By: Edward T. F. Wei PhD
It is important for McArdle people to erectile dysfunction nyc nizagara 50 mg amex try to best erectile dysfunction pills for diabetes discount 100mg nizagara fast delivery avoid becoming overweight (see section 4 zinc causes erectile dysfunction discount 100mg nizagara overnight delivery. Further reading: Most of the information about the production of energy in muscle cells in people unaffected by McArdle’s is based upon Molecular Biology of the Cell by Alberts et al erectile dysfunction age 80 order online nizagara. This is a university undergraduate degree level textbook erectile dysfunction surgery cost buy cheap nizagara 100mg line, and therefore quite complicated. In order to provide the reader with a comprehensive overview, the following chapter includes information on supplements which has been shown to be effective, to have no effect or a negative effect, and for which there is limited information. A brief description of the medical/scientific reason for these supplements is given. Reason why it might help McArdle’s: Amino acids are used to build proteins for body growth and maintenance. McArdle people may have a high requirement for amino acids which are used to build and repair muscle damage. Reason why it might help McArdle’s: proteins are broken down by the citric acid cycle and used to produce energy by oxidative phosphorylation (see section 6. How is it taken: orally as a supplement to the usual diet What were the results of clinical trials: Kushner (1990) studied three McArdle people before treatment. Form of the supplement: A powdered sachet made up in water as a drink (used by Beynon et al. Their theory was therefore that unless enough B6 is obtained from the diet, McArdle people may suffer from a B6 deficiency. Results of clinical trials: Pheonix (1998) studied a McArdle person who had been taking 50mg of vitamin B6 daily for two years. The ability of the participant was compared when he was given either vitamin B6 or a placebo. He felt less well when given placebo, but it did not seem to affect the strength of the muscles. No significant difference was seen with the B6 treatment compared to placebo treatment. It can be made by the body from the amino acids L-arginine, glycine, and L-methionine. Creatine supplements had previously been found to improve the ability to do intense exercise in people unaffected with McArdle’s and also people with mitochondrial myopathies (see section 2. They showed that McArdle people were able to exercise more easily after taking the creatine. When taking high dose creatine, the McArdle people reported that they felt muscle pain more frequently during exercise and the level of pain was higher. Vogerd (2002) felt that “An effective *creatine+ dosage without adverse effects may be between 60 and 150 mg/kg daily”, but that further trials were necessary. It was not possible to determine how creatine improved the ability to exercise as treatment did not increase creatine levels in the muscles. It was therefore possible that creatine was having a different, albeit positive effect upon the body (Vorgerd and Zange, 2007). In McArdle people, the liver form of the glycogen phosphorylase enzyme works perfectly well, so the body is able to store excess sugar as glycogen in the liver, and then convert it back into glucose which can be released into the blood when needed. A sugary drink can help, as the sugar is very rapidly absorbed through the stomach/intestine into the blood, and can quickly get to the muscle cells where it is needed (quickly in this case would be sometime between 5mins and 2 hours). In contrast, cornstarch takes much longer to absorb and for the body to break it down into sugar (Sweetman, 2009). If you tried drinking/eating cornstarch just before exercise, the sugar from the cornstarch would not be released until a long time after you had finished exercise, and would not provide any sugar for the muscles during exercise. The abstract said that it was an open trial which means that the participants knew if they were having the treatment or not which is much less scientifically/medically useful. It may be that no other trials of cornstarch have been performed because most researchers have decided based on the science that it would be unlikely to help, and therefore not bothered testing it. A total of 150mg (given as three doses of 50mg) was given to participants in the trial by Poels et al. Note: An intravenous injection of dantrolene sodium can be used as a treatment for malignant hyperthermia (Sweetman, 2009)(see section 12. Reason why it might help McArdle’s: Dantrolene sodium is a muscle relaxant, which works directly on the skeletal muscles (Sweetman, 2009). It was thought that dantrolene sodium might induce or improve the second-wind (Poels et al. There was also a case report that dantrolene sodium prevented rhabdomyolysis caused by exercise, in a person who had rhabdomyolysis and whose muscles quickly became tired during exercise (Haverkort-Poels et al. The researchers may have hoped that dantrolene sodium would have a similar positive effect on McArdle people. However, the overall conclusion was that “None of the patients experienced beneficial effect of dantrolene sodium medication” (Poels et al. Form of the supplement: D-ribose dissolved in water as a drink Reason why it might help McArdle’s: Ribose has several functions in the body. It is part of riboflavin, which is a building block of two components involved in aerobic energy metabolism. Initial studies suggested that ribose supplements did appear to help people with either myoadenylate deaminase deficiency (see section 2. Results of clinical trials: Several studies have been carried out in people unaffected by McArdle’s to see if ribose supplements help them exercise for longer, but in general they did not have much effect. There was no significant difference in ability to exercise before or after treatment. Reason why it might help McArdle’s: Sucrose is rapidly split into glucose and fructose within the muscle cells. Glucose and fructose can be used in glycolysis to provide energy (Fernandes, 2006). This removes the need to breakdown glycogen into glucose – which is requires muscle glycogen phosphorylase and does not occur in McArdle people (Fernandes, 2009). Having a sugary drink just before exercise can increase the level of glucose in the blood. Glucose in the blood can be transported and taken into the muscle cells, and used to produce energy for exercise. This source of glucose should prevent muscle cells running out of glucose, and reduce symptoms of McArdle’s which are normally induced by exercise; such as muscle pain and cramps. Form of the supplement used in the trials: sucrose powder dissolved in water to produce a drink. What were the results of clinical trials: Vissing and Haller (2003) gave McArdle people 660ml of a drink containing either 75g of sucrose or artificial sweeteners (as a placebo). Drinking sucrose increased the level of glucose in the blood, and made exercise easier for the McArdle people. The McArdle people who were given glucose had a lower heart rate and felt that exercise was easier compared to when they had the placebo. The exercise was a stationary bicycle (ergometer) which was cycled for 15 minutes. Andersen, Haller and Vissing then followed this up in 2008 with the following experiment. McArdle people were given either; 75 g of sucrose or a placebo 40 minutes before exercise, or 37 g of sucrose or a placebo 5 minutes before exercise. People were tested with each on different days but did not know which treatment they had each day. The results were that having either 75g or 37g of sucrose made exercise easier for McArdle people. However, taking of sucrose five minutes before exercise had a longer lasting positive effect than taking sucrose 40 minutes before exercise. The author’s conclusions were “This study shows that 37 g of sucrose ingested shortly before exercise has a marked and 82 prolonged effect on exercise tolerance in patients with McArdle disease. This treatment is more convenient for the patients and saves more calories than the currently recommended sucrose treatment. Cons: Having a sugary drink before exercise is a short term treatment, and can lead to weight gain (Amato, 2003; Quinlivan et al. Sugar isn’t a suitable treatment for McArdle people who have diabetes (Quinlivan et al. High levels of sucrose may prevent utilisation of fatty acids as a fuel for prolonged exercise (Amato, 2003)). Form of the supplement: It can be given orally as a tablet, or by intravenous injection. I think that treatment with verapamil was proposed as a way to reduce the increased heart rate which is usually seen in McArdle people when they exercise. These supplements have not been tested in clinical trials, and there is no clinical evidence that they could treat McArdle’s. Fatty acids can be broken down to produce energy, which provides energy for the second wind. This is an alternative method to produce energy than glycolysis (the breakdown of glycogen to glucose). I imagine that people would 83 take these supplements in the hope of improving the second wind phenomenon. B12 Vitamin B12 is a water soluble vitamin essential for the brain and nervous system, and also in formation of blood. L Alanine – an amino acid L Carnatine – made from a compound of several amino acids. There is no published data or any published hypotheses that CoQ10 supplements are of any benefit to McArdle people. The only relevant mention of CoQ10 was in conjunction with statin treatment (see 12. It was hypothesised that taking CoQ10 at the same time as statins may protect muscles against damage caused by the statins. She had been taking CoQ10 supplements for the past year and had felt these had led to improvement of her symptoms. There have been no clinical trials of CoQ10 supplements as a treatment for McArdle disease. An excessive level of some supplements may restrict absorption of other nutrients or vitamins, leading to a deficiency. It is possible to overdose on some supplements, especially those which are fat soluble, and this could have health risks. Historically is has been suggested that there may be several forms of McArdle disease, which I have summarised these below as four forms. It should be noted that no cases of the rare fatal infant form or milder form have been reported in the last ten years. A criticism of the papers which reported these two forms is that they were performed before genetic testing for McArdle disease was possible.
Insertion of subdural nique and leading causes erectile dysfunction buy discount nizagara 25 mg line, if so for erectile dysfunction which doctor to consult 50 mg nizagara free shipping, which one should be based on results of an strip electrodes for the investigation of temporal lobe epilepsy impotence trials france generic 100 mg nizagara overnight delivery. Intracranial electroencephalography with subdural grid electrodes: techniques impotence natural generic 50 mg nizagara with visa, complications erectile dysfunction age 27 purchase nizagara once a day, and outneuroimaging, and neuropsychological testing. Clinical outcome after complete or sive techniques varies among surgeons; as with other types of partial cortical resection for intractable epilepsy. Advancement in neuronavigation techniques for epilepsy surgery in children and adults. Intraventricular monitoring for temporal lobe epilepsy: report on technique and initial results in eight patients. The drawings in this chapter are original art by Elaine J Neurol Neurosurg Psychiatry. Responses to single pulse electrical stimulation identify epileptogenesis in the human brain in vivo. Interictal spike detection comparing subelectrocorticography in nonlesional medial temporal lobe epilepsy. Tailored resections in occipital electrocorticography: relation to clinical outcome in patients with temporal lobe epilepsy surgery guided by monitoring with subdural electrodes: lobe surgery. Comparison of depth and subdural electrodes mic approach to medically intractable epilepsy. All physiological and pathological consideration renders it improbable that the lesion has any direct relation with epilepsy. Penfield described successful control of Hughlings Jackson provided the intellectual foundations for seizures when he extended the resection to include the uncus the development of epilepsy neurosurgery. Based on a patient’s and hippocampus in patients whose anterior and lateral resectypical motor seizures, Rickman Godlee localized and opertions did not initially eliminate seizures. In addition, during ated upon a brain tumor in 1884, with Jackson, Ferrier, and the 1957 International Colloquium of Epilepsy at Bethesda, the neurosurgeon Victor Horsley present in the operating Maryland, Paulo Niemeyer described a creative surgical techroom. Two years later, Sir Victor Horsley performed his first nique to remove the amygdala and hippocampus by a transepilepsy surgery. Clinical observations made by Jackson associated “dreamy states” and psychical experience with lesions of the mesial temporal lobe. A crude sensation of smell or taste, generally of an that combines anatomical, clinical, and neuroimaging criteria unpleasant nature. Temporal lobe epilepsy without an identified epiquietly, or carry on simple automatic activities such as walkleptogenic lesion (termed cryptogenic, nonlesional, and ing. Habitual consist of lateralized buildup of rhythmic 5 to 7 Hz seizure seizures with limbic characteristics typically begin during the activity (30,31). C: A T2 sequence showing a large cystic lesion in left temporal lobe with sharply defined borders and no surrounding edema in a patient with low-grade temporal lobe tumor. One study evaluated the localizing value of abdominal auras in 491 consecutive patients with refractory epilepsy (38). In the temporal lobe, arising in or near an area with high epileptogenic potential. In involvement of amygdala was described in 11 of 29 autopsy fact, interictal discharges that exhibit a consistent unilateral cases (16). Extrahippocampal studies, being unilateral in 70% to 80% of cases and bilateral damage has also been described in the entorhinal cortex in in 20% to 30%. This group has detected, and there was adequate contralateral memory funcbeen termed cryptogenic, nonlesional, and paradoxical temtion on Wada memory test. In a involving nontemporal lobe structures making complete resecseries of 37 patients with dual pathology, the mean age of tion difficult. The pooled proportions weighted by number of patients are also represented by the large vertical bar. The the surgical group were seizure free at 1 year compared with authors found a similar diagnostic accuracy, with both stud8% in the medical group (P 0. Studies comparing source localdom after surgery averaging from 65% to 68% of patients. All but one study reported Seizure Outcome: Long-Term Outcome Studies more than 60% seizure freedom at 10 years follow-up. Evidence Report/Technology Assessment on Management of Treatment-Resistant Epilepsy, 2003. In patients with temporal pocampus were resected, the rate of seizure freedom lobe tumors, two studies report that 65% of patients remain decreased to 20% or less (99). Their results indicate that, in seizure free with follow-up of 9 years or more (21,64). In a patients with dual pathology, removal of both the lesion and series of 207 patients with brain tumors, of which 170 were in the atrophic hippocampus is the best surgical approach to the temporal lobe, 82% patients were free of disabling optimize the chance of becoming seizure free after surgery seizures after 1 year, and 81% remained seizure free over a 10(100). One study revealed that who had temporal lobe tumors were free of disabling seizures 78% of patients were seizure free in 14 patients with tempoafter surgery (94). A recent study reported Clinical Predictors of Surgical Outcome 75% of patients as Engel Class I at 16 years after surgery (21). Multiple studies have attempted to identify clinical factors these results were similar to two other studies that reported a that would predict outcomes after epilepsy surgery; the likelihood of remaining free of disabling seizures at 79% after results are often inconsistent (Table 82. By comstudies fail to control for clinical factors that are highly correparison, other authors reported that the likelihood of remainlated. A systematic review of psyassociation was found, the effect size was small, or the chosocial outcome after epilepsy surgery concluded that all association was weak. A study evaluating patients before and after temporal patients seizureand drug-free (cured). To address this quesresections found that in subjects with dominant hemisphere tion, Schmidt et al. In another meta-analysis, using more stringent selection criteTemporal lobe resections in the language-dominant hemiria, only 16% of patients with temporal lobe surgery patients sphere are also associated with declines in object naming. They also found that words Improves Quality of Life acquired later in life were more susceptible to being lost postoperatively than words learned earlier in life (112). The most common axis I diagnosis were anxiety disorimprovement is related to seizure control (108,109). However, a small series of five patients submitprevalence of depression in patients seizure free after surgery ted to nearly the same protocol showed disappointing results. In addition, a prospective, multicenter study none of the three survivors had seizure reduction (120). A recent study reported surgical outcome and lesions where longer durations of epilepsy are associated with rate of complications in 52 patients older than 50 years for worse outcomes. In addition, the authors also neuroimaging, and develop new treatment options for those found that neuropsychological deterioration was more prowho are not candidates for temporal lobe resections, such as nounced in the older subgroup, probably due to decreased brain stimulation and radiosurgery. Another future challenge will be the ability to offer surgical treatment to more people of the world. It is based on multiple X-ray beams from the opportunity to be evaluated and treated to reduce the a highly collimated radiation source oriented by stereotactic global burden of epilepsy. Practice parameter: temporal lobe and persisting seizures up to 2 years after the procedure. The localized neocortical resections for epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology, in assomechanisms underlying seizure control in patients submitted ciation with the American Epilepsy Society and the American Association to radiosurgery are not fully understood. Erkrankung des ammonshorns als aetiologiches moment der abdominal aura and its evolution: a study in focal epilepsies. Epilepsy and other convulsive diseases: their causes, sympmesial temporal lobe epilepsy with bilateral interictal spikes. Somato-motor, autonomic and electrocorticographic responses epilepsy with unitemporal versus bitemporal interictal epileptiform disto electrical stimulation of rhinencephalic and other structures in pricharges. Clinical seizure lateralization in orbito-insular, piriform and temporal cortex, hippocampus-fornix and mesial temporal lobe epilepsy: differences between patients with unitemamygdala. In: Engel electroencephalographic and neuropathological study of the brain in J, Jr. Volumetric magnetic resonance phy, neuropsychological testing, neuroimaging, surgical results, and imaging evidence of bilateral hippocampal atrophy in mesial temporal pathology. Outcome after temporal lobecmeasurements of the hippocampal formation and anterior temporal lobe: tomy in bilateral temporal lobe epilepsy. Temporal lobe tumoral seizures, psychosocial outcome and use of antiepileptic drugs. Defining the spectrum of internawith temporal lobe tumours and medically refractory focal epilepsy. Terminology and classification of the the prominent predictor of seizure-free outcome after temporal lobeccortical dysplasias. Surgical treatment of limbic pathological considerations in the surgical treatment of intractable epilepsy associated with extrahippocampal lesions: the problem of dual epilepsy associated with temporal lobe lesions. Race/ethnicity, sex, and socioecodual pathology in patients with lesional epilepsy. Long-term outbased volume studies in temporal lobe epilepsy: pathological correlations. Long-term seizures and quality of after dominant temporal lobectomy: age at onset of epilepsy and age of life after epilepsy surgery compared with matched controls. Management of Treatment-Resistant epilepsy surgery among 399 patients with nonlesional seizure foci includEpilepsy: Evidence Report/Technology Assessment No 77. Surgical treatment for refractory temtreatment of temporal lobe epilepsy in children. Long-term outcome after temporal lobe epilepsy: seizure response, adverse events, and verbal memory. Long term follow-up of the first knife radiosurgery for mesial temporal lobe epilepsy: report of five cases. While the majority arise in the temporal lobe, the history provides important antecedent factors related extratemporal foci are common particularly in childhood. The family hisneocortical epilepsies are a diverse group with a broad spectory will identify genetic syndromes that are not surgically trum of pathology, which present significant challenges to amenable. Assessment of developmental status is important in localizing the epileptogenic focus. The presurgical evaluation pediatric patients as catastrophic epilepsies associated with focuses on accurate and precise localization of the epileptodevelopmental stagnation or regression mandate more urgent genic zone so that complete resection can be achieved. Neurologic deficits on examination such as compilation of clinical, electrographic, and neuroimaging data hemiparesis or visual field defects raise suspicion of contralatare directed toward this goal. Epilepsy surgery should be advocated early in the course of Localizing Clinical Semiology medically intractable seizures (2). Early surgical management will prevent long-term disability, social maladjustment, and Frontal lobe epilepsy accounts for up to 30% of epilepsy surgimpaired quality of life. Timely surgical referral in childhood eries, second only to temporal lobectomies (6,7). An anterior is particularly important to improve cognitive development frontal wedge resection is illustrated in Figure 83. Complete inferior frontal gyrus induces speech arrest and tonic facial removal of the epileptogenic zone is the major prerequisite for contractions. Salivation and swallowing are characteristic feapostoperative seizure freedom (3,4). Patients generally fall tures of seizures arising in the frontal operculum, whereas into one of the three broad categories: (i) a discrete structural contralateral head and eye, tonic elevation, and contralateral lesion and concordant electrophysiology, (ii) an identifiable clonic movements of the arms and face occur with mesial developmental lesion with more diffuse abnormality and a less frontal or dorsolateral frontal seizures (12).
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Vagal Nerve Stimulation for Seizures A seizure disorder or epilepsy is a chronic condition that is characterized by recurrent seizures erectile dysfunction pump hcpc buy nizagara 50mg free shipping. It involves the insertion of a device similar to erectile dysfunction 31 years old buy nizagara discount a pacemaker under the skin on the left side of the chest erectile dysfunction treatment options injections generic 100 mg nizagara otc. This vagal nerve stimulator can send intermittent electrical signals to impotence word meaning purchase genuine nizagara online the brain by stimulating the left vagus nerve in the neck erectile dysfunction occurs at what age order 25 mg nizagara with mastercard. The vagus nerve is one of the cranial nerves that controls the muscles responsible for swallowing, coughing and voice sounds. Seizure activity may improve immediately, or it may improve over a two-year time period the vagal nerve stimulator works in two ways. It can also be activated to give extra stimulations manually between preprogrammed stimulations by placing a magnet over the stimulator and then removing the magnet. Programming of the generator is accomplished with a wand attached to a computer at the physician’s office. The additional handheld magnets supplied for manual stimulation of the system can damage credit cards, cell phones, and computer disks. The following section covers the procedure for the vagal nerve stimulation and possible problems and emergencies that may arise. For a student who requires vagal nerve stimulation, the following items should receive particular attention: Student’s underlying condition and possible problems associated with the condition or treatment. Whether student experiences auras, or can anticipate when seizures are about to occur. Other medications the student is taking and signs of adverse reactions or toxicity. Procedure for Activating Vagal Nerve Stimulation Note: Equipment and supplies provided by parents. The pager-style magnet comes with a belt clip so that the magnet and clip can be removed as a unit from the belt without coming apart. Always keep magnets at least 10 inches away from credit cards, televisions, computers, computer disks, microwave ovens, watches, or other magnets. If student senses a seizure is about to occur, place the magnet over the Pulse Generator site for one second and then move it away. To use the pager-style magnet, remove the belt clip and magnet from the belt and place the label against the Pulse Generator. To use the watch-style magnet, position the wrist so that the label can be placed over the generator. To temporarily stop stimulation (turn “off” the Pulse Generator) when student needs to sing or speak in public, while eating, or if stimulation is ever painful, put the magnet over the Pulse Generator and leave it there. The Pulse Generator will not stimulate while the magnet is in place over top of it, but it will start when the magnet is removed. The magnet should not be used for more than four hours in a row because it can decrease the Pulse Generator battery. Pass the magnet over the Pulse Generator for one second to see if it causes stimulation and is working. If stimulation ever hurts, hold the magnet in place to stop stimulation and contact school nurse and health care provider immediately. Reports having two nocturnal seizures (witnessed by her husband) since her last visit. Neurological examination shows a normal mental status, normal cranial nerves and a mild left hemiparesis and is unchanged from a year ago. He reports no change in his seizure control with approximately 1 to 2 seizures per month. They continue to consist of episodes of lip smacking with clouded consciousness lasting less than a minute. Impression: Partial seizures – doing well Plan: 1) Continue lamotrigine and valproate 2) Return in 6 months or prn change in seizure frequency Prior visit: 23 year old man returns for follow up having been seen 8 months ago. He continues to have fewer than 1seizure per week consisting of episodes lasting up to a minute of lip smacking and scratching hand movements for which he does not have a clear memory. She reports no further spells on treatment but complains that the medication sedates her and causes “foggy thinking. The patient’s physical examination and neurological examination are entirely normal. Workup at a local hospital revealed a right parietal mengioma that was surgically removed. She was treated with carbamazepine for 5 years with no further seizure activity and then medication was stopped. Three months after stopping the medication she had a grand mal seizure and was put back on carbamazepine which she continues to take. Discussed issues related to the risks of seizures during pregnancy versus the risks of continuing carbamazepine versus the risks of changing medications. Impression: Seizure disorder secondary to meningioma, well controlled on carbamazepine Plan: Continue carbamazepine Begin folate supplements Return once pregnant or prn. Occasionally family will report that she developed tonic-clonic activity and rarely she has been incontinent. Since she was last seen 3 months ago she has had spells of vocalization and automatisms almost every day but no tonic clonic seizures. Phenytoin, phenobarbital, valproic acid, and experimental medications have been tried in the past. Her current medications include carbamazepine and topiramate, with lorazepam as needed. She also takes an over-thecounter multivitamin and, occasionally, acetaminophen for headache. Her sister has been instructed on administering lorazepam when she is experiencing several consecutive seizures that occur over a 15-minute period or after her second bilaterally evolved focal seizure for the day. Her sister administers the lorazepam approximately once every 2 weeks but there is no regular pattern to it. One week, she may not require any lorazepam; the next week, she may require it several times. Mental status testing reveals poor calculations and difficulty with abstract thinking. His hospital course was complicated by several seizures that was treated with phenytoin. He presents now to your clinic with the main question of whether he needs to continue his anti-epileptic medications. All you have is the hospital discharge summary which indicates only the performance of neuroimaging. His medications include phenytoin, lisinopril, hydrochlorothiazide, and atorvastatin. He has midline gaze, mild dysarthria without aphasia, decreased fine finger motion on the right, and increased reflexes on the right. Assessment: Seizures secondary to hemorrhagic stroke Plan: Continue anti-seizure medication. She is a college student who says that she stayed up all night studying for an exam. Early the next morning, her roommate was awakened by the patient having a seizure. The patient says that she has occasional jerking movement s in the morning when brushing her teeth. The patient wants to know whether she needs to take medications to prevent these events from recurring. Given symptoms and family history, strong suspicion for juvenile myoclonic epilepsy. The semiology consists of an aura of gastric discomfort, head turning to the right, some autonomisms of hand movements, then loss of consciousness and tonic-clonic movements. Some auras do not progress to secondary generalization; all tonic-clonic seizures are preceded by an aura. She has been taking combination therapy of anti-epileptic medications, but they have not been able to achieve a seizure –free period for more than several months or have resulted in fatigue. Her migraine frequency is has been much reduced with the use of topirimate to about a few times per year. Pt reports being diagnosed with Migraine since age 18 and being prescribed with medication (he does not know the name) which did not help at that time. Pain is mostly throbbing, b/l frontal and behind the eyes, + photosensitivity, +N/V. He also complains of chronic back and neck pain for which uses Gabapentin with some improvement. Past Medical History Hypertension, Headache, Bipolar affective disorder Family History Diabetes Social History Smoking: Yes, 1 ppd. Motor Exam Muscle bulk: normal Overall muscle tone: normal Strength Strength 5/5 throughout. His typical seizures lasts 1 to a few minutes and is associated with generalized body shaking without urinary or bowel incontinence. Second time he was coming down stair and started to shake and was caught by his daughter. Other than shortness of breath when walking which is chronic, he denies any other symptoms. Past Surgical History: he has past surgical history that includes anesthesia arthroscopic shoulder disarticulation and carotid endarterectomy. Review of Systems: Extensive review of systems (10) was significant only for those items mentioned in History of Present Illness. Sensation: Light touch, vibration and temperature sensation was normal in all 4 extremities. These seizure-like activities that he had over Christmas do not seem like typical seizures. Review of Systems: Extensive review of systems (10) was performed via the patient questionnaire, it was significant for those items mentioned above, as well as: depression. Muscle strength was 5/5 except for 4+/5 distally on R arm, and 5/5 proximally and 4+/5 distally on R leg. At referral epilepsy centers, psychogenic non-epileptic Received 18 February 2009 attacks are by far the most common condition found to have been misdiagnosed as epilepsy, with an Accepted 19 February 2009 average delay of 7–10 years. There are many ‘‘red fiags” that can raise the suspicion of psychogenic Available online 21 February 2009 non-epileptic attacks. Syncope is the second most common condition misdiagnosed as epilepsy, and it is probably more common in outpatient populations. Conditions specific to children include nonepileptic staring spells, breath-holdNonepileptic seizures Differential diagnosis ing spells, and shudder attacks. The terminology on the tothe wrong diagnosis of epilepsy is unfortunately common. Various terms patients diagnosed with epilepsy who are seen at epilepsy centers, have been used, including pseudoseizures, nonepileptic seizures, 20% to 30% are found to have been misdiagnosed [1–3]. Strictly speaking, terms such as pseudocentage is astonishingly consistent across centers, countries, and seizures and nonepileptic seizures include both psychogenic and continents. On the other hand, the most common condition found at referral epilepsy centers a term such as psychogenic nonepileptic seizures should be preferred and epilepsy monitoring units, though syncope may be more combecause it adds the important connotation of a psychological orimon in a general neurology practice setting.
An overall approach to erectile dysfunction doctors staten island discount nizagara online visa evaluation and treatment of patients with chronic kidney disease is given in Guideline 2 erectile dysfunction pills cost effective 100 mg nizagara, and recommendations for individuals at increased risk of chronic kidney disease are given in Guideline 3 erectile dysfunction treatment mumbai buy discount nizagara on-line. Clinical applications are also given at the conclusion of each subsequent guideline erectile dysfunction treatment medscape order nizagara 25 mg amex. Finally erectile dysfunction how common order cheap nizagara on-line, additional recommendations for evaluation, diagnosis, and treatment of chronic kidney disease are given in Part 9. They include: widespread dissemination and easy access to the guidelines; educational interactive programs aimed at health professionals, patients, providers, administrators, manufacturers, and policy makers; information tools and systems to facilitate adherence; development of clinical performance measures; incorporation of guidelines into continuous quality improvement programs; development of quality assessment instruments; and update and review of the pertinent literature on an ongoing basis. Definition and Classification 65 markers of damage, and kidney function impairment. This would facilitate using administrative databases for epidemiological and outcomes surveys. The outcomes of individuals with various stages of chronic kidney disease are not defined. A cohort study of patients with chronic kidney disease would enable definition of the relationship between factors and outcomes of stages of chronic kidney disease. This would be particularly useful in defining the relationships among stages of chronic kidney disease, progression of chronic kidney disease, initiation and progression of cardiovascular disease, health service utilization, and barriers to care. An action plan for patients with chronic kidney disease also requires interventions during the earlier stages of kidney disease, irrespective of the cause of kidney disease. Definition and Classification 67 ing progression of kidney disease, cardiovascular disease risk reduction, preventing and treating complications of chronic kidney disease, and preparation for kidney replacement therapy. The definitive diagnosis of the type of kidney disease is based on biopsy or imaging studies. Biopsy and invasive imaging procedures are associated with a risk, albeit usually small, of serious complications. Therefore, these procedures are often avoided unless a definitive diagnosis would change either the treatment or prognosis. In most patients, well-defined clinical presentations and causal factors provide a sufficient basis to assign a diagnosis of chronic kidney disease. An approach to diagnosis, based on concepts elaborated on in this report, is given in Part 9. Diabetic kidney disease is a type of glomerular disease, but it is singled out here because it is the largest single cause of kidney failure. Because of the higher prevalence of type 2 diabetes, it is the more common cause of diabetic kidney disease. The clinical features, natural history and treatment for diabetic kidney disease are well known because it has been the subject of numerous epidemiological studies and clinical trials. Clinical trials have established a number of effective treatments to slow the development and progression of diabetic kidney disease, including strict glycemic control, angiotensinconverting enzyme inhibitors and angiotensin receptor blockers, blood pressure control, and perhaps dietary protein restriction. A variety of diseases, including other glomerular diseases, vascular diseases, tubulointerstitial diseases, and cystic diseases, are often grouped together under the label ‘‘nondiabetic kidney diseases’’ for the purpose of epidemiological studies and clinical trials. Amongst these, hypertensive nephrosclerosis and glomerular diseases are the second and third most common causes of kidney failure. The various diseases in this group differ widely based on history, clinical presentation, risk for progression, and response to treatment. Differentiation among the diseases can be difficult, often requiring kidney biopsy or invasive imaging studies. An approach to diagnosis, based on the history, and a review of clinical presentations of chronic kidney disease, are given in Part 9. Specific therapies are available to reverse abnormalities in structure and function for some types of chronic kidney disease: for example, immunosuppressive medications for autoimmune glomerular diseases, antibiotics for urinary tract infections, removal of urinary stones, relief of obstruction, and cessation of toxic drugs. A thorough search for ‘‘reversible causes’’ of decreased kidney function should be carried out in each patient with chronic kidney disease. Kidney disease in the transplant is probably the fourth largest cause of kidney failure. Definition and Classification 69 Both immunologic and non-immunologic factors appear to play an important role. The most common causes are chronic rejection, toxicity due to cyclosporine or tacrolimus, recurrent disease, and transplant glomerulopathy. In addition, differential diagnosis includes all the diseases that can occur in the native kidney. For a variety of reasons, especially the ease and safety of kidney biopsy, there is generally a much lower threshold for performing invasive procedures to establish a definitive diagnosis in kidney transplant recipients. Comorbidity is defined as conditions other than the primary disease (in this case, chronic kidney disease). Complications of chronic kidney disease, such as hypertension, anemia, malnutrition, bone disease and neuropathy, are not considered as comorbid conditions. Evaluation and management of these diseases is important for patients’ well being and may improve the course of chronic kidney disease. This is particularly important for patients with diabetes and high blood pressure, the leading causes of chronic kidney disease and cardiovascular disease in the United States. Unrelated diseases, which may lead to impairments of functioning and well-being but do not affect the course of chronic kidney disease. Cardiovascular disease is singled out from among the possible comorbid conditions to emphasize its complex relationship with chronic kidney disease, and its importance as a preventable cause of morbidity and mortality in patients with chronic kidney disease. In all cases, management of comorbid conditions must be integrated into the overall care of patients with chronic kidney disease. Factors associated with progression of kidney disease are discussed in Guideline 13. In diseases characterized by a quantifiable marker of damage—for example, albuminuria in diabetic kidney disease—progression, stability, or regression can be estimated by change in the marker. For most diseases, however, quantitative relationships between changes in markers and progression have not been established. Complications due to disorders in other organ systems are associated with worse outcomes. These include maintenance of the filtration barrier for plasma proteins (abnormalities include albuminuria and proteinuria), reabsorption or secretion of water or specific solutes (abnormalities include tubular syndromes), and various endocrine functions (erythropoietin deficiency causes anemia, parathyroid hormone excess causes bone disease, and vitamin D deficiency causes bone disease). Prevention and treatment of complications of chronic kidney disease includes specific therapies related to the pathogenesis of complications—for example, erythropoietin for anemia and vitamin D for bone disease. Treatment and prevention of cardiovascular disease in chronic kidney disease includes risk factor reduction as well as specific therapies for cardiovascular disease and should begin as early as possible. Patients require education and advance preparation to cope with the stresses of kidney failure, to choose 72 Part 4. All patients should probably be instructed to preserve suitable veins for possible future vascular access construction. The indications for initiation of kidney replacement therapy are based on the level of kidney function and presence of signs and symptoms of uremia. Patients with chronic kidney disease are prescribed a large number of medications. In addition, patients may take other medications, such as over-the-counter medications, ‘‘non-traditional’’ medications, vitamins and supplements, herbs, and drugs of abuse. A thorough review of the medication list and all other medications should be conducted at each visit. Drugs with potentially adverse effects on kidney function or complications of decreased kidney function should be discontinued if possible. Because of possible alterations in volume of distribution, protein binding, drug elimination, and drug-drug interactions in chronic kidney disease, therapeutic drug monitoring should be performed, if possible. A large amount of information is available to providers in texts, manuals, and databases for handheld computers. Interpretation may be facilitated by the similarity between the classification of levels of kidney function proposed in this guideline and the recommendations for pharmacokinetic studies of drugs in patients with decreased kidney function made by the Food and Drug Administration84 (on the Internet. Healthy people make choices that could ultimately shorten their lives, such as smoking, drinking or eating too much, not exercising, missing prescribed medications, and failing to get an annual physical. Those with chronic health conditions requiring lifestyle changes and clinician-initiated visits are more likely to be noncompliant. Definition and Classification 73 Because the terminology ‘‘noncompliance’’ or ‘‘nonadherence’’ often leads to prejudice and negative stereotyping, it is recommended that ‘‘self-management behaviors’’ be substituted. Frequently the primary care provider will make the diagnosis of chronic kidney disease. Referral to a nephrologist or other specialist for consultation or co-management should be made after diagnosis under the following circumstances: a clinical action plan cannot be prepared based on the stage of the disease, the prescribed evaluation of the patient cannot be carried out, or the recommended treatment cannot be carried out. These activities may not be possible either because the appropriate tools are not available or because the primary care physician does not have the time or information needed to do so. Subsequent guidelines will elaborate on the concepts in this guideline, but it is beyond the scope of these guidelines to provide specific instructions for evaluation and management. The ultimate goal is to develop specific guidelines for each action at each stage of disease. In principle, prevention of adverse outcomes of chronic kidney disease could be facilitated by evaluating individuals with risk factors, to enable earlier detection, and by risk factor reduction in individuals without chronic kidney disease, to prevent or slow the development of chronic kidney disease. In principle, the relationship between the risk factor and the outcome may be either causal or non-causal. Causal risk factors are determinants of the outcome, and successful intervention to reduce exposure to them would improve outcomes. Non-causal risk factors may be associated with the outcome through confounding or reverse causation. Interventions to reduce exposure to non-causal risk factors would not necessarily improve outcomes. A useful classification of risk factors has been used in cardiovascular disease epidemiology100 and is shown in Table 38. In addition, because it can be difficult to detect the onset of chronic kidney disease, some risk factors for faster progression may appear to be to susceptibility or initiation factors (Table 39). Note that progression factors may be associated with progression either because initial damage cannot be resolved or because damage is ongoing. In addition, numerous factors have been shown to be associated with worse outcomes in patients with kidney failure, (such as inadequate dialysis dose, temporary vascular access, anemia, and low serum albumin concentration). Textbooks and reviews list a large number of potential risk factors for chronic kidney disease. The difficulty of detecting the early stages of chronic kidney disease makes it difficult to determine whether the risk factors so far identified relate more to susceptibility, initiation, or progression. Table 40 contains a partial list of clinical and sociodemographic factors that have been implicated as susceptibility or initiation factors. For some of these factors (for example, diabetes), interventions (like strict glycemic control) have been proven to lower the risk of developing chronic kidney disease (Category I, Table 38). The prevalence of individuals at increased risk for development of chronic kidney disease has not been studied systematically. However, some idea of the magnitude of the problem can be obtained by reviewing data from recent publications (Table 42). It is beyond the scope of these guidelines to provide specific instructions for screening.