with myasthenia gravis . Low dose interferon - alpha is safe in patients

bral grey matter was normal. The posterior borders of these lesions were formed by the caudate nuclei, the anterior parts of the internal capsules being spared. The lesions reached the parietal periventricular areas. The necrotic areas were characterised by extensive loss of myelin with myelin laden gitter cells. On both sides a substantial number of neurons in the ventromedial parts of the putamen and in the nuclei accumbens showed central chromatolysis. No signs of neuronal degeneration were found in the rostrolateral parts of the putamen or in the caudate nuclei on both sides. The extensive coagulative necrosis of central white matter with spongiosis, sparing the U fibres, is in agreement with the diagnosis of delayed necrotising leukoencephalopathy.' The presence of gitter cells and reactive gliosis is compatible with onset of the disease about six to eight weeks before the patient's death. The absence of CSF pleiocytosis at the onset of delayed necrotising leukoencephalopathy suggests that a CNS leukaemic relapse was not important in its evolution. In the present case all symptoms of anterior cingulate syndrome as described by Cummings2 were present, but the clinical picture did not deteriorate to the most severe form of anterior cingulate syndrome-that is, the akinetic mutism strikingly characterised by Cairns et al as "a state of motionless, mindless wakefulness".4 In our patient verbal communication remained possible by writing and reading excluding global aphasia as the cause of his mutism. In children mutism is a rather non-specific symptom, which may occur in a wide variety of neurological diseases.5 The present finding suggests that in children with anterior cingulate syndrome mutism is associated with an extreme loss of initiative. This selectively affects the modalities of communication of which spontaneous speech and spontaneous writing seem to be the most vulnerable ones.