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Axons of postganglionic neurons branch many times close to their effector cells and have hundreds to thousands of varicosities, which contain transmitter(s) packed in vesicles. Excitation of the postganglionic neurons spreads over all its branches and invades all varicosities. Signal transmission from postganglionic neurons to most effector cells occurs through specific neuroeffector synapses. In the heart, acetylcholine released by parasympathetic cardiomotor axons reacts with junctional muscarinic receptors that are coupled via a intracellular second-messenger pathway to the cellular effectors. Arterioles and small arteries are influenced by neural release of noradrenaline and ATP from the varicosities of the vasoconstrictor axons. The ATP reacts with junctional purinoceptors and opens ligand-gated cation channels, which cause activation of voltage-sensitive calcium channels and resultant action potentials. Noradrenaline released from the postganglionic vasoconstrictor terminals reacts with junctionally and extrajunctionally located a-adrenoceptors leading to slow depolarization in some blood vessels. The influence exerted by autonomic neurons on their effector tissues may be modulated by local and remote non-neural signals. The mechanisms of neuroeffector transmission in different autonomic targets are diverse. As no exceptions have yet been found, it is not far-fetched to assume that neuroeffector transmission is specific for all target cells innervated by postganglionic neurons.
Roreitner scrutinizes Aristotle’s physiological description of perceptual processes, for which two alternative interpretations have been advocated in the past: it is either pneuma or blood which secures the communication between the peripheral organs of distal senses and the central organ. Roreitner assesses both these traditional interpretations and provides a third alternative according to which it is the body of blood-vessels rather than their content which provides this communication.
The cerebral microbleed (CMB) mimics form two types: those that contain blood products and those that do not (resembling CMBs because of shared signal intensity and morphology on gradient-recalled echo (GRE) MRI). This chapter describes both types, and outlines how these can be differentiated from true CMBs. It suggests a topographical approach to the recognition of CMB mimics on brain imaging. The GRE sequences used in the detection of CMBs are sensitive not only to blood breakdown products (deoxyhemoglobin, methemoglobin, hemosiderin and ferritin) but also to other paramagnetic substances such as calcium, manganese and iron, all of which may appear as foci of low signal. In lobar regions of the brain, common CMB mimics include vascular flow voids and hypointensities arising from partial volume artefact. The development of susceptibility-weighted imaging (SWI) has improved the detection of structures containing extravascular blood products, as well as those containing venous deoxygenated blood.
Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are used instead of conventional angiography for many cases requiring evaluation of the blood vessels. This chapter discusses the indications, diagnostic capabilities, and limitations of CTA of the upper and lower extremities, followed by images of important pathological findings. CTA, like conventional angiography, should be performed after traumatic injuries in patients whose injured extremity is pulseless, has a neurological deficit, has an expanding hematoma, or has a bruit or thrill. It can be used to detect most vascular lesions, including thrombus, aneurysm, arteriovenous fistulas, and injury to the vessel wall. CTA is useful in detecting traumatic injuries, with specificities from 87% to 98%. Suitable images require multidetector scanners and appropriate reconstruction software. Since CTA is not performed in real time but produces static images, it may be difficult to delineate vascular occlusion and other vascular injuries from vasospasm.
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