Paroxysmal Neurology: a Guide to Diagnosing Transient Neurologic Dysfunction in Adults and Adolescents.

Objective To explore the differences in brain protection between anterograde cerebral perfusion(ACP) and retrograde cerebral perfusion(RCP) in aortic arch surgery. Methods Aortic arch circulatory surgery, ACP and RCP techniques were searched at the Cochrane Library, PubMed, EMBASE, Wanfang Database and the Chinese Biomedical Database from January 2013 to December 2018. Cohort studies were then performed with early postoperative death, transient neurological dysfunction(TND), stroke, and transient ischemic attack(TIA). For each study, data on endpoints in the ACP and RCP groups were used to generate risk ratios(RR) and 95% confidence intervals(CI). The funnel chart was used to test publication bias. Results A total of 6 692 patients were enrolled in 12 studies, of which 3 902 patients received low-temperature circulatory arrest plus ACP, and 2 790 patients received low-temperature circulatory arrest plus RCP. Summary analysis showed that the early postoperative death(RR=0.83, 95%CI=0.51-1.35, P=0.46), stroke(RR=1.09, 95%CI=0.91-1.31, P=0.33), transient neurological dysfunction(RR=0.81, 95%CI=0.17-3.91, P=0.80) and transient ischemic attack(RR=1.00, 95%CI=0.74-1.34, P=1.00) in both groups were no significant differences(all P>0.05). Conclusion There are no significant differences in postoperative mortality and neurological dysfunction between antegrade cerebral perfusion and retrograde cerebral perfusion in the aortic arch surgery. Combined with hypothermic circulatory arrest, it can be selected according to the actual situation of aortic arch surgery. Key words: Aortic arch surgery Antegrade cerebral perfusion Retrograde cerebral perfusion Brain protection

Blood pressure (BP) fluctuation has been demonstrated to be closely associated with stroke. However, at present, no attention is paid to the BP fluctuation following total knee arthroplasty (TKA). The aim of this study is to investigate what is BP fluctuation patterns in stroke and transient ischemic attack (TIA) patients after primary TKA, compare clinical characteristics among different BP fluctuation patterns and determine whether it could predict the occurrence of a 90-day stroke. A retrospective study was conducted from February 1, 2011 to February 15, 2021. Stroke or TIA patients within 90 days after TKA were included. Data from a hospitalization management system were analyzed, including demographics, smoking status, comorbidities, medications, surgical variables, and 90-day stroke, mortality, and readmission rates. BP fluctuation patterns were defined based on the average BP in the first 3 days after TKA. A logistic regression analysis model was used to identify risk factors for 90-day stroke or TIA following TKA. Of the 1687 patients who underwent primary TKA, 4.0% (68/1687) experienced a 90-day stroke or TIA. A total of 63 patients met the inclusion criteria, with an average age of 67.5 years and 55.6% (35/63) female. The number of stroke or TIA patients in each BP fluctuation pattern (T1-T5) was 6 (9.5%), 5 (7.9%), 4 (6.3%), 13 (20.6%), and 35 (55.6%) respectively. Patients with a T5 pattern tended to be older and had a greater reduction in average systolic blood pressure (SBP) 3 days after surgery compared to other patterns. The T5 pattern was associated with a higher occurrence of stroke and a lower occurrence of TIA. Patients with a T5 pattern also had a longer length of stay within 90 days following TKA. After adjusting for confounding factors, average SBP fluctuation ≥40 mmHg and the T5 pattern of BP fluctuation remained risk factors for 90-day stroke or TIA after TKA. BP fluctuation patterns in the early postoperative period are associated with 90-day stroke and TIA following primary TKA.

Background: In patients with resolved symptoms, transient ischemic attack (TIA) is distinguished from ischemic stroke by neuroimaging evidence of acute infarction. DW-MRI has been shown to be more sensitive at detecting infarction than CT, but is not uniformly available in the acute setting. Hypothesis: We sought to identify predictors of stroke diagnosis among a cohort of clinically suspected TIA patients undergoing an accelerated diagnostic protocol in an emergency department observation unit (EDOU). Methods: We prospectively studied 189 patients treated in the EDOU of a single tertiary care academic medical center. Patients underwent DW-MRI of the brain (unless contraindicated), and bedside neurologist evaluation. A CT scan of the brain was considered optional prior to EDOU admission. We compared the odds of extremity weakness, sensory loss, facial droop, visual disturbance, slurred speech, aphasia, dizziness, and headache between patients with final diagnosis of stroke, TIA and mimic. This study was approved by the hospital IRB. Results: Thirty-one patients (16%) were diagnosed with an acute ischemic stroke, 85 (45%) TIA, and 73 (39%) mimic. Mean age was 64.8 years (SD = 15.5; range = 30-90). DW-MRI was performed on 92% of patients. A CT scan was also performed in 80% of patients diagnosed with stroke and 0 were diagnostic. Median ABCD2 scores were 4 for stroke and TIA (IQR 3-5) and 3 for mimic (IQR 2-4). Only headache symptoms predicted lower odds of stroke (OR 0.22; 95% CI: 0.05-0.96). Both headache (OR 1.44; 95% CI: 1.03-2.03) and visual disturbance (OR 3.14; 95% CI: 1.49-6.65) increased the odds of mimic diagnosis, but were also present in 13% and 10% of stroke patients respectively. Slurred speech (OR 0.48: 95% CI: 0.25-0.93); aphasia (OR 0.34 95% CI: 0.15-0.76) and facial droop (OR 90.36: 95% CI: 0.14-0.94) significantly predicted lower odds of mimic diagnosis. Conclusions: In our investigation of patients with transient neurologic dysfunction in an EDOU, stroke diagnosis was common and could not be predicted by clinical variables alone. Early DW-MRI should be considered in all TIA patients, especially those reporting slurred speech, aphasia or facial droop.

The authors have reviewed 150 consecutive carotid endarterectomies in 140 patients performed by three neurosurgeons. These were performed in two small community hospitals. There was an overall mortality rate of 1.3%; major or minor stroke was seen in 2.7% of patients and transient neurological dysfunction in 2.7%. Preoperative symptoms included major or minor stroke in 39.3% of patients and transient neurological dysfunction in 43.3%; 17.3% of patients were asymptomatic. The patients were continuously monitored intraoperatively with electroencephalography. There were two operative deaths, both related to myocardial infarction and both on the 2nd postoperative day. These statistics appear to compare favorably with those of series reported by major institutions. The average number of carotid endarterectomies per surgeon per year was 10. These were performed over a 7-year period (October, 1976, through November, 1983). Previous series have implied the need for higher frequency in performing the procedure to assure low morbidity and mortality rates. This series appears to offer evidence to the contrary. A key to these results has been that in 148 of the 150 operations, the primary surgeon has been assisted by one of the other two neurosurgeons. This affords the primary surgeon the benefit of excellent technical assistance, and also broadens the experience of the assisting surgeon, thereby allowing maximum experience from the small volume of cases.

Meningeal Disease Masquerading as Transient Ischemic Attack

Transient neurological dysfunction may be associated with uncommon disorders and should prompt consideration of a broad differential diagnosis when assessing patients with episodic symptoms. The most common causes of transient neurological dysfunction include transient ischemic attack (TIA), seizure disorder, and migraine and its variants. However, underlying unusual pathophysiological processes such as brain tumors can also cause transient neurological dysfunction. Here we present a case of a 68-year-old male with oligodendroglial gliomatosis cerebri (OGC) who presented with TIA-like symptoms. Brain magnetic resonance imaging revealed multiple diffuse T2 hyperintensities within the white and gray matter. Magnetic resonance spectroscopy was suggestive of gliomatosis cerebri and was particularly helpful in this case. The diagnosis of OGC was confirmed by histopathology and molecular genetic studies on brain biopsy tissue. In this report, we discuss the clinical and radiological characteristics of OGC and highlight the unusual presentation of this case.

Transient Neurologic Deficits: Can Transient Ischemic Attacks Be Discrimated from Migraine Aura without Headache?

Patients with "migraine aura without headache" can be separated from those with transient ischaemic attacks (TIA) on the basis of the onset of symptoms, which is generally gradual and which spread or intensify over minutes or hours, and from the typical migrainous nature of their visual symptoms. Fifty cases were prospectively identified and these were compared with 50 age matched patients with a TIA. Surprisingly, there were no significant differences in the prevalence of vascular risk factors and diseases in the two groups although those with TIAs tended to have more. Only one patient with "migraine aura without headache" suffered a subsequent vascular event (a myocardial infarction). Three patients with TIAs had strokes and two others died from vascular disease. Although the results are not conclusive, they do suggest that patients with the clinical characteristics of "migraine aura without headache" have a low risk of subsequent vascular events, lower than those with TIAs, despite perhaps having similar prevalence of vascular risk factors. Although their risk factors should be treated, patients with "migraine aura without headache" should be reassured and not subjected to inappropriate and potentially hazardous investigations and treatment.

Transient ischemic attacks (TIAs) are warning episodes predicting that such patients are at high risk for stroke which potentially could be life-threatening or leave an individual with substantial disability. TIAs result from large or small vessel disease, cardiogenic embolic events and hematological abnormalities. The patient’s past and current medical history provides necessary clues suggesting which investigational tests should be conducted. Every patient presenting with a TIA should have a total blood count, electrocardiogram, and a brain imaging study. Patients with anterior circulation symptoms should undergo noninvasive carotid testing, usually by carotid duplex ultrasonography, to determine if there is a surgically remediable carotid stenosis. Patients with posterior circulation TIAs should undergo magnetic resonance angiography (MRA) or a conventional arteriogram which, if positive, may be an indication for anti-platelet or anticoagulation therapy. Other testing depends on the presumptive etiology of the TIA. In general, a TIA should be considered as a serious warning of impending stroke that requires rapid and efficient investigations to define and remedy the reasons for the cerebral ischemic events. TIAs by definition may last up to 24 h, but usually are self-terminating after a few minutes. They are a serious warning of possible future strokes that may result in substantial morbidity and mortality. Once TIAs are diagnosed, the major goal is to reduce the risk of future strokes. Patients with TIAs usually present in the Emergency Room or doctor’s office. They may seek immediate medical care or relate the history of the TIA during a routine visit. As soon as a diagnosis of a TIA is considered, a careful past and current medical history should be taken to substantiate the diagnosis. Conditions which mimic TIAs need to enter into the differential diagnosis and, if necessary, be ruled out. For example, a Todd’s transient paralysis can follow a partial focal seizure. Migraine auras may also mimic TIAs, particularly in the elderly. Any space-occupying lesions and arteriovenous malfunction may first present with a TIA-like complaint. Peripheral nerve disease must be recognized since it can cause transient weakness and/or numbness affecting one limb.

Episodic transient neurological symptoms are an important set of problems presenting to a neurologist in his routine practice. Occasionally, detailed clinical history including past and family history supplemented with focused examination can bring out a rare cause for such symptoms. We describe in this report in a young male presenting with episodic focal neurological dysfunction, with family history of similar episodes in mother and brother. Examination showed features of pes cavus and peripheral neuropathy for which patient was asymptomatic. Mother and brother were established cases of hereditary neuropathy. Imaging on multiple occasions showed reversible white matter abnormalities. Clinical suspicion of X-linked Charcot-Marie-Tooth disease type 1 (CMT1X) was confirmed with detection of mutation in Gap Junction B1 (GJB1) gene, which codes for connexin 32 protein (c.425G>A; p.R142Q hemizygous mutation). Though this mutation has been already reported in CMTX patients, it has not been associated with transient neurological dysfunctions. This is probably the first reported case of CMTX patient with transient neurological dysfunction from India, whose family members had similar episodes.

Deep Hypothermia With Retrograde Cerebral Perfusion Versus Moderate Hypothermia With Antegrade Cerebral Perfusion for Arch Surgery

Background: The extracardiac Fontan procedure, a palliative intervention for single‐ventricle physiology, is associated with significant thromboembolism and bleeding risks. Warfarin has been the standard anticoagulant, but its limitations have prompted exploration of nonvitamin K oral anticoagulants, such as rivaroxaban.Objective: To compare the safety and efficacy of rivaroxaban vs. warfarin as postoperative anticoagulation in pediatric patients following the extracardiac Fontan procedure, focusing on thromboembolic events, bleeding complications, and treatment adherence.Methods: This retrospective cohort study included 369 pediatric patients (aged 3–17 years) who underwent the extracardiac Fontan procedure at a single center from 2015 to 2022, selected from 412 cases reviewed, with 43 excluded due to incomplete follow‐up or comorbidities. Patients received either warfarin (n = 177) or rivaroxaban (n = 192) for anticoagulation. Baseline characteristics, including age, sex, body weight, and pulmonary artery pressure, were comparable between groups. Anticoagulation was initiated on postoperative Day 1 per institutional protocol, excluding aspirin to standardize thromboembolism prevention due to high risk in nonanticoagulated patients. Warfarin was titrated to an international normalized ratio (INR) of 2.0–3.0, while rivaroxaban was dosed per European Medicines Agency guidelines. Outcomes included thromboembolic events (graft thrombosis, pulmonary embolism, and transient ischemic attacks [TIAs]), major and minor bleeding, mortality, and treatment discontinuation over a mean follow‐up of 5 years. TIAs were defined per American Heart Association guidelines as transient neurological dysfunction lasting less than 24 h without infarction on neuroimaging. Statistical analyses used Fisher’s exact test, Kaplan–Meier survival analysis, and multivariable logistic regression, with p < 0.05 indicating significance; the study was designed to detect a 3% difference in major bleeding. The limited number of thromboembolic events resulted in wide confidence intervals, limiting precision in between‐group comparisons.Results: Thromboembolic events occurred in 5.1% (n = 9) of warfarin patients and 2.1% (n = 4) of rivaroxaban patients (OR = 2.5, 95% CI: 0.8–8.2). Major bleeding was significantly higher with warfarin (3.4%, n = 6; 4 intracranial and 2 gastrointestinal) than rivaroxaban (0.5%, n = 1; gastrointestinal; OR = 7.0, 95% CI: 1.2–40.8). Minor bleeding rates were 9.0% (warfarin) vs. 5.7% (rivaroxaban). Two warfarin‐related deaths (intracranial hemorrhage and systemic embolism post‐TIA) were recorded; none occurred with rivaroxaban. Treatment discontinuation was higher with warfarin (5.1% vs. 0.5%).Conclusions: Rivaroxaban demonstrated a superior safety profile compared to warfarin, with significantly lower major bleeding rates, no associated mortality, and improved treatment adherence in pediatric Fontan patients. Its fixed‐dose regimen simplifies management, although implementation requires consideration of cost and formulation access. Risk‐stratified approaches and larger prospective trials are needed to optimize anticoagulation strategies.

Transient ischaemic attacks (TIAs) are caused by an ischaemic focal neurological deficit lasting less than 24 hours without structural brain injury, as determined by diffusion-weighted MRI. Ischaemic stroke, on the other hand, is associated with a structural brain lesion. Causes are a transient or permanent occlusion of a cerebral artery with regional reduction of tissue perfusion, ischaemia, and transient or permanent neurological dysfunction. Cerebral arteries may occlude due to atherosclerosis of large cerebrovascular arteries, microvascular cerebral disease, haemodynamically induced ischaemia in the presence of severe carotid stenosis, or cardiac or paradoxical embolism. Rarely, aortic or carotid dissection can cause TIA or stroke. Risk factors are age, arterial hypertension, diabetes, smoking, lipid disorders, atrial fibrillation, and aortic valve disease, as well as obstructive sleep apnoea. The diagnosis involves cerebral imaging with computer tomography or MRI, as well as colour-coded duplex sonography of the extracranial cerebral arteries. Treatment may involve intravenous thrombolysis or intra-arterial catheter-based thrombectomy or antihypertensive medication in those with blood pressure values above 220 mmHg systolic. Secondary prevention is similar to that of acute coronary syndromes, but also involves left atrial appendix occlusion in those at high bleeding risk, and a history of TIA or embolic stroke.

Leukoencephalopathy and Cortical Laminar Necrosis Associated with Intrathecal Methotrexate and Cranial Irradiation

Affective disorders are common sequelae of cerebrovascular events. A myriad of evidence demonstrates that clinically significant depression can often follow a stroke. However, less is known about the extent to which anxiety disorders present after these experiences, and in particular, post-traumatic stress disorder (PTSD) with panic attacks. To our knowledge, the association between transient ischemic attacks (TIAs) and PTSD with panic attacks has not been described in the literature. Here we describe a patient with depression and PTSD with panic attacks following a transient ischemic attack. Many non-psychiatric physicians learn about post-stroke depression so they are equipped to screen for it. However, to many physicians, PTSD with panic attacks usually conjures the image of an individual who experienced either trauma or rape. Therefore, it is important to increase the awareness of such complications after TIAs. Increased awareness of these TIA sequelae has important implications for detection by non-psychiatric healthcare providers. Furthermore, prompt recognition and treatment has important implications for patient quality of life.