Simple partial, and mainly motor seizures, with or without secondary generalization, accounted for 80% of the classifiable seizures but it was not possible to determine the seizure type in half of the cases. Factors that appeared to be predictive of seizure development were the presence of large cortical infarcts and the presence of apparently preserved cerebral tissue within the infarcted area. Seizures were rare in patients with lacunar infarction but the presence of associated leukoaraiosis increased the risk. The risk was also increased in patients with other medical problems known to lower seizure threshold, such as renal failure.

We have evaluated computed tomography (CT) and ultrasonography (US) in 41 patients with hepatic hydatid disease. CT was diagnostic in all patients, while US performed on 36 patients was diagnostic in 34. In the remaining two cases, heavy calcification in one and a large amount of intracavitary air in the other prevented accurate diagnosis. The US findings in the liver regarding cyst form (multilocular or unilocular), size and location were comparable to those of CT. CT detected associated extrahepatic cysts in the abdomen and pelvis in 11 patients while US performed on the same group of patients detected such cysts in seven patients. It is suggested that the entire abdomen and pelvis should be scanned in patients suspected of hydatid disease and when a hepatic lesion is suggestive of the disease.

ABSTRACT. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) has varying anatomical patterns dependent on the type of insult, the degree and duration of cerebral hypoxia, or presence and degree of hypoperfusion. Profound insults can affect the entire cerebral cortex or just the perirolandic cortex, the cerebellum and the deep grey matter structures. Less severe insults may affect only the watershed regions. The objective of this article is to review the anatomical patterns of non-perinatal HIEs by MRI. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) can be a devastating neurological injury and prompt recognition of it can result in significant changes in patient management. HIE insults develop in varying regions of the brain depending on the severity and duration of hypoperfusion or hypo-oxygenation [1]. Brain parenchyma changes have corresponding MR signal characteristics that are often obvious but can be subtle [2]. It is important for radiologists to be aware of the variations in the appearance of HIE in order to be alert to the diagnosis in subtle cases, recognise unusual patterns and be aware of the clinical ramifications.This review shows cases of HIE beyond the perinatal period. Aetiological factors and timing of imaging findings are delineated. The cases involve the usual HIE-specific neuroanatomical locations: the cerebral cortex, cerebellum, hippocampus, basal ganglia and thalamus. In addition, cases of HIE showing damage to the cerebral white matter and limbic system are demonstrated. Also, cases that mimic the appearance of HIE are presented. It is critical for a radiologist to be aware of potentially confounding cases.

This paper describes a prospective study of the diagnostic radiation doses received in a neonatal intensive care unit (NICU) for a representative radiological technique used at our institution for a number of years and a "low dose" technique similar to that recommended by the Commission of the European Communities (CEC). A 400 speed film-screen combination was used in both techniques. A total of 363 anteroposterior (AP) chest and abdominal films of 77 neonates were accrued. For each radiograph, the entrance skin dose (FSD), energy imparted (EI) and mean whole body dose were determined. For a neonatal AP chest, there was an 18% reduction in the mean ESD per radiograph from 20.0 muGy for the representative technique to 16.4 muGy for the low dose technique (p < 0.0005). The reduction in the mean EI per radiograph values for the two techniques from 7.9 muJ to 7.1 muJ (10%) was statistically significant at the p < 0.017 level, after compensating for the difference in mean field dimensions between the two patient cohorts. The mean whole body dose per radiograph reduction from 4.4 to 3.5 muGy (20%) was statistically significant at the p < 0.0028 level. It was determined that the ESD and EI could be fitted by an exponential function in the equivalent patient diameter, a single parameter indicative of neonate size. Absolute excess childhood cancer mortality risk per film was estimated using risk factors derived for fetal exposures. A "worst case" absolute excess mortality risk per chest radiograph was estimated to be 1.40 x 10(-7) for the conventional technique and was further reduced to 1.11 x 10(-7) for the low dose technique. A blind comparison of patient-matched film pairs for each technique was performed by three radiologists using criteria similar to those specified by the CEC. No statistically significant difference in clinical image quality was found between the two techniques.

The authors report a case of ossification of the ligamentum flavum at T-10 and T-11 associated with compressive myelopathy. Metrizamide myelography with computerized tomography allowed precise preoperative diagnosis and anatomic localization of the lesion. The patient had satisfactory and prompt improvement after surgical intervention.

A selective non-occlusive technique was developed for administration of BCNU (1,3-bis(2-chloroethyl)-1-nitrosourea) into the internal carotid artery of the dog, and the neuropathological effects in the brain were studied. One out of three dogs showed ipsilateral hemorrhagic necrotizing encephalitis at doses of 102 mg/sq m, and all of three dogs showed similar but more severe pathology at doses of 215 to 232 mg/sq m. This study and previous studies in the dog and monkey suggest definite thresholds above which cerebral toxicity occurs when BCNU is administered via the intracarotid route. Greater dilution of drug in the larger territory of supply of the human internal carotid artery allows somewhat higher doses in man. The pathology of the lesion induced by BCNU suggests a primary vascular injury as a pathogenic mechanism, consonant with similar findings following high-dose systemic BCNU administration in man. Investigators conducting ongoing and future trials of intracarotid BCNU in the human for the treatment of intracranial neoplasms should be especially vigilant for a similar toxic effect.

✓ This is a report of spontaneous regression of intracranial arteriovenous malformations (AVM's) in three female patients; two of these patients had complete angiographic disappearance of the AVM, including an instance of intimate association of the AVM with an astrocytoma. The AVM's in these two patients were unicompartmental medium- to large-sized lesions supplied by a single feeder and draining principally through one large vein; spontaneous thrombosis is suggested as a cause of the AVM regression. Partial regression in the third patient might have been partially due to embolism from a clot-filled aneurysm on the feeding vessel. The significance of such disappearance of AVM's in relation to persistence or otherwise of the neurological status of these patients is discussed.

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