MESOTHELIOMA CURCUMIN SLOWS DISEASE PROGRESSION

A common Asian spice and cancer-hampering molecules show promise in slowing the progression of mesothelioma, a cancer of the lung's lining often linked to asbestos. Scientists from Case Western Reserve University and the Georg-Speyer-Haus in Frankfurt, Germany, demonstrate that application of curcumin, a derivative of the spice turmeric, and cancer-inhibiting peptides increase levels of a protein inhibitor known to combat the progression of this cancer. Their findings appeared in the Aug. 14 online edition Clinical Cancer Research; the print version of the article will appear Oct. 1.

Malignant mesothelioma has received widespread notoriety because it occurs frequently in the lung linings of people exposed to asbestos. However, asbestos does not always cause this particular cancer that kills 43,000 people worldwide each year. Many mesothelioma patients were never exposed to asbestos.

"Mesothelioma is a disease that continues to have a significant burden worldwide, and the treatment option is really suboptimal. We must find better ways to treat it," said senior author Afshin Dowlati, MD, Professor of Medicine -- Hematology/Oncology, Case Western Reserve University School of Medicine, and member of the Case Comprehensive Cancer Center. "We now understand the mechanisms that drive cell proliferation and growth in malignant mesothelioma."

The culprit in sparking many cancers, particularly mesothelioma, is the intracellular protein and transcription factor STAT3 (signal transducer and activator of transcription 3). A signal transducer and activator is a pathway for instructing the growth and survival of cells, and a transcription factor is a protein that controls genetic information directing cells how to perform. STAT3 is notorious for sending signals to trigger the onset of human cancers and to fuel their continued growth. The great neutralizer of STAT3 is PIAS3 (protein inhibitor of activated STAT3). PIAS3 possesses the strength to inhibit and block STAT3's ability to cause cancer.

In this study, investigators assessed PIAS3 expression in tissue samples of mesothelioma solid tumors and the protein inhibitor's subsequent effects on STAT3 activity. Tissue samples came from three different locations in the country, and information logged for each specimen detailed how long the patient lived and the types of mesothelioma they had. Investigators then linked the levels of PIAS3 with STAT3 activity in each sample. Additionally, investigators examined the effects of curcumin and peptides extracted from PIAS3 segments on malignant mesothelioma cells in vitro.

"In those mesothelioma patients where PIAS3 is low, indeed STAT3 is activated," said Dowlati, Director of the Center for Cancer Drug Development at University Hospitals Seidman Cancer Center. "Mesothelioma patients who have low PIAS3 and high STAT3 have a greater chance of dying early. On the flip side, those patients with a high PIAS3 levels have a 44 percent decreased chance of dying in one year, which is substantial."

Investigators also found that curcumin and PIAS3 peptides raised PIAS3 levels, which brought down STAT3 activity and caused mesothelioma cells to die. Their study served as proof of principle about the effectiveness of these two compounds in treating malignant mesothelioma, a first step in moving a treatment toward clinical trials. Additionally, their findings demonstrated that PIAS3 could serve as a predictive marker for managing mesothelioma because the disease's tumors do not always progress in a consistent, predictable manner, even when tumor stages, grades and clinical presentations appear similar.

"Our findings suggest that PIAS3 expression positively affects survival in mesothelioma patients and that PIAS3 activation could become a therapeutic strategy," Dowlati said. "Our interest for the future is that we want to find better, more simple ways to increase intracellular levels of PIAS3 for malignant mesothelioma through the use of synthetic PIAS3 peptide or curcumin analogs. We must develop a curcumin analog that is absorbable by the human body. Currently, curcumin ingested as the spice turmeric has practically no absorption within the gut."

Their investigation also contributes to the overall body of scientific knowledge for all cancer.

"Our findings beg the question of what role PIAS3 could play in limiting STAT3 activation in other cancers as well," Dowlati said. "There is an opportunity to extend this discovery because a number of cancers are STAT3-activated."

POMEGRANATE DRUG TO AID ALZHEIMERS PARKINSONS DISEASE

Dr Olumayokun Olajide's research will look to produce compound derivatives of punicalagin for a drug that would treat neuro-inflammation and slow down the progression of Alzheimer's disease

The onset of Alzheimer's disease can be slowed and some of its symptoms curbed by a natural compound that is found in pomegranate. Also, the painful inflammation that accompanies illnesses such as rheumatoid arthritis and Parkinson's disease could be reduced, according to the findings of a two-year project headed by University of Huddersfield scientist Dr Olumayokun Olajide, who specialises in the anti-inflammatory properties of natural products.

Now, a new phase of research can explore the development of drugs that will stem the development of dementias such as Alzheimer's, which affects some 800,000 people in the UK, with 163,000 new cases a year being diagnosed. Globally, there are at least 44.4 million dementia sufferers, with the numbers expected to soar.

The key breakthrough by Dr Olajide and his co-researchers is to demonstrate that punicalagin, which is a polyphenol -- a form of chemical compound -- found in pomegranate fruit, can inhibit inflammation in specialised brain cells known as micrologia. This inflammation leads to the destruction of more and more brain cells, making the condition of Alzheimer's sufferers progressively worse.

There is still no cure for the disease, but the punicalagin in pomegranate could prevent it or slow down its development.

Dr Olajide worked with co-researchers -- including four PhD students -- in the University of Huddersfield's Department of Pharmacy and with scientists at the University of Freiburg in Germany. The team used brain cells isolated from rats in order to test their findings. Now the research is published in the latest edition of the journalMolecular Nutrition & Food Research and Dr Olajide will start to disseminate his findings at academic conferences.

He is still working on the amounts of pomegranate that are required, in order to be effective.

"But we do know that regular intake and regular consumption of pomegranate has a lot of health benefits -- including prevention of neuro-inflammation related to dementia," he says, recommending juice products that are 100 per cent pomegranate, meaning that approximately 3.4 per cent will be punicalagin, the compound that slows down the progression of dementia.

Dr Olajide states that most of the anti-oxidant compounds are found in the outer skin of the pomegranate, not in the soft part of the fruit. And he adds that although this has yet to be scientifically evaluated, pomegranate will be useful in any condition for which inflammation -- not just neuro-inflammation -- is a factor, such as rheumatoid arthritis, Parkinson's and cancer.

The research continues and now Dr Olajide is collaborating with his University of Huddersfield colleague, the organic chemist Dr Karl Hemming. They will attempt to produce compound derivatives of punicalagin that could the basis of new, orally administered drugs that would treat neuro-inflammation.

Dr Olajide has been a Senior Lecturer at the University of Huddersfield for four years. His academic career includes a post as a Humboldt Postdoctoral Research Fellow at the Centre for Drug Research at the University of Munich. His PhD was awarded from the University of Ibadan in his native Nigeria, after an investigation of the anti-inflammatory properties of natural products.

He attributes this area of research to his upbringing. "African mothers normally treat sick children with natural substances such as herbs. My mum certainly used a lot of those substances. And then I went on to study pharmacology!"

Role of physiotherapy in Parkinsons Disease

Parkinson's Disease

Parkinson’s disease is really a condition in which the amounts of chemical messengers in the brain are reduced. Many times, it causes reducedmobility, memory problems, muscle tremors, and difficulties performing everyday tasks. Physiotherapy for those who have Parkinson’s disease concentrates on increasing and looking after mobility whilst lowering the risk of falls.
Physio provide neurological physiotherapy treatment specific towards the needs of the individual. Our specialist physiotherapists know how Parkinson’s affect an individual and people close to them. Consequently, the majority of patients with Parkinson’s are noticed in their home environment with partners, relatives or carers present. 
Parkinson's disease affects approximately One in 500 of the general population. It's a progressive neurological condition affecting activities for example walking, talking, and writing.
Parkinson's disease occurs as a consequence of a reduction of nerve cells within the part of the brain referred to as substantia nigra. These cells have the effect of producing a chemical referred to as dopamine, which assists in the transmission of messages delivered to the parts of the brain that co-ordinate movement. Using the significant reduction in the amount of dopamine-producing cells, these areas of the brain are unable to function normally.
Classify the results of Parkinson's disease as motor and non-motor. 
Common motor symptoms observed in Parkinson's disease are:
• Tremor - usually begins in a single hand (the first symptom for 70% of individuals with Parkinson's disease).
• Slowness of motion - people with Parkinson's disease usually see that they have difficulty initiating movements or that performing movements takes longer.
• Stiffness or rigidity of muscles - individuals with Parkinson’s disease often find they have problems with activities for example standing up from a chair or allowing this to continue in bed.
• Postural instability - results in impaired balance and falls.
• Gait and posture disturbances:
o Shuffling gait.
o Decreased arm swing
o Stooped, forward-flexed posture
o Gait freezing - happens in tight, cluttered spaces, doorways or when initiating gait
• Other motor symptoms:
o Fatigue
o Mask-like, expressionless face with infrequent blinking
o Micrographia (small, cramped handwriting)
Various non-motor symptoms can also be experienced, for example:
• Sleep disturbance
• Constipation
• Urinary urgency
• Depression
Treatment for Parkinson’s Disease
While there is no cure for Parkinson's disease at the moment, drugs are used to attempt to control the symptoms. Within the majority of newly diagnosed people considerable improvements is possible by careful introduction of anti-Parkinson drugs. When only mild symptoms can be found, individuals may decide, along with their GP/consultant, to delay medications until their symptoms increase and instead depend on a healthy lifestyle, focusing on exercise, relaxation and diet. As Parkinson's disease is an extremely individual condition medicine is prescribed and adapted to individual needs. Reaction to medication varies from individual to individual and not every medication is going to be considered suitable for everyone.
Kinds of medication commonly used are:
• Levodopa
• Dopamine agonists
• COMT inhibitors
• MAO-B inhibitors
• Glutamate antagonists
• Anticholinergics
Surgery
Surgical treatment is available for some people with Parkinson’s disease, determined by symptoms. This includes:
• Deep brain stimulation
• Lesioning
Parkinson’s Disease Physiotherapy Treatment
Physiotherapy is essential in the management of Parkinson’s disease. Individuals with Parkinson’s disease usually have mobility problems and therefore are often at high-risk of falls. Physio try to increase mobility and recommend changes to the home environment to improve independence and safety. Consequently, patients with Parkinson’s disease can cope better from day-to-day and keep their independence.
Independence is increased with balance, stretching and strengthening exercises and provision of walking aids and equipment. Our physiotherapists will assess how a person performs activities for example; walking, going up and down stairs, getting away from a chair and becoming in and out of bed. Our physiotherapists canteach patients, their loved ones and carers, special strategies how do deal with common the signs of Parkinson’s. Family and carers usually see this advice and the practical handling techniques particularly helpful, with regards to helping individuals up out of bed, walking and overcoming freezing. 
Physio recommend a house assessment is performed so advice could be given regarding any changes which may be required. This will boost the safety and independence from the patient with Parkinson’s disease. In the home assessment our physiotherapists will give you advice and suitable tips about aids and adaptations to increase the independence and safety from the patient.
A specific falls prevention programme can be produced to be completed between treatment sessions. The house assessment, along with a falls prevention programme, will greatly increase safetyat home and lower the risk of falls.
Physio offer acupuncture,hydrotherapy, seating / wheelchair assessments and suggestions about postural management for people with Parkinson’s disease. Patients with Parkinson’s disease often enjoy physiotherapy because it increases their independence and reduces their anxiety about falling.

TOP HOMOEOPATHIC REMEDIES FOR MENIERES DISEASE

Meniere's disease is a disorder of the inner ear that causes episodes in which you feel as if you're spinning (vertigo), and you have fluctuating hearing loss with a progressive, ultimately permanent loss of hearing, ringing in the ear (tinnitus), and sometimes a feeling of fullness or pressure in your ear. In most cases, Meniere's disease affects only one ear.

Meniere's disease can occur at any age, but it usually starts between the ages of 20 and 50. It's considered a chronic condition, but various treatments can help relieve symptoms and minimize the long-term impact on your life.

Cause--The cause of Meniere's disease isn't understood. One popular theory that hasn't been proved is that Meniere's disease appears to be the result of the abnormal amount of fluid (endolymph) in the inner ear. This often shows on autopsies, but it's not clear that it causes the episodes.

Factors that affect the fluid, which might contribute to Meniere's disease, include:-Improper fluid drainage, perhaps because of a blockage or anatomic abnormality, Abnormal immune response,Allergies, Viral infection, Genetic predisposition,Head trauma,Migraines

Because no single cause has been identified, it's likely that Meniere's disease results from a combination of factors.

Symptoms--Signs and symptoms of Meniere's disease include:

·         Recurring episodes of vertigo. You have a spinning sensation that starts and stops spontaneously. Episodes of vertigo occur without warning and usually last 20 minutes to several hours, but not more than 24 hours. Severe vertigo can cause nausea and vomiting.

·         Hearing loss. Hearing loss in Meniere's disease may come and go, particularly early on. Eventually, most people have some permanent hearing loss.

·         Ringing in the ear (tinnitus). Tinnitus is the perception of a ringing, buzzing, roaring, whistling or hissing sound in your ear.

·         Feeling of fullness in the ear. People with Meniere's disease often feel pressure in the affected ears (aural fullness) or on the side of their heads.

After an episode, signs and symptoms improve and might disappear entirely. Episodes can occur weeks to years apart.

HOMOEOPATHIC REMEDIES

CHININUM SULPH 30- :- Chinimum sulph is one of the best indicated remedies for Meniere’s disease when periodicity of the attacks is marked.It is considered a specific for this condition.   The leading symptom for this medicine in most of the cases is tinnitus. There is an unusual sensation of roaring in the ears and it is invariably associated with vertigo. People in whom Chinimum sulph may be indicated generally have complaints of postural vertigo and heaviness in the ears. Vertigo could be very sudden in onset and in severe cases the person may fall down due to loss of balance. Generally, they may feel uncomfortable in standing posture. Chinimum sulph gives desired results when there is a considerable degree of hearing loss and affect the left ear

PHOSPHOROUS 200-:- Phosphorous is one of the top ranking drug in Meniere’s disease associated with echoing sounds in the ears.I have given Phosphorous in Meniere’s disease with equally good results. The unique feature for Phosphorous in these cases is the hearing impairment to human voices. Phosphorous may be indicated in lean, thin and stoop shouldered persons. Though there is no satisfactory evidence, but these complaints may be related to attack of typhoid fever. When asked in detail, the person may reveal that the first episode of vertigo and tinnitus had manifested just after typhoid fever. Phosphorous may be indicated in people who have a gradual hearing impairment. Vertigo may be felt on an attempt to rise from the bed. In severe cases, the person may faint during an attack of vertigo. People who need Phosphorous are generally restless physically and mentally. They may be easily affected by external stimuli like sharp noises, bright lights and this may trigger sudden attacks of vertigo. Tinnitus may be of echoing type, that is, all the sounds may have an echoing effect.

THERIDION 30- :- It is one of the most indicated remedies in Meniere’s disease with marked vertigo that comes on least motion and is associated with extreme nausea and vomiting .Theridion are generally sensitive to noises and may feel a sudden discomfort when they hear loud and unpleasant noises. The guiding symptom for Theridion to be prescribed is that, vertigo comes when the person closes the eyes. Theridion may be indicated in people who detest travelling because it triggers attacks of vertigo. There may be an uneasy sensation in the ears with fullness or heaviness in one or both ears.

AMMONIUM IODIDE 30- In younger people. Dull headache and vertigo

CHENOPODIUM 30- Deaf to the human voice. , but grat sensitivity to for other sounds and better for high pitched sounds. Buzzing in the ear

CHIN. SAL. 30- Deafness and tinnitus

NATRUM SAL. 200- Vertigo and deafness with noises in the ear. It is a good remedy if there is progressive deafness

Charcot Marie Tooth Disease An Inherited Neuropathy

Today's post from chronicpainreliefoptions.com (see link below) is both complex and easy to understand and talks in full about an inherited form of neuropathy with a strange name but serious problems. Charcot-Marie-Tooth Disease (CMT) is the nerve disease and it is yet another form of neuropathy that can take months if not years to diagnose. You may feel that because you haven't been told that your neuropathy is C.M.T. you don't need to read this article but believe me you'll recognise so many of the symptoms and treatments, you'll feel right at home here (although with C.M.T there is much more emphasis on muscular and foot problems). Many people learn that they have C.M.T. long after being told they have idiopathic neuropathy (no cause can be established) and have been sent home with the necessary pain prescription, to make the best of it, so it's important for your doctor or neurologist to at least rule it out. The treatment and symptoms are much the same as other neuropathies, so with a bit of luck, you won't be missing out due to a mis-diagnosis but nevertheless, establishing the true nature of your neuropathy is important to all concerned, if only because it validates your pain and discomfort. If you already have C.M.T. this article will fill you in on information you may not have received from your doctor - worth a read for everyone.

Charcot-Marie-Tooth – A Very Painful Disorder
By Jeffrey Bado, D.O. | September 3, 2016

HAVE YOU CONSIDERED THIS?

During my career as a specialist practicing General Internal Medicine, with a focus on Pain Management, I encountered many unusual causes of chronic pain. In most of those cases, the patients were referred to me for management of their chronic pain and had already been diagnosed by various sub-specialists.

One of the most challenging syndromes I faced in clinical practice was an inherited condition called Charcot-Marie-Tooth Disease (CMT). Due to the clinical frequency of this disorder I have decided to write this monograph entitled, “Charcot-Marie-Tooth – A Very Painful Disorder.”
All of the cases of CMT that were referred to me had a diagnosis and ample medical records.

Patients were usually referred to my practice as a last desperate attempt at their pain management.

Charcot-Marie-Tooth disease is a neurological disorder named after the three physicians who first described it in 1886 — Jean-Martin Charcot of France, Pierre Marie of France, and Howard Henry Tooth of the United Kingdom.

CMT is the most commonly inherited peripheral nerve disorder in the U.S. affecting about 1 in 2,500 people. It affects more than 250,000 Americans.

Since this condition is frequently undiagnosed, misdiagnosed or diagnosed very late in life, the true number of affected persons may actually be higher.

A “TRUE LIFE” CASE OF CMT…

Tracey (her name has been changed) came to my office on referral from a friend. She was siting patiently in the exam room with a “quad cane” at her side when I first interviewed her.

“Hello Tracey, I see you have brought a very extensive copy of your medical records with you. The records indicate that you have been diagnosed with Charcot-Marie-Tooth (CMT) disease.

How may I help you?” I said somewhat uncertain of just what her condition was.

“Yes, I have been to a number of Doctors for my condition. None of them seemed to know what I have. It took 7 years and 7 different Doctors before anyone could figure out my case,” she said with a frustrated tone of voice.

“Do you know what CMT is, Dr. Bado?”

It was never my style to pretend to know something when I didn’t…”Tracey, to be honest with you, I remember the name from medical school but I have never had a case with this disease.”

“But, if you will work with me, I will research what you have and on your next visit I will be fully acquainted with it,” I said a little embarrassed at my ignorance about her disorder.

Tracey smiled, “You are the first Doctor I met who admitted that they didn’t know what it was. I think you and I are going to do just fine.”

I was relieved that I had not disappointed her.

“Tracey, why don’t you tell me just how you feel and maybe I can begin some therapy today?” My goal with every new patient in my practice was to establish trust as early as possible.

I believe the best way to do that is to let a new patient tell their story without any time pressure or interruptions. Here is what she told me over the next hour…

Tracey had been in good health until she was in her mid-30s when she noticed she began to stumble without warning. This happened even when she was walking on flat surfaces that most people would not stumble on.

Her diagnosis of CMT had led to her falling, without warning, occasionally. She had embarrassed herself at several social gatherings with friends because of this.

Her husband had even accused her of drinking too much alcohol at a party where she had fallen…he was embarrassed too.

She went to her Family Doctor who could not find anything wrong with her. Her husband was becoming skeptical and did not want to go to social functions with her.

This put an additional strain on their already fragile marriage.

Over time her condition worsened. After a year she began to notice her feet were “numb” to the touch but felt as if they were always burning.

There were no visible physical changes to her feet though. She had always had “high arched” feet but was able to walk just fine.

Tracey found she was unable to wear high heeled shoes anymore as her ankles would “give out.” She went to another Family Doctor who spent 10 minutes with her and told her she was “just clumsy.”

On several occasions she went to the Emergency Room of her local community hospital when the burning of her feet became unbearable. The Doctor spent 2 minutes with her, ran a few blood tests looking for “arthritis”, and gave her some Motrin.

It didn’t help…she was getting worried.

Her social life was becoming unmanageable as she began to isolate herself due to her frequent stumbling and falls. Furthermore, she was unable to stand for long periods at work (she worked on an assembly line) and had to quit.

Her husband was sure she was just malingering since none of the Doctors could identify what was wrong with her. Her trust in him waned and she no longer wanted to be physically intimate with him.

By the time she was in her early forties she had pain in her feet all the time. Tracey had difficulty just walking around her home, and had fallen down the stairs from the second floor several times.

The Family Doctor she was seeing finally referred her to a Neurologist. In one visit he diagnosed her with CMT and told her the bad news…she had an incurable disease that will only get worse.

He offered her little in the way of pain relief. He told her she would just have to “live with the pain.”
Tracey considered suicide but, the recent birth of her grand-daughter kept her from attempting to end her life.

Tracey’s story with CMT is not unusual. Neuropathic conditions often have little in the way of observable abnormalities.

This makes it difficult for an untrained person to be able to relate to a person suffering from CMT. In fact, even Doctors are often fooled by the lack of physical findings.

Let’s discuss for a moment just what is happening to the human body with Charcot-Marie-Tooth disease. 

WHAT IS THE ANATOMY AND PHYSIOLOGY OF CMT?

In the normal human body, nerves are attached to muscles where the muscle is then “given instructions” for movement from the nerve. Nerves that are required to transmit signals rapidly are covered with a form of “insulation” called myelin.
Myelin allows the electrical signal to travel rapidly along the tail of the nerve called an axon.



If the myelin or the axon itself is in anyway disrupted, the transmission of the nerve signal is affected. If the nerve signal is affected the muscle that is relying on the signal for instructions will not function properly.

Walking is a very complicated function and requires precise coordination of the muscles of the legs and feet to occur.



Furthermore, the information from the bottom of the foot is sent up to the spinal cord and brain for precise adjustment of balance during walking. Simple numbness of the bottom of the foot can make walking difficult.

Numbness often preceeds weakness in people with CMT disease and may not be noticed by the person suffering from the disease in the early stages.







CMT can affect the myelin, the axon proper, or both. The more disruption of the myelin and axon, the more dysfunction that occurs.
The disease process is unrelenting in people with CMT and is not visible in the early stages.

In CMT there is a genetic alteration that renders the myelin dysfunctional and/or the mitchondria inside the axon defective (mitochondria manufacture energy). These 2 processes can result in what is called a neuropathy.

HOW DO YOU DIAGNOSE CMT?

The diagnosis of CMT is suspected when the following history, symptoms, physical signs, and diagnostic findings are manifested by a patient:

HISTORY
People with CMT will often relate a history of difficulty walking, running, unprovoked falling, leg weakness or numbness, hand weakness or numbness, and loss of fine motor movement of the fingers.

There may be a family history of similar symptoms (or perhaps even a diagnosis). It is not unusual for people to have a long delay in diagnosis if their examining Doctor has never seen a case.

SYMPTOMS AND SIGNS



1)Decreased sensitivity to heat, touch, or pain of the feet and/or hands.

2)Muscle weakness of the feet, lower legs, or hands.

3)Trouble with fine motor skills of the hands.

4)Foot drop

5)Loss of muscle mass of the lower legs.

6)Unprovoked tripping or falling.

7)Hammertoes

8)High Arched Feet

9)Flat Feet

10)Loss of Patellar and Achilles reflexes.

DIAGNOSTIC STUDIES
Needle Nerve Conduction/Electromyogram

The classic diagnostic study for CMT is a nerve conduction/electromyogram study (NC/EMG). This is performed by inserting needles into nerves and muscles of the areas already in pain and placing a small electrical charge through the needles to stimulate a nerve or muscle.

The response of the nerve or muscle is graphically recorded and interpreted by a physician.

The NC/EMG is an uncomfortable study. Imagine having needles inserted into areas that already are painful.
Few patients will subject themselves to more than one NC/EMG after having experienced the discomfort of the first.

The graphic findings are diagnostic for nerve or muscle dysfunction. The study is limited by the discomfort it causes, the precision of the needle insertion, and can only detect larger nerve fiber dysfunction.

Small nerve fiber abnormalities can be missed with this type of diagnostic study.
Neural Scanning

There is a fairly recent improvement in the detection of nerve dysfunction called Neural Scanning (NS). NS does not require needle punctures.

The electrical current in NS is applied via skin pad electrodes. The particular electrical frequency of stimulation used allows for the measurement of both large and small fiber nerves (remember needle NC/EMG can only measure large nerve fibers).

In this way, early detection of neuropathic changes in very small nerve fibers (called C fibers) can be detected with Neural Scanning. Furthermore, it is a painless way to stimulate nerve fibers.

I prefer this method of nerve and muscle stimulation as the patients tolerated it much better. They were more likely to allow me to recheck their results with repeat NS after they had been on therapy.
Most of my patients viewed the needle NC/EMG as torturous, but readily accepted multiple Neural Scans.

The following diagnostic studies are also performed at the discretion of the examining physician:
Nerve Biopsy: this looks at the health of the nerve microscopically. Obviously, the patient requires a minor surgical procedure for this, possibly causing more pain.
MRI imaging: usually of the feet and lower legs. This may show atrophy in a pattern consistent with demyelination or axonal injury.
X-Rays of the feet and/or hands: prolonged and severe neuropathy can actually result in resorption of the toes and fingers. By the time this test is positive the disease is usually quite advanced.
The definitive way to specifically diagnose CMT is with genetic testing.

Molecular genetic testing is currently available for CMT1A, CMT1B, CMT1D, CMT2E, CMT4A, CMT4E, CMT4F and CMTX.

The following section is an in depth review of the present combinations of genetic abnormalities found in CMT.

GENETIC SUBTYPES

Today, CMT is precisely diagnosed by genetic testing. There are many sub-types as assigned by the specific genetic defect.
Each sub-type is classified according to the specific genetic defect, where the main disorder resides (whether of the nerve axon or of the myelin sheath around the axon), age of onset, severity of dysfunction, and body parts affected.

The most recent classification is as follows:
CMT1A: A subtype of CMT1, called CMT1A (caused by a duplication in the PMP22 gene on chromosome 17) accounts for around 60 percent of CMT1 cases, making it the most common subtype of CMT1. The PMP22 gene encodes for peripheral myelin protein, and disruption of this gene leads to a dysfunctional myelin sheath on nerves.

CMT1A patients usually present with typical CMT onset within adolescence, but remain ambulatory with no reduced life expectancy.
CMT1B: CMT1B is the second most common subtype of CMT1. CMT1B is caused by a defect within the MPZgene, which lies on chromosome 1.

The MPZ gene produces myelin protein zero, and disruption of this gene also causes defects within the myelin sheath. CMT1B patients have onset and symptoms similar to those of CMT1A patients, although there is a wide range of variability within CMT1B.
CMT1C: caused by defects in the LITAF gene.
CMT1D: caused by defects in the ERG2 gene.
CMT1E: caused by defects in the PMP22 gene, which is also associated with CMT1A. Instead of having a duplication of the normal PMP22 gene, CMT1E patients harbor different genetic abnormalities called point mutations within the PMP22 gene.
CMT1F: caused by defects in the NEFL gene.
CMTX: caused by mutations in the gene for connexin 32, which normally codes for a protein located in myelin, the insulating sheath that surrounds nerve fibers.

Because this form of CMT is X-linked, it affects males more frequently than females (all other forms of CMT affect males and females equally).
CMT Type 2: (CMT2) is a subtype of CMT that is similar to CMT1 but is less common. CMT2 is typically autosomal dominant, but in some cases can be recessive.

CMT2 is caused by direct damage to the nerve axon itself in comparison to CMT1 which results from damage to the myelin sheath insulating the axon. CMT2 is commonly referred to as “axonal” CMT.

CMT2A is the most common subtype of CMT2 and is caused by defects in the MFN2 gene. The MFN2 gene encodes for Mitofusin 2, which is a protein involved in the fusion of cellular mitochondria.

Other more rare forms of CMT and their gene defects include:
CMT2B: caused by defects in the RAB7 gene.
CMT2C: caused by defects in the TRPV4 gene.
CMT2D: caused by defects in the GARS gene.
CMT2E: caused by defects in the NEFL gene.
CMT2H: caused by defects in the HSP27 gene.
CMT2I: caused by defects in the HSP22 gene.
CMT3: severe, early onset CMT is a sub-type of CMT that is a particularly severe variant of the disease. Other terms used to describe this variant include Dejerine-Sottas disease, and congenital hypomyelinating neuropathy.

Severe, early-onset CMT can be inherited in either an autosomal dominant or recessive pattern.

CMT3 is a severe neuropathy with generalized weakness sometimes progressing to profound disability, loss of or changes in sensation, curvature of the spine and sometimes mild hearing loss.

Severe, early-onset CMT begins in infancy or early childhood, and progresses slowly. Severe disability may eventually occur.

CMT3 is caused by defects in the genes for proteins found in axons or in the genes for proteins found in myelin. Some of these same genes also cause CMT1 and CMT2 such as PMP22, MPZ, and GJB.
CMT4: a rare subtype of CMT, a genetic, neurological disorder that causes damage to the peripheral nerves and tracts of nerve cell fibers that connect the brain and spinal cord to muscles and sensory organs. CMT4 is a subtype of CMT that is inherited in an autosomal recessive pattern.

CMT4 is caused by defects in the myelin sheath which insulates the axon. Symptoms are generally more severe than in CMT types 1 or 2.

There are sub-types for this severe type of CMT also:
CMT4A: caused by defects in the GDAP1 gene.
CMT4B: caused by defects in the genes MTMR2 (CMT4B1), or MTMR13 (CMT4B2).
CMT4C: caused by defects in the SH3TC2 gene.
CMT4D: caused by defects in the NDRG1 gene.
CMT4E: caused by defects in the EGR2 gene.
CMT4F: caused by defects in the PRX gene.
CMT4H: caused by defects in the FDG4 gene.
CMT4J: caused by defects in the FIG4 gene.
Obviously, the genetic types of CMT are very complex and really do not affect the treatment of the disease. 

WHAT IS THE TREATMENT OF CMT?
As CMT is presently incurable, treatment is aimed at reducing pain, limiting orthopedic complications, improving functionality, treating depression, and adjusting to the emotional/social isolation that can occur with this devastating illness.

I recommend my article on, “The 7 Best Treatments for Chronic Pain” as a starting point for therapy of CMT (click here to link to that article).

In addition to the therapies recommended in that article, the following are usually listed as therapies for CMT:
Physical Therapy
Shoe Orthotics (shoe inserts)
Leg Bracing
Selective Orthopedic Surgery (for limb deformity)
Effective treatment of pain is essential with CMT.

Simply instructing a patient that they must “live with it” is an insufficient response of a Doctor to a patient in chronic pain. Chronic pain causes negative physiologic changes to the immune system, nervous system, cardiovascular system, endocrine system, cerebrovascular system, and nearly every other system of the human body.

All cause mortality is also increased in people with under-treated chronic pain. This means that existing disorders are often made worse in the presence of chronic pain.
The effect of chronic pain on existing disorders is often under-reported since the cause of death is never “Undertreated Pain” but usually reflects the underlying disease process.
DESPITE ALL THAT HAS BEEN SAID, THERE IS HOPE…

Are you wondering what happened to “Tracey” (the case history I presented at the beginning of this long article)? Her outcome was one of the many successes in my Pain Management practice.

On the first long visit with Tracey I was able to establish that her pain was averaging an 8 or 9 out of 10 when not treated. My custom for my pain practice was to query a new patient as to what medicine in their past history worked best for their pain.

Thereafter, I would estimate the dose based on their usage history.

In Tracey’s case I took a pragmatic approach:

FIRST…I prescribed a short acting opiate pain medication to be taken every 4 hours while awake. This would mean that her starting dose would require 240 pills for the month (1 every 4 hours and 2 at bedtime so she could sleep 4 or more hours).
The “start low and go slow” mantra, that seems to have infiltrated the medical literature, didn’t make sense to me in a patient who was already opiate tolerant.

Nowhere else in medicine do we “start low and go slow” with a patient who already has historically demonstrated an effective dose. Can you imagine a patient with severe high blood pressure, who has been maintained on effective doses of medication, seeing a new Doctor and restarting their medications at the lowest dose possible?

They could have a complication doing this (such as a stroke).

Why is this done with opiate pain medications? It is done this way because the fear of inducing addiction (and potential legal reprisal) is more important to most present day physicians than effectively treating a patient’s pain.

The actual risk of addiction in a chronic pain patient (with whom there is no history of addiction) is less than 1%. The opiate “naysayers” seem to ignore this statistic in favor of political correctness.

Once I had established what dose of opiates would need to keep her pain at a “5” with the short acting opiate, I then converted Tracey to a combination of long acting opiate pain medicine as “background” coverage for her pain and short acting opiate pain medicine for “break-through” pain (the episodes where her pain intensified during the day).

This will often take several sequential visits. Most of my patients had their pain effectively treated within 3 months or less.

The format of using a combination of long acting opiate pain medication with short acting for “break-through” pain mirrors the way in which diabetics are treated with insulin. In a diabetic, a long acting insulin is given as “back-ground” coverage of their blood sugar.

Then, before each meal. a fingerstick blood sugar is checked and a “sliding scale” dose of short acting insulin is given to “cover” any spike in blood sugar. The dose of the insulin is never arbitrarily limited but is determined by how high the blood sugar is.

So it should be with the dosing of opiate pain medications.

SECOND…I considered starting Tracey on a slower to act medication that reduces pain conduction (such as Lyrica). It may take weeks to work so having the opiate pain medication gave immediate relief and hope.

The adjustment of the Lyrica dosing will take months due to each new dose requiring weeks of observation to see if it was reducing her pain.

THIRD…I also considered giving Tracey an anti-depressant that recycles both norepinephrine and serotonin (such as Cymbalta). This type of medicine has shown great promise in reducing pain and alleviating depression (of which most chronic pain patients suffer).

All of these medicines are prescribed with the consideration of potential side effects, drug interactions, previous tolerances, and whether the patient’s insurance will cover the cost of the medicines (a HUGE consideration when considering what medicines to choose).

Within 8 weeks I was able to lower Tracy’s chronic pain level to a “5” where she remained until I retired in January of 2013. She had been a patient of mine for over 7 years at the time I retired and her pain was well controlled throughout the entire period of time.

Don’t believe the misinformation that “long term” opiate therapy doesn’t work. Just ask “Tracey”…

If you are suffering with CMT (or any chronic pain syndrome for that matter) there is hope for you. You will need to find a physician who is willing to prescribe the medications you need.

Those Doctors are out there…don’t give up looking for them.

I hope you have enjoyed this rather long article on CMT. It has been my privilege to share this information with you.

If you have further questions or comments, please send me an email. I will promptly respond.

Wishing you joy and healing,

Jeff

http://chronicpainreliefoptions.com/charcot-marie-tooth-a-very-painful-disorder

HOMOEOPATHIC REMEDIES FOR HAND FOOT AND MOUTH DISEASE

Hand -foot-and-mouth disaese is a viral infection caused by  coxsackievirus A16. The coxsackievirus belongs to a group of viruses called nonpolio enteroviruses. Other types of enteroviruses sometimes cause hand-foot-and-mouth disease.

Oral ingestion is the main source of coxsackievirus infection and hand-foot-and-mouth disease. The illness spreads by person-to-person contact with an infected person's:

·         Nasal secretions or throat discharge

·         Saliva

·         Fluid from blisters

·         Stool

·         Respiratory droplets sprayed into the air after a cough or sneeze

Hand-foot-and-mouth disease is most common in children in child care settings because of frequent diaper changes and potty training, and because little children often put their hands in their mouths.

Although your child is most contagious with hand-foot-and-mouth disease during the first week of the illness, the virus can remain in his or her body for weeks after the signs and symptoms are gone. That means your child still can infect others.

Some people, particularly adults, can pass the virus without showing any signs or symptoms of the disease.

Outbreaks of the disease are more common in summer and autumn in the United States and other temperate climates. In tropical climates, outbreaks occur year-round.

Hand-foot-and-mouth disease isn't related to foot-and-mouth disease (sometimes called hoof-and-mouth disease), which is an infectious viral disease found in farm animals. You can't contract hand-foot-and-mouth disease from pets or other animals, and you can't transmit it to them.

Causes--The most common cause of hand-foot-and-mouth disease is infection with the coxsackievirus A16. The coxsackievirus belongs to a group of viruses called nonpolio enteroviruses. Other types of enteroviruses sometimes cause hand-foot-and-mouth disease.

Oral ingestion is the main source of coxsackievirus infection and hand-foot-and-mouth disease. The illness spreads by person-to-person contact with an infected person's:

·         Nasal secretions or throat discharge

·         Saliva

·         Fluid from blisters

·         Stool

·         Respiratory droplets sprayed into the air after a cough or sneeze

Symptoms--Hand-foot-and-mouth disease may cause all of the following signs and symptoms or just some of them. They include:

·         Fever

·         Sore throat

·         Feeling of being unwell (malaise)

·         Painful, red, blister-like lesions on the tongue, gums and inside of the cheeks

·         A red rash, without itching but sometimes with blistering, on the palms, soles and sometimes the buttocks

·         Irritability in infants and toddlers

·         Loss of appetite

The usual period from initial infection to the onset of signs and symptoms (incubation period) is three to six days. A fever is often the first sign of hand-foot-and-mouth disease, followed by a sore throat and sometimes a poor appetite and malaise.

One or two days after the fever begins, painful sores may develop in the mouth or throat. A rash on the hands and feet and possibly on the buttocks can follow within one or two days.

Risk factors--Hand-foot-and-mouth disease primarily affects children younger than age 10, often those under 5 years. Children in child care centers are especially susceptible to outbreaks of hand-foot-and-mouth disease because the infection spreads by person-to-person contact, and young children are the most susceptible.

Children usually develop immunity to hand-foot-and-mouth disease as they get older by building antibodies after exposure to the virus that causes the disease. However, it's possible for adolescents and adults to get the disease.

Complications--The most common complication of hand-foot-and-mouth disease is dehydration. The illness can cause sores in the mouth and throat, making swallowing painful and difficult.

Watch closely to make sure your child frequently sips fluid during the course of the illness. If dehydration is severe, intravenous (IV) fluids may be necessary.

Hand-foot-and-mouth disease is usually a minor illness causing only a few days of fever and relatively mild signs and symptoms. A rare and sometimes serious form of the coxsackievirus can involve the brain and cause other complications:

Viral meningitis. This is a rare infection and inflammation of the membranes (meninges) and cerebrospinal fluid surrounding the brain and spinal cord.

Encephalitis. This severe and potentially life-threatening disease involves brain inflammation caused by a virus. Encephalitis is rare.

HOMOEOPATHIC REMEDIES

MERCURIUS SOL 30- Merc sol is one of the leading remedies for hand foot and mouth disease . Here mouth sores can be very severe and the person is very sensitive to heat and cold. There may have a fever before getting the blisters and may alternate between getting too hot with perspiration and becoming chilled at night. Becoming too hot or too cold makes the patient worse in general. The blisters tend to be more painful at night. One of the characteristic symptoms of Mercurius is the tendency to drool or to have an excess of saliva in the mouth. The breath of the patient may be quite offensive with pus visible on the tonsils or else where in the mouth.

ANTIMONIUM TART. 30-Antimonium tart is another effective remedy for this diseases. In  the chill stage of fever--.gooseflesh and icy cold skin. Heat stage of fever.--the patient clings to those around and wants to be carried. He does not want to be touched or looked at.Thirstless despite the dry parched tongue.Sweat stage of fever-profuse , cold , clammy or sticky , dry, cracked, parched tongue with whitish discoloration in the centre. Tongue tip and sides clean, moist and red. Thrush. There is craving for apples or apple juice.

BORAX 3X—Borax is another top remedy for this disease . The patient refuses to talk during fever. Desire for cold drinks and cold food during fever.There is great heat and dryness of mouth with white ulcers. White fungus-like growth, they are tender.Ulcers bleed on touch and eating. Painful red blisters on tongue. Sore mouth prevents infants from nursing. Fear of downward motion. Startle easily. Very sensitive to sudden noises .

BELLADONNA 200-Belladonna is prescribed when there is high temperature, with flushed face and the eye is sensitive to light.There is severe headache with either restlessness or drowsiness. The  rash is red in colour with a feeling of heat and throbbing.

BRYONIA ALB. 30-Bryonia alb is prescribed when a dry cough develops if the fever persists for several days. There is thirst for large quantities of cold water with dry mouth. The child feels worse from motion. Constipation is also occurs .

APIS MELLIFICA 30-Apis mel is prescribed when the eruption is pink and puffy and very itchy, with stinging pains. The eyelids may become swollen. The child feels worse from warmth , and is irritable. There is no thirst.

RHUS TOXICODENDRON 30-Rhus tox is prescribed when severe itching occurs, which is worse from scratching and is relieved from warm bath or applying heat. The eyes may become inflamed and sticky. There is severe body pain and muscles feel very stiff, which is relieved by gentle movement or from warmth.The patient is restless both mentally and physically.

SULPHUR 200-Sulphur is prescribed when severe itching and burning occurs which is worse from scratching and washing. The symptoms worse from warmth. Both heat and chills are felt during fever. The child may feel drowsy in the afternoon and restless and hot at night.

Anal complaints – Seat of disease

Anal complaints

DIGESTIVE DISORDERS – Anal complaints – Seat (of) disease

People often suffer from anal complaints when they suffer from digestive disorders. It can also happen vice versa. To understand all about anal complaints, everyone should know about the anus and its functions. Any complaint of the anus makes everyone restless and won’t let them take their seat. Also, most of the anal complaints are left untreated or maltreated due to shyness or shamefulness to discuss/show the thing. For example, people may complain of pile mass in anus, but it may actually be a residual of fissure (sentinel pile – skin tag of linear crack). Likewise, some others may complain of pus discharging boil near the anus, but actually it may be an opening of fistula (tunnel passage from anal canal).

For normal good defecation, a good digestion is ultimately necessary i.e. all the way starting from the mastication of food in the mouth. Our digestive tract starts from the mouth (entry door of food) and ends in the anus (exit door). Any food which enters the stomach needs to pass through the coiled small intestines, where most of the nutrients get absorbed. For getting the nutrients and water absorbed, food passes slowly through this long route by swaying motion of the intestines. After reaching the caecum (first part of the large intestine), food has to ascend with ascending colon and arches left with transverse colon and descend with descending colon of large intestines. Finally it will enter the rectum and anal canal to get expelled.

Anus – is the external opening of the anal canal through which faeces (waste product of digestion) are evacuated. It is guarded and controlled by the anal sphincters.

Anal canal architecture – The anal canal is about 3.5 cms long and it starts from the lower end of the rectum and ends in the anus’ opening. The walls of the anus are well guarded with sphincter muscles which always keep it closed, except during defecation. It is also designed in such a manner to control the release of air (flatus) and watery stools i.e. airtight and leak proof.

The anal canal is anatomically divided into two parts (namely upper part and lower part) by pectinate line (bluish pink ring). These two parts are different from embryonic origin, i.e. the upper part is originated from endoderm and it is covered with mucous membranes like covering of the oral cavity. It will be pink or reddish in colour. This upper anal part is supplied by autonomic nervous system and doesn’t have pain sensitive nerve fibres. So, it responds only to fullness and tightness of intestines. The lower part of the anal canal originates from the ectoderm and is covered by skin. It is usually brown or pale white in colour. Unlike the upper part, it contains sebaceous glands, sweat glands and cutaneous pain sensitive spinal nerves like normal skin.

Defecation – The act of passing stool is called defecation. Defecation is aided by the rectum and anal canal. Defecation can be initiated by increasing abdominal pressure, straining at rectum and anal canal, mind, habits, etc. Anus with brain control controls the defecation process accordingly by time, place and circumstances. The waste products, called faeces, which are excrement discharge of the bowels, are expelled through the anus. The intestines usually secrete, excrete and absorb. But the rectum and anal canal have less work in dealing with this digested food. The absorption of water and minerals are low or very little in the rectum and anal canal.

Normal faeces usually have a water content of 60-70 per cent, fat 15-20 per cent, nitrogen 4-5 per cent, inorganic materials 10-20 per cent. The bile pigments colour the stool as brown or yellow. If the content of fat in the stool is more, it makes it pale and to float. The bile pigments and other wastages are usually excreted through faeces. So even during fasting, a small quantity of faeces will be passed on.

Importance of defecation – Defecation is discharge or evacuation of bacteria-rich faeces from the body. It is very much important in letting out the waste and unwanted toxic substances from the digestive tract to avoid toxicity. Everyone would have heard of headache, abdominal discomfort, poor appetite, sensation of vomiting, etc., when there is defective defecation. For getting energy, continuous support or intake of food is necessary, but if the stool is impacted or stagnated due to defective digestion and assimilation, then the process will make any one to reduce/avoid intake of food.

Dysfunctions causing anal complaints

Constipation is infrequent and inadequate defecation without satisfaction. It may be due to

• Failure in developing habits
• Controlling the urge for a prolonged period
• Low fibre foods with more spices and chillies
• Liver disorders with defective digestion
• Drugs impairing digestion
• Defective expulsion due to nervous disorders or nerve damages

Diarrhoea is commonly called increased motility of the bowels resulting in frequent evacuation of watery stools with uncontrollable purging. While caring for loss of minerals, the strain of the anus should also be considered. Forcible expulsion of diarrhoea from laxatives or enemas can cause anal complaints like piles and prolapse.

Incidences – One who deviates more from nature in diet, living and sitting habits will usually suffer with anal complaints. Anal problems are rare in children due to their bland diet, unless pathological. The incidence of anal complaints increases with age factor and occurs more commonly in the 20 to 30 age group. Females suffer more commonly than males. Sufferers are mostly

• Travellers who sit for long
• Sedentary workers
• Lovers of chillies and spices
• One who have is prone to constipation
• One who has or is prone to diarrhoea
• Sufferers of liver disorders

Other suspected reasons for development of anal complaints

• Erect posture of man – The evolution of man from an animal on four feet to a human being on two feet is considered one of the main causes for anal complaints, when compared to other animals
• Hereditary – development of piles is often noted to run in families
• Physiological – Pregnancy and delivery can cause increased venous pressure and weakness of the anal canal, so piles or constipation can occur
• Physical strain – exerting while passing stool, coughing, weight lifting, etc., can cause piles, prolapsed anus, etc.
• Pathological – pelvic and rectal tumours, liver and portal vein disorders can cause piles
• Infections in skin and mucous membranes of the anal canal can cause boils and proceed to fistulas
• Blood vessels – due to valvular damage or back flow or resistance pressure exerted by obstruction or disease can cause dilatation of blood vessels
• Ligaments – defective support of anal canal can cause prolapsed anus
• Worries and mental strain can also cause havoc to intestines and anus

Diagnosis & investigations – Diagnosis of anal complaints can be easily made on examination of the anus with finger palpation / proctoscope / sigmoidoscope / endoscopy / barium meal X-ray / biopsy / stool examination, etc. Other than anal complaints, anal examination is also done to detect prostate enlargement in males and to detect the changes in consistency of the uterus, ovaries, cervix, etc., in females.

Complications – if any complaint is left untreated or maltreated, then danger begins to unfold. Infection, bleeding, extreme painfulness, prolapse and strangulation may occur, complicating in their own way.

Cautions and precautions:

• Move more towards greens and nature
• Don’t be sedentary and sit idle for a long time
• Keep good diet for good digestion
• Take plenty of water
• Take plenty of fruits/fruit juices
• Follow regular bowel habits to avoid constipation and strain

Follow hygienic measures in cleaning and caring

Avoid cycling

Common complaints often faced in the anus are:

• Piles or haemorrhoids – dilatation of veins of the anal canal (upper or lower part)
• Fissures – tear in lower sensitive part of anus, which is very painful
• Fistula – tunnel passage developed from boil which gets opened internally into anal canal
• Anal stricture – constriction of the part with the feeling of tightness or compression
• Itchy skin lesions including recurrent boils, since the anus is more prone to bacteria
• Incontinence – defect in controlling or with holding or postponing the defecation process
• Congenital deformities – like miniature anus, imperforate anus

To avoid discomfort, pain, bleeding and unwanted progress of the disease, treatment should be taken at the earliest to heal with all precautionary measures in food, restriction of work/bed rest and juice fasting. Best results are often shown when one reverts to nature in food and habits rather than treatment.

for new hope

Dr. S. Chidambaranathan, BHMS, MD (Homeo)

Laxmi Homeo Clinic

24 E. New Mahalipatti Road

Madurai, TN 625 001

India

Tel:  +91-452-233-8833 | +91-984-319-1011 (Mob)

Fax: +91-452-233-0196

E-mail:  drcheena@yahoo.com

www.drcheena.com / www.drcheena.in

(Disclaimer: The contents of this column are for informational purpose only. The content is not intended to be a substitute for professional healthcare advice, diagnosis, or treatment. Always seek the advice of healthcare professional for any health problem or medical condition.)