GENERAL POINTS APPLICABLE IN ALL CASES

Understand the significance of coexisting medical and other problems, always liaising with the person’s medical and other health professionals.

Review the current situation before each exercise session.

Be aware that analgesic and anti-inflammatory medication could be masking physical deterioration.

Always begin by correcting postural faults and associated muscle malfunction.

Always focus on correct spine alignment and stability in preparation for exercising the extremities.

Ultimately provide an exercise programme appropriate to the individual’s level of fitness, so as to progressively increase strength and stamina and thereby build on the individual’s trust and confidence.

Specific points follow each medical condition.

EATING DISORDERS

These constitute a form of behavioural problem associated with physiological changes that may lead to physical disability. There is a disturbance of eating habits and of weight control behaviour.

Anorexia nervosa and bulimia nervosa comprise the vast majority of cases in the context of fitness for exercise. They are an important cause of morbidity in girls and young women but are much less common in men. The aetiology is complex and poorly understood but involves social, psychological and biological factors, and there is a genetic predisposition. Subjects have an exaggerated perception of their size and shape that they feel the need to reduce and control, either by starvation or by other less obvious means.

In anorexia nervosa there is self-starvation leading to marked weight loss. Subjects may be physically overactive to a punishing degree and develop various ruses to distract attention from their behaviour. They may wear voluminous clothing in the pockets of which they can conceal heavy objects when attending weight checks. There may be misuse of laxatives and diuretics to complement a regimen of strict dieting, or even frank starvation. Subjects may be seriously underweight with low muscle bulk and weakness, and low bone density with progressive osteoporosis. Thyroid underactivity, with cold extremities, cardiovascular depression with hypotension and bradycardia, constipation and amenorrhoea may develop. Many are chronically unwell, but even marked changes can usually be reversed, with the possible exception of reduced bone density. However, some may die from the physical complications or, ultimately, from suicide.

In bulimia nervosa self-starvation alternates with self-induced vomiting after eating large amounts of food. Weight may be normal but the bouts of vomiting may lead to dehydration and metabolic disturbances, including alkalosis and electrolyte depletion with cardiac arrhythmias and kidney damage. There may also be obvious dental damage from the frequent passage of gastric acid over the teeth during vomiting.

Management

Those with these eating disorders may see Pilates as an additional contribution to image control and to their overactive exercise regimens, and it is important to identify these motivating factors as well as the extent of any underlying physical abnormalities when initially assessing the suitability of such clients for Pilates exercise programmes, whether bulimic or, especially, anorexic.

Good teaching practice

This would include:

awareness of risks such as dehydration and electrolyte imbalance

avoidance of overactive regimens

a gradual building of strength and endurance.

OBESITY

This is an increasing problem in much of the developed world. In the United Kingdom, for example, 50% of the population is overweight and 20% is obese, as judged by body mass index (BMI) which is calculated by dividing body weight by height squared (kg/m²). If the normal BMI range is 18.5–24.9, then 25 or more is overweight, 30 or more is obese, 40 or more is extremely obese, and so on. Most weight gain occurs between the ages of 20 and 40. Whilst there may be specific causal factors in some cases, the aetiology generally involves behavioural and genetic factors.

Whilst obesity has become much more prevalent in the last 20 years, actual food intake has not been shown to increase over the same period, whereas there seems to have been an overall decrease in physical activity. However, it is important to realize that, although food intake may not have increased, its composition has been changing towards energy-dense foods that combine high fat and sugar content with low bulk. Increased appetite for food, and also alcohol, may also follow cessation of smoking. Such behavioural factors have now come to be regarded as of prime importance in the trend towards obesity.

Genetics factors may also operate and, whilst felt to be relatively much less common, may underlie the difference between abdominal (apple-shaped) and generalized hip and thigh (pear-shaped) body weight distribution.

Specific causes of weight gain should always be borne in mind, such as endocrine abnormalities of the thyroid and of the pituitary–adrenal systems. The numerous complications of weight gain – in particular, non-insulin dependent diabetes mellitus, hypertension, stroke, coronary heart disease, breathing problems, weight-related musculoskeletal disorders and arthritis, and urinary stress incontinence – are important factors to be taken into account when assessing clients for, and designing, their exercise programmes.

CHRONIC FATIGUE SYNDROME

This is the term now given to a loosely defined condition, other names for which include post-viral fatigue syndrome, myalgic encephalomyelitis (ME), epidemic neuromyasthenia and Icelandic disease.

There is an abnormal degree of muscle fatigue after (often minimal) physical or even mental exercise that may readily reach the point of exhaustion, following which recovery may be very slow. In addition to abnormal fatigability, there is a wide variety of features including headache, dizziness, poor concentration, impaired memory, irritability and sleep disturbance, together with muscle aches and, in some cases, fever and enlarged lymph glands. There may also be various cardiac or gastrointestinal symptoms such as palpitations, chest pain and tightness, abdominal pain and cramps, etc. Whilst there are often symptoms of anxiety and depression, women get chronic fatigue syndrome much more commonly than men, but for unknown reasons.

As much of this may occur after a viral illness, particularly influenza, and is normally short lived, a diagnosis of chronic fatigue syndrome is now made only after a duration of some 6 months, without necessarily any history of viral illness, but infectious mononucleosis (glandular fever), epidemic myalgia (Bornholm disease), hepatitis A (with or without clinical jaundice) and a wide variety of relatively mild viral illnesses have been implicated. Laboratory tests are usually normal, even though there may be a clear history typical of viraemia. Whilst the whole notion of this condition remains controversial, most medical authorities accept its existence, although it is still considered by some to constitute a wholly psychiatric disorder.

Management

This is based on behavioural and cognitive approaches aimed at gradually consistently increasing activity (graded exercise), and discouraging the tendency to rest rather than to exercise so as to improve confidence as well as stamina. The subject is encouraged to accept the need for exercise as the key to physical recovery. Some subjects respond to antidepressants of the serotonin reuptake inhibitor type such as fluoxetine (Prozac).

Not surprisingly, subjects with chronic fatigue syndrome may present, or be referred, for Pilates exercises and these can be expected to confer real benefit if the programme is carefully paced, depending on the severity of the features which must, of course, be regarded as very real to the subjects concerned. It is essential for the subject’s medical advisers to be aware of and to approve of what is proposed.

Faults in posture and muscles

These may include slouched position and overall muscle weakness. In particular, the spinal and posterior hip muscles may be affected due to prolonged periods of inactivity.

EPILEPSY

In epilepsy there is a tendency to recurrent seizures that are the effect of an electrical discharge in the brain and therefore a symptom of, rather than actual, brain disease. A single seizure is not epilepsy, although the recurrence rate after the first seizure is 70% in the first year, usually within the first couple of months.

In some cases it is only necessary to identify and eliminate certain triggering factors to control the condition. In others, only complex anticonvulsant medication programmes, or even brain surgery, can achieve adequate control. Triggering factors may include lack of sleep or other causes of fatigue, alcohol, or alcohol withdrawal, substance abuse, lights flickering at some critical frequency, as from a television screen or in a nightclub, and so on. Intercurrent infections or metabolic disturbances may also destabilize even well-controlled epileptics.

The aetiology of epilepsy covers an enormous variety of factors, congenital and acquired. In some disorders, seizures are the only symptoms, in others they are only one of several features. Primary generalized epilepsy usually develops in childhood or adolescence and is not associated with any structural, as opposed to functional, nervous system abnormality.

Secondary generalized epilepsy may be related to many factors, including a wide variety of drugs and metabolic disturbances, and certain uncommon genetic disorders.

Partial seizures arise from some abnormal focus in the cerebral cortex in the surface layer of the brain and affect first a limb or other localized area that will often progress to generalized seizures. Causes in otherwise fit people include previous head injury or following essential brain surgery. There may be a history of meningitis, encephalitis or certain tropical diseases, or genetic or degenerative conditions.

Major seizures, as classically associated with epilepsy, cause loss of consciousness with the patient falling to the ground with a history of ‘blackouts’, although this term often refers also to minor seizures without loss of consciousness.

A typical major seizure with tonic–clonic features may begin with a partial phase or aura that the patient may not subsequently recall. Rigidity with loss of consciousness follows, and injuries may occur if the patient falls to the ground or against something, especially if out of doors in traffic, etc. Breathing ceases and cyanosis may follow. This rigid tonic phase should soon give way to the clonic phase, with alternating muscular contractions and relaxations so that the whole body jerks violently. There follows a flaccid relaxed phase, breathing is resumed and the colour and general appearance improve. After a few more minutes, consciousness begins to return, but confusion and disorientation may persist for over half an hour or more and memory of the event may not return for several hours.

There may be headache and generalized malaise, and tongue biting and urinary, or even bowel, incontinence may have occurred. Such major seizures can be most alarming to a casual observer.

A partial seizure, much less dramatic or even obvious, comprises an episode of altered consciousness without physical collapse. A form of ‘blackout’ or ‘absence’ occurs, with blank staring, with or without involuntary movements of the eyes, lips, limbs, etc., all lasting a few minutes. Consciousness returns but again there may be residual confusion, drowsiness, etc. As with major seizures, there may be an aura that the patient can usually recall. An aura may comprise a variety of features, including alterations of mood, memory and perception, visual hallucinations, nausea and abdominal pain, etc. Such phenomena may also be familiar to migraine suffers.

Many other forms of seizure may be encountered involving only motor or sensory features of one side of the body or a limb.

Late onset epilepsy in older people is common and the incidence in those over 60 years is rising. The difference between fits and faints may be less clear and the condition may present as a cause of confusion in the elderly. Minor simple absences may recur several times in a day. More recently, they have become easier to control with specific anticonvulsant medication.

Little can be done for a person whilst a major seizure is occurring, except first aid and common sense manoeuvres to prevent injury and other secondary complications.

MULTIPLE SCLEROSIS

In multiple sclerosis (MS), the most common neurological cause of long-term disability, the body may be setting up an immune or antibody–antigen reaction to its own tissues, an autoimmune condition in which the cells of the central nervous system (CNS) concerned with the production of myelin are attacked. Myelin occurs, and has a protective and nutrient effect, in relation to nerve fibres throughout the CNS, comprising the brain and spinal cord but not the peripheral nerves. A basic immune reaction could create an inflammatory response leading to loss of the myelin-producing cells that occur throughout the CNS and result in areas of demyelination. Electrical insulation of nerve fibres is impaired, impulse conduction is affected and ultimately nerve fibres are destroyed and areas of scarring result. The brain stem, optic nerve and the spinal cord tend to be the first areas affected.

The condition starts with a relatively acute phase of inflammation that begins the process of nerve damage. This initial acute phrase often responds to corticosteroids, but in the established condition nerve fibres are destroyed both by inflammation and by the loss of their myelin sheaths. However, the whole notion of MS as an autoimmune condition has recently come back into question so it has to be accepted that, at present, its real cause remains unknown.

The majority of subjects have a relapsing and remitting course, others have a slowly progressive course, and some progress rapidly and severely to early death. Onset is rare before puberty or after the age of 60, and is commoner in women. Drug treatment, however, continues to be based on beta-interferon and other immunomodulating agents, although their effectiveness is disputed.

The demyelinating lesions cause features that come on over days or weeks and may resolve over weeks or months. Different patterns of progress are encountered and in some cases there may be years or decades between attacks that range between mild visual and sensory deficits to more disabling motor deficit, but significant intellectual impairment is unusual until late in the disease.

Management

Management during an acute relapse will usually require hospital inpatient treatment involving high dose steroids and immunosuppressive drugs. Longer term complications and disabilities require a range of measures involving occupational and physiotherapy, together with a possible array of medications targeting specific disabilities.

Those in lengthy remission with minimal established disability may present themselves for Pilates exercises, or may be referred by physiotherapists once remission is underway. Regular exercise can assist recovery of muscle strength, promote confidence building and create well-being.

Faults in posture and muscles

These may include any of the postural habits and faults described in Chapter 3. In addition, as the disease progresses, balance and posture deteriorate according to the individual’s specific disabilities.

PARKINSON’S DISEASE

This is the commonest of a group of degenerative neurological conditions. Its main features include slowness of movement, rigidity, loss of postural reflexes and the well-known tremors.

The classic features may be absent initially, there being only tiredness, aches and pains, mental slowness and depression. Later, tremor appears, usually unilaterally at first, perhaps in an upper limb, but later becoming generalized, affecting limbs, mouth, tongue, etc. Slowness of movement may develop gradually, as may rigidity, causing stiffness and a flexed posture. Impaired postural reflexes may lead eventually to a tendency to falls. Muscle strength, reflexes and sensation remain normal. Intellectual faculties also remain normal, at least initially, belying the physical appearance.

Management

This is based on drug therapy that can benefit especially the slowness of movement and rigidity. Neurosurgical intervention may be used to treat tremor that has not been helped by drug therapy. Physiotherapy benefits Parkinson’s disease subjects at all stages by helping to reduce rigidity and abnormal posture.

Although postural improvement is of great importance, it must performed under the guidance of the person’s health care professionals.

Faults in posture and muscles

These may include any of the postural faults described in Chapter 3. In addition, as the disease progresses, posture becomes flexed and rigid, and there is a tendency to fall.

DIABETES MELLITUS

Diabetes mellitus is a clinical syndrome characterized by a raised blood sugar level (hyperglycaemia) due to an absolute or relative deficiency of the hormone insulin. The mechanism of action and the effects of deficiency of insulin are complex and involve the metabolism not only of glucose and other carbohydrates, but also of protein and fat, with secondary effects on water and electrolyte balance.

Whilst death may follow an acute diabetic metabolic derangement, a more long-standing chronic derangement associated with poor metabolic control may cause irreversible cell damage, affecting the vascular system in particular, with a wide variety of manifestations that comprise the complications of diabetes.

Blood glucose levels are normally tightly regulated within a narrow range which represents a balance between, on the one hand, entry of glucose into the circulation from storage forms in the liver, together with intestinal absorption after meals, and, on the other hand, uptake of glucose by the tissues, mainly the skeletal muscles, but also, most importantly, the brain, for which glucose is the principal fuel that must therefore be continuously supplied.

Whilst glucagon and adrenaline are the hormones that act to maintain hepatic glucose output, if required, between meals, it is insulin that counteracts the marked rise in blood glucose that would otherwise follow immediately upon a meal, by suppressing liver glucose output and stimulating its uptake by muscle and fat.

Insulin is secreted by special pancreatic beta cells directly into the pancreatic vein, as also is glucagon from the pancreatic alpha cells. These are distinct from the main pancreatic glandular cells, which secrete digestive juices into the duodenum, together with bile from the liver via the pancreatic and common bile ducts. Adrenaline, from the suprarenal medulla, is secreted directly into the adrenal veins.

The hyperglycaemia of diabetes develops because of an absolute (Type 1 diabetes) or relative (Type 2 diabetes) deficiency of insulin. In Type 1 diabetes, the absolute deficiency of insulin is due to either immunological or unknown factors. In Type 2 diabetes one or more of a variety of widely differing factors may operate to create a state of resistance to the action of insulin. These range from pancreatic disease affecting the entire gland, genetic defects, drug-induced effects, hormonal antagonism from various glands such as the pituitary, adrenal cortical, thyroid, etc., and from the placenta in pregnancy. Gestational diabetes refers to hyperglycaemia diagnosed for the first time during pregnancy in predisposed individuals. It may or may not resolve after delivery.

Glycosuria, the appearance of sugar in the urine, occurs when blood glucose levels exceed a certain level, the renal threshold for a particular individual. The excretion of glucose requires an obligatory increased excretion of water leading to the classic features of thirst and the passing of large volumes of urine (polyuria). These features may be less dramatic in Type 2 diabetes as it develops slowly over months or years, during which the renal threshold also rises and the symptoms of thirst and polyuria are mild so that detection of the condition tends to be delayed.

Testing of urine for glucose at routine medical examinations is the usual procedure that first detects diabetes but glycosuria may then be due merely to a low renal threshold when it is termed renal glycosuria, is relatively harmless and often occurs during normal pregnancy. However, the diagnosis depends ultimately on measurement of blood glucose levels. Sometimes an unduly rapid rise in blood glucose levels after a meal may exceed the renal threshold causing a so-called alimentary glycosuria that, like renal glycosuria, is benign. However, glycosuria in pregnancy should always be followed up with blood glucose measurements to distinguish it from an actual gestational diabetic state.

Testing of urine for ketones is also a routine procedure. Ketonuria is not necessarily associated with diabetes unless combined with hyperglycaemia when the diagnosis of diabetes becomes highly likely. When diabetes is suspected, confirmatory blood testing for glucose is required. Random raised levels may be misleading and must always be supplemented by measurement of fasting levels or a glucose tolerance test where levels are measured serially after an intake of a standard amount of glucose.

The major clinical features of diabetes are therefore due initially to hyperglycaemia and include, in addition to thirst, dry mouth and polyuria, nocturia (passage of urine during the night), fatigue, nausea, headache, weight change and a preference for sweet foods. The glycosuria, together with a lowered resistance to infection, also predisposes to genital thrush. These features are all more common in Type 1 diabetes compared with Type 2 in which symptoms may be absent or comprise only chronic fatigue or malaise.

Physical signs, other than perhaps weight loss, may be absent in Type 1 diabetes, but over 70% of Type 2 diabetics are overweight, at least in developed countries, and hypertension is present in around 50%. Other contrasting features are outlined in Table 2.1.

Table 2.1 Contrasting features between Type 1 and Type 2 diabetes

	Type 1	Type 2
Age of onset	< 40 years	> 50 years
Duration of symptoms	Weeks	Months to years
Body weight	Normal or low	Obese
Ketonuria	Yes	No
Fatal without insulin	Yes	No
Family history	Uncommon	Yes
Complications (vascular etc.) present at diagnosis	No	25%