BACKGROUND: Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS. METHODS: We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm. RESULTS: Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients. CONCLUSIONS: We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.
BACKGROUND: Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS. METHODS: We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm. RESULTS: Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients. CONCLUSIONS: We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.