Using Single-Photon Emission Computerized Tomography on Patients With Positive Quantitative Electroencephalogram to Evaluate Chronic Mild Traumatic Brain Injury With Persistent Symptoms.

Background: Following mild traumatic brain injury (mTBI), also known as concussion, many patients with chronic symptoms (>3 months post injury) receive conventional imaging such as computed tomography (CT) or magnetic resonance imaging (MRI). However, these modalities often do not show changes after mTBI. We studied the benefit of triaging patients with ongoing symptoms >3 months post injury by quantitative electroencephalography (qEEG) and then completing a brain single positron emission computed tomography (SPECT) to aid in diagnosis and early detection of brain changes. Methods: We conducted a retrospective case review of 30 outpatients with mTBI. The patients were assessed by a neurologist, consented, and received a qEEG, and if the qEEG was positive, they consented and received a brain SPECT scan. The cases and diagnostic tools were collectively reviewed by a multidisciplinary group of physicians in biweekly team meetings including neurology, nuclear medicine, psychiatry, neuropsychiatry, general practice psychotherapy, neuro-ophthalmology, and chiropractic providers. The team noted the cause of injury, post injury symptoms, relevant past medical history, physical examination findings, and diagnoses, and commented on patients' SPECT scans. We then analyzed the SPECT scans quantitatively using the 3D-SSP software. Results: All the patients had cerebral perfusion abnormalities demonstrated by SPECT that were mostly undetectable by conventional imaging (CT/MRI). Perfusion changes were localized primarily in the cerebral cortex, basal ganglia, and cingulate cortex, and correlated with the patients' symptoms and examination findings. Qualitative and quantitative analyses yielded similar results. Most commonly, the patients experienced persistent headache, memory loss, concentration difficulties, depression, and cognitive impairment post mTBI. Because of their symptoms, most of the patients were unable to return to their previous employment and activity level. Conclusion: Our findings outline the physical basis of neurological and psychiatric symptoms experienced by patients with mTBI. Increased detection of mTBI can lead to development of improved targeted treatments for mTBI and its various sequelae.

Atrial fibrillation in patients with cryptogenic stroke.

BACKGROUND: Atrial fibrillation is a leading preventable cause of recurrent stroke for which early detection and treatment are critical. However, paroxysmal atrial fibrillation is often asymptomatic and likely to go undetected and untreated in the routine care of patients with ischemic stroke or transient ischemic attack (TIA). METHODS: We randomly assigned 572 patients 55 years of age or older, without known atrial fibrillation, who had had a cryptogenic ischemic stroke or TIA within the previous 6 months (cause undetermined after standard tests, including 24-hour electrocardiography [ECG]), to undergo additional noninvasive ambulatory ECG monitoring with either a 30-day event-triggered recorder (intervention group) or a conventional 24-hour monitor (control group). The primary outcome was newly detected atrial fibrillation lasting 30 seconds or longer within 90 days after randomization. Secondary outcomes included episodes of atrial fibrillation lasting 2.5 minutes or longer and anticoagulation status at 90 days. RESULTS: Atrial fibrillation lasting 30 seconds or longer was detected in 45 of 280 patients (16.1%) in the intervention group, as compared with 9 of 277 (3.2%) in the control group (absolute difference, 12.9 percentage points; 95% confidence interval [CI], 8.0 to 17.6; P<0.001; number needed to screen, 8). Atrial fibrillation lasting 2.5 minutes or longer was present in 28 of 284 patients (9.9%) in the intervention group, as compared with 7 of 277 (2.5%) in the control group (absolute difference, 7.4 percentage points; 95% CI, 3.4 to 11.3; P<0.001). By 90 days, oral anticoagulant therapy had been prescribed for more patients in the intervention group than in the control group (52 of 280 patients [18.6%] vs. 31 of 279 [11.1%]; absolute difference, 7.5 percentage points; 95% CI, 1.6 to 13.3; P=0.01). CONCLUSIONS: Among patients with a recent cryptogenic stroke or TIA who were 55 years of age or older, paroxysmal atrial fibrillation was common. Noninvasive ambulatory ECG monitoring for a target of 30 days significantly improved the detection of atrial fibrillation by a factor of more than five and nearly doubled the rate of anticoagulant treatment, as compared with the standard practice of short-duration ECG monitoring. (Funded by the Canadian Stroke Network and others; EMBRACE ClinicalTrials.gov number, NCT00846924.).

Reducing the delay in thrombolysis: is it necessary to await the results of renal function tests before computed tomography perfusion and angiography in patients with code stroke?

OBJECTIVE: We sought to determine the percentage of patients presenting with code stroke who would be excluded from computed tomography angiography, computed tomography perfusion, or both based on their emergency department laboratory results (creatinine and glomerular filtration rate) and the incidence of contrast-induced nephropathy in patients with code stroke who receive contrast. DESIGN: We conducted a retrospective analysis of our prospective code stroke database. SETTING: The study took place in an emergency department at a university medical center. RESULTS: A total of 131 consecutive patients with code stroke were identified. Of these, 11 (8.4%) would not have received contrast based on a creatinine level greater than 1.5 mg/dL on initial evaluation. However, 10 of these 11 patients (91%) had a history of renal disease. A total of 3% of patients who received contrast developed contrast-induced nephropathy. CONCLUSIONS: Our findings suggest that the use of contrast agents in patients with code stroke before availability of renal function tests appears safe in patients who do not have a known history of renal disease.

Association between serum ferritin level and perihematoma edema volume in patients with spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Preclinical evidence indicates that iron plays a key role in mediating neuronal injury and edema formation after intracerebral hemorrhage (ICH). However, the clinical role of iron in patients with ICH has not been well studied. We undertook this exploratory study to investigate the association of serum ferritin, as an indicator of body iron load, with perihematoma edema after ICH. METHODS: We retrospectively reviewed prospectively-collected clinical and laboratory data from 23 consecutive patients with acute spontaneous ICH who had a CT scan and serum ferritin checked on admission, and a follow-up CT scan 3 to 4 days afterward. We measured hematoma and edema volumes on admission and follow-up scans, and calculated the relative edema volume to correct for hematoma volume. We used Spearman correlation coefficient to determine the association of various variables with relative perihematoma edema volume. RESULTS: Whereas the median hematoma volume increased by approximately 28% from baseline to day 3 to 4, the relative edema volume almost doubled during this time period. We observed a significant positive correlation between serum ferritin and relative perihematoma edema volume on day 3 to 4 (r=0.78; P=0.002), but not at baseline; and little correlation between the changes in hematoma volumes and corresponding relative edema volumes (r=0.14). There was a trend for a positive correlation between body temperature and relative edema volumes. CONCLUSIONS: Our findings support the notion that delayed iron toxicity plays a role in causing brain injury and edema formation after ICH. These findings are preliminary and need to be further investigated in future studies.

Paradoxical clustering of brain metastases in an underperfused cerebral hemisphere.

OBJECTIVE: To describe a patient with a predominantly unilateral intracranial arterial stenosis who then developed metastatic lung cancer to the brain, with the tumors preferentially depositing in the underperfused cerebral hemisphere. DESIGN: Case report. SETTING: Inpatient neurology ward at a university medical center. Patient A 68-year-old woman with intracerebral arterial stenosis who then developed lung cancer with multiple metastases to the brain in an asymmetric arrangement. Main Outcome Measure The location of metastatic tumor deposits in relation to intracerebral arterial stenosis in the cerebral hemispheres of our patient. RESULTS: In this patient, most of the metastatic tumors were located in the underperfused cerebral hemisphere. CONCLUSIONS: This case demonstrates the concept that emboli washout by vigorous circulation is more important than direct delivery of embolic material in determining whether tumor cells will implant and grow in the brain.

Acute [corrected] stroke thrombolysis: an update [corrected].

Acute stroke therapy took a major step forward in 1996 after the approval of Intravenous (IV) tissue plasminogen activator (t-PA) by the US Food and Drug Administration for patients presenting within 3 hours of the onset of stroke symptoms. Since that time, there have been considerable advances in imaging techniques as well as the advent of devices to help in the management of acute stroke patients. As a result, the arsenal to treat acute stroke has grown, and the field of stroke as a subspecialty of neurology has emerged. Despite these advances, only 3% to 8% of eligible patients with acute stroke in the United States are administered thrombolytics.(1) We herein review the use of thrombolytics in stroke and provide an overview of the imaging advances, new devices, and recent trials that are shaping modern stroke therapy. Finally, we provide a practical approach to the management of acute stroke, specifically for the practicing cardiologist, who may encounter stroke during cardiac catheterization, post myocardial infarction (MI), and in a variety of other settings.