Diabecon

Thierry H. Le Jemtel, MD

• Henderson Chair Professor of Medicine
• Director, Heart Failure and Transplant Program
• Tulane University Heart and Vascular Institute
• New Orleans, Louisiana

Its function is to accept electrons at the end of the chain diabete signs purchase cheap diabecon on-line, and the water O2 formed is added to the cellular water diabetes mellitus erectile dysfunction purchase diabecon 60caps visa. In one location managing diabetes zorgtraject order diabecon from india, an oxidation reaction is poised to release electrons at very high energy; in another location metabolic disease symptoms in dogs order diabecon 60 caps mastercard, a potential electron acceptor waits to be reduced. Once the two terminals of the battery are connected by a wire, electrons flow from one compartment to the other through the wire, producing an electrical current or electricity. A light bulb or an electrical pump inserted into the circuit will run on the electricity generated. The mitochondrial electron transport chain operates according to the same principle. The electrons are passed along a series of protein and lipid carriers that serve as the wire. Mitchondrion All these components are in the inner membrane of the mitochondria as shown in Figure 1 13-3. This is similar to pumping any ion, such as Na+, across a membrane to create a gradient. The end result is that a proton gradient is normally maintained across the mitochondrial inner membrane. Enzymes are released from the damaged tissue, and lactic acidosis contributes to by serial measurements of protein precipitation and coagulation necrosis. They convert hemo several days previously globin to methemoglobin, which binds cyanide in the blood before reaching the tissues. Carbon Monoxide Carbon monoxide binds to cytochrome al a3 but less tightly than cyanide. Depending genin), which allows energy loss as heat to maintain a basal temperature around the kidneys, on the degree of salicylate neck, breastplate, and scapulae in newborns. These react rapidly with lipids to cause peroxidation, with proteins, and with other substrates, resulting in denaturation and precipitation in tissues. These small quantities are normally destroyed by protective enzymes such as catalase. In the special case of erythrocytes, large amounts of superoxide are generated by the spontaneous dissociation of the oxygen from hemoglobin (occurrence is 0. The processes that adequately detoxify the superoxide require a variety of enzymes and compounds, including superoxide dismutase, catalase, as well as glutathione peroxidase, vitamin E in membranes, and vitamin C in the cytoplasm. Mutations in these genes affect highly aerobic tissues (nerves, muscle), and the diseases exhibit characteristic mitochondrial pedigrees (maternal inheritance). Because the daily amount of creatinine in urine is constant per unit muscle mass, the amount of urinary creatinine can be used as a normalizing factor for other materials that are excreted. However, increases in creatinine levels in the bloodstream are indicative of renal problems. Diagnosis of Myocardial Infarctions with Creatine Kinase Isoforms A 62-year-old man was shoveling snow after a recent snowstorm. Shortly thereafter, he began to complain of chest pain, dizziness, and shortened breath. In myocardial infarctions, there is a blockage of blood flow to the heart, resulting in lysis of cardiac cells. Also, elevated serum levels of cardiac-specific troponins are most often used for rapid diagnosis of myocardial infarction (see Bridge to Pathology on page 184). During a myocardial infarction, the oxygen supply to an area of the heart is dramatically reduced, forcing the cardiac myocytes to switch to anaerobic metabolism. Which of the following enzymes is affected most directly by the active metabolite of this drug When nitroprusside is given in higher than usual doses, it may be accompanied by the administration of thiosulfate to reduce potential toxic side effects. Which complex asso ciated with electron transport or oxidative phosphorylation is most sensitive to the toxic byproduct that may accumulate with high doses of nitroprusside A patient has been exposed to a toxic compound that increases the permeability of mito chondrial membranes for protons. Oxaloacetate, produced from pyruvate, exits the mitochondrion after conver sion to malate. Glycogen synthesis and degradation occur primarily in liver and skeletal muscle, although other tissues, including cardiac muscle and the kidney, store smaller quantities. Glycogen is stored in the cytoplasm as either single granules (skeletal muscle) or as clusters of granules (liver). The granule has a central protein core with polyglucose chains radiating out ward to form a sphere 1-14-1). Glycogen granules composed entirely of linear chains have the highest density of glucose near the core. If the chains are branched, the glucose density is highest at the periphery of the granule, allowing more rapid release of glucose on demand. A Glycogen Granule Glycogen stored in the liver is a source of glucose mobilized during hypoglycemia. In white (fast-twitch) muscle fibers, the glucose is converted primarily to lactate, whereas in red (slow-twitch) muscle fibers, the glucose is completely oxidized. Glycogen Metabolism Glycogen Synthase Glycogen synthase forms the a1,4 glycosidic bond found in the linear glucose chains of the granule. Transfers the oligoglucose unit and attaches it with an a1,6 bond to create a branch. Branching Enzyme Branching enzyme is responsible for introducing al,6-linked branches into the granule as it grows. The process by which the branch is introduced is shown schematically in Figure 1-14-3. The glucose l-phosphate formed is con verted to glucose 6-phosphate by the same mutase used in glycogen synthesis 1-14-2). Glycogen Phosphorylase Glycogen phosphorylase breaks al,4 glycosidic bonds, releasing glucose l-phosphate from the periphery of the granule. Glycogen phosphorylase releases glucose 1-P from the periphery of the granule until it encounters the first branch points. Myophosphorylase Deficiency (McArdle Disease) Myophosphorylase is another name for the muscle glycogen phosphorylase. The episodes were somewhat ameliorated by drinking sucrose-rich soft drinks immediately before exercise. The latest episode occurred during her first spin class (stationary bicycling with a resistance load) at her local bicycle shop. She initially had extreme weakness in both legs and muscle cramps and later excreted red-brown urine. In subsequent sessions, in addition to the high-sucrose drink, she reduced the load on the bicycle and was better able to tolerate the initial phase of exercise. After 10-15 minutes, she experienced a "second wind" and was able to continue her exercise successfully, this woman has myophosphorylase deficiency and is unable to properly break down glyco gen to glucose 6-phosphate in her muscles. Without an adequate supply of glucose, sufficient energy via glycolysis for carrying out muscle contraction cannot be obtained, explaining why the muscles are not functioning well (weakness and cramps). The situation is improved by drinking the sucrose-containing drink, which provides dietary glucose for the muscles to use. Hepatic Glycogen Phosphorylase Deficiency (Hers Disease) Hepatic glycogen phosphorylase deficiency is usually a relatively mild disease because gluco neogenesis compensates for the lack of glycogenolysis I-14-5). The defi cient enzyme normally resides in the lysosome and is responsible for digesting glycogen-like material accumulating in endosomes.

Despite President Bushs pronouncement early on that he recognized that Congress also has an important oversight function to perform and his commitment that I will work with members of both parties to make sure this efort is thorough metabolic bone disease journal generic 60caps diabecon free shipping,71 our Committee faced a White House less willing to cooperate with a Senate investigation than any we have witnessed in our many years in this body somogyi effect diabetes in dogs purchase cheap diabecon on line. Tat is why we ultimately concluded that the Committee should issue subpoenas to the White House to produce the material that the Committee asked for during its investigation diabetes0rg buy discount diabecon on line. Unfortunately blood sugar too high purchase 60caps diabecon with amex, the Chairman disagreed with Senator Liebermans request to issue subpoenas, and so, the Committee did not obtain all that we believe was necessary for a comprehensive investigation. Tere are matters that we could not fully explore because of agency and Administration recalcitrance and, in some cases, intransigence. But one thing we do know is that because we were denied the opportunity to fully explore the role the White House played in preparing for and respond ing to Katrina, we have little insight into how the President and his staf monitored, man aged, and directed the governments disaster preparedness in the post-9/11 world, how they coordinated the rest of the federal bureaucracy in response to Katrina, or how leadership was exercised by the only entity in the federal government with the authority to order all the others to act. Without this information, the Committees investigation necessarily lacked the ability to fully and fairly analyze and assess a critical element of the response to Katrina. We have plenty of circumstantial evidence to believe that there were signifcant failures of leadership at the top and actions that should have been taken but were not. But there remain too many important questions that cannot be answered conclusively because the White House did not provide the information necessary to do so. Only through a thorough and comprehensive investigation of what went wrong could we be as sured that the government will know what steps are necessary to get it right the next time. The White House A Chronology of Efforts to Obtain Information from the White House On October 7, 2005, the Committee sent a letter, signed by Chairman Collins and Sena tor Lieberman, to White House Chief of Staf Andrew H. The letter was similar to those sent to over twenty federal agencies and Departments, as well as to the Governors of Louisiana, Mississippi and Alabama, the Mayors of New Orleans, Biloxi, Gulfport, and Mo bile, and a number of other state and local agencies. The goal of these letters was to help the Committee collect a comprehensive set of documents and information that would allow it to understand what those at all levels of all relevant governments did or didnt do to prepare for and respond to Hurricane Katrina. Some requests were basic, like those that asked the White House to identify its various components with emergency-preparedness and response responsibilities, to explain how the White House learns of and monitors hurricanes, and to provide an organizational chart of the relevant White House components. Others sought more detailed, Katrina-specifc information, such as how the White House and the President frst learned about the storm, who was responsible for processing requests from the Governors for emergency declarations, how much the White House understood about the vulnerability of New Orleans to fooding, and, perhaps most importantly, a description of what the White House specifcally did to prepare for and respond to the hurricane. Louisiana Governor Kathleen Blancos ofce, for example, produced over 8,000 pages of substantive documents, including a large number of e-mails to or from the Governor herself, and granted the Committee access to all six members of her staf with whom it requested interviews. Similarly, Mississippi Governor Haley Barbours ofce provided the information that the Committee asked for, including mate rial directly involving the Governors ofce and his staf, and the Committee interviewed both members of the Governors staf for whom it asked. The cooperation the Committee received from these ofces greatly enhanced the Committees ability to understand what happened, and helped ensure that it could be confdent in the Committee reports fndings and conclusions. Kelley, the White House started of well, pledging that [t]he Administration is commit ted to cooperating with your Committee. Kelleys letter and the accompanying documents made clear that the White House had little intention of giving the Committee what it had requested. His letter noted that the Committee had sought information and documents from other Executive Branch agencies and observed: As is customary for any examination of an issue addressed by many com ponents of the federal Government, the Administrations principal form of 677 Additional Views assistance will be through the production of information from those agencies and departments most directly involved in preparing for and responding to Hurricane Katrina. As is traditional for responses to Congressional Com mittee requests for information, the [White House] stands ready to assist your Committee in appropriate ways once the scope and content of the agencies and departments production of information can be assessed in relation to your Committees remaining requirements. As discussed further below, the views expressed by Kelley were neither customary nor traditional, but given them, it was not surprising that the near entirety of the nearly 4,000 accompanying pages of documents were publicly available. To make matters worse, the Committee soon learned that despite the White Houses sug gestion that the Committee seek its information elsewhere, the White House was in fact directing the federal agencies that were producing documents and witnesses for the Com mittees investigation to withhold from the Committee any material or testimony relating to the agencies or witnesses interactions with the White House. The Committee spent the next two months attempting to work these matters out at a staf level. Committee pressure yielded marginally more documents and a three-hour briefng from the White Houses Deputy Homeland Security Advisor, Ken Rapuano. In many cases, the White House produced multiple copies of the same widely distributed material. In short, the Committee did not receive information or documents showing what actually was going on within the White House and was still lef with little insight into the White Houses substantive actions in preparation for and response to Hurricane Katrina. Frustrated by the White Houses omissions (its failure to produce what the Committee had requested), as well as its commissions (its interference with productions and testimony from other agencies), the Committee sent Card a second letter on January 12, 2006. The 678 letter, again signed by both Chairman Collins and Senator Lieberman, expressed concern Hurricane Katrina: A Nation Still Unprepared about the White Houses response to the investigation. It assessed the status of the White House production this way: We have received several boxes of documents, which we do appreciate. As a result, to date, we have yet to receive the bulk of what we requested, and the Committee is unable to fully understand and assess actions involving White House personnel during the preparations for and response to Hurricane Katrina. The Committees letter saved its harshest language for its assessment of the White Houses directions to agency counsel to keep White House-related information from the Com mittee: This practice, Senators Collins and Lieberman wrote, simply must cease. The Committees letter also took issue with another of the White Houses arguments: Tat the White House was acting within tradition by telling the Committee that it must wait for the White Houses response until afer other agencies provided theirs: Respectfully, Chair man Collins and Senator Lieberman wrote: We are aware of no such tradition. Indeed, this Committee, as well as others, has repeatedly conducted investigations of matters involving this and previous White Houses and has never held White House requests in abeyance. In an efort to end the impasse, the Committee ofered the White House a signifcantly pared-down list of priorities and asked that it produce particular documents and provide specifc individuals for interviews by January 23, 2006. In a letter again signed by Kelley, the White House once again paid homage to Congresss important role in examining events surrounding Hurricane Katrina and the need for the Executive Branch to assist those inqui ries. Instead, it ofered to address the Committees requests through a combination of a briefng and ad ditional documents. While Kelleys letter suggested that this lef a wide area of inquiry open to the Committee, the reality was that it walled of documents and testimony involv ing virtually anyone in the White House who had any level of responsibility or involvement with Katrina, regardless of whether that person actually had anything to do with advising the President. On February 3, 2006, the Committee received its second briefng from Rapuano, and by February 8, it had in hand the additional documents the White House promised in its January 27 letter. Rapuanos briefng, while again helpful in answering questions about the activities of some of the federal agencies and about the White House, ofered few of the additional specifc details the Committee had sought about the White Houses actions. The documents did not difer markedly in type from those received already: The Committee had obtained virtually all of them previously from other agencies; consequently, they ofered little new insight. As an example, the Committee asked for all White House documents re lated to the deployment of federal troops to the Gulf region. Given the weighty implications of deploying our premier fghting force on domestic soil, and the controversies surrounding the timing of those deployments and the allegations that Governor Blanco was responsible for the delay, the Committee believed that access to this information from the White House was critical to understanding and informing the American people of this important part of the Katrina story. But the documents provided by the White House consisted mainly of situation reports, most of which already had been produced to the Committee by the Penta gon, and did not address the issue of troop deployment. Around the time of this exchange, the Committee gained virtually its only signifcant insight into what actually happened within the White House immediately before and afer Katrinas landfall. When the President declined to invoke that privilege, Brown testifed before the Committee on Friday, February 10, and shortly thereafer sat for a more detailed, transcribed interview with Com mittee staf. In both instances, Brown made clear that he saw the White House as a critical player in the preparations for and response to Hurricane Katrina. Brown testifed that, before landfall, he had conveyed to the President that, depending on where it struck, the storm could be catastrophic. Afer putting that testimony 680 together with what the investigation had already revealed about the federal governments Hurricane Katrina: A Nation Still Unprepared activities during the week afer landfall, Senator Lieberman concluded that the Committee would be remiss if it did not follow up on the multiple questions regarding White House action lef unanswered by Browns testimony and the rest of our investigation. In addition, the Committee failed to receive from federal agencies an unknown volume of responsive material as a result of White House orders to withhold anything related to or referencing virtually anyone of signifcance in the White House. Afer reviewing that response, Senator Lieberman wrote Chairman Collins on March 15, 2006, asking her to issue subpoenas to (1) the White House for the documents requested in their joint January 12, 2006, letter; (2) to fve members of the White House staf most involved in the response, ordering them to sit for Committee depositions; and (3) to each federal agency to which they previously sent request letters, compelling them to produce previously withheld White House-related material. Analysis of the White Houses Arguments We do not believe that the White House, or any Executive Branch agency, must automati cally turn over material to a Congressional committee simply because it has been asked to do so. During the Committees months of eforts to obtain the information sought from the White House, the White House provided no satisfactory reason for its limited response. We have already referenced the fallacy of the White Houses assertion that it appropriately directed the Committee elsewhere for its information. As noted above, Chairman Collins and Senator Lieberman rejected that argument in their January 12, 2006, letter to Card.

Subdural hematoma is characteristically caused by venous bleeding diabetes prevention wine buy genuine diabecon on line, most often from veins that join the cerebrum to venous sinuses within the dura diabetes diet guidelines 2014 discount 60 caps diabecon. The venous hemorrhage typically arrests early who diabetes definition 1999 buy diabecon 60caps low cost, but the volume of the hematoma gradually increases because of osmotic imbibing ofwater control diabetes naturally diet purchase diabecon 60caps on line. This results in a slowly enlarging tumor-like mass characterized clinically by gradual signs of cerebral compression occurring hours to days or even weeks after head injury. In newborns, the most likely agents are group B streptococci, Escherichia coli, and Listeria; in young adults, the most frequent agent is N meningitidis. In older adults, especially those with impaired resistance to infection, the most common etiologic agents are S. Because this slowly growing benign tumor arises from the arachnoidal cells of the meninges, it is actually external to the brain and is frequently amenable to surgical resection and complete cure. A meningomyelocele is a neural tube defect in which both the meninges and spinal cord are included in the herniated tissue. A meningocele is a defect in which the herniated membranes consist only of meninges, and spina bifida occulta does not manifest any apparent abnormalities. In neural tube defects, an increase in a-fetoprotein in both the maternal serum and the amniotic fuid is noted. An epidural hematoma is an arterial hemorrhage between the dura and the skull, most often resulting fromskull fracture and laceration of the middle meningeal artery. Epidural hematomas are characterized clinically by a short period ofconsciousness (lucid interval) followed by loss of consciousness and signs of cerebral compression. A subdural hematoma is venous hemorrhage underneath the dura, resulting from laceration of the bridging veins. Subdural hematomas are characterized clinically by gradual signs of cerebral compression occurring hours, days, or weeks after injury. Subarachnoid hemorrhage is commonly associated with rupture of a berry aneurysm in the circle of Willis. A transient ischemic attack is a brief episode of impaired neurologic function caused by a brief disturbance in cerebral circulation. The lesion shown in the illustrations is a glioblastoma multiforme, the most frequently occurring primary neoplasm of the central nervous system. The middle cerebral arteries are the most common sites of cerebral embolic occlusion in general, and, in this instance, the involvement is almost certainly left-sided. Middle cerebral artery lesions are manifest by contralateral upper extremity weakness and ipsilateral facial weakness. Also, in right-handed individuals, the left side ofthe cerebral cortex is usually dominant, and verbal aphasias are caused by left-sided lesions in the great majority of cases. Multiple sclerosis is the most common demyelinating disease and is characterized by destruction ofmyelin with relative preservation ofaxons. The disease is associated with plaques scattered irregularly throughout the central nervous system. Increased neutrophils, decreased glucose, and increased protein are characteristics of bacterial meningitis. Alzheimer disease is a major cause ofdementia and is characterized by relatively slow, progressive memory loss followed in later stages by motor problems, contractures, and paralysis. Degeneration of the upper and lower motor neurons is characteristic of amyotrophic lateral sclerosis. Dopamine depletion and depigmentation of the substantia nigra is characteristic of Parkinson disease. Pick bodies can be found in Pick disease, which clinically resembles Alzheimer disease. Parkinson disease, orparkinsonism, is characterized by a resting pill-rolling tremor, masked facies, slowness of movements, muscular rigidity, and a festinating (shufing) gait. This brain tumor has a very poor prognosis, with death occurring in less than 1 year. These can be further divided into true-positive results and false-positive results. These definitions depend on determination of the presence or absence of the disease by criteria other than the laboratory test. Similarly, these can be divided into true-negative results and false-negative results. They are also independent of the incidence of the disease, which is the occurrence of new cases in a defined interval of time. Sensitivity measures the extent to which a laboratory test is positive in patients. Ideally, sensitivity should be very high when a procedure is used as a screening test, because it is desirable to identify as many persons as possible with the disease. Specificity measures the extent to which a laboratory test is negative in healthy persons. For most analytic procedures, the point ofmaximum specificity is the highest test value that correctly identifies all subjects without the disease. Theyare dependent on the prevalence ofthe disease (in contrast to sensitivity and specificity). This value is a measure of the likelihood that a person with a positive test result actually hasthe disease. This value is a measure ofthelikelihoodthata person with a negative test resultis actually free ofthe disease. This type of variation describes variable laboratory results unrelated to disease processes. It is called diurnal variation when laboratory results vary systematically according to the time of day. In some instances, it is infuenced by variable factors, such as diet, exercise, posture, or the efects of smoking, alcohol, or medications. This type of variation describes the variability of repeated laboratory measurements on identical specimens over a specified time span. The measurements are most often repeated at daily intervals, thus assessing daily variability. What is the negative predictive value of disposal 1000 similarly preserved serum this test What is the likelihood that the S test will he develops a diagnostic procedure for the correctly identif a potential firefighter as disorder.

When the eye turns and travel through the superior orbital ssure medially diabetes journal submission diabecon 60 caps generic, the action of this muscle is to pull the to innervate the superior oblique muscle blood glucose you tube buy discount diabecon 60 caps line. When the eye is turned lat Unilateral or even bilateral abducens palsy erally diabetes term definition best 60caps diabecon, however diabetes vitamin pills cheap diabecon 60 caps overnight delivery, the action of the muscle is to is commonly seen as a false localizing sign in intort the eye (rotate it on its axis with the top patients with increased intracranial pressure. All of the other Although the long intracranial course of the extraocular muscles receive their innervation nerve is often cited as the cause of its predis through the oculomotor or third cranial nerve. From a clinical point of view, however, it be clear from the above that, whereas impair is important to remember that isolated unilat ment of mediolateral movements of the eyes eral or bilateral abducens palsy does not nec mainly indicates imbalance of the two cog essarily indicate a site of injury. The emergence nate rectus muscles, disturbances of upward or of the trochlear nerve from the dorsal mid downward movement are far more complex to brain just behind the inferior colliculus makes work out, as they result from dysfunction of it prone to injury by the tentorial edge (which the complex set of balanced contractions of the runs along the adjacent superior surface of the other four muscles. The course of all three ocular motor nerves It passes through the tentorial opening and through the cavernous sinus and superior or runs adjacent to the posterior communicating bital ssure means that they are often damaged artery, where it is subject to injury by posterior in combination by lesions at these sites. The nerve lesion of all three of these nerves unilaterally then runs through the cavernous sinus and su indicates injury in the cavernous sinus or supe perior orbital ssure to the orbit, where it di rior orbital ssure rather than the brainstem. The Head trauma causing a blowout fracture of superior branch innervates the superior rectus the orbit may trap the eye muscles, resulting muscle and the levator palpebrae superioris, in abnormalities of ocular motility unrelated to which raises the eyelid, and the inferior branch any underlying brain injury. The entrapment supplies the medial and inferior rectus and of the eye muscles is determined by forced inferior oblique muscles as well as the ciliary duction. The abducens nerve exits from the the globe) as described below in the exami base of the pons, near the midline. These af neal tumor) causes loss of vertical eye move ferents arise from cortical, tectal, and tegmen ments, usually beginning with upgaze. Each superior collicu greatly different from the types of inputs that lus contains a map of the visual world on the control alpha-motor neurons concerned with contralateral side of space, and electrical stim striated muscles, except the oculomotor mus ulation of a specic point in this visual map will cles do not contain muscle spindles and hence command a saccade to the corresponding point there is no somesthetic feedback. In nonmammalian vertebrates, such asthe oculomotor nuclei are surrounded by frogs, this area is called the optic tectum and is areas of the brainstem tegmentum containing the principal site for directing eye movement; premotor cell groups that coordinate eye move in mammals, it comes largely under the control 93,95,96 ments. The premotor area for regulating of the cortical system for directing eye move lateral saccades consists of the paramedian ments. However, it would effect is to allow conjugate lateral saccades to be incorrect to think of this area as a motor the ipsilateral side of space, and when neurons cortex. Unlike neurons in the primary motor in this area are inactivated by injection of local cortex, which re in relation to movements of anesthetic, ipsilateral saccades are slowed or the limbs in particular directions at particu eliminated. In addition, neurons in the dorsal lar joints, recordings from area 8 neurons in pontine nuclei relay smooth pursuit signals to awake, behaving monkeys indicate that they the occulus, and the medial vestibular nucleus do not re during most random saccadic eye and occulus are both important for holding movements. Inputsfromthesesystemscon ing tasks that require a saccade to a particular verge on the abducens nucleus, which contains part of space only when the saccadic eye two classes of neurons: those that directly in movement is part of a behavioral sequence that nervate the lateral rectus muscle (motor neu is rewarded. Axons from these latter neurons Area 8 projects widely to both the superior cross the midline at the level of the abducens colliculus as well as the premotor areas for ver nucleus and ascend on the contralateral side of tical and lateral eye movements, and to the 102 the brainstem to allow conjugate lateral gaze. Descend Thus, pontine tegmental lesions typically re ing axons from area 8 mainly run through the sult in the inability to move the eyes to the internal medullary lamina of the thalamus to ipsilateral side of space (lateral gaze palsy). Unilateral le portant in judging movement of objects in 101,103 sions of the rostral interstitial nuclei typically contralateral space. Cortex in this region reduce vertical saccades as well as causing plays a critical role in following movements 99,100 torsional nystagmus. Compression of the originating in that space, including movements Examination of the Comatose Patient 63 toward the ipsilateral space. Thus, following tensive vestibular input as well as somatosen 101 an object that travels from the left to the right sory and visual afferents. The output from engages the right parietal cortex (area 7) to x the occulus ensures the accuracy of saccadic attention on the object, the right area 8 to eye movements and contributes to pursuit eye produce a saccade to pick it up, the right oc movements and the ability to hold an eccen cipital cortex to follow the object to the right, tric position of gaze. The vestibulocerebellum and ultimately the left occipital cortex as well is also critical in learning new relationships to see the object as it enters the right side of between eye movements and visual displace space. Lesions of the vestibulocerebel gages a number of important cortical as well as lum cause ocular dysmetria (inability to perform brainstem pathways necessary to produce eye accurate saccades), ocular utter (rapid to-and movements. Hence, although the test is fairly fro eye movements), and opsoclonus (chaotic 105 sensitive for picking up oculomotor problems eye movements). It may be difficult to dis at a cortical and brainstem level, the interpre tinguish less severe cases of vestibulocerebellar tation of failure of optokinetic nystagmus is a function from vestibular dysfunction. First, visual feedback allows the rapid cor internuclear ophthalmoplegia, a condition that rection of errors in gaze. Second, the ocular occurs quite commonly in multiple sclerosis motor nuclei receive direct and relayed inputs and brainstem lacunar infarcts). Because the eye shows horizontal gaze-evoked nystagmus eyes must respond to changes in head position (slow phase toward the midline, rapid jerks very quickly to stabilize the visual image on laterally), while the adducting eye stops in the the retina, the direct vestibular input, which midline (if the lesion is complete) or fails to identies angular or linear acceleration of the fully adduct (if it is partial). The abducens only causes a bilateral internuclear ophthal nucleus is located at the same level as the moplegia, but also prevents vertical vestibulo vestibular complex, and it receives inputs from ocular responses or pursuit. In patientsthe vestibulocerebellum, including the oc with stupor or coma, testing of reex eyelid and 99 culus, paraocculus, and nodulus, receives ex ocular movements must suffice. Eliciting the corneal reex in coma in sleep, are maintained in a closed position by may require more vigorous stimulation than in tonic contraction of the orbicularis oculi mus an awake subject, but it is important not to cles. Corneal trauma tive state have alternating cycles of eyes open can be completely avoided by testing the cor ing and closing; see Chapter 9. Two to three raise and then release the eyelids, noting their drops of sterile saline are dropped on the 109 tone. Reex smoothly and gradually, a movement that can closure of both eyelids and elevation of both not be duplicated by an awake individual sim eyes (Bells phenomenon) indicates that the ulating unconsciousness. Absence of tone or reex pathways, from the trigeminal nerve and failure to close either eyelid can indicate facial spinal trigeminal nucleus through the lateral motor weakness. Blepharospasm, or strong re brainstem tegmentum to the oculomotor and sistance to eyelid opening and then rapid clo facial nuclei, remain intact. However, some sure, is usually voluntary, suggesting that the patients who wear contact lenses may have per patient is not truly comatose. In gic patients with either metabolic or structural other patients with an acute lesion of the des lesions may resist eye opening, as do some pa cending corticofacial pathways, the blink reex tients with a nondominant parietal lobe infarct. In pa midbrain level may result in loss of Bells phe tients with unilateral forebrain infarcts, the nomenon, but an intact blink response. In sion at the midpontine level may not only im cases of brainstem injury, the ptosis may be pair Bells phenomenon, but also cause the part of a Horners syndrome. Hold the eyelids gently in an open position Spontaneous blinking usually is lost in coma to observe eye position and movements in a as a function of the depressed level of con comatose patient. How ophthalmoscope held about 50 cm from the ever, in persistent vegetative state, it may re face and shined toward the eyes of the patient turn during cycles of eye opening (Chapter 9). Most pa bright light implies that the afferent sensory tients with impaired consciousness demon pathways are intact to the brainstem, but does strate a slight exophoria. If it is possible to ob not necessarily mean that they are active at a tain a history, ask about eye movements, as a forebrain level. Even patients with complete congenital strabismus may be misinterpreted destruction of the visual cortex may recover as dysconjugate eye movements due to a brain 107 reex blink responses to light, but not to stem lesion. Slowly roving eye or depth of the eyelid excursion during blink movements are typical of metabolic encepha ing occurs in patients with ipsilateral facial lopathy, and if conjugate, they imply an intact paresis. Examination of the Comatose Patient 65the vestibulo-ocular responses are then Eye movements in patients who are deeply tested by rotating the patients head (oculoce comatose may respond sluggishly or not at all to phalic reexes). In such cases, more suffered trauma, it is important rst to rule out intense vestibular stimulation may be obtained the possibility of a fracture or dislocation of the by testing caloric vestibulo-ocular responses. The on either side with both hands and using the ear canal is rst examined and, if necessary, thumbs to reach across to the eyelids and hold cerumen is removed to allow clear visualiza them open. The brisk, and when the head position is held at head of the bed is then raised to about 30 each extreme for a few seconds, the eyes should degrees to bring the horizontal semicircular gradually come back to midposition. Moving canal into a vertical position so that the re the head back to the opposite side then pro sponse is maximal. The eye movements sleepy, the canal may be irrigated with cool should be smooth and conjugate. The head is water (158Cto208C); this usually induces a then rotated in a vertical plane (as in head brisk response and may occasionally cause nodding) and the eyes are observed for vertical nausea and vomiting. During downward head it is rarely necessary to use caloric stimulation movement, the eyelids may also open (the in such patients. An emesis basin can be placed below the head to the right should cause the eyes to de ear, seated on an absorbent pad, to catch the viate to the left). The ice water is infused at a rate of untary control of gaze overcomes this reex about 10 mL/minute for 5 minutes, or until a response. After a response is ob consciousness, the oculocephalic reex should tained, it is necessary to wait at least 5 minutes predominate.

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