Hin: Gular, Umar
Ben: Jagya dumurMal, Tam,Kan: AthiTel: Udambaramu, PaidiGular fig, Cluster fig or Country fig, which is considered sacred, has golden coloured exudate and black bark. It is distributed all over India. Its roots are useful in treating dysentery. The bark is useful as a wash for wounds, highly efficacious in threatened abortions and recommended in uropathy. Powdered leaves mixed with honey are given in vitiated condition of pitta. A decoction of the leaves is a good wash for wounds and ulcers. Tender fruits (figs) are used in vitiated conditions of pitta, diarrhoea, dyspepsia and haemorrhages. The latex is administered in haemorrhoids and diarrhoea (Warrier et al, 1995). The ripe fruits are sweet, cooling and are used in haemoptysis, thirst and vomiting (Nadkarni, 1954; Aiyer et al, 1957; Moos, 1976). Nalpamaradi coconut oil, Candanasava, Valiya Arimedastaila, Dinesavalyadi Kuzhambu, Abhrabhasma, Valiya candanaditaila, etc. are some important preparations using the drug (Sivarajan et al, 1994).It is a moderate to large-sized spreading laticiferous, deciduous tree without many prominent aerial roots. Leaves are dark green and ovate or elliptic. Fruit receptacles are 2-5cm in diameter, sub- globose or pyriform arranged in large clusters on short leafless branches arising from main trunk or large branches. Figs are smooth or rarely covered with minute soft hairs. When ripe, they are orange, dull reddish or dark crimson. They have a pleasant smell resembling that of cedar apples. The bark is rusty brown with a fairly smooth and soft surface, the thickness varying from 0.5-2cm according to the age of the trunk or bark. Surface is with minute separating flakes of white tissue. Texture is homogeneously leathery (Warrier et al, 1995).Stem-bark gives gluanol acetate, -sitosterol, leucocyanidin-3-O- -D-glucopyrancoside, leucopelargonidin-3-O- -D-glucopyranoside, leucopelargonidin -3-O- -L-rhamnopyranoside, lupeol, ceryl behenate, lupeol acetate and -amyrin acetate. Stem- bark is hypoglycaemic and anti-protozoal. Gall is CVS active. Bark is tonic and used in rinder pest diseases of cattle. Root is antidysenteric and antidiabetic. Leaf is antibilious. Latex is antidiarrhoeal and used in piles. Bark and syconium is astringent and used in menorrhagia (Husain et al, 1992).2. Ficus microcarpa Linn. f. syn. F. retusa auct. Non. Linn.San: Plaksah; Hin,Ben: Kamarup;Mal: Ithi, Ithiyal;Tam: Kallicci, Icci;
Kan: Itti;
Tel: PlaksaPlaksah is the Ficus species with few branches and many adventitious roots growing downward. It is widely distributed throughout India and in Sri Lanka, S. China, Ryuku Isles and Britain. Plakasah is one of the five ingredients of the group panchvalkala i.e, five barks, the decoction of which is extensively used to clear ulcers and a douche in leucorrhoea in children. This decoction is administered externally and internally with satisfactory results. Plaksah is acclaimed as cooling, astringent, and curative of raktapitta doshas, ulcers, skin diseases, burning sensation, inflammation and oedema. It is found to have good healing property and is used in preparation of oils and ointments for external application in the treatment of ulcers (Aiyer and Kolammal, 1957). The stem-bark is used to prepare Usirasava, Gandhataila, Nalpamaradi taila, Valiya marmagulika, etc. (Sivarajan et al, 1994). The bark and leaves are used in wounds, ulcers, bruises, flatulent colic, hepatopathy, diarrhoea, dysentery, diabetes, hyperdipsia, burning sensation, haemaorrhages, erysipelas, dropsy, ulcerative stomatitis, haemoptysis, psychopathy, leucorrhoea and coporrhagia (Warrier et al,1995) F. microcarpa is a large glabrous evergreen tree with few aerial roots. Leaves are short- petioled, 5-10cm long, 2-6cm wide and apex shortly and bluntly apiculate or slightly emarginate. Main lateral nerves are not very prominent and stipules are lanceolate. Fruit receptacles are sessile and globose occurring in axillary pairs. It is yellowish when ripe without any characteristic smell. Bark is dark grey or brown with a smooth surface except for the lenticels. Outer bark is corky and crustaceous thin and firmly adherent to inner tissue. Inner bark is light and flesh coloured with firbrous texture (Warrier et al, 1995). It is also equated with many other species of the genus. viz. F. Singh and Chunekar, 1972; Kapoor and Mitra, 1979; Sharma, 1983).The bark contains tannin, wax and saponin. Bark is antibilious. Powdered leaves and bark is found very good in rheumatic headache. The bark and leaves are astringent, refrigerant, acrid and stomachic.3. Ficus benghalensis Linn.Eng: Banyan tree; San: Nyagrodhah, Vatah;Hin: Bat, Bargad;Ben: Bar, Bot; Mar: Vada; Mal: Peral, Vatavriksham;Tam: Alamaram, Peral;Kan: Ala;Tel: Peddamarri;Guj: VadBanyan tree is a laticiferous tree with reddish fruits, which is wound round by aerial adventitious roots that look like many legs. It is found in the Sub-Himalayan tract and Peninsular India. It is also grawn throughout India. It is widely used in treatment of skin diseases with pitta and rakta predominance. Stem-bark, root -bark, aerial roots, leaves, vegetative buds and milky exudate are used in medicine. It improves complexion, cures erysepelas, burning sensation and vaginal disorders, while an infusion of the bark cures dysentery, diarrhoea, leucorrhoea, menorrhagia, nervous disorders and reduces blood sugar in diabetes. A decoction of the vegetative buds in milk is beneficial in haemorrhages. A paste of the leaves is applied externally to abcesses and wounds to promote suppuration, while that of young aerial roots cure pimples. Young twigs when used as a tooth brush strengthen gum and teeth (Nadkarni, 1954; Aiyer and Kolammal, 1957; Mooss,1976). The drug forms an important constituent of formulations like Nalpamaradi Coconut oil, Saribadyasava, Kumkumadi taila, Khadi ra gulika, Valiyacandanadi taila, Candanasava, etc. (Sivarajan et al, 1994). The aerial roots are useful in obstinate vomiting and leucorrhoea and are used in osteomalacia of the limbs. The buds are useful in diarrhoea and dysentery. The latex is useful in neuralgia, rheumatism, lumbago, bruises, nasitis, ulorrhagia, ulitis, odontopathy, haemorrhoids, gonorrhoea, inflammations, cracks of the sole and skin diseases (Warrier et al, 1995).It is a very large tree up to 30m in height with widely spreading branches bearing many aerial roots functioning as prop roots. Bark is greenish white. Leaves are simple, alternate, arranged often in clusters at the ends of branches. They are stipulate, 10-20cm long and 5-12.5cm broad, broadly elliptic to ovate, entire, coriaceous, strongly 3-7 ribbed from the base. The fruit receptacles are axillary, sessile, seen in pairs globose, brick red when ripe and enclosing male, female and gall flowers. Fruits are small, crustaceous, achenes, enclosed in the common fleshy receptacles. The young bark is somewhat smooth with longitudinal and transverse row of lenticels. In older bark, the lenticels are numerous and closely spaced; outer bark easily flakes off. The fresh cut surface is pink or flesh coloured and exudes plenty of latex. The inner most part of the bark adjoining the wood is nearly white and fibrous (Warrier et al, 1995).The bark yields flavanoid compounds A, B and C; A and C are identified as different forms of a leucoanthocyanidin and compound B a leucoanthocyanin. All the 3 were effective as hypoglycaemic agents. Leaves give friedelin, -sitosterol, flavonoids- quercetin-3-galactoside and rutin. Heart wood give tiglic acid ester of taraxasterol. Bark is hypoglycemic, tonic, astringent, antidiarrhoeal and antidiabetic. Latex is antirheumatic. Seed is tonic. Leaf is diaphoretic. Root fibre is antigonorrhoeic. Aerial root is used in debility and anaemic dysentery (Husain et al, 1992)..4. Ficus religiosa Linn.Eng:Peepal tree, Sacred fig; San:Pippalah, Asvatthah; Hin:Pippal, Pipli, Pipar; Mal:ArayalBen: Asvatha;Tam: Arasu, Asvattam;Kan: Aswatha;Tel: Ravi; Mar: Ashvata, PimpalaPeepal tree or Sacred fig is a large deciduous tree with few or no aerial roots. It is common throughout India, often planted in the vicinity of the temples. An aqueous extract of the bark has an antibacterial activity against Staphylococcus aureus and Escherichia coli. It is used in the treatment of gonorrhoea, diarrhoea, dysentery, haemorrhoids and gastrohelcosis. A paste of the powdered bark is a good absorbent for inflammatory swellings. It is also good for burns. Leaves and tender shoots have purgative properties and are also recommended for wounds and skin diseases. Fruits are laxative and digestive. The dried fruit pulverized and taken in water cures asthma. Seeds are refrigerant and laxative. The latex is good for neuralgia, inflammations and haemorrhages (Warrier et al, 1995). Decoction of the bark if taken in honey subdues vatarakta (Nadkarni, 1954; Aiyer and Kolammal, 1957; Mooss, 1976; Kurup et al, 1979). The important preparations using the drug are Nalpamaradi taila, Saribadyasava, Candanasava, Karnasulantaka, Valiyamarma gulika etc (Sivarajan et al, 1994). branches bearing long petioled, ovate, cordate shiny leaves. Leaves are bright green, the apex produced into a linear-lanceolate tail about half as long as the main portion of the blade. The receptacles occurring in pairs and are axillary, depressed globose, smooth and purplish when ripe. The bark is grey or ash coloured with thin or membranous flakes and is often covered with crustose lichen patches. The outer bark is not of uniform thickness, the middle bark in sections appear as brownish or light reddish brown. The inner part consists of layers of light yellowish or orange brown granular tissue (Warrier et al, 1995).Bark gives -sitosterol and its glucoside. Bark is hypoglycaemic. Stem bark is antiprotozoal, anthelmintic and antiviral. Bark is astringent, antigonorrheic, febrifuge, aphrodisiac and antidysenteric. Syconium, leaf and young shoot is purgative (Husain et al, 1992).Agrotechnology: Ficus species can be cultivated in rocky areas, unused lands, or other wastelands of the farmyard. The plant is vegetatively propagated by stem cuttings. A few species are also seed propagated. Stem cuttings of pencil thickness taken from the branches are to be kept for rooting. Rooted cuttings are to be transplanted to prepared pits. No regular manuring is required. Irrigation is not a must as a plant is hardy. The plant is not attacked by any serious pests or diseases. Bark can be collected after 15 years. Ficus species generally has an economic life span of more than hundred years. Hence bark can be regularly collected from the tree. Root, bark, leaves, fruits and latex form the economic parts (Prasad et al,1995).... ficusAssociation areas interpret information received from sensory areas and prompt appropriate responses such as voluntary movement.... association area
During a bite by the female mosquito, one or more sporozoites – a stage in the life-cycle of the parasite – are injected into the human circulation; these are taken up by the hepatocytes (liver cells). Following division, merozoites (minute particles resulting from the division) are liberated into the bloodstream where they invade red blood cells. These in turn divide, releasing further merozoites. As merozoites are periodically liberated into the bloodstream, they cause the characteristic fevers, rigors, etc.
Malaria occurs in many tropical and subtropical countries; P. falciparum is, however, con?ned very largely to Africa, Asia and South America. Malaria is present in increasingly large areas; in addition, the parasites are developing resistance to various preventative and treatment drugs. The disease constitutes a signi?cant problem for travellers, who must obtain sound advice on chemoprophylaxis before embarking on tropical trips – especially to a rural area where intense transmission can occur. Transmission has also been recorded at airports, and following blood transfusion.
The World Health Organisation (WHO) has listed malaria as one of Europe’s top ten infectious diseases. In 1992, 20,000 cases were reported: this had risen to more than 200,000 by the late 1990s. The resurgence of malaria has been worldwide, in part the result of the development of resistant strains of the disease, and in part because many countries have failed (or been unable) to implement environmental measures to eliminate mosquitoes. Nearly 40 years ago the WHO forecast that by 1980 only four million people would be affected worldwide; now, at the beginning of the 21st century, around 500 million people a year are contracting malaria with about 3,000 people a day dying from the infection – as many as 70 per cent of them children under the age of ?ve, according to WHO ?gures. The apparently steady advance of global warming means that countries with temperate climates may well warm up su?ciently to enable malaria to become established as an ENDEMIC disease. In any case, the great increase in international air travel has exposed many more people to the risk of malaria, and infected individuals may not exhibit symptoms until they are back home. Doctors seeing a recent traveller with unexplained pyrexia and illness should consider the possibility of malarial infection.
Diagnosis is by demonstration of trophozoites – a stage in the parasite’s life-cycle that takes place in red blood cells – in thick/thin blood-?lms of peripheral blood. Serological tests are of value in deciding whether an individual has had a past infection, but are of no value in acute disease.
P. vivax and P. ovale infections cause less severe disease than P. falciparum (see below), although overall there are many clinical similarities; acute complications are unusual, but chronic ANAEMIA is often present. Primaquine is necessary to eliminate the exoerythrocytic cycle in the hepatocyte (liver cell).
P. falciparum Complications of P. falciparum infection include cerebral involvement (see BRAIN – Cerebrum), due to adhesion of immature trophozoites on to the cerebral vascular endothelium; these lead to a high death rate when inadequately treated. Renal involvement (frequently resulting from HAEMOGLOBINURIA), PULMONARY OEDEMA, HYPOTENSION, HYPOGLYCAEMIA, and complications in pregnancy are also important. In complicated disease, HAEMODIALYSIS and exchange TRANSFUSION have been used. No adequate controlled trial using the latter regimen has been carried out, however, and possible bene?ts must be weighed against numerous potential side-effects – for instance, the introduction of a wide range of infections, overload of the circulatory system with infused ?uids, and other complications.
P. malariae usually produces a chronic infection, and chronic renal disease (nephrotic syndrome) is an occasional sequel, especially in tropical Africa.
Gross SPLENOMEGALY (hyper-reactive malarious splenomegaly, or tropical splenomegaly syndrome) can complicate all four human Plasmodium spp. infections. The syndrome responds to long-term malarial chemoprophylaxis. BURKITT’S LYMPHOMA is found in geographical areas where malaria infection is endemic; the EPSTEIN BARR VIRUS is aetiologically involved.
Prophylaxis Malaria specialists in the United Kingdom have produced guidance for residents travelling to endemic areas for short stays. Drug choice takes account of:
risk of exposure to malaria;
extent of drug resistance;
e?cacy of recommended drugs and their side-effects;
criteria relevant to the individual (e.g. age, pregnancy, kidney or liver impairment). Personal protection against being bitten by
mosquitoes is essential. Permethrinimpregnated nets are an e?ective barrier, while skin barrier protection and vaporised insecticides are helpful. Lotions, sprays or roll-on applicators all containing diethyltoluamide (DEET) are safe and work when put on the skin. Their e?ect, however, lasts only for a few hours. Long sleeves and trousers should be worn after dark.
Drug prophylaxis should be started at least a week before travelling into countries where malaria is endemic (two or three weeks in the case of me?oquine). Drug treatment should be continued for at least four weeks after leaving endemic areas. Even if all recommended antimalarial programmes are followed, it is possible that malaria may occur any time up to three months afterwards. Medical advice should be sought if any illness develops. Chloroquine can be used as a prophylactic drug where the risk of resistant falciparum malaria is low; otherwise, me?oquine or proguanil hydrochloride should be used. Travellers to malaria-infested areas should seek expert advice on appropriate prophylactic treatment well before departing.
Treatment Various chemoprophylactic regimes are widely used. Those commmonly prescribed include: chloroquine + paludrine, me?oquine, and Maloprim (trimethoprim + dapsone); Fansidar (trimethoprim + sulphamethoxazole) has been shown to have signi?cant side-effects, especially when used in conjunction with chloroquine, and is now rarely used. No chemotherapeutic regimen is totally e?ective, so other preventive measures are again being used. These include people avoiding mosquito bites, covering exposed areas of the body between dusk and dawn, and using mosquito repellents.
Chemotherapy was for many years dominated by the synthetic agent chloroquine. However, with the widespread emergence of chloroquine-resistance, quinine is again being widely used. It is given intravenously in severe infections; the oral route is used subsequently and in minor cases. Other agents currently in use include me?oquine, halofantrine, doxycycline, and the artemesinin alkaloids (‘qinghaosu’).
Researchers are working on vaccines against malaria.... malaria
Naevus simplex Also known as ‘salmon patch’. About one-third of white children are born with macular pink areas of ERYTHEMA on the nape, brow or eyelids which usually disappear after a few months, but patches on the nape may persist.
Naevus ?ammeus Also known as ‘portwine stain’ and present at birth. It is unilateral, usually on the face, and may be extensive. It tends to darken with age and is permanent. Laser treatment is e?ective.
Strawberry naevus (cavernous haemangioma) is usually not present at birth but appears within a few weeks and grows rapidly, reaching a peak in size after 6–12 months, when the lobulated red nodule may resemble a ripe strawberry. Untreated, the naevus disappears spontaneously over several years. It may occur anywhere and may be very troublesome when occurring around an eye or on the ‘nappy’ area. If possible it should be left alone, but where it is causing problems other than simply cosmetic ones it is best treated by an expert. This may involve medical treatment with steroids or interferon or laser therapy.
Spider naevus is due to a dilated ARTERIOLE causing a minute red papule in the skin, the small branching vessels resembling spider legs. A few spider naevi are common in young people, but multiple naevi are common in pregnancy and may also be a warning sign of chronic liver disease.... naevus
The nervous system can be likened to a computer. The central processing unit – which receives, processes and stores information and initiates instructions for bodily activities – is called the central nervous system: this is made up of the brain and SPINAL CORD. The peripheral nervous system – synonymous with the cables that transmit information to and from a computer’s processing unit – has two parts: sensory and motor. The former collects information from the body’s many sense organs. These respond to touch, temperature, pain, position, smells, sounds and visual images and the information is signalled to the brain via the sensory nerves. When information has been processed centrally, the brain and spinal cord send instructions for action via motor nerves to the ‘voluntary’ muscles controlling movements and speech, to the ‘involuntary’ muscles that operate the internal organs such as the heart and intestines, and to the various glands, including the sweat glands in the skin. (Details of the 12 pairs of cranial nerves and the 31 pairs of nerves emanating from the spinal cord are given in respective texts on brain and spinal cord.)
Functional divisions of nervous system As well as the nervous system’s anatomical divisions, the system is divided functionally, into autonomic and somatic parts. The autonomic nervous system, which is split into sympathetic and parasympathetic divisions, deals with the automatic or unconscious control of internal bodily activities such as heartbeat, muscular status of blood vessels, digestion and glandular functions. The somatic system is responsible for the skeletal (voluntary) muscles (see MUSCLE) which carry out intended movements initiated by the brain – for example, the activation of limbs, tongue, vocal cords (speech), anal muscles (defaecation), urethral sphincters (urination) or vaginal muscles (childbirth). In addition, many survival responses – the most powerfully instinctive animal drives, which range from avoiding danger and pain to shivering when cold or sweating when hot – are initiated unconsciously and automatically by the nervous system using the appropriate neural pathways to achieve the particular survival reaction required.
The complex functions of the nervous system include the ability to experience emotions, such as excitement and pleasure, anxiety and frustration, and to undertake intellectual activities. For these experiences an individual can utilise many built-in neurological programmes and he or she can enhance performance through learning – a vital human function that depends on MEMORY, a three stage-process in the brain of registration, storage and recall. The various anatomical and functional divisions of the nervous system that have been unravelled as science has strived to explain how it works may seem confusing. In practical terms, the nervous system works mainly by using automatic or relex reactions (see REFLEX ACTION) to various stimuli (described above), supplemented by voluntary actions triggered by the activity of the conscious (higher) areas of the brain. Some higher functions crucial to human activity – for example, visual perception, thought, memory and speech – are complex and subtle, and the mechanisms are not yet fully understood. But all these complex activities rest on the foundation of relatively simple electrochemical transmissions of impulses through the massive network of billions of specialised cells, the neurones.... nervous system
Paralysis due to brain disease The most common form is unilateral palsy, or HEMIPLEGIA, generally arising from cerebral HAEMORRHAGE, THROMBOSIS or EMBOLISM affecting the opposite side of the BRAIN. If all four limbs and trunk are affected, the paralysis is called quadraplegia; if both legs and part of the trunk are affected, it is called paraplegia. Paralysis may also be divided into ?accid (?oppy limbs) or spastic (rigid).
In hemiplegia the cause may be an abscess, haemorrhage, thrombosis or TUMOUR in the brain. CEREBRAL PALSY or ENCEPHALITIS are other possible causes. Sometimes damage occurs in the parts of the nervous system responsible for the ?ne control of muscle movements: the cerebellum and basal ganglion are such areas, and lack of DOPAMINE in the latter causes PARKINSONISM.
Damage or injury Damage to or pressure on the SPINAL CORD may paralyse muscles supplied by nerves below the site of damage. A fractured spine or pressure from a tumour may have this e?ect. Disorders affecting the cord which can cause paralysis include osteoarthritis of the cervical vertebrae (see BONE, DISORDERS OF), MULTIPLE SCLEROSIS (MS), MYELITIS, POLIOMYELITIS and MENINGITIS. Vitamin B12 de?ciency (see APPENDIX 5: VITAMINS) may also cause deterioration in the spinal cord (see also SPINE AND SPINAL CORD, DISEASES AND INJURIES OF).
Neuropathies are a group of disorders, some inherited, that damage the peripheral nerves, thus affecting their ability to conduct electrical impulses. This, in turn, causes muscle weakness or paralysis. Among the causes of neuropathies are cancers, DIABETES MELLITUS, liver disease, and the toxic consequences of some drugs or metals – lead being one example.
Disorders of the muscles themselves – for example, muscular dystrophy (see MUSCLES, DISORDERS OF – Myopathy) – can disturb their normal working and so cause partial or complete paralysis of the part(s) affected.
Treatment The aim of treatment should be to remedy the underlying cause – for example, surgical removal of a displaced intervertebral
disc or treating diabetes mellitus. Sometimes the cause cannot be recti?ed but, whether treatable or not, physiotherapy is essential to prevent joints from seizing up and to try to maintain some tone in muscles that may be only partly affected. With temporary paralysis, such as can occur after a STROKE, physiotherapy can retrain the sufferers to use their muscles and joints to ensure mobility during and after recovery. Patients with permanent hemiplegia, paraplegia or quadraplegia need highly skilled nursing care, rehabilitative support and resources, and expert help to allow them, if possible, to live at home.... paralysis
Causes Blood supply to the brain may be interrupted by arteries furring up with ATHEROSCLEROSIS (which is accelerated by HYPERTENSION and DIABETES MELLITUS, both of which are associated with a higher incidence of strokes) or being occluded by blood clots arising from distant organs such as infected heart valves or larger clots in the heart (see BLOOD CLOT; THROMBOSIS). Hearts with an irregular rhythm are especially prone to develop clots. Patients with thick or viscous blood, clotting disorders or those with in?amed arteries – for example, in SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) – are particularly in danger of having strokes. Bleeding into the brain arises from areas of weakened blood vessels, many of which may be congenital.
Symptoms Minor episodes due to temporary lack of blood supply and oxygen (called TRANSIENT ISCHAEMIC ATTACKS OR EPISODES (TIA, TIE)) are manifested by short-lived weakness or numbness in an arm or leg and may precede a major stroke. Strokes cause sudden weakness or complete paralysis of the muscles controlled by the part of the brain affected, as well as sensory changes (e.g. numbness or tingling). In the worst cases these symptoms and signs may be accompanied by loss of consciousness. If the stroke affects the area of the brain controlling the larynx and throat, the patient may suffer slurring or loss of speech with di?culty in initiating swallowing. When the face is involved, the mouth may droop and the patient dribble. Strokes caused by haemorrhage may be preceded by headaches. Rarely, CVAs are complicated by epileptic ?ts (see EPILEPSY). If, on the other hand, numerous small clots develop in the brain rather than one major event, this may manifest itself as a gradual deterioration in the patient’s mental function, leading to DEMENTIA.
Investigations Tests on the heart or COMPUTED TOMOGRAPHY or ultrasonic scans (see ULTRASOUND) on arteries in the neck may indicate the original sites of distantly arising clots. Blood tests may show increased thickness or tendency to clotting, and the diagnosis of general medical conditions can explain the presence of in?amed arteries which are prone to block. Special brain X-rays show the position and size of the damaged brain tissue and can usually distinguish between a clot or infarct and a rupture of and haemorrhage from a blood vessel in the brain.
Management It is better to prevent a stroke than try to cure it. The control of a person’s diabetes or high blood pressure will reduce the risk of a stroke. Treatment with ANTICOAGULANTS prevents the formation of clots; regular small doses of aspirin stop platelets clumping together to form plugs in blood vessels. Both treatments reduce the likelihood of minor transient ischaemic episodes proceeding to a major stroke.
Once the latter has occurred, there is no e?ective treatment to reduce the damage to brain tissue. Function will return to the affected part of the body only if and when the brain recovers and messages are again sent down the appropriate nerves. Simple movements are more likely to recover than delicate ones, and sophisticated functions have the worst outlook. Thus, movement of the thigh may improve more easily than ?ne movements of ?ngers, and any speech impairment is more likely to be permanent. A rehabilitation team can help to compensate for any disabilities the subject may have. Physiotherapists maintain muscle tone and joint ?exibility, whilst waiting for power to return; occupational therapists advise about functional problems and supply equipment to help patients overcome their disabilities; and speech therapists help with diffculties in swallowing, improve the clarity of remaining speech or o?er alternative methods of communication. District nurses or home helps can provide support to those caring for victims of stroke at home. Advice about strokes may be obtained from the Stroke Association.... stroke
Symptoms: numbness, nerves may swell like iron rods. Infected nerves kill all sensation. In endemic areas, pins and needles in hands may call attention to it. A disease of nerves rather than skin. NOTIFIABLE DISEASE.
Many laymen and practitioners will never have seen a case. In the absence of modern medicine some good can be achieved by traditional remedies. Ancient Hindu and Chinese records refer to the use of Gotu Kola (internally and externally). Dr C.D. de Granpre? (1888) refers. (Martindale 27; p.441)
Oil of Chaulmoogra was used up to one hundred years ago before introduction of modern drugs. It fell into dis-use until discovered by a Director of Health in the Philippine Islands during World War I when he used it successfully in combination with camphor. In South America, where the disease is still active, Sarsaparilla has a long traditional reputation. Walnut oil is used as a dressing, in China. An anti- staphylococcal fraction has been isolated from the seeds of Psoralea corylifolia for use in leprosy. (Indian Journal of Pharmacy 26: 141, 1964)
Tea. Gotu Kola. Half a teaspoon to each cup boiling water; infuse 15 minutes. Drink freely. Stronger infusions may be used externally to cleanse ulceration.
Decoction. Combine: Sarsaparilla 1; Gotu Kola 1; Echinacea 2. Half an ounce to 1 pint water gently simmered 20 minutes. Dose: Half a cup 3 times daily.
Formula. Echinacea 2; Sarsaparilla 1; Gotu Kola 2. Dose. Powders 500mg. Liquid Extracts 3-5ml. Tinctures 5-10ml. Thrice daily.
Note: Antibody-positive cases of AIDS are vulnerable to leprosy, both diseases being caused by a similar bacterium.
To be treated by infectious diseases specialist. ... hansen’s disease
Infection is usually blood-born from dental abscess, tonsils, boil, or old wounds. Prompt modern hospital treatment is necessary to avoid thrombosis or necrosis of bone. Herbal medication can play a substantial supportive role. Differential diagnosis should exclude Infective Arthritis, Cellulitis, Rheumatic Fever, Leukaemia.
Symptoms. Affected bone painful and hot. Throbbing. Fever. Dehydration. Raised E.S.R. Severe general illness.
Treatment. Should enhance resistance as well as combat infection. Comfrey and Echinacea are principle remedies. Infected bone areas are not well supplied with blood, so oral antibiotics may not reach them; this is where topical herbal treatments can assist. Anti-bacterial drinks are available in the absence of conventional antibiotics.
To promote cell proliferation and callous formation: Comfrey root, Marigold, St John’s Wort, Arnica. (Madaus)
To stimulate connective tissue: Thuja.
Comfrey root. Potential benefit outweighs possible risk.
Teas. Nettles. Plantain. Silverweed, Yarrow. Boneset. Marigold petals. St John’s Wort. Comfrey leaves. Singly or in combination. Abundant drinks during the day.
Formula. Echinacea 2; Comfrey 1; Myrrh half; Thuja quarter. Dose – Liquid extracts: 2 teaspoons. Tinctures: 2-3 teaspoons. Powders: 750mg (three 00 capsules or half a teaspoon). Three or more times daily in water or honey.
Madaus: Tardolyt. Birthwort: a sodium salt of aristolochic acid.
Maria Treben: Yarrow and Fenugreek tea. Half cup Yarrow tea 4 times daily. To two of such cups, add half a teaspoon ground Fenugreek seeds.
Dr Finlay Ellingwood: Liquid Extract Echinacea 20-30 drops in water four times daily. And: Liquid Extract Lobelia 20-30 drops in water twice daily. Calcium Lactate tablets.
Topical. Comfrey root poultices to facilitate removal of pus, and to heal.
Diet. No solids. Fruit and milk diet for 5 days, followed by lacto-vegetarian diet. Herb teas as above. Plenty of water to combat dehydration.
Supplements. Daily. Vitamin B12 (50mcg), C (3g), D (500iu), E (1000iu). Calcium (1000-1500mg) taken as calcium lactate, Zinc.
General. Regulate bowels. Surgical treatment in a modern hospital necessary for removal of dead bone (sequestrum) and for adequate nursing facilities.
Treatment by a general medical practitioner or hospital specialist. ... osteomyelitis
Agnosia is usually associated with just one of the senses of vision, hearing, or touch and is described as visual, auditory, or tactile respectively. Some people, after a stroke that damages the right cerebral hemisphere, seem unaware of any disability in their affected left limbs. This is called anosognosia or sensory inattention. There is no specific treatment for agnosia, but some interpretative ability may return eventually.... agnosia
CANDIDA ALBICANS, also known as thrush or moniliasis. Candidiasis affects areas of mucous membrane in the body, most commonly the vagina and the inside of the mouth. In infants, it can occur in conjunction with nappy rash.
The fungus is normally present in the mouth and vagina but may multiply excessively if antibiotic drugs destroy the harmless bacteria that control its growth, or if the body’s resistance to infection is lowered.
Certain disorders, notably diabetes mellitus, and hormonal changes due to pregnancy or oral contraceptives, may also encourage its growth.
Candidiasis can be contracted by sexual intercourse with an infected partner.
The infection is far more common in women than in men.
Symptoms of vaginal infection include a thick, white discharge, genital irritation, and discomfort when passing urine.
Less commonly, the penis is infected in men, usually causing balanitis.
Oral candidiasis produces sore, creamy-yellow, raised patches in the mouth.
Candidiasis may spread to other moist areas of the body and may also affect the gastrointestinal tract, particularly in people with impaired immune systems.
Treatment for candidiasis is with topical preparations such as creams, pessaries, or lozenges, or with oral antifungal drugs.... candidiasis
Delays vary in severity and may affect the development of hand–eye coordination, walking, listening, language, speech, or social interaction. Delay may first be noticed by parents or detected during a routine developmental check.
There are many causes of developmental delay. A child who is late in most aspects of development usually has a generalized problem. This may be due to severe visual or hearing impairment, limited intellectual abilities (see learning difficulties), or damage to the brain before, during, or after birth.
Specific areas of delay may occur in movement and walking. Often there is no serious cause. However, specific causes may include muscular dystrophy and spina bifida. Delay in developing manipulative skills is often due to lack of adequate stimulation.
A lack of response to sound may be due to deafness. Autism is a rare cause of unresponsiveness to the human voice although hearing is normal. A hearing problem may cause delayed speech. Twins are often late talkers. Any generalized difficulty with muscle control can affect speech production; this may occur in children with cerebral palsy. Damage to, or structural defects of, the speech muscles, larynx (voice box), or mouth may also cause speech difficulties, as may any disorder affecting the speech area of the brain (see aphasia; dysarthria; dysphonia; speech disorders). Delay in bladder and bowel control have many possible causes (see encopresis; enuresis; soiling).
A child who shows signs of developmental delay should undergo a full assessment by a paediatrician.... developmental delay
Habitat: Kashmir, Himachal Pradesh, Tehri-Garhwal and other areas of northern India, at altitudes of 2,100-3,600 m.
English: Pindrow-Fir, Silver-Fir, The West-Himalayan Low-Level Fir.Ayurvedic: Taalisha (related sp.).Folk: Badar, Morinda, Raisalla, Ransla.Action: Uses similar to those of A. webbiana.
Terpenoids, flavonoids, glycosides and steroids of the leaf were found to have mast cell stabilizing action in rats. Terpenoids and flavonoids offered bronchoprotection against his- tamine challenge in guinea pigs. The ulcer protective action of petroleum ether, benzene and chloroform fraction has been attributed to steroidal contents. Terephthalic acid demethyl ester (TADE), isolated from the leaf, exhibited protection against inflammation and bronchospasm in guinea pigs. Ethanolic extract of leaves showed significant anxiolytic effects on all the paradigms of anxiety, barbiturate hypnosis potentiation.Pindrolactone, a lanostane-based triterpene lactone, isolated from the leaves, showed mild activity against Gram-positive bacteria but exhibited potent antibacterial activity against Gram-negative bacteria E. coli.... abies pindrowHabitat: Marshy areas throughout India, as a weed.
English: Blistering Ammannia.Ayurvedic: Agnipatri.Folk: Daadmaari. (Also known as Paashaanabheda.)Action: Stomachic, laxative, antirheumatic, febrifuge. Leaves— used externally for ringworm, herpic eruptions and other skin diseases; rubefacient.
Leaves contain lawsone. Plant extract—antibacterial. Extracts of stem, leaf and inflorescence are more effective as compared with the seed and root extract.... ammannia bacciferaAncylostoma braziliensis A nematode infection of dogs, which in humans causes local disease (larva migrans) only, generally on the soles of the feet. It is usually acquired by walking on beaches contaminated with dog faeces in places such as the Caribbean.... ancylostomiasis
In the wake of the devastating terrorist attacks on buildings in New York and Washington on 11 September 2001, modi?ed anthrax spores were sent by mail from an unidenti?ed source to some prominent Americans. Several people were infected and a few died. This was the ?rst known use of anthrax as a terror weapon.
Prevention is most important by disinfecting all hides, wool and hair coming from areas of the world. An e?cient vaccine is now available. Treatment consists of the administration of large doses of the broad-spectrum antibiotic, CIPROFLOXACIN. If bioterrorism is thought to be the likely source of anthrax infection, appropriate decontamination procedures must be organised promptly.
Symptoms
EXTERNAL FORM This is the ‘malignant pustule’. After inoculation of some small wound, a few hours or days elapse, and then a red, in?amed swelling appears, which grows larger till it covers half the face or the breadth of the arm, as the case may be. Upon its summit appears a bleb of pus, which bursts and leaves a black scab, perhaps 12 mm (half an inch) wide. The patient is feverish and seriously ill. The in?ammation may last ten days or so, when it slowly subsides and the patient recovers, if surviving the fever and prostration.
INTERNAL FORM This takes the form of pneumonia with haemorrhages, when the spores have been drawn into the lungs, or of ulcers of the stomach and intestines, with gangrene of the SPLEEN, when they have been swallowed.
It is usually fatal in two or three days. Victims may also develop GASTROENTERITIS or MENINGITIS.... anthrax
The speciality of anaesthesia broadly covers its provision for SURGERY, intensive therapy (intensive care), chronic pain management, acute pain management and obstetric analgesia. Anaesthetists in Britain are trained specialists with a medical degree, but in many countries some anaesthetists may be nurse practitioners working under the supervision of a medical anaesthetist.
The anaesthetist will assess the patient’s ?tness for anaesthesia, choose and perform the appropriate type of anaesthetic while monitoring and caring for the patient’s well-being, and, after the anaesthetic, supervise recovery and the provision of post-operative pain relief.
Anaesthesia may be broadly divided into general and local anaesthesia. Quite commonly the two are combined to allow continued relief of pain at the operation site after the patient awakens.
General anaesthesia is most often produced by using a combination of drugs to induce a state of reversible UNCONSCIOUSNESS. ‘Balanced’ anaesthesia uses a combination of drugs to provide unconsciousness, analgesia, and a greater or lesser degree of muscle relaxation.
A general anaesthetic comprises induction, maintenance and recovery. Historically, anaesthesia has been divided into four stages (see below), but these are only clearly seen during induction and maintenance of anaesthesia using inhalational agents alone.
(1) Onset of induction to unconsciousness
(2) Stage of excitement
(3) Surgical anaesthesia
(4) Overdosage
Induction involves the initial production of unconsciousness. Most often this is by INTRAVENOUS injection of a short-acting anaesthetic agent such as PROPOFOL, THIOPENTONE or ETOMIDATE, often accompanied by additional drugs such as ANALGESICS to smooth the process. Alternatively an inhalational technique may be used.
Maintenance of anaesthesia may be provided by continuous or intermittent use of intravenous drugs, but is commonly provided by administration of OXYGEN and NITROUS OXIDE or air containing a volatile anaesthetic agent. Anaesthetic machines are capable of providing a constant concentration of these, and have fail-safe mechanisms and monitors which guard against the patient’s receiving a gas mixture with inadequate oxygen (see HYPOXIC). The gases are adminstered to the patient via a breathing circuit either through a mask, a laryngeal mask or via ENDOTRACHEAL INTUBATION. In recent years, concerns about side-effects and pollution caused by volatile agents have led to increased popularity of total intravenous anaesthesia (TIVA).
For some types of surgery the patient is paralysed using muscle relaxants and then arti?cially ventilated by machine (see VENTILATOR). Patients are closely monitored during anaesthesia by the anaesthetist using a variety of devices. Minimal monitoring includes ELECTROCARDIOGRAM (ECG), blood pressure, PULSE OXIMETRY, inspired oxygen and end-tidal carbon-dioxide concentration – the amount of carbon dioxide breathed out when the lungs are at the ‘empty’ stage of the breathing cycle. Analgesic drugs (pain relievers) and local or regional anaesthetic blocks are often given to supplement general anaesthesia.
Volatile anaesthetics are either halogenated hydrocarbons (see HALOTHANE) or halogenated ethers (iso?urane, en?urane, des?urane and sevo?urane). The latter two are the most recently introduced agents, and produce the most rapid induction and recovery – though on a worldwide basis halothane, ether and chloroform are still widely used.
Despite several theories, the mode of action of these agents is not fully understood. Their e?cacy is related to how well they dissolve into the LIPID substances in nerve cells, and it is thought that they act at more than one site within brain cells – probably at the cell membrane. By whatever method, they reversibly depress the conduction of impulses within the CENTRAL NERVOUS SYSTEM and thereby produce unconsciousness.
At the end of surgery any muscle relaxant still in the patient’s body is reversed, the volatile agent is turned o? and the patient breathes oxygen or oxygen-enriched air. This is the reversal or recovery phase of anaesthesia. Once the anaesthetist is satis?ed with the degree of recovery, patients are transferred to a recovery area within the operating-theatre complex where they are cared for by specialist sta?, under the supervision of an anaesthetist, until they are ready to return to the ward. (See also ARTIFICIAL VENTILATION OF THE LUNGS.) Local anaesthetics are drugs which reversibly block the conduction of impulses in nerves. They therefore produce anaesthesia (and muscle relaxation) only in those areas of the body served by the nerve(s) affected by these drugs. Many drugs have some local anaesthetic action but the drugs used speci?cally for this purpose are all amide or ester derivatives of aromatic acids. Variations in the basic structure produce drugs with di?erent speeds of onset, duration of action and preferential SENSORY rather than MOTOR blockade (stopping the activity in the sensory or motor nerves respectively).
The use of local rather than general anaesthesia will depend on the type of surgery and in some cases the unsuitability of the patient for general anaesthesia. It is also used to supplement general anaesthesia, relieve pain in labour (see under PREGNANCY AND LABOUR) and in the treatment of pain in persons not undergoing surgery. Several commonly used techniques are listed below:
LOCAL INFILTRATION An area of anaesthetised skin or tissue is produced by injecting local anaesthetic around it. This technique is used for removing small super?cial lesions or anaesthetising surgical incisions.
NERVE BLOCKS Local anaesthetic is injected close to a nerve or nerve plexus, often using a peripheral nerve stimulator to identify the correct point. The anaesthetic di?uses into the nerve, blocking it and producing anaesthesia in the area supplied by it.
SPINAL ANAESTHESIA Small volumes of local anaesthetic are injected into the cerebrospinal ?uid through a small-bore needle which has been inserted through the tissues of the back and the dura mater (the outer membrane surrounding the spinal cord). A dense motor and sensory blockade is produced in the lower half of the body. How high up in the body it reaches is dependent on the volume and dose of anaesthetic, the patient’s position and individual variation. If the block is too high, then respiratory-muscle paralysis and therefore respiratory arrest may occur. HYPOTENSION (low blood pressure) may occur because of peripheral vasodilation caused by sympathetic-nerve blockade. Occasionally spinal anaesthesia is complicated by a headache, perhaps caused by continuing leakage of cerebrospinal ?uid from the dural puncture point.
EPIDURAL ANAESTHESIA Spinal nerves are blocked in the epidural space with local anaesthetic injected through a ?ne plastic tube (catheter) which is introduced into the space using a special needle (Tuohy needle). It can be used as a continuous technique either by intermittent injections, an infusion or by patient-controlled pump. This makes it ideal for surgery in the lower part of the body, the relief of pain in labour and for post-operative analgesia. Complications include hypotension, spinal headache (less than 1:100), poor e?cacy, nerve damage (1:12,000) and spinal-cord compression from CLOT or ABSCESS (extremely rare).... anaesthesia
Habitat: Kashmir and Himachal Pradesh up to 2,500 m.
English: Indian Belladonna, Indian Atropa.Ayurvedic: Suuchi.Unani: Luffaah, Luffaah-Barri, Yabaruj, Shaabiraj.Action: Highly poisonous; sedative, narcotic, anodyne, nervine, antispasmodic (used in paralysis); parkinsonism; encephalitis; carcinoma; spastic dysmenorrhoea; whooping cough, spasmodic asthma; colic of intestines, gall bladder or kidney, spasm of bladder and ureters; contraindicated in enlarged prostate.
Key application: In spasm and colic-like pain in the areas of the gastrointestinal tract and bile ducts. (German Commission E, The British Herbal Pharmacopoeia.) It is contraindicated in tachycardiac arrhythmias, prostate adenoma, glaucoma, acute oedema of lungs.A. belladonna L. (European sp. Belladonna, Deadly Nightshade) is cultivated in Kashmir and Himachal Pradesh.The herb contains tropane (tropine) or solanaceous alkaloids (up to 0.6%), including hyoscamine and atropine; flavonoids; coumarins; volatile bases (nicotine).Tropane alkaloids inhibit the para- sympathetic nervous system, which controls involuntary bodily activities; reduces saliva, gastric, intestinal and bronchial secretions, and also the activity of urinary tubules. Tropane alkaloids also increase the heart rate and dilate the pupils. These alkaloids are used as an additive to compound formulations for bronchitis, asthma, whooping cough, gastrointestinal hy- permotility, dysmenorrhoea, nocturnal enuresis and fatigue syndrome.Atropine provides relief in parkin- sonism and neurovegetative dystonia.The root is the most poisonous, the leaves and flowers less, and the berries the least. (Francis Brinker.)Dosage: Leaf, root—30-60 mg powder. (CCRAS.)... atropa acuminata royle exNutritional Profile Energy value (calories per serving): Moderate Protein: Low (cocoa powder) High (chocolate) Fat: Moderate Saturated fat: High Cholesterol: None Carbohydrates: Low (chocolate) High (cocoa powder) Fiber: Moderate (chocolate) High (cocoa powder) Sodium: Moderate Major vitamin contribution: B vitamins Major mineral contribution: Calcium, iron, copper
About the Nutrients in This Food Cocoa beans are high-carbohydrate, high-protein food, with less dietary fiber and more fat than all other beans, excepting soy beans. The cocoa bean’s dietary fiber includes pectins and gums. Its proteins are limited in the essential amino acids lysine and isoleucine. Cocoa butter, the fat in cocoa beans, is the second most highly saturated vegetable fat (coconut oil is number one), but it has two redeeming nutritional qualities. First, it rarely turns rancid. Second, it melts at 95°F, the temperature of the human tongue. Cocoa butter has no cholesterol; neither does plain cocoa powder or plain dark chocolate. Cocoa beans have B vitamins (thiamine, riboflavin, niacin) plus min- erals (iron, magnesium, potassium, phosphorus, and copper). All chocolate candy is made from chocolate liquor, a thick paste pro- duce by roasting and grinding cocoa beans. Dark (sweet) chocolate is made of chocolate liquor, cocoa butter, and sugar. Milk chocolate is made of choc- olate liquor, cocoa butter, sugar, milk or milk powder, and vanilla. White * These values apply to plain cocoa powder and plain unsweetened chocolate. Add- ing other foods, such as milk or sugar, changes these values. For example, there is no cholesterol in plain bitter chocolate, but there is cholesterol in milk chocolate. chocolate is made of cocoa butter, sugar, and milk powder. Baking chocolate is unsweetened dark chocolate. The most prominent nutrient in chocolate is its fat. Fat Content in One Ounce of Chocolate
| Saturated fat (g) | Monounsaturated fat (g) | Polyunsaturated fat (g) | Cholesterol (mg) | |
| Dark (sweet) | ||||
| chocolate | 5.6 | 3.2 | 0.3 | 0 |
| Milk chocolate | 5.9 | 4.5 | 0.4 | 6.6 |
| Baking chocolate | 9 | 5.6 | 0.3 | 0 |
| White chocolate | 5.5 | 2.6 | 0.3 | 0 |
The Most Nutritious Way to Serve This Food With low-fat milk to complete the proteins without adding saturated fat and cholesterol. NOTE : Both cocoa and chocolate contain oxalic acid, which binds with calcium to form cal- cium oxalate, an insoluble compound, but milk has so much calcium that the small amount bound to cocoa and chocolate hardly matters. Chocolate skim milk is a source of calcium.
Diets That May Restrict or Exclude This Food Antiflatulence diet Low-calcium and low-oxalate diet (to prevent the formation of calcium oxalate kidney stones) Low-calorie diet Low-carbohydrate diet Low-fat diet Low-fat, controlled-cholesterol diet (milk chocolates) Low-fiber diet Potassium-regulated (low-potassium) diet
Buying This Food Look for: Tightly sealed boxes or bars. When you open a box of chocolates or unwrap a candy bar, the chocolate should be glossy and shiny. Chocolate that looks dull may be stale, or it may be inexpensively made candy without enough cocoa butter to make it gleam and give it the rich creamy mouthfeel we associate with the best chocolate. (Fine chocolate melts evenly on the tongue.) Chocolate should also smell fresh, not dry and powdery, and when you break a bar or piece of chocolate it should break cleanly, not crumble. One exception: If you have stored a bar of chocolate in the refrigerator, it may splinter if you break it without bringing it to room temperature first.
Storing This Food Store chocolate at a constant temperature, preferably below 78°F. At higher temperatures, the fat in the chocolate will rise to the surface and, when the chocolate is cooled, the fat will solidif y into a whitish powdery bloom. Bloom is unsightly but doesn’t change the chocolate’s taste or nutritional value. To get rid of bloom, melt the chocolate. The chocolate will turn dark, rich brown again when its fat recombines with the other ingredients. Chocolate with bloom makes a perfectly satisfactory chocolate sauce. Dark chocolate (bitter chocolate, semisweet chocolate) ages for at least six months after it is made, as its flavor becomes deeper and more intense. Wrapped tightly and stored in a cool, dry cabinet, it can stay fresh for a year or more. Milk chocolate ages only for about a month after it is made and holds its peak flavor for about three to six months, depending on how carefully it is stored. Plain cocoa, with no added milk powder or sugar, will stay fresh for up to a year if you keep it tightly sealed and cool.
What Happens When You Cook This Food Chocolate burns easily. To melt it without mishap, stir the chocolate in a bowl over a pot of hot water or in the top of a double boiler or put the chocolate in a covered dish and melt it in the microwave (which does not get as hot as a pot on the store). Simple chemistry dictates that chocolate cakes be leavened with baking soda rather than baking powder. Chocolate is so acidic that it will upset the delicate balance of acid (cream of tartar) and base (alkali = sodium bicarbonate = baking soda) in baking powder. But it is not acidic enough to balance plain sodium bicarbonate. That’s why we add an acidic sour-milk product such as buttermilk or sour cream or yogurt to a chocolate cake. Without the sour milk, the batter would be so basic that the chocolate would look red, not brown, and taste very bitter.
How Other Kinds of Processing Affect This Food Freezing. Chocolate freezes and thaws well. Pack it in a moistureproof container and defrost it in the same package to let it reabsorb moisture it gave off while frozen.
Medical Uses and/or Benefits Mood elevator. Chocolate’s reputation for making people feel good is based not only on its caffeine content—19 mg caffeine per ounce of dark (sweet) chocolate, which is one-third the amount of caffeine in a five-ounce cup of brewed coffee—but also on its naturally occurring mood altering chemicals phenylethylalanine and anandamide. Phenylethylalanine is found in the blood of people in love. Anandamide stimulates areas of your brain also affected by the active ingredients in marijuana. (NOTE : As noted by the researchers at the Neurosci- ences Institute in San Diego who identified anandamide in chocolate in 1996, to get even the faintest hint of marijuana-like effects from chocolate you would have to eat more than 25 pounds of the candy all at once.) Possible heart health benefits. Chocolate is rich in catechins, the antioxidant chemicals that give tea its reputation as a heart-protective anticancer beverage (see tea). In addition, a series of studies beginning with those at the USDA Agricultural Research Center in Peoria, Illinois, suggest that consuming foods rich in stearic acid like chocolate may reduce rather than raise the risk of a blood clot leading to a heart attack. Possible slowing of the aging process. Chocolate is a relatively good source of copper, a mineral that may play a role in slowing the aging process by decreasing the incidence of “protein glycation,” a reaction in which sugar molecules ( gly = sugar) hook up with protein molecules in the bloodstream, twisting the protein molecules out of shape and rendering them unusable. This can lead to bone loss, rising cholesterol, cardiac abnormalities, and a slew of other unpleasantries. In people with diabetes, excess protein glycation may be one factor involved in complications such as loss of vision. Ordinarily, increased protein glyca- tion is age-related. But at the USDA Grand Forks Human Nutrition Research Center in North Dakota, agricultural research scientist Jack T. Saari has found that rats on copper-deficient diets experience more protein glycation at any age than other rats. A recent USDA survey of American eating patterns says that most of us get about 1.2 mg copper a day, considerably less than the Estimated Safe and Adequate Daily Dietary Intake (ESADDI) or 1.5 mg to 3 mg a day. Vegetarians are less likely to be copper deficient because, as Saari notes, the foods highest in copper are whole grains, nuts, seeds, and beans, including the cocoa bean. One ounce of dark chocolate has .25 mg copper (8 –17 percent of the ESADDI).
Adverse Effects Associated with This Food Possible loss of bone density. In 2008, a team of Australian researchers at Royal Perth Hos- pital, and Sir Charles Gairdner Hospital published a report in the American Journal of Clinical Nutrition suggesting that women who consume chocolate daily had 3.1 percent lower bone density than women who consume chocolate no more than once a week. No explanation for the reaction was proposed; the finding remains to be confirmed. Possible increase in the risk of heart disease. Cocoa beans, cocoa powder, and plain dark chocolate are high in saturated fats. Milk chocolate is high in saturated fats and cholesterol. Eating foods high in saturated fats and cholesterol increases the amount of cholesterol in your blood and raises your risk of heart disease. NOTE : Plain cocoa powder and plain dark chocolate may be exceptions to this rule. In studies at the USDA Agricultural Research Center in Peoria, Illinois, volunteers who consumed foods high in stearic acid, the saturated fat in cocoa beans, cocoa powder, and chocolate, had a lower risk of blood clots. In addition, chocolate is high in flavonoids, the antioxidant chemicals that give red wine its heart-healthy reputation. Mild jitters. There is less caffeine in chocolate than in an equal size serving of coffee: A five- ounce cup of drip-brewed coffee has 110 to 150 mg caffeine; a five-ounce cup of cocoa made with a tablespoon of plain cocoa powder ( 1/3 oz.) has about 18 mg caffeine. Nonetheless, people who are very sensitive to caffeine may find even these small amounts problematic. Allergic reaction. According to the Merck Manual, chocolate is one of the 12 foods most likely to trigger the classic food allergy symptoms: hives, swelling of the lips and eyes, and upset stomach.* The others are berries (blackberries, blueberries, raspberries, strawberries), corn, eggs, fish, legumes (green peas, lima beans, peanuts, soybeans), milk, nuts, peaches, pork, shellfish, and wheat (see wheat cer ea ls).
Food/Drug Interactions Monoamine oxidase (MAO) inhibitors. Monoamine oxidase inhibitors are drugs used to treat depression. They inactivate naturally occurring enzymes in your body that metabolize tyra- mine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. Caffeine is a substance similar to tyramine. If you consume excessive amounts of a caffeinated food, such as cocoa or chocolate, while you are taking an M AO inhibitor, the result may be a hypertensive crisis. False-positive test for pheochromocytoma. Pheochromocytoma, a tumor of the adrenal gland, secretes adrenalin, which the body converts to VM A (vanillylmandelic acid). VM A is excreted in urine, and, until recently, the test for this tumor measured the level of VM A in the urine. In the past, chocolate and cocoa, both of which contain VM A, were eliminated from the patient’s diet prior to the test lest they elevate the level of VM A in the urine and produce a false-positive result. Today, more finely drawn tests usually make this unnecessary. * The evidence link ing chocolate to allergic or migraine headaches is inconsistent. In some people, phenylet hylamine (PEA) seems to cause headaches similar to t hose induced by t yramine, anot her pressor amine. The PEA-induced headache is unusual in t hat it is a delayed react ion t hat usually occurs 12 or more hours after t he chocolate is eaten.... chocolate
Habitat: Throughout the plains of India in damp marshy areas.
English: Thyme-leaved Gratiola.Ayurvedic: Braahmi, Aindri, Nir- braahmi, Kapotavankaa, Bhaarati, Darduradalaa, Matsyaakshaka, Shaaluraparni, Mandukaparni (also equated with Centella asiatica Linn., synonym Hydrocotyle asiatica Linn. Umbelliferae, Apiaceae).Unani: Brahmi.Siddha/Tamil: Piramivazhukkai, Neerbrami.Folk: Jalaneem, Safed-Chammi.Action: Adaptogenic, astringent, diuretic, sedative, potent nervine tonic, anti-anxiety agent (improves mental functions, used in insanity, epilepsy), antispasmodic (used in bronchitis, asthma and diarrhoea).
Key application: In psychic disorders and as a brain tonic. (The Ayurvedic Pharmacopoeia of India; Indian Herbal Pharmacopoeia.)B. monnieri has been shown to cause prolonged elevated level of cerebral glutamic acid and a transient increase in GABA level. It is assumed that endogenous increase in brain glutamine maybe helpful in the process oflearn- ing.The herb contains the alkaloids brahmine, herpestine, and a mixture of three bases. Brahmine is highly toxic; in therapeutic doses it resembles strychnine. The herb also contains the saponins, monnierin, hersaponin, bacosides A and B. Bacosides A and B possess haemolytic activity. Her- saponin is reported to possess car- diotonic and sedative properties. It was found, as in case of reserpene, to deplete nor-adrenaline and 5-HT content of the rat brain.An alcoholic extract of the plant in a dose of 50 mg/kg produced tranquil- izing effect on albino rats and dogs, but the action was weaker than that produced by chlorpromazine.Dosage: Whole plant—1-3 g powder. (API Vol. II.)... bacopa monnieriHin: Akasgaddah;
Mal: Kadamba, KollankovaTam: Akashagarudan, Gollankovai;Tel: Murudonda, NagadondaCorallocarpus is a prostrate or climbing herb distributed in Punjab, Sind, Gujarat, Deccan, Karnataka and Sri Lanka. It is monoecious with large root which is turnip-shaped and slender stem which is grooved, zigzag and glabrous. Tendrils are simple, slender and glabrous. Leaves are sub-orbicular in outline, light green above and pale beneath, deeply cordate at the base, angled or more or less deeply 3-5 lobed. Petiole is long and glabrous. Male flowers are small and arranged at the tip of a straight stiff glabrous peduncle. Calyx is slightly hairy, long and rounded at the base. Corolla is long and greenish yellow. Female flowers are usually solitary with short, stout and glabrous peduncles. Fruit is stalked, long, ellipsoid or ovoid. Seeds are pyriform, turgid, brown and with a whitish corded margin. It is prescribed in later stages of dysentery and old veneral complaints. For external use in chronic rheumatism, it is made into a liniment with cumin seed, onion and castor oil. It is used in case of snakebite where it is administered internally and applied to the bitten part. The root is given in syphilitic rheumatism and later stages of dysentery. The plant is bitter, sweet, alexipharmic and emetic. The root is said to possess alterative and laxative properties (Kirtikar and Basu, 1988). Root contains a bitter principle like Breyonin (Chopra et al, 1980).Agrotechnology: Cucurbits can be successfully grown during January-March and September- December. For the rainfed crop, sowing can also be started after the receipt of the first few showers.Pits of 60cm diameter and 30-45cm depth are to be taken at the desired spacing. Well rotten FYM or vegetable mixture is to be mixed with topsoil in the pit and seeds are to be sown at 4-5/pit. Unhealthy plants are to be removed after 2 weeks and retained 2-3 plants/pit. FYM is to be applied at 20-25t/ha as basal dose along with half dose of N (35kg/ha) and full dose of P (25kg) and K (25kg). The remaining dose of N (35kg) can be applied in 2 equal split doses at fortnightly intervals. During the initial stages of growth, irrigation is to be given at an interval of 3-4 days and at alternate days during flowering and fruiting periods. For trailing cucumber, pumpkin and melon, dried twigs are to be spread on the ground. Bitter gourd, bottle gourd, snake gourd and ash gourd are to be trailed on Pandals. Weeding and raking of the soil are to be conducted at the time of fertilizer application. Earthing up may be done during rainy season. The most dreaded pest of cucurbits is fruit flies which can be controlled by using fruit traps, covering the fruits with polythene, cloth or paper bags, removal and destruction of affected fruits and lastly spraying with Carbaryl or Malathion 0. 2% suspension containing sugar or jaggery at 10g/l at fortnightly intervals after fruit set initiation. During rainy season, downy mildew and mosaic diseases are severe in cucurbits. The former can be checked by spraying Mancozeb 0.2%. The spread of mosaic can be checked by controlling the vectors using Dimethoate or Phosphamidon 0.05% and destruction of affected plants and collateral hosts. Harvesting to be done at least 10 days after insecticide or fungicide application (KAU,1996).... cucurbitsExamination of the ear includes inspection of the external ear. An auriscope is used to examine the external ear canal and the ear drum. If a more detailed inspection is required, a microscope may be used to improve illumination and magni?cation.
Tuning-fork or Rinne tests are performed to identify the presence of DEAFNESS. The examiner tests whether the vibrating fork is audible at the meatus, and then the foot of the fork is placed on the mastoid bone of the ear to discover at which of the two sites the patient can hear the vibrations for the longest time. This can help to di?erentiate between conductive and nerve deafness.
Hearing tests are carried out to determine the level of hearing. An audiometer is used to deliver a series of short tones of varying frequency to the ear, either through a pair of headphones or via a sound transducer applied directly to the skull. The intensity of the sound is gradually reduced until it is no longer heard and this represents the threshold of hearing, at that frequency, through air and bone respectively. It may be necessary to play a masking noise into the opposite ear to prevent that ear from hearing the tones, enabling each ear to be tested independently.
General symptoms The following are some of the chief symptoms of ear disease: DEAFNESS (see DEAFNESS). EARACHE is most commonly due to acute in?ammation of the middle ear. Perceived pain in this region may be referred from other areas, such as the earache commonly experienced after tonsillectomy (removal of the TONSILS) or that caused by carious teeth (see TEETH, DISORDERS OF). The treatment will depend on the underlying cause. TINNITUS or ringing in the ear often accompanies deafness, but is sometimes the only symptom of ear disease. Even normal people sometimes experience tinnitus, particularly if put in soundproofed surroundings. It may be described as hissing, buzzing, the sound of the sea, or of bells. The intensity of the tinnitis usually ?uctuates, sometimes disappearing altogether. It may occur in almost any form of ear disease, but is particularly troublesome in nerve deafness due to ageing and in noise-induced deafness. The symptom seems to originate in the brain’s subcortical regions, high in the central nervous system. It may be a symptom of general diseases such as ANAEMIA, high blood pressure and arterial disease, in which cases it is often synchronous with the pulse, and may also be caused by drugs such as QUININE, salicylates (SALICYLIC ACID and its salts, for example, ASPIRIN) and certain ANTIBIOTICS. Treatment of any underlying ear disorder or systemic disease, including DEPRESSION, may reduce or even cure the tinnitis, but unfortunately in many cases the noises persist. Management involves psychological techniques and initially an explanation of the mechanism and reassurance that tinnitus does not signify brain disease, or an impending STROKE, may help the person. Tinnitus maskers – which look like hearing aids – have long been used with a suitably pitched sound helping to ‘mask’ the condition.
Diseases of the external ear
WAX (cerumen) is produced by specialised glands in the outer part of the ear canal only. Impacted wax within the ear canal can cause deafness, tinnitis and sometimes disturbance of balance. Wax can sometimes be softened with olive oil, 5-per-cent bicarbonate of soda or commercially prepared drops, and it will gradually liquefy and ‘remove itself’. If this is ineffective, syringing by a doctor or nurse will usually remove the wax but sometimes it is necessary for a specialist (otologist) to remove it manually with instruments. Syringing should not be done if perforation of the tympanic membrane (eardrum) is suspected. FOREIGN BODIES such as peas, beads or buttons may be found in the external ear canal, especially in children who have usually introduced them themselves. Live insects may also be trapped in the external canal causing intense irritation and noise, and in such cases spirit drops are ?rst instilled into the ear to kill the insect. Except in foreign bodies of vegetable origin, where swelling and pain may occur, syringing may be used to remove some foreign bodies, but often removal by a specialist using suitable instrumentation and an operating microscope is required. In children, a general anaesthetic may be needed. ACUTE OTITIS EXTERNA may be a di?use in?ammation or a boil (furuncle) occurring in the outer ear canal. The pinna is usually tender on movement (unlike acute otitis media – see below) and a discharge may be present. Initially treatment should be local, using magnesium sulphate paste or glycerine and 10-per-cent ichthaminol. Topical antibiotic drops can be used and sometimes antibiotics by mouth are necessary, especially if infection is acute. Clotrimazole drops are a useful antifungal treatment. Analgesics and locally applied warmth should relieve the pain.
CHRONIC OTITIS EXTERNA producing pain and discharge, can be caused by eczema, seborrhoeic DERMATITIS or PSORIASIS. Hair lotions and cosmetic preparations may trigger local allergic reactions in the external ear, and the chronic disorder may be the result of swimming or use of dirty towels. Careful cleaning of the ear by an ENT (Ear, Nose & Throat) surgeon and topical antibiotic or antifungal agents – along with removal of any precipitating cause – are the usual treatments. TUMOURS of the ear can arise in the skin of the auricle, often as a result of exposure to sunlight, and can be benign or malignant. Within the ear canal itself, the commonest tumours are benign outgrowths from the surrounding bone, said to occur in swimmers as a result of repeated exposure to cold water. Polyps may result from chronic infection of the ear canal and drum, particularly in the presence of a perforation. These polyps are soft and may be large enough to ?ll the ear canal, but may shrink considerably after treatment of the associated infection.
Diseases of the middle ear
OTITIS MEDIA or infection of the middle ear, usually occurs as a result of infection spreading up the Eustachian tubes from the nose, throat or sinuses. It may follow a cold, tonsillitis or sinusitis, and may also be caused by swimming and diving where water and infected secretions are forced up the Eustachian tube into the middle ear. Primarily it is a disease of children, with as many as 1.5 million cases occurring in Britain every year. Pain may be intense and throbbing or sharp in character. The condition is accompanied by deafness, fever and often TINNITUS.
In infants, crying may be the only sign that something is wrong – though this is usually accompanied by some localising manifestation such as rubbing or pulling at the ear. Examination of the ear usually reveals redness, and sometimes bulging, of the ear drum. In the early stages there is no discharge, but in the later stages there may be a discharge from perforation of the ear drum as a result of the pressure created in the middle ear by the accumulated pus. This is usually accompanied by an immediate reduction in pain.
Treatment consists of the immediate administration of an antibiotic, usually one of the penicillins (e.g. amoxicillin). In the majority of cases no further treatment is required, but if this does not quickly bring relief then it may be necessary to perform a myringotomy, or incision of the ear drum, to drain pus from the middle ear. When otitis media is treated immediately with su?cient dosage of the appropriate antibiotic, the chances of any permanent damage to the ear or to hearing are reduced to a negligible degree, as is the risk of any complications such as mastoiditis (discussed later in this section). CHRONIC OTITIS MEDIA WITH EFFUSION or glue ear, is the most common in?ammatory condition of the middle ear in children, to the extent that one in four children in the UK entering school has had an episode of ‘glue ear’. It is characterised by a persistent sticky ?uid in the middle ear (hence the name); this causes a conductive-type deafness. It may be associated with enlarged adenoids (see NOSE, DISORDERS OF) which impair the function of the Eustachian tube. If the hearing impairment is persistent and causes problems, drainage of the ?uid, along with antibiotic treatment, may be needed – possibly in conjunction with removal of the adenoids. The insertion of grommets (ventilation tubes) was for a time standard treatment, but while hearing is often restored, there may be no long-term gain and even a risk of damage to the tympanic membrane, so the operation is less popular than it was a decade or so ago. MASTOIDITIS is a serious complication of in?ammation of the middle ear, the incidence of which has been dramatically reduced by the introduction of antibiotics. In?ammation in this cavity usually arises by direct spread of acute or chronic in?ammation from the middle ear. The signs of this condition include swelling and tenderness of the skin behind the ear, redness and swelling inside the ear, pain in the side of the head, high fever, and a discharge from the ear. The management of this condition in the ?rst instance is with antibiotics, usually given intravenously; however, if the condition fails to improve, surgical treatment is necessary. This involves draining any pus from the middle ear and mastoid, and removing diseased lining and bone from the mastoid.
Diseases of the inner ear
MENIÈRE’S DISEASE is a common idiopathic disorder of ENDOLYMPH control in the semicircular canals (see EAR), characterised by the triad of episodic VERTIGO with deafness and tinnitus. The cause is unknown and usually one ear only is affected at ?rst, but eventually the opposite ear is affected in approximately 50 per cent of cases. The onset of dizziness is often sudden and lasts for up to 24 hours. The hearing loss is temporary in the early stages, but with each attack there may be a progressive nerve deafness. Nausea and vomiting often occur. Treatment during the attacks includes rest and drugs to control sickness. Vasodilator drugs such as betahistine hydrochloride may be helpful. Surgical treatment is sometimes required if crippling attacks of dizziness persist despite these measures. OTOSCLEROSIS A disorder of the middle ear that results in progressive deafness. Often running in families, otosclerosis affects about one person in 200; it customarily occurs early in adult life. An overgrowth of bone ?xes the stapes (the innermost bone of the middle ear) and stops sound vibrations from being transmitted to the inner ear. The result is conductive deafness. The disorder usually affects both ears. Those affected tend to talk quietly and deafness increases over a 10–15 year period. Tinnitus often occurs, and occasionally vertigo.
Abnormal hearing tests point to the diagnosis; the deafness may be partially overcome with a hearing aid but surgery is eventually needed. This involves replacing the stapes bone with a synthetic substitute (stapedectomy). (See also OTIC BAROTRAUMA.)... ear, diseases of
The outer coat consists of the sclera and the cornea; their junction is called the limbus. SCLERA This is white, opaque, and constitutes the posterior ?ve-sixths of the outer coat. It is made of dense ?brous tissue. The sclera is visible anteriorly, between the eyelids, as the ‘white of the eye’. Posteriorly and anteriorly it is covered by Tenons capsule, which in turn is covered by transparent conjunctiva. There is a hole in the sclera through which nerve ?bres from the retina leave the eye in the optic nerve. Other smaller nerve ?bres and blood vessels also pass through the sclera at di?erent points. CORNEA This constitutes the transparent, colourless anterior one-sixth of the eye. It is transparent in order to allow light into the eye and is more steeply curved than the sclera. Viewed from in front, the cornea is roughly circular. Most of the focusing power of the eye is provided by the cornea (the lens acts as the ‘?ne adjustment’). It has an outer epithelium, a central stroma and an inner endothelium. The cornea is supplied with very ?ne nerve ?bres which make it exquisitely sensitive to pain. The central cornea has no blood supply – it relies mainly on aqueous humour for nutrition. Blood vessels and large nerve ?bres in the cornea would prevent light from entering the eye. LIMBUS is the junction between cornea and sclera. It contains the trabecular meshwork, a sieve-like structure through which aqueous humour leaves the eye.
The middle coat (uveal tract) consists of the choroid, ciliary body and iris. CHOROID A highly vascular sheet of tissue lining the posterior two-thirds of the sclera. The network of vessels provides the blood supply for the outer half of the retina. The blood supply of the choroid is derived from numerous ciliary vessels which pierce the sclera in front and behind. CILIARY BODY A ring of tissue extending 6 mm back from the anterior limitation of the sclera. The various muscles of the ciliary body by their contractions and relaxations are responsible for changing the shape of the lens during ACCOMMODATION. The ciliary body is lined by cells that secrete aqueous humour. Posteriorly, the ciliary body is continuous with the choroid; anteriorly it is continuous with the iris. IRIS A ?attened muscular diaphragm that is attached at its periphery to the ciliary body, and has a round central opening – the pupil. By contraction and relaxation of the muscles of the iris, the pupil can be dilated or constricted (dilated in the dark or when aroused; constricted in bright light and for close work). The iris forms a partial division between the anterior chamber and the posterior chamber of the eye. It lies in front of the lens and forms the back wall of the anterior chamber. The iris is visible from in front, through the transparent cornea, as the ‘coloured part of the eye’. The amount and distribution of iris pigment determine the colour of the iris. The pupil is merely a hole in the centre of the iris and appears black.
The inner layer The retina is a multilayered tissue (ten layers in all) which extends from the edges of the optic nerve to line the inner surface of the choroid up to the junction of ciliary body and choroid. Here the true retina ends at the ora serrata. The retina contains light-sensitive cells of two types: (i) cones – cells that operate at high and medium levels of illumination; they subserve ?ne discrimination of vision and colour vision; (ii) rods – cells that function best at low light intensity and subserve black-and-white vision.
The retina contains about 6 million cones and about 100 million rods. Information from them is conveyed by the nerve ?bres which are in the inner part of the retina, and leave the eye in the optic nerve. There are no photoreceptors at the optic disc (the point where the optic nerve leaves the eye) and therefore there is no light perception from this small area. The optic disc thus produces a physiological blind spot in the visual ?eld.
The retina can be subdivided into several areas: PERIPHERAL RETINA contains mainly rods and a few scattered cones. Visual acuity from this area is fairly coarse. MACULA LUTEA So-called because histologically it looks like a yellow spot. It occupies an area 4·5 mm in diameter lateral to the optic disc. This area of specialised retina can produce a high level of visual acuity. Cones are abundant here but there are few rods. FOVEA CENTRALIS A small central depression at the centre of the macula. Here the cones are tightly packed; rods are absent. It is responsible for the highest levels of visual acuity.
The chambers of the eye There are three: the anterior and posterior chambers, and the vitreous cavity. ANTERIOR CHAMBER Limited in front by the inner surface of the cornea, behind by the iris and pupil. It contains a transparent clear watery ?uid, the aqueous humour. This is constantly being produced by cells of the ciliary body and constantly drained away through the trabecular meshwork. The trabecular meshwork lies in the angle between the iris and inner surface of the cornea. POSTERIOR CHAMBER A narrow space between the iris and pupil in front and the lens behind. It too contains aqueous humour in transit from the ciliary epithelium to the anterior chamber, via the pupil. VITREOUS CAVITY The largest cavity of the eye. In front it is bounded by the lens and behind by the retina. It contains vitreous humour.
Lens Transparent, elastic and biconvex in cross-section, it lies behind the iris and in front of the vitreous cavity. Viewed from the front it is roughly circular and about 10 mm in diameter. The diameter and thickness of the lens vary with its accommodative state. The lens consists of: CAPSULE A thin transparent membrane surrounding the cortex and nucleus. CORTEX This comprises newly made lens ?bres that are relatively soft. It separates the capsule on the outside from the nucleus at the centre of the lens. NUCLEUS The dense central area of old lens ?bres that have become compacted by new lens ?bres laid down over them. ZONULE Numerous radially arranged ?bres attached between the ciliary body and the lens around its circumference. Tension in these zonular ?bres can be adjusted by the muscles of the ciliary body, thus changing the shape of the lens and altering its power of accommodation. VITREOUS HUMOUR A transparent jelly-like structure made up of a network of collagen ?bres suspended in a viscid ?uid. Its shape conforms to that of the vitreous cavity within which it is contained: that is, it is spherical except for a shallow concave depression on its anterior surface. The lens lies in this depression.
Eyelids These are multilayered curtains of tissue whose functions include spreading of the tear ?lm over the front of the eye to prevent desiccation; protection from injury or external irritation; and to some extent the control of light entering the eye. Each eye has an upper and lower lid which form an elliptical opening (the palpebral ?ssure) when the eyes are open. The lids meet at the medial canthus and lateral canthus respectively. The inner medial canthus is ?xed; the lateral canthus more mobile. An epicanthus is a fold of skin which covers the medial canthus in oriental races.
Each lid consists of several layers. From front to back they are: very thin skin; a sheet of muscle (orbicularis oculi, whose ?bres are concentric around the palpebral ?ssure and which produce closure of the eyelids); the orbital septum (modi?ed near the lid margin to form the tarsal plates); and ?nally, lining the back surface of the lid, the conjunctiva (known here as tarsal conjunctiva). At the free margin of each lid are the eyelashes, the openings of tear glands which lie within the lid, and the lacrimal punctum. Toward the medial edge of each lid is an elevation known as the papilla: the lacrimal punctum opens into this papilla. The punctum forms the open end of the cannaliculus, part of the tear-drainage mechanism.
Orbit The bony cavity within which the eye is held. The orbits lie one on either side of the nose, on the front of the skull. They a?ord considerable protection for the eye. Each is roughly pyramidal in shape, with the apex pointing backwards and the base forming the open anterior part of the orbit. The bone of the anterior orbital margin is thickened to protect the eye from injury. There are various openings into the posterior part of the orbit – namely the optic canal, which allows the optic nerve to leave the orbit en route for the brain, and the superior orbital and inferior orbital ?ssures, which allow passage of nerves and blood vessels to and from the orbit. The most important structures holding the eye within the orbit are the extra-ocular muscles, a suspensory ligament of connective tissue that forms a hammock on which the eye rests and which is slung between the medial and lateral walls of the orbit. Finally, the orbital septum, a sheet of connective tissue extending from the anterior margin of the orbit into the lids, helps keep the eye in place. A pad of fat ?lls in the orbit behind the eye and acts as a cushion for the eye.
Conjunctiva A transparent mucous membrane that extends from the limbus over the anterior sclera or ‘white of the eye’. This is the bulbar conjunctiva. The conjunctiva does not cover the cornea. Conjunctiva passes from the eye on to the inner surface of the eyelid at the fornices and is continuous with the tarsal conjunctiva. The semilunar fold is the vertical crescent of conjunctiva at the medial aspect of the palpebral ?ssure. The caruncle is a piece of modi?ed skin just within the inner canthus.
Eye muscles The extra-ocular muscles. There are six in all, the four rectus muscles (superior, inferior, medial and lateral rectus muscles) and two oblique muscles (superior and inferior oblique muscles). The muscles are attached at various points between the bony orbit and the eyeball. By their combined action they move the eye in horizontal and vertical gaze. They also produce torsional movement of the eye (i.e. clockwise or anticlockwise movements when viewed from the front).
Lacrimal apparatus There are two components: a tear-production system, namely the lacrimal gland and accessory lacrimal glands; and a drainage system.
Tears keep the front of the eye moist; they also contain nutrients and various components to protect the eye from infection. Crying results from excess tear production. The drainage system cannot cope with the excess and therefore tears over?ow on to the face. Newborn babies do not produce tears for the ?rst three months of life. LACRIMAL GLAND Located below a small depression in the bony roof of the orbit. Numerous tear ducts open from it into predominantly the upper lid. Accessory lacrimal glands are found in the conjunctiva and within the eyelids: the former open directly on to the surface of the conjunctiva; the latter on to the eyelid margin. LACRIMAL DRAINAGE SYSTEM This consists of: PUNCTUM An elevated opening toward the medial aspect of each lid. Each punctum opens into a canaliculus. CANALICULUS A ?ne tube-like structure run-ning within the lid, parallel to the lid margin. The canaliculi from upper and lower lid join to form a common canaliculus which opens into the lacrimal sac. LACRIMAL SAC A small sac on the side of the nose which opens into the nasolacrimal duct. During blinking, the sac sucks tears into itself from the canaliculus. Tears then drain by gravity down the nasolacrimal duct. NASOLACRIMAL DUCT A tubular structure which runs down through the wall of the nose and opens into the nasal cavity.
Visual pathway Light stimulates the rods and cones of the retina. Electrochemical messages are then passed to nerve ?bres in the retina and then via the optic nerve to the optic chiasm. Here information from the temporal (outer) half of each retina continues to the same side of the brain. Information from the nasal (inner) half of each retina crosses to the other side within the optic chiasm. The rearranged nerve ?bres then pass through the optic tract to the lateral geniculate body, then the optic radiation to reach the visual cortex in the occipital lobe of the brain.... eye
Astigmatism (See ASTIGMATISM.)
Blepharitis A chronic in?ammation of the lid margins. SEBORRHOEA and staphylococcal infection are likely contributors. The eyes are typically intermittently red, sore and gritty over months or years. Treatment is di?cult and may fail. Measures to reduce debris on the lid margins, intermittent courses of topical antibiotics, steroids or systemic antibiotics may help the sufferer.
Blepharospasm Involuntary closure of the eye. This may accompany irritation but may also occur without an apparent cause. It may be severe enough to interfere with vision. Treatment involves removing the source of irritation, if present. Severe and persistent cases may respond to injection of Botulinum toxin into the orbicularis muscle.
Cataract A term used to describe any opacity in the lens of the eye, from the smallest spot to total opaqueness. The prevalence of cataracts is age-related: 65 per cent of individuals in their sixth decade have some degree of lens opacity, while all those over 80 are affected. Cataracts are the most important cause of blindness worldwide. Symptoms will depend on whether one or both eyes are affected, as well as the position and density of the cataract(s). If only one eye is developing a cataract, it may be some time before the person notices it, though reading may be affected. Some people with cataracts become shortsighted, which in older people may paradoxically ‘improve’ their ability to read. Bright light may worsen vision in those with cataracts.
The extent of visual impairment depends on the nature of the cataracts, and the ?rst symptoms noticed by patients include di?culty in recognising faces and in reading, while problems watching television or driving, especially at night, are pointers to the condition. Cataracts are common but are not the only cause of deteriorating vision. Patients with cataracts should be able to point to the position of a light and their pupillary reactions should be normal. If a bright light is shone on the eye, the lens may appear brown or, in advanced cataracts, white (see diagram).
While increasing age is the commonest cause of cataract in the UK, patients with DIABETES MELLITUS, UVEITIS and a history of injury to the eye can also develop the disorder. Prolonged STEROID treatment can result in cataracts. Children may develop cataracts, and in them the condition is much more serious as vision may be irreversibly impaired because development of the brain’s ability to interpret visual signals is hindered. This may happen even if the cataracts are removed, so early referral for treatment is essential. One of the physical signs which doctors look for when they suspect cataract in adults as well as in children is the ‘red re?ex’. This is observable when an ophthalmoscopic examination of the eye is made (see OPHTHALMOSCOPE). Identi?cation of this red re?ex (a re?ection of light from the red surface of the retina –see EYE) is a key diagnostic sign in children, especially young ones.
There is no e?ective medical treatment for established cataracts. Surgery is necessary and the decision when to operate depends mainly on how the cataract(s) affect(s) the patient’s vision. Nowadays, surgery can be done at any time with limited risk. Most patients with a vision of 6/18 – 6/10 is the minimum standard for driving – or worse in both eyes should
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bene?t from surgery, though elderly people may tolerate visual acuity of 6/18 or worse, so surgery must be tailored to the individual’s needs. Younger people with a cataract will have more demanding visual requirements and so may opt for an ‘earlier’ operation. Most cataract surgery in Britain is now done under local anaesthetic and uses the ‘phaco-emulsi?cation’ method. A small hole is made in the anterior capsule of the lens after which the hard lens nucleus is liqui?ed ultrasonically. A replacement lens is inserted into the empty lens bag (see diagram). Patients usually return to their normal activities within a few days of the operation. A recent development under test in the USA for children requiring cataract operations is an intra-ocular ?exible implant whose magnifying power can be altered as a child develops, thus precluding the need for a series of corrective operations as happens now.
Chalazion A ?rm lump in the eyelid relating to a blocked meibomian gland, felt deep within the lid. Treatment is not always necessary; a proportion spontaneously resolve. There can be associated infection when the lid becomes red and painful requiring antibiotic treatment. If troublesome, the chalazion can be incised under local anaesthetic.
Conjunctivitis In?ammation of the conjunctiva (see EYE) which may affect one or both eyes. Typically the eye is red, itchy, sticky and gritty but is not usually painful. Redness is not always present. Conjunctivitis can occasionally be painful, particularly if there is an associated keratitis (see below) – for example, adenovirus infection, herpetic infection.
The cause can be infective (bacteria, viruses or CHLAMYDIA), chemical (e.g. acids, alkalis) or allergic (e.g. in hay fever). Conjunctivitis may also be caused by contact lenses, and preservatives or even the drugs in eye drops may cause conjunctival in?ammation. Conjunctivitis may addtionally occur in association with other illnesses – for example, upper-respiratory-tract infection, Stevens-Johnson syndrome (see ERYTHEMA – erythema multiforme) or REITER’S SYNDROME. The treatment depends on the cause. In many patients acute conjunctivitis is self-limiting.
Dacryocystitis In?ammation of the lacrimal sac. This may present acutely as a red, painful swelling between the nose and the lower lid. An abscess may form which points through the skin and which may need to be drained by incision. Systemic antibiotics may be necessary. Chronic dacryocystitis may occur with recurrent discharge from the openings of the tear ducts and recurrent swelling of the lacrimal sac. Obstruction of the tear duct is accompanied by watering of the eye. If the symptoms are troublesome, the patient’s tear passageways need to be surgically reconstructed.
Ectropion The lid margin is everted – usually the lower lid. Ectropion is most commonly associated with ageing, when the tissues of the lid become lax. It can also be caused by shortening of the skin of the lids such as happens with scarring or mechanical factors – for example, a tumour pulling the skin of the lower lid downwards. Ectropion tends to cause watering and an unsightly appearance. The treatment is surgical.
Entropion The lid margin is inverted – usually the lower lid. Entropion is most commonly associated with ageing, when the tissues of the lid become lax. It can also be caused by shortening of the inner surfaces of the lids due to scarring – for example, TRACHOMA or chemical burns. The inwardly directed lashes cause irritation and can abrade the cornea. The treatment is surgical.
Episcleritis In?ammation of the EPISCLERA. There is usually no apparent cause. The in?ammation may be di?use or localised and may affect one or both eyes. It sometimes recurs. The affected area is usually red and moderately painful. Episcleritis is generally not thought to be as painful as scleritis and does not lead to the same complications. Treatment is generally directed at improving the patient’s symptoms. The in?ammation may respond to NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) or topical CORTICOSTEROIDS.
Errors of refraction (Ametropia.) These will occur when the focusing power of the lens and cornea does not match the length of the eye, so that rays of light parallel to the visual axis are not focused at the fovea centralis (see EYE). There are three types of refractive error: HYPERMETROPIA or long-sightedness. The refractive power of the eye is too weak, or the eye is too short so that rays of light are brought to a focus at a point behind the retina. Longsighted people can see well in the distance but generally require glasses with convex lenses for reading. Uncorrected long sight can lead to headaches and intermittent blurring of vision following prolonged close work (i.e. eye strain). As a result of ageing, the eye becomes gradually long-sighted, resulting in many people needing reading glasses in later life: this normal process is known as presbyopia. A particular form of long-sightedness occurs after cataract extraction (see above). MYOPIA(Short sight or near sight.) Rays of light are brought to a focus in front of the retina because the refractive power of the eye is too great or the eye is too short. Short-sighted people can see close to but need spectacles with concave lenses in order to see in the distance. ASTIGMATISMThe refractive power of the eye is not the same in each meridian. Some rays of light may be focused in front of the retina while others are focused on or behind the retina. Astigmatism can accompany hypermetropia or myopia. It may be corrected by cylindrical lenses: these consist of a slice from the side of a cylinder (i.e. curved in one meridian and ?at in the meridian at right-angles to it).
Keratitis In?ammation of the cornea in response to a variety of insults – viral, bacterial, chemical, radiation, or mechanical trauma. Keratitis may be super?cial or involve the deeper layers, the latter being generally more serious. The eye is usually red, painful and photophobic. Treatment is directed at the cause.
Nystagmus Involuntary rhythmic oscillation of one or both eyes. There are several causes including nervous disorders, vestibular disorders, eye disorders and certain drugs including alcohol.
Ophthalmia In?ammation of the eye, especially the conjunctiva (see conjunctivitis, above). Ophthalmia neonatorum is a type of conjunctivitis that occurs in newborn babies. They catch the disease when passing through an infected birth canal during their mother’s labour (see PREGNANCY AND LABOUR). CHLAMYDIA and GONORRHOEA are the two most common infections. Treatment is e?ective with antibiotics: untreated, the infection may cause permanent eye damage.
Pinguecula A benign degenerative change in the connective tissue at the nasal or temporal limbus (see EYE). This is visible as a small, ?attened, yellow-white lump adjacent to the cornea.
Pterygium Overgrowth of the conjunctival tissues at the limbus on to the cornea (see EYE). This usually occurs on the nasal side and is associated with exposure to sunlight. The pterygium is surgically removed for cosmetic reasons or if it is thought to be advancing towards the visual axis.
Ptosis Drooping of the upper lid. May occur because of a defect in the muscles which raise the lid (levator complex), sometimes the result of ageing or trauma. Other causes include HORNER’S SYNDROME, third cranial nerve PALSY, MYASTHENIA GRAVIS, and DYSTROPHIA MYOTONICA. The cause needs to be determined and treated if possible. The treatment for a severely drooping lid is surgical, but other measures can be used to prop up the lid with varying success.
Retina, disorders of The retina can be damaged by disease that affects the retina alone, or by diseases affecting the whole body.
Retinopathy is a term used to denote an abnormality of the retina without specifying a cause. Some retinal disorders are discussed below. DIABETIC RETINOPATHY Retinal disease occurring in patients with DIABETES MELLITUS. It is the commonest cause of blind registration in Great Britain of people between the ages of 20 and 65. Diabetic retinopathy can be divided into several types. The two main causes of blindness are those that follow: ?rst, development of new blood vessels from the retina, with resultant complications and, second, those following ‘water logging’ (oedema) of the macula. Treatment is by maintaining rigid control of blood-sugar levels combined with laser treatment for certain forms of the disease – in particular to get rid of new blood vessels. HYPERTENSIVE RETINOPATHY Retinal disease secondary to the development of high blood pressure. Treatment involves control of the blood pressure (see HYPERTENSION). SICKLE CELL RETINOPATHY People with sickle cell disease (see under ANAEYIA) can develop a number of retinal problems including new blood vessels from the retina. RETINOPATHY OF PREMATURITY (ROP) Previously called retrolental ?broplasia (RLF), this is a disorder affecting low-birth-weight premature babies exposed to oxygen. Essentially, new blood vessels develop which cause extensive traction on the retina with resultant retinal detachment and poor vision. RETINAL ARTERY OCCLUSION; RETINAL VEIN OCCLUSION These result in damage to those areas of retina supplied by the affected blood vessel: the blood vessels become blocked. If the peripheral retina is damaged the patient may be completely symptom-free, although areas of blindness may be detected on examination of ?eld of vision. If the macula is involved, visual loss may be sudden, profound and permanent. There is no e?ective treatment once visual loss has occurred. SENILE MACULAR DEGENERATION (‘Senile’ indicates age of onset and has no bearing on mental state.) This is the leading cause of blindness in the elderly in the western world. The average age of onset is 65 years. Patients initially notice a disturbance of their vision which gradually progresses over months or years. They lose the ability to recognise ?ne detail; for example, they cannot read ?ne print, sew, or recognise people’s faces. They always retain the ability to recognise large objects such as doors and chairs, and are therefore able to get around and about reasonably well. There is no e?ective treatment in the majority of cases. RETINITIS PIGMENTOSAA group of rare, inherited diseases characterised by the development of night blindness and tunnel vision. Symptoms start in childhood and are progressive. Many patients retain good visual acuity, although their peripheral vision is limited. One of the characteristic ?ndings on examination is collections of pigment in the retina which have a characteristic shape and are therefore known as ‘bone spicules’. There is no e?ective treatment. RETINAL DETACHMENTusually occurs due to the development of a hole in the retina. Holes can occur as a result of degeneration of the retina, traction on the retina by the vitreous, or injury. Fluid from the vitreous passes through the hole causing a split within the retina; the inner part of the retina becomes detached from the outer part, the latter remaining in contact with the choroid. Detached retina loses its ability to detect light, with consequent impairment of vision. Retinal detachments are more common in the short-sighted, in the elderly or following cataract extraction. Symptoms include spots before the eyes (?oaters), ?ashing lights and a shadow over the eye with progressive loss of vision. Treatment by laser is very e?ective if caught early, at the stage when a hole has developed in the retina but before the retina has become detached. The edges of the hole can be ‘spot welded’ to the underlying choroid. Once a detachment has occurred, laser therapy cannot be used; the retina has to be repositioned. This is usually done by indenting the wall of the eye from the outside to meet the retina, then making the retina stick to the wall of the eye by inducing in?ammation in the wall (by freezing it). The outcome of surgery depends largely on the extent of the detachment and its duration. Complicated forms of detachment can occur due to diabetic eye disease, injury or tumour. Each requires a specialised form of treatment.
Scleritis In?ammation of the sclera (see EYE). This can be localised or di?use, can affect the anterior or the posterior sclera, and can affect one or both eyes. The affected eye is usually red and painful. Scleritis can lead to thinning and even perforation of the sclera, sometimes with little sign of in?ammation. Posterior scleritis in particular may cause impaired vision and require emergency treatment. There is often no apparent cause, but there are some associated conditions – for example, RHEUMATOID ARTHRITIS, GOUT, and an autoimmune disease affecting the nasal passages and lungs called Wegener’s granulomatosis. Treatment depends on severity but may involve NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), topical CORTICOSTEROIDS or systemic immunosuppressive drugs.
Stye Infection of a lash follicle. This presents as a painful small red lump at the lid margin. It often resolves spontaneously but may require antibiotic treatment if it persists or recurs.
Sub-conjunctival haemorrhage Haemorrhage between the conjunctiva and the underlying episclera. It is painless. There is usually no apparent cause and it resolves spontaneously.
Trichiasis Inward misdirection of the lashes. Trichiasis occurs due to in?ammation of or trauma to the lid margin. Treatment involves removal of the patient’s lashes. Regrowth may be prevented by electrolysis, by CRYOTHERAPY to the lid margin, or by surgery.
For the subject of arti?cial eyes, see under PROSTHESIS; also GLAUCOMA, SQUINT and UVEITIS.... eye, disorders of
Scientists have engineered appropriate genes from other organisms into BACTERIA, or sometimes plants, to accelerate this natural evolutionary process. For e?ective ‘digestion of waste’, a micro-organism must quickly and completely digest organic waste without producing unpleasant smells or noxious gases, be non-pathogenic and be able to reproduce in hostile conditions. For example, American researchers have discovered an anaerobic bacterium that neutralises dangerous chlorinated chemical compounds such as trichlorethane, which can pollute soil, into a harmless molecule called ethens. But the bacteria do not thrive in soil. So the dechlorinating genes in this bacterium are transferred to bacteria that are acclimatised to living in toxic areas and can more e?ciently carry out the required detoxi?cation. Other research has been aimed at detoxifying the byproducts of DDT, a troublesome and resistant pollutant. Bioremediation should prove to be an environmentally friendly and cost-e?ective alternative to waste incineration or chemically based processes for washing contaminated soils.... bioremediation
Habitat: Coastal areas of Bengal, Bihar and Western and Eastern Peninsula.
English: Palmyra Palm, Brab tree.Ayurvedic: Taala, Taada, Trinraj, Mahonnata, Lekhyapatra. Siddha/Tamil: Panai, Panaimaram.Action: Fresh sap—diuretic, cooling, antiphlegmatic, laxative, anti- inflammatory. Slightly fermented juice is given in diabetes. Palm- jaggery—used as an energy food for convalscents. Ash of dry spadix—antacid, antibilious (used in heartburn). Young root, terminal buds, leaf-stalks—used in gastritis and hiccups.
The sap is given as a tonic to asthmatic and anaemic patients. Jaggery is given for anaemia, for diseases characterized by a marked loss of potassium. Palm candy is used in coughs and pulmonary affections and as a laxative for children.The Ayurvedic Pharmacopoeia ofIn- dia recommends dried male inflorescence in dysuria.Jaggery solution may be used in hypertension and oedema due to heart and liver diseases, also as a food for typhoid patients.The sap is an excellent source of biologically available riboflavin.Aqueous MeOH extract of young shoots contains heat-stable toxin; edible part of young shoot, neurotoxic to rats, but not hepatotoxic.Dosage: Dried male inflorescence— 1-3 g (API Vol. III.)... borassus flabelliferUses Glycerin has many and varied uses. Numerous substances, such as carbolic acid, tannic acid, alum, borax, boric acid and starch, are dissolved in it for application to the body. It is frequently applied along with other remedies to in?amed areas for its action in extracting ?uid and thus diminishing in?ammation.... glycerin
The control centre of the whole nervous system is the brain, which is located in the skull or cranium. As well as controlling the nervous system it is the organ of thought, speech and emotion. The central nervous system controls the body’s essential functions such as breathing, body temperature (see HOMEOSTASIS) and the heartbeat. The body’s various sensations, including sight, hearing, touch, pain, positioning and taste, are communicated to the CNS by nerves distributed throughout the relevant tissues. The information is then sorted and interpreted by specialised areas in the brain. In response these initiate and coordinate the motor output, triggering such ‘voluntary’ activities as movement, speech, eating and swallowing. Other activities – for example, breathing, digestion, heart contractions, maintenance of BLOOD PRESSURE, and ?ltration of waste products from blood passing through the kidneys – are subject to involuntary control via the autonomic system. There is, however, some overlap between voluntary and involuntary controls.... brain
Habitat: Throughout India as a weed in cultivated areas and waste places, particularly in the temperate regions up to an altitude of 4,200 m.
English: Shepherd's Purse, St. James's Wort.Folk: Mumiri.Action: The herb or its juice extracts are employed to check menorrhagia and haemorrhages from renal and genitourinary tract. Also used in diarrhoea and dysentery and as a diuretic.
Key application: In symptom-based treatment of mild menorrhagia and metrorrhagia. (German Commission E.) The British Herbal Pharmacopoeia reported antihaem- orrhagic action.Aerial parts contain flavonoids, polypeptides, choline, acetylcholine, histamine and tyramine.The extract of dried or green plant causes strong contraction of the small intestines and uterus of guinea pigs. A quarternary ammonium salt has been isolated from the herb which is reported to be responsible for its pharmacological activity.Young leaves contain vitamin A (5,000 IU/100 g) and ascorbic acid (91 mg/100 g); among other constituents are hesperidin and rutin, which reduced permeability of blood vessel walls in white mice. A neoplasm inhibitory substance has been identified as fumaric acid. An inhibitory effect of the extracts of the herb on Ehrlich solid tumour in mice was found to be due to the fumaric acid.Major constituent of the essential oil is camphor.... capsella bursa-pastorisHabitat: Cultivated as a condiment crop.
English: Bird Chilli.Ayurvedic: Katuviraa.Unani: Surkh Mirch.Siddha/Tamil: Musi Milagay.Action: See Capsicum annuum.
Key application: Externally, in painful muscle spasms in areas of shoulder, arm and spine; for treating arthritis, rheumatism, neuralgia, lumbago and chilbains. (German Commission E.) The British Pharmacopoeia reported rubefacient and vasostimulant action.The plant contains hydroxybenzoic acid, hydroxycinnamic acid and ascorbic acid. Fruits contain up to 1% of capsaicin.... capsicum frutescensRarely, 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
The imaging systems of COMPUTED TOMOGRAPHY (CT) and magnetic resonance imaging (see MRI) have powerful computer techniques underlying them.
Computerised statistical analysis of study data, population databases and disease registries is now routine, leading to enhanced understanding of the interplay between diseases and the population. And the results of research, available on computerised indexes such as MEDLINE, can be obtained in searches that take only seconds, compared with the hours or days necessary to accomplish the same task with its paper incarnation, Index Medicus.
Medical informatics The direct computerisation of those activities which are uniquely medical – history-taking, examination, diagnosis and treatment – has proved an elusive goal, although one hotly pursued by doctors, engineers and scientists working in the discipline of medical informatics. Computer techniques have scored some successes: patients are, for example, more willing to be honest about taboo areas, such as their drug or alcohol consumption, or their sexual proclivities, with a computer than face to face with a clinician; however, the practice of taking a history remains the cornerstone of clinical practice. The examination of the patient is unlikely to be supplanted by technological means in the foreseeable future; visual and tactile recognition systems are still in their infancy. Skilled interpretation of the result by machine rather than the human mind seems equally as remote. Working its way slowly outwards from its starting point in mathematical logic, ARTIFICIAL INTELLIGENCE that in any way mimics its natural counterpart seems a distant prospect. Although there have been successes in computer-supported diagnosis in some specialised areas, such as the diagnosis of abdominal pain, workable systems that could supplant the mind of the generalist are still the dream of the many developers pursuing this goal, rather than a reality available to doctors in their consulting rooms now.
In therapeutics, computerised prescribing systems still require the doctor to make the decision about treatment, but facilitate the process of writing, issuing, and recording the prescription. In so doing, the system can provide automated checks, warning if necessary about allergies, potential drug interactions, or dosing errors. The built-in safety that this process o?ers is enhanced by the superior legibility of the script that ensues, reducing the potential for error when the medicine is dispensed by the nurse or the pharmacist.
Success in these individual applications continues to drive development, although the process has its critics, who are not slow to point to the lengthier consultations that arise when a computer is present in the consulting room and its distracting e?ect on communication with the patient.
Underlying these many software applications lies the ubiquitous personal computer – more powerful today than its mainframe predecessor of only 20 years ago – combined with networking technology that enables interconnection and the sharing of data. As in essence the doctor’s role involves the acquisition, manipulation and application of information – from the individual patient, and from the body of medical knowledge – great excitement surrounds the development of open systems that allow di?erent software and hardware platforms to interact. Many problems remain to be solved, not least the fact that for such systems to work, the whole organisation, and not just a few specialised individuals, must become computer literate. Such systems must be easy to learn to use, which requires an intuitive interface between user(s) and system(s) that is predictable and logical in its ordering and presentation of information.
Many other issues stand in the way of the development towards computerisation: standard systems of nomenclature for medical concepts have proved surprisingly di?cult to develop, but are crucial for successful information-sharing between users. Sharing information between existing legacy systems is a major challenge, often requiring customised software and extensive human intervention to enable the previous investments that an organisation has made in individual systems (e.g. laboratory-result reporting) to be integrated with newer technology. The beginnings of a global solution to this substantial obstacle to networking progress is in sight: the technology that enables the Internet – an international network of telephonically linked personal computers – also enables the establishment of intranets, in which individual servers (computers dedicated to serving information to other computers) act as repositories of ‘published’ data, which other users on the network may ‘browse’ as necessary in a client-server environment.
Systems that support this process are still in early stages of development, but the key conceptualisations are in place. Developments over the next 5–10 years will centre on the electronic patient record available to the clinician on an integrated clinical workstation. The clinical workstation – in essence a personal computer networked to the hospital or practice system – will enable the clinician to record clinical data and diagnoses, automate the ordering of investigations and the collection of the results, and facilitate referral and communication between the many professionals and departments involved in any individual patient’s care.
Once data is digitised – and that includes text, statistical tables, graphs, illustrations and radiological images, etc. – it may be as freely networked globally as locally. Consultations in which live video and sound transmissions are the bonds of the doctor-patient relationship (the techniques of telemedicine) are already reality, and have proved particularly convenient and cost-e?ective in linking the patient and the generalist to specialists in remote areas with low population density.
As with written personal medical records, con?dentiality of personal medical information on computers is essential. Computerised data are covered by the Data Protection Act 1984. This stipulates that data must:
be obtained and processed fairly and lawfully.
be held only for speci?ed lawful purposes.
•not be used in a manner incompatible with those purposes.
•only be recorded where necessary for these purposes.
be accurate and up to date.
not be stored longer than necessary.
be made available to the patient on request.
be protected by appropriate security and backup procedures. As these problems are solved, concerns about
privacy and con?dentiality arise. While paper records were often only con?dential by default, the potential for breaches of security in computerised networks is much graver. External breaches of the system by hackers are one serious concern, but internal breaches by authorised users making unauthorised use of the data are a much greater risk in practice. Governing network security so that clinical users have access on a need-to-know basis is a di?cult business: the software tools to enable this – encryption, and anonymisation (ensuring that clinical information about patients is anonymous to prevent con?dential information about them leaking out) of data collected for management and research processes – exist in the technical domain but remain a complex conundrum for solution in the real world.
The mushroom growth of websites covering myriad subjects has, of course, included health information. This ranges from clinical details on individual diseases to facts about medical organisations and institutes, patient support groups, etc. Some of this information contains comments and advice from orthodox and unorthodox practitioners. This open access to health information has been of great bene?t to patients and health professionals. But web browsers should be aware that not all the medical information, including suggested treatments, has been subject to PEER REVIEW, as is the case with most medical articles in recognised medical journals.... information technology in medicine
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
Severe and extensive burns are most frequently produced by the clothes – for example, of a child – catching ?re. This applies especially to cotton garments, which blaze up quickly. It should be remembered that such a ?ame can immediately be extinguished by making the individual lie on the ?oor so that the ?ames are uppermost, and wrapping him or her in a rug, mat or blanket. As prevention is always better than cure, particular care should always be exercised with electric ?res and kettles or pots of boiling water in houses where there are young children or old people. Children’s clothes, and especially night-clothes, should be made of non-in?ammable material: pyjamas are also much safer than nightdresses.
Severe scalds are usually produced by escape of steam in boiler explosions. Cigarettes are a common cause of ?res and therefore of burns; people who have fallen asleep in bed or in a chair while smoking may set ?re to the bed or chair. Discarded, unextinguished cigarettes are another cause.
Degrees of burns Burns are referred to as either super?cial (or partial-thickness) burns, when there is su?cient skin tissue left to ensure regrowth of skin over the burned site; and deep (or full-thickness) burns, when the skin is totally destroyed and grafting will be necessary.
Symptoms Whilst many domestic burns are minor and insigni?cant, more severe burns and scalds can prove to be very dangerous to life. The main danger is due to SHOCK, which arises as a result of loss of ?uid from the circulating blood at the site of a serious burn. This loss of ?uid leads to a fall in the volume of the circulating blood. As the maintenance of an adequate blood volume is essential to life, the body attempts to compensate for this loss by withdrawing ?uid from the uninjured areas of the body into the circulation. If carried too far, however, this in turn begins to affect the viability of the body cells. As a sequel, essential body cells, such as those of the liver and kidneys, begin to suffer, and the liver and kidneys cease to function properly. This will show itself by the development of JAUNDICE and the appearance of albumin in the urine (see PROTEINURIA). In addition, the circulation begins to fail with a resultant lack of oxygen (see ANOXIA) in the tissues, and the victim becomes cyanosed (see CYANOSIS), restless and collapsed: in some cases, death ensues. In addition, there is a strong risk of infection occurring. This is the case with severe burns in particular, which leave a large raw surface exposed and very vulnerable to any micro-organisms. The combination of shock and infection can all too often be life-threatening unless expert treatment is immediately available.
The immediate outcome of a burn is largely determined by its extent. This is of more signi?cance than the depth of the burn. To assess the extent of a burn in relation to the surface of the body, what is known as the Rule of Nine has been evolved. The head and each arm cover 9 per cent of the body surface, whilst the front of the body, the back of the body, and each leg each cover 18 per cent, with the perineum (or crutch) accounting for the remaining 1 per cent. The greater the extent of the burn, the more seriously ill will the victim become from loss of ?uid from his or her circulation, and therefore the more prompt should be his or her removal to hospital for expert treatment. The depth of the burn, unless this is very great, is mainly of import when the question arises as to how much surgical treatment, including skin grafting, will be required.
Treatment This depends upon the severity of the burn. In the case of quite minor burns or scalds, all that may be necessary if they are seen immediately is to hold the part under cold running water until the pain is relieved. Cooling is one of the most e?ective ways of relieving the pain of a burn. If the burn involves the distal part of a limb – for example, the hand and forearm – one of the most e?ective ways of relieving pain is to immerse the burned part in lukewarm water and add cold water until the pain disappears. As the water warms and pain returns, more cold water is added. After some three to four hours, pain will not reappear on warming, and the burn may be dressed in the usual way. Thereafter a simple dressing (e.g. a piece of sterile gauze covered by cotton-wool, and on top of this a bandage or adhesive dressing) should be applied. The part should be kept at rest and the dressing kept quite dry until healing takes place. Blisters should be pierced with a sterile needle, but the skin should not be cut away. No ointment or oil should be applied, and an antiseptic is not usually necessary.
In slightly more severe burns or scalds, it is probably advisable to use some antiseptic dressing. These are the cases which should be taken to a doctor – whether a general practitioner, a factory doctor, or to a hospital Accident & Emergency department. There is still no general consensus of expert opinion as to the best ‘antiseptic’ to use. Among those recommended are CHLORHEXIDINE, and antibiotics such as BACITRACIN, NEOMYCIN and polymixin. An alternative is to use a Tulle Gras dressing which has been impregnated with a suitable antibiotic.
In the case of severe burns and scalds, the only sound rule is immediate removal to hospital. Unless there is any need for immediate resuscitation, such as arti?cial respiration, or attention to other injuries there may be, such as fractures or haemorrhage, nothing should be done on the spot to the patient except to make sure that s/he is as comfortable as possible and to keep them warm, and to cover the burn with a sterile (or clean) cloth such as a sheet, pillowcases, or towels wrung out in cold water. If pain is severe, morphine should be given – usually intravenously. Once the victim is in hospital, the primary decision is as to the extent of the burn, and whether or not a transfusion is necessary. If the burn is more than 9 per cent of the body surface in extent, a transfusion is called for. The precise treatment of the burn varies, but the essential is to prevent infection if this has not already occurred, or, if it has, to bring it under control as quickly as possible. The treatment of severe burns has made great advances, with quick transport to specialised burns units, modern resuscitative measures, the use of skin grafting and other arti?cial covering techniques and active rehabilitation programmes, o?ering victims a good chance of returning to normal life.
CHEMICAL BURNS Phenol or lysol can be washed o? promptly before they do much damage. Acid or alkali burns should be neutralised by washing them repeatedly with sodium bicarbonate or 1 per cent acetic acid, respectively. Alternatively, the following bu?er solution may be used for either acid or alkali burns: monobasic potassium phosphate (70 grams), dibasic sodium phosphate (70 grams) in 850 millilitres of water. (See also PHOSPHORUS BURNS.)... burns and scalds
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