Abstract

BACKGROUND: Selective craniocerebral hypothermia, used in the acute period of brain damage, ensures the development of positive clinical effects (rapid and persistent reduction of neurological deficit, increased consciousness, and maintenance of normothermy in feverish patients). The safety and efficacy of craniocerebral hypothermia in the acute period of cerebrovascular lesions prompted the use of craniocerebral cooling in patients with chronic disorders of consciousness. For this category of patients, the craniocerebral hypothermia technique has been developed, which requires careful study including its effect on overall metabolism.
 AIMS: To determine the nature of the metabolic response to craniocerebral hypothermia procedures in patients in a vegetative state and minimal conscious state.
 MATERIALS AND METHODS: A pilot study was conducted from February 3, 2021 until March 3, 2022. This study included 34 patients who were in a state of chronic disorders of consciousness, CRS-R score of 8 (vegetative state and minimally conscious state), after severe brain damage (stroke, 25; brain injury, 5; anoxic brain injuries, 4). Hypothermia was induced using the ATG-01 device, lowering the temperature of the scalp to 47C with a cooling procedure lasting for 120 min. The indirect calorimetry method was conducted before cooling and after 105 min of the craniocerebral hypothermia session. Statistical analysis was performed using the program StatTech v. 2.6.5 (StarTech LLC, Russia).
 RESULTS: Craniocerebral cooling provided a decrease in the temperature of the frontal cortex of the large hemispheres already after 30 min from 36.4C to 34.90.41C in the left hemisphere and 34.70.47C in the right hemisphere. By the 120th minute, the temperature in the left hemisphere reached 34.00.40C, and that in the right hemisphere reached 33.30.51C, decreasing by 2.4C and 3.1C, respectively. Subsequently, 30 min after the completion of craniocerebral hypothermia, the brain temperature remained lowered by 0.7C. Changes in the level of metabolism under the influence of craniocerebral hypothermia were of a multidirectional nature. In 24 patients (70.59%), the resting energy expenditure (REE) index increased to varying degrees by the end of the cooling procedure, and in 10 participants, it decreased. A significant spread of data allowed only a descriptive analysis of the results obtained during a 120-min craniocerebral hypothermia session.
 CONCLUSIONS: Chronic disorders of consciousness are largely associated with severe damage of the cerebral cortex. It can be assumed that in patients who reacted with a decrease in REE to the induction of hypothermia, at least metabolic activity in the intact parts of the cerebral cortex was preserved to a certain extent, which may indicate some level of rehabilitation potential. The lack of expression of the reactions of the general metabolism to craniocerebral cooling may be due to the fact that the severe damage to the cerebral cortex excluded the selectivity of hypothermic exposure.

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