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To elucidate the mechanism of excessive size of the head in Sotos syndrome, serial neuroimaging features from birth were reviewed in two patients. Macrocephaly shortly after birth was attributed to increased volume of the cerebral parenchyma itself (megalencephaIon). Subsequent excessive size of the head was related to retention of cerebrospinal fluid in the ventricles and the subarachnoid spaces. Thus, macrocephaly in Sotos syndrome reflects two different mechanisms. The value of serial evaluation of intracranial structures is emphasized. [Neural Res 1998; 20: 149–152]

A 55-year-old man with traumatic acute subdural hematoma (SDH) was managed nonsurgically because of having isolated mild headache that resolved within a week. However, the patient developed an acute onset of amnestic aphasia 12 days post-trauma. Although the SDH itself did not increase in volume, remarkable swelling of the ipsilateral cerebral hemisphere was observed on CT scanning. Craniotomy was required since the main component of the SDH was solid and partially organized. Post-operative recovery from his speech disturbance was delayed, necessitating speech therapy for more than two months. Additionally, decreased cerebral blood flow on the affected side was observed even 3 months after injury. Symptomatic subacute SDH exclusively presenting as focal neurological deficits, though very rare,is worthwhile to be kept in mind as a pitfall in nonsurgical management of acute SDH.

A patient who suffered rapid deterioration due to cerebral vasospasm 18 days after aneurysmal subarachnoid haemorrhage is reported. Unusually delayed onset of ischaemic neurological deficits and its preventative management is discussed.

An eight-month-old boy with clinical features of acute encephalopathy with symmetrical low-density areas in the thalami and the putamen on computed tomography is presented. These particular computed tomography features suggest potential aetiology common to acute encephalopathy with low-density areas in the thalami and infantile bilateral striatal necrosis with an acute onset The therapeutic consideration of these conditions is also discussed.

A case of acute subdural haematoma caused by ruptured arteriovenous malformation is reported. At surgery, there was no association with intracerebral haematoma or definite subarachnoid haemorrhage. The mechanism of acute subdural haematoma in the present case was considered to be rupture of an arteriolized bridging vein drained by arteriovenous malformation. [Neurol Res 1993; 15: 353-355]

A 52-year-old male underwent lumboperitoneal shunting after external decompressive craniectomy. His postoperative course was accompanied by remarkable displacement of the intracranial structures to the opposite side of craniectomy. This phenomenon, probably caused by the siphon effect of cerebrospinal fluid shunting, resolved after cranioplasty. This observation- provides the evidence casting doubt on the presence of the siphon effect due to atmospheric pressure in patients without the association of skull defect or open cranial sutures.

Chronic subdural haematoma in adults has been treated by percutaneous subdural tapping using a subdural needle. In order to prevent recurrence, the procedure including replacement of the haematoma with oxygen, irrigation using relatively small amounts of saline, and additional drainage for one hour proved to be simple and reliable. The detailed technique is illustrated, and sequential computed tomography scans in six patients treated with this procedure are presented.