Targeted application of hypothermia may provide neuroprotective benefits in the hours after a Concussion or mTBI.
Upon further validation, selective brain cooling could be a potential clinical tool in the minimization of symptoms and pathological changes after concussion.
Selective brain cooling applied post-trauma and craniectomy improved neurological function and reduced structural damage and may be therefore an alternative to complication-burdened systemic hypothermia.
Induced hypothermia (IH) continues to become a more prevalent treatment modality in neurocritical care. Reducing core temperature has been shown to protect brain tissue during injury and disease.
Therapeutic hypothermia is reported to be effective at lowering intracranial pressure; however, its efficacy in improving neurological outcome is not fully demonstrated. This review suggests that therapeutic hypothermia had increased benefits in patients with haematoma-type injuries as opposed to those with diffuse injury and contusions. It also suggests that cooling should recommence if rebound intracranial hypertension is observed.
Conclusively, TTM (Targeted Temperature Management) is still in the center of neuroprotective treatments in TBI. This therapy is expected to mitigate ischemic and reperfusional pathophysiology and to reduce intracranial pressure in TBI.
…results suggest that posttraumatic hypothermia is an effective method to prevent dendrite degeneration and spine loss and preserve learning and memory function after severe TBI.
Mild to moderate hypothermia reduces the intracranial pressure (ICP). Randomized control trials for short-term hypothermia indicate no benefit in outcome after severe TBI, whereas longer-term hypothermia could be of benefit by reducing ICP.
Promoting the long-term survival of newborn cells during neurogenesis is a compelling goal for the treatment of TBI… These results suggest that MHT-mediated neurogenesis may have an important therapeutic potential for the endogenous repair of TBI.
This work demonstrates the feasibility of using a non-invasive method to induce brain hypothermia using a portable collar. This device demonstrated an optimal safety profile and represents a potentially useful method for the administration of mild hypothermia and temperature control (i.e., treatment of hyperpyrexia) in cardiac arrest and critically ill neurologic patients.
The use of mild hypothermia and/or targeted temperature management has revolutionized neonatal neurocritical care, impacted the neurocritical care of comatose adults after cardiac arrest, and the care of patients with a variety of other acute neurological insults such as severe TBI, stroke, spinal cord injury and subarachnoid hemorrhage. If temperature control is important to mTBI and concussion, it could have a substantial impact on mTBI outcomes, and in a very high risk group for the occurrence of multiple concussions. This seminal work throws down the gauntlet on an important area of future investigation and one very worthy of answers as we capitalize on the golden age of TBI research.
…brain temperature is an important variable for mTBI outcome and that mildly elevated temperatures at the time of injury result in persistent cognitive deficits. Importantly, cooling to normothermia after mTBI prevents the development of long-term cognitive deficits caused by hyperthermia. Reducing temperature to normothermic levels soon after mTBI represents a rational approach to potentially mitigate the long-term consequences of mTBI.
Emerging research on the long-term impact of concussions on athletes has allowed public recognition of the potentially devastating effects of these and other mild head injuries. Mild traumatic brain injury (mTBI) is a multifaceted disease for which management remains a clinical challenge. Recent pre-clinical and clinical data strongly suggest a destructive synergism between brain temperature elevation and mTBI; conversely, brain hypothermia, with its broader, pleiotropic effects, represents the most potent neuro-protectant in laboratory studies to date. Although well-established in selected clinical conditions, a systemic approach to accomplish regional hypothermia has failed to yield an effective treatment strategy in traumatic brain injury (TBI). Furthermore, although systemic hypothermia remains a potentially valid treatment strategy for moderate to severe TBIs, it is neither practical nor safe for mTBIs. Therefore, selective head-neck cooling may represent an ideal strategy to provide therapeutic benefits to the brain.
Collectively, these findings indicate that even mild hypothermia or the blunting free radical damage, even when performed in a delayed period, is protective in repetitive mTBI. In sum, the present study continues to confirm the damaging consequences of repetitive brain injury while suggesting that some of its damaging consequences can be targeted with relatively innocuous therapeutic approaches that include mild hypothermia.
Brain temperature management was performed mainly in young patients, and the outcome on discharge was favorable in patients who received brain temperature management. Particularly, patients who need craniotomy for removal of hematoma were a good indication of therapeutic hypothermia. Improvement of therapeutic outcomes with widespread temperature management in TBI patients is expected
Appropriate thermoregulation of the brain for individual patients with various types of TBI are important.
For severe traumatic brain injury (TBI) patients, no effective treatment method replacing hypothermia therapy has emerged, and hypothermia therapy still plays the major role. To increase its efficacy, first, early introduction is important.
Sport-related concussions are heterogeneous and require an individualized clinical approach.
Together, these data suggest that local hypothermia is an effective treatment for edema formation and BBB disruption via the upregulation of TJ proteins and the suppression of TNF-α and IL-1β.
Candidate therapies selected for research include drugs that are aimed at reducing the acute and delayed effects of the traumatic incident, stem cell therapies aimed at brain repair, and selective brain cooling to stabilize cerebral metabolism. Each of these efforts can also focus on combination therapies targeting multiple mechanisms of neuronal injury.
In conclusion, hypothermia induced early may reduce neuronal cell damage in the reperfusion injury, which was induced after ASDH removal.
Following repetitive injury, cerebral vascular reactivity was dramatically preserved by either therapeutic intervention or the combination thereof compared to control group in which no intervention was employed. Similarly, APP density was significantly lower in the therapeutic intervention group compared in controls. Although the individual use of FK506 or hypothermia exerted significant protection, no additive benefit was found when both therapies were combined. In sum, the current study demonstrates that the exacerbated pathophysiological changes associated with repetitive mTBI can be therapeutically targeted.
Therapeutic hypothermia may protect the injured central nervous system by targeting the detrimental consequences of the innate immune response to injury.
Cooling can reduce primary injury and prevent secondary injury to the brain after insults in certain clinical settings and in animal models of brain insult. The mechanisms that underlie the protective effects of cooling – also known as therapeutic hypothermia – are slowly beginning to be understood.Hypothermia influences multiple aspects of brain physiology in the acute, subacute and chronic stages of ischaemia. It affects pathways leading to excitotoxicity, apoptosis, inflammation and free radical production, as well as blood flow, metabolism and blood-brain barrier integrity. Hypothermiamay also influence neurogenesis, gliogenesis and angiogenesis after injury. It is likely that no single factor can explain the neuroprotection provided by hypothermia, but understanding its myriad effects may shed light on important neuroprotective mechanisms.
These neuropathological results demonstrate that relatively mild elevations in temperature associated with peri-traumatic events may affect the long-term functional consequences of mTBI. Because individuals exhibiting mildly elevated core temperatures may be predisposed to aggravated brain damage after mTBI or concussion, precautions should be introduced to target this important physiological variable.
Mild hypothermia therapy with whole-body cooling had a greater effect on the suppression of free radical production than selective head cooling. However, selective head cooling might be an appropriate indication for patients with circulatory instability after resuscitation, because it provides neuroprotection similar to that of whole-body cooling.
The review indicated that therapy should be conducted for at least 24 hours, with temperatures ranging between 32° and 33°C and a rewarming period of < 24 hours.
… authors of prior studies have determined that hypothermic interventions following longer delays are less efficacious.
…prolonged treatment with hypothermia (12-48 hours) showed longer lasting neuroprotective benefits than shorter periods of therapy.
Our pilot study demonstrated that the cooling head cover was effective in rapidly achieving brain cooling and establishing a favorable brain-to-body temperature gradient. Our overall goal is to significantly improve the outcome of brain injured military personnel by rapidly inducing moderate cerebral (28-32°C) hypothermia but mild systemic (32-35°C) hypothermia to maximize the neuro-protective potentials yet minimize the systemic hypothermia induced complications.
These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit.
Treatment with the cooling device was well tolerated by all participants. The technique had measurable effects on core body temperature (rectal) and tympanic temperature (may reflect temperature at the external ear and skin rather than intracranial). It can be considered as a simple therapeutic approach to patients with suspected stroke in the prehospital setting.
These results indicate that 34°C SBC is effective in protecting against acute brain damage and related neurological dysfunction.
Therapeutic hypothermia may improve functional outcome by attenuating trauma-induced oligodendrocyte cell death, subsequent demyelination, and circuit dysfunction.
the best available evidence to date supports the use of early prophylactic mild-to-moderate hypothermia in patients with severe TBI (Glasgow Coma Scale score < or = 8) to decrease mortality and improve rates of good neurologic recovery. This treatment should be commenced as soon as possible after injury (e.g., in the emergency department after computed tomography) regardless of initial ICP, or before ICP is measured.
These results indicate that moderate brain injury produces temperature-sensitive acute, as well as more long-lasting vascular perturbations associated with secondary injury mechanisms.
Convective head cooling reduced MRS brain temperature and core brain was cooled.
In conclusion, the noninvasive SBC described here is a safe method of administering therapeutic hypothermia, which can reduce ICP and improve prognosis without severe complications in patients with severe TBI.
helmet delivers initial rapid and selective brain cooling and maintains a significant temperature gradient between the core and brain temperatures throughout the hypothermic period to provide sufficient regional hypothermia yet minimize systemic complications.
The present data demonstrate that moderate postinjury brain hypothermia can provide protection from sensorimotor and cognitive behavioral deficits as well as neuropathology in a model of traumatic brain injury associated with early neuronal and microvascular injury.
Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons
…craniocerebral hypothermia should be employed in skull-brain injury patients as soon as the presence of a space-occupying intracranial formation requiring a surgical intervention is excluded, or immediately thereafter. The reduction of cerebral metabolism during the colling can be indirectly demonstrated by EEG changes and evoked potentials recordings.