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IN26-TU-02 Hyperbaric oxygen treatment (HBOT) in neurology
S22
19th World Congress of Neurology, Invited Abstracts / Journal of the Neurological Sciences 285 S1 (2009) S5–S56
IN26-TU-02 Hyperbaric oxygen treatment (HBOT) in neurology
IN27 – Stroke 6: what is hot in stroke?
M.G. Grønning. Dep. of Neurology and Dep. of Occup Med, Haukeland University Hospital, Bergen, Norway
IN27-TU-01 Risk and predicting factors concentrating on modifiable factors
During hyperbaric oxygen treatment (HBOT) patients breathe pure oxygen at pressures greater than 1 atmosphere absolute (ATA) in a specially designed pressure chamber, most commonly at pressures of 2–2.5 ATA. In this way the partial pressure of oxygen and oxygen supply to tissues increase. Oxygen at high pressure has bacteriostatic effects and direct effects on inflammatory processes and angiogenesis. In this way the healing of some ischemic and inflammatory processes is enhanced. The side effects are rare, but HBOT is associated with the risk of barotrauma of the ears, sinuses and lungs, temporary myopia, and toxic effects of oxygen on the lung and CNS. HBOT is internationally accepted as treatment for decompression sickness (DCS) and arterial gas embolism (AGE) which are caused by free gas or “bubbles”. The two entities have different pathogenesis but are clinically difficult to distinguish. The central nervous system and the musculoskeletal system are most often involved, and the symptoms vary from very mild to paralysis and death. According to Divers Alert Network more than 85% of the patiens with DCI have neurologic symptoms and/or pain. Recompression and HBOT enhance the diffusion of inert gas out of any bubbles and reduce the bubble volume. The prognosis is often favourable, although around 50% have some residual symptoms. HBOT has also been considered as adjunctive therapy for the treatment of other neurologic disorders like ischaemic stroke, traumatic brain injury, migraine, cluster headache, cerebral palsy and multiple sclerosis, in which ischemia, deranged vasoregulation and inflammmatory processes are involved. However, the clinical trials are charactericed by diverging methodology, outcome variables and follow-up time, and there is only a very few doubleblinded studies. The clinical trials have so far given little evidence of positive effects of HBOT in these disorders.
Y. Shinohara. Department of Internal Medicine and Neurology, Federation of National Public Service Personnel Mutual Aid Associations, Tachikawa Hospital, Tokyo, Japan
IN26-TU-03 Hypothermia and the Cerebral Circulation J.K.J. Rhodes. Anaesthesia, Critical Care and Pain Medicine, University of Edinburgh, Edinburgh, United Kingdom Hypothermia has profound effects on the brain function but importantly is potentially protective against both focal and global injuries. Aspects of the biochemical response to acute ischaemia and trauma, which are associated with poor outcome, can be inhibited by cooling. Unlike many pharmacological treatments which tend to antagonise a single neurochemical process, hypothermia offers a simple method of inhibiting multiple pathological processes simultaneously. It therefore has the potential, if applied correctly, to improve outcomes after acute brain injuries, were drug trials have so far failed. The systemic cooling of patients after acute brain injury is an established treatment modality in many neuro-intensive care units. It is a strategy for protecting the injured brain that makes intuitive sense and can reduce both intracranial pressure and the potential for ischaemic secondary insults. Basic science evidence also suggests that cooling can attenuate many secondary biochemical cascades that are activated after acute injury. However, despite these multiple lines of supportive evidence there is as yet no confirmation from a high quality randomised controlled trial (RCT) that prophylactic hypothermia improves outcome or reduces mortality. This talk will look at the potentially beneficial effects of hypothermia on the biochemistry of acute brain injury, consider the reasons for the failure to demonstrate clinical efficacy and review the supportive data from meta-analysis, suggesting how hypothermia might be best delivered. Finally I will introduce EuroTherm 3235, a European Society of Intensive Care Medicine funded multicentre RTC investigating prophylactic hypothermia in (traumatic brain injury), which draws on the lessons from the available literature.
Together with neuroimaging, endovascular treatment and so on, modification of risk factors and management of predicting factors for stroke are currently very hot areas. Control of hypertension is effective for primary and secondary prevention of stroke. Nowadays, the focus is on the optimum level of target blood pressure and the selection of appropriate antihypertensives, depending on age, complications etc. Regarding dyslipidemia, the MEGA study revealed that the combination of low-dose statin (pravastatin) with dietary control is effective for primary prevention of coronary heart disease and cerebral infarction compared with dietary control alone. Very-highdose statin (SPARCL using atorvastatin) is effective for preventing recurrence of stroke. Further, JELIS subgroup analysis showed that the combination of low-dose statin (pravastatin 10 mg or simvastatin 5 mg) with EPA is effective for secondary prevention of stroke. Regarding anti-diabetics, the PROactive study showed that pioglitazone is effective for secondary, but not primary, prevention of stroke. Therefore, aggressive treatment with pioglitazone together with antiplatelets may be recommended. Stopping smoking and heavy drinking, and detection and management of atrial fibrillation are also important for stroke prevention, as are early detection and management of predicting factors such as asymptomatic cerebral infarction, silent carotid stenosis, chronic kidney disease and so on. In Japan, we have a unique brain check-up system nicknamed brain dock. Among more than 3000 “normative persons” (mean age 55 years old) examined in brain dock, almost 25% showed abnormalities on MRI, MRA, or carotid sonography. During 3-year follow-up, subjects in whom carotid stenosis or silent cerebral infarction was detected developed ischemic stroke or hemorrhagic stroke significantly more frequently than did subjects in whom they were not detected. IN27-TU-02 What progress have we made in acute stroke treatment? W. Hacke. Universitaetsklinikum Heidelberg, Direktor der Neurologischen Klinik, Heidelberg, Germany IN27-TU-03 TIA revisited P.M. Rothwell. Department of Clinical Neurology, University of Oxford, Oxford, United Kingdom About 20–30% of stroke patients report a preceding TIA or minor stroke. These “warning” events provide an opportunity for prevention, but the time window is short – nearly half of all prior TIAs occur within 7 days of the stroke – and cohort studies report stroke risks of 5–10% during the 7days after a TIA. If these early recurrent strokes could be prevented, then urgent investigation and treatment would be justified. Not all patients with suspected TIA need to be seen urgently – many genuine TIAs have a low early risk of stroke and validated scores (ABCD system) are now available to identify high and low risk cases. Several treatments are effective long-term secondary prevention after TIA and ischaemic stroke, including antiplatelet agents, blood pressure lowering drugs, statins, anticoagulation for atrial fibrillation, and endarterectomy for ≥50% symptomatic carotid stenosis. Use of all of these interventions in appropriate patients would be predicted to reduce the long-term group risk of recurrent stroke by 80–90%. Given the likelihood that at least some of this benefit would also be seen with urgent
19th World Congress of Neurology, Invited Abstracts / Journal of the Neurological Sciences 285 S1 (2009) S5–S56
IN26-TU-02 Hyperbaric oxygen treatment (HBOT) in neurology
IN27 – Stroke 6: what is hot in stroke?
M.G. Grønning. Dep. of Neurology and Dep. of Occup Med, Haukeland University Hospital, Bergen, Norway
IN27-TU-01 Risk and predicting factors concentrating on modifiable factors
During hyperbaric oxygen treatment (HBOT) patients breathe pure oxygen at pressures greater than 1 atmosphere absolute (ATA) in a specially designed pressure chamber, most commonly at pressures of 2–2.5 ATA. In this way the partial pressure of oxygen and oxygen supply to tissues increase. Oxygen at high pressure has bacteriostatic effects and direct effects on inflammatory processes and angiogenesis. In this way the healing of some ischemic and inflammatory processes is enhanced. The side effects are rare, but HBOT is associated with the risk of barotrauma of the ears, sinuses and lungs, temporary myopia, and toxic effects of oxygen on the lung and CNS. HBOT is internationally accepted as treatment for decompression sickness (DCS) and arterial gas embolism (AGE) which are caused by free gas or “bubbles”. The two entities have different pathogenesis but are clinically difficult to distinguish. The central nervous system and the musculoskeletal system are most often involved, and the symptoms vary from very mild to paralysis and death. According to Divers Alert Network more than 85% of the patiens with DCI have neurologic symptoms and/or pain. Recompression and HBOT enhance the diffusion of inert gas out of any bubbles and reduce the bubble volume. The prognosis is often favourable, although around 50% have some residual symptoms. HBOT has also been considered as adjunctive therapy for the treatment of other neurologic disorders like ischaemic stroke, traumatic brain injury, migraine, cluster headache, cerebral palsy and multiple sclerosis, in which ischemia, deranged vasoregulation and inflammmatory processes are involved. However, the clinical trials are charactericed by diverging methodology, outcome variables and follow-up time, and there is only a very few doubleblinded studies. The clinical trials have so far given little evidence of positive effects of HBOT in these disorders.
Y. Shinohara. Department of Internal Medicine and Neurology, Federation of National Public Service Personnel Mutual Aid Associations, Tachikawa Hospital, Tokyo, Japan
IN26-TU-03 Hypothermia and the Cerebral Circulation J.K.J. Rhodes. Anaesthesia, Critical Care and Pain Medicine, University of Edinburgh, Edinburgh, United Kingdom Hypothermia has profound effects on the brain function but importantly is potentially protective against both focal and global injuries. Aspects of the biochemical response to acute ischaemia and trauma, which are associated with poor outcome, can be inhibited by cooling. Unlike many pharmacological treatments which tend to antagonise a single neurochemical process, hypothermia offers a simple method of inhibiting multiple pathological processes simultaneously. It therefore has the potential, if applied correctly, to improve outcomes after acute brain injuries, were drug trials have so far failed. The systemic cooling of patients after acute brain injury is an established treatment modality in many neuro-intensive care units. It is a strategy for protecting the injured brain that makes intuitive sense and can reduce both intracranial pressure and the potential for ischaemic secondary insults. Basic science evidence also suggests that cooling can attenuate many secondary biochemical cascades that are activated after acute injury. However, despite these multiple lines of supportive evidence there is as yet no confirmation from a high quality randomised controlled trial (RCT) that prophylactic hypothermia improves outcome or reduces mortality. This talk will look at the potentially beneficial effects of hypothermia on the biochemistry of acute brain injury, consider the reasons for the failure to demonstrate clinical efficacy and review the supportive data from meta-analysis, suggesting how hypothermia might be best delivered. Finally I will introduce EuroTherm 3235, a European Society of Intensive Care Medicine funded multicentre RTC investigating prophylactic hypothermia in (traumatic brain injury), which draws on the lessons from the available literature.
Together with neuroimaging, endovascular treatment and so on, modification of risk factors and management of predicting factors for stroke are currently very hot areas. Control of hypertension is effective for primary and secondary prevention of stroke. Nowadays, the focus is on the optimum level of target blood pressure and the selection of appropriate antihypertensives, depending on age, complications etc. Regarding dyslipidemia, the MEGA study revealed that the combination of low-dose statin (pravastatin) with dietary control is effective for primary prevention of coronary heart disease and cerebral infarction compared with dietary control alone. Very-highdose statin (SPARCL using atorvastatin) is effective for preventing recurrence of stroke. Further, JELIS subgroup analysis showed that the combination of low-dose statin (pravastatin 10 mg or simvastatin 5 mg) with EPA is effective for secondary prevention of stroke. Regarding anti-diabetics, the PROactive study showed that pioglitazone is effective for secondary, but not primary, prevention of stroke. Therefore, aggressive treatment with pioglitazone together with antiplatelets may be recommended. Stopping smoking and heavy drinking, and detection and management of atrial fibrillation are also important for stroke prevention, as are early detection and management of predicting factors such as asymptomatic cerebral infarction, silent carotid stenosis, chronic kidney disease and so on. In Japan, we have a unique brain check-up system nicknamed brain dock. Among more than 3000 “normative persons” (mean age 55 years old) examined in brain dock, almost 25% showed abnormalities on MRI, MRA, or carotid sonography. During 3-year follow-up, subjects in whom carotid stenosis or silent cerebral infarction was detected developed ischemic stroke or hemorrhagic stroke significantly more frequently than did subjects in whom they were not detected. IN27-TU-02 What progress have we made in acute stroke treatment? W. Hacke. Universitaetsklinikum Heidelberg, Direktor der Neurologischen Klinik, Heidelberg, Germany IN27-TU-03 TIA revisited P.M. Rothwell. Department of Clinical Neurology, University of Oxford, Oxford, United Kingdom About 20–30% of stroke patients report a preceding TIA or minor stroke. These “warning” events provide an opportunity for prevention, but the time window is short – nearly half of all prior TIAs occur within 7 days of the stroke – and cohort studies report stroke risks of 5–10% during the 7days after a TIA. If these early recurrent strokes could be prevented, then urgent investigation and treatment would be justified. Not all patients with suspected TIA need to be seen urgently – many genuine TIAs have a low early risk of stroke and validated scores (ABCD system) are now available to identify high and low risk cases. Several treatments are effective long-term secondary prevention after TIA and ischaemic stroke, including antiplatelet agents, blood pressure lowering drugs, statins, anticoagulation for atrial fibrillation, and endarterectomy for ≥50% symptomatic carotid stenosis. Use of all of these interventions in appropriate patients would be predicted to reduce the long-term group risk of recurrent stroke by 80–90%. Given the likelihood that at least some of this benefit would also be seen with urgent