ALL ABOUT REHAB: PAIN &OTHERS

a week after

2011-02-01T19:49:00.003+07:00

Diabetic foot

2011-01-31T21:30:00.004+07:00

Dry Eye Syndrome

2010-11-13T10:35:00.001+07:00

Author: C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
Coauthor(s): Erdem Yuksel, MD, Fellow, Department of Ophthalmology, Massachusetts Eye Research and Surgery Institute, Medical School of Gazi University; Fahd Anzaar, MD, Fellow, Massachusetts Eye Research and Surgery Institute; Clinical Research and Education Coordinator, Ocular Immunology and Uveitis Foundation; Anthony S Ekong, MD, Consulting Staff, Department of Ophthalmology, Marshfield Clinic
Contributor Information and Disclosures

Updated: May 13, 2009

Introduction

Background

Dry eye is a multifactorial disease of the tears and the ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface.¹Dry eye is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.¹

The tear layer covers the normal ocular surface. Generally, it is accepted that the tear film is made up of 3 intertwined layers, as follows:

A superficial thin lipid layer (0.11 µm) is produced by the meibomian glands, and its principal function is to retard tear evaporation and to assist in uniform tear spreading.
A middle thick aqueous layer (7 µm) is produced by the main lacrimal glands (reflex tearing), as well as the accessory lacrimal glands of Krause and Wolfring (basic tearing).
An innermost hydrophilic mucin layer (0.02-0.05 µm) is produced by both the conjunctiva goblet cells and the ocular surface epithelium and associates itself with the ocular surface via its loose attachments to the glycocalyx of the microplicae of the epithelium. It is the hydrophilic quality of the mucin that allows the aqueous to spread over the corneal epithelium.

The lipid layer produced by the meibomian glands acts as a surfactant, as well as an aqueous barrier (retarding evaporation of the underlying aqueous layer), and provides a smooth optical surface. It may also act as a barrier against foreign particles and may also have some antimicrobial properties. The glands are holocrine in nature, and so the secretions contain both polar lipids (aqueous-lipid interface) and nonpolar lipids (air-tear interface) as well as proteinaceous material. All of these are held together by ionic bonds, hydrogen bonds, and van der Waals forces. The secretions are subject to neuronal (parasympathetic, sympathetic, and sensory sources), hormonal (androgen and estrogen receptors), and vascular regulation. Evaporative loss is predominantly due to meibomian gland dysfunction (MGD).

The aqueous component is produced by the lacrimal glands. This component includes about 60 different proteins, electrolytes, and water. Lysozyme is the most abundant (20-40% of total protein) and also the most alkaline protein present in tears. It is a glycolytic enzyme that is capable of breaking down bacterial cell walls. Lactoferrin has antibacterial and antioxidant functions, and the epidermal growth factor (EGF) plays a role in maintaining the normal ocular surface and in promoting corneal wound healing. Albumin, transferrin, immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) are also present.

Aqueous tear deficiency (ATD) is the most common cause of dry eye, and it is due to insufficient tear production. The secretion of the lacrimal gland is controlled by a neural reflex arc, with afferent nerves (trigeminal sensory fibers) in the cornea and the conjunctiva passing to the pons (superior salivary nucleus), from which efferent fibers pass, in the nervus intermedius, to the pterygopalatine ganglion and postganglionic sympathetic and parasympathetic nerves terminating in the lacrimal glands.

Keratoconjunctivitis sicca (KCS) is the name given to this ocular surface disorder. KCS is subdivided into Sjögren syndrome (SS) associated KCS and non-SS associated KCS. Patients with aqueous tear deficiency have SS if they have associated xerostomia and/or connective tissue disease. Patients with primary SS have evidence of a systemic autoimmune disease as manifested by the presence of serum autoantibodies and very severe aqueous tear deficiency and ocular surface disease. These patients, mostly women, do not have a separate, identifiable connective tissue disease. Subsets of patients with primary SS lack evidence of systemic immune dysfunction, but they have similar clinical ocular presentation. Secondary SS is defined as KCS associated with a diagnosable connective tissue disease, most commonly rheumatoid arthritis but also SLE and systemic sclerosis.

Non-SS KCS is mostly found in postmenopausal women, in women who are pregnant, in women who are taking oral contraceptives, or in women who are on hormone replacement therapy (especially estrogen only pills). The common denominator here is a decrease in androgens, either from reduced ovarian function in the postmenopausal female or from increased levels of the sex hormone binding globulin in pregnancy and birth control pill use. Androgens are believed to be trophic for the lacrimal and meibomian glands. They also exert potent anti-inflammatory activity through the production of transforming growth factor beta (TGF-beta), suppressing lymphocytic infiltration.

Lipocalins (previously known as tear-specific prealbumin), which are present in the mucous layer, are inducible lipid-binding proteins produced by the lacrimal glands that lower the surface tension of normal tears. This provides stability to the tear film and also explains the increase in surface tension that is seen in dry eye syndromes characterized by lacrimal gland deficiency. Lipocalin deficiency can lead to the precipitation in the tear film, forming the characteristic mucous strands seen in patients with dry eye symptomatology.

The glycocalyx of the corneal epithelium contains the transmembrane mucins (glycosylated glycoproteins present in the glycocalyx) MUC1, MUC4, and MUC16. These membrane mucins interact with soluble, secreted, gel-forming mucins produced by the goblet cells (MUC5AC) and also with others like MUC2. The lacrimal gland also secretes MUC7 into the tear film.

These soluble mucins move about freely in the tear film (a process facilitated by blinking and electrostatic repulsion from the negatively charged transmembrane mucins), functioning as clean-up proteins (picking up dirt, debris, and pathogens), holding fluids because of their hydrophilic nature, and harboring defense molecules produced by the lacrimal gland. Transmembrane mucins prevent pathogen adherence (and entrance) and provide a smooth lubricating surface, allowing lid epithelia to glide over corneal epithelia with minimal friction during blinking and other eye movements. Recently, it has been suggested that the mucins are mixed throughout the aqueous layer of tears (owing to their hydrophilic nature) and, being soluble, move freely within this layer.

Mucin deficiency (caused by damage to the goblet cells or the epithelial glycocalyx), as seen in Stevens-Johnson syndrome or after a chemical burn, leads to poor wetting of the corneal surface with subsequent desiccation and epithelial damage, even in the presence of adequate aqueous tear production.

Pathophysiology

A genetic predisposition in SS associated KCS exists as evident by the high prevalence of human leukocyte antigen B8 (HLA-B8) haplotype in these patients. This condition leads to a chronic inflammatory state, with the production of autoantibodies, including antinuclear antibody (ANA), rheumatoid factor, fodrin (a cytoskeletal protein), the muscarinic M3 receptor, or SS-specific antibodies (eg, anti-RO [SS-A], anti-LA [SS-B]), inflammatory cytokine release, and focal lymphocytic infiltration (ie, mainly CD4⁺ T cells but also B cells) of the lacrimal and salivary gland, with glandular degeneration and induction of apoptosis in the conjunctiva and lacrimal glands. This results in dysfunction of the lacrimal gland, with reduced tear production, and loss of response to nerve stimulation and less reflex tearing. Active T lymphocytic infiltrate in the conjunctiva also has been reported in non-SS associated KCS.

Both androgen and estrogen receptors are located in the lacrimal and meibomian glands. SS is more common in postmenopausal women. At menopause, a decrease in circulating sex hormones (ie, estrogen, androgen) occurs, possibly affecting the functional and secretory aspect of the lacrimal gland. Forty years ago, initial interest in this area centered on estrogen and/or progesterone deficiency to explain the link between KCS and menopause. However, recent research has focused on androgens, specifically testosterone, and/or metabolized androgens.

It has been shown that in meibomian gland dysfunction, a deficiency in androgens results in loss of the lipid layer, specifically triglycerides, cholesterol, monounsaturated essential fatty acids (eg, oleic acid), and polar lipids (eg, phosphatidylethanolamine, sphingomyelin). The loss of polar lipids (present at the aqueous-tear interface) exacerbates the evaporative tear loss, and the decrease in unsaturated fatty acids raises the melting point of meibum, leading to thicker, more viscous secretions that obstruct ductules and cause stagnation of secretions. Patients on antiandrogenic therapy for prostate disease also have increased viscosity of meibum, decreased tear break-up time, and increased tear film debris, all indicative of a deficient or abnormal tear film.

Various proinflammatory cytokines that may cause cellular destruction, including interleukin 1 (IL-1), interleukin 6 (IL-6), interleukin 8 (IL-8), TGF-beta, TNF-alpha, and RANTES, are altered in patients with KCS. IL-1 beta and TNF-alpha, which are present in the tears of patients with KCS, cause the release of opioids that bind to opioid receptors on neural membranes and inhibit neurotransmitter release through NF-K b production. IL-2 also binds to the delta opioid receptor and inhibits cAMP production and neuronal function. This loss of neuronal function diminishes normal neuronal tone, leading to sensory isolation of the lacrimal gland and eventual atrophy.

Proinflammatory neurotransmitters, such as substance P and calcitonin gene related peptide (CGRP), are released, which recruit and activate local lymphocytes. Substance P also acts via the NF-AT and NF-K b signaling pathway leading to ICAM-1 and VCAM-1 expression, adhesions molecules that promote lymphocyte homing and chemotaxis to sites of inflammation. Cyclosporin A is an NK-1 and NK-2 receptor inhibitor that can downregulate these signaling molecules and is a novel addition to the therapeutic armamentarium for dry eye, being used to treat both aqueous tear deficiency and meibomian gland dysfunction. It has been shown to improve the goblet cell counts and to reduce the numbers of inflammatory cells and cytokines in the conjunctiva.

These cytokines, in addition to inhibiting neural function, may also convert androgens into estrogens, resulting in meibomian gland dysfunction, as discussed above. An increased rate of apoptosis is also seen in conjunctival and lacrimal acinar cells, perhaps due to the cytokine cascade. Elevated levels of tissue-degrading enzymes called matrix metalloproteinases (MMPs) are also present in the epithelial cells.

Mucin synthesizing genes, designated MUC1-MUC17, representing both transmembrane and goblet-cell secreted, soluble mucins, have been isolated, and their role in hydration and stability of the tear film are being investigated in patients with dry eye syndrome. Particularly significant is MUC5AC, expressed by stratified squamous cells of the conjunctiva and whose product is the predominant component of the mucous layer of tears. A defect in this and other mucin genes may be a factor in dry eye syndrome development. In addition to dry eye, other conditions, such as ocular cicatricial pemphigoid, Stevens-Johnson syndrome, and vitamin A deficiency, which lead to drying or keratinization of the ocular epithelium, eventually lead to goblet cell loss. Both classes of mucins are decreased in these diseases, and, on a molecular level, mucin gene expression, translation, and posttranslational processing are altered.

Normal production of tear proteins, such as lysozyme, lactoferrin, lipocalin, and phospholipase A2, is decreased in KCS.

Frequency

United States

Dry eye is a very common disorder affecting a significant percentage (approximately 10-30%) of the population, especially those older than 40 years.

In the United States, an estimated 3.23 million women and 1.68 million men, a total of 4.91 million people, aged 50 years and older are affected.

International

The frequency of dry eye in other countries closely parallels that of the United States.

Mortality/Morbidity

Dry eye may be complicated by sterile or infectious corneal ulceration, particularly in patients with SS. Ulcers are typically oval or circular, less than 3 mm in diameter, and located in the central or paracentral cornea. Occasionally, corneal perforation may occur. In rare cases, sterile or infectious corneal ulceration in dry eye syndrome can cause blindness. Other complications include punctate epithelial defects (PEDs), corneal neovascularization, and corneal scarring.

Race

The frequency and the clinical diagnosis of dry eye are greater in the Hispanic and Asian populations than in the Caucasian population.

Sex

Dry eye may be slightly more common in women. KCS associated with SS (a type of dry eye) is believed to affect 1-2% of the population, and 90% of those affected are women.

Clinical

History

Ocular irritation of dry sensation, burning, itching, pain, foreign body sensation, photophobia, and blurred vision are common in patients with dry eye. These symptoms are often exacerbated in smoky or dry environments, by indoor heating, or by excessive reading or computer use. These symptoms are quantified objectively in the Ocular Surface Disease Index (OSDI) questionnaire, which lists 12 symptoms and grades each on a scale of 1-4.

In KCS, symptoms tend to be worse toward the end of the day, with prolonged use of the eyes, or with exposure to extreme environmental conditions. Patients with meibomian gland dysfunction may complain of redness of the eyelids and conjunctiva, but, in these patients, the symptoms are worse on awakening in the morning.

Paradoxically, some patients with dry eye syndrome complain of too much tearing. When evidence of dry eye syndrome exists, this symptom often is explained by excessive reflex tearing due to severe corneal surface disease from the dryness.

Certain systemic medications also decrease tear production, such as antihistamines, beta-blockers, and oral contraceptives.

Past medical history may be significant for coexisting connective tissue disease, rheumatoid arthritis, or thyroid abnormalities. A thorough review of systems should be obtained, asking specifically about dry mouth.

Physical

Signs of a dry eye include the following:

Bulbar conjunctival vascular dilation
Decreased tear meniscus
Irregular corneal surface
Decreased tear break-up time
Punctate epithelial keratopathy
Corneal filaments
Increased debris in the tear film
Conjunctival pleating
Superficial punctuate keratitis, with positive fluorescein staining
Mucous discharge
Corneal ulcers in severe cases

Symptoms often do not correlate with signs.

In severe cases, there may be an epithelial defect or a sterile corneal infiltrate or ulcer. Secondary infectious keratitis also can develop. Both sterile and infectious corneal perforations can occur.

Causes

The International Dry Eye WorkShop (DEWS) recently developed a 3-part classification of dry eye, based on etiology, mechanisms, and disease stage.¹

The classification system, which is updated as an etiopathogenic classification by the DEWS Subcommittees, formulated by the National Eye Institute (NEI)/Industry Dry Eye Workshop Report in 1995, distinguishes 2 main categories (or causes) of dry eye states, as follows: an aqueous deficiency state and an evaporative state.

Deficient aqueous production
- Sjogren syndrome dry eye
  - Primary
  - Secondary
- Non-Sjogren syndrome dry eye
  - Lacrimal gland deficiency
  - Lacrimal gland duct obstruction
  - Reflex hyposecretion
  - Systemic drugs
Evaporative
- Intrinsic causes
  - Meibomian gland dysfunction
  - Disorders of lid aperture
  - Low blink rate
  - Drug action (eg, Accutane)
- Extrinsic causes
  - Vitamin A deficiency
  - Topical drugs and preservatives
  - Contact lens wear
  - Ocular surface disease (eg, allergy)

Deficient aqueous production can be further classified as follows:

Non-Sjögren syndrome
- Primary lacrimal gland deficiencies
  - Idiopathic
  - Age-related dry eye
  - Congenital alacrima (eg, Riley-Day syndrome)
  - Familial dysautonomia
- Secondary lacrimal gland deficiencies
  - Lacrimal gland infiltration
  - Sarcoidosis
  - Lymphoma
  - AIDS
  - Graft vs host disease
  - Amyloidosis
  - Hemochromatosis
  - Lacrimal gland infectious diseases
  - HIV diffuse infiltrative lymphadenopathy syndrome
  - Trachoma
  - Systemic vitamin A deficiency (xerophthalmia) – Malnutrition, fat-free diets, intestinal malabsorption from inflammatory bowel disease, bowel resection, or chronic alcoholism
  - Lacrimal gland ablation
  - Lacrimal gland denervation
- Lacrimal obstructive disease
  - Trachoma
  - Ocular cicatricial pemphigoid
  - Erythema multiforme and Stevens-Johnson syndrome
  - Chemical and thermal burns
  - Endocrine imbalance
  - Postradiation fibrosis
- Medications – Antihistamines, beta-blockers, phenothiazines, atropine, oral contraceptives, anxiolytics, antiparkinsonian agents, diuretics, anticholinergics, antiarrhythmics, topical preservatives in eye drops, topical anesthetics, and isotretinoin
- Reflex hyposecretion – Reflex sensory block and reflex motor block
  - Neurotrophic keratitis - Fifth nerve/ganglion section/injection/compression
  - Corneal surgery - Limbal incision (eg, extracapsular cataract extraction), keratoplasty, refractive surgery (eg, PRK, LASIK, RK)
  - Infective - Herpes simplex keratitis, herpes zoster ophthalmicus
  - Topical agents - Topical anesthesia
  - Systemic medications – Beta blockers, atropine-like drugs
  - Chronic contact lens wear
  - Diabetes
  - Aging
  - Trichloroethylene toxicity
  - Cranial nerve VII (CN VII) damage
  - Multiple neuromatosis
Sjögren syndrome
- Primary (no associated connective tissue disease [CTD])
- Secondary (associated CTD)
  - Rheumatoid arthritis
  - Systemic lupus erythematosus
  - Progressive systemic sclerosis (scleredema)
  - Primary biliary cirrhosis
  - Interstitial nephritis
  - Polymyositis and dermatomyositis
  - Polyarteritis nodosa
  - Hashimoto thyroiditis
  - Lymphocytic interstitial pneumonitis
  - Idiopathic thrombocytopenic purpura
  - Hypergammaglobulinemia
  - Waldenstrom macroglobulinemia
  - Wegener granulomatosis

Evaporative loss can be further classified as follows:

Intrinsic causes
- Meibomian gland disease
  - Reduced number - Congenital deficiency, acquired meibomian gland dysfunction
  - Replacement - Distichiasis, distichiasis lymphedema syndrome, metaplasia
  - Meibomian gland dysfunction
    - Hypersecretory - Meibomian seborrhea
    - Hyposecretory - Retinoid therapy
    - Obstructive – Simple, primary or secondary to local disease (eg, anterior blepharitis), systemic disease (eg, acne rosacea, seborrheic dermatitis, atopy, ichthyosis, psoriasis), syndromes (eg, anhidrotic ectodermal dysplasia, ectrodactyly syndrome, Turner syndrome), and systemic toxicity (eg, 13-cis retinoic acid, polychlorinated biphenyls); or cicatricial, primary or secondary to local disease (eg, chemical burns, trachoma, pemphigoid, erythema multiforme, acne rosacea, VKC, AKC)
- Low blink rate
  - Physiological phenomenon, such as during performance of tasks that require concentration (eg, working at a computer or a microscope)
  - Extrapyramidal disorder, such as Parkinson disease (decreasing dopaminergic neuron pool)
- Disorders of eyelid aperture and eyelid/globe congruity
  - Exposure (eg, craniostenosis, proptosis, exophthalmos, high myopia)
  - Lid palsy
  - Ectropion
  - Lid coloboma
- Drug action (eg, Accutane)
Extrinsic causes
- Vitamin A deficiency
  - Development disorder of goblet cells
  - Lacrimal acinar damage
- Topical drugs and preservatives (surface epithelial cell damage)
- Contact lens wear
- Ocular surface disease (eg, allergy)

A classification of dry eye on the basis of mechanisms includes tear hyperosmolarity and tear film instability.

For a classification of dry eye on the basis of severity, the Delphi Panel Report was adopted and modified as a third component of the DEWS.¹See Table.

Table. Dry Eye Severity levels^1,2

Open table in new window

[ CLOSE WINDOW ]

Table

Dry Eye Severity level	1	2	3	4 (Must have signs and symptoms.)
Discomfort, severity & frequency	Mild and/or episodic; occurs under environmental stress	Moderate episodic or chronic, stress or no stress	Severe frequent or constant without stress	Severe and/or disabling and constant
Visual symptoms	None or episodic mild fatigue	Annoying and/or activity-limiting episodic	Annoying, chronic and/or constant, limiting activity	Constant and/or possibly disabling
Conjunctival injection	None to mild	None to mild	+/–	+/++
Conjunctival staining	None to mild	Variable	Moderate to marked	Marked
Corneal staining (severity/location)	None to mild	Variable	Marked central	Severe punctate erosions
Corneal/tear signs	None to mild	Mild debris, decreased meniscus	Filamentary keratitis, mucus clumping, increased tear debris	Filamentary keratitis, mucus clumping, increased tear debris, ulceration
Lid/meibomian glands	MGD variably present	MGD variably present	Frequent	Trichiasis, keratinization, symblepharon
TFBUT (sec)	Variable	≤10	≤5	Immediate
Schirmer score (mm/5 min)	Variable	≤10	≤5	≤2

Dry Eye Severity level	1	2	3	4 (Must have signs and symptoms.)
Discomfort, severity & frequency	Mild and/or episodic; occurs under environmental stress	Moderate episodic or chronic, stress or no stress	Severe frequent or constant without stress	Severe and/or disabling and constant
Visual symptoms	None or episodic mild fatigue	Annoying and/or activity-limiting episodic	Annoying, chronic and/or constant, limiting activity	Constant and/or possibly disabling
Conjunctival injection	None to mild	None to mild	+/–	+/++
Conjunctival staining	None to mild	Variable	Moderate to marked	Marked
Corneal staining (severity/location)	None to mild	Variable	Marked central	Severe punctate erosions
Corneal/tear signs	None to mild	Mild debris, decreased meniscus	Filamentary keratitis, mucus clumping, increased tear debris	Filamentary keratitis, mucus clumping, increased tear debris, ulceration
Lid/meibomian glands	MGD variably present	MGD variably present	Frequent	Trichiasis, keratinization, symblepharon
TFBUT (sec)	Variable	≤10	≤5	Immediate
Schirmer score (mm/5 min)	Variable	≤10	≤5	≤2

Scoliosis

2010-10-05T21:35:00.007+07:00

Cerebral Palsy Research with Low Level Laser Therapy

2010-09-02T15:03:00.000+07:00

Bonnie L Brandes, MEd

Cerebral palsy (CP) is a postural and movement disorder caused by brain malformation or injury in the prenatal, perinatal (around birth), or
postnatal time period. The illness is non-progressive within the brain, but musculoskeletal and other tissues affected by the condition can
continue to weaken.
n the United States CP is the major disability affecting children’s functional development, with a prevalence of 1.5 to 2.0 cases per 1000. The
affected child is often unable to control motor functions normally. The illness is also associated with cognitive impairment and other
developmental disabilities. The child may have difficulties speaking, seeing, hearing, learning, and becoming independent depending on the
location and severity of the brain damage.

Many patients have normal intelligence, but communication skills are diminished because of speech and motor difficulties. It is therefore most
important not to underestimate the child’s intellect; he or she should be given every opportunity to learn. Lower life expectancy is related to
severe disabilities, such as mental retardation, necessity for tube feedings, and seizures, but otherwise, normal life expectancy may be expected.

Although a definitive cure does not yet exist, therapy, education, and technology can improve the child’s functioning and quality of life. The last
section of this paper reports on treatment successes using low level laser therapy.

Risk Factors

In approximately 25% to 40% of children with CP, birth was at less than 37 weeks gestation. Those with birth weight less than 1500 g (3.3
pounds) are at the highest risk. Damage to the periventricular white matter of the brain is the most common cause of CP in preterm infants. In
more than 30% of children with CP, etiology or risk factors are unknown.

Types of CP

CP can be classified according to the dominant motor characteristics—spastic, hypotonic, athetotic, dystonic, and ataxic, or by the pattern of limb
damage—monoplegia, diplegia, triplegia, hemiplegia, or quadriplegia.

Another way to classify the disease is by the two physiological types, pyramidal (spastic) and extra pyramidal (nonspastic). Pyramidal/spastic CP
is caused by damage in the corticospinal pathways of the brain. It accounts for 70% to 80% of all cases. In approximately 30% of cases, there is
cognitive impairment. The most conspicuous feature is increased muscle tone; other features include hyperreflexia, clonus (involuntary muscular
contractions), and persistent primitive reflexes, including Babinski.

Extrapyramidal (nonspastic) CP is caused by nerve damage outside of the pyramidal tracts in the basal ganglia or the cerebellum. There are two
subtypes, dyskinetic and ataxic. The disability is global, with inadequate regulation of muscle tone, poor control over posture, and abnormal
coordination.

Hypotonic CP, characterized by motor delays, is classified as CP only when myopathy and neuropathy have been ruled out as causes. Infants
with this CP have a marked decrease in muscle tone and a significant delay in motor milestones. Problems in feeding result from weak facial and
mouth muscles.

There are persistent primitive reflex patterns and hyperreflexia.

Different combinations of CP types are seen in some children.

Diagnosis of CP

Diagnosis is made mainly from clinical observation. Major signs include delayed motor milestones, abnormal neurological exam, persistence of
primitive reflexes, and abnormal postural reactions. No single abnormality is conclusive. Generally, the more severely ill child is diagnosed by the
age of six months, or later when symptoms are milder. The earlier the diagnosis, the sooner the child’s abnormal behavior can be understood by
the parents, allowing time to plan for long-term management.

Brain damage documented by cranial ultrasound, CAT scan, or MRI can facilitate diagnosis. When a child with identified lesions shows delayed
motor milestones, abnormal muscle tone, and retained primitive reflexes, an earlier diagnosis can be made. A series of examinations noting
progression is also useful in diagnosis.

Persistence of primitive reflexes is a hallmark of the condition. Most primitive reflexes are integrated within the first four to eight months of life, but
they may persist into adulthood in CP. Persistence of these reflexes adversely affects muscle tone and limb position, preventing the development
of voluntary motor movements. There may also be failure to develop protective reflexes such as parachute response or asymmetrical response.

In the neurological examination, the following are significant: abnormal muscle tone, weakness, deep tendon reflexes, clonus persisting beyond
12 months, and side to side asymmetries in muscle tone or functional abilities.

Prognosis

Predicting future abilities or disabilities is difficult at the time of diagnosis, leading to a “wait-and-see” approach.

Prediction of Ambulation:

How can the child’s ambulation potential be predicted? Sala and Grant present three categories of predictors: primitive reflexes and postural
reactions, gross motor skills, and type of CP. (1)

Persistence in these primitive reflexes by two years of age—asymmetrical tonic neck reflex (ATNR), symmetrical tonic neck reflex (STNR), Moro
reflex, tonic labyrinthine reflex, and to a lesser degree, positive supporting reflex—have been shown to be associated with inability to ambulate.
The same is true of abnormal postural reactions of foot placement and parachute reactions. (1)

In the category of gross motor skills, Jones and Morgan (2) report the following: In all types of CP, independent sitting by age 2 was found to be
reliably predictive for eventual walking. Achievement of head balance before nine months, ability to put weight on hands while prone and rolling
from supine to prone by 18 months, and motor control of crawling by 30 months were also found to be predictors of ambulation.

For type of CP as a predictor, Sala and Grant report the following: spastic hemiplegia, very good prognosis; spastic diplegia, good prognosis
(over 85%); spastic quadriplegia, much less favorable, with a wide range outcomes. (1)

Classifications of Severity:

In defining severity, a 5-level Gross Motor Function Measure has been developed by Rosenbaum, et al. (3) In Level 1 the patient walks without
restrictions (some limitations in advanced gross motor skills); Level II, able to walk without devices; Level III: able to walk with mobility devices;
Level IV, self mobility with limitations (power mobility); Level V, self mobility severely limited, even with technology. Parents often seek categories
of mild, moderate, and severe. Jones et al gives the following rule of thumb: mild – walking without assistance; moderate – requires medications,
bracing, and adaptive equipment to ambulate; severe – only mobile in a wheelchair. (2)

Success of LLLT (Low Level Laser Therapy) in Treating CP

Several clinical studies have been published concerning treatment of CP by soft laser, including application to acupuncture points on the scalp.
Scalp acupuncture was developed in China by Dr. Jiao Shunfa in 1971. Combining acupuncture in clinical practice and modern anatomy and
physiology, Dr. Shunfa developed a methodology based on 16 scalp areas. Studies have shown that scalp acupuncture increases cerebral
blood flow. (4) The World Health Organization reviewed and standardized scalp acupuncture in 1984.

In an early prospective study in 2001 - 2002, Fadaie and Khan performed a seven month treatment program of children with cerebral palsy and
other brain damage, applying laser therapy at scalp acupuncture points. (5) Seventeen boys and 12 girls, aged 5 months through 11 years,
were treated at the Fazal Hospital in Lahore, Pakistan.

Results showed significant improvement:

16 with brain damage and spasticity: six recovered fully, six had mild to moderate improvement, four had no improvement.
6 with brain damage and flaccidity or normal musculature: all six showed improved muscle function.
29 with brain damage and speech disorders: one showed great improvement; seven showed mild to moderate improvement; 21 showed little
improvement.
4 with brain damage and epileptic fits: Two showed improvement, but frequency of fits increased. It was concluded that treatment with laser
acupuncture should be continued, but with longer inter-session intervals and use of anti-epileptic medication. In a subsequent study in 2003 –
2004, no increase in epileptic fits was noted. (6)
10 children with cortical blindness: four recovered completely.
5 with impaired hearing or deafness: all five improved.
2 with autism: autism improved little, although other mental faculties improved.
Best results were noted in children less than two years old; the second best results were in ages less than 5. In ages 5 through 10, results were
poor. For the one subject 11 years old, results were very poor.

In a larger study conducted on children with cerebral palsy in 2003 through 2006 at Children’s Hospital in Lahore, Pakistan, 250 children were
treated with Aculaser therapy directed at acupuncture sites, including sites on the skull. (7) Aculaser therapy consists primarily of low level laser
therapy, acupuncture, and physical therapy. A minimum of 15 treatments for a minimum of six weeks was given to each of the children, who were
classified according to type of CP.

Results showed significant improvement:

171 children with spasticity and stiffness: 147 showed marked improvement (87% success).
126 with epileptic fits: 91 showed a significant reduction in intensity, frequency, and duration of fits (72% success).
48 children with cortical blindness: 30 showed improvement (63% success).
105 with hearing difficulty: 63 showed marked improvement (60% success).
190 with speech disorders, 122 showed improvement (64% success).
96 with hemiplegia, 71 showed improvement in movement, tone, and power (74% success).
76 with quadriplegia, 52 showed improvement in gross and fine motor functions (69% success).
58 with paraplegia of lower limbs, 44 showed improvement in weight bearing, standing, and movement (76% success).
Children given a break in treatment for one month to one year did not show any reversal of symptoms.

As in the earlier study, best results were noted in children less than two years old; the second best results were in ages less than 5.
Similar successful results were demonstrated by the same group in another study using Aculaser therapy. (6) For the scalp, a red diode laser
was used with a wavelength 650 nm, power of 5mW, and duration of 30 - 45 seconds. For body and auricular points, a HeNe laser was used with
a wavelength 632.8, power of 30 mW, and duration of 15 seconds.

It is concluded from these studies that the low level laser can be a valuable therapy in reducing the degree of disability in persons with CP.

Success Story:

Annie, age 6-1/2 years, received three Quantum Reflex Integration sessions during a three month period. The sessions included using the
Quantum Wave Laser with the "Unwinding" protocol (developed by Paul Weisbart), QRI laser acu-points, and QRI laser reflex integration
techniques for active primary reflexes. Primary reflexes that were addressed: Moro, Babinski, Leg Cross Flexion, Spinal Galant, Spinal Perez,
Hands Grasping, Automatic Gait, and Tonic Labyrinthine.

Annie's mother stimulated QRI acu-points manually as a home program times 3 - 4 times a week for approximately 30-40 minutes each session.
Mother does not have access to a laser between therapist sessions.

After the first session, Mom reported that Annie's ability to jump on a mini trampoline improved from 0 inches to 3 inches, with some assistance
for balance. Also after the first session, Annie's balance and endurance in walking without braces improved.

After three sessions, Mother reports that Annie has more confidence and better balance, and has met her first goal of jumping off the ground
independently. She has continued to improve in mobility and strength as demonstrated by her ability to walk around the yard without braces and
move a chair from one area to another. She now is able to pump her legs while swinging on a swing set, walk up steps of 4" without assistance
or holding on to a rail, and has increased the length of her stride.

Previous therapies include Physical Therapy and Occupational Therapy; current therapies and programs include QRI, Physical Therapy and
Occupational Therapy.

QRI Home Training Programs allow parents and therapists to successfully give their children possibilities, options, and successful
outcomes using soft lasers and reflex integration.

References:

1. Sala DA, Grant AD. Prognosis for Ambulation in Cerebral Palsy. Developmental Medicine and Child Neurology. 2008;37(11):1020-1026.

2. Jones MW, Morgan E, Shelton JE, Thorogood C. Cerebral Palsy: Introduction and Diagnosis (Part I). J Pediatr Health Care. 2007;21(3):146-152.

3. Rosenbaum PL, Walter SD, Hanna SE, Palisani RJ et al. Prognosis for gross motor function in cerebral palsy. JAMA. 2002;288:1357-1363.

4. Jing L, Jianhua X, Guirong D. Clinical study on effect of scalp acupuncture in treating acute cerebral hemorrhage. Chinese Journal of Integrative
Medicine. 1993;5(2):141.

5. Fadaie M; Khan M, Shah S. Application of Laser Acupuncture in Children with Cerebral Palsy. Majid Fadaie, Medical Acupuncturist, Lic AC (China) and
Malik Khan, pediatric neurosurgeon, Children’s Hospital, Lahore, Pakistan. 2002.

6. Anwar S, Khan M et al. Role of Aculaser Therapy in Cerebral Palsy Children. Anwar Shah’s First CP & Paralysis Clinic and Research Center. Lahore,
Pakistan. 2004.

7. Anwar S, Khan M et al. Treating cerebral palsy with Aculaser therapy. Anwar Shah’s First CP & Paralysis Clinic and Research Center, Lahore, Pakistan.
2006.

Sweet Vallen, juvenile rheumatoid arthritis

2010-07-18T08:44:00.006+07:00

Flare and swaleen a week a go

A week after. No flare, reduce edema. Transcutaneus and scann mode low level laser.

She just 6 y o. Came to me with swollen at all fingers and both knee. Yesterday, the 2nd laser application. At the 1st , just transcutaneus for 1 hour. Yestesday I found the finger and knees not flare anymore. I gave ½ hour transcutaneus, 15 minutes scan for both knee, and the fingers. At the end of the treatment, she could moved her knee and fingers without tears.

I couldn’t ask how her pain number by pain scale. I’ll try next time.

Juvenile Rheumatoid Arthritis: Follow-up

2010-07-15T10:52:00.001+07:00

Juvenile Rheumatoid Arthritis: Follow-up
Author: C Egla Rabinovich, MD, MPH, Associate Professor and Co-Division Chief, Department of Pediatrics, Division of Pediatric Rheumatology, Duke University Medical Center
Contributor Information and Disclosures
Updated: Apr 7, 2010

Follow-up
Further Inpatient Care
Further inpatient care is required for persisting fevers of unknown origin or when children with known juvenile idiopathic arthritis (JIA) have severe exacerbation of disease. Admit for evaluation any child who loses the ability to walk for unknown reasons. Development of pericarditis in children with systemic juvenile idiopathic arthritis is usually an indication for admission.
Further Outpatient Care
Patients may have a gradually responsive disease (particularly those with pauciarticular juvenile idiopathic arthritis).
A small number of patients with pauciarticular juvenile idiopathic arthritis develop aggressive arthritis confined to a single joint; such patients may require more intensive medical treatment and physical therapy.
Some patients with polyarticular juvenile idiopathic arthritis demonstrate rapid response to treatment; however, most have prolonged courses, requiring frequent adjustments in medical and nonmedical therapy. Some have sufficient problems with activities of daily living, and they may benefit from courses of outpatient (and sometimes inpatient) rehabilitation.
Inpatient & Outpatient Medications
See Medication.
Transfer
Consider outpatient evaluation in a pediatric rheumatology center for all patients with known and suspected disease. Inpatient care for individuals with intercurrent illnesses may best be carried out at local hospitals; complications from juvenile idiopathic arthritis usually indicate transfer to a hospital with a pediatric rheumatology center.
Treatment of macrophage activation syndrome (MAS) is a medical emergency and should be done by physicians familiar with this complication.
Deterrence/Prevention
No prevention methods are known. The best means of deterrence is compliance with recommended treatment. As many as one half of patients may not comply with every detail of recommended treatment. Persisting noncompliance is a problem that increases risk of morbidity. Parents of such patients often admit noncompliance only to the child's primary care physician, rather than to a pediatric subspecialty team. The continued monitoring of compliance by the primary care physician, together with continuing communication between the pediatric subspecialist and primary physician, is an important part of the treatment of children with juvenile idiopathic arthritis and any chronic illness.
Complications
The following complications may occur:
• Systemic-onset juvenile idiopathic arthritis
o Pericarditis (patients often presenting with orthopnea and responsive to intravenous corticosteroid treatment)
o Hemolytic anemia
o Disseminated intravascular coagulopathy (DIC), often present at a low level of activity: The levels of D-dimer and fibrinogen may be elevated; their return to reference range levels is observed with successful treatment.
o MAS
 This is a rare, but important, complication, in which numbers of all 3 bloodlines become rapidly decreased. Hypofibrinogenemia, thrombocytopenia, and elevated aspartate aminotransferase levels are hallmarks.
 Hypotension, CNS disease, and marked hepatosplenomegaly may be noted as complications of a release of massive amounts of cytokines.
 Bone marrow aspiration may reveal histiocytic consumption of bone marrow precursors, which confirms the diagnosis and excludes malignancy. One does not need to see the histiocytic consumption for diagnosis of MAS.
 MAS often responds to cyclosporin A, and some case reports have detailed response to anakinra.
o Endarteritis resulting in circulatory compromise of the digits with threatened autoamputation
 This complication is even more rare than MAS.
 Central administration of prostaglandin E1 may be of potential benefit, similar to its use for patients with scleroderma and endarteritis.
• Pauciarticular juvenile idiopathic arthritis
o Knee flexion contractures: This complication requires splinting at night, in addition to medical treatment, to restore range of motion, allow recovery of muscle strength, and avoid subluxation of the joint. Intra-articular corticosteroid injection should be strongly considered.
o Uveitis
 Often asymptomatic, patients are typically young girls who have positive levels of antinuclear antibody (ANA).
 In such patients, evaluation using a slit-lamp examination by a pediatric ophthalmologist every 4 months can detect early disease.
 Treatment with topical corticosteroid medication and with mydriatic agents (to prevent closed-angle glaucoma) often can prevent progression of disease to development of calcium deposition in the lens (band keratopathy) and adhesions of the iris to the lens (posterior synechiae), in which an irregular pupillary margin develops.
 Such complications may herald a chronic active disease, in which vision is threatened; immunosuppressive agents, such as methotrexate or cyclosporin, may help to control chronic uveitis. Infliximab can be effective in some patients who are resistant to immunosuppressive agents.
o Leg length discrepancy (can result from neovascularization of growth plates of an affected knee)
 The problem may not be detected in patients with a knee flexion contracture until the contracture is corrected.
 Treatment consists of a shoe lift on the nonaffected side.
• Polyarticular juvenile idiopathic arthritis
o Skeletal abnormalities - Increased size of epiphyses, accelerated bone age, narrowed joint spaces, swan-neck and/or boutonniere deformities, and joint subluxation
o Cervical spine involvement
 Difficulty flexing the spine may create a problem for intubation prior to surgery; inform anesthesiologists of the patient's diagnosis. Screening cervical spine radiography (in both flexion and extension) may help screen for potential difficulties during induction of anesthesia.
 High-level subluxation is a potential complication.
Prognosis
Some studies suggest that many children with juvenile idiopathic arthritis can lead productive lives. However, other studies suggest many patients, particularly those with polyarticular disease, may have problems with active disease throughout adulthood, with sustained remission attained in a minority of patients. Early hip or wrist involvement, symmetric disease (even in pauciarticular patients), presence of rheumatoid factor, and prolonged active disease have been associated with poor long-term outcomes.
Children with systemic disease tend to have either complete responsiveness to medical therapy or development of a polyarticular course that tends to be refractive to medical treatment, with disease persisting into adulthood.
Most children with pauciarticular disease demonstrate eventual permanent remission; a small number progress to persisting polyarticular disease.
Patient Education
Educating the patient, family, and school personnel (eg, classroom teachers, physical education teachers, nurses) about juvenile idiopathic arthritis and its presentation, treatment, and potential effects is continually necessary. Members of the pediatric rheumatology team in pediatric rheumatology clinics are the best educators about juvenile idiopathic arthritis. Another important source of information is the American Juvenile Arthritis Organization, a council of the Arthritis Foundation.
For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education articles Juvenile Rheumatoid Arthritis and Understanding Rheumatoid Arthritis Medications.
Miscellaneous
Medicolegal Pitfalls
The major medicolegal pitfall lies in diagnosing juvenile idiopathic arthritis (JIA) when another problem exists (eg, infection, malignancy, orthopedic problem). Whenever possible, referral to a pediatric rheumatologist can help address this issue. Careful attention to presenting history and initial physical examination findings can lower the likelihood of such a pitfall. However, the chance of such a pitfall can never be eliminated completely.
At the time of diagnosis, inform parents and/or caregivers of the possible need to revise the diagnosis of juvenile idiopathic arthritis should new symptoms, physical findings, or unusual laboratory results develop.
Special Concerns
Chronic illness imposes burdens on families, who may vary in their abilities to cope. Social workers can help provide assessment and assist families in finding resources (including counseling). Remind parents and/or caregivers to bring all questions to the pediatric rheumatology team, who can often help. Any unusual symptom may signal a new complication of disease or adverse effect of medication. In the current health care environment, managed care can result in initial denial of services (eg, physical therapy), resulting in delays in treatment with subsequent morbidity. Advocacy by the primary care physician and pediatric rheumatologist can help point out the need for such services.

Acknowledgments
The authors and editors of eMedicine gratefully acknowledge Michael L Miller, MD, to the original writing and development of this article.

Juvenile Rheumatoid Arthritis: Treatment & Medication

2010-07-15T10:43:00.003+07:00

Juvenile Rheumatoid Arthritis: Treatment & Medication

Author: C Egla Rabinovich, MD, MPH, Associate Professor and Co-Division Chief, Department of Pediatrics, Division of Pediatric Rheumatology, Duke University Medical Center
Contributor Information and Disclosures

Updated: Apr 7, 2010

Treatment

Medical Care

Medical care of children with juvenile rheumatoid arthritis (JRA) must be provided in the context of a team-based approach, considering all aspects of their illness (eg, physical functioning in school, psychological adjustment to disease). Using medications in the absence of an appropriate physical therapy program and attention to problematic social issues of the family is not successful. Success of medications is monitored best with repeated physical examinations and history. Both the number of joints involved and the duration of morning stiffness should demonstrate continued decrease, with elimination reflecting success.

Surgical Care

Surgery is not usually needed; however, some children with persisting pauciarticular juvenile rheumatoid arthritis, despite medical treatment, may benefit from intra-articular steroid injection. Such injections may also be effective in treating temporomandibular arthritis in children with polyarticular juvenile rheumatoid arthritis. Usually, delay joint replacement (often of the hips, in patients with polyarticular juvenile rheumatoid arthritis) until bone growth has completed, which is reflected by epiphyseal closure. The consistent effective use of medical treatment has consigned synovectomy to a rarely used intervention. Large leg length discrepancies may need surgical treatment.

Consultations

The subspecialty team includes the following:

Pediatric rheumatologist (when available)
Nurses (who help with education)
Physical and occupational therapists: Nonmedical approaches (eg, physical and occupational therapy) are an important part of treatment. At presentation, arthritis may be so active as to preclude the use of an aggressive program of muscle strengthening. Nevertheless, the use of pain modalities during this period may permit the gradual introduction of an active program of exercises and stretching.
Social workers: Social work evaluation helps to determine how well each family is coping with their child's disease in terms of emotional and financial resources. Social workers can offer invaluable guidance for helping children to maintain healthy relationships both within their families and at school. Transition programs for adolescents with arthritis can help prepare them for higher education and future vocations.

Pediatric ophthalmologists help provide slit-lamp examinations to exclude uveitis. Pediatric orthopedic surgeons can offer consultation when orthopedic diagnoses are being considered. The development of profound anemia or a drop in 2 or more cell lines may require the help of a pediatric hematologist. A pediatric gastroenterologist may help with hepatic abnormalities or symptoms suggesting inflammatory bowel disease.

Diet

No specific diet helps in the treatment of juvenile rheumatoid arthritis. However, because active juvenile rheumatoid arthritis has been associated with decreased osteoblastic activity and a risk of osteopenia, encourage the inclusion of at least 3 servings of calcium-rich foods each day. Consider behavioral intervention when poor calcium intake persists.

Activity

Encourage patients to be as active as possible. Except in individuals with severe systemic disease, bed rest is not a part of the treatment. In fact, the more active the patient the better the long-term prognosis is. Children may experience increased pain during routine physical activities. As a result, these children must be allowed to self-limit their activities, particularly during physical education classes. A consistent physical therapy program, with attention to stretching exercises, pain modalities, joint protection, and home exercises, can help ensure that patients are as active as possible.

Medication

Classes of medications are suggested below, and specific drugs are covered in detail by category. See the therapeutic algorithm below

One set of suggested algorithms for the treatment of patients with juvenile arthritis. This should not be considered dogmatic because treatment is not standardized and remains empiric and, at times, controversial.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to treat all subtypes of juvenile rheumatoid arthritis (JRA). They may help with pain and decrease swelling. They are often used in conjunction with second-line agents. These medications are effective because of inhibition of prostaglandin synthesis. Naproxen is listed below as an example of an NSAID used in treatment; other NSAIDs commonly used include ibuprofen, tolmetin, diclofenac, and indomethacin. In addition, sulfasalazine is sometimes used as a second anti-inflammatory drug in some children with persisting pauciarticular and polyarticular disease. Its use may be considered as an intermediate step prior to adding a second-line drug such as methotrexate (MTX).

Aspirin is no longer the drug of first choice because of the increased frequency of gastric toxicity and hepatotoxicity when compared to other NSAID medications, along with its association with Reye syndrome. The discovery that cyclooxygenase (COX) in gastric and intestinal endothelium (ie, COX-1) is different in structure from that in leukocytes (ie, COX-2) has led to the development of anti-inflammatory drugs specific for COX-2. COX-2 inhibitors have been found to be effective in treatment of adults with rheumatoid arthritis. Studies of COX-2 inhibitors in persons with juvenile idiopathic arthritis are underway. Besides the benefit of greatly reducing gastric toxicity (although hepatotoxicity remains a possible adverse event), COX-2 inhibitors do not inhibit platelet aggregation. Thus, these agents may find a role in the treatment of inflammatory conditions in which a bleeding diathesis is a potential problem, such as in the postoperative setting.

NSAIDs alone are usually adequate for treatment of pauciarticular disease. However, an aggressive arthritis sometimes develops in this subtype, requiring the need to add a second-line drug. Various second-line drugs have been used in addition to first-line NSAIDs. Gold salt injections were used until approximately 15 years ago, when studies by the Pediatric Rheumatology Collaborative Study Group demonstrated the efficacy of oral (PO) MTX; these injections are not currently used for most children. Subsequent studies have demonstrated that some children with polyarticular arthritis unresponsive to PO MTX benefit from subcutaneous (SC) or intramuscular (IM) administration. The use of high-dose intravenous (IV) steroids as a therapeutic bridge in selected patients has been beneficial in some patients, particularly during an early period before MTX may have a full therapeutic effect.

Etanercept, a biologic agent administered SC twice weekly and containing a receptor to tumor necrosis factor (TNF) ligated to an Fc portion of immunoglobulin, has been found to be effective in controlling polyarticular arthritis not controlled by conventional medical treatment. Adalimumab is another anti-TNF agent now approved for use in juvenile idiopathic arthritis. These medications are for those children treated by pediatric rheumatology centers who are unresponsive to treatment including conventional second-line drugs.

Abatacept is a biological immune modulator with a delayed onset of action (4 mo) that may be useful in polyarticular disease.

Finally, the treatment of systemic juvenile idiopathic arthritis may require, in addition to treatment with NSAIDs, the careful use of either PO or high-dose pulse IV corticosteroids. Such treatment is best reserved for patients in whom definite arthritis has developed to avoid premature treatment in a patient who may prove to have a disease other than juvenile rheumatoid arthritis. Corticosteroids may be avoided with the use of anakinra, which is relatively new, inhibits interleukin (IL)-1 activity, and appears to have unique efficacy on the systemic signs and symptoms of systemic juvenile idiopathic arthritis. Rilonacept (anti-IL-1) may be an alternative treatment that is being studied, as is tocilizumab, which is anti-IL-6. Thalidomide has also been reported to be useful in these children.

Juvenile Rheumatoid Arthritis: Differential Diagnoses & Workup

2010-07-15T10:40:00.002+07:00

Juvenile Rheumatoid Arthritis: Differential Diagnoses & Workup

Differential Diagnoses

Other Problems to Be Considered

Many conditions may manifest with arthritis of brief duration. Postinfectious arthritis typically affects large joints. This syndrome is clinically indistinguishable from the early phase of juvenile idiopathic arthritis (JIA), particularly because onset of juvenile idiopathic arthritis may be triggered by viral infections; a duration longer than 6 weeks eventually differentiates juvenile idiopathic arthritis. Patients with acute lymphocytic leukemia can present with joint pain and arthritis. Expansion of lymphoblasts in bone metaphyses results in pain, which is typically severe and may awaken a child from sleep.

Thrombocytopenia is rare in persons with juvenile idiopathic arthritis; its presence also suggests the possibility of leukemia. The differential count in juvenile idiopathic arthritis often demonstrates a relative lymphopenia, presumably because of egress of activated lymphocytes from circulation into synovium. Lymphocytosis is uncharacteristic of juvenile rheumatoid arthritis and raises the possibility of leukemia, particularly when a neutropenia is present.

Enthesitis-related arthritis, or spondyloarthropathy, is a chronic disease characterized by periods of inflammation of tendons and ligaments, particularly at the area of insertion into bone (entheses). Often, children and adolescents with spondyloarthropathy present with arthritis, making the distinction between subtypes difficult. Furthermore, some children occasionally develop a disease that appears to be a combination of the 2 diseases. Nevertheless, although enthesitis can be observed in persons with pauciarticular and polyarticular juvenile rheumatoid arthritis, the eventual evolution of arthritis to a predominant enthesitis is more characteristic of spondyloarthropathy. The presence of the human leukocyte antigen (HLA) B27 is helpful in suggesting the diagnosis. However, radiographic changes observed in adults (eg, sclerosis of the sacroiliac joints, bamboo spine) are rare in childhood and adolescence.

Workup

Laboratory Studies

No laboratory studies are diagnostic for juvenile idiopathic arthritis (JIA).

All laboratory study findings may be normal in children with juvenile idiopathic arthritis. Diagnosis is based on the physical finding of arthritis. Laboratory studies help exclude other underlying diagnosis, classify the type of arthritis, and help evaluate for extra-articular manifestations of juvenile idiopathic arthritis. Initial evaluation should include the following:

Inflammatory markers

Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) are usually elevated in children with systemic juvenile rheumatoid arthritis (JRA) and may be elevated or normal in those with polyarticular disease; however, it is often within the reference range in those with pauciarticular disease.
When elevated, inflammatory markers may be used to monitor success of medical treatment.

CBC count with differential and platelet count

Lymphopenia is not uncommon because of emigration of activated lymphocytes out of the circulation into synovium.
Neutropenia is uncommon and, particularly with lymphocytosis or thrombocytopenia, raises the possibility of acute lymphocytic leukemia.
Thrombocytopenia may also be observed in persons with systemic lupus erythematosus (SLE) presenting with arthritis, as well as marrow occupying malignancies. Thrombocytosis reflects inflammatory state and often mirrors inflammatory markers in juvenile idiopathic arthritis.
Anemia may result from chronic active juvenile rheumatoid arthritis; often microcytic, anemia is usually refractive to treatment with iron.

Alanine aminotransferase (ALT) test: Obtain ALT levels to exclude the possibility of hepatitis (viral or autoimmune) prior to initiating treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) or methotrexate (MTX), which can cause hepatotoxicity.
Urinalysis with microscopic examination: Perform a urinalysis to exclude the possibility of infection (as a trigger of juvenile rheumatoid arthritis or transient postinfectious arthritis) and nephritis (observed in individuals with SLE). Urinalysis should be monitored in children on chronic NSAIDs. Serum creatinine levels should be obtained prior to initiation of treatment with NSAIDs.
Antinuclear antibody (ANA)

ANA is observed in as many as 50% of children with juvenile idiopathic arthritis, particularly in those with oligoarticular or polyarticular rheumatoid factor–negative subtypes.
A positive ANA is a marker for increased risk of anterior uveitis. Children younger than 6 years at arthritis onset with a positive ANA finding are in the highest risk category for development of uveitis and need slit lamp screening every 3-4 months.
Very high titers may sometimes be associated with evolution to other rheumatic disease (eg, SLE).
Titers otherwise do not correlate with disease activity.

Rheumatoid factor

Rheumatoid factor is found to be present in less than 10% of children with juvenile idiopathic arthritis. It is very rarely found in those with systemic juvenile idiopathic arthritis. Rheumatoid factor is a marker for early erosive disease and persistence of arthritis into adulthood.
Rheumatoid nodules may be seen in those with rheumatoid factor–positive disease
Compared with adults who have rheumatoid factor, children are at less risk for rheumatoid lung involvement and vasculitis.

Other laboratory tests for systemic juvenile rheumatoid arthritis include the following:

Total protein and albumin levels are often decreased during active disease.
Fibrinogen and D-dimer levels are often elevated in individuals with active disease.
A falling sedimentation rate, along with normalization or falling WBC, low platelets, elevated liver function test findings, increased ferritin and triglycerides with low fibrinogen and associated erratic fevers, hemorrhages (disseminated intravascular coagulation–like pattern) are indicative of development of macrophage activating syndrome (MAS) in particularly in those with systemic onset juvenile idiopathic arthritis.

Other laboratory tests to consider include the following:

ACE elevation may be indicative of sarcoidosis.
Antistreptolysin 0 (AS0) and anti-DNAse B elevations may indicate acute rheumatic fever or poststreptococcal arthritis.

Imaging Studies

The following imaging studies are indicated:

Radiography of affected joints: When only a single joint is affected, radiography is important to exclude other diseases, such as osteomyelitis or septic arthritis.
Bone scanning: When physical findings do not document definite arthritis, consider bone scanning as a means of identifying a potential focus of osteomyelitis or other abnormality.
MRI

Perform MRI of the affected joint, with gadolinium injection to enhance inflamed synovium.
MRI is helpful when considering trauma in the differential diagnosis.
MRI of the temporal-mandibular joint (TMJ) is useful in diagnosing TMJ inflammatory arthritis.

CT scanning of long bones: Perform when considering osteoid osteoma in a child with lower extremity pain (often at night) and unremarkable findings on physical examination.
Echocardiography

This is performed in a child with possible systemic juvenile rheumatoid arthritis and with fevers.
Perform echocardiography in an individual who has orthopnea by history or a rub to exclude pericarditis.

In a person who has nonspecific rash, adenopathy, and possible mucocutaneous changes, perform echocardiography to exclude coronary arterial dilation resulting from (possibly atypical) Kawasaki disease.
In an individual who has findings suggestive of SLE (eg, nephritis, pleuritic chest pain, thrombocytopenia), perform echocardiography to exclude valvular disease, although mild dilation may be seen in some patients with systemic juvenile rheumatoid arthritis.

Other Tests

Perform dual-energy radiograph absorptiometry (DXA) scanning to document osteopenia in children with polyarticular juvenile rheumatoid arthritis.

Procedures

The following procedures are indicated:

Arthrocentesis: Perform arthrocentesis to exclude septic arthritis in a child with monoarticular swelling.
Synovial biopsy: This procedure may be helpful to exclude other diagnoses, particularly when the knee is affected (eg, villonodular synovitis, granulomatous arthritis).
Pericardiocentesis: Perform this in an ICU setting to treat severe pericarditis.

Histologic Findings

Synovial biopsy may reveal synovial infiltration with plasma cells, mature B lymphocytes, and T lymphocytes, with areas of synovial thickening and fibrosis.

Juvenile Rheumatoid Arthritis

2010-07-15T10:38:00.000+07:00

Juvenile Rheumatoid Arthritis

Updated: Apr 7, 2010

Introduction

Background

Juvenile rheumatoid arthritis (JRA) is the most common rheumatological disease in children and is one of the most common chronic diseases of childhood. It represents a group of disorders that all share the clinical manifestation of chronic joint inflammation. The etiology is largely unknown, and the genetic component is complex, making clear distinctions between the various subtypes difficult. As a result, various classification criteria are recognized, with different benefits and limitations. A new nomenclature, juvenile idiopathic arthritis (JIA), is increasingly used and is replacing the term juvenile rheumatoid arthritis.

The American College of Rheumatology classifies juvenile rheumatoid arthritis into 3 distinct subtypes: pauciarticular juvenile rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, and systemic JRA. Other childhood arthritis such as juvenile ankylosing spondylitis and psoriatic arthritis are classified under spondyloarthropathies.

In 1997, the International League of Associations for Rheumatology (ILAR) conducted a consensus conference during which they proposed the nomenclature juvenile idiopathic arthritis. The classification criteria include psoriatic arthritis and enthesitis-related arthritis, which encompasses juvenile ankylosing spondylitis, arthritis associated with inflammatory bowel disease, reactive arthritis, and spondyloarthropathies. This has resulted in some confusion in the literature; when reviewing existing literature, consider whether authors are referring to the juvenile rheumatoid arthritis or juvenile idiopathic arthritis nomenclature because this affects the population being discussed and thus the generalizability of the results.

This article focuses on oligoarticular juvenile idiopathic arthritis (pauciarticular juvenile rheumatoid arthritis), polyarticular juvenile idiopathic arthritis, both rheumatoid factor positive and negative (polyarticular JRA), and systemic juvenile idiopathic arthritis (systemic JRA).

Gathering Club for COPD and laryngectomee's

2010-07-02T11:31:00.003+07:00

METABOLISM DURING EXERCISE - AEROBIC VS. ANAEROBIC

2010-05-23T17:20:00.000+07:00

Metabolically, there are two types of exercise, aerobic and anaerobic. Aerobic exercise uses oxygen as energy substrate to metabolize food to adenosine triphosphate (ATP) (see box below, METABOLIC CHANGES DURING AEROBIC AND ANAEROBIC EXERCISE). When the supply of oxygen is no longer sufficient to meet the needs of exercising muscles, anaerobic metabolism begins. In anaerobic metabolism, glucose is converted to ATP without oxygen, and lactic acid is generated as a by-product. A healthy person can perform aerobic exercise for several hours; in contrast, pure anaerobic exercise can only be sustained for a few minutes before severe dyspnea and fatigue set in.

During short bursts of activity, such as sprinting, energy may be obtained only anaerobically. Otherwise, anaerobic metabolism occurs in addition to ongoing aerobic metabolism. Typically, anaerobic metabolism begins approximately midway between resting and maximal oxygen consumption. The point at which anaerobic metabolism begins is called the anaerobic threshold (AT). AT can be identified by a typical pattern of changes in the blood and in expired gases (see the next section).

METABOLIC CHANGES DURING AEROBIC AND ANAEROBIC EXERCISE

During aerobic exercise, both glucose and fatty acids are metabolized. One molecule of glucose utilizes 6 molecules of oxygen and produces 6 molecules of carbon dioxide, for a metabolic respiratory quotient (RQ) of I.O. For fatty acids, 23 molecules of oxygen are used for every 16 molecules of carbon dioxide produced, giving an RQ of 0.71. The average RQ during mild to moderate exercise (before anaerobic threshold) is approximately 0.85.

By contrast, anaerobic metabolism produces only 2 molecules of ATP per molecule of glucose; at the same time 2 molecules of lactic acid are produced, which, when buffered, generate carbon dioxide in excess of that from aerobic metabolism.

AEROBIC METABOLISM

C₆H₁₂O₆ + 6 02 ----> 6 CO₂ + 6 H₂O + 36 ATP (RQ = 1.0)
(Glucose)

C₁₆H₃₂O₂ + 23 0₂ ----> 16 CO₂ + 16 H₂O + 130 ATP (RQ = 0.71)
(Fatty acid)

ANAEROBIC METABOLISM

Glucose + 2 ADP ----> 2 H⁺ lactate + 2 ATP (Lactic acid)

H⁺ lactate^- + Na⁺HCO^-₃ ---> Na⁺ lactate^- + H₂CO₃

H₂CO₃ ---> H₂O + CO₂

Chapter 12: Exercise Physiology

Lawrence Martin, M.D.

Energy Supply

2010-05-23T16:55:00.003+07:00

Energy supply

a. ATP à ADP + energy

b. Creatine phosphate + ADP à creatine + ATP (anaerobic , alactic)

c. Glucose + ADP à lactic + ATP (anaerobic, lactic)

d. Glucose + oxygen + ADP à carbon dioxide + ATP + water (aerobic, alactic)

e. Fat + oxygen + ADP à carbon dioxide + ATP + water (aerobic, alactic)

Classification of maximum activity of various duration together with energy – supplying system for this activity
duration	Classification (aerobic/ anaerobic)	Enrtgy supplied by	Observations
1-4 sec	Anaerobic, alactic	ATP
4-20 sec	Anaerobic, alactic	ATP +CP
20 – 45 sec	Anaerobic, alactic	ATP + CP +	High lactate production
	+ anaerobic, lactic	Muscle glycogen	High lactate production
45-120 sec	Anaerobic, alactic	Muscle glycogen	with increasing
			duration,
			decreasing lactate
			production
120- 140 sec	Aerobic + anaerobic,	Muscle glycogen	ditto
	lactic
240-600 sec	Aerobic	Muscle glycogen	With increasing
		+ fatty acids	Duration higher
Etc			Share of fats

Various substrates for energy supply and their characteristics
Substrate	breakdown	availability	Speed of energy production
Creatine phosphate (CP)	Anaerobic, alactic	Very limited	Very fast
Glycogen or glucose	Anaerobic, lactic	limited	fast
Glucose or glycogen	Aerobic, alactic	limited	slow
Fatty acids	Aerobic, alactic	unlimited	sluggish

Reference:

Training Lactate Pulse-Rate by Peter GJM Janssen

Parkinson’s disease

2010-05-22T20:59:00.000+07:00

MedlinePlus Topics

Parkinson's disease is a disorder of the brain that leads to shaking (tremors) and difficulty with walking, movement, and coordination.

Causes

Parkinson's disease was first described in England in 1817 by Dr. James Parkinson. The disease most often develops after age 50. It is one of the most common nervous system disorders of the elderly. Sometimes Parkinson's disease occurs in younger adults, but is rarely seen in children. It affects both men and women.

In some cases, Parkinson's disease occurs in families. When a young person is affected, it is usually because of a form of the disease that runs in families.

Nerve cells use a brain chemical called dopamine to help control muscle movement. Parkinson's disease occurs when the nerve cells in the brain that make dopamine are slowly destroyed. Without dopamine, the nerve cells in that part of the brain cannot properly send messages. This leads to the loss of muscle function. The damage gets worse with time. Exactly why the brain cells waste away is unknown. Parkinson's in children may occur because the nerves are not as sensitive to dopamine. Parkinson's is rare in children.

The term "parkinsonism" refers to any condition that involves the types of movement changes seen in Parkinson's disease. Parkinsonism may be caused by other disorders (such as secondary parkinsonism) or certain medications.

Symptoms

The disorder may affect one or both sides of the body. How much function is lost can vary.

Symptoms may be mild at first. For instance, the patient may have a mild tremor or a slight feeling that one leg or foot is stiff and dragging.

Symptoms include:

Automatic movements (such as blinking) slow or stop
Constipation
Difficulty swallowing
Drooling
Impaired balance and walking
Lack of expression in the face (mask-like appearance)
Muscle aches and pains (myalgia)
Problems with movement

Difficulty starting or continuing movement, such as starting to walk or getting out of a chair
Loss of small or fine hand movements (writing may become small and difficult to read, and eating becomes harder)
Shuffling gait
Slowed movements

Rigid or stiff muscles (often beginning in the legs)
Shaking, tremors

Tremors usually occur in the limbs at rest, or when the arm or leg is held out
Tremors go away during movement
Over time, tremor can be seen in the head, lips, tongue, and feet
May be worse when tired, excited, or stressed
Finger-thumb rubbing (pill-rolling tremor) may be present

Slowed, quieter speech and monotone voice
Stooped position

Other symptoms:

Anxiety, stress, and tension
Confusion
Dementia
Depression
Fainting
Hallucinations
Memory loss
Oily skin (seborrhea)

Exams and Tests

The health care provider may be able to diagnose Parkinson's disease based on your symptoms and a physical examination. However, the symptoms can be difficult to assess, particularly in the elderly. The signs (tremor, change in muscle tone, problems walking, unsteady posture) become more clear as the illness progresses.

An examination may show:

Difficulty starting or finishing voluntary movements
Jerky, stiff movements
Muscle atrophy
Parkinson's tremors
Variation in heart rate

Reflexes should be normal.

Tests may be needed to rule out other disorders that cause similar symptoms.

Treatment

There is no known cure for Parkinson's disease. The goal of treatment is to control symptoms.

Medications control symptoms, mostly by increasing the levels of dopamine in the brain. At certain points during the day, the helpful effects of the medication often wears off, and symptoms can return. Your doctor need to be change the:

Type of medication
Dose
Amount of time between doses
How the medications are taken

Work closely with your doctors and therapists to adjust the treatment program. Never change or stop taking any medications without talking with your doctor.

Many medications can cause severe side effects, including hallucinations, nausea, vomiting, diarrhea, and delirium. Monitoring and follow-up by the health care provider is important.

Eventually, symptoms such as stooped posture, frozen movements, and speech difficulties may not respond very well to drug treatment.

Medications used to treat symptoms of Parkinson's disease are:

Levodopa (L-dopa), Sinemet, levodopa and carbidopa (Atamet)
Pramipexole (Mirapex), ropinirole (Requip), bromocriptine (Parlodel)
Selegiline (Eldepryl, Deprenyl), rasagiline (Azilect)
Amantadine or anticholinergic medications -- to reduce early or mild tremors
Entacapone -- to prevent the breakdown of levodopa

Lifestyle changes that may be helpful for Parkinson's disease:

Good general nutrition and health
Exercising, but adjusting the activity level to meet changing energy levels
Regular rest periods and avoiding stress
Physical therapy, speech therapy, and occupational therapy
Railings or banisters placed in commonly used areas of the house
Special eating utensils
Social workers or other counseling services to help you cope with the disorder and get assistance (such as Meals-on-Wheels)

Less commonly, surgery may be an option for patients with very severe Parkinson's disease who no longer respond to many medications. These surgeries do not cure Parkinson's, but may help some patients:

In deep brain stimulation (DBS), the surgeon implants electrical stimulators in specific areas of the brain to help with movement.
Another type of surgery destroys brain tissues that cause Parkinson's symptoms.

Support Groups

Support groups may help you cope with the changes caused by the disease.

See: Parkinson's disease - support group

Outlook (Prognosis)

Untreated, the disorder will get worse until a person is totally disabled. Parkinson's may lead to a deterioration of all brain functions, and an early death.

Most people respond to medications. How much the medications relieve symptoms, and for how long can be very different in each person. The side effects of medications may be severe.

Possible Complications

Difficulty performing daily activities
Difficulty swallowing or eating
Disability (differs from person to person)
Injuries from falls
Pneumonia from breathing in (aspirating) saliva
Side effects of medications

When to Contact a Medical Professional

Call your health care provider if:

You have symptoms of Parkinson's disease
Symptoms get worse
New symptoms occur

Also tell the health care provider about medication side effects, which may include:

Changes in alertness, behavior or mood
Delusional behavior
Dizziness
Hallucinations
Involuntary movements
Loss of mental functions
Nausea and vomiting
Severe confusion or disorientation

Also call your health care provider if the condition gets worse and home care is no longer possible.

Alternative Names

Paralysis agitans; Shaking palsy

References

Lang AE. When and how should treatment be started in Parkinson disease? Neurology. 2009;72(7 Suppl):S39-43.

Miyasaki JM, Shannon K, Voon V, Ravina B, Kleiner-Fisman G, Anderson K, et al. Practice Parameter: evaluation and treatment of depression, psychosis, and dementia in Parkinson's disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;66:996-1002.

Pahwa R, Factor SA, Lyons KE, Ondo WG, Gronseth G, Bronte-Stewart H, et al. Practice Parameter: treatment of Parkinson disease with motor fluctuations and dyskinesia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;66:983-995.

Suchowersky O, Reich S, Perlmutter J, Zesiewicz T, Gronseth G, Weiner WJ. Quality Standards Subcommittee of the American Academy of Neurology. Practice Parameter: diagnosis and prognosis of new onset Parkinson disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006.66:968-975.

Weaver FM, Follett K, Stern M, et al. Bilateral deep brain stimulation vs best medical therapy for patients with advanced Parkinson disease: a randomized controlled trial. JAMA. 2009;301(1):63-73.

Update Date: 7/4/2009

Updated by: Daniel B. Hoch, PhD, MD, Assistant Professor of Neurology, Harvard Medical School, Department of Neurology, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

Exercises For The Parkinson Patient

2010-05-20T21:11:00.000+07:00

Just as running water does not freeze, so moving muscles do not freeze.

Know the facts. The maintenance of normal muscle tone and function is an important aspect of the treatment of parkinsonism. In part, medication administered for your illness achieves this goal. However, to realize the full benefit of the medication daily exercise and activity are essential. This booklet outlines some of the exercises capable of maintaining muscle power and tone and preventing deformities of the limbs and spine. Their daily performance has proved most beneficial to patients with this illness.

TEN BASIC EXERCISES FOR THE PARKINSON PATIENT

1. Bring the toes up with every step you take. In Parkinson's disease, "you never make a move", without lifting the toes.

2. Spread the legs (10 inches) when walking or turning, to provide a wide base, a better stance, and to prevent falling. It may not look "beautiful," but neither does falling.

3. For greater safety in turning, use small steps, with feet widely separated. Never cross one leg over the other when turning. Practice walking a few yards and turn. Walk in the opposite direction and turn. Do so fifteen minutes a day.

4. Practice walking into tight corners of a room, to overcome fear of close places.

5. To insure good body balance, practice rapid excursions of the body. Backward, forward and to the right and left, five minutes, several times a day. Don't look for a wall when you think you are falling. It may not be there. Your body will always be there to protect you, if you will practice balance daily.

6. When the legs feel frozen or "glued" to the floor, a lift of the toes eliminates muscle spasm and the fear of falling. You are free to walk again.

7. Swing the arms freely when walking. It helps to take body weight off the legs, lessens fatigue, and loosens the arms and shoulders.

8. If getting out of a chair is difficult, rise with "lightning speed," to overcome the "pull of gravity." Sitting down should be done slow, with body bent sharply forward, until one touches the seat. Practice this at least a dozen times a day.

9. If the body lists to one side, carry a shopping bag loaded with books or other weights in the opposite hand to decrease the bend.

10. Any task that is difficult, such as buttoning a shirt. or getting out of bed, if practiced 20 times it day, becomes easier the 21st time.

FOR TIGHT MUSCLES AND POOR POSTURE

STANDING

1. Stand ln front of a wall, facing it about 8" away. Raise arms and reach as high as possible toward the top of the wall. Lean toward the wall and stretch.

2. With your back to the wall, alternate raising legs as high as possible by bending the knee as if marching in place.

3. Holding on to something secure, squat down as far as possible, bending knees; then come up.

SITTING

1. Sitting in straight-back chair, place your arms behind the chair and bring your shoulders back as far as possible; raise your head up and look at the ceiling.

2. Sitting In the same chair, grip the ends of a broom or mop stick with both hands, try to raise it over your head until you get it behind your head. Keep head and shoulders as erect as possible.

3. Sitting in same chair, place one leg at a time on another chair and press the knee straight. Keep it there 15 minutes. Try both legs together.

4. Sitting in a chair, raise legs up from the knee alternately, as if stamping your feet.

LYING ON A FIRM BED OR FLOOR

1. Lie on the floor or bed, flat on your back; try to press your body to the floor as flat as possible. Move your head from right to left as far as possible. Make sure your head, shoulders, back, and knees touch the surface.

2. Lie on the floor or bed on your abdomen. Do the following one by one:

Put your hands behind back and look up to ceiling, trying to raise your chest off the floor.
Kick your legs alternately, as if swimming.
Turn your head from right to left.

FOR BETTER BALANCE

1. Stand with hands on hips, feet spread apart:

Practice marching in place
Practice raising leg straight out to the rear.
Practice raising leg out to the side.
Practice drawing a circle with the leg.

2. Standing with hands at side, feet spread apart:

Lean forward and back
Lean to both sides
Lean in a circular motion and reverse the motion

FOR WALKING

1. When walking, REMEMBER:

Take as large a step as possible
Raise your toes as you step forward, hitting ground with your heels
Keep legs apart and posture straight
Swing arms and look straight ahead - your feet know where the floor is located.

2. Collect a dozen magazines; lay them out in a straight line. Space them so that you can take as long a step as possible. Practice walking over these magazines without stepping on them.

3. For a better swing to arms, walk holding a rolled magazine in each hand; keep elbows straight.

4. Practice walking sideways, backwards, and take big steps.

FOR TURNING

1. When practicing turning:

Keep feet spread-apart and head high
Use small steps; rock front side to side
Raise legs from the knees

2. If you feel glued to the floor:

Raise your head, relax back on your heels and raise your toes
Rock from side to side, bend knees slightly and straighten up and lift your toes
It sometimes helps if the arms are raised in a sudden short motion

FOR GETTING IN AND OUT OF A CHAIR

1. If you become glued a few steps before you reach the chair, try this: Don't aim for the chair but some object past it. Pass the chair as closely as possible and as you go by it sit down.

2. To sit down, bend forward as far as possible and sit down slowly. Get close to the chair. Do not fall into the chair.

3. To get up, move to the edge of the chair, bend forward and push up vigorously using your arms; try to count 1 2 3 GO! If you have a favorite armchair, raise the back legs with 4" blocks. This will help you to get up easily. Don't let people drag you up by your arms, but help you by pulling you under your arms, or with a slight push on your back.

FOR GETTING OUT OF BED

1. Place blocks under the legs of the head of the bed. This will elevate the head of the bed, & make it easier for you to sit up and swing the legs off the bed.

2. A knotted rope tied to the foot of the bed can help you to pull yourself up.

3. To get to a sitting position, shift the body down and rock yourself by vigorously, throwing your arms and legs toward the side of the bed.

FOR USING YOUR ARMS AND HANDS

1. Practice buttoning and unbuttoning your clothes; practice cutting food and writing. Squeeze a ball or work with "Silly Putty." Keep your fingers busy many times a day. Tear paper; take coins out of the pocket; play the piano.

2. Always try to dress yourself completely. Use shoehorns, elastic laces, or extra-long shoelaces to get a better grip. Dress in the most relaxed and comfortable position, sitting or standing, but make sure you are in a safe position.

3. To keep elbows straight and shoulders loose, install a pulley in doorway, place a chair under it or slightly in front. Stretch your arms and shoulders in all directions. By working the pulley when seated, you can get a more vigorous pull.

FOR GREATER SAFETY IN BATHTUB AND TOILET

If it is difficult to sit down in a bathtub, try the following:

1. Place a bench, stool or chair inside the tub; have the legs sawed off to tub height. Sit on the chair and soap yourself. Use shower to rinse, or rubber shower extension.

2. Bathtub grab bars are available. Purchase only those that attach securely.

3. Raised toilet seats are commercially available.

4. Toilet armrest for getting on and off the toilet are available.

FOR SPEECH, FACE AND CHEWING DIFFICULTIES

1. Practice singing and reading aloud with forceful lip movements. Talk into a tape recorder, if one is available.

2. Practice making faces in front of a mirror. Recite the alphabet and count numbers with exaggerated facial motions. Massage your face with vigor when washing and bathing.

3. When chewing food, chew hard and move the food around; avoid swallowing large lumps.

The previously outlined general exercises and suggestions are designed to help you. They are ancillary to medical treatment which should be carried out in consultation with your physician. In special instances where other diseases are associated with parkinsonism, your physician may wish to limit the intensity of your physical activity. Conversely, more intensive physical therapy may be indicated and in some instances should be done under the direction of a physical therapist.

All activities possible should be engaged in: work, walking, shopping, house chores, gardening, visiting, senior clubs, church organizations, travel, theater, swimming, sports, gymnasium, health clubs, "Y" activities, etc.

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