Solian

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By H. Topork. Hamline University.

The paired posterior horns extend pos- scending tracts conduct motor impulses from the brain to teriorly and the paired anterior horns project anteriorly generic 100mg solian free shipping medicine 4211 v. Lateral horns are prominent only in Specific nerve pathways allow for reflexive movements the thoracic and upper lumbar regions discount solian 100 mg without a prescription adhd medications 6 year old. The transverse bar of rather than those initiated voluntarily by the brain. Move- gray matter that connects the paired horns across the center of ments of this type are not confined to skeletal muscles; re- the spinal cord is called the gray commissure. Within the gray flexive movements of cardiac and smooth muscles control commissure is the central canal. It is continuous with the ven- heart rate, breathing rate, blood pressure, and digestive ac- tricles of the brain and is filled with cerebrospinal fluid. Spinal nerve pathways are also involved in swal- lowing, coughing, sneezing, and vomiting. Spinal Cord Tracts Impulses are conducted through the ascending and descending Structure of the Spinal Cord tracts of the spinal cord within the columns of white matter. The spinal cord extends inferiorly from the position of the fora- men magnum of the occipital bone to the level of the first lum- bar vertebra (L1). It is somewhat flattened posteroventrally, making it oval in cross section. 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 385 Medulla oblongata C1 C2 Cervical spinal nerve C3 Cervical plexus C4 Cervical spinal C5 enlargement C6 C7 C8 T1 Brachial plexus T2 Arachnoid T3 T4 T5 Dura mater T6 Cervical enlargement T7 T8 Thoracic spinal nerve T9 Dura mater T10 Lumbar enlargement Lumbar spinal T11 enlargement Dura mater Conus medullaris T12 Filum terminale Conus medullaris L1 Cauda equina Lumbar spinal L2 Cauda equina nerve L3 Filum terminale L4 L5 Lumbar plexus S1 S2 S3 (b) S4 Sacral plexus S5 (a) FIGURE 11. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 386 Unit 5 Integration and Coordination Posterior horn Posterior funiculus Posterior median Lateral funiculus sulcus Gray commissure Posterior root of spinal nerve Central canal Lateral horn Spinal ganglion Paras Anterior horn Anterior root Anterior median Anterior funiculus fissure Spinal nerve of spinal nerve (a) Posterior horn Central canal Anterior horn Spinal ganglion Spinal nerve (b) FIGURE 11. The spinal cord has six columns of white matter called funiculi ated and are named according to their origin and termination. The two anterior funiculi are lo- brain and spinal cord or cross over within the medulla oblongata cated between the two anterior horns of gray matter, to either or the spinal cord. The crossing over of nerve tracts is referred to side of the anterior median fissure (fig. Each funiculus consists of both ascending and descending Descending tracts are grouped according to place of origin as tracts. The nerve fibers within the tracts are generally myelin- either corticospinal or extrapyramidal. Corticospinal (pyramidal) tracts descend directly, without synaptic interruption, from the cerebral cortex to the lower motor neurons. 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 387 Cerebrum Sensory cortex Motor cortex of cerebrum of cerebrum Cerebrum Corticospinal tract Thalamus Midbrain Sections of brain Midbrain Sections of brain Pons Pons Sensory fibers decussate Medulla oblongata Medulla Motor fibers oblongata decussate Section of cervical spinal cord Section of cervical spinal cord Motor impulse to skeletal muscle Sensory impulse from skin receptors FIGURE 11. Most (about 85%) of The corticospinal tracts appear to be particularly important in the corticospinal fibers decussate in the pyramids of the medulla voluntary movements that require complex interactions between the motor cortex and sensory input. The remaining 15% do not cross from ample, is impaired when the corticospinal tracts are damaged one side to the other. The fibers that cross compose the lateral in the thoracic region of the spinal cord, whereas involuntary breath- corticospinal tracts, and the remaining uncrossed fibers compose ing continues. Damage to the pyramidal motor system can be de- the anterior corticospinal tracts. Because of the crossing of fibers tected clinically by the presence of Babinski’s reflex, in which stimulation of the sole of the foot causes extension (upward move- from higher motor neurons in the pyramids, the right hemisphere ment) of the great toe and fanning out of the other toes. Babinski’s re- primarily controls the musculature on the left side of the body, flex is normally present in infants because neural control is not yet whereas the left hemisphere controls the right musculature. Nervous Tissue and the © The McGraw−Hill Anatomy, Sixth Edition Coordination Central Nervous System Companies, 2001 388 Unit 5 Integration and Coordination TABLE 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 389 FIGURE 11. The remaining descending tracts are extrapyramidal tracts that originate in the brain stem region. Electrical stimulation of the cerebral cortex, the cerebellum, and the basal nuclei indi- rectly evokes movements because of synaptic connections within extrapyramidal tracts. Neurostimulation of the reticular formation by the cerebrum or cerebellum either facilitates or inhibits the ac- tivity of lower motor neurons (depending on the area stimu- lated) (fig.

Resting membrane potentials (Em) are shown at the bottom of each column and amplitude (mV) and time (ms) at the bottom right with phenobarbitone solian 100 mg mastercard medicine zyrtec, can precipitate seizures quality 100 mg solian treatment vertigo. Although still used in refractory myo- clonic epilepsy, when its depressant effect on the spinal cord may be significant, clonazepam, like phenobarbitone, is rarely used now, but the more recently introduced 1:5 benzodiazepine clobazam is quite often used as an adjunct (not in the United States). While there is some belief and evidence that clonazepam and clobazam are more effective than other benzodiazepines as anticonvulsants nothing is known specifically about their modes of action that supports this view. The reported inhibitory effects of B & Bs on a calcium-sensitive NTrelease in synaptosomes is difficult to evaluate in terms of their in vivo anticonvulsant activity. THE EPILEPSIES 347 Valproic acid (sodium valproate) Introduced initially for absence seizures, this drug is now known to be effective in and used to treat tonic±clonic seizures and most types of epilepsy. It was found to inhibit GABA transaminase and so elevate GABA concentrations and inhibition. This is achieved, however, over a slower time-course than its anti-seizure effect, especially experimentally, which is now thought to be due to its phenytoin-like, use-dependent block of sodium channels. Since, unlike phenytoin, the full effect of valproate takes some weeks to develop, its slower effect on GABA metabolism and activity should not be ignored. NEW AEDs Most of these have been used mainly as add-on therapy although some are now being used alone. Lamotrigine One unwanted side-effect of phenytoin is its anti-folate activity. A programme of synthetic chemistry to manipulate the structure of the anti-folate compound pyri- methium to try to replace that property with anticonvulsant activity resulted in the synthesis of lamotrigine. It proved to be an effective AED in partial and generalised epilepsy but experience has found it also to be of value in absence seizures. Experimentally it was shown to reduce the release of glutamate and to a lesser extent GABA, induced in small brain slices by veratridine, a sodium ion channel opener. It now appears that its primary effect is prolonging the inactivation of sodium channels in a use-dependent manner much like phenytoin, although in a recent study of intra- cellularly recorded activity of striatal neurons in the rat corticostriatal slice preparation some differences emerged. While both drugs reduced experimentally induced repetitive firing, phenytoin was more effective against those induced by direct current activation of the neurons and also inhibited the EPSPs induced by the direct application of glutamate. Vigabatrin (g vinyl GABA) This drug is chemically related to GABA, is an irreversible inhibiter of GABA transaminase and appears to produce its antiepileptic effect through that mechanism. Not only does it increase brain GABA levels in animals it also elevates them up to threefold in human CSF and in the occipital cortex of normal and epileptic patients as shown by nuclear magnetic resonance spectroscopy. An interesting decrease in glutamate may be secondary to the rise in GABA. It is effective in partial and secondary generalised epilepsy, but since its mode of action requires the regeneration of new enzyme (GABA-t) its effect far outlasts its plasma life. A worrying intramyelinic oedema in rat nerves has fortunately not been seen in humans or primates. Attaching nipecotic acid to a lipophilic component to increase brain penetration resulted in tiagabine. Surprisingly, it appears to act preferentially on the GABA transporter GAT1 which, although found on astrocytes, is more associated with nerve terminals. Microdialysis in rats shows it increases extracellular GABA and prolongs the post-excitatory hyperpolarisation of neurons. It has proved effective in partial and secondary generalised epilepsy but prolonged post- and possibly presynaptic actions of the increased GABA could present problems. Gabapentin This drug, which is a cyclohexone analogue of GABA, was synthesised in the hope that it would be an agonist for GABA receptors which could cross the blood±brain barrier. Its efficacy in drug-resistant partial and secondary generalised epilepsy means that it certainly must enter the brain but it does not bind to GABA receptors. Despite this, it appears to increase GABA brain levels in epileptic patients and weak potentiation of GAD and inhibition of GABA-t have been described. It does not appear to affect sodium or calcium channels even though experimentally chronic dosing blocks repetitive neuronal firing.

Unlike autonomic ganglia elsewhere in the body effective solian 50 mg symptoms urinary tract infection, where they function mainly as relay-distribution centers for signals transmitted from the brain and spinal cord order solian 50mg overnight delivery medicine expiration, enteric The Enteric Division of the ANS Functions as a ganglia are interconnected to form a nervous system with Minibrain in the Gut mechanisms for the integration and processing of informa- tion like those found in the CNS. This is why the ENS is The ENS is a minibrain located close to the effector sys- sometimes referred to as the “minibrain-in-the-gut. Effector systems of the digestive tract are the musculature, secretory glands, and blood vessels. Rather than crowding the vast numbers of neurons required Myenteric and Submucous Plexuses for controlling digestive functions into the cranium as part Are Parts of the ENS of the cephalic brain and relying on signal transmission over long and unreliable pathways, the integrative micro- The ENS consists of ganglia, primary interganglionic fiber circuits are located at the site of the effectors. The circuits tracts, and secondary and tertiary fiber projections to the CHAPTER 26 Neurogastroenterology and Gastrointestinal Motility 457 effector systems (i. These structural components of the ENS are inter- ing several seconds can be recorded in cell bodies of enteric laced to form a plexus. These synaptic events may be excitatory most obvious constituents of the ENS (see Fig. The postsynaptic potentials (EPSPs) or inhibitory postsynaptic myenteric plexus, also known as Auerbach’s plexus, is lo- potentials (IPSPs). They can be evoked by experimental cated between the longitudinal and circular muscle layers stimulation of presynaptic axons, or they may occur spon- of most of the digestive tract. Presynaptic inhibitory and facilitatory events known as Meissner’s plexus, is situated in the submucosal can involve axoaxonal, paracrine, or endocrine forms of region between the circular muscle and mucosa. The sub- transmission, and they occur at both fast and slow synaptic mucous plexus is most prominent as a ganglionated net- connections. Neurons in submucosal submucous plexus and applying electrical shocks to stimu- ganglia send fibers to the myenteric plexus and also receive late presynaptic axons and release the neurotransmitter at synaptic input from axons projecting from the myenteric the synapse. The interconnections link the two networks into a functionally integrated nervous system. Enteric Slow EPSPs Have Specific Properties Mediated by Metabotropic Receptors Sensory Neurons, Interneurons, and Motor The slow EPSP in Figure 26. The heuristic model for the ENS is the same as that for the Slowly activating depolarization of the membrane poten- brain and spinal cord (Fig. In fact, the ENS has as tial with a time course lasting longer than 2 minutes after many neurons as the spinal cord. Repetitive dis- rons, interneurons, and motor neurons in the ENS are con- charge of action potentials reflects enhanced neuronal ex- nected synaptically for the flow of information from sensory citability during the EPSP. The record shows hyperpolariz- neurons to interneuronal integrative networks to motor neu- ing after-potentials associated with the first four spikes of rons to effector systems. As the slow EPSP develops, the hyperpolarizing the activity of each effector system into meaningful behavior after-potentials are suppressed and can be seen to recover of the integrated organ. Bidirectional communication occurs at the end of the spike train as the EPSP subsides. Slow EPSPs are mediated by multiple chemical messen- SYNAPTIC TRANSMISSION gers acting at a variety of different metabotropic receptors. Multiple kinds of synaptic transmission occur in the micro- Different kinds of receptors, each of which mediates slow circuits of the ENS. Both fast synaptic potentials with du- synaptic-like responses, are found in varied combinations Central nervous system Enteric Effector nervous system systems Interneurons Muscle Sensory Reflexes Motor Secretory epithelium neurons FIGURE 26. Sensory Information processing neurons, interneurons, and motor neu- rons are synaptically interconnected to form the microcircuits of the ENS. As Gut behavior in the CNS, information flows from Motility pattern sensory neurons to interneuronal inte- Secretory pattern grative networks to motor neurons to Circulatory pattern effector systems. B, The fast EPSPs were SPs, fast EPSPs, and slow IPSPs all occur in en- also evoked by single electrical shocks applied to the axon that teric neurons. A, The slow EPSP was evoked by repetitive electri- synapsed with the recorded neuron. Two fast EPSPs were evoked cal stimulation of the synaptic input to the neuron.

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