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The clinical and autopsy findings of a two and a half year-old infant with Toxocara sp. infection of the brain and granulomatous lesions in the liver are reported. The cause of death was non-accidental injury. The relationship between Toxocara infection and behavioural disorders is discussed.

Opsoclonus is an involuntary eye movement disorder in which there are chaotic, usually conjugate, multidimensional saccadic eye movements. In this paper 2 cases of opsoclonus are reported, as a paraneoplastic phenomenon in association with oat cell carcinoma of the lung. It has previously been hypothesized that opsoclonus results from dysfunction of a group of premotor neurons in the brainstem called omnipause neurons. We describe the location of these cells in man by homology with animal studies, and describe the light microscopic appearance of these neurons in the 2 cases of opsoclonus. Although these neurons appeared normal it is still possible that their function was disturbed as a result of metabolic or neurotransmitter abnormalities.

✓ A case of a benign cyst within the fourth ventricle is described. The histology of the cyst wall lining resembled that of an enterogenous cyst of the spinal cord. The relationship between this cyst, colloid cysts of the third ventricle, and enterogenous cysts of the spinal cord is discussed.

SUMMARY The brains from 12 babies up to 21/2 years of age, who died after repeated nonaccidental injury to the head, were subjected to detailed neuropathological examination. The nine brains from infants under 5 months showed contusional tears-slit like lesions in the white matter surrounded by astrocytes and associated with evidence of old and recent haemorrhage. The three brains from infants over 5 months showed white matter lesions similar to those seen in adults after closed head injury, including damage in the dorsolateral quadrant of the brain stem without axonal hemispheric damage, which may have been a result of whiplash injury after shaking. In addition, all the brains examined showed diffuse gliosis.This paper draws attention to contusional tears and other white matter lesions, which the authors believe are manifestations of mechanical damage produced by trauma. The long term neurological and intellectual defects observed in patients suffering non-accidental injury early in life are increasingly being recognised, although it is difficult to identify the extent to which these are due to social or neuropathological factors. We suggest that the white matter damage we describe has an important role.

SUMMARY Diffuse axonal injury typified by retraction balls and axonal swellings was identified in the brains of a series of infants, 5 months old and younger, who had suffered closed head injuries.These axonal discontinuities were shown by using Nauomenko and Feigin's silver method, which is particularly useful for showing fine axons such as those found in the developing brain.Diffuse axonal injury in early infancy may occur in the same way as that described in adults. The low incidence of intracerebral haematomata suggests that recurrent trauma to the head from a combination of direct contact and shaking results in axonal damage to the poorly myelinated axons and that blood vessels are rarely damaged.Closed head injury in early infancy (5 months of age and younger) produces focal lesions, contusional tears, and diffuse astrocytic reaction.1 2 Contusions, typical of adult closed head injuries, are not seen because of the smooth inner surface of the infant skull. The diffuse degeneration of the white matter first defined by Strich3 is now commonly known as diffuse axonal injury and is a recognised distinct clinicopathological entity in adult closed head injury.4 Diffuse axonal injury has not been described in infants under 5 months of age.We describe diffuse axonal injury in a series of infants 5 months old and younger who had suffered serious closed head injuries. Intracerebral haemorrhages are rarely seen in abused infants, indicating that small blood vessels are not commonly torn at the time of trauma. Material and methodsThe brains of nine infants (cases 1-9 from Calder et al, 1984) and one additional case (10), all of which had been subject to non-accidental injury and had died of head injury, were studied.

SUMMARY The spinal cords of 10 cases of motor neuron disease were compared with those of six age-matched controls using myelin and silver impregnation methods, and the Marchi reaction for myelin degradation products. These studies revealed striking asymmetry in involvement of the lateral and anterior corticospinal tracts, without concordance in the pattern of involvement of these crossed and uncrossed corticospinal pathways. In addition there was prominent involvement of the posterior and anterior spinocerebellar tracts, but less marked abnormality was seen in the reticulospinal pathways. These findings highlight the asymmetrical involvement of the upper and lower motor neuron components of the motor system that is a characteristic feature of the disease, and demonstrate that involvement of the spinocerebellar system is a frequent finding.Motor neuron disease is a progressive and fatal disorder of the motor system, characterised by clinical and pathological features of coexistent upper and lower niotor neuron degeneration.1-4 Involvement of the motor system may be strikingly asymmetrical.5 Sensory involvement is not evident to ordinary clinical examination but, in some cases, paraesthesiae have been noted,6 ' and subclinical abnormalities have been found in teased fibre preparations of sensory peripheral nerves.8 In the spinal cord the major abnormalities comprise loss of anterior horn cells and degeneration of the crossed and uncrossed corticospinal tracts.9'-1 Degeneration of the spinocerebellar tracts has been described in familial cases'2 but is thought to be infrequent in the more common sporadic form of the disease.2 3 13 However, no systematic pathological study has been made of noncorticospinal pathways in the spinal cord in sporadic motor neuron disease.In a previous study we showed that

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