Perspectives in Medicine最新文献

Sleep is the most conspicuous alteration of cerebral function during the circadian rhythm. It is composed of a cyclic sequence of stages defined on the basis of electrophysiological parameters. The underlying functional activity of the human brain is reflected by sleep correlated changes of cerebral blood flow (CBF), CBF velocity and cerebral metabolism (CM). Transcranial Doppler sonography (TCD) allows to analyze the rapid adaptation processes of cerebral hemodynamics due to TCD capabilities for high temporal resolution and continuous recording during sleep using modern ultrasonic probes with special fixation devices. After the onset of sleep there is a significant progressive reduction of CBF velocity from the waking state to slow wave sleep. The beginning of REM sleep is accompanied by a marked increase in CBF velocity. Furthermore, TCD enables the assessment of perfusion changes in pathological sleep conditions. In sleep apnea syndrome an apnea-associated increase in CBF velocity occurs, which is attributed to apnea-related hypercapnia, whereas a rapid normalization of flow velocity occurs at the end of each apneic episode. TCD is a useful method for long-term and on-line monitoring of dynamic changes in cerebral perfusion during normal sleep and in sleep disorders.

Intravascular papillary endothelial hyperplasia (IPEH), also known as Masson's tumor, is a rare, generally considered a non neoplastic vascular lesion, caused by an abnormal endovascular proliferation of endothelial cells.

We describe, as far as we know, the first case of this lesion, localized at the origin of the internal carotid artery, which was responsible for an ischemic stroke. Although this entity is very rare, it is important for the clinician to become familiar with this lesion, since the complete removal of the lesion is the only treatment of choice. A partial removal may lead to further clinical events.

Neurological deterioration can occur in 13–38% of patients with acute ischemic stroke due to hemodynamic and non-hemodynamic causes. Several non-hemodynamic mechanisms can lead to ischemic lesion extension and subsequent neurological worsening, including infections, cerebral edema, hemorrhagic conversion of infarction and metabolic disorders. The most common hemodynamic causes related to infarct expansion, leading to neurologic deterioration in the setting of acute cerebral ischemia are the following: (i) cardiac complications, (ii) arterial reocclusion, (iii) intracranial arterial steal phenomenon, and (iv) cerebral microembolization. The present review aims to address the underlying mechanisms and potential clinical implications of the hemodynamic causes of neurological deterioration in patients with acute cerebral ischemia. The contribution of neurosonology in detection of changes in cerebral hemodynamics in real-time are also going to be discussed. Finally, potential treatment strategies for specific causes of hemodynamic deterioration in acute ischemic stroke patients are reported.

Major cardio- and cerebrovascular events often occur in individuals without known preexisting cardiovascular disease. The prevention of such events, including the accurate identification of those at risk, remains a serious public health challenge. Scoring equations to predict those at increased risk have been developed using cardiovascular risk factors, but they tend to overestimate the risk in low-risk populations and underestimate it in high-risk populations. This overview discusses the possible role of ultrasound for an optimized prevention of stroke and focusses on (1) the importance of embolic signals in asymptomatic carotid stenosis, (2) the detection of unstable carotid plaques using duplex ultrasonography, and (3) the role of the ankle–brachial index for the stroke risk prediction in the acute stage and for secondary prevention.

Background

The hypothesis that cerebral embolism plays no role in late septic encephalopathy and septic shock is based on indirect clinical evidence in the literature. The goal of this study was to prove the hypothesis that cerebral embolism plays no role in the pathophysiology of sepsis by direct evidence.

Methods

To examine this hypothesis, 20 patients with a late septic encephalopathy and septic shock were examined for direct evidence of ongoing cerebral embolism with transcranial Doppler for 30 min. Clinical data analysis included age, gender, cause of sepsis (gram-positive or -negative microorganisms), an index of severity of illness (the APACHE II score) and outcome (survivor/non survivor). Cerebral embolism was quantified by embolus detection software.

Findings

The study revealed no ongoing cerebral embolism during sepsis.

Conclusion

Cerebral micro-embolism plays no role in cerebral dysfunction during sepsis. This negative finding has an important clinical repercussion, because if transcranial Doppler exams should reveal ongoing cerebral embolism in septic shock, the embolism cannot be attributed to the septic shock itself rather it would indicate for a vigorous search for an embolic source.

Introduction

Chronic cerebrospinal venous insufficiency (CCSVI) is a newly suggested cause for multiple sclerosis (MS) detected by color-coded Doppler sonography. Our aim was to evaluate the relationship between CCSVI and MS compared to the control group.

Methods

The study was performed on 84 MS patients and 115 healthy subjects. The presence of at least two of the extra- and/or intra-cranial Zamboni's criteria was considered positive for evidence of CCSVI.

Results

Although the total number of MS patients with any detectable CCSVI criterion was significantly higher than the controls (22.6% vs. 10.4%, P = 0.019), only one out of 84 patients fulfilled the Zamboni's criteria (1.2% vs. none, P = 0.422).

Conclusion

Our results do not support the presence of a relationship between MS and CCSVI criteria defined by Zamboni.