SUMMARY Basal ganglia calcification was found as an incidental finding in 42 out of 7000 patients who underwent computed tomography. The calcification showed on plain skull radiography when the maximum density on computed tomography exceeded 100 Hounsfield units. The 26 patients with basal ganglia calcification detected on computed tomography who were available for follow-up, were investigated with matched controls. No clinical features of basal ganglia calcification were noted. Twenty-four patients had no significant metabolic abnormality and two patients had parathyroid disorder identified.Basal ganglia calcification identified radiographically has been associated with any one of 24 conditionsl 2 (table) with treatable parathyroid disease being the most common of these associations.3 Computed tomography (CT) has identified basal ganglia calcification more sensitively than plain skull radiographs,2 4-9 but the incidence of disease including parathyroid disorder in the CT group has been less.2 4-7 This study was carried out to correlate radiographically basal ganglia calcification on CT with that on plain skull radiographs; to attempt to define any systemic metabolic mechanism of basal ganglia calcification formation; and to investigate the possibility of early detection of treatable parathyroid disease.

A series of 118 patients with diffuse traumatic brain swelling was studied retrospectively in order to compare the clinical findings in children with those in adults, and to determine the occurrence of neurological deterioration and outcome. The computerized tomography (CT) picture of absent third ventricle and basal cisterns was used to identify the cases. Although this condition has been associated with children, we found the same number of children and adults (59 cases each). Secondary deterioration (decline in consciousness, the development of new focal neurological signs, or an increase in intracranial pressure) occurred in 40% of cases and was more common in adults than children. Features that were significantly associated with deterioration were the presence of prolonged coma (> 1 hour) after the injury, CT signs of diffuse axonal injury or subarachnoid hemorrhage, or a recorded episode of hypotension. A moderate or good recovery at 6 months was achieved by 70 patients (59%), but 45 patients had a poor outcome (severe disability in nine, vegetative state in three, and death in 33) and this was often a consequence of secondary deterioration. In three patients, the outcome was not known. The combination of a severe initial injury, secondary insult, and diffuse swelling is associated with a poor outlook, particularly in adults. The CT appearance of diffuse swelling may develop more readily in children because of the lack of cerebrospinal fluid available for displacement. In children, diffuse swelling may have a relatively benign course unless there is a severe primary injury or a secondary hypotensive insult.

SUMMARY Computed tomography demonstrated a haematoma in the region of the basal ganglia in 61 of 2000 head injured patients. In 41 the haematoma occurred as an isolated lesion while in 20 there was another associated intracranial haematoma. Clinical and radiological differences within these groups are discussed. The patients with basal ganglia haematoma were more severely injured than those in a group who had an intracranial haematoma evacuated by craniotomy and the findings closely resembled those of a group of patients who had sustained diffuse brain damage. They share many features with those of patients with diffuse white matter injury and have a worse prognosis than other traumatic intracranial haematomas.Computed tomography (CT) has proved to be of enormous value in the assessment of traumatic intracranial haematomas and has led to improved clinical management with significant reductions in morbidity and mortality.' CT also demonstrates the effects of diffuse brain injury, though unfortunately the outcome for patients shown to have suffered this type of damage has not been similarly improved. It is only since the advent of CT that one has been able to identify in life small haematomas in the region of the basal ganglia. Basal ganglia haematomas were infrequently described before the scanning era2 and most reports since have concerned very large lesions.3 This study investigates the cause of injury, the clinical features, the CT appearances, and the outcome of a series of patients with basal ganglia haematoma, and considers the possible mechanisms responsible for these haematomas. It also assesses how the features of this group compare with those in a surgically treated group of patients with traumatic intracranial haematoma, and with a group of patients who sustained diffuse brain injury. The scans of 2000 of the head injured patients admitted during the period 1979-1983 were reviewed retrospectively by one of us (PM) and 61 were found to have a haematoma in the basal ganglia region. These patients were then sub-divided into a group in which the basal ganglia haematoma occurred as an isolated lesion (41) and one in which the haematoma was associated with another intracranial haematoma (20). The former group were further sub-divided by CT appearances into those with normal intracranial pressure (20) and those with evidence of raised intracranial pressure (18); that is presence or absence of the 3rd ventricle with or without absent basal cisterns, such findings being consistent with an intracranial -pressure of >20 mm Hg.4 Three patients had a large isolated basal ganglia haematoma causing midline displacement of >5 mm with resulting direct ventricular compression, and were considered separately. In the associated group, the second haematoma was intracerebral in 11, subdural in five and extradural in four.Clinical information concerning age, cause of accident, lucid intervals, focal signs and conscious levels (Glasgow Coma Scale5) were obtained from a retrospective analysis of the case records and this infor...

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S U MM AR Y The carotid angiograms of 96 patients who had died from non-missile head injury were reviewed and assessed for evidence of arterial spasm, slowing of the cerebral circulation, and the presence of intracranial haematoma. As bilateral angiography had been done in 44 cases the results are based on a correlation between the angiographic appearances and the presence or absence of ischaemic brain damage in the cortex of 140 cerebral hemispheres. There was a significant relationship between spasm alone, the presence of intracranial haematoma alone, or their combination, and ischaemic damage in the ipsilateral cortex. Apart from an association between the more severe grades of spasm and slowing of circulation in the group with ischaemia within arterial territories, there was none between slowing of the circulation or the combination of slowing with either spasm or haematoma and ischaemic brain damage.We have reported previously the association between ischaemic brain damage and arterial spasm or slowing of the cerebral circulation in a series of 33 fatally head-injured patients (Macpherson and Graham, 1973). We have now extended the series by a further 63 cases and, in addition, have investigated the possible role of intracranial haematoma in the genesis of ischaemic brain damage in the total 96 patients. MethodsThe series comprised 96 patients who died in the Institute of Neurological Sciences in Glasgow as a result of non-missile head injury, on whom carotid angiography had been carried out before any surgical treatment and on whom a full neuropathological examination was performed subsequently. There were 79 males and 17 females, aged from 8 months to 73 years, and with a survival time after injury ranging from six hours to seven months. ANGIOGRAPHYThe technique used was that described previously