Magnetic Resonance Imaging (MRI)

Diffusion MR imaging provides unique information about the physiologic state of ischemic tissue. It is highly sensitive and specific in the detection of acute and hyperacute ischemic stroke and has greatly improved the diagnosis and treatment of acute stroke. The DWI abnormality provides information about clinical outcome and final infarct size. Diffusion combined with perfusion MR imaging provides information about the operational ischemic penumbra and final infarct size. Diffusion MR imaging seems to be promising in the evaluation of candidates for thrombolysis.

We describe a method that directly relates tissue neuropathological analysis to medical imaging. Presently, only indirect and often tenuous relationships are made between imaging (such as MRI or x-ray computed tomography) and neuropathology. We present a biochemistry-based, quantitative neuropathological method that can help to precisely quantify information provided by in vivo proton magnetic resonance spectroscopy (1HMRS), an emerging medical imaging technique.

Although cerebellar alterations have been consistently noted in the addiction literature, the pathophysiology of this link remains unclear. The cerebellum is commonly classified as a motor structure, but human functional neuroimaging along with clinical observations in cerebellar stroke patients and anatomical tract tracing in non-human primates suggests its involvement in cognitive and affective processing. A comprehensive literature search on the role of the cerebellum in addiction was performed.

Functional magnetic resonance imaging (fMRI) experiments are more complex compared with standard radiological imaging, involving additional data streams and hardware along with complex analysis methods. Here, we propose guidelines based around mitigating risks associated with the complexities of the technique at the level of the individual imaging protocol, including workable and effective quality assurance/quality control procedures and rigorous, predefined, analysis pipelines.

There is increasing interest in the application of quantitative magnetic resonance imaging (MRI) methods to drug development, but as yet little standardization or best practice guidelines for its use in this context. Pharmaceutical trials are subject to regulatory constraints and sponsor company processes, including site qualification and expectations around study oversight, blinding, quality assurance and quality control (QA/QC), analysis and reporting of results.

Nalbuphine, an agonist-antagonist kappa-opioid, produces brief analgesia followed by enhanced pain/hyperalgesia in male postsurgical patients. However, it produces profound analgesia without pain enhancement when co-administration with low dose naloxone. To examine the effect of nalbuphine or nalbuphine plus naloxone on activity in brain regions that may explain these differences, we employed pharmacological magnetic resonance imaging (phMRI) in a double blind cross-over study with 13 healthy male volunteers.

The behavioral response to pain is driven by sensory and affective components, each of which is mediated by the CNS. Subjective pain ratings are used as readouts when appraising potential analgesics; however, pain ratings alone cannot enable a characterization of CNS pain circuitry during pain processing or how this circuitry is modulated pharmacologically. Having a more objective readout of potential analgesic effects may allow improved understanding and detection of pharmacological efficacy for pain.

We used functional magnetic resonance imaging (fMRI) to determine whether similar brain regions activate during noxious hot and cold stimulation. Six male subjects underwent whole brain fMRI during phasic delivery of noxious hot (46 degrees C) and noxious cold (5 degrees C) stimulation to the dorsum of the left hand. Mid-brain regions activated included thalamus, basal ganglia and insula. Cortical areas activated included cingulate, somatosensory, premotor and motor cortices, as well as prefrontal and inferior parietal cortex.

A dramatic increase in the use and dependence of prescription opioids has occurred within the last 10 years. The consequences of long-term prescription opioid use and dependence on the brain are largely unknown, and any speculation is inferred from heroin and methadone studies. Thus, no data have directly demonstrated the effects of prescription opioid use on brain structure and function in humans.