Mind Injury

Recently resolved bankruptcy court litigation involving asbestos-product maker W.R.Grace & Co. will likely benefit the thousands of sick individuals who have brought mesothelioma lawsuits against the company.

According to The Daily Inter Lake, W.R. Grace recently ended bankruptcy court litigation that has dragged on since 2001 and agreed to a $19.5 million that will fund the Libby Medical Program and transfer to a local Libby Medical Plan Trust. This will ensure that the Libby Medical Program – which was a voluntary operation started by W.R.Grace that could have been shut down at any time – will remain open.

The bankruptcy settlement also will establish a separate Asbestos Personal Injury Trust as part of the company’s reorganization plan. Up to two asbestos trusts to compensate asbestos and mesothelioma personal injury claimants and property owners can be established under the reorganization plan.

W.R. Grace announced that the trusts will cover costs for any current and future asbestos claims. When initially filing for bankruptcy, the company said it had been named in 110,000 asbestos-related lawsuits.

If you or a loved one has been harmed by loose asbestos fibers, call Sokolove Law today to learn more about possibly pursuing an asbestos or mesothelioma lawsuit.

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Tysabri Brain Infection Lawsuit News – 2/22/2012: Please contact us today if you took Tysabri and suffered unusual side effects or other injuries.

Tysabri Brain Infection Lawsuit: The brain directs every voluntary activity in the body (motor functions and the musculoskeletal system), stimulates respiration, oversees digestion, manages growth and development, ensures tissue repair, and serves as Grand Central Station for the nervous system. (The brain contains 6 mil­lion nerve cells, fully half of the body’s entire supply.) The brain is our in­terpreter of the outside world, monitoring information supplied by our five senses. It is also, of course, the center of our thoughts, feelings, and emo­tions. In fact, it is specially constructed for processing that complex mix.

The human brain is divided into two sections—a newer, outer layer called the neocortex or the cerebral cortex, and a more primitive interior re­gion known as the Old Brain or archipallium. The neocortex, called “neo” because it is believed to have evolved more recently, is the seat of percep­tion, learning, cognition, conscience, and morality. The Old Brain, includ­ing the hippocampus and brain stem, is where our moods and emotions dominate—fear, anxiety, happiness, love, excitement, and so on. All mam­mals have the equivalent of our Old Brain, but the large, overdeveloped, multi-wrinkled outside (the neocortex) sets humans apart.

Specialized nerve cells called neurons are the fundamental structure of the brain. The human brain has 100 billion neurons, and each one has as many as 100,000 links to other neurons. It transmits billions of messages between neurons every second. To get over the gap, or synapse, between neurons, those messages rely on chemicals known as neurotransmitters. Neurons store neurotransmitters, releasing them in response to electri­cal signals. The neurotransmitter then attaches to receptors on nearby neu­rons, triggering another electrical signal. This is the way moods, thoughts, emotions, and impulses move throughout the brain. Receptors on neurons are specific to certain neurotransmitters—like a lock and key.

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Tysabri Brain Infection Lawsuit: You never get any more neurons than you are born with. In fact, the brain loses nerve cells as it ages (and in the event of brain injury). Aging also cuts down on the number of extensions from the neu­rons (dendrites) that connect to other neurons, so communication between brain cells gets more difficult the older you get. Levels of some of the neurotransmitters charged with carrying positive feel­ings decrease. In addition, by age forty-five, levels of a powerful enzyme that is responsible for breaking down several types of neurotransmitters increase. The stepped-up breakdown can throw your brain chemistry out of balance and lead to, among many other things, a decrease in the general level of brain activity, inter­ference with the ability to think and remember, and depression.

Certainly, none of this has to mean senility or the loss of mental function that we (wrongly) associate with getting older. You have plenty of neurons to keep you mentally strong for your entire life if you care for them well; and providing the materials for all the neu­rotransmitters you need is within your control. But aging can mean that your brain chemistry tips out of balance more easily if you don’t provide proper nutrition. Looking at it another way, people may get away with sloppy eating habits in their youth, but those habits eventually catch up with them.

The disproportionate opportunities for failure, rather than success, make it that much more crucial that our brains get a constant supply of the correct neurotransmitters, and the raw materials for making them, in order to keep working smoothly. By and large, neurotransmitters become inactive once they’re delivered a message, and they need to be replenished. Though they exist throughout the body, they cannot move into the brain from out­side it, in order to protect it from fluctuations of neurotransmitters in the blood. Instead, they are made “on site”—in the brain, where and when they are needed. (It is also possible to have too much of a particular neurotrans­mitter, and breakdown is an important step in controlling this. Your body will make only what it needs from available materials.)

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Tysabri Brain Infection Lawsuit: Neurotransmitters are made from amino acids (the building blocks of all proteins), which we get from the food we eat. Poor diet, then, can leave us without the ability to make the chemical messengers necessary for healthy brain function. Optimal nutrition, through high-quality food and, as necessary, supplements, maintains balance in the brain, which allows for a plentiful supply of the appropriate neurotransmitters and a general mood of well-being and comfort. Your brain physically changes in response to your experiences. Neu­rons develop new connections thanks to new sensations and even thoughts. While you learn something, or try something new, or go through something for the first time, your brain actually grows or alters its structure to accommodate that information.

An electron microscope is an imposing instrument, about six feet high, housed inside a small darkened room designed exclusively for this instrument and the support equipment it requires—high voltage trans­formers, vacuum pumps, and a liquid nitrogen tank. A heavy steel col­umn about ten inches in diameter rises up to the ceiling from a workstation console, encrusted with buttons, switches, knobs, flashing indicator lights, digital numerical displays, and video monitors. Sprout­ing out of the top of the column is a heavy, two-inch-diameter electrical cable, which delivers 100,000 volts to the electron gun at the top of the column. Liquid nitrogen billows out a white cold fog spilling down from the top of the column in the darkened room like liquid oxygen from a rocket on the launchpad at dawn.

After placing the sample in the microscope and energizing the electron gun, Morest sees shadowy patterns come into focus on a phos­phorescent screen. Anyone not trained in interpreting these shadowy patterns would see nothing more than grey doodles on a glowing yel- low-green background. But the electron microscopist, with his head pressed against the column to look at the glowing screen through a thick glass window, is transported inside a cell of this rat’s brain. The tiny slice is now expanded into an immense new universe. Turning wheels simul­taneously with both hands he moves the grid, scanning acres of cellular territory for hours, completely absorbed in the new world he is seeing. Hours later he emerges from the room with a telltale flat spot embossed into the center of his forehead from pressing it against the column.

Increasing the magni­fication in an electron microscope is like seeing the ground spinning below as you descend swinging from a parachute, bringing greater and greater detail as you approach the ground. Mo rest must keep his bear­ings through all of these dizzying twists, maintaining a conceptual thread back through the slicing process to the way the tissue was ori­ented in the brain of the rat He will have to analyze hundreds of sections to reconstruct the three-dimensional cellular structure correctly, a pro­cess requiring months or years of work.

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Some research­ers suggest that augmenting these beneficial actions of microglia would be the best therapy Microglia do indeed target and kill neurons that are infected with the disease-causing prions and thus they do damage neu­ral circuitry, but in doing so they may protect the brain by limiting the spread of the diseased prion. Microglia also engulf the deposits of PrP outside neurons, thus eliminating or slowing the accumulation of PrP plaques. Once infected by prion, however, the ability of microglia to consume particles of PrP becomes impaired. Dysfunctional microglia might even contribute to the disease, making some people more suscep­tible to prion infection than others.

This is essential for synaptic transmission and to prevent glu­tamate from rising to toxic levels. In CJD, microglia transform to take over this vital function as astrocytes become infected and die. The trans­porter molecule in the cell membrane that absorbs the n euro transmitter glutamate into astrocytes starts to be synthesized in microglia during prion infection. Now equipped with the glutamate transporter of astro­cytes, microglia step in for their fallen glial comrades to lower the toxic levels of this neurotransmitter in damaged brain tissue. This protects neurons from death due to overstimulation by the excess glutamate.

Finally, microglia could be helpful in diagnosing prion disease. Microglia develop distinct cellular changes in response to prion infec­tion, and these alterations can be detected with appropriate diagnostic techniques. Much as monitoring changes in blood cell count informs doctors of the type and severity of infections in the body, one can imag­ine that careful monitoring of changes in microglia could provide criti­cal insight into infection in the brain. Interestingly, current evidence suggests that oligodendrocytes are not capable of supporting replication of the infectious prion protein. Tin’s resistance sets them apart from both neurons and astrocytes. However, oligodendrocytes and myelin suffer damage in prion disease. Other studies indicate that oligodendrocytes are killed by oxidative injury ac­companying prion infection.

Our use of the term or terms Tysabri Brain Infection Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Tysabri Class Action Lawsuit News – 2/22/2012:You deserve to be compensated if you took Tysabri and suffered side effects that the public was not warned about. Contact us today and we will arrange a free consultation with a lawyer experienced in pharmaceutical and medical device ligation that can advise you of your legal rights.

Tysabri Class Action Lawsuit: Recall that PrP is a normal protein in neurons that becomes mutated and infectious in prion disease. The biological role of the normal PrP in cells is still mysterious. In 2005 it was reported that normal PrP is found in purified myelin and in oligodendrocytes. In 2007, Frank Baumann and colleagues from the University Hospital of Zurich, Switzerland, re­ported that a mutation in a particular part of PrP caused myelin break­down in both the central and peripheral nervous systems of mice. This study suggests that myelin integrity must be maintained by some un­known action of the normal PrP in myelin. By studying the role of PrP in myelin, we may learn more about the normal function of this protein in cells.

How do the 100 billion neurons in our brain allow us to remember who we are; to learn, think, and dream; to be stirred by passion or rage; to ride a bike or conjure meaning from inked patterns on paper; or to pluck out instantly a mothers voice from the muddle of a noisy crowd? What goes wrong with neural circuits in schizophrenia or depression, or in dreadful diseases like Alzheimer’s, multiple sclerosis, chronic pain, or paralysis?

We are on the cusp of a new understanding of the brain that trans­forms a century of conventional thinking about the brain, specifically the role of the brains neurons. Crowding around the computer screen in a darkened room in 1990, scientists watched information passing through peculiar brain cells, bypassing neurons and communicating without using electrical impulses. Until this discovery scientists had presumed that information in the brain flowed only through neurons by using electricity. In fact, a mere 15 percent of the cells in our brain are neurons. The rest of our brain cells—called glia—have been over­looked as little more than packing material stuffed between the electric neurons. “Housekeeping cells” they were called. Dismissed as cellular domestic servants, glia were neglected for more than a century after they were discovered.

A neuron from the brain of a genius was indistinguishable from one taken from a typical brain. And on average, there were just as many neurons in Einstein’s creative cerebral cortex as in the cortex of men not noted for being unusually creative. But there was one difference in the data. The number of cells that were not neurons was off the charts in all four areas of Einsteins brain. On average, the samples from normal brain tissue had one cell that was not a neuron for every two neurons counted, but the samples from Einsteins brain had nearly twice as many nonneuronal cells, about one for every neuron. The biggest difference was seen in the sample of parietal cortex from the dominant side of Einsteins brain, the region where abstract concepts, visual imagery, and complex thinking take place. Was this a fluke? Diamond calculated the mathematical odds that this difference could have happened by chance, considering the range of variation in the control tissue samples. In all the regions sampled from Einsteins brain the odds that the difference could have occurred by chance were small.

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Tysabri Class Action Lawsuit: The rest of the brain is white matter. This glistening-white brain tissue is a mass of millions of tightly bundled communication lines connecting neurons between distant points in the brain. These vital communication lines are packed beneath the grey matter cortex, much like tightly wound fibers beneath the leather skin of a baseball. White matter in the brain, like white space on paper, is easily dismissed as something defining the areas between the functional components, but recently this naive view has been changing. Unraveling this part of the brain is such a daunting task that only in the last few years have new brain imaging techniques allowed scientists to venture into the white matter realm. As we will see later, these new findings are changing fundamental concepts about how the brain processes and stores information—how we learn. Here inside the blank white regions of brain, glia are the heart of the mechanism.

A revolution in our understanding of how the brain is built, how it functions, how it fails in mental illness and disease, and how it is repaired has been ignited with the recent exploration of these long- neglected brain cells. Glia are the key to understanding this new view of the brain. There is little or no information available about these cells to nonscientists, so we can begin our inquiry with about as much knowl­edge as the pioneering scientists who discovered these various odd brain cells. Since the answers are known to only a few specialists, we can ex­perience the same puzzles, clues, and revelations as the scientists who sleuthed out these peculiar cells in the brain. When these clues are as­sembled, will they reveal another brain working in parallel with our neuronal brain?

Before venturing further, it is essential that we proceed from a common base of knowledge about how the brain operates at the level of cells and circuits. The nervous system works by sending electrical impulses down a wire-like axon at top speeds of 200 miles per hour. Impulses travel through some axons, such as pain fibers, much more slowly—only 2 miles per hour, the pace of our footsteps in a slow walk. This explains the build-up to the full painful sensation when you accidentally hit your thumb with a hammer. The reason for the hundred-fold increase in transmission speed through our high-speed nerve fibers is that they are wrapped with electrical insulation, called myelin. In contrast, pain fibers are uninsulated thread-like axons.

Neurons are not fused to one another like copper wires soldered in a circuit; instead, each neuron in your brain is an island unto itself. Each of these neuronal islands communi­cates by sending a message to another neuron across a tiny gulf of the saltwater that bathes every cell in your body. Because of this gulf of separation, information is not passed on to the next neuron in a circuit by electricity. Instead, the neuron floats chemical messages across the gulf to reach the neuron on the other side. This gulf is the synapse, and the neurons on either side are called presynaptic or postsynaptic neu­rons, depending on whether they are the sending or receiving shore of the gulf. The presynaptic neuron is always the one sending the message from its axon tip; the postsynaptic neuron receives messages across the synapse through its root-like dendrites.

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Tysabri Class Action Lawsuit: The messages are sent in the form of a chemical substance called a neurotransmitter. Microscopic “bottles” inside neurons, called synaptic vesicles, are filled with neurotransmitter molecules. Each synaptic vesi­cle is a tiny sphere too small to see with a light microscope; they are visible only under the high-power magnification of an electron micro­scope. The messages are not floated across the synaptic gulf in these spherical bottles, as you might expect; instead, their contents are dumped into the gulf and diffuse across to the opposite shore. Synaptic vesicles accumulate inside the axon right next to the cell membrane at the tip.

Like cellular water balloons, one or more synaptic vesicles are smashed against the cell membrane of the axon by the force of the electrical im­pulse when it arrives, releasing the vesicles contents into the cellular sea. The neurotransmitter then flows across the synaptic gulf to reach the postsynaptic neuron on the other side.

Sentinel molecules along the shore of the postsynaptic neuron are specially designed to detect the neurotransmitter substance in the syn­aptic gulf. These neurotransmitter receptors are large protein molecules acting as biological nanomachines. In each neurotransmitter receptor there is a passageway that can open into the dendrite of the receiving neuron when neurotransmitter is detected. When the tunnel through the receptor opens briefly, charged ions floating in solution leak out, reducing the voltage inside the postsynaptic neuron. This brief drop in voltage in the postsynaptic neuron is the receiving signal, called the postsynaptic potential. If the synaptic voltage change is big enough, the voltage drop triggers the postsynaptic neuron to fire an impulse out its own axon to signal the next neuron in the circuit. This may seem an awkward way to design a nervous system, but consider the engineering challenge facing Nature: to build a powerful, high-speed biological com­puter using nothing other than cells—tiny bags of saltwater.

So the nerve impulse speeds down an axon, releasing neurotrans­mitter when it reaches the end. The neuro transmitter flows across the synaptic gulf and activates neurotransmitter receptors on the postsyn­aptic neuron, causing a voltage drop in the recipient neuron that will make it fire an electric impulse down its own axon to release neurotrans­mitter onto dendrites of the next neuron in the circuit in relay fashion. To reduce the time it takes for neuro transmitter to diffuse across the syn apse, the gulf of separation is infinitesimally narrow (25 billionths of a meter). The synaptic cleft is so narrow, in fact, it is impossible to see the separation through the most powerful light microscopes. This fact caused decades of controversy in the field of neuroscience until the elec­tron microscope proved that every synapse in the body has a gulf of separation between the pre- and postsynaptic neurons. A message passes across the synapse in about one-tenth of an eye blink, but compared with the two hundred mile per hour speed of the neural impulse, the synapse slows information flow much like a toll booth on a turnpike.

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Tysabri Class Action Lawsuit: When your doctor taps his rubber mallet below your knee to test your knee-jerk reflex, you are seeing a circuit in action that controls the vital coordination crucial for you to walk. Should you stub your toe as you are walking, this misstep will jerk the tendon below your kneecap, just as your doctor does with his mallet. To avoid stumbling, you must now quickly swing your lower leg forward to catch your fall mid-stride. It is vital that this entire sensory-motor reflex is executed in a split sec­ond of time, otherwise you will trip and fall.

To execute this lightning-speed response, there is only one synapse in the entire circuitry controlling the vital reflex that keeps you on your toes. When nerve endings in your kneecap tendon sense a sudden tug from a stubbed toe (or doctor’s mallet), they shoot impulses at two hun­dred miles per hour up the axon from the nerve endings into your spine. There is no time to send signals to your brain; instead, there in your spinal cord a single synapse separates this sensory neuron (bringing information about your leg motion into your spine) from a motor neu­ron that will fire electrical impulses down to your leg muscle to jerk your lower leg forward in a flash—one synapse separating us from falling on our face. (The messages will be relayed by other nerve circuits to your brain, but they arrive after your leg muscles have already responded, and you have no conscious control over what has happened. This is why the doctors mallet triggering the knee-jerk reflex always delights us with surprise as we watch our leg react automatically.)

Synapses do much more than connect neurons; they enable flexibility of information processing. Synapses permit adjustments in functional connections based on experience. The process of learning is more finely regulated than simply making and breaking synapses: the strength of a synaptic connection can be finely tuned in a process called synaptic plas­ticity. How? The molecular changes that strengthen or weaken a synaptic connection are intensely studied by neuroscientists interested in memory and learning, but in principle, the mechanisms are quite simple. Either by releasing a bit more neurotransmitter from the pre-synaptic ending when an impulse arrives, or by adjusting the sensitivity of the postsynaptic neuron receiving the neurotransmitter signal, the same input to a syn­apse can produce greater or lesser voltage change in the postsynaptic neuron, thereby weakening or strengthening the connection.

But there is one additional crucial aspect to this process of synaptic transmission: cleanup. Communication across a synapse would fail if the synaptic gulf were not cleared of n euro transmitter quickly to permit another message to be sent. It was long understood that glia bordering the synaptic cleft carried out this cleanup operation. Protein molecules in the glial membrane pump the neurotransmitter out of the synaptic cleft and into the astrocyte—one of the four major kinds of glial cells— where it is reprocessed. After filtering out the neurotransmitter and re­cycling it into an inert form that cannot be confused as a signal, the astrocyte surrounding a synapse delivers the reprocessed substance back to the presynaptic nerve terminal. The neuron then carries out a simple chemical reaction to convert the inert neurotransmitter back into active neurotransmitter and repackages it into synaptic vesicles.

If neurotransmitter is not taken up efficiently, communication across a synapse will fail because the gulf will become saturated with stale mes­sages. If neurotransmitter is taken up too quickly, the message will ap­pear too briefly to have full effect on the postsynaptic cell. If the energy requirements of the neuron cannot be met by the nutrients supplied by astrocytes, the neuron will run out of gas. Astrocytes are thus in a posi­tion of control.

Our use of the term or terms Tysabri Class Action Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Tysabri Lawyers News – 2/22/2012: Tysabri may be linked to serious negative side effects. If you took Tysabri and believe you suffered negative side effects as a result, contact us today so that we can make arrangements for a free consultation with a law firm that is investigating cases related to the side effects of Tysabri.

Tysabri Lawyers: Like sponges, astrocytes absorb discarded potassium ions from the space around neurons, sucking them into their own cytoplasm. Potas­sium ions are released by neurons when they fire an electrical impulse. Accumulating these excess positive charges inside astrocytes does not create a problem for glial function, because glia do not communicate by firing electrical impulses. Removing the excess potassium is essential for recharging neurons.

How do astrocytes collect and dispose of the excess potassium ions? Astrocytes are connected to one another in avast multicellular network through protein channels called gap junctions. Gap junctions not only couple astrocytes together like snaps on a jacket, they allow potassium to flow freely through the channels and between adjacent glial cells. These gap-junction connections between astrocytes allow them to si­phon off potassium from around a neuron that is actively dumping po­tassium ions as it fires impulses, dispersing the excess positive ions into the network of astrocytes, The community of glial cells, coupled by gap junctions, works cooperatively to maintain the proper potassium ion concentration outside neurons. To dispose of the excess potassium, spe­cialized astrocytes have structures called end feet. These cellular exten­sions grasp small blood vessels like the clinging feet of a bat. Through these end feet, astrocytes dump the accumulated potassium into the bloodstream, as if it were ridding the brain of the waste generated by neuronal activity.

The consequences of glia failing to maintain potassium ions at the proper concentration outside neurons are obvious. During high states of neuronal activity—the extreme being a brain seizure—the potassium concentration builds up around neurons quickly, and its removal by astrocytes is crucial. Without astrocytes sopping up potassium ions, the brain will run out of electrical power. When it is unable to fully recharge its neuronal batteries, the brain waves go flat. In comparison to normal brain waves, these flattened brain waves, called spreading depression, are much like the dim flash of a camera strobe, too feeble to work prop­erly. These depressed waves are seen in EEG recordings accompanying many pathological conditions.

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Tysabri Lawyers : Recent research has found that astrocytes markedly change their calcium signaling in animals in which seizures have been induced ex­perimentally. Normally the amount of calcium signaling between astro­cytes in brain cortex is relatively moderate, but after a seizure these astrocytes typically show large oscillations in calcium signals. They sweep through the cortex in strong waves, presumably releasing more glutamate and tipping the brain toward seizure. The evidence suggests that these changes in astrocyte calcium signaling are permanent changes following repeated seizures, rather than echoes in the wake of increased calcium signaling in astrocytes induced during the seizure itself. Possi­bly this change in astrocyte calcium signaling after seizure could be beneficial, but early research suggests that damping the excessive astro­cyte signaling with drugs improves the outcome and limits the death of neurons in animal models of epilepsy.

As mentioned previously, interesting new research reveals that patients with bipolar disorder and schizophrenia also have fewer oligo­dendrocytes, the myelinating cell of the brain. These glial cells wrap axons with myelin, but they are not thought to be involved in glutamate regulation. Nevertheless, too much glutamate can be just as toxic to myelinating glia as it is for neurons. This could be another way glia par­ticipate in mental illness, because when the myelin insulation becomes frayed, so does mental function.

Excess glutamate in the brain may be one of the main causes of death of myelinating glia in the brains of people suffering overproduction of this neurotransmitter. The effects of glutamate on myelinating glia might influence cognitive function even though these cells are not associated with synapses. When one considers that prefrontal lobotomy works by severing the connections to the forebrain, and seeing how the process completely changes a persons personality, it is not difficult to imagine how a pathological loss of myelinating glial cells in these forebrain tracts could lead to psychiatric disorders such as schizophrenia and other mental impairments. Breaking the insulation 011 critical communication cables in the brain will disrupt communication as effectively as severing the cable.

Electroconvulsive shock has a therapeutic effect on clinical depres­sion and schizophrenia by resetting brain waves, but electroconvulsive shock therapy may also activate a beneficial injury response in the brain. Since astrocytes and microglia are the first line of defense in any brain injury, it is obvious why altered glia would be seen in regions of the brain giving rise to seizures. This injury response of glia to brain seizure may also be one of the cellular mechanisms that explains the changed brain function induced by electroshock therapy. Both microg­lia and astrocytes release growth factors in response to brain stress and injury. These growth factors sustain neurons under neurotoxic condi­tions that would normally kill them, and in the healthy brain these glial- derived growth factors promote neuronal growth and health. Both microglia and astrocytes release many different natural inflammatory agents to aid in the healing process, and all of these glial responses prob­ably contribute to the therapeutic effect of electroshock treatment.

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Tysabri Lawyers: This neurovascular unit, as the astrocyte-capillary-neuron group is now called, is also intimately involved in another form of pain and disability suffered by millions of people. Migraines are debilitating vascular head­aches originating within the brain. Electrical impulses spreading to other regions of the brain change nerve cell activity and together with the resulting disturbances in local blood flow cause symptoms that can include visual disturbance, numbness, tingling, and dizziness. This spreading depression of brain waves was described previously in asso­ciation with epilepsy. The same phenomenon occurs in migraine, and here too, astrocytes have a role in the process.

These vascular headaches are caused by blood vessels in the brain dilating excessively and triggering pain and inflammation in the sur­rounding regions. The inflammation triggers the trigeminal nerve, re­sulting in a severe throbbing headache originating in the meninges, the skin-like cells that cover the brain. The senses become hypersensi­tive, so that normal sound and light cause excruciating pain. Nausea, vomiting, loss of appetite, and mood disturbances can accompany mi­graine attacks, and patients often experience auras, visual halos and hallucinations caused by abnormal nerve cell activity in blood-starved cortical regions where vision is processed.

Migraines occur on a periodic basis and they disproportionately affect women. Hormonal effects are thus suspected to have a role in migraine, but it is also in part an inherited disorder. Once we know more about the molecular mechanisms astrocytes use to sense neural activity and control brain waves and local blood flow, new treatments may be devised to control the problem at its source rather than simply trying to blunt the painful aftereffects when the intricate cooperation between neuron, glia, and blood vessel goes awry.

Still, it is surprising that the long-held and well-accepted role of glia as first responders to neuronal injury did not stimulate more vigorous research into exploiting glia for new investigative methods and treat­ments for brain disease and injury. Neuroscientists and the scientific establishment (research funding agencies, editors at scientific journals, and even biomedical companies) were slow to move in this promising direction. Few who marvel at the wondrous new imaging of functional activity in the human brain appreciate that they are seeing the power of glia at work in the brain, both in health and in sickness, as they promote information processing and sustain neuronal function.

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Tysabri Lawyers: People with Ashlyns congenital condition, called CIPA (congenital insensitivity to pain with anhidrosis), usually die before the age of twenty-five. Injury or infection will take them. They have no gag reflex, never feel the tickle to sneeze or the scratchy throat to cough. Never—no matter how severe her injury or what the cause—can Ashlyn tell the doctor where it hurts. Such children are insensible to an inflamed ap­pendix or an ear infection, so the infections rage undetected. As babies they never cry out in pain or develop the alarm and panic reflex at the sight of their own blood. To these babies blood is merely a curiosity. Sadly, grotesquely, but understandably, her own blood was a gruesome plaything for baby Ashlyn. These people, normal in every other respect, suffer painlessly and die prematurely because of a genetic defect that weakens and kills their pain neurons before birth.

In contrast to this puzzle of injury without pain, many people suffer the converse: pain without injury. Chronic pain is not the warning slap of acute pain that saves us from further injury. That pain subsides on its own. Strangely, chronic pain often develops after an injury has healed. It intensifies when there are no longer any noxious or injurious signals to excite pain neurons, yet these neurons scream out in gut-wrenching pain nevertheless. The ceaseless intense pain controls the lives of such chronic sufferers. Pain robs them of sleep and blots out all pleasure from their lives by imposing constant misery. A normally pleasant touch or sensation ignites raging flames of pain. Putting on a pair of socks may be unbearable.

Some patients are forced to accumulate and consume such large quantities of painkillers that the police become suspicious. Doctors who treat patients suffering chronic pain can attract scrutiny from the au­thorities for the high volume of narcotic drugs they must dispense to relieve these patients’ agonies—doses of narcotic drugs that could be fatal for a person without tolerance. At the risk of drawing unwanted attention from police and health insurance companies, many doctors are compelled to limit the dosage of pain medications to levels they know are no longer effective for the patient grown tolerant to them.

With an increasing appreciation of glia in nervous system function, some pain researchers have begun examining the most improbable of suspects, and they have found the culprit. These scientific sleuths were awakened to the improbable realization that the source of chronic pain is not in pain neurons themselves, but rather in glia. This insight is not only leading to new treatments for chronic pain; it is cracking the case of drug addiction to heroin and other narcotics.

Our use of the term or terms Tysabri Lawyers is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Tysabri Side Effects News – 2/22/2012: If you were prescribed drug name and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

Tysabri Side Effects: Before considering chronic pain and the role of glia, we need to under­stand some fundamentals of pain circuitry. It may come as a surprise to learn that your pain neurons are not located in your brain. They are not inside your spinal cord either, where you will find the motor neurons that issue commands to your muscles. Pain neurons are squeezed like an afterthought between each vertebra of the bony spinal column that rises as a series of bumps down the center of your back. In the space between each bone in your backbone there is a sack of pain neurons. You have one sack of pain neurons on each side of the spinal column at each seg­ment in your articulated spine.

In four-legged creatures, there is ample room for a small sack of pain neurons stashed between each vertebral joint, but as humans rose up on two hind legs our vertebrae became stacked vertically, compressing the elastic disc of padding between each bone in our backbone. Our spine also became distorted away from the strong arched backbone of other four-legged animals—a horse for example—into a wispy bent S shape, creating kinks at our lower back and neck. These are the vulnerable points for neck and back pain that we humans endure in exchange for trading hooves for hands. Many of us suffer neck and back pain as a result of a herniated or compressed disk squeezing this sack of pain neurons between backbones. This pain is both agonizing and damaging.

The nerve cells inside these sacks are unusual. Their cell bodies are round crystalline globes like gel-filled balloons. Pain neurons have no dendrites, but instead a slender string of an axon extends from each bal­loon and passes, bundled together with strings from other sense neu­rons, through our nerves to reach the skin or muscle somewhere on our bodies. Here the tiny nerve endings fray apart and become specialized into microscopic sensory organs that can sense touch, pressure, heat, cold, irritating chemicals, and substances released by skin cells damaged by sunburn, abrasion or cuts.

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Tysabri Side Effects: These nerve sensors also monitor the inside of our bodies. Some of them send their axons into muscle, where their tips spiral around individual muscle fibers, wrapping them like clinging vines. The tiny tendrils feel the stretch and strain of fibers in our muscles. They report back vital information to our unconscious brain on the tension and position of every muscle in our body. Without this delicate and intricate unconscious sensation, we could not move or even stand up balanced on two legs.

Each globular nerve cell also sends another axon into the spinal cord. Thus, sensory neurons have two axons, like two arms, one extend­ing to the periphery where its fingers react to stimulation, and the other penetrating the spinal cord, where it signals what it has detected. The axons penetrate the top (or dorsal surface) of the spinal cord, giving these sensory neurons the name dorsal root ganglion (DRG) neurons. The left and right halves of your body are mirrored, so you have a dorsal root ganglion nerve sack on the left and right sides of your spine be­tween each bump in your backbone.

The axons entering the dorsal surface of your spine then communi­cate through synapses to neurons inside your spinal cord. (The spinal column is your backbone, which shields your spinal cord. The spinal cord is an extension of your brain tissue running like a cord down your back inside these back bones. As mentioned earlier, it is part of your central nervous system, or CNS.) These spinal neurons are linked by a chain of neurons to the opposite side of your spinal cord. Sensations from the right side of your body are channeled across to the left side of your spinal cord, just as commands from the right side of your brain control movement of limbs on the left side of your body. Spinal cord neurons on this side then send axons up to your brain. After reaching the thalamus, the major switch box for information flow into and out of your cerebral cortex, neurons carry the pain signals to your cerebral cortex and to emotional processing centers of your brain, where you perceive the sensation of pain and associate the appropriate emotional reactions with it.

Pain can be stopped by silencing the pain neurons in the skin, as a dentist does when he injects Novocain into your gums. Novocain blocks the ion channels that spark nerve impulses. If there are no nerve im­pulses, no signals of pain will reach the spinal cord, and the tooth can be pulled painlessly. Pain caused by injury is protective, but there is another type of pain that develops mysteriously and intensifies even after the injury has healed. This “neuropathic” pain transforms protective pain into an agonizing disease. Chronic pain develops because of changes in pain circuits in the central nervous system after injury and healing. Neuroscientists know that pain neurons in people suffering chronic pain become hyperexcit- able after healing from injury. The slightest touch or change in tempera­ture sets these neurons firing barrages of nerve impulses that signal intense pain to the brain. The neurons also fire abnormally in bursts of high intensity all on their own. Like a broken record, cycles of nerve impulses scream pain over and over again without any stimulus to trig­ger them.

What causes these pain neurons to spin out of control? After an in­jury to the body or an infection, cells involved in the body’s defense and healing release powerful chemicals called inflammatory cytokines and chemokines. Drugs like ibuprofen and aspirin bring relief by blocking the action of these cytokines. Inflammatory cytokines act in many ways, and one of the consequences for pain fibers is heightened sensitivity. This is natures way of telling us to take it easy until we are healed. We are all familiar with this phenomenon when we feel the region sur­rounding the site of injury become tender and painful. Also, we have all experienced the painful reaction to light and sounds while suffering a severe headache. Our senses become heightened to the point of pain. If the inflammatory condition does not resolve, however, pain and hyper­sensitivity will persist even after the injury has healed.

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Tysabri Side Effects : People suffering chronic pain often describe their misery as raw nerves, but the latest research suggests that chronic pain goes beyond nerve cells. For many pain sufferers, the source of their chronic, un­reachable pain is glia. Linda Watkins, a pain researcher from the Univer­sity of Colorado at Boulder, began to suspect microglia as the source of chronic pain that develops after nerve injury. She recognized that glia have no involvement in transmitting normal pain, but chronicpain that develops after an injury heals might be another matter.

To test this theory that microglia may cause chronic pain, all one must do is block the normal reaction of microglia to injury and then test the animals to see whether numbing the glial response to injury brings relief from chronic pain. Watkins and colleagues conducted tests on rats with chronic pain that had been caused by spinal cord injury. She then administered a drug, minocycline, that targets microglia, preventing their activation and cytokine release in response to injury. Watkins and several other researchers found that injecting this drug into the spinal fluid relieves rats of chronic pain caused by spinal cord injury almost immediately. The experiments proved that the rats receiving the drug experienced greatly reduced chronic pain as a result of blocking micro­glial response to injury.

Other work is extending the findings on microglia and chronic pain to astrocytes by using minocycline. After all, responding to injury and infection is one of the shared functions of astrocytes and microglia. After injury, astrocytes proliferate and begin to express the skeletal pro­tein GFAP at high levels, a cellular remodeling that allows astrocytes to change their shape and motility. Like microglia, astrocytes have many receptors for injury-related signals released by neurons, and in response, astrocytes release growth factors, cytokines, and chemokines that can contribute to chronic pain in some circumstances.

Microglia and astrocytes perform many vital functions after injury, however. Eliminating glial reaction to injury entirely would likely have many undesirable consequences. If we knew more about how microglia sense neural injury and the detailed mechanisms that control their many responses during injury, healing, and development of chronic pain, po­tent new pain medications could be developed to bring relief to chronic pain sufferers without sacrificing the healing functions of glia.

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Tysabri Side Effects: One of the signals damaged nerve cells are known to broadcast when they are in distress is a chemical called fractalkine. This molecule is tethered on the surface of neurons and released like signal flares upon injury or distress. Microglia have special receptors to detect these frac­talkine distress signals. When the sensory receptor proteins on micro­glia sense fractalkines, the glial cells quickly move toward the injury and flood the area with cytokines. This response normally resolves after a period of weeks as the injury heals, but in some unfortunate cases, the microglia do not stop saturating the tissue with cytokines. The injury maybe healed, but the painful injury response continues at full rage.

After administering a drug that dampens the microglial sensors for fractalkine, Watkins and her colleagues tested how sensitive the rat was to pain. There are several well established tests for assessing pain accu­rately and humanely—for example, placing the rat’s tail on a heating pad and turning up the temperature gradually until the rat flicks the tail away. In rats suffering chronic pain as a result of previous nerve injury, even the slightest change in temperature causes the animal to flick its tail away quickly. Other tests using fine bristles of precisely calibrated stiff­ness to touch the skin can accurately gauge sensitivity to pain. Normally these bristles are painless, but in rats (and people) suffering chronic pain the slightest touch becomes excruciatingly painful, like poking an open wound. After researchers treated the rats with the drug blocking the fractalkine receptors on their microglia, the tests showed that the rats were released from the grip of chronic pain. Since the microglia could not receive the fractalkine distress signal sent by injured neurons, they did not release the inflammatory and painful cytokines.

This is an astonishing transition in medical science, for here is a painkiller that does not act on pain neurons; it brings relief from chronic pain by acting on nonneuronal cells. It is as if a door has been cracked open into a room filled with an entirely new stock of drugs to cure chronic pain. Some of these glia-targeted drugs are currently undergo­ing clinical trials in people suffering constant, uncontrollable pain.

Beyond the simple consequence that a small brain with fewer neu­rons and glia will have diminished mental capacity, one need only con­sider the crucial role of glia in orchestrating nervous system development to foresee the multiple devastating consequences of alcohol attacking fetal glia. As we will discuss in the next chapter, glia are the infrastruc­ture of the fetal brain, the scaffolding upon which the fetal nervous system is built. Glia provide trophic factors to promote transformation of immature cells into appropriate types of neurons and sustain those neurons after development. Glia lay down molecules in tracts to guide axons to form appropriate connections that will make functional cir­cuits. Glia promote the formation of synapses. Glia take up neuro­transmitters and maintain the vital salt and nutrient concentration surrounding neurons at the proper levels. Glia protect the brain from infection. Glia control migration of cells during development The loss of glia poisoned by alcohol will have a multitude of negative conse­quences on the developing brain.

Our use of the term or terms Tysabri Side Effects is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Tysabri Lawsuit News – 2/22/2012: You deserve to be compensated if you took Tysabri and suffered side effects that the public was not warned about. Contact us today and we will arrange a free consultation with a lawyer experienced in pharmaceutical and medical device ligation that can advise you of your legal rights.

Tysabri Lawsuit : Glia outnumber neurons six to one, but the exact ratio differs in dif­ferent parts of the nervous system. Just as the ratio of men to women is one to one on average, the exact ratio of men to women ranges widely in different areas. For example, the sex ratio maybe ten men to one woman in barbershops and just the opposite in fabric stores. Along nerves or in white matter tracts in the brain, the ratio of glia to neurons can be one hundred to one, because one axon can be ensheathed by myelin-forming glial cells spaced roughly one millimeter apart along the full length of the axon. In the human frontal cortex, the ratio of astrocytes to neurons is four to one, but whales and dolphins have seven astrocytes for every neuron in their gigantic forebrains. This glia to neuron ratio is larger than seen in the frontal cortex of any other mammal. No one knows why this is the case. Whales and dolphins are highly social creatures and very intelligent. Perhaps, as with Einsteins cortex, the larger proportion of glia somehow contributes to the animal’s obvious intelligence. But whales may also need more abundant glial cells to sustain their neurons in a healthy state during their long breath-holding dives to the ocean depths.

Small-diameter axons are not studded with Schwann cell “pearls,” yet they are not naked. These tiny axons are cabled together by huge globular cells grasping bunches of slender axons like a fistful of spa­ghetti. The anatomists called these fist-like cells “nonmyelinating” Schwann cells, to distinguish them from the pearl-type “myelinating” Schwann cell. These protective non myelinating Schwann cells assure that none of the most fragile slender axons in nerves are ever left bare. The nonmyelinating Schwann cells also undermine the clever idea that axons are formed in embryonic development by connecting to­gether Schwann cells to form the axon tube, because one nonmyelinat­ing Schwann cell engulfs a dozen or more small-diameter axons inside itself. Some pioneering neuroscientists suspected that these glial cells in our nerves must have a hidden function, but what the function might be was unclear.

When an axon reaches its target—for example, the synapse onto a muscle fiber that will make the muscle twitch—the entire tip of the axon is completely engulfed by another glial cell that seals off the nerve junc­tion like shrink wrap. This cell is called the “terminal” Schwann cell or “perisynaptic” Schwann cell (“perisynaptic” meaning “surrounding the synapse”). Until recently this was essentially the function most scientists presumed it served: sealing off the nerve ending. In recent years, that naive view has crumbled with the discovery that these terminal Schwann cells can sense and control information flow from nerve to muscle.

For now we should understand that Schwann cells come in three basic types: (1) myelinating, (2) nonmyelinating, and (3) terminal. Al­though these cells look completely different, they are all called Schwann cells simply because early anatomists recognized that none of them was a type of nerve cell. As will become apparent, each of these Schwann cells performs entirely different functions, and our nerves will fail to work properly if any one of them is defective. This static picture belies the dynamic nature of Schwann cells: they react with rapid changes in their structure and undergo cell division in response to nerve injury Schwann cells must perform all the functions of the various specialized glia found in the central nervous system (CNS).

Schwann cells were ignored for decades because there was no reason to imagine that they could have any function in information flow through our nerves, but the mystery of what I had just seen was before me on the computer screen: Schwann cells all along the axon in our experiment had somehow detected impulses flowing through the nerve fiber. How were the Schwann cells picking up the signals from electrical impulses in the axons? An even more intriguing question was, why would Schwann cells all along the axon need to tap into the information flowing through the nerve cell? And what would they do with the infor­mation they gleaned? These questions lay ahead of us as I flipped off the switch and watched the Schwann cell lights dim slowly, returning the screen to the shadowy darkness of silent neurons.

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Tysabri Lawsuit: The early anatomists looked closely for cells resembling Schwann cells inside the brain and spinal cord, but without success. Ultimately, however, the search led to the discovery of oligodendrocytes. These were the last glial cells discovered, and these odd brain cells were a great puzzle to anatomists. Like astrocytes, these glial cells are found only inside the brain and spinal cord, never in the nerves of our body. When the mystery of oligodendrocytes was finally solved, the most widely appreciated and intricate form of neuron-glia interaction was revealed—an elegant partnership between axon and glia that is absolutely essential for high-speed impulse conduction. This is myelin.

Oligodendrocytes are seen almost everywhere in the brain, but they are especially numerous in white matter tracts. White matter streaks through the core of the brain of animals with backbones (fish, amphib­ians, reptiles, birds, mammals, and humans). This white matter consists of the information trunk lines formed by thousands of axons bundled together to carry information between distant parts of the brain. Under a microscope, anatomists could easily see why the trunk lines were spar­kling white. Each axon was coated with a substance that reflected light brilliantly. In the focused beams of the light microscope, an axon looks like the branch of a tree encased in a crystalline sheath of ice deposited in a winter storm.

Vertebrates have a far more complex nervous system than inverte­brates. The vertebrate nervous system is also centralized, that is, concen­trated into a brain and spinal cord. In lower animals like crabs or slugs, neurons are bunched together like grapes wherever they are needed. There are clusters of neurons at each segment of the articulated tail of a lobster and knots of neurons near the mouth parts of slugs to operate structures for feeding, for example. But in animals with backbones, the brain is concentrated into one massive supercomputer encased inside a thick armor of bone. The backbones of vertebrate animals protect their vital spinal cord. This cerebral concentration of brain power and com­plexity could not have occurred without this fundamental difference in glia separating vertebrates from invertebrates. Glia—not neurons—are responsible for this biological revolution.

Some invertebrates, such as squid, which can move quickly, have developed an ingenious method to overcome the absence of myelin. Through the course of evolution, squid and some other invertebrates have greatly enlarged the diameter of critical axons that are essential for the life-saving reflexes needed to escape predators. The principle is sim­ple: you can get more water through a fire hose than a garden hose, even if both are leaky. The giant axons in squid are so enormous that they can be seen with the naked eye as you clean squid in preparing calamari for dinner. They look like damp cotton strings about a millimeter in diam­eter, stuck to the underside of the squid mantle, which is the fleshy part of the squid. The mantle is designed to squeeze quickly like the rubber bulb of a turkey b as ter. The spurt of water squirting out a small opening propels the squid suddenly to escape a predator. The giant axons offer less resistance to electric current, enabling more rapid flow of nerve impulses to trigger this quick escape from a predator s jaws.

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Tysabri Lawsuit: The brains isolation behind the blood-brain barrier deprives it of access to the vital immune system that fights infection and disease, for the immune cells circulating in our blood and lymph do not penetrate the tightly sealed walls of blood vessels in the brain and spinal cord. How then does the brain resist attack by microorganisms and toxins?

The answer is that the brain has its own exclusive guard, a special class of glial cells called microglia, the smallest and most dynamic of all glia. Each microglia can transform from a latent multi branched solitary cell into a highly mobile amoeboid cell when it detects the danger of infection or injury Squeezing between tangles of dendrites and axons as they rush to kill the invader, microglia attack and devour any harmful organism. These cells are no doubt tunneling through your brain at this very moment like tiny worms through fertile garden soil. Their mission accomplished, they transform back again into stationary multibranched cells, camouflaged like the apple-throwing guard trees in The Wizard of Oz, looking like just another part of the landscape.

These microglia, “microglue cells,” constitute 5 to 20 percent of the entire glial population in the brain. This means that there is nearly one microglial cell for every neuron. Each neuron has, in effect, its own pri­vate bodyguard. Some of these cells wrap themselves around a particular neuron, protecting it like a Secret Service agent shielding the president from a bullet. So stealthy in their disguise are these quick-change artists that fifteen years ago, scientists were still debating whether they existed. Dr. Alois Alzheimer, who described the degenerative disease that now bears his name, encountered these cells in his studies of diseased brains. He studied them with intense interest because they accumulated in large numbers around the senile plaques in brain tissue that are the hallmark of Alzheimer’s disease.

Microglia will track down and pounce on a bacterium, virus, or cel­lular debris and devour it, but they also attack using chemical weapons. Some of the chemical agents they release—for example the excitatory neurotransmitter glutamate, cytokines, reactive oxygen, and nitrogen species—are particularly harmful to neurons in high concentrations. Like all defending armies and soldiers, microglia are both saviors and potential enemies. Collateral damage caused by microglia is the source of many neurological disorders. They also carry out mercy missions, bringing aid to neurons by dispensing neuroprotective chemicals to in­jured nerve cells.

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Tysabri Lawsuit: The many branches of these bushy cells are encrusted with an array of cell sensors always on the lookout for signals of danger and disease. They have receptors for immunological recognition molecules, beacons of self and nonself that identify foreign cells invading the brain. They also have certain sensors like those on neurons (neurotransmitter recep­tors and ion channels) that allow microglia not only to detect invading cells and toxic conditions, but also to monitor neuronal function and remain alert to possible neuronal distress.

Considering their armament of toxic weapons, their array of sensors that can respond to disease and monitor neuronal states, and their abil­ity to secrete healing proteins that repair neurons, microglia deserve closer attention. As we’ve seen, microglia are equipped with powerful enzymes that enable them to cut through the matrix of proteins that bind cells into a tissue as they rush to attack an invading organism. There is evidence that they can also apply these weapons to strip synap­tic connections from neurons—not only in disease, but also in rewiring circuits in learning. Microglia, it appears, maybe able to unplug the con­nections between neurons.

Astrocytes are everywhere in the brain and spinal cord, but they are not present in the nerves of the peripheral nervous system. They are found in the optic nerve because the eye forms during embryonic devel­opment as a swelling growing out from the brain, and it is in fact part of the brain. Astrocytes support neurons in several ways. They provide a physical matrix for structural support, they deliver energy to neurons and re­move their waste products, and they react to brain injury by forming scars. Like all living cells, astrocytes have an electrical voltage, but they do not fire nerve impulses. However, their constant battery-like voltage can strengthen or weaken slowly in some interesting circumstances.

The cell membrane is the barrier between battery poles in a neuron, separating the inside from the outside of the cell. Inside the nerve cell there is an excess of negative charges, giving the nerve cell a voltage of “0.1 volt. If this imbalance of ions across the neuronal membrane ever depletes to zero, the neuron battery is dead and it will be electrically si­lent, unable to fire an electrical impulse. This is where astrocytes come into play, for they are vital in maintaining the proper balance of ions in the space between cells in our brain. By controlling these charged ions outside the neuron, glia recharge the battery and help control the power source for neurons.

Our use of the term or terms Tysabri Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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At a dinner party the other night, I was asked about what I did for work. I replied, “I’m inasbestos awareness and advocacy.”

Blank stare.

“We’re trying to get the word out about the dangers of asbestos. Most people don’t realize how dangerous it is, and that it’s not a banned substance in the United States. We’re trying to change that.”

“What is asbestos anyway? Isn’t it an old chemical they used to make in the 1950s?”

This person, a well-educated woman in her 40s, is like the majority of people we here at Ban Asbestos Now meet. Folks who have a vague idea that asbestos is somehow “bad,” but really have no clue what it is (a naturally occurring mineral), how widespread its use was (and still is), and how inhaling it can lead to severely debilitating and fatal illnesses such as mesothelioma and lung cancer.

And even if they are aware of asbestos and its dangers, most do not realize that it is not currently a banned substance in the US, as it is in almost 60 other nations, including those of the European Union. And they are probably also not aware that despite diminished use here in the US, asbestos continues to kill more than 10,000 people a year in the US alone.

We want to change that. And we are, but we need help to do it.

Ban Asbestos Now researches and develops content to educate and inform about asbestos awareness, has been running a letter writing campaign that allows readers to send a letter to their Congressperson urging them to ban asbestos, and continually supports grassroots efforts that raise funds for mesothelioma research, such as the Miles for Meso 8k road race.

We could probably not do this if we were not backed by the Sokolove Law Firm.

You see, asbestos law firms have stepped in to fight for the victims of asbestos cancer when the U.S. government has been unable or unwilling to do so. As difficult as it is to believe, the government is beholden to corporate America. And the corporations that dealt in asbestos, and profited mightily from it, were some of the richest and most powerful in the world.

Civil justice law firms like Sokolove Law are not beholden to corporations. They are only answerable to the individuals who hire them. So when a pipefitter who has lost his lung capacity and possibly his life to the negligence of a company that makes billions in profits each year, who is going to help him fight?

Asbestos law firms are not the only organizations fighting for this cause. Asbestos advocacy groups such as ADAO and MARF are making significant contributions to the gain traction in Congress towards a definitive and lasting ban on asbestos, as well as educate the public on the dangers of asbestos and raise funding for mesothelioma treatments.

While some people might be predisposed to think that all law firms are greedy and selfish (an assumption that’s not true!) we believe that the only way to make real and lasting changes in the asbestos landscape is to have all voices join together and make a difference. The louder we are, the more they will listen.

Asbestos

A Zoloft lawsuit has been filed against Pfizer by a Chicago woman claiming the antidepressant drug taken by her mother during pregnancy caused her to be born with birth defects.

According to the Madison Record, Angela Rife claims that she was born on December 1991 with congenital birth defects, including cleft palate and cleft lip that was caused by Zoloft medication given to her mother during the pregnancy.

The Zoloft lawsuit, which was filed on December 5, 2011, alleges that the drug maker knew about the risks associated with pregnant women taking Zoloft and failed to properly test the antidepressant. Rife also claims that Pfizer failed to warn patients of these risks despite having knowledge of them.

The complaint charges the drug maker for fraud, misrepresentation and negligent and careless breach of duty.

If you were born with a birth defect due to the use of Zoloft or anotherdangerous drug, contact Sokolove Law to learn about your options and receive a free legal consultation.

Zoloft Lawsuit

A Zoloft lawsuit has been filed against drug maker Pfizer by a group of parents who claim the antidepressant caused their children to be born with severe birth defects, including heart damage.

According to the Madison Record, six couples filed Zoloft lawsuits on December 2, 2011 and allege that, despite the medical studies published on the dangers of drugs similar to Zoloft in pregnant women, the mothers were all prescribed the antidepressant drug during their pregnancies. thedangerous drug lawsuits claim that Pfizer was aware of the possible risks Zoloft posed, and that the company did not properly design or test their antidepressant.

The Zoloft lawsuits also claims that the drug did not have proper labeling to warn consumers about the possibility of birth defects associated with its use in pregnant women, and that Pfizer violated Consumer Protection Laws.

The drug maker is being charged with breach of implied warranties, fraud, misrepresentation and negligence.

If you or a loved one has been harmed by Zoloft or another dangerous drug, contact Sokolove Law for a free legal consultation and to learn about your options.

Zoloft Lawsuit

Actos Lawsuit News – 2/14/2012: If you were prescribed Actos and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

Actos Lawsuit: Because of the risk of recurrence of bladder cancer after cystectomy, patients require careful follow-up and evaluation after surgery has been completed. Your doctor will establish a specific follow-up schedule for your particular situation and strict compliance with follow-up visits is mandatory to ensure that if the cancer recurs after surgery, it is detected and treated as early as possible. In general, patients treated for superficial disease are followed every 3 to 6 months by cystoscopic evaluation (examination of the urinary tract with a cystoscope to detect cancer or other problems) and urine cytology

Bladder cancer recurrence following radical cystectomy can either be local or distant. Local recurrence refers to the recurrence of a tumor at the site of the surgery or in the nearby (regional) lymph nodes. In general, early stage bladder cancer that is confined to the bladder is associated with a low risk of local recurrence (3% to 6%). In contrast, higher stage tumors that invade the deeper layers of the bladder wall, regional lymph nodes, or nearby organs carry a much higher risk for local tumor recurrence.

Distant recurrence of bladder cancer refers to the recurrence of the cancer in distant sites from the bladder. It has been reported that up to 50% of patients undergoing cystectomy for muscle-invasive bladder cancer eventually develop distant recurrence of the disease (usually within 3 years after cystectomy). Most commonly, distant recurrence involves spread of the cancer to bone, lung, or liver. Patients who develop distant recurrence are treated with combination systemic chemotherapy, with either M-VAC or GC as the standard regimen.

In discussing the role of CAM therapies for the management of cancer, it is important to differentiate between CAM therapies that purport to “cure” cancer as opposed to those therapies that are used in palliative cancer care to provide relief from cancer-related symptoms and improve the patient’s quality of life. Unlike some conventional cancer treatments that have been demonstrated to cure patients with certain types of cancers, currently there is a lack of sufficient scientific evidence to support the conclusion that any specific type of CAM modality can cure cancer. Patients who fail to draw a distinction between the “care versus cure” aspects of CAM therapies may delay seeking or may completely abandon potentially curative mainstream cancer treatments in hope that a particular CAM therapy may be a “magic bullet” for curing their cancer. On the other hand, complementary therapies have become an important aspect of palliative cancer care by helping cancer patients better cope with cancer-related symptoms and side-effects and, thereby, improving quality of life. In fact, many cancer centers in the United States and other Western countries have integrated complementary therapies into their mainstream treatment strategies for palliative cancer care in an emerging field of cancer practice known as integrative oncology.

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Actos Lawsuit: Conventional cancer treatments such as chemotherapy, radiation therapy, and surgery are often associated with severe side-effects that can significantly impact the patient’s quality of life and interfere with routine activities of daily living, in general, side-effects of conventional cancer treatments may include nausea/vomiting, fatigue, anxiety, depression, pain, sleep disturbances, loss of appetite, dry mouth, gastrointestinal disturbances, and peripheral neuropathy. Conventional treatments may not always be completely effective in relieving cancer-related symptoms and, in some cases, the treatments themselves may cause additional side-effects. Complementary therapies, when used in conjunction with conventional mainstream treatments can help patients better cope with cancer-related symptoms and side-effects and also improve physical and emotional well-being and overall quality of life.

In general, patients with severe mood disturbances (e.g., panic attacks; suicide ideation) require immediate psychological evaluation and treatment to stabilize their acute condition before CAM therapies may be considered. For most patients with mild to moderate anxiety and mood disturbances, CAM therapies are a useful adjunct to conventional treatments for managing psychological distress. Techniques such as mind-body interventions, acupuncture, and music therapy are generally safe when performed by qualified, experienced practitioners and can help cancer patients better cope with feelings of anxiety, fear, hopelessness, and depression. Although some herbs and dietary supplements (e.g., Kava Kava; St. John’s Wort; Passionflower) have been reported to relieve anxiety and mood disturbances, some experts have discouraged the use of these products in cancer patients because they may interfere with drugs used to treat cancer (chemotherapeutic agents) and/or other medications that patients may be taking. Patients should discuss the risks and benefits of using any herbal medications/dietary supplements with their oncologist before taking any of these products, particularly if they are undergoing chemotherapy, radiation therapy, or surgery.

Pain is a common symptom that can affect many cancer patients. Most often, the source of the pain is the tumor itself. Cancer-related pain may be caused by spread of the tumor to other tissues and organs or may result from compression of the tumor on a nerve or the spinal cord. In general, acute cancer-related pain is most responsive to conventional mainstream treatments which may involve medications (e.g., narcotic analgesics; steroids) or, in severe cases, (e.g., tumor causing spinal cord compression; tumor associated with abdominal obstruction), emergent surgery may be required to relieve the acute pain.

Some cancer patients who undergo surgery to remove a tumor develop persistent neuropathic pain due to injury of nerves during the surgical procedure. In general, severe neuropathic pain may be difficult to control with conventional pain management treatment modalities. There is some evidence that acupuncture, when used in conjunction with conventional pain management strategies, may be effective for the management of persistent neuropathic pain that may develop in some patients after cancer surgery.

Actos Lawsuit: Additional Information and Resources

Actos Lawsuit: Nausea and vomiting are relatively common side-effects in patients undergoing cancer chemotherapy. When used in conjunction with standard treatments, CAM therapies may offer patients additional relief from chemotherapy-induced nausea and vomiting. A 1998 National Institutes of Health (NIH) Consensus Conference concluded that there is clear evidence supporting the efficacy of acupuncture for controlling nausea and vomiting associated with cancer chemotherapy. Other CAM therapies that may help cancer patients better cope with chemotherapy-induced nausea and vomiting.

Evidence from epidemiological studies strongly supports a relationship between dietary factors and the risk for developing certain types of cancers. In general, a diet that is rich in certain food constituents (e.g., fruits, vegetable, fiber) appears to be protective against the development of cancer. In contrast, excessive consumption of other dietaiy substances (e.g., animal fats, alcohol) appears to increase the risk of certain types of cancers. Some vitamins that possess antioxidant properties (e.g., vitamins A, C, and E) may protect against certain types of cancers by protecting the body’s cells from damage by certain compounds known as free radicals.

The diagnosis of any type of cancer is a frightening, life-altering event for both the patient and their family. The potential for a diminished quality of life for newly diagnosed cancer patients becomes an immediate, pressing concern when confronted with anxiety, fear, pain, the prospect of a long course of treatments that may cause significant side effects, and the possibility that the treatments may not work. It is critically important, however, for cancer patients and their families to address and learn to cope with the physical, emotional, and social issues that, if ignored and left to “fester”, can rapidly lead to a significantly reduced quality of life.

Actos Lawsuit: News and Information from related Sources

Actos Lawsuit: Over the years, cancer specialists and other allied health-care professionals have come to realize that addressing a cancer patient’s quality of life issues is an integral component of a comprehensive, overall cancer treatment strategy. From a practical perspective, that means developing an effective treatment plan that aims not only to control and/or to eradicate the patient’s cancer with medical and/or surgical therapy but, at the same time, also takes into consideration critical issues of supportive care throughout the course of treatment and offers the patient the best chances of maintaining a reasonably high level quality of life. In fact, most cancer specialists now consider supportive care as an essential component of an overall, effective cancer treatment plan.

If sleep disturbances begin to affect your functional ability and diminish your quality of life, a variety of options are available to deal with the problem. These treatment options include learning new sleep habits (improved sleep hygiene practices); complementary therapies (e.g., relaxation techniques, biofeedback, meditation); and the use of prescription sleep medications. If lack of sleep is affecting your quality of life and interfering with your activities of daily living, talk with your doctor about developing an individualized treatment plan to help improve your quality of sleep.

Fatigue is perhaps the most common and potentially debilitating symptom experienced by cancer patients that can have a significant negative impact on routine activities of daily living and diminish quality of life. Fatigue may be attributed to a variety of causes including side-effects of cancer treatments (e.g., chemotherapy, radiation therapy), anemia, sleep deprivation resulting from insomnia, chronic pain, inadequate nutrition, and lack of physical exercise. In many cases, a combination of factors contributes to fatigue, exhaustion, and a general lack of energy. It is important to notify your cancer specialist or primary health care provider if you begin to experience bouts of fatigue lasting a few days or longer.

A variety of strategies are available to overcome the problem of fatigue in cancer patients. Fatigue related to anemia (low numbers of red blood cells) can be treated with blood transfusions and drugs, such as erythropoietin (e.g., Procrit) that promote the production of red blood cells. Fatigue not related to anemia may be managed with lifestyle modifications such as proper nutrition, regular exercise, and improved sleep hygiene practices.

In the past, cancer patients were usually advised to “relax”, “take it easy¹¹ and “don’t overdo it”. More recently, however, doctors are beginning to realize the potential benefits of physical exercise for cancer patients undergoing treatment as well as for cancer survivors. Researchers are continuing to explore the effect of physical exercise on survival rates for various types of cancers. In general, the potential benefits of physical activity for patients suffering from chronic diseases include enhanced physical and mental function and improved quality of life. For cancer patients, the potential benefits of exercise also include decreased fatigue, improved appetite, better toleration of side effects of chemotherapy and radiation therapy and improved quality of life.

Actos Lawsuit: Information and News

Actos Lawsuit: One of the most common symptoms experienced by cancer patients is unintentional weight loss which can lead to malnutrition, increased susceptibility to infections, reduced quality of life, and shorter survival time. The underlying causes of unintentional weight loss in cancer patients may be attributed to a variety of factors including loss of appetite associated with chemotherapy and/or radiation therapy and psychological disturbances such as depression which has been found to affect up to 25% of cancer patients.

From a metabolic perspective, unintentional weight loss may be understood by the increased energy (calories) required by cancer cells to grow and spread as well as the increased energy requirements of the body to mount an effective response to fight the cancer. A net loss in weight occurs when the body uses more calories from stored energy reserves than is available from calories ingested from nutrients in the diet. Metabolic changes in cancer can also cause a condition called cachexia – a generalized wasting condition involving the loss of muscle mass and fat Cachexia may develop even in people with good nutritional intake due to the failure of the body to absorb nutrients. Symptoms of cachexia, which affects about 50% of all cancer patients, include loss of appetite, weight loss, wasting of muscle mass, generalized fatigue, and significantly reduced capacity to perform routine activities of daily living.

The management of weight loss in cancer patients usually involves nutritional counseling to ensure an adequate intake of calories. Nutritional counseling can also help cancer patients develop new eating habits to prevent further weight loss including eating foods that are rich in calories or protein; eating smaller meals more frequently throughout the course of the day; “snacking” between meals; and drinking high-calorie liquid nutritional supplements (e.g., Boost, Ensure, Sustacal). In some cases, medications such as megestrol acetate (Megace) or dexamethasone (Decadron) may be prescribed to stimulate the appetite.

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Actos Lawsuit