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To the Editor: We would like to correct an error in the article on the reliability of the NINDS Myotatic Reflex Scale.1 On page 971 of the article, the authors cite our study on …

Sudden loss of consciousness and cardiorespiratory disorders occurred in 43 of 254 patients with subarachnoid hemorrhage. Two patients had ventricular fibrillation, 37 had one or more episodes with a disturbance of respiratory rhythm that required assisted ventilation, and 4 died suddenly without recorded vital signs. Sixteen patients recovered after resuscitation. The outcome could not be predicted at an early stage from the anatomic type of hemorrhage on CT, the initial presence or absence of brainstem reflexes, or the type of cardiorespiratory disorder. Spontaneous respiration and responsiveness returned within 1 hour in all patients who recovered.

We used decision analysis to approach the dilemma “surgery or not?” in patients with incidental intracranial saccular aneurysms. To decide if a patient should undergo surgery, the following factors are of primary importance: age and general health of the patient, chance of rupture of the aneurysm, surgical mortality and morbidity, and patient preference for immediate and long-term risks. In a fictitious patient (a woman of 45 with migraine, otherwise healthy), surgery was the option with the greatest expected utility. Sensitivity analysis showed the influence of different factors. Other patients are also discussed, and “break-even” points for age versus surgical results are given.

Fifty-seven of 176 prospectively studied patients with aneurysmal subarachnoid hemorrhage (SAH) developed delayed cerebral ischemia. Clinical features included hemispheric focal signs (13), decrease in level of consciousness (14), or both (30), and mutism (15). Forty-seven patients showed hypodense lesions on CT in one (19) or multiple vascular territories (22), or diffusely in one or both hemispheres (6). Twenty-eight had symmetric decrease in ventricular size. Of 18 autopsied patients, only 1 had a purely univascular lesion. The clinical, CT, and pathologic features suggest that delayed cerebral ischemia after SAH is a multivascular or diffuse process in most patients.