The place of computed tomography and lumbar puncture in suspected bacterial meningitis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D H Mellor.
Explore the source record for details and available documents.
Three boys with hemimegalencephaly are reported. Two suffered neonatal convulsions and the third presented with seizures at seven months. In each case the EEG was grossly abnormal, with spike and wave activity. All three have significant developmental delay and demonstrate other manifestations of the condition: macrocephaly in two, contralateral hemiparesis in one and one boy has ipsilateral facial hemihypertrophy and linear naevus. Hemimegalencephaly can be recognised on cranial ultrasonography, and the seizures may respond to benzodiazepine therapy.
Explore the source record for details and available documents.
Two cases of influenza A encephalitis seen during an outbreak of influenza types A/England/427/88 (H3N2) and A/Taiwan/1/86 (H1N1) in December 1989 are described. In both children the encephalitis developed within three days of the respiratory symptoms and both became comatose within 48 hours. Virological studies showed that the patients had had a recent influenza A infection. Symmetrical localised hypodense lesions within the thalami and pons were demonstrated in both cases on computed tomography of the brain and striking findings in the pons in one case on magnetic resonance imaging. Influenza A encephalitis is not easy to recognise clinically and serological confirmation can only be made after 10 days. Imaging may provide evidence in the acute stage to support a diagnosis of influenza encephalitis during influenza outbreaks.
To investigate the role of magnetic resonance imaging (MRI) in neurological disorders, 115 children were studied in two groups. Group A (78 patients) was studied by paired computed tomography and MRI cranial scans. Group B (37 patients) was studied by paired computed tomography assisted myelography (CTM) and MRI spinal scans. In group A, the scans were generally equivalent for supratentorial tumours and for investigating fits, hydrocephalus, benign intracranial hypertension, and cerebral atrophies, but MRI scanning was superior for posterior fossa tumours and cysts. In group B, MRI scans were superior for intramedullary spinal tumours, spinal dysraphic problems with tethering or syrinx, and were complementary to CTM in diastematomyelia.
Nine patients with congenital ocular motor apraxia (COMA) are presented and the natural history of this condition is considered. Two presented in early infancy, before the onset of the head thrust, and the means of establishing the diagnosis at this age are discussed. All exhibited motor delay in infancy which lessened, but did not completely resolve, with time. Conceptual delay, particularly with speech, affected all in early childhood. Three had agenesis of the corpus callosum and 2 cerebellar abnormalities. The autopsy of one infant showed cerebellar cortical dysplasia. The pathogenesis of COMA remains unknown and it is possible that agenesis of the corpus callosum and cerebellar hypoplasia are markers indicative of early CNS maldevelopment and not an integral part of the mechanism of COMA.
Fifty-three infants with delayed visual maturation (DVM) are presented. These have been classified according to their ocular and systemic features into three groups: DVM as an isolated anomaly, in association with mental retardation, and ocular abnormalities accompanied by DVM. The clinical features are discussed, particularly regarding the time and speed of visual improvement in the three groups. Infants with DVM who experienced difficulties in the perinatal period have an increased risk of developing permanent neurological sequelae.
The topography of the brain-stem (ABR), middle latency (MLR) and cortical (ACR) evoked responses was investigated in children with normal speech and language development and those with either a language or motor speech disorder. The aim was to determine whether it is possible to discriminate between the groups of children in terms of the evoked potential characteristics. There were significant inter-group differences, particularly relating to the amplitude of the different responses. The ABR in both the language and motor speech groups exhibited smaller amplitudes for waves I, III and V than the control group, with no change in latency. Two explanations were suggested; firstly abnormal functioning of the peripheral hearing mechanism even though the hearing thresholds were normal which could be a secondary effect due to deprivation of normal speech and language development; and secondly far-field recording effects due to differences in the electrical conductivity of tissue and the distance separating the generator site and recording electrodes. The MLR in the motor speech group was significantly larger at the mastoid and temporal electrode sites than either the control or language groups. This was considered to be an enhanced myogenic response like the other exaggerated brain-stem reflexes seen in congenital suprabulbar paresis. Significantly larger amplitudes of the ACR were also recorded from the motor speech group at the Cz electrode site. This was thought to be due to underactivity of some normal cortical inhibitory system and not a direct result of increased MLR amplitude. The ACR in the language disordered children exhibited an abnormal left temporal hemispheric dominance and a more inverted or 'dissimilar' wave form at the T3 electrode site on the correlation analysis. These findings suggest impaired functioning of the left temporal cortex in our children who have failed to develop language normally. We feel that this has more significance for the language abnormality than the low amplitude ABRs which were observed in both the language and motor speech disordered children.
The author visited ten paediatric neurology departments in the U.K. as part of a travelling scholarship. He was particularly interested in the way services were organized, and was able to make comparisons and note those features which seemed desirable. It seemed to him that: there should be a considerable overlap between paediatric neurology and handicapped childrens' services with the paediatric neurologist an active member of the local child development centre team; paediatric neurologists should be closely involved in the diagnosis and treatment of acute neurological disorders; minimum staffing for a regional paediatric neurology service for a total population of 2 million or more would be two consultant paediatric neurologists and appropriate supporting staff; different centres have opted for inpatient facilities either in a separate paediatric neurology ward, or in general paediatric wards: there are advantages and disadvantages for each option; school clinics and clinics in other hospital centres are valuable; neuroradiology, neurosurgery, neurophysiology and neuropathology should ideally be present in the hospital providing the paediatric neurology service; regular professional contact with other doctors in the neurosciences is important; junior posts in paediatric neurology would usually be filled by paediatricians in training but certain centres could be asked to appoint a career senior registrar from time to time depending on consultant paediatric neurologist requirements; and creation of lecturerships in paediatric neurology would help to encourage academic research in the subject.
Two half-brothers with tuberous sclerosis (TS) presented with polycystic kidneys in early childhood, before the classical stigmata became apparent. Their father shows no evidence of the disease. The older boys subsequently developed adenoma sebaceum at nine years and the younger boy developed infantile spasms. Hypertension occurred in both cases but neither showed evidence of renal failure. Extensive renal cyst formation in TS is rare, but when it does occur it differs from both infantile and adult-type polycystic disease. TS should be considered in the differential diagnosis of renal enlargement, haematuria and hypertension in childhood.
A total of 107 children who had been hospitalized following a febrile convulsion were enrolled into the trial. By random allocation, 55 children were treated with pyridoxine hydrochloride (20 mgs twice daily) and the remaining 52 children were treated with a placebo until there had been either a further convulsion or a year had passed without recurrence. Eighty children were adequately followed up and of these, 17 had a recurrent febrile convulsion while receiving medication. Recurrences occurrences occurred in 7 of the 38 children receiving pyridoxine and in 10 of the 42 children receiving placebo (X2 = .346, p greater than 0.5). Initial tryptophan load tests had been abnormal in 34 children, and of these, recurrences occurred in 3 of the 17 who received pyridoxine and in 3 of the 17 who received placebo. It has yet to be shown that pyridoxine supplementation protects children from recurrent febrile convulsions.
We report a girl who developed an encephalitic illness with visual loss after two years treatment for acute lymphoblastic leukaemia. The visual loss was found to be due to bilateral macular degeneration. She later developed radiological evidence of intracranial calcification and temporal lobe epilepsy. A second episode of encephalitis occurred when she had been off all antileukaemic treatment for three years and this left her with a right hemiparesis. Investigation suggested involvement with both measles virus and Toxoplasma gondii as a cause for these illnesses.
In a family with a history of two neonatal deaths, propionicacidaemia was diagnosed retrospectively from stored plasma as the cause of the second death during the mother's next pregnancy. Amniocentesis was performed and a culture of amniotic cells was assayed for propionyl CoA carboxylase activity. The absence of any detectable propionyl CoA carboxylase activity allowed the prenatal diagnosis of propionicacidaemia to be made. Treatment with biotin and a modified aminoacid diet was started in the immediate postnatal period. Investigation of propionyl CoA carboxylase in leucocytes from the parents, siblings and other relations of the patient failed to demonstrate intermediate enzyme activities in even the parents, who were presumably heterozygotes for this condition.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.