John B. Selhorst

Improved confidence of outcome prediction in severe head injury A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure

An analysis of clinical signs, singly or in combination, multimodality evoked potentials (MEPs), computerized tomography scans, and intracranial pressure (ICP) data was undertaken prospectively in 133 severely head-injured patients to ascertain the accuracy, reliability, and relative value of these indicants individually, or in various combinations, in predicting one of two categories of outcome. Erroneous predictions, either falsely optimistic (FO) or falsely pessimistic (FP), were analyzed to gain pathophysiological insights into the disease process. Falsely optimistic predictions occurred because of unpredictable complications, whereas FP predictions were due to intrinsic weakness of the indicants as prognosticators. A combination of clinical data, including age, Glasgow Coma Scale (GCS) score, pupillary response, presence of surgical mass lesions, extraocular motility, and motor posturing predicted outcome with 82% accuracy, 43% with over 90% confidence. Nine percent of predictions were FO and 9% FP. The GCS score alone was accurate in 80% of predictions, but at a lower level of confidence (25% at the over-90% level), with 7% FO and 13% FP. Computerized tomography and ICP data in isolation proved to be poor prognostic indicants. When combined individually with clinical data, however, they increased the number of predictions made with over 90% confidence to 52% and 55%, respectively. Data from MEPs represented the most accurate single prognostic indicant, with 91% correct predictions, 25% at the over-90% confidence level. There were no FP errors associated with this indicant. Supplementation of the clinical examination with MEP data yielded optimal prognostic power, an 89% accuracy rate, with 64% over the 90% confidence level and only 4% FP errors. The clinical examination remains the strongest basis for prognosticating outcome in severe head injury, but additional studies enhance the reliability of such predictions.

Papilledema after acute head injury.

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.

Sarcoid optic neuropathy

Three patients presented with unilateral progressive optic neuropathy. None of these patients had signs or symptoms referable to the chiasm or eye, thus confining their decline in vision to the optic nerve. Clinical and neuroradiographic evidence suggested a meningioma involving the optic nerve at the orbital-canalicular junction in one patient and the intracranial optic nerve in another patient. Surgical exploration in both patients, however, revealed a noncaseating granuloma. Decline in vision from granulomatous invasion of the retrobulbar optic nerve is an uncommon manifestation of sarcoidosis. Review of our patients findings suggests that a nonsurgical diagnosis of sarcoid optic neuropathy may have been tenable.

Anterior Ischemic Optic Neuropathy with Internal Carotid Artery Occlusion

We examined three patients who had anterior ischemic optic neuropathy and ipsilateral internal carotid artery occlusion. Each patient had transient cerebral ischemic attacks associated with the occluded carotid artery. In two patients there attacks were in temporal proximity to the anterior ischemic optic neuropathy. Carotid angiography showed retrograde filling of the ophthalmic artery through the external carotid artery demonstrating altered perfusion and, perhaps, hypoperfusion of the distal optic nerve head.

Ventriculostomy for hydrocephalus in cerebellar hemorrhage.

In a matter of hours the neurologic status of two hypertensive patients deteriorated to coma. Cranial computed tomography (CT) showed mild to moderate cerebellar hemorrhage and secondary hydrocephalus. Ventriculostomy resulted in clinical improvement within 20 minutes and obviated the need for suboccipital craniectomy. Both patients made a very satisfactory recovery. Similar patients have occasionally been observed by others. Ventriculostomy should be considered for patients with cerebellar hemorrhage who have hydrocephalus by CT scan and undergo progressive neurologic deterioration. Because the frequency of improvement and the risk of upward cerebellar herniation following ventriculostomy is unknown, immediate surgical evacuation of the hemorrhage should be anticipated.

Retinopathy after tilorone hydrochloride.

Two patients, a 34-year-old woman and a 50-year-old woman, received tilorone HCl, an experimental antitumor drug. After taking the drug orally (total dose, 152 g), the first patient developed corneal subepithelial infiltrates and toxic retinopathy characterized by fine pigment mottling of the peripheral fundus and macula with mild arteriolar narrowing. Although visual acuity was 6/6 (20/20) throughout treatment, Goldmann perimetry showed marked peripheral constriction of the visual fields and results of an electroretinogram and an electro-oculogram were abnormal. After taking the drug orally (total dose, 189 g), the second patient developed corneal subepithelial infiltrates, severe bilateral arteriolar narrowing, and mild pigment mottling of the macula. ERG and EOG were moderately attenuated. Visual fields by Goldman perimetry were within normal limits. Tilorone HCl, like chloroquine, may be an antioxidant that affects the free radical scavenging mechanism of the retinal pigment epithelium. Extensive testing should be done on all patients taking tilorone HCl in order to detect the initial manifestations of retinopathy.