Positron emission tomography (Pet)

PET (Positron emission tomography) gives insights into the function of the living brain as well as its structure. It uses the principles of computerized tomography in that Y-ray detectors are located around the head and the source is a positron-emitting compound either inhaled or injected, which enters the brain in described Figure. Compounds used involve receptor ligands, neurotransmitters and glucose analogs that are used for studying brain activity. Usually they are radio labeled with 116C, 137N, 158O or 189F that substitute for hydrogen. These isotopes have tiny half-lives decaying to the elements parts with atomic number one less; for instance:

The positron (e⁺, the antiparticle of the electron) travels a short distance before colliding with an electron (e^-). The two particles annihilate with the production of two Y-ray photons that shoot off in exactly against directions. These are detected simultaneously via a pair of detectors 180? apart. This coincidence detection permits localization of the site of the Y-ray emission that is among 2 and 8 mm from the positron source which is depending on the isotope used.

Spatial resolution of the Positron emission tomography is about 4–8 mm not as good as Computer assisted tomography but it can be used to follow brain events over time.

                                    Figure:  Positron emission tomography (PET).

The importance of Positron emission tomography in functional studies is described through the use of the nonmetabolizable analog of glucose, 2-deoxyglucose (2-DG). This molecule crosses the blood–brain barrier is transported into phosphorylated and neurons to 2-DG-6-phosphate, so it remains in the cell. Moreover, it cannot be metabolized additional. This means it acts as a marker for local glucose uptake and thus of neuron activity. Imaging the distribution of [189F] 2-DG although subjects engage in sensory cognitive or motor tasks reveals how these functions are localized in the brain. Associated studies show in which during transient increases in neuronal activity the increment in local cerebral oxygen consumption (as measured through 158O PET) does not match the increase in glucose utilization as probable from 2-DG PET. This implies in which short periods of brain activity can be supported through glycolysis.