How Early To Take Pregnancy Test

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View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..What Are Diabetes Blood Test Strips What Are Diabetes Blood Test Strips :: what are the symptoms of diabetes type 2 - The 3 Step Trick that Reverses Diabetes .TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..Walmart Diabetic Test Strips Treatment Diabetes Alternative Diabetes Treatment Walmart Diabetic Test Strips ::The 3 Step Trick that Reverses Diabetes .What's in a Name? What Every Consumer Should Know About Foods and Flavors; 4 Medication Safety Tips for Older Adults; FDA: Cutting-Edge Technology Sheds Light on .National diabetes education program Diabetic Shoes Covered By Medicare :: national diabetes education program - The 3 Step Trick that Reverses Diabetes .

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TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..What's in a Name? What Every Consumer Should Know About Foods and Flavors; 4 Medication Safety Tips for Older Adults; FDA: Cutting-Edge Technology Sheds Light .National diabetes education program Diabetic Shoes Covered By Medicare :: national diabetes education program - The 3 Step Trick that Reverses Diabetes .What Are Diabetes Blood Test Strips What Are Diabetes Blood Test Strips :: what are the symptoms of diabetes type 2 - The 3 Step Trick that Reverses Diabetes .View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..Walmart Diabetic Test Strips Treatment Diabetes Alternative Diabetes Treatment Walmart Diabetic Test Strips ::The 3 Step Trick that Reverses Diabetes .

NEW HORIZON IN HEART FAILURE INVESTIGATIONAL DRUG POISED TO CHANGE CARDIOLOGY

An investigational new heart failure drug could be poised to change the face of cardiology based on Hot Line results presented today at ESC Congress 2014

Findings from the PARADIGM-HF trial, published simultaneously in the New England Journal of Medicine, "are extraordinarily powerful and compelling; they are destined to change the management of patients with chronic heart failure for years to come," said Milton Packer, MD, co-primary author of the study from University of Texas Southwestern Medical Center, in Dallas, Texas USA.

"This really is an astonishing result and a real breakthrough for patients with heart failure," added John McMurray, MD, the other co-primary author, from the University of Glasgow, UK.

The new agent, an angiotensin receptor-neprilysin inhibitor (ARNI) known as LCZ696, has already been granted Fast Track status by the United States Food and Drug Administration (FDA) -- a designation which can expedite the review of new medicines intended to treat serious or life-threatening conditions. Fast Track designation also allows for rolling submission in the US, which Novartis said it expects to complete by the end of 2014. The company said it aims to file in Europe in early 2015.

"To say that we are excited is an understatement. We are absolutely thrilled," said Dr. Packer.

"Given the survival advantage of LCZ696 over currently available drugs, once this drug becomes available, it would be difficult to understand why physicians would continue to use traditional angiotensin converting-enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) for the treatment of heart failure."

PARADIGM-HF (Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure) first made headlines this spring when the trial was stopped early by an independent data monitoring committee based on evidence of the "overwhelming benefit" of LCZ696 compared to enalapril, an ACE inhibitor.

"We were surprised and delighted that the magnitude of the superiority was so great that the trial was stopped early by the ethical committee. That was an amazing event," said Dr. Packer.

Today, full details of the findings are being released for the first time.

"The magnitude of the advantage of LCZ696 over enalapril on cardiovascular mortality was at least as large as that of enalapril over placebo during long-term treatment," Dr. Packer reported. "This robust finding provides strong support for using this new approach instead of ACE inhibitors or ARBs in the treatment of chronic heart failure."

PARADIGM-HF randomized 8,399 patients with class II to IV heart failure and an ejection fraction if 40% or less to either LCZ696 200 mg twice daily (n=4,187), or enalapril 10 mg twice daily (n=4,212), in addition to recommended therapy.

When the trial was stopped early, after a median follow-up of 27 months, death from cardiovascular causes or hospitalisation for heart failure (the primary composite outcome) had occurred in 21.8% of the LCZ696 group and 26.5% of the enalapril group (hazard ratio [HR] 0.80; p=0.0000002).

Compared to enalapril, LCZ696 reduced the risk of death from cardiovascular causes by 20% (13.3% vs 16.5%; HR 0.80; p<0.0001), and the risk of hospitalisation for heart failure by 21% (12.8% vs 15.6%; HR 0.79; p<0.0001), noted Dr. Packer. This effect was consistent across all prespecified subgroups.

Secondary outcomes were also significantly improved by LCZ696, including all-cause mortality (17.0% vs 19.8%; HR 0.84; p<0.001) and symptoms and physical limitations of heart failure measured on the Kansas City Cardiomyopathy Questionnaire (p=0.001).

"The superiority of LCZ696 over enalapril was not accompanied by important safety concerns," added Dr. Packer. The LCZ696 group had more symptomatic hypotension compared to the enalapril group (14% vs 9.2%, p< 0.001) however this rarely required the discontinuation of treatment. In fact, fewer patients in the LCZ696 group stopped their study medication for any adverse event (10.7% vs 12.3%, P=0.03).

Importantly, LCZ696 was not associated with an increased risk of serious angioedema, which was the main safety concern observed with a related medication -- omapatrilat -- in the OVERTURE trial.

Omapatrilat's association with life-threatening angioedema is related to its inhibition of ACE, neprilysin and aminopeptidase P, whereas LCZ696 avoids inhibition of ACE and aminopeptidase P. "LCZ696 was specifically designed to minimise the risk of serious angioedema by combining the neprilysin inhibitor sacubitril (AHU377) and the ARB valsartan," explained Dr. Packer.

Findings of the PARADIGM-HF trial are particularly striking when considered in the context of the current standard of care in heart failure, concluded Professor McMurray.

"The superiority of LCZ696 wasn't over placebo -- it was over the gold-standard dose of the gold-standard ACE inhibitor, the absolute corner-stone of guideline-recommended, conventional therapy," he said. "On top of that, these incremental benefits were obtained in patients fully treated with the other key pharmacological therapies for this condition such as beta-blockers and mineralocorticoid receptor antagonists. All that you can ask of any new therapy in heart failure (or other chronic diseases) is to make patients live longer, stay out of hospital and feel better -- and those are exactly the benefits we demonstrated with LCZ696."

How the nerve is damaged

This description is something I can understand:-

Myelin Layer

The myelin layer is a white fatty and protein covering that insulates and protects a nerve fiber. The concept of myelin can be thought of as similar to the insulating coatings that typically surround electrical wiring. Just like insulators are needed to protect electrical wires, myelin is needed to protect our nerve fibers which incidentally, conduct electrical current also.

Myelin is made up of roughly about 80% fat, and about 20% protein. In addition to protecting our nerves, having a myelin covering or sheath allows nerve signals to be transported much quicker and more effectively. When the myelin sheath is damaged, impulses do not get transmitted through the nerve as quickly as it should. In addition, much like a damaged insulator covering can result in frayed wiring, a compromised myelin sheath can result in the underlying nerves becoming damaged as well. Neuropathy symptoms are often the result of this damage.

Originally from www.LivingWithPeripheralNeuropathy.com

Unconfusing the Comfreys

Thanks to Susun Weed for elaborating on this troublesome mix up in this issue of the
Wise Woman's Ezine.

Are There Non Opioid Alternatives For Nerve Pain

Today's post from medscape.com (see link below) is an important one because it highlights the dilemmas facing doctors and patients alike when it comes to medicating severe neuropathic pain. The situation at the moment is clear: there is a global (but mainly North American) outcry at the use and abuse of opioid-strength medications and this has triggered a frantic search amongst the scientific community for non-opioid medications that are both strong and effective enough to combat nerve pain at its worst. This article is directed at trainee doctors and nurses and examines the problem in a sensible and well-balanced way and for that reason it's very interesting for neuropathic patients who have no option at the moment but to use the only means available for suppressing their pain and that is the opioid family of medications. It may seem a little technical but it will provide you with so much information about the thinking behind nerve pain drug prescription.

Non-Narcotic Options for Pain Relief with Chronic Neuropathic Conditions
Donna V. Wright, MS, RN, FNP
Journal for Nurse Practitioners. 2008;4(4):263-270.

Neuropathic pain is a misunderstood, usually inadequately treated condition. This article discusses the types of pain, mechanisms of pain, diagnosis, and rationale for treating neuropathic pain. The importance of working with patients to achieve their functioning goals is also addressed.

Tom Jacobson, a bail bondsman, is not getting adequate pain relief from hydrocodone/acetaminophen 10/500 (Lortab) four times a day. He is suffering from chronic low back pain with peripheral neuropathy secondary to a motor vehicle accident. He knows that his back pain is a long-term condition (with chronic pain, the recommended daily dose of acetaminophen is 2000 mg to minimize the risk of liver damage; therefore, increasing his daily doses is not an option). He has tried the generic equivalent with less acetaminophen and with less than satisfactory results. He does not want to take the next step up the pain ladder to oxycodone/acetaminophen (Percocet) at this time. He knows that in South Carolina, by changing his prescription to a schedule II medication, he will be required to obtain a new prescription monthly and that his nurse practitioner can no longer prescribe independently of her physician preceptor (in 29 states, prescription of scheduled drugs requires physician collaboration.)[1] This increase in required medical supervision and possible change of caregiver can be a deterrent for some patients. The most important consideration for Tom is the nature of his work. He does not believe that he can function effectively in his role unless he feels "totally in control." The nature of narcotic medications makes this a concern.

To better understand some of the mechanisms of neuropathic pain, a review of the types of pain, the mechanisms, the diagnosis, and the treatment of neuropathic pain is in order. Cadden describes three types of pain: acute, chronic, and acute on chronic.[2] Tom is experiencing chronic pain, which simplifies his care. When chronic pain sufferers have acute pain as well as chronic pain, they are at risk for undertreatment of pain. Table 1 reviews terms used to describe pain. There are basically three ways to treat pain: alter the central pain perception (inhibit mechanisms of pain perception in the dorsal horn of the spinal cord"'how most narcotics work), modify the pain source, and block transmission of pain impulses by modulating the transmission of the pain impulse.[2] The last mechanism is the area in which we will focus.

"Chronic neuropathic pain is the net result of sensory input greater than the central inhibitory response" the uniqueness of chronic neuropathic pain is that its multiple etiologies share a common pathway."[5] The pain signal is processed via the dorsal horn of the spinal cord and transmitted in the central nervous system (CNS). After an injury, the healing process may be altered and actually increase rather than decrease the pain response. The development of dendritic growth (neuroplasticity) can increase the number of alternate neural pathways, which may actually increase the sensitivity to pain. These alternate pathways may have an accumulation of Na+ channels that become "leaky" and fire spontaneously or with very little provocation. "Neurons fire, or spontaneously produce electrical impulses on a regular basis" they may fire more or less slowly depending on whether or not they are excited or inhibited from firing by various types of chemicals called neurotransmitters" naturally occurring chemicals i.e. substance P, glutamate and aspartate excite neurons responsible for pain transmission" drugs that block the action of these substances diminish our awareness of pain. Our body's narcotic chemicals in the brain and the spinal cord inhibit the transmission of pain impulses."[6] By decreasing the rate of impulse firing, these chemicals can help modulate the pain response. The chemicals or neurotransmitters involved are commonly affected by anticonvulsants, antidepressants, neuroleptics, and antiarrythmics (ie, betabockers, sodium channel blockers, acetycholinesterase inhibitors) ( Table 2 , Table 3 ). This very simplified explanation helps provide rationale for the diagnostic criteria and the management of neuropathic pain.

The initial goals for diagnosis according to Gilron[8] include: rule out treatable conditions (ie, a neoplasm), confirm the diagnosis of neuropathic pain, and identify the clinical features (ie, insomnia) that help individualize treatment. Neuropathic pain is most frequently diagnosed by history and examination. A common presentation would be a level of pain intensity that is disproportionate to the injury received. There may be a history of sensory disturbance (numbness, abnormal sensations, itching, burning, pricking) that worsens as the day progresses. This pain pattern may initially follow a dermatonal distribution but can begin to deviate as neuronal plastic changes advance. The development of new "leaky" neural pathways (neuroplasticity) after an injury can set the stage for development of chronic burning or electric (tingling, shocking, jolting) sensations. These overly sensitive pathways can become "exquisitely painful" or sensitive to sensations that are normally not considered painful (allodynia). Other manifestations of neuropathic pain are dysesthesia, altered or abnormal sensations, paresthesias, or hyperalgias. These pains can occur spontaneously due to regrowth connections to sympathetic nerve fibers or can be evoked. It may become difficult for the sufferer to perform his or her usual daily activities.

It is important to determine which medications or treatments have been attempted. Acetaminophen and nonsteroidal antiinflammatories (NSAIDs) are usually not effective. Concurrent alcohol or substance use and abuse issues can complicate treatment. This delayed symptomology combined with a tendency for the pain path to follow a dermatonal distribution meet the diagnositic criteria for neuropathic pain.[9]

On physical examination, disturbances in light touch, response to pin pricks, vibration, and proprioception may be noted. Sensory disturbances may be beyond the discrete nerve territory. There may be pain with a straight-leg raise exam, which suggests irritation of a lumbar root; Phalen's test or Tinell's sign may be positive (usually indicates carpal tunnel). Deep tendon reflexes may be abnormal. A skin examination may show temperature, color, and hair growth changes, along with abnormal sweating.[8] Stimulus-evoked hypersensitivities may be present and can occur in areas that have loss of sensation. "The symptoms most associated with neuropathic pain were dysesthesias, evoked pain, paroxysmal pain, thermal pain, autonomic complaints, and descriptions of the pain as being sharp, hot or cold, with high sensitivity."[10] It is common for there to be a relatively modest demonstration of clinical neurological deficits or an essentially normal examination.[10]

Confirmatory diagnostics include computed tomography (CT) scans and magnetic resonance images (MRIs) that may show compromised nerve root pathways and structural damage; electromyography and nerve conduction studies, which can show the extent of neuroplastic changes; quantitative sensory testing (QST "' measures sensory thresholds for pain, touch, vibration, and temperature); and three-phase nuclear medicine bone scans that may help diagnose complex regional pain syndrome (CRPS).[10] During the diagnostic phase, a physiatrist (a physician who specializes in physical and rehabilitation medicine) can be an invaluable ally who can perform and interpret many of these examinations as well as suggest other diagnostic tests that might be appropriate.

Once the diagnosis has been confirmed, the practitioner may want to consider using conservative nonpharmacologic treatment options. These options can be crucial if the patient has a history of alcohol and/or substance abuse. Consider the physical conditions and activities that may increase pain. Watch the patient walk, move, and transfer. Large wallets, improper shoes (especially heels and boots), inappropriate canes and walkers, and gaits that favor one leg or another can increase neuropathic pain. Also, evaluate physical activities that may be exacerbating pain. Riding lawnmowers, all-terrain vehicles, and post-hole diggers are among the common culprits.

Physical therapy may be an appropriate referral for gait training; to determine the need for assistive devices; to determine whether use of a TENS (transcutaneous electrical nerve stimulation) unit would be appropriate; to initiate the use of massage, therapeutic exercises, cold, heat, hydrotherapy, electrical stimulation, or light therapy; to improve the general physical condition and reduce stress levels;[9] or to assist with the development of a set of guidelines for patient activity. A physiatrist may not only be able to assist in confirming the diagnosis but also in performing nerve blocks (injection of an anesthetic to "deaden" a specific nerve pathway), facet injections (use of a corticosteroid to decrease inflammation around a nerve root), and in recommending appropriate physiologic therapies.

The other specialists that you may wish to consult include a pain clinic referral[9] (a facility supervised by a physician, usually an anesthesiologist, who specializes in pain management) for nerve blocks and other injections; a chiropractor[9] (a practitioner who uses spinal manipulation to treat disorders of the nervous system); or a homeopath[9] (a practitioner who uses a system of therapeutics based on the theory that "like cures like"). Due to the emotional impact of chronic pain, a referral to a behavioral therapist may be appropriate. This therapist may suggest various therapies to improve the patient's coping level, reduce stress, and raise the pain threshold, which include relaxation, biofeedback, distraction, or attendance at a support group.[9] "Early referrals for nerve blocks and injections can promote the effectiveness of physiotherapy and pain rehabilitation."[8] While you hate to discourage activity with chronic pain, management of pain requires that the patient achieve a balance between activity and rest.

What pharmacologic options are available for the nurse practitioner who wants to help his or her patients maintain their functional levels? "Pharmacologic interventions follow the guidelines of the three-step analgesic ladder for pain control as developed by the World Health Organization (WHO). Step 1: Mild pain is usually treated with aspirin, acetaminophen, or nonsteroidal antiinflammatories (NSAIDs).[11] This is usually not an appropriate treatment level for neuropathic pain. Step 2: "Step 2 of the WHO three-step ladder includes mild opiates" along with the adjuvant medications."[9] In this instance, the nurse practitioner may be delaying or minimizing the use of stronger opiods (i.e. morphine) which are reserved for moderate-to-severe pain (Step 3 of the WHO ladder). This combination can decrease the incidence of side effects and increase the functional level of patients. Which medication is best? Table 4 suggests options. However, the bottom line is "how functional is your patient with this medication?" Current guidance is that for neuropathic pain, "tricyclic antidepressants are the initial drugs of choice" .amitryptyline, nortriptyline, imipramine, or desipramine." "Second line medications are anticonvulsants that include phenytoin, carbamazepine, and valproic acid" . (they) are especially helpful in cases of neuralgia and paresthesia."[15] Atypical anticonvulsants have had a role in neuropathic pain treatment, ie, gabapentin (Neurontin). The Food and Drug Administration (FDA) also has recommendations based on research.

Antidepressants should be used with caution in patients whose psychiatric history is unknown. A patient with an undiagnosed bipolar disorder can be placed in a hypomanic state or in a state of rapid cycling subsequent to initiation of an antidepressant.[15] Tricyclic antidepressants, ie, amitriptyline (Elavil) have been used as an adjunctive in treatment of neurogenic pain. They are believed to inhibit reuptake of serotonin and norepinephrine. Amitriptyline has multiple drug effects and antiarrythmic effects. Dosing this medication at bedtime can help reduce the impact of sedation. It is a pregnancy category D.[15] It is investigational for adjunctive analgesia with phantom limb pain, migraine, diabetic peripheral neuropathy, peripheral neuropathy pain, and post herpetic neuralgia.[14] Doxepin (Sinequan) works similarly to amitriptyline but with more sedation. Its pregnancy category is NR.[15] Nortriptyline can be used for chronic severe neurogenic pain.[14] Desipramine is investigational for severe neuropathic pain.[14] Imipramine has been used for severe neuropathic pain but has a seizure risk with high therapeutic dosages.[14]

Other antidepressants used for pain control include venlafaxine (Effexor), which potentiates neurotransmitter activity in the CNS, especially serotonin and norepinephrine with weak potentiation of dopamine. This medication should not be discontinued abruptly. It is a pregnancy category C.[15] Duloxetine (Cymbalta) works similarly to venlafaxine. It was the first medication to have FDA approval for diabetic peripheral neuropathy. With duloxetine, you must use caution with severe renal and hepatic disease. It is a pregnancy category C (Lilly insert). With any medication that increases serotonin levels, be aware of the risk of serotonin syndrome. This is especially true when "triptans" (medications used to prevent migraines) and SSRIs (selective serotonin reuptake inhibitors) are used together.[13]

Anticonvulsants have been considered second line for neuropathic pain. One of the most commonly used drugs is gabapentin (Neurontin). It is believed to be a competitive and reversible inhibitor of acetycholinesterase, which decreases the available acetycholine for nerve impulse transmission. The dosage needs to be reduced if the patient has altered renal function. It is a pregnancy category C.[15] It is considered an investigation drug for neuropathic pain and prevention of migraines. It has been approved for treatment of post herpetic neuralgia (PHN). It can be dosed up to 1800 mg/day in three divided doses.[14] Pregabalin (Lyrica) has obtained FDA indications for post herpetic neuralgia, diabetic peripheral neuropathy, and primary fibromyalgia syndrome. It is believed to be a GABA analog that reduces calcium dependent release of several neurotransmitters. The dosing for pregabalin is more linear than that of gabapentin (Pfizer insert).[13]

Another anticonvulsant, carbamazepine (Tegretol) is commonly used for trigeminal neuralgia and restless leg syndrome. It reduces the post tetanic potentiation of synaptic transmissions (it possibly depresses activity in the nucleus ventralis anterior of thalamus, thus decreasing polysynaptic responses).[14] This medication is well known for its multiple drug interactions, especially with warfarin, tricyclic antidepressants, and monamine oxidase inhibitors. It is a pregnancy category D.[15] Valproic acid (Depakene) acts by increasing levels of GABA, an inhibitory transmitter. It may also improve membrane stability by affecting the potassium channel. It has been used for prophylaxis of migraine headache.[14] Concerns include decreased hepatic function, multiple drug interactions, and that it is pregnancy category D.[15] Phenytoin (Dilantin) has also been indicated for neuretic pain"'migraine, trigeminial neuralgia, Bell's palsy. This medication acts by stabilizing neuronal membranes by decreasing the influx of sodium ions across the cell membranes in the motor cortex during generation of nerve impulses. Concerns include hydantoin hypersensitivity, slowed cardiac conduction, and hepatic dysfunction. This medication is also a pregnancy category D.[15] It is considered investigational for trigeminal neuralgia.[14] In theory, any anticonvulsant could be used as an adjuvant. However, be wary of medications not commonly used for pain control. In my practice, the drug Gabitril (tiagabine) has precipitated seizures in nonepileptic patients and should not be used "off label." In fact, an FDA alert was issued February 28, 2005 discouraging off-label use of this medication due to seizure risk in nonepileptics.[13]

Other medications that can be used include skeletal muscle relaxants, ie, lioresal (Baclofen), which has a twofold effect. It inhibits transmission of monosynaptic and polysynaptic reflexes and it causes muscle relaxation. It has indications for analgesia and trigeminal neuralgia. This medication should not be withdrawn abruptly.[15] Its function is related to GABA with CNS depressant effects. It is investigational for trigeminal neuralgia, prevention of migraines, and neuropathic pain.[14] Chloroxazone (Parafon forte) modifies the central perception of pain through its sedative effects. Possible side effects can include angioedema and anaphylaxis.[15]

Do not overlook topical analgesics. In fact, some authors suggest that topical lidocaine should be the first pharmacologic intervention.[8] The three classes most commonly used include[5]:

Local anesthetics "' lidocaine and mexiletine (Mexitil) interfere with the exchange of sodium in the sodium channel. (Some patients find Biofreeze effective at decreasing pain.)

Formulations containing antiinflammatories

Topical capsaicin "' depletes substance p and decreasing transmission of pain impulses.

Consider having a compounding pharmacist tailor topical medications. Consult with the pharmacist regarding the specific compounds and their concentration. Table 5 provides a reference for discussion. Topicals are ideal when patients desire decreased side effects and decreased liver involvement.

Another consideration when choosing an adjuvant is the associated conditions that interfere with pain management. Has the patient recently started on a "statin" for lowering cholesterol levels? Does the patient also suffer from arthritis, muscle spasms, restless leg syndrome, insomnia, diabetes mellitus, or depression? Sometimes treating other conditions allows medications for chronic pain syndromes to work more effectively. Comorbidities may point to appropriate adjuvants. Tricyclic antidepressants are helpful if insomnia is a concern. Baclofen has been known to help with neuropathic pain due to its neurotransmitter and CNS effects. "Steroids have been and continue to be administered by multiple routes for complex regional pain syndrome therapy."[12] Methylprednisolone (Medrol dose pak) is an antiinflammatory and immunosuppressant that can provide significant relief when inflammation is present. It is not for long-term use.[15] "Nonsteroidal anti-inflammatory drugs, physical therapy, accupuncture, antidepressants, and antiepileptics have been used as adjunctive treatment for chronic low back pain."[12] Clonidine (Catapress) stimulates the alpha andrenergic receptors in the CNS, which inhibits the sympathetic vasomotor center and decreases nerve impulse transmission, thus decreasing pain. Side effects include bradycardia and hypotension. This medication has been used for post herpetic neuralgia and restless leg syndrome.

"Pain management requires ongoing evaluation, patient education and reassurance. Diagnostic evaluation of treatable underlying conditions (eg, spinal cord compression, herniated disc, neoplasm) should occur concurrently with pain management."[8] For many patients with neuropathic pain, the nurse practitioner who has developed a comprehensive plan of care and has a strong network for referrals can be the most appropriate primary care provider. However, severe intractable pain may require referral to a pain clinic or neurosurgeon (if significant damage is identified during diagnostic studies). In most cases, "treatments with the lowest risk of adverse effects should be tried first."[8]

There is both an art and a science to pain management. Rowbotham states that the "Treatment of complex regional pain syndrome is largely empirical."[12] Sometimes trial and error is the best guide with any neuropathic pain. Both the practitioner and the patient need a willingness to try various options. If "pain is whatever the person experiencing the pain says it is, existing whenever the patient says it does,"[17] perhaps optimal functioning can be defined similarly. Can optimal functioning be defined as being achieved when the patient can satisfactorily perform at their chosen activity level? My bail bondsman, Tom, is a case in point. After multiple trials, he started using pregabalin as an adjuvant. His pain was more controlled, he felt as if he was "in control," and he became better able to function without excessive sedation. An unqualified success. 

There is both an art and a science to pain management. Rowbotham states that the "Treatment of complex regional pain syndrome is largely empirical."[12] Sometimes trial and error is the best guide with any neuropathic pain. Both the practitioner and the patient need a willingness to try various options. If "pain is whatever the person experiencing the pain says it is, existing whenever the patient says it does,"[17] perhaps optimal functioning can be defined similarly. Can optimal functioning be defined as being achieved when the patient can satisfactorily perform at their chosen activity level? My bail bondsman, Tom, is a case in point. After multiple trials, he started using pregabalin as an adjuvant. His pain was more controlled, he felt as if he was "in control," and he became better able to function without excessive sedation. An unqualified success. 

References (click to open)
Journal for Nurse Practitioners. 2008;4(4):263-270. © 2008 Elsevier Science, Inc.

http://webcache.googleusercontent.com/search?q=cache:DtqGKvHZDuoJ:www.medscape.com/viewarticle/576064+&cd=1&hl=en&ct=clnk&gl=nl&client=firefox-b-ab

HOMOEOPATHIC REMEDIES FOR VITILIGO AND LEUCODERMA

Vitiligo  is a disease that causes the loss of skin color in blotches. The extent and rate of color loss from vitiligo is unpredictable. It can affect the skin on any part of your body. It may also affect hair, the inside of the mouth and even the eyes.

Normally, the color of hair, skin and eyes is determined by melanin. Vitiligo occurs when the cells that produce melanin die or stop functioning.

Vitiligo affects people of all skin types, but it may be more noticeable in people with darker skin. The condition is not life-threatening or contagious. It can be stressful or make you feel bad about yourself.

Causes--Vitiligo occurs when melanin-forming cells (melanocytes) die or stop producing melanin — the pigment that gives your skin, hair and eyes color. The involved patches of skin become lighter or white. Doctors don't know why the cells fail or die. It may be related to:

 A disorder in which your immune system attacks and destroys the melanocytes in the skin

  Family history (heredity)

 A trigger event, such as sunburn, stress or exposure to industrial chemicals

On the other hand Leucoderma has different cause of onset. The difference in vitiligo and Leucoderma is only their onset. Vitiligo is self-generated while Leucoderma can occur after a cut, a burn or after allergy from some chemical. So basically cause of Leucoderma can be said accidental. Leucoderma cure is possible faster than vitiligo cure.

Symptoms--The main sign of vitiligo and leucoderma is color (pigment) loss that produces light or white patches on your skin. Usually, the discoloration first shows on sun-exposed areas, such as the hands, feet, arms, face and lips.

Vitiligo and leucoderma signs include:

Skin discoloration

  Premature whitening or graying of the hair on your scalp, eyelashes, eyebrows or beard (usually before age 35)

  Loss of color in the tissues that line the inside of your mouth and nose (mucous membranes)

  Loss of or change in color of the inner layer of the eyeball (retina)

  Discolored patches around the armpits, navel, genitals and rectum

Vitiligo can start at any age, but most often appears before age 20.

Depending on the type of vitiligo you have, the discolored patches may cover:

Many parts of your body. With this most common type, called generalized vitiligo, the discolored patches often progress similarly on corresponding body parts (symmetrically).

Only one side or part of your body. This type, called segmental vitiligo, tends to occur at a younger age, progress for a year or two, then stop.

One or only a few areas of your body. This type is called localized (focal) vitiligo.

It's difficult to predict how your disease will progress. Sometimes the patches stop forming without treatment. In most cases, pigment loss spreads and eventually involves most of your skin. Rarely, the skin gets its color back.

HOMOEOPATHIC REMEDIES

Homoeopathic remedies are found to be very effective for the treatment of vitiligo and leucoderma. Some of the important remedies are given below.

TUBERCULINUM 200- Treatment should be started with this remedy. A dose of 200 potency should be given every month along with the following remedies

ARS . SULPH. FLAVATUM 6- Vitiligo or leucoderma  especially at mucocutaneous junction. It is one of the top remedies for vitiligo and leucoderma. The skin is  very dry, cracked , scaly and blackish in appearance. Leucoderma that occurs along with eruptions, especially on the outer as well as inner side of the left wrist.

HYDROCOTYLE 3X- If Ars sulph flav fails this remedy may be tried. It should be used for a long  time.

BARYTA CARBONICUM 30--Baryta Carbonicum is an excellent  medicine for leucoderma with burning sensation. It acts well when white patches are present along with intolerable itching and tingling over the whole body at night. Baryta Carbonicum is most indicated when a person has sensations like pricks of burning needles along with itching and crawling on the skin. The person feels good in a warm atmosphere; while exposure to cold makes him feel unwell.

 

BARYTA MURIATICA 30-Barta mur. is best for leucoderma having small spots. The patient  has small spots and whitish patches all around his head, nape of the neck, abdomen and thighs. These white spots are often associated with itchy eruptions all over the exposed parts of the body

CALCAREA CARB 30--Calcarea Carb is a top grade constitutional homeopathic medicine for Vitiligo and Leucoderma  It is prescribed to patients of Vitiligo with milky white spots on skin. These white spots can appear anywhere on the body. There  is a  tendency to free perspiration over the head, neck and chest. Next is intolerance to cold weather. Certain peculiar cravings may be present are – eggs, lime, pencils. Person needing Calcarea Carb may show tendency to catch cold easily. Weakness of bone may also be found. Easily fatigued by exertion . Tendency to chronic constipation and obesity also guides the selection of Calcarea Carb in vitiligo. On mental sphere the person may shows a number of fears. The prominent fears among them are fear of misfortune, of contagious disease, of losing reason and of insanity.

BORAX 30- Borax is prescribed when white skin with red patches occurs.

ARSENICUM ALB 30--Arsenic Album is  another effective  remedy for vitiligo or leucoderma  in persons prone to dry, rough skin. The skin shows whitish spots and skin is dry, dirty and rough. The skin complaint alternating with respiratory complaints like asthma is a strong pointer for using homeopathic medicine Arsenic Album. In general sphere warmth is a relieving factor for persons needing Arsenic album. Warm applications over skin and warm drinks are highly desirable. Burning sensations in varying body parts may also be noticed. Extreme exhaustion may also be present. There are peculiar constitutional symptoms that allow us to select Arsenic Album in vitiligo treatment. The most prominent out of these are fears and anxieties. This remedy is often indicated in persons who have fears including that of death,  disease,  germs and of catching infection. Patients requiring Arsenic Album are highly anxious personalities. They may show anxieties  about health,  trifles and anxiety about others. Marked restlessness is often seen on both mental and physical planes in persons needing Arsenic Album. Next distinctive feature for selecting Arsenic Album in vitiligo is fastidiousness. Person demanding extreme neatness and order in everything are yet another suitable subjects requiring Arsenic Album.

CAUSTICUM 30—Causticum is best for leucoderma  from burns.

SEPIA 30--Sepia is another important remedy for vitiligo or leucoderma  treatment.   Constitutional symptoms that indicate the use of  sepia are – having an indifferent approach towards life and family. They show aversion towards family members and friends who were once loved with great affection. They lack interest in doing any work. Tendency to avoid both Physical or mental labor is present . They are constantly depressed with marked irritability, weeping tendency, desire to be alone and an aversion to consolation or sympathy. The use of Sepia must also be thought in women with menstrual irregularities or those around menopausal age with tendency to hot flushes. It is also useful for vitiligo at the tip os penis

NITRIC ACID 30-Nitric acid is prescribed when Vitiligo or Leucoderma occurs  especially at mucocutaneous junction. Discoloured zigzag patches on the skin. The base looks like raw flesh.

SILICEA 30- Silicea  is another top remedy for  vitiligo or leucoderma .  The constitutional  symptoms that indicate the use of  Silicea are –   pale and waxy skin; tendency to excessive perspiration on hands and feet; tendency to eruptions with pus formation in various body parts; tendency to catch cold on frequent basis; lean, thin physical makeup . There are few characteristic mind symptoms that need attention when selecting Silicea. The main mind symptom are timidity and an under-confident nature. Silicea may be thought of in people who seem under-confident, fear public speaking, are timid and bashful. Obstinate behavior and stubbornness may also indicate its use .

PSORALEA CORYL. 3X- 5 drops daily is an excellent remedy for vitiligo or leucoderma.. It is used externally in the form of oil. After applying the oil , exposure to sun rays must be avoided .

STAPHYSAGRIA 30-Staphysagria is prescribed when Vitiligo is present  at the tip of penis. Itching, scratching changes location of itching occurs.

SULPHUR 200-Sulphur is a deep acting homeopathic medicine used frequently in treatment of varying skin diseases including vitiligo or leucoderma. It goes deep inside the basic root cause to annihilate the disease in its complete extent. The persons requiring homeopathic medicine Sulphur usually show a philosophical mind set. They are popularly referred as ‘ragged philosophers’. Their mind is constantly occupied with various theories and plans. As a result they suffer from mental fatigue and absent mindedness. They take little or no care for their physical appearance and even show aversion to bathing. Persons who have suffered a lot from skin troubles, itchy skin with long term use of ointments are also likely to be benefited from use of homeopathic medicine Sulphur. Apart from all above said symptoms burning sensations in various body parts may be present along with white spots on skin.  An extra ordinary craving for sweets may also be shown as a constitutional symptom.

Summer Herbal Intensive

I am offering an Herbal Intensive for adults this Summer. It will be once a week (Wednesdays) for seven weeks, 9am - 3pm. I am very excited and I hope some of you can join me.

It will take place where I work, Great Hollow Wilderness School, in New Fairfield, CT. The land is enchanted and we will get to see plenty of it, since this course will not take place indoors. We will be on the land for the entire time aside from snippets where we may need a kitchen. All other heating will be over a campfire.

We will learn first hand from the plants, and use all our senses to gain information. We will hike through different habitats and examine them. We will learn some simple botany, plant families, and practical herbal wisdom. We will teach each other, get wet in the river, harvest and prepare medicinal and edible plants growing in abundance. We will cover a lot of material, yet it will be simple, digestible and applicable in everyday life. Indexing, journaling, and homework will be implemented. We will also be exploring herbal energetics, vocabulary for the herbalist, and probably a few unknown surprises too. :)

Herbal Intensive for beginners, ages 18 + 

Wednesdays June 24 - August 5, 9 am - 3 pm

Fee $ 450, deposit required

For registration go here

To learn more about Great Hollow Homeschool go here

To learn about all of Great Hollow go here

Green Blessings!