<![CDATA[Armstrong Neurology - Neurology Spectrum]]>Wed, 21 Feb 2018 06:45:49 -0800Weebly<![CDATA[Prevagen]]>Fri, 03 Feb 2017 18:45:26 GMThttp://hickoryneurology.net/neurology-spectrum/prevagen

ConsumerLab.com Answers

Does Prevagen really improve memory?

According to the company’s website, people who use people Prevagen (Quincy Bioscience) can “experience improved memory, a sharper mind, and clearer thinking. Unfortunately, no peer-reviewed studies have been published to back up these claims. In addition, the FDA has warned Quincy Bioscience in the past against claiming Prevagen could treat conditions such as head injuries and Alzheimer's disease and for failing to report adverse reactions, and the FTC has charged Prevagen's markets with making false and unsubstantiated claims. The FDA has also claimed that the key ingredient, apoaequorin, a synthetic protein, is not an acceptable ingredient in a dietary supplement. 

Prevagen touts that it’s the only supplement containing apoaequorin, a protein that it says was originally plucked from a jellyfish in the Puget Sound and which aging brains “need for healthy function.” But the lawsuit filed in January against Quincy Bioscience asserts that this protein does just about as much for the brain as a royale with cheese (and other assorted run-of-the-mill proteins):
Prevagen cannot work as represented because apoaequorin, the only purported active ingredient in Prevagen, is completely destroyed by the digestive system and transformed into common amino acids no different than those derived from other common food products such as chicken, cold cuts, hamburgers, etc.
The brain supplement’s website shares three studies under its research tab. One of studies lists Mark Y. Underwood, the president of Quincy Bioscience, who said in an interview with TINA.org that all clinical trials were done in-house.

When the FDA came knocking
The FDA sent Underwood a warning letter in 2012 over the alleged illegal marketing of Prevagen as a drug without the agency’s approval. The letter also noted that the product did not satisfy the definition of a dietary supplement because the only dietary ingredient on the label — “synthetically produced apoaequorin” — did not qualify as such.
Perhaps most importantly, the FDA said an inspection found that the company had received more than 1,000 adverse health events associated with the product, but failed to report serious cases, including seizures and strokes, to the agency as required. The unreported events and complaints were submitted to Quincy Bioscience between May 2008 and December 2011. Underwood said “less than two dozen” of the more than 1,000 adverse health events were “serious.”
Underwood said the company has made “adjustments” to its reporting procedure regarding adverse health events. Since August 2010, the FDA has received more than 50 adverse event reports related to Prevagen products, documents obtained by TINA.org through a Freedom of Information Act (FOIA) request show. But he refuted much of what the FDA alleged in its 2012 letter and said that the company stands by its advertising and clinical trials. He declined to comment on the class-action lawsuit.

<![CDATA[Ozanezumab Yields Disappointing Results for Treating Amyotrophic Lateral Sclerosis]]>Thu, 01 Oct 2015 17:47:22 GMThttp://hickoryneurology.net/neurology-spectrum/ozanezumab-yields-disappointing-results-for-treating-amyotrophic-lateral-sclerosisseptember-30-2015by-thomas-s-maychicago-september-30-2015-ozanezumab-a-monoclonal-antibody-has-demonstrated-disappointiCHICAGO -- September 30, 2015 -- Ozanezumab, a monoclonal antibody, has demonstrated disappointing efficacy results against the neurite outgrowth inhibitor protein Nogo-A in patients with amyotrophic lateral sclerosis (ALS), according to results of a phase 2 study presented at the 140th Annual Meeting of the American Neurological Association (ANA).

<![CDATA[New therapy for Multiple Sclerosis!]]>Tue, 18 Nov 2014 03:27:47 GMThttp://hickoryneurology.net/neurology-spectrum/new-therapy-for-multiple-sclerosisFDA Approves Lemtrada™ (alemtuzumab) for Relapsing MS - UPDATENovember 14, 2014

UPDATED November 17, 2014

The U.S. Food and Drug Administration has approved Lemtrada™ (alemtuzumab, Genzyme, a Sanofi Company) as a disease-modifying therapy for people with relapsing forms of MS. Lemtrada is given as intravenous infusions – for 5 consecutive days initially and for 3 consecutive days one year later. Because of its safety profile, the prescribing information indicates that use of Lemtrada should generally be reserved for people who have had an inadequate response to two or more MS therapies.

<![CDATA[EyeWire - The Game]]>Sat, 14 Jun 2014 15:47:31 GMThttp://hickoryneurology.net/neurology-spectrum/eyewire-the-gameEyeWire is a game to map the brain from Seung Lab at MIT. Anyone can play and you need no scientific background. Over 100,000 people from 130 countries already do. Together we are mapping the 3D structure of neurons; advancing our quest to understand ourselves.
<![CDATA[AVM - New concepts for the best management.]]>Fri, 13 Jun 2014 00:25:21 GMThttp://hickoryneurology.net/neurology-spectrum/june-12th-2014New Study Supports Conservative Management Over Intervention for Unruptured Brain AVMsFitzgerald, Susan

During up to 12 years of follow-up, the risk of a nonfatal stroke or death due to brain arteriovenous malformation, arterial aneurysm, or intervention was lower for patients treated medically compared with those who underwent neurosurgical excision, endovascular embolism, stereotactic radiotherapy, or a combination of these therapies.

Patients with an unruptured brain arteriovenous malformation (AVM) who received conservative medical management fared better in the long term than patients who underwent an intervention, according to a population-based study from Scotland.

During up to 12 years of follow-up, the risk of a nonfatal stroke or death due to brain AVM, arterial aneurysm, or intervention was lower for patients treated medically compared with those who underwent neurosurgical excision, endovascular embolism, stereotactic radiotherapy, or a combination of these therapies.

The Scottish study, published in the April 23/30 edition of Journal of the American Medical Association (JAMA), included 204 patients, 103 of whom underwent an intervention and 101 who did not. The patients, who were at least 16 years old, were diagnosed with an unruptured brain AVM during 1999–2003 or 2006–2010.

Using anonymous data from the Scottish National Health Service, researchers followed the patients prospectively. The patients who underwent an intervention tended to be younger, more likely to have presented with seizures, and less likely to have a large brain AVM (exceeding 6 cm) than those who did not get an intervention.

The study's primary outcome was death or sustained morbidity due to any cause by measure of the Oxford Handicap Scale.

“During a median follow-up of 6.9 years, the rate of progression to the primary outcome was lower with conservative management during the first 4 years of follow-up (36 versus 39 events; a relative risk reduction of 41 percent) but rates were similar thereafter,” the researchers reported.

When it came to the secondary outcome measure — nonfatal symptomatic stroke or death due to brain AVM, associated arterial aneurysm or intervention — “the rate of the secondary outcome was lower with conservative management during 12 years of follow-up (14 versus 38 events; a relative risk reduction of 63 percent),” according to the researchers. Seven symptomatic strokes occurred within 30 days of intervention.

<![CDATA[New therapies for stroke.]]>Sun, 16 Oct 2011 00:17:25 GMThttp://hickoryneurology.net/neurology-spectrum/new-therapies-for-stroke_PARIS—The ARISTOTLE trial took center stage at the recent European Society of Cardiology (ESC) Congress here, with results showing the experimental oral factor Xa inhibitor apixaban was superior to warfarin in patients with atrial fibrillation (AF).

Apixaban reduced the risk of stroke or systemic embolism, the primary endpoint, by 21 percent, compared with warfarin. Additionally, it was associated with a 31 percent reduction in major bleeding and an 11 percent reduction in all-cause mortality versus the vitamin K antagonist, reported Christopher B. Granger, MD, professor of medicine and director of the cardiac care unit at Duke University Medical Center in Durham, NC.

The results of the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) study was simultaneously published Aug. 28 in the online edition of The New England Journal of Medicine.

[Neurology Today]
<![CDATA[New potential model for Multiple Sclerosis]]>Wed, 17 Aug 2011 18:58:54 GMThttp://hickoryneurology.net/neurology-spectrum/new-potential-model-for-multiple-sclerosisJapanese macaque monkeys infected with a newly identified virus develop a progressive disease characterized by paresis in one or more limbs, ataxia, or ocular motor paresis — providing a potential new animal model for multiple sclerosis research.

The multiple sclerosis (MS) community has a surprising and important new animal model, the Japanese macaque monkey, which could provide a tantalizing new clue to the etiology of the human disease. The monkey develops an MS-like demyelinating disease after infection with a newly characterized virus, according to a study that appeared online before print in the Annals of Neurology.

“The new model offers the opportunity to try to understand the pathogenesis in an animal a lot closer to humans, and to test therapeutics,” said Neurology Today Associate Editor Kenneth L. Tyler, MD, who was not involved in the research. “It also raises the possibility that a related virus could potentially be playing a role in human disease,” said Dr. Tyler, the Reuler-Lewin Family Professor and chair of neurology at the University of Colorado-Denver.

[Neurology Today]

<![CDATA[Medical Watchdog Groups Asks FDA to Withdraw Donepezil 23 Mg]]>Sun, 31 Jul 2011 14:41:57 GMThttp://hickoryneurology.net/neurology-spectrum/medical-watchdog-groups-asks-fda-to-withdraw-donepezil-23-mg
_Shortly after patent protection on donepezil (Aricept) expired late in 2009, the manufacturer introduced a new version containing a higher dose, with advertisements claiming it was effective for treating mild, moderate, and severe Alzheimer disease (AD).

But several leading AD researchers have expressed serious doubts about the drug‘s effectiveness and safety at the higher 23 mg dose. And Public Citizen, a medical watchdog organization, has filed a petition with the FDA to request that the drug marketed as Aricept 23 be withdrawn immediately.

“Aricept went off patent last year, so in order to maintain a proprietary drug they came up with a dose formulation that you couldn‘t easily duplicate by taking two [standard dose] 10 mg pills,” said David S. Knopman, MD, professor of neurology at Mayo Clinic in Rochester, MN. “If the higher dose were more effective, I would have no objection, but the clinical trial conducted by Aricept‘s sponsors failed to meet basic standards for demonstration of efficacy. I would like to see the scientific leadership of the neurologic community go on record as objecting to this misleading interpretation of the clinical trial data.”

Donepezil, manufactured by the Japanese drug company Eisai in partnership with Pfizer, was recording sales of about $2 billion a year before the expiration of the patent opened the way for less expensive generic versions of the drug. Eisai predicted generic competition would cut sales by 60 percent within three years.

[Neurology Today]
<![CDATA[Something to meditate on.]]>Tue, 28 Jun 2011 08:34:56 GMThttp://hickoryneurology.net/neurology-spectrum/something-to-meditate-on_  Imagine you are almost dozing in a lounge chair outside, with a magazine on your lap. Suddenly, a fly lands on your arm. You grab the magazine and swat at the insect. What was going on in your brain after the fly landed? And what was going on just before?

Many neuroscientists have long assumed that much of the neural activity inside your head when at rest matches your subdued, somnolent mood. In this view, the activity in the resting brain represents nothing more than random noise, akin to the snowy pattern on the television screen when a station is not broadcasting. Then, when the fly alights on your forearm, the brain focuses on the conscious task of squashing the bug.

But recent analysis produced by neuroimaging technologies has revealed something quite remarkable: a great deal of meaningful activity is occurring in the brain when a person is sitting back and doing nothing at all.
It turns out that when your mind is at rest—when you are daydreaming quietly in a chair, say, asleep in a bed or anesthetized for surgery—dispersed brain areas are chattering away to one another. And the energy consumed by this ever active messaging, known as the brain’s default mode, is about 20 times that used by the  brain when it responds consciously to a pesky fly or another outside stimulus. Indeed, most things we do consciously, be it sitting down to eat dinner or making a speech, mark a departure from the baseline activity of the brain default mode.

[Scientific American: The Brain's Dark Energy]     ]]>
<![CDATA[Unusual outbreak of neuropathy at a pork-processing plant.]]>Thu, 23 Jun 2011 19:32:40 GMThttp://hickoryneurology.net/neurology-spectrum/unusual-outbreak-of-neuropathy-at-a-pork-processing-plant
In the fall of 2007, the Minnesota Department of Health was notified of 11 cases of an unexplained neurological illness, all linked to a pork processing plant, Quality Pork Processors, Inc., in Austin, MN. The cluster of workers had been experiencing similar symptoms, including fatigue, pain, numbness, and tingling in their extremities as well as weakness. The symptoms were described as more sensory than motor, and all patients had evidence of polyradiculoneuropathy with signs of nerve root irritation.

An epidemiological investigation revealed that the only commonality between cases was their exposure to a pork brain extraction procedure involving compressed air. As relatives of the cases remained asymptomatic and all cultures for known pathogens were negative, the etiology of the syndrome seemed not to be infectious.

Clinically, the syndrome was most akin to chronic inflammatory demyelinating polyneuropathy. Laboratory tests corroborated the clinical findings, revealing inflammation of peripheral nerves and nerve roots; however, these cases also had features clinically distinct from chronic inflammatory demyelinating polyneuropathy as well as laboratory testing revealing a novel immunoglobulin G immunostaining pattern. This suggested that the observed inflammation was the result of 1 or more unidentified antigens.

This syndrome was ultimately dubbed progressive inflammatory neuropathy and was theorized to be an autoimmune reaction to aerosolized porcine neural tissue. Since the investigation's outset, 18 cases of progressive inflammatory neuropathy have been identified at the Minnesota pork processing plant, with 5 similar cases at an Indiana plant and 1 case at a Nebraskan plant.

The plants in which cases have been identified have since stopped the use of compressed air in removing pork brains. All cases have stabilized or improved, with some requiring immunosuppressive and analgesic treatment. The study of progressive inflammatory neuropathy is ongoing, and the details of this investigation highlight the value of epidemiological principles in the identification and containment of outbreaks while researchers attempt to uncover the unique pathophysiology and potential etiology of the illness. Mt Sinai J Med 76:442-447, 2009. (c) 2009 Mount Sinai School of Medicine.