Therapeutic hypothermia and acute brain injury

The neuroprotective effects of therapeutic hypothermia (TH) have been recognized for decades, but these have generally failed to translate these into improved outcome in clinical studies. Here, we provide an overview of the putative mechanisms of hypothermia-induced neuroprotection, the technical considerations for the clinician wishing to use TH, and review the evidence for the clinical application of TH after acute brain injury (ABI).Although TH is increasingly used as a tool in the management of intracranial hypertension, its role in different ABI types is not yet fully established. Many questions remain regarding the logistics of cooling (including length of treatment), and how best to manage complications of therapy, particularly shivering. The only level I evidence for its benefit lies in adult cardiac arrest and neonatal hypoxic-ischaemic encephalopathy. Further high-quality studies are needed to assess the role of TH in other ABI types.     

Therapeutic hypothermia and acute brain injury

Secondary brain injury has devastating effects on morbidity, mortality and good functional outcomes. Neuroprotection is multimodal, with decades of preclinical and small clinical studies showing the benefits of therapeutic hypothermia. The basic scientific principles have merit, yet large randomized controlled trials fail to show a clear benefit. This article will review the basic science the practical aspects of delivering targeted temperature management and evaluate the evidence behind its use for acute brain injuries. With a lack of high-quality evidence for hypothermia, recent consensus statements are shifting the paradigm away from hypothermia to the maintenance of normothermia and prevention of pyrexia.     

Therapeutic hypothermia and acute brain injury

Secondary brain injury has devastating effects on morbidity, mortality and good functional outcomes. Neuroprotection is multimodal, with decades of preclinical and small clinical studies showing the benefits of therapeutic hypothermia. The basic scientific principles have merit, yet large randomized controlled trials fail to show a clear benefit. This article will review the basic science – the practical aspects of delivering targeted temperature management and evaluate the evidence behind its use for acute brain injuries. With a lack of high-quality evidence for hypothermia, recent consensus statements are shifting the paradigm away from hypothermia to the maintenance of normothermia and prevention of pyrexia.     

Therapeutic hypothermia for brain injury

Therapeutic hypothermia has an evolving role in the management of patients with brain injury. It is recognized as an integral part of post-resuscitation care following cardiac arrest and its place in managing other forms of brain injury is under ongoing investigation. This article reviews the definitions, proposed mechanisms of benefit, current clinical indications and physiological consequences of mild–moderate therapeutic hypothermia as it relates to brain injury.     

Occlusive arteriopathy and brain tumor

Four cases with the association of occlusive arteriopathy and brain tumor are presented. A clinical analysis of these cases and cases reported in the literature revealed that occlusive arteriopathy at the base of the brain was often associated with a slowly growing basal tumor in children. Possible causes of occlusive arteriopathy in these cases were compression of the circle of Willis by a slowly growing basal tumor, secondary artial occlusive changes by radiation therapy for a basal tumor, or vasculopathy associated with neurocutaneous syndrome. Symptoms of sudden onset or episodic nature suggest the presence of occlusive arteriopathy rather than the mass effect of a tumor. Cerebral angiography is mandatory whenever computerized tomography (CT), performed to rule out recurrence of a basal tumor, shows an ischemic lesion with low-density areas without any evidence of mass effect of the tumor. Cerebral angiography is also necessary when a basal tumor is suspected in children, particularly in cases associated with neurocutaneous syndrome and a basal tumor. Care should be taken not to scarify the abnormal vascular network at the base of the brain at the time of operation, because it is considered to be functioning as collateral circulation. The potential hazards of radiotherapy to radiation-induced occlusive changes of the circle of Willis must be considered in treating a benign basal brain tumor in children. Even in adults, repeated large doses of irradiation could cause occlusive arteriopathy.     

Asymptomatic brain tumor detected at brain check-up

Brain check-up was performed in 4000 healthy subjects who underwent medical and radiological examinations for possible brain diseases in our hospital from April 1996 to March 2000. Magnetic resonance imaging revealed 11 brain tumors which consisted of six meningiomas, three pituitary adenomas, one astrocytoma, and one epidermoid cyst. The detection rate of incidental brain tumor in our hospital was 0.3%. Nine patients underwent surgery, with one case of morbidity due to postoperative transient oculomotor nerve paresis. The widespread use of brain check-up may increasingly detect asymptomatic brain tumors. Surgical indications for such lesions remain unclear, and the strategy for treatment should be determined with consideration of the patient's wishes.     

Calcified metastatic brain tumor

The case of a 57-year-old woman with a calcified metastatic brain tumor, histologically confirmed to be a squamous cell carcinoma, is reported. This patient is unusual because this metastatic squamous cell carcinoma contained an extraordinary huge conglomerated calcification, that was well-defined radiographically. This case is documented with a discussion of the pathogenesis of the calcification.     

Radiation-induced cerebrovasculopathy of the distal middle cerebral artery and distal posterior cerebral artery--case report

A 15-year-old girl underwent partial removal of a pituitary adenoma followed by local irradiation of the brain with a total of 70 Gy through two lateral opposing ports. Twenty years later, she experienced frequent transient ischemic attacks with left sensory disturbance. Cerebral angiography revealed stenoses of the right distal middle cerebral artery (MCA) and the right distal posterior cerebral artery without net-like vessels. There was a severe decrease of vasoreactivity in the right hemisphere. Right superficial temporal artery (STA)-MCA anastomosis was performed. Her neurological deficits were resolved and perfusion reserve capacity had markedly improved 6 months later. We recommend STA-MCA anastomosis in such cases.     

Treatment of delayed brain injury after pituitary irradiation

Treatment for delayed brain injury after pituitary irradiation is discussed. Six cases with delayed brain injury were treated with a combination of dexamethasone or betamethasone, with heparin, glycerol, dextran 40 and some vasodilators. Two cases with temporal lobe syndrome were treated in the early stages of brain injury for a period of over 12 months were almost completely cured, another two cases with chiasma syndrome were treated in the relatively late stages, showed a partial improvement. One case which was irradiated 120 GY during 13 years did not improve. The final case treated with steroids for a short period also resulted in failure and the patient underwent an operation for the removal of the necrotic mass three years after the radiotherapy. Steroid therapy started in the early stages of brain injury after irradiation for over the 12 months is thought to be effective. Heparin therapy was also effective in one out of three cases, but in one of the cases subarachnoid hemorrhage from a traumatic aneurysm occurred during the therapy. In an acute phase, showing edematous change of the injured brain, the administration of glycerol is also thought to be useful. But the effectiveness of the other medicines containing some vasodilators was obscure or doubtful. We propose the following: (1) A meticulous observation is essential for the patients who received high doses of irradiation to diagnose brain injury in the early reversible stage. (2) Steroids should be given immediately in this reversible stage of brain injury before the irreversible "necrosis" occurs. (3) Steroids should be maintained for a long period over 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

Therapeutic effect of nimodipine on experimental brain injury

Objective: To study the therapeutic effect of nimodipine on experimental brain injury. Methods: Experimental and control rabbits were subjected to a dosed head injury. In one group nimodipinewas given intravenously and the effect evaluated by electron microscopy, brain water content, calcium levels,transcranial Doppler, and intracranial pressure monitoring. Results: In rabbits treated with nimodipine the level of neuronal cytosolic free calcium was markedly decreased.There were less cellular damage and less spasm of the middle cerebral artery seen on electron microscopy. No difference regarding intracranial pressure changes between the two groups was noted. Conclusions: Nimodipine has a protective action on brain injury by blocking a series of pathological reactions induced by neuronal calcium overload, and by reducing the spasm of brain vessels and improving cerebral blood flow.