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However, 2 weeks later, she reported transient visual obscuration on standing and hissing sound in the right ear. Her visual acuity had decreased to 20/30 in the left eye and funduscopic examination revealed a progression of the papilledema and newly developed macular star in both eyes. Goldmann perimetry also documented further aggravation of the enlarged blind spot. Furthermore, the visual acuity had decreased in the left eye with newly developed macular star in both eyes. Three days later, her visual acuity deteriorated further to 20/30 in the right eye. After the operation, she reported mild headache on standing for several days, probably due to low-pressure syndrome, but the tinnitus, visual obscuration, and diplopia disappeared over the following several days. Follow-up funduscopy 10 days after the operation showed a marked improvement of the papilledema (figure 3A). The enlarged blind spots on Goldmann perimetry also resolved (figure 3B) along with improvement of the bilateral abduction limitation. Transient visual obscurations usually last less than a minute, and are often precipitated on standing from a stooped posture. Follow-up of 57 patients from five to 41 years and a profile of 14 patients with permanent severe visual loss. At the age of 6 years and 10 months, he was admitted to a local hospital because of vomiting and nonfebrile unilateral headache. Blood tests (complete blood count, C-reactive protein, electrolytes, blood urea nitrogen, creatinine, glucose, serum bicarbonate and pH, anion gap, transaminase, and urine culture) were within normal limits. Based on these results and on clinical observation, common medical and surgical causes (viral illness, gastroenteritis, diabetes, intestinal obstruction) were ruled out. A presumptive diagnosis of migraine with aura was made after 2 months by a pediatric neurologist because of several episodes of unilateral pulsatile headache and vomiting (one to two episodes per week). Pallor, poorly defined abnormal ocular movements, and transitory unresponsiveness were also reported by his parents. Five months later, the patient was brought to the Emergency Department of our hospital because of recurrent and long-lasting episodes of headache beginning the same day. He had four episodes of nausea, vomiting, pallor, and unilateral (right-sided or left-sided) pulsatile headache, each one lasting from 5 to more than 30 minutes. The prescribed treatment was ineffective, and the child was considered to be in a migraine aura status by his pediatrician. A critical episode was observed during clinical examination: the child reported a sudden feeling of sickness and a severe unilateral pulsatile headache, followed by nausea. Left eyelid myoclonus followed, and the child described a short-lasting sensation of blindness. Then his head turned toward the right and he became unresponsive for about 20 seconds. Other rare etiologies to consider are vascular syndromes (Klippel-Trenaunay-Weber, arteriovenous malformations of the brain), familial dysautonomia. This child showed prolonged and severe autonomic symptoms (nausea, vomiting, pallor, bradycardia) that are mainly due to acute cerebral insults, but can also be diagnosed as status migrainosus or autonomic status epilepticus. In his personal history, we can identify shorter but similar episodes, suggesting that the two latter hypotheses are most likely correct. Migraine and epilepsy are highly comorbid conditions that may share the same pathophysiology, but the nature of their association is unclear. In our patient, autonomic symptoms could be related to a basilar-type migraine rather than to an aura. Differential diagnosis between seizure and migraine could be complicated by the presence of headache in both. A clinical diagnosis of autonomic status epilepticus was made, and a rectal dose of 0. Crises are focal, initially characterized by a complaint from the child of not feeling well, followed by autonomic signs or symptoms frequently characterized by emetic symptoms (nausea, retching, vomiting), paleness (or, less often, cyanosis or facial blushing), mydriasis (or, less often, miosis), coughing, hypersalivation, urinary and fecal incontinence, and cardiorespiratory and thermoregulatory alterations. During seizure evolution, the child can become flaccid and unresponsive in 20% of cases (ictal syncope), with tonic eye and head deviation. Speech arrest, visual hallucinations, oropharyngolaryngeal movements, and behavioral disturbances occur less frequently. Usually, autonomic manifestations are generated by activation or inhibition of parts of the central autonomic network that involves the insular cortex, medial prefrontal cortex, amygdala, hypothalamus, and ventrolateral medulla. Therefore, ictal discharges may easily activate the lower threshold autonomic centers. The child had a complete recovery and was kept under medical supervision for 1 day. The epileptiform activity is characterized by spikes or spike-wave complexes of great amplitude, with multifocal localization predominating in the posterior regions. Children have normal physical and neuropsychological development and the risk of epilepsy in adult life appears no higher than in the general population. There is no evidence of the superiority of any antiepileptic drug, and carbamazepine and valproic acid are both widely used. Because of autonomic status epilepticus and bradycardia in our patient, valproic acid therapy was started and symptoms resolved completely. Most general practitioners and pediatricians are not familiar with the notion that prominent autonomic symptoms and signs may occur as epileptic seizure manifestations of occipital origin. As a consequence, this diagnosis can be easily missed and have potentially lifethreatening sequelae. Ictal bradycardia is seen primarily in association with focal seizures, particularly involving the temporal and limbic lobes. In our case, an intrarectal dose of diazepam was rapidly effective in normalizing heart rate, possibly preventing a cardiorespiratory arrest, with all its consequences. Our case illustrates the efficacy of an intrarectal dose of diazepam in case of ictal bradycardia, possibly preventing a cardiorespiratory arrest. Although more studies are needed on the subject, supportive family management should also include specific education about autonomic status epilepticus symptoms. Autonomic seizures and autonomic status epilepticus peculiar to childhood: diagnosis and management. Panayiotopoulos syndrome: epidemiological and clinical characteristics and outcome. Benign childhood focal epilepsies: assessment of established and newly recognized syndromes. Panayiotopoulos syndrome: a benign childhood autonomic epilepsy frequently imitating encephalitis, syncope, migraine, sleep disorder, or gastroenteritis. Neurology 72 April 14, 2009 207 e71 Management dilemmas Despite the ever-increasing number of randomized controlled trials for treatment of neurologic diseases, individual patients present unique clinical dilemmas, and it can be challenging to determine how best to apply the findings from large studies in individual cases. In the field of vascular neurology, for example, clinical trial data are perhaps more extensive than in any other neurologic subspecialty, yet significant controversy persists over how to interpret these data. In the cases in this section, the authors describe the management of patients with cerebrovascular disease, exploring both how existing data can be used to guide complex clinical reasoning and the limitations of existing data when applied to individual patients. In the emergency room, it was noted that visual blurring resolved with right eye closure, but his ophthalmologic examination was otherwise normal. He reported no headache, neck pain, prior trauma, prior transient neurologic deficit, or palpitations. There was no history to suggest seizure, and the monocular visual deficit and lack of headache would be atypical (albeit not impossible) for complex migraine. Extraocular muscle weakness causing ocular misalignment can cause the phenomenon of blurred vision resolving with closure of one eye, but no extraocular muscle weakness was detected on examination. Abrupt onset of unilateral blurred vision with contralateral face and arm weakness suggests simultaneous retinal and ipsilateral frontal hemispheric ischemia. Potential etiologies include embolism or hypoperfusion due to pathology of the internal carotid artery, aortic arch, or heart.

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The decision between a tricyclic antidepressant and an anticonvulsant should be made according to the typical side-effect profile. Tramadol, a weak opioid analgesics, which due to its specific mode of action is not regarded as an opioid in many countries, and is therefore unrestricted, will be sufficient for most patients. If the above therapeutic strategies fail, it might be worthwhile to send the patient to a referral hospital that has dedicated pain therapists. The therapy of choice in such incidences is regional anesthesia using epidural catheters. This technique is usually applied for major surgery or certain surgical Management of Postherpetic Neuralgia procedures, when no general anesthesia is possible or necessary. Therefore, such an invasive treatment would only be justified with refractory excruciating pain, in order to control pain for a limited time period until the spontaneous reduction of pain occurs. Lidocaine patches are small, bandage-like patches that contain the topical pain-relieving medication, lidocaine. If this is not possible due to side effects, the tricyclic antidepressant or the anticonvulsant should be combined with a weak opioid. Apart from targeting the peripheral nerves, the epidural or intrathecal space may be used to apply analgesics. Unfortunately, this catheter technique is not able to reduce pain in the long term. With this treatment, the patient may have short-term or even long-term pain reduction. All these techniques are outside the scope of this manual because they are highly sophisticated, very expensive, and require lengthy experience in pain management. This treatment is effective for prolonged periods Maged El-Ansary of time but is not permanent. With careful use of the technique, the complication rate for this patient group can be acceptable. In the emergency room, he was conscious but not able to move his legs or left arm. He was complaining of severe burning pain in his right hand and deep aching pain in both of his upper extremities. There was severe hyperesthesia, hyperalgesia, and dynamic allodynia as well as impaired cold sensation in the 4th and 5th fingers and on the ulnar side of his right hand. Within 4 years, the neuropathic pain started gradually to resolve, and gabapentin was successfully tapered off. Case report 2 Shabana, an Afghan housewife from Jalalabad in her late thirties, came to a psychiatric outpatient clinic escorted by her husband. History taking revealed that she had had a sudden attack of vertigo, slurred speech, and motor weakness in her left extremities 3 years earlier. Most of her symptoms had subsided within 2 days, but the motor weakness had persisted for weeks. Neurological examination revealed slight clumsiness and ataxia in her left arm, but muscle strength was regarded as normal. A conspicuous decrease in cold and pain sensibility was noticed on her right cheek, and in the lower two-thirds of her left arm as compared to the contralateral side. Based on the history and clinical findings, a tentative diagnosis of central neuropathic pain due to a low brainstem infarct was made. It has been estimated that the annual incidence of spinal cord injury in different countries throughout the world varies from 15 to 40 cases per million. Although central neuropathic pain is relatively uncommon, its impact should not be underestimated, because it is difficult to treat and causes disability and suffering to those affected. A common feature of central neuropathic pain is altered function of the spinothalamic tract, which mediates temperature and pain sensations. Patients usually experience constant spontaneous pain, but they can also have pain paroxysms (brief attacks of pain), evoked pain (pain caused by a stimulus), and allodynia (innocuous stimuli are sensed as painful). A lesion in the brainstem causes abnormal cranial nerve findings on the ipsilateral side, whereas abnormal findings in the limbs and trunk are due to a contralateral lesion. Below-level pain is typically constant, severe, and difficult to treat and represents central deafferentation-type neuropathic pain. Examples of common visceral nociceptive pains in these patients are pain caused by bowel impaction or distension of the bladder. These symptoms are important to recognize in management of the patient with spinal cord injury. In advanced countries, road traffic accidents rank highest among the etiological factors for traumatic spinal cord injury. According to an epidemiological study conducted in Haryana, India, the predominant cause of injury was falling from a height (45%), followed by motor vehicle accidents (35%). In people with asymptomatic cervical spinal stenosis, a fall or a sudden deceleration force can cause a contusion in the cervical cord, even without any bone or joint trauma. Syringomyelia is a cystic cavitation of the central spinal cord, most commonly in the cervical region. Neurosurgical treatment is considered only in cases with recent and quick progression. In some patients, phantom limb pain is maintained by stump pain (a peripheral pain at the site of amputation). In mirror therapy, patients are instructed to use the mirror in such a way that the reflected image of the intact limb seems to appear in the place of the amputated or affected extremity. It most often affects the shoulder and is related to changed dynamics due to motor weakness on the affected side. The prevalence of central pain in patients with traumatic brain injury is not known. A curious feature is the manifestation of pain in body regions that are not associated with local or spinal injury. It was previously called thalamic pain according to the typical location of the lesion, but it can also be due to cortical (parietal cortex), subcortical, internal capsule (posterior limb), or brainstem lesion. The most common pain quality is Central Neuropathic Pain 193 hematomas usually present with headache and progressive neurological symptoms, but central neuropathic pain is an uncommon symptom in these cases. The cornerstones of the diagnosis are a detailed history of development of symptoms and relieving and aggravating factors, and a careful neurological examination including sensory testing to touch, pinprick, cold, warmth, and vibration. Careful clinical examination is usually sufficient for this process, such as diagnosing musculoskeletal pain or pain due to local infection. Diagnostic studies, such as neuroimaging and cerebrospinal fluid analysis, may provide useful information in reaching an accurate diagnosis, but they may not be available. Spinal and cerebral abscesses, spinal traumas with partial cord lesion, and spinal tumors are examples of conditions with radically improved prognosis with active surgical treatment. History of trauma before the onset of weakness of the limbs and sensory changes, including central pain, is suggestive of partial cord lesion. If there is an unstable lesion of the vertebral column, quick stabilizing surgery may prevent complete paralysis, and the same is true with laminectomies in spinal contusion with partial paresis. The first line of therapy, after a thorough assessment, is information and education, for both the patient and the family. Difficulties in urination, constipation, dry mouth, and dizziness are typical side effects, which may prevent further dose escalation. If side effects (dizziness, headache, ataxia, or nystagmus) appear, the dose should be reduced. Pregabalin has been shown effective for spinal cord injury pain, but it is not available in every country. It is still not known whether treatment of the pain has any modifying effect on the duration of central neuropathic pain. She has a history of a single episode of bronchopneumonia, for which she was hospitalized and received intravenous antibiotics at the age of 2 months. On examination she is 79% of her expected weight for her age, with generalized lymphadenopathy, severe oral candidiasis extending into her pharynx, and a 3-cm hepatomegaly. The history and examination should attempt to delineate the area where pain is occurring.

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The uncus, which represents the bulging medial surface of the amygdala within the medial temporal lobe, usually sits over the tentorial opening, and its medial surface may even be grooved by the tentorium. Excess mass in one compartment can lead to herniation of the cingulate gyrus under the falx. Note the vulnerability of the oculomotor nerve to both herniation of the medial temporal lobe and aneurysm of the posterior communicating artery. The basilar artery is tethered at the top to the posterior cerebral arteries, and at its lower end to the vertebral arteries. As a result, either upward or downward herniation of the brainstem puts at stretch the paramedian feeding vessels that leave the basilar at a right angle and supply the paramedian midbrain and pons. The posterior cerebral arteries can be compressed by the medial temporal lobes when they herniate through the tentorial notch. Compression of the oculomotor nerve by either of these structures results in early injury to the pupillodilator fibers that run along its dorsal surface37; hence, a unilateral dilated pupil frequently heralds a neurologic catastrophe. The other ocular motor nerves are generally not involved in early transtentorial herniation. The trochlear nerves emerge from the dorsal surface of the midbrain just caudal to the inferior colliculi. These slender fiber bundles wrap around the lateral surface of the midbrain and follow the third nerve through the petroclinoid ligament into the cavernous sinus. Because the free edge of the tentorium sits over the posterior edge of the inferior colliculi, severe trauma that displaces the brainstem back into the unyielding edge of the tentorium may result in hemorrhage into the superior cerebellar peduncles and the surrounding parabrachial nuclei. Usually, a small portion of the cerebellar tonsils protrudes into the aperture (and may even be grooved by the posterior lip of the foramen magnum). However, when the cerebellar tonsils are compressed against the foramen magnum during tonsillar herniation, compression of the tissue may compromise its blood supply, causing tissue infarction and further swelling. Patterns of Brain Shifts That Contribute to Coma There are seven major patterns of brain shift: falcine herniation, lateral displacement of the diencephalon, uncal herniation, central transtentorial herniation, rostrocaudal brainstem deterioration, tonsillar herniation, and upward brainstem herniation. The first five patterns are caused by supratentorial mass lesions, whereas tonsillar herniation and upward brainstem herniation usually result from infratentorial mass lesions, as described below. The cingulate gyrus and the pericallosal and callosomarginal arteries are compressed against the falx and may be displaced under it. The compression of the pericallosal and callosomarginal arteries causes ischemia in the medial wall of the cerebral hemisphere that swells and further increases the compression. Eventually, the ischemia may advance to frank infarction, which increases the cerebral mass effect further. Note that the course of the oculomotor nerve takes it along the medial aspect of the temporal lobe where uncal herniation can compress its dorsal surface. However, the abducens nerves are rarely damaged by supratentorial or infratentorial mass lesions unless they invade the cavernous sinus or displace the entire brainstem downward. The foramen magnum, at the lower end of the posterior fossa, is the only means by which brain tissue may exit from the skull. Hence, just as progressive enlargement of a supratentorial mass lesion inevitably results in herniation through the tentorial opening, continued downward displacement either from an expanding supratentorial or infratentorial mass lesion ultimately causes herniation of the cerebellum and the brainstem through the foramen magnum. The key sign associated with uncal herniation is an ipsilateral fixed and dilated pupil due to compression of the dorsal surface of the oculomotor nerve. There is usually also evidence of some impairment of ocular motility by this stage, but it may be less apparent to the examiner as the patient may not be sufficiently awake either to complain about it or to follow commands on examination (i. However, examining oculocephalic responses by rotating the head usually will disclose eye movement problems associated with third nerve compression. A second key feature of uncal herniation that is sufficient to cause pupillary dilation is impaired level of consciousness. This may be due to the distortion of the ascending arousal systems as they pass through the midbrain, distortion of the adjacent diencephalon, or perhaps stretching of blood vessels perfusing the midbrain, thus causing parenchymal ischemia. Nevertheless, the impairment of arousal is so prominent a sign that in a patient with a unilateral fixed and dilated pupil and normal level of consciousness, the examiner must look for another cause of pupillodilation. Pupillary dilation from uncal herniation with a preserved level of consciousness is rare enough to be the subject of case reports. Hence, the side of paresis is not helpful in localizing the lesion, but the side of the enlarged pupil accurately identifies the side of the herniation over 90% of the time. The headaches became more severe, and toward the end of the eighth month she sought medical assistance. Her physicians planned to admit her to hospital, perform an elective cesarean section, and then operate on the tumor. During the night she complained of a more severe headache and rapidly became lethargic and then stuporous. Examination revealed complete loss of vision including ability to appreciate light but with retained pupillary light reflexes. Over the following week she gradually regained some central vision, after which it became clear that she had severe prosopagnosia (difficulty recognizing faces). Central transtentorial herniation is due to pressure from an expanding mass lesion on the diencephalon. If the mass effect is medially located, the displacement may be primarily downward, in turn pressing downward on the midbrain, although the mass may also have a substantial lateral component shifting the diencephalon in the lateral direction. Hemorrhage into a large frontal lobe tumor caused transtentorial herniation, compressing both posterior cerebral arteries. The patient underwent emergency craniotomy to remove the tumor, but when she recovered from surgery she was cortically blind. Hence, even small degrees of displacement may stretch and compress important feeding vessels and reduce blood flow. In addition to accounting for the pathogenesis of coma (due to impairment of the ascending arousal system at the diencephalic level), the ischemia causes local swelling and eventually infarction, which causes further edema, thus contributing to gradually progressive displacement of the diencephalon. In severe cases, the pituitary stalk may even become partially avulsed, causing diabetes insipidus, and the diencephalon may buckle against the midbrain. The earliest and most subtle signs of impending central herniation tend to begin with compression of the diencephalon. Less commonly, the midbrain may be forced downward through the tentorial opening by a mass lesion impinging upon it from the dorsal surface. Rostrocaudal deterioration of the brainstem may occur when the distortion of the brainstem compromises its vascular supply. Paramedian ischemia may contribute to loss of consciousness, and postmortem injection of the basilar artery demonstrates that the paramedian arteries are at risk of necrosis and extravasation. However, in postmortem series, venous infarction is a rare contributor to brainstem injury. This may occur quite suddenly, as in cases of subarachnoid hemorrhage, when a large pressure wave drives the cerebellar tonsils against the foramen magnum, compressing the caudal medulla. The patient suddenly stops breathing, and blood pressure rapidly increases as the vascular reflex pathways in the lower brainstem attempt to perfuse the lower medulla against the intense local pressure. A similar syndrome is sometimes seen when lumbar puncture is performed on a patient whose intracranial mass lesion has exhausted the intracranial compliance. Upward brainstem herniation may also occur through the tentorial notch in the presence of a rapidly expanding posterior fossa lesion. The dorsal midbrain compression results in impairment of vertical eye movements as well as consciousness.

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Neglect can range in severity, can vary from testing session to testing session, and may be specific to a particular region of space. Neglect can occur for objects in contralesional space with respect to the viewer (egocentric), to a stimulus (allocentric), or to the environment [79]. Neglect may also be specific to a type of task (perceptual versus motor) or sensory modality (visual, tactile, auditory) and may be apparent on some tasks but not others within a given sensory modality [80]. A number of investigators have proposed theories to account for neglect in adult patients with brain injury. Neglect could result from excessive attention to one side of the world or failure to direct attention away from that side of the world. While the final result might appear the same, these are theoretically distinct possibilities and both have been suggested as the mechanism for neglect. Mesulam proposed that spatial attention relies upon a distributed network within each hemisphere, centered in the inferior parietal lobule but receiving polymodal sensory input from other parietal regions as well as information about motivational valence from cingulate cortex and basal forebrain, motor information from frontal eye fields, and general arousal modulation from the reticular activating formation. However, he suggested that the two hemispheres are not equally involved in spatial attention. Rather, the right hemisphere is more active in attentional tasks and may attend to all of extrapersonal space, while the left hemisphere only attends to right space [81]. Heilman also supported the right hemisphere as being dominant for attention, demonstrating that the right parietal lobe is active in attention to either hemifield, while the left parietal lobe only responds to stimuli in the contralateral hemifield [82]. In their views, this accounts for the greater persistence and severity of neglect following right hemisphere injury as compared to left hemisphere insults. Kinsbourne proposed asymmetric involvement of the hemispheres in attention, although he suggested that each hemisphere generates a vector of spatial attention directed contralaterally and inhibits the opposite hemisphere [83]. He accounted for the frequency of neglect after right hemisphere injury by claiming left hemisphere dominance for attention. Another way of conceptualizing neglect is a failure to disengage attention from one part of the visual world. Using this framework Posner and colleagues argued that three steps must occur, "disengaging from the current focus of attention, moving attention to the location of the target, and engaging the target," and that parietal lobe injury impairs the disengage function in the contralesional visual field [84]. Numerous studies have provided support for this account of neglect using a cuing paradigm [85]. A valid cue appears on the same side as the target and an invalid cue appears on the side opposite the target. Subjects are consistently slower to respond to targets preceded by an invalid cue than a valid cue, and this is interpreted as a measure of the difficulty in disengaging attention from the location to which it was initially cued. However, subjects with neglect are much slower to respond to targets when the invalid cue is presented in contralesional space than ipsilesional space (for example, in left hemifield when the lesion is in the right parietal lobe), suggesting that the asymmetric disengage deficit accounts for the behavior of neglect. It is important to note, however, that neglect can be subtle and can require close observation as well as formal testing to be identified. Qualitative assessment in the neuropsychological evaluation is often obtained through object copying tasks or drawing of symmetrical figures. Quantitative assessments of visual neglect include line bisection tests, in which the patient is asked to indicate the midpoint of a line, and cancellation tasks in which the patient is provided a page with numerous small targets and is asked to mark out a particular target stimulus. Assessment of sensory neglect begins with unilateral presentation of stimuli and asking the patient to state the presence and location of the stimulus. Failure to detect stimulation on one side may indicate neglect or may be due to a primary sensory disturbance. For auditory modalities, the examiner stands behind the patient and provides gentle auditory stimulation. If the patient detects unilateral stimulation accurately, the examiner should also assess for extinction, in which the patient fails to detect simultaneous stimulation on the side contralateral to his or her lesion but will report perception of the ipsilateral stimulus. Visuospatial neglect has been reported in children following neonatal or pediatric stroke, but few studies have characterized this phenomenon in detail [87, 88]. In an ongoing study of 65 children who experienced unilateral arterial ischemic stroke or parenchymal hemorrhage in the neonatal period or later in childhood, chronic visuospatial neglect was assessed using five tasks: line bisection. Almost half (30/65) of the children exhibited mild spatial neglect on at least one task, and the frequency of neglect did not differ significantly between children with right hemisphere injury as compared to left hemisphere injury or between children with neonatal brain injury as compared to children who experienced brain injury later in childhood. Line bisection and conjunction search were the most sensitive tasks for the detection of neglect but did not detect neglect in all subjects. Overall, this study demonstrates that mild chronic visuospatial neglect is common following stroke in children and suggests that the right hemispheric dominance for visuospatial attention seen in adults is not yet consolidated in children. Executive Functioning Executive functions refer to a collection of higherorder cognitive abilities that coordinate and regulate other mental activities. Examples of executive functions include deciding on a plan of action, sequencing steps toward a goal, regulating behaviors, selective inhibition of responding, response preparation, cognitive flexibility, set maintenance, and organizing time and space. Executive functions allow us to start and stop behaviors, monitor our performance, adapt to changing conditions, and develop new strategies as needed. These functions allow an individual to engage in purposeful, goal-directed, independent behavior [46]. Aspects of attention and working memory are related to executive functioning, and successful performance of these tasks is often dependent on these abilities. Executive dysfunction is quite common in patients who have sustained strokes and is considered to be a core neuropsychological deficit following cerebrovascular injury [51]. Although often described as "frontal functions," executive deficits can occur as a result of injury to non-frontal brain regions. In fact, executive dysfunction is common even in individuals whose strokes did not cause damage to the frontal lobes [51]. Behavioral manifestations of executive dysfunction can present as hypoactivity. Executive dysfunction can manifest cognitively as impaired response initiation and/or suppression, poor rule deduction, poor set maintenance and/or set shifting, difficulty with self-monitoring, and impaired concept formation, problem-solving, or planning abilities (see [51] for a review of these syndromes in stroke). Executive functioning deficits can severely impede progress in rehabilitation of stroke, if the patient cannot benefit from feedback or generalize rehabilitation strategies into their daily living. A recent study demonstrated that executive functioning deficits are prevalent in the early phases of stroke and are an excellent predictor of long-term impairment [90]. Therefore, assessment of these skills should be included in the early phases of stroke recovery. Assessment of executive functioning should be multifaceted and should include standardized assessment measures and qualitative observations on test-taking strategies. As Lezak notes, "A major obstacle to examining the executive functions is the paradoxical need to structure a situation in which patients can show 6 Cerebrovascular Disease 113. Presence of neglect was determined by comparison to normal distribution of performance by age-matched controls. Subject omitted more targets from the left hemifield than the right (c) and cancelled left-sided targets significantly later than right-sided targets (d). Subjects with neglect are depicted in black and subjects without neglect are shown in gray. Formal testing of executive dysfunction following stroke can vary depending on presenting symptomatology and concerns. If possible and necessary, evaluation should include formal assessment of attention, working memory, speed of processing, response time, impulse control, planning, organization, problem solving, mental flexibility, concept formation, cognitive set maintenance, and generativity. Higher-Order Visual Processing Skills Stroke can impact visual processing in a variety of ways, ranging from very subtle to gross impairment. Damage to the visual cortex or portions of the visual pathway beginning at the optic nerve can lead to visual field defects or, in severe cases, cortical blindness. Higher-level visual processing deficits can also occur in the absence of gross visual impairment. Research studies have found that between 34 and 75% of patients with stroke had impairment on higher-order visual tasks [90, 96], underscoring the need to evaluate these functions. Therefore, the neuropsychological assessment of stroke should include measurement of higher-order visual processing skills. Deficits in higher-order visual processing skills are often due to posterior right hemisphere lesions; however, damage to other regions can also have an impact. Deficits can occur in the identification and localization of objects within the visual field, defined by anatomically distinct visual systems often referred to as the "what" (i. Object recognition ("what") is mediated by occipitotemporal structures (ventral stream), while object location ("where") is mediated by occipito-parietal structures (dorsal stream) [97]. Arterial ischemic strokes affecting the posterior cerebral artery territory can lead to visuoperceptual deficits, while strokes affecting the posterior division of the middle cerebral artery territory may also result in visuospatial deficits.

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Erythrocytapheresis compared with whole blood phlebotomy for the treatment of hereditary haemochromatosis. Central nervous system manifestations include confusion, somnolence, dizziness, headache, coma, and parenchymal hemorrhage. Pulmonary complications include hypoxemia, diffuse alveolar hemorrhage, and respiratory failure. The pathogenesis is unclear, but may relate to cell rigidity, size, rheological properties, high metabolic activity causing local hypoxia, cytoadhesive interactions, and endothelial damage. Compared to lymphoid blasts, myeloid blasts are larger, less deformable, and their cytokine products are more prone to activate inflammation and endothelial cell adhesion molecule expression. Other studies have reported no benefit and raised concerns that leukocytapheresis might delay start of induction chemotherapy. Limitations to these studies include the retrospective, observational nature of the publications, and having moderate to high risk of confounding bias. Thus, leukocytapheresis may still have a therapeutic role in patients presenting with leukostasis. However, chemotherapy should not be postponed and is required to prevent rapid re-accumulation of circulating blasts. Platelet, cryoprecipitate and/or plasma transfusion, however, may be given if the patient has thrombocytopenia and/or coagulopathy prior to the procedure. In patients <10 kg, manual whole blood exchange may be performed instead of using the automated cell separators. Early complications of hyperleukocytosis and leukapheresis in childhood acute leukemias. Leukapheresis and cranial irradiation in patients with hyperleukocytic acute myeloid leukemia: no impact on early mortality and intracranial hemorrhage. The effect of therapeutic leukapheresis on early complications and outcomes in patients with acute leukemia and hyperleukocytosis: a propensity score-matched study. Apheresis principles in a patient with chronic myeloid leukemia during pregnancy: challenges in cell separation and assessing transcript levels. Leukapheresis reduces 4-week mortality in acute myeloid leukemia patients with hyperleukocytosis - a retrospective study from a tertiary center. Leukapheresis and low-dose chemotherapy do not reduce early mortality in acute myeloid leukemia hyperleukocytosis: a systematic review and meta-analysis. How we approach a patient with symptoms of leukostasis requiring emergent leukocytapheresis. Management of chronic myeloid leukemia in the setting of pregnancy: when is leukocytapheresis appropriate? Endothelial cell activation by myeloblasts: molecular mechanisms of leukostasis and leukemic cell dissemination. Hyperleucocytosis in paediatric acute myeloid leukaemia - the challenge of white blood cell counts above 200 x 109/l. Extracorporeal elimination of large lipoproteins is hypothesized to stop further organ damage. However, these systems are optimized for the elimination of small to mid-sized apoB100-positive lipoproteins and efficacy can be reduced with chylomicronemia. For patients treated prophylactically, chronic therapy for years has been reported. A systematic review of the epidemiology, pathophysiology and current management of hyperlipidemic pancreatitis. Systematic review of hypertriglyceridemia-induced acute pancreatitis: a more virulent etiology. The role of apheresis in hypertriglyceridemia-induced acute pancreatitis: a systematic review. Plasmapheresis for Preventing Complication of Hypertriglyceridemia: A Case Report and Review of Literature. Therapeutic plasma exchange for hypertriglyceridemia induced pancreatitis: a rapid and practical approach. Clincal features and treatment of hypertriglyceridemia-induced acute pancreatitis during pregnancy: a retrospective study. Therapeutic plasma exchange in patients with chylomicronemia syndrome complicated by acute pancreatitis. Plasma exchange treatment for acute hyperlipidemic pancreatitis with falsely low levels of serum triglycerides - a case report. Plasmapheresis therapy has no triglyceride-lowering effect in patients with hypertriglyceridemic pancreatitis. Diabetic ketoacidosis-induced hypertriglyceridemic acute pancreatitis treated with plasmapheresis-recipe for biochemical disaster management. Therapeutic plasma exchange in patients with severe hypertriglyceridemia: a multicenter study. Relationship between plasma triglyceride level and severity of hypertriglyceridemic pancreatitis. Role of therapeutic plasma exchange in the treatment of severe hypertriglyceridemia: an experience. As blood viscosity rises, a nonlinear increase in shear stress in small blood vessels, particularly at low initial shear rates, produces damage to fragile venular endothelium such as that of the eye and other mucosal surfaces. Other manifestations include congestive heart failure (related to plasma volume overexpansion), respiratory compromise, coagulation abnormalities, anemia, fatigue, peripheral polyneuropathy, and anorexia. Early diagnosis, which can usually be made from the funduscopic exam, is crucial to prevent further progression. Patients with constitutional symptoms, hematological compromise, and bulky disease should be considered for chemotherapy +/- immunotherapy. A combination of bendamustine and rituximab has been recommended as first line therapy for bulky disease, while dexamethasone-rituximab-cyclophosphamide has been suggested as an alternative, especially in the setting of non-bulky disease. Other regimens include proteasome inhibitors (bortezomib and carfilzomib), nucleoside analogs (fludarabine and cladribine), and ibrutinib. IgM is 80% intravascular and serum viscosity rises steeply with increasing IgM levels. Thus, a relatively small reduction in IgM concentration has a significant effect on lowering serum viscosity. A transient increase in IgM level after rituximab therapy (flares), has been reported in 30-70% of patients within 4 weeks of treatment initiation. Cascade filtration and membrane filtration techniques have been described and may have similar efficacy in removing M-protein. The reduction in IgM may be less than the theoretical reduction of an ideal solute (Miyamoto, 2018). When patients are maintained at a level under their symptomatic threshold, clinical manifestations of the syndrome usually are prevented. Prediction of immunoglobulin M reduction via simple dose of therapeutic plasma exchange and double filtration plasmapheresis using membrane separation in patients with hyperviscosity syndrome caused by Waldenstrom macroglobulinemia. Roughly >10% of patients can present as rapidly progressive crescentic glomerulonephritis. When there are symptoms, the classic presentation for the disease is gross hematuria occurring shortly after an upper respiratory infection (synpharyngitic) or, when asymptomatic, discovery of microscopic hematuria with or without proteinuria. Factors associated with disease progression are hypertension, persistent proteinuria >1000 mg/day, and elevations in serum creatinine. Numerous authors have found that improvement only occurred in the presence of cellular crescents, and not in sclerotic, scarred glomeruli. The pathogenesis of IgA nephropathy: What is new and how does it change therapeutic approaches? Coexistence of atypical hemolytic uremic syndrome and crescentic IgA nephropathy treated with eculizumab: a case report.

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Morgan, and Priscilla Powell Type 1 Diabetes Overview of Type 1 Diabetes Type 1 diabetes (T1D) or insulin-dependent diabetes is an endocrine disorder of insulin deficiency secondary to pancreatic -cell destruction. Exogenous insulin replacement is imperfect and results in variable blood glucose levels with risk of glucose excess or hyperglycemia, and glucose insufficiency or hypoglycemia. An intensive regimen of self-care behaviors helps minimize blood glucose fluctuations through frequent blood glucose monitoring, insulin replacement via subcutaneous injections, or insulin pump therapy, along with diet and exercise requirements. Near-normal metabolic control, as measured by the glycosylated hemoglobin (HbA1c) assay, can significantly reduce micro- and macrovascular damage and other disease complications thought secondary to fluctuations in blood glucose concentrations. During the past 25 years, studies of cognitive dysfunction and cerebral anatomical status have increased dramatically. Interestingly, despite the statistical sensitivity afforded by over 600 patients, cognitive domains of learning and memory, motor speed, divided and selected attention, and language were unaffected. Slowed psychomotor efficiency and diminished mental flexibility may be core features that underlie broader cognitive dysfunction. When cognitive dysfunction is found, impairments are greater with accompanying microvascular and macrovascular complications, an indication that 415 C. Hypoglycemic Effects on Adult T1D Cognition the landmark Diabetes Control and Complications Trial [3] demonstrated that near-normal metabolic control significantly reduces the progression of microvascular retinopathy and other disease complications. However, intensive treatment also relates to a threefold increase in transient severe hypoglycemia that can result in seizures or coma. Milder hypoglycemia is more common; approximately half of T1D individuals may experience mild hypoglycemia below 70 mg/dL up to 10% of the time [12]. Acute hypoglycemia can be particularly dangerous since patients may be unaware of their diminished cognitive capacity. Neuroglycopenic effects, including slowed P300 markers of diminished attention, often precede adrenergic counterregulation, i. Insufficient glucose disrupts normal neuronal functioning and initially is related to reduced cerebral blood flow, particularly to the frontal cortex [19, 20] followed by two to four times greater cerebral hyperperfusion as a compensatory mechanism. Despite rebound hyperperfusion, glucose availability increases by only 3% in children [21]. Animal studies reveal severe hypoglycemia, characterized by an absence of all neuroelectric activity for several minutes, is necessary to produce neuronal death. Although neuronal necrosis is unlikely to result from most hypoglycemic episodes, cerebral potentiation or sensitization effects may occur in response to significant alterations in cerebral blood flow. Transient cerebral hypoperfusion may become persistent if counterregulatory mechanisms become impaired. Recurrent episodes of hypoglycemia are associated with persistent cerebral hypoperfusion to the frontal cortex and basal ganglia in youth [22], regardless of blood glucose level at the time of assessment, age, or chronic hyperglycemia, as indexed by glycosylated hemoglobin. Congruently, detection of hypoglycemic effects may be secondary to the type and sensitivity of the neuroimaging technique or alternatively to the proportion of vulnerable populations included in any individual study, such as youth with earlier disease onset who may be uniquely vulnerable to hypoglycemic insult. Recurrent hypoglycemia appears associated with reduced gray matter density, thought to presage later cognitive difficulties, in brain regions associated with language and limbic memory structures and in the cerebellum associated with executive skills of attention and planning [25]. This pattern is consistent with transient hypoglycemic effects of slowed information processing and executive functioning [6, 26]. Better description of the isolated effects of severe hypoglycemia will be possible with consideration of these study design issues, particularly subject sampling. Recurrent hypoglycemic seizures or coma were unrelated to decline in any of eight cognitive domains studied. Meta-analysis also fails to document cognitive differences between groups of patients with and without recurrent severe hypoglycemia [6]. The damaging effects of hypoglycemia appear limited to their immediate acute cognitive effects with no discernible lasting performance complications in most individuals, despite much speculation and concern in the earlier neurocognitive literature. However, debate still exists as to possible enduring hypoglycemic effects in youth with disease onset before the age of 7. An early study found acute hyperglycemia at 300 mg/dL caused reduced speed of information processing [27] along with a trend toward reduced verbal fluency, an executive functioning skill [28]. These effects were transient, subtle and not as pronounced in magnitude as those that occurred during mild hypoglycemia. Subjects were generally unaware of hyperglycemic impairments, similar to the effects of mild hypoglycemia. Interestingly, an optimal glucose range for cognitive functioning was found between 70 and 180 mg/dL; cognitive deterioration of up to 30% begins at either end of the glucose continuum, with a steeper decline during hypo- than hyperglycemia. Undetermined was the level of hyperglycemia necessary to produce impairments comparable in magnitude to those of hypoglycemia [29, 30]. Deterioration of up to 9% of baseline levels occurs and chronic hyperglycemia is the sole predictor of slower functioning. Neither recurrent severe hypoglycemia nor treatment regimen related to performance. The possibility is raised that better metabolic control might reduce mild cognitive decline much as it forestalls micro- and macrovascular complications. Beyond glycohemoglobin indices of chronic hyperglycemia, others have found the presence of retinopathic and neuropathic complications, a proxy marker of chronic hyperglycemia, relates to increasingly slower psychomotor efficiency over time [6, 31, 32]. Chronic hyperglycemia appears to exert a lasting detrimental cognitive effect, whether indexed by glycohemoglobin assay or microvascular disease complications. Like hypoglycemia, acute hyperglycemia appears associated with disruption of cerebral vascular status. Animal models show initial hypoperfusion of approximately 25% after glucose injection is followed by an increase in cerebral blood flow that is two to four times greater than baseline, thought secondary to increased plasma osmolality [31]. Reduced white matter volume in T1D also relates to slowed attention and executive functioning [33]. Differences in gray matter density, measured by voxel-based morphometry, also are associated with advanced diabetic retinopathy [32]. Trends of reduced gray matter volume in the left middle frontal gyrus, right inferior frontal gyrus, right occipital lobe, and cerebellum are found in patients with proliferative retinopathy but not those without. Reductions in white and gray matter occur near "water-shed" areas of the medial cerebral artery and posterior cerebral artery, and suggest relative hypoperfusion as an instigating factor [35]. Patients with T1D experience generalized reduction in white and gray matter volume, and ultimately whole brain volume, with white matter differences more reliably detected and related to slowed psychomotor functioning, diminished attention, and speed of information processing. Cognitive Effects of Pediatric T1D Children and adolescents (<18 years) with type 1 diabetes also experience mild cognitive dysfunction. Similar studies of newly diagnosed adults have not been conducted to conclusively establish the length of disease duration necessary to detect psychomotor slowing. Older age predicted brain volume loss and change to the basal ganglia [23], consistent with an "accelerated aging" hypothesis of diabetes [40], even in youth. Despite the smaller magnitude of neurocognitive effects, the pervasiveness of cognitive difficulties [36, 38] along with glucose and attentional fluctuations that may occur in the classroom could nevertheless exert a significant impact on learning and achievement. Indeed, only 68% of young adults at follow-up completed compulsory 12-year education versus 85% of controls [23]. Nevertheless, youth with later disease onset still show small but broad neurocognitive sequelae that mirror the effects reported in overall pediatric samples, including spared memory and learning skills [36]. Compared to these transient effects of hyperglycemia, chronic hyperglycemic effects are less well documented in children. Poorer metabolic control is related to reduced visuospatial and math performance, disrupted attention, and memory and executive deficits [39]. Although reversible, effects may linger for up to 45 min after resumption of normoglycemia, an extended period of diminished capability that could impact complex skills required in a classroom, much like effects on adult driving skills [14].

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Hematopoietic growth factors and androgens are often used as adjunctive therapies. Corticosteroids (prednisone at 1 mg/kg) are used as first line therapy and are associated with significant response rates ($40%). No well-defined treatment schedules exist, however 1-24 treatments were reported in the literature. Warm autoantibodies consist of IgG hemolysins that react optimally at 378C and are directed primarily against the red cell Rh antigens. It usually arises in reaction to an infection (polyclonal autoantibodies) or to a lymphoproliferative disorder (monoclonal autoantibodies). The cold-reactive IgM autoantibody produced after Mycoplasma pneumonia infection usually has anti-I specificity, whereas the autoantibody associated with Epstein-Barr virus infection (infectious mononucleosis) frequently has anti-i specificity. The thermal amplitude is defined as the highest temperature at which the antibody reacts with its cognate antigen. A cold autoantibody with high thermal amplitude could, therefore, be active within a range of temperatures attainable in vivo. The thermal amplitude of a cold agglutinin may be more predictive of the severity of hemolysis than its titer. Prednisone suppresses antibody production and down-regulates Fc-receptor-mediated red cell destruction in the spleen. Various immunosuppressive/immunomodulatory agents have been used for patients with refractory hemolysis; rituximab has recently shown promise. If indicated by more severe hemolysis/anemia, treatment primarily involves avoiding exposure to cold. Prednisone is usually ineffective, as is splenectomy, because the liver is the dominant site of destruction of C3b-sensitized red cells. Apheresis treatment may buy time until immunosuppressive therapy takes effect or if other treatments have failed. Anecdotal evidence of favorable results has been described in some cases of IgG hemolysis. The rational seems clear but clinical data are limited to case reports that do not always show improvement. Technical notes If the thermal amplitude of an IgM cold autoantibody is such that agglutination occurs at room temperature, red cell agglutination may occur within the cell separator and tubing. In these situations, therapy may require a controlled, high temperature setting of 378C both in the room and within the extracorporeal circuit. Endemic areas are the coastal and inland regions of the northeast, as well as northern Midwest particularly Wisconsin and Minnesota. The disease is usually transmitted from an animal reservoir to humans by the bites of ixodid ticks, most commonly between May through October. Several cases of neonatal babesiosis acquired by transplacental transmission have been reported. The incubation period is usually 1-3 weeks, with longer incubation period (6-9 weeks) reported with transfusion transmission. Asymptomatic infection, as suggested by the disparity between seroprevalence and the number of reported cases. It is uncertain whether patients experiencing asymptomatic babesial infection are at risk for any complications. Mild-moderate illness, most common presentation, characterized by the gradual onset of malaise and fatigue followed by intermittent fever and one or more of the following: chills, sweat, anorexia, headaches, myalgia, arthralgia and cough. The illness usually lasts for several weeks to months, occasionally with prolonged recovery that can last more than a year. Excessive cytokine production is thought to be a major cause of severe babesiosis and is associated with tissue pathology that can lead to significant end-organ damage and can result in persistent relapsing disease or death. The detection of IgM is indicative of recent infection while IgG titer of 1:1024 or greater usually signify active or recent infection. Titers generally return to 1:64 or less within 8 to 12 months but may persist for years. Current management/treatment Primary therapy for mild to moderate disease includes antibiotic combination. Most people can be successfully treated with atovaquone and azithromycin administered for 7 to 10 days. Combination of quinine sulfate and clindamycin, the first drug combination used in this disease, is equally effective but associated with more adverse reactions. Thus, this combination should be used when patients do not respond well to atovaquone and azithromycin. In severe disease, the combination of quinine sulfate and clindamycin, given 7-10 days is the treatment of choice. In persistent relapsing disease, antibiotics should be given for a minimum of six weeks and for at least two weeks after the last positive blood smear. The specific level to which parasitemia must be reduced to elicit the maximum therapeutic effect is not defined. Increased capillary permeability and intravascular volume deficits predispose to cellular shock due to diminished perfusion of major organs. Disruption of the sodium-potassium membrane pump results in an intracellular sodium shift contributing to the progressive hypovolemia. Heat injury causes release of inflammatory mediators, including complement, kinins, and histamine, with subsequent vasodilation and capillary leakage. Myocardial depression with decreased contractility and inappropriate cardiac output may be associated with hemodynamic fragility. Acute Respiratory Distress Syndrome may complicate the clinical picture whether related to inhalational injury or excessive edema with increasing fluid resuscitation attempts. Affected patients have suppressed leukocyte chemotactic function and lymphocyte suppression, both of which contribute to susceptibility to life threatening infections, in addition to the loss of the important barrier of normal skin. Circulating mediators have been implicated in majority of these physiologic derangements although the exact mechanisms or humoral ``factor(s)' remain enigmatic. Decreased levels of fibronectin in severely burned patients have been correlated with impaired function of the reticuloendothelial system and phagocytosis. Microembolization of tissue debris, bacteria, and byproducts of disseminated intravascular coagulation are other potential contributors to the pathophysiology of burn shock. Current management/treatment the mainstay of treatment in the immediate post-burn period is aggressive intravenous fluid resuscitation. Patients with full-thickness burns, inhalation injury or delay in resuscitation may have greater fluid requirements. The most common solution is lactated Ringers; other solutions such as hypertonic saline, or colloids such as 5% albumin or hydroxyethyl starch, are also incorporated into different fluid resuscitation strategies. Replacement with donor plasma hypothetically could facilitate decrease in capillary permeability, and improve intravascular oncotic pressure, which might improve response to fluid resuscitation, urine output, and possibly immune function. Although the specific mediators of burn injury in the circulation are not precisely characterized, the literature implicates circulating component(s). For example, cross perfusion studies from burned to unburned dogs caused a decrease cardiac output in the unburned animals; in vitro studies from the sera of human burn patients demonstrate that specific immune cellular abnormalities can be reversed when the cell is removed from the burn environment, such as placement in plasma from a healthy individual. Of the limited published case series, a variety of favorable physiologic effects were reported with respect to fluid resuscitation, urine output, cardiac function and immune benefits. Thanks to potent immunosuppression, survival and quality of life have improved since then, although infection, malignancies, and allograft rejection continue to threaten long-term survival. Chronic rejection or allograft vasculopathy occurs months to years after transplant and its mechanism is poorly understood. It is characterized by progressive intimal thickening of the coronary arteries leading to late graft failure. Current management/treatment the approach to rejection prophylaxis in heart transplantation is based on three principles: a) the period with the highest risk for rejection is within the first 3-6 months posttransplant when immune reactivity is strongest; b) lower doses of several drugs or combinations of drug and apheresis is preferable to large doses of a single agent in order to minimize side-effects; and c) drug-induced profound immunosuppression carries serious side-effects such as infection and malignancy. Induction therapy with antilymphocyte antibodies is used by many transplant centers in the early postoperative period. Maintenance immunosuppression uses three classes of drugs: calcineurin-inhibitor (cyclosporine or tacrolimus), antiproliferative agent (mycophenolate mofetil or azathioprine) and corticosteroids. In addition to drug-specific side effects, cardiac allograft recipients have a high risk of developing infections, the major cause of death in the first post-transplant year.

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Additional reported changes have included decreased swelling, pain, and paresthesias. Additional reported changes have included resolution of skin lesions and decreased pruritis. Improvement of early symptoms in one patient reported to have occurred within 3 days of initiation of treatment. This fact sheet includes abstracts in the summary of published reports and considers them in determining the recommendation grade and category. Symptoms of myelitis include paraparesis and sensory loss below the lesion, sphincter loss, dyesthesia, and radicular pain; symptoms of optic neuritis include ocular pain, visual field deficits, and positive phenomena; and symptoms of hypothalamic and brainstem involvement, which occur in 15% of patients, include hiccoughs (hiccups), intractable nausea, and respiratory failure. Monophasic course is associated with younger age at disease onset and equal male:female predominance. The majority of incidents is accidental and occurs at home, most often involving children under the age of six. The physician can choose from a vast array of methods to enhance removal of the toxin, depending on specific characteristics of the agent and the route of exposure. Induced emesis, gastric lavage, and oral administration of activated charcoal may be used to minimize gastrointestinal absorption of ingested substances. Whole-bowel irrigation, another technique available for gastro-intestinal decontamination, is particularly useful for removing poorly absorbed agents that are not adsorbed to charcoal. Comprehensive lists of drugs and chemicals removed with dialysis and hemoperfusion have been compiled. The clinical benefit can be achieved only if toxin levels can be reduced to concentrations below the threshold for tissue damage. Reports of the successful use of apheresis in the treatment of various drug overdoses and poisonings are generally anecdotal. There are also case reports of the failure of plasma exchange to remove substances bound to proteins and lipids such as barbiturates, chlordecone, aluminum, tricyclic antidepressants, benzodiazipines, quinine, and phenytoin. Very early initiation of the treatment (less than 30 hours) resulted in the best outcomes. There are anecdotal reports on the use of immunadsorption to treat poisoning with toxins such as botulin toxin. There is increasing number of biological drugs such as monoclonal antibodies (pharmacokinetic half-life typically 10 to 30 days with potentially longer pharmacodynamic half-life) with rare but potentially serious side effects. Technical notes the replacement fluid chosen should be one that contains enough protein to draw toxin into the blood compartment for elimination; albumin is such an agent and generally acts as an effective replacement fluid. Some venoms also cause coagulopathy, in which case the use of plasma should be considered. Major syndromes are classified according to the affected central nervous system anatomy but an international workshop consensus statement called for a combination of immunohistochemistry and Western immunoblotting for proper diagnosis. Autoantibodies reactive against Purkinje cell cytoplasm react on Western blot analysis with 34-kDa and 62-kDa Purkinje cell proteins and are referred to as ``anti-Yo' antibodies. The onset of symptoms, including truncal and limb ataxia, dysarthria (which may be severe), and downbeating nystagmus may precede the diagnosis of cancer by months to years. A serum anti-Hu antibody and rapidly developing symptoms of encephalomyelitis will likely lead to a diagnosis of small cell lung cancer within several months. The onset is often abrupt in adults and may beaccompanied by nausea and vomiting, and then progress to truncal ataxia, generalized myoclonus, altered mental status, and sometimes to stupor and coma. Paraneoplastic Stiff-Person Syndrome, associated with antibodies to the 128 kDa synaptic vesicle-associated protein amphiphysin. It is associated with small cell lung cancer, cervix carcinoma and malignant melanoma. Most patients have serum autoantibodies to the retinal photoreceptor protein recoverin. A large number of additional antibodies associated with paraneoplastic syndromes of the central and peripheral nervous systems and the neuromuscular junction have been described and extensively reviewed. Neurological improvement or worsening may correlate with tumor response or relapse. Aggressive immunosuppression early in the course is recommended in patients who are identified prior to a tumor diagnosis or whose tumors do not yet require specific anti-cancer therapy. Description of the disease Polyneuropathy can present as acute, subacute, or chronic process with initial sensory symptoms of tingling, prickling, burning or bandlike dysesthesias in the balls of the feet or tips of the toes. Nerve fibers are affected according to axon length, without regard to root or nerve trunk distribution. The polyneuropathies are diverse in timing, severity, mix of sensory and motor features, and presence or absence of positive symptoms. The diagnosis can be established based on electrophysiological studies and the presence of monoclonal proteins. Corticosteroids alone tend to be more effective in IgG- and IgA- polyneuropathies with a response rate of 40 to 60%. Combination therapy with low dose cyclophosphamide and prednisone given monthly over 6 months improves clinical outcome irrespective of antibody specificity or class. Polyneuropathies with IgG monoclonal protein resistant to this treatment have been successfully treated with cyclosporine A and carmustine. However, this was not confirmed in a small randomized trial and when compared to interferon alpha. These new therapies are likely to change the therapeutic approach if the benefits are confirmed in larger trials. While some measures did not reach statistical significance, the observed differences were clinically significant. The heterogeneity of the IgG group, which included patients with more treatment refractory axonal neuropathy, may have adversely affected the observed results. The patient may continue to improve over weeks following cessation of plasma exchange. If the level of paraprotein is correlative to the polyneuropathy then it can be monitored to evaluate the frequency of treatment. However, the titer of the paraprotein may not correlate with the clinical disease state. Severe symptoms often last several weeks to months or longer and then gradually subside. The major clinical manifestations include chorea, hypotonia and emotional lability. Elevated levels of antineuronal antibodies and/or anti-basal ganglia antibodies have been reported in both. It is very important to differentiate the two since their treatment can be different. However, azithromycin prophylaxis should not routinely be recommended because of emerging resistant streptococci. Both genders are equally affected with the mean age of onset in the sixth and seventh decade of life. The patients present with skin lesions typically flaccid blisters which can be recurrent and relapsing. The blisters can be located on the entire body surface as well as on the mucous membranes of the mouth. A large surface of skin can be affected at any given point leading to situations akin to severe burn. Pathology of pemphigus vulgaris is characterized by the in vivo deposition of an autoantibody on the keratinocyte cell surface. This antibody, which is also present in the circulation, is typically directed against a 130-kDa protein (desmoglein 3). Histology reveals the presence of a suprabasilar intraepidermal split with acantholysis. Current management/treatment the treatment of pemphigus vulgaris, especially in its severe form, is challenging. Introduction of corticosteroids reduced the mortality rate from 70 to 100% to a mean of 30%. However, long-term administration of high doses of corticosteroids can be associated with severe adverse effects. They are often used in combination with other immunosuppressant agents such as azathioprine, methotrexate, and cyclophosphamide. In addition, some newer experimental technologies involve cholinergic receptor agonists, desmoglein 3 peptides and a p38 mitogen activated protein kinase inhibitor. All reported patients have received high-dose systemic corticosteroids and immunosuppressive agents which either produced life-threatening adverse effects or failed to control the disease.

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Each of the recommendations is submitted to a focused review of the scientific evidence. Final notes from the participants are considered, and a final document is elaborated. After this process is completed, the document is sent for publication in a peer-reviewed journal. Feedback can occur either as the service is being provided (concurrent feedback) or after that service has been provided (retrospective feedback). There are three basic stages of evaluation: (i) evaluation during the development of guidelines and before their full dissemination and implementation (inception evaluation); (ii) evaluation of health care programs within which guidelines play a central role (guidelines-program evaluation); and (iii) evaluation of the effects of guidelines within defined health care environments (scientific evaluation). Other studies show that physicians are generally positive about guidelines but that they do not integrate them into their practices to a large extent. Identified were: (i) awareness, (ii) familiarity, (iii) agreement, (iv) self-efficacy, (v) outcome expectancy, (vi) ability to overcome the inertia of previous practice, and (vii) absence of external barriers to perform recommendations. For example, Canadian family physicians show little resistance to guidelines and appear to need less threat of external control to incorporate them into their practice. Finally, potentially effective dissemination and education techniques developed in high-resource settings may also have to undergo some changes to be feasible in a specific low-resource setting. It may be inevitable to make certain evidence-based approaches to diagnosis and treatment optional. Grading methods take into account the study design, benefits and harms, and outcome. A guide to the Canadian Medical Association handbook on clinical practice guidelines. The same care and considerations must be taken into account, with a history and relevant clinical examination. The needle is inserted perpendicularly to the skin and advanced slightly under the artery. It is possible that anxiety and apprehension may appear within the period of acute pain, for example, the fear of surgery and anesthesia that could form part of the treatment. Practical consequences As part of preparation for surgery, interventions such as relaxation techniques, a good explanation of the procedure and possible outcomes, and an optimistic outlook have been proven to be helpful. Relaxation techniques can minimize psychological agitation patterns such as a high heart rate and inner restlessness. Additionally, patients have to cope with pain due to a tumor, as well as pain that may arise during the course of the treatment. Caring for the ill person is often very difficult for the family because of financial problems. A difficult financial situation and poor access to medical, nursing, or other social services can affect the process of healing negatively. At the time of diagnosis, there is often a loss of control and helplessness in the face of possible physical disfigurement, accompanying pain, and possible financial implications for adequate treatment, not least the fear and uncertainty surrounding the prospect of an untimely death. Chronic back pain, in most cases, is musculoskeletal in origin, accompanied by poor coping skills along with other "yellow flags. For example, a diagnosis of "nonspecific back pain" leads to an extreme uncertainty on the part of the patient, often leading to increased fear of serious pathology and the desire for repeated diagnostic procedures. Often there is an iatrogenic component when repeated investigations are ordered-partly because the patient insists on it, and partly because the physician may be uncertain: "Is there a tumor or a serious disk prolapse causing the pain? Practical consequences A comprehensive compilation of all available findings, as well as discussion with colleagues about previous diagnosis and treatment, can be useful to get a complete picture about the patient. After considering all possible factors including psychiatric comorbidity or risks of chronification, a treatment plan can be developed. Chronic pain and psychopathology: research findings and theoretical considerations. Practical consequences Important in the treatment of headache is describing to the patient that stress can lead to an increase in the intensity and frequency of the headache. Sensitization is a basic learning mechanism that describes an increased neural response when stimuli of constant intensity are simply repeated. If this were true, only large bone metastases that extend into the periosteum should be painful. But experience teaches otherwise: fortunately, painful bone metastases usually have not yet destroyed the compacta. Thus, when they are treated causally by radiation or chemotherapy, the stability of the bone is still preserved. Rolf-Detlef Treede In the aura phase, many patients are hypersensitive to external stimuli such as light, sound, smell, or touch. For example, evoked cerebral potential studies have shown that the normal response decrement upon repetitive application of visual stimuli is absent in migraine sufferers. Practical consequences Tissue damage restricted to the bone marrow can be a source of intense nociceptive input. However, treatment here does not necessarily have to be by analgesics; instead, radiation or chemotherapy may actually eliminate the cause of this pain. Insights on neuropathic pain There has been a long-standing debate on how to define "neuropathic pain. As with any other alarm system, there are two possible ways the alarm can be activated: (a) it is a true alarm signaling an actual event; (b) it is a false alarm, caused by a defect in the alarm system. The usual pain after tissue damage is a case of true alarm by the nociceptive system. In case of neuropathic pain, it is a false alarm caused by some kind of damage to the nociceptive system. Practical consequences Currently none, but in the future it may be possible to alleviate chronic pain conditions by treatment modalities that enhance habituation without being directly analgesic. Immediately after birth, cutaneous withdrawal reflexes are lively and occur with very low threshold, such as mild touch by a pointed object. As soon as a child is able to understand verbal instructions, faces pain scales can be used in a similar fashion as visual analogue scales in adults. Practical consequences If a patient reports pain in a part of the body that is not damaged, consider neuropathic pain as a possibility. To verify this clinical hypothesis, evidence should be sought to demonstrate the underlying damage to the nociceptive system. Insights on pain in old age and dementia Pain thresholds and pain-evoked brain potentials have been studied in healthy volunteers up to the age of 100 years. For demented people, Practical consequences Many people maintain normal functions of their nociceptive system way into old age. For example, the homeopathic remedies Arnica and Hypericum may be useful prior to and after surgery. Guide to Pain Management in Low-Resource Settings Chapter 49 Profiles, Doses, and Side Effects of Drugs Used in Pain Management Barbara Schlisio the following drug list is a selection of commonly used drugs for pain management. The selection reflects recommendations of the "Essential Drug List for Cancer" from Makarere University and the health ministry in Uganda for the treatment of cancer patients, which appear to be a reasonable drug selection for treatment of the most common pain syndromes encountered by nonspecialists in a low-resource setting. This overview explains the mode of action as well as typical side effects of drugs. This means that safety is an issue to be considered when selecting a drug: the possible positive effects must always be balanced against possible side effects. In pain of low to moderate intensity, they may give sufficient pain control as a single therapy, but in moderate to severe pain they should only be used in combination with opioids. Renal failure is a more frequent and serious complication and is mostly associated with long-term use, especially in patients with a history of previous renal impairment and hypovolemia.

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If the patient is suspected to be suffering from a supratentorial mass, determine how se- vere the symptoms are and estimate how rapidly they are worsening. If the patient is deeply comatose, or if transtentorial herniation is evolving rapidly in a stuporous patient, it is necessary to treat intracranial hypertension first. The patient may initially be hyperventilated by a mask and Ambu bag while waiting for appropriate personnel and equipment to intubate the patient. An arterial sample for blood gas analysis should also be taken after hyperventilation is begun. On the other hand, this method raises the differential between mean arterial pressure and cerebral perfusion pressure,54 and the net effect on brain perfusion is difficult to measure and may vary among patients. Mannitol also lowers blood viscosity, increasing cerebral perfusion, and may also act as a free radical scavenger. In patients with brain tumors, whether primary or metastatic, subdural or epidural hematomas and empyemas, or other mass lesions that incite neovascularization with blood vessels that lack a blood-brain barrier, adrenal corticosteroids dramatically reverse signs and symptoms of herniation. Substantial clinical improvement is seen within 6 to 12 hours even though changes in water content of the brain may not be seen for days. The typical initial dose is 10 mg of dexamethasone, although as much as 100 mg of dexamethasone can be given safely as an intravenous bolus. Steroids decrease the transfer constant of substances across a disrupted blood-brain barrier within an hour, and they may increase clearance of edema fluid in the extracellular space, but substantial changes in brain water are not seen for many hours or days. The brain edema in stroke is largely cytotoxic, rather than vasogenic, and steroids do not produce the dramatic amelioration of the symptoms of brain edema seen in patients with tumors. Furthermore, the hyperglycemic effects of steroids may actually deleteriously affect the outcome. The scan will demonstrate the nature of the supratentorial mass lesion and often determines the degree of transtentorial herniation as well. If a subdural or epidural hematoma is identified, it should be evacuated immediately. If one of these lesions is suspected clinically and the patient is deteriorating rapidly, a neurosurgeon should be contacted at the time of imaging. For brain tumors, it is sometimes best to allow the steroids to reduce the level of edema for several days prior to surgery. An endotracheal tube should be in place, and the patient ventilated to PaO2 at greater than 100 mm Hg. In patients suffering from cerebral tumors or abscess, continue dexamethasone (typically 4 mg Approach to Management of the Unconscious Patient 323 every 6 hours, although doses up to 24 mg every 6 hours may be used if clinically necessary) or an equivalent steroid. Measure electrolytes frequently if mannitol or saline is being given, because the use of these drugs can result in severe electrolyte imbalance. Some investigators have advocated barbiturate anesthesia to treat severe intracranial hypertension from head injury. In one protocol, a loading dose of 10 mg/kg is given over 30 minutes followed by 5 mg/kg over 60 minutes for three doses. The patient is then maintained at 1 to 3 mg/kg/hour to maintain the pentobarbital level at 3 to 4 mg/dL. This technique requires extremely careful monitoring of vital signs and should be carried out only in an intensive care unit. There are reports of decreases in mortality with the use of barbiturate anesthesia in head injuries, drownings, cerebral infarction, and other supratentorial mass lesions. It is not simply through anesthesia, since in experimental animals gas anesthesia appears to have no such salutary effect. The clinical usefulness of barbiturate therapy for coma must be regarded as still in the stage of experimental evaluation. It may improve outcome in the former,77 but while it may be lifesaving in the latter, functional outcome is often poor especially in the elderly. In patients with infratentorial mass or destructive lesions causing coma, one may elicit a history of occipital headache or complaints of vertigo, diplopia, or other symptoms and signs suggesting brainstem dysfunction. Frequently, however, the onset of the coma is sudden and headache occurs only moments before the patient loses consciousness. If the onset of the headache is accompanied by vomiting, one should suspect an infratentorial lesion, as acute vomiting is less common with supratentorial masses in adults. Characteristic oculovestibular abnormalities including skew deviation, dysconjugate gaze, fixed gaze palsies, or dysconjugate responses to oculocephalic and oculovestibular testing are strong presumptive evidence of an infratentorial lesion. Cranial nerve palsies are often present and abnormal respiratory patterns usually are present from onset. The major problem in differential diagnosis arises when a patient with a supratentorial mass lesion has progressed far enough to arrive at the pontine or medullary level of coma. In this instance, it is virtually impossible to distinguish by physical examination between the effects of supratentorial and infratentorial masses. Metabolic coma can usually be distinguished from destructive or compressive lesions because the pupils remain reactive. At times it is impossible to distinguish on clinical grounds an intrinsic brainstem lesion (such as infarction from basilar artery occlusion) from an extrinsic compressive lesion (such as cerebellar hematoma), but the treatment is different: surgery for compressive lesions73 and thrombolysis for acute vascular occlusions. Some reports describe successful surgical evacuation of brainstem hematomas,81 particularly when the hemorrhage is due to a cavernous angioma. Primary pontine hemorrhages (those due to hypertension) usually are not treated surgically, particularly when the patient is comatose. When motor signs (decorticate or decerebrate rigidity) appear, they are usually symmetric. If the patient is stuporous rather than comatose, asterixis, myoclonus, and tremor are common, and in comatose patients the presence of repetitive seizures, either focal or generalized, provide presumptive evidence of metabolic dysfunction. Many patients with metabolic coma either hyper- or hypoventilate, but it is rare to see the abnormal respiratory patterns that characterize infratentorial mass or destructive lesions (see page 50). The first is in differentiating patients with the diencephalic stage of supratentorial masses from those with metabolic coma. In the absence of focal motor signs, one may initially suspect metabolic coma even in patients who have a supratentorial mass lesion with early central herniation. In this instance, the preservation of intact and symmetric pupillary and oculovestibular responses provides strong presumptive evidence for metabolic rather than structural disease. It is stupor and coma caused by metabolic brain disease that most challenges the internist, neurologist, or general physician likely to be reading this monograph. If patients suffer from major damage caused by supra- or infratentorial mass lesions or destructive lesions, specific treatment often involves a surgical or intravascular procedure. If psychogenic unresponsiveness is the problem, the ultimate management of the patient rests with a psychiatrist. In metabolic brain disease, however, the task of preserving the brain from permanent damage rests with the physician of first contact. The physician should first evaluate the vital signs, provide adequate ventilation and arterial pressure, and then draw blood for metabolic studies. Those metabolic encephalopathies that are most likely to produce either irreversible brain damage or a quick demise but are potentially treatable include drug overdose, hypoglycemia, metabolic or respiratory acidosis (from several causes), hyperosmolar states, hypoxia, bacterial meningitis or sepsis, and severe electrolyte imbalance. It is important to secure an arterial sample for blood gas analysis, although emergency management may have to begin even before laboratory results are returned. Both acidosis and alkalosis can cause cardiac arrhythmias, but acute metabolic acidosis is more likely to be lethal; however, pH is not an independent predictor of mortality in critically ill patients with metabolic acidosis. Instead, urgent treatment of the underlying cause of the acidosis is probably the best approach. Relieve hypoxia immediately by ensuring an adequate airway and delivering sufficient oxygen to keep the blood fully oxygenated. Such patients should be given 100% oxygen and hyperventilated to increase blood oxygenation. Hyperbaric oxygenation may improve the situation, and if a hyperbaric chamber is available, it should probably be utilized for patients with life-threatening exposure. Severe anemia (hematocrit less than 25) in a comatose patient should be treated with transfusion of whole blood or packed red cells.

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