In this report the authors describe a noninvasive transcranial method of determining the flow velocities in the basal cerebral arteries. Placement of the probe of a range-gated ultrasound Doppler instrument in the temporal area just above the zygomatic arch allowed the velocities in the middle cerebral artery (MCA) to be determined from the Doppler signals. The flow velocities in the proximal anterior (ACA) and posterior (PCA) cerebral arteries were also recorded at steady state and during test compression of the common carotid arteries. An investigation of 50 healthy subjects by this transcranial Doppler method revealed that the velocity in the MCA, ACA, and PCA was 62 +/- 12, 51 +/0 12, and 44 +/- 11 cm/sec, respectively. This method is of particular value for the detection of vasospasm following subarachnoid hemorrhage and for evaluating the cerebral circulation in occlusive disease of the carotid and vertebral arteries.

✓ Present knowledge of the still controversial pathogenetic, ultrastructural, diagnostic, and treatment aspects of chronic subdural hematomas is reviewed.

The end-tidal carbon dioxide partial pressure (PCO2) response curves for the flow velocity in the middle cerebral artery were studied in 31 normal subjects with transcranial Doppler techniques. An exponential curve with an exponent of 0.034 mm Hg-1 was found to be a good fit to the recorded data. By means of this relationship, recordings of flow velocity in cerebral arteries can be normalized to a standard value of PCO2. Physiological aspects of cerebrovascular reactivity to PCO2 and the clinical implications of the PCO2 response curve are discussed. The normal material provides a reference for assessing pathological responses.

A consecutive series of 32 adult patients with chronic subdural hematoma was studied in respect to postoperative cerebral reexpansion (reduction in diameter of the subdural space) after burr-hole craniostomy and closed-system drainage. Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. Our study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly.