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Triphasic waves in a patient with brainstem hemorrhage modified by hemispheric infarct

We recently encountered an elderly patient who developed triphasic waves (TWs) in the electroencephalography (EEG) in association with a hypertensive brainstem hemorrhage that subsequently became attenuated on the side of a major hemispheric infarct. A 74-year-old man was hospitalized in a comatose state. Examination showed mid-dilated and non-reacting pupils, absence of Doll’s eye movements and extensor plantar responses. His blood pressure was 190/ 110 mmHg. The computed tomography (CT) scan revealed a large brainstem hematoma, involving the midbrain, pons and the upper medulla (Fig. 1a). A small part of the bleed was seen extending into the thalamus on the right side. The arterial pH was 7.39, with a PaO2 of 57.9 mmHg, PaCO2 of 40 mmHg and bicarbonate of 23.7 mM/l. The patient was started on assisted ventilation, which normalized the blood gases. Measurements of serum sodium, calcium, glucose, urea, creatinine osmolality, hemocrit, platelet count, coagulation profile, bilirubin, aspartate aminotransferase, alkaline phosphatase and ammonia levels were normal. The EEG showed a background activity of 7–8 Hz, which reacted poorly to alerting and nociceptive stimuli. At times during the recording, there were trains of generalized TWs, that were bilaterally symmetrical and synchronous, and better expressed over the anterior head regions (Fig. 1b). The patient remained in a state of coma and required continued ventilatory support. Regular monitoring of the blood gases and metabolic parameters revealed normal findings. A repeat EEG still showed the TWs, which now were markedly attenuated over the left hemisphere (Fig. 2a). A repeat CT scan disclosed a fresh large infract in the left middle cerebral artery territory. The brain stem revealed large hypodense areas, corresponding to the resolution of the bleed (Fig. 2b). The patient expired. The family did not consent for autopsy. Triphasic waves have previously been documented in association with focal brainstem and diencephalic lesions. Aguglia et al. (1990) examined seven patients (two with craniopharyngioma, three with thalamic glioma and two with pontine stroke), who exhibited TWs in the absence of concomitant metabolic abnormalities. Townsend and Drury (1991) reported a patient with brainstem infarction and coma, who had TWs on the EEG. The hypertensive hemorrhage in our patient involved predominantly the pons and midbrain, and extended into the right thalamus. In the absence of any metabolic abnormalities, it may be concluded that the TWs in our patient resulted from the brainstem–dencephalic pathology. The anatomical substrate and the pathophysiological mechanism involved in the generation of TWs are obscure. Bickford and Butt (1955) postulated dysfunction of thalamocortical pathways in the genesis of TWs. Based on the neuropathological findings in a patient with TWs in association with cerebral carcinomatosis, Miller et al. (1986) concluded that TWs were the result of diffuse cortical dysfunction, rather than because of the involvement of subcortical structures. The attenuation of pre-existing TWs over the side of cerebral hemispheric damage as observed in our patient suggests that fairly functional cortex and subcortical white matter are required for the expression of TWs. Figure 2 Subsequent investigations: (a) EEG dated 2 December 2002 reveals marked attenuation of the amplitude of the triphasic waves over the left hemisphere, (b) CT dated 7 December 2002 shows a large infarct in the left middle cerebral artery territory involving the frontal, parietal and temporal lobes, insula and subcortical white matter, and resolving brainstem hemorrhage. Figure 1 Initial investigations: (a) CT dated 11 November 2002 shows hemorrhage involving pons and midbrain, and (b) EEG dated 13 November 2002 shows intermittent trains of generalized triphasic waves that are frontally dominant, symmetric and synchronous. Letters to the Editor 789