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INTODUCTION-

Osteomyelitis is an infection in a bone. Infections can reach a bone by traveling through the bloodstream or spreading from nearby tissue. Infections can also begin in the bone itself if an injury exposes the bone to germs.

Smokers and people with chronic health conditions, such as diabetes or kidney failure, are more at risk of developing osteomyelitis. People who have diabetes may develop osteomyelitis in their feet if they have foot ulcers.

Although once considered incurable, osteomyelitis can now be successfully treated. Most people need surgery to remove areas of the bone that have died. After surgery, strong intravenous antibiotics are typically needed.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones in the arms or legs) are large, dense bones that provide strength, structure and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis is not more common in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes.
• Patients receiving hemodialysis.
• People with weakened immune systems.
• People with sickle cell disease.
• Intravenous drug abusers.
• The elderly.

CAUSES-

It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends coming out through the skin.
• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.
• Bacteria in the bloodstream (bacteremia), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.
• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a direct bone infection.

Most cases of osteomyelitis are caused by staphylococcus bacteria, types of germs commonly found on the skin or in the nose of even healthy individuals.

Germs can enter a bone in a variety of ways, including:

• The bloodstream. Germs in other parts of your body — for example, in the lungs from pneumonia or in the bladder from a urinary tract infection — can travel through your bloodstream to a weakened spot in a bone.
• Injuries. Severe puncture wounds can carry germs deep inside your body. If such an injury becomes infected, the germs can spread into a nearby bone. Germs can also enter the body if you have broken a bone so severely that part of it is sticking out through your skin.
• Surgery. Direct contamination with germs can occur during surgeries to replace joints or repair fractures.

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Risk factors

Your bones are normally resistant to infection, but this protection lessens as you get older. Other factors that can make your bones more vulnerable to osteomyelitis may include:

Recent injury or orthopedic surgery

A severe bone fracture or a deep puncture wound gives bacteria a route to enter your bone or nearby tissue. A deep puncture wound, such as an animal bite or a nail piercing through a shoe, can also provide a pathway for infection.

Surgery to repair broken bones or replace worn joints also can accidentally open a path for germs to enter a bone. Implanted orthopedic hardware is a risk factor for infection.

Circulation disorders

When blood vessels are damaged or blocked, your body has trouble distributing the infection-fighting cells needed to keep a small infection from growing larger. What begins as a small cut can progress to a deep ulcer that may expose deep tissue and bone to infection.

Diseases that impair blood circulation include:

• Poorly controlled diabetes
• Peripheral artery disease, often related to smoking
• Sickle cell disease

Problems requiring intravenous lines or catheters

There are a number of conditions that require the use of medical tubing to connect the outside world with your internal organs. However, this tubing can also serve as a way for germs to get into your body, increasing your risk of an infection in general, which can lead to osteomyelitis.

Examples of when this type of tubing might be used include:

• Dialysis machine tubing
• Urinary catheters
• Long-term intravenous tubing, sometimes called central lines

Conditions that impair the immune system

If your immune system is affected by a medical condition or medication, you have a greater risk of osteomyelitis. Factors that may suppress your immune system include:

• Cancer treatment
• Poorly controlled diabetes
• Needing to take corticosteroids or drugs called tumor necrosis factor inhibitors

Illicit drugs

People who inject illegal drugs are more likely to develop osteomyelitis because they may use nonsterile needles and are less likely to sterilize their skin before injections.

Complications

Osteomyelitis complications may include:

• Bone death (osteonecrosis). An infection in your bone can impede blood circulation within the bone, leading to bone death. Areas where bone has died need to be surgically removed for antibiotics to be effective.
• Septic arthritis. Sometimes, infection within bones can spread into a nearby joint.
• Impaired growth. Normal growth in bones or joints in children may be affected if osteomyelitis occurs in the softer areas, called growth plates, at either end of the long bones of the arms and legs.
• Skin cancer. If your osteomyelitis has resulted in an open sore that is draining pus, the surrounding skin is at higher risk of developing squamous cell cancer.

SYMPTOM-

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The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area.
• Swelling, redness and warmth in the infected area.
• Fever.
• Nausea, secondarily from being ill with infection.
• General discomfort, uneasiness, or ill feeling.
• Drainage of pus (thick yellow fluid) through the skin.

Additional symptoms that may be associated with this disease include:

• Excessive sweating.
• Chills.
• Lower back pain (if the spine is involved).
• Swelling of the ankles, feet, and legs.
• Loss or decrease of motion of a joint.
• Changes in gait (walking pattern that is a painful, yielding a limp) or unwillingness to bear weight in children.

TREATMENT-

Treatment focuses on stopping infection in its tracks and preserving as much function as possible. Most people with osteomyelitis are treated with antibiotics, surgery, or both.

Antibiotics help bring the infection under control and often make it possible to avoid surgery. People with osteomyelitis usually get antibiotics for several weeks through an IV, and then switch to a pill.

More serious or chronic osteomyelitis requires surgery to remove the infected tissue and bone. Osteomyelitis surgery prevents the infection from spreading further or getting so bad that amputation is the only remaining option.

physical therapy approach-

Physical  therapists can play a vital role in the screening process for osteomyelitis.  Individuals who present with signs and symptoms of infection, possibly causing osteomyelitis, should be referred to a physician for further diagnostic testing.  These signs and symptoms are included in the above section. Prevention is another area in cases of osteomyelitis where physical therapists can play an important role.  Chronic osteomyelitis is often a result of complication of treatment with open fractures, therefore, prevention of infection is highly important^[3].  Since the role of nutrition is vital in cases of infection, patient need to be properly educated on proper nutrition in early post-surgical intervention due to the fact that most infections occur in the immediate post-operative period^[3].  Individuals who are at risk for developing osteomyelitis should also be taught proper preventative measures and be aware of early warning signs that infection may be present such as, excessive pus present coming from incision line, redness, extreme tenderness, increased skin temperature near area of injury or surgical procedure, and symptoms of nausea or vomiting. If treated surgically for osteomyelitis, physical therapy may be indicated post-operatively to address any impairments in strength, ROM, proprioception, etc. as well as treatment for any functional limitations or disability secondary to infection.

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The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps). Myopathies are grouped as follows:
congenital myopathies: characterized by developmental delays in motor skills; skeletal and facial abnormalities are occasionally evident at birth
muscular dystrophies: characterized by progressive weakness in voluntary muscles; sometimes evident at birth
mitochondrial myopathies: caused by genetic abnormalities in mitochondria, cellular structures that control energy; include Kearns-Sayre syndrome, MELAS and MERRF
glycogen storage diseases of muscle: caused by mutations in genes controlling enzymes that metabolize glycogen and glucose (blood sugar); include Pompe’s, Andersen’s and Cori’s diseases
myoglobinurias: caused by disorders in the metabolism of a fuel (myoglobin) necessary for muscle work; include McArdle, Tarui, and DiMauro diseases
dermatomyositis: an inflammatory myopathy of skin and muscle
myositis ossificans: characterized by bone growing in muscle tissue
familial periodic paralysis: characterized by episodes of weakness in the arms and legs
polymyositis, inclusion body myositis, and related myopathies: inflammatory myopathies of skeletal muscle
neuromyotonia: characterized by alternating episodes of twitching and stiffness; and
stiff-man syndrome:  characterized by episodes of rigidity and reflex spasms
common muscle cramps and stiffness, and
tetany:  characterized by prolonged spasms of the arms and legs

Symptoms-

There are several different types of genetic myopathies, most of which have similar symptoms. These include:

• Muscle weakness
• Motor delay
• Respiratory impairment
• Bulbar muscle dysfunction (malfunction of the muscles responsible for swallowing and speech)

Bulbar muscle dysfunctions can be especially apparent in congenital myopathies (those present from birth), and can result in severe impairments to swallowing and speech abilities. Congenital myopathies also are characterized by developmental motor delays and, at times, facial or skeletal abnormalities.

Acquired myopathies may have symptoms similar to those of genetic myopathies and also may include:

• Muscle weakness
• Muscle soreness (myalgias)
• Cramps
• Stiffness
• Muscle wasting around the shoulders and hips

Causes and Risk Factors

Patients who have a blood relative with a genetic myopathy have an increased risk for developing the condition. Depending on how the myopathy is inherited, men can be at greater risk than women of developing the condition. Myopathies carried on the X chromosome affect more men than women, while those carried on chromosomes other than the sex chromosome affect both men and women equally.

Patients may be at increased risk of developing acquired myopathy if they have an autoimmune disorder, metabolic or endocrine disorder, are on certain drugs or are exposed to certain toxins.

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Classification

Myopathies may be divided into two main categories: inherited and acquired. The temporal course, the pattern of muscle weakness, and the absence or presence of a family history of myopathy help distinguish between the two types. An early age of onset with a relatively longer duration of disease suggests an inherited myopathy, and a sudden or subacute presentation at a later age is more consistent with an acquired myopathy. Inherited myopathies can be further subclassified as muscular dystrophies, congenital myopathies, mitochondrial myopathies, and metabolic myopathies. Acquired myopathies can be subclassified as inflammatory myopathies, toxic myopathies, and myopathies associated with systemic conditions. The more commonly seen inherited and acquired myopathies are listed in Box 1.

Box 1 Common Causes of Myopathy
Acquired Myopathies
Inflammatory Myopathy Polymyositis Dermatomyositis Inclusion body myositis
Infection Viral infections (HIV, influenza virus, Epstein-Barr virus) Bacterial pyomyositis (Staphylococcus aureus and streptococci are common organisms) Spirochete (Lyme disease) Parasitic infections such as trichinosis
Toxic Myopathy Medications Steroids Cholesterol-lowering medications: statins, fibrates, niacin, and ezetimibe Propofol Amiodarone Colchicine Chloroquine Antivirals and protease inhibitors Omeprazole Tryptophan Toxins Alcohol Toluene
Myopathy Associated with Systemic Diseases Endocrine disorders Thyroid Parathyroid Pituitary or adrenal dysfunction Systemic inflammatory diseases Systemic lupus erythematosus Rheumatoid arthritis Scleroderma Sjögren’s syndrome Mixed connective disease Sarcoidosis Electrolyte imbalance Potassium or magnesium abnormalities Hypophosphatemia Critical illness myopathy Nondepolarizing neuromuscular blocking agents Steroids Amyloid myopathy Primary amyloidosis Familial amyloidosis (TTR mutation)
Inherited Myopathies
Muscular Dystrophy Dystrophinopathy (Duchenne muscular dystrophy,Becker muscular dystrophy) Myotonic dystrophy 1 and 2 Facioscapulohumeral muscular dystrophy Oculopharyngeal muscular dystrophy Limb girdle muscular dystrophy
Congenital Myopathy Nemaline myopathy Central core myopathy
Metabolic Myopathy Acid maltase or acid alpha-1,4-glucosidase deficiency (Pompe’s disease) Glycogen storage disorders 3-11 Carnitine deficiency Fatty acid oxidation defects Carnitine palmitoyl transferase deficiency
Mitochondrial Myopathy Myoclonic epilepsy and ragged red fibers (MERRF) Mitochondrial myopathy, lactic acidosis, and strokes (MELAS) Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) Progressive external ophthalmoplegia (PEO)

DIAGNOSIS-

The clinical history is essential in identifying the presence of a myopathy and narrowing down the differential diagnosis. In particular, the patient should be questioned about medication and recreational drug history (especially alcohol), chemical exposures, exercise intolerance, childhood development, and family history of muscle disease or developmental motor delay.

Laboratory Testing

Serologic testing, which can indicate muscle damage, includes elevations in creatine phosphokinase (CPK), aldolase, lactate dehydrogenase (LDH), and liver function enzymes. A screening panel of laboratory tests may also be obtained to rule out more common causes of myopathy, which are listed in. In cases suspected to be a primary inflammatory myopathy, specific autoantibodies can be considered to determine the prognosis and rule out associated conditions. For example, the presence of anti-Jo antibody in dermatomyositis predicts a superimposed interstitial lung disease. In addition, these patients should also be evaluated for an underlying systemic autoimmune disease with an extensive autoimmune panel and angiotensin-converting enzyme (ACE) levels. In myopathies that are accompanied by polyneuropathy, renal involvement, and a restrictive cardiomyopathy, immunofixation electrophoresis studies in the serum and urine should be considered to rule out the possibility of amyloid disease. Genetic testing is available for some inherited myopathies. These are listed in

Box 2 Laboratory Evaluation for Suspected Myopathy
Confirm the Presence of Muscle Disease Creatine phosphokinase Aldolase Liver function tests Lactate dehydrogenase levels
Identify Etiology Complete blood count with differential Complete metabolic panel Thyroid function tests Parathyroid hormone level Sedimentation rate C-reactive protein and antinuclear antibody panel
Suspected Inflammatory Etiology Myositis-specific autoantibodies Anti–double stranded DNA antibody Anti-Scl 70 antibody Anti-SSA and SSB antibodies Anti-ribonucleoprotein antibody Rheumatoid factor Anti-PM1 antibody Angiotensin-converting enzyme levels
Suspected Mitochondrial or Metabolic Myopathy Serum lactate, pyruvate, ammonia, coenzyme Q10 levels Ischemic forearm lactate test Carnitine levels
Suspected Amyloid Myopathy Immunofixation electrophoresis of monoclonal proteins in serum and urine

Table 2 Commercially Available Genetic Tests in Diagnosis of a Myopathy

Myopathies with Known Genetic Defects	Gene Abnormalities	Pattern of Inheritance
Duchenne muscular dystrophy	Dystrophin gene	X-linked recessive
Becker muscular dystrophy	Dystrophin gene	X-linked recessive
Emery-Dreifuss muscular dystrophy	Emerin gene	X-linked recessive
Limb girdle muscular dystrophy	Lamin A/C Calpain Dysferlin Fukutin related protein	Some are autosomal dominant and others are recessive
Facioscapulohumeral muscular dystrophy	D4Z4 deletion	Autosomal dominant
Oculopharyngeal muscular dystrophy	GCG repeat expansion in poly A binding protein 2 gene	Autosomal dominant
Myotonic dystrophy 1 and 2	DMPK gene for type 1 CNBP (ZNF9) gene for type 2	Autosomal dominant
Mitochondrial myopathy	Specific point mutation analysis for diseases like MELAS POLG1 sequencing for MERRF available Southern blot analysis for mtDNA deletions and mtDNA sequencing	Maternally inherited. But other can be inherited as autosomal dominant or recessive disease
Amyloid myopathy from familial causes	Transthyretin mutation	Autosomal dominant
Statin myopathy (predictor of increased susceptibility)	SLCO1B1 gene	Unknown

MELAS, mitochondrial myopathy, lactic acidosis, and strokes; MERRF, myoclonic epilepsy and ragged red fibers; mtDNA, mitochondrial DNA.

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Ischemic Forearm Test

A traditional test used in the evaluation of a suspected metabolic myopathy is the ischemic forearm test. This is performed by obtaining baseline serum ammonia and lactate levels taken from the forearm. The patient then exercises that arm for 1 minute, after which repeat serum lactate and blood ammonia levels are measured. This is repeated at several intervals (1, 2, 5, and 10 minutes). In normal muscle, the resultant ischemia causes a 3- to 5-fold rise in lactate levels. In contrast, patients with glycogen storage disorders demonstrate no change in lactate levels after exercise.

Electrodiagnostic Studies

The electromyogram (EMG) is an electrical study of the nerves and muscles that plays an important role in confirming the presence, duration, and severity of a myopathy. The study can also disclose special findings such as myotonic potentials. This is the electrical equivalent of clinical myotonia, which is manifested as impaired relaxation of muscles after forceful contraction; for example, patients cannot release objects from their grip. Myotonic potentials have the characteristic sound of a dive bomb on EMG and can help point toward the diagnosis of myotonic dystrophy when found in the appropriate muscles.

Although integral in the evaluation of a myopathy, the EMG can be normal in mild myopathies, steroid myopathies, and a number of metabolic myopathies. Therefore, it is important to remember that a normal EMG does not exclude the presence of a myopathy.

Muscle Biopsy

Histopathologic examination of muscle may be helpful in determining the specific type of muscle disease, especially in patients with a suspected inflammatory or infectious myopathy. Selecting the optimal muscle to biopsy is very important because factors such as severe weakness and technical artifacts can hamper an accurate histologic diagnosis. The ideal muscle that should be sampled is one that is clinically involved but still antigravity in strength, because more-severe weakness can lead to unhelpful, nonspecific findings of fibrosis. Also avoid muscles that have been examined by an EMG because the needle portion of the electrical study might have caused local damage, which can result in spurious findings. Common biopsy sites include the biceps and deltoid muscles in the upper extremity and the quadriceps and gastrocnemius muscles in the lower extremity.

TREATMENT-

Treatments for the myopathies depend on the disease or condition and specific causes. Supportive and symptomatic treatment may be the only treatment available or necessary for some disorders. Treatment for other disorders may include drug therapy, such as immunosuppressives, physical therapy, bracing to support weakened muscles, and surgery.

The treatment of myopathies is multidisciplinary and depends on the type of myopathy. Certain types of myopathies can be treated with immune-suppressant agents and IVIG. Most myopathies require the use of supportive services, such as physical and occupational therapy, pulmonary medicine, cardiology, dietary management, and speech/swallowing therapists. Surgical treatment of spine and limb deformities is used in long-standing cases.

While there is no cure for genetic myopathy, many different treatment options are available to manage the symptoms. Treatments for both genetic and endocrine myopathy are most effective when the disease is diagnosed early and a comprehensive treatment plan is overseen by a knowledgeable medical team, such as those at Cedars-Sinai’s Neuromuscular Disorders Program.

For acquired myopathies due to the immune system, such as dermatomyositis and polymyositis, medications that work to reduce the body’s immune response and decrease inflammation, such as corticosteroids or other immunosuppressants, can help manage some symptoms. Physical therapy, supportive devices such as braces, and sometimes surgery may also be used as treatment tools.

Treatment of metabolic, toxic and endocrine-related myopathy generally focuses on the underlying cause of the condition. Medication or surgery may be used to address the symptoms.

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INTRODUCTION-

Myasthenia gravis (MG) is a relatively rare acquired, autoimmune disorder caused by an antibody-mediated blockade of neuromuscular transmission resulting in skeletal muscle weakness. The autoimmune attack occurs when autoantibodies form against the nicotinic acetylcholine postsynaptic receptors at the neuromuscular junction of skeletal muscles Although the chief target of the autoimmune attack in most cases is the skeletal muscle nicotinic acetylcholine receptor (nAChR), other antigenic targets that are components of the neuromuscular junction (NMJ) have also been implicated.

Myasthenia gravis (MG) is a neuromuscular disorder that causes weakness in the skeletal muscles, which are the muscles your body uses for movement. It occurs when communication between nerve cells and muscles becomes impaired. This impairment prevents crucial muscle contractions from occurring, resulting in muscle weakness.

According to the Myasthenia Gravis Foundation of America, MG is the most common primary disorder of neuromuscular transmission. It’s a relatively rare condition that affects between 14 and 20 out of every 100,000 people in the United States.

SYMPTOM-

Muscle weakness caused by myasthenia gravis worsens as the affected muscle is used. Because symptoms usually improve with rest, muscle weakness can come and go. However, the symptoms tend to progress over time, usually reaching their worst within a few years after the onset of the disease.

Although myasthenia gravis can affect any of the muscles that you control voluntarily, certain muscle groups are more commonly affected than others.

Eye muscles

In more than half of people who develop myasthenia gravis, their first signs and symptoms involve eye problems, such as:

• Drooping of one or both eyelids (ptosis)
• Double vision (diplopia), which may be horizontal or vertical, and improves or resolves when one eye is closed

Face and throat muscles

In about 15% of people with myasthenia gravis, the first symptoms involve face and throat muscles, which can:

• Impair speaking. Your speech might sound soft or nasal, depending on which muscles have been affected.
• Cause difficulty swallowing. You might choke easily, making it difficult to eat, drink or take pills. In some cases, liquids you’re trying to swallow come out your nose.
• Affect chewing. The muscles used for chewing might wear out halfway through a meal, particularly if you’ve been eating something hard to chew, such as steak.
• Change facial expressions. For example, your smile might look like a snarl.

Neck and limb muscles

Myasthenia gravis can also cause weakness in your neck, arms and legs. Weakness in your legs can affect how you walk. Weak neck muscles make it hard to hold up your head.

Weakness associated with MG typically gets worse with more activity and improves with rest. Symptoms of MG can include:

• trouble talking
• problems walking up stairs or lifting objects
• facial paralysis
• difficulty breathing due to muscle weakness
• difficulty swallowing or chewing
• fatigue
• hoarse voice
• drooping of eyelids
• double vision

Not everyone will have every symptom, and the degree of muscle weakness can change from day to day. The severity of the symptoms typically increases over time if left untreated.

When to see a doctor

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Talk to your doctor if you have difficulty:

• Breathing
• Seeing
• Swallowing
• Chewing
• Walking
• Using your arms or hands
• Holding up your head.

CAUSES-

Antibodies

Your nerves communicate with your muscles by releasing chemicals (neurotransmitters) that fit precisely into receptor sites on the muscle cells at the nerve-muscular junction.

In myasthenia gravis, your immune system produces antibodies that block or destroy many of your muscles’ receptor sites for a neurotransmitter called acetylcholine With fewer receptor sites available, your muscles receive fewer nerve signals, resulting in weakness.

Antibodies can also block the function of a protein called a muscle-specific receptor tyrosine kinase . This protein is involved in forming the nerve-muscular junction. Antibodies that block this protein can lead to myasthenia gravis.

Thymus gland

The thymus gland is a part of your immune system situated in the upper chest beneath your breastbone. Researchers believe the thymus gland triggers or maintains the production of the antibodies that block acetylcholine.

Large in infancy, the thymus gland is small in healthy adults. In some adults with myasthenia gravis, however, the thymus gland is abnormally large. Some people with myasthenia gravis also have tumors of the thymus gland (thymomas). Usually, thymomas aren’t cancerous (malignant), but they can become cancerous.

Other causes

Some people have myasthenia gravis that isn’t caused by antibodies blocking acetylcholine or the muscle-specific receptor tyrosine kinase. This type of myasthenia gravis is called antibody-negative myasthenia gravis. Antibodies against another protein, called lipoprotein-related protein 4, can play a part in the development of this condition.

Rarely, mothers with myasthenia gravis have children who are born with myasthenia gravis (neonatal myasthenia gravis). If treated promptly, children generally recover within two months after birth.

Some children are born with a rare, hereditary form of myasthenia, called congenital myasthenic syndrome.

Factors that can worsen myasthenia gravis

• Fatigue
• Illness
• Stress
• Some medications — such as beta blockers, quinidine gluconate, quinidine sulfate, quinine, phenytoin, certain anesthetics and some antibiotics
• Pregnancy
• Menstrual periods

DIAGNOSIS-

Your doctor will perform a complete physical exam, as well as take a detailed history of your symptoms. They’ll also do a neurological exam. This may consist of:

• checking your reflexes
• looking for muscle weakness
• checking for muscle tone
• making certain your eyes move properly
• testing sensation in different areas of your body
• testing motor functions, like touching your finger to your nose

Other tests that can help your doctor diagnose the condition include:

• repetitive nerve stimulation test
• blood testing for antibodies associated with MG
• edrophonium (Tensilon) test: a drug called Tensilon (or a placebo) is administered intravenously, and you’re asked to perform muscle movements under doctor observation
• imaging of the chest using CT scans or MRI to rule out a tumor

Treatment options for myasthenia gravis-

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There is no cure for MG. The goal of treatment is to manage symptoms and control the activity of your immune system.

Medication

Corticosteroids and immunosuppressants can be used to suppress the immune system. These medications help minimize the abnormal immune response that occurs in MG.

Additionally, cholinesterase inhibitors, such as pyridostigmine (Mestinon), can be used to increase communication between nerves and muscles.

Thymus gland removal

Removal of the thymus gland, which is part of the immune system, may be appropriate for many patients with MG. Once the thymus is removed, patients typically show less muscle weakness.

According to the Myasthenia Gravis Foundation of America, between 10 and 15 percent of people with MG will have a tumor in their thymus. Tumors, even those that are benign, are always removed because they may become cancerous.

Plasma exchange

Plasmapheresis is also known as a plasma exchange. This process removes harmful antibodies from the blood, which may result in an improvement in muscle strength.

Plasmapheresis is a short-term treatment. The body continues to produce the harmful antibodies and weakness may recur. Plasma exchange is helpful before surgery or during times of extreme MG weakness.

Intravenous immune globulin

Intravenous immune globulin (IVIG) is blood product that comes from donors. It’s used to treat autoimmune MG. Although it’s not entirely known how IVIG works, it affects the creation and function of antibodies.

Lifestyle changes

There are some things you can do at home to help alleviate symptoms of MG:

• Get plenty of rest to help minimize muscle weakness.
• If you’re bothered by double vision, talk to your doctor about whether you should wear an eye patch.
• Avoid stress and heat exposure, as both can worsen symptoms.

These treatments cannot cure MG. However, you’ll typically see improvements in your symptoms. Some individuals may go into remission, during which treatment is not necessary.

Tell your doctor about any medications or supplements you take. Some drugs can make MG symptoms worse. Before taking any new medication, check with your doctor to ensure it’s safe.

PHYSICAL THERAPY APPROACH-

Rehabilitation alone or in combination with other forms of treatment can relieve or reduce symptoms for some people with MG.

MG patients should find the optimal balance between physical activity and rest. It is not possible to cure the weakness by active physical training. However, most MG patients are more passive than they need to be. Physical activity and physical training of low to medium intensity is recommended.

One study showed a clear benefit from a strength training exercise program for a group of patients with mild to moderate MG, concluding “physical training can be carried out safely in mild MG and provides some improvement of muscle force”.

Physical exercise is well tolerated in patients with well regulated Myasthenia Gravis. Aerobic exercise and mild strength training can be advised and should be supervised.

Balance strategy training maybe effective in improving balance and more research into this domain has to be done

General advice for exercise programs for people with MG:

• Aim to strengthen large muscle groups, particularly proximal muscles of shoulders and hips
• Advise patient to do the exercises at their “best time of day” ie. when not feeling tired – for the majority of MG patients this will be morning
• If a patient is taking pyridostigmine, exercise at peak dose ie. 1.5 to 2 hours after taking a dose
• Moderate intensity of exercise only: the patient should not experience worsening of MG symptoms (eg. ptosis or diplopia) during exercise
• General aerobic exercise is also valuable, helping with respiratory function as well stamina

EXERCISE CONSIDERATIONS FOR INDIVIDUALS WITH MYASTHENIA GRAVIS–

When engaging in exercise, individuals with MG must be cautious. They must consider the time of day in which they exercise, type of exercise, duration of exercise, and the environment in which they exercise.

Because fatigue is a common symptom of MG, individuals with this condition should exercise in the morning when they have the most energy and are least fatigued, since muscular weakness is usually heightened in the evening. 4 Being conscious of timing to avoid fatigue not only applies to exercise, but also to the eating schedules of individuals with MG. Chewing is essentially an exercise which works the muscles of the jaw. If these muscles experience too much fatigue, individuals may be at greater risk of choking because their food is inadequately chewed. To combat this, meals should also be planned with the largest meals of the day coinciding with the time at which the individual is least fatigued.

Additionally, “Excessive heat can bring on muscle weakness as well as other MG symptoms.” 6 As a result, exercise sessions are best limited to the mornings when temperatures are lower, or performed in indoor facilities to avoid hot, humid outdoor environments.

To ensure safety while exercising, PACE is a suitable guideline to follow. 8

P- Planning daily activities
A- Adapting the home, adequate rest, assistive equipment, asking for help
C- Conserving energy, check-ups with doctor, cool temperature
E- Emotional stability, exercising in moderation, eliminating unnecessary daily tasks

EXERCISE PRESCRIPTION

Although there are no set guidelines for exercise intensity, duration and load for individuals with MG, regular to moderate exercise in the form of walking swimming, jogging or recreational sports can combat muscle weakness. 6 Exercise should be repeated, yet only performed at a level which falls short of muscular fatigue. 6

In a physiotherapy clinic, exercise progression should be based on the needs of each individual. Some cases of MG are less progressive, meaning individuals may be able to tolerate more exercise, while in other circumstances, less exercise may be advisable.

All strengthening exercises should progress first from range of motion exercises to emphasize flexibility to exercises using light resistance in the form of a thera-band and finally to full resistance exercises using machines and free weights. A general exercise prescription for an average individual is 3 sets of 10 repetitions, while no distinct guidelines exist for individuals with MG, starting with a lower prescription of 3 sets of 5 repetitions may be advisable.

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INTRODUCTION-

Bone fractures are a common injury and the healing process is complex. Bone is one of a few tissues that is able to heal without forming a fibrous scar. There are two types of fracture healing – indirect (secondary) and direct healing (primary)

Fracture of 4th Metacarpal Bone

Direct healing occurs when the bony fragments are fixed together with compression. There is no callus formation. The bony ends are joined and healed by osteoclast and osteoblast activity.

ndirect healing is more common than direct healing and involves both endochondral and intramembranous bone healing. Anatomical reduction and stable conditions are not required for indirect healing to occur. Rather, there is a small amount of motion and weight bearing at the fracture, which causes a soft callus to form, leading on to secondary bone formation. It should be noted though that too much load/movement can result in delayed healing or non-union, which occurs in 5-10% of all fractures.

Indirect healing usually occurs with:

• non operative fracture treatment
• operative treatments where some motion occurs at the fracture site, such as:
  • Intramedullary nailing
  • External fixation
  • Internal fixation of comminuted fractures.

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PHSESE OF FRACTURE HEALING-

Inflammatory phase (duration: hours–days): Broken bones result in torn blood vessels and the formation of a blood clot or haematoma. The inflammatory reaction results in the release of cytokines, growth factors and prostaglandins, all of which are important in healing. The fracture haematoma becomes organised and is then infiltrated by fibrovascular tissue, which forms a matrix for bone formation and primary callus.

Reparative phase (duration: days-weeks): A thick mass of callus forms around the bone ends, from the fracture haematoma. Bone-forming cells are recruited from several sources to form new bone, which can be seen on radiographs within 7-10 days after injury . Soft callus is organised and remodelled into hard callus over several weeks. Soft callus is plastic and can easily deform or bend if the fracture is not adequately supported. Hard callus is weaker than normal bone but is better able to withstand external forces and equates to the stage of “clinical union”, i.e. the fracture is not tender to palpation or with movement.

Remodelling phase (duration: months-years): This is the longest phase and may last for several years. During remodelling, the healed fracture and surrounding callus responds to activity, external forces, functional demands and growth. Bone (external callus) which is no longer needed is removed and the fracture site is smoothed and sculpted until it looks much more normal on an x-ray (Figure 9). The epiphyses gradually realign and residual angulation may be slowly corrected, in accordance with the rules of remodelling.

With the continued migration of osteoblasts and osteoclasts, the hard callus undergoes repeated remodeling – termed ‘coupled remodeling.’ This ‘coupled remodeling’ is a balance of resorption by osteoclasts and new bone formation by osteoblasts. The center of the callus is ultimately replaced by compact bone, while the callus edges become replaced by lamellar bone. Substantial remodeling of the vasculature occurs alongside these changes. The process of bone remodeling lasts for many months, ultimately resulting in regeneration of the normal bone structure.

An important point to expand on is endochondral ossification, which is the name given for the process of conversion of cartilage to bone. As described above, this occurs during the formation of bony callus, in which the newly formed collagen-rich cartilaginous callus gets replaced by immature bone. This process is also the key to the formation of long bones in the fetus, in which the bony skeleton replaces the hyaline cartilage model. The second type of ossification also occurs in the fetus; this is intramembranous ossification; this is the process by which mesenchymal tissue (primitive connective tissue) is converted directly to the bone, which no cartilage intermediate. This process takes place in the flat bones of the skull.

CLINICAL SIGNIFICANCE-

Primary bone healing is the reestablishment of the cortex without the formation of a callus. It occurs if a fracture is adequately “fixed” through reduction, immobilization, and rehabilitation. Secondary bone healing, as described above, occurs through the formation of a callus and subsequent remodeling.

By reducing and fixating, the clinician moves the two ends of the fracture into close apposition, which results in the minimal formation of granulation tissue and callus. ‘Cutting cones’ of osteoclasts cross the fracture site to the resorbed damaged bone, and ‘forming zones’ of osteoblasts lay down new bone.

Reduction and fixation of fractures can be either open or closed. If treated as closed, this happens without the need to make an incision into the skin. Open refers to the need/choice to open the skin with a surgical incision. If a fracture pattern appears stable, then the most appropriate method is closed. Options for this would be to use a cast (e.g., plaster of Paris), a brace or a splint. Open reduction tends to be the choice with unstable fractures and commonly occurs alongside internal fixation – hence the term ORIF. Internal fixation involves the use of surgical implants to hold the two ends of the fracture closely opposed. Commonly used methods of internal fixation include plating, screws, wires, and intramedullary nails. A final method of external fixation is also an option, and this involves the placing of pins through the skin, which are then held in place by an external ‘scaffold.’ This method tends to be used in complex fractures and can serve as a temporary option before internal fixation.

Multiple factors affect fracture healing, which can broadly categorize into local and systemic categories.

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Local factors:

• Fracture characteristics – excessive movement, misalignment, extensive damage and soft tissues caught within fracture ends can lead to delayed or non-union
• Infection – it can lead to poor healing and delayed or non-union.
• Blood supply – reduced blood supply to the fracture site can lead to delayed or non-union.

Systemic factors (the presence of any of these factors predisposes to poor healing)

• Advanced age
• Obesity
• Anemia
• Endocrine conditions – Diabetes mellitus, Parathyroid disease, and Menopause
• Steroid administration
• Malnutrition
• Smoking

Fractures have significant mortality and morbidity; therefore a multi-disciplinary approach is essential for good outcomes.

There are multiple methods that the interprofessional team can utilize to promote/stimulate fracture healing, including:

• Dietary supplements – calcium, protein, Vitamins C, and D
• Bone stimulators – which can be electrical, electromagnetic, and ultrasound. The current effectiveness of these methods is still equivocal, and this area requires further research.
• Bone graft – this involves the use of bone to help provide a scaffold to the newly forming bone. This graft can be from the patient’s body (autograft) or from a deceased donor (allograft).

What Can Hinder Bone Healing? 

A wide variety of factors can slow down the healing process. These include:

• Movement of the bone fragments; weightbearing too soon
• Smoking, which constricts the blood vessels and decreases circulation
• Medical conditions, such as diabetes, hormone-related problems or vascular disease
• Some medications, such as corticosteroids and other immunosuppressants
• Fractures that are severe, complicated or become infected
• Advanced age
• Poor nutrition or impaired metabolism
• Low levels of calcium and vitamin D
  

What Helps Promote Bone Healing?

If a bone will be cut during a planned surgical procedure, some steps can be taken pre- and postoperatively to help optimize healing. The surgeon may offer advice on diet and nutritional supplements that are essential to bone growth. Smoking cessation and adequate control of blood sugar levels in people living with diabetes are important. Smoking and high glucose levels interfere with bone healing. 

For all patients with fractured bones, immobilization is a critical part of treatment because any movement of bone fragments slows down the initial healing process. Depending on the type of fracture or surgical procedure, the surgeon may use some form of fixation (such as screws, plates or wires) on the fractured bone and/or a cast to keep the bone from moving. During the immobilization period, weightbearing is restricted as instructed by the surgeon. 

Once the bone is adequately healed, physical therapy often plays a key role in rehabilitation. An exercise program designed for the patient can help in regaining strength and balance and can assist in returning to normal activities.

PHYSICAL THERAPY FOR BONE HEALING-

Physiotherapy should start immediately after the fracture has been immobilised. Physiotherapy during fracture healing will concentrate on:

• Promoting healing
• Encouraging weight bearing
• Maintaining strength of weakened muscles
• Maintaining range of movement of the affected and surrounding joints
• Reducing pain
• Reducing swelling

After your fracture has healed and/or your cast has been removed physiotherapy is continued for 3-12 months or until you have regained your full level of function.The aims of physiotherapy are to:

• Progress weight bearing activities
• Return to full function
• Return strength and full range of movement to muscles / joints
• Focus on sport-specific rehabilitation
• Optimise the range of movement at the affected joint

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INTRODUCTION-

Depression is classified as a mood disorder. It may be described as feelings of sadness, loss, or anger that interfere with a person’s everyday activities.

It’s also fairly common. The Centers for Disease Control and Prevention (CDC) estimates that 8.1 percent of American adults ages 20 and over had depression in any given 2-week period from 2013 to 2016.

Depression is a common illness worldwide, with more than 264 million people affected(1). Depression is different from usual mood fluctuations and short-lived emotional responses to challenges in everyday life. Especially when long-lasting and with moderate or severe intensity, depression may become a serious health condition. It can cause the affected person to suffer greatly and function poorly at work, at school and in the family. At its worst, depression can lead to suicide. Close to 800 000 people die due to suicide every year. Suicide is the second leading cause of death in 15-29-year-olds.

Although there are known, effective treatments for mental disorders, between 76% and 85% of people in low- and middle-income countries receive no treatment for their disorder(2). Barriers to effective care include a lack of resources, lack of trained health-care providers and social stigma associated with mental disorders. Another barrier to effective care is inaccurate assessment. In countries of all income levels, people who are depressed are often not correctly diagnosed, and others who do not have the disorder are too often misdiagnosed and prescribed antidepressants.The burden of depression and other mental health conditions is on the rise globally. A World Health Assembly resolution passed in May 2013 has called for a comprehensive, coordinated response to mental disorders at the country level.

CAUSES-

There are several possible causes of depression. They can range from biological to circumstantial.

Common causes include:

• Family history. You’re at a higher risk for developing depression if you have a family history of depression or another mood disorder.
• Early childhood trauma. Some events affect the way your body reacts to fear and stressful situations.
• Brain structure. There’s a greater risk for depression if the frontal lobe of your brain is less active. However, scientists don’t know if this happens before or after the onset of depressive symptoms.
• Medical conditions. Certain conditions may put you at higher risk, such as chronic illness, insomnia, chronic pain, or attention-deficit hyperactivity disorder (ADHD).
• Drug use. A history of drug or alcohol misuse can affect your risk.

other risk factors for depression include:

• low self-esteem or being self-critical
• personal history of mental illness
• certain medications
• stressful events, such as loss of a loved one, economic problems, or a divorce

Many factors can influence feelings of depression.

Types and symptoms-

Depending on the number and severity of symptoms, a depressive episode can be categorized as mild, moderate or severe.

A key distinction is also made between depression in people who have or do not have a history of manic episodes. Both types of depression can be chronic (i.e. over an extended period) with relapses, especially if they go untreated.

Recurrent depressive disorder: this disorder involves repeated depressive episodes. During these episodes, the person experiences depressed mood, loss of interest and enjoyment, and reduced energy leading to diminished activity for at least two weeks. Many people with depression also suffer from anxiety symptoms, disturbed sleep and appetite, and may have feelings of guilt or low self-worth, poor concentration and even symptoms that cannot be explained by a medical diagnosis.

Depending on the number and severity of symptoms, a depressive episode can be categorized as mild, moderate or severe. An individual with a mild depressive episode will have some difficulty in continuing with ordinary work and social activities but will probably not cease to function completely. During a severe depressive episode, it is unlikely that the sufferer will be able to continue with social, work or domestic activities, except to a limited extent.

Bipolar affective disorder: this type of depression typically consists of both manic and depressive episodes separated by periods of normal mood. Manic episodes involve elevated or irritable mood, over-activity, pressure of speech, inflated self-esteem and a decreased need for sleep.

Depression test-

There isn’t a single test to diagnose depression. But your healthcare provider can make a diagnosis based on your symptoms and a psychological evaluation.

In most cases, they’ll ask a series of questions about your:

• moods
• appetite
• sleep pattern
• activity level
• thoughts

Because depression can be linked to other health problems, your healthcare provider may also conduct a physical examination and order blood work. Sometimes thyroid problems or a vitamin D deficiency can trigger symptoms of depression.

Don’t ignore symptoms of depression. If your mood doesn’t improve or gets worse, seek medical help. Depression is a serious mental health illness with the potential for complications.

If left untreated, complications can include:

• weight gain or loss
• physical pain
• substance use problems
• panic attacks
• relationship problems
• social isolation
• thoughts of suicide
• self-harm

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Contributing factors and prevention-

Depression results from a complex interaction of social, psychological and biological factors. People who have gone through adverse life events (unemployment, bereavement, psychological trauma) are more likely to develop depression. Depression can, in turn, lead to more stress and dysfunction and worsen the affected person’s life situation and depression itself.

There are interrelationships between depression and physical health. For example, cardiovascular disease can lead to depression and vice versa.Prevention programmes have been shown to reduce depression. Effective community approaches to prevent depression include school-based programmes to enhance a pattern of positive thinking in children and adolescents. Interventions for parents of children with behavioural problems may reduce parental depressive symptoms and improve outcomes for their children. Exercise programmes for the elderly can also be effective in depression prevention.

Types of depression-

Depression can be broken into categories depending on the severity of symptoms. Some people experience mild and temporary episodes, while others experience severe and ongoing depressive episodes.

There are two main types: major depressive disorder and persistent depressive disorder.

Major depressive disorder

Major depressive disorder is the more severe form of depression. It’s characterized by persistent feelings of sadness, hopelessness, and worthlessness that don’t go away on their own.

In order to be diagnosed with clinical depression, you must experience 5 or more of the following symptoms over a 2-week period:

• feeling depressed most of the day
• loss of interest in most regular activities
• significant weight loss or gain
• sleeping a lot or not being able to sleep
• slowed thinking or movement
• fatigue or low energy most days
• feelings of worthlessness or guilt
• loss of concentration or indecisiveness
• recurring thoughts of death or suicide

There are different subtypes of major depressive disorder, which the American Psychiatric Association refers to as “specifiers.”

These include:

• atypical features
• anxious distress
• mixed features
• peripartum onset, during pregnancy or right after giving birth
• seasonal patterns
• melancholic features
• psychotic features
• catatonia

Persistent depressive disorder

Persistent depressive disorder (PDD) used to be called dysthymia. It’s a milder, but chronic, form of depression.

In order for the diagnosis to be made, symptoms must last for at least 2 years. PDD can affect your life more than major depression because it lasts for a longer period.

It’s common for people with PDD to:

• lose interest in normal daily activities
• feel hopeless
• lack productivity
• have low self-esteem

Depression can be treated successfully, but it’s important to stick to your treatment plan.

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Treatment for depression

Living with depression can be difficult, but treatment can help improve your quality of life. Talk to your healthcare provider about possible options.

You may successfully manage symptoms with one form of treatment, or you may find that a combination of treatments works best.

It’s common to combine medical treatments and lifestyle therapies, including the following:

Medications

Your healthcare provider may prescribe:

• antidepressants
• antianxiety
• antipsychotic medications

Each type of medication that’s used to treat depression has benefits and potential risks.

Psychotherapy

Speaking with a therapist can help you learn skills to cope with negative feelings. You may also benefit from family or group therapy sessions.

Light therapy

Exposure to doses of white light can help regulate your mood and improve symptoms of depression. Light therapy is commonly used in seasonal affective disorder, which is now called major depressive disorder with seasonal pattern.

Alternative therapies

Ask your healthcare provider about acupuncture or meditation. Some herbal supplements are also used to treat depression, like St. John’s wort, SAMe, and fish oil.

Talk with your healthcare provider before taking a supplement or combining a supplement with prescription medication because some supplements can react with certain medications. Some supplements may also worsen depression or reduce the effectiveness of medication.

Exercise

Aim for 30 minutes of physical activity 3 to 5 days a week. Exercise can increase your body’s production of endorphins, which are hormones that improve your mood.

Avoid alcohol and drugs

Drinking or misusing drugs may make you feel better for a little bit. But in the long run, these substances can make depression and anxiety symptoms worse.

Learn how to say no

Feeling overwhelmed can worsen anxiety and depression symptoms. Setting boundaries in your professional and personal life can help you feel better.

Take care of yourself

You can also improve symptoms of depression by taking care of yourself. This includes getting plenty of sleep, eating a healthy diet, avoiding negative people, and participating in enjoyable activities.

Sometimes depression doesn’t respond to medication. Your healthcare provider may recommend other treatment options if your symptoms don’t improve.

These include electroconvulsive therapy (ECT), or repetitive transcranial magnetic stimulation (rTMS) to treat depression and improve your mood.

Physical Therapy Management

One of the biggest things a physical therapist can do for their patients is to be aware of the signs and symptoms of depression and some of the common disorders associated with depression. If the therapist is sensitive to the signs and symptoms of depression they can document it in the plan of care and then notify the physician so the patient can get the appropriate medical treatment, if necessary. Also, because patients with depression may be emotionally unstable, recognizing the signs and symptoms of depression can help you in approaching different situations and then redirecting the patient toward other activities, instructions or more positive topics of conversation.

Exercise has been shown to benefit patients with mild to moderate mood disorders, especially anxiety and depression. When performing aerobic exercise your body releases endorphins from the pituitary gland which are responsible for relieving pain and improving mood. These endorphins can also lower cortisol levels which have been shown to be elevated in patients with depression. Additionally, exercise increases the sensitivity of serotonin in the same way antidepressants work, allowing for more serotonin to remain in the nerve synapse. Exercise can be aerobic or resistive in nature, as both have been shown to be beneficial in a variety of patient types. Anyone with depression can participate in an exercise program no matter how old or young they are, as long as proper supervision is provided. Exercise is an excellent option for treatment when taking anti-depressants is not an option due to their side effects. Depression symptoms can be decreased significantly after just one session but the effects are temporary. An exercise program must be continued on a daily basis to see continued effects. As a person continues to exercise they may experiences changes in their body type which can help to improve self esteem and body image issues they may have been having. Some other benefits of regular physical exercise include:

• Reduces/prevents functional declines associated with ageing
• Maintains/improves cardiovascular function
• Aids in weight loss and weight control
• Improves function of hormonal, metabolic, neurologic, respiratory, and hemodynamic systems
• Alteration of carbohydrate/lipid metabolism results in favourable increase in high-density lipoproteins
• Strength training helps to maintain muscle mass and strength
• Reduces age-related bone loss; reduction in risk for osteoporosis
• Improves flexibility, postural stability, and balance; reduction in risk of falling and associated injuries
• Psychological benefits (preserves cognitive function, alleviates symptoms/behaviours of depression, improves self awareness, promotes sense of well-being)
• Reduces disease risk factors
• Improves functional capacity
• Improves immune function
• Reduces age-related insulin resistance
• Reduces incidence of some cancers
• Contributes to social integration
• Improves sleep pattern

Because of depression’s effect on the neuromusculoskeletal system, research has shown that treating a patient’s underlying depression can lead to better improvements in their pain. Physical therapists can implement other strategies into their practice to further improve the effects of therapy beyond the benefits of exercise.

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INTRODUCTION-

Epilepsy is a chronic disorder, the hallmark of which is recurrent, unprovoked seizures. A person is diagnosed with epilepsy if they have two unprovoked seizures (or one unprovoked seizure with the likelihood of more) that were not caused by some known and reversible medical condition like alcohol withdrawal or extremely low blood sugar.

The seizures in epilepsy may be related to a brain injury or a family tendency, but often the cause is completely unknown. The word “epilepsy” does not indicate anything about the cause of the person’s seizures or their severity.

A mild seizure may be difficult to recognize. It can last a few seconds during which you lack awareness.

Stronger seizures can cause spasms and uncontrollable muscle twitches, and can last a few seconds to several minutes. During a stronger seizure, some people become confused or lose consciousness. Afterward you may have no memory of it happening.

There are several reasons you might have a seizure. These include:

• high fever
• head trauma
• very low blood sugar
• alcohol withdrawal

Having seizures and epilepsy can affect one’s safety, relationships, work, driving, and so much more. Public perception and treatment of people with epilepsy are often bigger problems than actual seizures.

Epilepsy is a fairly common neurological disorder that affects 65 million people around the world. In the United States, it affects about 3 million people.

Anyone can develop epilepsy, but it’s more common in young children and older adults. It occurs slightly more in males than in females.

CAUSES-

Epilepsy has no identifiable cause in about half the people with the condition. In the other half, the condition may be traced to various factors, including:

• Genetic influence. Some types of epilepsy, which are categorized by the type of seizure you experience or the part of the brain that is affected, run in families. In these cases, it’s likely that there’s a genetic influence. Researchers have linked some types of epilepsy to specific genes, but for most people, genes are only part of the cause of epilepsy. Certain genes may make a person more sensitive to environmental conditions that trigger seizures.
• Head trauma. Head trauma as a result of a car accident or other traumatic injury can cause epilepsy.
• Brain conditions. Brain conditions that cause damage to the brain, such as brain tumors or strokes, can cause epilepsy. Stroke is a leading cause of epilepsy in adults older than age 35.

Infectious diseases. Infectious diseases, such as meningitis, AIDS and viral encephalitis, can cause epilepsy. Prenatal injury. Before birth, babies are sensitive to brain damage that could be caused by several factors, such as an infection in the mother, poor nutrition or oxygen deficiencies. This brain damage can result in epilepsy or cerebral palsy. Developmental disorders. Epilepsy can sometimes be associated with developmental disorders, such as autism and neurofibromatosis.

SYMPTOM-

Seizures are the main symptom of epilepsy. Symptoms differ from person to person and according to the type of seizure.

Focal (partial) seizures

A simple partial seizure doesn’t involve loss of consciousness. Symptoms include:

• alterations to sense of taste, smell, sight, hearing, or touch
• dizziness
• tingling and twitching of limbs

Complex partial seizures involve loss of awareness or consciousness. Other symptoms include:

• staring blankly
• unresponsiveness
• performing repetitive movements

Generalized seizures

Generalized seizures involve the whole brain. There are six types:

Absence seizures, which used to be called “petit mal seizures,” cause a blank stare. This type of seizure may also cause repetitive movements like lip smacking or blinking. There’s also usually a short loss of awareness.

Tonic seizures cause muscle stiffness.

Atonic seizures lead to loss of muscle control and can make you fall down suddenly.

Clonic seizures are characterized by repeated, jerky muscle movements of the face, neck, and arms.

Myoclonic seizures cause spontaneous quick twitching of the arms and legs.

Tonic-clonic seizures used to be called “grand mal seizures.” Symptoms include:

• stiffening of the body
• shaking
• loss of bladder or bowel control
• biting of the tongue
• loss of consciousness

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DIAGNOSIS-

If you suspect you’ve had a seizure, see your doctor as soon as possible. A seizure can be a symptom of a serious medical issue.

Your medical history and symptoms will help your doctor decide which tests will be helpful. You’ll probably have a neurological examination to test your motor abilities and mental functioning.

In order to diagnose epilepsy, other conditions that cause seizures should be ruled out. Your doctor will probably order a complete blood count and chemistry of the blood.

Blood tests may be used to look for:

• signs of infectious diseases
• liver and kidney function
• blood glucose levels

Electroencephalogram (EEG) is the most common test used in diagnosing epilepsy. First, electrodes are attached to your scalp with a paste. It’s a noninvasive, painless test. You may be asked to perform a specific task. In some cases, the test is performed during sleep. The electrodes will record the electrical activity of your brain. Whether you’re having a seizure or not, changes in normal brain wave patterns are common in epilepsy.

Imaging tests can reveal tumors and other abnormalities that can cause seizures. These tests might include:

• CT scan
• MRI
• positron emission tomography (PET)
• single-photon emission computerized tomography

Epilepsy is usually diagnosed if you have seizures for no apparent or reversible reason.

RISK FACTOR-

Certain factors may increase your risk of epilepsy:

• Age. The onset of epilepsy is most common in children and older adults, but the condition can occur at any age.
• Family history. If you have a family history of epilepsy, you may be at an increased risk of developing a seizure disorder.
• Head injuries. Head injuries are responsible for some cases of epilepsy. You can reduce your risk by wearing a seat belt while riding in a car and by wearing a helmet while bicycling, skiing, riding a motorcycle or engaging in other activities with a high risk of head injury.
• Stroke and other vascular diseases. Stroke and other blood vessel (vascular) diseases can lead to brain damage that may trigger epilepsy. You can take a number of steps to reduce your risk of these diseases, including limiting your intake of alcohol and avoiding cigarettes, eating a healthy diet, and exercising regularly.

Dementia. Dementia can increase the risk of epilepsy in older adults. Brain infections. Infections such as meningitis, which causes inflammation in your brain or spinal cord, can increase your risk. Seizures in childhood. High fevers in childhood can sometimes be associated with seizures. Children who have seizures due to high fevers generally won’t develop epilepsy. The risk of epilepsy increases if a child has a long seizure, another nervous system condition or a family history of epilepsy.

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COMPLICATION-

Having a seizure at certain times can lead to circumstances that are dangerous to yourself or others.

• Falling. If you fall during a seizure, you can injure your head or break a bone.
• Drowning. If you have epilepsy, you’re 15 to 19 times more likely to drown while swimming or bathing than the rest of the population because of the possibility of having a seizure while in the water.
• Car accidents. A seizure that causes either loss of awareness or control can be dangerous if you’re driving a car or operating other equipment. Many states have driver’s license restrictions related to a driver’s ability to control seizures and impose a minimum amount of time that a driver be seizure-free, ranging from months to years, before being allowed to drive.
• Pregnancy complications. Seizures during pregnancy pose dangers to both mother and baby, and certain anti-epileptic medications increase the risk of birth defects. If you have epilepsy and you’re considering becoming pregnant, talk to your doctor as you plan your pregnancy.

Most women with epilepsy can become pregnant and have healthy babies. You’ll need to be carefully monitored throughout pregnancy, and medications may need to be adjusted. It’s very important that you work with your doctor to plan your pregnancy.

Emotional health issues. People with epilepsy are more likely to have psychological problems, especially depression, anxiety and suicidal thoughts and behaviors. Problems may be a result of difficulties dealing with the condition itself as well as medication side effects.

Other life-threatening complications of epilepsy are uncommon, but may happen, such as:

• Status epilepticus. This condition occurs if you’re in a state of continuous seizure activity lasting more than five minutes or if you have frequent recurrent seizures without regaining full consciousness in between them. People with status epilepticus have an increased risk of permanent brain damage and death.
• Sudden unexpected death in epilepsy (SUDEP). People with epilepsy also have a small risk of sudden unexpected death. The cause is unknown, but some research shows it may occur due to heart or respiratory conditions. People with frequent tonic-clonic seizures or people whose seizures aren’t controlled by medications may be at higher risk of SUDEP. Overall, about 1 percent of people with epilepsy die of SUDEP.

TREATMENT-

Most people can manage epilepsy. Your treatment plan will be based on severity of symptoms, your health, and how well you respond to therapy.

Some treatment options include:

• Anti-epileptic (anticonvulsant, antiseizure) drugs: These medications can reduce the number of seizures you have. In some people, they eliminate seizures. To be effective, the medication must be taken exactly as prescribed.
• Vagus nerve stimulator: This device is surgically placed under the skin on the chest and electrically stimulates the nerve that runs through your neck. This can help prevent seizures.
• Ketogenic diet: More than half of people who don’t respond to medication benefit from this high fat, low carbohydrate diet.
• Brain surgery: The area of the brain that causes seizure activity can be removed or altered.

Research into new treatments is ongoing. One treatment that may be available in the future is deep brain stimulation. It’s a procedure in which electrodes are implanted into your brain. Then a generator is implanted in your chest. The generator sends electrical impulses to the brain to help decrease seizures.

Another avenue of research involves a pacemaker-like device. It would check the pattern of brain activity and send an electrical charge or drug to stop a seizure.

Minimally invasive surgeries and radiosurgery are also being investigated.

Medications for epilepsy–

Most people with epilepsy can become seizure-free by taking one anti-seizure medication, which is also called anti-epileptic medication. Others may be able to decrease the frequency and intensity of their seizures by taking a combination of medications.

Many children with epilepsy who aren’t experiencing epilepsy symptoms can eventually discontinue medications and live a seizure-free life. Many adults can discontinue medications after two or more years without seizures. Your doctor will advise you about the appropriate time to stop taking medications.

Finding the right medication and dosage can be com

plex. Your doctor will consider your condition, frequency of seizures, your age and other factors when choosing which medication to prescribe. Your doctor will also review any other medications you may be taking, to ensure the anti-epileptic medications won’t interact with them.

Your doctor likely will first prescribe a single medication at a relatively low dosage and may increase the dosage gradually until your seizures are well-controlled.

Anti-seizure medications may have some side effects. Mild side effects include:

• Fatigue
• Dizziness
• Weight gain
• Loss of bone density
• Skin rashes
• Loss of coordination
• Speech problems
• Memory and thinking problems

More-severe but rare side effects include:

• Depression
• Suicidal thoughts and behaviors
• Severe rash
• Inflammation of certain organs, such as your liver

To achieve the best seizure control possible with medication, follow these steps:

• Take medications exactly as prescribed.
• Always call your doctor before switching to a generic version of your medication or taking other prescription medications, over-the-counter drugs or herbal remedies.
• Never stop taking your medication without talking to your doctor.
• Notify your doctor immediately if you notice new or increased feelings of depression, suicidal thoughts, or unusual changes in your mood or behaviors.
• Tell your doctor if you have migraines. Doctors may prescribe one of the anti-epileptic medications that can prevent your migraines and treat epilepsy.

At least half the people newly diagnosed with epilepsy will become seizure-free with their first medication. If anti-epileptic medications don’t provide satisfactory results, your doctor may suggest surgery or other therapies. You’ll have regular follow-up appointments with your doctor to evaluate your condition and medications.

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PHYSIOTHERAPY

Apart from medications and surgery, these potential therapies offer an alternative for treating epilepsy

Vagus nerve stimulation. In vagus nerve stimulation, doctors implant a device called a vagus nerve stimulator underneath the skin of your chest, similar to a heart pacemaker. Wires from the stimulator are connected to the vagus nerve in your neck. The battery-powered device sends bursts of electrical energy through the vagus nerve and to your brain. It’s not clear how this inhibits seizures, but the device can usually reduce seizures by 20 to 40 percent. Most people still need to take anti-epileptic medication, although some people may be able to lower their medication dose. You may experience side effects from vagus nerve stimulation, such as throat pain, hoarse voice, shortness of breath or coughing.

Ketogenic diet. Some children with epilepsy have been able to reduce their seizures by following a strict diet that’s high in fats and low in carbohydrates.

In this diet, called a ketogenic diet, the body breaks down fats instead of carbohydrates for energy. After a few years, some children may be able to stop the ketogenic diet — under close supervision of their doctors — and remain seizure-free.

Consult a doctor if you or your child is considering a ketogenic diet. It’s important to make sure that your child doesn’t become malnourished when following the diet.

Side effects of a ketogenic diet may include dehydration, constipation, slowed growth because of nutritional deficiencies and a buildup of uric acid in the blood, which can cause kidney stones. These side effects are uncommon if the diet is properly and medically supervised.

Following a ketogenic diet can be a challenge. Low-glycemic index and modified Atkins diets offer less restrictive alternatives that may still provide some benefit for seizure control.

Deep brain stimulation. In deep brain stimulation, surgeons implant electrodes into a specific part of your brain, typically your thalamus. The electrodes are connected to a generator implanted in your chest or your skull that sends electrical pulses to your brain and may reduce your seizures.

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INTRODUCTION-

Parkinsonism is a disease that occurs when a person has symptoms and brain dysfunction commonly associated with Parkinson’s disease but also has other symptoms related to an additional condition or cause.Parkinsonism is any condition that causes a combination of the movement abnormalities seen in Parkinson’s disease — such as tremor, slow movement, impaired speech or muscle stiffness — especially resulting from the loss of dopamine-containing nerve cells (neurons).

Parkinson’s disease (PD) is a neurodegenerative disorder characterized primarily by loss of dopamine neurons in the substantia nigra. Symptoms generally develop on one body side slowly over years but the progression may differ from one person to another due to the diversity of the disease. People with PD may experience tremor, mainly at rest (described as pill rolling tremor in hands), bradykinesia, limb rigidity, gait and balance problems. Prevalence is approximately 200 cases per 100,000 population, and the incidence is about 25 cases per 100,000 population, but these figures might show differences from one region of the world to another.

CAUSES-

Parkinsonism can be caused by Parkinson’s disease itself as well as another underlying condition.

Other causes associated with Parkinsonism include:

• Corticobasal degeneration: This condition causes dementia as well as affected movements, usually on one side. A person may also be unable to make controlled muscle movements.
• Dementia with Lewy bodies: This condition causes changes in overall alertness as well as visual hallucinations. This condition is the second most common cause of dementia after Alzheimer’s disease, according to Johns Hopkins Medicine.
• Multiple system atrophy: This condition affects coordination and autonomic dysfunction, including bowel and bladder incontinence.
• Progressive supranuclear palsy: This condition causes dementia, frequent backward falls, and problems moving the eyes up and down in addition to Parkinson’s disease symptoms.

The conditions above are the four most common causes of Parkinsonism, according to University of Texas Southwestern Medical Center. The number of people with these conditions is about one-fourth of the amount of people who have Parkinson’s disease itself.

Another, less common condition called vascular Parkinsonism also exists. This condition causes multiple, small strokes that can affect a person’s balance, walking, and memory.

Parkinsonism is also sometimes the result of taking certain medications. Doctors call this condition drug-induced Parkinsonism. Examples of drugs that could cause it include aripiprazole (Abilify), haloperidol (Haldol), and metoclopramide (Reglan).

Ideally, if a person has drug-induced Parkinsonism, they can slowly reduce the dosages of these medicines. However, that may not always be possible, and a person should not stop taking a medication without their doctor’s approval.

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SYMPTOM-

A person with Parkinsonism usually starts developing symptoms at anywhere from age 50 to 80, according to the University of Texas Southwestern Medical Center.

Parkinson’s disease can cause varying and progressive symptoms throughout its course. Some of the most common symptoms associated with the disease include:

• difficulty showing facial expressions
• muscle stiffness
• slowed, affected movements
• speech changes
• tremor, especially of one hand

A person with Parkinsonism may have some, but not all, of the symptoms listed above. This is because they also have an additional disorder that affects the brain’s functioning.

For example, people with Parkinsonism often do not have the hand tremor that affects many people with Parkinson’s disease.

Other symptoms associated with Parkinsonism include:

• dementia
• issues with the autonomic nervous system, such as problems with controlled movements or spasms
• early problems with balance
• rapid onset and progression of symptoms

Each underlying cause of Parkinsonism, such as dementia with Lewy bodies, also has its own unique set of symptoms.

DIAGNOSIS-

No single test exists for doctors to diagnose Parkinsonism.

A doctor will start by taking a person’s health history and review their current symptoms. They will ask for a medication list to determine if any medicines could be causing the symptoms.

A doctor will likely also order blood testing to check for underlying potential causes, such as thyroid or liver problems. A doctor will also order imaging scans to examine the brain and body for other causes, such as a brain tumor.

Doctors can perform a test that tracks the movement of dopamine in the brain. This is known as the DaT-SPECT test.

The test uses radioactive markers designed to track dopamine in the brain. This allows a doctor to watch the release of dopamine in a person’s brain and identify the areas of the brain that do or do not receive it.

Because Parkinsonism does not respond to typical treatments and can have a variety of symptoms, doctors can have difficulty coming to a quick diagnosis. It may take time for doctors to rule out other conditions and begin to make treatment recommendations.

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TREATMENT-

One of the most commonly prescribed medications to treat Parkinson’s disease is levodopa. This medication is related to dopamine and can increase the amount of dopamine available in the brain.

However, people with Parkinsonism not only have problems producing dopamine, but they also have damaged or destroyed cells that cannot respond to dopamine. As a result, levodopa may not work as well to reduce their symptoms.

Doctors can find Parkinsonism challenging to treat because the symptoms of the condition do not always respond as well or at all to medications that boost dopamine.

As a result, treatments for Parkinsonism depend upon the “plus” disease that a person has. For example, if a person has corticobasal degeneration and related muscle spasms, a doctor may prescribe antidepressants and botulinum toxin A (BOTOX) injections.

Treatments for Parkinsonism usually aim to help reduce a person’s symptoms whenever possible to help them maintain independence. Doctors often recommend physical and occupational therapy because they can help a person keep their muscles strong and improve balance.

PHYSICAL THERAPY FOR PARKINSON

Exercise

Exercise has been proven to maintain health and well-being in Parkinson’s and now importantly it is shown to play a big role in addressing secondary prevention (focusing on strength, endurance, flexibility, functional practice and balance). Exercise for neuroprotection focuses on endurance and uses motor learning principles approaches, such as mental imagery and dual task training. Neuroprotection training, to be effective, should be introduced in the early stages, but helps at all stages. It involves complex, powerful and intensive exercises.

Exercise undertaken in a group setting has the added value of providing a social connection to those becoming increasingly isolated as the condition progresses, or for those who are newly diagnosed, so they can see the benefits of maintaining exercise and activity. A group environment also permits time for people to ask questions and discuss their symptoms and own management strategies with one another.

Movement Strategy Training

Basal ganglia disorders cause deficits in the generation of internal (automatic) behavior. Strategies (physical or attentional cues and combined strategies) can help overcome some of the resultant problems, hence have become an increasingly utilised method of intervention for people with Parkinson’s.

Music-based movement therapy is a promising intervention that needs some further research. It is interesting since it combines cognitive movement strategies, cueing techniques, balance exercises and physical activity. The focus is on enjoying moving and not on the mobility limitation which might appeal more to the patients than standard exercises.

We can see immediately the effects of external cueing and attention on improving step length, freezing and turning during walking tasks, and in activities of daily living. A Systematic Review and Meta-Analyses suggests better outcomes with short-term physiotherapy on the symptoms of freezing of gait in Parkison’s patient. However, further randomized control trial studies are still needed.Literature suggests that robot-assisted gait technology has better results in addressing the freezing of gait for Parkinson’s patients. However, more research is needed in this field.

Depending on the cognitive state of the individual, they may be able to learn how to self-instruct in the use of an internal cue or strategy. If less able, the cue or strategy has to come from an external source e.g. a visual strip on the ground, the rhythmic beat of a metronome.

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INTRODUCTION-

Insomnia is a common sleep disorder that can make it hard to fall asleep, hard to stay asleep, or cause you to wake up too early and not be able to get back to sleep. You may still feel tired when you wake up. Insomnia can sap not only your energy level and mood but also your health, work performance and quality of life.

Insomnia is the most common of all sleep disorders, according to the American Psychiatric Association (APA). In fact, the APA states that about one-third of all adults report insomnia symptoms. But between 6 to 10 percent of all adults have symptoms severe enough for them to be diagnosed with insomnia disorder.

The condition can be short-term (acute) or can last a long time (chronic). It may also come and go.Acute insomnia lasts from 1 night to a few weeks. Insomnia is chronic when it happens at least 3 nights a week for 3 months.

TYPES OF INSOMNIA –

There are two types of insomnia: primary and secondary.

• Primary insomnia: This means your sleep problems aren’t linked to any other health condition or problem.
• Secondary insomnia: This means you have trouble sleeping because of a health condition (like asthma, depression,arthitis, heartburn)

CAUSES-

Causes of primary insomnia include:

• Stress related to big life events, like a job loss or change, the death of a loved one, divorce, or moving
• Things around you like noise, light, or temperature
• Changes to your sleep schedule like jet lag, a new shift at work, or bad habits you picked up when you had other sleep problems

Causes of secondary insomnia include:

• Mental health issues like depression and anxiety
• Medications for colds, allergies, depression, high blood pressure, and asthma
• Pain or discomfort at night
• Caffeine, tobacco, or alcohol use
• Hyperthyroidism and other endocrine problems
• Other sleep disorders, like sleep apnea or restless legs syndrome.

SYMPTOM-

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Symptoms

Insomnia symptoms may include:

• Difficulty falling asleep at night
• Waking up during the night
• Waking up too early
• Not feeling well-rested after a night’s sleep
• Daytime tiredness or sleepiness
• Irritability, depression or anxiety
• Difficulty paying attention, focusing on tasks or remembering
• Increased errors or accidents
• Ongoing worries about sleep

Risk factors for insomnia

Insomnia can occur at any age and is more likely to affect women than men.

According to the National Heart, Lung, and Blood Institute (NHLBI)Trusted Source, people with certain risk factors are more likely to have insomnia. These risk factors include:

• high levels of stress
• emotional disorders, such as depression or distress related to a life event
• lower income
• traveling to different time zones
• sedentary lifestyle
• changes in work hours, or working night shifts

Certain medical conditions, such as obesity and cardiovascular disease, can also lead to insomnia. Menopause can lead to insomnia as well. Find out more about the causes of — and risk factors for — insomnia.

DIAGNOSIS-

Depending on your situation, the diagnosis of insomnia and the search for its cause may include:

• Physical exam. If the cause of insomnia is unknown, your doctor may do a physical exam to look for signs of medical problems that may be related to insomnia. Occasionally, a blood test may be done to check for thyroid problems or other conditions that may be associated with poor sleep.
• Sleep habits review. In addition to asking you sleep-related questions, your doctor may have you complete a questionnaire to determine your sleep-wake pattern and your level of daytime sleepiness. You may also be asked to keep a sleep diary for a couple of weeks.
• Sleep study. If the cause of your insomnia isn’t clear, or you have signs of another sleep disorder, such as sleep apnea or restless legs syndrome, you may need to spend a night at a sleep center. Tests are done to monitor and record a variety of body activities while you sleep, including brain waves, breathing, heartbeat, eye movements and body movements.

TREATMENT-

Meditation

Meditation is a natural, easy, drug-free method for treating insomnia. According to the National Sleep Foundation, meditation can help improve the quality of your sleep, as well as make it easier to fall asleep and stay asleep.

MANY CONDITIONS CONTRIBUTE TO INSOMNIA THESE ARE:-

anxiety

depression

digestive problems

pain

Many apps and videos are available to help you meditate.

Melatonin

The hormone melatonin is naturally produced by the body during the sleep cycle. People often take melatonin supplements in hopes of improving their sleep.

Studies are inconclusiveTrusted Source regarding whether melatonin can actually help treat insomnia in adults. There’s some evidence that supplements may slightly decrease the time it takes you to fall asleep but more research is needed.

Melatonin is generally thought to be safe for a short period of time, but its long-term safety has yet to be confirmed.

It’s always best to work with your doctor when deciding to take melatonin.

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MEDICATION-

sedative-a drug that subues excitement and calms the without inducing sleep, though drowsiness maybe produced.

hypnotic- a drug that induces and/ or maintains sleep, simila to normal arousable sleep .

PHYSICAL THERAPY

To integrate sleep health in prevention, health promotion, and wellness interventions, therapists should:

1. Assess overall sleep health and screen for risk of sleep disorders.
2. Refer for additional assessment if individual is identified as at increased risk for a sleep disorder.
3. Provide sleep hygiene education.
4. Provide an appropriate exercise program.
5. Consider positioning to promote sleep quality.
6. Address bed mobility issues.

Getting a full night sleep is critical to a healthy lifestyle. Sometimes we all have difficulty sleeping to due to a number of factors: stressful lives, chronic pain, our busy schedules. Many of our physical therapy patients come to us with physical pain or limitations that can also impact their quality of life…including their ability to rest.

Conducting an assessment or a screening to determine a patient’s sleep deficits provides an overview of their sleep profile and habits before going to sleep and after waking. Known as sleep hygiene, it is characterized by the National Sleep Foundation as “...a variety of different practices and habits that are necessary to have good nighttime sleep quality and full daytime alertness.” Conducted by a physical therapist, assessment is part of understanding how physical conditions, body positioning and limitations to mobility can affect sleep. Additional factors may include a discussion on ergonomics: the type of bed and mattress used, number of pillows, body positioning for sleeping, etc.

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INTRODUCION-

Gout is a common form of inflammatory arthritis that is very painful. It usually affects one joint at a time (often the big toe joint). There are times when symptoms get worse, known as flares, and times when there are no symptoms, known as remission. Repeated bouts of gout can lead to gouty arthritis, a worsening form of arthritis.

There is no cure for gout, but you can effectively treat and manage the condition with medication and self-management strategies.

Gout is a general term for a variety of conditions caused by a buildup of uric acid. This buildup usually affects your feet.

If you have gout, you’ll probably feel swelling and pain in the joints of your foot, particularly your big toe. Sudden and intense pain, or gout attacks, can make it feel like your foot is on fire.

SYMPTOM-

Gout flares start suddenly and can last days or weeks. These flares are followed by long periods of remission—weeks, months, or years—without symptoms before another flare begins. Gout usually occurs in only one joint at a time. It is often found in the big toe. Along with the big toe, joints that are commonly affected are the lesser toe joints, the ankle, and the knee.

Some people have too much uric acid in their blood, but no symptoms. This is called asymptomatic gout.

Acute gout symptoms come on quickly from the buildup of uric acid crystals in your joint and last for 3 to 10 days. You’ll have intense pain and swelling, and your joint may feel warm. Between gout attacks you won’t have any symptoms.

If you don’t treat gout, it can become chronic. Hard lumps called tophi can eventually develop in your joints and the skin and soft tissue surrounding them. These deposits can permanently damage your joints.

Prompt treatment is important to prevent gout from turning chronic.

Symptoms in the affected joint(s) may include:

• Pain, usually intense.
• Swelling.
• Redness.
• Heat.

The buildup of uric acid in your blood from the breakdown of purines causes gout.

Certain conditions, such as blood and metabolism disorders or dehydration, make your body produce too much uric acid.

A kidney or thyroid problem, or an inherited disorder, can make it harder for your body to remove excess uric acid.

You’re more likely to get gout if you:

• are a middle-aged man or postmenopausal woman
• have parents, siblings, or other family members with gout
• eat too much purine-rich food, such as red meats, organ meats, and certain fish
• drink alcohol
• take medications such as diuretics and cyclosporine
• have a condition like high blood pressure, kidney disease, thyroid disease, diabetes, or sleep apnea

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ETIOLOGY-

Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body. The body makes uric acid when it breaks down purines, which are found in your body and the foods you eat. When there is too much uric acid in the body, uric acid crystals (monosodium urate) can build up in joints, fluids, and tissues within the body. Hyperuricemia does not always cause gout, and hyperuricemia without gout symptoms does not need to be treated.

Gout occurs when urate crystals accumulate in your joint, causing the inflammation and intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in your blood.

Your body produces uric acid when it breaks down purines — substances that are found naturally in your body.

Purines are also found in certain foods, such as steak, organ meats and seafood. Other foods also promote higher levels of uric acid, such as alcoholic beverages, especially beer, and drinks sweetened with fruit sugar (fructose).

Normally, uric acid dissolves in your blood and passes through your kidneys into your urine. But sometimes either your body produces too much uric acid or your kidneys excrete too little uric acid. When this happens, uric acid can build up, forming sharp, needlelike urate crystals in a joint or surrounding tissue that cause pain, inflammation and swelling.

Risk factors

You’re more likely to develop gout if you have high levels of uric acid in your body. Factors that increase the uric acid level in your body include:

• Diet. Eating a diet rich in meat and seafood and drinking beverages sweetened with fruit sugar (fructose) increase levels of uric acid, which increase your risk of gout. Alcohol consumption, especially of beer, also increases the risk of gout.
• Obesity. If you’re overweight, your body produces more uric acid and your kidneys have a more difficult time eliminating uric acid.
• Medical conditions. Certain diseases and conditions increase your risk of gout. These include untreated high blood pressure and chronic conditions such as diabetes, metabolic syndrome, and heart and kidney diseases.
• Certain medications. The use of thiazide diuretics — commonly used to treat hypertension — and low-dose aspirin also can increase uric acid levels. So can the use of anti-rejection drugs prescribed for people who have undergone an organ transplant.
• Family history of gout. If other members of your family have had gout, you’re more likely to develop the disease.
• Age and sex. Gout occurs more often in men, primarily because women tend to have lower uric acid levels. After menopause, however, women’s uric acid levels approach those of men. Men are also more likely to develop gout earlier — usually between the ages of 30 and 50 — whereas women generally develop signs and symptoms after menopause.
• Recent surgery or trauma. Experiencing recent surgery or trauma has been associated with an increased risk of developing a gout attack.

Complications

People with gout can develop more-severe conditions, such as:

• Recurrent gout. Some people may never experience gout signs and symptoms again. Others may experience gout several times each year. Medications may help prevent gout attacks in people with recurrent gout. If left untreated, gout can cause erosion and destruction of a joint.
• Advanced gout. Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi (TOE-fie). Tophi can develop in several areas such as your fingers, hands, feet, elbows or Achilles tendons along the backs of your ankles. Tophi usually aren’t painful, but they can become swollen and tender during gout attacks.
• Kidney stones. Urate crystals may collect in the urinary tract of people with gout, causing kidney stones. Medications can help reduce the risk of kidney stones.

Prevention

During symptom-free periods, these dietary guidelines may help protect against future gout attacks:

• Drink plenty of fluids. Stay well-hydrated, including plenty of water. Limit how many sweetened beverages you drink, especially those sweetened with high-fructose corn syrup.
• Limit or avoid alcohol. Talk with your doctor about whether any amount or type of alcohol is safe for you. Recent evidence suggests that beer may be particularly likely to increase the risk of gout symptoms, especially in men.
• Get your protein from low-fat dairy products. Low-fat dairy products may actually have a protective effect against gout, so these are your best-bet protein sources.
• Limit your intake of meat, fish and poultry. A small amount may be tolerable, but pay close attention to what types — and how much — seem to cause problems for you.
• Maintain a desirable body weight. Choose portions that allow you to maintain a healthy weight. Losing weight may decrease uric acid levels in your body. But avoid fasting or rapid weight loss, since doing so may temporarily raise uric acid levels.

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TREATMENT-

Gout can be effectively treated and managed with medical treatment and self-management strategies. Your health care provider may recommend a medical treatment plan to

• Manage the pain of a flare. Treatment for flares consists of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, steroids, and the anti-inflammatory drug colchicine.
• Prevent future flares. Making changes to your diet and lifestyle, such as losing weight, limiting alcohol, eating less purine-rich food (like red meat or organ meat), may help prevent future attacks. Changing or stopping medications associated with hyperuricemia (like diuretics) may also help.
• Prevent tophi and kidney stones from forming as a result of chronic high levels of uric acid. Tophi are hard, uric acid deposits under the skin. For people with frequent acute flares or chronic gout, doctors may recommend preventive therapy to lower uric acid levels in the blood using drugs like allopurinol, febuxostat, and pegloticase.

In addition to medical treatment, you can manage your gout with self-management strategies. Self-management is what you do day to day to manage your condition and stay healthy, like making healthy lifestyle choices. The self-management strategies described below are proven to reduce pain and disability, so you can pursue the activities important to you.

Gout foods to avoid

Certain foods are naturally high in purines, which your body breaks down into uric acid. Most people don’t have a problem with high-purine foods, but if your body has trouble releasing excess uric acid, you may want to avoid foods and drinks like these:

• red meats
• organ meats
• certain seafood
• alcohol

Sugar-sweetened beverages and foods containing the sugar fructose can also be problematic, even though they don’t contain purines.

Certain foods help reduce uric acid levels in the body.

Gout home remedies

Some gout-relief methods don’t come in a bottle from your pharmacy. Evidence from studies suggests that these natural remedies may help lower uric acid levels and prevent gout attacks:

• tart cherries
• magnesium
• ginger
• apple cider vinegar
• celery
• nettle tea
• dandelion
• milk thistle seeds

Gout surgery

Gout can typically be treated without surgery. But after many years, this condition can damage the joints, tear the tendons, and cause infections in the skin over the joints.

Hard deposits, called tophi, can build up on your joints and in other places, like your ear. These lumps may be painful and swollen, and they can permanently damage your joints.

Three surgical procedures treat tophi:

• tophi removal surgery
• joint fusion surgery
• joint replacement surgery

Which one of these surgeries your doctor recommends depends on the extent of the damage, where the tophi are located, and your personal preferences.

PHYSIOTHERAPY MANAGEMENT –

Physical therapy management of gout falls under preferred practice pattern 4E: Impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation.  

The physical therapist should be aware that any patient with a history of gout, hyperuricemia, and/or a septic joint presentation should be refered for medical evaluation prior to treatment.

During acute exacerbations the physical therapist should focus on reinforcement of management program and splinting, orthotics, or other assistive devices to protect the affected joint(s).

A 2002 study in the Journal of Rheumatology found that the use of cryrotherapy to alleviate the pain associated with acute bouts of gout may be effective.

During intercritical phases physical therapists may offer assistance with maintinance of ROM, strength, and function.  The physical therapist can also assist the patient in the creation of a suitable exercise routine and keeping thier weight under control.

There is a Randomized Clinical Trial which suggests that Electroacupuncture in combination with blood letting puncture and cupping has relatively good results as a treatment for Gout. The treatment is effective mostly because the blood uric acid decreased significantly after the treatment was given to the patients.

There is another study about Electroacupuncture combined with local blocking therapy on acute gouty arthritis that shows an improvement in health status of the patients. This treatment is positive and it also decreases blood uric acid levels.

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Introduction-

The human immunodeficiency virus (HIV) is an enveloped retrovirus that contains 2 copies of a single-stranded RNA genome. It causes the acquired immunodeficiency syndrome (AIDS) that is the last stage of HIV disease.

1. Four to 10 weeks after the HIV enters the body, the patient may complain of symptoms of primary infection.
2. After the primary infection, a long chronic HIV infection occurs, which can last for decades.

AIDS is mainly characterized by opportunistic infections and tumors ( as a result of immunodeficiency) which are usually fatal without treatment.

HIV is a virus that damages the immune system. The immune system helps the body fight off infections. Untreated HIV infects and kills CD4 cells, which are a type of immune cell called T cells. Over time, as HIV kills more CD4 cells, the body is more likely to get various types of infections and cancers. HIV is transmitted through bodily fluids that include:

• blood
• semen
• vaginal and rectal fluids
• breast milk

• HIV continues to be a major global public health issue, having claimed more than 32 million lives so far.
• With increasing access to effective HIV prevention, diagnosis, treatment and care (including for opportunistic infections) HIV infection has become a manageable chronic health condition, enabling people living with HIV to lead long and healthy lives.
• There were approximately 37.9 million people living with HIV at the end of 2018.
• Concerted international efforts to respond to HIV had lead to an increased coverage of services. In 2018, 62% of adults and 54% of children living with HIV in low- and middle-income countries were receiving lifelong antiretroviral therapy (ART).
• Between 2000 and 2018, new HIV infections fell by 37% and HIV-related deaths fell by 45%, with 13.6 million lives saved due to ART. This achievement was the result of great efforts by national HIV programmes supported by civil society and international development partners.

AIDS-

AIDS is a disease that can develop in people with HIV. It’s the most advanced stage of HIV. But just because a person has HIV doesn’t mean they’ll develop AIDS. HIV kills CD4 cells. Healthy adults generally have a CD4 count of 500 to 1,500 per cubic millimeter. A person with HIV whose CD4 count falls below 200 per cubic millimeter will be diagnosed with AIDS. A person can also be diagnosed with AIDS if they have HIV and develop an opportunistic infection or cancer that’s rare in people who don’t have HIV. An opportunistic infection, such as pneumonia, is one that takes advantage of a unique situation, such as HIV. Untreated, HIV can progress to AIDS within a decade. There’s no cure for AIDS, and without treatment, life expectancy after diagnosis is about three yearsTrusted Source. This may be shorter if the person develops a severe opportunistic illness. However, treatment with antiretroviral drugs can prevent AIDS from developing. If AIDS does develop, it means that the immune system is severely compromised. It’s weakened to the point where it can no longer fight off most diseases and infections. That makes the person vulnerable to a wide range of illnesses, including:

• pneumonia
• tuberculosis
• oral thrush, a fungal infection in the mouth or throat
• cytomegalovirus (CMV), a type of herpes virus
• cryptococcal meningitis, a fungal infection in the brain
• toxoplasmosis, a brain infection caused by a parasite
• cryptosporidiosis, an infection caused by an intestinal parasite
• cancer, including Kaposi’s sarcoma (KS) and lymphoma

The shortened life expectancy linked with untreated AIDS isn’t a direct result of the syndrome itself. Rather, it’s a result of the diseases and complications that arise from having an immune system weakened by AIDS.

etiology-

The cause of this infectious disease is the human immunodeficiency virus (HIV) which can be classified into HIV-1 and HIV-2.

• HIV-1 is more globally expanded and virulent. It originated in Central Africa.
• HIV-2 is much less virulent and comes from West Africa.
• Both viruses are related antigenically to immunodeficiency viruses found primarily in primates.

HIV is a variation of a virus that infects African chimpanzees. Scientists suspect the simian immunodeficiency virus (SIV) jumped from chimps to humans when people consumed infected chimpanzee meat. Once inside the human population, the virus mutated into what we now know as HIV. This likely occurred as long ago as the 1920s. HIV spread from person to person throughout Africa over the course of several decades. Eventually, the virus migrated to other parts of the world. Scientists first discovered HIV in a human blood sample in 1959. It’s thought that HIV has existed in the United States since the 1970s, but it didn’t start to hit public consciousness until the 1980s.

Signs and symptoms–

The symptoms of HIV vary depending on the stage of infection. Though people living with HIV tend to be most infectious in the first few months after being infected, many are unaware of their status until the later stages. In the first few weeks after initial infection people may experience no symptoms or an influenza-like illness including fever, headache, rash or sore throat.

As the infection progressively weakens the immune system, they can develop other signs and symptoms, such as swollen lymph nodes, weight loss, fever, diarrhoea and cough. Without treatment, they could also develop severe illnesses such as tuberculosis (TB), cryptococcal meningitis, severe bacterial infections, and cancers such as lymphomas and Kaposi’s sarcoma.

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DIGNOSIS –

Several different tests can be used to diagnose HIV. Healthcare providers determine which test is best for each person.

Antibody/antigen tests

Antibody/antigen tests are the most commonly used tests. They can show positive results typically within 18–45 daysTrusted Source after someone initially contracts HIV. These tests check the blood for antibodies and antigens. An antibody is a type of protein the body makes to fight an infection. An antigen, on the other hand, is the part of the virus that activates the immune system.

Antibody tests

These tests check the blood solely for antibodies. Between 23 and 90 daysTrusted Source after transmission, most people will develop detectable HIV antibodies, which can be found in the blood or saliva. These tests are done using blood tests or mouth swabs, and there’s no preparation necessary. Some tests provide results in 30 minutes or less and can be performed in a healthcare provider’s office or clinic. Other antibody tests can be done at home:

• OraQuick HIV Test. An oral swab provides results in as little as 20 minutes.
• Home Access HIV-1 Test System. After the person pricks their finger, they send a blood sample to a licensed laboratory. They can remain anonymous and call for results the next business day.

If someone suspects they’ve been exposed to HIV but tested negative in a home test, they should repeat the test in three months. If they have a positive result, they should follow up with their healthcare provider to confirm.

Nucleic acid test (NAT)

This expensive test isn’t used for general screening. It’s for people who have early symptoms of HIV or have a known risk factor. This test doesn’t look for antibodies; it looks for the virus itself. It takes from 5 to 21 days for HIV to be detectable in the blood. This test is usually accompanied or confirmed by an antibody test. Today, it’s easier than ever to get tested for HIV.

WHO-

HIV can be diagnosed through rapid diagnostic tests that provide same-day results. This greatly facilitates early diagnosis and linkage with treatment and care. People can also use HIV self-tests to test themselves. However, no single test can provide a full HIV diagnosis; confirmatory testing is required, conducted by a qualified and  trained health or community worker at a community centre or clinic. HIV infection can be detected with great accuracy using WHO prequalified tests within a nationally approved testing strategy.

Most widely-used HIV diagnostic tests detect antibodies produced by the person as part of their immune response to fight HIV. In most cases, people develop antibodies to HIV within 28 days of infection. During this time, people experience the so-called “window” period –  when HIV antibodies haven’t been produced in high enough levels to be detected by standard tests and when they may have had no signs of HIV infection, but also when they may transmit HIV to others. After infection, an individual may transmit HIV transmission to a sexual or drug-sharing partner or for pregnant women to their infant during pregnancy or the breastfeeding period.

Following a positive diagnosis, people should be retested before they are enrolled in treatment and care to rule out any potential testing or reporting error. Notably, once a person diagnosed with HIV and has started treatment they should not be retested.

While testing for adolescents and adults has been made simple and efficient, this is not the case for babies born to HIV-positive mothers. For  children less than 18 months of age, serological testing is not sufficient to identify HIV infection – virological testing must be provided as early as birth or at 6 weeks of age). New technologies are now becoming available to perform this test at the point of care and enable same-day results, which will accelerate appropriate linkage with treatment and care.

SYMPTOM-

After the first month or so, HIV enters the clinical latency stage. This stage can last from a few years to a few decades. Some people don’t have any symptoms during this time, while others may have minimal or nonspecific symptoms. A nonspecific symptom is a symptom that doesn’t pertain to one specific disease or condition. These nonspecific symptoms may include:

• headaches and other aches and pains
• swollen lymph nodes
• recurrent fevers
• night sweats
• fatigue
• nausea
• vomiting
• diarrhea
• weight loss
• skin rashes
• recurrent oral or vaginal yeast infections
• pneumonia
• shingles

As with the early stage, HIV is still infectious during this time even without symptoms and can be transmitted to another person. However, a person won’t know they have HIV unless they get tested. If someone has these symptoms and thinks they may have been exposed to HIV, it’s important that they get tested. HIV symptoms at this stage may come and go, or they may progress rapidly. This progression can be slowed substantially with treatment. With the consistent use of this antiretroviral therapy, chronic HIV can last for decades and will likely not develop into AIDS, if treatment was started early enough.

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DIFFERENTIAL DIAGNOSIS –

Many individuals with HIV/AIDS may remain asymptomatic for years, with a mean time of 10 years between exposure and development. Virtually, all the findings in the initial onset of AIDS may be found/mimic other diseases such as:

• Fever
• Headaches
• Night sweats
• Fatigue
• HTN
• Back pain
• Pulmonary complications ex. cough and SOA
• GI complaints (change in bowel habits and function)
• Cutaneous complaints (dry skin, new rashes, nail bed changes)
• Poor wound healing
• Thrush
• Easy Bruising
• Weight loss
• Herpes Simplex virus
• Cytomegalovirus
• Lymphoma

 All of these signs/symptoms may be associated with other diseases, a combination of complaints is more suggestive of HIV infection than any one symptom alone.

TREATMENT –

HIV can be suppressed by  treatment regimens composed by a combination of 3 or more ARV drugs. Current ART does not cure HIV infection but  highly  suppresses viral replication within a person’s body and allows an individual’s immune system  recovery to strengthen and regain the capacity to fight off infections.

Since 2016, WHO recommended that all people living with HIV be provided with lifelong ART, including children, adolescents and adults, and pregnant and breastfeeding women, regardless of clinical status or CD4 cell count. By the end of 2019, 185 countries had already adopted this recommendation, covering 99% of all people living with HIV globally.

• WHO updated its HIV treatment guidelines in 2018 and 2019 to reflect the latest scientific advances.  

The current  HIV treatment guidelines include new ARV options with better tolerability, higher efficacy, and lower rates of treatment discontinuation when compared with previous recommended medicines. In 2019, WHO recommends the use of dolutegravir-based or low-dose efavirenz for first-line therapy. DTG should also be used in 2^nd line therapy , if not used in 1^st line and darunavir/ritonavir is recommended as the anchor drug in third- line  or a alternative option second-line therapy.

By mid-2020, transition to dolutegravir has been implemented  in 100  low- and middle-income countries and is expected to improve the durability of the treatment and the quality of care for people living with HIV. Despite improvements, limited options remain for infants and young children. For this reason, WHO and partners are coordinating efforts to enable a faster and more effective development and introduction of age-appropriate paediatric formulations of  new ARV drugs.

In addition, 1 in each 3 people living with HIV present to care with advanced disease, usually with  severe clinical  symptoms, low CD4 cell counts, and at high risk of develop serious illness and death. To reduce this risk, WHO recommends that these individuals receive a “package of care” that includes screening tests and drug prophylaxis for  the most common serious infections that can cause severe morbidity and death, such as TB and cryptococcal meningitis, in addition to rapid ART initiation.

Globally, 25.4 million people living with HIV were receiving ART in 2019. This equates to a global ART coverage rate of 67%. However, more efforts are needed to scale up treatment, particularly for children and adolescents. Only 53% of children were receiving ART at the end of 2019.

Expanding access to treatment is at the heart of a set of targets for 2020, which aim to bring the world back on track to end the AIDS epidemic by 2030.

PHYSIOTHERAPY APPROACH –

Physical Therapists play an important role in treating conditions that limit the patient’s movement and function.

• Goals will be set to improve the quality of life and keep the patient active in both his/her life and in the community.
• Patients with HIV develop many of the functional limitations that any other patient may have, such as sports-related injuries or arthritis. In addition to managing impairments, these patients may have problems with the disease process, infections, and/or side effects of the medication.
• A physical therapist will develop a plan of care to help the patient improve his/her ability to do daily activities, improve heart health, improve balance, reduce pain, and maintain healthy body weight.
• In addition, this plan of care, a proper home exercise program will be prescribed to achieve goals set by the patient or physical therapist. A qualitative study by deBoer et al. suggests that collaborating physiotherapists on the interprofessional health care team would help in addressing the unique requirements of patients living with HIV.

In addition to improving the above mentioned positive benefits, the therapist must also address the following issues:

• Quality of life issues
• Work environment
• Community management skills (how to access transportation, socialisation opportunities, shopping, banking, ability to access and negotiate health care and insurance systems)
• Integumentary care

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