Abstract-Arterial hypertension is a major risk factor for stroke, and retinal vessels can be regarded as a mirror of the cerebral vasculature. Whether vascular remodeling of retinal arterioles with ageing and hypertension plays a role in cerebrovascular risk stratification has not yet been adequately addressed. In study 1, retinal arteriolar structure was assessed in 182 normotensive volunteers and 117 patients with essential hypertension. In study 2, we compared retinal arteriolar structure among 74 normotensive volunteers, 47 patients with treated essential hypertension, and 18 subjects with a history of a cerebrovascular event. Retinal arteriolar structure was assessed using scanning laser Doppler flowmetry and automatic full-field perfusion imaging analysis. In study 1, wall:lumen ratio of retinal arterioles revealed a significant correlation with age (rϭ0.198; Pϭ0.001). In study 2, wall:lumen ratio was highest in patients with a history of a cerebrovascular event compared with treated hypertensive and normotensive subjects (0.46Ϯ0.08, 0.36Ϯ0.14, and 0.35Ϯ0.12; Pϭ0.007). When the treated group with hypertension was divided into 2 subgroups according to the quality of blood pressure control, patients with poor blood pressure control showed higher wall:lumen ratio than subjects with good blood pressure control (0.40Ϯ0.13 versus 0.31Ϯ0.13; Pϭ0.025). Thus, assessment of wall:lumen ratio of retinal arterioles emerged as an attractive tool to identify treated patients with hypertension with increased cerebrovascular risk.

When caring for critically ill patients needing central venous catheterization, nursing staff and physicians should be aware of this potentially lethal complication.

This article represents the update of ‘European Stroke Initiative Recommendations for Stroke Management’, first published in this Journal in 2000. The recommendations are endorsed by the 3 European societies which are represented in the European Stroke Initiative: the European Stroke Council, the European Neurological Society and the European Federation of Neurological Societies.

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Background: Peripheral facial nerve palsy is the most common functional disturbance of a cranial nerve. 60-75% of cases are idiopathic.Methods: This review is based on a selective literature search proceeding from the current, updated German-language guideline on the diagnosis and treatment of idiopathic facial nerve palsy.Results: The recommended drug treatment consists of prednisolone 25 mg bid for 10 days, or 60 mg qd for 5 days followed by a taper to off in decrements of 10 mg per day. This promotes full recovery (number needed to treat [NNT] = 10; 95% confidence interval [6; 20]) and lessens the risk of late sequelae such as synkinesia, autonomic disturbances, and contractures. Virostatic drugs are optional in severe cases (intense pain or suspicion of herpes zoster sine herpete) and mandatory in cases of varicella-zoster virus (VZV) infection. Corneal protection with dexpanthenol ophthalmic ointment, artificial tears, and a nocturnal moistureretaining eye shield has been found useful in practice. In cases of incomplete recovery with residual facial weakness, both static and microsurgical dynamic methods can be used to restore facial nerve function. Conclusion:Because 25-40% of cases of facial nerve palsy are not idiopathic, differential diagnosis is very important; key diagnostic methods include a clinical neurological examination, otoscopy, and a lumbar puncture for cerebrospinal fluid examination. High-level evidence supports corticosteroid treatment for the idiopathic form of the disorder.

Peer-trained students pass written exam and OSCE as efficient as postgraduates-trained students. Self-assessed learning success is equally rated in both groups.

Figure.Taste test [number of taste strips (out of 32) correctly identified; (A) and self-rated dysgeusia (in % of the visual analogue scale; (B) before (black bars) and after (white bars) therapy (means, standard errors of means; zinc group, n = 26; placebo group. n = 24).

Hepatitis C virus (HCV) infection is often associated with abnormal immunological responses. We describe four patients with vasculitic neurological signs and symptoms following HCV infection. A 56-year-old woman with HCV infection developed peripheral neuropathy characterized by asymmetric distal painful hypesthesia, dysesthesia and moderate motor weakness of the lower limbs. Serological examinations revealed cryoglobulinemia and low levels of complement C4. A biopsy of the sural nerve revealed vasculitic neuropathy. HCV infection associated immunomediated vasculitis was diagnosed. While steroid therapy was ineffective, treatment with interferon-alpha improved the neuropathy considerably without, however, eliminating HCV infection. A 62-year-old man with HCV infection developed peripheral sensory neuropathy. Complement C3 was slightly diminished. Nerve biopsy revealed vasculitic neuropathy. A 71-year-old woman developed chronic symmetric sensomotor polyneuropathy. HCV hepatitis followed blood transfusions. Cryoglobulins tested positive, consistent with type II cryoglobulinemia. Complements C3 and C4 were diminished. Inflammatory infiltrates in the sural nerve biopsy specimen led to the diagnosis of chronic vasculitic disorder. A 55-year-old woman with HCV infection developed vasculitis of the skin, connective tissue, visceral organs, and kidney, leading to hemodialysis. Neurologically she developed severe apathy and drowsiness, myoclonic jerks, exaggerated deep tendon reflexes, and positive pyramidal signs. Magnetic resonance imaging of the brain showed diffuse increased signal abnormalities involving supra- and infratentorial white matter suggesting cerebral vasculitis. Cryoglobulins were positive, complements C3 and C4 slightly diminished (54 mg/dl, 4.3 mg/dl). Supportive therapy resulted in neurological improvement. Treatment with interferon-alpha was discontinued because of agranulocytosis. In patients with peripheral neuropathy or signs of leucencephalopathy, a hepatitis C associated vasculitis should be considered in the differential diagnosis.