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Sjogren’s (SHOW-grins) syndrome is a disorder of your immune system identified by its two most common symptoms — dry eyes and a dry mouth.

The condition often accompanies other immune system disorders, such as rheumatoid arthritis and lupus. In Sjogren’s syndrome, the mucous membranes and moisture-secreting glands of your eyes and mouth are usually affected first — resulting in decreased tears and saliva.

Although you can develop Sjogren’s syndrome at any age, most people are older than 40 at the time of diagnosis. The condition is much more common in women. Treatment focuses on relieving symptoms.

epidemiology

Internationally, comparative studies between different ethnic groups have suggested that Sjögren syndrome is a homogeneous disease that occurs worldwide with similar prevalence and affects 1-2 million people.

The female-to-male ratio of Sjögren syndrome is 9:1. Sjögren syndrome can affect individuals of any age but is most common in elderly people. Onset typically occurs in the fourth to fifth decade of life.

Symptoms

The two main symptoms of Sjogren’s syndrome are:

• Dry eyes. Your eyes might burn, itch or feel gritty — as if there’s sand in them.
• Dry mouth. Your mouth might feel like it’s full of cotton, making it difficult to swallow or speak.

Some people with Sjogren’s syndrome also have one or more of the following:

• Joint pain, swelling and stiffness
• Swollen salivary glands — particularly the set located behind your jaw and in front of your ears
• Skin rashes or dry skin
• Vaginal dryness
• Persistent dry cough
• Prolonged fatigue

Causes

Sjogren’s syndrome is an autoimmune disorder. Your immune system mistakenly attacks your body’s own cells and tissues.

Scientists aren’t certain why some people develop Sjogren’s syndrome. Certain genes put people at higher risk of the disorder, but it appears that a triggering mechanism — such as infection with a particular virus or strain of bacteria — is also necessary.

In Sjogren’s syndrome, your immune system first targets the glands that make tears and saliva. But it can also damage other parts of your body, such as:

• Joints
• Thyroid
• Kidneys
• Liver
• Lungs
• Skin
• Nerves

Prognosis

Sjögren syndrome carries a generally good prognosis. In patients who develop a disorder associated with Sjögren syndrome, the prognosis is more closely related to the associated disorder (eg, SLE, lymphoma). Interestingly, primary Sjögren syndrome is associated with lower cardiovascular risk factors and lower risk of serious cardiovascular events such as myocardial infarction and stroke, in comparison with SLE.​ 

Although salivary and lacrimal function generally stabilize, the presence of SSA and/or hypocomplementemia may predict a decline in function.

Morbidity and mortality

Morbidity associated with Sjögren syndrome is mainly associated with the gradually decreased function of exocrine organs, which become infiltrated with lymphocytes. The increased mortality rate associated with the condition is primarily related to disorders commonly associated with Sjögren syndrome, such as SLE, RA, and primary biliary cirrhosis. Patients with primary Sjögren syndrome who do not develop a lymphoproliferative disorder have a normal life expectancy. 

Risk factors

Sjogren’s syndrome typically occurs in people with one or more known risk factors, including:

• Age. Sjogren’s syndrome is usually diagnosed in people older than 40.
• Sex. Women are much more likely to have Sjogren’s syndrome.
• Rheumatic disease. It’s common for people who have Sjogren’s syndrome to also have a rheumatic disease — such as rheumatoid arthritis or lupus.

Complications

The most common complications of Sjogren’s syndrome involve your eyes and mouth.

• Dental cavities. Because saliva helps protect the teeth from the bacteria that cause cavities, you’re more prone to developing cavities if your mouth is dry.
• Yeast infections. People with Sjogren’s syndrome are much more likely to develop oral thrush, a yeast infection in the mouth.
• Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal damage.

Less common complications might affect:

• Lungs, kidneys or liver. Inflammation can cause pneumonia, bronchitis or other problems in your lungs; lead to problems with kidney function; and cause hepatitis or cirrhosis in your liver.
• Lymph nodes. A small percentage of people with Sjogren’s syndrome develop cancer of the lymph nodes (lymphoma).
• Nerves. You might develop numbness, tingling and burning in your hands and feet (peripheral neuropathy).

History

The clinical presentation of Sjögren syndrome may vary. Most patients are women, and onset is usually at age 40-60 years, but the syndrome also can affect men and children. The onset is insidious. The first symptoms in primary Sjögren syndrome can be easily overlooked or misinterpreted, and diagnosis can be delayed for as long as several years.

Xerophthalmia (dry eyes) and xerostomia (dry mouth) are the main clinical presentations in adults. Bilateral parotid swelling is the most common sign of onset in children.

Extraglandular involvement in Sjögren syndrome falls into two general categories: periepithelial infiltrative processes and extraepithelial extraglandular involvement. Periepithelial infiltrative processes include interstitial nephritis, liver involvement, and bronchiolitis and generally follow a benign course.

Extraepithelial extraglandular involvement in Sjögren syndrome is related to B-cell hyperreactivity, hypergammaglobulinemia, and immune complex formation and includes palpable purpura, glomerulonephritis, and peripheral neuropathy. These latter manifestations occur later in the course of Sjögren syndrome and are associated with a higher risk of transformation to lymphoma.

Symptoms of Sjögren syndrome can decrease the patient’s quality of life in terms of its physical, psychological, and social aspects.

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Sicca symptoms (dry eyes and dry mouth)

Although dry eyes and dry mouth are the most common symptoms in patients with Sjögren syndrome, most patients who report these symptoms have other underlying causes. The incidence of sicca symptoms increases with age. Indeed, more than one third of elderly persons have sicca symptoms. Whether this is part of the normal aging process (associated with fibrosis and atrophy observed on some lip biopsy studies) or is due to the accumulation of associated illnesses and medications is unclear. 

Common medications that can cause sicca symptoms in any age group include antidepressants, anticholinergics, beta blockers, diuretics, and antihistamines. Anxiety can also lead to sicca symptoms. Women who use hormone replacement therapy may be at increased risk of dry eye syndrome. 

Patients may describe the effects dry mouth in the following ways:

• Inability to eat dry food (eg, crackers) because it sticks to the roof the mouth
• Tongue sticking to the roof of the mouth
• Putting a glass of water on the bed stand to drink at night (and resulting nocturia)
• Difficulty speaking for long periods of time or the development of hoarseness
• Higher incidence of dental caries and periodontal disease
• Altered sense of taste
• Difficulty wearing dentures
• Development of oral candidiasis with angular cheilitis, which can cause mouth pain

Dry eyes may be described as red, itchy, and painful. However, the most common complaint is that of a gritty or sandy sensation in the eyes. Symptoms typically worsen throughout the day, probably due to evaporation of the already scanty aqueous layer. Some patients awaken with matting in their eyes and, when severe, have difficulty opening their eyes in the morning. Blepharitis can also cause similar morning symptoms.

Parotitis

Patients with Sjögren syndrome may have a history of recurrent parotitis, often bilateral. Although in some patients the parotid glands become so large that the patients report this as a problem, more often the examining physician discovers them.

Cutaneous symptoms

Nonvasculitic cutaneous manifestations in Sjögren syndrome include the following  :

• Dryness
• Eyelid dermatitis
• Pruritus
• Erythema annulare

Cutaneous vasculitis, such as palpable purpura, develops in some patients with Sjögren syndrome, especially those with hypergammaglobulinemia or cryoglobulinemia.  Raynaud phenomenon is observed in approximately 20% of patients.

Pulmonary symptoms

Patients with Sjögren syndrome can develop dryness of the tracheobronchial mucosa (xerotrachea), which can manifest as a dry cough.  Less often, patients develop dyspnea from an interstitial lung disease that is typically mild. Patients may develop recurrent bronchitis or even pneumonitis (infectious or noninfectious).

Gastrointestinal symptoms

Dryness of the pharynx and esophagus frequently leads to difficulty with swallowing (deglutition), in which case patients usually describe food becoming stuck in the upper throat.  Lack of saliva may lead to impaired clearance of acid and may result in gastroesophageal reflux and esophagitis.

Abdominal pain and diarrhea can occur. Rarely, patients develop acute or chronic pancreatitis, as well as malabsorption due to pancreatic insufficiency. However, caution is advised when interpreting laboratory results because an elevated amylase level may arise from the parotid gland.

Patients with gastritis should be tested for Helicobacter pylori infection, because of its association with gastric mucosa–associated lymphoid tissue lymphomas.

Patients with Sjögren syndrome are at increased risk for delayed gastric emptying, which can cause early satiety, upper abdominal discomfort, nausea, and vomiting. 

Cardiac symptoms

Pericarditis and pulmonary hypertension, with their attendant symptomatology, can occur in Sjögren syndrome.  Orthostatic symptoms related to dysfunction of autonomic control of blood pressure and heart rate is associated with increased severity of Sjögren syndrome. 

Neurologic symptoms

The occurrence of central nervous system (CNS) and spinal cord involvement in Sjögren syndrome is estimated by various studies to be 8-40%, with manifestations including myelopathy, optic neuropathy, seizures, cognitive dysfunction, and encephalopathy.  Attempts must be made to distinguish other causes of these symptoms, including concomitant SLE, multiple sclerosis, cerebrovascular disease, and Alzheimer disease.

Sensory, motor, or sensorimotor peripheral neuropathy, often subclinical, can be detected in up to 55% of unselected patients with Sjögren syndrome.  Symptoms of distal paresthesias may be present. Cranial neuropathies can develop, particularly trigeminal neuropathy or facial nerve palsy. Mononeuritis multiplex should prompt a search for a vasculitis.

Progressive weakness and paralysis secondary to hypokalemia due to underlying renal tubular acidosis can occur and is potentially treatable. 

Renal symptoms

Renal calculi, renal tubular acidosis, and osteomalacia, nephrogenic diabetes insipidus, and hypokalemia can occur secondary to tubular damage caused by interstitial nephritis, the most common form of renal involvement in Sjögren syndrome.

Interstitial cystitis, with symptoms of dysuria, frequency, urgency, and nocturia, is strongly associated with Sjögren syndrome. 

Glomerulonephritis can be caused by Sjögren syndrome but is uncommon and is usually attributable to another disorder, such as SLE or mixed cryoglobulinemia.

Additional symptoms

Nasal dryness can result in discomfort and bleeding. Women may also have a dry vagina, which can lead to dyspareunia, vaginitis, and pruritus.

Patients with Sjögren syndrome may report fatigue, joint pain, and, sometimes, joint swelling. A careful review of systems must be performed to differentiate these from the manifestations of other disorders (see DDx). Fibromyalgia is common in patients with Sjögren syndrome, with a prevalence of about 31%. 

Women with Sjögren syndrome may have a history of recurrent miscarriages or stillbirths, and women and men may have a history of venous or arterial thrombosis. These are related to the presence of antiphospholipid antibodies (eg, lupus anticoagulant or anticardiolipin antibodies).

Secondary Sjogren syndrome

Secondary Sjögren syndrome appears late in the course of the primary disease. However, in some patients, primary Sjögren syndrome may precede SLE by many years. Secondary Sjögren syndrome is usually mild, and sicca symptoms are the main feature. Unlike patients with primary Sjögren syndrome, persons with the secondary type have significantly fewer systemic manifestations. These manifestations include the following:

• Salivary gland swelling
• Lung involvement
• Nervous system involvement
• Renal involvement
• Raynaud phenomenon
• Lymphoproliferative disorders

In secondary Sjögren syndrome, symptoms of the primary disease predominate. Secondary Sjögren syndrome does not modify the prognosis or outcome of the basic disease. Polyarteritis nodosa and Sjögren syndrome may also coexist, perhaps best viewed as an overlap syndrome. 

Approach Considerations

No curative agents for Sjögren syndrome exist. The treatment of the disorder is essentially symptomatic.

Skin and vaginal dryness

Patients should use skin creams, such as Eucerin, or skin lotions, such as Lubriderm, to help with dry skin. Vaginal lubricants, such as Replens, can be used for vaginal dryness. Vaginal estrogen creams can be considered in postmenopausal women. Watch for and treat vaginal yeast infections.

Arthralgias and arthritis

Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) can be taken for arthralgias. Consider hydroxychloroquine if NSAIDs are not sufficient for the synovitis occasionally associated with primary Sjögren syndrome. However, hydroxychloroquine does not relieve sicca symptoms. Patients with RA associated with Sjögren syndrome likely require other disease-modifying agents.

Additional treatment considerations

In patients with major organ involvement, such as lymphocytic interstitial lung disease, consider therapy with steroids and immunosuppressive agents, such as cyclophosphamide.

While cyclophosphamide and similar agents may be helpful for treating serious manifestations of Sjögren syndrome or disorders associated with Sjögren syndrome, clinicians should understand that these agents are also associated with the development of lymphomas.

Long-term anticoagulation may be needed in patients with vascular thrombosis related to antiphospholipid antibody syndrome.

In a small group of patients with primary Sjögren syndrome, mycophenolate sodium reduced subjective, but not objective, ocular dryness and significantly reduced hypergammaglobulinemia and RF.

Among the biologic therapies, the greatest experience in primary Sjögren syndrome is with rituximab, an anti-CD20 (which is expressed on B-cell precursors) monoclonal antibody. Anti-B–cell strategies, particularly rituximab, have a promising effect in the treatment of patients with severe extraglandular manifestations of Sjögren syndrome.

Reports on the use of rituximab in patients with primary Sjögren syndrome have emerged in the literature. In a double-blind, randomized, placebo-controlled trial, Meijer et al found that rituximab significantly improved saliva flow rate, lacrimal gland function, and other variables in patients with primary Sjögren syndrome.

In an open-label clinical trial, modest improvements were noted in patient-reported symptoms of fatigue and oral dryness. However, no significant improvement in the objective measures of lacrimal and salivary gland function was noted, despite effective depletion of blood B cells. In a randomized, placebo-controlled, parallel-group study of 120 patients with primary Sjögren syndrome, treatment with rituximab did not alleviate disease activity or symptoms at week 24, although it did alleviate some symptoms at weeks 6 and 16. 

Rituximab appears promising in the treatment of vasculitis and intravenous immunoglobulin (IVIG)–dependent ataxic neuropathy. Results from the AIR registry (French) indicated that rituximab appears to be effective in cryoglobulinemia or vasculitis-related peripheral nervous system involvement in primary Sjögren syndrome.

In a prospective study of 78 patients with primary Sjögren syndrome treated with rituximab, significant improvement in extraglandular manifestations was reported, as measured by EULAR [European League Against Rheumatism] Sjögren Syndrome Disease Activity Index (ESSDAI) (disease activity score) and overall good tolerance reported.  Several smaller studies of rituximab revealed improvement of arthralgias, regression of parotid gland swelling, and improvement of immune-related thrombocytopenia.

Of the TNF inhibitors, both etanercept and infliximab have failed to demonstrate significant benefit in Sjögren syndrome.

Combination therapy with leflunomide and hydroxychloroquine resulted in a significant decrease in ESSDAI scores and caused no serious adverse events, in a small phase 2a randomized clinical trial from the Netherlands. At 24 weeks, the mean difference in ESSDAI score in the leflunomide-hydroxychloroquine group (n=21), compared with the placebo group (n=7), was –4.35 points after adjustment for baseline values.

Fewer data are available with regard to the role of anti-CD22, anti-BAFF, anti-IL-1, type 1 interferon, and anti-T–cell agents in treatment of primary Sjögren syndrome, with further investigations ongoing. The overall paucity of evidence in therapeutic studies in primary Sjögren syndrome suggests that much larger trials of the most promising therapies are necessary. The investigators concluded that further evaluation of leflunomide–hydroxychloroquine combination therapy in larger clinical trials is warranted.

Emergency department care

The diagnosis of Sjögren syndrome can be made from the ED if the index of suspicion is high. Patients may present with mild symptoms (eg, eye grittiness, eye dryness or discomfort, dry mouth, recurrent caries). Bilateral parotid gland swelling is also a common presentation.

Patients with known Sjögren syndrome should not be taken lightly for their complaint of dry eyes or dry mouth, as these chronic problems can be very distressing and obtrusive.

Inpatient care

Give attention to artificial lubricants and humidified oxygen for intubated and/or sedated patients with Sjögren syndrome.

Outpatient care

Encourage patients with Sjögren syndrome to be active. In addition, patients should be encouraged to avoid exacerbation of dryness symptoms (eg, through smoking or exposure to low-humidity environments). All patients with Sjögren syndrome should be monitored by an ophthalmologist and dentist, in addition to their rheumatologist. Certain patients may be candidates for punctal occlusion, which is usually performed by an ophthalmologist.

Monitoring

Most patients with Sjögren syndrome can be monitored at follow-up visits every 3 months and, if the patient is stable, up to every 6 months. Patients with active problems or in whom an emerging associated illness is a concern can be seen as often as monthly.

Surgical Therapy

Occlusion of the lacrimal puncta can be corrected surgically. Electrocautery and other techniques can be used for permanent punctal occlusion.

During surgery, the anesthesiologist should administer as little anticholinergic medication as possible and use humidified oxygen to help avoid inspissation of pulmonary secretions. Good postoperative respiratory therapy should also be provided. Patients are at higher risk for corneal abrasions, so ocular lubricants should be considered.

Biopsies that may be performed in association with Sjögren syndrome include the following:

• Minor salivary gland biopsy – For diagnostic purposes
• Parotid gland biopsy – If malignancy is suggested
• Biopsy of an enlarged lymph node – To help rule out pseudolymphoma or lymphoma

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Acute disseminated encephalomyelitis (ADEM) is a rare kind of inflammation that affects the brain and spinal cord, usually in children. It damages the coating that protects nerve fibers, called myelin.

Symptoms may be severe, but they can be treated. Most people make a full recovery and don’t have another attack.

Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory demyelinating condition that predominately affects the white matter of the brain and spinal cord. The disorder manifests as an acute-onset encephalopathy associated with polyfocal neurologic deficits and is typically self-limiting.  ADEM bears a striking clinical and pathological resemblance to other acute demyelinating syndromes (ADS) of childhood, including multiple sclerosis (MS). ADEM in children is readily distinguishable from alternative diagnoses on the basis of clinical features and findings on neuroimaging and laboratory investigations. However, given that ADEM lacks a specific identified biological marker rendering a reliable laboratory diagnosis, long-term follow-up is important as there are instances where an illness initially diagnosed as ADEM is ultimately replaced with a diagnosis of MS. 

The onset of ADEM usually occurs in the wake of a clearly identifiable febrile prodromal illness or immunization and in association with prominent constitutional signs and encephalopathy of varied degrees. ADEM is typically a monophasic disease of pre-pubertal children; whereas, MS is typically a chronic relapsing and remitting disease of young adults. Abnormalities of findings on cerebrospinal fluid (CSF) immunoglobulin studies are less common in ADEM. However, the division between these processes is indistinct, suggesting a clinical continuum. Moreover, other conditions along the suggested continuum include optic neuritis, transverse myelitis, and neuromyelitis optica – clinical entities that may occur as manifestations of either MS or ADEM. ^[2] Other boundaries of ADEM merge indistinctly with a wide variety of inflammatory encephalitic and vasculitic illnesses as well as monosymptomatic, postinfectious illnesses that should remain distinctfromADEM, such as acute cerebellar ataxia (ACA). A furtherindistinct boundary is shared by ADEM and Guillain-Barré syndrome as manifested in cases of Miller-Fisher syndrome and encephalomyeloradiculoneuropathy (EMRN).

Susceptibility to either ADEM or MS is likely the product of multiple factors, including a complex interrelationship of genetics and exposure to infectious agents and other environmental factors. Of particular interest are the indications that susceptibility to either condition is in part age-related. Most cases of ADEM possibly occur as the result of an inflammatory response provoked by pre-pubertal infection with a virus, vaccine, or other infectious agent. Typically, the manifestations of ADEM occur quickly after this pre-pubertal febrile systemic illness and are monophasic. In a minority of cases, patients with ADEM experience one or two pre-pubertal recurrences followed by remission. MS, on the other hand, typically manifests as a relapsing-remitting illness in ensuing adolescence or young adulthood, a significant and unexplained latency of effect with apparent permanency of immune dysregulation. Bouts of MS occur without a febrile prodrome. Uncommonly, MS develops in pre-pubertal individuals andADEMdevelops in post-pubertal individuals. In very rare instances, individuals manifest pre-pubertal ADEM and, after long latency, MS in adolescence.

epidemiology

Few studies have provided incidence data from other countries, thus little is known about occurrence throughout the world. Genetic factors, prevalence of infectious pathogens, immunization status, degree of skin pigmentation, diet, and other factors may influence risk.

History

Clinically, acute disseminated encephalomyelitis (ADEM) is usually readily distinguishable from multiple sclerosis (MS) by the presence of certain clinical features, including the following:

• History of preceding infectious illness or immunization, although a clear preceding event may be absent in up to a quarter of patients. 
• Association with constitutional symptoms and signs, such as fever
• Prominence of cortical signs such as mental status changes and seizures
• Comparative rarity of posterior column abnormalities, which are common in MS
• Age younger than 11-12 years in ADEM and age older than 11-12 years in MS

ADEM is more common in the winter months, with most cases occurring between October and March. Typical cases of ADEM arise 1-2 days to several weeks after a childhood infectious illness.

• There is usually a clearly defined phase of afebrile improvement lasting 2-21 days or more before onset of neurologic findings.
• Generally, patients have shown partial or complete recovery from the prodromal illness at the time of onset of ADEM.
• Whether latencies of longer than 21 days implicate a particular febrile illness as the prodrome of ADEM is unclear. Clinical experience suggests that this is possible.
• Most of the large envelope-bearing viruses that figured prominently in older series of ADEM, of which measles was a particularly virulent example, no longer figure importantly in the etiology of ADEM because these diseases are prevented by vaccination.
• Most cases encountered now occur in the wake of respiratory or gastrointestinal illness presumed to be of viral etiology, although a specific virus is seldom identified.
• Documentation of at least 1 fever-free day is especially suggestive of ADEM, although such a hiatus is also found in post-infectious vasculitides.
• Occasionally, ADEM may occur in the wake of several weeks of fever of unknown origin.
• Some patients have premonitory pain in the back prior to the development of ADEM-related inflammatory myelitis.
• Various vaccines have been suggested as the exogenous provocation of cases of ADEM.
  • This remains a controversial subject, although clear evidence exists for the role of the Pasteur rabies vaccine and compelling, although somewhat less conclusive evidence exists for the role of other vaccines.
  • The overall effect of the introduction of vaccinations for measles and other encephalomyelitogenic viruses has been a marked reduction in the number of severe or fatal cases of ADEM.
  • Measles was associated with ADEM in about 1 out of 800 cases, and in many of these cases, ADEM that was often particularly severe. Measles-associated ADEM had a high rate of both morbidity and mortality.
• A cause-and-effect relationship between a possible prodrome and ADEM is more difficult to establish in cases where longer or very short intervals exist between a possible exogenous stimulus and inflammatory result.
  • Latencies longer than 50 days have been suggested for infections or vaccines but are difficult to prove. 
  • Relationships are also difficult to determine when a febrile systemic process is rapidly followed by neurologic deterioration because such cases may represent meningoencephalitis.
    • Approximately 25% of cases lack a clearly-defined prodrome.
    • Some of these cases are possible examples of longer than 20 days of latency from prodrome to ADEM, especially in prepubertal children, with imaging changes suggesting ADEM, with negative CSF immune profile, and with rapid and complete recovery.
    • Another subgroup with poorly-defined prodrome but low risk for recurrence are children or adolescents manifesting subacute-onset syndromes that combine neuropsychiatric abnormalities and movement disorders and imaging changes suggestive of ADEM. The course in these cases, which could be termed Johnson syndrome, is often prolonged or even progressive, improving with high-dose intravenous corticosteroids.

The first signs of ADEM usually include abrupt onset encephalopathy (alteration in consciousness or behavioral change unexplained by fever, systemic illness or postictal symptoms. Rapid-onset encephalopathy is typically associated with multifocal neurologic symptoms.

• In most cases, the clinical course is rapidly progressive and typically develops over hours to maximum deficits within days (mean of 4.5 days). A minority of cases show continued deterioration of function for periods as long as 4 weeks.
• Strictly speaking, encephalopathy, unexplained by fever, should be present for a diagnosis of ADEM, though it may not be the presenting sign. A single institution follow-up study (at least 5.5 y for each individual) of 52 young individuals (age range 10 mo to 19 y) who presented with their first bout of an acute central nervous system demyelinating disease included 26 children ultimately diagnosed with MS and 24 diagnosed with ADEM. Encephalopathy was the presenting sign in 42% of those with a follow-up diagnosis of ADEM but none of the individuals with a follow-up diagnosis of MS. 
• Convulsive seizures occur around the onset of ADEM in as many as 35% of cases.
• Meningismus may be present and has been reported in up to 30% of cases.
• Although almost any portion of the CNS may be clinically involved, certain systems appear to be particularly prone to dysfunction; thus, the descending white matter motor tracts, optic nerves, and spinal cord are particularly commonly involved.
• ADEM-associated optic neuritis is typically bilateral, although the onset in a second eye may follow onset in the first by days to months. Bilaterality may provide a degree of reassurance with regard to MS risk as optic neuritis in MS is frequently unilateral. Visual evoked responses may discern abnormalities in a second eye before clinical deterioration in vision is discernible.
  • A wide variety of cranial nerve abnormalities may occur in addition to optic nerve disease.
  • Long tract signs (eg, clonus, increased muscle stretch reflexes, upgoing toes) are present early in as many as 85% of cases.
  • In some instances, reflexes may be lost at the onset. When this is caused by transverse myelitis, the evolution of disease after spinal shock replaces absent reflexes with increased muscle stretch reflexes within a few days or more. A small number of cases manifest loss of reflexes as a sign of associated peripheral nerve disease with ADEM, a condition termed EMRN. Some of these EMRN cases are associated with evidence for acute infection with Epstein-Barr virus.
    • Weakness may be hemiparetic, double hemiparetic, diparetic, or generalized and symmetric. Fairly symmetric leg weakness is seen in many cases of ADEM-related transverse myelitis with associated abnormalities of bowel and bladder function.

Some ADEM presentations are fulminant.

• Fulminant ADEM is more likely to manifest in children younger than 3 years, with rapid evolution of a low state of function and demonstration of severe edema on neuroimaging. Such cases have become uncommon with widespread vaccination against childhood illnesses.
• Transverse myelitis (TM) may begin rapidly and be associated with severe edema, usually in the cervical region. ADEM-related TM must be distinguished from TM associated with MS, vascular accidents, and directly infectious conditions, including enterovirus. It must also be distinguished from neuromyelitis optica (NMO), which may present with TM in isolation. NMO is a condition for which a biological marker (anti-AQP4 IgG in serum and/or CSF) has been identified.
  • Child/adolescent NMO represents approximately 5% of cases of NMO. Onset is a median range of 10-14 y and the vast majority of these patients are girls or young women. The median number of spinal levels involved is 10 vertebral segments.  Motor signs are usually more prominent than sensory signs. CNS lesions may be demonstrated on scans and mental status changes may be noted.
• Acute administration of very high-dose intravenous corticosteroids may possibly close the blood-brain barrier and subtend the development of edema, which may, in these fulminant cases, account for the high risk for permanent morbidity.

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There are unusual presentations for possible ADEM that have uncertain classification. More literature is supporting a continuum of acute demyelinating diseases in childhood and adulthood.

• Cases of pediatric patients diagnosed with neuromyelitis optica presenting with a clinical and radiographic evidence of ADEM have been reported. 
• Cases of patients with anti-NMDA receptor encephalitis and ADEM-like lesions on MRI have also been reported. 
• Additionally, pediatric cases of ADEM followed by recurrent or monophasic optic neuritis have been described. 
• Young children may manifest a rapidly progressive demyelinating illness that may be fatal within days to weeks and is almost universally associated with profound permanent psychomotor deficits in those who survive. Brain images differ from those typical of juvenile MS and may demonstrate confluent symmetric areas (butterfly pattern) of bright signal abnormality on T2-weighted sequences.
  • Fulminant presentation with lesions showing significant degrees of ring enhancement after contrast administration may also be found.
  • Malignant brain edema may be present, manifested by sulcal and ventricular effacement.
• Some patients with the large tumor-like lesions, acute MS, or Schilder disease presentations during childhood or adolescence do remarkably well as compared to adults with similar presentations.
• The classification of rare severe infantile cases, exhibiting features suggesting either severe acute MS or hyperacute ADEM, remains in doubt.
  • Nonetheless, pathological confirmation that some of these cases are MS has been published, and hyperacute adult cases with similar clinical and radiographic manifestations have been reported. 
  • Some of these cases display more generalized T2-weighted abnormalities on MRI and may represent cases of what has been referred to as acute toxic encephalopathy.
  • Emphasizing that scan results do not reliably distinguish every case of MS from ADEM is important, but in most cases, reliable inferences may be drawn. Extensive white matter involvement may be found in young infants that some would label as MS  while others would label it hyperacute ADEM.
• Rarely, childhood, adolescent, or adult MS manifests as large unilateral or multiple tumor-like mass lesions that may appear cystic and may impart mass effects (albeit atypically and, if present, unexpectedly mildly). The lesions are steroid responsive and may recur in other locations, such as the contralateral paraventricular white matter.
  • These lesions may represent an intermediate entity between MS and ADEM. Other differential considerations are neoplasm, systemic lupus erythematosus (SLE) and other vasculitic illnesses, progressive multifocal leukoencephalomyelitis, and Schilder myelinoclastic diffuse sclerosis.
  • Schilder disease (diffuse sclerosis) is sometimes considered an MS variant, and the uncertain diagnostic status is beyond the scope of this review. Detailed discussion of that entity is available in the Neurology section of the Medscape Reference journal.

Recurrence may occur during the taper of corticosteroid therapy initiated for ADEM. This phenomenon is not thought to represent a second or independent bout of illness; it usually responds to increasing the corticosteroid dosage and prolonging the ensuing taper.

The appearance of small new lesions on MRI within a month of presentation must also be interpreted with caution, and this may be seen in ADEM.

Although long tapers are sometimes required and more than one taper-related worsening occurs in a small number of patients, recovery is achieved within 2-12 months without further recurrence.

A rare subgroup of patients exists who cannot be weaned entirely from anti-inflammatory therapy. Most of the 8 examples one of the authors (RSR) has encountered were in boys, and the onset of illness usually occurred at age 2-6 years.

• Mental status changes, visual disturbance, and pyramidal weakness are typical findings; seizures occur in most cases.
• Imaging changes resemble those found in cases of typical ADEM (ie, multiple plaques at the grey-white junction and in deep white matter), a feature that distinguishes these cases from chronic cases considered a manifestation of Schilder disease.
• The CSF immune profile remains normal despite recurrences, although myelin basic protein may be elevated.
• The neurologic abnormalities in this group improve significantly with intravenous methylprednisolone treatment (20 mg/kg/d for 3 successive doses) followed by oral methylprednisolone (2 mg/kg/d) with slow taper to achieve alternate-day dosing.
• Trouble is encountered during the taper, each patient having a particular threshold for recurrence. In most of the authors’ cases, this threshold is encountered when the daily methylprednisolone dose is lowered to approximately 12-14 mg every other day.
• The neurologic worsening responds to higher corticosteroid doses, but this threshold effect cannot be overcome, and steroid therapy has been continued in these patients for periods as long as 8 years.
• Although prolonged daily steroid therapy is generally well tolerated, osteopenia may develop, and one of the authors’ patients developed vertebral compression fractures.

In 2007, the International Pediatric Multiple Sclerosis Study Group (IPMSSG) proposed operational definitions for the pediatric acquired demyelinating diseases (including ADEM) in attempts to improve consistency in terminology for clinical and research purposes. These guidelines were revised in 2013 and are outlined below. 

• The criteria requires that a child must meet all of the following to be accurately classified as pediatric ADEM:
  • A first, polyfocal clinical CNS event with presumed inflammatory demyelinating cause
  • Encephalopathy that cannot be explained by fever
  • No new clinical and MRI findings emerge 3 months or more after onset
  • Brain MRI is abnormal during the acute phase
  • Typical findings on brain MRI (discussed below) that include diffuse, poorly demarcated large lesions involving the cerebral white matter; T1 hypointense lesions of the white matter are rare; deep gray matter lesions may be present.

Recurrent ADEM was previously defined as a new event of ADEM with a recurrence of the initial symptoms and signs 3 or more months after the first ADEM event. Based upon the 2013 consensus criteria from IPMSSG, this entity is now included under the entity known as multiphasic ADEM.

Multiphasic ADEM

• Individuals who have experienced typical ADEM are at risk for recurrence. As many as 10% of children with an initial diagnosis of ADEM experience another ADEM attack, typically within the first 2-8 years after the initial attack. 
• Included under the entity of “multiphasic ADEM” are new events of ADEM 3 months or more after the initial attack that can be associated with new or re-emergence of prior clinical and/or MRI findings. 
  • Relapsing disease that follows a second ADEM attack is, by definition, no longer consistent with a diagnosis of multiphasic ADEM. Typically, these cases represent a chronic neuro-inflammatory disorder (such as MS or NMO).

Physical

Irritability and lethargy are common first signs of acute disseminated encephalomyelitis (ADEM). Fever returns and headache is present in up to half of cases. Meningismus is also detected in approximately one third of cases. Over the course of minutes to weeks, multifocal neurologic abnormalities develop. The interval from onset of symptoms to maximum deficit is varied but is typically seen at a mean of 4-7 days. Among the most common abnormalities are long tract signs, acute hemiparesis, cranial nerve abnormalities (including visual loss), ataxia, and mental status abnormalities. Mental status disturbances include lethargy, fatigue, confusion, irritability, obtundation, and coma. Focal or generalized seizures occur as an early sign in a minority of cases.

Weakness (roughly 75% of cases) is more commonly discerned than sensory defects. The combinations of these signs may suggest cortical, subcortical, brainstem, cranial nerve, or spinal cord localization. Long tract signs develop in more than half of all cases. Cranial nerve palsies (including vision loss) are found in a wide range of cases (23-89%) of childhood ADEM.  Mental or psychiatric disturbances, seizures, and cranial nerve palsies are significantly less common in adolescents or adults with a first or second bout of MS and in many adults with an illness labeled ADEM. Sensory changes may be underappreciated in young children; however, posterior column deficits and hemisensory changes are possibly much less common than in adult cases of ADEM or in early bouts of adolescent or adult MS. Band or girdle dysesthesia or Lhermitte’s sign are seldom if ever found in cases of childhood ADEM.

Ataxia is found in 28-65% of childhood ADEM cases,  to differ from cases of ACA because it is more commonly appendicular with nystagmus or generalized ataxia than the distinctive gait/trunk ataxia of ACA. Extrapyramidal disorders such as choreoathetosis or dystonia are sometimes observed.

Signs and symptoms found in cases of ADEM:

• Alteration in personality
• Abnormal consciousness
• Ataxia (appendicular more than axial or gait)
• Cranial nerve palsies
• Hallucinations
• Headache
• Language disturbances
• Meningeal signs
• Nystagmus
• Psychiatric abnormalities
• Optic neuritis
• Ophthalmoparesis
• Seizures, focal or generalized
• Sensory loss/dysesthesia
• Visual field deficits
• Vomiting

Causes

Acute disseminated encephalomyelitis (ADEM) may develop in the wake of a wide variety of infectious illnesses or immunizations, especially those associated with large envelope-bearing viruses. Among the agents most commonly identified by titer rise suggesting responsibility for the prodromal phase are Ebstein-Barr virus, cytomegalovirus, herpes simplex virus (HSV), and mycoplasma; however, a particular agent is identified only in a minority of ADEM cases.

ADEM is somewhat more common in the colder months of the year, during which these various viral illnesses are more prevalent. Prior to widespread immunization programs, measles was the most common associated illness. Now, most cases occur in the wake of respiratory or gastrointestinal illnesses that are presumed to be of viral etiology; specific viral agents are seldom identified.

The hiatus between onset of viral symptoms and onset of ADEM may range from 2-21 days. The two phases of illness are typically separated by a phase of recovery from fever and other constitutional manifestations of the initial infectious phase of illness. ADEM may possibly arise after intervals as long as 30 or more days after an infectious prodrome. The longer the interval between the presumed prodrome and ADEM, the less certain one can be of the etiologic association. A minority of cases lack a prodromal phase. Establishing the etiologic role of immunizations has proven controversial.

Clear links between the Pasteur rabies vaccine and ADEM have been established. Immunizations less frequently associated with ADEM include pertussis, measles,  Japanese B virus, tetanus, influenza, hepatitis B, diphtheria, rubella, pneumococcus, varicella, smallpox, poliomyelitis, and human papillomavirus. 

The provocation provided by an infectious agent likely requires participation of other genetic or immuno-experiential factors of the individual in order to give rise to ADEM. These factors likely include genetically or experientially determined aspects of immunoregulation, particularly T-helper cell function. Alves-Leon et al have found that the alleles HLA DQB1*0602, DRB1*1501, and DRB1*1503 confer genetic susceptibility to acute disseminated encephalomyelitis. 

Medical Care

Acute disseminated encephalomyelitis (ADEM) is often treated with high-dose intravenous corticosteroids, to which it appears to be responsive. One common protocol is 20-30 mg/kg/d of methylprednisolone (maximum dose of 1 g/d) for 3-5 days. Improvement may be observed within hours but usually requires several days. An oral taper for 4-6 weeks or some other interval is sometimes appended.

• Though there is conflicting data, at least two studies have presented data suggesting that steroid taper of 3 weeks or less may increase the risk of relapse in ADEM.
• Taper-related recurrence occurs in as many as 3-5% of cases and usually responds to prolongation of taper. Similar phenomena occur in other postinfectious diseases, such as Guillain-Barré syndrome or opsoclonus-myoclonus. A subset of patients manifest repeated recurrences that prevent discontinuation of corticosteroids or necessitate changing to various steroid-sparing treatments such as cyclophosphamide or beta-interferons. This rare and interesting subgroup tends to have onset of disease before 6 years of age, and despite recurrence, these children do not manifest evidence for CSF immune profile (ie, IgG index, IgG synthetic rate, oligoclonal bands) abnormality. The relationship of this group to patients with ADEM or MS or some other form of inflammatory CNS illness remains unclear.

The chief alternative therapy is intravenous immune globulin (IVIG).  It is administered as 2 g/kg intravenously as a single dose or over the course of 3-5 days. IVIG may be preferable in instances where meningo-encephalitis cannot be excluded based upon the hypothesis that corticosteroids might worsen the course of infection.

Available published information concerning efficacy is inadequate to accurately assess much concerning the impact of either form of therapy, although it appears likely that both forms of therapy increase the pace of initial recovery. Whether these forms of therapy influence times to final outcome or extent of final recovery is not known.

Theoretically, very high-dose corticosteroids (30-50 mg/kg) administered intravenously at presentation to patients with transverse myelitis may be advantageous from the vantage point of its capacity to close the blood-brain barrier and limit swelling. Marked cord swelling may account for poor outcome in some cases of transverse myelitis because of circulatory impairment and cord infarction. The same argument may hold true for severe cerebral ADEM such as tends to arise in some young children (< 3 y old) who also may have marked permanent neurologic impairments after severe ADEM.

There is as yet no convincing evidence that treatment with the combination of intravenous corticosteroids and IVIG confers any advantage in such cases, although this approach is employed by some clinicians.

Severe ADEM has also been treated, apparently successfully, with such alternative approaches as (1) combination of intravenous corticosteroids and IVIG, (2) cyclosporin, (3) cyclophosphamide, or (4) plasma exchange/plasmapheresis.  Greater understanding of trimolecular complex regulation, adhesion molecules, and inflammatory cytokines may permit development of more specific and effective ADEM therapies. The polymorphism of the human major histocompatibility complex and apparent heterogeneity of T cell response to autoantigens render this a daunting project, although anti-cytokines represent an intriguing avenue of therapeutic research.

Surgical Care

Surgical treatment for severely elevated intracranial pressure has been undertaken for cases of AHLE, hemorrhagic brain purpura, and non-Reye syndrome, examples of what have been termed obscure encephalopathies of infancy. Some of these cases were likely examples of hyperacute ADEM. Surgical interventions have ranged from placement of pressure bolts to decompression of the intracranial fossae by unroofing of the cranium. Outcome of such interventions was mixed.

Although such severe cases were regularly noted in the medical literature from the 1920s until the mid 1970s, few examples have been noted since that time. Prevalence clearly has dramatically decreased. Because these severe cases often followed measles, mumps, and other diseases for which effective vaccines have been developed and because the disappearance of such cases has followed the availability and use of such vaccines (earlier disappearance in the United States and Western Europe, subsequent disappearance in Asia and the Middle East), this change in prevalence likely reflects the removal of pathogens that are provocative of such severe forms of ADEM.

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Introduction

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Lesions to the central nervous system (brain or spinal cord) can lead to both positive and/ or negative upper motor neurone syndrome (UMNS) features:

Positive Component	Negative Component
Exaggerated Tendon Reflexes	Spastic Co-Contractions
Released Reflexes	Motor Weakness
Babinski Sign	Slowed Movements
Increased Tone	Loss of Dexterity
Clonus	Loss of Selective Motor Control
Spastic Dystonia

Spasticity is seen to be a positive feature of upper motor neuron syndrome. This is because it is due to a loss of inhibition of the lower motor neuron pathways, rather than a loss of connection to the lower motor neuron (or other pathways). This results from disordered sensorimotor control of movement due to a lesion of the upper motor neuron which regulate muscle control. Therefore, there is an imbalance of the signals between the central nervous system (CNS) and muscles, presenting as intermittent or sustained involuntary activation of muscles.

All muscles have some tone to maintain function, for example, activation of antigravity muscles to maintain sitting or standing postures. In an individual with spasticity, there is a velocity-dependent increase in muscle tone to passive movement. This creates an inability to stretch muscles or coordinate movements effectively.

This inhibition can result from central nervous system pathology, such as:

• Cerebral Palsy
• Multiple Sclerosis
• Motor neurone disease
• Stroke
• Hypoxic Brain Injury
• Traumatic Brain Injury
• Parkinson’s Disease
• Spinal cord injury
• Spinal cord compression
• Metastesis / tumour

Spasticity can have an impact on an individual’s function, affecting upper and lower limbs, as well as trunk. If this is not managed effectively, it can lead to fixed deformity contractures (changes to soft tissue), which affect skin care, comfort and hygiene, as well as complications for daily tasks.

The management of spasticity needs to be carefully considered as some patients rely on aspects of spasticity to allow them to maintain enough tone for functions such as standing or walking. Physiotherapy management may include facilitating individuals to utilise this to maintain weight bearing and ambulation to decrease their risk of developing osteoporosis, strengthen muscles, help improve circulation and promote overall mental health.

Definition

The most well-known and referenced description of spasticity is the physiological definition proposed by Lance in 1980. 

‘Spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome’

More recently, a definition from Pandyan et al (2005)  states that spasticity is:

‘Disordered sensorimotor control, resulting, resulting from an upper motor neuron lesion (UMN), presenting as an intermittent or sustained involuntary activations of muscles .

Classification of Spasticity into various components of spasticity into sub-definitions:

1. Intrinsic Tonic Spasticity: Exaggeration of the tonic component of the stretch reflex (manifesting as increased tone),
2. Intrinsic Phasic Spasticity: Exaggeration of the phasic component of the stretch reflex (manifesting as tendon hyper-reflexia and clonus), and
3. Extrinsic Spasticity: Exaggeration of extrinsic flexion or extension spinal reflexes.

Epidemiology

Spasticity affects approximately:

• 35% of those with stroke,
• more than 90% with CP
• about 50% of TBI patients
• 40% of SCI patients
• between 37% and 78% of MS patients.

Anatomy and Etiology

A UMN injury leads to loss of inhibition downstream and hypersensitivity of the reflex arc within the spinal cord. Primary impairments from an upper motor neuron lesion (UMNL) are usually due to the disruption of supraspinal control of descending pathways that control excitatory and inhibitory influences on proprioceptive, cutaneous and nociceptive spinal reflexes.

The Inhibitory System

Corticoreticular Spinal Tract: These tracts travel with, but are separate from, the Corticospinal Tract, and are responsible for the facilitation of the inhibitory area within the medulla called the ventromedial reticular formation. Here, the Dorsal Reticulospinal Tract originates, which is responsible for an inhibitory action on both the stretch and flexor reflexes.

The Excitatory System

The bulbopontine tegmentum gives rise to the Medial Reticulospinal Tract and, acting weakly with the Vestibulospinal Tract, is excitatory to both stretch and extensor reflexes and like the Dorsal Reticulospinal Tract, is also inhibitory to the flexor reflexes.

Different Lesions and Their Presentations

The signs and symptoms between Cortical UMN Lesions and Spinal Cord UMN Lesions vary due to the location of where the disruption has taken place. 

Normal

Both the inhibitory system (Corticospinal Tract and Dorsoreticulospinal Tract) and excitatory systems (Medial Reticulospinal and Vestibulospinal Tract) are in dynamic balance and therefore the inhibition to the spinal cord is easily adjusted according to demand.

Corticospinal Tract Lesion

Although the Corticospinal Tract has an inhibitory influence on stretch and flexor reflex, the main inhibitory system produced by the Dorsal Reticulospinal Tract remains intact and therefore the balance of excitatory and inhibitory influences are maintained.

Internal Capsule Lesion

Leads to interruption of both the Corticospinal Tract and Corticoreticular Tract pathways that are responsible for the inhibitory response and some loss of inhibition to stretch and flexor stretches. The excitatory systems from both the Medial Reticulospinal and Vestibulospinal Tract are more dominant which leads to the facilitation of extensor and stretch reflexes but inhibition of flexors.

Incomplete Spinal Cord Lesion

Signs and symptoms will vary dependant on site and extent. If the inhibitory system is affected then there will be an unopposed excitatory drive to stretch and extensor reflexes with partial inhibition of flexor reflexes.

Complete Spinal Cord Lesion

Spinal reflexes are unopposed due to the complete loss of supraspinal control. Both flexor and extensor reflexes are disinhibited and therefore people may experience both flexor and extensor spasms.

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Clinical Presentation

On physical exam, hallmark findings include

• high muscle tone in muscle groups such as the shoulder adductors; elbow, wrist, and finger flexors; and forearm pronators. In the lower extremities, the increased tone is especially prominent in the hip adductors, knee flexors and extensors, and plantar flexors and invertors of the ankle. Antigravity muscles are predominantly affected.
• Patients may report difficulty with footwear if their spasticity involves constant, high tone of the extensor hallucis longus or long toe flexors.
• Spasticity varies with speed of movement (velocity dependent); meaning the faster the muscle is moved or stretched, the greater the resistance to stretch or passive elongation is felt.
• Clonus, spastic co-contractions, and spastic dystonia may be evident. i.e., Clonus is defined as an alternating muscle contraction and relaxation of the agonist and antagonist muscles. Spastic co-contractions are abnormal antagonist contractions that present during voluntary agonist effort. Spastic dystonia is a muscle contraction that is present at rest, leading to a constant clinical posture that is highly sensitive to stretch. 
• Clasp knife phenomenon: Limb initially resists movement and then suddenly gives way 
• Stroking Effect: Stroking the surface of the antagonist muscle may reduce tone in spasticity. 

Permanent loss of joint range has been known to occur 3-6 weeks after both stroke and brain injury and therefore it is important that spasticity is identified early on in the assessment in order for it to be monitored and managed as required. In a person with hemiplegia the lower limb pattern is plantar flexion and inversion of the ankle with hamstring tightness limiting knee range of motion as well as adductor spasticity. Upper limb presentation is usually shoulder adduction, internal rotation, elbow flexion, forearm pronation with wrist and elbow flexion. 

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Outcome measures

Useful objective measures to monitor changes in spasticity can include:

Subjective:

• Pain:
  • Numeric Pain Scale (e.g. for pain, comfort, stiffness)
  • Observing grimacing / pulling away
• Arm A and Arm B
• LegA

Objective:

• Resting Position: photographs, description, measuring bony landmarks
• Passive range of movement
  • Adductor Tone Rating
• Active range of movement
• Muscle strength: Oxford Scale
• Spasms:
  • Modified Penn Spasm Frequency Scale
  • Clonus and Spasm Score
• Function
  • Walking: 10m times walk
  • Transfers: Times up and go
  • Upper Limb Function: 9 hole peg test
  • Speech: Speech comprehension score 
  • Walking and Falls Score
• Muscle tone: Ashworth Scale / Modified Ashworth Scale, Tardieu (outlined below)

Ashworth Scale

The Ashworth scale is the most widely used assessment tool to measure resistance to limb movement in a clinic setting, although it is unable to distinguish between the neural and non-neural components of increased tone.

The scale is as follows:

Ashworth Scale
Grade	Description
0	No increase in muscle tone
1	Slight increase in tone giving a catch when the limb is moved
2	More marked increase in tone but limb easily moved
3	Considerable increase in tone – passive movement difficult
4	Limb is rigid in flexion or extension

Modified Ashworth Scale

Modified Ashworth Scale’ scores exhibited better reliability when measuring upper extremities than lower. The scale is as below:

Modified Ashworth Scale
Grade	Description
0	No increase in muscle tone
1	Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part(s) is moved in flexion or extension
1+	Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM
2	More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
3	Considerable increase in muscle tone, passive movement difficult
4	Affected part(s) rigid in flexion or extension

Tardieu Scale

This scale quantifies muscle spasticity by assessing the response of the muscle to stretch applied at specified velocities. Grading is always performed at the same time of day, in a constant position of the body for a given limb. For each muscle group, reaction to stretch is rated at a specified stretch velocity. 

Tardieu
Velocity to Stretch
V1	As slow as possible
V2	Speed of the limb segment falling (with gravitational pull)
V3	At a fast rate (>gravitational pull)
Quality of Muscle Reaction
0	No resistance throughout passive movement
1	Slight resistance throughout,with no clear catch at a precise angle.
2	Clear catch at a precise angle followed by release
3	Fatiguable Clonus (< 10 secs) occurring at a precise angleFatiguable Clonus (< 10 secs) occurring at a precise angle
4	Unfatiguable Clonus (> 10 secs) occurring at a precise angle
5	Joint immobile
Spasticity Angle
R1	Angle of catch seen at Velocity V2 or V3
R2	Full range of motion achieved when muscle is at rest and tested at V1 velocity

Management

It important to consider the triggers of spasticity when planning interventions. There are a number of stimuli which can exacerbate spasticity, some may need multidisciplinary input alongside implementing physiotherapy management. These include:

• Skin: pressure ulcers, ingrown toe nails
• Bladder or bowel: constipation, full bladder
• Pain / discomfort: restrictive clothing, wheelchair straps, catheter straps
• Seating / positioning
• Fatigue
• Infections: UTI, pneumonia, skin
• Stress
• Disease progression
• Menstruation
• Other medical condistions (e.g. kidney stones)
• Ill fitting orthotics

Physiotherapy

Spasticity is one of the components of the UMN syndrome but should not be considered in isolation when it comes to management strategies. It is essential that management targets identified impairments to function and is always patient focused rather than aimed at reducing the degree of spasticity Planned interventions should consider a balance between movement and positioning. This includes:

• Standing
  • Standing frame
  • Treadmill training (body-weight supported if needed)
  • Tilt table
• Active exercises
• Passive movements
• Functional electrical stimulation
• 24 hour positioning management
• Splinting and the use of orthotics
• Stretches

Considerations for managing spasticity :

• Client care:
  • Preventing or treating contractures
  • Monitoring skin to preventing pressure areas
  • Positioning of trunk, head and limbs in supine and in chair/ wheel chair
    • If possible, standing promotes anti-gravity muscle activity in the trunk and lower limbs. It also maintains or improves soft tissue and joint flexibility and modulation of the neural component of spasticity.
  • Orthotics to maintain / improve available range
• Movement improvement:
  • The unmasking of voluntary movements previously covered by significant spasticity in cases of incomplete lesions
  • Accelerating the “spontaneous” recovery process
  • Modifying the “immature” motor pattern
  • Using new recovery techniques to promote guided neuroplasticity, e.g. robotic rehabilitation
  • New functional pattern in moving and walking.
• ADL’s and transfers
  • Getting around
  • Putting on clothes
  • Personal hygiene
  • Driving, etc.
  • Occupation
• Quality of life
  • Independent living
  • social and professional reintegration
  • Task specific activities can have a positive psychological effect

Patients should be educated on maintaining a daily stretching and range of motion program. In addition to the patient, the family and caregivers should be educated about proper positioning, daily skin inspection, an adequate and regular bowel/bladder regimen, avoiding noxious stimuli, and identifying signs of infection and pain.

Pharmacological

Some individuals may benefit from medications to manage spasticity. These can be generalised, focal or intrathecal interventions.

If the spasticity is widespread then systemic medication is used. This includes:

• Dantrolene (Dantrium)
• Baclofen (Lioresal and others)
• Tizanidine (Zanaflex)
• Diazepam (Vallium)
• Benzodiazepines
• Gabapentin
• Pregabalin
• Canabinoids

If the spasticity is locallised then local medication is used. This includes:

• Boutulinum Toxin (Botox)
• Regional Nerve Block

Intrathecal medications can also be used. These include:

• Baclofen
• Phenol

Medication
Baclofen	The most common systemic agent. Baclofen acts on the receptors of excitatory nerve terminals, in particular the ‘GABA B G-Protein receptor. Once the baclofen has attached to this G-Protein on the pre-synaptic terminal, potassium channels open while calcium channels close, hyperpolarising the cell. The inability for calcium to enter the cell means the release of glutamate, an excitatory neurotransmitter, is prohibited.
Tizanidine	Follows the same mechanism as Baclofen, however attaches to the a2 adrenoreceptor on the pre-synaptic cell membrane.
Botulinum Toxin (Botox)	Injected locally into muscle. Prevents the excytotic release of acetylcholine at the level of the neuromuscular junction which further prevents release of calcium from the sarcoplasmic reticulum which leads to excitation-contraction coupling.
Diazepam (Vallium)	Less common. Increases the effect of GABA, an inhibitory neurotransmitter, that is released from inhibitory interneurons which decreases the excitability within the post-synaptic nerve terminal.
Dantrolene	Provided orally. Blocks the release of calcium from the sarcoplasmic reticulum within the muscle which prevents excitation-contraction coupling.

Considerations of medication:

• Optimise timings of sessions alongside medications
• Exposing weakness in limbs of trunk
• Monitor effects and when dose may need adjusting
• Side effects, such as fatigue

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Definition

Amputation is defined as surgical removal or loss of body part such as arms or limbs in part or full.

Prevalence

One million limb amputations are reported globally each year. And as of 2017, 57.7 million people across the globe have been living with traumatic amputation. Approximately 185,000 amputations occur in United States each year according to the amputee coalition. And also, as of April 2021, United states has over 2 million Americans living with amputation, and another 28 million at a risk of surgical amputation due to undelaying causes.

Data from Stanford Healthcare shows 49% rise in total number of amputations during the time of COVID-19 pandemic, during March 2020 to February 2021.

Causes of Amputations

There are several conditions that can lead to amputation.

• Severe infection with extensive tissue damage
• Gangrene
• Trauma resulting from accident or injury, such as crush or blast wound
• Congenital/ Paediatric limb deficiency undergoing conversion amputation
• Congenital deformities of digits or limbs
• Congenital extra digits or limbs
• Necrosis or Necrotizing Fasciitis
• Cellulitis
• Peripheral Arterial Disease
• Frostbite
• Malignant/ cancerous tumor in bone or muscle of the limb e.g. Osteosarcoma
• Conditions that affect blood flow for example Diabetes

Levels of Amputation

Upper Limb 

• Forequarter
• Shoulder Disarticulation (SD)
• Transhumeral (Above Elbow AE)
• Elbow Disarticulation (ED)
• Transradial (Below Elbow BE)
• Hand/ Wrist Disarticulation
• Transcarpal (Partial Hand PH)
• Transmetacarpal

Lower Limb

• Hemicorporectomy
• Hemipelvectomy/ Hindquarter amputation
• Hip Disarticulation
• Short transfemoral(above knee)
• Transfemoral (above Knee)
• Long transfemoral (above knee)
• Knee Disarticulation
• Short transtibial (below knee)
• Transtibial (below knee)
• Long transtibial (below knee)
• Ankle Disarticulation (Symes)
• Tansmetatarsal
• Partial Foot/ray resection
• Toe disarticulation
• Partial Toe

Pre-Surgical Evaluation

1. General system review- Cardiovascular & Respiratory
2. Nutritional status
3. Diabetes Control if appropriate
4. Bowel & Bladder Function
5. Past medical history
6. Social history
7. Pre-morbid mobility
8. Strength & Condition of Healthy limb
9. Psychological assessment to access emotion impact of amputation
10. Home & work place assessment to make sure, everything is in accordance for patients maximal self reliance
11. Explanation of post-operative regimen.

Surgery for Amputation

Anesthesia is the first step to any surgery. During amputation, choice of anesthesia depends on the type of amputation, described above on levels of amputation. Two option of anesthesia for amputation are general anesthesia or epidural anesthesia.

While performing amputation, special care is to be taken to make sure the procedure does not hamper the functioning of remaining limb. It is vital to condition, shorten & smoothen the remaining bone, so there is a healthy stump that in future can take the load of a prosthetic limb and reduce complication risk.

Muscle is sutured to the bone at the distal residual bone so maximal strength of the remaining limb can be retained. This procedure is known as myodesis.

Distal stabilization of the muscles is always recommended, allowing for effective muscle contraction and reduced atrophy. This in turn allows for a greater functional use of the stump and maintains soft tissue coverage of the remnant bone. As the procedure for amputation is completed, the wound us sealed by performing myoplasty: suture to opposite muscle in the residual limb to to each other and to the periosteum or to the distal end of the cut bone for weight bearing purposes; and is covered with a bandage. A drainage tube might be placed to drain all excess fluid. Hence, every possible measure is taken to reduce risk of infection.

Ideal Stump

1. Skin flaps: skin should be mobile, sensation intact, no scars
2. Muscles are divided 3 to 5 cm distal to the level of bone resection
3. Nerves are gently pulled and cut cleanly, so that they retract well proximal to the bone level to reduce the complication of neuroma

Stump care

• For hygiene and skin care see handout on amputations
• A hip flexion contracture may develop because of elevation to reduce swelling
• Stump bandaging is done to ‘cone’ the stump, thereby preventing oedema, which occurs because there is no muscle pump and the stump hangs
• Swelling must be prevented to allow proper attachment of the prosthesis, and the prevention of pressure sores
• The stump sock is put on first, then the prosthesis
• The prosthesis must be cleaned and maintained (children who are still growing, grow out of their prostheses)

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Complications of Amputation

• Edema & Swelling
• Wounds Infection
• Pain (phantom limb)
• Muscle weakness
• Muscle Tightness & contractures
• Joint Instability
• Autonomic dysfunction
• for more detailed information on post-operative complications following an amputation.

Post Surgical Evaluation

• General system review- Cardiovascular & Respiratory
• Nutritional status
• Diabetes Control if appropriate
• Bowel & Bladder Function
• Strength & Condition of Healthy limb
• Psychological assessment to access emotion impact of amputation
• Signs of Infection
• Type of pain(Incisional, phantom, other)
• Level of Pain(VAS 1 – 10)
• Functional status (Bed mobility, transfers, sitting, standing, walking, balance)
• Strength and/or pain of the un-amputated limb

Post-operative Care

• Maintain function in the remaining leg and stump to maintain peripheral circulation
• Maintain respiratory function (important with smokers and those patients under general anaesthesia)
• Prepare for mobility rehabilitation

Pain in Amputation

Residual Limb pain and phantom limb pain are the two essential types of pain, post amputation.

Residual Limb Pain

Residual limb pain has three main cause:

1. Very likely post operative pain
2. Peripheral nerve neuroma formation at the end of cut peripheral nerve
3. Prosthetic pain caused by ill fitting prosthesis

Phantom Limb Pain

Phantom limb pain is defined as “pain that is localized in the region of the removed body part.” Cause of Phantom limb pain is not fully understood , but it is distressing and has a significant impact on patients life.

Psychological Implications of Amputation

• Loss of limb has a huge psychological impact on ones mental health, as if the person has lost a loved one. It is difficult to cope with loss of sensation and function from the amputated limb. It also changes your (patients) and other peoples perception of your (patients) body image, which can lead to depression and anxiety as negative thoughts are very common.
• Psychological well being of the patient is vital to a good rehabilitation process. Hence, it is the duty of a physiotherapist/ physical therapist to acknowledge patients concerns with good knowledge of natural grieving process.^[1][2]

Fall Risk Post Amputation

• Patient undergone amputation is at a higher risk of fall especially when they try to get up from the bed or chair and they have forgotten about the absence of the limb. These falls can cause injury to the surgical site, leading to prolonged healing.^[1]
• To deal with the risk of fall, it is mandatory to place a walker besides the patient. This reminds the patient to use assistance for transfers.

Goals of Post-operative Physiotherapy Management

1. Patient education on amputation and rehabilitation post amputation.
2. Maintenance of respiratory & cardiovascular status both pre- & post- surgery
3. Proper positioning of amputated limb to maintain the limb in right anatomical position.^[10]
4. Maintaining/improving strength of unamputated limb
5. Residual Limb care
6. Balance training
7. Transfer Training
8. Mobility Training
9. Prosthetic training

Post-operative Physiotherapy Management

1. Start with respiratory maintenance with pain control for amputated limb. Also start strengthening the unamputated limb to maintain its strength.
2. Teach the patient to wrap the residual limb correctly.
3. Prevent hip flexion contracture by avoiding prolonged sitting & guiding patient to spend more time in prone position.
4. For proper positioning avoid side lying position, maintain the residual limb in extension at hip & knee.
5. Start balance training
6. Procced to mobility training initially with a walker followed by crutches.
7. Start strengthening of the residual limb before proceeding to prosthetic training

Pre- Prosthetic Evaluation

1. Social History of patient
2. Financial status
3. Cause of amputation
4. Cardiopulmonary status examination
5. Scar healing assessment
6. Sensory assessment
7. Residual limb length & shape
8. Emotional status of patient for acceptance of amputation and body image
9. Vascularity (pulse, color of limb, temperature, edema/swelling, pain & tropic changes
10. Range of motion
11. Muscle strength
12. Pain (residual & phantom)
13. Functional status ( transfers, mobility, activities of daily living)

Please find below links to more detailed pages on the management of amputees

• Pain Management
• Pre-Fitting Management of the Patient with a Lower Limb Amputation
• Post-fitting Management
• Prosthetic Rehab
• High level Rehab
• Clinical Guidelines: Mental Health Amputees

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More to do with patients with amputation

1. Berger’s Exercises

• Stimulates collateral blood flow in the patient’s leg
• It is performed for 20 min.
• The leg is elevated until the toes go white, then lowered, then level
• Repeat 2-3 times to improve collateral circulation

2. Connective Tissue Massage

3. Dynamic Stump Exercises

4. Balance and Gait Retraining

• Improve static and dynamic balance
• Use parallel bars, walking frame then Crutches (in that order)
• Therapist stands on the amputation side, using a belt around the patient’s waist to support
• Rest if the patient feels tired

5. Short Wave Diathermy (SWD)

Through the pelvis to warm the arteries (contraindicated in patients with arterial insufficiency because the warmth leads to increased metabolism, causing a greater demand for nutrients, which are not available)

Walking Again Post Amputation/ Mobility Aids

• The choice of mobility aids depends on the level of fitness, strength, balance skills of the individual:
  • Walking frame
  • Axillary crutches
  • Elbow crutches
  • Walking stick 
• For bilateral lower limb amputees a wheelchair is often indicated (high energy expenditure during gait with prostheses)

Prosthetic Training

Prosthetic training is vital for smooth and energy efficient living, while performing all of daily living activities.

Below is step by step guidance to prosthetic training:

• Accepting weight of the
• body on each leg is vital to prosthetic training
• work on strengthening unamputated limb along with residual limb
• Teach the patient to balance on both legs and than on one leg
• Teach walking with prosthetic first with use of walker followed by crutches and stick
• Further proceed to independent prosthetic training.
• Teach the patient to adapt to environmental demands while walking

Introduction

The loss of a lower limb has severe implications for a person’s mobility, and ability to perform activities of daily living . This negatively impacts their participation and integration into society. The ultimate goal of rehabilitation after limb loss is to ambulate successfully with the use of a prosthesis and to return to a high level of social reintegration. Prosthetic rehabilitation is a complex task that ideally requires input from a transdisciplinary rehabilitation team. However, most often physiotherapists are in charge of the physical rehabilitation process.

Overview of the Rehabilitation Process

The rehabilitation process of the lower limb amputee consists of nine phases, namely:

1. Pre-operative
2. Amputation surgery
3. Acute post-surgical
4. Pre-prosthetic
5. Prosthetic prescription
6. Prosthetic training
7. Community integration
8. Vocational rehabilitation and
9. Follow up.

Table 1: Phases of amputee rehabilitation: Modified from Esquenazi & Meier cited in Esquenazi.

Phase	Hallmark	Link
Pre-Operative	Assess body condition, patient education, surgical level discussion, postoperative prosthetic plans	Assessment of the amputee
Amputation Surgery/Reconstruction	Length, myoplastic closure, soft tissue coverage, nerve, handling, rigid dressing
Acute Post-Surgical	Wound healing, pain control, proximal body motion, emotional support
Pre-Prosthetic	Shaping, shrinking, increase muscle strength, restore patient locus of control	Post-fitting management of the amputee
Prosthetic Prescription	Team consensus on prosthetic prescription and fabrication	Prosthetics
Prosthetic Training	Increase prosthetic wearing and functional utilisation	Gait in prosthetic rehabilitation
Community Integration	Resumption of roles in family and community activities. Emotional equilibrium and healthy coping strategies. Recreational activities.
Vocational Rehabilitation	Assess and plan vocational activities for the future. May need further education, training or job modification.
Follow-up	Life-long prosthetic, functional, medical assessment and emotional support

Throughout all of these phases, a rehabilitation treatment plan is utilised to guide the care of an individual who has undergone an amputation. The treatment plan is based on an evaluation by all specialties involved in the rehabilitation process and acts as a guide for all team members to address goals important to the patient and family. The level of rehabilitation intervention is contemplated from the date of admission to the hospital and determined after the amputation surgery and prior to discharge from the hospital. The rehabilitative process includes:

• Ongoing medical assessment of impairments, and
• Therapy interventions to address disabilities or activity limitation

Below we define this more detailed team-focused rehabilitation process in 8 phases:

	Patient Journey	The Team Management	Physiotherapy Management
1.	Pre-operative	Subjective assessment – History of present condition; Past medical history; Drug history; Social History.Objective assessment – Range of movement (ROM); Muscle power; Limb for amputation; Pulses; Skin integrity.Collaborating all findings to decide on the most appropriate level of amputation for the individual and, if they are likely to become a limb wearer, which level of amputation would be most appropriate.	The focus is on the objective assessment looking at ROM and muscle power. Using assessment findings, knowledge of prosthetic componentry and gait patterns, provide a clinically reasoned recommended level of amputation to the consultant. Provide patient with appropriate exercises to aid post-amputation mobility.
2.	Amputation surgery/reconstruction	Amputation surgery and reconstruction is the responsibility of the surgeon.
3.	Acute post-operative	Medical care; Wound care; Discharge planning; Rigid dressing used rigid material such as plaster of Paris applied immediately after surgery and kept in place for 5-7 days (only for below knee and below elbow).	Post-operative chest physiotherapy. Transfer practice and specific exercises to improve strength; increase exercise tolerance; maintain ROM.
4.	Pre-prosthetic rehabilitation	Monitoring patient progress; counselling if required; Patient goals; deciding on prosthetic prescription with the whole team and all appropriate information [including how the patient has managed with Early walking aids (EWA) and patient goals ]	Early walking aids (EWA) can be used to help decide on a patient’s suitability for a prosthetic limb.Exercise therapy to prepare the limb for a prosthesis.Liaison with the whole team regarding pre-fitting management of the amputee.
5.	Prosthetic prescription	Casting and measuring – Prosthetists cast and measure a patient’s residuum.Fitting of the prosthesis –  Prosthetists fit the primary prosthesis to the patient, ensuring the alignment and length are correct in standing and walking.	The physiotherapist may be needed to assist in the cast appointment, to ensure a neutral alignment of the pelvis is obtained.Physiotherapy provides intervention on mobility guidance, static balance and weight-bearing.
6.	Prosthetic Training	Prosthetists will help problem solve and adjust prosthesis as required.	The physiotherapist takes a lead role at this stage. Beginning with educating the patient about donning and doffing the prosthesis, skin integrity and weight-bearing areas on their residuum. A gait rehabilitation programme can then commence.
7	Discharge Management	The occupational therapists take a large role in this phase to aid the resumption of roles in family, recreational and community activities. They will also assist with vocational rehabilitation by assessing and planning vocational activities for the future. May need further education, training or job modification. Counsellors will be involved with emotional equilibrium and healthy coping strategies.	The physiotherapist should ensure that they include education for ongoing management, strategies for coping and training for resuming functional activities.
8.	Follow up	Patient will be reviewed regularly by the consultant the physiotherapist, and the prosthetic team.Assessing the individual is still suitable for prosthetic use, the prosthetic prescription is still the most appropriate option for the patient and any required changes are made to the prosthesis as the patient changes.	The consultant and/or prosthetist may ask for physiotherapy input. For example, if the patient is having a change of prescription, their goals have changed, their mobility has decreased/increased. The physiotherapist may be required to re-commence a gait rehabilitation programme with the patient or advice only may be required.

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Psychological Assessments or Psychological Tests are verbal or written tests formed to evaluate a person’s behaviour. Many types of Psychological tests help people understand various dynamics of the human being. It helps us understand why someone is good at something, while the other is good at another. However, Humans are complex beings which can’t be defined and classified under certain branches. The subjective nature of humans and individual differences has quite often raised criticism in psychological testing.

The classification of the types of psychological tests is as follows:

• As per the nature of psychological tests in terms of standardized and non-testing method of testing
• As per the functions of psychological tests such as intelligence tests, personality tests, interest inventories, aptitude tests, etc.

Characteristics of Psychological Tests

Here are the key characteristics of Psychological Tests:

• Reliability: The psychological assessment/test must produce the same result no matter when it’s taken.
• Validity: The psychological test must measure what it’s been created to assess.
• Objectivity: The assessment must be free from any personal bias for its scoring, interpretation of scoring or administration.
• Standardization: The test must be standardized in terms of its place, material and time for the assessment as well as its environment.

Types of Psychological Tests

Now that you know about their origins, let’s explore the top and most popular psychological tests.

Here are the major nine types of Psychological tests:

1. Personality Tests
2. Achievement Tests
3. Attitude Tests
4. Aptitude Tests
5. Emotional Intelligence Tests
6. Intelligence Tests
7. Neuropsychological Tests
8. Projective Tests
9. Observation (Direct) Tests

Types of Intelligence Tests

The pioneer of Intelligence Tests, Alfred Binet was the first one to construct the IQ test for assessing French students to identify which students need special assistance. He soon realized that a few students could solve much more advanced questions which an average student couldn’t. He then realized that various factors play a role in assessing the intelligence of a person which makes the term multi-dimensional. He then constructed the Binet-Simon test which was revised and given the name Stanford-Binet test which became the standard intelligence test in the U.S. Soon, many intelligence tests were formed for different groups of people. Psychologists started intervening the possible variables and Psychology tests like Wechsler Intelligence Scales, Raven’s Progressive Matrices, etc. 

Here are the major types of intelligence tests:

• Wechsler Individual Achievement Test
• Woodcock Johnson III Tests of Cognitive Disabilities
• Wechsler Adult Intelligence Scale
• Stanford-Binet Intelligence Scale
• Peabody Individual Achievement Test
• Universal Nonverbal Intelligence
• Differential Ability Scales

Personality Tests

Earlier, Phrenology (the measurement of the bumps on the skulls) was used to assess someone’s personality. A personality test evaluates our behaviours, emotions, behavioural and environmental traits, attitudes and even clinical disturbances in people. Each personality test is used to measure a certain variable or compare two variables. For example, adolescent emotional problems or psychopathologies are screened using The Minnesota Multiphasic Personality Inventory (MMPI-A). There are various versions of the MMPI depending on the sample type you want to test. 

Another unique type of personality test is the projective assessment. Very commonly used Projective assessments are the Thematic Apperception Test and the Rorschach Inkblot test. These projective psychological tests are formed to test the response of a person to a certain stimulus which elicits different hidden emotions, underlying thoughts or beliefs using pictures.

Here are the types of personality tests in psychology:

• Objective Tests of Personality: MMPI
• Projective Tests of Personality: Rorschach Inkblot Test ,The Thematic Apperception Test

Aptitude Tests

As mentioned above, humans have certain abilities and specialities. A person who has a creative bent of mind might not necessarily have a calculative brain. Such different abilities and interests are tested using aptitude tests. It is used to predict the future scope of a person or tests whether a person possesses a certain skill set. However, speaking of human complexities again, humans are incomprehensive and unpredictable in their ways which always leaves some room for ambiguity. Various aptitude tests are given to students and employees. Many capability tests also come under aptitude tests. (For eg.: Assessment of Edward who wants to become a police officer. For such an alert, courageous and risk-taking job, Edward must possess certain skills and abilities for being selected.) Some common forms of aptitude tests used are the Graduate Management Admission Test (GMAT), Graduate Record Examination (GRE), Scholastic Assessment Test (SAT), amongst others.

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Speed and Power Tests

Another type of Psychological tests on our list is the speed and power tests. It is a test where the performance is being measured based primarily upon the speed with which one works. The example can be tests of clerical ability. The other alternative can be where the test is difficult and the applicant or the person is given as much time as he/she wants. This type of tests where the person’s score is based exclusively upon his/her ability to answer the question correctly irrespective of the time he/she has taken is known as power test. An example can be of tests like Tweezers Dexterity Test etc. 

Emotional Intelligence Test

Have you ever felt like you impulsively shout at someone or cry without any reason? These emotions of anger and sadness is what we need to control and monitor. We need to identify our emotions and regulate them without being influenced by others. An Emotional Intelligence test taps various emotions through situations presented to the test-taker. An emotional intelligence  test requires a person’s honesty in it to accurately evaluate a person’s EQ [Emotional Quotient] and suggest ways to improve it. It is often noted that people who have higher EQ are much more content and successful than people otherwise. Even though emotional intelligence can overlap with other aspects like personality or genetic compositions, Emotional Intelligence of a person tends to fluctuate or change. It often requires constant consciousness in your actions and evaluation of its consequences. 

“When dealing with people, remember you are not dealing with creatures of logic, but with creatures of emotion.” – Dale Carnegie

Neuropsychological Tests

Now scroll up to the beginning of the blog where we mentioned different perceptions. These perceptions are due to the different neurological structures and pathways our brain has. These tests are designed to measure the cognitive workings of a person. How would you test if you have a strong or a weak memory? Neuropsychological tests are the most essential form among the many types of psychological tests used for assessing diseases like Alzheimer’s, Brain injury, Emotional disorders, such as depression or anxiety. It is important for doctors to know the core of the problem to cure it. Neurological tests assess factors like Memory, Language, Executive functioning, Dementia, Visuospatial Function, etc.

Individual and Group Tests

There are a number of tests which are meant to be performed individually. Such tests are called individual tests and these tests are preferred for vocational guidance and counselling and for clinical and diagnostic work with emotionally disturbed persons. As individual tests are more costly, therefore they are less used in the industry than the group tests. An example of an individual psychological test can be the Stanford -Binet intelligence scale. On the contrary, some tests are usually designed for a purpose so that they can be administered to a large number of people in the industry. The examples of group tests can be Purdue Vocational Achievement Tests, the Adaptability Test and the Wonderlic Personnel Test. 

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Essay and Objectives Tests

The essay tests are probably one of the oldest methods of psychological tests that are created to check the candidate’s ability to organise and articulate his or her thoughts clearly and of course logically. It is Lord Macaulay who has been credited with introducing this concept for the Indian Administrative Services or IAS. On the other hand, the objective test has one correct answer and does not require or ask for any sort of long extensive answers/explanation from the candidates. These tests are generally used to check the mental ability or mental power of the candidate and reasoning and clarity of the concepts above all. 

Uses of Psychological Testing

Psychological Tests are mainly used to analyse the mental abilities and attributes of an individual, including personality, achievement, ability and neurological functioning. Here are the central and most important uses of Psychological Testing:

• Detection of Specific Behavior
• Psychological Diagnosis
• Tools in Academic Placements
• Screening Job Candidates
• Individual Differences
• Research
• To Promote Self-awareness and Understanding
• Psychometrics/Career Assessment Tests
• Organizational Development

History of Psychological Testing

Originally created by Francis Baton as a group of tests, Psychological testing methods can be traced way back to 2200 B.C in China when an emperor tested his officials to know whether they were suitable for his office. Since then many Chinese dynasties have seen such tests unfold into more formal ones with various levels. These tests created an impression in the world and soon every country started following them. Fast forward to the time when the whole world was struck with World War I, this era served as a critical crunch in the psychological world. Many types of psychological tests were designed to evaluate soldiers for the army and to filter soldiers who were suffering from ‘shellshock’ or PTSD. Such intense screenings might come off as archaic in today’s world, but it was a landmark in psychology because it gave rise to the World’s first Personality Test.

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Functional assessments have become an integral part of the comprehensive rehabilitation medicine evaluation. Descriptions of improvements in function have been consistently performed since rehabilitation medicine developed after World War II. Unfortunately, previously utilized methods lacked the consistency required to study rehabilitation outcomes accurately.

Functional assessment measures an individual’s level of function and ability to perform specific tasks on a safe and dependable basis over a defined period. A detailed assessment should include a pertinent clinical history; a neurologic and musculoskeletal evaluation, a physical effort determination, and a comprehensive evaluation of behaviors that might impact physical performance. Assessments must be valid, reliable, and reproducible. They can be self-administered questionnaires or clinician administered.

From a research standpoint, functional assessments provide supporting evidence to develop, improve and attest to different evidence-based treatments. In the clinical setting, these instruments are commonly used to set rehabilitation goals, to develop specific therapeutic interventions and to monitor clinical changes.

In 2014, functional assessments took a different direction when the Improving Medicare Post-Acute Care Transformation Act of 2014 (the IMPACT Act) was signed into law seeking to connect findings on the baseline assessment to functional outcomes. This required that Long-Term Care Hospitals (LTCHs), Skilled Nursing Facilities (SNFs), Home Health Agencies (HHAs) and Inpatient Rehabilitation Facilities (IRFs) to report and submit standardized patient assessment data, including quality measures and standardized patient assessment data elements. The collection of this information permitted the exchange of information among providers on specific functional domains that included functional status, cognitive function, and mental status among some. The final goal intended to enhanced rehabilitation outcomes through share decision making, care coordination and improved discharge planning.

Relevance To Clinical Practice

The scope of practice in Rehabilitation Medicine is wide and includes an array of conditions such as neurological (stroke, TBI, neurodegenerative), musculoskeletal (joint pain, tendinopathies, ligamentous injuries, balance dysfunction) pain syndromes, medical (deconditioning, cardiopulmonary), rheumatologic (Rheumatoid Arthritis, Osteoarthritis, Connective Tissue Disorders), among others.

Commonly used assessments include:

Activities of daily living (Table 1A) measures the performance of basic functional skills required to care for oneself independently. They measure basic daily activities (eating, grooming, bathing, dressing, continence) mobility (gait, transfers) and cognition. Examples include: 

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• Barthel Index
• Functional Independence Measure (FIM)
• Functional Independence Measure for Children (WeeFIM)
• GG Functional Abilities and Goal 
• specific Functional Scale
• Canadian Occupational Performance Measure
• Lawton’s Instrumental Activities of Daily Living among others
• WHO International Classification of Functioning, Disability, and Health (ICF)
• International Classification of Functioning, Disability and Health for Children and Youth (ICF-CY)

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An exercise tolerance test (also called a stress test) shows how well your heart handles physical activity. While exercising on a treadmill or stationary bike, a healthcare provider will measure your heart rate, blood pressure, and breathing while monitoring an electrocardiogram (ECG), a test that records your heart’s electrical signals.

Exercise tolerance tests are generally used to detect certain heart conditions or determine safe levels of exercise for people with existing heart conditions.

This article provides an overview on what an exercise tolerance test entails and how to understand the test’s results.

Purpose of an Exercise Tolerance Test

Exercise tolerance tests evaluate how hard your heart works when it’s under the stress of physical activity.

When we exercise, our hearts pump harder and faster to deliver blood and oxygen throughout the body.¹ It’s often easier to detect certain heart conditions while your heart is working hard, since the heart may appear to be working normally while at rest.

After hooking a patient up to a blood pressure cuff and ECG during exercise on a treadmill or stationary bike, healthcare providers can monitor your:

• Heart rate
• Blood pressure
• Breathing
• Level of exertion

Not everyone needs an exercise tolerance test. They’re mainly used to detect a heart condition or monitor a preexisting heart condition. For example, a healthcare provider may recommend this test:

• If you have symptoms like chest pain or shortness of breath that could indicate a heart condition
• If you have an irregular heartbeat
• To determine a safe exercise plan for patients recovering from heart surgery
• To see if treatments you’re receiving for heart disease are working well

Recap

An exercise tolerance test can demonstrate your heart’s ability to endure physical exercise. This in-office exam is often used to help detect heart conditions and determine appropriate treatments or exercise plans for existing heart patients.⁴

Limitations of an Exercise Tolerance Test

As with any medical test, exercise tolerance tests have some limitations. For example:

• Exercise tolerance tests can help detect an artery blockage in coronary artery disease, but they can’t predict things like how much of the artery has thickened or if and when a person may have a heart attack.
• Exercise tolerance test results aren’t always 100% accurate and can vary based on equipment used, experience of the healthcare professional conducting the test, and other factors. Some people may get a false-positive result, indicating a heart condition when there is none.

With this in mind, your healthcare provider will typically use the results of an exercise tolerance test along with other information, like your symptoms, medical history, and results of other tests, to make a determination or diagnosis.

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Recommendations for Exercise Testing

The U.S. Preventive Services Task Force recommends against routine exercise tolerance testing for people who don’t have any heart symptoms and are at low risk for developing heart disease. This is because the risk of false-positive findings can result in unnecessary further testing, treatment, or worry.

Risks of an Exercise Tolerance Test

An exercise tolerance test is a relatively safe test.

That said, sometimes increasing your heart rate through exercise can cause symptoms like dizziness, chest pain, or nausea. A healthcare provider will closely monitor you throughout the test to reduce the chances of this happening and quickly treat any issues that may come up.

In addition, people with certain preexisting heart disease can experience complications like an irregular heartbeat or even a heart attack. To be safe, your healthcare provider would likely not recommend an exercise tolerance test if you have any of the following heart conditions:⁷

• Unstable angina (chest discomfort caused by poor blood flow)
• Uncontrolled arrhythmia (an irregular heartbeat)
• Pulmonary hypertension (a type of high blood pressure)
• Severe aortic stenosis (narrowing of the main artery)
• Congestive heart failure (a condition in which the heart doesn’t pump blood as well as it should)
• Pulmonary embolism (a clot in the arteries of a lung)
• Aortic dissection (a tear in the main artery)
• Another acute illness

Before the Test

There’s not much preparation needed for an exercise tolerance test. Your healthcare provider will give you a set of guidelines to follow, which may include these instructions:⁸

• Avoid eating a heavy meal or consuming anything other than water within a few hours of the test.
• Avoid consuming caffeine the day before the test.
• Wear loose-fitting clothing and comfortable walking shoes.
• Continue to take any usual medication unless otherwise advised by a healthcare provider.

During the Test

Exercise tolerance tests take place at a healthcare provider’s office or at a hospital and will be overseen by a medical professional. They are relatively quick and painless, minus any potential minor discomfort felt while exercising. The test itself should take about 15–20 minutes. 

Here’s what you can expect:⁹

1. Equipment used will include a treadmill or exercise bike, ECG machine connected to electrodes (wires), a blood pressure cuff, and a pulse oximeter to measure blood oxygen levels.
2. The small electrodes will be stuck to the skin of your chest or shoulders and attached to the ECG machine to measure your heartbeat and heart waves. In addition, the blood pressure cuff will be wrapped around your arm, and the pulse oximeter sensor will be clipped to your finger. 
3. You’ll then be asked to start exercising on the treadmill or bike at an easy pace. Gradually, the speed and incline are increased while the ECG monitors your body and heart’s reaction to the stress of exercise.
4. You may be asked to breathe into a mouthpiece that will measure how much air you’re breathing out.

Before, during, and after the test, your ECG, heart rate, blood pressure, and breathing will be monitored and recorded.

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After the Test

When the test is done, you’ll be able to sit or lie down for several minutes until your heart rate returns to its normal resting state. You may be offered a glass of water or towel while you cool down.

If your blood pressure substantially rose during the test, or if the healthcare provider noticed any other concerning symptoms, you may be monitored for a few additional minutes.

After getting clearance, you’ll be free to return home and await the test results, which usually come back within a couple of days.

Interpreting Results of an Exercise Tolerance Test

After the test is performed, your healthcare provider will look over the results. They’ll be evaluating factors like:¹⁰

• Your ECG reading
• Blood pressure changes
• Heartbeat changes
• Any symptoms reported or noted during the test
• Your estimated exercise capacity 

After summarizing these items, your provider will go over the results with you and offer a conclusion based on their interpretation. Possible results include:¹¹

• Positive (or abnormal): This means the test found potential evidence of a heart condition.
• Negative (or normal): This means the test didn’t find any evidence of a heart condition.
• Inconclusive or uninterpretable: This indicates the test was unable to determine if a heart condition is present. In this case, the equipment may have malfunctioned, or you were unable to complete the test.
• Goal achieved: If you took the test to help establish a safe exercise plan following a heart diagnosis or surgery, your healthcare provider might have set some fitness goals that you were able to meet.

Recap

Stress tests give your healthcare provider important information about the likelihood of a heart problem and to recommend next steps for you. Ultimately, your healthcare provider is the best source of information about interpreting your stress test results.

Follow-Up

Depending on the results, your healthcare provider may want to speak with you about further testing, alternative testing, or treatment options.

In some cases, more appointments or testing may be necessary to:

• Confirm your exercise tolerance test result
• Seek additional information after your exercise tolerance test result

Follow-up tests may include:

• MRI (magnetic resonance imaging) heart scan to evaluate the structure of your heart
• CT coronary scan to look at the arteries that supply blood to your heart
• Myocardial perfusion scan to provide a visual on how well the heart is pumping
• Nuclear stress test to measure the blood flow to your heart

Summary

An exercise tolerance test is one way to record your heart’s response to the stress of physical exercise. It measures the heart’s electrical activity, heart rate, blood pressure, and breathing while you’re on a treadmill or exercise bike.

Exercise tolerance tests may be used to diagnose certain heart conditions, monitor heart attack recovery, or form an appropriate fitness plan for heart disease or surgery patients. Your healthcare provider may recommend this test if you report symptoms of potential heart disease, such as chest pain or shortness of breath. This test generally isn’t recommended for people at low risk of developing heart disease.

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Key facts by WHO-

• Over 1 billion people live with some form of disability.
• The number of people with disability are dramatically increasing. This is due to demographic trends and increases in chronic health conditions, among other causes.
• Almost everyone is likely to experience some form of disability – temporary or permanent – at some point in life.
• People with disability are disproportionately affected during the COVID-19 pandemic.
• When people with disability access health care, they often experience stigma and discrimination, and receive poor quality services.
• There is an urgent need to scale up disability inclusion in all levels of the health system, particularly primary health care.

overview

A disability is any condition of the body or mind (impairment) that makes it more difficult for the person with the condition to do certain activities (activity limitation) and interact with the world around them (participation restrictions).

There are many types of disabilities, such as those that affect a person’s:

• Vision
• Movement
• Thinking
• Remembering
• Learning
• Communicating
• Hearing
• Mental health
• Social relationships

Although “people with disabilities” sometimes refers to a single population, this is actually a diverse group of people with a wide range of needs. Two people with the same type of disability can be affected in very different ways. Some disabilities may be hidden or not easy to see.

Disability is part of being human. Almost everyone will temporarily or permanently experience disability at some point in their life. Over 1 billion people – about 15% of the global population – currently experience disability, and this number is increasing due in part to population ageing and an increase in the prevalence of noncommunicable diseases. 

Disability results from the interaction between individuals with a health condition, such as cerebral palsy, Down syndrome and depression, with personal and environmental factors including negative attitudes, inaccessible transportation and public buildings, and limited social support.

A person’s environment has a huge effect on the experience and extent of disability. Inaccessible environments create barriers that often hinder the full and effective participation of persons with disabilities in society on an equal basis with others. Progress on improving social participation can be made by addressing these barriers and facilitating persons with disabilities in their day to day lives.

Disability can be:

• Related to conditions that are present at birth and may affect functions later in life, including cognition (memory, learning, and understanding), mobility (moving around in the environment), vision, hearing, behavior, and other areas. These conditions may be
  • Disorders in single genes (for example, Duchenne muscular dystrophy);
  • Disorders of chromosomes (for example, Down syndrome); and
  • The result of the mother’s exposure during pregnancy to infections (for example, rubella) or substances, such as alcohol or cigarettes.
• Associated with developmental conditions that become apparent during childhood (for example, autism spectrum disorder and attention-deficit/hyperactivity disorder or ADHD)
• Related to an injury (for example, traumatic brain injury or spinal cord injuryexternal icon).
• Associated with a longstanding condition (for example, diabetes), which can cause a disability such as vision loss, nerve damage, or limb loss.
• Progressive (for example, muscular dystrophy), static (for example, limb loss), or intermittent (for example, some forms of multiple sclerosisexternal icon).

Magnitude of disability –

About 15% of the world’s population lives with some form of disability, of whom 2-4% experience significant difficulties in functioning. The global disability prevalence is higher than previous WHO estimates, which date from the 1970s and suggested a figure of around 10%.

As per the country’s latest statistics, an estimated 2.1 percent of the Indian population has a disability; a humbling figure of over 26 million people. A person can face disability — intellectually and physically — at any point in their life from medical complications or life-altering events.

Epidemiology 

Epidemiology of Intellectual Disability and Comorbid Conditions Epidemiology is essentially the study of a disorder in a given population. Knowledge of the distribution of a disorder in a population can increase understanding of the causes and how best to manage it.

Management

Increasing evidence suggests that, as a group, people with disabilities experience poorer levels of health than the general population. By improving access to quality, affordable health care services, health outcomes for people with disabilities can be improved. Primary health-care services with the support of specialists can provide health services to people with disability. Health services should be focused for the following health conditions:   

Primary health conditions: A primary health condition is the possible starting point for impairment can lead to a wide range of impairments, including mobility, sensory, mental, and communication impairments.

Secondary conditions: Secondary conditions occur in addition to (and are related to) a primary health condition, and are both predictable and therefore preventable; such as depression is a common secondary condition in people with disabilities, osteoporosis is common in people with a spinal cord injury or cerebral palsy.

Co-morbid conditions occur in addition to (and are unrelated to) a primary health condition associated with disability. One study indicated that adults with developmental disabilities had a similar or greater rate of chronic health conditions such as high blood pressure, cardiovascular disease, and diabetes (due to increased physical inactivity) than people without disabilities.

Age-related conditions: The ageing process for some groups of people with disabilities begins earlier than usual and they may experience age related health conditions (such as osteoporosis, loss of strength and balance) more frequently.

Risk behaviours: People with disabilities have higher rates of engaging in risky behaviours such as smoking, alcohol conumption, poor diet and physical inactivity as compare to general population.

Violence :People with disabilities are at greater risk of violence than those without disabilities.

Unintentional injury: People with disabilities are at higher risk of unintentional injury from road traffic crashes, burns, falls, and accidents related to assistive devices.

Assistive technologies and assistive devices such as crutches, prostheses, wheelchairs, and tricycles in mobility impairments; hearing aids and cochlear implants for hearing impairments; ocular devices, talking books, and software for screen magnification and reading for people with visual impairments may be advised according to the user and the user’s environment.

Rehabilitation: It is an important aspect of management for people with disability. It involves combined and coordinated use of medical, social, educational, and vocational measures for training or retraining the individual to the highest possible level of functional ability.

Community-based rehabilitation (CBR) was initiated by WHO to enhance the quality of life for people with disabilities and their families; meet their basic needs; and ensure their inclusion and participation. CBR is implemented through the combined efforts of people with disabilities, their families and communities, and relevant government and non-government health, education, vocational, social and other services.  

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Role of Physiotherapy for disabled people

Disabled people spend their time in same position which affect their range of motion,when body is not mobile,that sedentary life style can affect the health and also weight of disabled people.With the help of physiotherapist the person with disability can stretch and strengthen muscles,this will help to give them more mobility and give positive impact on overall body.

• Decrease Pain: physiotherapist not only help the people to keep them fit but also help to reduce pain and stress.
• Physiotherapist prescribed mobility equipments to help disabled people stand and walk without help of other people like family members or friends.
• Physiotherapist asses, diagnose and provide exercise programs to strengthen the muscles.

For example

Strengthening exercises improve function, quality of life and reduce risk of injury.

Balance exercise helps in preventing falls

Relaxation exercise helps patient to calm mind and progressive muscle relaxation (PMR) relax muscle and reduce tension.

Flexibility exercise increase range of motion, decrease pain and stiffness.

      “During exercise endorphins release to energize mood, relieve stress and also boost self esteem”.

The Equality Act 2010 states “that disabled people should be treated equally, and protection from discrimination applies in many situations such as education, employment, exercise of public functions, goods, services, facilities and transport”.

Goals

• Education:

Should have the right to quality education at all levels of disabled people.

• Employment: 

Disabled people have the right to work in an open and accessible environment.

• Health care: 

They have right to highest standard of health care without discrimination.

Conclusion

People with disabilities have a higher rate of needs than non-disabled. The result indicates the importance of needs and wants of parents and patients should be respected so that the parents play an active role. There is a need to increase the rehabilitation center and staff to make them accessible for their needs in rural areas. Disabled people face problems in dealing with healthcare facilities, the barriers increase when a person is disabled and it can be decreased by giving them education and facilities which are easily accessible.

Occupational therapists ensure the people recovering from disability and promote physical and mental health through therapeutic use of everyday activities. They teach self care skills (cooking, eating, dressing) and enable them to return to their life.

On the other hand, Physiotherapists help the disabled people through exercise, manual therapy, electrotherapy, mobilization, manipulation for the management of pain and improve the range of motion.

legislation and act related to disablility

The Department administers the following three Acts:-

1. The Rights of Persons with Disabilities Act, 2016
2. The National Trust for the Welfare of Persons with Autism, Cerebral Palsy, Mental Retardation and Multiple Disabilities Act, 1999
3. Rehabilitation Council of India Act, 1992

The Rights of Persons with Disabilities (RPwD) Act, 2016

The RPwD Act, 2016 was enacted on 28.12.2016 which came into force from 19.04.2017. The salient features of the Act are:-

1. Responsibility has been cast upon the appropriate governments to take effective measures to ensure that the persons with disabilities enjoy their rights equally with others.
2. Disability has been defined based on an evolving and dynamic concept.
3. The Act covers the following specified disabilities:-

1. Physical Disability
   1. Locomotor Disability
      1. Leprosy Cured Person
      2. Cerebral Palsy
      3. Dwarfism
      4. Muscular Dystrophy
      5. Acid Attack Victims
   2. Visual Impairment
      1. Blindness
      2. Low Vission
   3. Hearing Impairment
      1. Deaf
      2. Hard of Hearing
   4. Speech and Language Disability
2. Intellectual Disability
   1.  Specific Learning Disabilities
   2. Autism Spectrum Disorder
3. Mental Behaviour (Mental Illness)
4. Disability caused due to-
   1. Chronic Neurological Conditions such as-
      1. Multiple Sclerosis
      2. Parkinson’s Disease
   2. Blood Disorder-
      1. Haemophilia
      2. Thalassemia
      3. Sickle Cell Disease
5. Multiple Disabilities

1. Additional benefits have been provided for persons with benchmark disabilities and those with high support needs.
2. Every child with benchmark disability between the age group of 6 and 18 years shall have the right to free education.
3. 5% reservation in seats in Government and Government aided higher educational institutions for persons with benchmark disabilities.
4. Stress has been given to ensure accessibility in public buildings (both Government and private) in a prescribed time-frame.
5. 4% reservation in Government jobs for certain persons or class of persons with benchmark disability.
6. The Act provides for grant of guardianship by District Court or any authority designated by the State Government under which there will be joint decision – making between the guardian and the persons with disabilities.
7. Broad based Central & State Advisory Boards on Disability to be set up as policy making bodies.
8. The Act provides for strengthening of the Office of Chief Commissioner of Persons with Disabilities and State Commissioners of Disabilities which will act as regulatory bodies and Grievance Redressal agencies and also monitor implementation of the Act. These Offices will be assisted by an Advisory Committee comprising of experts in various disabilities.
9. Creation of National and State Fund to provide financial support to the persons with disabilities.
10. The Act provides for penalties for offences committed against persons with disabilities.
11. Designated special Courts to handle cases concerning violation of rights of PwDs.

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THE NATIONAL POLICY FOR PERSONS WITH DISABILITIES, 2006

Recognizing that the Persons with Disabilities constitute a valuable human resource for the country and that a majority of such persons can lead a better quality of life if they have equal opportunities and effective access to rehabilitation measures, the Government, with a view to create an environment that provides such persons equal opportunities for protection of their rights and full participation in society, formulated and brought out the National Policy for Persons with Disabilities.

2. With focus on Prevention of Disabilities and Rehabilitation Measures, the Policy provides for the following:-

I.      Prevention of Disabilities

II.     Rehabilitation Measures

II A. Physical Rehabilitation Strategies :

• Early Detection and Intervention
• Counselling & Medical Rehabilitation
• Assistive Devices
• Development of Rehabilitation Professionals

II B. Education for Persons with Disabilities

II C. Economic Rehabilitation of Persons with Disabilities :

• Employment in Government Establishments
• Wage employment in Private Sector
• Self-employment

III.    Provisions for Women with Disabilities

IV.   Provisions for Children with Disabilities

V.    Barrier-free Environment

VI.   Issue of Disability Certificates

VII.  Social Security

VIII. Promotion of Non-Governmental Organizations (NGOs)

IX.   Collection of regular information on Persons with Disabilities

X.    Research

XI.   Sports, Recreation and Cultural life

XII.  Amendments to existing Acts dealing with the Persons with Disabilities

4. Accordingly, the principal areas of intervention under the Policy are :  Prevention, Early-detection and Intervention; Programmes of Rehabilitation; Human Resource Development; Education of Persons with Disabilities; Employment; Barrier free-environment; Social Protection; Research; Sports, Recreation and Cultural Activities.

5.       The following mechanism is in place for implementation of the National Policy:

        i. Department of Empowerment of Persons with Disabilities, Ministry of Social Justice & Empowerment is the nodal Department to coordinate all             matters relating to implementation of the Policy.

1.  The Central Coordination Committee, with stakeholder representation, coordinates matters relating to implementation of the National Policy. There is a similar Committee at the State level.
2. The Ministries of Home Affairs; Health & Family Welfare; Rural Development; Urban Development; Youth Affairs & Sports; Railways; Science & Technology; Statistics & Programme Implementation; Labour; Panchayati Raj and Women & Child Development and Departments of Elementary Education & Literacy, Secondary & Higher Education; Road Transport & Highways; Public Enterprises; Revenue; Information Technology and Personnel & Training are also identified for implementation of the policy.
3.  Panchayati Raj Institutions and Urban Local Bodies are associated in the functioning of the District Disability Rehabilitation Centres. They are required to play a crucial role in the implementation of the National Policy to address local level issues.
4. The Chief Commissioner for Persons with Disabilities at Central level and State Commissioners at the State level, play key role in implementation of the National Policy, apart from their respective statutory responsibilities.

UNITED NATIONS CONVENTION ON THE RIGHTS OF PERSONS WITH DISABILITIES (UNCRPD), 2006

The Convention was adopted by UN General Assembly on December 13, 2006 and opened for signing by the State Parties on March 30, 2007. Adoption of the Convention has really imparted empowerment to Persons with Disabilities across the globe to demand their rights and make State, private and civil society agencies accountable for enjoying their rights.

2. India is one of the few first countries which ratified the Convention. Consequent upon signing the Convention on March 30, 2007, India  ratified the Convention on 01.10.2007. The Convention has come into force from May 3, 2008. The Convention places the following three important obligations on each State Party: –

a) Implementation of the provisions of the Convention;

b) Harmonization of the country laws with the Convention and

c) Preparation of a Country Report.

3. Taking concrete measures for effective implementation of the Convention, all the concerned Central Ministries were requested to implement the provisions of the Convention as might be applicable to each of them. Similarly, all the Chief Ministers of States and Administrators of UTs were also requested to examine different provisions/obligations under the Convention as might relate to them and to take effective steps for their early implementation. The State Governments/UT Administrators were also asked to furnish a status report in this regard so that the same could be utilized towards preparing the Country Report. Rigorous monitoring and follow-up was being done in this regard so as to fulfill obligations of the Convention. India’s First Country Report was submitted to UN Committee on Rights of Persons in November, 2015.

Incheon Strategy

Incheon Strategy “To make the Right Real” for Persons with Disabilities in Asia and Pacific. The Ministers and representative of members and associate members of the United Nations Economic and Social Commission for Asia and the Pacific (ESCAP) assembled at the High Level Inter Governmental meeting on the final review of the implementation of the Asian and Pacific Decade of Disabled Persons, 2003-2012 held at Incheon, Korea from 29th October – 2 nd November, 2012 and adopted the Incheon Strategy “Make the Right Real” for Persons with Disabilities in Asia and the Pacific. The ESCAP in its 69th Session held from 25th April – 1 st May, 2013 passed the resolution endorsing the Ministerial declaration and Incheon Strategy.

2. The Incheon Strategy to make the Right Real for Persons with Disabilities in Asia and Pacific sets out the following 10 goals:-

1. Reduce Poverty and enhance work and employment prospects;
2. Promote participation in political processes and in decision making;
3. Enhance access to the physical environment, public transportation, knowledge, information and communication;
4. Strengthen social protection;
5. Expand early intervention and education of children with disabilities;
6. Ensure gender equality and women‟s empowerment;
7. Ensure disability-inclusive disaster risk reduction and management;
8. Improve the reliability and comparability of disability data;
9. Accelerate the ratification and implementation of the Convention on the Rights of Persons with Disabilities and harmonisation of National Legislation with the Convention; and x. Advance sub-regional, regional and inter-regional co-operation.

3. The Incheon Strategy spells out Action Plans at the regional, sub-regional and regional levels to achieve the above goals and also contains the core indicators for tracking the progress of implementation.

4.  In order to oversee implementation of the Incheon Strategy, the UNESCAP has constituted a Working Group on the Asian and Pacific Decade for Persons with Disabilities, 2013-2022. The Working Group consists for Government representatives from 15 member countries including India and 15 Civil Society Organisations in the Asia and Pacific Region. The First meeting of the Working Group was held at Incheon, Korea during 25-26 February, 2014. The Second Session of the Working Group was held in Delhi during 2-3 March, 2015 hosted by Department of Empowerment of Persons with Disabilities in association with UNESCAP Secretariat. Third and Fourth Session of the Working Group were held in Bangkok.

5. Subsequently, high-level inter-Governmental meeting was held on mid-point review of the Asia Pacific Decade for Persons with Disabilities in Beijing from 27^th November to 1^st December, 2017. After deliberations in the meeting, Beijing Declaration was adopted which outlines action plan for the State parties to achieve the targets of Incheon Strategy in the next five years.

Scheme

Research and Development

The Department of Empowerment of Persons with Disabilities has launched a new Central sector scheme on “Research on disability related technology, products and issues‟. In January, 2015 with the objective to promote research of service models and programmes on the basis of life cycle needs, holistic development of the individuals and their families and creating an enabling environment for the empowerment of the persons with disabilities and promote research in prevention and prevalence of disability and the application of science & technology for the development of indigenous, appropriate aids and appliances.

The scheme has 2 components

(i) Research and Development of assistive technology and product development devices; and

(ii) Scheme for study/research/survey/internship and periodical collection of data related to disability. The State Governments, the national institutes under the Department have been requested to submit their proposal in accordance with the scheme. Until 2017-18 the scheme was implemented as a standalone scheme of the Department. From the year 2018-19 it has become part of the umbrella scheme SIPDA.

2. The Department has developed guidelines for grant of financial assistance for R&D projects under SIPDA.

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Polymyalgia rheumatica is an inflammatory disorder that causes muscle pain and stiffness, especially in the shoulders and hips. Signs and symptoms of polymyalgia rheumatica (pol-e-my-AL-juh rue-MAT-ih-kuh) usually begin quickly and are worse in the morning.

Most people who develop polymyalgia rheumatica are older than 65. It rarely affects people under 50.

This condition is related to another inflammatory condition called giant cell arteritis. Giant cell arteritis can cause headaches, vision difficulties, jaw pain and scalp tenderness. It’s possible to have both conditions together.

Polymyalgia rheumatica (PMR) is a relatively common chronic inflammatory condition of unknown etiology that affects elderly individuals. It is characterized by proximal myalgia of the hip and shoulder girdles with accompanying morning stiffness that lasts for more than 1 hour.  Approximately 15% of patients with PMR develop giant cell arteritis (GCA), and 40-50% of patients with GCA have associated PMR. Despite the similarities of age at onset and some of the clinical manifestations, the relationship between GCA and PMR is not yet clearly established. 

Pathophysiology

The cause of polymyalgia rheumatica (PMR) is unknown. PMR is closely linked to giant cell arteritis (GCA, temporal arteritis), although it is controversial whether GCA and PMR are two separate diseases or part of the same spectrum of disease. One hypothesis is that in a genetically predisposed patient, an environmental factor, possibly a virus, causes monocyte activation, which helps determine the production of cytokines that induce manifestations characteristic of PMR and GCA. However, although several infectious agents have been investigated as possible triggers, results are inconclusive. 

Immunogenetic studies support a polygenic basis for GCA and PMR. Occurrence in siblings and increased prevalence in those of Northern European heritage suggest a genetic role in the pathophysiology of the disease. Although most studies confirm an association between HLA-DRB1*04 alleles and GCA, the strength of this association with PMR varies between different populations. Interleukin (IL)–1 and tumor necrosis factor–alpha (TNF-α) gene polymorphisms have weak association with GCA and PMR. In Spain, an IL-6 polymorphism was associated with the expression of PMR symptoms in GCA patients. Additionally, in this Spanish population, the RANTES polymorphism was associated with PMR and not GCA. 

Pathologically, GCA and PMR are similar, except that significant vascular involvement does not occur in pure PMR. Synovitis, bursitis, and tenosynovitis around the joints, especially the shoulders, hips, knees, metacarpal phalangeal joints, and wrists, are seen in PMR. Inflammation is thought to start within the synovium and bursae, with recognition of an unknown antigen by dendritic cells or macrophages.

Systemic macrophage and T-cell activation are characteristic of both GCA and PMR. Patients often have an elevated IL-6 level, which is likely responsible for the systemic inflammatory response in both GCA and PMR. Most studies in PMR show that a decrease in the level of circulating IL-6 correlates with remission of clinical symptoms. Data on other circulating cytokines (eg, IL-1, IL-2, TNF-α, IL-10) are too scant to draw any conclusions. However, studies do show that interferon-gamma (IFN-γ) is expressed in nearly 70% of temporal artery biopsy samples from patients with GCA but is not detected in patients with isolated PMR, suggesting IFN-γ may be crucial to the development of GCA. 

Although PMR causes severe pain and stiffness in the proximal muscle groups, no evidence of disease is present on muscle biopsy. Muscle strength and electromyographic findings are normal. Instead, the inflammation is at the level of the synovium and bursae, with MRI studies revealing periarticular inflammation as well as bursitis in the bursae associated with both the shoulder and hip girdles. 

Some evidence suggests the presence of cell-mediated injury to the elastic lamina in the blood vessels in the affected muscle groups. A prospective study of 35 patients with isolated PMR noted vascular (¹⁸F) fluorodeoxyglucose positron emission tomography (FDG-PET) imaging at diagnosis in 31% of patients, predominantly at the subclavian arteries, but at a much lower intensity than in GCA patients. Increased FDG uptake in the shoulders was seen in 95% of the patients, in the hips in 89%, and in the spinous processes of the cervical and lumbar vertebrae (correlating with interspinous bursitis) of 51% of the patients with isolated PMR. 

A study of circadian variation in PMR found that plasma concentrations of IL-6, IL-8, TNF-α, and IL-4 peaked between 4 and 8 am in both untreated patients and controls, although levels of those cytokines were higher throughout the day in patients. The peak in cytokines matched the early-morning peak of pain and stiffness in untreated patients. In addition, melatonin levels were consistently higher in patients than in controls and varied with time, peaking around 2 am, suggesting that melatonin stimulates cytokine production, which in turn accounts at least partly for PMR symptoms. 

PMR is a clinical diagnosis based on the complex of presenting symptoms and the exclusion of the other potential diseases . Corticosteroids are considered the treatment of choice, and a rapid response to low-dose corticosteroids is considered pathognomonic. Patients who are at risk for relapse, have steroid-related adverse effects, or need prolonged steroid therapy may benefit from the addition of methotrexate or tocilizumab. 

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Etiology

The exact cause (or causes) of polymyalgia rheumatica (PMR) is unknown. The disease is more common among northern Europeans, which may indicate a genetic predisposition. Other risk factors for PMR are an age of 50 years or older and the presence of GCA. PMR has been reported as a rare complication of cancer therapy with immune checkpoint inhibitors (eg, nivolumab).

An autoimmune process may play a role in PMR development. PMR is associated with the HLA-DR4 haplotype. A high level of IL-6 is associated with increased disease activity.

History

Patients with polymyalgia rheumatica (PMR) were often in good health prior to disease onset, which is abrupt in about 50% of patients. In most patients, symptoms appear first in the shoulder girdle. In the remainder, the hip or neck are involved at onset. At presentation, symptoms may be unilateral but they usually become bilateral within a few weeks.

The symptoms include pain and stiffness of the shoulder and hip girdle. The stiffness may be so severe that the patient may have a great difficulty rising from a chair, turning over in bed, or raising the arms above shoulder height. Stiffness after periods of rest (gel phenomenon) as well as morning stiffness of more than 1 hour typically occurs.

Muscle weakness is not a feature of PMR. However, this can be difficult to assess in the setting of pain, especially if symptoms are protracted and untreated, resulting in disuse atrophy.

Patients may also describe distal peripheral joint swelling or, more rarely, limb edema. Carpal tunnel syndrome can occur in some patients. Most patients report systemic features as listed below.

Several diagnostic criteria for PMR exist. One set of diagnostic criteria is as follows  :

• Age of onset 50 years or older
• Erythrocyte sedimentation rate ≥40 mm/h
• Pain persisting for ≥1 month and involving 2 of the following areas: neck, shoulders, and pelvic girdle
• Absence of other diseases capable of causing the same musculoskeletal symptoms
• Morning stiffness lasting ≥1 hour
• Rapid response to prednisone (≤20 mg)

In 2012, the European League Against Rheumatism and the American College of Rheumatology published new provisional classification criteria for PMR in patients aged 50 or older with bilateral shoulder aching and elevated inflammatory markers. These are not diagnostic criteria, but rather are designed for enrolling patients into clinical trials of new treatments for PMR. This collaborative initiative resulted in a scoring algorithm based on the following criteria:

• Morning stiffness >45 minutes (2 points)
• Hip pain/limited range of motion (1 point)
• Absence of rheumatoid factor and/or anti–citrullinated protein antibody (anti-CCP) (2 points)
• Absence of peripheral joint pain (1 point)

A score of ≥4 points has a 68% sensitivity and 78% specificity for discriminating PMR from other comparison patients. There is also an additional ultrasound criteria (1 point if positive findings), which can add up to a score of ≥5 points that is associated with a 66% sensitivity and 81% specificity for PMR. 

Systemic findings in more than 50% of patients are as follows:

• Low-grade fever and weight loss
• Malaise, fatigue, and depression
• Difficulty rising from bed in the morning
• Difficulty getting up from the toilet or out of a chair
• Difficulty completing daily life activitiesHigh, spiking fevers (rare, should prompt evaluation for underlying infection, malignancy, or vasculitis)

Musculoskeletal findings are as follows  :

• Morning stiffness for ≥1 hour, often more prolonged
• Muscle stiffness after prolonged inactivity
• Synovitis of proximal joints and periarticular structures
• Peripheral arthritis (in 25% of patients)
• Carpal tunnel syndrome (in about 15% of patients)
• Distal extremity swelling (in approximately 12%)
• Possible development of arthralgia and myalgia up to 6 months after onset of systemic symptoms

Many investigators believe that nonerosive synovitis and tenosynovitis are responsible for many symptoms of PMR.

Physical Examination

PMR is a clinical diagnosis based on the complex of the presenting symptoms and exclusion of the other potential diseases. The symptoms and signs of PMR are nonspecific, and objective findings on physical examination are often lacking.

General symptoms are as follows:

• Fatigued appearance
• Low-grade temperature
• Distal extremity swelling with pitting edema

Musculoskeletal findings are as follows:

• Normal muscle strength; no muscle atrophy typically present at initial presentation
• Pain in the shoulder and hip with movement; active range of motion may be decreased because of pain
• Transient synovitis of the knee, wrist, and sternoclavicular joints; a more peripheral nonerosive arthritis may be seen in some cases
• Tenderness to palpation with decreased active range of motion in the musculature of the proximal hip/leg and/or shoulder/arm girdle

In later stages, disuse muscle atrophy with proximal muscle weakness may occur. Contractures of the shoulder capsule may lead to limitation of passive and active movements.

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Symptoms

The signs and symptoms of polymyalgia rheumatica usually occur on both sides of the body and might include:

• Aches or pain in your shoulders
• Aches or pain in your neck, upper arms, buttocks, hips or thighs
• Stiffness in affected areas, particularly in the morning or after being inactive for a time
• Limited range of motion in affected areas
• Pain or stiffness in your wrists, elbows or knees

You might also have more-general signs and symptoms, including:

• Mild fever
• Fatigue
• A general feeling of not being well (malaise)
• Loss of appetite
• Unintended weight loss
• Depression

Risk factors

Risk factors for polymyalgia rheumatica include:

• Age. Polymyalgia rheumatica affects older adults almost exclusively. It most often occurs between ages 70 and 80.
• Sex. Women are about two to three times more likely to develop the disorder.
• Race. Polymyalgia rheumatica is most common among white people whose ancestors were from Scandinavia or northern Europe.

Complications

Symptoms of polymyalgia rheumatica can greatly affect your ability to perform everyday activities, such as:

• Getting out of bed, standing up from a chair or getting out of a car
• Combing your hair or bathing
• Getting dressed

Diagnosis

A physical exam, including joint and neurological exams, and test results can help your doctor determine the cause of your pain and stiffness. During the exam, he or she might gently move your head and limbs to assess your range of motion.

Your doctor might reassess your diagnosis as your treatment progresses. Some people initially given a diagnosis of polymyalgia rheumatica are later reclassified as having rheumatoid arthritis.

Tests your doctor might recommend include:

• Blood tests. Besides checking your complete blood counts, your doctor will look for two indicators of inflammation — erythrocyte sedimentation rate (sed rate) and C-reactive protein. However, in some people with polymyalgia rheumatica, these tests are normal or only slightly high.
• Imaging tests. Increasingly, ultrasound is being used to distinguish polymyalgia rheumatica from other conditions that cause similar symptoms. MRI can also identify other causes of shoulder pain, such as joint changes.

Monitoring for giant cell arteritis

Your doctor will monitor you for signs and symptoms that can indicate the onset of giant cell arteritis. Talk to your doctor immediately if you have any of the following:

• New, unusual or persistent headaches
• Jaw pain or tenderness
• Blurred or double vision or visual loss
• Scalp tenderness

If your doctor suspects you might have giant cell arteritis, he or she will likely order a biopsy of the artery in one of your temples. This procedure, performed during local anesthesia, involves removing a small sample of the artery, which is then examined for inflammation.

Treatment

Treatment usually involves medications to help ease your signs and symptoms. Relapses are common.

Medications

• Corticosteroids. Polymyalgia rheumatica is usually treated with a low dose of an oral corticosteroid, such as prednisone (Rayos). You’ll likely start to feel relief from pain and stiffness within the first two or three days.After the first two to four weeks of treatment, your doctor might begin to gradually decrease your dosage depending on your symptoms and the results of blood tests. Because of potential side effects, the goal is to keep you on as low a dose as possible without triggering a relapse in your symptoms.Most people with polymyalgia rheumatica need to continue the corticosteroid treatment for a year or more. You’ll need frequent follow-up visits with your doctor to monitor how the treatment is working and whether you have side effects.Long-term use of corticosteroids can result in serious side effects, including weight gain, loss of bone density, high blood pressure, diabetes and cataracts. Your doctor will monitor you closely for problems. He or she might adjust your dose and prescribe treatments to manage reactions to corticosteroid treatment.
• Calcium and vitamin D. Your doctor will likely prescribe daily doses of calcium and vitamin D supplements to help prevent bone loss as a result of corticosteroid treatment. The American College of Rheumatology recommends 1,000 to 1,200 milligrams of calcium supplements and 600 to 800 international units of vitamin D supplements for anyone taking corticosteroids for three months or more.
• Methotrexate. Joint guidelines from the American College of Rheumatology and the European League Against Rheumatism suggest using methotrexate (Trexall) with corticosteroids in some patients. This is an immune-suppressing medication that’s taken by mouth. It might be useful early in the course of treatment or later, if you relapse or don’t respond to corticosteroids.

Medication Summary

The goals of therapy in polymyalgia rheumatica (PMR) are to control painful myalgia, to improve muscle stiffness, and to resolve constitutional features of the disease. Oral corticosteroids are the first line of treatment. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful as adjuncts to corticosteroids during tapering, or alone in mild cases; however, because they are associated with increased drug-related morbidity, they should be used with caution, especially in elderly patients. Steroid-sparing agents may be beneficial.

The interleukin-6 receptor antagonist tocilizumab is approved for use in giant cell arteritis and has demonstrated benefit for PMR in several case series and retrospective studies.  However, controlled trials are needed to fully establish the efficacy of tocilizumab in PMR, and it has not yet been approved for this indication by the US Food and Drug Administration.

Physical therapy

Most people who take corticosteroids for polymyalgia rheumatic return to their previous levels of activity. However, if you’ve had a long stretch of limited activity, you might benefit from physical therapy. Talk with your doctor about whether physical therapy is a good option for you.

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Penis captivus allegedly occurs when a penis becomes stuck in a vagina during sexual intercourse. Reports of this happening are incredibly rare.

Very few reports have documented the existence of penis captivus. What reports there are have led many people to question whether it really happens.

The penis becoming stuck in the vagina is one possible outcome of a condition called vaginismus, in which the vagina involuntarily closes due to muscle spasms in the pelvic floor.

If penis captivus occurs, the effect is likely very temporary. If both partners relax and give it some time, the muscles should relax, allowing the couple to separate.

Is it common?

It sounds like the stuff of urban legend, but it’s possible for a penis to get stuck inside a vagina during intercourse. This condition is called penis captivus, and it’s a  occurrence. It’s so rare, in fact, that anecdotal reports are the only way doctors and health experts know it happens.

It’s unclear how often penis captivus occurs because couples may be able to disconnect from one another before medical attention is necessary. And they may never report the incident to a doctor.

In the event that you find yourself unable to disengage from intercourse, it’s important to stay calm. Knowing what’s happening can help you and your partner wait out penis captivus.

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How can it occur?

During arousal, the penis fills with blood, becoming erect in preparation for sexual intercourse. For females, the walls of the vagina relax and the vulva lubricates in preparation for sexual penetration.

The vaginal walls are made up of muscular tissue, which expands and contracts at different times during sex, such as during an orgasm. These contractions can be very strong, and they are sometimes stronger than usual.

In some rare cases, the vagina may contract with enough force to latch onto the penis. This could make it difficult for the partners to separate.

However, after these vaginal contractions come to an end, the vaginal walls will relax. The time that it takes for this to happen varies. The blood will eventually flow away from the penis, and it will become smaller and softer. When either or both of these things occur, the partners should be able to separate.

Due to the lack of medical documentation, it may be safe to assume that penis captivus — when it does occur — is a temporary phenomenon that may only cause fleeting discomfort.

What to do if it occurs

If either partner feels penis captivus starting to happen, they should try to stay calm. Added stress can lead to more muscular tension, which can make the phenomenon last longer.

It is important not to try to force the penis out of the vagina. Doing so can hurt one or both partners. It is also important not to try to open the vagina or pry the penis out manually.

Taking deep breaths may help both partners become or remain calm. Distracting each other or making a joke out of the situation can also relieve the tension and reduce arousal in the genitals.

Staying calm and allowing the muscles in both bodies to relax can help resolve the issue as soon as possible without complication.

If this phenomenon does occur, it will likely only last for a moment before the penis and vagina relax.

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