• D G Grosset, J Straiton, I McDonald, M Cockburn, and R Bullock.
• Institute of Neurological Sciences, Glasgow, Scotland.
• J. Neurosurg. 1993 Feb 1; 78 (2): 183-7.

AbstractBlood flow velocity was recorded from the middle or anterior cerebral and extracranial internal carotid arteries using transcranial Doppler sonography (TCD) in 121 unselected consecutive patients with acute aneurysmal subarachnoid hemorrhage (SAH). Recordings were made daily or every 2nd day after SAH for a 14-day period. The highest recorded velocity was greater in the 47 patients who developed a delayed ischemic neurological deficit (186 +/- 6 cm sec-1; mean +/- standard error of the mean) than in the 74 patients who did not develop a neurological deficit (149 +/- 5 cm sec-1) (p < 0.001, Mann-Whitney test). Peak velocity recordings can thus assist in the diagnosis of delayed ischemic neurological deficit; however, peak velocity was often recorded only after the onset of neurological deficit. When only those readings made before the onset of neurological deficit were considered, there was no significant difference in peak velocity between the groups (157 +/- 8 cm sec-1 vs. 149 +/- 5 cm sec-1, respectively). Alternative TCD parameters for predicting delayed neurological deficit were therefore sought. The rate of increase in TCD velocity, recorded during the first few days after SAH, was significantly higher in the patients who later developed a neurological deficit. A maximum velocity increase of 65 +/- 5 cm sec-1 per 24-hour period was recorded in patients who later developed a neurological deficit, compared to 47 +/- 3 cm sec-1 24 hrs-1 in patients who did not develop a delayed neurological deficit (p = 0.003). A rise of more than 50 cm sec-1 24 hrs-1 identifies those patients who are most likely to develop a delayed ischemic neurological deficit after SAH. This can be applied prospectively to individual cases. Serial TCD studies in the early period after SAH are thus of value to identify patients who can be selected for prophylactic therapy, which may prevent or ameliorate development of delayed ischemic neurological deficits.

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