as that sustained during military combat; and mild, repetitive TBI, as seen in boxers and National Football League (NFL) players to learn what measures need to be taken to identify risk and incidence early and reduce long-term complications.
Mild, repetitive TBI, as is seen in boxers, football players, and occasionally military veterans who suffer multiple blows to the head, is most often associated with CTE, or a condition called “boxer’s dementia.” Boxing scoring includes a record of knockouts, providing researchers with a starting point in interpreting an athlete’s risk. But no such records exist for NFL players or soldiers on the battlefield.
Dr. Gandy and the authors of the Nature Reviews Neurology piece suggest recruiting large cohorts of players and military veterans in multi-center trials, where players and soldiers maintain a TBI diary for the duration of their lives. The researchers also suggest a genome-wide association study to clearly identify risk factors of CTE. “Confirmed biomarkers of risk, diagnostic tools, and long-term trials are needed to fully characterize this disease and develop prevention and treatment strategies,” said Dr. Gandy.
Amyloid imaging, which has recently been approved by the U.S. Food and Drug Administration, may be useful as a monitoring tool in TBI, since amyloid plaques are a hallmark symptom of AD-type neurodegeneration. Amyloid imaging consists of a PET scan with an injection of a contrast agent called florbetapir, which binds to amyloid plaque in the brain, allowing researchers to visualize plaque deposits and determine whether the diagnosis is CTE or AD, and monitor progression over time. Tangle imaging is expected to be available soon, complementing amyloid imaging and providing an affirmative diagnosis of CTE. Dr. Gandy and colleagues recently reported the use of amyloid imaging to exclude AD in a retired NFL player with memory problems under their care at Mount Sinai.
Clinical diagnosis and evaluation of mild, repetitive TBI is a challenge, indicating a significant need for new biomarkers to identify damage, report the authors. Measuring cerebrospinal fluid (CSF) may reflect damage done to neurons post-TBI. Previous research has identified a marked increase in CSF biomarkers in boxers when the CSF is taken soon after a fight, and this may predict which boxers are more likely to develop detrimental long-term effects. CSF samples are now only obtained by invasive lumbar puncture; a blood test would be preferable.
"Biomarkers would be a valuable tool both from a research perspective in comparing them before and after injury and from a clinical perspective in terms of diagnostic and prognostic guidance," said Dr. Gandy. "Having the biomarker information will also help us understand the mechanism of disease development, the reasons for its delayed progression, and the pathway toward effective therapeutic interventions."
Currently, there are no treatments for boxer’s dementia or CTE, but these diseases are preventable. “With more protective equipment, adjustments in the rules of the game, and overall education among athletes, coaches, and parents, we should be able to offer informed consent to prospective sports players and soldiers. With the right combination of identified genetic risk factor, biomarkers, and better drugs, we should be able to dramatically improve the outcome of TBI and prevent the long-term, devastating effects of CTE,” said Dr. Gandy.
(Source: mountsinai.org)
Surprisingly, yes.
The modern lobotomy originated in the 1930s, when doctors realized that by severing fiber tracts connected to the frontal lobe, they could help patients overcome certain psychiatric problems, such as intractable depression and anxiety. Over the next two decades, the procedure would become simple and popular, completed by poking a sharpened tool above the eyeball. According to one study, about two thirds of patients showed improvement after surgery.
Unfortunately, not all lobotomy practition-ers were responsible, and the technique left some patients with severe side effects, including seizures, lethargy, changes in personality, and incontinence. In response, doctors refined their techniques. They replaced the lobotomy with more specialized approaches: the cingulotomy, the anterior capsulotomy, and the subcaudate tractotomy. Studies of these procedures found evidence of benefit for at least one fourth of patients suffering from problems such as OCD and depression.
Even with the risk of side effects, those in the field still say the procedures were by and large successful. “I feel that the principle behind ablative surgery was somewhat exonerated by the research findings, which showed that it worked for very specific indications,” says Konstantin Slavin, president of the American Society for Stereotactic and Functional Neurosurgery, and professor at the University of Illinois at Chicago.
By the 1980s, lobotomies had fallen out of fashion. “In general, the entire functional neurosurgery field moved away from destruction—from ablative surgery,” Slavin says. A then-new technique called deep-brain stimulation made ablative surgery obsolete. In the procedure, a surgeon drills holes in the head and inserts electrodes into the neural tissue. When current passes through the leads, they activate or inactivate patches of the brain. “The attractive part is that we don’t destroy the tissue,” Slavin says. Doctors can also adjust treatment if a patient suffers side effects. They can turn the current down or suspend it altogether—so as to “give the brain a holiday,” as Slavin calls it.
Most deep-brain stimulation is now used to treat movement disorders such as Parkinson’s Disease. The surgical treatment of patients with OCD is FDA-approved but reserved only for extreme cases. Slavin and his colleagues have been examining broader uses in an ongoing study. “Within the next five years, we hope we’ll have a definitive answer of whether or not it works.”