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SummaryCerebral haemodynamic changes in 17 patients with cerebral arteriovenous malformations (AVMs), who showed hypoperfusion on single-photon emission computed tomography (SPECT) before endovascular treatment, were studied after embolization. Nine of them had non-haemorrhagic clinical manifestations and the other eight had a history of intracranial haemorrhage. Obliteration of AVMs was nearly total in six patients and partial in eleven.New low density lesions on X-ray computed tomography (CT) developed in 3 of 6 patients after nearly total obliteration and one of 11 patients after partial obliteration.The first SPECT after embolization showed diminished hypoperfusion in 11 of 13 patients without new low density lesions and one of 4 patients with new low density lesions. Diminution of hypoperfusion was seen even in two patients who underwent SPECT study immediately after the embolization. Cerebral circulation was improved in five of eight patients with low density lesions before embolization and in nine of eleven patients after partial obliteration. Hypoperfused state in the haemorrhagic group tended to remain unchanged compared with that in the non-haemorrhagic group. The hypoperfused area was expanded after embolization in three patients with new cerebral infarction.It is important for improvement of cerebral circulation to reduce the shunt flow without causing new infarction due to the embolization itself. In one of two patients who had a hyperperfused area surrounding the AVM after embolization, an unexpected and abnormal degree of brain swelling and haemorrhage occurred at the end of the surgery 20 days after the embolization. In the other patient, total extirpation was successfully performed after confirming disappearance of hyperperfusion in the follow-up SPECT.SPECT allows repeated measurement of the cerebral blood flow pattern easily and safely, and is useful for AVM management.

We report three cases of traumatic microbleeds evaluated by sequential observation. Hypo-intensities on T2* gradient echo imaging (T2*GEI) appeared just 2-3 h after the injury (the hyper-acute period). However, these hypo-intensities on T2*GEI disappeared or became obscure 2-6 days after the injury (the subacute period). A follow-up MRI again revealed clear hypo-intensities on T2*GEI 1-3 months after the injury (the chronic period). Our cases indicate that hypo-intensities on T2*GEI might change dynamically from the hyper-acute to the chronic period. The differences of susceptibility effects by hematoma age might be the cause of this dynamic change.

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