Dean S. Karnaze

Triphasic waves: a reassessment of their significance.

Electroencephalograms and case histories of 50 patients with triphasic waves were reviewed. EEGs were studied for slowed dominant activity, anteriorly dominant triphasic waves, anterior-posterior lag time and bursts of triphasic waves. Etiologies of triphasic waves were: hepatic (28), azotemia (10), anoxia (10) and hyperosmolarity (2). Sixteen hepatic and two azotemic patients showed all of these characteristic EEG features. Triphasic waves demonstrating all of these features are highly characteristic of but are not pathognomonic for hepatic encephalopathy. Prognosis correlated best with the type of hepatic injury and deteriorating renal function. We postulate that triphasic waves are generated by the same thalamocortical volleys which normally induce spindles.

EEG monitoring of clinical coma The compressed spectral array

Twenty-four comatose patients were studied by 16-hour compressed spectral array (CSA), made from four-channel portable EEG recordings. Causes of coma included head injury (15), anoxia (6), and brainstem strokes (3). CSA was classified on the basis of frequency and alternating or nonalternating patterns. Alternating CSA was significantly associated with survival (p < 0.005) in the head-injured and anoxic group combined, and in the head-injured subgroup (p < 0.013). The prognostic value of CSA equaled the Glasgow Coma Scale or neurologic examination and occasionally added prognostic information.

Auditory evoked potentials in coma after closed head injury A clinical‐neurophysiologic coma scale for predicting outcome

We studied auditory evoked potentials in 45 head-injured patients. All but three were comatose or stuporous at the time of study. Preservation of brainstem auditory or long-latency auditory evoked potentials predicted good outcome. The Glasgow coma scale (GCS), the clinical subtotal of the neurophysiologic coma scale (NPCS), and the NPCS had predictive accuracies of 71%, 82%, and 82%. Although there were 22 falsely pessimistic predictions with the GCS and 9% with the clinical subtotal of the NPCS, there were no falsely pessimistic predictions with the NPCS.

Assessment of median nerve somatosensory evoked potentials in cerebral ischemia.

Seventy patients with cerebral ischemia (21 with transient ischemic attack and 49 with stroke) were studied with short-latency median nerve somatosensory evoked potentials to characterize the evoked potentials in all ischemic patients and to investigate their efficacy for prognosis in stroke. Within 72 hours of symptom onset, all 70 patients received a scaled neurologic function score, with a maximum of 50 points. Somatosensory evoked potential abnormalities were found in 10% (2/19), 42% (15/36), and 93% (14/15) of all patients with initial neurologic examinations who had normal (50 points), mild-moderate (30-49 points), and severe deficits (less than or equal to 29 points), respectively. Thirty-seven of the 49 stroke patients were available for a follow-up neurologic assessment. Eight-nine percent (8/9) of the stroke patients with poor outcome had somatosensory evoked potential abnormalities; 82% (9/11) of the stroke patients with severe neurologic deficits at onset had poor outcome. Results demonstrate that somatosensory evoked potential abnormalities are common in patients with cerebral ischemia but that somatosensory evoked potential findings are not significantly better than a detailed neurologic examination in predicting outcome from stroke.

Abnormal visual evoked potentials in myotonic dystrophy

Pattern-shift visual evoked potentials (VEPs) were recorded in 17 patients with myotonic dystrophy. Abnormalities of latency or amplitude were found in 10 patients (59%) with no obvious retinal or other significant ocular abnormality. All patients had a visual acuity of 20/30 or better. Since most patients had bilateral VEP abnormalities, localization of the disturbance was not certain.

Short-latency somatosensory evoked potentials correlate with the severity of the neurological deficit and sensory abnormalities following cerebral ischemia

Short-latency somatosensory evoked potentials (SSEPs) were studied in 49 patients who had suffered hemispheric or thalamic ischemia, including 6 patients with transient ischemic attacks (TIAs) and 3 patients with reversible ischemic neurological deficits (RINDs). SSEPs were abnormal in 30 patients (61%). SSEP abnormalities correlated with the presence of sensory deficit and the degree of neurological deficit. SSEPs were normal following TIA but were abnormal in 2 of 3 patients with RINDs. SSEPs were abnormal in some patients without sensory deficits suggesting that sensory pathways may be affected when clinically inapparent.

Short-latency somatosensory evoked potentials in myotonic dystrophy: Evidence for a conduction disturbance

Short-latency somatosensory evoked potentials were recorded in 13 patients with myotonic dystrophy (MyD). The MyD were compared with age-matched controls. The mean conduction latency between the brachial plexus and dorsal column nuclei (EP-N14) was significantly longer for the MyD. Results suggest an afferent conduction disturbance in MyD.