Lancet neurology
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The past decade has resulted in a rapid increase in knowledge of mechanisms underlying brain injury induced by intracerebral haemorrhage (ICH). Animal studies have suggested roles for clot-derived factors and the initial physical trauma and mass effect as a result of haemorrhage. The coagulation cascade (especially thrombin), haemoglobin breakdown products, and inflammation all play a part in ICH-induced injury and could provide new therapeutic targets. ⋯ There are conflicting data on the role of ischaemia in ICH and there is uncertainty over the role of clot removal in ICH therapy. The next decade should bring further information about the underlying mechanisms of ICH-induced brain injury and new therapeutic interventions for this severe form of stroke. This review addresses our current understanding of the mechanisms underlying ICH-induced brain injury.
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Cerebral hyperperfusion syndrome (CHS) after carotid endarterectomy is characterised by ipsilateral headache, hypertension, seizures, and focal neurological deficits. If not treated properly it can result in severe brain oedema, intracerebral or subarachnoid haemorrhage, and death. Knowledge of CHS among physicians is limited. ⋯ Treatment strategies are directed towards regulation of blood pressure and limitation of rises in cerebral perfusion. Complete recovery happens in mild cases, but disability and death can occur in more severe cases. More information about CHS and early institution of adequate treatment are of paramount importance in order to prevent these potentially severe complications.
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Low-grade gliomas (LGG) are not benign neoplasms. Patients with LGG eventually die as a consequence of this disease. ⋯ Breakthroughs in molecular biology have improved our understanding of tumours and have led to the development of novel treatments and better prognoses. Ongoing clinical trials will help to elucidate the optimum management of patients with LGG.
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The traditional view of dementia is that the features most important to accurate diagnosis and management are cognitive decline and functional disability. Behavioural and psychological symptoms have generally been thought to be of secondary importance, but new evidence suggests that these are important determinants of patients' distress, carer burden, and outcome in dementia; they can also be valuable diagnostic pointers to the underlying pathological cause and disease diagnosis. ⋯ Although pharmacological management is a commonly used option, it is often limited in its effects and can be associated with a substantial risk of side-effects. Progress in understanding the pathophysiological mechanisms underpinning behavioural and psychological symptoms in dementia will assist in developing more effective treatment approaches.
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Dementia is one of the major causes of dependency after stroke. The prevalence of poststroke dementia (PSD)-defined as any dementia occurring after stroke-is likely to increase in the future. In community-based studies, the prevalence of PSD in stroke survivors is about 30% and the incidence of new onset dementia after stroke increases from 7% after 1 year 48% after 25 years. ⋯ In developed countries, the proportion of patients with presumed Alzheimer's disease among those with PSD is between 19% and 61%. Patients with PSD have high mortality rates and are likely to be functionally impaired. These patients should be treated according to the current guidelines for stroke prevention.