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  • Pediatric Pulmonary Clinical Pharmacy Specialist, Riley Hospital for Children at Indiana University Health, Indianapolis, Indiana

Multi-infarct transient ischemic attack: a community-based case-control dementia: a computed tomographic study spasms hiccups discount urispas 200 mg visa. Neuro-Behcet’s disease in Caucasians: a leukoencephalopathy: a neuropathologic confirmation muscle relaxant 800 mg purchase generic urispas line. Alzheimer’s disease amyloid gene in hereditary cerebral Kanazawa M spasms upper back purchase urispas on line, Sanpei K muscle relaxant high blood pressure generic 200 mg urispas with mastercard, Kasuga K. Neurological complications in the medullary arteries in Binswanger’s disease brains: a Behcet’s syndrome. Eur Neurol 2003; in Wegener’s granulomatosis: an analysis of 324 consecutive 49:67–71. Review of the literature and functional outcome after stroke associated with small vessel thorough study of 142 cases. Diagnosis and management of isolated angiitis of the dysfunction during attack and recovery in two ‘pure’ cases. Early lacunar strokes disturbance of verbal memory: a clinicoanatomical study with complicated polyarteritis nodosa: thrombotic a new method of computed tomographic stereotaxic lesion microangiopathy. A clinical comparative study of correlated with magnetic resonance imaging in subcortical multiple sclerosis and neuro-Behcet’s syndrome. Meningo-encephalitis of Behcet’s disease: prevention of cranial ischemic complications in giant cell Case report with pathological findings. Acta controlled multicentre study of memantine in mild to Neuropathol (Berl) 1995; 89:116–21. Incidence and risk factors of transient global amnesia: elevated signal intensity in the left vascular dementia and Alzheimer’s disease in a defined elderly medial temporal lobe in 7 of 10 patients. Idiopathic granulomatous angiitis of the central nervous system: diagnostic challenges. Focal signs, such as hemiparesis, may or may not be present, and, Subdural hematomas, which typically, but not always, when present, may be quite mild. Rarely seizures may occur occur secondary to head trauma, may present acutely, sub(Annegers et al. In all acute hematomas, blood may be demonstrated for a week three varieties, blood accumulates between the dura and or two, after which, with hemolysis, a proteinaceous fluid arachnoid; in acute subdural hematomas, this is generally remains. In chronic cases the fluid has the same imaging due to arterial bleeding, whereas subacute and chronic subcharacteristics as the cerebrospinal fluid. Acute subdural hematoma typically occurs in the setting of a traumatic brain injury, and is often accompanied by Course other intracranial injuries, such as diffuse axonal injury, contusions, intracerebral hemorrhages, and subarachnoid Acute subdural hematomas tend to rapidly enlarge and hemorrhage. Patients may develop delirium or may presmay become immediately life-threatening. Chronic subdural hematomas tend to trauma, the latent interval between the trauma and the undergo a very gradual progression. With progression, uncal herniation may occur with the developEtiology ment of an ipsilateral third nerve palsy and hemiparesis. Chronic subdural hematoma may be caused by trivial Most cases of subdural hematoma occur secondary to head injury and, indeed, anywhere from one-quarter to trauma, either due to a blow to the head or to an one-half of patients may not recall any head trauma acceleration–deceleration injury. After a and severe, for example in a motor vehicle accident; however, latent interval of months to years patients gradually develop in the elderly the trauma need not be severe and indeed may a dementia, which is often accompanied by headache appear trivial. Acute subdural hematomas generally occur (Arieff and Wetzel 1964; Black 1984; Ishikawa et al. Subacute and chronic submay occur (Cameron 1978) and, rarely, chronic subdural dural hematomas, however, typically appear secondary to p11. Importantly, however, some judgment is required here before ascribing a dementia to a chronic subdural hematoma: whereas a thick chronic hematoma that grossly compresses the underlying cortex may reasonably be held accountable for a dementia, a thin structure that barely compresses the underlying cortex might well be incidental and in such cases it is appropriate to look for other causes of dementia. Regardless of the source of the bleeding, blood accutime may be required for the gradual re-expansion of the mulates in the ‘virtual space’ between the dura and the arachchronically compressed cortex and, hence, clinical noid. In cases in which the hematoma is relatively small, the fluid may simply be resorbed, with little in the way of anatomic sequelae (Dolinskas et al. These encapsulated fluid colinjury’, given the extensive vascular injury it could also be lections tend to very gradually enlarge, probably as a result of called ‘diffuse vascular injury’. These injuries are typically bleeding from fragile capillaries found in the pseudomemaccompanied by other traumatic lesions, such as contubrane itself (Markwalder 1981), and it is this gradual enlargesions, intracerebral hemorrhages, etc. Simple old age also increases the risk of a chronic Clinical features subdural hematoma, and this may be because the normal atrophy seen with age leads to a stretching of the bridging Typically, patients are rendered immediately unconscious veins, thus making them more vulnerable to rupture. Some may never regain consciousness; those that do may develop a persistent vegetaDifferential diagnosis tive state (Levin et al. Other sequelae, as immediately suggests the diagnosis; however, as noted in discussed in Section 7. Dementia pugilistica is a distinct syndrome that occurs 2003) in the centrum semiovale, corpus callosum, internal secondary to repeated blows to the head and is charactercapsules, dorsolateral quadrants of the brainstem, and the ized by dementia, ataxia, and parkinsonism. Clinical features Course the onset of symptoms is gradual and occurs anywhere Most improvement is seen over the first 6 months postfrom 5 to 40 years after there has been an accumulation of injury, with some further, but less substantial, progress a sufficient number of blows to the head, which, in the case over the following 6 months; after a year, however, little of professional boxers, equates to perhaps a dozen or so further spontaneous improvement may be expected. Thus, although some boxers may develop this disorder while they are still professionally active, in most cases symptoms are delayed until long after the boxer has Etiology left the ring. Clinically (Corsellis 1989; Critchley 1957; Harvey and With either a sudden impact or merely a severe ‘whiplash’ Davis 1974; Jordan 1987; McLatchie et al. Axons acutely display retraction balls and microglial clusthe dementia itself is non-specific, except perhaps for an ters and, over time, microglial scars appear. Etiology Neuropathologic findings are described in the classic paper by Corsellis et al. The cerebral cortex is atrophied and the ventricles are enlarged; cerebellar atroAs noted earlier, diffuse axonal injury occurs as part of the phy is also present. Microscopically, there are widespread syndrome of traumatic brain injury and in many cases it neurofibrillary tangles, which are identical to those found may be very difficult to determine how great a part diffuse in Alzheimer’s disease (Roberts 1988; Schmidt et al. Cell loss is found in the substantia nigra and in normal or displays only findings consistent with diffuse the locus ceruleus, but Lewy bodies are absent. The mechaxonal injury, and here one may confidently ascribe the anism whereby repeated blows to the head induce these clinical findings to this etiology. Treatment Differential diagnosis the overall treatment of the delirium and dementia of Not all dementias occurring long after repeated head injury traumatic brain injury is discussed in Section 7. The amnesia seen in concussion extends in a retrograde fashion for up to hours and in an anterograde fashion from minutes to, in rare cases, hours (Fisher 1966; Martland 1928). In a very small minority of cases, concussion may be associated with a grand mal seizure occurring within seconds of the impact; also known as ‘concussive convulsions’, these events do not recur and do not portend the development of epilepsy (McCrory et al. Although the grosser aspects of concussion clear immediately, there may be some subtle and mild difficulty with memory and concentration that typically resolves gradually within a week (McCrea et al. In a minority of cases, concussion may be followed by the post-concussion syndrome (Lishman 1968; Mapothar Figure 11. Headache tends to be severe and may be continuous or had a traumatic subarachnoid hemorrhage followed by the episodic; it may be dull and continuous, or throbbing, and gradual development of a communicating hydrocephalus. Clinically, although perhaps having a ‘magnetic’ gait, such Fatigue may be constant or may become evident only when patients do not develop parkinsonism; furthermore, on patients exert themselves. Dizziness may consist of mere imaging, the ventricular dilation will be out of all proportion light-headedness or there may be a true vertigo; when verto any cortical atrophy. Chronic subdural hematoma must tigo is present, patients may complain that it is exacerbated also be considered but is readily diagnosed on imaging. Irritability may be prominent, and Treatment patients may complain of great difficulty controlling their tempers. Anxiety may also be seen but appears less comthe general treatment of dementia is discussed in Section mon. In cases in which parkinsonism is prominent, considhyperacusis, and hyperhidrosis, which at times may be eration may be given to a trial of levodopa. When symptoms persist for more than 3 years, a in a minority a post-concussion syndrome will develop. Post-concussion syndrome, also known as post-concussional disorder, is characterized by headache, difficulty with concentration and memory, fatigue, dizziness, various admixEtiology tures of depression, irritability and anxiety, and other symptoms, such as photophobia. Patients may experience delirium, axonal injury underlying the post-concussion syndrome, drowsiness, ataxia, headache, nausea and vomiting, and, in head trauma sufficient to cause a concussion may also, a small minority, seizures (Oliff et al. Symptoms especially in the elderly, alcoholics, and those on warfarin, undergo a gradual, spontaneous resolution. In patients who received Post-traumatic stress disorder may follow an assault whole-brain irradiation, there may be delirium, drowsiinvolving a blow to the head, but here one finds evidence of ness, headache, and nausea. By contrast, in those subjected a re-experiencing of the event, as in dreams or waking to focal irradiation there may be focal signs appropriate to memories, symptoms not typical of the post-concussion the irradiated area.


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Standard treatment is with metronidazole (500 mg orally twice a day for 7 days) or gel (0 muscle relaxant and alcohol cheap urispas 200 mg line. Adolescent females may develop a number of genital conditions that may or may not be related to muscle relaxant otc usa discount 200mg urispas amex sexual behavior [52] muscle relaxant side effects purchase urispas 200 mg mastercard. For example muscle relaxant walgreens buy generic urispas on-line, the Epstein–Barr virus can be transmitted via intimate contact with a sex partner and lead to infectious mononucleosis. Hepatitis A and hepatitis B can be sexually transmitted and vaccination for both these viruses is recommended, as previously noted. Also as noted earlier, Group A Streptococcus may cause vaginal discharge and can be due to autoinoculation or sexual contact from a pharyngeal site. A forgotten, retained tampon (or other objects) can lead to foreign body vaginitis characterized by a very malodorous 332 D. Omar vaginal discharge; cognitively limited patients can vaginally insert a variety of objects, much like that noted with young children. Clinicians may also find such conditions as tinea cruris, contact dermatitis, or molluscum contagiosum. Contact dermatitis can involve any part of the genitals and can be due to contact and sensitization from a variety of materials such as latex condoms or diaphragms, sexual lubricants, spermicides, deodorant soaps, bubble bath or bath salts, douches, underclothing dyes, patterned toilet tissue, “feminine hygiene” sprays or suppositories. Removal of the offending agent is needed along with sitz baths, topical compresses (Burrow’s solution), and/or mild topical steroids. For example, intense vulvar pruritus (often worse at night) with excoriations can be found with the presence of the eggs (“nits”) or active adult forms of Phthirius pubis that are evident on examination of pubic hair with a hand lens; these nits may also be found on perineum, axillary hair, or eyelashes. Pubic lice are acquired from sexual contact but may also be spread with fomites, such as bedding or clothes that are shared, such as with infected siblings and thus, involve children. Treatment is with 1% permethrin with second-line treatments such as use of lindane or pyrethrin; repeat the treatment in 7–10 days to kill lice hatched from the initial treatment. Another infestation that may occur is due to the mite, Sarcoptes scabiei, in which female mites burrow in the stratum corneum to deposit eggs leading to intense pruritus (worse at night) that can also result in various skin lesions, such as papules, vesicles, pustules, and burrows and linear or “S”-shaped tunnels may be seen on the hands (especially finger webs), wrists, axillae, belt line, and areolae. The diagnosis is with microscopic examination of material scraped with a scalpel blade from non-excoriated lesions placed on a glass slide and covered with a cover slip, look for mites, eggs, or feces. Treat with 5% permethrin cream that is applied from the neck down for 8–14 h and repeated in 7–10 days to kill the mites that hatched from eggs after the initial treatment. Treat all members in the family and clean infested clothes and bedding; alternatively clothes and bedding can be stored in a plastic bag for 72 h. Menstrual Disorders/Concerns Any adolescent female may present with a variety of breast or menstrual disorders [52, 58]. A recent study of adolescent females with Down syndrome, autism, and cerebral palsy noted a link between behavioral problems (as mood changes) and irregular menstrual bleeding, especially in those with autism [64]. Females with trisomy 21 have increased incidence for thyroid disorders that may lead to amenorrhea or dysfunction uterine bleeding. The presence of Turner 20 Sexuality and Gynecological Care 333 syndrome should be considered in any adolescent female with short stature and amenorrhea because of premature ovarian failure. Youth with various neurodevelopmental disorders may be prescribed neuroleptic medication or anticonvulsants that may lead to drug-induced menstrual dysfunction [65]. In youth with severe cognitive limitations, education by the clinician may be confined to hygiene improvement and sex abuse prevention. The clinician may need to recommend various means to control problematic menstruation and related hygiene concerns; these recommendations may include behavioral modification training, use of non-steroidal anti-infiammatory drugs, prescription of hormonal treatment. Perceived abnormalities may prompt the request for cosmetic surgery that may or may not be needed in attempts to prove one’s self-esteem. Counseling can also help this vulnerable patient prevent unnecessary surgery, as noted with the recent trend for cosmetic surgery in those under 18 years of age, as breast augmentation and liposuction [66]. Contraception Sexually active youth and those not having sex, but presenting with questions, should receive accurate and balanced information about contraception [1, 31, 49, 52]. In addition to pregnancy prevention, oral contraceptives can be presented as medication useful in treatment of a variety of conditions, including dysmenorrhea, dysfunctional uterine bleeding [52, 58]. As noted, the au courant media and social networking of the Internet are promoting a promiscuous society without fear of consequences from unprotected sex with multiple partners. Such instruction should also include accurate information about emergency contraception. Methods such as the intravaginal ring and barrier contraception are often not the ideal choice for those with developmental disabilities unless this female possesses the physical and cognitive abilities to use the ring as directed or the barrier contraceptive with each act of coitus [49, 61–65, 67–69]. There may be concerns with estrogen-containing contraceptives because of risks for thromboembolic events or concerns with Depo-Provera because of risks for increased menstrual bleeding or loss of bone density. Those with anorexia nervosa or if wheelchair bound may not be good candidates for prolonged Depo-Provera use [49, 68–71]. Nevertheless, the most popular contraceptive for adolescent females with developmental disabilities (such as cognitive limits) is often depo-medroxy-progesterone acetate (Depo-Provera), because of its high contraceptive efficacy for 3 months with each dose, its intramuscular administration, and its side effect of amenorrhea. Omar medications, the risks of potential side effects must be balanced with the potential benefits of their use. Thus, the clinician should provide careful, comprehensive counseling regarding contraception to these adolescent females. Concerns of fertility exist in the minds of adolescent and adult females with disabilities and should be addressed by the clinician in discussion with the patient or in actual testing as warranted by the specific situation [72]. Finally, the topic of sterilization for severely disabled youth remains a very controversial and complex topic in today’s diverse society [54, 73–75]. Sexual Dysfunction As the adolescent female progresses toward adulthood, issues of physical sexual expression and reproductive capacity become more important and, thus, sexuality education should be available from an informed, sensitive, and caring clinician who is not embarrassed with such topics. Discussion of sexuality can be complicated by cognitive dysfunction noted in various disabilities (see Table 20. Concerns of general society regarding the sexuality of adolescents including those with mental retardation and other disabilities have been present since H. However, it is clear that healthy sexual functioning is an important part of healthy as well as joyful living, and a major cause of sexual dysfunction is lack of knowledge about normal sexuality. Removal of the offending medications and replacement with those having less or absence adverse effect on sexual functioning are often helpful in this regard. Sexual dysfunction that arises in adolescence may continue into adulthood when society becomes more accepting of sexual function in general. It is a general principle of medicine that pathophysiologic disorders (as diabetes mellitus, hypertension, Table 20. Sexual pain disorder/dyspareunia (due to vaginitis, lichen sclerosus, imperforated hymen, pelvic infiammatory disease, congenital genital disorders, endometriosis, others) 4. Orgasmic dysfunction (anorgasmia) 20 Sexuality and Gynecological Care 335 Table 20. The same principle applies to the development and correction of sexual dysfunction in adolescents. Failure to correct problems and disorders in adolescence typically leads to the worsening of these conditions in adulthood and with earlier complications or sequelae. Youth with visible deformities may experience interference with sexual expression and need special counseling in this regard; these deformities include amputations, ostomies, paraplegia, or abnormal genitalia [1, 31]. Youth with colostomies can be anxious about the odor from the ostomy while those with arthritis may be in pain, or a youth with spinal cord lesions may have painful bed sores. Youth may be bullied by others especially if they appear different from peers because of having cognitive limitations, physical deformities, and/or mental disorders. Feelings of being inadequate and problems with sexual performance may arise in any youth or adult with regard to their sexual lives. However, perhaps the major discomfort is found in parents and society in general when considering the sexuality of their children with various disabilities (Table 20. Conclusions Adolescence brings complex challenges for parents, clinicians, society, and for the teenagers as well [79]. Consideration of healthy sexuality in adolescents including those with disabilities remains a controversial concept for contemporary society [80]. Adolescent females are involved in a wide variety of voluntary and forced sexual behavior, and the existence of neurodevelopmental disabilities does not negate these issues nor does it negate the importance of healthy sexuality functioning for these youth [85–88]. The 2002 National Survey of Family Growth reports that 47% of never-married female adolescents (aged 15–19 years) have been sexually active in contrast to 46% of the same age males [80].

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Anticonvulsant properties of Other side effects spasms caused by anxiety order urispas 200 mg, including bone demineralization spasms define purchase urispas with a visa, growth acetone spasms translation discount 200 mg urispas mastercard, a brain ketone elevated by the ketogenic diet spasms liver buy 200mg urispas free shipping. Antioxidant study, both by virtue of its clinical utility as well as the potencapacity contributes to protection of ketone bodies against oxidative damtial insights to be gleaned from analyzing its effective and age induced during hypoglycemic conditions. Are purines mediators of the anticonvulsant/ neuroprotective effects of ketogenic dietsfi Benefits of the nonfasting ketogenic diet effects of two ketogenic diets in childhood epilepsy. A clinical electroencephalographic Practice Committee of the Child Neurology Society; Practice Committee of correlation of seizures on a ketogenic diet. Successful treatment of ommendations of the International Ketogenic Diet Study Group. Landau-Kleffner syndrome with mitoacross the blood-brain barrier as a cause of persistent hypoglycorrhachia, chondrial respiratory chain-complex I deficiency. In addition, safety and tolerability issues trials showed improved control in adults with intractable parassociated with both the acute and chronic side effects and tial seizures who were not candidates for epilepsy surgery toxicity complications further diminish the effectiveness of (22–24). Each stimulation period is preceded by 2 seconds of ramp-up time and followed by 2 seconds of ramp-down time. Zabara likened 1996 Second randomized active control these contractions to convulsions. This theory was commercial approval proved in his first canine studies (21), and a company— February 2009 50,000 implants worldwide for Cyberonics, Inc. Currently, three leads are available: the Model 302, Perennia model leads are not yet available in all countries. The median reducstimulation of the vagus nerve had different effects on the fretion in seizure frequency was 45%, with seizure frequency quency of partial seizures (26,27). E03 acute-study patients (27) (N 114 implanted) had epilepsy for an average of 22 years. Real-World Outcomes Seizure frequency was reduced by at least half in 31% of patients in the high-stimulation group, compared with 14% in In addition to the clinical trial data, real-world outcome studthe low-stimulation group. Patients in rates from the literature for studies reporting on at least the high-stimulation group either aborted or decreased 59. One patient receiving with an additional 13% of patients having a seizure frequency high stimulation became seizure free, and 23. Seizure-free periods increased apy also successfully stopped a case of refractory generalized every year; one patient continued to be seizure free after convulsive status epilepticus in a patient 13 years of age (66). A prospective, open evaluation of 64 patients Another report among three children admitted to the intensive reported results for up to 5 years of follow-up (35). In this ment option among this patient population irregardless of age population with refractory seizures, 44% experienced a sub(67–72). Seizure frequency reductions among these studies stantial reduction in severity and frequency over a long ranged from 40% to 70% (67–69,71,72). Small, prospective studies report similar results patients of different ages (75) recommended age-related stimas well as additional benefits beyond seizure reduction such as ulation adjustments based on age-related changes seen in reduced postictal periods and seizure duration (37,38). Additional pediatric studies reported that higher output currents might be required, particularly when lower pulse durations are used (76–78). A retrospective study of 46 children implanted under Electrical stimulation of the peripheral vagus nerve requires the age of 18 (median age of 12. Verbal performance, alertness, motor and cognitive functions, and general behavior improved, sometimes dramatically (45,47,56,62,63). Hypersynchronized Chapter 70: Vagus Nerve Stimulation Therapy 801 cortical and thalamocortical neuronal interactions characterfrequency bands (99), interictal epileptiform activity, or the ize seizures; therefore, it was postulated that desynchronizing waking or sleep background rhythms (22,99–101). Most central projections of the vagus of magnetic extra stimulation in abolishing seizures (102). However, this population was quite different stem nuclei are known to influence seizure susceptibility from that in the earlier adult series. Cerebrospinal fluid samples nephrine release by the locus ceruleus is antiepileptogenic. A pilot study of three through neuronal networks that project from brain stem adults showed activation of the right thalamus, right posto forebrain structures. Vagal projections to noradrenergic terotemporal cortex, left putamen, and left inferior cerebellum and serotonergic neuromodulatory systems of the brain may (107). Patients with cardiac conduction disorders were derived from the clinical trial experience, not from an undernot studied in the controlled trials. Patients with other seizure types or epilepsy prevent exacerbation of this condition (126). The watchdog timer is an internal monitor that limits the number of pulses Hospitalization for implantation of the device is preceded by to be delivered without an “off” time to prevent excess evaluations by a neurologist and by a surgeon with experience stimulation. Fracture of the of bradycardia, asystole, or both mandate initial lead testing electrode, related to fatigue at the junction between contact in the operating room (24,133,134); the anesthesiologist and the lead wire, was a common problem with early devices should be notified immediately before this test. Substitution of a quadrifilar wire and, later, a following intraoperative bradycardia has been shown to be trifilar lead body coil improved electrode tolerance that had safe, with no change in cardiac rhythm upon initiation of postbeen compromised by repetitive neck motion. Correct placement of the lead electrodes around Model 302 but has a lead body designed with three high the vagus nerve is critical. Two methods have been developed fatigue silicone tubes; the bifurcation is still caudal to the to help confirm correct placement of the electrodes intraopanchor tether, but designed with a smoother transition to eratively (136), depending on the type of anesthesia used for facilitate a smooth strain relief bend. For patients receiving general anesthesia, the structed with a trifilar lead body coil and a continuous bilularynx and vocal cords can be monitored by fiberoptic men lead body silicone tube with the bifurcation cephalad to endoscopy for contraction of the left lateral larynx wall and the anchor tether; this design makes the handling characterisvocal cord tightening. For patients being implanted under tics of the Perennia lead feel stiffer during the implantation local and regional anesthesia, stimulation intensities can be procedure compared with the Model 302 and 304 leads. Incisional infections are unusual and generally respond to Prophylactic antibiotics may be administered both in the antibiotic therapy. The patient can be diswith or without infection occurs in 1% to 2% of implantacharged after the procedure, which usually lasts for less than tions and resolves with aspiration and antibiotics; the rare 1 hour, or can be observed overnight. Discharge education cases of refractory infection require removal of the generashould include care of the incisions and use of the magnet. However, one case of deep wound infection associated clinical studies, the generator’s output current was kept at with implantation of the generator was reported to be man0 mA for the first 2 weeks; however, programmed stimulaaged successfully with open wound treatment without tion is now being initiated at 0. Unilateral vocal cord paralthe first 3 months of stimulation unless an early response is ysis, which accompanies approximately 1% of implants, noted. The subsequent stimulation schedule is ulator is actually delivering a pulse (Table 70. At each visit, the generaence hoarseness or a change in vocal quality and tingling over tor and the battery are assessed for end of service; the battery’s the left cervical region on delivery of the electrical pulse. Inhalation of ipratropium bromide or lowering of the stimulus systemic adverse effects or cognitive side effects (160,161); frequency or current is recommended. No substantial effects in some patients, memory, alertness, mood, and communication on cardiac function were reported during clinical studies (24,26, have been shown to improve (100,162–166). An analysis of total mortality and sudden death QoL independent of treatment effect on seizure frequency, as in epileptic patients (to August 1996) revealed the expected well as increased daytime vigilance, have also been reported rate in individuals with severe, intractable epilepsy (149,150). The severe dysseizure or improve the postictal phase empowers the patient phoric or psychotic conditions emerged once seizure frequency and provides a sense of control over epilepsy. Children between $15,000 and $25,000) can be prohibitive without with a history of dysphagia may experience swallowing difficoverage by a third-party payer. These cost benefits are sustained over time and are sufficient to cover or exceed the cost of the device. Diagnosing refractory epilepsy: response to work because of health-related concerns (P 0. Predictors of pharmacoresistant which further reflect positive changes in the QoL of both epilepsy. Antiepileptic drug therapy in the United States: a review of formed among patients both with and without the device clinical studies and unmet needs. Unexpected places: how did vagus nerve stimulation become a treatment for epilepsyfi Prevention of intractable partial seizures by intermittent vagal stimulation in humans: preliminary results. Vagus nerve stimulation dramatically improve the overall treatment of all patients with therapy for partial-onset seizures: a randomized active-control trial. A randomized controlled trial of chronic vagus nerve stimulation for treatseizure types. Earlier use of adjunctive vagus nerve stimulation therapy for refractory epilepsy.


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