How to control Epilepsy Seizure?

 Classification, Investigations and Treatment of Epilepsy:

The classification of epilepsy brings together the seizure semiology and other aspects of the history and investigations. The International League against Epilepsy classified epilepsies as:

• Idiopathic – Thought to be primarily genetic with generalized seizures, sometimes group as more specific syndromes. Account for about 10-20% of cases.
• Symptomatic – Partial onset seizures associated with a structural lesion, such as rumour, cortical dysplasia, infection, head injury or trauma – about 30-40% of cases. The combination of the site of seizure onset and the underlying pathology leads to the diagnosis: for example: post traumatic frontal lobe epilepsy’ or temporal lobe epilepsy due to mesial temporal sclerosis or symptomatic occipital lobe epilepsy secondary to an arteriovenous malformation’.
• Cryptogenic – Partial onset seizures for which no cause has been found. Account for about 50% of patients.

With developments in understanding, particularly in genetics, limitations with this general practical classification have arisen – for example familial frontal onset epilepsy (associated with a mutation in the gene encoding the neuronal nicotinic acetylcholine receptor (nAChR) alpha-4 subunit) is idiopathic yet partial onset epilepsy. Newer proposals und consideration suggest the classification should move to genetic, structural/metabolic’ or unknown cause rather than the groups given above.

Selected Idiopathic Epilepsy Syndromes (by age of onset)

1. Childhood absence epilepsy (common)

• Absence seizures begin between 4 and 12 years of age. Family history in 40% of patients. The absence may occur many times a day with duration of 5-15 seconds.
• Frequent episodes lead to falling off in scholastic performance.
• Attacks rarely present beyond adolescence.
• In 30% of children, adolescence may bring tonic/clonic seizures.
• Distinction of absences from complex partial seizures is straightforward; the latter are longer 30 seconds or more  and followed by headache, lethargy, confusion and automatism. EEG finds 3 Hz spike and wave.

2. Juvenile Myoclonic Epilepsy (Common)

Myoclonic jerks begin in teenage years, typically in the morning. Develop tonic/clonic seizures, often with sleep deprivation, in late teens. Occasionally have absence seizures. EEG frequently finds 4-5 polyspike and wave discharges.

EPILEPSY INVESTIGATION
Investigations are directed at:

• Corroborating the diagnosis of epilepsy
• Classifying the type of epilepsy
• Looking for an underlying cause
• Eliminating alternative diagnoses

The relative emphasis of these elements will depend on the clinical situation. For most patients the clinical diagnosis of a seizure is secure and the emphasis is to seek the cause and to classify the epilepsy to direct treatment. In others the main concern is whether the episodes are seizures or an alternative diagnosis.

1. Neuroimaging

All adults and all with focal onset seizures should be scanned. MRI brain imaging is more sensitive than CT and many lesions, for example small turnouts, cortical dysplasia or hippocampal sclerosis will be missed on CT.

2. EEG

• Standard interictal EEG is relatively insensitive – though this varies according to the type of epilepsy (it is very sensitive in childhood absence epilepsy).The interpretation of abnormalities requires caution; 0.5% of the normal population have interictal spikes or sharp waves (epileptic discharges) as compared to 30% of patients after their first seizure.
• The pattern of abnormalities can point towards a focal or generalized onset and can supplement the clinical classification.
• Sleep deprived EEG increases the yield but with the risk of provoking a seizure. EEG shortly after a seizure is more likely to find an abnormality.
• Ambulatory EEG recording increases the chance of finding an abnormality and of recording a clinical event. The gold standard investigation is simultaneous EEG monitoring and video monitoring (video telemetry).

3. Eliminating Alternatives

• ECG should be done in all patients with seizures. This is a simple cheap test and a small number of epilepsy mimics can be identified this way, e.g. prolonged QT syndrome.
• Prolonged ECG may be useful in patients with possible cardiac syncope especially in patients with sleep associated events. Implantable loop recorders can be used when patients have infrequent events.
• Head up tilt table testing is often helpful in the diagnosis of neurocardiogenic syncope.
• Metabolic investigation to consider includes fasting glucose for insulinoma and synacthen test for Addison’s disease.

4. Advanced Investigation

• Volumetric MRI can identify hippocampal sclerosis not apparent on conventional imaging.
• Functional imaging, using ictal and inter-ictal SPECT may be helpful in identifying an epileptogenic focus when evaluating patients for surgery.
• Advanced EEG techniques for example using sphenoidal electrodes or recording from surgically inserted intracranial grid or depth electrodes can help localize a focus before surgery.

EPILEPSY TREATMENT

• Basic principles: Most patients respond to anticonvulsant drug therapy. Drug treatment should be simple, preferably using one anticonvulsant (monotherapy). Polytherapy should be avoided to minimize adverse effects and drug interactions.
• Treatment aims to prevent seizures without side effects though this is not always achieved.
• Surgery is an option in a small number on non-responders.
• Teratogenicity: It is important to consider the teratogenetic risks when starting any anticonvulsant in a woman of childbearing age. Large prospective studies have established rates of major congenital malformations for widely used drugs: those on no medication, carbamazepine or lamotrigine had similar rates of around 3%; in valproate monotherapy the rate was significantly higher at 6%; polytherapy overall was about 6%, and 9% if valproate was one of the drugs.
• Interactions: Many anticonvulsants (especially carbamazepine, phenytoin, phenobarbitone) induce liver enzymes to increase metabolism of other drugs (notably the oral contraceptive, warfarin and other anticonvulsants); valproate inhibits liver enzymes.
• Blood levels: Monitoring levels is useful for phenytoin because of the difficult pharmacokinetics. Other blood levels can occasionally be useful to check the patient is taking the medication or for toxicity.

1. Drug choice:

• Idiopathic Generalized Epilepsy:  sodium valproate; lamotrigine; topiramate; levetiracetam; phenytoin.
• Partial (Focal) Epilepsy:  lamotrigine; carbamazepine; sodium valproate; Phenytoin; Phenobarbitone; Levetiracetam;Topiramate;Tiagabine; Zonisamide; Oxcarbazepine; Gabapentin; pregabalin; lacosamide.
• Those drugs asterisked are typically used for monotherapy others as add-on therapy when control sub-optimal. The choice of anticonvulsant will be a balance between efficacy, adverse efficacy, teratogenicity and drug interactions and the patient should be involved in this decision.

2. Lifestyle Issues: Generally there should be as few restrictions as possible. Patient should be made aware of potential triggers to avoid – sleep deprivation, excess alcohol, and, where relevant flashing lights (though most patients are not photosensitive). Sensible precautions – showering rather.

Braner Pain Clinics specialize in chronic pain management, neurology, neurological testing and disability. Our main clinic is conveniently located in Falls Church, Virginia near the Beltway(495).  Call Now at: (703) 573-1282 and Call at Toll Free Number:1 (877) 573-1282

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ARE YOU SUFFERING FROM HEADACHE?

Pain Relief Management Treatment:

Headache is the common disease. Mostly, human beings are suffering from Chronic Headache Disease. The commonest form of headache experienced by 70% of males and 90% of females at some time in their lives. Most causes of adult headache may occur in children. The specific headache cause is Tension Type Headache and Migraine Headache.

The clinician must not take a complaint of headache lightly; the younger the child, the more likely the presence of an underlying organic disease. Pyrexia may not only represent a mild constitutional’ upset, but may result from meningitis, encephalitis or cerebral abscess. The presence of neck stiffness and/or impaired conscious level indicates the need for urgent investigation.

In a child with unexplained headache, CT or MRI scan should be performed if the headache is acute or progressive or if there are other features (increase in head circumference, change in personality or decline in school performance).

Specific Types of Headache:

1.    TENSION TYPE HEADACHE

2.    MIGRAINE TYPE HEADACHE

 

TENSION TYPE HEADACHE

• Characteristics: Diffuse, dull, aching, band-like headache, worse on touching the scalp and aggravated noise; associated with tension but not with other physical symptoms. Attacks may be chronic or episodic. Depressions commonly co-exist.
• Duration: Many hours’ days.
• Frequency: Infrequent or daily; worse towards the end of the day. May persist over years.
• Mechanism: ‘Muscular‘ due to persistent contraction, e.g. clenching teeth, head posture, furrowing of brow. Some overlap with transformed migraine.
• Treatment: Reassurance. Attempt to reduce psychological stress and analgesic over-use medication-overuse headache). Amitriptyline and other tricyclic antidepressants or b-blockers.

MIGRAINE TYPE HEADACHE

Migraine is a common often familial disorder characterized by unilateral throbbing headache.

• Onset: Childhood or early adult life.
• Incidence: Affects 5-10% of the population.
• Female: Male Ratio: 2:1
• Family History: Obtained in 70% of all sufferers.
• Two recognizable forms exist
• Specific diagnostic criteria are required for migraine with and without aura.

MIGRAINE WITH AURA

An aura or warning of visual, sensory or motor type followed by headache throbbing, unilateral, worsened by bright light, relieved by sleep, associated with nausea and, occasionally, vomiting.

MIGRAINE WITHOUT AURA (COMMON MIGRAINE)

The aura is absent. The headache has similar features, but it is often poorly localized and its description may merge with that of ‘tension’ headache.

The aura of migraine may take many forms. The visual forms comprise: flashing lights, zigzags (fortifications), scintillating scotoma (central vision)  and may precede visual field defects. Such auras are of visual (occipital) cortex origin.

The headache is recurrent, lasting from 2 to 48 hours and rarely occurring more frequently than twice weekly. In migraine equivalents the aura occurs without ensuing headache.

Specific Types of Migraine with Aura

Basilar: Characterized by bilateral visual symptoms, unsteadiness, dysarthria, vertigo, Limb Paraesthesia  even tetra paresis. Loss of consciousness may ensue and precede the onset of headache. This form of migraine affects young women.

Hemiplegic: Characterized by an aura of unilateral paralysis (hemiplegia) which unusually persist for some days after the headache has settled. Often misdiagnosed as a ‘stroke’. When familial, mendelian dominant inheritance is noted. Recovery is the rule.

Retinal

• Unilateral (monocular) visual loss which is reversible and followed by headache.
• Ophthalmological examination between episodes is normal.

Precipitating Factors in Migraine

• Dietary: alcohol, chocolate and cheese (contain tyramine).
• Hormonal: often premenstrual or related to oral contraceptive (nuctuations in oestrogen)’
• Stress, physical fatigue, exercise, sleep deprivation and minor head trauma.

 Diagnosis

Clinical history with

• Occasional positive family history
• Travel sickness or migraine variants (abdominal pains) in childhood
• Onset in childhood, adolescence, early adult life or menopause

Distinguish 

• Partial (focal) epilepsy (in hemiplegic or hemi sensory migraine)
• Transient ischaemic attack (in hemiplegic or hemi sensory migraine)
• Arteriovenous malformation  gives well localized but chronic headache
• Hypoglycaemia

Management

1. Identification and avoidance of precipitating factors

2. Treatment of acute attacks:

• Simple analgesics (e.g. aspirin) with metoclopramide to enhance reduced absorption during an attack. If vomiting is prominent anti-emetic (domperidone or prochlorperazine) and analgesic can be helpful.
• Sumatriptan (a selective 5HTI agonist) and other Triptans e.g. Naratriptan, Rizatriptan and Zolmitriptan – effectively reverse dilatation in extracranial vessels. Given orally or subcutaneously.
• Ergotamine widespread action on 5HT receptors reversing dilatation. Give orally or by inhalation, injection or by suppository.
• MethyIprednisolone i.m. or i. v. will halt the attack when prolonged (status migrainosus).

3. Prophylaxis: use only for frequent and severe attacks

• Pizotifen   (5HT2 receptor blocker)
• Propranolol (beta adrenergic receptor blocker)
• Calcium antagonists (verapamil), antidepressants (amitriptyline) and anticonvulsants, (topiramate or sodium valproate).

Medication Overuse Headaches

Some patients with episodic tension headache or migraine find their headache pattern changes so that they have headaches most days. Many such patients take regular analgesics and/or Triptans and this overuse (>14 days a month) can cause medication overuse headaches (MOB). These do not respond to prophylactic agents and will improve on stopping the regular analgesics; this can take some weeks and headaches can be worse in the short-term.

Transformed Migraine

If patients with migraine go on to develop chronic daily headache without overusing medication this is transformed migraine. It usually responds to migraine prophylactic agents.

Fitness Tips For Health

IS THERE AN IDEAL AGE FOR FITNESS?

Many studies have been conducted in old folks, but the changes in Neurogenesis and interconnection are just as dramatic as in young people. There seem to be more long lasting effects while the brains are still developing. For instance in children with ADHD, exercises may be a substitute or a supplement for drugs.  In general until about 20 years of age, the frontal lobes are not completely developed and exercises may speed up the executive functions, math, logic, reading, etc.  That knowledge from kids is making many educators to request more P.T in schools.  The hope of educators is that kids can develop a love for sports early in life to avoid the fate that their grandparents are now facing due to physical inactivity.  Current and early studies suggest that people that exercise, delay or suppress the development of Alzheimer Disease.

HOW MUCH, HOW OFTEN AND WHAT MODALITY OF EXERCISE IS APPROPRIATE?

Researchers don’t know the straight answer yet. So far the strength training, toning and weight lifting, have no effect on cognition.  There is no consensus about how much is too much. Recent discoveries have shown long lasting effects that include: improved mood decreased anxiety, improved sleep pattern, reduced stress and elevated self-‘esteem. That is why some people call it “endorphin high”, that make you feel good during and right after the exercise session. It is kind of the “Prozac”, “Ritalin” effect.

DOES THE BRAIN CAN TELL HOW MUCH EXERCISE  IS SUFFICIENT?

The motivation for exercises is still under genetic control.  Recent studies indicate that the brain governs how much activity the body is ready for, just similar to how make people hungry  to become overweight.  The brain uses signals from the muscles as a guide. Therefore the brain of lazy people often encourages some inactivity.  Indeed, some researchers are beginning to wonder if genes that make a person vulnerable to depression also make exercise less pleasant.  Perhaps this may explain why is almost impossible to promote a healthy lifestyle, as information about the positive effects of exercises is not enough.  People just hate exercises.  Perhaps would be better to explain how the genes control our experience of exercise. Start knowing yourself first, before taking the decision to join a fancy gym, to invest in expensive equipment to obtain the benefit of exercise.

Remember that an aggressive, intense, vigorous program won’t give an instantaneous psychological improvement.  More important is the ability to achieve a sustained exercise routine. The research indicates that one have to stick to a chosen program for atleast 2 months to see the best chances to feel better. Develop a habit that with time becomes enjoyable to continue.

CHANGING FROM FAT TO FIT

When we exercise, we don’t benefit our body muscles, but our heart muscles and our brain neurons do.

TYPE OF EXERCISES

• Aerobics
• Strength training
• Aerobics stimulates the CVS rushing blood to the ear, the brain and the rest of the body.
• Strength training can reduce and sometimes reverse some of the body decline of bone and muscle mass.

LIVE LONGER

According to a study done on 17000 middle age Harvard Graduates, found that those individuals who exercised on regular basis, reduced the risk of dying prematurely by 25%. Other studies on people older than 50, who exercised, lived between 1.3 to 3.7 years longer than the sedentary ones. The more vigorous the physical activity the longer the prolongation of life.

HEAL FASTER

Research at the Ohio State University found after dividing 35-70 years of age in 2 groups. Group one attended a supervised exercise program for weeks.  The second group sedentary people as model. At the end of the first month, they produce wounds on the arms of both groups as volunteers, then monitored the speed of healing in both groups. The wounds of those who exercised healed about 25% faster

INCREASE SEXUAL FUNCTION

On average, by age 50, one third of Americans men, suffer some form of impotence. Newer drugs such as Viagra and Cialis help erectile dysfunction by increasing blood now to the penis , but studies have found the exercises are more long lasting beneficial in those who participated in frequent vigorous exercises  were at least one third less likely to suffer erectile dysfunction.

HAVE FEWER HOT FLASHES

About 75% of women in the US experience hot flashes during menopause and 25% still get them even ten or more years afterward.  1 n the past the medical health providers eated this condition with hormone replacement, giving Estrogens and Progesterone. But starting in 2002, millions of women discontinue such hormone therapy due to many undesirable side effects.  A study done in 1998 a Swedish researcher studied 800 women ages 55-56 and found that those who exercised at least 2 hours a week experienced less hot flashes. It has been postulated that one reason might be the release of Endorphins that may counter the hormonal imbalance that produce these menopausal symptoms.

BE PAIN FREE

Although exercises alone cannot eliminate all the aches and pains of getting older, it can reduce muscle, tendon, bone and joint pains. Researchers at Stanford University compared group of 60 plus of runners  with a group of sedentary elders; they found that after adjusting for age, height, gender and health status, the runners experienced less musculoskeletal pains over 14 years.

SAVE MONEY

Chronic diseases cost the US, billions of dollars in health care and lost productivity every year. But a study by the Health Partner Research Foundation has found that people older than 50 that exercise for at least 30 minutes 3 times a week, actually saved an average of 2200 dollars a year in medical bills.

THE CURRENT SCIENTIFIC KNOWLEDGE ON PHYSICAL EXERCISES

THE REGULAR PHYSICAL EXERCISES INCREASE THE FOLLOWING:

• Mental and psychological health
• The efficiency of Insulin activity
• Oxygen supply to the body
• Immunological defenses
• The levels of Growth Hormone
• The muscle mass and coordination
• Endorphin production and release to fight pain
• The eye sight
• The memory and intellect
• The Calcium uptake and fixation
• The Glucose Tolerance
• The bone density
• The HDL (good) Cholesterol
• The intestinal transit to prevent constipation
• The Lipoprotein Balance
• The Pulmonary function
• The Neurotransmitter pool and efficiency(NE, DA,5-HT,ACTH)
• The quality of Sleep
• The sexual activity
• The slow down aging.

It is estimated that each hour of Physical Exercises, prolong 2 hours of life expectal.

THE REGULAR PHYSICAL EXERCISES DECREASE THE FOLLOWING:

• Blood pressure
• Blood glucose
• Chronic inflammation
• Infection frequency and severity
• Obesity
• Coronary Diseases
• Type I1 Diabetes
• Gall Bladder Disease
• Hernias
• Slow down chronic Arthritis
• Frequency and Severity of chronic headaches
• Chronic Back and Neck Stiffness and Pain.

ON EXERCISES (continues)

• Kidney Stones
• Muscle weakness and easy failings
• Osteoporosis
• Arthralgias and Myalgias
• Mental Depression
• Chronic Constipation
• Dementia
• Chronic fatigue
• Scoliosis due to muscle spasm
• Insomnia
• Vascular insufficiency
• Certain cancers
• Erectile dysfunction

TO BE BENEFICIAL HOW TO DO THE EXERCISES?

• Every day or at least every other day
• First thing in the morning
• At least for half an hour
• Not to be boring, tedious or dangerous
• Not to be expensive

WHAT MODALITY TO CHOOSE?

• Walking, slow to start  and then progressive as tolerated
• Running slowly under pleasant temperature
• Bicycling
• Skating
• Skiing
• Dancing
• Swimming or simply walking in water.

IF THERE IS NO TIME OR DESIRE WHAT ARE SOME ALTERNATIVES

• Get your next car with standard gear shift
• Cars with manual windows and seat adjustments
• Avoid TV and Garage remote controllers
• Avoid the Elevator and electric escalators
• Try public transportation
• Commute on bicycle
• When parking leave your car the farthest possible, so you have to walk
• Avoid electric saws, screwdrivers or tooth brush
• Avoid watching prolonged TV shows
• Avoid any sport events in sitting position
• “Do not exercise with the only purpose of losing weight.”
• Remember: there is no age limit

FREQUENT EXCUSES NOT TO EXERCISE:

• I am no longer in the age
• I need to rest
• I get tired and fatigued easily
• It is dangerous to walk or run
• My doctor does no approve
• I do not have time
• It is boring to exercise alone.

 

SOME SCIENTIFIC EVIDENCE OF REGULAR PHYSICAL EXERCISES

“Physical activity can save your eye sight” say the experts at the Wisconsin University. Physical Activity lowers the risk of age-related macular degeneration by as much as 70%. The exercise may control inflammation and blood vessel abnormalities that have been linked to the disease.

Exercises can make you “smarter”. Experiments with fifth grade children put to PE by Charles Hillerman, concluded that sports boost student’s intellect. There is rapidly growing movement showing that Exercise can make people smarter. Recently  some researchers have announced they have coaxed the human brain into growing new nerve cells (neurons), simply by putting subjects on a three-month aerobic work-out regimen. Other researchers have found that vigorous exercises  can make existing neurons to form a dense , interconnected webs that make the brain function faster and more efficient.

There are now clues, that physical activity can prevent dementia like Alzheimer’s, Attention Deficit (ADHD) and other cognitive disorders. These and other facts about Sports and Scholar Achievements are really not new. We know it was common in ancient Greece in which fitness and learning was equally important. The Greek knew there was connection between “mind and body” when they stated “mens Sana et corpora Sana”. We now realize that aerobics makes the heart pump more oxygen to the brain and the rest of the body. With the help of brain scanning tools and knowledge of biochemistry, researchers have found that the effects of exercises are more profound and complex than previously thought.

Every time a muscle contracts and rests, sends out chemicals, including a protein called IGF-1 , that travels through the blood stream into the brain. IGF-1 acts as mediator of the body’s neurotransmitter factory. IGF-1 stimulates the production of other chemicals including BDF (Brain Derived Neurotrophic Factor). Raten, author of an incoming book “SPARK” calls BDNF a “miracle-grow” for the brain. With habitual aerobics the neuron starts to branch out to produce webs to communicate each other in new ways. In other words, the more abundant the BDNF is, the greater the capacity to learn. Most individuals can keep BDNF pool fairly constant throughout the adulthood; but as they age their individual neurons start to die off slowly. Until about 10 years ago scientists were convinced that the loses were permanent; that those dead neurons were not able to be replaced by the brain. But new research in animal models has shown the neurogenesis thus occur, especially in certain parts of the brain through aerobic exercises. It has been shown that the STEM CELLS do transform into full-grown, functional neurons. Most of the neurogenesis has been observed by Scott Small at Columbia University and Fred Isage, a neurobiologist al Salk Institute in the Dentate Gyrus, a region of the Hippocampus by way of creation of blood vessels (vasogenesis).

The Hippocampus which is located under the Temporal Lobes helps the brain to match names to faces.  As the psychologist Arthur Kramer puts it, physical activity not only slows down the aging process but perhaps a matter of reversing it. The other area of interest is the executive function of the Frontal Lobes the site of higher thoughts, decision making, planning and so forth. In general new growth of neuron can happen throughout the rest of the brain.

Furthermore, new population of neurons also means new population of blood vessels, thus reducing the chance of some multiple frequent and silent ischemic events leading to strokes that are usually silent and contribute to declining cognition.

Other researchers have found that athletes have more abundant Atrocities, the kind of cells that support the neurons conducting the neurotransmitter chemicals that convey messages from cell to cell. Among those neurotransmitters are DA, Serotonin (5-HT),NE. So doing a work up, helps with the concentration, release and increasing impulsivity

The nice thing about exercises is that we don’t have to wait several weeks to feel the benefit of neurogenesis; many additional benefits from them appear almost immediately, as early as 30 minutes and continue serendipitously during the rest of the day.

Individuals feel the sensation of well being, enthusiasm, confidence, etc. It is important to know that the commitment for fitness needs to be maintained, so the neurogenesis and its connection remain the same through the years when the training stops, the astrocite web starts to decline again.

ON CALCIUM METABOLISM AND OSTEOPOROSIS

Symptoms And Treatment of Osteoporosis:

Most of the body Calcium (Ca++) is extracellular (in serum) in ionized form. Ca++ is extremely important for maintaining: Skeletal metabolism, nerve, and muscle function and cell activity. The intracellular Ca++ functions as cytoplasmic second – messenger and moves in and out of the cell membrane through the Calcium channels. The normal Calcium serum levels is 8.5 to 10.5 mg/dl around 40 % of circulating Calcium is bound to proteins (Albumin 90%) and as anions, such as Phosphate, Citrate and Sulfate. The extracellular Calcium is tightly regulated by HORMONES and its concentration is indirectly affected by the Parathyroid  (PTH) hormone, by stimulating the renal reabsorption.

How is the extracellular Ca++ metabolized?

• From the daily Calcium intake of 1000 mg, 100 mg are excreted in feces and 200 mg in urine. From the guts some 300 mg are absorbed and moved to the Calcium pool mediated by Vitamin D and from this pool 100 mg a re moved back to the guts again for excretion Likewise from the Calcium pool, 8800 mg are reabsorbed by the kidneys and 200 mg are excreted in urine. In addition, 200 mg are moved from the skeleton to the Calcium Pool mediated by the PTH and also 200 mg are reabsorbed back by the bones.

• Calcium deficiency can be produced by physical inactivity, immobilization, and certain environment like the astronauts subjected to prolonged lack of gravity.

• Calcium intestinal absorption may also be reduced in certain diseases such as: chronic diarrhea, malaria absorption conditions, rapid intestinal transit, use of steroids or Phenytoin treatment of Epilepsy

CALCIUM MAINTENANCE AND REPLACEMENT

The FDA daily allowance is 1000 mg/d in adults less than 50 y, 1200 mg\d for those more than 50 y and 1300 mg\d  for healthy adolescents. More than 99% of total body calcium is sequestered in bones and teeth.

HYPER CALCEMIA

Hypercalcemia is the result of: 

• Increased skeletal re sorption
• Increased intestinal absorption
• Increased PTH activity

The main signs and symptoms of primary Hyperparathyroidism are: fatigue, weakness ,  thirst, frequent urination, calcium kidney stones formation ,  hematuria, bone loss (osteoporosis), joint pain, bone pain, loss appetite, heartburn, acid  gastric reflux , peptic  ulcer disease, chronic  constipation, low mental concentration, forgetfulness and mental depression. The most common cause of hypercalcemia in hospitalized patients is CANCER. Malignancy may occur due to increased secretion of PTH activity or due to bone meta Stasis. Hypercalcemia may also result for increase in Calcium production in certain diseases such as: Sarcoidosis, tuberculosis, crohn”s disease, and lymphomas. For which the best treatment is with glucocorticoides (Prednisolone and hydrocortisone) Otherwise the treatment of hypercalcemia, in general, are Biphosphonates Intravenously. Examples of Biphosphonates are Pamidronates (Aradia) and Zoledronic acid (Zometa).

HYPOCALCEMIA

Hypocalcemia is calcium deficiency in those cases with calcium serum level < than 8.5 mg/dl. The treatment for acute hypocalcemia is CALCIUM GLUCONATE IV, 10% solution, containing 9.3 mg Ca/ ml. Dose 10-15 mg/kg of body wt. over 4-6 hours. For faster infusion use l0mI of 10% solution diluted in 50 ml of 5% dextrose in water (D 5 W) over 5 minutes. For Hypocalcemic TETANY or laryngospasm: CALCIUM CHLORIDE (CaCl) is given. 10% solution containing 1.36 mEq Ca2++/ ml, IV at rate of less than 1 ml/minute to prevent cardiac arrhythmia.

Caution:  Calcium Gluconate may give a generalized burning sensation due to vasodilation, which also can lead to arterial hypotension. The alternate treatment is CALCIUM GLUPECTATE 22% solution, containing 18 mg Ca2++/ml in a volume of 5-20 ml IV for severe Tetany. Mild and chronic hypocalcemia can be treated with oral calcium and vitamin D combination. Oral Calcium preparation are Calcium Carbonate, Citrate, Phosphonate, Lactate, and Gluconate in doses of 1-2 G/day up to 3-6 G /day.

 

TREATMENT AND PREVENTION FOR OSTEOPENIA OR OSTEPOROSIS.

 CALCIUM CARBONATES

ACTONEL (Risedronel Sodium). ACTONEL is a biphosphonate, it is available in tabs 5, 30, 35, 75 and150 mg once a week dose packs. Dose as follows: 5mg/day, 35 mg/week, or 75 mg /day for 2 days once a month or 150 mg once a month. Actonel and other biphosphonates are indicated both for treatment or prevention of Osteoporosis in menopausal, postmenopausal females as well as Osteporosis in males. ACTONEL is also available as ACTONEL PLUS CALCIUM as a blister package containing 28-day course therapy per wee k as follows: #4 ACTONEL 35 mg tablets for the first day and # 24 Calcium Carbonate 1250 mg tablets for days 2 to 7h. Either kind of ACTONEL, for the first day dose has to be taken with Sounces of plain water, 30 minutes before the first meal or drink of the day. Another biphosphonate is BONIVA (Ibandronate). In general the biphosphonates act as inhibitors of osteoclasts-mediated bone resorption thus inducing osteoblast activity to favor bone mass. The recommended dose of BONIVA is 100-150 mgs once a month or 2.5 mg per day along with 400 IU of Vitamin D3 plus 500 mg of Calcium. Dose of 2.5 mg a day reduces the incidence of second bone fracture. Another biphosphonate is FOSAMAX ( Alendronate) available in tablets 5, 10, 35 and 70 mgs. It is also available as FOSAMAX PLUS VIT D3, strengths 7Omg/ 2800 IU and 7Omg/5600 IU tabs. The recommended dose is one tablet once a week or 10 mg tabs per day.

CALCIUM ACETATE

Phospho-LO gel caps 667 mg. Mostly indicated in concomitant hyper phosphatemia in end-stage renal failure (dyalisis). Dose: 2 gel caps with each meal.

CALCIUM CITRATE (Active Ca). Usually mixed with Vitamin D3, Vitamin K, Mg 100 mg and calcium 200mg. Take 4 tabs/day with meals.

OTHER TREATMENTS:

Calcitonin, Calcitriol and Genestein aglycone.

• MIACALCIN (Calcitonin-Salmon) Calcitonin is a polypeptide hormone secreted by cells of the Thyroid gland. When provided reduces calcium in serum and reduces and reduces calcium bone resorption. It is used both in hypocalcaemia and postmenopausal osteoporosis. Dose for the latter 100 IU subcutaneous or IM every other day. Simultaneous give Calcium Carbonate 105 Gm and Vit D 400 IU per day. MIALCALCIN is also available as Nasal Spray, one spray (200 IU) per day. Monitor effectiveness of treatment with periodic lumbar vertebral bone density studies, also periodic analysis of serum Calcium, Magnesium and Alkaline Phosphatase levels, and also 24 hours urinary calcium and phosphates levels.

• RECALTROL (Calcitriol) Occurs naturally in humans. It is the active form of Vitamin D3 (cholecalciferol).

• FOSTEUM (Genestein Aglycone). It is given as a dietary management of metabolic process of Osteopenia and Osteoporosis. Genetein is obtained from soy, citrated zinc and cholecalciferol (Vit D3).

Mild hypocalcemia is usually asymptomatic. Moderate to severe hypocalcemia usually presents as: Tingling sensation, paresthesias, cramps, increased neuromuscular excitation, tetany, laringospasm, and even tonic-clonic seizures. If low calcium is concomitant to low PTH activity the symptoms may include: Total body hair loss (alopecia totalis) starting in infancy, grooved finger nails, cataracts, brain basal ganglia calcifications, mental depression, chronic anxiety, and delusions. Hypocalcemia may also be present in Vitamin D deficiency, poor nutrition, starvation, and mal absorption disorders. Some cases of chronic hypocalcemia in adults may follow thyroid gland surgery or radiation.

CALCIUM AND PHOSPHATE METABOLISM

Calcium and phosphate homeostasis is regulated by PTH and 1,25 dihydro Vitamin D (Calcitriol) through the effects of the kidneys, the intestines and the PTH gland. The l,25 dihydro Vitamin D is the only active Vitamin D. It is formed from the inert 25 OH vitamin D3, which is stored in fat tissue as a reserve.

VITAMIN D

Vitamin D is critical to preserve bones but it is also important to protect the body from certain diseases like cancer s of the Prostate, Breast and Colon, also other conditions like Non-Hodgeking Lymphoma, Rheumatoid Arthritis, Type II Diabetes, Macular Degeneration, Multiple Sclerosis (MS), Fibromyalgia, Gingivitis and others. It also promotes the efficiency of the immune system, regulates the cell growth, and has also anti-inflammatory properties. There are basically two kinds of Vita min D: From animal source, CALCIFEROL (Vitamin D3, and from plants source, ERGOCALCIFEROL (Vita min D2). Vitamin D is soluble in fat just as Vitamin A, Vitamin E, and Vitamin K are. The normal, recommended daily dose is 800-1000 international units (IU). The major natural sources of Vitamin D are fish, especially Salmon, Tuna, Sardines, Mackerel, and Cod Liver. The following are the people more at risk for Vitamin D deficiency: Older adults, people with limited sun exposure, the use of skin screen products, fair skin (less melanin), some mal absorption diseases such as Crohn’s , pancreatic deficiency, cystic fibrosis, sprue, liver diseases and post gastric by-pass surgery.

ON CALCIUM METABOLISM AND OSTEOPOROSIS

Symptoms and Treatment Of Osteoporosis:

Most of the body Calcium (Ca++) is extracellular (in serum) in ionized form. Ca++ is extremely important for maintaining: Skeletal metabolism, nerve, and muscle function and cell activity. The intracellular Ca++ functions as cytoplasmic second – messenger and moves in and out of the cell membrane through the Calcium channels. The normal Calcium serum levels is 8.5 to 10.5 mg/dl around 40 % of circulating Calcium is bound to proteins (Albumin 90%) and as anions, such as Phosphate, Citrate and Sulfate. The extracellular Calcium is tightly regulated by HORMONES and its concentration is indirectly affected by the Parathyroid (PTH) hormone, by stimulating the renal reabsorption.

How is the extracellular Ca++ metabolized?

• From the daily Calcium intake of 1000 mg, 100 mg are excreted in feces and 200 mg in urine. From the guts some 300 mg are absorbed and moved to the Calcium pool mediated by Vitamin D and from this pool 100 mg a re moved back to the guts again for excretion Likewise from the Calcium pool, 8800 mg are reabsorbed by the kidneys and 200 mg are excreted in urine. In addition, 200 mg are moved from the skeleton to the Calcium Pool mediated by the PTH and also 200 mg are reabsorbed back by the bones.

• Calcium deficiency can be produced by physical inactivity, immobilization, and certain environment like the astronauts subjected to prolonged lack of gravity.

• Calcium intestinal absorption may also be reduced in certain diseases such as: chronic diarrhea, malaria absorption conditions, rapid intestinal transit, use of steroids or Phenytoin treatment of Epilepsy

CALCIUM MAINTENANCE AND REPLACEMENT

The FDA daily allowance is 1000 mg/d in adults less than 50 y, 1200 mg\d for those more than 50 y and 1300 mg\d for healthy adolescents. More than 99% of total body calcium is sequestered in bones and teeth.

HYPER CALCEMIA

Hypercalcemia is the result of:

• Increased skeletal re sorption

• Increased intestinal absorption

• Increased PTH activity

The main signs and symptoms of primary Hyperparathyroidism are: fatigue, weakness , thirst, frequent urination, calcium kidney stones formation , hematuria, bone loss (osteoporosis), joint pain, bone pain, loss appetite, heartburn, acid gastric reflux , peptic ulcer disease, chronic constipation, low mental concentration, forgetfulness and mental depression. The most common cause of hypercalcemia in hospitalized patients is CANCER. Malignancy may occur due to increased secretion of PTH activity or due to bone meta Stasis. Hypercalcemia may also result for increase in Calcium production in certain diseases such as: Sarcoidosis, tuberculosis, crohn”s disease, and lymphomas. For which the best treatment is with glucocorticoides (Prednisolone and hydrocortisone) Otherwise the treatment of hypercalcemia, in general, are Biphosphonates Intravenously. Examples of Biphosphonates are Pamidronates (Aradia) and Zoledronic acid (Zometa).

HYPOCALCEMIA

Hypocalcemia is calcium deficiency in those cases with calcium serum level < than 8.5 mg/dl. The treatment for acute hypocalcemia is CALCIUM GLUCONATE IV, 10% solution, containing 9.3 mg Ca/ ml. Dose 10-15 mg/kg of body wt. over 4-6 hours. For faster infusion use l0mI of 10% solution diluted in 50 ml of 5% dextrose in water (D 5 W) over 5 minutes. For Hypocalcemic TETANY or laryngospasm: CALCIUM CHLORIDE (CaCl) is given. 10% solution containing 1.36 mEq Ca2++/ ml, IV at rate of less than 1 ml/minute to prevent cardiac arrhythmia.

Caution: Calcium Gluconate may give a generalized burning sensation due to vasodilation, which also can lead to arterial hypotension. The alternate treatment is CALCIUM GLUPECTATE 22% solution, containing 18 mg Ca2++/ml in a volume of 5-20 ml IV for severe Tetany. Mild and chronic hypocalcemia can be treated with oral calcium and vitamin D combination. Oral Calcium preparation are Calcium Carbonate, Citrate, Phosphonate, Lactate, and Gluconate in doses of 1-2 G/day up to 3-6 G /day.

TREATMENT AND PREVENTION FOR OSTEOPENIA OR OSTEPOROSIS.

CALCIUM CARBONATES

ACTONEL (Risedronel Sodium). ACTONEL is a biphosphonate, it is available in tabs 5, 30, 35, 75 and150 mg once a week dose packs. Dose as follows: 5mg/day, 35 mg/week, or 75 mg /day for 2 days once a month or 150 mg once a month. Actonel and other biphosphonates are indicated both for treatment or prevention of Osteoporosis in menopausal, postmenopausal females as well as Osteporosis in males. ACTONEL is also available as ACTONEL PLUS CALCIUM as a blister package containing 28-day course therapy per wee k as follows: #4 ACTONEL 35 mg tablets for the first day and # 24 Calcium Carbonate 1250 mg tablets for days 2 to 7h. Either kind of ACTONEL, for the first day dose has to be taken with Sounces of plain water, 30 minutes before the first meal or drink of the day. Another biphosphonate is BONIVA (Ibandronate). In general the biphosphonates act as inhibitors of osteoclasts-mediated bone resorption thus inducing osteoblast activity to favor bone mass. The recommended dose of BONIVA is 100-150 mgs once a month or 2.5 mg per day along with 400 IU of Vitamin D3 plus 500 mg of Calcium. Dose of 2.5 mg a day reduces the incidence of second bone fracture. Another biphosphonate is FOSAMAX ( Alendronate) available in tablets 5, 10, 35 and 70 mgs. It is also available as FOSAMAX PLUS VIT D3, strengths 7Omg/ 2800 IU and 7Omg/5600 IU tabs. The recommended dose is one tablet once a week or 10 mg tabs per day

CALCIUM ACETATE

Phospho-LO gel caps 667 mg. Mostly indicated in concomitant hyper phosphatemia in end-stage renal failure (dyalisis). Dose: 2 gel caps with each meal.

CALCIUM CITRATE (Active Ca). Usually mixed with Vitamin D3, Vitamin K, Mg 100 mg and calcium 200mg. Take 4 tabs/day with meals.

OTHER TREATMENTS: Calcitonin, Calcitriol and Genestein aglycone.

• MIACALCIN (Calcitonin-Salmon) Calcitonin is a polypeptide hormone secreted by cells of the Thyroid gland. When provided reduces calcium in serum and reduces and reduces calcium bone resorption. It is used both in hypocalcaemia and postmenopausal osteoporosis. Dose for the latter 100 IU subcutaneous or IM every other day. Simultaneous give Calcium Carbonate 105 Gm and Vit D 400 IU per day. MIALCALCIN is also available as Nasal Spray, one spray (200 IU) per day. Monitor effectiveness of treatment with periodic lumbar vertebral bone density studies, also periodic analysis of serum Calcium, Magnesium and Alkaline Phosphatase levels, and also 24 hours urinary calcium and phosphates levels.

• RECALTROL (Calcitriol) Occurs naturally in humans. It is the active form of Vitamin D3 (cholecalciferol).

• FOSTEUM (Genestein Aglycone). It is given as a dietary management of metabolic process of Osteopenia and Osteoporosis. Genetein is obtained from soy, citrated zinc and cholecalciferol (Vit D3).

Mild hypocalcemia is usually asymptomatic. Moderate to severe hypocalcemia usually presents as: Tingling sensation, paresthesias, cramps, increased neuromuscular excitation, tetany, laringospasm, and even tonic-clonic seizures. If low calcium is concomitant to low PTH activity the symptoms may include: Total body hair loss (alopecia totalis) starting in infancy, grooved finger nails, cataracts, brain basal ganglia calcifications, mental depression, chronic anxiety, and delusions. Hypocalcemia may also be present in Vitamin D deficiency, poor nutrition, starvation, and mal absorption disorders. Some cases of chronic hypocalcemia in adults may follow thyroid gland surgery or radiation.

CALCIUM AND PHOSPHATE METABOLISM

Calcium and phosphate homeostasis is regulated by PTH and 1,25 dihydro Vitamin D (Calcitriol) through the effects of the kidneys, the intestines and the PTH gland. The l,25 dihydro Vitamin D is the only active Vitamin D. It is formed from the inert 25 OH vitamin D3, which is stored in fat tissue as a reserve.

VITAMIN D

Vitamin D is critical to preserve bones but it is also important to protect the body from certain diseases like cancer s of the Prostate, Breast and Colon, also other conditions like Non-Hodgeking Lymphoma, Rheumatoid Arthritis, Type II Diabetes, Macuiar Degeneration, Multiple Sclerosis (MS), Fib romyalgia, Gingivitis and others. It also promotes the efficiency of the immune system, regulates the cell growth, and has also anti inflammatory properties. There a re basically two kinds of Vita min D: From animal source, CALCIFEROL (Vitamin D3, and from plants source, ERGOCALCIFEROL (Vita min D2). Vitamin D is soluble in fat just as Vitamin A, Vitamin E, and Vitamin K are. The normal, recommended daily dose is 800-1000 international units (IU). The major natural sources of Vitamin D are fish, especially Salmon, Tuna, Sardines, Mackerel, and Cod Liver. The following are the people more at risk for Vitamin D deficiency: Older adults, people with limited sun exposure, the use of skin screen products, fair skin (less melanin), some mal absorption diseases such as Crohn’s , pancreatic deficiency, cystic fibrosis, sprue, liver diseases and post gastric by-pass surgery.

Complex Regional Pain Syndrome

Symptoms And Treatment of CRPS:

The current knowledge of the cause of CRPS is damage to:

• The C and A delta nerve fibers.
• The Somatic nerves.
• The CNS pathways (as it happens in strokes and spinal cord injuries).
• The C & A delta fibers reside in the dorsal roots and conduct the nociceptive pain, as they innervate mostly the soft tissues and bones. Those fibers seem to activate the afferent pathways, involved in:
• The discriminatory  pain signals ,( location, intensity and quality).
• The affective system (the unpleasant sensation of the stimulus).
• The sympathetic (autonomic system).
• The immune system.

SIGNS AND SYMPTOMS OF CPRS

According to the International Association of the Study of Pain (IASP)I, the signs and symptoms of CRPS are:

• Abnormality of pain processing: (Allodynia, Hyperalgesia, hyperpathia).
• Skin changes in color and temperature (bluish, reddish or paleness).
• Neurogenic edema, due to vasomotor and sudomotor dysregulation.
• A motor syndrome (weakness and eventually disuse muscle atrophy).

Patients with typical CRPS may present numerous other symptoms, such as:

• Tremors
• Spasms
• Dystonia
• Myoclonus
• Parasomnias
• Reduced concentration
• Gastroparesis
• Dysphagia
• Hoarseness of voice

  Less Frequent:

• Presyncopes Episodes
• Rash
• Pruritus
• Headaches
• Blurry Vision

CRPS incidence is 40/17000 for females and 11.9/100000 for males, and is more frequent in the ages of 37-64 years.  The more frequent causes of CRPS are bone fractures, muscle and ligament sprains, soft tissue trauma, surgery, etc. The set of symptoms vary, but is usually out of proportions (exaggerated) for the extension of initial injury. It does not follow a sensible anatomical distribution and may spread in characteristic pattern over time. The extraterritoriality of the pain may be due to diffuse wallerian degeneration.

The persistent pain may be maintained by:

• Neuromas
• Poorly healed fractures
• Brachial plexus traction injuries of UE.
• Chronic root irritation (radicuiitis)
• Failure of inhibition at the dorsal horn level.

NEUROBILOGY OF CRPS

The nerve injury seems to activate the GLIAL cells (microgia, astrocytes and oligodendrocytes). For a long time glial cells consider to be just inactive, non neuronal cells of tissue support of the NS. The current knowledge is that the GLIAL cells become activated after nerve injury and once activated release proinflammatory CYTOKINES, such as:

• Tumor Necrosis Factor (TNF)
• Reactive Oxygen Species (ROS)
• Nitrous Oxyde (NO)
• Excitatory Amino acids (EAA)
• Prostaglandins (PG)
• Interleukin 1
• Interleukin 6

Once such cytokines are released in the Dorsal and Ventral Horns of the spinal cord, are responsible for the development, spread and maintenance of neuropathic pain. Other important molecules of the inflammatory “soup” at the site of injury coming from the blood and, invade the immune cells, and include:

• Proton
• Serotonin
• Bradykinin
• Epinephrine
• Lipoxoxygenases
• Brain Derived Neurotropic Factor(BDVF) Adenosine
• Neurotropins
• Substance P and Calcitonin
• Generated Peptides(CGRP)

DOES THE IMMUNE SYSTEM HAVE ANY ROLE IN CRPS?

The answer is YES. Both microglia and astrocytes are the primary immune component in the CNS and become activated by nerve and tissue damage or by inflammation and act in persistent pain states . The presence of proinflammatory cytokines can be measured in CSF along with Glutamates and Nitric Oxyde metabolites.

TREATMENT OF CRPS

At the time of this discussion, standard therapy for CRPS is limited. Early diagnosis is the most important, especially:

• Traction injuries
• Recurrent disc disease
• Poorly healed fractures
• Neuromas, etc.. Some of the earliest procedures are sympathetic blockades, while the patient has sympathetically maintained pain;
• Many early CRPS cases are misdiagnosed and labeled as fibromyalgias when symptoms may arise from brachia| and cervical plexitis, frequently common in automobile accidents.
• The use of Opiod pain medications is not usually effective, but if any has to be used, Methadone at low doses is the most adequate.
• GABA agonists are good in certain cases, such as Pregabalin, Cymbalta and amitriptyline.
• One of the newest medicines being tried is KETAMINE.
• It is necessary to do a basic EKG and if possible a 2-D echocardiogram, and a neuropsychological evaluation.
• The protocol is to use 10 sessions of 4 hours IV infusion of 200 milligrams of Ketamine as an outpatient; monitoring the BP, Pulse and EKG monitoring. Give Valium or Versedl, plus Clo nidine. At the end of the session give 2 mgs of Ativan, po.
• Result is about 80% of patients obtain 6080 %  pain relief that may last for two to three months.
• Give a buster at one month and at 3 months
• Other approaches in the near future are: Lidocaine infussiions, Propentofylline, a phosphodiesterase inhibitor that can block the activation of  microglia. Other alternative to be tried is Thalidomide and Chyoneurolysis of neuromas that now is able to be seen under MRI or ultrasound.

Is Arthritis Limiting You ?

Osteoarthritis And Rheumatoid Arthritis

Arthritis is a painful joint condition that affects a reported 32.9 million  American  adults.  Though  it commonly occurs in adults however, children can also be affected.

Arthritis can occur in an injured or diseased joint. A joint is where the ends of two or more bones meet. The bone ends of a joint are covered with cartilage, a smooth material that cushions the bone and allows the joint to move smoothly without pain.

Types of Arthritis

Though there are more than a hundred different types of arthritis, the two most common types are called osteoarthritis and rheumatoid arthritis.

Osteoarthritis

Osteoarthritis is found in the joints of older people and in injured or overused joints of younger individuals. It is commonly found in the knee, hips, and spine. In this type of arthritis, the cartilage covering the joint begins to wear away. Occasionally, bone growths called “spurs“, can develop in the joint. The resulting inflammation in the joint causes pain and swelling.

Rheumatoid Arthritis

Rheumatoid arthritis, another common form of arthritis, is a long lasting disease in which the joint lining swells. This swelling invades surrounding tissues and causes chemical substances to attack and destroy the joint surface. Though rheumatoid arthritis is commonly found in the hands and feet, it can also occur in the knees, hips, and elbows. Swelling, pain, and stiffness are present even when the joint is not used. Though rheumatoid arthritis can affect anyone, more than seventy percent of those with this disease are above thirty.

Treatment of Arthritis

• The main approach to treating arthritis centers on pain relief, increased motion, and increased strength.
• Many over-the-counter medications, including aspirin, ibuprofen, and naproxen can be used to control pain and inflammation associated with arthritis.
• Prescription medications are also available if over-the-counter medications are not effective.
• People with arthritic joints can use canes, crutches, and walkers to help relieve the stress placed on arthritic joints.
• Exercising and physical therapy can also be helpful in decreasing stiffness and in strengthening muscles around the joints.

Surgical Treatment

If these methods of treatment are not successful, surgery is recommended.

• The type of surgery depends on the extent of arthritis in the joints, its type, and the physical condition of the patient.
• Surgical procedures include removal of the diseased or damaged joint lining, realignment of the joints, total joint replacement, and fusion of the bone ends of a joint to prevent joint motion and relieve joint pain.
• Though there is no present cure for arthritis, researchers continue to make progress in finding the underlying causes for the major types of arthritis.
• Still, people with arthritis can continue to perform normal activities.
• Various exercise programs, anti-inflammatory drugs, and weight reduction programs for obese people are ways to reduce pain, stiffness, and improve function.
• In persons with severe cases of arthritis, orthopedic surgery can often provide dramatic pain relief and restore lost joint function.
• A total joint replacement, for example, can usually enable a person with severe arthritis in the hip or the knee to walk around without pain or stiffness.
• Consult your orthopedic doctor if you are having symptoms typical of arthritis.

ARTHRITIS OF THE ELBOW

Elbow Pain : Symptoms, Causes And Treatment

Symptoms

How many times a day do you bend your elbow? A person usually bends their elbow hundreds of times a day. Now imagine if every time you bent your elbow, you felt the pain of arthritis.

For many Americans, this scenario is all too true. Arthritis of the elbow can cause pain not only when they bend their elbow, but also when they straighten it. The most common cause of arthritis of the elbow is rheumatoid arthritis (RA). Osteoarthritis (OA or “wear-and-tear” arthritis) and trauma can also cause arthritis in the elbow joint. RA is a disease of the joint linings, or synovia. As the joint lining swells, the joint space narrows.

Causes

The disease gradually destroys the bones and soft tissues. Usually, RA affects both elbows, as well as other joints such as the hand, wrist and shoulder. OA affects the cushioning cartilage on the ends of the bones that enables them to move smoothly in the joint. As the cartilage is destroyed, the bones begin to rub against each other. Loose fragments within the joint may accelerate degeneration. Trauma or injury to the elbow can also damage the articular cartilage. This eventually leads to the development of post traumatic arthritis. Usually, this form of arthritis is confined to the injured joint.

In the early stages of RA, pain may been primarily on the outer side of the joint. Pain generally worsens as you turn (rotate) your forearm. The pain of OA may intensify as you extend your arm. Pain that continues during the night or when you are at rest indicates a more advanced stage of OA. In addition to pain, one may experience swelling, inability to perform daily activities because the elbow gives away, inability to straighten or bend the elbow, locking of the elbow, and stiffness in the elbow. At times, both elbows are involved or pain can occur at the wrist, shoulders, and elbow; this is indicative of RA.

Treatment

The initial treatment is non-surgical and depends on the type of arthritis.

• Your physician will discuss the options with you and develop an individualized program of medical and physical activities.
• Among the therapies that can be used are: activity modification; since, OA may be linked to repetitive overuse of the joint, modifying job or sports activities can be helpful. Intermittent periods of rest can relieve stress on the elbow.
• Painkillers, such as acetaminophen or ibuprofen can provide short-term pain relief. More potent agents can be prescribed to treat RA.
• These include antimalarial agents, gold salts, immunosuppressive drugs, and corticosteroids. An injection of a corticosteroid into the joint can often help.
• Physical therapy is another treatment option; heat or cold applications and gentle exercises may be prescribed.
• A splint worn at night, or one that permits movement as it protects the elbow from stresses, may also be helpful.
• Other assistine devices, such as handle extensions, can be used to maintain daily activities.

If your arthritis does not respond to the above treatments, you and your physician may discuss surgical options. Because several nerves are near the elbow, a skilled orthopedic surgeon should be consulted. Surgery usually results in improved pain control and increased range of motion.

Procedure

The exact procedure will depend on the type of arthritis you have, the stage of the disease, your age, expectations, and activity requirements. Arthroscopy, a procedure involving pencil-sized instruments and two or three small incisions, allows the surgeon to remove bone spurs, loose fragments, or a portion of the diseased synovium. This procedure can be used to treat both RA and OA. Another procedure is called a synovectomy; here, the surgeon removes the diseased synovium. Sometimes, a portion of bone is also removed to provide a greater range of motion. This procedure is often used in the early stages of RA. In an osteotomy, part of the bone is removed to relieve pressure on the joint. This procedure is often used to treat OA. In an arthroplasty, the surgeon creates an artificial joint using either an internal prosthesis or an external fixation device. A total joint replacement is usually reserved for patients over 60 years old or patients with RA in advanced stages.

ON CANNABIS AND CANNABINOIDS

Medicinal Uses of Cannabis and Cannabinoids:

MEDICAL CANNABIS

Cannabis was legalized in Montana in 2004.  It already has achieved semi-legal status in 14 states of the Union as per the date of this paper. Cannabis status at Federal level remains schedule I, under the Controlled Substance Act. So far the major reasons for medical use has been chronic pain, muscle spasm, nausea, vomitting, inflammation, glaucoma and insomnia. Currently some 2500 medical practitioners in Montana alone have been registered to grow and recommend  the  use of Cannabis to patients.

CANNABINOIDS

Cannabinoids are synthetic forms of the main psychoactive ingredients of cannabis. The chemical designation of cannabis is tetra -hydro- cannabinol-delta-9 (CTR) Cannabinoids have been prescribed in the US since 1986.  One of them is dronabinol, marketed  as MARINOL and has been downgraded from schedule I1 to schedule III in
1999, due to low street value. It is listed for nausea and vomiting associated with cancer
chemotherapy, and appetite improvement in AIDS.  Another synthetic cannabinoid, racemic nabilone is marketed in the USA as CESAMET. It was also approved for chemotherapy-related symptoms.  Another product currently used in Canada and Europe is a cannabis extract used  as oral spray (Savitex).  Since this is a product completely extracted from the cannabis plant Savitex is currently in phase III of drug testing in the USA.

GENERAL CONSIDERATIONS

Cannabis  receptors were identified in 1988. There are two general receptors: Type CB I,generally in the CNS and CB2 generally in the immune system. Almost all cannabinoids are anti-inflammatories.  From a technical stand point, there is no evidence that cannabis has drug-interactions with OPIODS. The toxicity of cannabis is extremely low. However,
psyquiatric side effects can be severe in certain persons with underlying psyquiatric conditions, such as Schizophrenia, specially when used in adolescence. There have been some reports that cannabis use under age 20 may have a negative effect on the maturing of the CNS.

On the other hand there  are many small studies favoring cannabis used for seizures,polyneuropathies, anxiety and chronic pain. A few other potential good use of cannabis are symptoms management of MS, spasticity, fatigue, appetite and sleep. According to the United Nations, cannabis is the most widely used illicit drug in the world. Cannabis use has been traced as far back to the III millennium B.C. In modem times, cannabis has been used for numerous other purposes such as: recreational, religious, spiritual as well as medical. The possession, use, share, transport and distribution cannabis preparations containing psychoactive substances became illegal in most parts of the world in the early 20 century. Cannabis indigenous to Central and South Asia. Some other names for cannabis: hashish, hem, marijuana, marihuana and mariguana.