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15 Weeks Pregnant Baby Bump

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Fluoroquinolone Antibiotics And Neuropathy A Report

Today's important post from the Journal of Investigative Medicine at hic.sagepub.com (see link below) is another piece of the jigsaw showing how dangerous fluoroquinolone antibiotics can be for people whether living with, or prone to, nerve damage (neuropathy). It's quite long but worth reading because it's very important to check what sort of antibiotics your doctor is prescribing. Permanent neuropathy from an antibiotic is no joke and is so easily avoided - it's in your own interests to check the label on the box and question your doctor's choice afterwards.
 

Permanent Peripheral Neuropathy
A Case Report on a Rare but Serious Debilitating Side-Effect of Fluoroquinolone Administration
Published July 27, 2014, doi: 10.1177/2324709614545225 Journal of Investigative Medicine High Impact Case Reports April-June 2014 vol. 2 no. 2 2324709614545225

Jacquelyn K. Francis, BA1
Elizabeth Higgins, MD1
1Albany Medical College, Albany, NY, USA
Jacquelyn K. Francis, Albany Medical College, 47 New Scotland AvenueAlbany, NY 12208, USA. Email: francij@mail.amc.edu

Abstract

The health risks and side effects of fluoroquinolone use include the risk of tendon rupture and myasthenia gravis exacerbation, and on August 15, 2013, the Food and Drug Administration updated its warning to include the risk of permanent peripheral neuropathy. We present a case of fluoroquinolone-induced peripheral neuropathy in a patient treated for clinically diagnosed urinary tract infection with ciprofloxacin antibiotic.

Introduction

While there has been success in recent years in decreasing the numbers of unnecessary antibiotic administrations,1 still rampant in medical practice is the inappropriate use of antibiotics. Fluoroquinolones administration is no different. These bactericidal agents are capable of central nervous system (CNS) penetration,2 with an impressive treatment profile that includes an enhanced spectrum of activity, high oral bioavailability, high serum drug concentration that parallels that of intravenous drug administration, and rapid mechanism of action. It is for this reason that physicians favor these drugs for treatment of simple infections, which range from uncomplicated urinary tract infections (UTIs) and gastrointestinal infections to lower respiratory infections and pneumonias. According to established guidelines, however, these antibiotics are recommended as drugs of last resort and for treatment of cases refractory to other safer antibiotic alternatives. Reports in recent years of the adverse drug events of these drugs are on the rise, with not only an overrepresentation of common antibiotic complaints, including diarrhea, nausea, and headache that occur at rates higher than most other antimicrobials on the market,3 but there is also mounting evidence suggesting the potential for long-term adverse peripheral nervous system (PNS) effects from fluoroquinolone usage. The need for physicians to be judicious when prescribing these drugs is therefore paramount.

Case Presentation

A 57-year-old Caucasian female presented to outpatient clinic with complaints of dysuria, polyuria, and urinary urgency. Urinalysis showed 2+ leukocytes and trace blood. Based on her clinical presentation, she was treated for UTI with a ciprofloxacin regimen of 250 mg twice a day for 5 days. Subsequent urine culture showed no evidence of organism, and against advice for reevaluation, she was lost to follow-up. She presented 2 months later reporting whole body burning and alopecia. The burning, she claimed, started 2 or 3 days after completion of the prescribed course of ciprofloxacin. The burning lasted 3 weeks and resolved only to recur, unrelentingly, 3 weeks later. She had been unable to adorn clothing during this time, for she said this triggered whole body burning. At the point wherein she was finally able to wear clothing, she presented to the clinic. Hydration and Epsom salt soaks provided no relief. She reported pain of 10/10. Her past medical history is significant for trigeminal neuralgia, in remission for 12 years. The patient was on no medications at the time of her visit. She has no specific medication allergies, but does get gastrointestinal symptoms with opioids, namely, fentanyl. Physical examination was unremarkable. Vitals at the time that she was seen included the following: blood pressure 132/78 mm Hg, temperature of 97°F, heart rate of 60 beats per minute, respirations of 18. Her body mass index was 17.94, down from 20.3 two months earlier. On detailed neurologic examination, cranial nerves II through XII were intact bilaterally. There was no pronator drift of outstretched arms. There was some muscle wasting in biceps; however, overall tone was normal. Strength was full bilaterally. Reflexes were 2+ and symmetric at the biceps, triceps, knees, and ankles. Plantar responses were flexor. Light touch and pinprick produced pain and paresthesias diffusely in the upper and lower extremities; however, position sense and vibration sense were intact in fingers and toes. Rapid alternating movements and fine finger movements were intact. There was no dysmetria on finger-to-nose and heel-knee-shin. There were no abnormal or extraneous movements. Romberg was absent. The patient’s posture was normal. Gait was steady with normal, though tentative, steps, base, arm swing, and turning. Heel and toe walking were normal. Tandem gait was normal. She had no discernable rash or skin lesions.

Subsequent complete blood work analysis to check for an electrolyte abnormality basis of her complaints was unremarkable. Her complete blood count was normal with a hematocrit of 41%. Her vitamin B12 level was 258 pg/mL, with a normal range of 200 to 900 pg/mL. Her thyroid stimulating hormone level was 2.05, with a normal range of 0.4 to 6.0. Her immunoglobulin levels were normal. Her vitamin D level was 13 nmol/L (optimal >30 nmol/L). Copper level was 98 mg (normal 50-80 mg). Vitamin E was normal at 12.7 µg/mL (normal range = 5.5-17 µg/mL). Vitamin B1 was normal at 5.4 µg/dL (normal range = 2.5-7.5 µg/dL).

Her blood work and further questioning could provide no new medical etiology for her symptoms, and so the patient was subsequently sent for complete neurological workup. Workup included heavy metal toxicity screening to assess for possible heavy metal exposure to lead, mercury, cadmium, and zinc. Electrophysiological studies were also done to assess neuromuscular nerve action potential transmission, a test that could discern a neuromuscular disorder etiology. Three-millimeter skin punch biopsy to assess for small fiber density and possible neurologic process were also done. These tests were all negative. Neurological workup could not determine a unique cause of her symptoms. It was concluded that if her symptoms were neurologic-based, it was, in fact, a multifocal process.

Two years after the initial onset of symptoms, the patient continues to suffer from polyneuropathies chronologically related to ciprofloxacin use. At her most recent visit, she describes constant pain of 7/10 and is unable, she states, to ambulate for more than 2 minutes, without intense shooting pains up and down her lower extremities. She describes “pins and needles” up and down her legs and thighs radiating to her buttocks and feet. She claims that her upper body and abdomen have now been spared of such feelings. She describes severe alopecia and ambulates now with a broad-based gait. She describes being on permanent disability because of her condition. The rest of her physical examination remains unchanged. There are no gross neurological deficits discernible on neurologic examination. The patient remains on amitriptyline 20 mg daily for control of her pain symptoms.

Discussion

Fluoroquinolones are fluorinated quinolones, the only bactericidal agent in the antibiotic class capable of directly inhibiting DNA synthesis. They do this by promoting cleavage of bacterial DNA in the DNA–enzyme complexes of DNA gyrase and topoisomerase IV.2 Generally, gram-negative antibacterial activity correlates with inhibition of DNA gyrase, and gram-positive antibacterial activity corresponds with inhibition of DNA type IV topoisomerase.2,4 With the introduction of these drugs in the 1960s, physicians were able, for the first time, to treat severe gram-negative infections orally.3 The first successful fluorination of part of the quinolone drug in 1986, in the form of norfloxacin, brought with it the capability of crossing the blood–brain barrier and achieving CNS penetration.5 This and the already great treatment profile in the form of enhanced spectrum of activity, high oral bioavailability, high serum drug concentration comparable to intravenous infusion, and rapid mechanism of action added to the popularity of these drugs ultimately resultingin the indiscriminate use of these drugs. The enhanced treatment profile of these drugs came at a price however, with adverse effects so severe that use of many fluoroquinolones since then being restricted or the drugs withdrawn from the market entirely.6,7

One of the challenges of diagnosing a patient with fluoroquinolone-associated peripheral neuropathy is the diffuse, confusing, and delayed array of symptoms that can occur. A 1996 study first brought these adverse effects to light.7 While patients on the fluorinated drugs exhibited less side effects than those associated with first-generation quinolone predecessors, such as nausea and gastrointestinal disturbances, 0.9% to 1.6% experienced adverse reactions relating to the peripheral and central nervous system, including headache, dizziness, drowsiness, agitation, psychosis, and convulsions, as well as peripheral sensory disturbances, symptoms that had never been complained of prior, at least not on any significant scale. Of these patients, 81% had symptoms occurring within 1 week of drug administration, with paresthesia being the mainly reported symptom. Five years later, a 2001 study found that contrary to previous reports suggesting that fluoroquinolone-associated PNS events are mild and short term, 80% of study participants reported severe events that typically involved multiple organ systems, especially the PNS, with symptom onset as early as 24 hours within initiation of treatment. 58% of these cases had symptoms lasting greater than 1 year.8

Another 2001 formal study that sought to assess the prevalence of fluoroquinolone-induced PNS adverse side effects highlighted the severity of these effects. The study concluded that there was a high association between fluoroquinolone antibiotics and severe, long-term adverse PNS and multiple organ system effects that included PNS sensory symptoms (91%), peripheral neuropathy motor symptoms (55%), and CNS effects (75%). Over 80% of the patients surveyed had sequalae stemming from fluoroquinolone use that lasted for greater than 1 year.9 A subset of these patients and their adverse drug events are included in Table 1.


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Table 1.

15 of the 45 Total Reported Cases of Fluoroquinolone-Associated Events in the Literature6.

Despite these seemingly significant numbers and overwhelming reports from patients, physicians continue to prescribe fluoroquinolone antibiotics unsystematically, against US Food and Drug Administration recommendations. The pressures of health care facilities and patients alike to increase patient turnaround and quickly alleviate symptoms may compound this problem 10.

As highlighted in the aforementioned case, the peripheral neuropathy reported with fluoroquinolone administration can be severe, debilitating, and permanent. It is for this reason that physicians need to practice due diligence when prescribing not only antibiotics, but any drug. Physicians also need to practice vigilance in the event of an adverse reaction. They can do this with careful follow-up of patients and ensure that patients are aware of all the side effects that may be associated with their prescribed drug. Patients need to know what to look for and where to go in the event that one of these symptoms become manifest. It is our hope that the updated FDA warning and presentation of this case will encourage physicians to be more conscientious of their treatment selections.

Take Home Points

The FDA recommends that fluoroquinolones be used as a drug of last resort and for treatment of cases refractory to other safer antibiotic alternatives.

The FDA updated their black box warnings on all fluoroquinolones to stress the rapidity of onset and permanence of peripheral neuropathy associated with their use.

Physicians should be aware of the risks and side effects associated with the drugs that are prescribed and be able to inform patients of the risks associated with the use of these drugs.

Physicians should always aim to administer the least broad spectrum antibiotic possible based on known sensitivities and regional resistance patterns.

Article Notes

Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).

References
1.↵
US Food and Drug Administration. FDA drug safety communication: FDA requires label changes to warn of risk for possibly permanent nerve damage from antibacterial fluoroquinolone drugs taken by mouth or by injection. http://www.fda.gov/Drugs/DrugSafety/ucm365050.htm. Accessed August 15, 2013.
2.↵
Scheld M. Quinolone therapy for infections of the central nervous system. Rev Infect Dis. 1989;11(suppl 5):S1194-S1202.
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Turnidge J. Pharmacokinetics and pharmacodynamics of fluoroquinolones. Drugs. 1999;58(suppl 2):29-36.
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Hooper DC,
Wolfson JS. Mechanisms of Quinolone Action and Bacterial Killing. Quinolone Antimicrobial Agents. 2nd ed. Washington, DC: American Society for Microbiology; 1993:53-57.
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Kelentey B,
Kerr M,
Tao Z,
Purushotham KR,
Humphreys-Beher MG,
Zelles T. Inhibition of rat parotid gland growth response induced by chronic isoproterenol following treatment with quinolone antibiotic. Mol Cell Biochem. 1996;165:55-63.
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Cohen JS. Peripheral neuropathy associated with fluoroquinolones. Ann Pharmacother. 2001;35:1540-1547.
Abstract/FREE Full Text
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Hedenmalm K,
Spigset O. Peripheral sensory disturbances related to treatment with fluoroquinolones. J Antimicrob Chemother. 1996;37:831-837.
Abstract/FREE Full Text
8.↵
Gold L,
Igra H. Levofloxacin-induced tendon rupture: a case report and review of the literature. J Am Board Fam Pract. 2003;16:458-460.
FREE Full Text
9.↵
Mandell L,
Tillotson G. Safety of fluoroquinolones: an update. Can J Infect Dis. 2002;13:54-61.
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10.↵
Linder JA,
Huang ES,
Steinman MA,
Gonzales R,
Stafford RS. Fluoroquinolone prescribing in the United States: 1995 to 2002. Am J Med. 2005;118:259-268.
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WARTS AND HOMEOPATHIC MANAGEMENT

                                                                      WARTS

                A warts or verrucae are a localized, benign epidermal growth caused by a DNA virus (humanwart virus of the group of papova viruses). It is a contagious condition and occurs mostly in children and adulthood.

TYPES:-

                Clinically, warts are of the following types.

1.       PLAIN WARTS (VERRUCA PLANA):-

-          They are round or polygonal, small in size (1-5 mm).

-          These type are occur mostly over the hands or the face.

-          These are usually multiple, smooth, slightly elevated and usually of the colour of skin or slightly pigmented.

2.       COMMON WARTS (VERRUCA VULGARIS):-

-          They are larger in size (even up to 1 cm in diameter).

-          Its darker in colour and occur mostly over the back of the hands or the knees.

-          Their surface is rough and horny.

3.       PLANTER WARTS (VERRUCA PLANTARIS):-

-          They occur over the ball of the foot or the heel.

-          They appear as a small, shiny, horny papule but soon change into a round, flat lesion.

-          In many ways, they resemble common warts in size and shape but these are painful.

-          They differ from corn in that a wart bleeds on scratching whereas a corn does not bleed.

4.       CONDYLOMATA ACUMINATA:-

-          They also resemble common warts in size but differ in shape (filiform or digitate) and the site.

-          They occur either over the mucocutaneous junction of the external genitalia or around the anus region.

-          These are usually multiple and often called veneral warts.

TREATMENT:-

-          A wart should be either destroyed by chemical or electrical cautery or removed surgically.

-          Chemicals that may be used for cautery are phenol (95 percent), trichloracetic acid(50 percent), carbon dioxide snow, salicylic acid, phodophyline (25 percent in spirit) and glacial acetic acid,

-          Recurrences are common.

HOMEOPATHIC TREATMENT:-

                 In homeopathy we have some wonderful medicines for any types of warts. The medicines names are given below.

1.       BARYTA CARB.

2.       BELLADONNA.

3.       CALCAREA CARB.

4.       CALCAREA SULPH.

5.       CAUSTICUM.

6.       DUL CAMARA.

7.       MERC SOUL.

8.       NATRUM SULPH.

9.       NITRIC ACID.

10.   SULPHUR.

11.   THUJA.

12.   BENZOIC ACID.

13.   BOVISTA.

14.   FLOURIC ACID.

15.   MAGNESIUM SULPH.

16.   MEDORRIHINUM.

17.   NATRUM CARB.

18.   LACHESIS.

19.   PHOSPHORIC ACID.

20.   PSORINUM.

21.   RHUS TOXI.

22.   SEPIA.

23.   SILICEA.

High Blood Pressure And Pregnancy

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HOMOEOPATHIC REMEDIES FOR DIABETES INCLUDING DIABETIC FOOT AND DIABETIC NEPHROPATHY

Diabetes mellitus refers to a group of diseases that affect how your body uses blood sugar (glucose). Glucose is vital to your health because it's an important source of energy for the cells that make up your muscles and tissues. It's also your brain's main source of fuel.

If you have diabetes, no matter what type, it means you have too much glucose in your blood, although the causes may differ. Too much glucose can lead to serious health problems.

Chronic diabetes conditions include type 1 diabetes and type 2 diabetes. Potentially reversible diabetes conditions include prediabetes — when your blood sugar levels are higher than normal, but not high enough to be classified as diabetes — and gestational diabetes, which occurs during pregnancy but may resolve after the baby is delivered.

Causes --To understand diabetes, first you must understand how glucose is normally processed in the body.

How insulin works

Insulin is a hormone that comes from a gland situated behind and below the stomach (pancreas).

·        The pancreas secretes insulin into the bloodstream.

·        The insulin circulates, enabling sugar to enter your cells.

·        Insulin lowers the amount of sugar in your bloodstream.

·        As your blood sugar level drops, so does the secretion of insulin from your pancreas.

The role of glucose

Glucose — a sugar — is a source of energy for the cells that make up muscles and other tissues.

·        Glucose comes from two major sources: food and your liver.

·        Sugar is absorbed into the bloodstream, where it enters cells with the help of insulin.

·        Your liver stores and makes glucose.

·        When your glucose levels are low, such as when you haven't eaten in a while, the liver breaks down stored glycogen into glucose to keep your glucose level within a normal range.

Causes of type 1 diabetes

·        The exact cause of type 1 diabetes is unknown. What is known is that your immune system — which normally fights harmful bacteria or viruses — attacks and destroys your insulin-producing cells in the pancreas. This leaves you with little or no insulin. Instead of being transported into your cells, sugar builds up in your bloodstream.

·        Type 1 is thought to be caused by a combination of genetic susceptibility and environmental factors, though exactly what many of those factors are is still unclear.

Causes of prediabetes and type 2 diabetes

·        In prediabetes — which can lead to type 2 diabetes — and in type 2 diabetes, your cells become resistant to the action of insulin, and your pancreas is unable to make enough insulin to overcome this resistance. Instead of moving into your cells where it's needed for energy, sugar builds up in your bloodstream.

·        Exactly why this happens is uncertain, although it's believed that genetic and environmental factors play a role in the development of type 2 diabetes. Being overweight is strongly linked to the development of type 2 diabetes, but not everyone with type 2 is overweight.

Causes of gestational diabetes

·        During pregnancy, the placenta produces hormones to sustain your pregnancy. These hormones make your cells more resistant to insulin.

·        Normally, your pancreas responds by producing enough extra insulin to overcome this resistance. But sometimes your pancreas can't keep up. When this happens, too little glucose gets into your cells and too much stays in your blood, resulting in gestational diabetes.

Symptoms--Some of the signs and symptoms of type 1 and type 2 diabetes are:

·        Increased thirst

·        Frequent urination

·        Extreme hunger

·        Unexplained weight loss

·        Presence of ketones in the urine (ketones are a byproduct of the breakdown of muscle and fat that happens when there's not enough available insulin)

·        Fatigue

·        Irritability

·        Blurred vision

·        Slow-healing sores

·        Frequent infections, such as gums or skin infections and vaginal infections

Although type 1 diabetes can develop at any age, it typically appears during childhood or adolescence. Type 2 diabetes, the more common type, can develop at any age, though it's more common in people older than 40.

HOMOEOPATHIC REMEDIES

Homoeopathic remedies are very safe for treating diabetes and its complications without any side effects . Some of the important remedies are given below-Along with the following remedies consider the constitutional drug for a permanent cure.

ABROMA AUGUSTA Q - Abroma Augusta is the top Homeopathic medicine to treat Diabetes Mellitus. Its use is highly recommended in those patients who are losing flesh and suffer from extreme weakness due to Diabetes Mellitus. The patients who can greatly benefit from this Homeopathic medicine have an increased thirst with dryness of mouth. They also have an increased appetite and the urination is very frequent day and night. Excessive weakness is felt after urination. Homeopathic medicine Abroma Augusta is also of great help in treating sleeplessness in a person with Diabetes. Another sphere in which this Homeopathic remedy yields good results is skin complaints like boils and carbuncles in a diabetic patient. Burning sensation in the whole body is a prominent general symptom that can be found in persons requiring Abroma Augusta

CEPHALANDRA INDICA Q- A specific remedy for diabetes. Dryness of mouth. Great thirst for large quantities of cold water

PHOSPHORUS 200--Phosphorus is a Homeopathic medicine of great help for treating Diabetes Mellitus, though its use depends completely on the constitutional symptoms of the patient. Homeopathic medicine Phosphorus is a remedy of great help for weakness of vision in a diabetic patient

RHUS AROMATICA Q- Rhus aromatic is an effective remedy for diabetes. Passing large quantities of urine of low specific gravity

SYZYGIUM JAMBOLANUM Q-Syzygium Jambolanum is among the best Homeopathic remedies for the treatment of Diabetes Mellitus. It acts promptly and efficiently in decreasing the sugar levels. Excessive thirst and excessive urination are always present in the patient. Homeopathic medicine Syzygium Jambolanum also gives wonderful results in treatment of long-standing ulcers in a diabetic patient

PHASEOLUS 3X—Diabetes with heart disease

PHOSPHORIC ACID Q-Phosphoric Acid is an excellent Homeopathic remedy for extreme weakness, either mental or physical, in a diabetic patient. Such patients feel exhausted all the time. They have a weak memory and are forgetful. Some sort of history of grief may be found in patients requiring this Homeopathic medicine. For numbness of feet in patients of Diabetes Mellitus, Phosphoric Acid is the best Homeopathic remedy

MEMORDICA CHARANTIA Q- An excellent specific remedy for diabetes.

GYMNEMA SYLVESTRE Q--Gymnema Sylvestre is a Homeopathic medicine of great help for patients of Diabetes Mellitus who are losing weight with weakness and exhaustion. In such patients, this Homeopathic remedy works as a tonic resulting in improvement of overall health. With Homeopathic medicine Gymnema Sylvestre,the patient puts on weight and feels energeti

URANIUM NITRICUM 3X- Diabetes with weakness and losing flesh

DIABETIC FOOT

SECALE COR 30- An excellent remedy for diabetic gangrene . Dry gangrene of toe. Dusky blue tinge. Skin feels cold to touch yet covering not tolerated. Warmth aggravatio

ARSENICUM ALBUM 30- Diabetic gangrene. Burning and soreness , relieved by warmth. Fetid smell from the wound. Restlessness

APIS MELLIFICA 30-Spreading cellulitis with burning stinging pain. Sensitive. Blebs are seen

ANTIMONIUM CRUDUM 30- Callosities are seen. Dry gangrene

CARBO VEGETABIS 30- Carbuncles and boils becomes gangrenous. Wet , purple and icy cold gangrene.Moist gangrene. There is great prostration

HEPAR SULPH 30- Blebs are seen. Very sensitive to touch

LACHESIS 200- Bluish purple surroundings around gangrene. Traumatic

RHUS TOX 30- Spreading cellulitis

SULPHURIC ACID-30- Blue and purple surroundings of the gangrene. Bleeding under the skin

THIOSINAMINUM 30-Specific for callosities. Dry gangrene

TARENTULA CUB 30- Painful and inflamed abscess with a tendency to gangrene

ECHINACEA Q- Emitting a foul smell from gangrene . 5 drops in a little of water every 2 hours . Externally wash with a Echinacea lotion. It act as a cleaning and antiseptic agent.

DIABETES NEPHROPATHY

LYCOPODIUM CLAVATUM 30—Lycopodium is an effective remedy for diabetic nephropathy. Urine scanty , cries before urinating, red sand in urine, must strain, suppressed or retained. Urine milky and turbid. Sometimes haematuria . Urine is burning and hot. The right kidney is mainly affected. The patient experiences impotency.The patient likes warm food and drink, also there is intense craving for sweets.

SERUM ANGUILLAE 6X—Serum Anguilae is one of the best remedies for diabetes nephropathy. It is very effective in acute nephritis. Kidney failure. It is prescribed when hypertension and oliguria without oedema is present. Urine contains albumin.

ARALIA HISPIDA 30-Aralia hispida is found to be effective for diabetes nephropathy. There is dropsy of renal origin. Urinary tract infection is present. Urine is scanty leading to complete suppression of urine. Renal diseases with constipation.

AMPELOPSIS QUINQUEFOLIA 30- Ampelopsis quinquefolia is another effective remedy for diabetes nephropathy. There is uraemia or uremic coma. Vomiting, purging, tenesmus , cold sweat and collapse are the leading symptoms. 

CUPRUM ARSENITUM 3x-Cuprum ars is also a very effective remedy for diabetes nephropathy. There is kidney inefficiency and uremia. The urine smell like garlic. Urine of high specific gravity increased, acetones and diacetic acid.

CUPRUM ACETICUM 3X- In Cuprum aceticum the tongue is pale , coated with lot of mucus. Anemia. Pulse rapid. The patient is chilly. Breathlessness with dry cough. Cannot eat or drink without retching.

ARSENICUM ALBUM- 30-Arsenic alb. Is also an effective remedy for diabetes nephropathy. Urine is scanty, burning when urinating. Albuminuria. Epithelial cells, cylindrical clots of fibrin and globules of pus and blood in urine. Feeling weakness in abdomen after urination. Retention of urine. Urine black as if mixed with dung.

Sleep Deprivation And Neuropathy

Today's post from beating-diabetes.com (see link below) is aimed at diabetics with neuropathy but applies to all of us living with nerve problems. It talks about a problem that millions of people with neuropathic symptoms have and that is sleep deprivation. You don't need telling how important a good night's rest is for your general health and feeling of well-being and if the symptoms of neuropathy regularly disrupt your sleep it can affect your whole life, leading to all sorts of problems during the waking hours. This article gives some very helpful advice as to how to tackle the problem. The solution doesn't always lie with prescription sleeping pills; there may be other ways of improving what can seem an insurmountable problem. Lack of sleep is a vastly underrated aspect of living with neuropathy and all good advice is welcome.
 

Diabetic Neuropathy and Sleep
Written By: Paul - May• 11•14

Diabetic neuropathy can develop into a nagging intrusiveness that will undermine you ability to enjoy a good night’s sleep. And lack of sleep will exacerbate the painful symptoms of neuropathy. What can you do about it?

Peripheral neuropathy is damage to the nerves in the feet and legs. When it is caused by long-term diabetes it is called diabetic neuropathy.

This nerve damage can cause a loss of feeling in the feet or symptoms such as tingling, numbness, burning, and pain. These symptoms come and go and can be quite intensive and disturbing from time to time.

It is permanent, so once it’s happened you cannot improve it by controlling your diabetes better. However, you can allay the symptoms (and prevent the damage getting worse) through a change in diet and exercise.
Sleep disturbances

As it can be very intrusive, neuropathy can disturb your sleep in a number of ways.

The pain and weird sensations (especially in the legs) of neuropathy can make it hard to fall asleep.

Many people find themselves focusing on their pain during the evening when daytime distractions are at a minimum which makes it more difficult to get to asleep. The pain can also kick in during the night and wake you up.

Neuropathy has been linked with sleep apnoea syndrome, ie pauses in breathing during sleep.

A meta-analysis published online in late 2013 by three Japanese researchers indicates that patients with diabetic neuropathy are twice as likely to have apnoea compared to diabetic patients who do not have neuropathy. This, however, does not mean that neuropathy is a cause of sleep apnoea.

The relationship between neuropathy and sleep is a two-way street. While neuropathy can cause your sleep to be disturbed, sleep that is disturbed (for other reasons) can make the symptoms of neuropathy worse.

In addition, being deprived of sleep can lower your pain threshold and your ability to tolerate pain, which makes your neuropathic pain feel worse.
Overcoming the effects of neuropathy on sleep

There are several things you can do to overcome the intrusiveness of neuropathy:

[1] You can use medicines, both over-the-counter and prescription medications. However these can cause drowsiness during the day, as well as other side affects and can cause dependency.

[2] You can try non-pharmacological treatments such as cognitive behavioural therapy, relaxation techniques, stress management, and acupuncture.

[3] You can follow the tips below for getting a good night’s sleep. This is probably the best thing you can do.
Getting a good night’s sleep despite your neuropathy

There are several things you can do to get a good night’s sleep. You may find some or all of the following useful: 

Keep your blood glucose under control using diet and, if necessary, medications.

Get some exercise every day.

Go to bed at about the same time each night so you adhere to a regular sleep/wake schedule.

Make sure your bed is large and comfortable with a good mattress and supportive pillows.

Elevate the bed sheets so that they are not in direct contact with your legs and feet. You can do this using wire frames to create a tunnel for your feet under the blankets.

Ensure your room is cool (18 degrees Centigrade) and well ventilated.
Sleep in the dark in a noise free room (or use a blindfold and/or ear plugs).

Develop a bedtime ritual (eg, taking a warm bath, reading light material).

Limit or eliminate caffeine four to six hours before bed and minimize daytime use.

Avoid smoking, especially near bedtime or if you awake in the middle of the night.

Avoid alcohol and heavy meals before going to bed.

Turn off your TV, smartphone, iPad, and computer a few hours before your bedtime.

Adopt relaxation techniques to help induce sleep such as setting an hour aside before bedtime to relax and unwind. Try meditation or deep breathing exercise.

http://beating-diabetes.com/index.php/diabetic-neuropathy-and-sleep/

Accepting The Pain Of Neuropathy And Moving Forward

Today's post from instituteforchronicpain.org (see link below) is a self-help article with a difference - it makes sense! Most self-help articles are well-meaning but stuffed with clichés and so-called new age philosophy and go over most people's heads. What we need is to know why we need to become proactive in our health problem and why that will do us good. This article sets out to explain how not fighting our pain (as we're expected to do) is the first step towards learning to live with it and improve it. Worth a read...even for cynics.

Finding Hope in Acceptance  
Author: Murray J. McAllister, PsyDPosted on August 26, 2013

At first thought, it might seem crazy to accept that your pain is chronic. When I bring it up with patients, many of them tell me, not without some irritation in their voice, “I’ll never give up hope of finding someone who can fix me!” Indeed, it’s common to think that accepting the chronicity of your pain is the same thing as giving up hope that you’ll ever get better. So, why in the world would you ever want to accept that your pain is chronic?

Contrary to what you might think, accepting that your pain is chronic is the first step in actually getting better. It opens up a whole new way of getting better, a way that takes into account the realities of your pain condition. As such, it’s a new and more realistic way to have hope.

To understand the point more clearly, let’s briefly review two different models of healthcare – two different ways that we get better when having an illness or injury. These two models are what we might call the ‘acute medical model’ and the ‘rehabilitation model.’ The latter is sometimes called the ‘self-management model.’ (For a more thorough review of these models of healthcare, click on this post here.) 


Acute Medical Model

The acute medical model of healthcare is what most of us think of when we go to see a healthcare provider. When sick or injured, we go to a provider who determines what’s wrong and provides a treatment that cures us. The healthcare provider is an expert who usually knows more about the condition and the treatments than we do. The treatments themselves are usually medications or procedures that act on us. We don’t typically get better by doing things ourselves. Rather, it’s the treatments that get us better and we rely on healthcare providers to provide us with those treatments. Lastly, getting better in the acute medical model is usually thought of as getting cured. We return to our usual state of health — how we were before we became ill or injured.

Hope of getting better within the acute medical model lies in finding the right healthcare provider who knows what’s wrong and knows how to cure you. In this model, hope lies external to you. You find it in the expertise and treatments of a healthcare provider.

Now there’s nothing wrong with the acute medical model. It’s all well and good when we have a condition for which there actually is a cure. Indeed, it’s likely the best thing to do. But, what do you do when you have a condition for which there is no cure?

Rehabilitation Model

The answer to the question, of course, isn’t to give up hope and do nothing. There’s actually a different way of getting better. It’s the rehabilitation model of care. It requires, however, redefining how to get better and even redefining what it means to get better.

In the rehabilitation model of care, the emphasis is on what you, the patient, do to get better — not on what the healthcare provider does to get you better. Specifically, the focus is on the patient acquiring the abilities to make healthy changes, which, when done over time, have a positive impact on the chronic health condition that you have. These changes fall into two categories: a) changes in health behaviors, or what’s often referred to as lifestyle change, and b) changes in coping, or what’s often referred to as stress management. The goal of learning and engaging in these health behaviors over time is two-fold: you reduce the symptoms of the condition and you reduce the impact that the chronic health condition has on you. In other words, you get so good at self-managing the condition that it no longer is as problematic as it once was. As a consequence, you can move on with the rest of your life, engaging in the meaningful activities of life – such as work, family activities, social and recreational activities.

Notice that the rehabilitation model doesn’t promise a cure. The reason is that the conditions for which the rehabilitation model is best suited are those conditions that are chronic. They have no cure. Nonetheless, the patient does get better in very real and meaningful ways.

Notice too that hope gets redefined. It allows for having hope even when there is no cure. Finding a cure is not the only way to get better. Therefore there’s still hope. It’s just a different way to have hope, a hope that realistically takes into account the chronic nature of the condition you have, but nonetheless points to how to how you still can get better.

The conditions for which the rehabilitation model is best suited are chronic conditions, where there is no cure, such as chronic pain syndromes, diabetes, heart disease, and spinal cord injuries, among others.

Finding Hope in Acceptance

Acceptance that your pain is chronic is the first step in pursuing the rehabilitation model of care. Rehabilitation is hard work. It also takes time. You don’t do it if you think that a cure is just around the corner. Once you recognize, though, that your chronic pain really is chronic, it becomes your life-saver – or life-retriever. You start to get your life back. You learn how to self-manage your pain and you practice it to the point that you move on with the rest of your life. Your life doesn’t have to be about chronic pain.

Patients can keep their life on hold when they insist on finding hope only in a cure. They seek out appointment after appointment, attempting to find the right specialist who will know what to do to make their pain go away. Oftentimes, they seek out surgeries or interventional procedures that seem as if they might be a cure, but aren’t. Each time they seek out a new specialist, there is hope. Each time, though, it gets dashed because there really is no cure for chronic pain. Chronic pain really is chronic.

The point, here, is not a criticism of such patients. What we are describing makes sense if you think of healthcare as only the acute medical model. If we think of healthcare providers as specialists who fix us when sick or injured, it makes all the sense in the world to look for the right one who can do the job – even if you have to try one after another. It’s a hard lesson to learn when realizing that it’s only sometimes that healthcare providers act like a mechanic. A lot of the time, we have no fixes. So, again, I’m not judging when I describe patients who fail to accept that their pain is chronic. We can all understand how it happens. They are trying to find hope in a cure.

What if, though, at the end of the day, the hope is really a false hope? It can become a vicious cycle that leads to depression and oftentimes more pain. Hope is found with each new procedure, but each procedure fails to cure the pain and so hope is dashed. If hope is defined by finding a cure, and if there really is no cure, then you are left helpless – and hopeless.

Maybe it’s best to find a new way to have hope.

You find it by accepting that chronic pain really is chronic. You accept that you are not going to get better by finding a cure. Rather, you accept that you are going to get better by learning to self-manage it. You learn how to make healthy changes in your life that, when done over time, reduce your symptoms and reduce the impact that chronic pain has on your life. You get so good at managing chronic pain that it is no longer the preoccupying problem that it once was. Your life consists of the stuff of life and chronic pain comes along for the ride, but remains in the side car.

It’s okay if you don’t know how to do it yet. Most patients have to learn how to do it. Oftentimes, I remind patients that you’re not born with the knowledge of how to self-manage pain successfully. People have to learn it. And it’s okay if you don’t know how and have to learn it.

What matters, though, is that you learn how. It’s possible to learn how to self-manage pain and do it successfully. People learn how to do it everyday in chronic pain rehabilitation programs. And you can too.

You just have to first accept that your chronic pain is really chronic.

(For more information, please see: “What is chronic pain?” or “Why the healthcare system refuses to accept the chronicity of chronic pain.”)

http://www.instituteforchronicpain.org/blog/finding-hope-acceptance/

GINKGO BILOBA FOR ALZHEIMERS DISEASE AND CARDIOVASCULAR DISEASE

Botanical name-Ginkgo biloba Linn

Family- Ginkgoaceae

Common name- Maidenhair tree

Ginkgos are large trees, normally reaching a height of 20–35 m (66–115 ft), with some specimens in China being over 50 m (160 ft). The tree has an angular crown and long, somewhat erratic branches, and is usually deep rooted and resistant to wind and snow damage. Young trees are often tall and slender, and sparsely branched; the crown becomes broader as the tree ages. During autumn, the leaves turn a bright yellow, then fall, sometimes within a short space of time (one to 15 days). A combination of resistance to disease, insect-resistant wood and the ability to form aerial roots and sprouts makes ginkgos long-lived, with some specimens claimed to be more than 2,500 years old.

Leaves: The characteristic greenish-yellow leaves are fan-shaped and composed of two or more distinct lobes; the Latin species name biloba refers to this fact. The common name of maidenhair tree pertains to the similarity of the leaves to those of maidenhair ferns (Adiantum species). In autumn, the leaves of Ginkgo biloba turn a beautiful golden hue before falling to the ground.

Seeds: It takes 20-35 years for maidenhair trees to reach maturity and start bearing seeds. Male and female trees are separate; male trees have pollen-producing catkins while female trees, once fertilised, bear rounded, yellowish seeds with a fleshy outer coat (resembling a plum in appearance). These fall to the ground in the autumn and as the seed coat decays it exudes a rancid butter-like smell

Part used – Leaves

Chemical constituents-- The constituents of primary interest in Ginkgo leaf are ginkgolides and flavonoids. Ginkgolides (ginkgolides A, B, C, J, and M) are diterpenes. Flavonoids present in Ginkgo leaf include flavones, biflavones, flavonols, tannins, and associated glycosides. In general, flavonoids are principally found in the leaves, although they are also present in many other parts of the plant. There are about 20 flavonoid glycosides along with glucosides, quercetin and kaempferol 3-rhamnosides and 3-rutinosides, p-coumaric esters of glucorhamnosides of quercetin, kaempferol and biflavones. The biflavones are amentoflavone, bilobetol, 5-methoxybilobetol, ginkgetin, isoginkgetin, and sciadopitysin, bilobalides. Ginkgo leaves also contain flavan-3-ols, proanthocyanins and poly-isoprenoid - derived betulaprenols in unusually high amounts. Other compounds of interest in the leaf include ginnon, ginnol, 2-hexenal, and bilobalide.

Therapeutic  uses--Ginkgo biloba has been used medicinally for thousands of years. Today, it is one of the top-selling herbs in the United States.

Ginkgo is used for the treatment of numerous conditions, many of which are under scientific investigation. Available evidence supports ginkgo for managing dementia, anxiety, schizophrenia, and cerebral insufficiency (insufficient blood flow to brain).

Evidence for other uses is either lacking or mixed. Further research is needed for all uses of ginkgo.

Although ginkgo is generally well tolerated, it should be used cautiously in people with clotting disorders or taking blood thinners, or prior to some surgical or dental procedures, due to reports of bleeding.

HOMOEOPATHIC USES

First time the Homoeopathic proving was done in the year 1933 by Dr. E.A.Maury with the M.T. on seven subjects ( 5 men, 2 women) then six persons and Dr. KORSAKOFF on two men. An auto experimentation was undertaken by Dr. E.G.IVOR of New Zealand in 1971. Homoeopathically proved main symptoms are --- General lameness with chill. Unreasonable fear with rapid flow of words. Suppressed anger. Intellectual weakness.

 Heaviness of the frontal region of head.Vertigo. Sensation of troubles vision with a veil before the eyes.Buzzing in ears.Vesiculous eruptions, burning, prurigious. Great muscular weakness. Asthma

Here, it is interesting to know, that many Homoeopathic pharmaceuticals in India and abroad have spearheaded research on Ginkgo biloba and Ginkgo biloba Mother Tincture is being used globally for Cardio- Vascular disease, neurological problems.

1.       Improves cerebral circulation and pheripheral vascular problems

2.      Improves in age related forgetfulness

3.      Useful in weakness of memory, difficulty in thinking, insomnia, heaviness in frontal region, vertigo, buzzing sensation

4.    Inhibits Prolye endopeptidase (PEP), plays an important role in learning and memory process, depression and senile dementia

5.       Useful in Alzheimer's patients

6.    Inhibits platelet activation factor (PAF), thereby reduces the chances of blood clotting leading to various inflammations and allergic changes