New Electrocardiographic Changes in Patients Diagnosed with Pulmonary Embolism.

BACKGROUND: The electronic medical record is a relatively new technology that allows quick review of patients' previous medical records, including previous electrocardiograms (ECGs). Previous studies have evaluated ECG patterns predictive of pulmonary embolism (PE) at the time of PE diagnosis, though none have examined ECG changes in these patients when compared with their previous ECGs. OBJECTIVE: Our aim was to identify the most common ECG changes in patients with known PE when their ECGs were compared with their previous ECGs. METHODS: A retrospective chart review of patients diagnosed with PE in the emergency department was performed. Each patient's presenting ECG was compared with their most recent ECG obtained before diagnosis of PE. RESULTS: A total of 352 cases were reviewed. New T wave inversions, commonly in the inferior leads, were the most common change found, occurring in 34.4% of cases. New T wave flattening, also most commonly in the inferior leads, was the second most common change, occurring in 29.5%. A new sinus tachycardia occurred in 27.3% of cases. In 24.1% of patients, no new ECG changes were noted, with this finding more likely to occur in patients younger than 60 years. CONCLUSIONS: The most common ECG changes when compared with previous ECG in the setting of PE are T wave inversion and flattening, most commonly in the inferior leads, and occurring in approximately one-third of cases. Approximately one-quarter of patients will have a new sinus tachycardia, and approximately one-quarter will have no change in their ECG.

Rapid prototyping for neuroscience and neural engineering.

Rapid prototyping (RP) is a useful method for designing and fabricating a wide variety of devices used for neuroscience research. The present study confirms the utility of using fused deposition modeling, a specific form of RP, to produce three devices commonly used for basic science experimentation. The accuracy and precision of the RP method varies according to the type and quality of the printer as well as the thermoplastic substrate. The printer was capable of creating device channels with a minimum diameter of 0.4 or 0.6mm depending on the orientation of fabrication. RP enabled the computer-aided design and fabrication of three custom devices including a cortical recording/stroke induction platform capable of monitoring electrophysiological function during ischemic challenge. In addition to the recording platform, two perfusion chambers and a cranial window device were replicated with sub-millimeter precision. The ability to repeatedly modify the design of each device with minimal effort and low turn-around time is helpful for oft-unpredictable experimental conditions. Results obtained from validation studies using both the cortical recording platform and perfusion chamber did not vary from previous results using traditional hand-fabricated or commercially available devices. Combined with computer-aided design, rapid prototyping is an excellent alternative for developing and fabricating custom devices for neuroscience research.

Electrophysiological response dynamics during focal cortical infarction.

While the intracellular processes of hypoxia-induced necrosis and the intercellular mechanisms of post-ischemic neurotoxicity associated with stroke are well documented, the dynamic electrophysiological (EP) response of neurons within the core or periinfarct zone remains unclear. The present study validates a method for continuous measurement of the local EP responses during focal cortical infarction induced via photothrombosis. Single microwire electrodes were acutely implanted into the primary auditory cortex of eight rats. Multi-unit neural activity, evoked via a continuous 2 Hz click stimulus, was recorded before, during and after infarction to assess neuronal function in response to local, permanent ischemia. During sham infarction, the average stimulus-evoked peak firing rate over 20 min remained stable at 495.5+/-14.5 spikes s-1, indicating temporal stability of neural function under normal conditions. Stimulus-evoked peak firing was reliably reduced to background levels (firing frequency in the absence of stimulus) following initiation of photothrombosis over a period of 439+/-92 s. The post-infarction firing patterns exhibited unique temporal degradation of the peak firing rate, suggesting a variable response to ischemic challenge. Despite the inherent complexity of cerebral ischemia secondary to microvascular occlusion, complete loss of EP function consistently occurred 300-600 s after photothrombosis. The results suggest that microwire recording during photothrombosis provides a simple and highly efficacious strategy for assessing the electrophysiological dynamics of cortical infarction.

A method for monitoring intra-cortical motor cortex responses in an animal model of ischemic stroke.

Neuroplasticity is believed to play a key role in functional recovery after stroke. Neuroplastic effects can be monitored at the cellular level via e.g. neurotransmitter assessment, but these studies require sacrifice of the animal. FMRI can be used to assess functional neuronal performance, but the spatial and temporal resolution is far from the single cell level. The objective was to establish an effective method for short-term analysis of single and multi-unit electrophysiological function before, during and after stroke. We instrumented one rat with a 16-ch array in the primary motor cortex (100 microm wire diameter) to monitor cortical activity. A bipolar cuff electrode was implanted around the Ulnar nerve in the contralateral forelimb to provide a controlled electrical stimulus input to the sensory-motor system. A 3 mm diameter ischemic infarct was created immediately posterior to the electrode array by light activation of a photosensitive dye (Rose Bengal, 1.3 mg/100 mg body weight) at the cortical surface. M1 activity in response to the peripheral electrical stimulus was recorded before, during and after the cortical ischemic infarct. At 425 min following ischemic infarct the peak peri-stimulus time response had decreased to 30 +/- 11% (electrodes placed 1.5 mm from the infarct core) of the activity before the ischemic onset. The mean response latency increased from 30.1 +/- 4.5 ms (before infarct) to 40.6 +/- 8.5 ms (at 425 min). This dynamic view of neuroplasticity may eventually assist in optimizing acute stroke therapies and optimize functional recovery further.