Marc Randall

Long-Term Results of Carotid Artery Stents to Manage Symptomatic Carotid Artery Stenosis and Factors That Affect Outcome

Background—Limited data are available about the long-term outcomes of the use of carotid artery stents in symptomatic patients and the impact of patient variables on the durability of endovascular carotid procedures. Outcome data previously reported from registry series mix symptomatic and asymptomatic patients. We present analysis of long-term follow-up, with independent neurological assessment, for patients with symptomatic high-grade carotid lesions undergoing stenting to identify patients at risk of recurrence. Methods and Results—Prospectively collected data on 563 carotid stenting procedures in a single center were analyzed. Univariate and multivariate techniques were used to identify risk groups and beneficial technical adaptations. Ipsilateral stroke rates for all patients were 4.8%, 7.0%, and 9.5% at 30 days, 1 year, and 4 years, respectively. The rates improved to 2.7%, 4.1%, and 4.5% when patients were treated with optimal therapy. Retinal events had a lower risk of long-term recurrent ipsilateral stroke (hazard ratio=0.228, CI=0.082 to 0.632, P=0.004) than cerebral events. A recurrent or residual stenosis of >50% had a statistically significant effect on long-term stroke recurrence in multivariate analysis (hazard ratio=2.187, CI=1.173 to 4.078, P=0.014). Conclusions—Patients with retinal presentations are a lower risk group to treat. Residual stenosis or restenosis >50% has a statistically significant trend to an increased risk of recurrence for ipsilateral stroke in the long term in this population. In our patients, a combination of procedural modifications and pharmacological changes seems to improve outcomes.

‘Dystextia’: onset of difficultly writing mobile phone texts determines the time of acute ischaemic stroke allowing thrombolysis

At 16:24, an ambulance was asked to attend an 18-year-old man found collapsed at home. First responders arrived at the patients house at 16:30, followed by a paramedic ambulance at 16:45. Paramedics along with the patient and his sister left the house at 17:04 in a blue-light ambulance and arrived at our acute stroke service at 17:15. His sister said that he had spoken normally on the phone at approximately 13:00. A friend had phoned at 16:15 and found his speech was ‘slurred’, so went to his house, found him face down on the floor and called an ambulance. Paramedics found him alert with normal vital signs. Pupils were equal and reactive but speech was very slurred, and there was right face, arm and leg weakness. On arrival at hospital, he was alert with eyes open but severe dysphasia was present and he was limited to making incomprehensible sounds and following very simple instructions with visual …

Stretch syncope: Reflex vasodepressor faints easily mistaken for epilepsy

The pathophysiology of stretch syncope is demonstrated through the clinical, electrophysiological, and hemodynamic findings in three patients. Fifty-seven attacks were captured by video/EEG monitoring. Simultaneous EEG, transcranial (middle cerebral artery) doppler, and continuous arterial pressure measurements were obtained for at least one typical attack of each patient. They all experienced a compulsion to precipitate their attacks. Episodes started with a stereotyped phase of stretching associated with neck torsion and breath holding, followed by a variable degree of loss of consciousness and asymmetric, recurrent facial and upper limb jerks in the more prolonged episodes. Significant sinus tachycardia coincided with the phase of stretching and was followed within 9-16 seconds by rhythmic generalized slow wave abnormalities on the EEG in attacks with impairment of consciousness. Transcranial doppler studies showed a dramatic drop in cerebral perfusion in the middle cerebral arteries during the episodes. The combination of the stereotyped semiology of the attacks, the pseudofocal myoclonic jerking, and the rhythmic generalized slow wave EEG abnormalities with the tachycardia make differential diagnosis from epilepsy challenging.

Outcome After Clipping and Coiling for Aneurysmal Subarachnoid Hemorrhage in Clinical Practice in Europe, USA, and Australia

BACKGROUND Within randomized clinical trials (RCTs), coiling of the ruptured aneurysm to prevent rebleeding results in better outcomes than clipping in patients with aneurysmal subarachnoid hemorrhage (aSAH). OBJECTIVE To study the association of coiling and clipping with outcome after aSAH in daily clinical practice. METHODS In this controlled, nonrandomized study, we compared outcomes after endovascular coiling and neurosurgical clipping of ruptured intracranial aneurysms in an administrative dataset of 7658 aSAH patients (22 tertiary care hospitals from Europe, USA, Australia; 2007-2013). Because the results contradicted those of the randomized trials, findings were further explored in a large clinical dataset from 2 European centers (2006-2016) of 1501 patients. RESULTS In the administrative dataset, the crude 14-d case-fatality rate was 6.4% (95% confidence interval [CI] 5.6%-7.2%) after clipping and 8.2% (95% CI 7.4%-9.1%) after coiling. After adjustment for age, sex, and comorbidity/severity, the odds ratio (OR) for 14-d case-fatality after coiling compared to clipping was 1.32 (95% CI 1.10-1.58). In the clinical dataset crude 14-d case fatality rate was 5.7% (95% CI 4.2%-7.8%) for clipping and 9.0% (95% CI 7.3%-11.2%) for coiling. In multivariable logistic regression analysis, the OR for 14-d case-fatality after coiling compared to clipping was 1.7 (95% CI 1.1-2.7), for 90-d case-fatality 1.28 (95% CI 0.91-1.82) and for 90-d poor functional outcome 0.78 (95% CI 0.6-1.01). CONCLUSION In clinical practice, coiling after aSAH is associated with higher 14-d case-fatality than clipping and nonsuperior outcomes at 90 d. Both options need to be considered in aSAH patients. Further studies should address the reasons for the discrepancy between current data and those from the RCTs.

Trigeminal neuralgia: no laughing matter

A 21-year-old right-handed man was referred to neurology in autumn 2009. He had been a university student for 1 year, with his studies progressing well until Easter 2009, when his work had deteriorated. His writing had become muddled with frequent spelling mistakes and he was diagnosed with dyslexia. In June, he developed severe generalised headaches, which did not respond to simple analgesics. The pain progressed to a right-sided facial pain with a sharp electric shock quality and was diagnosed as trigeminal neuralgia: his general practitioner started carbamazepine, which was ineffective. The pain had been constant for the previous 8 weeks, with no nausea or vomiting. ### Question 1 What are the causes of acquired dyslexia and how would you investigate it? ### Comment ‘Dyslexia’ is commonly used to refer to a developmental reading disability. In contrast, acquired dyslexia, sometimes termed ‘alexia’ to highlight the distinction, indicates a difficulty in reading in someone who previously read normally. Acquired dyslexias can be divided into: The deep dyslexias are seen in semantic dementia and with lesions (strokes and tumours) affecting the dominant hemisphere temporal and parietal lobes. A non-dominant hemisphere lesion can cause alexia by two mechanisms. ### Question 2 What are the typical symptoms of trigeminal neuralgia …