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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.

Monday, June 15, 2015



Maps of the lymphatic system: old (left) and updated to reflect the new discovery. Image courtesy University of Virginia Health System.


Up until now, diagrams and maps showed the human lymphatic system ending at the base of the skull, with the tonsils, adenoids, and cervical lymph nodes. The brain itself, it has long been thought, has no direct connection to the lymphatic system. But that conventional wisdom has now been challenged by a team of researchers at the University of Virginia, who have identified a system of lymphatic vessels in the meninges.


In a paper published in the June 1 online edition of Nature, Jonathan Kipnis, PhD, a professor of neuroscience and director of the Center for Brain Immunology and Glia, his postdoctoral fellow Antoine Louveau, PhD, and their colleagues described how they identified these vessels.


It all started with an experiment Dr. Louveau was conducting on mouse meninges. After developing a method to mount them on a single slide and examine them as a whole, he noticed vessel-like patterns in the distribution of immune cells on those slides. He tested them for classic markers of lymphatic endothelial cells (LEC) — and there they were. Preliminary experiments suggested that a similar structure exists in humans, long unnoticed because of how closely it tracks the dural sinuses (sagittal and transverse).


“These structures express all of the molecular hallmarks of lymphatic endothelial cells, are able to carry both fluid and immune cells from the cerebrospinal fluid, and are connected to the deep cervical lymph nodes,” they wrote in the paper. “The discovery of the central nervous system lymphatic system may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.”


Dr. Kipnis said the current discovery could have many implications and requires further characterization in humans. “I think that in any neurologic condition where the immune system is involved, these vessels could be playing a role,” he said. “For example, there are immune abnormalities in autism, and we don't understand why. Alzheimer’s disease involves immune abnormalities. And there are many others.”


The newly discovered lymphatic system of the brain could play a role in understanding the pathogenesis of MS as well, Dr. Kipnis said.  “For example, lymphatic vessels are known in peripheral tumors to affect the state of T-cell activation; maybe it’s the same in the brain. There could be abnormal drainage of brain proteins into the lymph nodes; the presence of too many of them might trigger an explosive immune response. Or these vessels could become clogged and not drain cells as they should, triggering an accumulation of cells in the brain. We just need to start exploring. Remember, the current manuscript is not addressing the role of these vessels in any of the neurological disorders, but instead just describes their structure and some function.”


The next steps, said Lawrence Steinman, MD, FAAN, a professor of neurology and neurological sciences, pediatrics, and genetics at Stanford University, should include mapping the nuances of the heretofore undiscovered lymphatic system of the brain. “There will need to be experiments to determine whether there are new targets and new mechanisms to be discovered within this system, or whether it is, as I suspect, no different than the skin or kidney or any other organ in terms of how the immune system attacks it.”


After that, Dr. Kipnis said, will come exploration of the newly characterized system’s role in disease pathogenesis.  “Once we understand what role, if any, these vessels play in the initiation of disease, we could target them and see if it is possible to somehow alter the progression of the disease.”


Look for the full article, with expert commentary, in the July 2 issue of Neurology Today. To read more about the link between the immune system and neurologic disease, browse our archives here.

Monday, June 08, 2015




An adjuvanted herpes zoster subunit vaccine was 97.2 percent effective at reducing the risk of herpes zoster in adults aged 50 years and older, researchers reported in the April 28 online edition of the New England Journal of Medicine. What’s more, the vaccine remained between 96.6 and 97.9 percent effective among adults aged 70 years or older.


The results suggest that the new vaccine could be highly effective at preventing shingles and its complications, such as post-herpetic neuralgia, in older adults. In particular, people over age 70, who are at increased risk for shingles and in whom the vaccine has demonstrated high efficacy, stand to benefit, study author Thomas C. Heineman, MD, PhD, director of global clinical development of vaccines at GlaxoSmithKline, the vaccine’s manufacturer, told Neurology Today.


“This is very encouraging from the point of view of older people,” he said, “because the incidence of shingles increases as you age, and so do the incidence and severity of its complications. Therefore, a vaccine that remains highly effective even as people age into their 60s, 70s, and beyond is certainly a benefit for the public.”


Zostavax, the live attenuated herpes zoster vaccine, is approximately 51.3 percent effective against herpes zoster and 66.5 percent effective against post-herpetic neuralgia in adults aged 60 or older, according to figures cited in the study. But its efficacy against the virus decreases with age, and it is only 37.5 percent in those aged 70 or older.


The new vaccine, which contains varicella-zoster virus glycoprotein E and the currently unlicensed AS01B adjuvant system (called HZ/su), was shown to have an acceptable safety profile and to elicit a robust immune response that persisted for at least three years in phase 1 and 2 clinical trials, Dr. Heineman and his colleagues reported. For the randomized, placebo-controlled phase 3 trial, they assigned 15,411 participants to receive either the vaccine (7,698 participants) or placebo (7,713). Participants received two intramuscular doses of the vaccine or placebo two months apart.


During a mean follow-up of 3.2 years, herpes zoster was confirmed in six patients in the vaccine group and 210 participants in the placebo group (incidence rate, 0.3 vs. 9.1 per 1,000 person-years). The vaccine was 97.2 percent effective in the entire cohort (95% confidence interval [CI], 93.7 to 99.0; p<0.001), and efficacy remained between 96.6 and 97.9 percent when the researchers stratified the results by age, separating out participants in their 50s, 60s, and 70s.


There were significantly more reports of injection-site and systemic reactions — including pain, redness, and swelling at the injection site, as well as fatigue, fever, gastrointestinal symptoms, headache, myalgia, and shivering — within seven days after inoculation in the vaccine group compared with the placebo group. Grade 3 symptoms — those that prevented normal everyday activities — were reported in 17 percent of those receiving the vaccine and 3.2 percent of those receiving placebo. The majority of these were injection-site reactions, and median durations ranged from one to three days. The proportion of participants who had serious adverse events, potential immune-mediated diseases, or who died during follow-up were similar in both groups (103 in the vaccine group vs. 128 in the placebo group).


“There have been hypothetical concerns that adjuvanted vaccines may be associated with an increased risk of autoimmune diseases. But with this vaccine, there was no imbalance between the vaccine and placebo groups with regard to serious adverse events, autoimmune diseases, or deaths,” said Dr. Heineman.


Given these results, the vaccine “has the potential, once it’s approved, to dramatically reduce the number of shingles cases, especially in the elderly,” he said. “It also has the potential to prevent most of the misery caused by the various complications of shingles, including post-herpetic neuralgia, which can be quite common.


“It is a very interesting and, I think, unexpected finding that even in the oldest population we studied, people over 70, there was no indication of a decline in efficacy,” he added. “With most vaccines, the effectiveness declines with age, presumably because as people get older, their immune responses to vaccinations become less robust. We did not see that effect here. That’s a very important result, because it potentially provides the basis for better addressing other vaccine-preventable diseases in the elderly, for which the necessary immune responses have been harder to attain.”


And because the adjuvanted subunit vaccine does not contain live virus, it may potentially be used in immunocompromised patients, for instance those who have had an autologous stem cell transplant. For these patients, the risk for herpes zoster is higher but the live attenuated vaccine is contraindicated, Dr. Heineman noted. “Over the next year or so we’ll have more data on the vaccine’s safety, immunogenicity, and efficacy in immunocompromised people, who may someday substantially benefit from it,” he said.


Look for the full story, with expert commentary, in the July 2 issue of Neurology Today. For more coverage of herpes zoster, browse our archives here.


Image via NIAID on Flickr.