Common abnormalities on neuroimaging were white matter lesions (60%) and cerebral atrophy (59%). Results: Over a nine-year period, 105 patients with TWs were included. EEG analysis included semiquantitative evaluation of TWs, background activity, and EEG reactivity. Methods: Consecutive adult encephalopathic patients with TWs on EEG and neuroimaging were included.
We hypothesized that specific EEG characteristics are predictive of outcome. The aim of this study was to determine the clinical and EEG characteristics in encephalopathic patients with TWs. Significance: In contrast to clinical, EEG and neuroimaging findings, non-reactive EEG patterns predicted death in encephalopathic patients with TWs.Ībstract = "Objective: Triphasic waves (TWs) are a frequent electroencephalography (EEG) finding in encephalopathy, yet their origin and prognostic significance are not well understood. Conclusions: These results suggest that TWs are a marker of structural brain disease coupled with toxic-metabolic perturbations, and that etiologies or underlying pathologies were not predictive for outcome while non-reactive EEG was independently associated with death. Absent EEG background reactivity and respiratory failure were independently associated with death (OR 3.73, 95%CI 1.08-12.80, p= 0.037 and OR 6.47, 95%CI 1.98-21.12, p= 0.02). Pathologic conditions included infections (56%), renal (50%) and liver insufficiency (12%), and respiratory failure (20%). When receiving oxygen insufflation, hypoxia-induced respiration failed leading to central hypopnea, acute pCO2 increase and stupor.Objective: Triphasic waves (TWs) are a frequent electroencephalography (EEG) finding in encephalopathy, yet their origin and prognostic significance are not well understood. We conclude that our patient suffered from chronic alveolar hypoventilation due to severe neuropathy which resulted in chronic moderate hypercapnia, with respiration triggered by hypoxia alone. Moreover, this case illustrates the danger of oxygen insufflation in patients with chronic alveolar hypoventilation. This case demonstrates that hypercapnia may induce acute-onset triphasic waves in the EEG which are readily reversible within minutes after assisted ventilation. Upon bag-valve-mask ventilation, the triphasic waves disappeared within 2–3 min, and the EEG showed a normal awake state prior to sedation intubation. Upon post hoc review, the EEG during the night after admission showed normal sleep patterns which were replaced by triphasic waves just about 10 min before the patient was found to be stuporous. Polysomnography revealed alveolar hypoventilation, and non-invasive assisted bilevel ventilation treatment was initiated before the patient was discharged home. After several days, the patient was extubated without any new-onset neurological deficit. Emergency bag-valve mask ventilation was started, the patient was intubated, and transferred to the intensive care unit. Blood gas analysis showed carbon dioxide partial pressure (pCO2) of 85.6 mmHg and oxygen partial pressure (pO2) of 75.6 mmHg. At a routine check, the patient was found stuporous. Oxygen insufflation was initiated by the doctor-on-call and the patient’s vigilance was repeatedly tested throughout the night. During the first evening after admission, SatO2 repeatedly dropped below 80%. At time of admission, a borderline oxygen saturation (SatO2) of around 80% was recorded, attributable to his chronic neuromuscular disease. The patient was referred to our hospital and admitted to the EEG monitoring unit for differential diagnosis of recurrent episodes of loss of consciousness. We report on a 27-year-old male with severe sensory and motor neuropathy, tetraparesis, ataxia, dysarthria, and cognitive impairment of yet unknown etiology since the age of 14 years. Here, we present a case report of acute-onset triphasic waves induced by hypercapnia.
Although typically associated with metabolic encephalopathy or post-hypoxic damage, they are unspecific in respect of the etiology of brain dysfunction. Triphasic waves are commonly seen in the EEG of patients with encephalopathy.