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Friday, July 17, 2015



Some children and adolescents with traumatic brain injury (TBI) take longer to recover than others, and injury severity is not always to blame. Now, investigators at the University of California, Los Angeles (UCLA) offer a possible explanation: Injury-related damage to myelin and white matter in the corpus callosum may contribute to prolonged TBI symptoms in kids and teens, they write in the July 15 issue of the Journal of Neuroscience. And they propose that this type of axonal injury, as seen on brain imaging, may serve as a biomarker to identify patients at risk of persistent symptoms following TBI.


For the study, Christopher C. Giza, MD, director of the UCLA Steve Tisch BrainSPORT Program and a professor of pediatrics and neurosurgery at UCLA’s David Geffen School of Medicine and Mattel Children’s Hospital, and colleagues administered a series of computerized tasks to 32 children and adolescents aged eight to 19 who had experienced a moderate to severe TBI one to five months prior. The tests measured processing speed, short-term memory, verbal learning, and cognitive flexibility.


They then administered high angular resolution diffusion-weighted imaging (DWI) to measure how quickly the axons were able to transmit information across brain hemispheres (interhemispheric transfer times) and evaluate the structure of the white matter. They compared the results with those of a control group of 31 healthy, age-matched kids and teens.


“We suspected that trauma was damaging the myelin and slowing the brain’s ability to translate information, interfering with patients’ capacity to learn,” Dr. Giza explained in a news release.


He and his colleagues found that 16 patients (50 percent) in the TBI group showed signs of damage to the myelin. These patients also had 14 percent lower scores on cognitive testing, less structural integrity in the corpus callosum, and their axons transmitted information three times more slowly. The remaining 16 patients with TBI had less or no damage to myelin, and had comparable interhemispheric transfer times to the healthy control children. They performed 8.5 percent better on cognitive tests than the TBI patients with myelin damage, but not as well as the healthy controls, who performed 4 percent better still.


“Our data…support the theory that TBI can cause extensive and prolonged damage to myelin integrity, impairing the function of those tracts,” the researchers wrote.


“This study reveals that there is a subset of pediatric [moderate to severe] TBI patients during the post-acute phase of injury who have markedly impaired CC [corpus callosum] functioning and structural integrity that is associated with poor neurocognitive functioning,” they concluded.


The results suggest that using DWI to evaluate white matter integrity and axonal damage could help predict a patient’s prognosis following TBI, and guide the clinician in monitoring patients accordingly, Dr. Giza and his colleagues said. In future research, they plan to look at how these potential biomarkers change within the first year after injury, when patients with persistent symptoms begin to regain some cognitive function.


For more coverage of traumatic brain injury research, browse our archives here.


Image: Susceptibility-weighted image (SWI) from a subject with traumatic brain injury. The venous vasculature appears dark on the images due to deoxygenated hemoglobin. A dark microbleed lesion appears in the left thalamus resulting from the traumatic brain injury.

Thursday, July 09, 2015




Stroke takes a toll on cognitive function both in the short and long term, according to a study published in the July 7 issue of the Journal of the American Medical Association (JAMA).


The study included 23,572 people over the age of 45 who were enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study. The subjects had no cognitive impairment at enrollment between 2003 and 2007, and they were followed through March 2013. Over a median follow-up of 6.1 years, 515 participants survived a stroke.


The researchers assessed global cognition using the Six-Item Screener (SIS) — a brief test of temporal orientation and recall with a range of 0 to 6, with higher scores indicating better cognitive performance — and administered tests to evaluate new learning, verbal memory, and executive function. They then compared these results with the patients’ pre-stroke rate of cognitive decline.


Among the findings, stroke was associated with an acute decline in global cognition on the SIS (0.10 points; 95% confidence interval [CI], 0.04-0.17), as well as in new learning (1.80 points; 95% CI, 0.73-2.86) and verbal memory (0.6 points; 95% CI, 0.13-1.07). Compared with those who remained stroke-free, stroke survivors had faster declines in global cognition (0.06 points per year faster; 95% CI, 0.03-0.08) and executive function (0.63 points per year faster) over the study period, compared with their pre-stroke rates.


The authors noted that the declines, while modest, are likely clinically meaningful — a point echoed by Philip B. Gorelick, MD, MPH, and David Nyenhuis, PhD, both of the Hauenstein Neuroscience Center at Saint Mary’s Health Care and the Michigan State University College of Human Medicine, in an accompanying editorial in JAMA. “Few persons can afford to lose any cognitive capacity over time,” they wrote.


In past research, declines in cognition and executive function have been linked to a significantly increased risk of mortality, dementia, depression, and accelerated functional decline, and subsequent institutionalization and caregiver burden, the study authors noted.


Dr. Gorelick and Dr. Nyenhuis pointed out that the new research does not provide information about “the mechanism whereby stroke was associated with continued cognitive decline, the possible role of stroke and cardiovascular risk factors, possible interactions with neurodegenerative disease, and the means to prevent such decline” — areas that should be explored in future studies, they wrote. “It is likely that many different sources of prior damage to the brain (e.g., stroke, trauma, hypertension, diabetes) increase vulnerability to subsequent brain disease, cognitive decline, and dementia,” they added.


What does this mean for the clinician? Doctors should be vigilant in looking for signs of stroke or silent stroke on neuroimaging, Drs. Gorelick and Nyenhuis said, “because these findings may be harbingers of future complications such as recurrent stroke, cognitive impairment, or disability.” Doing so can, in turn, help clinicians better manage the patient, whether by ordering formal neuropsychological testing or by intensifying vascular risk management to safeguard against stroke, heart attack, cognitive loss, and overall disability.


For more coverage of stroke and cognitive decline, browse our archives here.


Image by National Heart Lung and Blood Institute (NIH), via Wikimedia Commons.

Monday, June 29, 2015




Acute stroke robs patients of nearly eight years of cognitive function overnight, researchers report in a new study published in the May 21 online edition of Stroke. The study, which was designed to look at whether stroke contributes to racial differences in cognitive decline, also found that the immediate impact of stroke on cognition was the same for black and white adults, suggesting that stroke frequency and impact do not account for racial disparities in the rates of cognitive impairment and dementia.


“As we search for the key drivers of the known disparities in cognitive decline between blacks and whites, we focus here on the role of ‘health shocks’ such as strokes,” said lead author Deborah Levine, MD, MPH, an assistant professor of medicine at the University of Michigan Medical School, in a news release. Past studies have shown that older non-Hispanic blacks have an approximately twofold risk of cognitive impairment or dementia, including Alzheimer’s disease, than older non-Hispanic whites, the study authors noted.


“Although we found that stroke does not explain the difference, these results show the amount of cognitive aging that stroke brings on, and therefore the importance of stroke prevention to reduce the risk of cognitive decline,” Dr. Levine said.


The study looked at data on 4,908 adults — 453 black, 4,455 white — aged 65 and older, with a mean age of 74, who were enrolled in the nationally representative Health and Retirement Study with linked Medicare data between 1998 and 2010. At baseline, the participants had no history of stroke, dementia, or other cognitive problems. They participated in periodic assessments of global cognition using a modified version of the Telephone Interview for Cognitive Status (TICS), which assesses global cognition, learning, and memory — the cognitive domains commonly affected by stroke.


They found that 34 of 453 black patients (7.5 percent) and 300 of 4,455 white subjects (6.7 percent) experienced a stroke over a mean of 4.1 years of follow-up. Both black and white patients showed a significant (1.21-point) decline in cognitive function after stroke (p<0.001), corresponding to 7.9 years of cognitive aging. The effect of stroke on cognition did not differ by race (p=0.52), even though black patients had greater cognitive decline than white patients over the course of the study, with a difference of 1.47 points (95% confidence interval [CI], 1.21-1.73).


“We found no evidence that black-white differences in cognition are explained by blacks’ increased incidence of stroke or a greater detrimental effect of stroke on their cognitive health,” the researchers concluded. However, they added, “results cannot be generalized to younger individuals or those with severe cognitive impairment.”


Possible contributors to racial differences in cognitive decline that warrant further examination include socioeconomic factors, education quality, genetic or biological factors, access and use of health care, and vascular risk factors, among others, they said.


To learn more about the latest stroke research, browse our archives here.


Image via Allan Ajifo on Flickr.

Wednesday, June 24, 2015



Can leg-compressing “skinny” jeans cause neuropathy? A paper published in the June 22 online edition of the Journal of Neurology, Neurosurgery & Psychiatry suggests it can. In the featured case study, a 35-year-old woman developed swelling in the lower legs, global weakness of ankle and toe movements, and numbness in the lower legs and feet after spending several hours in a squat position while wearing a pair of “skinny” jeans. The woman was treated with intravenous hydration and was able to walk unaided four days later, at which point she was discharged from the hospital.


Past reports of neuropathy caused by tight clothing have been limited to damage to the lateral cutaneous nerve of the thigh, the study authors from Royal Adelaide Hospital in Australia, noted. “The present case represents a new neurological complication of wearing tight jeans,” they wrote.


One day before she presented to the hospital with severe weakness in both ankles, the young woman had been helping a relative move. She told physicians that she had spent several hours in a squatting position to empty out her relative’s cupboards. She was wearing a pair of skinny jeans, which she said felt increasingly tight and uncomfortable as time passed. Later that evening, she noticed bilateral foot drop and foot numbness. She tripped and fell, and spent several hours lying on the ground before she was found.


When she arrived at the hospital, her calves were so swollen that her jeans needed to be cut from her legs. She had severe global weakness of ankle and toe movements, as well as impaired sensation in her lower legs and feet.


Nerve conduction studies showed conduction block in both common peroneal nerves (a branch of the sciatic nerve, which supplies movement and sensation to the lower leg, foot, and toes) and diminished compound muscle action potential (electrical activity in the muscles) of the tibial nerves. External compression caused by prolonged squatting is a known cause of common peroneal neuropathies, the researchers noted. This was likely exacerbated by the patient’s wearing skinny jeans, which may have caused a compartment syndrome, reducing the blood supply to the leg muscles and causing the muscles to swell and the nearby nerves to become compressed.


The patient was given intravenous fluids, and her swelling and lower limb function improved significantly. She was able to walk unaided at the time of hospital discharge four days later.


This is not the first anecdotal report to suggest that too-tight denim can cause temporary nerve damage. Neurology Today Associate Editor Orly Avitzur, MD, MBA, FAAN, a clinical assistant professor of neurology at New York Medical College in Valhalla, NY, has reported extensively on meralgia paresthetica, or “tingling thigh syndrome,” which can occur when tight clothing compresses the femoral cutaneous nerve. This compression can cause numbness and prickly, tingling, burning, or painful sensations in the outer thighs.


Removing the offending garment can help ease the pain, but if the nerve compression is severe, symptoms can last for weeks or even months, according to Dr. Avitzur.


To learn more about neuropathy and nerve pain, browse our archives here.


Image via Wikimedia Commons.

Wednesday, June 17, 2015



The US Food and Drug Administration (FDA) announced June 12 that it had approved an implantable deep brain stimulation (DBS) device for Parkinson’s disease (PD) and essential tremor.


The device, called the Brio Neurostimulation System and manufactured by St. Jude Medical, Inc. in St. Cloud, MN, is the second DBS device to gain FDA approval to treat symptoms of PD and essential tremor, including difficulty walking, balance problems, and tremors, in patients for whom symptoms are not adequately controlled with medication.


Both the Brio Neurostimulation System and the previously approved neurostimulator, the Activa Deep Brain Stimulation Therapy System manufactured by Medtronic, have the same mechanism of action, Carlos Peña, PhD, director of the Division of Neurological and Physical Medicine Devices in the Office of Device Evaluation at the FDA’s Center for Devices and Radiological Health, told Neurology Today in an email. The Activa neurostimulator was approved in 1997 for essential tremor and approval was expanded to include an indication for Parkinson’s disease in 2002.


“The approval of the Brio system provides Parkinson’s disease and essential tremor patients with another choice for managing their symptoms,” Dr. Peña said.

The small, battery-powered rechargeable electrical pulse generator is implanted under the skin of the upper chest, with wire leads that attach to electrodes placed in different brain regions depending on whether the patient is being treated for PD or essential tremor, the FDA explained in a news release. It delivers a continuous stream of low-intensity electrical pulses to interrupt brain signals causing motor symptoms. These can be adjusted as needed by health care professionals.


In two clinical studies, the DBS stimulation system was found to be safe and effective. One trial included 136 patients with PD and the other, 127 patients with essential tremor. In both cases, patients’ symptoms were not adequately controlled with medication. PD patients who used the device in addition to medication showed a statistically significant improvement in motor symptoms at three months, according to the FDA, while essential tremor patients experienced statistically significant improvement at six months and were able to control their symptoms without the use of medications.


“The results of the clinical studies demonstrated a clinically meaningful improvement in ‘on’ time with the Brio System in patients with advanced Parkinson’s disease,” Dr. Peña said. “Essential tremor patients with unilateral or bilateral disabling medication-refractory upper extremity tremor observed a reduction in tremor. Most subjects with the device also reported improvements in their quality of life, such as increased mobility, ability to perform daily activities, and general well-being.”


Serious adverse events included intracranial bleeding, infection, and dislocation of the device lead under the skin, the FDA reported.


Dr. Peña added that in the Parkinson’s study, “the results demonstrated no significant differences in adverse event rates between patients implanted with the device who received stimulation compared to the control group of patients who received the device without stimulation. In the essential tremor study, the rate of device-related or procedure-related adverse events within 6 months post-implant compared favorably to historical controls. In both studies, intracranial bleeding was observed at rates comparable to risks known for these devices.”


For more coverage of DBS for Parkinson’s disease, browse our archives here.


Image via St. Jude Medical, Inc.