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A man in his fifties with advanced Parkinson´s disease was admitted with increasing motor fluctuations including dyskinesias, as well as hallucinations and delusions. After reduction of oral dopaminergic treatment, the dyskinesias improved, but the psychotic symptoms persisted. They were perceived as levodopa-induced, despite concurrent prominent bradykinetic-rigid symptoms. Dopaminergic treatment was therefore discontinued. He subsequently developed hyperthermia, severe generalised rigidity and akinesia, and autonomic instability. Parkinsonism-hyperpyrexia syndrome was diagnosed, and continuous intraduodenal levodopa/carbidopa infusion was initiated. Despite this, he had several episodes of respiratory distress requiring mechanical ventilation, as well as bradycardia and a single asystole. Although motor and autonomic dysfunction slowly improved, severe akinetic-rigid and neuropsychiatric symptoms persisted, with poor response to increased levodopa. On vital indication, electroconvulsive therapy was performed with clear improvement of mobility and mental state. A hip fracture requiring surgery necessitated discontinuation of ECT, which failed to show equivalent effect when resumed. His condition was considered terminal and all active treatment ceased, resulting in death a few weeks later.Parkinsonism-hyperpyrexia syndrome can develop if dopaminergic treatment is reduced abruptly and excessively. Coexistence of confusion and/or psychosis and clear bradykinetic-rigid symptoms should alarm the clinician. Dopaminergic treatment should not be discontinued, but given intraduodenally. ECT can be effective if started sufficiently early and administered frequently.

Background/case presentation A man in his fifties with advanced Parkinson´s disease was admitted with increasing motor fluctuations including dyskinesias, as well as hallucinations and delusions. After reduction of oral dopaminergic treatment, the dyskinesias improved, but the psychotic symptoms persisted. They were perceived as levodopa-induced, despite concurrent prominent bradykinetic-rigid symptoms. Dopaminergic treatment was therefore discontinued. He subsequently developed hyperthermia, severe generalised rigidity and akinesia, and autonomic instability. Parkinsonism-hyperpyrexia syndrome was diagnosed, and continuous intraduodenal levodopa/carbidopa infusion was initiated. Despite this, he had several episodes of respiratory distress requiring mechanical ventilation, as well as bradycardia and a single asystole. Although motor and autonomic dysfunction slowly improved, severe akinetic-rigid and neuropsychiatric symptoms persisted, with poor response to increased levodopa. On vital indication, electroconvulsive therapy was performed with clear improvement of mobility and mental state. A hip fracture requiring surgery necessitated discontinuation of ECT, which failed to show equivalent effect when resumed. His condition was considered terminal and all active treatment ceased, resulting in death a few weeks later. Interpretation Parkinsonism-hyperpyrexia syndrome can develop if dopaminergic treatment is reduced abruptly and excessively. Coexistence of confusion and/or psychosis and clear bradykinetic-rigid symptoms should alarm the clinician. Dopaminergic treatment should not be discontinued, but given intraduodenally. ECT can be effective if started sufficiently early and administered frequently.

Objective Early blood pressure-lowering treatment appears to be beneficial in patients with acute intracerebral haemorrhage and potentially in ischaemic stroke. We used a new method for analysis of vascular events in the Scandinavian Candesartan Acute Stroke Trial to see if the effect was dependent on the timing of treatment. Methods Scandinavian Candesartan Acute Stroke Trial was a randomized controlled and placebo-controlled trial of candesartan within 30 h of ischaemic or haemorrhagic stroke. Of 2029 patients, 231 (11.4%) had a vascular event (vascular death, nonfatal stroke or nonfatal myocardial infarction) during the first 6 months. The modified Rankin Scale (mRS) score following a vascular event was used to categorize vascular events in order of severity: no event (n = 1798), minor (mRS 0-2, n = 59), moderately severe (mRS 3-4, n = 57) and major event (mRS 5-6, n = 115). We used ordinal logistic regression for analysis and adjusted for predefined prognostic variables. Results Candesartan had no overall effect on vascular events (adjusted common odds ratio 1.11, 95% confidence interval 0.84-1.47, P = 0.48), and the effects were the same in ischaemic and haemorrhagic stroke. Among the patients treated within 6 h, the adjusted common odds ratio for vascular events was 0.37, 95% confidence interval 0.16-0.84, P = 0.02, and there was no heterogeneity of effect between ischaemic and haemorrhagic strokes. Conclusion Ordinal analysis of vascular events showed no overall effect of candesartan in the subacute phase of stroke. The effect of treatment given within 6 h of stroke onset appears promising, and will be addressed in ongoing trials. Ordinal analysis of vascular events is feasible and can be used in future trials.

Uncertainty persists over the effects of blood pressure-lowering treatment in acute intracerebral hemorrhage (ICH). We assessed the effects of treatment with candesartan in acute ICH and according to different types of hematoma.Post-hoc analysis of the Scandinavian Candesartan Acute Stroke Trial, a randomized- and placebo-controlled, double-masked trial of candesartan in patients with any stroke within the acute phase (30 hours) and high systolic blood pressure (≥140 mm Hg). We collected baseline computed tomography scans of participants with ICH, and characterized hematoma volume (planimetric approach), location (deep versus lobar or infratentorial), hemisphere side, and presence of intraventricular hemorrhage. The trial's 2 coprimary effect variables were the composite endpoint of vascular death, stroke or myocardial infarction, and functional outcome at 6 months according to the modified Rankin scale. We used Cox, ordinal, and binary logistic regression for analysis and adjusted for key, predefined prognostic variables.Of 274 participants with ICH, computed tomography scans were available in 205 patients (74.8%). There were no significant differences between the candesartan and placebo groups with respect to hematoma volume (median 15.6 mL versus 13.5 mL, P = .96), deep location (77% versus 72%, P = .64), right hemisphere (49% versus 51%, P = .46), and presence of intraventricular hemorrhage (18% versus 11%, P = .22). Candesartan was associated with a significant increase in poor functional outcome in patients with deep hematoma (adjusted common odds ratio 2.27, 95% confidence interval 1.23-4.18, P = .009, P for interaction .015), but there was no differential effect on functional outcome or vascular events in any of the other imaging subgroups.Candesartan was not associated with any beneficial effect when initiated in the acute phase of ICH, a possible adverse effect on functional outcome in patients with deep hematomas cannot be ruled out by this study alone.

Carotid Artery Stenosis (CAS) is a marker of systemic atherosclerosis and patients with CAS are at high risk of vascular events in multiple vascular locations, including ipsilateral ischemic stroke. Both medical and surgical therapies have been demonstrated effective in reducing this risk. The optimal management for patients with asymptomatic carotid artery stenosis remains controversial. In patients with symptomatic CAS ≥70%, CEA has been demonstrated to reduce the risk of stroke. With the risk of recurrent stroke being particularly high in the first 2 weeks after the first event, Carotid Endarterectomy (CEA) or carotid angioplasty with stenting provides maximal benefits to patients with symptomatic CAS ≥70% if performed within this «2-week» target. Several large ongoing trials are currently comparing the risks and benefits of carotid revascularization versus medical therapy alone.

What is the role of dual antiplatelet therapy after high risk transient ischaemic attack or minor stroke? Specifically, does dual antiplatelet therapy with a combination of aspirin and clopidogrel lead to a greater reduction in recurrent stroke and death over the use of aspirin alone when given in the first 24 hours after a high risk transient ischaemic attack or minor ischaemic stroke? An expert panel produced a strong recommendation for initiating dual antiplatelet therapy within 24 hours of the onset of symptoms, and for continuing it for 10-21 days. Current practice is typically to use a single drug

Acute stroke is a leading cause of death and disability in the developed world. Among survivors, the risk of stroke recurrence is highest within the first few days, and up to 15% will be affected within the first year. In the case of noncardioembolism, antiplatelets, such as aspirin, clopidogrel, and the combination of aspirin and dipyridamole, remain the mainstay of treatment. Aspirin given immediately is beneficial, but when combined with clopidogrel is associated with a higher risk of bleeding. Dual antiplatelet therapy of aspirin and dipyridamole was no more effective than clopidogrel in reducing stroke recurrence. In symptomatic extracranial atherosclerosis, surgery within 2 weeks of the index event will benefit, but in strokes due to intracranial atherosclerosis and small vessel disease, medical therapy alone is recommended. The purpose of this review is to discuss the various trials of antiplatelet therapies in acute and long-term stroke prevention in mechanisms excluding cardioembolism.

Background The Scandinavian Candesartan Acute Stroke Trial (SCAST) showed no beneficial clinical effects of blood pressure lowering with the angiotensin receptor blocker candesartan in the acute phase of stroke. In the present analysis we wanted to see if the effects of blood pressure lowering are harmful in the subgroup of patients with carotid artery stenosis. Methods SCAST was a randomized- and placebo-controlled, double-masked trial of 2029 patients with acute stroke and high systolic blood pressure (≥140 mmHg). Of 1733 patients with ischemic stroke 993 underwent carotid artery imaging, and the degree of stenosis was categorized as no/insignificant (0–49%, n = 806), moderate (50–69%, n = 97) or severe (=70%, n = 90). The trial's two co-primary effect variables were the composite end-point of vascular death, stroke or myocardial infarction, and functional outcome at six-months, according to the modified Rankin Scale. Results Among patients with moderate or severe carotid artery stenosis the vascular end-point occurred in 9 of 87 patients (10·3%) treated with candesartan and in 17 of 100 controls (17·0%), and there was no evidence of a different risk in patients with severe stenosis (adjusted hazard ratio 0·74, 95% confidence interval 0·28–1·96, P = 0·54). For functional outcome there was also no clear difference, although in patients with severe stenosis the risk of a poor outcome was somewhat higher than in any of the other groups (adjusted odds ratio 2·24, 95% confidence interval 0·71–7·09, P = 0·16). Progressive stroke also occurred more often in patients with carotid artery stenosis treated with candesartan (10 of 87 patients (11·5%) vs. 4 of 100 patients (4·0%)), with a trend towards an increased risk with increasing severity of stenosis ( P-value for linear trend = 0·04). Conclusions There is no clear evidence that the effect of candesartan is qualitatively different in patients with carotid artery stenosis, but there are signals that patients with severe stenosis are at particularly high risk of stroke progression and poor functional outcome.

Background and Purpose— The Scandinavian Candesartan Acute Stroke Trial (SCAST) found no benefits of blood pressure–lowering treatment with candesartan in acute stroke. We have investigated whether the effect of treatment is different in different subtypes of ischemic stroke. Methods— SCAST was a randomized- and placebo-controlled trial of candesartan in 2029 patients presenting within 30 hours of ischemic or hemorrhagic stroke and systolic blood pressure ≥140 mm Hg. Ischemic stroke subtype was categorized by the Oxfordshire Community Stroke Project classification. There were 2 primary effect variables: the composite vascular end point of vascular death, myocardial infarction, or stroke during the first 6 months and functional outcome at 6 months. Results— A total of 1733 patients with ischemic stroke were included: total anterior circulation infarcts in 129, partial anterior in 850, posterior in 236, and lacunar in 510 patients. For functional outcome there was a significant trend toward a better effect of candesartan in patients with larger infarcts (total anterior circulation or partial anterior circulation) than in patients with smaller infarcts (lacunar infarction; P =0.02). For the composite vascular end point, there were no differences in treatment effect. Conclusions— The results suggest that the effect of blood pressure–lowering treatment with candesartan may differ according to different types of acute ischemic stroke, but this needs to be confirmed in future trials. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00120003.

BACKGROUND There is no sound scientific documentation of current guidelines for the treatment of cerebral infarction assumed to be due to patent foramen ovale. In this article, we present a young patient with this condition. In addition, we provide a general overview of the prevalence, recommended assessment and indications for treatment of patent foramen ovale in ischaemic stroke patients. METHOD The article is based on a non-systematic search in PubMed. We emphasise three recently published randomised trials on the subject. RESULTS Transoesophageal echocardiography with saline contrast is the gold standard for detecting patent foramen ovale. Just who will benefit from the diagnosis and treatment of this condition remains unclear, however. None of the three randomised studies of antithrombotic treatment versus transcatheter closure in patients who have suffered ischaemic stroke show a difference in outcomes, but subgroup analyses indicate that closure in young patients (age

Background Hypercoagulability leading to arterial or venous thrombosis and embolism in patients with cancer is a known phenomenon. Material and methods We describe a 62 year old woman with a clinical course compatible with catastrophic antiphospholipid syndrome but seronegative findings and mucinous lung cancer. The case is discussed with reference to literature from a non-systematic PubMed search. Results and interpretation Diagnoses of cerebral and cardiac infarcts, deep venous thrombosis and lung embolism led to a diagnosis of lung cancer by biopsy and positron emission tomography (PET). Early recurrence of venous and arterial thromboses or poor response to anticoagulation and antiplatelets should initiate cancer search in the assessment of such stroke patients. Especially the combination of venous and arterial thromboses should raise suspicion of cancer. PET and surgical cancer treatment should be evaluated at an early stage.

Background and Purpose— Early and intensive blood pressure–lowering treatment seems to be beneficial in patients with acute hemorrhagic stroke and high blood pressure. We wanted to see if similar benefits can be shown from a later and more gradual blood pressure lowering, using data from the Scandinavian Candesartan Acute Stroke Trial (SCAST). Methods— SCAST was a randomized- and placebo-controlled, double-masked trial of candesartan given for 7 days, in 2029 patients with acute stroke and systolic blood pressure ≥140 mm Hg. We assessed the effects of candesartan in the 274 patients with hemorrhagic stroke, using the trial’s 2 coprimary effect variables: the composite vascular end point of vascular death, stroke or myocardial infarction, and functional outcome at 6 months, according to the modified Rankin Scale. We used Cox proportional hazards models and ordinal regression for analysis and adjusted for key, predefined prognostic variables. Results— There was no association between treatment with candesartan and risk of vascular events (17 of 144 [11.8%] versus 13 of 130 [10.0%]; hazard ratio, 1.36; 95% confidence interval, 0.65–2.83; P =0.41). For functional outcome we found evidence of a negative effect of candesartan (common odds ratio, 1.61; 95% confidence interval, 1.03–2.50; P =0.036). Conclusions— There was no evidence that blood pressure–lowering treatment with candesartan is beneficial during the first week of hemorrhagic stroke. Instead, there were signs that such treatment may be harmful, but this needs to be verified in larger studies. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00120003.

Raised blood pressure is common in ischaemic stroke and intracerebral haemorrhage and is an independent risk factor for unfavourable outcome. Yet, the approach to blood pressure management represents an unresolved issue in acute stroke treatment. The aim of this review is to present the current knowledge regarding the management of raised blood pressure in patients with acute ischaemic stroke or intracerebral haemorrhage. In ischaemic stroke, several large clinical trials have tested the efficacy of several strategies that lower blood pressure. Overall, blood pressure lowering in the acute phase has no beneficial effect and should not be included in routine clinical practice apart from when treating patients with very raised blood pressure or those who are eligible for thrombolytic treatment. These findings in patients with acute ischaemic stroke are in contrast with those in intracerebral haemorrhage. A recent clinical trial has strongly suggested a clinical benefit of blood pressure lowering during the first few hours in intracerebral haemorrhage, which have led to changes in international guidelines. An important unanswered question in blood pressure management in the acute phase of ischaemic stroke involves the first few hours, when there is still penumbral tissue at risk. Forthcoming trials may help to answer this remaining issue.

Stroke is the second most common cause of death and the most common cause of disability worldwide. Up to 30% of ischaemic strokes are caused by carotid atherosclerosis, usually due to thromboemboli from an atherosclerotic plaque at the carotid bifurcation. High blood pressure is an important risk factor for atherosclerosis, the development of unstable carotid plaques, and ischaemic strokes. Differentiation between asymptomatic and symptomatic carotid atherosclerosis is critical to treatment management because of the difference in natural history. Intensive medical treatment including blood pressure lowering medication reduces the risk of both primary and secondary vascular events in patients at risk. This review summarises recent data on blood pressure management in patients with carotid artery stenosis.

We thank Gioia and colleagues for their insightful and valuable comments. We agree that we have not accounted for all important predictors of prognosis, such as hematoma volume, but the equal distribution of stroke severity (Scandinavian Stroke Scale), stroke syndrome subtype (Oxfordshire Community Stroke Project classification), and blood pressure should go some way to assure that randomization was successful in achieving balance …

Background Vascular damage in the central hand knob area can mimic peripheral motor nerve deficits. Case presentation We describe the case of a woman presenting with apparent peripheral neuropathy. Brain magnetic resonance imaging and computed tomography angiography revealed an infarct in the precentral hand knob area, with significant stenosis in the right proximal middle cerebral artery trunk. Subsequent 3-Tesla magnetic resonance imaging of the brain suggested cerebral angiitis. The patient experienced improved hand function following combined glucocorticoid and cyclophosphamide treatment. Conclusion Vascular damage in the hand knob area should be considered when evaluating peripheral motor nerve deficits in the presence of normal nerve conduction velocities. The diagnosis of cerebral angiitis remains a major challenge for clinicians.

There is no sound scientific documentation of current guidelines for the treatment of cerebral infarction assumed to be due to patent foramen ovale. In this article, we present a young patient with this condition. In addition, we provide a general overview of the prevalence, recommended assessment and indications for treatment of patent foramen ovale in ischaemic stroke patients.The article is based on a non-systematic search in PubMed. We emphasise three recently published randomised trials on the subject.Transoesophageal echocardiography with saline contrast is the gold standard for detecting patent foramen ovale. Just who will benefit from the diagnosis and treatment of this condition remains unclear, however. None of the three randomised studies of antithrombotic treatment versus transcatheter closure in patients who have suffered ischaemic stroke show a difference in outcomes, but subgroup analyses indicate that closure in young patients (age50 years) with a large foramen ovale reduces the number of recurrent ischaemic events. Two other randomised studies of antithrombotic treatment alone versus closure are presently ongoing.For stroke patients with patent foramen ovale, the choice between lifelong antithrombotic therapy alone and transcatheter closure is a difficult one. Treatment with antiplatelet agents remains the first choice in most cases. Well-designed studies are needed to identify which patients will benefit most from closure.

Background and purpose Our population-based long-term follow-up of young ischaemic stroke patients and controls showed 10-fold increased mortality and fivefold increased arterial event rate nearly 12 years after study inclusion. We now assess memory, anxiety, depression and sleep in relation to employment and functional outcome, treatment goals and results from a last alive–dead survey. Methods Patients (n = 232) ≤ 49 years with an index-stroke between 1988 and 1997 were retrospectively selected and compared with age- and sex-matched controls (n = 453). At follow-up from 2004 to 2005, 144 (77%) of 187 patients were clinically examined. Self-assessment information about memory problems, anxiety, depression, sleeping problems, education and employment was compared with answers from standardized questionnaires from 167 controls. Functional outcome was measured by the modified Rankin Scale (mRS). Results Patients compared with controls had more memory problems (41.0% vs. 5.4%, P

Background Cerebellar and cerebral infarctions caused by the syndrome of cervical rib with thrombosis of subclavian artery are very unusual. Case presentation We report the case of a 49-year-old male patient with a right cervical rib compression leading to subclavian arterial thrombosis and both cerebellar and cerebral infarctions secondary to retrograde thromboembolisation. Follow-up imaging revealed partial resolution of the thrombosis after combined anti-coagulant and anti-platelet therapy. The cervical rib and first costa were surgically removed to prevent additional events. Conclusion Cervical rib vascular compression should be promptly diagnosed and treated in order to avoid further complications, including cerebrovascular ischemic events.

Hypercoagulability leading to arterial or venous thrombosis and embolism in patients with cancer is a known phenomenon.We describe a 62 year old woman with a clinical course compatible with catastrophic antiphospholipid syndrome but seronegative findings and mucinous lung cancer. The case is discussed with reference to literature from a non-systematic PubMed search.Diagnoses of cerebral and cardiac infarcts, deep venous thrombosis and lung embolism led to a diagnosis of lung cancer by biopsy and positron emission tomography (PET). Early recurrence of venous and arterial thromboses or poor response to anticoagulation and antiplatelets should initiate cancer search in the assessment of such stroke patients. Especially the combination of venous and arterial thromboses should raise suspicion of cancer. PET and surgical cancer treatment should be evaluated at an early stage.