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Insulin plays a major role in metabolism of carbohydrate cheap amantadine 100 mg visa, Insulin is secreted into the portal circulation and trans- fat order 100mg amantadine with mastercard, and protein (Box 27–1). These foodstuffs are broken ported to the liver, where about half is used or degraded. The down into molecules of glucose, lipids, and amino acids, re- other half reaches the systemic circulation, where it circulates spectively. The molecules enter the cells and are converted to mainly in an unbound form and is transported to body cells. When car- tivates receptors on the cell membranes of about 80% of body rying out its metabolic functions, the overall effect of insulin cells. Liver, muscle, and fat cells have many insulin receptors is to lower blood glucose levels, primarily by the following and are primary tissues for insulin action. After insulin– mechanisms: receptor binding occurs, cell membranes become highly per- 1. In the liver, insulin acts to decrease breakdown of meable to glucose and allow rapid entry of glucose into the glycogen (glycogenolysis), formation of new glucose cells. The cell membranes also become more permeable to from fatty acids and amino acids (gluconeogenesis), amino acids, fatty acids, and electrolytes such as potassium, and formation of ketone bodies (ketogenesis). Cellular metabolism is altered same time, it acts to increase synthesis and storage of by the movement of these substances into the cells, activation glycogen and fatty acids. In adipose tissue, insulin acts to decrease breakdown proteins between intracellular compartments, changes in the of fat (lipolysis) and to increase production of glycerol amounts of proteins produced, and perhaps other mechanisms. In muscle tissue, insulin acts to decrease protein break- effects (eg, utilization and storage of glucose, amino acids, and down and amino acid output and to increase amino fatty acids) and inhibit catabolic processes (eg, breakdown of acid uptake, protein synthesis, and glycogen synthesis. After binding to insulin and enter- ing the cell, receptors may be degraded or recycled back to the cell surface. Regulation of Insulin Secretion Insulin is cleared from circulating blood in 10 to 15 min- utes because of rapid binding to peripheral tissues or meta- Insulin, the only hormone that decreases blood sugar, regu- bolic breakdown. The insulin that does not combine with lates the amount of glucose available for cellular metabolism receptors is metabolized in the liver, kidneys, plasma, and and energy needs, during both fasting and feeding. Insulin Cell membrane Pancreas Insulin Glucose Insulin receptor Figure 27–1 Normal glucose metabolism. Once insulin binds with receptors on the cell membrane, glucose can move into the cell, promoting cellular metabolism and energy production. Blood concentrations of triglycerides, cholesterol, cle, adipose tissue, the heart, and some smooth muscle organs, and phospholipids are also increased. The high blood lipid con- such as the uterus; it must be present for muscle and fat tissues centration probably accounts for the atherosclerosis that tends to to use glucose for energy. If excess glucose is present after this need is met, can use as fuel, some fatty acids are converted into ketones. Ex- it is converted to glycogen and stored for future energy needs or cessive amounts of ketones produce acidosis and coma. The excess glucose transported to Protein Metabolism liver cells is converted to fat only after glycogen stores are sat- • Insulin increases the total amount of body protein by increas- urated. When insulin is absent or blood glucose levels are low, ing transport of amino acids into cells and synthesis of pro- these stored forms of glucose can be reconverted. The basic mechanism of these effects is especially important in restoring blood sugar levels by breaking unknown. Fat Metabolism • Lack of insulin causes protein breakdown into amino acids, • Insulin promotes transport of glucose into fat cells, where which are released into the bloodstream and transported to the it is broken down. One of the breakdown products is alpha- liver for energy or gluconeogenesis. The lost proteins are not re- glycerophosphate, which combines with fatty acids to form placed by synthesis of new proteins and protein wasting causes triglycerides. This is the mechanism by which insulin promotes abnormal functioning of many body organs, severe weakness, fat storage. Glucose is the major stimulus of insulin secretion; others The two major classifications are type 1 and type 2. Although include amino acids, fatty acids, ketone bodies, and stimula- both are characterized by hyperglycemia, they differ in tion of beta2-adrenergic receptors or vagal nerves. Other types of dia- cose is more effective than intravenous glucose because betes may be induced by disease processes, certain drugs, glucose or food in the digestive tract induces the release of and pregnancy.

This convergence is quite specific because no when the peroneal stimulus intensity was increased convergence has been detected between femoral Ia far above 1 × MT (Marque purchase amantadine 100mg with visa, Pierrot-Deseilligny & afferents and low-threshold afferents in the poster- Simonetta-Moreau best amantadine 100mg, 1996), argues against an IPSP ior tibial and plantar nerves or various cutaneous evoked in motoneurones, because an IPSP should afferents. This finding, together with the potency of depress the H reflex as well (see pp. It is the group I excitation, raises the question whether therefore suggested that the suppression seen in the the organisation of the excitation of quadriceps presence of corticospinal stimulation is due to disfa- motoneurones from the pretibial flexors is unique cilitation resulting from inhibition of propriospinal in the lumbar enlargement. Peripheral inhibitory inputs to lumbar Cutaneous effects propriospinal neurones Cutaneous inhibition has only been disclosed in the presence of cortical stimulation (p. The absence of depression these effects were mediated through propriospinal was observed in 95% of motor units and contrasts neurones. Projections of group I afferents from intrinsic foot muscles to motoneurone pools of TA, quadriceps and triceps surae. Ia afferents from intrinsic plantar foot muscles have monosynaptic Ia and non-monosynaptic excitatory projections to tibialis anterior (TA) motoneurones (MN), and monosynaptic Ia excitatory and non-monosynaptic inhibitory projections to quadriceps (Q) and gastrocnemius-soleus (GS) MNs. Vertical dashed and dotted lines indicate the latency of the monosynaptic excitation and of the non-monosynaptic effect, respectively. Evidence has been presented that heteronymous group I excitation, it is likely to be this suppression presumably reflects disfacilitation of group I origin. Here again, the low threshold and of the motoneurone due to inhibition of excitatory abrupt onset of the inhibition (see Fig. Group I inhibition from foot muscles Medium-latency reciprocal inhibition Stimulation of the tibial nerve at the ankle elicits During voluntary dorsiflexion of the foot, group aweak heteronymous monosynaptic Ia facilitation Ivolleys in the common peroneal nerve evoke a in all leg and thigh muscles, followed by inhibi- medium-latency inhibition of the soleus H reflex tion 3–5 ms later in triceps surae and quadriceps (1–3 ms longer than disynaptic reciprocal Ia inhi- (Fig. This medium-latency inhibition is super- suppresses the H reflexes of soleus and quadriceps imposed on the disynaptic reciprocal Ia inhibition at rest (Fig. Because it is not produced whereitappears∼50msbeforetibialisanteriorEMG by separate stimulation of cutaneous afferents and activity, and is correlated with the strength of tonic has the same low threshold as the monosynaptic dorsiflexion (Crone & Nielsen, 1989). Because of its 498 Lumbar propriospinal system low threshold, it was again assumed that this inhibi- verge onto premotoneurones interposed in the cor- tion could be mediated through a disynaptic path- ticospinal pathway to quadriceps motoneurones way with interneurones located at different spinal (Marchand-Pauvert, Simonetta-Moreau & Pierrot- segments than motoneurones. It is readily facilitates the quadriceps MEP, sparing the initial facilitatedduringtonicvoluntarydorsiflexion(Crone part of the MEP (Fig. This is than the sum of effects of separate stimuli and, here anotherindicationthatthegroupIinputtothispath- again, the initial part of the corticospinal peak was wayisrelativelyweakandthesupraspinalinputrela- not facilitated (Fig. Finally,spa- ever, there is no evidence that these interneurones tial facilitation between corticospinal and group I belong to the system of short-axoned lumbar pro- volleys has also allowed the disclosure of excitatory priospinal neurones located rostral to motoneu- connections between leg muscles (from gastrocne- rones. Indeed, the central delay of the tibial nerve- mius medialis to tibialis anterior, and vice versa), induced inhibition of extensors, assessed with the connectionsthatwererarelydetectedintheabsence Hreflex (Fig. It was therefore not possible to be cer- tain of the central delay of the extra facilitation of Corticospinal control of peripheral excitation thecorticospinalpeak,andtodeterminewhetherthe centraldelayislongerthemorecaudalthemotoneu- Spatial facilitation between peripheral and rone pool. Thus, so far, it has not been demon- corticospinal volleys strated that the premotoneurones transmitting cor- The same spatial facilitation technique as in the ticospinal excitation are lumbar propriospinal neu- upper limb has been used to demonstrate that rones, even though this is probable. The finding that corticospinal and common peroneal volleys con- peripheral inhibition of propriospinal neurones can Organisation and pattern of connections 499 MEP H Reflex MEP (a) 150 (b) (c) 20 Corticospinal 100 0 Inhibitory 50 IN 0 2 4 6 25 30 35 40 45 ISI CPN-TMS (ms) PN Latency (ms) 7 9 11 13 ISI CPN-FN (ms) Ia Q Q MN VL MU 12 10 Group I (d ) (e) FN CPN 0 0 TA 28. Corticospinal fibres have monosynaptic excitatory projections to quadriceps (Q) motoneurones (MNs), propriospinal neurones (PN) and feedback inhibitory interneurones (IN) (the latter projection being the more potent, as indicated by the thickest line). The conditioned responses (expressed as a percentage of the control responses) are plotted against the interstimulus interval (ISI) between CPN and TMS (upper abscissa) and CPN and femoral nerve (FN) stimuli (lower abscissa, in italics), the two abscissae being aligned to start at the simultaneous arrival of conditioning and test volleys at the segmental level of the Q MN pool. Dashed and dotted lines in (c)–(e) indicate the onset of the MEP (c)orthe corticospinal peak ((d), (e)) and of the extra facilitation on combined stimulation, respectively. Modified from Marchand-Pauvert, Simonetta-Moreau & Pierrot-Deseilligny (1999), with permission. Overall the dominant effect of corticospinal volleys on the lumbar propriospinal Convergence of corticospinal and peripheral system seems to be excitation of feedback inhibi- volleys onto inhibitory interneurones tion. This could explain the results obtained during During a weak voluntary contraction of quadriceps, contraction (see below). Motor tasks and physiological This contrasts with the progressive decline of the implications group I facilitation of the H reflex (Fig.

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Onset of action is 30 minutes after oral administration and 1 to 2 minutes after IV injection best 100mg amantadine. Muscle Because of variations in the degree of hepatic metabolism order amantadine 100mg, ****************************** cell clients vary widely in the dosages required to maintain a ther- apeutic response. A Atenolol, metoprolol, and nadolol have the same actions, uses, and adverse effects as propranolol, but they have long half-lives and can be given once daily. They are excreted by the kidneys, and dosage must be reduced in clients with renal Muscle contraction impairment. Calcium Channel Blocking Agents Muscle cell Calcium channel blockers act on contractile and conductive tis- sues of the heart and on vascular smooth muscle. For these cells B to function normally, the concentration of intracellular calcium must be increased. This is usually accomplished by movement of extracellular calcium ions into the cell (through calcium channels in the cell membrane) and release of bound cal- Calcium-blocking drugs cium from the sarcoplasmic reticulum in the cell. Thus, calcium plays an important role in maintaining vasomotor tone, myo- cardial contractility, and conduction. Calcium channel block- ing agents prevent the movement of extracellular calcium into Muscle the cell. As a result, coronary and peripheral arteries are dilated, cell myocardial contractility is decreased, and the conduction system is depressed in relation to impulse formation (auto- maticity) and conduction velocity (Fig. C In angina pectoris, the drugs improve the blood supply to Figure 53–1 Calcium channel blockers: mechanism of action. In atrial fibrillation or flutter and other supraven- (C) When calcium channels are blocked by drug molecules, muscle tricular tachydysrhythmias, diltiazem and verapamil slow the contraction is decreased because calcium ions cannot move through rate of ventricular response. In hypertension, the drugs lower the cell membrane into the muscle cell. Most also have short elimination used for angina or hypertension, and only diltiazem and verap- half-lives (<5 hours), so doses must be given three or four amil are used to manage supraventricular tachydysrhythmias. In clients with CAD, the drugs are effective as monotherapy Amlodipine (30 to 50 hours), bepridil (24 hours), and felodi- but are commonly prescribed in combination with beta block- pine (11 to 16 hours) have long elimination half-lives and there- ers. In addition, nimodipine is approved for use only in sub- fore can be given once daily. The drugs are metabolized in the arachnoid hemorrhage, in which it decreases spasm in cerebral liver, and dosage should be reduced in clients with severe liver blood vessels and limits the extent of brain damage. Seven of these are chemically dihydropyridines, Contraindications include second- or third-degree heart of which nifedipine is the prototype. Bepridil, diltiazem, and block, cardiogenic shock, and severe bradycardia, heart fail- verapamil differ chemically from the dihydropyridines and ure, or hypotension. Nifedipine and related drugs act mainly on vascu- with milder bradycardia, heart failure, or hypotension and lar smooth muscle to produce vasodilation, whereas verapamil with renal or hepatic impairment. CHAPTER 53 ANTIANGINAL DRUGS 781 Adjunctive Antianginal Drugs Elevated cholesterol is a significant risk factor for coronary atherosclerosis and angina and the risk is directly related to In addition to antianginal drugs, several other drugs may be the degree of elevation. Cardiac enzyme levels, such as tro- used to control risk factors and prevent progression of myo- ponin, creatine kinase (CK), lactate dehydrogenase (LDH), cardial ischemia to myocardial infarction and sudden cardiac and aspartate aminotransferase (AST), should all be nor- death. This drug has become the standard of care be- • During an acute attack, assess the following: cause of its antiplatelet (ie, antithrombotic) effects. Chest pain is non- ommended doses vary from 81 mg daily to 325 mg daily specific. It may be a symptom of numerous disorders, or every other day; apparently all doses are beneficial in such as pulmonary embolism, esophageal spasm or reducing the possibility of myocardial reinfarction, inflammation (heartburn), costochondritis, or anxiety. For example, what was the client by clients who are unable to lower serum cholesterol lev- doing, thinking, or feeling just before the onset of chest els sufficiently with a low-fat diet. The goal is usually to reduce the • Has the client had invasive procedures to diagnose serum cholesterol level below 200 mg/dL and low- or treat his or her coronary artery disease (CAD) density lipoprotein cholesterol to below 130 mg/dL. Because beta blockers and calcium channel blockers are used to man- age hypertension as well as angina, one of these drugs Nursing Diagnoses may be effective for both disorders.

The sen- ing between hemifields produced greater ip- sorimotor representation for the skin and for silesional activations during the second PET as- flexible movements changes its extent cheap 100 mg amantadine, in- sociated with improvements in tests of neglect creasing soon after reading and decreasing if and everyday spatial skills safe 100 mg amantadine. In patients with TBI, as discussed, PET and Sign language activates primary and associ- fMRI can assess the effects of working mem- ation auditory cortex. A very high memory load, which is as- cochlear implants given to prelingually deaf sociated with greater dorsolateral prefrontal subjects may depend on whether the auditory 184 Neuroscientific Foundations for Rehabilitation cortex has been partially usurped by another Monaminergic Agents modality, such as visual, somatosensory, or other afferents associated with, lip reading for Fluoxetine 20 mg, a selective serotonin reup- example. Greater hypometabolism in primary take inhibitor, and fenozolone (20 mg), an am- auditory cortex by resting PET was associated phetamine-like drug that increases monamine with less likelihood of cross-modal input and, transmission, was given to healthy subjects dur- after training, higher hearing capability after ing an fMRI task that compared rest to two fist cochlear implantation. The executive mo- tor regions are rich in monaminergic receptors NEUROPHARMACOLOGIC (see Chapter 1). Serotonin activates both py- MODULATION ramidal cells and GABAergic inhibitory in- terneurons. The neurotransmitter may inhibit For rehabilitationists, a major goal for func- Purkinje cell firing. Using the same task, an- tional neuroimaging is to use techniques to vi- other SSRI, paroxetine 20 mg, but not 60 mg, sualize the physiologic activity of medications produced the same fMRI change in activation and their potential for modulating cerebral re- and improved hand speed modestly for the 9- organization. No modulation of may have a negative, although less obvious, im- cortical activation was found for passive move- pact on functional outcomes. Thus, increasing brain concentrations of The ability to screen drugs for potential pos- monamines may promote motor learning. A few studies on the S1M1 response during active ankle dor- have shown that available medications can in- siflexion in a healthy subject. Responses to a regional activation in S1M1 and SMA suggests drug may be state dependent. Actions of neurotransmitters responsiveness to a medication may be pre- and modulators (see Chapter 1) can be stud- dicted by regional fMRI activation stud- ied by functional neuroimaging and cortical ies. For example, a measure of acetyl- nucleus, which is a major projection for corti- cholinesterase activity201 may prove useful in costriatal fibers. Functional magnetic resonance imaging and Other Agents TMS also may demonstrate the negative im- pact of certain drugs. For example, some alco- Piracetam is a -aminobutyric acid derivative, holics show unusual activation patterns as they or nootropic agent, available in Europe and carry out working memory tasks. A PET study showed that 2400 mg of the drug abuse is seen frequently especially among drug twice a day increased rCBF during a patients with TBI and spinal cord injury, the word-repetition task in mildly to moderately impact may be appreciated through brain map- impaired aphasic subjects at the end of 6 weeks ping paradigms. SUMMARY The drug group also improved in more subtests of language function. The mechanism of action The strength of the relationships between is uncertain, but presumably piracetam aids practice by patients with brain and spinal le- learning in subjects with spared nodes in the sions, mechanisms of activity-dependent plas- language pathways. A larger study is needed to ticity, and alterations in the maps acquired by make that determination. More work, to date, has gone into colleagues evaluated the effects of drugs with demonstrating plasticity than in trying to ex- differing actions on rapidly induced motor tract the elements of training that best induce plasticity. As they activated the corticocortical connections maps of cognitive and sensorimotor tasks are of pyramidal neurons of the motor cortex to defined for healthy subjects and patients with elicit either a thumb flexor or an extensor a CNS or PNS injury, however, rehabilitation- movement. The subjects then practiced mak- ists will better recognize the pathways that sub- ing movements in the opposite direction, until serve recovery and the effects of physical, cog- TMS over the same scalp location elicited a re- nitive, and pharmacologic interventions on sponse in that direction. Imaging may reveal how spe- NMDA receptors and decreases cortical ex- cific pharmacologic agents affect motor and citability,200 reduced the activity-dependent mental processes. Amphetamine enhanced the practice clever paradigms allow clinicians to use these time required for reversal of direction. The re- tools as physiologic measures of the effects of versals lasted approximately an hour, but were intensity and duration of an intervention. Transcranial Electrical and Magnetic Stimulation of the Brain magnetic stimulation, fMRI, NIRS, and other and Spinal Cord. New York: Raven Press, 1993:187– techniques can become the tools of rehabilita- 200. Karl A, Birbaumer N, Lutzenberger W, Cohen LG, tionists for the study of hypotheses about train- Flor H. Carefully designed experi- cortex in upper extremity amputees with phantom ments and clinical trials that incorporate these limb pain. Roux F, Boulanouar K, Ibarrola D, Tremoulet M, proach to neurorehabilitation. Functional MRI and intraoper- ative brain mapping to evaluate brain plasticity in patients with brain tumours and hemiparesis.

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