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D. Faesul. Texas A&M University, Kingsville.

Somatasensory Evoked Potentials Somatasensory evoked potentials (SSEP) and motor evoked potentials (MEP) have become common intraoperative mechanisms for monitoring spinal cord function during spinal surgery in idiopathic adolescent scoliosis cialis black 800mg visa impotence at 70. Their use in children with CP has not been as well defined discount cialis black 800 mg line erectile dysfunction medicine name in india, with early reports sug- gesting that they are not reliable. As with every test obtained in the treatment of individuals, the fact that a test can be done does not mean that it should be done. Specifically, even though children with CP technically can have spinal cord monitoring, we have to ask what we hope to gain from these data. If children are ambulatory, an aggressive approach similar to that in idiopathic adolescent scoliosis would indicate that all cor- rective force from instrumentation should be removed if spinal cord moni- toring detects spinal cord dysfunction. For the Unit rod, this would involve bending the rod to allow some deformity as a way of decreasing its correc- tive force or, alternatively, considering removal of the rod. If a hook and rod system is used, it should usually be removed because the rods provide some longitudinal force and the hooks may cause direct compression of the spinal cord. If sublaminar wires are in place, they should not be removed, as their removal is more dangerous and likely to cause more injury than just tight- ening the wires in place. Clearly, the 1-mm or even 2-mm thickness of sub- laminar wires would never cause a significant compression of the spinal cord; therefore, there is no rational reason indicating that the risk of removing the wires would be of any benefit. There could potentially have been damage from inserting the wires, but their removal would only increase the risk of more damage. If hooks were used, they should be removed because the vol- ume of the hook is such that it definitely can place potential pressure on the spinal cord. These children should also be given an immediate bolus of cor- ticosteroids to prevent further secondary damage from spinal cord swelling. This problem could was instrumented to T1 (Figure C9. The rod was have been avoided by bending the rod anteriorly at the tip left in the normal position but the end was slightly or by wiring it to C6 and C7. Another option would have prominent, as the kyphosis extended into the cervical been to cut the rod at the end of the original procedure spine (Figure C9. The rod formed a bursa over the and connect the individual rods with the two rod con- end and, by 1 year after surgery, she complained of pain nectors. This is the least preferred approach because loss at the end of the rod (Figure C9. The goal of surgery for children with total body involvement is to correct the spinal deformity so they can sit well. The risk of poor sitting and decu- bitus formation is such that, in the worst cases where children are completely paralyzed, they will still be better off with a corrected body posture. The use of spinal cord monitoring has much less benefit in severely involved children. The treatment we would consider is to increase the blood pressure if it is low and perhaps give corticosteroids; however, the risk–benefit ratio of this would have to be seriously considered. We always raise the blood pressure if it goes below a mean of 60 mmHg, and spinal cord monitoring would not provide additional information, as this is part of our required protocol without the spinal cord monitoring. In 30 patients, 20 of whom were monitored, 3 false positives of the spinal cord monitoring occurred. None of these children had any noticeable neurologic change, and except for giving corticosteroids to 2 of these children, no change in the treatment was made. Also, in 340 children with CP who had spinal fusions, only 2 neurologic deficits occurred, and both were associated with infections in the postoperative recovery period. Intra- operative spinal cord monitoring would not have helped to detect either of these deficits. Based on this experience, we believe intraoperative monitor- ing of the spinal cord in nonambulatory children with CP adds no beneficial gain to the care of these children and, as a consequence, is not indicated. Postoperative Complications Many reports in the literature evaluate the outcome of spinal fusions in chil- dren with CP. Many of these authors report major and minor complications. It is impossible to determine any reasonable rate of complication from these reports because there is no clear definition of what constitutes a major or a minor complication. In general, most surgeons would consider a deep wound infection a major complication because it significantly delays children’s re- covery and requires much effort from surgeons.

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The thyroid gland secretes the thy- Thyroid hormones (principally T3 ) modulate cellular energy production and roid hormones tetraiodothyronine utilization through their ability to increase the gene transcription of many pro- (T4) and triiodothyronine (T3) (see teins involved in intermediary metabolism cheap cialis black 800 mg without prescription herbal remedies erectile dysfunction causes, including enzymes in the TCA cycle Fig discount cialis black 800 mg online erectile dysfunction statistics by age. They increase the rate of ATP utilization by Na , most active form of the hormone. They also affect the efficiency of energy trans- thesized and secreted in approximately 10 formations, so that either more fuel must be oxidized to maintain a given level of times greater amounts than T3. Hepatocytes (liver cells) and other cells contain a deiodi- ATP, or more ATP must be expended to achieve the desired physiological nase that removes one of the iodines from response. Teefore, in spite of a very good T4, converting it to T3. T3 exerts its effects on appetite, reflects his increased caloric requirements and a less efficient utiliza- tissues by regulating the transcription of tion of fuels. The result is an enhanced oxidation of adipose tissue stores as well specific genes involved in energy metabo- as a catabolic effect on muscle and other protein-containing tissues. An activated sympathetic nervous system leads to a more rapid and forceful heartbeat (tachycardia and palpitations), increased nervousness (anxiety and insomnia), tremulousness (a sense of shakiness or jitteriness), and other symptoms. CHAPTER 19 / CELLULAR BIOENERGETICS: ATP AND O2 357 Congestive heart failure occurs Cora Nari. Cora Nari was in left ventricular heart failure (LVF) when when the weakened pumping she presented to the hospital with her second heart attack in 8 months. The action of the ischemic left ventricu- diagnosis of LVF was based, in part, on her rapid heart rate (104 lar heart muscle causes back pressure to beats/min) and respiratory rate. On examining her lungs, her physician heard res- increase in the vessels which bring oxy- piratory rales, caused by inspired air bubbling in fluid that had filled her lung air genated blood from the lungs to the left side spaces secondary to LVF. This condition is referred to as congestive heart failure. The pressure inside these pul- monary vessels eventually reaches a critical Cora Nari’s rapid heart rate (tachycardia) resulted from a reduced capacity of level above which water from the blood her ischemic, failing left ventricular muscle to eject a normal amount of blood into moves down a “pressure gradient” from the the arteries leading away from the heart with each contraction. The resultant drop capillary lumen into alveolar air spaces of in intraarterial pressure signaled a reflex response in the central nervous system the lung (transudation). The patient experi- that, in turn, caused an increase in heart rate in an attempt to bring the total amount ences shortness of breath as the fluid in the of blood leaving the left ventricle each minute (the cardiac output) back toward a air spaces interferes with oxygen exchange more appropriate level to maintain systemic blood pressure. The hypoxia then stimu- workload of the heart with diuretics and other “load reducers,” attempts to improve lates the respiratory center in the central the force of left ventricular contraction with digitalis and other “inotropes,” and the nervous system, leading to a more rapid administration of oxygen by nasal cannula to reduce the injury caused by lack of respiratory rate in an effort to increase the oxygen content of the blood. As the patient blood flow (ischemia) to the viable heart tissue in the vicinity of the infarction. These sounds represent the bubbling of inspired air as it enters the fluid-filled pul- Active Transport and Cell Death. Most of us cannot remember monary alveolar air spaces. But exactly how cells die from a lack of oxygen is an intriguing question. Pathologists generally describe two histologically distinct types of cell death: Hypoxia necrosis and apoptosis (programmed cell death). Cell death from a lack of O2, such as occurs during a myocardial infarction, can be very rapid, and is considered necro- 2 Decreased mitochondrial sis. The lack of ATP for the active transport of Na and Ca triggers some of the electron transport chain death cascades leading to necrosis (Fig. The influx of Na and loss of the Na gradient across the plasma membrane is Decreased ATP and an early event accompanying ATP depletion during interruption of the O2 supply. For example, the Increased Na+ Increased Ca2+ Na /H exchanger, which normally pumps out H generated from metabolism in exchange for extracellular Na , can no longer function, and intracellular pH may Cellular swelling drop. The increased intracellular H may impair ATP generation from anaerobic glycolysis. As a consequence of increased intracellular ion concentrations, water Mitochondrial Increased plasma permeability enters the cells and hydropic swelling occurs. Swelling is accompanied by the membrane permeability transition release of creatine kinase MB subunits, troponin I, and troponin C into the blood. These enzymes are measured in the blood as indicators of a myocardial infarction Fig. Swelling is an early event and is considered a reversible death.

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CSF is the fluid that circu- tends to multiply in motor neurons in the spinal cord buy cialis black 800mg on-line erectile dysfunction za, lates in and around the brain and spinal cord cialis black 800 mg line erectile dysfunction pills comparison. This fluid leading to paralysis, including paralysis of the breathing is taken from the space below the spinal cord to avoid muscles. Because the spinal cord is Polio has been virtually eliminated in many countries only about 18 inches long and ends above the level of through the use of vaccines against the disease—first the the hip line, a lumbar puncture or spinal tap is usually injected Salk vaccine developed in 1954, followed by the done between the third and fourth lumbar vertebrae, at Sabin oral vaccine. A goal of the World Health Organiza- about the level of the top of the hipbone. The sample tion (WHO) is the total eradication of polio by worldwide that is removed can then be studied in the laboratory vaccination programs. Anesthetics or medications are Tumors Tumors that affect the spinal cord commonly sometimes injected into the space below the cord. The arise in the support tissue in and around the cord. They anesthetic agent temporarily blocks all sensation from are frequently tumors of the nerve sheaths, the meninges, the lower part of the body. Symptoms are caused by pressure on the thesia has an advantage for certain types of procedures or cord and the roots of the spinal nerves. These include THE NERVOUS SYSTEM: THE SPINAL CORD AND SPINAL NERVES 191 Box 9-1 Hot Topics Spinal Cord Injury: Crossing the DivideSpinal Cord Injury: Crossing the Divide pproximately 11,000 new cases of spinal cord injury occur ◗ Using neurotrophins to induce repair in damaged nerve tissue. Aeach year in the United States, the majority involving males Certain types of neuroglia produce chemicals called neu- ages 16 to 30. Because neurons show little, if any, capacity to re- rotrophins (e. Intravenous injec- The factor called Nogo is an example. Successfully transplanted donor duces swelling at the site of injury and improves recovery. Spinal tains the cell bodies of the sensory neurons. A ganglion cord tumors are diagnosed by magnetic resonance imag- (GANG-le-on) is any collection of nerve cell bodies lo- ing (MRI) or other imaging techniques, and treatment is cated outside the CNS. Fibers from sensory receptors 9 by surgery and radiation. The ventral roots of the spinal nerves are a combina- Injuries Injury to the spinal cord may result from tion of motor (efferent) fibers that supply muscles and wounds, fracture or dislocation of the vertebrae, hernia- glands (effectors). The cell bodies of these neurons are lo- tion of intervertebral disks, or tumors. The most common cated in the ventral gray matter (ventral horns) of the causes of accidental injury to the cord are motor vehicle cord. Because the dorsal (sensory) and ventral (motor) accidents, falls, sports injuries (especially diving acci- roots are combined to form the spinal nerve, all spinal dents), and job-related injuries. Branches of the Spinal Nerves Damage to the cord may cause paralysis or loss of sen- Each spinal nerve continues only a short distance away sation in structures supplied by nerves below the level of from the spinal cord and then branches into small poste- injury. Different degrees of loss are named using the root rior divisions and larger anterior divisions. The larger an- -plegia, meaning “paralysis,” for example: terior branches interlace to form networks called plexuses (PLEK-sus-eze), which then distribute branches ◗ Monoplegia (mon-o-PLE-je-ah)—paralysis of one limb to all parts of the body (see Fig. The three main ◗ Diplegia (di-PLE-je-ah)—paralysis of both upper or plexuses are described as follows: both lower limbs ◗ Paraplegia (par-ah-PLE-je-ah)—paralysis of both lower ◗ The cervical plexus supplies motor impulses to the limbs muscles of the neck and receives sensory impulses from ◗ Hemiplegia (hem-e-PLE-je-ah)—paralysis of one side the neck and the back of the head. The phrenic nerve, of the body which activates the diaphragm, arises from this plexus. Box 9-1, Spinal Cord Injury: Crossing the Divide, con- ◗ The lumbosacral (lum-bo-SA-kral) plexus supplies tains information on treatment of these injuries. The largest branch in this plexus is the sciatic (si-AT-ik) nerve, which leaves the dorsal part of the pelvis, passes beneath the gluteus ◗ The Spinal Nerves maximus muscle, and extends down the back of the There are 31 pairs of spinal nerves, each pair numbered thigh. At its beginning, it is nearly 1 inch thick, but it according to the level of the spinal cord from which it soon branches to the thigh muscles; near the knee, it arises (see Fig. Each nerve is attached to the spinal forms two subdivisions that supply the leg and the foot. On each dorsal root is a marked swelling Dermatomes Sensory neurons from all over the skin, of gray matter called the dorsal root ganglion, which con- except for the skin of the face and scalp, feed information 192 CHAPTER NINE C-2 extremities. It affects both sensory and C-2 motor function, causing symptoms of pain and paralysis.

The translocated gene new location cheap cialis black 800 mg amex erectile dysfunction fpnotebook, the proto-oncogene may be controlled by a more active promoter is now under the control of the promoter and cialis black 800 mg with visa erectile dysfunction caused by medications, therefore, overexpressed (increased amounts of the protein product may be region for the immunoglobulin heavy chain produced). If only a portion of the proto-oncogene is translocated, it may be gene, which leads to inappropriate and over- expressed as a truncated protein with altered properties, or it may fuse with expression of c-myc. The result may be another gene and produce a fusion protein containing portions of what normally uncontrolled cell proliferation and tumor were two separate proteins. The truncated or fusion protein would be hyperac- development. All subtypes of Burkitt’s lym- phoma contain this translocation. Barr virus infection of B cells is also associ- • The proto-oncogene may be amplified (Fig. The cell may cells contain the Philadelphia chro- be transformed and exhibit an abnormal pattern of growth. Rather than inserting mosome, typical of chronic myel- an oncogene, a virus may simply insert a strong promoter into the host cell ogenous leukemia (CML). This promoter may cause an increased or untimely expression of a nor- chromosome results from a reciprocal mal proto-oncogene. As a consequence, a The important point to remember is that transformation results from abnormali- fusion protein is produced containing the N- ties in the normal growth regulatory program caused by gain-of-function mutations terminal region of the Bcr protein from chro- in proto-oncogenes. However, loss-of-function mutations also must occur in the mosome 22 and the C-terminal region of the tumor suppressor genes, repair enzymes, or activators of apoptosis for full transfor- Abl protein from chromosome 9. Mutations in Repair Enzymes region and is constitutively active. When active, Abl stimulates the Ras pathway of sig- Repair enzymes are the first line of defense preventing conversion of chemical nal transduction, leading to cell proliferation. DNA repair enzymes are tumor suppressor genes in the sense that errors repaired before replication do not become mutagenic. DNA damage is constantly occurring from exposure to sun- The oncogene N-myc (a cell prolif- light, background radiation, toxins, and replication error. If DNA repair enzymes eration transcription factor, related to c-myc) is amplified in some neu- are absent, mutations accumulate much more rapidly, and once a mutation develops roblastomas, and amplification of the erb-B2 in a growth regulatory gene, a cancer may arise. As an example, inherited mutations oncogene (a growth factor receptor) is asso- in the tumor suppressor genes brca1 and brca2 predispose women to the develop- ciated with several breast carcinomas. CHAPTER 18 / THE MOLECULER BIOLOGY OF CANCER 321 Proto-oncogene Promoter Coding region Normal DNA A. Gene amplification Mutation in Mutation in coding region promoter causes Expression of multiple copies causes production excessive expression of the proto-oncogene of hyperactive protein Strong promoter Gene Gene or enhancer X B. Y Gene rearrangement Proto-oncogene Proto-oncogene or is now under a portion of it is control of strong fused with another promoter or enhancer gene Fusion protein is either overproduced or hyperactive Fig. The mutations may be point mutations, deletions, or insertions. The proto-oncogene and the resulting oncogene are shown in blue. The protein products of these genes play roles in DNA repair, recombination, Although mutations in both the and regulation of transcription. A second example, HNPCC (hereditary non-poly- brca1 and brca2 genes are linked to posis colorectal cancer), was previously introduced in Chapter 13. It results from breast cancer development in women, there are some fundamental differ- inherited mutations in enzymes involved in the DNA mismatch repair system. ONCOGENES there are some differences in the diseases expressed by mutations within these genes. Proto-oncogenes control normal cell growth and division. These genes encode For example, brca1 mutations are also linked proteins that are growth factors, growth factor receptors, signal transduction pro- to ovarian cancer and brca2 mutations are teins, transcription factors, cell cycle regulators, and regulators of apoptosis not.

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