Ischemic stroke, resulting from insufficient blood supply to the brain, is among the leading causes of death and disability worldwide. A potentially severe complication of the disease itself or its treatment aiming to restore optimal blood flow is hemorrhagic transformation (HT) increasing morbidity and mortality. Detailed summaries can be found in the literature on the pathophysiological background of hemorrhagic transformation, the potential clinical risk factors increasing its chance, and the different biomarkers expected to help in its prediction and clinical outcome. Clinicopathological studies also contribute to the improvement in our knowledge of hemorrhagic transformation. We summarized the clinical risk factors of the hemorrhagic transformation of ischemic strokes in terms of risk reduction and collected the most promising biomarkers in the field. Also, auxiliary treatment options in reperfusion therapies have been reviewed and collected. We highlighted that the optimal timing of revascularization treatment for carefully selected patients and the individualized management of underlying diseases and comorbidities are pivotal. Another important conclusion is that a more intense clinical follow-up including serial cranial CTs for selected patients can be recommended, as clinicopathological investigations have shown HT to be much more common than clinically suspected.

The signs and symptoms of acute alcohol intoxication resemble those of vertebrobasilar stroke. Due to their shared symptoms including double vision, nystagmus, dysarthria, and ataxia, the differential diagnosis of alcohol intoxication and vertebrobasilar stroke may pose a challenge. Moreover, if alcohol intoxication and stroke occur simultaneously, the signs and symptoms of stroke may be attributed to the effects of alcohol, leading to delayed stroke diagnosis and failure to perform reperfusion therapy. Three cases of alcohol intoxication and stroke are presented. The first patient (female, 50 years old) had dysarthria, nystagmus and trunk ataxia on admission. Her blood alcohol level was 2.3‰. The symptoms improved after forced diuresis, but 5.5 h later progression was observed, and the patient developed diplopia and dysphagia in addition to her initial symptoms. Angiography showed occlusion of the basilar artery. Intraarterial thrombolysis was performed. The second patient (male, 62 years old) developed diplopia, dysarthria and trunk ataxia after consuming 4-units of alcohol, and his symptoms were attributed to alcohol intoxication. Two hours later, neurological examination revealed dysphagia and mild right-sided hemiparesis, which questioned the causal relationship between the symptoms and alcohol consumption. Cerebral CT was negative, and intravenous thrombolysis was administered. The third patient (male, 55 years old) consumed 10 units of alcohol before falling asleep. Three hours later, his relatives tried to wake him up. He was unresponsive, which was attributed to alcohol intoxication. When he woke up 8 h later, right-sided hemiparesis and aphasia were observed, and cerebral CT already revealed irreversible ischemic changes. Our cases show that alcohol consumption may interfere with stroke diagnosis by mimicking the signs and symptoms of vertebrobasilar stroke. Moreover, attributing the symptoms of stroke to alcohol intoxication may delay stroke diagnosis resulting in failure of reperfusion therapy. Based on our observations we conclude that stroke should be considered in the case of worsening symptoms, dysphagia, hemiparesis and disproportionately severe signs that cannot be attributed to the amount of alcohol consumed. In the case of ambiguity, ambulance should be called, and if stroke cannot be excluded, specific therapy should be administered.

Use of transcranial Doppler has undergone much development since its introduction in 1982, making the technique suitable for general use in intensive care units. The main application in intensive care units is to assess intracranial pressure, confirm the lack of cerebral circulation in brain death, detect vasospasm in subarachnoid haemorrhage, and monitor the blood flow parameters during thrombolysis and carotid endarterectomy, as well as measuring stenosis of the main intracranial arteries in sickle cell disease in children. This review summarises the use of transcranial Doppler in intensive care units.

Introduction: Redo carotid endarterectomy (CEA) and carotid stenting (CAS) are often performed when there is evidence of post-procedural restenosis. The incidence of restenosis after carotid reconstruction is not negligible, ranging from 5 to 33%. The diagnosis of significant internal carotid artery (ICA) restenosis is usually based on duplex ultrasound (US) criteria, mostly on peak-systolic flow velocity (PSV). However, there have been no generally accepted duplex US criteria for carotid restenosis after CAS or CEA.Methods: In this systematic review, the PubMed/ Medline and Scopus databases were screened to find trials that reported duplex US criteria for significant restenosis after CEA and/or CAS. Only those reports were analyzed in which the restenoses were also assessed by CT/MR or digital subtraction angiography as comparators for duplex US.Results: Fourteen studies met the predetermined search criteria and were included in this review. In most studies, PSV thresholds for significant in-stent ICA restenosis after CAS were higher than those for significant stenosis in non-procedurally treated (native) ICA. Many fewer studies investigated the US criteria for ICA restenosis after CEA. Despite the heterogeneous data, there is a consensus to use higher flow velocity thresholds for assessment of stenosis in stented ICA than in native ICA; however, there have been insufficient data about the flow velocity criteria for significant restenosis after CEA. Although the flow velocity thresholds for restenosis after CAS and CEA seem to be different, the large studies used the same duplex criteria to define restenosis after the two procedures. Moreover, different studies used different flow velocity thresholds to define ICA restenosis, leading to variable restenosis rates.Discussion: We conclude that (1) further examinations are warranted to determine appropriate duplex US criteria for restenosis after CAS and CEA, (2) single duplex US parameter cannot be used to reliably determine the degree of ICA restenosis, (3) inappropriate US criteria used in large studies may have led to false restenosis rates, and (4) studies are required to determine if there is a benefit from redo carotid artery procedure, such as redo-CEA or redo-CAS, starting with prospective risk stratification studies using current best practice non-invasive care alone.