Perspectives in Medicine最新文献

We investigated the distribution of wall shears stress (WSS) within the carotid artery bifurcation of healthy volunteers and patients with internal carotid artery stenosis. WSS was determined by flow-sensitive 4D MRI and correlated with bifurcation angle, vessel tortuosity and the ratio of the diameter of the common (CCA) and internal carotid artery (ICA). Critical WSS occurred at the posterior wall of the physiologically dilated ICA bulb and the incidence of critical WSS values was dependent from individual bifurcation geometry. Moreover, we found that ICA stenosis changed physiological WSS distribution whereas carotid endarterectomy partially restored physiological WSS conditions.

Background

Current protocols stress the importance of short-term diagnosis and treatment in recent TIA or minor stroke. The risk of a recurrent event can be predicted with embolus detection. Studies have shown that the presence of micro-emboli is associated with an increased risk of recurrent events. We explored in our patient population the effect of a zero-tolerance regime for cerebral embolism on outcome.

Methods

Patients with a recent TIA or minor stroke were assigned to a study group or control group. Both groups were treated according to European Stroke guidelines, including prompt start of anti-thrombotic therapy, statins and short-term carotid arteries duplex scanning. The study group was subjected to TCD (Delica 9 series, Shenzen Delicate Electronics Co., LTD., China) embolus detection as soon as possible (EDS, SMT Medical, Wuerzburg, Germany). If emboli were detected, treatment was started immediately to stop cerebral embolization. This was achieved by either an altered drug regimen (clopidogrel) or angioplasty or carotid endarterectomy within one or two days. If carotid intervention was indicated in the control group, it was performed within two weeks, according to European guidelines.

Results

133 patients were enrolled in the study with three months follow-up. 61 patients were subjected to the control group, 72 patients were enrolled in the study group. Recurrent events occurred in 10.2% and 3.0%, respectively (p = 0.145).

Conclusion

The current study shows a non-significant reduction in recurrent events in the study group. Probably sample size in this pilot study was insufficient to detect a significant decline. Nevertheless, the results show that embolus detection is feasible and the zero-tolerance regime may enhance the outcome of TIA and minor stroke patients. The findings support the start of a multicenter randomized trial to assess the clinical value of emboli detection in TIA and stroke care.

Background

Optic Neuritis (ONe) is common in Multiple Sclerosis (MS). The aim of this study was to evaluate the Optic Nerve (ONr) and its vascularisation in MS patients with and without previous ONe and in Healthy Controls (HC).

Methods

We performed high-resolution echo-color ultrasound examination in 50 subjects (29 MS patients and 21 HC). By a suprabulbar approach we measured the ONr diameter at 3 mm from the retinal plane and at another unfixed point. We assessed the flow velocities of Ophthalmic Artery (OA), Central Retinal Artery (CRA) and Central Retinal Vein (CRV) measuring the Peak Systolic Velocity (PSV) and the End Diastolic Velocity (EDV) for the arteries and the Maximal Velocity (MaxV), Minimal Velocity (MinV) and mean Velocity (mV) for the veins. The Pulsatility Index (PI) and the Resistive Index (RI) were also calculated.

Results

No significant variation for OA supply was found as well as no significant variation for CRA supply, while significant higher PI in the CRV of non-ONe MS eyes vs. both HC and ONe MS eyes was measured. We found that ONr diameter was decreased significantly from HC to non-ONe MS eyes and ONe MS eyes.

Conclusions

Ultrasound examination of ONr and its vascularisation is feasible and can demonstrate ON atrophy. The increase of CRV PI in unaffected eyes of MS patients is intriguing and seems not associated to ONr atrophy. Larger studies are needed to confirm these results.

Background

Sickle cell disease (SCD) may impair intellectual activity; 25% of SCD patients have a significant cognitive deficit. Our aim was to verify in a cohort of children with HbSS if the presence of silent strokes or altered Time Averaged Mean velocities of Maximum blood flow (TAMM) detected by Transcranial Color Doppler (TCD) Sonography are indicators of impaired intellectual ability.

Methods

Thirty-five consecutive SCD patients (17 males; mean age: 8.6 ± 3.22) were subdivided into two groups according to neuro-psycological deficits. Cognitive function was assessed by WISC III (for the children aged 6–16 years) and WPPSI (for the children aged 4–6 years). All patients underwent a TCD scan of the main intracranial arteries, in order to detect any increase of TAMM velocities (normal <170 cm/s; altered >170 cm/s) and a cerebral MRI to reveal any silent stokes.

Results

According to the neuro-psycological evaluation, 29/35 (82.8%) patients (Group 1) had a “normal” Total Intelligence Quotient (TIQ ≥70), while 6/35 (17.2%) patients (Group 2) were defined intellectually impaired (TIQ <69).

TCD detected altered velocities in 8/35 (22.8%) patients. No significant differences were found in the percentage of altered TAMM velocities between the two groups (Fisher's exact test: p = 0.42).

MRI detected silent ischemic lesions in 14/35 patients (40.0%). No significant differences were found in silent stroke frequencies (Fisher's exact test: p = 0.25) between Group 1 and Group 2.

Conclusion

With the limitations of the study sample, according to our results, altered TAMM values and silent strokes do not seem to be indicators of impaired intellectual ability in SCD patients.

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.