Trichloroethylene (TCE) is a common chemical in paint removers, gun cleaners, correction fluid, aerosol cleaning products, and dry cleaning.

“Earth provides enough to satisfy every man’s needs, but not every man’s greed.” ― Mahatma Gandhi.

What is Parkinson’s disease?

Parkinson’s disease is a progressive neurological disorder that affects movement. A loss of dopamine-producing cells in the brain causes the condition, which leads to a lack of dopamine, a neurotransmitter responsible for coordinating movement.

Common symptoms of Parkinson’s disease include the following:

• Tremors in the arms, hands, legs, or head
• Stiff muscles with contractions for a long time
• Slow movements
• Balance and coordination challenges, sometimes resulting in falls
• Impaired balance and coordination, sometimes leading to falls

Other symptoms may include:

• Emotional changes such as depression
• Swallowing, speaking, or chewing challenges
• Constipation or urinary problems
• Skin problems

Individuals with Parkinson’s disease often develop a so-called Parkinsonian gait. Here, the patient tends to lean forward, taking small and quick steps. There may be reduced arm swinging, too. Many need help initiating (or continuing) movement.

There is no cure for Parkinson’s disease, but tools are available to help manage symptoms and improve quality of life. Such interventions may include medications (for example, dopamine agonists or levodopa, and non-medication interventions, including physical therapy, exercise, and speech therapy.

What causes Parkinson’s disease?

The basal ganglia is a brain region that regulates movement. The most prominent Parkinson’s disease symptoms occur when nerve cells in the basal ganglia, an area of the brain that controls movement, become impaired or die.

These nerve cells (neurons) normally produce an important brain chemical — dopamine. When the neurons die or become impaired, they produce less dopamine, which causes movement problems associated with the disease.

Second, patients with Parkinson’s disease also lose nerve endings that make norepinephrine. This neurotransmitter is a primary chemical messenger of the sympathetic system, controlling functions such as blood pressure and heart rate.

This neurotransmitter loss may contribute to some of the non-movement Parkinson’s features, including irregular blood pressure, fatigue, diminished food movement through the gut, and a sudden blood pressure drop upon sitting or lying.

Third, those with Parkinson’s disease have many brain cells with Lewy bodies and unusual clumps of the protein alpha-synuclein. Researchers are working to understand better the relationship between alpha-synuclein and genetic variants impacting Parkinson’s and Lewy body dementia.

Researchers believe Parkinson’s disease is the product of a combination of environmental and genetic factors. There are several risk-increasing genes, with mutations causing the brain’s hallmark loss of dopamine-producing cells. The Mayo Clinic reminds us that such mutations are uncommon (except in rare cases with many family members affected by Parkinson’s disease).

Environmental factors such as exposure to toxins (including pesticides) and head injuries are associated with an increased risk of Parkinson’s disease.

Aging is another risk factor for Parkinson’s disease. The disease is more common in people over the age of 60. Finally, men are more likely than women to develop the condition.

Parkinson’s disease is probably secondary to a complex interplay between genetics, aging, and environmental exposures.

A common chemical and Parkinson’s disease risk

The number of individuals with Parkinson’s disease has doubled over the last three decades. It may double again (from 6.9 million in 2015 to 14.2 million) by 2040.

The causes of Parksin’s disease are entirely clear. As discussed above, certain genetic mutations can increase risk, as can head trauma. However, these risk factors don’t explain the vast majority of cases. There are some less visible factors.

Could a common chemical used in paint removers, gun cleaners, dry cleaning, aerosol cleaning products, decaffeinating coffee, and correction fluid be a key to understanding the recent dramatic increase in Parkinson’s disease?

An international group of researchers recently reported the disturbing results of its review of previous research:

Trichloroethylene is associated with as much as a 500 percent increased risk for Parkinson’s disease.

What is TCE?

It is invisible, a highly volatile liquid, and seemingly everywhere. It is invisible, a highly volatile liquid, and seemingly everywhere. First synthesized in a lab in 1864, the chemical trichloroethylene (TCE) was first used for commercial production in 1920. TCE has commercial, industrial, military, and medical applications.

Among its uses are:

• Producing refrigerants
• Cleaning electronics
• Degreasing engine parts
• Anesthetic and analgesic (limited use)
• Gun cleaners
• Correction fluid
• Dry cleaning. A similar chemical (perchloroethylene) is currently more widely used. The current researchers pointedly observe that, in anaerobic conditions, perchloroethylene often transforms into TCE.”

The researchers remind us that we don’t have to have occupational exposure to come into contact with TCE. Exposure can occur through the air (indoor or outdoor) or groundwater. The substance evaporates from the underlying solid and groundwater and often enters our workplaces, homes, and schools undetected.

Animal studies indicate the potential peril, with TCE exposure causing selective loss of dopamine-producing nerve cells. Studies dating back to 1960 show a TCE: Parkinson’s disease association.

Unfortunately, the chemical was ubiquitous in the 1970s; 10 million Americans worked with chemical or organic solvents daily. If you want to see an exhaustive list of the occupations and industries in which TCE exposure still occurs, please go here:

Trichloroethylene: An Invisible Cause of Parkinson’s Disease?

The etiologies of Parkinson’s disease (PD) remain unclear. Some, such as certain genetic mutations and head trauma, are…

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TCE problem scope

I decided to write this piece after seeing this figure from the research paper:

“TCE contaminates up to one-third of US drinking water, and has polluted groundwater in over 20 countries on five continents. The substance is found in half of the 1300 most toxic “Superfund” sites that are in a federal cleanup program, including 15 in California’s Silicon Valley; there TCE was used to clean electronics.”

While the United States military no longer uses TCE, several contaminated sites exist, including Marine Corps Base Camp Lejeune in North Carolina. Researchers discovered TCE and PCE in drinking water at 280 times the recommended safety standards at Camp Lejeune.

The current review highlights seven cases of people who developed Parkinson’s disease after likely exposure to TCE. For example, National Basketball Association player Brian Grant developed symptoms of Parkinson’s disease in 2006 at age 34.

Grant lived at Camp Lejeune as a child. He bathed in, drank, and swam in contaminated water. His father died of esophagus carcinoma, cancer that is associated with TCE. Grant created a foundation to support and inspire folks with Parkinson’s disease.

In 2014, the International Agency for Research on Cancer updated its classification of TCE to Group 1. This assignment means that there is sufficient evidence that the substance causes kidney cancer (and that there is some evidence that it leads to liver cancer and non-Hodgkin’s lymphoma.

My take — TCE and Parkinson’s disease

This study was eye-opening, even as these authors acknowledge that TCE’s role in Parkinson’s disease is “far from definitive.” For example, TCE exposure is often combined with toxin exposure or unmeasured genetic risk factors. No causal relationship is proven; most of us exposed to TCE never get Parkinson’s disease.

Secondly, there can be recall bias: Those with Parkinson’s disease may be more likely to recall their exposure to the toxin.

Of course, we need more research and cleanup of contaminated sites. I hope to have contributed to spreading the word about the potential harms of TCE exposure. Still, given the known connection with some cancer types, I hope to stay clear of trichloroethylene.

The post Parkinson’s: What’s Behind the Fastest-Growing Brain Disease? appeared first on Medika Life.

Today we learn how that substance — cerebrospinal fluid or CSF — washes in and out of our brain tissues in waves, helping to remove waste products. The cerebrospinal spinal fluid also bathes our brain with proteins or growth factors, facilitating normal development.

Decay theory of memory fading

When we learn something new, we create a neurochemical memory trace. The decay theory posits that our memory fades secondary to the passage of time, with information becoming less available for later retrieval as time goes by; the memory strength simply wears away.

Columbia University (USA) psychologist Edward Thorndike first coined the descriptor “decay theory” in The Psychology of Learning in 1914. Active rehearsal of the information can counteract the memory fading.

Memories fade like old photographs

Why do our memories, like old photographs, fade in quality over time? Not only do our recollections become less accurate over time, but we also experience decreases vibrancy and other visual qualities.

Are you like me? I sometimes have a memory that feels like I am reliving the moment. On other occasions, the details are remarkably fuzzy. An example of the former? After I had an emotionally significant event, getting engaged at New York’s Rainbow Room at Rockefeller Center, I have a good recall of the event, but everything has faded in my mind.

As events are forgotten or stored in memory, Boston College researchers wondered how their visual features evolve? Study participants reported changes in their memories akin to using a filter to edit a photograph on Instagram.

The researchers went a step further, inquiring if forgetting is similar to applying a filter to our experiences and whether the emotional significance of the event would change which filter we apply.

Here are the findings, as detailed by study author Rose Cooper:

“Memories seem to fade literally: people consistently remembered visual scenes as being less vibrant than originally experienced.” She continues, adding, “we had expected that memories would get less accurate after a delay, but we did not expect that there would be this qualitative shift in the way that they remembered them.”

Furthermore, negative emotions study participants experienced when viewing images raised the chances that they would accurately recall the images but did not influence memory fading.

In summary, the researchers discovered that the vibrancy of low-level details — colors and shapes, for example — fades in memory while we keep the general gist of the experience.

The fading appeared less for memories subjectively rated as more robust. Emotional memories did not influence the fading amount but did impact the likelihood with which the subjects remembered an exposure. My Rainbow is recalled, but not vividly.

What drives the memory fading? Do we forget over time, or is new material interfering with new information?

Cerebrospinal fluid basics

Researchers recently reversed memory loss in mice by injecting them with a brain fluid from younger peers. First, let’s take a quick look at that fluid, or cerebrospinal fluid (CSF).

The CSF is a body fluid surrounding the brain and cushion in the skull. Maiken Nedergaard and colleagues discovered that cerebrospinal fluid also acts as a lymph system in the brain.

Via a series of elegant experiments analyzing mice brains, the researchers visualized cerebrospinal fluid entering and flowing through the brain, ultimately draining into the same ducts used by the lymphatic system of the rest of the body.

The cerebrospinal fluid clears harmful amyloid-beta from the brain. The substance is associated with Alzheimer’s disease and other neurological conditions. While Nedergaard and co-investigators honed in on this protein, other leftover proteins are likely also removed.

In summary, cerebrospinal (spinal) fluid washes in and out of the crevices of our brains in waves. The process is central to waste removal.

Reversing memory loss in mice

Researchers reversed memory loss by injecting cerebrospinal fluid from younger mice peers.

Using a tiny tube and pump, the scientists infused cerebrospinal fluid from young adult mice into the brains of 18-month-old animals — the equivalent to about 60 years for humans — over seven days.

Imaging revealed higher levels of myelin, a fatty sheath that covers and protects nerve cells from damage. The injections led to practical changes, too: The elderly mice improved at a fear-conditioning task. The refreshed mice remembered a tone, and a flashing light meant a small electric shock was coming.

Growth factors and memory rejuvenation

Growth factors that can restore nerve cell function are the likely agents of memory improvement. Stimulated cells — oligodendrocytes — made more myelin, creating stronger connections between the nerve cells.

Genes normally expressed in oligodendrocytes appeared revved up or upregulated in the old mice who had received cerebrospinal fluid from young mice.

The researchers also found changes in gene expression in a structure important for memory, the hippocampus. The gene Fgf17 decreases activity with age; the CSF infusion restored function.

This research is stunning. With all of the troubles in the world, it is heartening to see brilliant scientists opening doors to a future where we may be able to improve memory. It is also disturbing. I hope we someday don’t go down this road; gene editing sounds much more appealing to me, especially for those with dementia.

Until we get a drug targeting memory in humans, I will continue to focus on a healthy diet, adequate sleep, regular physical activity, limiting alcohol consumption, and challenging my brain with activities such as my new Haydn Piano Sonatas.

The post Can We Reverse Memory Loss with Brain Liquid From Younger Folks? appeared first on Medika Life.

Causes of transverse myelitis include infections, immune system disorders, and other disorders that may damage or destroy myelin, the fatty white insulating substance that covers nerve cell fibers.  Inflammation within the spinal cord interrupts communications between nerve fibers in the spinal cord and the rest of the body, affecting sensation and nerve signaling below the injury.  Symptoms include pain, sensory problems, weakness in the legs and possibly the arms, and bladder and bowel problems.  The symptoms may develop suddenly (over a period of hours) or over days or weeks.

Transverse myelitis can affect people of any age, gender, or race.  It does not appear to be genetic or run in families.  A peak in incidence rates (the number of new cases per year) appears to occur between 10 and 19 years and 30 and 39 years.  It is estimated that about 1,400 new cases of transverse myelitis are diagnosed each year in the United States.

Although some people recover from transverse myelitis with minor or no residual problems, the healing process may take months to years.  Others may suffer permanent impairments that affect their ability to perform ordinary tasks of daily living.  Some individuals will have only one episode of transverse myelitis; other individuals may have a recurrence, especially if an underlying illness caused the disorder.

There is no cure for transverse myelitis.  Treatments to prevent or minimize permanent neurological deficits include corticosteroid and other medications that suppress the immune system, plasmapheresis (removal of proteins from the blood), or antiviral medications.

What causes transverse myelitis?

The exact cause of transverse myelitis and extensive damage to nerve fibers of the spinal cord is unknown in many cases.  Cases in which a cause cannot be identified are called idiopathic.  However, looking for a cause is important, as some will change treatment decisions.  

The discovery of circulating antibodies to the proteins aquaporin-4 and anti-myelin oligodendrocyte point to a definite cause in some individuals with transverse myelitis.  Antibodies are proteins produced by cells of the immune system that bind to bacteria, viruses, and foreign chemicals to prevent them from harming the body.  In autoimmune disorders, antibodies incorrectly bind to normal body proteins.  Aquaporin-4 is a key protein that carries water through the cell membrane of neural cells.  The myelin oligodendrocyte glycoprotein sits on the outer layer of myelin.  

A number of conditions appear to cause transverse myelitis, including:

• Immune system disorders.  These disorders appear to play an important role in causing damage to the spinal cord.  Such disorders are:
  • aquaporin-4 autoantibody associated neuromyelitis optica
  • multiple sclerosis
  • post-infectious or post-vaccine autoimmune phenomenon, in which the body’s immune system mistakenly attacks the body’s own tissue while responding to the infection or, less commonly, a vaccine
  • an abnormal immune response to an underlying cancer that damages the nervous system; or
  • other antibody-mediated conditions that are still being discovered.
• Viral infections.  It is often difficult to know whether direct viral infection or a post-infectious response to the infection causes the transverse myelitis. Associated viruses include herpes viruses such as varicella zoster (the virus that causes chickenpox and shingles), herpes simplex, cytomegalovirus, and Epstein-Barr; flaviviruses such as West Nile and Zika; influenza, echovirus, hepatitis B, mumps, measles, and rubella. 
• Bacterial infections such as syphilis, tuberculosis, actinomyces, pertussis, tetanus, diphtheria,  and Lyme disease.  Bacterial skin infections, middle-ear infections, campylobacter jejuni gastroenteritis, and mycoplasma bacterial pneumonia have also been associated with the condition.
• Fungal infections in the spinal cord, including Aspergillus, Blastomyces, Coccidioides, and Cryptococcus.
• Parasities, including Toxoplasmosis, Cysticercosis, Shistosomiasis, and Angtiostrongyloides.

• Other inflammatory disorders that can affect the spinal cord, such as sarcoidosis, systemic lupus erythematosus, Sjogren’s syndrome, mixed connective tissue disease, scleroderma, and Bechet’s syndrome.
• Vascular disorders such as arteriovenous malformation, dural arterial-venous fistula, intra spinal cavernous malformations, or disk embolism.

In some people, transverse myelitis represents the first symptom of an autoimmune or immune-mediated disease such as multiple sclerosis or neuromyelitis optica.  (Multiple sclerosis, or MS, is disease that causes distinctive lesions, or plaques, that primarily affect parts of the brain, spinal cord, and optic nerve—the nerve that carries information from the eye to the brain.  Neuromyelitis optica, or NMO, is an autoimmune disease of the central nervous system that predominantly affects the optic nerves and spinal cord.)  ”Partial” myelitis—affecting only a portion of the cord cross-section—is more characteristic of multiple sclerosis.  Neuromyelitis optica is much more likely as an underlying condition when the myelitis is “complete” (causing severe paralysis and numbness on both sides of the spinal cord). 

What are the symptoms of transverse myelitis?

Transverse myelitis may be either acute (developing over hours to several days) or subacute (usually developing over one to four weeks). 

Four classic features of transverse myelitis are:

• Weakness of the legs and arms.  People with transverse myelitis may have weakness in the legs that progresses rapidly.  If the myelitis affects the upper spinal cord it affects the arms as well.  Individuals may develop paraparesis (partial paralysis of the legs) that may progress to paraplegia (complete paralysis of the legs), requiring the person to use a wheelchair.  
• Pain.  Initial symptoms usually include lower back pain or sharp, shooting sensations that radiate down the legs or arms or around the torso.
• Sensory alterations.  Transverse myelitis can cause paresthesias (abnormal sensations such as burning, tickling, pricking, numbness, coldness, or tingling) in the legs, and sensory loss.  Abnormal sensations in the torso and genital region are common.  Sometimes the shooting sensations occur when the neck is bent forward and resolve when the neck is brought back to normal position (a condition called Lhermitte’s phenomenon).
• Bowel and bladder dysfunction.  Common symptoms include an increased frequency or urge to use the toilet, incontinence, difficulty voiding, and constipation.

Many individuals also report experiencing muscle spasms, a general feeling of discomfort, headache, fever, and loss of appetite, while some people experience respiratory problems.  Other symptoms may include sexual dysfunction and depression and anxiety caused by lifestyle changes, stress, and chronic pain.

The segment of the spinal cord at which the damage occurs determines which parts of the body are affected.  Damage at one segment will affect function at that level and below.  In individuals with transverse myelitis, myelin damage most often occurs in nerves in the upper back, causing problems with leg movement and bowel and bladder control, which require signals from the lower segments of the spinal cord.

How is transverse myelitis diagnosed?

Physicians diagnose transverse myelitis by taking a medical history and performing a thorough neurological examination.  The first step in evaluating a spinal cord condition is to rule out causes that require emergency intervention, such as trauma or a mass putting pressure on the cord.  Other problems to rule out include herniated or slipped discs, stenosis (narrowing of the canal that holds the spinal cord), abscesses, abnormal collections of blood vessels, and vitamin deficiencies.  Tests that can indicate a diagnosis of transverse myelitis and rule out or evaluate underlying causes include:

• Magnetic resonance imaging (MRI) uses a strong magnetic field and radio waves to produce a cross sectional view or three-dimensional image of tissues, including the brain and spinal cord.  A spinal MRI will almost always confirm the presence of a lesion within the spinal cord, whereas a brain MRI may provide clues to other underlying causes, especially MS.  In some instances, computed tomography (CT), which uses x-rays and a computer to produce cross-section images of the body or an organ, may be used.  Often an injection of a contrast agent is given in the middle of the scan to determine whether the contrast agent leaks out into the spinal cord. Such leakage is a telltale feature of inflammation.
• Blood tests may be performed to rule out various disorders such as HIV infection, vitamin B12 deficiency, and many others.  Blood is tested for the presence of autoantibodies (anti- aquaporin-4, anti-myelin oligodendrocyte) and a host of  antibodies associated with cancer (paraneoplastic antibodies) that may be found in people with transverse myelitis.
• Lumbar puncture (also called spinal tap) uses a needle to remove a small sample of the cerebrospinal fluid that surrounds the brain and spinal cord.  In some people with transverse myelitis, the cerebrospinal fluid contains more protein than usual and an increased number of white blood cells (leukocytes) that help the body fight infections.  A spinal tap is important to identify or rule out infectious causes.  

If none of these tests suggests a specific cause, the person is presumed to have idiopathic transverse myelitis.  In occasional cases, initial testing using MRI and lumbar puncture may show normal results but may need to be repeated in 5-7 days.

How is transverse myelitis treated?

Treatments are designed to address infections that may cause the disorder, reduce spinal cord inflammation, and manage and alleviate symptoms.  

Initial treatments and management of the complications of transverse myelitis

• Intravenous corticosteroid drugs may decrease swelling and inflammation in the spine and reduce immune system activity.  Such drugs may include methylprednisolone or dexamethasone (usually administered for 3 to 7 days and sometimes followed by a tapering off period).  These medications may also be given to reduce subsequent attacks of transverse myelitis in individuals with underlying disorders. 
• Plasma exchange therapy (plasmapheresis) may be used for people who don’t respond well to intravenous steroids.  Plasmapheresis is a procedure that reduces immune system activity by removing plasma (the fluid in which blood cells and antibodies are suspended) and replacing it with special fluids, thus removing the antibodies and other proteins thought to be causing the inflammatory reaction.
• Intravenous immunoglobulin (IVIG) is a treatment thought to reset the immune system.  IVIG is a highly concentrated injection of antibodies pooled from many healthy donors that bind to the antibodies that may cause the disorder and remove them from circulation.
• Pain medicines that can lessen muscle pain include acetaminophen, ibuprofen, and naproxen.  Nerve pain may be treated with certain antidepressant drugs (such as duloxetine), muscle relaxants (such as baclofen, tizanidine, or cyclobenzaprine), and anticonvulsant drugs (such as gabapentin or pregabalin).
• Antiviral medications may help those individuals who have a viral infection of the spinal cord.
• Medications can treat other symptoms and complications, including incontinence, painful muscle contractions called tonic spasms, stiffness, sexual dysfunction, and depression.

Following initial therapy, it is critical part to keep the person’s body functioning while hoping for either complete or partial spontaneous recovery of the nervous system.  This may require placing the person on a respirator in the uncommon scenario where breathing is significantly affected.  Treatment is most often given in a hospital or in a rehabilitation facility where a specialized medical team can prevent or treat problems that afflict paralyzed individuals. 

Prevention of future transverse myelitis episodes

Most transverse myelitis only occurs once (called monophasic).  In some cases chronic (long-term) treatment with medications to modify the immune system response is needed.  Examples of underlying disorders that may require long-term treatment include multiple sclerosis and neuromyelitis optica.  Treatment of MS with immumodulatory or immunosuppressant medications may be considered when it is the cause of myelitis.   These medications include alemtuzumab, dimethyl fumarate, fingomilod, glatiramer acetate, interferon-beta, natalizumab, and teriflunomide, among others.

Immunosuppressant treatments are used for neuromyelitis optica spectrum disorder and recurrent episodes of transverse myelitis that are not caused by multiple sclerosis. They are aimed at preventing future myelitis attacks (or attacks at other sites) and include steroid-sparing drugs such as mycophenolate mofetil, azathioprine, and rituximab.

Rehabilitative and long-term therapy

Many forms of long-term rehabilitative therapy are available for people who have disabilities resulting from transverse myelitis.  Strength and functioning may improve with rehabilitative services, even years after the initial episode.  Rehabilitative therapy teaches people strategies for carrying out activities in new ways in order to overcome, circumvent, or compensate for permanent disabilities.  Although rehabilitation cannot reverse the physical damage resulting from transverse myelitis, it can help people, even those with severe paralysis, become as functionally independent as possible and attain the best possible quality of life.

Common neurological deficits resulting from transverse myelitis include severe weakness, spasticity, or paralysis; incontinence, and chronic pain.  In some cases these may be permanent.  Such deficits can substantially interfere with a person’s ability to carry out everyday activities such as bathing, dressing, and performing household tasks.   Individuals with lasting neurological defects from transverse myelitis typically consult with a range of rehabilitation specialists, who may include physiatrists (physicians specializing in physical medicine and rehabilitation), physical therapists, occupational therapists, vocational therapists, and mental health care professionals.

• Physical therapy can help retain muscle strength and flexibility, improve coordination, reduce spasticity, regain greater control over bladder and bowel function, and increase joint movement.  It also can help to reduce the likelihood of pressure sores developing in immobilized areas.  Individuals are also taught to use assistive devices such as wheelchairs, canes, or braces as effectively as possible. 
• Occupational therapy teaches people new ways to maintain or rebuild their independence by participating in meaningful, self-directed, everyday tasks such as bathing and dressing.  Therapists teach people how to function at the highest level possible, by developing coping strategies, suggesting changes in their homes to improve safety (such as installing grab bars in bathrooms), and changing obstacles in their environment that interfere with normal activity.
• Vocational therapy involves offering instructions to help people develop and promote work skills, identify potential employers, and assist in job searches.  Vocational therapists act as mediators between employees and employers to secure reasonable workplace accommodations.
• Psychotherapy for people living with permanent includes strategies and tools to deal with stress and a wide range of emotions and behaviors. 

What is the prognosis?

Most people with transverse myelitis have at least partial recovery, with most recovery taking place within the first 3 months after the attack.  For some people, recovery may continue for up to 2 years (and in some cases, longer).  However, if there is no improvement within the first 3 to 6 months, complete recovery is unlikely (although partial recovery can still occur and still requires rehabilitation). 

Aggressive acute treatment and physical therapy have been shown to improve outcomes.  Some individuals are left with moderate disability (such as trouble walking, nerve sensitivity, and bladder and bowel problems) while others may have permanent weakness, spasticity, and other complications.  Myelitis attacks with neuromyelitis optica spectrum disorder (NMOSD) tend to be more severe and are associated with less recovery than attacks with multiple sclerosis.  Research has shown that a rapid onset of symptoms generally results in poorer recovery.

Many people with transverse myelitis experience only one episode although recurrent or relapsing transverse myelitis does sometimes occur, particularly when an underlying cause (such as MS or NMOSD) can be found.  Some people recover completely and then experience a relapse.  Others begin to recover and then suffer worsening of symptoms before recovery continues. 

In all cases of transverse myelitis, physicians will evaluate possible underlying causes such as MS, NMOSD, or sarcoidosis, since most people with these underlying conditions can experience a relapse or worsen when acute treatment is discontinued.  These individuals should be treated with preventative care to reduce the chance of future relapses. 

Resources

For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute’s Brain Resources and Information Network (BRAIN) at:

BRAIN
P.O. Box 5801
Bethesda, MD 20824
800-352-9424

Information also is available from the following organizations:

Transverse Myelitis Association
1787 Sutter Parkway
Powell, OH 43605-4884
855-380-3330

Cody Unser First Sep Foundation
P.O. Box 56696
Albuquerque, NM 87187
505-792-9551

Christopher and Dana Reeve Foundation
636 Morris Turnpike, Suite 3A
Short Hills, NU 07078
800-225-0292

The Guthy-Jackson Charitable Foundation
10525 Vista Sorrento Parkway, Suite 210
San Diego, CA 92121
858-638-7638

National Organization for Rare Disorders (NORD)
55 Kenosia Avenue
Danbury, CT 06810
203-744-0100

National Library of Medicine
8600 Rockville Pike
Bethesda, MD 20894
301-594-5983
888-346-3656

The post Understanding Transverse Myelitis appeared first on Medika Life.

These aneurysms can occur anywhere in the brain. Some small aneurysms may not show signs and are usually detected during imaging tests for other medical conditions. The signs and symptoms of an unruptured cerebral aneurysm will partly depend on its size and rate of growth. A larger aneurysm that is steadily growing may produce symptoms such as numbness, pain above and behind the eye, and paralysis on one side of the face.

Immediately after an aneurysm ruptures, an individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness.

What are the symptoms?

Unruptured aneurysm
Most cerebral aneurysms do not show symptoms until they either become very large or rupture.  Small unchanging aneurysms generally will not produce symptoms. 

A larger aneurysm that is steadily growing may press on tissues and nerves causing:

• pain above and behind the eye
• numbness
• weakness
• paralysis on one side of the face
• a dilated pupil in the eye
• vision changes or double vision.

Ruptured aneurysm
When an aneurysm ruptures (bursts), one always experiences a sudden and extremely severe headache (e.g., the worst headache of one’s life) and may also develop:

• double vision
• nausea
• vomiting
• stiff neck
• sensitivity to light
• seizures
• loss of consciousness (this may happen briefly or may be prolonged)
• cardiac arrest.

Leaking aneurysm
Sometimes an aneurysm may leak a small amount of blood into the brain (called a sentinel bleed).  Sentinel or warning headaches may result from an aneurysm that suffers a tiny leak, days or weeks prior to a significant rupture.  However, only a minority of individuals have a sentinel headache prior to rupture. 

If you experience a sudden, severe headache, especially when it is combined with any other symptoms, you should seek immediate medical attention.

How are aneurysms classified?

Type
There are three types of cerebral aneurysms: 

• Saccular aneurysm.  A saccular aneurysm is a rounded sac containing blood, that is attached to a main artery or one of its branches.  Also known as a berry aneurysm (because it resembles a berry hanging from a vine), this is the most common form of cerebral aneurysm.  It is typically found on arteries at the base of the brain.  Saccular aneurysms occur most often in adults.
• Fusiform aneurysm.  A fusiform aneurysm balloons or bulges out on all sides of the artery. 
• Mycotic aneurysm.  A mycotic aneurysm occurs as the result of an infection that can sometimes affect the arteries in the brain.  The infection weakens the artery wall, causing a bulging aneurysm to form.  

Size
Aneurysms are also classified by size: small, large, and giant. 

• Small aneurysms are less than 11 millimeters in diameter (about the size of a large pencil eraser).
• Large aneurysms are 11 to 25 millimeters (about the width of a dime).
• Giant aneurysms are greater than 25 millimeters in diameter (more than the width of a quarter).

What causes a cerebral aneurysm?

Cerebral aneurysms form when the walls of the arteries in the brain become thin and weaken.  Aneurysms typically form at branch points in arteries because these sections are the weakest.  Occasionally, cerebral aneurysms may be present from birth, usually resulting from an abnormality in an artery wall.           

Risk factors for developing an aneurysm

Sometimes cerebral aneurysms are the result of inherited risk factors, including:

• genetic connective tissue disorders that weaken artery walls
• polycystic kidney disease (in which numerous cysts form in the kidneys)
• arteriovenous malformations (snarled tangles of arteries and veins in the brain that disrupt blood flow.  Some AVMs develop sporadically, or on their own.)
• history of aneurysm in a first-degree family member (child, sibling, or parent).

Other risk factors develop over time and include:

• untreated high blood pressure
• cigarette smoking
• drug abuse, especially cocaine or amphetamines, which raise blood pressure to dangerous levels. Intravenous drug abuse is a cause of infectious mycotic aneurysms.
• age over 40.

Less common risk factors include:

• head trauma
• brain tumor
• infection in the arterial wall (mycotic aneurysm).

Additionally, high blood pressure, cigarette smoking, diabetes, and high cholesterol puts one at risk of atherosclerosis (a blood vessel disease in which fats build up on the inside of artery walls), which can increase the risk of developing a fusiform aneurysm.

Risk factors for an aneurysm to rupture

Not all aneurysms will rupture.  Aneurysm characteristics such as size, location, and growth during follow-up evaluation may affect the risk that an aneurysm will rupture. In addition, medical conditions may influence aneurysm rupture.

Risk factors include:

• Smoking.  Smoking is linked to both the development and rupture of cerebral aneurysms. Smoking may even cause multiple aneurysms to form in the brain.
• High blood pressure.  High blood pressure damages and weakens arteries, making them more likely to form and to rupture. 
• Size.  The largest aneurysms are the ones most likely to rupture in a person who previously did not show symptoms.
• Location.  Aneurysms located on the posterior communicating arteries (a pair of arteries in the back part of the brain) and possibly those on the anterior communicating artery (a single artery in the front of the brain) have a higher risk of rupturing than those at other locations in the brain.
• Growth.  Aneurysms that grow, even if they are small, are at increased risk of rupture.
• Family history.  A family history of aneurysm rupture suggests a higher risk of rupture for aneurysms detected in family members.
• The greatest risk occurs in individuals with multiple aneurysms who have already suffered a previous rupture or sentinel bleed.

Diagnosing cerebral aneurysms

Most cerebral aneurysms go unnoticed until they rupture or are detected during medical imaging tests for another condition. 

If you have experienced a severe headache or have any other symptoms related to a ruptured aneurysm your doctor will order tests to determine if blood has leaked into the space between the skull bone and brain. 

Several tests are available to diagnose brain aneurysms and determine the best treatment. These include: 

• Computed tomography (CT).  This fast and painless scan is often the first test a physician will order to determine if blood has leaked into the brain.  CT uses x-rays to create two-dimensional images, or “slices,” of the brain and skull.  Occasionally a contrast dye is injected into the bloodstream prior to scanning to assess the arteries, and look for a possible aneurysm.  This process, called CT angiography (CTA), produces sharper, more detailed images of blood flow in the brain arteries.  CTA can show the size, location, and shape of an unruptured or a ruptured aneurysm. 
• Magnetic resonance imaging (MRI).   An MRI uses computer-generated radio waves and a magnetic field to create two- and three-dimensional detailed images of the brain and can determine if there has been bleeding into the brain.  Magnetic resonance angiography (MRA) produces detailed images of the brain arteries and can show the size, location, and shape of an aneurysm. 
• Cerebral angiography.  This imaging technique can find blockages in arteries in the brain or neck.  It also can identify weak spots in an artery, like an aneurysm.  The test is used to determine the cause of the bleeding in the brain and the exact location, size, and shape of an aneurysm.  Your doctor will pass a catheter (long, flexible tube) typically from the groin arteries to inject a small amount of contrast dye into your neck and brain arteries.  The contrast dye helps the X-ray create a detailed picture of the appearance of an aneurysm and a clear picture of any blockage in the arteries. 
• Cerebrospinal fluid (CSF) analysis.  This test measures the chemicals in the fluid that cushions and protects the brain and spinal cord (cerebrospinal fluid).  Most often a doctor will collect the CSF by performing a spinal tap (lumbar puncture), in which a thin needle is inserted into the lower back (lumbar spine) and a small amount of fluid is removed and tested.   The results will help detect any bleeding around the brain.  If bleeding is detected, additional tests would be needed to identify the exact cause of the bleeding. 

What are the complications of a ruptured cerebral aneurysm?

Aneurysms may rupture and bleed into the space between the skull and the brain (subarachnoid hemorrhage) and sometimes into the brain tissue (intracerebral hemorrhage). These are forms of stroke called hemorrhagic stroke.  The bleeding into the brain can cause a wide spectrum of symptoms, from a mild headache to permanent damage to the brain, or even death.  

After an aneurysm has ruptured it may cause serious complications such as:

• Rebleeding.  Once it has ruptured, an aneurysm may rupture again before it is treated, leading to further bleeding into the brain, and causing more damage or death.    
• Change in sodium level.  Bleeding in the brain can disrupt the balance of sodium in the blood supply and cause swelling in brain cells.  This can result in permanent brain damage. 
• Hydrocephalus.  Subarachnoid hemorrhage can cause hydrocephalus.  Hydrocephalus is a buildup of too much cerebrospinal fluid in the brain, which causes pressure that can lead to permanent brain damage or death.  Hydrocephalus occurs frequently after subarachnoid hemorrhage because the blood blocks the normal flow of cerebrospinal fluid. If left untreated, increased pressure inside the head can cause coma or death. 
• Vasospasm.  This occurs frequently after subarachnoid hemorrhage when the bleeding causes the arteries in the brain to contract and limit blood flow to vital areas of the brain.  This can cause strokes from lack of adequate blood flow to parts of the brain.

Seizures.  Aneurysm bleeding can cause seizures (convulsions), either at the time of bleed or in the immediate aftermath.  While most seizures are evident, on occasion they may only be seen by sophisticated brain testing.  Untreated seizures or those that do not respond to treatment can cause brain damage.

How are cerebral aneurysms treated?

Not all cerebral aneurysms require treatment.  Some very small unruptured aneurysms that are not associated with any factors suggesting a higher risk of rupture may be safely left alone and monitored with MRA or CTA to detect any growth.  It is important to aggressively treat any coexisting medical problems and risk factors.

Treatments for unruptured cerebral aneurysms that have not shown symptoms have some potentially serious complications and should be carefully weighed against the predicted rupture risk.

Treatment considerations for unruptured aneurysms
A doctor will consider a variety of factors when determining the best option for treating an unruptured aneurysm, including:

• type, size, and location of the aneurysm
• risk of rupture
• the person’s age and health
• personal and family medical history
• risk of treatment.

Individuals should also take the following steps to reduce the risk of aneurysm rupture:

• carefully control blood pressure
• stop smoking
• avoid cocaine use or other stimulant drugs. 

Treatments for unruptured and ruptured cerebral aneurysms
Surgery, endovascular treatments, or other therapies are often recommended to manage symptoms and prevent damage from unruptured and ruptured aneurysms.

Surgery
There are a few surgical options available for treating cerebral aneurysms.  These procedures carry some risk such as possible damage to other blood vessels, the potential for aneurysm recurrence and rebleeding, and a risk of stroke. 

• Microvascular clipping.  This procedure involves cutting off the flow of blood to the aneurysm and requires open brain surgery.  A doctor will locate the blood vessels that feed the aneurysm and place a tiny, metal, clothespin-like clip on the aneurysm’s neck to stop its blood supply.  Clipping has been shown to be highly effective, depending on the location, size, and shape of the aneurysm.  In general, aneurysms that are completely clipped do not recur. 

Endovascular treatment

• Platinum coil embolization.  This procedure is a less invasive procedure than microvascular surgical clipping.  A doctor will insert a hollow plastic tube (a catheter) into an artery, usually in the groin, and thread it through the body to the brain aneurysm.  Using a wire, the doctor will pass detachable coils (tiny spirals of platinum wire) through the catheter and release them into the aneurysm.  The coils block the aneurysm and reduce the flow of blood into the aneurysm. The procedure may need to be performed more than once during the person’s lifetime because aneurysms treated with coiling can sometimes recur.
• Flow diversion devices.  Other endovascular treatment options include placing a small stent (flexible mesh tube) similar to those placed for heart blockages, in the artery to reduce blood flow into the aneurysm.  A doctor will insert a hollow plastic tube (a catheter) into an artery, usually in the groin, and thread it through the body to the artery on which the aneurysm is located.   This procedure is used to treat very large aneurysms and those that cannot be treated with surgery or platinum coil embolization.    

Other treatments

Other treatments for a ruptured cerebral aneurysm aim to control symptoms and reduce complications.  These treatments include

• Antiseizure drugs (anticonvulsants).  These drugs may be used to prevent seizures related to a ruptured aneurysm. 
• Calcium channel-blocking drugs.  Risk of stroke by vasospasm can be reduced with calcium channel-blocking drugs.
• .   A shunt, which funnels cerebrospinal fluid from the brain to elsewhere in the body, may be surgically inserted into the brain following rupture if the buildup of cerebrospinal fluid (hydrocephalus) is causing harmful pressure on surrounding brain tissue. 

Rehabilitative therapy.   Individuals who have suffered a subarachnoid hemorrhage often need physical, speech, and occupational therapy to regain lost function and learn to cope with any permanent disability. 

What is the prognosis?

An unruptured aneurysm may go unnoticed throughout a person’s lifetime and not cause symptoms.

After an aneurysm bursts, the person’s prognosis largely depends on:

• age and general health
• preexisting neurological conditions
• location of the aneurysm
• extent of bleeding (and rebleeding)
• time between rupture and medical attention
• successful treatment of the aneurysm.

About 25 percent of individuals whose cerebral aneurysm has ruptured do not survive the first 24 hours; another 25 percent die from complications within 6 months.  People who experience subarachnoid hemorrhage may have permanent neurological damage.  Other individuals recover with little or no disability.  Diagnosing and treating a cerebral aneurysm as soon as possible will help increase the chances of making a full recovery. 

Recovery from treatment or rupture may take weeks to months. 

Additional resources

Offsite Links
Please note that the links below are to information and materials not hosted on Medika’s servers and are as such, not subject to our Terms of Use

BRAIN
P.O. Box 5801
Bethesda, MD 20824
800-352-9424

Information also is available from the following organizations:

Brain Aneurysm Foundation
269 Hanover Street, Building 3
Hanover, MA 02339
Tel: 781-826-5556; 888-BRAIN02 (272-4602)
office@bafound.org

American Stroke Association: A Division of American Heart Association
7272 Greenville Avenue
Dallas, TX 75231-4596
Tel: 888-4STROKE (478-7653)
Fax: 214-706-5231
strokeinfo@heart.org

American Association of Neurological Surgeons
5550 Meadowbrook Drive
Rolling Meadows, IL 60008-3852
Tel: 847-378-0500/888-566-AANS (2267)
Fax: 847-378-0600
info@aans.org

Joe Niekro Foundation
26780 N. 77th St.
Scottsdale, AZ 85252
Tel: 602-318-1013 
info@joeniekrofoundation.com

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