In infancy and childhood, tumours within the spinal canal arc rarer than in adult life. Because of the relative rarity of neoplasms primarily involving meninges or nerve roots, pain is less common than in adult cases, and this, combined with the difficulty in examining young children and frequent failure to think of the possibility, means that the diagnosis is often delayed. It must be considered in all cases of limb weakness and sphincter disturbance and careful examination including sensory testing must be made. The spine must be examined for tenderness and mobility and for cutaneous stigmata of the kind associated with dermoid and epidermoid cysts. Head tilt is often seen with cervical cord lesions. Localized stiffness of the spine may be the presenting symptom of intraspinal tumours. Progression of weakness to complete paralysis can occur very rapidly in children with intraspinal tumours, so that delay in diagnosis is dangerous.

The three main types of intraspinal tumour seen in childhood are congenital tumours, such as dermoid cysts and teratomas, intramedullary gliomas such as the ependymoma, and extradural masses including spread of neuroblastoma, neurofibroma or reticuloses, and rarer lesions such as extradural abscess and haematoma.
When a spinal tumour is suspected detailed x-rays of the spine are needed with CSF examination and contrast myelography. Exploratory laminectomy should follow localization of a tumour. Extradural and subdural tumours can usually be completely excised, often with marked improvement in paralysis. Intrinsic tumours of the cord may not be operable and radiotherapy may then be indicated.

Brain abscess in children arises in several different ways. Spread of infection from other sites is an important source, either by direct or venous extension from infection in the middle ear, mastoid or sinuses, or by blood-born metastasis from infection in lungs, pleura or elsewhere. Compound fracture of the skull causing contaminated fragments of bone or foreign bodies to enter the brain is an unusual mechanism. A rare but important group are the abscesses, usually cerebellar, resulting from infection in dermoid or epidermoid cysts due to entry of bacteria via a congenital dermal sinus. The commonest type of brain abscess of childhood seen in many centres today, with improvement in the treatment of respiratory and ear infections, is the ‘paradoxical’ cerebral abscess associated with congenital cyanotic heart disease.

In the infective type of brain abscess a history of recent ear or chest infection may be obtained, but this may have been obscured by treatment. The clinical features of brain abscess itself include those of infection (fever, malaise, leucocytosis and meningism), which may be mild or absent, those of raised intracranial pressure which are more consistent and may develop rapidly, and focal neurological features related to the site of the abscess. Hemiplegia, aphasia, visual field defects, convulsions, and cerebellar features may be found. The EEG may be of localizing value and x-rays may help by showing signs of raised intracranial pressure or sources of infection in mastoids, sinuses or chest. The CSF is usually abnormal with increased white cells, mainly polymorphonuclear, in acute abscesses, but in more chronic cases may show little pleocytosis. The protein level is usually moderately raised, and the sugar normal or slightly reduced. The fluid is sterile in most cases, and may be under very high pressure, particularly with a cerebellar abscess.

In patients with cyanotic congenital heart disease who develop cerebral abscess the clinical picture is of convulsions, focal neurological features or signs of raised intracranial pressure. Symptoms and signs of previous infection are often absent. Headache, vomiting and lethargy are common. Focal neurological signs, such as hemiplegia, aphasia or hemianopia, appearing in patients with cyanotic congenital heart disease should probably always be regarded as due to cerebral abscess until proved otherwise.

Localization of cerebral abscess by ventricular air studies may be needed in order to plan appropriate treatment. The focus of infection, when known, must be eradicated by medical treatment with appropriate antibiotics and surgery if indicated. The methods of surgical treatment of abscess include repeated tapping through a burr-hole and total excision. Changes in the size of the abscess cavity can be followed by x-rays after injection of opaque medium. Complete excision of the abscess is in many centres giving way to a policy of aspiration, which has the advantage of leaving a smaller scar.

In this syndrome of varied, and often indefinite, aetiology raised intracranial pressure develops in the absence of an intracranial space-occupying lesion, and is usually transient. The symptoms are non-specific with headache, vomiting, internal strabismus and papilloedema. There is often a history of otitis media and some cases may be due to thrombosis of a lateral dural sinus secondary to infection, possibly with spread to other venous sinuses, although this is rarely proved. The association with otitis explains the earlier name ‘Otitic hydrocephalus’, but this is inappropriate since the lateral ventricles are small or normal. Trauma and endocrine disturbances have been incriminated in some cases. A similar transient intracranial hypertension may occur during treatment with tetracycline, nalidixic acid, and also during the withdrawal of ACTH or steroid therapy. The condition is usually self-limited, and without sequelae, but in severe cases prolonged intracranial hypertension threatens vision. Repeated lumbar puncture and corticosteroids have been used in treatment, and rarely surgical decompression is needed.

It is important to distinguish this syndrome from raised intracranial pressure due to space-occupying lesions. The latter is often associated with signs of cerebellar dysfunction and special x-rays usually show ventricular enlargement, neither of which is found in benign intracranial hypertension. The diagnosis can only be safely made by exclusion, usually by ventriculography, which shows the lateral ventricles to be small or normal in size with no evidence of a tumour in the posterior fossa or elsewhere.

This is a rare disease which starts like an attack of ordinary epidemic hepatitis. The symptoms, however, become much more severe, with headache, delirium, vomiting, diarrhoea and high fever. The disease is commoner in older children and young adults. Some cases follow anaesthesia and phosphorus poisoning, others upon what appears to be an acute hepatitis; the virus of homologous serum jaundice may also be responsible. Toxic hepatitis progressing to necrosis has followed the use of drugs including amine oxidase inhibitors and halothanes.

The child, who has been drowsy and vomiting, becomes gradually delirious and jaundiced, the urine being deeply bile-stained and the motions pale and frequent. What was at first thought to be infective hepatitis is now seen to be a graver illness. Delirium is present. The liver, which at first was easily palpable, shrinks beneath the costal margin. There may be haemorrhages in the mucous membranes and purpuric patches in the skin. Renal failure may occur, Air-hunger and coma rapidly supervene, death taking place in the severe cases.
The dietary content and fluid balance should be carefully controlled. Infusions of salt-free plasma albumin are indicated in hypoproteinaemia but protein in the oral diet should be restricted. Glucose may be infused intravenously. Steroids and transfusion of fresh blood are used in severe cases, but the prognosis is poor when coma is established.
Congenital obliteration of the bile ducts or bile canaliculi

Urticaria is a type reaction of the skin, which takes its name from the Latin word for nettle, the sting of which it clearly resembles. The reaction, which is vascular, can easily be reproduced by the injection or iontophoresis of histamine, itself a constituent of the nettle sting. Urticarial eruptions are always transient and rarely persist for longer than 8-10 hours, their extent and size is variable. In a small number of cases the mucosae may be involved leading rarely to gross swelling of the lips, abdominal pain and oedema of the larynx which may be severe enough to require urgent tracheostomy, if there is not prompt improvement after the injection of noradrenalin.

Many agents, physical, chemical and biological, will produce urticaria, certain of these, but by no means all, act as allergens. Thus many drugs, including morphine, codeine, chloroquine and quinine, possess the property of releasing histamine from mast cells, when given in appropriate dosage. Peptones and similar products of the hydrolytic digestion of proteins in food are also histamine releasers, and may therefore, give rise to attacks of ‘hives’ (uticaria) if absorbed; many foods will produce urticaria in children, e.g. strawberries, shell-fish.

Sunlight, cold and pressure are among the less common causes of urticaria, but stroking the skin will be followed by urticaria or dermatographia; about 6 per cent of otherwise normal individuals react in this way at some time in their lives, including childhood. Penicillin allergy may be accompanied by dermatographia.

Bites and stings often produce urticarial reactions, and in some children, this is followed by the appearance of papules which persist after the urticarial element has faded. These lesions are intensely pruritic and represent the delayed hypersensitivity (cellular) immune reaction, to the bites of bed-bugs, fleas, biting flies, mites and other noxious arthropods. This papular urticaria will persist until either the child is removed from the environment, or the cause is dealt with by liberal sprinkling of the arthropod’s haunts and breeding places with an appropriate pesticide such as dicophane. Hairs from certain caterpillars, e.g. the processional, will produce an intensely pruritic urticaria, which may persist for several days after the victim has visited the oakwood; or other habitat favoured by the moth.

It is chiefly in the severe cases of rheumatic carditis that pericarditis occurs and along with it there are always changes in the endocardium and the myocardium (pancarditis). Often there is mediastinitis as well, and there may be pleurisy and pneumonia. The pericarditis is either dry with localized or widespread to-and-fro friction sounds, or it causes a sudden effusion which may be serous or serofibrinous.-Ihe effusion is sterile and rarely sufficient in amount to compress the heart; it is reabsorbed spontaneously. Adherence of the pericardium may follow one or more attacks of pericarditis, but chronic constrictive pericarditis is almost never rheumatic in origin.

CLINICAL  PICTURE
The child has a pale and anxious face. Fever and tachycardia are present. Pain may be felt in the chest over the praecordium or it may be due to an associated pleurisy. When there is a large effusion, the heart sounds may be muffled, and on percussion dullness becomes evident in the second intercostal spaces close to the sternum. Radiological examination shows the heart shadow to be greatly enlarged and the left border is seen to be convex. An effusion similar to that in the pericardium appears at the base of the left pleura and this causes an area of dullness and bronchial breathing at the left base near the midline (Ewart’s sign). A similar but smaller effusion may occur in the right pleura. Erythema marginatum and nodules may be present. In about two-thirds of the acute cases there are characteristic changes in the electrocardiogram

TREATMENT
Is directed to the relief of pain and distress. Cardiac decompression is needed only in the rare cases of high-pressure effusion. Corticosteroids appear to have a beneficial effect in the acute phase.

Pericarditis in Still’s disease
In some 10 per cent of cases of Still’s disease, electrocardiographic changes and sometimes friction sounds provide evidence of pericarditis, and pericardial adhesions are usually found at autopsy. The pericardial inflammation probably occurs in the acute phases of the disease but does not otherwise affect the prognosis. Endocardial and myocardial changes do not develop in these cases unless there happens to be co-existing acute rheumatic infection.

There is no clear line between the anxiety states and the behaviour disorders, the distinction being based on the prominence of symptoms. The behaviour disorders are usually taken as those in which normal social patterns are not achieved. Ultimately, the child may defy normal authority and may seem to be completely indifferent towards his social obligations. While anxiety and unhappiness may be less obvious, it should not be assumed that they are absent.
Children whose behaviour is so disordered that they need treatment include those showing violent temper tantrums, a tendency to steal, aggressiveness towards others, and, in the psychopathic state, an apparent lack of concern regarding the harm they do.
A detailed discussion of juvenile delinquency and of the law in relation to juvenile offenders is outside the scope of this chapter, but one or two points deserve mention . Stott and others have shown that there is a high correlation between broken homes and the more severe behaviour disorders. This is understandable when the acceptance of good parental authority is seen as an essential part of normal development. Almost as important as this, is that parents and children should remain closely in contact whenever possible, and particularly during the formative years of early childhood.
Chronic or recurrent illness remains one of the commoner causes of separation in early childhood, and all is not well with the child who seems happier in hospital than he is at home. Every effort should be made to avoid long separations, and to mitigate these by making parents’ visits a real contact and a link between home and hospital. Bowlby’s work has underlined these points, but since the disordered behaviour does not occur in hospital, but after the child goes home, there is still a risk of complacency.

Gross mental disorder in early childhood was formerly regarded as excessively rare. More recently, increasing interest in the problems of the so-called autistic child have tended to focus attention to an extent suggesting that the condition is not uncommon. A recent survey giving the most authoritative figure available in this country suggests that there is a prevalence rate of 4-5 per 10,000, and that these children probably account for something of the order of 7 per cent of the severely subnormal population (Lotter, 1966). As a comparison: fewer blind children but more deaf children than this number need special education adapted to their handicap.

The terminology of this condition raises difficulties. The term ‘autism’ originated from Bleuler early this century as an attribute of many of his schizophrenic patients; Kanner (1943) used the diagnostic label ‘early infantile autism’, but similar cases were reported by Bender (1958). An attempt has been made to clarify the diagnostic criteria by selecting those points most frequently observed (Creak et al., 1961).

Nevertheless, it will often be the family doctor or paediatrician who will be consulted first on behalf of a young child whose development is not proceeding along the normal lines. The outstanding feature in such children is their lack of contact. They appear neither to look for nor to listen to the ordinary signals which pass all the time between mothers and their children. They are often rightly described as ‘living in a world of their own’. Speech fails to develop beyond a simple level, while in some cases a sharp regression in the form of a social withdrawal and loss of such speech as has been acquired may occur. Thus, the differential diagnosis becomes of critical importance; for example, deafness must be excluded.
Since communication is such a vital factor in any child’s development, it is easy to suppose that a child with retarded speech may be mentally handicapped or suffering from a progressive process involving cerebral degeneration. Certainly some forms of cerebral degeneration may result in a similar clinical picture, seen as a passing phase, but it will be short-lived, in the sense that it is soon superseded by gross and progressive interference with normal function and activity.

The autistic child appears to be set in a pattern of behaviour which is repetitive and limited to certain chosen activities, interference with which provokes an excessive protest reaction. Often such reactions as motor hyperactivity, screaming and constant restlessness take over without any obvious provocation. Sleep may be disturbed, and much of this activity may continue before sleep, or even during the night after a short spell of natural sleep.
Thus, the question of day care or institutionalization may be brought in at an early stage. Many parents find themselves torn between the wish to care for such a child at home and the emotional cost to themselves and the rest of the family of doing so.

Since the aetiology is so uncertain, treatment cannot be precise and specific. However, residential units for the special study of this condition now exist in many parts of the country, and the help of child psychiatrists, experienced in this particular problem, should be sought early, rather than when all else has failed. There is also an increasing number of day units, often attached as a special class in a school helping other kinds of handicapped children. Intensive psychotherapy has sometimes appeared to check the degree of withdrawal and social disintegration which plays such havoc with the child’s learning capacity. Once the diagnosis is clarified, drugs can play a useful part in controlling hyperactivity and sleeplessness. They have largely superseded the physical methods so often successful in adult schizophrenia, such as convulsant therapy or insulin.
The possibility of organic factors may yet reveal what it is that makes these children so astonishingly like each other, and so unlike the rest of the world. Meanwhile, early diagnosis, continued watchful care, and therapy where practicable, together with continued counselling of parents, can go some way towards relieving a very severe problem for both the affected child and the other members of his family.

In general, sleep difficulties recede after infancy, perhaps because the very young child often rests in his nursery school, while the older child goes to bed a good deal later than he did 30 years ago.
Evening entertainment such as radio and television play a large part in children’s lives, and in some families seem to have replaced entirely their interest in reading or being read to at bedtime. It is commoner nowadays to meet fatigued children who drop asleep during the day than wakeful children who are afraid of the dark and cannot get off to sleep. Perhaps television also provides sufficient alarm, so that the imagination need not create its own dreadful images. Perhaps, also, parents are less dogmatic over timing the evening meal, and allowing children a night-light.
A temporary sleep disturbance can be helped to right itself with the aid of sedatives, particularly should it arise in association with an immediate and environmental factor. Sedatives used over long periods may only serve to conceal the underlying anxiety state, and psychiatric help for this basic anxiety, rather than drugs for insomnia, should be sought.

Symptomatic hypoglycaemia in the newborn is seen most commonly in full-term infants of low birth-weight, who have presumably undergone intrauterine growth retardation. The symptoms most commonly occur during the first 3-4 days of life, premonitory signs of apathy, weak cry and reluctance to feed may precede the appearance of ashen pallor, twitching, apnoeic attacks or frank convulsions. The symptoms are corrected by the use of intravenous 50 per cent glucose, 2 ml per kg body weight, followed by a slow infusion of 10 per cent glucose.
In the routine management of newborn infants, the possibility of neonatal hypoglycaemia is a not uncommon problem. It has been suggested that very early feeding of low birth-weight full-term infants will prevent symptomatic hypoglycaemia. There is little doubt that the general incidence can be reduced by this technique, but it is doubtful whether it provides invariable protection. Where the diagnosis is suspected blood should be taken for plasma glucose determination, but treatment with oral and intravenous glucose should not be withheld until the result is known. In the absence of laboratory facilities a rough estimate may be made with a glucose oxidase impregnated test paper | Dextrostix),