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Treatment – Parkinson Canada

Posted: September 23, 2016 at 4:45 pm

The main treatment for Parkinsons is drug therapy. Surgical techniques are also available for some people.

Drug therapy

The decision to take medication depends on the individual and on a variety of factors such as

Consult your doctor to help choose the medication that will best suit your individual situation. See info sheet: Parkinson’s Medications…What you need to know!(PDF)

The purpose of drug therapy is to relieve symptoms and improve quality of life. Drugs will not stop the progression of the disease. Drugs can help you function on a daily basis; but may cause side effects that need to be managed. Finding the right balance may take time. It is important to contact your doctor to report benefits or problems you may be experiencing. Taking your medication at the right time every day is very important. Parkinson Canada has developed theI have Parkinsons Medication Card(PDF)to help keep track of drugs. For a copy, contact [email protected].

Surgical options

Surgical treatment for Parkinsons can be beneficial for some people. Surgery is not a standard treatment for everyone with Parkinsons; but can be considered after drug therapy has been tried. Procedures involve inserting a probe into the brain and targeting specific areas that may control tremor or involuntary movements. Talk with your neurologist to determine whether you might be a candidate for surgery. A comprehensive assessment will need to be done before a decision is made.

Deep Brain Stimulation for Parkinson Disease: An Expert Consensus and Review of Key Issues.

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Hormone Therapy for Breast Cancer Fact Sheet – National …

Posted: September 22, 2016 at 5:46 am

What are hormones?

Hormones are substances that function as chemical messengers in the body. They affect the actions of cells and tissues at various locations in the body, often reaching their targets through the bloodstream.

The hormones estrogen and progesterone are produced by the ovaries in premenopausal women and by some other tissues, including fat and skin, in both premenopausal and postmenopausal women. Estrogen promotes the development and maintenance of female sex characteristics and the growth of long bones. Progesterone plays a role in the menstrual cycle and pregnancy.

Estrogen and progesterone can also promote the growth of some breast cancers, which are called hormone-sensitive (or hormone-dependent) breast cancers.

How do hormones stimulate the growth of breast cancer?

Hormone-sensitive breast cancer cells contain proteins known as hormone receptors that become activated when hormones bind to them. The activated receptors cause changes in the expression of specific genes, which can lead to the stimulation of cell growth.

To determine whether breast cancer cells contain hormone receptors, doctors test samples of tumor tissue that have been removed by surgery. If the tumor cells contain estrogen receptors, the cancer is called estrogen receptor-positive (ER-positive), estrogen-sensitive, or estrogen-responsive. Similarly, if the tumor cells contain progesterone receptors, the cancer is called progesterone receptor-positive (PR- or PgR-positive). Approximately 70 percent of breast cancers are ER-positive. Most ER-positive breast cancers are also PR-positive (1).

Breast cancers that lack estrogen receptors are called estrogen receptor-negative (ER-negative). These tumors are estrogen-insensitive, meaning that they do not use estrogen to grow. Breast tumors that lack progesterone receptors are called progesterone receptor-negative (PR- or PgR-negative).

What is hormone therapy?

Hormone therapy (also called hormonal therapy, hormone treatment, or endocrine therapy) slows or stops the growth of hormone-sensitive tumors by blocking the bodys ability to produce hormones or by interfering with hormone action. Tumors that are hormone-insensitive do not respond to hormone therapy.

Hormone therapy for breast cancer is not the same as menopausal hormone therapy or female hormone replacement therapy, in which hormones are given to reduce the symptoms of menopause.

What types of hormone therapy are used for breast cancer?

Several strategies have been developed to treat hormone-sensitive breast cancer, including the following:

Blocking ovarian function: Because the ovaries are the main source of estrogen in premenopausal women, estrogen levels in these women can be reduced by eliminating or suppressing ovarian function. Blocking ovarian function is called ovarian ablation.

Ovarian ablation can be done surgically in an operation to remove the ovaries (called oophorectomy) or by treatment with radiation. This type of ovarian ablation is usually permanent.

Alternatively, ovarian function can be suppressed temporarily by treatment with drugs called gonadotropin-releasing hormone (GnRH) agonists, which are also known as luteinizing hormone-releasing hormone (LH-RH) agonists. These medicines interfere with signals from the pituitary gland that stimulate the ovaries to produce estrogen.

Examples of ovarian suppression drugs that have been approved by the U.S. Food and Drug Administration (FDA) are goserelin (Zoladex) and leuprolide (Lupron).

Blocking estrogen production: Drugs called aromatase inhibitors can be used to block the activity of an enzyme called aromatase, which the body uses to make estrogen in the ovaries and in other tissues. Aromatase inhibitors are used primarily in postmenopausal women because the ovaries in premenopausal women produce too much aromatase for the inhibitors to block effectively. However, these drugs can be used in premenopausal women if they are given together with a drug that suppresses ovarian function.

Examples of aromatase inhibitors approved by the FDA are anastrozole (Arimidex) and letrozole (Femara), both of which temporarily inactivate aromatase, and exemestane (Aromasin), which permanently inactivates the enzyme.

Blocking estrogens effects: Several types of drugs interfere with estrogens ability to stimulate the growth of breast cancer cells:

Because SERMs bind to estrogen receptors, they can potentially not only block estrogen activity (i.e., serve as estrogen antagonists) but also mimic estrogen effects (i.e., serve as estrogen agonists). Most SERMs behave as estrogen antagonists in some tissues and as estrogen agonists in other tissues. For example, tamoxifen blocks the effects of estrogen in breast tissue but acts like estrogen in the uterus and bone.

How is hormone therapy used to treat breast cancer?

There are three main ways that hormone therapy is used to treat hormone-sensitive breast cancer:

Adjuvant therapy for early-stage breast cancer: Research has shown that women treated for early-stage ER-positive breast cancer benefit from receiving at least 5 years of adjuvant hormone therapy (2). Adjuvant therapy is treatment given after the main treatment (surgery, in the case of early-stage breast cancer) to increase the likelihood of a cure.

Adjuvant therapy may include radiation therapy and some combination of chemotherapy, hormone therapy, and targeted therapy. Tamoxifen has been approved by the FDA for adjuvant hormone treatment of premenopausal and postmenopausal women (and men) with ER-positive early-stage breast cancer, and anastrozole and letrozole have been approved for this use in postmenopausal women.

A third aromatase inhibitor, exemestane, is approved for adjuvant treatment of early-stage breast cancer in postmenopausal women who have received tamoxifen previously.

Until recently, most women who received adjuvant hormone therapy to reduce the chance of a breast cancer recurrence took tamoxifen every day for 5 years. However, with the advent of newer hormone therapies, some of which have been compared with tamoxifen in clinical trials, additional approaches to hormone therapy have become common (35). For example, some women may take an aromatase inhibitor every day for 5 years, instead of tamoxifen. Other women may receive additional treatment with an aromatase inhibitor after 5 years of tamoxifen. Finally, some women may switch to an aromatase inhibitor after 2 or 3 years of tamoxifen, for a total of 5 or more years of hormone therapy.

Decisions about the type and duration of adjuvant hormone therapy must be made on an individual basis. This complicated decision-making process is best carried out by talking with an oncologist, a doctor who specializes in cancer treatment.

Treatment of metastatic breast cancer: Several types of hormone therapy are approved to treat hormone-sensitive breast cancer that is metastatic (has spread to other parts of the body).

Studies have shown that tamoxifen is effective in treating women and men with metastatic breast cancer (6). Toremifene is also approved for this use. The antiestrogen fulvestrant can be used in postmenopausal women with metastatic ER-positive breast cancer after treatment with other antiestrogens (7).

The aromatase inhibitors anastrozole and letrozole can be given to postmenopausal women as initial therapy for metastatic hormone-sensitive breast cancer (8, 9). These two drugs, as well as the aromatase inhibitor exemestane, can also be used to treat postmenopausal women with advanced breast cancer whose disease has worsened after treatment with tamoxifen (10).

Neoadjuvant treatment of breast cancer: The use of hormone therapy to treat breast cancer before surgery (neoadjuvant therapy) has been studied in clinical trials (11). The goal of neoadjuvant therapy is to reduce the size of a breast tumor to allow breast-conserving surgery. Data from randomized controlled trials have shown that neoadjuvant hormone therapiesin particular, aromatase inhibitorscan be effective in reducing the size of breast tumors in postmenopausal women. The results in premenopausal women are less clear because only a few small trials involving relatively few premenopausal women have been conducted thus far.

No hormone therapy has yet been approved by the FDA for the neoadjuvant treatment of breast cancer.

Can hormone therapy be used to prevent breast cancer?

Yes. Most early breast cancers are ER-positive, and clinical trials have studied whether hormone therapy can be used to prevent breast cancer in women who are at increased risk of getting the disease.

A large NCI-sponsored randomized clinical trial called the Breast Cancer Prevention Trial found that tamoxifen, taken for 5 years, reduced the risk of developing invasive breast cancer by about 50 percent in postmenopausal women who were at increased risk of getting the disease (12). A subsequent large randomized trial, the Study of Tamoxifen and Raloxifene, which was also sponsored by NCI, found that 5 years of raloxifene reduces breast cancer risk in such women by about 38 percent (13).

As a result of these trials, both tamoxifen and raloxifene have been approved by the FDA to reduce the risk of developing breast cancer in women at high risk of the disease. Tamoxifen is approved for use regardless of menopausal status. Raloxifene is approved for use only in postmenopausal women.

The aromatase inhibitor exemestane has also been found to reduce the risk of breast cancer in postmenopausal women at increased risk of the disease. After 3 years of follow-up in another randomized trial, women who took exemestane were 65 percent less likely than those who took a placebo to develop breast cancer (14). Longer follow-up studies will be necessary to determine whether the risk reduction with exemestane remains high over time, as well as to understand any risks of exemestane treatment. Although exemestane has been approved by the FDA for treatment of women with ER-positive breast cancer, it has not been approved for breast cancer prevention.

What are the side effects of hormone therapy?

The side effects of hormone therapy depend largely on the specific drug or the type of treatment (5). The benefits and risks of taking hormone therapy should be carefully weighed for each woman.

Hot flashes, night sweats, and vaginal dryness are common side effects of hormone therapy. Hormone therapy also disrupts the menstrual cycle in premenopausal women.

Less common but serious side effects of hormone therapy drugs are listed below.



Ovarian suppression

Aromatase inhibitors


A common switching strategy, in which patients take tamoxifen for 2 or 3 years, followed by an aromatase inhibitor for 2 or 3 years, may yield the best balance of benefits and harms of these two types of hormone therapy (15).

Can other drugs interfere with hormone therapy?

Certain drugs, including several commonly prescribed antidepressants (those in the category called selective serotonin reuptake inhibitors, or SSRIs), inhibit an enzyme called CYP2D6. This enzyme plays a critical role in the use of tamoxifen by the body because it metabolizes, or breaks down, tamoxifen into molecules, or metabolites, that are much more active than tamoxifen itself.

The possibility that SSRIs might, by inhibiting CYP2D6, slow the metabolism of tamoxifen and reduce its potency is a concern given that as many as one-fourth of breast cancer patients experience clinical depression and may be treated with SSRIs. In addition, SSRIs are sometimes used to treat hot flashes caused by hormone therapy.

Researchers have found that women taking certain SSRIs together with tamoxifen have decreased blood levels of active tamoxifen metabolites. Because of this, many experts suggest that patients who are taking antidepressants along with tamoxifen should discuss treatment options with their doctors. For example, doctors may recommend switching from an SSRI that is a potent inhibitor of CYP2D6 (such as paroxetine) to one that is a weaker inhibitor (such as sertraline) or that has no inhibitory activity (such as venlafaxine or citalopram), or they may suggest that their postmenopausal patients take an aromatase inhibitor instead of tamoxifen.

Other medications that inhibit CYP2D6 include the following:

People who are prescribed tamoxifen should discuss the use of all other medications with their doctors.

Where can someone find more information about drugs used in hormone therapy for breast cancer?

NCI’s Drug Information Summaries provide consumer-friendly information about certain drugs that are approved by the FDA to treat cancer or conditions related to cancer. For each drug, topics covered include background information, research results, possible side effects, FDA approval information, and ongoing clinical trials. The Drug Information Summaries include information about drugs that have been approved for breast cancer.

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Ulcerative Colitis – causes, symptoms, treatment – Southern Cross

Posted: September 21, 2016 at 12:45 am

Ulcerative colitis may be suspected when a person has experienced symptoms of rectal bleeding, intermittent diarrhoea and abdominal pain. As part of the diagnosis the doctor will take a full medical history and conduct a physical examination. The doctor may request that blood tests and specimens of the bowel motion are taken.

In ulcerative colitis, blood test results will often indicate anaemia and signs of inflammation in the body. Samples of bowel motions will often indicate the presence of blood, pus and mucous.

If ulcerative colitis is suspected,endoscopy may be recommended. Endoscopy is the most important diagnostic test used to diagnose ulcerative colitis. During this test a small flexible tube (an endoscope) with a fibre-optic camera at its tip is passed into the rectum and colon. The doctor is able to see the lining of the rectum and colon on a television screen and can look for signs of inflammation and ulceration that may indicate ulcerative colitis. Small tissue samples (biopsies) from the lining of the colon and rectum can be taken for testing. Ulcerative colitis can be diagnosed by the characteristic abnormalities of this tissue.

X-ray tests using barium (a chalky liquid that is able to be seen on x-rays) can be helpful in determining how much of the colon is affected by ulcerative colitis. The barium is administered into the rectum and colon via a tube inserted through the anus. A series of x-rays is taken, showing the outline of the inside of the colon and highlighting any abnormalities.

Treatment for ulcerative colitis aims to prevent complications of the condition by reducing inflammation and maintaining periods of remission. The type of treatment recommended will depend on the extent and severity of the condition. A persons age, general health, lifestyle and personal choice will also be taken into account. In very mild cases, modification of the diet and stress reduction may be all that are required to effectively manage symptoms. However, in severe cases, surgery to remove the colon and rectum may be required.Treatment options include:

Stress reduction

While stress does not cause ulcerative colitis, it can worsen symptoms in some people. Developing techniques to reduce stress can be helpful in managing the condition.


Alternative therapies Some people have found that therapies such as massage, yoga, acupuncture and naturopathy have helped to manage their condition. It is advisable to discuss these with the doctor before starting them.

Medications Treatment for ulcerative colitis usually involves the use of anti-inflammatory medications containing a medication known as 5-aminosalicylic acid (5-ASA). Examples of these medications include sulphasalazine (Salazopyrin), mesalazine (Pentasa, Asacol) and olsalazine (Dipentum). These reduce inflammation in the colon and rectum leading to a reduction in symptoms. These medications are usually taken on a long-term basis and can help prevent flare-ups.

Medications to suppress the immune system may be recommended. Examples of these include azathioprine (Imuran) and cyclosporin (Neoral). Infliximab (Remicade) – a new type of medication that modifies immune system function – is available for people with active ulcerative colitis whose symptoms are not adequately controlled with 5-ASA and corticosteroid medications. However, use of infliximab may be restricted by its high cost.

Severe flare-ups of ulcerative colitis may require hospitalisation. Corticosteroid medications, such as budesonide (Entocort CIR) and prednisone (Apo-Prednisone) may be required and can be given either by mouth (orally), through a drip (intravenously) or into the rectum (as an enema or suppository). Antibiotics may be required if infection is present in the colon.

Dehydration caused by profuse diarrhoea may need to be treated by giving fluids through a drip. Medications to relieve pain and diarrhoea may also be given.

Loss of blood through the rectum over a long period of time can lead to anaemia. Iron tablets may be prescribed to correct the anaemia and prevent its recurrence. In cases of severe blood loss, blood transfusions may be required.

Surgery In severe cases, where medication and supportive treatment have not been successful in controlling the condition, or where the side effects of medications are intolerable, surgery may be required. Approximately 20% of all people with extensive ulcerative colitis will require surgery at some stage. There are three main surgical techniques for the treatment of ulcerative colitis.

Total proctocolectomy and ileostomy – This involves removing the entire colon and rectum. The end of the small intestine is brought out onto the wall of the abdomen. A collection bag is placed over the opening and faecal matter will pass into it. The bag is emptied by the person as required. The ileostomy is permanent. This type of surgery offers a permanent cure for ulcerative colitis.

Sub-total colectomy and ileorectal anastomosis – This is where most of the colon is removed, but the rectum is retained. The lower end of the small intestine is joined to the upper end of the rectum.

Ileoanal anastomosis (Pouch operation) – The entire colon and rectum are removed. A section of the small intestine is used to make a small pouch where faecal matter can be stored. The pouch is then attached to the anus. This surgical technique does not require a permanent ileostomy.

Carson De-Witt, R. (2006) Ulcerative Colitis. The Gale Encyclopaedia of Medicine. Third Edition. Jacqueline L. Longe, Editor. Farmington Hills, MI. Thompson Gale. Crohn’s & Colitis New Zealand (2011). Ulcerative Colitis (PDF).

Crohn’s & Colitis New Zealand (2011). Surgery in IBD (PDF).

Schoenfield, A., Wu, J.W. (2013). Ulcerative Colitis. New York: WebMD LLC. O’Toole, J.M. (Ed) 2013) Mosby’s Dictionary of Medicine, Nursing & Health Professionals (9th ed) St. Louis:elsevier Mosby.

Last Reviewed May 2013

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Treatment – Cerebral palsy – Mayo Clinic

Posted: September 17, 2016 at 6:46 pm

Children and adults with cerebral palsy require long-term care with a medical care team. This team may include:

Medications that can lessen the tightness of muscles may be used to improve functional abilities, treat pain and manage complications related to spasticity or other cerebral palsy symptoms.

It’s important to talk about drug treatment risks with your doctor and discuss whether medical treatment is appropriate for your child’s needs. Medication selection depends on whether the problem affects only certain muscles (isolated) or the whole body (generalized). Drug treatments may include the following:

Isolated spasticity. When spasticity is isolated to one muscle group, your doctor may recommend onabotulinumtoxinA (Botox) injections directly into the muscle, nerve or both. Botox injections may help to improve drooling. Your child will need injections about every three months.

Side effects may include pain, mild flu-like symptoms, bruising or severe weakness. Other more-serious side effects include difficulty breathing and swallowing.

Generalized spasticity. If the whole body is affected, oral muscle relaxants may relax stiff, contracted muscles. These drugs include diazepam (Valium), dantrolene (Dantrium) and baclofen (Gablofen).

Diazepam carries some dependency risk, so it’s not recommended for long-term use. Its side effects include drowsiness, weakness and drooling.

Dantrolene side effects include sleepiness, weakness, nausea and diarrhea.

Baclofen side effects include sleepiness, confusion and nausea. Note that baclofen may also be pumped directly into the spinal cord with a tube. The pump is surgically implanted under the skin of the abdomen.

Your child also may be prescribed medications to reduce drooling. Medications such as trihexyphenidyl, scopolamine or glycopyrrolate (Robinul, Robinul Forte) may be helpful, as can Botox injection into the salivary glands.

A variety of nondrug therapies can help a person with cerebral palsy enhance functional abilities:

Physical therapy. Muscle training and exercises may help your child’s strength, flexibility, balance, motor development and mobility. You’ll also learn how to safely care for your child’s everyday needs at home, such as bathing and feeding your child.

For the first 1 to 2 years after birth, both physical and occupational therapists provide support with issues such as head and trunk control, rolling, and grasping. Later, both types of therapists are involved in wheelchair assessments.

Braces or splints may be recommended for your child. Some of these supports help with function, such as improved walking. Others may stretch stiff muscles to help prevent rigid muscles (contractures).

Occupational therapy. Using alternative strategies and adaptive equipment, occupational therapists work to promote your child’s independent participation in daily activities and routines in the home, the school and the community.

Adaptive equipment may include walkers, quadrupedal canes, seating systems or electric wheelchairs.

Speech and language therapy. Speech-language pathologists can help improve your child’s ability to speak clearly or to communicate using sign language.

Speech-language pathologists can also teach your child to use communication devices, such as a computer and voice synthesizer, if communication is difficult.

Another communication device may be a board covered with pictures of items and activities your child may see in daily life. Sentences can be constructed by pointing to the pictures.

Speech therapists may also address difficulties with muscles used in eating and swallowing.

Surgery may be needed to lessen muscle tightness or correct bone abnormalities caused by spasticity. These treatments include:

Orthopedic surgery. Children with severe contractures or deformities may need surgery on bones or joints to place their arms, hips or legs in their correct positions.

Surgical procedures can also lengthen muscles and tendons that are proportionally too short because of severe contractures. These corrections can lessen pain and improve mobility. The procedures may also make it easier to use a walker, braces or crutches.

Some children and adolescents with cerebral palsy use some form of complementary or alternative medicine.

For example, hyperbaric oxygen therapy is widely promoted for cerebral palsy treatment despite limited evidence of efficacy. This and other unproven therapies for cerebral palsy should be viewed with skepticism. Controlled clinical trials involving therapies such as hyperbaric oxygen therapy, resistance exercise training using special clothing, assisted motion completion for children and certain forms of electrical stimulation have been inconclusive or showed no benefit to date, and the therapies are not accepted mainstream clinical practice.

Stem cell therapy is being explored as a treatment approach for cerebral palsy, but research is still assessing whether such approaches are safe and effective. Studies in the U.S. and elsewhere are examining the safety and tolerability of umbilical cord blood stem cell infusion in children with cerebral palsy.

Aug. 25, 2016

Treatment – Cerebral palsy – Mayo Clinic

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Hormone Replacement Therapy – What You Need to Know

Posted: at 6:46 pm

This material must not be used for commercial purposes, or in any hospital or medical facility. Failure to comply may result in legal action.

What is it? Hormone replacement therapy (HRT) is a treatment for women who have low hormone levels, like a woman going through menopause. HRT is also called estrogen (es-tro-jin) replacement therapy or ERT. With HRT a woman takes estrogen, and often progestin (pro-jes-tin), to help the symptoms caused by low hormone levels in her body.

What are hormones and how do they work?

What are the reasons I may not have enough estrogen?

What are the signs and symptoms of a low estrogen level? You can have physical and emotional changes when your estrogen level is low.

Will HRT help these symptoms? You may choose to take HRT to help or prevent the symptoms of low estrogen. Hot flashes and night sweats will occur less often and may possibly go away if you take estrogen. Estrogen helps prevent vaginal dryness and thinning of the tissue inside the vagina. Your chances of breaking a bone are much lower if you take estrogen. HRT may also improve your mood and memory. HRT may reduce your risk of heart disease.

Is HRT safe?

Are there side effects with HRT? Following are possible side effects of HRT.

How long do I need to take HRT? Bone loss is highest during the early years after menopause. To get the best results, HRT should start soon after the beginning of menopause. You should continue with HRT for at least 7 to 10 years. You and your caregiver can decide how long you should take HRT. You will need long-term treatment if you are trying to prevent heart disease or osteoporosis. Bone loss will begin right away when you stop taking HRT.

How do I take HRT?

Are there other ways to prevent bone loss or heart disease without HRT? Eating foods that are rich in calcium and low in fat is one way to control bone loss and heart disease. Caregivers may give you medicine to prevent bone loss or heart disease. Other ways to prevent bone loss and heart disease are to exercise regularly and to limit the amount of alcohol that you drink. You should not have more than 1 drink a day. A drink is 1 1/2 ounces of whiskey, 5 ounces of wine, or 12 ounces of beer (regular or light). If you smoke, you should quit.

How often should I see my caregiver if I take HRT? Call your caregiver if you are bleeding from your vagina or have other side effects that are bothering you. You should see your caregiver every year for a check up. Your caregiver may want you to have the following tests.

Where can I get more information about HRT? You can call or write the following organizations for more information.

You have the right to help plan your care. To help with this plan you must learn about hormone replacement therapy. You can then discuss the treatment options with caregivers. Work with them to decide what care will be used to treat your decreasing estrogen levels. You always have the right to refuse treatment.

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My Experience with Bells Palsy All Things Galindo

Posted: at 5:43 am

This page chronicles my experience with and recovery from Bells Palsy. Ill continue to add my most current Bells Palsy Post (BPP) to the bottom.

For links to helpful Bells Palsy-related sites, check out my Bells Palsy Information and Resources page.

Last modified on 2011-02-27 15:20:57 GMT. 4 comments. Top.

Hi, Im David. is my personal blog. I was diagnosed on Wednesday, April 9th, 2008 with Bells Palsy, a paralysis of the facial nerve. The result is that its pretty much impossible for me to control the muscles on the right side of my face. In the few days since this appeared, Ive researched several different informational sites and read others stories of their experiences with Bells Palsy. Among the many tips, suggestions and advice was the recommendation to document my progress with pictures. I figure I can do that here on my blog. That way, I can hopefully measure my improvement and share my frustrations and achievements. Also, if someone else with this condition comes along and reads this, maybe it will provide them with some helpful information.

Here is a picture taken of me last Sunday, April 6th. I was hiking the Wind Cave trail at Usery Pass in Mesa, Arizona.

Heres a not-so-brief timeline of my past week:

I have a slight headache in the morning, but the weather is great and the hike at Usery Pass is a lot of fun. Other than the headache, I feel great. Later in the day, I begin to notice that when I eat, I am losing my sense of taste on the right side of my tongue. It also kind of feels like that feeling after you burn your tongue on hot food, sort of numb and tingly. It is about this time that my headache comes back and the area at the base of my skull, behind my right ear, starts aching and feeling sore.

Its springtime here in the desert, with everything blooming like crazy so I figure maybe its allergies (which I dont normally have), dust or the dryness that is causing the headache. I take some ibuprofen, which seems to help, and go to bed.

Back to work on Monday. I work in the training department for a large domain registrar and hosting company in Arizona. Pretty much a normal day. Busy, with lots of projects going on. Again, Im feel pretty good most of the day. Near the end of today, the headache and aching return and Im feeling pretty worn out.

Wrapping up the final touches on a pilot project at work. A lot of time working at the computer with earphones in, listening to Pandora and NPR. Ive got plans to meet some friends for happy hour at B-Dubs (aka Buffalo Wild Wings) after work, between 5 and 5:30pm.

I show up at happy hour, eat a dozen wings and have two Blue Moons (its a beer). The loss of taste and numbness in my tongue seem a little more pronounced. I stay for a couple of hours. Before I leave, Im laughing at someones joke and I notice the muscles on the right side of my face are kind of sluggish. Im starting to think maybe I have a sinus infection or something. I go home, watch American Idol and go to bed.

I wake up in the morning and my face doesnt feel right. My right eye is dry and kind of goopy. I make some coffee and I find Im not able to drink very well. While getting ready for work, I look in the mirror and noticed that my right eye and the right side of my mouth are drooping down. This is when I start to get a little scared. Ive been seeing several commercials lately about recognizing the signs of a stroke and its the first thing that comes to mind. I finish getting ready, and brush my teeth, with obvious difficulty spitting out the toothpaste. I decide to go Urgent Care before going to work.

I get to Urgent Care, explain what Ive been experiencing and that I think I might have some kind of sinus infection or maybe pink eye. The doctor looks at me and says, Im almost 100% sure youve got Bells Palsy. He does some other tests to eliminate a possible stroke or other condition.

This usually clears up on its in 8 to 10 weeks. Eight to ten weeks. Thats two to two and a half months. Not what I was expecting. Theyre not sure what causes Bells Palsy, but its probably due to some kind of trauma or infection to Cranial Nerve 7.

I go to work, and as you can probably guess, Im pretty self-conscious about how I look. Im trying to talk to people with the good side of my face, and I feel the obligation to explain whats been going on. Most people say they wouldnt have noticed if I hadnt pointed it out. More on the experience at work later.

Ive been prescribed an anti-viral medication, five times a day for the next ten days. I also need to follow up with my regular doctor next week. Since my right eye doesnt close on its own, I have to use artificial tears to keep my eye moist letting it dry out can damage the cornea. In addition to the artificial tears, Ive purchased an eye patch to wear whenever the eye gets tired. Plus, it gives me the opportunity to let out my inner pirate. Arrrggghhh!!

My head and the area behind my ear are still aching on and off. With ibuprofen, eye drops and my eye patch, Im off to bed.

I must have rolled over while I was sleeping during the night and slept on the eye patch. When I woke up, the area around my eye was a little swollen and there was this nice ring around my eye from the patch. Ill have to be more careful with that going forward.

Today at work, it seemed that the loss of muscular control became a little more pronounced while Ive been speaking. Bs and Ps are the letters that seem to cause the most problem.

I had a couple of training sessions that I was scheduled to facilitate. All I could do was suck it up and work through it. The people I work with have been incredibly supportive. Thats one thing that I think is most important. Having a few people to confide in when the confidence and optimism takes a dip. Considering everything, it was a really good day.

About the same as yesterday. There are moments throughout the day when I seem to feel small improvements. My right eye is much more sensitive to light so I have a couple of the fluorescent bulbs removed from the overhead lighting to dim my office a bit. Ive been wearing glasses while working at the computer and that seems to help as well. Still, I find myself getting fatigued quickly and I end up going home early today. Im hoping with the weekend to rest and recuperate that Ill feel better by Monday.

Here I am this morning with my first pictures since this all started. My goal is to take the same series of pictures throughout the recovery process. Hopefully I can see some progress soon.

Straight face: 04-12-2008

Smile: 04-12-2008

Eyes Closed: 04-12-2008

Raised Eyebrows: 04-12-2008

Ill ask my doctor when I see him what level of paralysis Im experiencing.

Im still deciding how often to post progress pictures but probably not daily. Its kind of like the saying about a watched pot never boils. I dont want to be discouraged by not seeing improvements fast enough. I also think about those that are trying to lose weight. If you look at the scale too frequently it can be a de-motivator. So , with that, maybe once or twice a week.

Aside from that, Ill share more as often as I can. The appointment with regular doctor is Monday morning and well see what he recommends.

Last modified on 2011-02-28 03:13:44 GMT. 0 comments. Top.

For the last four or five days, Ive been coping with my Bells Palsy. This is Day 5 and my 2nd Bells Palsy Post (BPP-2). The whole process up to this point has been exhausting and at times, frustrating. Still, Im feeling optimistic and hopeful. I should probably be resting more and thats something Im going to work on in the days and weeks ahead.

That being said, I still want to get out and do stuff. I was invited to breakfast this morning with friends at the Hanger Cafe. The restaurant is close to home and is at Chandler Municipal Airport. I had a good and easy-to-eat breakfast of scrambled eggs, potato cubes and bacon strips.

After a breakfast, I was able to take a short flight in the friends plane. It was windy and a little bumpy but definitely a fun flight. Now, you may be thinking that this sites [former] name,, implies that Im a pilot. I am not. The story behind that is a longer story than I intend to tell right now. However, I actually was a Flying Galindo today. AND as seen in the following pictures, I was ACTUALLY FLYING THE PLANE!

OK, so it was me basically making small turns and keeping the nose of the plane level but I was FLYING!

So, here I am, 5 days into Bells Palsy and still able to have a good time.

Last modified on 2010-02-21 17:26:02 GMT. 3 comments. Top.

Today is Monday and a visit to my primary care provider. Last Wednesday, when I woke up with this facial paralysis, I went to a local Urgent Care center for my initial Bells Palsy diagnosis. I was pretty happy with the service and attention there, but I still felt I should make an appointment to see my regular doctor fairly soon. So this morning, before work, I went to my appointment.

My doctor is a pretty cool guy. He happens to be from Michigan and from my home town of Tecumseh. It was about ten years ago , after an unfortunate mountain biking incident (translation: crash and bruised ribs), that I was referred to his office. Anyway, he has a good way of telling me everythings gonna be cool while compare stories of our last visits to the mittened-state.

So today was no different. We went over what had been happening over the last week and he recommended a slightly different course of action to help my recovery go a little smoother. Still, its a matter of time and patience. Because Ive got complete paralysis on the right side Im still looking at several weeks. The good news is: he told me not to worry; that Im going to make a full recovery. Then Ill be able to do things like this again!:

Oh, I took more progress pictures today. I think its too soon to notice any difference so Im not going to post those here now. However, check this one out:

Nice look, huh?

I bought the eye patch last week. Its been really helpful when Ive needed to let my eye rest and to keep wind and dust out of my eye. I think I mentioned before about the drying of my eye due to it not blinking or closing fully. After putting some artificial tears in the eye, the patch (along with a small gauze square underneath) makes it a lot more comfortable.

So you think Id be dying to wear this cool pirate-looking thing out in public, right? No, not really. Ive been pretty self-conscious about it. Until today, I either wore my reading glasses or just held the eye shut to help with the discomfort. When I tried to use the mouse at my computer with my right hand AND hold my right eye shut you get the picture. I was all twisted up. I finally broke down and started wearing the eye patch at work today at work. It was still a long day, but it was easier to bear.

More than ever, Im learning humility and to be humble.

Last modified on 2010-02-21 17:31:01 GMT. 0 comments. Top.

Today was dry day here in Arizona. Here are the current readings here in Chandler:

See the time and temperature? 80 degrees at 7:25 in the evening. See the humidity? 9% Thats dry.

Now, you may be thinking , Yes thats dry, but you live in the desert. Why do you bring it up?

Normally, its fairly dry. But this is REALLY dry. Everybodys been complaining of dry eyes and dry sinuses. For me, Ive been sneezing a lot and had to take extra special care of my eye today. In addition to that, its really windy today which only aggravates the situation. My eye patch and the gel eye drops really helped today.

Aside from that, not much else to report today, but Im doing ok. Ill write more tomorrow on where Im at with my BP.

Well, I think Im going to relax and finish watching American Idol. And Vote for Jason Castro -hes of Colombian descent, like me. Got to support the heritage right?

Last modified on 2010-04-18 17:29:36 GMT. 0 comments. Top.

Its been a week since I woke up and found my face wasnt working quite right. In that week, Ive learned a lot about this condition called Bells Palsy and I continue to learn more. Ive found theres this world-wide community of people suffering from it. Still, its surprising that outside of that community, not many people are aware of Bells palsy. Or if they are, there are a ton of misconceptions, both good and bad.

The most important things Ive learned are that having a positive attitude, being patient and just giving things time to heal are really the best and only course of action. In some ways, thats contrary to the way that I normally functionI tend to try to find ways to fix or mend things. That alone is teaching me something greater than I probably could have learned otherwise.

Today I drove to my companys Scottsdale office to facilitate some testing classes Ive been coordinating. The commute is 35 to 50 minutes depending on traffic. I sometimes like these drives before getting in front of a group because I get to spend a little more time listening to music. Music has always been important to me and one of my favorite bands, Journey, was in the CD player this morning.

Now, those that know me, are aware of the fact that I occasionally like to do a little karaoke now and then. And those that know me REALLY well, know that one of my more important hobbies is writing, singing and recording my own songs in my spare-bedroom studio.

In the last week, with the way my mouth was, or rather, wasnt working, I havent really felt like singing a note. This morning on my drive to work, with Journeys Dont Stop Believin playing loud over the speakers, I sang for the first time in 8 days.

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It felt a little odd at first, trying to form the words and the hearing in my right ear getting boomy at times, but it went ok. All in all, it was a good release.

Before leaving for work this morning, I took the following pictures. I added a couple of profile pictures to illustrate my smile on both sides. I think that I notice a difference in how people react depending on the side they see first. Others tell me thats not the case. To be honest, Im really not sure.

When I look at these pictures and compare them with my earlier post, things look much the same as they did then. One small but optimistic sign is that it appears my right eye is closing a little more. Thats a big deal when you understand how much time Ive been spending making sure my cornea doesnt dry out or get damaged.

Tomorrow, Im going to share pictures of what Im beginning to call my Bells Palsy Survival Kit. I love Ziploc bags. They rank up there with Velcro and Nougat!

Last modified on 2010-02-24 05:30:34 GMT. 0 comments. Top.

My temporary facial paralysis brings on some additional issues. My right eye doesnt fully close on its own and stay moist. My sinus on the right side has the a similar drying problem. Same problem with my lips. Here are a few things that have become part of my daily maintenance kit and travel nicely in a quart-size Ziploc freezer bag:

Thera Tears Lubricant Eye Drops, Saline nasal spray, Burts Bees Beeswax Lip Balm, tissues, Eye patch, Gauze pad (for under the eye patch).

In addition to these, at night I use: Thera Tears Liquid Gel Eye Drops (longer lasting for overnight use), more gauze and medical tape to close the eye over night. I admit it becomes a chore at times but these are things that have helped me feel a little more comfortable

I try to take my lunch to work a few days a week. It only takes a little planning and usually ends up being healthier, more cost-effective and satisfying anyway. Right now, the right side of my mouth doesnt open as wide or control food in the same way. Having smaller, bite size options seems to work best:

Having straws and a good napkin come in handy as well. I cant wait until I can eat a big messy slice of pizza again.

Last modified on 2008-04-19 22:44:48 GMT. 0 comments. Top.

Today is one week since my first set of pictures. I thought it might be interesting to compare where Im at today side-by-side with those I took last Saturday morning.

Im not going to analyze them too much. For me, I know that most of the improvement is with my right eye. Its closing just slightly better which really helps with keeping it from drying out.

The pictures in the right column were taken Saturday, April 12th, 2008, with the exception of the side profile smiling photos. I decided to start adding that perspective on Wednesday, April 16th, 2008.

The pictures in the right column were taken today, Saturday, April 19th, 2008.

Its still really dry here in Arizona, but you cant beat the temperature:

If youre someplace where its cold right now, dont be too jealous. Were just a few weeks away from daily triple-digits!!

Last modified on 2008-04-24 03:40:48 GMT. 0 comments. Top.

Its been three days since my last post and four since my last set of pictures. With the busy week Ive been having, I took a couple days off working on my computer at home. The good news is: Im starting to get some movement back. It started as a twitch around my right eye Monday morning.

Im feeling the ability to show a little more expression. However, I realize at the end of each day how much energy my body is using to recover and regenerate this nerve thats been damaged. For anybody reading that has experienced this, you can probably relate. Ive been pretty tired at the end of each day where I cant wait to get home and just close my eyes for awhile. Today was no exception, but Ill take being tired if it means Im getting better.

Guess what Monday happened to be? My 39th birthday. The improvement may have been small, but for me, was quite an impressive gift.

As before, the pictures in the left column were taken Saturday, April 12th, 2008 (except the side profile smiling photos).

The pictures in the right column were taken this evening, Wednesday, April 23rd, 2008.

More pictures

Last modified on 2010-04-18 18:14:41 GMT. 0 comments. Top.

Today is two weeks since my first set of pictures tracking my recovery from Bells Palsy. Im really glad I decided to take the pictures, even though I admit it was really hard for me to look at them at first. At the most difficult moments during the last 18 days, I was able to compare and notice the slight changes in the pictures. This made it was easier for me to keep my spirits up.

The muscles around my right eye are starting to respond more now. The right side of my mouth is turning up just ever so slightly which is helpful when youre trying to smile. I went to wedding last night and, though I felt fairly good, it still feels awkward when I know that emotions like laughter and happiness dont appear like they should. The sense of taste on the right side of my tongue is still subdued (best way I can describe it). Im hoping that comes back soon because food in general has tasted bland since this all began. My speech is pretty close to normal. However, the last couple of hours in the evening I started feeling really fatigued trying to say certain words. It reminds me that I still have a way to go.

Todays pictures were taken after spending quite a bit of time working on my blog and its template. I notice my right eye in the eyes closed shot is slightly open Im going to have to let it rest for awhile after I finish this post.

The following pictures in the left column were taken Saturday, April 12th, 2008 (except the side profile smiling photos).

The pictures in the right column were taken this afternoon, Saturday, April 26rd, 2008.

Last modified on 2010-04-18 18:17:07 GMT. 0 comments. Top.

As I walked into my office yesterday afternoon, a co-worker, after not seeing me for a day, exclaimed David! Your face is back! Prior to having Bells Palsy and the way we playfully joke with each other at work, a comment like that would probably have been followed by a witty punch line. This time however, it was sincere. And it was nice to hear too.

The word on the street is that my smile is returning to the right side of my face. All the things that make a smile possible mouth turning up, squinting of the eye, raising the eyebrow are returning to normal, a wrinkle at a time. Who would have thought wrinkles were a good thing? I do now.

After three weeks, I think the following pictures are a significant milestone. Im doing my best to take natural-looking photos. If it looks like Im smirking I apologize.

Pictures in the left column were taken Saturday, April 12th, 2008 (except where noted on the side profile smiling photos).

Pictures in the right column were taken this morning, Wednesday, April 30th, 2008.

Read this article:
My Experience with Bells Palsy All Things Galindo

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Lost & Found: What Brain Injury Survivors Want You to Know

Posted: at 5:43 am

Barbara J. Webster, Lash & Associates

I need a lot more rest than I used to. Im not being lazy. I get physical fatigue as well as a brain fatigue. It is very difficult and tiring for my brain to think, process, and organize. Fatigue makes it even harder to think.

My stamina fluctuates, even though I may look good or all better on the outside. Cognition is a fragile function for a brain injury survivor. Some days are better than others. Pushing too hard usually leads to setbacks, sometimes to illness.

Brain injury rehabilitation takes a very long time; it is usually measured in years. It continues long after formal rehabilitation has ended. Please resist expecting me to be who I was, even though I look better.

I am not being difficult if I resist social situations. Crowds, confusion, and loud sounds quickly overload my brain, it doesnt filter sounds as well as it used to. Limiting my exposure is a coping strategy, not a behavioral problem.

If there is more than one person talking, I may seem uninterested in the conversation. That is because I have trouble following all the different lines of discussion. It is exhausting to keep trying to piece it all together. Im not dumb or rude; my brain is getting overloaded!

If we are talking and I tell you that I need to stop, I need to stop NOW! And it is not because Im avoiding the subject, its just that I need time to process our discussion and take a break from all the thinking. Later I will be able to rejoin the conversation and really be present for the subject and for you.

Try to notice the circumstances if a behavior problem arises. Behavior problems are often an indication of my inability to cope with a specific situation and not a mental health issue. I may be frustrated, in pain, overtired or there may be too much confusion or noise for my brain to filter.

Patience is the best gift you can give me. It allows me to work deliberately and at my own pace, allowing me to rebuild pathways in my brain. Rushing and multi-tasking inhibit cognition.

Please listen to me with patience. Try not to interrupt. Allow me to find my words and follow my thoughts. It will help me rebuild my language skills.

Please have patience with my memory. Know that not remembering does not mean that I dont care.

Please dont be condescending or talk to me like I am a child. Im not stupid, my brain is injured and it doesnt work as well as it used to. Try to think of me as if my brain were in a cast.

If I seem rigid, needing to do tasks the same way all the time; it is because I am retraining my brain. Its like learning main roads before you can learn the shortcuts. Repeating tasks in the same sequence is a rehabilitation strategy.

If I seem stuck, my brain may be stuck in the processing of information. Coaching me, suggesting other options or asking what you can do to help may help me figure it out. Taking over and doing it for me will not be constructive and it will make me feel inadequate. (It may also be an indication that I need to take a break.)

You may not be able to help me do something if helping requires me to frequently interrupt what I am doing to give you directives. I work best on my own, one step at a time and at my own pace.

If I repeat actions, like checking to see if the doors are locked or the stove is turned off, it may seem like I have OCD obsessive-compulsive disorder but I may not. It may be that I am having trouble registering what I am doing in my brain. Repetitions enhance memory. (It can also be a cue that I need to stop and rest.)

If I seem sensitive, it could be emotional lability as a result of the injury or it may be a reflection of the extraordinary effort it takes to do things now. Tasks that used to feel automatic and take minimal effort, now take much longer, require the implementation of numerous strategies and are huge accomplishments for me.

We need cheerleaders now, as we start over, just like children do when they are growing up. Please help me and encourage all efforts. Please dont be negative or critical. I am doing the best I can.

Dont confuse Hope for Denial. We are learning more and more about the amazing brain and there are remarkable stories about healing in the news every day. No one can know for certain what our potential is. We need Hope to be able to employ the many, many coping mechanisms, accommodations and strategies needed to navigate our new lives. Everything single thing in our lives is extraordinarily difficult for us now. It would be easy to give up without Hope.

Created with the assistance of the “Amazing” Brain Injury Survivor Support Group of Framingham, MA.

Excerpted from Lost & Found: A Survivor’s Guide for Reconstructing Life After a Brain Injury by Barbara J. Webster. 20ll by Lash & Associates Publishing/Training Inc. Used with permission. Click here for more information about the book.

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Lost & Found: What Brain Injury Survivors Want You to Know

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Brain – Wikipedia, the free encyclopedia

Posted: at 5:43 am

This article is about the brains of all types of animals, including humans. For information specific to the human brain, see Human brain. For other uses, see Brain (disambiguation).

The brain is an organ that serves as the center of the nervous system in all vertebrate and most invertebrate animals. Only a few invertebrates such as sponges, jellyfish, adult sea squirts and starfish do not have a brain; diffuse or localised nerve nets are present instead. The brain is located in the head, usually close to the primary sensory organs for such senses as vision, hearing, balance, taste, and smell. The brain is the most complex organ in a vertebrate’s body. In a typical human, the cerebral cortex (the largest part) is estimated to contain 1533 billion neurons,[1] each connected by synapses to several thousand other neurons. These neurons communicate with one another by means of long protoplasmic fibers called axons, which carry trains of signal pulses called action potentials to distant parts of the brain or body targeting specific recipient cells.

Physiologically, the function of the brain is to exert centralized control over the other organs of the body. The brain acts on the rest of the body both by generating patterns of muscle activity and by driving the secretion of chemicals called hormones. This centralized control allows rapid and coordinated responses to changes in the environment. Some basic types of responsiveness such as reflexes can be mediated by the spinal cord or peripheral ganglia, but sophisticated purposeful control of behavior based on complex sensory input requires the information integrating capabilities of a centralized brain.

The operations of individual brain cells are now understood in considerable detail but the way they cooperate in ensembles of millions is yet to be solved.[2] Recent models in modern neuroscience treat the brain as a biological computer, very different in mechanism from an electronic computer, but similar in the sense that it acquires information from the surrounding world, stores it, and processes it in a variety of ways, analogous to the central processing unit (CPU) in a computer.[3]

This article compares the properties of brains across the entire range of animal species, with the greatest attention to vertebrates. It deals with the human brain insofar as it shares the properties of other brains. The ways in which the human brain differs from other brains are covered in the human brain article. Several topics that might be covered here are instead covered there because much more can be said about them in a human context. The most important is brain disease and the effects of brain damage, covered in the human brain article because the most common diseases of the human brain either do not show up in other species, or else manifest themselves in different ways.

The shape and size of the brain varies greatly in different species, and identifying common features is often difficult.[4] Nevertheless, there are a number of principles of brain architecture that apply across a wide range of species.[5] Some aspects of brain structure are common to almost the entire range of animal species;[6] others distinguish “advanced” brains from more primitive ones, or distinguish vertebrates from invertebrates.[4]

The simplest way to gain information about brain anatomy is by visual inspection, but many more sophisticated techniques have been developed. Brain tissue in its natural state is too soft to work with, but it can be hardened by immersion in alcohol or other fixatives, and then sliced apart for examination of the interior. Visually, the interior of the brain consists of areas of so-called grey matter, with a dark color, separated by areas of white matter, with a lighter color. Further information can be gained by staining slices of brain tissue with a variety of chemicals that bring out areas where specific types of molecules are present in high concentrations. It is also possible to examine the microstructure of brain tissue using a microscope, and to trace the pattern of connections from one brain area to another.[7]

The brains of all species are composed primarily of two broad classes of cells: neurons and glial cells. Glial cells (also known as glia or neuroglia) come in several types, and perform a number of critical functions, including structural support, metabolic support, insulation, and guidance of development. Neurons, however, are usually considered the most important cells in the brain.[8] The property that makes neurons unique is their ability to send signals to specific target cells over long distances.[8] They send these signals by means of an axon, which is a thin protoplasmic fiber that extends from the cell body and projects, usually with numerous branches, to other areas, sometimes nearby, sometimes in distant parts of the brain or body. The length of an axon can be extraordinary: for example, if a pyramidal cell, (an excitatory neuron) of the cerebral cortex were magnified so that its cell body became the size of a human body, its axon, equally magnified, would become a cable a few centimeters in diameter, extending more than a kilometer.[9] These axons transmit signals in the form of electrochemical pulses called action potentials, which last less than a thousandth of a second and travel along the axon at speeds of 1100 meters per second. Some neurons emit action potentials constantly, at rates of 10100 per second, usually in irregular patterns; other neurons are quiet most of the time, but occasionally emit a burst of action potentials.[10]

Axons transmit signals to other neurons by means of specialized junctions called synapses. A single axon may make as many as several thousand synaptic connections with other cells.[8] When an action potential, traveling along an axon, arrives at a synapse, it causes a chemical called a neurotransmitter to be released. The neurotransmitter binds to receptor molecules in the membrane of the target cell.[8]

Synapses are the key functional elements of the brain.[11] The essential function of the brain is cell-to-cell communication, and synapses are the points at which communication occurs. The human brain has been estimated to contain approximately 100 trillion synapses;[12] even the brain of a fruit fly contains several million.[13] The functions of these synapses are very diverse: some are excitatory (exciting the target cell); others are inhibitory; others work by activating second messenger systems that change the internal chemistry of their target cells in complex ways.[11] A large number of synapses are dynamically modifiable; that is, they are capable of changing strength in a way that is controlled by the patterns of signals that pass through them. It is widely believed that activity-dependent modification of synapses is the brain’s primary mechanism for learning and memory.[11]

Most of the space in the brain is taken up by axons, which are often bundled together in what are called nerve fiber tracts. A myelinated axon is wrapped in a fatty insulating sheath of myelin, which serves to greatly increase the speed of signal propagation. (There are also unmyelinated axons). Myelin is white, making parts of the brain filled exclusively with nerve fibers appear as light-colored white matter, in contrast to the darker-colored grey matter that marks areas with high densities of neuron cell bodies.[8]

Except for a few primitive organisms such as sponges (which have no nervous system)[14] and cnidarians (which have a nervous system consisting of a diffuse nerve net[14]), all living multicellular animals are bilaterians, meaning animals with a bilaterally symmetric body shape (that is, left and right sides that are approximate mirror images of each other).[15] All bilaterians are thought to have descended from a common ancestor that appeared early in the Cambrian period, 485-540 million years ago, and it has been hypothesized that this common ancestor had the shape of a simple tubeworm with a segmented body.[15] At a schematic level, that basic worm-shape continues to be reflected in the body and nervous system architecture of all modern bilaterians, including vertebrates.[16] The fundamental bilateral body form is a tube with a hollow gut cavity running from the mouth to the anus, and a nerve cord with an enlargement (a ganglion) for each body segment, with an especially large ganglion at the front, called the brain. The brain is small and simple in some species, such as nematode worms; in other species, including vertebrates, it is the most complex organ in the body.[4] Some types of worms, such as leeches, also have an enlarged ganglion at the back end of the nerve cord, known as a “tail brain”.[17]

There are a few types of existing bilaterians that lack a recognizable brain, including echinoderms, tunicates, and acoelomorphs (a group of primitive flatworms). It has not been definitively established whether the existence of these brainless species indicates that the earliest bilaterians lacked a brain, or whether their ancestors evolved in a way that led to the disappearance of a previously existing brain structure.[18]

This category includes arthropods, molluscs, and numerous types of worms. The diversity of invertebrate body plans is matched by an equal diversity in brain structures.[19]

Two groups of invertebrates have notably complex brains: arthropods (insects, crustaceans, arachnids, and others), and cephalopods (octopuses, squids, and similar molluscs).[20] The brains of arthropods and cephalopods arise from twin parallel nerve cords that extend through the body of the animal. Arthropods have a central brain, the supraesophageal ganglion, with three divisions and large optical lobes behind each eye for visual processing.[20] Cephalopods such as the octopus and squid have the largest brains of any invertebrates.[21]

There are several invertebrate species whose brains have been studied intensively because they have properties that make them convenient for experimental work:

The first vertebrates appeared over 500million years ago (Mya), during the Cambrian period, and may have resembled the modern hagfish in form.[32] Sharks appeared about 450Mya, amphibians about 400Mya, reptiles about 350Mya, and mammals about 200Mya. Each species has an equally long evolutionary history, but the brains of modern hagfishes, lampreys, sharks, amphibians, reptiles, and mammals show a gradient of size and complexity that roughly follows the evolutionary sequence. All of these brains contain the same set of basic anatomical components, but many are rudimentary in the hagfish, whereas in mammals the foremost part (the telencephalon) is greatly elaborated and expanded.[33]

Brains are most simply compared in terms of their size. The relationship between brain size, body size and other variables has been studied across a wide range of vertebrate species. As a rule, brain size increases with body size, but not in a simple linear proportion. In general, smaller animals tend to have larger brains, measured as a fraction of body size. For mammals, the relationship between brain volume and body mass essentially follows a power law with an exponent of about 0.75.[34] This formula describes the central tendency, but every family of mammals departs from it to some degree, in a way that reflects in part the complexity of their behavior. For example, primates have brains 5 to 10 times larger than the formula predicts. Predators tend to have larger brains than their prey, relative to body size.[35]

All vertebrate brains share a common underlying form, which appears most clearly during early stages of embryonic development. In its earliest form, the brain appears as three swellings at the front end of the neural tube; these swellings eventually become the forebrain, midbrain, and hindbrain (the prosencephalon, mesencephalon, and rhombencephalon, respectively). At the earliest stages of brain development, the three areas are roughly equal in size. In many classes of vertebrates, such as fish and amphibians, the three parts remain similar in size in the adult, but in mammals the forebrain becomes much larger than the other parts, and the midbrain becomes very small.[8]

The brains of vertebrates are made of very soft tissue.[8] Living brain tissue is pinkish on the outside and mostly white on the inside, with subtle variations in color. Vertebrate brains are surrounded by a system of connective tissue membranes called meninges that separate the skull from the brain. Blood vessels enter the central nervous system through holes in the meningeal layers. The cells in the blood vessel walls are joined tightly to one another, forming the bloodbrain barrier, which blocks the passage of many toxins and pathogens[36] (though at the same time blocking antibodies and some drugs, thereby presenting special challenges in treatment of diseases of the brain).[37]

Neuroanatomists usually divide the vertebrate brain into six main regions: the telencephalon (cerebral hemispheres), diencephalon (thalamus and hypothalamus), mesencephalon (midbrain), cerebellum, pons, and medulla oblongata. Each of these areas has a complex internal structure. Some parts, such as the cerebral cortex and the cerebellar cortex, consist of layers that are folded or convoluted to fit within the available space. Other parts, such as the thalamus and hypothalamus, consist of clusters of many small nuclei. Thousands of distinguishable areas can be identified within the vertebrate brain based on fine distinctions of neural structure, chemistry, and connectivity.[8]

Although the same basic components are present in all vertebrate brains, some branches of vertebrate evolution have led to substantial distortions of brain geometry, especially in the forebrain area. The brain of a shark shows the basic components in a straightforward way, but in teleost fishes (the great majority of existing fish species), the forebrain has become “everted”, like a sock turned inside out. In birds, there are also major changes in forebrain structure.[38] These distortions can make it difficult to match brain components from one species with those of another species.[39]

Here is a list of some of the most important vertebrate brain components, along with a brief description of their functions as currently understood:

The most obvious difference between the brains of mammals and other vertebrates is in terms of size. On average, a mammal has a brain roughly twice as large as that of a bird of the same body size, and ten times as large as that of a reptile of the same body size.[50]

Size, however, is not the only difference: there are also substantial differences in shape. The hindbrain and midbrain of mammals are generally similar to those of other vertebrates, but dramatic differences appear in the forebrain, which is greatly enlarged and also altered in structure.[51] The cerebral cortex is the part of the brain that most strongly distinguishes mammals. In non-mammalian vertebrates, the surface of the cerebrum is lined with a comparatively simple three-layered structure called the pallium. In mammals, the pallium evolves into a complex six-layered structure called neocortex or isocortex.[52] Several areas at the edge of the neocortex, including the hippocampus and amygdala, are also much more extensively developed in mammals than in other vertebrates.[51]

The elaboration of the cerebral cortex carries with it changes to other brain areas. The superior colliculus, which plays a major role in visual control of behavior in most vertebrates, shrinks to a small size in mammals, and many of its functions are taken over by visual areas of the cerebral cortex.[50] The cerebellum of mammals contains a large portion (the neocerebellum) dedicated to supporting the cerebral cortex, which has no counterpart in other vertebrates.[53]

The brains of humans and other primates contain the same structures as the brains of other mammals, but are generally larger in proportion to body size.[57] The most widely accepted way of comparing brain sizes across species is the so-called encephalization quotient (EQ), which takes into account the nonlinearity of the brain-to-body relationship.[54] Humans have an average EQ in the 7-to-8 range, while most other primates have an EQ in the 2-to-3 range. Dolphins have values higher than those of primates other than humans,[55] but nearly all other mammals have EQ values that are substantially lower.

Most of the enlargement of the primate brain comes from a massive expansion of the cerebral cortex, especially the prefrontal cortex and the parts of the cortex involved in vision.[58] The visual processing network of primates includes at least 30 distinguishable brain areas, with a complex web of interconnections. It has been estimated that visual processing areas occupy more than half of the total surface of the primate neocortex.[59] The prefrontal cortex carries out functions that include planning, working memory, motivation, attention, and executive control. It takes up a much larger proportion of the brain for primates than for other species, and an especially large fraction of the human brain.[60]

The brain does not simply grow, but rather develops in an intricately orchestrated sequence of stages.[61] It changes in shape from a simple swelling at the front of the nerve cord in the earliest embryonic stages, to a complex array of areas and connections. Neurons are created in special zones that contain stem cells, and then migrate through the tissue to reach their ultimate locations. Once neurons have positioned themselves, their axons sprout and navigate through the brain, branching and extending as they go, until the tips reach their targets and form synaptic connections. In a number of parts of the nervous system, neurons and synapses are produced in excessive numbers during the early stages, and then the unneeded ones are pruned away.[61]

For vertebrates, the early stages of neural development are similar across all species.[61] As the embryo transforms from a round blob of cells into a wormlike structure, a narrow strip of ectoderm running along the midline of the back is induced to become the neural plate, the precursor of the nervous system. The neural plate folds inward to form the neural groove, and then the lips that line the groove merge to enclose the neural tube, a hollow cord of cells with a fluid-filled ventricle at the center. At the front end, the ventricles and cord swell to form three vesicles that are the precursors of the forebrain, midbrain, and hindbrain. At the next stage, the forebrain splits into two vesicles called the telencephalon (which will contain the cerebral cortex, basal ganglia, and related structures) and the diencephalon (which will contain the thalamus and hypothalamus). At about the same time, the hindbrain splits into the metencephalon (which will contain the cerebellum and pons) and the myelencephalon (which will contain the medulla oblongata). Each of these areas contains proliferative zones where neurons and glial cells are generated; the resulting cells then migrate, sometimes for long distances, to their final positions.[61]

Once a neuron is in place, it extends dendrites and an axon into the area around it. Axons, because they commonly extend a great distance from the cell body and need to reach specific targets, grow in a particularly complex way. The tip of a growing axon consists of a blob of protoplasm called a growth cone, studded with chemical receptors. These receptors sense the local environment, causing the growth cone to be attracted or repelled by various cellular elements, and thus to be pulled in a particular direction at each point along its path. The result of this pathfinding process is that the growth cone navigates through the brain until it reaches its destination area, where other chemical cues cause it to begin generating synapses. Considering the entire brain, thousands of genes create products that influence axonal pathfinding.[61]

The synaptic network that finally emerges is only partly determined by genes, though. In many parts of the brain, axons initially “overgrow”, and then are “pruned” by mechanisms that depend on neural activity.[61] In the projection from the eye to the midbrain, for example, the structure in the adult contains a very precise mapping, connecting each point on the surface of the retina to a corresponding point in a midbrain layer. In the first stages of development, each axon from the retina is guided to the right general vicinity in the midbrain by chemical cues, but then branches very profusely and makes initial contact with a wide swath of midbrain neurons. The retina, before birth, contains special mechanisms that cause it to generate waves of activity that originate spontaneously at a random point and then propagate slowly across the retinal layer. These waves are useful because they cause neighboring neurons to be active at the same time; that is, they produce a neural activity pattern that contains information about the spatial arrangement of the neurons. This information is exploited in the midbrain by a mechanism that causes synapses to weaken, and eventually vanish, if activity in an axon is not followed by activity of the target cell. The result of this sophisticated process is a gradual tuning and tightening of the map, leaving it finally in its precise adult form.[62]

Similar things happen in other brain areas: an initial synaptic matrix is generated as a result of genetically determined chemical guidance, but then gradually refined by activity-dependent mechanisms, partly driven by internal dynamics, partly by external sensory inputs. In some cases, as with the retina-midbrain system, activity patterns depend on mechanisms that operate only in the developing brain, and apparently exist solely to guide development.[62]

In humans and many other mammals, new neurons are created mainly before birth, and the infant brain contains substantially more neurons than the adult brain.[61] There are, however, a few areas where new neurons continue to be generated throughout life. The two areas for which adult neurogenesis is well established are the olfactory bulb, which is involved in the sense of smell, and the dentate gyrus of the hippocampus, where there is evidence that the new neurons play a role in storing newly acquired memories. With these exceptions, however, the set of neurons that is present in early childhood is the set that is present for life. Glial cells are different: as with most types of cells in the body, they are generated throughout the lifespan.[63]

There has long been debate about whether the qualities of mind, personality, and intelligence can be attributed to heredity or to upbringingthis is the nature and nurture controversy.[64] Although many details remain to be settled, neuroscience research has clearly shown that both factors are important. Genes determine the general form of the brain, and genes determine how the brain reacts to experience. Experience, however, is required to refine the matrix of synaptic connections, which in its developed form contains far more information than the genome does. In some respects, all that matters is the presence or absence of experience during critical periods of development.[65] In other respects, the quantity and quality of experience are important; for example, there is substantial evidence that animals raised in enriched environments have thicker cerebral cortices, indicating a higher density of synaptic connections, than animals whose levels of stimulation are restricted.[66]

The functions of the brain depend on the ability of neurons to transmit electrochemical signals to other cells, and their ability to respond appropriately to electrochemical signals received from other cells. The electrical properties of neurons are controlled by a wide variety of biochemical and metabolic processes, most notably the interactions between neurotransmitters and receptors that take place at synapses.[8]

Neurotransmitters are chemicals that are released at synapses when an action potential activates themneurotransmitters attach themselves to receptor molecules on the membrane of the synapse’s target cell, and thereby alter the electrical or chemical properties of the receptor molecules. With few exceptions, each neuron in the brain releases the same chemical neurotransmitter, or combination of neurotransmitters, at all the synaptic connections it makes with other neurons; this rule is known as Dale’s principle.[8] Thus, a neuron can be characterized by the neurotransmitters that it releases. The great majority of psychoactive drugs exert their effects by altering specific neurotransmitter systems. This applies to drugs such as cannabinoids, nicotine, heroin, cocaine, alcohol, fluoxetine, chlorpromazine, and many others.[67]

The two neurotransmitters that are used most widely in the vertebrate brain are glutamate, which almost always exerts excitatory effects on target neurons, and gamma-aminobutyric acid (GABA), which is almost always inhibitory. Neurons using these transmitters can be found in nearly every part of the brain.[68] Because of their ubiquity, drugs that act on glutamate or GABA tend to have broad and powerful effects. Some general anesthetics act by reducing the effects of glutamate; most tranquilizers exert their sedative effects by enhancing the effects of GABA.[69]

There are dozens of other chemical neurotransmitters that are used in more limited areas of the brain, often areas dedicated to a particular function. Serotonin, for examplethe primary target of antidepressant drugs and many dietary aidscomes exclusively from a small brainstem area called the Raphe nuclei.[70]Norepinephrine, which is involved in arousal, comes exclusively from a nearby small area called the locus coeruleus.[71] Other neurotransmitters such as acetylcholine and dopamine have multiple sources in the brain, but are not as ubiquitously distributed as glutamate and GABA.[72]

As a side effect of the electrochemical processes used by neurons for signaling, brain tissue generates electric fields when it is active. When large numbers of neurons show synchronized activity, the electric fields that they generate can be large enough to detect outside the skull, using electroencephalography (EEG)[73] or magnetoencephalography (MEG). EEG recordings, along with recordings made from electrodes implanted inside the brains of animals such as rats, show that the brain of a living animal is constantly active, even during sleep.[74] Each part of the brain shows a mixture of rhythmic and nonrhythmic activity, which may vary according to behavioral state. In mammals, the cerebral cortex tends to show large slow delta waves during sleep, faster alpha waves when the animal is awake but inattentive, and chaotic-looking irregular activity when the animal is actively engaged in a task. During an epileptic seizure, the brain’s inhibitory control mechanisms fail to function and electrical activity rises to pathological levels, producing EEG traces that show large wave and spike patterns not seen in a healthy brain. Relating these population-level patterns to the computational functions of individual neurons is a major focus of current research in neurophysiology.[74]

All vertebrates have a bloodbrain barrier that allows metabolism inside the brain to operate differently from metabolism in other parts of the body. Glial cells play a major role in brain metabolism by controlling the chemical composition of the fluid that surrounds neurons, including levels of ions and nutrients.[75]

Brain tissue consumes a large amount of energy in proportion to its volume, so large brains place severe metabolic demands on animals. The need to limit body weight in order, for example, to fly, has apparently led to selection for a reduction of brain size in some species, such as bats.[76] Most of the brain’s energy consumption goes into sustaining the electric charge (membrane potential) of neurons.[75] Most vertebrate species devote between 2% and 8% of basal metabolism to the brain. In primates, however, the percentage is much higherin humans it rises to 2025%.[77] The energy consumption of the brain does not vary greatly over time, but active regions of the cerebral cortex consume somewhat more energy than inactive regions; this forms the basis for the functional brain imaging methods PET, fMRI,[78] and NIRS.[79] The brain typically gets most of its energy from oxygen-dependent metabolism of glucose (i.e., blood sugar),[75] but ketones provide a major alternative source, together with contributions from medium chain fatty acids (caprylic[80] and heptanoic[81] acids), lactate,[82]acetate,[83] and possibly amino acids.[84]

From an evolutionary-biological perspective, the function of the brain is to provide coherent control over the actions of an animal. A centralized brain allows groups of muscles to be co-activated in complex patterns; it also allows stimuli impinging on one part of the body to evoke responses in other parts, and it can prevent different parts of the body from acting at cross-purposes to each other.[85]

To generate purposeful and unified action, the brain first brings information from sense organs together at a central location. It then processes this raw data to extract information about the structure of the environment. Next it combines the processed sensory information with information about the current needs of an animal and with memory of past circumstances. Finally, on the basis of the results, it generates motor response patterns that are suited to maximize the welfare of the animal. These signal-processing tasks require intricate interplay between a variety of functional subsystems.[85]

The invention of electronic computers in the 1940s, along with the development of mathematical information theory, led to a realization that brains can potentially be understood as information processing systems. This concept formed the basis of the field of cybernetics, and eventually gave rise to the field now known as computational neuroscience.[86] The earliest attempts at cybernetics were somewhat crude in that they treated the brain as essentially a digital computer in disguise, as for example in John von Neumann’s 1958 book, The Computer and the Brain.[87] Over the years, though, accumulating information about the electrical responses of brain cells recorded from behaving animals has steadily moved theoretical concepts in the direction of increasing realism.[86]

The essence of the information processing approach is to try to understand brain function in terms of information flow and implementation of algorithms.[86] One of the most influential early contributions was a 1959 paper titled What the frog’s eye tells the frog’s brain: the paper examined the visual responses of neurons in the retina and optic tectum of frogs, and came to the conclusion that some neurons in the tectum of the frog are wired to combine elementary responses in a way that makes them function as “bug perceivers”.[88] A few years later David Hubel and Torsten Wiesel discovered cells in the primary visual cortex of monkeys that become active when sharp edges move across specific points in the field of viewa discovery for which they won a Nobel Prize.[89] Follow-up studies in higher-order visual areas found cells that detect binocular disparity, color, movement, and aspects of shape, with areas located at increasing distances from the primary visual cortex showing increasingly complex responses.[90] Other investigations of brain areas unrelated to vision have revealed cells with a wide variety of response correlates, some related to memory, some to abstract types of cognition such as space.[91]

Theorists have worked to understand these response patterns by constructing mathematical models of neurons and neural networks, which can be simulated using computers.[86] Some useful models are abstract, focusing on the conceptual structure of neural algorithms rather than the details of how they are implemented in the brain; other models attempt to incorporate data about the biophysical properties of real neurons.[92] No model on any level is yet considered to be a fully valid description of brain function, though. The essential difficulty is that sophisticated computation by neural networks requires distributed processing in which hundreds or thousands of neurons work cooperativelycurrent methods of brain activity recording are only capable of isolating action potentials from a few dozen neurons at a time.[93]

Furthermore, even single neurons appear to be complex and capable of performing computations.[94] So, brain models that don’t reflect this are too abstract to be representative of brain operation; models that do try to capture this are very computationally expensive and arguably intractable with present computational resources. However, having said this, the Human Brain Project is trying to build a realistic, detailed computational model of the entire human brain. It remains to be seen what level of success they can achieve in the time frame of the project and the wisdom of it has been publicly contested, with high-profile scientists on both sides of the argument.

One of the primary functions of a brain is to extract biologically relevant information from sensory inputs. The human brain is provided with information about light, sound, the chemical composition of the atmosphere, temperature, head orientation, limb position, the chemical composition of the bloodstream, and more. In other animals additional senses may be present, such as the infrared heat-sense of snakes, the magnetic field sense of some birds, or the electric field sense of some types of fish. Moreover, other animals may develop existing sensory systems in new ways, such as the adaptation by bats of the auditory sense into a form of sonar. One way or another, all of these sensory modalities are initially detected by specialized sensors that project signals into the brain.[8]

Each sensory system begins with specialized receptor cells, such as light-receptive neurons in the retina of the eye, vibration-sensitive neurons in the cochlea of the ear, or pressure-sensitive neurons in the skin. The axons of sensory receptor cells travel into the spinal cord or brain, where they transmit their signals to a first-order sensory nucleus dedicated to one specific sensory modality. This primary sensory nucleus sends information to higher-order sensory areas that are dedicated to the same modality. Eventually, via a way-station in the thalamus, the signals are sent to the cerebral cortex, where they are processed to extract biologically relevant features, and integrated with signals coming from other sensory systems.[8]

Motor systems are areas of the brain that are directly or indirectly involved in producing body movements, that is, in activating muscles. Except for the muscles that control the eye, which are driven by nuclei in the midbrain, all the voluntary muscles in the body are directly innervated by motor neurons in the spinal cord and hindbrain.[8] Spinal motor neurons are controlled both by neural circuits intrinsic to the spinal cord, and by inputs that descend from the brain. The intrinsic spinal circuits implement many reflex responses, and contain pattern generators for rhythmic movements such as walking or swimming. The descending connections from the brain allow for more sophisticated control.[8]

The brain contains several motor areas that project directly to the spinal cord. At the lowest level are motor areas in the medulla and pons, which control stereotyped movements such as walking, breathing, or swallowing. At a higher level are areas in the midbrain, such as the red nucleus, which is responsible for coordinating movements of the arms and legs. At a higher level yet is the primary motor cortex, a strip of tissue located at the posterior edge of the frontal lobe. The primary motor cortex sends projections to the subcortical motor areas, but also sends a massive projection directly to the spinal cord, through the pyramidal tract. This direct corticospinal projection allows for precise voluntary control of the fine details of movements. Other motor-related brain areas exert secondary effects by projecting to the primary motor areas. Among the most important secondary areas are the premotor cortex, basal ganglia, and cerebellum.[8]

In addition to all of the above, the brain and spinal cord contain extensive circuitry to control the autonomic nervous system, which works by secreting hormones and by modulating the “smooth” muscles of the gut.[8] The autonomic nervous system affects heart rate, digestion, respiration rate, salivation, perspiration, urination, and sexual arousal, and several other processes. Most of its functions are not under direct voluntary control.

Perhaps the most obvious aspect of the behavior of any animal is the daily cycle between sleeping and waking. Arousal and alertness are also modulated on a finer time scale, though, by an extensive network of brain areas.[8]

A key component of the arousal system is the suprachiasmatic nucleus (SCN), a tiny part of the hypothalamus located directly above the point at which the optic nerves from the two eyes cross. The SCN contains the body’s central biological clock. Neurons there show activity levels that rise and fall with a period of about 24 hours, circadian rhythms: these activity fluctuations are driven by rhythmic changes in expression of a set of “clock genes”. The SCN continues to keep time even if it is excised from the brain and placed in a dish of warm nutrient solution, but it ordinarily receives input from the optic nerves, through the retinohypothalamic tract (RHT), that allows daily light-dark cycles to calibrate the clock.[100]

The SCN projects to a set of areas in the hypothalamus, brainstem, and midbrain that are involved in implementing sleep-wake cycles. An important component of the system is the reticular formation, a group of neuron-clusters scattered diffusely through the core of the lower brain. Reticular neurons send signals to the thalamus, which in turn sends activity-level-controlling signals to every part of the cortex. Damage to the reticular formation can produce a permanent state of coma.[8]

Sleep involves great changes in brain activity.[8] Until the 1950s it was generally believed that the brain essentially shuts off during sleep,[101] but this is now known to be far from true; activity continues, but patterns become very different. There are two types of sleep: REM sleep (with dreaming) and NREM (non-REM, usually without dreaming) sleep, which repeat in slightly varying patterns throughout a sleep episode. Three broad types of distinct brain activity patterns can be measured: REM, light NREM and deep NREM. During deep NREM sleep, also called slow wave sleep, activity in the cortex takes the form of large synchronized waves, whereas in the waking state it is noisy and desynchronized. Levels of the neurotransmitters norepinephrine and serotonin drop during slow wave sleep, and fall almost to zero during REM sleep; levels of acetylcholine show the reverse pattern.[8]

For any animal, survival requires maintaining a variety of parameters of bodily state within a limited range of variation: these include temperature, water content, salt concentration in the bloodstream, blood glucose levels, blood oxygen level, and others.[102] The ability of an animal to regulate the internal environment of its bodythe milieu intrieur, as pioneering physiologist Claude Bernard called itis known as homeostasis (Greek for “standing still”).[103] Maintaining homeostasis is a crucial function of the brain. The basic principle that underlies homeostasis is negative feedback: any time a parameter diverges from its set-point, sensors generate an error signal that evokes a response that causes the parameter to shift back toward its optimum value.[102] (This principle is widely used in engineering, for example in the control of temperature using a thermostat.)

In vertebrates, the part of the brain that plays the greatest role is the hypothalamus, a small region at the base of the forebrain whose size does not reflect its complexity or the importance of its function.[102] The hypothalamus is a collection of small nuclei, most of which are involved in basic biological functions. Some of these functions relate to arousal or to social interactions such as sexuality, aggression, or maternal behaviors; but many of them relate to homeostasis. Several hypothalamic nuclei receive input from sensors located in the lining of blood vessels, conveying information about temperature, sodium level, glucose level, blood oxygen level, and other parameters. These hypothalamic nuclei send output signals to motor areas that can generate actions to rectify deficiencies. Some of the outputs also go to the pituitary gland, a tiny gland attached to the brain directly underneath the hypothalamus. The pituitary gland secretes hormones into the bloodstream, where they circulate throughout the body and induce changes in cellular activity.[104]

According to evolutionary theory, individuals are genetically programmed to behave in ways that ensure survival and reproductive success. This overarching goal of genetic fitness translates into a set of specific survival-promoting behaviors, such as seeking food, water, shelter, and a mate.[105] The motivational system in the brain monitors the current state of satisfaction of these goals, and activates behaviors to meet any needs that arise. The motivational system works largely by a rewardpunishment mechanism. When a particular behavior is followed by favorable consequences, the reward mechanism in the brain is activated, which induces structural changes inside the brain that cause the same behavior to be repeated later, whenever a similar situation arises. Conversely, when a behavior is followed by unfavorable consequences, the brain’s punishment mechanism is activated, inducing structural changes that cause the behavior to be suppressed when similar situations arise in the future.[106]

Most organisms studied to date utilize a rewardpunishment mechanism: for instance, worms and insects can alter their behavior to seek food sources or to avoid dangers.[107] In vertebrates, the reward-punishment system is implemented by a specific set of brain structures, at the heart of which lie the basal ganglia, a set of interconnected areas at the base of the forebrain.[48] There is substantial evidence that the basal ganglia are the central site at which decisions are made: the basal ganglia exert a sustained inhibitory control over most of the motor systems in the brain; when this inhibition is released, a motor system is permitted to execute the action it is programmed to carry out. Rewards and punishments function by altering the relationship between the inputs that the basal ganglia receive and the decision-signals that are emitted. The reward mechanism is better understood than the punishment mechanism, because its role in drug abuse has caused it to be studied very intensively. Research has shown that the neurotransmitter dopamine plays a central role: addictive drugs such as cocaine, amphetamine, and nicotine either cause dopamine levels to rise or cause the effects of dopamine inside the brain to be enhanced.[108]

Almost all animals are capable of modifying their behavior as a result of experienceeven the most primitive types of worms. Because behavior is driven by brain activity, changes in behavior must somehow correspond to changes inside the brain. Theorists dating back to Santiago Ramn y Cajal argued that the most plausible explanation is that learning and memory are expressed as changes in the synaptic connections between neurons.[109] Until 1970, however, experimental evidence to support the synaptic plasticity hypothesis was lacking. In 1971 Tim Bliss and Terje Lmo published a paper on a phenomenon now called long-term potentiation: the paper showed clear evidence of activity-induced synaptic changes that lasted for at least several days.[110] Since then technical advances have made these sorts of experiments much easier to carry out, and thousands of studies have been made that have clarified the mechanism of synaptic change, and uncovered other types of activity-driven synaptic change in a variety of brain areas, including the cerebral cortex, hippocampus, basal ganglia, and cerebellum.[111] Brain-derived neurotrophic factor (BDNF) and physical activity appear to play a beneficial role in the process.[112]

Neuroscientists currently distinguish several types of learning and memory that are implemented by the brain in distinct ways:

The field of neuroscience encompasses all approaches that seek to understand the brain and the rest of the nervous system.[8]Psychology seeks to understand mind and behavior, and neurology is the medical discipline that diagnoses and treats diseases of the nervous system. The brain is also the most important organ studied in psychiatry, the branch of medicine that works to study, prevent, and treat mental disorders.[118]Cognitive science seeks to unify neuroscience and psychology with other fields that concern themselves with the brain, such as computer science (artificial intelligence and similar fields) and philosophy.[119]

The oldest method of studying the brain is anatomical, and until the middle of the 20th century, much of the progress in neuroscience came from the development of better cell stains and better microscopes. Neuroanatomists study the large-scale structure of the brain as well as the microscopic structure of neurons and their components, especially synapses. Among other tools, they employ a plethora of stains that reveal neural structure, chemistry, and connectivity. In recent years, the development of immunostaining techniques has allowed investigation of neurons that express specific sets of genes. Also, functional neuroanatomy uses medical imaging techniques to correlate variations in human brain structure with differences in cognition or behavior.[120]

Neurophysiologists study the chemical, pharmacological, and electrical properties of the brain: their primary tools are drugs and recording devices. Thousands of experimentally developed drugs affect the nervous system, some in highly specific ways. Recordings of brain activity can be made using electrodes, either glued to the scalp as in EEG studies, or implanted inside the brains of animals for extracellular recordings, which can detect action potentials generated by individual neurons.[121] Because the brain does not contain pain receptors, it is possible using these techniques to record brain activity from animals that are awake and behaving without causing distress. The same techniques have occasionally been used to study brain activity in human patients suffering from intractable epilepsy, in cases where there was a medical necessity to implant electrodes to localize the brain area responsible for epileptic seizures.[122]Functional imaging techniques such as functional magnetic resonance imaging are also used to study brain activity; these techniques have mainly been used with human subjects, because they require a conscious subject to remain motionless for long periods of time, but they have the great advantage of being noninvasive.[123]

Another approach to brain function is to examine the consequences of damage to specific brain areas. Even though it is protected by the skull and meninges, surrounded by cerebrospinal fluid, and isolated from the bloodstream by the bloodbrain barrier, the delicate nature of the brain makes it vulnerable to numerous diseases and several types of damage. In humans, the effects of strokes and other types of brain damage have been a key source of information about brain function. Because there is no ability to experimentally control the nature of the damage, however, this information is often difficult to interpret. In animal studies, most commonly involving rats, it is possible to use electrodes or locally injected chemicals to produce precise patterns of damage and then examine the consequences for behavior.[125]

Computational neuroscience encompasses two approaches: first, the use of computers to study the brain; second, the study of how brains perform computation. On one hand, it is possible to write a computer program to simulate the operation of a group of neurons by making use of systems of equations that describe their electrochemical activity; such simulations are known as biologically realistic neural networks. On the other hand, it is possible to study algorithms for neural computation by simulating, or mathematically analyzing, the operations of simplified “units” that have some of the properties of neurons but abstract out much of their biological complexity. The computational functions of the brain are studied both by computer scientists and neuroscientists.[126]

Computational neurogenetic modeling is concerned with the study and development of dynamic neuronal models for modeling brain functions with respect to genes and dynamic interactions between genes.

Recent years have seen increasing applications of genetic and genomic techniques to the study of the brain [127] and a focus on the roles of neurotrophic factors and physical activity in neuroplasticity.[112] The most common subjects are mice, because of the availability of technical tools. It is now possible with relative ease to “knock out” or mutate a wide variety of genes, and then examine the effects on brain function. More sophisticated approaches are also being used: for example, using Cre-Lox recombination it is possible to activate or deactivate genes in specific parts of the brain, at specific times.[127]

The oldest brain to have been discovered was in Armenia in the Areni-1 cave complex. The brain, estimated to be over 5,000 years old, was found in the skull of a 12 to 14-year-old girl. Although the brains were shriveled, they were well preserved due to the climate found inside the cave.[128]

Early philosophers were divided as to whether the seat of the soul lies in the brain or heart. Aristotle favored the heart, and thought that the function of the brain was merely to cool the blood. Democritus, the inventor of the atomic theory of matter, argued for a three-part soul, with intellect in the head, emotion in the heart, and lust near the liver.[129] Hippocrates, the “father of medicine”, came down unequivocally in favor of the brain. In his treatise on epilepsy he wrote:

Men ought to know that from nothing else but the brain come joys, delights, laughter and sports, and sorrows, griefs, despondency, and lamentations. … And by the same organ we become mad and delirious, and fears and terrors assail us, some by night, and some by day, and dreams and untimely wanderings, and cares that are not suitable, and ignorance of present circumstances, desuetude, and unskillfulness. All these things we endure from the brain, when it is not healthy…

The Roman physician Galen also argued for the importance of the brain, and theorized in some depth about how it might work. Galen traced out the anatomical relationships among brain, nerves, and muscles, demonstrating that all muscles in the body are connected to the brain through a branching network of nerves. He postulated that nerves activate muscles mechanically by carrying a mysterious substance he called pneumata psychikon, usually translated as “animal spirits”.[129] Galen’s ideas were widely known during the Middle Ages, but not much further progress came until the Renaissance, when detailed anatomical study resumed, combined with the theoretical speculations of Ren Descartes and those who followed him. Descartes, like Galen, thought of the nervous system in hydraulic terms. He believed that the highest cognitive functions are carried out by a non-physical res cogitans, but that the majority of behaviors of humans, and all behaviors of animals, could be explained mechanistically.[131]

The first real progress toward a modern understanding of nervous function, though, came from the investigations of Luigi Galvani, who discovered that a shock of static electricity applied to an exposed nerve of a dead frog could cause its leg to contract. Since that time, each major advance in understanding has followed more or less directly from the development of a new technique of investigation. Until the early years of the 20th century, the most important advances were derived from new methods for staining cells.[132] Particularly critical was the invention of the Golgi stain, which (when correctly used) stains only a small fraction of neurons, but stains them in their entirety, including cell body, dendrites, and axon. Without such a stain, brain tissue under a microscope appears as an impenetrable tangle of protoplasmic fibers, in which it is impossible to determine any structure. In the hands of Camillo Golgi, and especially of the Spanish neuroanatomist Santiago Ramn y Cajal, the new stain revealed hundreds of distinct types of neurons, each with its own unique dendritic structure and pattern of connectivity.[133]

In the first half of the 20th century, advances in electronics enabled investigation of the electrical properties of nerve cells, culminating in work by Alan Hodgkin, Andrew Huxley, and others on the biophysics of the action potential, and the work of Bernard Katz and others on the electrochemistry of the synapse.[134] These studies complemented the anatomical picture with a conception of the brain as a dynamic entity. Reflecting the new understanding, in 1942 Charles Sherrington visualized the workings of the brain waking from sleep:

The great topmost sheet of the mass, that where hardly a light had twinkled or moved, becomes now a sparkling field of rhythmic flashing points with trains of traveling sparks hurrying hither and thither. The brain is waking and with it the mind is returning. It is as if the Milky Way entered upon some cosmic dance. Swiftly the head mass becomes an enchanted loom where millions of flashing shuttles weave a dissolving pattern, always a meaningful pattern though never an abiding one; a shifting harmony of subpatterns.

In the second half of the 20th century, developments in chemistry, electron microscopy, genetics, computer science, functional brain imaging, and other fields progressively opened new windows into brain structure and function. In the United States, the 1990s were officially designated as the “Decade of the Brain” to commemorate advances made in brain research, and to promote funding for such research.[136]

In the 21st century, these trends have continued, and several new approaches have come into prominence, including multielectrode recording, which allows the activity of many brain cells to be recorded all at the same time;[137]genetic engineering, which allows molecular components of the brain to be altered experimentally;[127]genomics, which allows variations in brain structure to be correlated with variations in DNA properties[138] and neuroimaging.

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Atopic eczema | DermNet New Zealand

Posted: September 14, 2016 at 8:48 am

Home Topics AZ Atopic eczema

Author: Dr Amy Stanway, Department of Dermatology, Waikato Hospital, February 2004.

Atopic eczema is a chronic, itchy skin condition that is very common in children but may occur at any age. It is also known as eczema, atopic dermatitis and neurodermatitis. It is the most common form of dermatitis.

Atopic eczema usually occurs in people who have an ‘atopic tendency’. This means they may develop any or all of three closely linked conditions; atopic eczema, asthma and hay fever (allergic rhinitis). Often these conditions run within families with a parent, child or sibling also affected. A family history of asthma, eczema or hay fever is particularly useful in diagnosing atopic eczema in infants.

Atopic eczema arises because of a complex interaction of genetic and environmental factors. These include defects in skin barrier function making the skin more susceptible to irritation by soap and other contact irritants, the weather, temperature and non-specific triggers: see Causes of atopic eczema.

There is quite a variation in the appearance of atopic eczema between individuals. From time to time, most people have acute flares with inflamed, red, sometimes blistered and weepy patches. In between flares, the skin may appear normal or suffer from chronic eczema with dry, thickened and itchy areas.

The presence of infection or an additional skin condition, the creams applied, the age of the person, their ethnic origin and other factors can alter the way eczema looks and feels.

There are however some general patterns to where the eczema is found on the body according to the age of the affected person.

More images of atopic eczema and flexural dermatitis.

Atopic eczema affects 15-20% of children but is much less common in adults. It is impossible to predict whether eczema will improve by itself or not in an individual. Sensitive skin persists life-long.

It is unusual for an infant to be affected with atopic eczema before the age of four months but they may suffer from infantile seborrhoeic dermatitis or other rashes prior to this. The onset of atopic eczema is usually before two years of age although it can manifest itself in older people for the first time.

Atopic eczema is often worst between the ages of two and four but it generally improves after this and may clear altogether by the teens.

Certain occupations such as farming, hairdressing, domestic and industrial cleaning, domestic duties and care-giving expose the skin to various irritants and, sometimes, allergens. This aggravates atopic eczema. It is wise to bear this in mind when considering career options it is usually easier to choose a more suitable occupation from the outset than to change it later.

Treatment of atopic eczema may be required for many months and possibly years.

It nearly always requires:

In some cases, management may also include one of more of the following:

Longstanding and severe eczema may be treated with an immunosuppressive agent.

Originally posted here:
Atopic eczema | DermNet New Zealand

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Atopic Dermatitis / Eczema – Allergy UK

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Eczema, also known as atopic eczema or atopic dermatitis, is a skin condition causing inflammation and intense irritation. Eczema symptoms tend to be caused by dry skin. The skin becomes hot, itchy and inflamed; it may also be red and appear irritated. Atopy, or being atopic, means having a genetic tendency for your immune system to make increased levels of IgE antibodies to certain allergens. An atopic individual is likely to have more than one allergic condition during their lifetime, such as eczema, asthma, hay fever or food allergy.

In young children, patches of dry, scaly skin, or (less commonly) wet, weepy skin, can appear anywhere on the body. In older children, the eczema usually appears on wrists, ankles, elbows, knees and face, including the eyelids. In adults, it may localise, affecting the face, hands, neck and scalp although it can affect any part of the body.

Skin that is affected by eczema gets sore and broken when it is scratched, it can look wet and may bleed. Scratching is hard to avoid since the main distressing symptom of eczema is unbearable itching but once the skin gets broken and cracked, infections can set in, causing even more discomfort. Those with severe eczema often feel cold when others are hot. This is because the skin is the largest organ of the body and one of its roles is helping to regulate body temperature. Conversely, being hot in bed causes severe irritation.

This skin condition can affect any age range and it is thought to be caused by a defect in the skin barrier that makes it more susceptible to inflammation and allows allergens and bacteria to make contact with the immune system.

Eczema can affect ones quality of life significantly and may also affect sleep patterns. Whilst this can make you irritable and frustrated, good management can help alleviate these problems. This skin condition is well understood and dermatologists (skin doctors) have developed effective skin treatment regimens to control and manage the symptoms. It can take some time to find the most suitable therapy for each individual, often causing embarrassment and daily frustration with the symptoms in the meantime. Many people do not understand that eczema is neither infectious nor contagious.

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Generally, GPs can diagnose eczema and differentiate whether you have eczema or another skin condition. Seasons of the year (for example, in winter), or even emotional responses (such as stress), may cause eczema to worsen. However, a large number of eczema sufferers are not able to link a cause to their symptoms. It is essential that any known triggers are avoided and sometimes keeping a trigger symptom diary at home may help you to realise what might be causing flares. Important things to consider include bubble baths, shampoos, make-up products, chemicals such as cleaning products and occupational irritants such as hairdressing products or heavy oils and lubricants used in the motor industry or allergens, such as latex gloves, leather, cement or certain plants.

If further investigation is needed, or the skins condition is not improving with barrier protection and prescribed treatment, your GP may make a referral to see a dermatologist to pinpoint the exact cause of the condition. Allergy patch tests can identify substances causing contact allergy. Allergy tests (either skin prick testing or a specific IgE blood test) may help to identify airborne or food allergens involved in flares, as many people with atopic dermatitis/eczema may also have asthma, allergic rhinitis/hay fever. Allergens that trigger these may also trigger symptoms in eczema, such as house dust mite, animal dander, mould spores, pollen or foods. You may need to be referred to an allergy clinic for skin prick or specific IgE blood tests.

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No. Children are born with the tendency to have eczema and many things can make their eczema worse. These are known as triggers for the eczema. Foods can be triggers for eczema especially in infants but the foods are not the primary cause of the eczema. If a food is found to make eczema worse, excluding that food may significantly improve symptoms but not cure the condition. A food that is not eaten often but causes symptoms may be easier to identify than one that is eaten daily, such as milk/dairy products, wheat or soya.

Some patients with the IgE-associated variety of AEDS suffer from worsening of their skin symptoms after contact with certain airborne allergens, such as house dust mite, pollens, or animal hairs, and improve after appropriate allergen avoidance strategies are introduced.

Emollient lotions and creams are prescribed for eczema and dry skin, and are, in their simplest form, mixtures of oil and water. Some emollients may also contain slight amounts of antibacterial chemicals (to avoid infection in broken skin), or steroids (to reduce inflammation).

Emollient products range in their consistency, from being runny lotions to thick creams, and while they can be a very cooling and soothing treatment for eczema, the stickiness of the thicker products can sometimes make them a source of annoyance. It is important to find a product that is suitable for you.

Dry skin is more susceptible to eczema, and once the skin barrier is broken, it is open to potential infection and further irritation from allergens and other chemical irritants. Scratching also causes the body to release histamine, which further aggravates the symptoms. Emollients work to reduce eczema symptoms by creating a protective barrier on the top layer of the skin, moisturising it and reducing water loss. The oil also provides lubrication so that the dry skin, which is often itchy and rough, will not be as easily irritated.

Although emollients do not stop the underlying cause of eczema, they calm and soothe the skin, and give it time to repair itself. For emollients to work effectively, they need to be used as part of a regular treatment regimen. This means that they should be applied at set times of day, and should be used whether they appear to be needed or not.

Eczema can flare up at any time, in some instances due to infection, hormonal changes, stress or allergens, but also for no obvious reason. Even when emollients are used, there may be times when eczema seems to get worse. However, regular treatment can help to minimise the number and severity of flare ups.

Emollients should be continued, even when all traces of eczema have vanished. By keeping the skin moisturised, it will be better hydrated and with less chance of the skin barrier being broken, the risk of allergens and other irritants causing eczema is reduced.

Emollients are available as lotions, creams, ointments, shower and bath products and soap substitutes. These products should be used every day as emollients support the skins barrier function by helping it to retain water and form a protective layer against allergens or bacteria. They can also help to relieve the itchy symptoms typical of eczema.

Water can have a drying effect on skin and so emollients are also available as bath products, which help to hydrate and protect the skin while soaking in the water, although it is no longer advised to soak for more than 15 minutes. In addition, soap can also make eczema worse because it dries the skin further. Soap substitute emollients can also be prescribed, which can be rubbed on and rinsed off skin just like liquid soap.

You may find that you are prescribed several creams if your eczema symptoms vary and different creams may be more suitable for different times. For example, you may prefer to use a less oily cream during the day and use a thicker cream or ointment treatment at night. Ointment also have the advantage of needing less or no preservatives, to which a few people can eventually react.

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It is sometimes necessary to apply topical corticosteroids (e.g. hydrocortisone), as these reduce inflammation in the skin.

Many people worry when steroids are mentioned as a treatment option because of stories they may have heard in the media, particularly related to anabolic steroid abuse in sports. These, however, are not the same steroids that are used as medical treatments and, when used as directed by a physician, steroids have an important role to play in treating a range of ailments, including eczema.

Topical steroids are safe to use but it is important to always follow the instructions provided, making sure you understand which areas you apply the cream to and exactly how much. If you have any questions, then ask your doctor or nurse for further advice and information.

Steroid creams only need to be applied to the inflamed areas of skin. One fingertip of cream (where the cream is squeezed along the fingertip as far as the first joint) is usually enough to cover an area of skin twice the size of an adults hand. Fingertip units are used as a guide for the amounts needed for different parts of the body.

Sometimes emollients and other creams (i.e. steroids and antibiotics) are needed in combination. It is important to leave an adequate gap between applying the different creams to allow one cream to be absorbed before applying another, ideally at least 10 minutes. If creams are applied too soon after each other they may be diluted so healing and control of the symptoms can take longer. Steroid creams, when used for a long time at a high dose, can cause skin to be thinned. This will not happen when steroid creams are prescribed at the appropriate strength, with less potent steroids being prescribed on the face than on the body. It is also important to use steroid creams as early into flares as possible, as this will avoid the need for higher strength preparations, required when the eczema is severe. Doctors are also increasingly using steroid creams proactively for only a couple of days a week (weekend therapy), even when the eczema is well controlled, to prevent future flares, as this has been shown to reduce the amount of steroids needed in the long-term.

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Sometimes, special pyjama-like garments (known as wet wraps) that are used for children, may also help certain areas of your body that have not responded to the usual topical application of emollients and steroids. Wet wraps can also be useful if you suffer from itch at night and cannot sleep, allowing you to have a better quality of sleep during times when the eczema is particularly bad. There are various ways of applying these garments and your nurse or doctor will be able to demonstrate the best way of application.

It important to follow the advice of your treating practitioner for the length of time of wet wrap treatment, and it is important to have your skin re-assessed when the treatment comes to an end.

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Calcineurin inhibitors are an alternative to steroid creams. There are two different preparations, Tacrolimus (0.03% and 0.1%) and 1% Pimecrolimus (also known as Protopic and Elidel), licensed for use in children over the age of two. Like steroid creams, they reduce the skin inflammation and can lessen itching.

These creams are suitable for use on almost every part of the body, as they do not thin the skin and are often used when steroids have proved unsuccessful, or are not suitable, for example, on sensitive skin around the eyes. Emollients should continue to be used as well as these creams.

A common side effect of these creams is a short-lived burning sensation on application, which is harmless and generally settles down after a few applications. These drugs are thought to be safe and effective in the short-term but their safety for long-term use has yet to be proven.

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There are many other types of dermatitis/eczema, which are non-atopic, i.e. not triggered by allergens or related to allergy, such as seborrhoeic; pompholyx; irritant contact; gravitational/asteototic; discoid/nummular. Information on these is available from

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Excerpt from:
Atopic Dermatitis / Eczema – Allergy UK

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