One in two homeless people has had a traumatic brain injury.

by Joe Gramigna

More than half of people who are homeless or dwell in unstable housing may have experienced a traumatic brain injury, according to results of a systematic review and meta-analysis published in The Lancet Public Health.

“Health care providers should be aware of the burden of TBI in this population,” Jacob L. Stubbs, BKin, a PhD student in the department of psychiatry at the University of British Columbia, Vancouver, told Healio Psychiatry. “Identifying a history of serious injury or new TBIs may allow for more targeted care. However, more research is urgently needed to better understand this issue.”

According to Stubbs and colleagues, a previous systematic review and previous studies have suggested that the lifetime incidence and prevalence of TBI in homeless and marginally housed individuals might be significantly higher than the general population. However, they noted that the present study is the first meta-analysis to their knowledge to evaluate TBI prevalence and incidence in these specific populations.

The researchers searched for original research studies that reported data on the association between TBI and one or more health- or function-related outcome measures, or on the prevalence or incidence of TBI. They included studies with clearly identifiable groups or subgroups of individuals who were homeless, seeking services for homeless people or marginally housed.

Among 21 studies with data from 11,417 individuals, the lifetime prevalence of any severity of TBI in homeless and marginally housed individuals was 53.4% (95% CI, 47.6-59.1). Among 12 studies with data from 6,302 individuals, the lifetime prevalence of moderate or severe TBI was 24.9% (95% CI, 16.3-35.9). Several factors significantly moderated estimated lifetime prevalence of any severity of TBI — the definition of TBI, the method used to determine TBI history and the age of the sample. The researchers noted that TBI was consistently associated with poorer self-reported mental and physical health, higher suicide risk and suicidality, memory concerns and increased criminal justice system involvement and health service use.

“Confirmation of structural brain damage caused by TBI might facilitate triage and referral to specialized services, such as cognitive rehabilitation, which could improve functional outcomes,” the researchers wrote. “Furthermore, imaging findings might positively inform the patient-caregiver relationship (eg, by increasing understanding of challenging behaviors that might be attributable to damage visible on neuroimaging).”

In a related editorial, Jesse T. Young, PhD, MPH, BSc, and Nathan Hughes, PhD, of Murdoch Children’s Research Institute in Melbourne, Australia, offered potential solutions to ameliorate the burden of TBIs among this population.

“Given the increasing evidence for a potential causal relationship, a randomized controlled trial investigating the effect of a housing intervention on TBI incidence is both feasible and warranted,” they wrote. “The Housing First model, in which homeless people are provided immediate access to permanent, noncontingent housing, has been found to reduce hospital contact for injury. Establishing the effectiveness of a Housing First approach in preventing TBI among people at risk of housing instability should be a public health priority for researchers and policy makers.”

Stubbs JL, et al. Lancet Public Health. 2019;doi:10.1016/S2468-2667(19)30188-4.
Young JT, Hughes N. Lancet Public Health. 2019;doi:10.1016/S2468-2667(19)30225-7.

https://www.healio.com/psychiatry/violence-trauma/news/online/%7B3684f5f6-57bc-4a44-92f2-1739e4a3f85e%7D/one-in-two-homeless-people-has-a-tbi?utm_source=selligent&utm_medium=email&utm_campaign=psychiatry%20news&m_bt=1162769038120

Experimental PET scan detects abnormal tau protein in brains of living former NFL players


CTE is a neurodegenerative disease that has been associated with a history of repetitive head impacts, including those that may or may not be associated with concussion symptoms in American football players. The image is in the public domain.

Summary: PET imaging of former NFL players who exhibited cognitive decline and psychiatric symptoms linked to CTE showed higher levels of tau in areas of the brain associated with the neurodegenerative disease. Using an experimental positron emission tomography (PET) scan, researchers have found elevated amounts of abnormal tau protein in brain regions affected by chronic traumatic encephalopathy (CTE) in a small group of living former National Football League (NFL) players with cognitive, mood and behavior symptoms. The study was published online in the New England Journal of Medicine.

Source: Boston University School of Medicine

The researchers also found the more years of tackle football played (across all levels of play), the higher the tau protein levels detected by the PET scan. However, there was no relationship between the tau PET levels and cognitive test performance or severity of mood and behavior symptoms.

“The results of this study provide initial support for the flortaucipir PET scan to detect abnormal tau from CTE during life. However, we’re not there yet,” cautioned corresponding author Robert Stern, PhD, professor of neurology, neurosurgery and anatomy and neurobiology at Boston University School of Medicine (BUSM). “These results do not mean that we can now diagnose CTE during life or that this experimental test is ready for use in the clinic.”

CTE is a neurodegenerative disease that has been associated with a history of repetitive head impacts, including those that may or may not be associated with concussion symptoms in American football players. At this time, CTE can only be diagnosed after death by a neuropathological examination, with the hallmark findings of the build-up of an abnormal form of tau protein in a specific pattern in the brain. Like Alzheimer’s disease (AD), CTE has been suggested to be associated with a progressive loss of brain cells. In contrast to AD, the diagnosis of CTE is based in part on the pattern of tau deposition and a relative lack of amyloid plaques.

The study was conducted in Boston and Arizona by a multidisciplinary group of researchers from BUSM, Banner Alzheimer’s Institute, Mayo Clinic Arizona, Brigham and Women’s Hospital and Avid Radiopharmaceuticals. Experimental flortaucipir PET scans were used to assess tau deposition and FDA-approved florbetapir PET scans were used to assess amyloid plaque deposition in the brains of 26 living former NFL players with cognitive, mood, and behavior symptoms (ages 40-69) and a control group of 31 same-age men without symptoms or history of traumatic brain injury. Results showed that the tau PET levels were significantly higher in the former NFL group than in the controls, and the tau was seen in the areas of the brain which have been shown to be affected in post-mortem cases of neuropathologically diagnosed CTE.

Interestingly, the former player and control groups did not differ in their amyloid PET measurements. Indeed, only one former player had amyloid PET measurements comparable to those seen in Alzheimer’s disease.

“Our findings suggest that mild cognitive, emotional, and behavioral symptoms observed in athletes with a history of repetitive impacts are not attributable to AD, and they provide a foundation for additional research studies to advance the scientific understanding, diagnosis, treatment, and prevention of CTE in living persons, said co-author, Eric Reiman, MD, Executive Director of Banner Alzheimer’s Institute in Phoenix, Arizona. “More research is needed to draw firm conclusions, and contact sports athletes, their families, and other stakeholders are waiting.

With support from NIH, the authors are working with additional researchers to conduct a longitudinal study called the DIAGNOSE CTE Research Project in former NFL players, former college football players, and persons without a history of contact sports play to help address these and other important questions. Initial results of that study are expected in early 2020.

Experimental PET scan detects abnormal tau protein in brains of living former NFL players

Risk of later developing dementia is doubled after a concussion

High school football player in for the touchdown.; Shutterstock ID 408266332; Purchase Order: –

Researchers reported on Monday in the journal JAMA Neurology that dementia was a possible complication following concussion even if the patient did not lose consciousness.

Scientists from the University of California, San Francisco (UCSF) tracked more than one-third of a million American veterans, and found that the likelihood of dementia more than doubled following concussion.

After adjusting for age, sex, race, education and other health conditions, they found that concussion without loss of consciousness led to 2.36 times the risk for dementia.

According to the study, these risks were slightly elevated for those in the loss-of-consciousness bracket (2.51 times) and were nearly four times higher (3.77 times) for those with the more serious moderate-to-severe traumatic brain injury.

In the total of 357,558 participants, whose average age was 49, half had been diagnosed with traumatic brain injury, of which 54 percent had concussion. The study followed participants for an average of 4.2 years, and 91 percent were male and 72 percent were white.

“There are several mechanisms that may explain the association between traumatic brain injury and dementia,” said the study’s senior author Kristine Yaffe, professor with the UCSF departments of neurology, psychiatry, and epidemiology and biostatistics.

“There’s something about trauma that may hasten the development of neurodegenerative conditions. One theory is that brain injury induces or accelerates the accumulation of abnormal proteins that lead to neuronal death associated with conditions like Alzheimer’s disease,” said Yaffe.

“It’s also possible that trauma leaves the brain more vulnerable to other injuries or aging processes,” said Yaffe, “but we need more work in this area.”

http://www.xinhuanet.com/english/2018-05/08/c_137162226.htm

Frequently heading the ball in soccer is more dangerous to the brain than acute concussions

Frequent soccer ball heading is a common and under recognized cause of concussion symptoms, according to a study of amateur players led by Albert Einstein College of Medicine researchers. The findings run counter to earlier soccer studies suggesting concussion injuries mainly result from inadvertent head impacts, such as collisions with other players or a goalpost. The study was published in Neurology, the medical journal of the American Academy of Neurology.

“The prevailing wisdom is that routine heading in soccer is innocuous and we need only worry about players when they have unintentional head collisions,” says study leader Michael L. Lipton, M.D., Ph.D., professor of radiology and of psychiatry and behavioral sciences at Einstein and director of MRI Services at Montefiore. “But our study suggests that you don’t need an overt collision to warrant this type of concern. Many players who head the ball frequently are experiencing classic concussion symptoms such as headache, confusion, and dizziness during games and practice, even though they are not actually diagnosed with concussion. Concussion sufferers should avoid additional collisions or head impacts during the following days or weeks, when their risk of incurring a second concussion is extremely high. Because these injuries go unrecognized and unmanaged, there may be important clinical consequences for the short and long term.”

Studies clearly show that single or repeated concussion causes neurologic problems. But little is known about the effects of frequent but lesser impacts, such as those experienced while heading a soccer ball. Some research, notably a recent study of adolescent players published in JAMA Pediatrics, suggest that heading is not a common cause of concussion. “However, these studies did not actually measure heading, and thus they were unable to separate the relative contributions of intentional and unintentional head impacts,” says Dr. Lipton.

In the current study, a part of the Einstein Soccer Study, Dr. Lipton and his colleagues asked 222 adult amateur soccer players (80 percent men, ages 18 to 55) to fill out online questionnaires on their soccer-related activities during the previous two weeks, including details about heading and other unintentional head impacts and any resulting headaches, pain and dizziness as well as more severe symptoms, such as feeling dazed, needing medical attention, and becoming unconscious. Some of the 222 players filled out questionnaires for more than a single two-week span, resulting in a total of 470 questionnaires during a nine-month period in 2013-2014.

Approximately 35 percent of the participants reported one unintentional head impact, and 16 percent reported more than one such impact. The median number of headings during the two-week reporting period for all respondents was 40.5. Twenty percent of the participants reported experiencing moderate-to-very severe concussion symptoms, with 18 percent reporting severe and 7 percent very severe symptoms. Although these symptoms were more strongly connected with unintentional head impacts, heading was shown to be an independent risk factor for concussion symptoms.

“This finding is consistent with one of our previous studies, where 30 percent of soccer players who’d had more than 1,000 headings per year had a higher risk of microstructural changes in the brain’s white matter, typical of traumatic brain injury, and worse cognitive performance,” says Dr. Lipton

In the new study, players who headed the most were the most susceptible to concussion. “The extent to which lesser degrees of exposure to heading lead to cumulative injury over time is not known and deserves further study,” Dr. Lipton says. “Our findings certainly indicate that heading is more than just a ‘sub-concussive’ impact, and that heading-related concussions are common. We need to give people who have these injuries proper care and make efforts to prevent multiple head impacts, which are particularly dangerous.”

The study is titled, “Symptoms from Repeated Intentional and Unintentional Head Impact in Soccer Players.” Other contributors are Walter F. Stewart, Ph.D., M.P.H., at Sutter Health Research, Walnut Creek, CA; Namhee Kim, Chloe Ifrah, Richard B. Lipton, M.D., Tamar Glattstein, and Mimi Kim, Sc.D., all at Einstein; and Molly E. Zimmerman, Ph.D., at Einstein and Fordham University, Bronx, NY.

http://www.einstein.yu.edu/news/releases/1218/soccer-ball-heading-may-commonly-cause-concussion-symptoms/

New evidence that traumatic brain injury increases the risk of dementia 3 decades later

by Tessa Gregory

Traumatic brain injury (TBI) has been associated with dementia, but the association has not been studied over a long period of time. Anna Nordström and Peter Nordström from Umeå University in Sweden recently published a study in PLOS Medicine that investigates this gap in knowledge.

In the new study, the researchers tracked all diagnoses of dementia and TBI in Swedish nationwide databases from 1964 through 2012. They used the data to make comparisons within three groups of patients. In one group, 164,334 people with TBI were compared with control participants who did not have TBI. In the second group, 136,233 people with TBI who were later diagnosed with dementia were compared with control participants who did not develop dementia, and in a third group, the researchers studied 46,970 sibling pairs with one sibling having a TBI.

The researchers found that in the first year after TBI, the risk of dementia increased by four- to sixfold. Thereafter, the risk decreased rapidly but was still significant more than 30 years after the TBI.

“The results indicate that a TBI could increase the risk for dementia even more than 30 years after the incident,” the authors say. “To our knowledge, no previous prospective study with similar power and follow-up time has been reported.”

Reference: Nordström A, Nordström P (2018) Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study. PLoS Med 15(1): e1002496. https://doi.org/10.1371/journal.pmed.1002496

http://researchnews.plos.org/2018/01/30/diagnosing-dementia-brain-damage-linked-to-increased-dementia-risk-for-decades-after-injury/

Risk of suicide increases 3X after a concussion

New research published in the Canadian Medical Association Journal shows that even mild concussions sustained in ordinary community settings might be more detrimental than anyone anticipated; the long-term risk of suicide increases threefold in adults if they have experienced even one concussion. That risk increases by a third if the concussion is sustained on a weekend instead of a weekday—suggesting recreational concussions are riskier long-term than those sustained on the job.

“The typical patient I see is a middle-aged adult, not an elite athlete,” says Donald Redelmeier, a senior scientist at the University of Toronto and one of the study’s lead authors. “And the usual circumstances for acquiring a concussion are not while playing football; it is when driving in traffic and getting into a crash, when missing a step and falling down a staircase, when getting overly ambitious about home repairs—the everyday activities of life.”

Redelmeier and his team wanted to examine the risks of the concussions acquired under those circumstances. They identified nearly a quarter of a million adults in Ontario who were diagnosed with a mild concussion over a timespan of 20 years—severe cases that resulted in hospital admission were excluded from the study—and tracked them for subsequent mortality due to suicide. It turned out that more than 660 suicides occurred among these patients, equivalent to 31 deaths per 100,000 patients annually—three times the population norm. On average, suicide occurred almost six years after the concussion. This risk was found to be independent of demographics or previous psychiatric conditions, and it increased with additional concussions.

For weekend concussions, the later suicide risk increased to four times the norm. Redelmeier and his fellow researchers had wondered whether the risk would differ between occupational and recreational concussions. They did not have information about how the concussions happened, so they used day of the week as a proxy. Although they do not know why weekend risk is indeed higher, they suspect it may be because on weekends medical staff may not be as available or accessible or people may not seek immediate care.

Although the underlying causes of the connection between concussion and suicide are not yet known, Redelmeier says that there were at least three potential explanations. A concussion may be a marker but not necessarily a mechanism of subsequent troubles—or, in other words, people who sustain concussions may already have baseline life imbalances that increase their risks for depression and suicide. “But we also looked at the subgroup of patients who had no past psychiatric history, no past problems, and we still found a significant increase in risk. So I don’t think that’s the entire story,” he notes. One of the more likely explanations, he says, is that concussion causes brain injury such as inflammation (as has been found in some studies) from which the patient may never fully recover. Indeed, a study conducted in 2014 found that sustaining a head injury leads to a greater risk of mental illness later in life. The other possibility is that some patients may not give themselves enough time to get better before returning to an ordinary schedule, leading to strain, frustration and disappointment—which, in turn, may result in depression and ultimately even suicide.

Lea Alhilali, a physician and researcher at the Barrow Neurological Institute who did not participate in this study, uses diffusion tensor imaging (an MRI technique) to measure the integrity of white matter in the brain. Her team has found similarities between white matter degeneration patterns in patients with concussion-related depression and noninjured patients with major depressive disorder—particularly in the nucleus accumbens, or the “reward center” of the brain. “It can be difficult to tease out what’s related to an injury and what’s related to the circumstances surrounding the trauma,” Alhilali says. “There could be PTSD, loss of job, orthopedic injuries that can all influence depression. But I do believe there’s probably an organic brain injury.”

Alhilali points to recent studies on chronic traumatic encephalopathy (CTE), a progressive degenerative brain disease associated with repeated head traumas. Often linked to dementia, depression, loss of impulse control and suicide, CTE was recently diagnosed in 87 of 91 deceased NFL players. Why, then, she says, should we not suspect that concussion causes other brain damage as well?

This new study may only represent the tip of the iceberg. “We’re only looking at the most extreme outcomes, at taking your own life,” Redelmeier says. “But for every person who dies from suicide, there are many others who attempt suicide, and hundreds more who think about it and thousands more who suffer from depression.”

More research needs to be done; this study was unable to take into account the exact circumstances under which the concussions were sustained. Redelmeier’s research examined only the records of adults who sought medical attention, it did not include more severe head injuries that required hospitalization or extensive emergency care. To that extent, his findings may have underestimated the magnitude of the absolute risks at hand.

Yet many people are not aware of these risks.

Redelmeier is adamant that people should take concussions seriously. “We need to do more research about prevention and recovery,” he says. “But let me at least articulate three things to do: One, give yourself permission to get some rest. Two, when you start to feel better, don’t try to come back with a vengeance. And three, even after you’re feeling better, after you’ve rested properly, don’t forget about it entirely. If you had an allergic reaction to penicillin 15 years ago, you’d want to mention that to your doctor and have it as a permanent part of your medical record. So, too, if you’ve had a concussion 15 years ago.”

http://www.scientificamerican.com/article/a-single-concussion-may-triple-the-long-term-risk-of-suicide1/

Migraine headaches in the NFL



Jets linebacker Lorenzo Mauldin (55) wears special contact lenses and a helmet shade to prevent migraines.

By ZACH SCHONBRUN

FWhen he woke last Sunday morning, Jeremy Kerley sensed trouble already coming on. Fitful sleep is often his trigger, he said. The migraine eventually hit him like an anvil late in last week’s game against the Giants.

His eyes grew blurry and he felt what he described as a “sharp, shooting, throbbing pain.” He wanted to sit down. He wanted to lie down. He knew he needed to leave the field.

Kerley, the Jets’ punt returner, departed to the locker room and did not return. As the Jets came from behind to beat the Giants in overtime, he was receiving intravenous fluids and oxygen to help relieve the anguish from a struggle that has afflicted him since high school.

For Kerley, migraines are the silent menace that constantly lurks. They ambush him almost once a month, even though he rarely talks about it. He knew his grandfather got them; only recently, he discovered that his dad did, too. He just never knows when they will affect him.

Though Kerley is one of approximately 38 million Americans who suffer from them, migraines are not something that is openly discussed in N.F.L. locker rooms. They are far more common in women, and often minimized as simply a headache, a stigma that Kerley acknowledged could make it difficult to pull himself out of a game.

But those who do struggle with migraines — which the Migraine Research Foundation considers a neurological disease, like epilepsy — understand the plight. When Kerley felt a severe headache coming on last season after a game at Minnesota, his teammate Percy Harvin patted him on the back.

“I know how you feel,” Harvin said quietly. He has struggled with migraines throughout his career.

Kerley did the same thing earlier this season, after linebacker Lorenzo Mauldin revealed that he had had migraines since adolescence. Kerley gave him recommendations about nutritional supplements that he found helpful, like fish oil and magnesium. Mauldin also now takes prescription medication to both relieve and prevent severe headaches.

He said that light could often trigger his migraine episodes, so Mauldin wears special contact lenses and a protective shade on his helmet.

“It hurts because it’s pulsating and you can’t really stop it,” Mauldin said. “With a bruise or something, you can put alcohol or peroxide over it and it’ll be fine. Or if you’ve hurt a muscle, you can ice it. But you can’t put ice over a migraine.”

In September, a migraine forced Ohio State quarterback Cardale Jones to the emergency room, something that is not uncommon, said Dr. Melissa Leber, the director of emergency department sports medicine at the Icahn School of Medicine at Mount Sinai. She typically treats patients intravenously. But that often cannot relieve the crippling symptoms right away.

“Some people can’t even get out of bed,” Leber said. “Others can function just while not feeling well. It really runs the gamut for how debilitating it can be.”

Migraines are thought to be related to the brain’s trigeminal nerve, which can grow hypersensitive and cause pain signals to fire throughout the brain, typically concentrated around the eyes or temples. Though migraines are strongly hereditary, showing up in people who have had no sports history, they are often clinically similar to post-traumatic headaches, like the headaches that arise after a concussion, according to Dr. Tad Seifert, a neurologist at Norton Healthcare in Louisville, Ky.

During the summer, Seifert led a study of 74 high school football players in the Louisville area and found that 33.8 percent of them suffered from migraines, a rate twice that of the normal population. The rate rose to 37.5 percent in players who reported having sustained a concussion once in their lives, and 40.7 percent in those who reported multiple concussions.

“The elephant in the room is whether there is some influence of contact sports and the development of frequent or chronic headache later in life,” Seifert said. “And if so, how much?”

Seifert, who also chairs an N.C.A.A. task force on headaches, said that he expected to publish a similar report involving 834 Division I athletes in the spring. Though he would not go into detail about the results, he said that it looked to be “very similar to what we’ve found in this sample of high school players.” Mauldin, it should be noted, sustained a concussion earlier this season.

There is no cure for migraines, and sufferers often go the rest of their lives “controlling” the issue, Seifert said, comparing it to those dealing with high blood pressure or diabetes. What concerns him, though, are the studies that have shown that people with migraines are more susceptible to concussions, and when they do sustain one, it takes them longer to recover.

“We know that the migraine brain is just wired differently,” Seifert said. “And we know that it’s a brain that is hypersensitive to external injury. And those pain receptors that are in overdrive — it takes that much longer to calm down and return to baseline.”

In the time it takes for the receptors to settle, though, the pain can bring a linebacker to his knees.

“When they pop up out of nowhere, you start to feel a sensation like in between the middle of your forehead,” Mauldin said. “But it’s in the back of your head as well. It’s like somebody’s punching you in the side of the head.”

Kerley said he had yet to receive a migraine disease diagnosis, but he thinks it could be related to difficulties he regularly has with sleeping, being someone who has sleep apnea. When he feels a headache coming on, he has a nasal spray that he said often cured his symptoms within a half-hour. But last Sunday, it was too late.

“If you don’t catch it while it’s early, it could get pretty bad,” Kerley said. “Mine got there.”

Air evacuation following traumatic brain injury may worsen outcomes for patients.


Over the past 15 years, more than 330,000 US soldiers have suffered a traumatic brain injury. Many were evacuated by air for further treatment. A new study has found evidence that such air evacuations may pose a significant added risk, potentially causing more damage to already injured brains.

Over the past 15 years, more than 330,000 U.S. soldiers have suffered a traumatic brain injury (TBI). It is one of the leading causes of death and disability connected to the country’s recent conflicts in Afghanistan and Iraq. Many of these patients were evacuated by air from these countries to Europe and the U.S. for further treatment. In general, these patients were flown quickly to hospitals outside the battle zone, where more extensive treatment was available.

But now a new study by researchers at the University of Maryland School of Medicine has found evidence that such air evacuations may pose a significant added risk, potentially causing more damage to already injured brains. The study is the first to suggest that air evacuation may be hazardous for TBI patients. The study was published in the Journal of Neurotrauma.

“This research shows that exposure to reduced barometric pressure, as occurs on military planes used for evacuation, substantially worsens neurological function and increases brain cell loss after experimental TBI — even when oxygen levels are kept in the normal range. It suggests that we need to carefully re-evaluate the cost-benefit of air transport in the first days after injury,” said lead researcher Alan Faden, MD, the David S. Brown Professor in Trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Neurology, and Neurosurgery, and director, Shock, Trauma and Anesthesiology Research Center (STAR) as well as the National Study Center for Trauma and Emergency Medical Services.

About a quarter of all injured soldiers evacuated from Afghanistan and Iraq have suffered head injuries.

Faden and his colleagues tested rats that were subjected to TBI, using a model that simulates key aspects of human brain injury. Animals were exposed to six hours of lowered air pressure, known as hypobaria, at levels that simulated conditions during transport; control animals were exposed to normal pressure. All the animals received extra oxygen to restore normal oxygen concentrations in the blood. In another study, animals received oxygen, either as in the first study or at much higher 100 percent concentration, which is often used during military air evacuations. On its own, low air pressure worsened long-term cognitive function and increased chronic brain inflammation and brain tissue loss. Pure oxygen further worsened outcomes.

Faden and his colleagues believe the findings raise concerns about the increased use of relatively early air evacuation, and suggest that this potential risk should be weighed against the benefits of improved care after evacuation. It may be necessary, he says, to change the current policy for TBI patients and delaying air evacuation in many cases.

In an accompanying editorial, Patrick Kochanek, MD, a leading expert on TBI and trauma care at the University of Pittsburgh, called the findings “highly novel and eye-opening,” and said that they could have “impactful clinical relevance for the field of traumatic brain injury in both military and civilian applications.”

Faden and colleagues believe that one of the mechanisms by which hypobaria worsens TBI is by increasing persistent brain inflammation after injury. They are currently examining how this process occurs and have tested treatments that can reduce the risks of air evacuation. Early results are promising. Scientists suspect that breathing pure oxygen could worsen TBI by increasing production of dangerous free radicals in the brain. After brain injury, these free radicals flood the site of injury, and pure oxygen may further boost these levels. Several recent studies from trauma centers, including from the R Adams Cowley Shock Trauma Center at the University of Maryland Medical Center, have found evidence that using 100 percent oxygen in trauma patients may be counterproductive.

Journal Reference:

Jacob W Skovira, Shruti V Kabadi, Junfang Wu, Zaorui Zhao, Joseph DuBose, Robert E Rosenthal, Gary Fiskum, Alan I Faden. Simulated Aeromedical Evacuation Exacerbates Experimental Brain Injury. Journal of Neurotrauma, 2015; DOI: 10.1089/neu.2015.4189

http://www.sciencedaily.com/releases/2015/11/151130110013.htm

7 Very Bizarre (and Very Rare) Psychotic Hallucinations

brain

The many documented cases of strange delusions and neurological syndromes can offer a window into how bizarre the brain can be.

It may seem that hallucinations are random images that appear to some individuals, or that delusions are thoughts that arise without purpose. However, in some cases, a specific brain pathway may create a particular image or delusion, and different people may experience the same hallucination.

In recent decades, with advances in brain science, researchers have started to unravel the causes of some of these conditions, while others have remained a mystery.

Here is a look at seven odd hallucinations, which show that anything is possible when the brain takes a break from reality.

1. Alice-in-Wonderland syndrome
This neurological syndrome is characterized by bizarre, distorted perceptions of time and space, similar to what Alice experienced in Lewis Carroll’s “Alice’s Adventures in Wonderland.”

Patients with Alice-in-Wonderland syndrome describe seeing objects or parts of their bodies as smaller or bigger than their actual sizes, or in an altered shape. These individuals may also perceive time differently.

The rare syndrome seems to be caused by some viral infections, epilepsy, migraine headaches and brain tumors. Studies have also suggested that abnormal activity in parts of the visual cortex that handle information about the shape and size of objects might cause the hallucinations.

It’s also been suggested that Carroll himself experienced the condition during migraine headaches and used them as inspiration for writing the tale of Alice’s strange dream.

English psychiatrist John Todd first described the condition in an article published in the Canadian Medical Association Journal in 1955, and that’s why the condition is also called Todd’s syndrome. However, an earlier reference to the condition appears in a 1952 article by American neurologist Caro Lippman. The doctor describes a patient who reported feeling short and wide as she walked, and referenced “Alice’s Adventures in Wonderland” to explain her body image illusions.

2. Walking Corpse Syndrome
This delusion, also called Cotard’s Syndrome, is a rare mental illness in which patients believe they are dead, are dying or have lost their internal organs.

French neurologist Jules Cotard first described the condition in 1880, finding it in a woman who had depression and also symptoms of psychosis. The patient believed she didn’t have a brain or intestines, and didn’t need to eat. She died of starvation.

Other cases of Cotard’s syndrome have been reported in people with a range of psychiatric and neurological problems, including schizophrenia, traumatic brain injury and multiple sclerosis.

In a recent case report of Cotard’s syndrome, researchers described a previously healthy 73-year-old woman who went to the emergency room insisting that she was “going to die and going to hell.” Eventually, doctors found the patient had bleeding in her brain due to a stroke. After she received treatment in the hospital, her delusion resolved within a week, according to the report published in January 2014 in the journal of Neuropsychiatry.

3. Charles Bonnet syndrome
People who have lost their sight may develop Charles Bonnet syndrome, which involves having vivid, complex visual hallucinations of things that aren’t really there.

People with this syndrome usually hallucinate people’s faces, cartoons, colored patterns and objects. It is thought the condition occurs because the brain’s visual system is no longer receiving visual information from the eye or part of the retina, and begins making up its own images.

Charles Bonnet syndrome occurs in between 10 and 40% of older adults who have significant vision loss, according to studies.

4. Clinical lycanthropy
In this extremely rare psychiatric condition, patients believe they are turning into wolves or other animals. They may perceive their own bodies differently, and insist they are growing the fur, sharp teeth and claws of a wolf.

Cases have also been reported of people with delusional beliefs about turning into dogs, pigs, frogs and snakes.

The condition usually occurs in combination with another disorder, such as schizophrenia, bipolar disorder or severe depression, according to a review study published in the March issue of the journal History of Psychiatry in 2014.

5. Capgras delusion
Patients with Capgras delusion believe that an imposter has replaced a person they feel close to, such as a friend or spouse. The delusion has been reported in patients with schizophrenia, Alzheimer’s disease, advanced Parkinson’s disease, dementia and brain lesions.

One brain imaging study suggested the condition may involve reduced neural activity in the brain system that processes information about faces and emotional responses.

6. Othello syndrome
Named after Shakespeare’s character, Othello syndrome involves a paranoid belief that the sufferer’s partner is cheating. People with this condition experience strong obsessive thoughts and may show aggression and violence.

In one recent case report, doctors described a 46-year-old married man in the African country Burkina Faso who had a stroke, which left him unable to communicate and paralyzed in half of his body. The patient gradually recovered from his paralysis and speaking problems, but developed a persistent delusional jealousy and aggression toward his wife, accusing her of cheating with an unidentified man.

7. Ekbom’s syndrome
Patients with Ekbom’s syndrome, also known as delusional parasitosis or delusional infestations, strongly believe they are infested with parasites that are crawling under their skin. Patients report sensations of itching and being bitten, and sometimes, in an effort to get rid of the pathogens, they may hurt themselves, which can result in wounds and actual infections.

It’s unknown what causes these delusions, but studies have linked the condition with structural changes in the brain, and some patients have improved when treated with antipsychotic medications.

http://www.livescience.com/46477-oddest-hallucinations.html