The recurrence of a disease after an apparent recovery, or the return of symptoms after a remission.
Causes There is an inherited element: parents, children or siblings of schizophrenic sufferers have a one in ten chance of developing the disorder; a twin has a 50 per cent chance if the other twin has schizophrenia. Some BRAIN disorders such as temporal lobe EPILEPSY, tumours and ENCEPHALITIS seem to be linked with schizophrenia. Certain drugs – for example, AMPHETAMINES – can precipitate schizophrenia and DOPAMINE-blocking drugs often relieve schizophrenic symptoms. Stress may worsen schizophrenia and recreational drugs may trigger an attack.
Symptoms These usually develop gradually until the individual’s behaviour becomes so distrubing or debilitating that work, relationships and basic activities such as eating and sleeping are interrupted. The patient may have disturbed perception with auditory HALLUCINATIONS, illogical thought-processes and DELUSIONS; low-key emotions (‘?at affect’); a sense of being invaded or controlled by outside forces; a lack of INSIGHT and inability to acknowledge reality; lethargy and/or agitation; a disrespect for personal appearance and hygiene; and a tendency to act strangely. Violence is rare although some sufferers commit violent acts which they believe their ‘inner voices’ have commanded.
Relatives and friends may try to cope with the affected person at home, but as severe episodes may last several months and require regular administration of powerful drugs – patients are not always good at taking their medication
– hospital admission may be necessary.
Treatment So far there is no cure for schizophrenia. Since the 1950s, however, a group of drugs called antipsychotics – also described as NEUROLEPTICS or major tranquillisers – have relieved ?orid symptoms such as thought disorder, hallucinations and delusions as well as preventing relapses, thus allowing many people to leave psychiatric hospitals and live more independently outside. Only some of these drugs have a tranquillising e?ect, but their sedative properties can calm patients with an acute attack. CHLORPROMAZINE is one such drug and is commonly used when treatment starts or to deal with an emergency. Halperidol, tri?uoperazine and pimozide are other drugs in the group; these have less sedative effects so are useful in treating those whose prominent symptoms are apathy and lethargy.
The antipsychotics’ mode of action is by blocking the activity of DOPAMINE, the chemical messenger in the brain that is faulty in schizophrenia. The drugs quicken the onset and prolong the remission of the disorder, and it is very important that patients take them inde?nitely. This is easier to ensure when a patient is in hospital or in a stable domestic environment.
CLOZAPINE – a newer, atypical antipsychotic drug – is used for treating schizophrenic patients unresponsive to, or intolerant of, conventional antipsychotics. It may cause AGRANULOCYTOSIS and use is con?ned to patients registered with the Clorazil (the drug’s registered name) Patient Monitoring Service. Amisulpride, olanzapine, quetiapine, risperidone, sertindole and zotepine are other antipsychotic drugs described as ‘atypical’ by the British National Formulary; they may be better tolerated than other antipsychotics, and their varying properties mean that they can be targeted at patients with a particular grouping of symptoms. They should, however, be used with caution.
The welcome long-term shift of mentally ill patients from large hospitals to community care (often in small units) has, because of a lack of resources, led to some schizophrenic patients not being properly supervised with the result that they fail to take their medication regularly. This leads to a recurrence of symptoms and there have been occasional episodes of such patients in community care becoming a danger to themselves and to the public.
The antipsychotic drugs are powerful agents and have a range of potentially troubling side-effects. These include blurred vision, constipation, dizziness, dry mouth, limb restlessness, shaking, sti?ness, weight gain, and in the long term, TARDIVE DYSKINESIA (abnormal movements and walking) which affects about 20 per cent of those under treatment. Some drugs can be given by long-term depot injection: these include compounds of ?upenthixol, zuclopenthixol and haloperidol.
Prognosis About 25 per cent of sufferers recover fully from their ?rst attack. Another 25 per cent are disabled by chronic schizophrenia, never recover and are unable to live independently. The remainder are between these extremes. There is a high risk of suicide.... schizophrenia
As described by the French physician, Charcot, over 100 years ago, it is not infectious. Symptom-free periods may extend for months, even years, though relapses may be triggered by emotional crises, physical injury, the contraceptive pill, influenza and other infections.
While the cause is unknown, some studies have revealed a link between the disorder and the distemper virus in dogs. Others have linked the disease with mercury toxicity from amalgam dental fillings shown to generate electromotive forces which propel ionised mercury particles into the body from teeth. A further link is persistent infective sinusitis.
MS is high in families that eat excessive meat fat, butter and dairy products but with too little vegetable fat (corn, Soya, sunflower oil, etc). Linoleic acid levels in the blood of MS patients are abnormally low, especially during relapse. (Schwartz JH, Bennett B. Int Arch Allergy Appl Immunol 45; 899-904, 1973) Evening Primrose oil is claimed to make up the deficiency. Ethnic peoples with a diet wholly of fish (Eskimos) seldom develop this disease.
While cure is not possible, herbal medicine may in some cases arrest deterioration. Treatment of severe nerve conditions should be supervised by neurologists and practitioners whose training prepares them to recognise serious illness and to integrate herbal and supplementary intervention safely into the treatment plan.
Nerve sheaths require calcium; herbs to increase its levels: Oats, Lobelia, Horsetail.
Evening Primrose oil makes good a deficiency of linoleic acid (Vitamin F) for efficient function of the brain.
Alternatives:– Tablets/capsules. Black Cohosh, Cramp bark, Prickly Ash, Skullcap, Ginseng.
Formula. Ginkgo 2; Prickly Ash 1; Black Cohosh; Ginger quarter. Dose: Liquid Extracts: one 5ml teaspoon. Tinctures: two 5ml teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon). Thrice daily.
Formula, for pain. Lobelia 1; Ladyslipper 1; Ginger quarter. Dose: Liquid Extracts: 30-60 drops. Tinctures: one 5ml teaspoon. Powders: 250-500mg.
Rue tea. Traditional remedy for MS.
Evening Primrose: 4 × 500mg capsules, daily.
Aromatherapy. Spinal massage. 10 drops oils of Rosemary and Lavender in egg-cup Almond oil (or other vegetable oil).
Purslane herb. A rich source of non-fish EPA – suitable for a vegetarian approach.
Diet. A diet rich in essential fatty acids appears to arrest deterioration. (MS Unit, Central Middlesex Hospital, London)
High protein, low fat with oily fish. Lecithin. Sugar-free. Gluten-free (see Gluten diet). Cholesterol- free (avoid milk and dairy products). Grape juice. Dandelion coffee. One tablespoon Cod Liver oil daily. Red beet. Vegetable oils (safflower, sunflower, etc). Avoid coffee and caffeine stimulants.
Vitamins. Dismutase enzymes (see entry). B-complex, B3, B6. Vitamin C, 500-1000mg. Vitamin E, 200iu. Daily. Some authorities advise maximum dosage of Vitamin B12.
Minerals. Dolomite. Manganese. Zinc.
Information. Multiple Sclerosis Society, 25 Effie Road, London SW6 1EE, UK. Send SAE. ... multiple sclerosis
Dengue haemorrhagic fever This is a more severe form of the disease which usually occurs in young children; it is largely con?ned to the indigenous population(s) of south-east Asia. It is accompanied by signi?cant complications and mortality. Immunological status of the host is considered important in pathogenesis.... dengue
Louse-borne relapsing fever is an EPIDEMIC disease, usually associated with wars and famines, which has occurred in practically every country in the world. For long confused with TYPHUS FEVER and typhoid fever (see ENTERIC FEVER), it was not until the 1870s that the causal organism was described by Obermeier. It is now known as the Borrelia recurrentis, a motile spiral organism 10–20 micrometres in length. The organism is transmitted from person to person by the louse, Pediculus humanus.
Symptoms The incubation period is up to 12 days (but usually seven). The onset is sudden, with high temperature, generalised aches and pains, and nose-bleeding. In about half of cases, a rash appears at an early stage, beginning in the neck and spreading down over the trunk and arms. JAUNDICE may occur; and both the LIVER and the SPLEEN are enlarged. The temperature subsides after ?ve or six days, to rise again in about a week. There may be up to four such relapses (see the introductory paragraph above).
Treatment Preventive measures are the same as those for typhus. Rest in bed is essential, as are good nursing and a light, nourishing diet. There is usually a quick response to PENICILLIN; the TETRACYCLINES and CHLORAMPHENICOL are also e?ective. Following such treatment the incidence of relapse is about 15 per cent. The mortality rate is low, except in a starved population.
Tick-borne relapsing fever is an ENDEMIC disease which occurs in most tropical and sub-tropical countries. The causative organism is Borrelia duttoni, which is transmitted by a tick, Ornithodorus moubata. David Livingstone suggested that it was a tick-borne disease, but it was not until 1905 that Dutton and Todd produced the de?nitive evidence.
Symptoms The main di?erences from the louse-borne disease are: (a) the incubation period is usually shorter, 3–6 days (but may be as short as two days or as long as 12); (b) the febrile period is usually shorter, and the afebrile periods are more variable in duration, sometimes only lasting for a day or two; (c) relapses are much more numerous.
Treatment Preventive measures are more di?cult to carry out than in the case of the louse-borne infection. Protective clothing should always be worn in ‘tick country’, and old, heavily infected houses should be destroyed. Curative treatment is the same as for the louse-borne infection.... relapsing fever
The most widely prescribed type of antidepressants are the tricyclics, so-called because their molecular structure includes three rings. The other commonly used types are named after the actions they have on chemicals in the brain: the SELECTIVE SEROTONIN-REUPTAKE INHIBITORS (SSRIS) and the MONOAMINE OXIDASE INHIBITORS (MAOIS) – see also below. All types of antidepressant work in similar ways. Tricyclic antidepressants have cured depression in millions of people, but they can cause unpleasant side-effects, particularly in the ?rst couple of weeks. These include SEDATION, dry mouth, excessive sweating, CONSTIPATION, urinary problems, and impotence (inability to get an erection). Up to half of all people prescribed tricyclic drugs cannot tolerate the side-effects and stop treatment before their depression is properly treated. More seriously, tricyclics can upset the rhythm of the heart in susceptible people and should never be given in the presence of heart disease.
The SSRIs are newer, coming into wide use in the late 1980s. They increase the levels in the brain of the chemical messenger SEROTONIN, which is thought to be depleted in depression. Indeed, the SSRIs are as e?ective as tricyclics and, although they can cause nausea and excessive sweating at ?rst, they generally have fewer side-effects. Their main disadvantage, however, is that they cost much more than the most commonly used tricyclic, amitriptyline. On the other hand, they are more acceptable to many patients and they cause fewer drop-outs from treatment – up to a quarter rather than a half. The money saved by completed, successful treatment may outweigh the prescribing costs. SSRIs have been reported as associated with an increased risk of suicide.
Another group of antidepressants, the MAOIs, have been in use since the late 1950s.
They are stimulants, rather than sedatives, and are particularly helpful for people who are physically and mentally slowed by depression. They work well but have one big disadvantage – a dangerous interaction with certain foods and other drugs, causing a sudden and very dangerous increase in blood pressure. People taking them must carry an information card explaining the risk and listing the things that they should avoid. Because of this risk, MAOIs are not used much now, except when other treatments have failed. A new MAOI, moclobemide, which is less likely to interact and so cause high blood pressure, is now available.
LITHIUM CARBONATE is a powerful antidepressant used for intractable depression. It should be used under specialist supervision as the gap between an e?ective dose and a toxic one is narrow.
St John’s Wort is a popular herbal remedy which may be e?ective, but which is handicapped by di?erences of strength between di?erent preparations or batches. It can interact with a number of conventional drugs and so needs to be used cautiously and with advice.
In general, antidepressants work by restoring the balance of chemicals in the brain. Improved sleep and reduced anxiety are usually the ?rst signs of improvement, particularly among people taking the more sedative tricyclic drugs. Improvement in other symptoms follow, with the mood starting to lift after about two weeks of treatment. Most people feel well by three months, although a few residual symptoms, such as slowness in the mornings, may take longer to clear up. People taking antidepressants usually want to stop them as soon as they feel better; however, the risk of relapse is high for up to a year and most doctors recommend continuing the drugs for around 4–6 months after recovery, with gradual reduction of the dose after that.
Withdrawal reactions may occur including nausea, vomiting, headache, giddiness, panic or anxiety and restlessness. The drugs should be withdrawn gradually over about a month or longer (up to six months in those who have been on maintenance treatment).
A wide range of antidepressant drugs is described in the British National Formulary. Examples include:
Tricyclics: amitryptyline, imipramine, doxepin.
MAOIs: phenelzine, isocarboxazid.
SSRIs: citalopram, ?uoxetine, paraxtene. (Antidepressant drugs not in these three
groups include ?upenthixol, mertazapine and venlafaxine.)... antidepressant drugs
Rarely, an enlarged gland may be the result of cancer in the thyroid.
Treatment A symptomless goitre may gradually disappear or be so small as not to merit treatment. If the goitre is large or is causing the patient di?culty in swallowing or breathing, it may need surgical removal by partial or total thyroidectomy. If the patient is de?cient in iodine, ?sh and iodised salt should be included in the diet.
Hyperthyroidism is a common disorder affecting 2–5 per cent of all females at some time in their lives. The most common cause – around 75 per cent of cases – is thyrotoxicosis (see below). An ADENOMA (or multiple adenomas) or nodules in the thyroid also cause hyperthyroidism. There are several other rare causes, including in?ammation caused by a virus, autoimune reactions and cancer. The symptoms of hyperthyroidism affect many of the body’s systems as a consequence of the much-increased metabolic rate.
Thyrotoxicosis is a syndrome consisting of di?use goitre (enlarged thyroid gland), over-activity of the gland and EXOPHTHALMOS (protruding eyes). Patients lose weight and develop an increased appetite, heat intolerance and sweating. They are anxious, irritable, hyperactive, suffer from TACHYCARDIA, breathlessness and muscle weakness and are sometimes depressed. The hyperthyroidism is due to the production of ANTIBODIES to the TSH receptor (see THYROTROPHIN-STIMULATING HORMONE (TSH)) which stimulate the receptor with resultant production of excess thyroid hormones. The goitre is due to antibodies that stimulate the growth of the thyroid gland. The exoph-
thalmos is due to another immunoglobulin called the ophthalmopathic immunoglobulin, which is an antibody to a retro-orbital antigen on the surface of the retro-orbital EYE muscles. This provokes in?ammation in the retro-orbital tissues which is associated with the accumulation of water and mucopolysaccharide which ?lls the orbit and causes the eye to protrude forwards.
Although thyrotoxicosis may affect any age-group, the peak incidence is in the third decade. Females are affected ten times as often as males; the prevalence in females is one in 500. As with many other autoimmune diseases, there is an increased prevalence of autoimmune thyroid disease in the relatives of patients with thyrotoxicosis. Some of these patients may have hypothyroidism (see below) and others, thyrotoxicosis. Patients with thyrotoxicosis may present with a goitre or with the eye signs or, most commonly, with the symptoms of excess thyroid hormone production. Thyroid hormone controls the metabolic rate of the body so that the symptoms of hyperthyroidism are those of excess metabolism.
The diagnosis of thyrotoxicosis is con?rmed by the measurement of the circulating levels of the two thyroid hormones, thyroxine and TRIIODOTHYRONINE.
Treatment There are several e?ective treatments for thyrotoxicosis. ANTITHYROID DRUGS These drugs inhibit the iodination of tyrosine and hence the formation of the thyroid hormones. The most commonly used drugs are carbimazole and propylthiouricil: these will control the excess production of thyroid hormones in virtually all cases. Once the patient’s thyroid is functioning normally, the dose can be reduced to a maintenance level and is usually continued for two years. The disadvantage of antithyroid drugs is that after two years’ treatment nearly half the patients will relapse and will then require more de?nitive therapy. PARTIAL THYROIDECTOMY Removal of three-quarters of the thyroid gland is e?ective treatment of thyrotoxicosis. It is the treatment of choice in those patients with large goitres. The patient must however be treated with medication so that they are euthyroid (have a normally functioning thyroid) before surgery is undertaken, or thyroid crisis and cardiac arrhythmias may complicate the operation. RADIOACTIVE IODINE THERAPY This has been in use for many years, and is an e?ective means of controlling hyperthyroidism. One of the disadvantages of radioactive iodine is that the incidence of hypothyroidism is much greater than with other forms of treatment. However, the management of hypothyroidism is simple and requires thyroxine tablets and regular monitoring for hypothyroidism. There is no evidence of any increased incidence of cancer of the thyroid or LEUKAEMIA following radio-iodine therapy. It has been the pattern in Britain to reserve radio-iodine treatment to those over the age of 35, or those whose prognosis is unlikely to be more than 30 years as a result of cardiac or respiratory disease. Radioactive iodine treatment should not be given to a seriously thyrotoxic patient. BETA-ADRENOCEPTOR-BLOCKING DRUGS Usually PROPRANOLOL HYDROCHLORIDE: useful for symptomatic treatment during the ?rst 4–8 weeks until the longer-term drugs have reduced thyroid activity.
Hypothyroidism A condition resulting from underactivity of the thyroid gland. One form, in which the skin and subcutaneous tissues thicken and result in a coarse appearance, is called myxoedema. The thyroid gland secretes two hormones – thyroxine and triiodothyronine – and these hormones are responsible for the metabolic activity of the body. Hypothyroidism may result from developmental abnormalities of the gland, or from a de?ciency of the enzymes necessary for the synthesis of the hormones. It may be a feature of endemic goitre and retarded development, but the most common cause of hypothyroidism is the autoimmune destruction of the thyroid known as chronic thyroiditis. It may also occur as a result of radio-iodine treatment of thyroid overactivity (see above) and is occasionally secondary to pituitary disease in which inadequate TSH production occurs. It is a common disorder, occurring in 14 per 1,000 females and one per 1,000 males. Most patients present between the age of 30 and 60 years.
Symptoms As thyroid hormones are responsible for the metabolic rate of the body, hypothyroidism usually presents with a general sluggishness: this affects both physical and mental activities. The intellectual functions become slow, the speech deliberate and the formation of ideas and the answers to questions take longer than in healthy people. Physical energy is reduced and patients frequently complain of lethargy and generalised muscle aches and pains. Patients become intolerant of the cold and the skin becomes dry and swollen. The LARYNX also becomes swollen and gives rise to a hoarseness of the voice. Most patients gain weight and develop constipation. The skin becomes dry and yellow due to the presence of increased carotene. Hair becomes thinned and brittle and even baldness may develop. Swelling of the soft tissues may give rise to a CARPAL TUNNEL SYNDROME and middle-ear deafness. The diagnosis is con?rmed by measuring the levels of thyroid hormones in the blood, which are low, and of the pituitary TSH which is raised in primary hypothyroidism.
Treatment consists of the administration of thyroxine. Although tri-iodothyronine is the metabolically active hormone, thyroxine is converted to tri-iodothyronine by the tissues of the body. Treatment should be started cautiously and slowly increased to 0·2 mg daily – the equivalent of the maximum output of the thyroid gland. If too large a dose is given initially, palpitations and tachycardia are likely to result; in the elderly, heart failure may be precipitated.
Congenital hypothyroidism Babies may be born hypothyroid as a result of having little or no functioning thyroid-gland tissue. In the developed world the condition is diagnosed by screening, all newborn babies having a blood test to analyse TSH levels. Those found positive have a repeat test and, if the diagnosis is con?rmed, start on thyroid replacement therapy within a few weeks of birth. As a result most of the ill-effects of cretinism can be avoided and the children lead normal lives.
Thyroiditis In?ammation of the thyroid gland. The acute form is usually caused by a bacterial infection elsewhere in the body: treatment with antibiotics is needed. Occasionally a virus may be the infectious agent. Hashimoto’s thyroiditis is an autoimmune disorder causing hypothyroidism (reduced activity of the gland). Subacute thyroiditis is in?ammation of unknown cause in which the gland becomes painful and the patient suffers fever, weight loss and malaise. It sometimes lasts for several months but is usually self-limiting.
Thyrotoxic adenoma A variety of thyrotoxicosis (see hyperthyroidism above) in which one of the nodules of a multinodular goitre becomes autonomous and secretes excess thyroid hormone. The symptoms that result are similar to those of thyrotoxicosis, but there are minor di?erences.
Treatment The ?rst line of treatment is to render the patient euthyroid by treatment with antithyroid drugs. Then the nodule should be removed surgically or destroyed using radioactive iodine.
Thyrotoxicosis A disorder of the thyroid gland in which excessive amounts of thyroid hormones are secreted into the bloodstream. Resultant symptoms are tachycardia, tremor, anxiety, sweating, increased appetite, weight loss and dislike of heat. (See hyperthyroidism above.)... goitre
Tumours All masses cause varying combinations of headache and vomiting – symptoms of raised pressure within the inexpansible bony box formed by the skull; general or localised epileptic ?ts; weakness of limbs or disordered speech; and varied mental changes. Tumours may be primary, arising in the brain, or secondary deposits from tumours arising in the lung, breast or other organs. Some brain tumours are benign and curable by surgery: examples include meningiomas and pituitary tumours. The symptoms depend on the size and situation of the mass. Abscesses or blood clots (see HAEMATOMA) on the surface or within the brain may resemble tumours; some are removable. Gliomas ( see GLIOMA) are primary malignant tumours arising in the glial tissue (see GLIA) which despite surgery, chemotherapy and radiotherapy usually have a bad prognosis, though some astrocytomas and oligodendronogliomas are of low-grade malignancy. A promising line of research in the US (in the animal-testing stage in 2000) suggests that the ability of stem cells from normal brain tissue to ‘home in’ on gliomal cells can be turned to advantage. The stem cells were chemically manipulated to carry a poisonous compound (5-?uorouracil) to the gliomal cells and kill them, without damaging normal cells. Around 80 per cent of the cancerous cells in the experiments were destroyed in this way.
Clinical examination and brain scanning (CT, or COMPUTED TOMOGRAPHY; magnetic resonance imaging (MRI) and functional MRI) are safe, accurate methods of demonstrating the tumour, its size, position and treatability.
Strokes When a blood vessel, usually an artery, is blocked by a clot, thrombus or embolism, the local area of the brain fed by that artery is damaged (see STROKE). The resulting infarct (softening) causes a stroke. The cells die and a patch of brain tissue shrinks. The obstruction in the blood vessel may be in a small artery in the brain, or in a larger artery in the neck. Aspirin and other anti-clotting drugs reduce recurrent attacks, and a small number of people bene?t if a narrowed neck artery is cleaned out by an operation – endarterectomy. Similar symptoms develop abruptly if a blood vessel bursts, causing a cerebral haemorrhage. The symptoms of a stroke are sudden weakness or paralysis of the arm and leg of the opposite side to the damaged area of brain (HEMIPARESIS), and sometimes loss of half of the ?eld of vision to one side (HEMIANOPIA). The speech area is in the left side of the brain controlling language in right-handed people. In 60 per cent of lefthanders the speech area is on the left side, and in 40 per cent on the right side. If the speech area is damaged, diffculties both in understanding words, and in saying them, develops (see DYSPHASIA).
Degenerations (atrophy) For reasons often unknown, various groups of nerve cells degenerate prematurely. The illness resulting is determined by which groups of nerve cells are affected. If those in the deep basal ganglia are affected, a movement disorder occurs, such as Parkinson’s disease, hereditary Huntington’s chorea, or, in children with birth defects of the brain, athetosis and dystonias. Modern drugs, such as DOPAMINE drugs in PARKINSONISM, and other treatments can improve the symptoms and reduce the disabilities of some of these diseases.
Drugs and injury Alcohol in excess, the abuse of many sedative drugs and arti?cial brain stimulants – such as cocaine, LSD and heroin (see DEPENDENCE) – can damage the brain; the effects can be reversible in early cases. Severe head injury can cause localised or di?use brain damage (see HEAD INJURY).
Cerebral palsy Damage to the brain in children can occur in the uterus during pregnancy, or can result from rare hereditary and genetic diseases, or can occur during labour and delivery. Severe neurological illness in the early months of life can also cause this condition in which sti? spastic limbs, movement disorders and speech defects are common. Some of these children are learning-disabled.
Dementias In older people a di?use loss of cells, mainly at the front of the brain, causes ALZHEIMER’S DISEASE – the main feature being loss of memory, attention and reasoned judgement (dementia). This affects about 5 per cent of the over-80s, but is not simply due to ageing processes. Most patients require routine tests and brain scanning to indicate other, treatable causes of dementia.
Response to current treatments is poor, but promising lines of treatment are under development. Like Parkinsonism, Alzheimer’s disease progresses slowly over many years. It is uncommon for these diseases to run in families. Multiple strokes can cause dementia, as can some organic disorders such as cirrhosis of the liver.
Infections in the brain are uncommon. Viruses such as measles, mumps, herpes, human immunode?ciency virus and enteroviruses may cause ENCEPHALITIS – a di?use in?ammation (see also AIDS/HIV).
Bacteria or viruses may infect the membrane covering the brain, causing MENINGITIS. Viral meningitis is normally a mild, self-limiting infection lasting only a few days; however, bacterial meningitis – caused by meningococcal groups B and C, pneumococcus, and (now rarely) haemophilus – is a life-threatening condition. Antibiotics have allowed a cure or good control of symptoms in most cases of meningitis, but early diagnosis is essential. Severe headaches, fever, vomiting and increasing sleepiness are the principal symptoms which demand urgent advice from the doctor, and usually admission to hospital. Group B meningococcus is the commonest of the bacterial infections, but Group C causes more deaths. A vaccine against the latter has been developed and has reduced the incidence of cases by 75 per cent.
If infection spreads from an unusually serious sinusitis or from a chronically infected middle ear, or from a penetrating injury of the skull, an abscess may slowly develop. Brain abscesses cause insidious drowsiness, headaches, and at a late stage, weakness of the limbs or loss of speech; a high temperature is seldom present. Early diagnosis, con?rmed by brain scanning, is followed by antibiotics and surgery in hospital, but the outcome is good in only half of affected patients.
Cerebral oedema Swelling of the brain can occur after injury, due to engorgement of blood vessels or an increase in the volume of the extravascular brain tissue due to abnormal uptake of water by the damaged grey (neurons) matter and white (nerve ?bres) matter. This latter phenomenon is called cerebral oedema and can seriously affect the functioning of the brain. It is a particularly dangerous complication following injury because sometimes an unconscious person whose brain is damaged may seem to be recovering after a few hours, only to have a major relapse. This may be the result of a slow haemorrhage from damaged blood vessels raising intracranial pressure, or because of oedema of the brain tissue in the area surrounding the injury. Such a development is potentially lethal and requires urgent specialist treatment to alleviate the rising intracranial pressure: osmotic agents (see OSMOSIS) such as mannitol or frusemide are given intravenously to remove the excess water from the brain and to lower intracranial pressure, buying time for de?nitive investigation of the cranial damage.... brain, diseases of
Causes In Malta and the Mediterranean littoral, the causative organism is the bacterium Brucella melitensis which is conveyed in goat’s milk. In Great Britain, the US and South Africa, the causative organism is the Brucella abortus, which is conveyed in cow’s milk: this is the organism which is responsible for contagious abortion in cattle. In Great Britain brucellosis is largely an occupational disease and is now prescribed as an industrial disease (see OCCUPATIONAL DISEASES), and insured persons who contract the disease at work can claim industrial injuries bene?t. The incidence of brucellosis in the UK has fallen from more than 300 cases a year in 1970 to single ?gures.
Symptoms The characteristic features of the disease are undulating fever, drenching sweats, pains in the joints and back, and headache. The liver and spleen may be enlarged. The diagnosis is con?rmed by the ?nding of Br. abortus, or antibodies to it, in the blood. Recovery and convalescence tend to be slow.
Treatment The condition responds well to one of the tetracycline antibiotics, and also to gentamicin and co-trimoxazole, but relapse is common. In chronic cases a combination of streptomycin and one of the tetracyclines is often more e?ective.
Prevention It can be prevented by boiling or pasteurising all milk used for human consumption. In Scandinavia, the Netherlands, Switzerland and Canada the disease has disappeared following its eradication in animals. Brucellosis has been eradicated from farm animals in the United Kingdom.... brucellosis
Crohn’s disease is rare in the developing world, but in the western world the incidence is increasing and is now 6–7 per 100,000 population. Around 80,000 people in the UK have the disorder with more than 4,000 new cases occurring annually. Commonly Crohn’s disease starts in young adults, but a second incidence surge occurs in people over 70 years of age. Both genetic and environmental factors are implicated in the disease – for example, if one identical twin develops the disease, the second twin stands a high chance of being affected; and 10 per cent of sufferers have a close relative with in?ammatory bowel disease. Among environmental factors are low-residue, high-re?ned-sugar diets, and smoking.
Symptoms and signs of Crohn’s disease depend on the site affected but include abdominal pain, diarrhoea (sometimes bloody), ANOREXIA, weight loss, lethargy, malaise, ANAEMIA, and sore tongue and lips. An abdominal mass may be present. Complications can be severe, including life-threatening in?ammation of the colon (which may cause TOXAEMIA), perforation of the colon and the development of ?stulae between the bowel and other organs in the abdomen or pelvis. If Crohn’s disease persists for a decade or more there is an increased risk of the victim developing colon cancer. Extensive investigations are usually necessary to diagnose the disease; these include blood tests, bacteriological studies, ENDOSCOPY and biopsy, and barium X-ray examinations.
Treatment As with ulcerative colitis, treatment is aimed primarily at controlling symptoms. Physicians, surgeons, radiologists and dietitians usually adopt a team approach, while counsellors and patient support groups are valuable adjuncts in a disease that is typically lifelong. Drug treatment is aimed at settling the acute phase and preventing relapses. CORTICOSTEROIDS, given locally to the affected gut or orally, are used initially and the effects must be carefully monitored. If steroids do not work, the immunosuppressant agent AZATHIOPRINE should be considered. Antidiarrhoeal drugs may occasionally be helpful but should not be taken during an acute phase. The anti-in?ammatory drug SULFASALAZINE can be bene?cial in mild colitis. A new generation of genetically engineered anti-in?ammatory drugs is now available, and these selective immunosuppressants may prove of value in the treatment of Crohn’s disease.
Diet is important and professional guidance is advisable. Some patients respond to milk- or wheat-free diets, but the best course for most patients is to eat a well-balanced diet, avoiding items that the sufferer knows from experience are poorly tolerated. Of those patients with extensive disease, as many as 80 per cent may require surgery to alleviate symptoms: a section of affected gut may be removed or, as a lifesaving measure, a bowel perforation dealt with.
(See APPENDIX 2: ADDRESSES: SOURCES OF INFORMATION, ADVICE, SUPPORT AND SELFHELP – Colitis; Crohn’s disease.)... crohn’s disease
Psychiatrists like to categorise mental illnesses because mental signs and symptoms do occur together in clusters or syndromes, each tending to respond to certain treatments. The idea that illnesses can be diagnosed simply by recognising their symptom patterns may not seem very scienti?c in these days of high technology. For most common mental illnesses, however, this is the only method of diagnosis; whatever is going wrong in the brain is usually too poorly understood and too subtle to show up in laboratory tests or computed tomography scans of the brain. And symptom-based definitions of mental illnesses are, generally, a lot more meaningful than the vague lay term ‘nervous breakdown’, which is used to cover an attack of anything from AGORAPHOBIA to total inability to function.
There is still a lot to learn about the workings of the brain, but psychiatry has developed plenty of practical knowledge about the probable causes of mental illness, ways of relieving symptoms, and ways of aiding recovery. Most experts now believe that mental illnesses generally arise from di?erent combinations of inherited risk and psychological STRESS, sometimes with additional environmental exposure – for example, viruses, drugs or ALCOHOL.
The range of common mental illnesses includes anxiety states, PHOBIA, DEPRESSION, alcohol and drug problems, the EATING DISORDERS anorexia and bulimia nervosa, MANIC DEPRESSION, SCHIZOPHRENIA, DEMENTIA, and a group of problems related to coping with life that psychiatrists call personality disorders.
Of these mental illnesses, dementia is the best understood. It is an irreversible and fatal form of mental deterioration (starting with forgetfulness and eventually leading to severe failure of all the brain’s functions), caused by rapid death of brain cells and consequent brain shrinkage. Schizophrenia is another serious mental illness which disrupts thought-processes, speech, emotions and perception (how the brain handles signals from the ?ve senses). Manic depression, in which prolonged ‘highs’ of extremely elevated mood and overexcitement alternate with abject misery, has similar effects on the mental processes. In both schizophrenia and manic depression the sufferer loses touch with reality, develops unshakeable but completely unrealistic ideas (delusions), and hallucinates (vividly experiences sensations that are not real, e.g. hears voices when there is nobody there). This triad of symptoms is called psychosis and it is what lay people, through fear and lack of understanding, sometimes call lunacy, madness or insanity.
The other mental illnesses mentioned above are sometimes called neuroses. But the term has become derogatory in ordinary lay language; indeed, many people assume that neuroses are mild disorders that only affect weak people who cannot ‘pull themselves together’, while psychoses are always severe. In reality, psychoses can be brief and reversible and neuroses can cause lifelong disability.
However de?ned and categorised, mental illness is a big public-health problem. In the UK, up to one in ?ve women and around one in seven men have had mental illness. About half a million people in Britain suffer from schizophrenia: it is three times commoner than cancer. And at any one time, up to a tenth of the adult population is ill with depression.
Treatment settings Most people with mental-health problems get the help they need from their own family doctor(s), without ever seeing a psychiatrist. General practictitioners in Britain treat nine out of ten recognised mental-health problems and see around 12 million adults with mental illness each year. Even for the one in ten of these patients referred to psychiatrists, general practitioners usually handle those problems that continue or recur.
Psychiatrists, psychiatric nurses, social workers, psychologists, counsellors and therapists often see patients at local doctors’ surgeries and will do home visits if necessary. Community mental-health centres – like general-practice health centres but catering solely for mental-health problems – o?er another short-cut to psychiatric help. The more traditional, and still more common, route to a psychiatrist for many people, however, is from the general practititioner to a hospital outpatient department.
Specialist psychiatric help In many ways, a visit to a psychiatrist is much like any trip to a hospital doctor – and, indeed, psychiatric clinics are often based in the outpatient departments of general hospitals. First appointments with psychiatrists can last an hour or more because the psychiatrist – and sometimes other members of the team such as nurses, doctors in training, and social workers – need to ask lots of questions and record the whole consultation in a set of con?dential case notes.
Psychiatric assessment usually includes an interview and an examination, and is sometimes backed up by a range of tests. The interview begins with the patient’s history – the personal story that explains how and, to some extent, why help is needed now. Mental-health problems almost invariably develop from a mixture of causes – emotional, social, physical and familial – and it helps psychiatrists to know what the people they see are normally like and what kind of lives they have led. These questions may seem unnecessarily intrusive, but they allow psychiatrists to understand patients’ problems and decide on the best way to help them.
The next stage in assessment is the mental-state examination. This is how psychiatrists examine minds, or at least their current state. Mental-state examination entails asking more questions and using careful observation to assess feelings, thoughts and mental symptoms, as well as the way the mind is working (for example, in terms of memory and concentration). During ?rst consultations psychiatrists usually make diagnoses and explain them. The boundary between a life problem that will clear up spontaneously and a mental illness that needs treatment is sometimes quite blurred; one consultation may be enough to put the problem in perspective and help to solve it.
Further assessment in the clinic may be needed, or some additional tests. Simple blood tests can be done in outpatient clinics but other investigations will mean referral to another department, usually on another day.
Further assessment and tests
PSYCHOLOGICAL TESTS Psychologists work in or alongside the psychiatric team, helping in both assessment and treatment. The range of psychological tests studies memory, intelligence, personality, perception and capability for abstract thinking. PHYSICAL TESTS Blood tests and brain scans may be useful to rule out a physical illness causing psychological symptoms. SOCIAL ASSESSMENT Many patients have social diffculties that can be teased out and helped by a psychiatric social worker. ‘Approved social workers’ have special training in the use of the Mental Health Act, the law that authorises compulsory admissions to psychiatric hospitals and compulsory psychiatric treatments. These social workers also know about all the mental-health services o?ered by local councils and voluntary organisations, and can refer clients to them. The role of some social workers has been widened greatly in recent years by the expansion of community care. OCCUPATIONAL THERAPY ASSESSMENT Mental-health problems causing practical disabilities – for instance, inability to work, cook or look after oneself – can be assessed and helped by occupational therapists.
Treatment The aims of psychiatric treatment are to help sufferers shake o?, or at least cope with, symptoms and to gain or regain an acceptable quality of life. A range of psychological and physical treatments is available.
COUNSELLING This is a widely used ‘talking cure’, particularly in general practice. Counsellors listen to their clients, help them to explore feelings, and help them to ?nd personal and practical solutions to their problems. Counsellors do not probe into clients’ pasts or analyse them. PSYCHOTHERAPY This is the best known ‘talking cure’. The term psychotherapy is a generalisation covering many di?erent concepts. They all started, however, with Sigmund Freud (see FREUDIAN THEORY), the father of modern psychotherapy. Freud was a doctor who discovered that, as well as the conscious thoughts that guide our feelings and actions, there are powerful psychological forces of which we are not usually aware. Applying his theories to his patients’ freely expressed thoughts, Freud was able to cure many illnesses, some of which had been presumed completely physical. This was the beginning of individual analytical psychotherapy, or PSYCHOANALYSIS. Although Freud’s principles underpin all subsequent theories about the psyche, many di?erent schools of thought have emerged and in?uenced psychotherapists (see ADLER; JUNGIAN ANALYSIS; PSYCHOTHERAPY). BEHAVIOUR THERAPY This springs from theories of human behaviour, many of which are based on studies of animals. The therapists, mostly psychologists, help people to look at problematic patterns of behaviour and thought, and to change them. Cognitive therapy is very e?ective, particularly in depression and eating disorders. PHYSICAL TREATMENTS The most widely used physical treatments in psychiatry are drugs. Tranquillising and anxiety-reducing BENZODIAZEPINES like diazepam, well known by its trade name of Valium, were prescribed widely in the 1960s and 70s because they seemed an e?ective and safe substitute for barbiturates. Benzodiazepines are, however, addictive and are now recommended only for short-term relief of anxiety that is severe, disabling, or unacceptably distressing. They are also used for short-term treatment of patients drying out from alcohol.
ANTIDEPRESSANT DRUGS like amitriptyline and ?uoxetine are given to lift depressed mood and to relieve the physical symptoms that sometimes occur in depression, such as insomnia and poor appetite. The side-effects of antidepressants are mostly relatively mild, when recommended doses are not exceeded – although one group, the monoamine oxidase inhibitors, can lead to sudden and dangerous high blood pressure if taken with certain foods.
Manic depression virtually always has to be treated with mood-stabilising drugs. Lithium carbonate is used in acute mania to lower mood and stop psychotic symptoms; it can also be used in severe depression. However lithium’s main use is to prevent relapse in manic depression. Long-term unwanted effects may include kidney and thyroid problems, and short-term problems in the nervous system and kidney may occur if the blood concentration of lithium is too high – therefore it must be monitored by regular blood tests. Carbamazepine, a treatment for EPILEPSY, has also been found to stabilise mood, and also necessitates blood tests.
Antipsychotic drugs, also called neuroleptics, and major tranquillisers are the only e?ective treatments for relieving serious mental illnesses with hallucinations and delusions. They are used mainly in schizophrenia and include the short-acting drugs chlorpromazine and clozapine as well as the long-lasting injections given once every few weeks like ?uphenazine decanoate. In the long term, however, some of the older antipsychotic drugs can cause a brain problem called TARDIVE DYSKINESIA that affects control of movement and is not always reversible. And the antipsychotic drugs’ short-term side-effects such as shaking and sti?ness sometimes have to be counteracted by other drugs called anticholinergic drugs such as procyclidine and benzhexol. Newer antipsychotic drugs such as clozapine do not cause tardive dyskinesia, but clozapine cannot be given as a long-lasting injection and its concentration in the body has to be monitored by regular blood tests to avoid toxicity. OTHER PHYSICAL TREATMENTS The other two physical treatments used in psychiatry are particularly controversial: electroconvulsive therapy (ECT) and psychosurgery. In ECT, which can be life-saving for patients who have severe life-threatening depression, a small electric current is passed through the brain to induce a ?t or seizure. Before the treatment the patient is anaesthetised and given a muscle-relaxing injection that reduces the magnitude of the ?t to a slight twitching or shaking. Scientists do not really understand how ECT works, but it does, for carefully selected patients. Psychosurgery – operating on the brain to alleviate psychiatric illness or di?cult personality traits – is extremely uncommon these days. Stereo-tactic surgery, in which small cuts are made in speci?c brain ?bres under X-ray guidance, has super-seded the more generalised lobotomies of old. The Mental Health Act 1983 ensures that psychosurgery is performed only when the patient has given fully informed consent and a second medical opinion has agreed that it is necessary. For all other psychiatric treatments (except another rare treatment, hormone implantation for reducing the sex drive of sex o?enders), either consent or a second opinion is needed – not both. TREATMENT IN HOSPITAL Psychiatric wards do not look like medical or surgical wards and sta? may not wear uniforms. Patients do not need to be in their beds during the day, so the beds are in separate dormitories. The main part of most wards is a living space with a day room, an activity and television room, quiet rooms, a dining room, and a kitchen. Ward life usually has a certain routine. The day often starts with a community meeting at which patients and nurses discuss issues that affect the whole ward. Patients may go to the occupational therapy department during the day, but there may also be some therapy groups on the ward, such as relaxation training. Patients’ symptoms and problems are assessed continuously during a stay in hospital. When patients seem well enough they are allowed home for trial periods; then discharge can be arranged. Patients are usually followed up in the outpatient clinic at least once.
TREATING PATIENTS WITH ACUTE PSYCHIATRIC ILLNESS Psychiatric emergencies – patients with acute psychiatric illness – may develop from psychological, physical, or practical crises. Any of these crises may need quick professional intervention. Relatives and friends often have to get this urgent help because the sufferer is not ?t enough to do it or, if psychotic, does not recognise the need. First, they should ring the person’s general practitioner. If the general practitioner is not available and help is needed very urgently, relatives or friends should phone the local social-services department and ask for the duty social worker (on 24-hour call). In a dire emergency, the police will know what to do.
Any disturbed adult who threatens his or her own or others’ health and safety and refuses psychiatric help may be moved and detained by law. The Mental Health Act of 1983 authorises emergency assessment and treatment of any person with apparent psychiatric problems that ful?l these criteria.
Although admission to hospital may be the best solution, there are other ways that psychiatric services can respond to emergencies. In some districts there are ‘crisis intervention’ teams of psychiatrists, nurses, and social workers who can visit patients urgently at home (at a GP’s request) and, sometimes, avert unnecessary admission. And research has shown that home treatment for a range of acute psychiatric problems can be e?ective.
LONG-TERM TREATMENT AND COMMUNITY CARE Long-term treatment is often provided by GPs with support and guidance from psychiatric teams. That is ?ne for people whose problems allow them to look after themselves, and for those with plenty of support from family and friends. But some people need much more intensive long-term treatment and many need help with running their daily lives.
Since the 1950s, successive governments have closed the old psychiatric hospitals and have tried to provide as much care as possible outside hospital – in ‘the community’. Community care is e?ective as long as everyone who needs inpatient care, or residential care, can have it. But demand exceeds supply. Research has shown that some homeless people have long-term mental illnesses and have somehow lost touch with psychiatric services. Many more have developed more general long-term health problems, particularly related to alcohol, without ever getting help.
The NHS and Community Care Act 1990, in force since 1993, established a new breed of professionals called care managers to assess people whose long-term illnesses and disabilities make them unable to cope completely independently with life. Care managers are given budgets by local councils to assess people’s needs and to arrange for them tailor-made packages of care, including services like home helps and day centres. But co-ordination between health and social services has sometimes failed – and resources are limited – and the government decided in 1997 to tighten up arrangements and pool community-care budgets.
Since 1992 psychiatrists have had to ensure that people with severe mental illnesses have full programmes of care set up before discharge from hospital, to be overseen by named key workers. And since 1996 psychiatrists have used a new power called Supervised Discharge to ensure that the most vulnerable patients cannot lose touch with mental-health services. There is not, however, any law that allows compulsory treatment in the community.
There is ample evidence that community care can work and that it need not cost more than hospital care. Critics argue, however, that even one tragedy resulting from inadequate care, perhaps a suicide or even a homicide, should reverse the march to community care. And, according to the National Schizophrenia Fellowship, many of the 10–15 homicides a year carried out by people with severe mental illnesses result from inadequate community care.
Further information can be obtained from the Mental Health Act Commission, and from MIND, the National Association for Mental Health. MIND also acts as a campaigning and advice organisation on all aspects of mental health.... mental illness
Acute gastritis is an in?ammatory reaction of the gastric mucosa to various precipitating factors, ranging from physical and chemical injury to infections. Acute gastritis (especially of the antral mucosas) may well represent a reaction to infection by a bacterium called Helicobacter pylori. The in?ammatory changes usually go after appropriate antibiotic treatment for the H. pylori infection. Acute and chronic in?ammation occurs in response to chemical damage of the gastric mucosa. For example, REFLUX of duodenal contents may predispose to in?ammatory acute and chronic gastritis. Similarly, multiple small erosions or single or multiple ulcers have resulted from consumption of chemicals, especialy aspirin and antirheumatic NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS).
Acute gastritis may cause anorexia, nausea, upper abdominal pain and, if erosive, haemorrhage. Treatment involves removal of the o?ending cause.
Chronic gastritis Accumulation of cells called round cells in the gastric mucosal characterises chronic gastritis. Most patients with chronic gastritis have no symptoms, and treatment of H. pylori infection usually cures the condition.
Atrophic gastritis A few patients with chronic gastritis may develop atrophic gastritis. With or without in?ammatory change, this disorder is common in western countries. The incidence increases with age, and more than 50 per cent of people over 50 may have it. A more complete and uniform type of ATROPHY, called ‘gastric atrophy’, characterises a familial disease called PERNICIOUS ANAEMIA. The cause of the latter disease is not known but it may be an autoimmune disorder.
Since atrophy of the corpus mucosa results in loss of acid- and pepsin-secreting cells, gastric secretion is reduced or absent. Patients with pernicious anaemia or severe atrophic gastritis of the corpus mucosa may secrete too little intrinsic factor for absorption of vitamin B12 and so can develop severe neurological disease (subacute combined degeneration of the spinal cord).
Patients with atrophic gastritis often have bacterial colonisation of the upper alimentary tract, with increased concentration of nitrite and carcinogenic N-nitroso compounds. These, coupled with excess growth of mucosal cells, may be linked to cancer. In chronic corpus gastritis, the risk of gastric cancer is about 3–4 times that of the general population.
Postgastrectomy mucosa The mucosa of the gastric remnant after surgical removal of the distal part of the stomach is usually in?amed and atrophic, and is also premalignant, with the risk of gastric cancer being very much greater than for patients with duodenal ulcer who have not had surgery.
Stress gastritis Acute stress gastritis develops, sometimes within hours, in individuals who have undergone severe physical trauma, BURNS (Curling ulcers), severe SEPSIS or major diseases such as heart attacks, strokes, intracranial trauma or operations (Cushing’s ulcers). The disorder presents with multiple super?cial erosions or ulcers of the gastric mucosa, with HAEMATEMESIS and MELAENA and sometimes with perforation when the acute ulcers erode through the stomach wall. Treatment involves inhibition of gastric secretion with intravenous infusion of an H2-receptorantagonist drug such as RANITIDINE or FAMOTIDINE, so that the gastric contents remain at a near neutral pH. Despite treatment, a few patients continue to bleed and may then require radical gastric surgery.
Gastric ulcer Gastric ulcers were common in young women during the 19th century, markedly fell in frequency in many western countries during the ?rst half of the 20th century, but remained common in coastal northern Norway, Japan, in young Australian women, and in some Andean populations. During the latter half of this century, gastric ulcers have again become more frequent in the West, with a peak incidence between 55 and 65 years.
The cause is not known. The two factors most strongly associated with the development of duodenal ulcers – gastric-acid production and gastric infection with H. pylori bacteria – are not nearly as strongly associated with gastric ulcers. The latter occur with increased frequency in individuals who take aspirin or NSAIDs. In healthy individuals who take NSAIDs, as many as 6 per cent develop a gastric ulcer during the ?rst week of treatment, while in patients with rheumatoid arthritis who are being treated long term with drugs, gastric ulcers occur in 20–40 per cent. The cause is inhibition of the enzyme cyclo-oxygenase, which in turn inhibits the production of repair-promoting PROSTAGLANDINS.
Gastric ulcers occur especially on the lesser curve of the stomach. The ulcers may erode through the whole thickness of the gastric wall, perforating into the peritoneal cavity or penetrating into liver, pancreas or colon.
Gastric ulcers usually present with a history of epigastric pain of less than one year. The pain tends to be associated with anorexia and may be aggravated by food, although patients with ‘prepyloric’ ulcers may obtain relief from eating or taking antacid preparations. Patients with gastric ulcers also complain of nausea and vomiting, and lose weight.
The principal complications of gastric ulcer are haemorrhage from arterial erosion, or perforation into the peritoneal cavity resulting in PERITONITIS, abscess or ?stula.
Aproximately one in two gastric ulcers heal ‘spontaneously’ in 2–3 months; however, up to 80 per cent of the patients relapse within 12 months. Repeated recurrence and rehealing results in scar tissue around the ulcer; this may cause a circumferential narrowing – a condition called ‘hour-glass stomach’.
The diagnosis of gastric ulcer is con?rmed by ENDOSCOPY. All patients with gastric ulcers should have multiple biopsies (see BIOPSY) to exclude the presence of malignant cells. Even after healing, gastric ulcers should be endoscopically monitored for a year.
Treatment of gastric ulcers is relatively simple: a course of one of the H2 RECEPTOR ANTAGONISTS heals gastric ulcers in 3 months. In patients who relapse, long-term inde?nite treatment with an H2 receptor antagonist such as ranitidine may be necessary since the ulcers tend to recur. Recently it has been claimed that gastric ulcers can be healed with a combination of a bismuth salt or a gastric secretory inhibitor
for example, one of the PROTON PUMP INHIBITORS such as omeprazole or lansoprazole
together with two antibiotics such as AMOXYCILLIN and METRONIDAZOLE. The long-term outcome of such treatment is not known. Partial gastrectomy, which used to be a regular treatment for gastric ulcers, is now much more rarely done unless the ulcer(s) contain precancerous cells.
Cancer of the stomach Cancer of the stomach is common and dangerous and, worldwide, accounts for approximately one in six of all deaths from cancer. There are marked geographical di?erences in frequency, with a very high incidence in Japan and low incidence in the USA. In the United Kingdom around 33 cases per 100,000 population are diagnosed annually. Studies have shown that environmental factors, rather than hereditary ones, are mainly responsible for the development of gastric cancer. Diet, including highly salted, pickled and smoked foods, and high concentrations of nitrate in food and drinking water, may well be responsible for the environmental effects.
Most gastric ulcers arise in abnormal gastric mucosa. The three mucosal disorders which especially predispose to gastric cancer include pernicious anaemia, postgastrectomy mucosa, and atrophic gastritis (see above). Around 90 per cent of gastric cancers have the microscopic appearance of abnormal mucosal cells (and are called ‘adenocarcinomas’). Most of the remainder look like endocrine cells of lymphoid tissue, although tumours with mixed microscopic appearance are common.
Early gastric cancer may be symptomless and, in countries like Japan with a high frequency of the disease, is often diagnosed during routine screening of the population. In more advanced cancers, upper abdominal pain, loss of appetite and loss of weight occur. Many present with obstructive symptoms, such as vomiting (when the pylorus is obstructed) or di?culty with swallowing. METASTASIS is obvious in up to two-thirds of patients and its presence contraindicates surgical cure. The diagnosis is made by endoscopic examination of the stomach and biopsy of abnormal-looking areas of mucosa. Treatment is surgical, often with additional chemotherapy and radiotherapy.... stomach, diseases of
Clinical course The incubation period of enteric fever is 7–21 days. Early symptoms include headache, malaise, dry cough, constipation and a slowly rising fever. Despite the fever, the patient’s pulse rate is often slow and he or she may have an enlarged SPLEEN. In the second week of illness, organisms invade the bloodstream again and symptoms progress. In general, symptoms of typhoid fever are more severe than those of paratyphoid fever: increasing mental slowness and confusion are common, and a more sustained high fever is present. In some individuals, discrete red spots appear on the upper trunk (rose spots). By the third week of illness the patient may become severely toxic, with marked confusion and delirium, abdominal distension, MYOCARDITIS, and occasionally intestinal haemorrage and/or perforation. Such complications may be fatal, although they are unusual if prompt treatment is given. Symptoms improve slowly into the fourth and ?fth weeks, although relapse may occur.
Diagnosis Enteric fever should be considered in any traveller or resident in an ENDEMIC area presenting with a febrile illness. The most common di?erential diagnosis is MALARIA. Diagnosis is usually made by isolation of the organism from cultures of blood in the ?rst two weeks of illness. Later the organisms are found in the stools and urine. Serological tests for ANTIBODIES against Salmonella typhi antigens (see ANTIGEN) (the Widal test) are less useful due to cross-reactions with antigens on other bacteria, and diffculties with interpretation in individuals immunised with typhoid vaccines.
Treatment Where facilities are available, hospital admission is required. Antibiotic therapy with chloramphenicol or amoxyacillin is e?ective. However, the potential toxicity of the former and the widespread resistance that has developed to both these antibiotics has led to the use of QUINOLONES such as CIPROFLOXACIN as the initial therapy for enteric fever in the UK and in areas where resistant organisms are common. A few individuals become chronic carriers of the organisms after they have recovered from the symptoms. These people are a potential source of spread to others and should be excluded from occupations that involve handling food or drinking-water.
Prolonged courses of antibiotic therapy may be required to eradicate carriage.
Prevention Worldwide, the most important preventive measure is improvement of sanitation and maintenance of clean water supplies. Vaccination is available for travellers to endemic areas.... enteric fever
Abnormal drowsiness may be the result of a head injury, high fever, meningitis, uraemia (excess urea in the blood due to kidney failure), or liver failure.
Alcohol or drugs may also produce this effect.
In a person with diabetes mellitus, drowsiness may be due to hypoglycaemia or to hyperglycaemia.
Abnormal drowsiness should be treated as a medical emergency.... drowsiness
Symptoms may include extravagant spending, repeatedly starting new tasks; sleeping less; increased appetite for food, alcohol, sex, and exercise; outbursts of inappropriate anger, laughter, or sudden socializing; and delusions of grandeur. If symptoms are mild, the condition is called hypomania.
Severe mania usually needs treatment in hospital with antipsychotic drugs. Relapses may be prevented by taking lithium or carbamazepine.... mania
Doctors make the diagnosis of depression when they believe a patient to be ill with the latter condition, which may affect physical health and in some instances be life-threatening. This form of depression is common, with up to 15 per cent of the population suffering from it at any one time, while about 20 per cent of adults have ‘medical’ depression at some time during their lives – such that it is one of the most commonly presenting disorders in general practice. Women seem more liable to develop depression than men, with one in six of the former and one in nine of the latter seeking medical help.
Manic depression is a serious form of the disorder that recurs throughout life and is manifested by bouts of abnormal elation – the manic stage. Both the manic and depressive phases are commonly accompanied by psychotic symptoms such as delusions, hallucinations and a loss of sense of reality. This combination is sometimes termed a manic-depressive psychosis or bipolar affective disorder because of the illness’s division into two parts. Another psychiatric description is the catch-all term ‘affective disorder’.
Symptoms These vary with the illness’s severity. Anxiety and variable moods are the main symptoms in mild depression. The sufferer may cry without any reason or be unresponsive to relatives and friends. In its more severe form, depression presents with a loss of appetite, sleeping problems, lack of interest in and enjoyment of social activities, tiredness for no obvious reason, an indi?erence to sexual activity and a lack of concentration. The individual’s physical and mental activities slow down and he or she may contemplate suicide. Symptoms may vary during the 24 hours, being less troublesome during the latter part of the day and worse at night. Some people get depressed during the winter months, probably a consequence of the long hours of darkness: this disorder – SEASONAL AFFECTIVE DISORDER SYNDROME, or SADS – is thought to be more common in populations living in areas with long winters and limited daylight. Untreated, a person with depressive symptoms may steadily worsen, even withdrawing to bed for much of the time, and allowing his or her personal appearance, hygiene and environment to deteriorate. Children and adolescents may also suffer from depression and the disorder is not always recognised.
Causes A real depressive illness rarely has a single obvious cause, although sometimes the death of a close relative, loss of employment or a broken personal relationship may trigger a bout. Depression probably has a genetic background; for instance, manic depression seems to run in some families. Viral infections sometimes cause depression, and hormonal disorders – for example, HYPOTHYROIDISM or postnatal hormonal disturbances (postnatal depression) – will cause it. Di?cult family or social relations can contribute to the development of the disorder. Depression is believed to occur because of chemical changes in the transmission of signals in the nervous system, with a reduction in the neurochemicals that facilitate the passage of messages throughout the system.
Treatment This depends on the type and severity of the depression. These are three main forms. PSYCHOTHERAPY either on a one-to-one basis or as part of a group: this is valuable for those whose depression is the result of lifestyle or personality problems. Various types of psychotherapy are available. DRUG TREATMENT is the most common method and is particularly helpful for those with physical symptoms. ANTIDEPRESSANT DRUGS are divided into three main groups: TRICYCLIC ANTIDEPRESSANT DRUGS (amitriptyline, imipramine and dothiepin are examples); MONOAMINE OXIDASE INHIBITORS (MAOIS) (phenelzine, isocarboxazid and tranylcypromine are examples); and SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) (?uoxetine – well known as Prozac®, ?uvoxamine and paroxetine are examples). For manic depression, lithium carbonate is the main preventive drug and it is also used for persistent depression that fails to respond to other treatments. Long-term lithium treatment reduces the likelihood of relapse in about 80 per cent of manic depressives, but the margin between control and toxic side-effects is narrow, so the drug must be carefully supervised. Indeed, all drug treatment for depression needs regular monitoring as the substances have powerful chemical properties with consequential side-effects in some people. Furthermore, the nature of the illness means that some sufferers forget or do not want to take the medication. ELECTROCONVULSIVE THERAPY (ECT) If drug treatments fail, severely depressed patients may be considered for ECT. This treatment has been used for many years but is now only rarely recommended. Given under general anaesthetic, in appropriate circumstances, ECT is safe and e?ective and may even be life-saving, though temporary impairment of memory may occur. Because the treatment was often misused in the past, it still carries a reputation that worries patients and relatives; hence careful assessment and counselling are essential before use is recommended.
Some patients with depression – particularly those with manic depression or who are a danger to themselves or to the public, or who are suicidal – may need admission to hospital, or in severe cases to a secure unit, in order to initiate treatment. But as far as possible patients are treated in the community (see MENTAL ILLNESS).... depression
Visceral leishmaniasis (kala-azar) A systemic infection caused by Leishmania donovani which occurs in tropical and subtropical Africa, Asia, the Mediterranean littoral (and some islands), and in tropical South America. Onset is frequently insidious; incubation period is 2–6 months. Enlargement of spleen and liver may be gross; fever, anaemia, and generalised lymphadenopathy are usually present. Diagnosis is usually made from a bone-marrow specimen, splenic-aspirate, or liver-biopsy specimen; amastigotes (Leishman-Donovan bodies) of L. donovani can be visualised. Several serological tests are of value in diagnosis.
Untreated, the infection is fatal within two years, in approximately 70 per cent of patients. Treatment traditionally involved sodium stibogluconate, but other chemotherapeutic agents (including allupurinol, ketoconazole, and immunotherapy) are now in use, the most recently used being liposomal amphotericin B. Although immunointact persons usually respond satisfactorily, they are likely to relapse if they have HIV infection (see AIDS/HIV).
Cutaneous leishmaniasis This form is caused by infection with L. tropica, L. major,
L. aethiopica, and other species. The disease is widely distributed in the Mediterranean region, Middle East, Asia, Africa, Central and South America, and the former Soviet Union. It is characterised by localised cutaneous ulcers
– usually situated on exposed areas of the body. Diagnosis is by demonstration of the causative organism in a skin biopsy-specimen; the leishmanin skin test is of value. Most patients respond to sodium stibogluconate (see above); local heat therapy is also used. Paromomycin cream has been successfully applied locally.
Mucocutaneous leishmaniasis This form is caused by L. braziliensis and rarely L. mexicana. It is present in Central and South America, particularly the Amazon basin, and characterised by highly destructive, ulcerative, granulomatous lesions of the skin and mucous membranes, especially involving the mucocutaneous junctions of the mouth, nasopharynx, genitalia, and rectum. Infection is usually via a super?cial skin lesion at the site of a sand?y bite. However, spread is by haematogenous routes (usually after several years) to a mucocutaneous location. Diagnosis and treatment are the same as for cutaneous leishmaniasis.... leishmaniasis
Most of these drugs act by blocking DOPAMINE receptors. As a result they can give rise to the extrapyramidal effects of PARKINSONISM and may also cause HYPERPROLACTINAEMIA.
Troublesome side-effects may require control by ANTICHOLINERGIC drugs. The main antipsychotic drugs are: (i) chlorpromazine, methotrimeprazine and promazine, characterised by pronounced sedative effects and a moderate anticholinergic and extrapyramidal e?ect; (ii) pericyazine, pipothiazine and thioridazine, which have moderate sedative effects and marked anticholinergic effects, but less extrapyramidal effects than the other groups; (iii) ?uphenazine, perphenazine, prochlorperazine, sulpiride and tri?uoperazine, which have fewer sedative effects and fewer anticholinergic effects, but more pronounced extrapyramidal effects.... neuroleptics
The symptoms depend upon the site of the infection. General symptoms such as fever, weight loss and night sweats are common. In the most common form of pulmonary tuberculosis, cough and blood-stained sputum (haemoptysis) are common symptoms.
The route of infection is most often by inhalation, although it can be by ingestion of products such as infected milk. The results of contact depend upon the extent of the exposure and the susceptibility of the individual. Around 30 per cent of those closely exposed to the organism will be infected, but most will contain the infection with no signi?cant clinical illness and only a minority will go on to develop clinical disease. Around 5 per cent of those infected will develop post-primary disease over the next two or three years. The rest are at risk of reactivation of the disease later, particularly if their resistance is reduced by associated disease, poor nutrition or immunosuppression. In developed countries around 5 per cent of those infected will reactivate their healed tuberculosis into a clinical problem.
Immunosuppressed patients such as those infected with HIV are at much greater risk of developing clinical tuberculosis on primary contact or from reactivation. This is a particular problem in many developing countries, where there is a high incidence of both HIV and tuberculosis.
Diagnosis This depends upon identi?cation of mycobacteria on direct staining of sputum or other secretions or tissue, and upon culture of the organism. Culture takes 4–6 weeks but is necessary for di?erentiation from other non-tuberculous mycobacteria and for drug-sensitivity testing. Newer techniques involving DNA ampli?cation by polymerase chain reaction (PCR) can detect small numbers of organisms and help with earlier diagnosis.
Treatment This can be preventative or curative. Important elements of prevention are adequate nutrition and social conditions, BCG vaccination (see IMMUNISATION), an adequate public-health programme for contact tracing, and chemoprophylaxis. Radiological screening with mass miniature radiography is no longer used.
Vaccination with an attenuated organism (BCG – Bacillus Calmette Guerin) is used in the United Kingdom and some other countries at 12–13 years, or earlier in high-risk groups. Some studies show 80 per cent protection against tuberculosis for ten years after vaccination.
Cases of open tuberculosis need to be identi?ed; their close contacts should be reviewed for evidence of disease. Adequate antibiotic chemotherapy removes the infective risk after around two weeks of treatment. Chemoprophylaxis – the use of antituberculous therapy in those without clinical disease – may be used in contacts who develop a strong reaction on tuberculin skin testing or those at high risk because of associated disease.
The major principles of antibiotic chemotherapy for tuberculosis are that a combination of drugs needs to be used, and that treatment needs to be continued for a prolonged period – usually six months. Use of single agents or interrupted courses leads to the development of drug resistance. Serious outbreaks of multiply resistant Mycobacterium tuberculosis have been seen mainly in AIDS units, where patients have greater susceptibility to the disease, but also in developing countries where maintenance of appropriate antibacterial therapy for six months or more can be di?cult.
Streptomycin was the ?rst useful agent identi?ed in 1944. The four drugs used most often now are RIFAMPICIN, ISONIAZID, PYRAZINAMIDE and ETHAMBUTOL. Three to four agents are used for the ?rst two months; then, when sensitivities are known and clinical response observed, two drugs, most often rifampicin and isoniazid, are continued for the rest of the course. Treatment is taken daily, although thrice-weekly, directly observed therapy is used when there is doubt about the patient’s compliance. All the antituberculous agents have a range of adverse effects that need to be monitored during treatment. Provided that the treatment is prescribed and taken appropriately, response to treatment is very good with cure of disease and very low relapse rates.... nature of the disease tuberculosis has
Symptoms The onset may be sudden or insidious. In the acute form there is severe diarrhoea and the patient may pass up to 20 stools a day. The stools, which may be small in quantity, are ?uid and contain blood, pus and mucus. There is always fever, which runs an irregular course. In other cases the patient ?rst notices some irregularity of the movement of the bowels, with the passage of blood. This becomes gradually more marked. There may be pain but usually a varying amount of abdominal discomfort. The constant diarrhoea leads to emaciation, weakness and ANAEMIA. As a rule the acute phase passes into a chronic stage. The chronic form is liable to run a prolonged course, and most patients suffer relapses for many years. SIGMOIDOSCOPY, BIOPSY and abdominal X-RAYS are essential diagnostic procedures.
Treatment Many patients may be undernourished and need expert dietary assessment and appropriate calorie, protein, vitamin and mineral supplements. This is particularly important in children with the disorder. While speci?c nutritional treatment can initiate improvement in CROHN’S DISEASE, this is not the case with ulcerative colitis. CORTICOSTEROIDS, given by mouth or ENEMA, help to control the diarrhoea. Intravenous nutrition may be required. The anaemia is treated with iron supplements, and with blood infusions if necessary. Blood cultures should be taken, repeatedly if the fever persists. If SEPTICAEMIA is suspected, broad-spectrum antibiotics should be given. Surgery to remove part of the affected colon may be necessary and an ILEOSTOMY is sometimes required. After recovery, the patient should remain on a low-residue diet, with regular follow-up by the physician, Mesalazine and SULFASALAZINE are helpful in the prevention of recurrences.
Patients and their relatives can obtain help and advice from the National Association for Colitis and Crohn’s Disease.... ulcerative colitis
However, calling a condition psychosomatic implies something more – the primacy of the psyche over the soma. Going back to the in?uential theories and practice of PSYCHOANALYSIS as expounded from the 1930s, many diseases have been proposed as the result of psychological factors.These have included PEPTIC ULCER, ULCERATIVE COLITIS, ASTHMA, PSORIASIS and others. In this view, much physical disorder is due to repressed or excessive emotions. Likewise it is also argued that whereas some people express psychological distress via psychological symptoms (such as anxiety, depression and so on), others develop physical symptoms instead – and that they are also at greater risk of physical disease.
The trouble with this view is that medical advances repeatedly show that it goes too far. Stress certainly causes physical symptoms – for example, DYSPEPSIA – but the belief that it caused peptic ulcers vanished with the discovery of the true cause: colonisation of the stomach by the bacterium, Helicobacter pylori. Of course, stress and social adversity affect the risk of many diseases. For example, the incidence of heart disease among UK government employees (civil servants) has been shown to be in?uenced by their social class and their degree of job satisfaction. But we do not know how this works. Some argue that social adversity and stress in?uence how the heart functions (‘He died of a broken heart’). Stress can also affect IMMUNITY but it cannot cause AIDS/HIV and we do not know if there is a link running from stress to abnormal immune function to actual illness.
We can say that psychological factors provoke physical symptoms, and often even explain how this can happen. For example, when you are anxious you produce more epinephrine (adrenaline), which gives rise to chest pain, ‘butter?ies in the stomach’ and PALPITATION. These symptoms are not ‘all in the mind’, even if the trigger is a psychological one. People who are depressed are more likely to experience nearly every physical symptom there is, but especially pain and fatigue. Taken as a whole, psychologically induced symptoms are an enormous burden on the NHS and probably responsible for more doctor visits and sickness absence than any other single cause. Also we can be con?dent that social adversity and stress powerfully in?uence the outcome of many illnesses; likewise, a vast range of unhealthy activities and behaviours such as smoking, excessive alcohol intake, excessive eating, and so on. But we must be careful not to assume that our emotions directly cause our illnesses.... psychosomatic diseases
The causes of anorexia are unclear, but the condition may be linked to a lack of self-worth that leads to excessive concern over physical appearance. Normal dieting may develop into starvation.
In the early stages, sufferers may be overactive and exercise excessively. They are obsessed with food, and often make complicated meals for their families, but are reluctant to eat socially and manage to avoid eating the meals themselves. As weight loss continues, they become tired and weak, the skin becomes dry, lanugo hair (fine, downy hair) grows on the body, and normal hair becomes thinner. Starvation leads to amenorrhoea in many women. Some anorexics sometimes make themselves vomit or take laxative drugs or diuretic drugs to promote weight loss (see bulimia). Chemical imbalances as a result of starvation with or without vomiting can cause potentially fatal cardiac arrhythmias.
Hospital treatment is often necessary and is usually based on a closely controlled feeding programme, combined with psychotherapy or family therapy. For some people, antidepressant drugs may be helpful. Many sufferers relapse after treatment, and long-term psychotherapy is required.... anorexia nervosa
Abnormalities in brain biochemistry, or in the structure and/or function of certain nerve pathways within the brain, could underlie manic–depressive illness. An inherited tendency is also an established causative factor.Severe manic–depressive illness often needs hospital treatment. Antidepressant drugs and/or ECT are used to treat depression, and antipsychotic drugs are given to control manic symptoms. Carbamazepine or lithium may be used to prevent relapse.
Group therapy, family therapy, and individual psychotherapy may be useful in treatment. Cognitive–behavioural therapy may also be helpful. With treatment, more than 80 per cent of patients improve or remain stable. Even those with severe illness may be restored to near normal health with lithium.... manic–depressive illness
The syndrome is caused by an immune response and usually develops only in people with a genetic predisposition. Most patients have the -B27 tissue type (see histocompatability antigens). The syndrome’s development is induced by infection: usually nongonococcal urethritis, but sometimes bacillary dysentery. Reiter’s syndrome usually starts with a urethral discharge, which is followed by conjunctivitis and then arthritis. The arthritis usually affects 1 or 2 joints (usually the knee and/or ankle) and is often associated with fever and malaise. Attacks can last for several months. Tendons, ligaments, and tissue in the soles of the feet may also become inflamed. Skin rashes are common.
Diagnosis is made from the symptoms.
Analgesic drugs and nonsteroidal antiinflammatory drugs relieve symptoms but may have to be taken for a long period.
Relapses occur in about 1 in 3 cases.... reiter’s syndrome
Today, yellow fever is contracted only in Central America, parts of South America, and a large area of Africa. Eradication of the causative mosquito from populated areas has greatly reduced its incidence.
Yellow fever is characterised by a sudden onset of fever and headache, often with nausea and nosebleeds and, despite the high fever, a very low heart-rate. In
more serious cases, the fever is higher and there is severe headache and pain in the neck, back, and legs. Damage may occur rapidly to the liver and kidneys, causing jaundice and kidney failure. This may be followed by severe agitation and delirium, leading to coma and death.
Vaccination confers long-lasting immunity and should always be obtained before travel to affected areas. A single injection of the vaccine gives protection for at least 10 years. Reactions to the vaccine are rare and are usually trivial, although children under the age of 1 should not be vaccinated.
During yellow fever epidemics, diagnosis is simple. A diagnosis can be confirmed by carrying out blood tests to isolate the causative virus or to find antibodies to the virus.
No drug is effective against the yellow fever virus; treatment is directed at maintaining the blood volume.
Transfusion of fluids is often necessary.
Many patients recover in about 3 days and, in mild to moderate cases, complications are few.
Relapses do not occur and one attack confers lifelong immunity.
Overall, however, about 10 per cent of victims die.... yellow fever
BI-RADS (Breast Imaging Reporting and Data System) a standardized system of terminology, report organization, assessment, and classification for mammography and ultrasound or MRI of the breast. BI-RADS reporting enables radiologists to communicate results to the referring physician clearly and consistently, with a final assessment and specific management recommendations.
The success of BI-RADS has inspired several other systems of the same kind: TI-RADS (Thyroid Imaging Reporting and Data System); LI-RADS (Liver Imaging Reporting and Data System); and PI-RADS (Prostate Imaging Reporting and Data System).... bipolar affective disorder
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