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Daffner RH best 80mg tadapox, Lupetin AR best 80 mg tadapox, Dash N et al (1986) MRI in the de- primary and secondary signs. Am J Roentgoenol 167:121-126 tection of malignant infiltration of bone marrow. McIntyre J, Moelleken S, Tirman P (2001) Mucoid degenera- Roentgoenol 146:353-358 tion of the anterior cruciate ligament mistaken for ligamentous 62. Skeletal Radiol 30:312-315 Assessment of knee cartilage in cadavers with dual-detector spi- 81. Bergin D, Morrison WB, Carrino JA et al (2004) Anterior cru- ral CT arthrography and MR imaging. Radiology 222:430-436 ciate ligament ganglia and mucoid degeneration: coexistence 63. Brown TR, Quinn SF (1993) Evaluation of chondromalacia of and clinical correlation. Am J Roentgoenol 182:1283-1287 the patellofemoral compartment with axial magnetic reso- 82. Nguyen B, Brandser E, Rubin DA (2000) Pains, strains, and nance imaging. Skeletal Radiol 22: 325-328 fasciculations: lower extremity muscle disorders. Disler DG, McCauley TR, Wirth CR et al (1995) Detection of Imaging Clin N Am 8:391-408 knee hyaline cartilage defects using fat-suppressed three-di- 83. Khan KM, Bonar F, Desmond PM et al (1996) Patellar tendi- mensional spoiled gradient-echo MR imaging: comparison nosis (jumper’s knee) : findings at histopathologic examina- with standard MR imaging and correlation with arthroscopy. Gagliardi JA, Chung EM, Chandnani VP et al (1994) nificance of magnetic resonance imaging findings. Am J Detection and staging of chondromalacia patellae: relative ef- Sports Med 27:345-349 ficacies of conventional MR imaging, MR arthrography, and 85. Zeiss J, Saddemi SR, Ebraheim NA (1992) MR imaging of the CT arthrography. Am J Roentgoenol 163:629-636 quadriceps tendon: normal layered configuration and its im- 66. Recht MP, Kramer J, Marcelis S et al (1993) Abnormalities of portance in cases of tendon rupture. Am J Roentgoenol articular cartilage in the knee: analysis of available MR tech- 159:1031-1034 niques. Sonin AH, Pensy RA, Mulligan ME et al (2002) Grading ar- sonography in the assessment of synovial tissue of the knee ticular cartilage of the knee using fast spin-echo proton densi- joint in rheumatoid arthritis: a preliminary experience. Kramer J, Recht MP, Imhof H et al (1994) Postcontrast MR arthritis of the knee: value of gadopentetate dimeglumine-en- arthrography in assessment of cartilage lesions. De Smet AA, Norris MA, Yandow DR et al (1993) MR diag- lonodular synovitis and related lesions: the spectrum of imag- nosis of meniscal tears of the knee: importance of high signal ing findings. Am J Roentgoenol 172:191-197 in the meniscus that extends to the surface. Hayes CW, Brigido MKI, Jamadar DA, Propeck T (2000) 161:101-107 Mechanism-based pattern approach to classification of com- 71. Kaplan PA, Nelson NL, Garvin KL et al (1991) MR of the knee: plex injuries of the knee depicted at MR imaging. Radio the significance of high signal in the meniscus that does not Graphics 20:S121-S134 clearly extend to the surface. Amis AA (1991) Functional anatomy of the anterior cruciate postoperative meniscus: potential MR imaging signs. Wascher DC, Markolf KL, Shapiro MS, Finerman GA (1993) MR and arthrographic findings after arthroscopic repair. Direct in vitro measurement of forces in the cruciate liga- Radiology 180:517-522 ments. JBJS 75-A:377-386 the postoperative meniscus of the knee: a study comparing 94. Kaplan PA, Walker CW, Kilcoyne RF et al (1992) Occult frac- conventional arthrography, conventional MR imaging, MR ture patterns of the knee associated with anterior cruciate lig- arthrography with iodinated contrast material, and MR ament tears: assessment with MR imaging.

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The brain has an extensive vascular supply through the paired internal carotid and vertebral arteries that unite at the cerebral arterial circle (circle of Willis) (see chapter 16 and fig 80mg tadapox amex. The brain of a newborn is especially sensitive to oxygen depri- vation or to excessive oxygen discount tadapox 80mg with mastercard. If complications arise during childbirth and the oxygen supply from the mother’s blood to the baby is interrupted while it is still in the birth canal, the infant may be still- born or suffer brain damage that can result in cerebral palsy, epilepsy, paralysis, or mental retardation. PET scans are of value in studying neurotransmitters The CNS is composed of gray and white matter. Gray matter and neuroreceptors, as well as the substrate metabolism of the brain. From each of these regions, dis- as the outer convoluted cortex layer of the cerebrum and cerebel- tinct functional structures are formed. In addition, specialized gray matter clusters of nerve cells marized in table 11. It consists of aggregations of dendrites and myelinated axons, along with associated neuroglia. What characteristics do the brain and spinal cord have in scribed in the previous section, neurons communicate with one common? Explain how the study of neuropeptides can enhance un- and dendrites within the brain. Using specific examples, describe the metabolic require- called neuropeptides. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 360 Unit 5 Integration and Coordination (a) (b) FIGURE 11. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 Chapter 11 Nervous Tissue and the Central Nervous System 361 (c) Cerebrum Corpus callosum Cerebellum Lateral ventricle Pons Medulla oblongata Spinal cord (d) FIGURE 11. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 362 Unit 5 Integration and Coordination (a) (b) FIGURE 11. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 Chapter 11 Nervous Tissue and the Central Nervous System 363 creases rapidly and the cortex enlarges out of proportion to the CEREBRUM underlying white matter. The con- cluding the perception of sensory impulses, the instigation of volutions effectively triple the area of the gray matter, which is voluntary movement, the storage of memory, thought processes, composed of nerve cell bodies. The cerebrum is also concerned with in- Recent studies indicate that increased learning is accom- stinctual and limbic (emotional) functions. Although the number of neurons is Objective 13 Describe the structure of the cerebrum and established during prenatal development, the number of list the functions of the cerebral lobes. The number of cytoplasmic extensions from the cell body of a neuron Objective 14 Define the term electroencephalogram and determines the extent of action potential conduction and the as- discuss the clinical importance of the EEG. Four of these lobes appear on the surface of the cephalon, is the largest and most obvious portion of the brain. It cerebrum and are named according to the overlying cranial accounts for about 80% of the mass of the brain and is responsi- bones (fig. The reasons for the separate cerebral lobes, as ble for the higher mental functions, including memory and rea- well as two cerebral hemispheres, have to do with specificity of son. The cerebrum consists of the right and left hemispheres, function (table 11. A portion of the meninges The frontal lobe forms the anterior portion of each cerebral called the falx (falks) cerebri extends into the longitudinal fis- hemisphere (fig. Each cerebral hemisphere contains a central cavity, the lat- central sulcus (fissure of Rolando) separates the frontal lobe eral ventricle (fig. The central sulcus extends at right angles and filled with cerebrospinal fluid. The lateral sulcus (fissure of Sylvius) extends laterally from the inferior sur- The two cerebral hemispheres carry out different functions. The frontal lobe’s functions include initiating voluntary the two hemispheres and permits a sharing of learning and memory. The frontal lobes also mediate responses related to mem- proven successful, it results in the cerebral hemispheres functioning ory, emotions, reasoning, judgment, planning, and verbal as separate structures, each with its own information, competing for communication. A more recent and effective technique of controlling epileptic seizures is a precise laser treatment of the corpus callosum. The surface layer, re- Parietal Lobe ferred to as the cerebral cortex, is composed of gray matter that The parietal lobe lies posterior to the central sulcus of the frontal is 2–4 mm (0. An important sensory area called the postcentral gyrus bral cortex is the thick white matter of the cerebrum, which (see figs.

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These are responsible for the active signalling properties of nerve cells and are discussed below (see Hille 1992 cheap 80mg tadapox, for a comprehensive account) purchase 80 mg tadapox with mastercard. This chapter concerns function, rather than structure, and hence does not systematically follow the structural classification. It is a transient electrical signal generated by the opening of voltage-gated Na‡ channels. These are normally shut at rest (or largely so), but are opened when the nerve cell membrane is depolarised by (e. Since the entry of Na‡ ions further depolarises the membrane, so opening more Na‡ channels, the process becomes regenerative once the threshold potential is exceeded: this is the potential at which the rate of Na‡ entry exceeds the rate of K‡ efflux (and/or Cl7 entry). Repolarisation results (in the first instance) from the inactivation of the Na‡ channels Ð that is, as the depolarisation is maintained, the channels close again (though at a slower rate than that at which they open). Recovery then requires that they progress back from the inactivated state to the resting closed state: this takes a little time, so the action potential becomes smaller and eventually fails during high frequency stimulation or during sustained depolarisation Ð a process of accommodation. Local anaesthetics and some anti-epileptic drugs such as phenytoin and carbemaze- pine act by blocking Na‡ channels. Many of these have a higher affinity for the inactivated state of the Na‡ channel than for the resting or open states. This provides a rationale for the use of phenytoin and carbemazepine in controlling epileptic discharges. In unmyelinated fibres (including the squid axon, where the ionic currents responsible for the action potential were first elucidated, see Fig. These may be sustained or transient (inactivating) in kinetic behaviour. However, K‡ channels are normally absent from nodes of Ranvier and action potential repolarisation in myelinated fibres results solely from Na‡ channel inactivation. Thus, blocking K‡ channels with drugs such as tetraethyl- ammonium or 4-aminopyridine (Fig. They can also improve conduction in myelinated fibres following demyelination (e. Cooling the nerve has a similar effect to blocking K‡ channels: hence MS patients are very sensitive to temperature. CALCIUM CHANNELS: TRANSMITTER RELEASE When an action potential arrives at the axon terminal, it induces the release of a chemical transmitter. Transmitter release is a Ca2‡-dependent process (see Chapter 4) and requires a charge of Ca2‡. This is provided through the action potential-induced 38 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION Table 2. A variety of Ca2‡ channels have been described, characterised by their kinetics, single-channel properties, pharmacology (especially sensitivity to different toxins) and molecular structure (Table 2. Those primarily responsible for transmitter release belong to the N (a1B), P/Q (a1A) and R classes (a1E). So far, no pharmacological agents capable of uniquely modifying Ca2‡ channels involved in transmitter release have been described (other than polypeptide toxins). These, and other (L-type, T-type), Ca2‡ channels are also variably present in neurons somata and/or dendrites, where they contribute to the regulation of neural activity in other ways (see below). REGULATION OFCa2‡ CHANNELS BY NEUROTRANSMITTERS N and P/Q channels are susceptible to inhibition by many neurotransmitters and extra- cellular mediators that act on receptors coupling to Pertussis toxin-sensitive G-proteins (primarily Go) Ð for example, noradrenaline (via a2 receptors), acetylcholine (via M2 and M4 muscarinic receptors), GABA (via GABA-B receptors), opioid peptides (via m=d receptors) and adenosine (via A2 receptors) (see Fig. Inhibition results from the release of the bg subunits of the trimeric (abg) G-protein following its activation by the receptor. The bg subunit then binds to the Ca2‡ channel in such a way as to shift its voltage sensitivity to more positive potentials, so that the channels do not open as readily during a rapid membrane depolarisation. One interpretation of this is that the binding of the bg subunits is itself voltage- dependent. This is thought to provide the principal mechanism responsible for presynaptic inhibition, whereby neurotransmitters inhibit their own release (autoinhibition) during high-frequency synaptic transmission. This process can be replicated by applying exogenous transmitters or their analogues (see Fig. Records show intra- axonal recordings from (a) a regenerating sciatic nerve axon following nerve crush; (b) a normal sciatic nerve axon; and (c) a demyelinated ventral root axon after treatment with lysopho- sphatidylcholine.

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