Transient Neurological Symptoms Research Articles

Migraine and Patent Foramen Ovale: Barking up the Wrong Tree?

Migraine and Patent Foramen Ovale: Barking up the Wrong Tree?

ED50 and ED90 of intrathecal hyperbaric 2% prilocaine in ambulatory knee arthroscopy.

Hyperbaric 2% prilocaine (HP) is increasingly used for spinal anesthesia in day-case surgery. The aim of this prospective double-blind study was to determine the effective dose (ED)50 and the ED90 of HP for patients undergoing knee arthroscopy. Doses of HP were determined using an up-and-down sequential allocation technique. Sequences were analyzed by isotonic regression analysis. A subsequent observational study was performed with the calculated ED90 in 50 patients to confirm the initial result and to describe the induced blockade effects and side effects. Times corresponding to onset and duration of sensory and motor block, surgical data, and side effects were recorded. The ED50 was estimated at 28.9 mg (95% confidence interval [CI]: 26.5 to 35.3) and the ED90 was estimated to be 38.5 mg (95% CI: 35.7 to 39.5). A 40 mg dose of HP provided efficient anesthesia in 46 patients (92%, 95% CI: 82 to 98). The average (SD) time to effective anesthesia was 14.5 (3.9) min. Complete sensory block at level T12 was obtained after ten minutes in 44 of 50 patients. The average (SD) duration of the sensory block was 205 (36.1) min. Maximal level of sensory block was obtained at the T8-T11 levels in 41 of 50 patients without hemodynamic instability. A Bromage 3 score was obtained in 40 of the 46 patients who achieved successful anesthesia after 30 min. Patients did not experience urinary retention, nor were any signs of transient neurologic symptoms observed. This study determined the ED50 of HP is 28.9 mg and suggests that a 40-mg dose of HP is adequate to provide successful spinal anesthesia for outpatient knee arthroscopy.

Cerebral amyloid angiopathy: a transient ischaemic attack mimic

Cerebral amyloid angiopathy is a commonly occurring condition that is not familiar to most clinicians. A common presenting feature may be transient focal neurological symptoms leading to the potential for clinical misdiagnosis as transient ischaemic attack. This may result in the inappropriate use of anti-platelets and anticoagulants or radiological misdiagnosis. It is also being increasingly recognised as an important cause of spontaneous intracerebral haemorrhage and cognitive impairment in the elderly. Cerebral amyloid angiopathy can be diagnosed based on clinical and radiological findings, but clinicians need a high index of suspicion to ensure appropriate investigations are requested. In this article we aim to cover the pathophysiology, clinical findings, radiological appearances and approach to management of cerebral amyloid angiopathy.

C2 compressive osteochondroma with transient neurologic symptoms in a pediatric patient

C2 compressive osteochondroma with transient neurologic symptoms in a pediatric patient

Acute kidney injury due to decompression illness.

Decompression illness is a rare but serious complication of diving caused by intravascular or extravascular gas bubble formation. We report the first case of acute kidney injury in a 27-year-old diver following three rapid ascents. He presented with transient neurological symptoms and abdominal pain followed by rapidly progressive acute kidney injury (creatinine peak 1210 µmol/L) due to arterial air emboli. He received supportive care and 100% oxygen followed by hyperbaric therapy and recovered fully. Arterial air emboli caused by rapid decompression can affect multiple organs including the kidneys. Early transfer to a hyperbaric unit is important as complications may present delayed.

Posterior reversible encephalopathy syndrome: differences between pregnant and non-pregnant patients.

Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiologic entity not yet understood, that presents with transient neurologic symptoms and particular radiological findings. Few papers show the differences between pregnant and non-pregnant patients. We review the cases of 38 women diagnosed with PRES, in order to find significant differences between pregnant (18) and non-pregnant (20) patients. We found differences among the age of patients (25.83 years old in pregnant and 29.31 years old in non pregnant; P=0.001); in the mean of highest systolic blood pressure, that was higher in non-pregnant group (185:162 mmHg; P=0.121); and in creatinine levels that was higher in non-pregnant group (3.47:1.04 mg/dL; P=0.001). To our knowledge, just a few papers analyzed whether PRES syndrome presented in the same way in pregnant and non-pregnant patients. The differences and the possible pathophisiology of this syndrome still remain enigmatic.

Intrathecal 1% 2-chloroprocaine vs. 0.5% bupivacaine in ambulatory surgery: a prospective, observer-blinded, randomised, controlled trial

This prospective, observer-blinded, randomised, multicentre study aimed at determining the non-inferiority of 50 mg of plain 1% 2-chloroprocaine vs. 10 mg of 0.5% plain bupivacaine in terms of sensory block onset time at T10 after spinal injection. The study hypothesis was that the difference in onset times of sensory block to T10 between the two drugs is ≤ 4 min. One hundred and thirty patients undergoing lower abdominal or lower limb procedures (≤ 40 min) were randomised to receive one of two treatments: 50 mg of plain 1% 2-chloroprocaine (Group C, n = 66) or 10 mg of plain 0.5% bupivacaine (Group B, n = 64). Times to sensory and motor block onsets, maximum sensory block level, readiness for surgery, regression of sensory and motor blocks, first analgesic requirements, unassisted ambulation, home discharge, and side effects after 24 h and 7 days were registered blindly. Chloroprocaine was comparable with plain 0.5% bupivacaine in terms of time to sensory block at T10 level. Group C showed faster onsets of motor block (5 vs. 6 min), maximum sensory block level (8.5 vs. 14 min), resolution of sensory (105 vs. 225 min) and motor (100 vs. 210 min) blocks, unassisted ambulation (142.5 vs. 290.5 min), first analgesic requirement (120 vs. 293.5 min), and home discharge (150 vs. 325 min) (all comparisons, P < 0.05). No chloroprocaine patient developed transient neurological symptoms. Spinal anaesthesia with 50 mg of plain 1% 2-chloroprocaine is similar to 10 mg of plain 0.5% bupivacaine in terms of onset of sensory block at T10 but shows quicker recovery from anaesthesia than with 0.5% bupivacaine.

Transient CNS Deficits and Migrainous Auras in Individuals Without a History of Headache

To demonstrate that benign transient focal neurological symptoms represent equivalents of migraine auras without headache. Benign focal neurological symptoms suggesting cerebral dysfunction are common and usually prompt an extensive diagnostic workup, but their etiology is often not elucidated. We hypothesized that benign transient focal neurological symptoms represent equivalents of migraine auras without headache, even in subjects who have never experienced migraine headaches. We led a cross-sectional study and identified individuals who presented at least 1 episode of unexplained transient focal neurological symptoms suggestive of cerebral dysfunction, but no history of migraine headache, among physicians and inpatients of an academic hospital. Cortical hyperexcitability, assessed by occipital transcranial magnetic stimulation (oTMS), was used as a marker of possible migraine auras without headache. Frequency of transient focal neurological symptoms suggestive of cerebral dysfunction among the physicians who responded was 9% (21/233), vs 0.09% (6/690) of inpatients. Most episodes resembled typical visual migrainous auras. Motor, sensory, and language dysfunction were more common among inpatients than among physicians. oTMS induced phosphenes in 12/16 (75%) subjects and in none of 10 controls. Benign focal neurological symptoms were common in our population and likely represent migraine aura without headache. Non-visual symptoms are less common and lead to medical consultation. oTMS is abnormal in most cases, supporting the diagnosis of migraine aura without headache and helping separate this benign condition from transient ischemic attacks.

Clinical Associations and Causes of Convexity Subarachnoid Hemorrhage

It has been previously found noted that ≈15% to 20% of subarachnoid hemorrhage (SAH) is nonaneurysmal. Nontraumatic convexity SAH (cSAH) is increasingly recognized. Data concerning incidence and associations are scant. We identified all SAH-coded cases from South Australian public hospitals between January 2005 and July 2011. Electronic discharge summaries were reviewed, and cases of cSAH were ascertained. Clinical and radiological features were recorded, and pathogenesis was assigned. Of 742 cases with SAH, 41 (6%) cases were cSAH, giving a minimum population annual incidence of 5.1 per million (95% confidence interval, 3.7-7.0). Median age was 70 years (interquartile range, 48-79). Commonest causes were cerebral amyloid angiopathy (39%), reversible cerebral vasoconstriction syndrome (17%), cerebral venous sinus thrombosis (10%), large-vessel stenotic atherosclerosis (10%), and posterior reversible encephalopathy syndrome (5%). No cause was identified in 20% (mostly elderly patients with incomplete evaluation). Most (63%) presented with transient neurological symptoms. Many (49%) were misdiagnosed as transient ischemic attacks and treated inappropriately with antithrombotics. cSAH comprises a significant proportion of SAH. Commonest causes are cerebral amyloid angiopathy in the elderly and reversible cerebral vasoconstriction syndrome in the young, but differential diagnosis is broad. Misdiagnosis is common and leads to potentially harmful treatments.

Abstract W P173: The Use of Mass Spectroscopy-Based Proteomics to Identify Novel Biomarkers of Cerebral Ischemia

Background: Cerebral ischemia and its mimics are often difficult to differentiate. While MRI is the gold standard for stroke diagnosis, a marker for TIA remains elusive. Proteomics offers a unique method to identify biomarkers of ischemic disease. Through the use of mass spectrometry-based proteomics, we analyzed the serum of patients with transient neurologic symptoms in our emergency department to determine candidate proteins to serve as indicators of cerebral ischemia. Methods: Patients with transient neurologic symptoms were prospectively enrolled and their serum was obtained. Mass spectrometry was performed on the samples, and the results were searched against the Human Uniport database to identify the most likely proteins. The student’s t-test was utilized to compare protein levels between the different clinical conditions, and significance was determined by using the Benjamini-Hochberg false discovery rate (FDR) controlling procedure for multiple comparison adjustments. Results: Twenty patients with TIAs, fifteen patients with minor strokes, and twelve control patients (i.e. migraine, seizure) were enrolled. Ceruloplasmin (p = 0.00027) and complement component C8 gamma chain (p = 0.00105) were increased in TIA and minor stroke compared with the control group, while platelet basic protein (p = 0.00010) was decreased. TIA patients tended to have higher Ig kappa chain 6 region AG and platelet basic protein levels and lower apolipoprotein F levels than stroke patients (p &lt;0.05), but these differences were not significant after FDR adjustments. Conclusions: Mass spectroscopy-based proteomics is a potential new tool to help identify biomarkers for cerebral ischemia. Ultimately, a panel of proteins may serve as a marker for cerebral ischemia or TIA. We have identified three candidate proteins as possible indicators for cerebral ischemia. Larger studies are needed to confirm our results.

Abstract T P183: Transient Neurological Symptoms with MRI Evidence of Infarction in an Emergency Department Observation Unit

Background: Transient symptoms with infarction (TSI) is distinguished from transient ischemic attack (TIA) by the presence of diffusion-weighted imaging (DWI) lesions on MRI. We report a series of patients with DWI lesions identified in an emergency department observation unit (EDOU) TIA protocol. Methods: Patients were treated in the ED of a tertiary care center (annual census=100,000 visits). In the first 3 months of operation of an EDOU for TIA, 50 patients met inclusion criteria of sudden/transient neurological deficit in the absence of known metabolic or cardiac source. Patients were excluded from the study if they demonstrated: persistent or stuttering deficits; fever &gt;100.4F, heart rate &lt;60 or &gt;100 bpm; SBP &gt;180 or &lt;100mmHg; pulse ox &lt;93%; or positive CT. Evaluation included: laboratory analyses; CT/MRI/MRA of the head/neck; EKG; echocardiogram, and neurology consult. MR data (ED 1.5T MR unit) include: DWI, ADC, GRE, and T2FLAIR images. Patients with TSI, were identified by the presence of 1 or more DWI bright and ADC dark lesions on ED MRI. All patients completed CT and MR imaging within &lt; 24 hours of admission. This study was approved by the hospital IRB. Results: TSI was identified in 10/50 EDOU patients (Mdn age 72.5, ABCD2 score 5). Two patients demonstrated infarcts in multiple vascular territories. Table 1 illustrates patient demographics, comorbidities, presentations, and outcome. Fifty percent of TSI patients were admitted from EDOU, 3 patients returned to the ED within 30 days , and no 30 day distinct recurrent events, such as recurrent stroke were identified. Conclusions: EDOU for TIA including DW-MRI resulted in TSI diagnosis in 20% of patients. In the TSI cases identified, infarct locations were heterogeneous; vascular and/or cardiac etiology must be considered. Longitudinal analysis is recommended to further assess the relationship between presentation, TSI risk, risk of recurrent stroke, and need for hospital admission.

Management of Symptomatic Carotid Disease in 2014

Extracranial carotid artery stenosis accounts for up to 12 % of stroke, the third leading cause of death in industrialized nations. Carotid stenoses leading to transient or permanent neurologic or retinal symptoms within the preceding 6 months are deemed symptomatic and require prompt noninvasive evaluation and treatment. Preventive medical therapy is standard for symptomatic carotid stenosis and continues to evolve. Landmark trials have proven carotid endarterectomy (CEA) superior to medical therapy for stroke prevention in symptomatic lesions. Modern investigations have proven carotid artery stenting (CAS) non-inferior to CEA, and the strength of the combined data has led to a class I recommendation for CEA or CAS in patients with high grade symptomatic carotid stenosis, provided the risk of perioperative events is acceptable. Evidence-based modern management of symptomatic carotid stenosis is reviewed here.

Results of percutaneous closure of patent foramen ovale with the GORE® septal occluder

The aim of this study was to evaluate the safety and efficacy of the GORE(®) Septal Occluder (GSO) at 1-, 6-, and 12-month follow-up in patients with a clinical indication for patent foramen ovale (PFO) closure. Limited data are available regarding the safety and efficacy of the GSO for PFO closure. Sixty consecutive patients with an embolic event, migraine, or risk of decompression sickness were enrolled. Transesophageal or transthoracic echocardiography and clinical follow-up were performed at 1, 6 and 12 months after implantation. All patients received 100 mg aspirin and 75 mg clopidogrel for 6 months. Procedures were technically successful in 98.3% (59/60). In one case, the anterior interatrial septal rim proved too short to allow safe GSO implantation and, instead, a different occluder was implanted. One patient developed transient neurological symptoms during the procedure without evidence for a stroke by magnetic resonance imaging. At 6-month follow-up, the closure rate was 86.6% (52/60). The complete closure rate after 1 year was 93.3% (56/60). Stroke, thrombus formation and atrial fibrillation (AF)/flutter occurred in 1 (1.7%), 1 (1.7%), and 5 (8.3%) patients, respectively. PFO closure with the GSO is accompanied by a high technical success rate and closure rates similar to other currently used devices. The incidence of AF was higher than reported with most other devices. This may be a chance finding but warrants further investigation in larger trials.

Magnetic resonance imaging in patients with transient ischemic attack.

Magnetic resonance imaging in patients with transient ischemic attack.

Importance of transient neurological attacks (TNAs)

Transient neurological attacks (TNAs) are attacks with temporary (< 24 h) neurological symptoms, and reported in 1975. Ischemic cerebral infarction often occurres after transient neurological symptoms which are not sometimes involved in transient ischemic attack (TIA) criteria. The purpose of this study was to clarity transient neurological symptoms before the onset of ischemic stroke. Consecutive acute stroke and TIA patients within 7 days of onset between July 2011 and December 2012 were studied. Questionnaire survey of transient neurological symptoms was done and we investigated the history of transient neurological symptoms and divided the patients into three groups, TIA group (history of TIA), TNAs group (history of TNAs), and no past history group. We compared clinical characteristics, the rate of posterior circulation lesions, and number of attacks among three groups. 184 patients (male 112 patients, mean 73 years old) were enrolled into the present study. TNAs group had 13 (7%) patients, and TIA had 20 (11%). Neurological symptoms of TNAs group were 5 (38%) transient dizziness, 3 (23%) disturbance of consciousness, 2 (23%) weakness of legs, 1 (8%) sensory disturbance of legs, 1 (8%) gait disturbance, and 1 (8%) sensory disturbance of lips. Five (38%) TNAs group had multiple attacks. In 33 transient neurological symptom patients, 17 (52%) patients did not have hospital visit, and 7 (21%) patient did not have antiplatelet and anticoagulant drug. TNAs group more frequently had hyperlipidemia, diabetes mellitus, and posterior circulation lesions among three groups. 20% posterior circulation lesion patients had TNAs history, and posterior circulation might be examined in TNAs patients.

Acute myocardial infarction

A 62-year-old man was woken by a prolonged and very intensive episode of retrosternal pain. His past medical history included a prostate cancer treated 2 years before with radical prostatectomy and radiation therapy. Thirty minutes after the onset of symptoms, his wife called the regulatory centre of medical emergency (Service d’Aide Medicale d’Urgence). Before the arrival of the physician-staffed ambulance, she noted that her husband became apparently confused and no more complained of chest pain. She did not witness a transient loss of consciousness. When the rescue staff arrived to patient’s home, vital signs were as follows: blood pressure 155/95 mmHg, heart rate 95 beats/min, respiration rate 18 breaths/min and oxygen saturation 96%. Physical examination ruled out focal neurological and congestive heart failure signs. A 12-lead ECG showed a marked ST-segment elevation in anterior leads associated with an inferior ST-segment depression. Sublingual nitrates were ineffective on these ST-segment alterations. Despite neurological symptoms and the absence of persistent chest pain, he was treated like a ST-segment elevation myocardial infarction. Consequently, he received 250 mg of intravenous aspirin, 3000 UI of intravenous enoxaparin and 600 mg of clopidogrel. He arrived to catheterization laboratory 45 min after the first medical contact. Coronary angiogram performed via a right transradial approach demonstrated a culprit lesion on the mid-left anterior descending artery (LAD) coronary artery segment (Fig. 1). The blood flow was thrombolysis in myocardial infarction (TIMI 1) in the distal LAD segment. The remaining coronary tree was free from noticeable plaque. Thrombus aspiration followed by a direct bare-metal stent stenting restored a TIMI 3 blood flow. The brain computed tomography (CT) scan performed immediately after percutaneous coronary intervention was normal. At admission to the ICU of cardiology, haemodynamic status was stable. It remains an anterograde and a mild retrograde amnesia. He remembered the last evening, but did not remember having chest pain or coronary angiogram. He repeated continuously the same questions. Personal knowledge was spared; he was able to provide information about his past history. Physical examination did not find other cognitive impairment, focal neurological or cardiac signs. A second 12-lead ECG revealed a resolve of ST-segment alterations and the emergence of Q waves on anterior leads. Transthoracic echocardiography evaluated left ventricular ejection fraction at 45% with an area at risk concerning apical and mid (anterior, septal and lateral) segments of the left ventricle. Biological parameters ruled out hypoglycemia and unknown diabetes or dyslipidemia. Troponin peak rose to 29mg/l (normal less than 0.1mg/l) and B-type natriuretic peptide was in the normal range. The amnesic gap resolved within 12 h from the onset of symptoms. A transient global amnesia following anterior ST-segment elevation myocardial infarction was finally diagnosed. The patient was discharged from hospital on the third day with a usual postmyocardial infarction treatment. The transient neurological symptoms were explored by a cerebral MRI performed 4 weeks later, which excluded any ischemic event in the vertebrobasilar territory (Fig. 2).

Causes and consequences of sports concussion.

Concussion in sports is a topic that is receiving increasing amounts of publicity and attention. Increasing recognition of concussion as well as improving understanding of the short- and long-term physiologic effects of concussion have resulted in widespread legislation governing the recognition and treatment of sports concussion. The increasing amount of medical research in the field and oftentimes subjective symptoms of concussion leave many ethical questions to be answered.

Migraine with Aura Phenomenology and Length

About 30 % of patients with migraine suffer from episodes of migraine with aura. Migraine with aura is characterized by transient focal neurologic symptoms, visual, sensory, or dysphasic, more rarely motor or brainstem, called ‘aura’ that are usually followed by a full migraine. The symptoms of the aura phase develop usually progressively over minutes and generally last for 5 to 60 minutes, although in a significant proportion of patients can be longer. The presumed substrate of migraine with aura is cortical spreading depression (CSD), a primarily neuronal phenomenon that causes a progressive shutdown of the cerebral cortex, starting from the occipital area and spreading onward at a speed of 2 to 3 mm per minute. The susceptibility to generate a CSD seems to be an intrinsic property of the migrainous brain.

Familial hemiplegic migraine and spreading depression.

Familial hemiplegic migraine (FHM) is an autosomal dominantly inherited subtype of migraine with aura, characterized by transient neurological signs and symptoms. Typical hemiplegic migraine attacks start in the first or second decade of life. Some patients with FHM suffer from daily recurrent attacks since childhood. Results from extensive studies of cellular and animal models have indicated that gene mutations in FHM increase neuronal excitability and reduce the threshold for spreading depression (SD). SD is a transient wave of profound neuronal and glial depolarization that slowly propagates throughout the brain tissue and is characterized by a high amplitude negative DC shift. After induction of SD, S218L mutant mice exhibited neurological signs highly reminiscent of clinical attacks in FHM type 1 patients carrying this mutation. FHM1 with ataxia is attributable to specific mutations that differ from mutations that cause pure FHM1 and have peculiar consequences on cerebellar Cav2.1 currents that lead to profound Purkinje cell dysfunction and neuronal loss with atrophy. SD in juvenile rats produced neuronal injury and death. Hormonal factors involved in FHM affect SD initiation and propagation. The data identify SD as a possible target of treatment of FHM. In addition, FHM is a useful model to explore the mechanisms of more common types of migraine.

Branching Enzyme Deficiency

The neuromuscular presentation of glycogen branching enzyme deficiency includes a severe infantile form and a late-onset variant known as adult polyglucosan body disease. Herein, we describe 2 patients with adult acute onset of fluctuating neurological signs and brain magnetic resonance imaging lesions simulating multiple sclerosis. A better definition of this new clinical entity is needed to facilitate diagnosis. To describe the clinical presentation and progression of a new intermediate variant of glycogen branching enzyme deficiency and to discuss genotype-phenotype correlations. Clinical, biochemical, morphological, and molecular study of 2 patients followed up for 6 years and 8 years at academic medical centers. The participants were 2 patients of non-Ashkenazi descent with adult acute onset of neurological signs initially diagnosed as multiple sclerosis. Clinical course, muscle and nerve morphology, longitudinal study of brain magnetic resonance imaging, and glycogen branching enzyme activity and GBE1 molecular analysis. Molecular analysis showed that one patient was homozygous (c.1544G>A) and the other patient was compound heterozygous (c.1544G>A and c.1961-1962delCA) for GBE1 mutations. Residual glycogen branching enzyme activity was 16% and 30% of normal in leukocytes. Both patients manifested acute episodes of transient neurological symptoms, and neurological impairment was mild at age 45 years and 53 years. Brain magnetic resonance imaging revealed nonprogressive white matter lesions and spinocerebellar atrophy similar to typical adult polyglucosan body disease. GBE1 mutations can cause an early adult-onset relapsing-remitting form of polyglucosan body disease distinct from adult polyglucosan body disease in several ways, including younger age at onset, history of infantile liver involvement, and subacute and remitting course simulating multiple sclerosis. This should orient neurologists toward the correct diagnosis.