The best studied and most prevalent comorbidity is insomnia with ma jor depression anxiety symptoms quiz buy fluvoxamine overnight. On the basis of longitudinal studies anxiety effects discount fluvoxamine online master card, insomnia is now established as a risk fac tor for major depression anxiety symptoms 5 yr old buy fluvoxamine paypal. Not all people with insomnia have a depression diagnosis; however anxiety 34 weeks pregnant best 50 mg fluvoxamine, studies have found that 15 to 20 percent of people diagnosed with insomnia have major depression (Ford and Kamerow, 1989; Breslau et al. A variety of polysomnographic abnormalities have been found with other psychiatric disorders (Benca, 2005a). Most potential mechanisms for sleep changes in psychiatric disorders deal specifically with insomnia and depres sion. Possible mechanisms include neurotransmitter imbalance (cholinergic aminergic imbalance), circadian phase advance, and hypothalamic-pituitary adrenal axis dysregulation (Benca, 2005a). Recent evidence implicating regions of the frontal lobe has emerged from imaging studies using positron emission tomography. Because the amygdala also plays a role in sleep regulation (Jones, 2005), this finding suggests that sleep and mood disorders may be manifestations of dysregulation in overlapping neuro circuits. The authors hypothesize that increased metabolism in emotional pathways with depression may increase emotional arousal and thereby adversely affect sleep (Nofzinger et al. Treatment Comorbid psychiatric and sleep disorders are treated by a combination of medication and/or psychotherapy (Krahn, 2005; Benca, 2005a). A major problem is underdiagnosis and undertreatment of one or both of the comorbid disorders. One of the disorders may be missed or may be mistak enly dismissed as a condition that will recede once the other is treated. In the case of depression, for example, sleep abnormalities may continue once the depression episode has remitted (Fava, 2004). If untreated, residual insomnia is a risk factor for depression recurrence (Reynolds et al. Further, because sleep and psychiatric disorders, by themselves, are disabling, the treatment of the comorbidity may reduce needless disability. Insomnia, for example, worsens outcomes in depres sion, schizophrenia, and alcohol dependence. Treatment of both conditions can improve a patient’s functioning and possibly improve adherence with therapy (Vincent and Hameed, 2003). Another concern is that medication for one disorder might exacerbate the other. Insomnia and Psychiatric Disorders As mentioned above insomnia is associated with depression, acting as both a risk factor and a manifestation (Ford and Kamerow, 1989; Livingston et al. Several studies done were longitudinal in design, including one that tracked more than 1, 000 male physicians for 40 years (Chang et al. Another study, which followed 1, 007 young adults at a health maintenance organization for 3. This figure is based on 16 percent of the sample who developed depression with a history of insomnia at baseline, as compared with 4. Insomnia is also a predictor of acute suicide among patients with mood disorders (Fawcett et al. The striking association between insomnia and depression in so many studies suggests that insomnia is also an early marker for the onset of depression, and the two may be linked by a common pathophysiology. Although the pathophysiological relationship is not known, researchers are focusing on overlapping neural pathways for anxiety, arousal, and/or circa dian disturbance (Benca, 2005b). One hypothesis is that common pathways are the amygdala and other limbic structures of the brain (Nofzinger et al. Another hypothesis is that chronic insomnia increases activity of the hypothalamic-pituitary-adrenal axis, which in turn contributes to depres sion (Perlis et al. The close association of insomnia and depression also raises the tantalizing possibility that treating insomnia may prevent some cases of depression (Riemann and Voderholzer, 2003), but limited data are available. The biological basis for the relationship between insomnia and new onset psychiatric disorders (other than depression) is also not known. In many cases narcolepsy arises during the mid to late teenage years; however, fre quently initial diagnosis is not correct, resulting in delays in diagnosis of 15 to 25 years after the onset of symptoms (Broughton et al. Onset of narcolepsy can also have a negative impact on school performance (see Chap ter 4). In most cases, naps are refreshing, but the rested feeling only lasts a short time. When severe, sleepiness can manifest as automatic behavior, a con tinuation of activities in a semiautomatic manner when sleepy, with no subsequent memory. Mean sleep latency of less than 8 minutes and two or more sleep onset rhythmic eye movement periods is diagnostic for narcolepsy. Sleep logs or actigraphy for the preceding 2 weeks can be helpful to exclude chronic sleep deprivation. It must also be conducted after withdrawal of psycho tropic medications (generally more than 2 weeks). Idiopathic and recurrent hypersomnia cases are not strongly associated with human leukocyte antigen. The first, idiopathic hypersomnia with prolonged sleep time, is a rare disorder and is characterized by the following: • Excessive daytime sleepiness occurs, as described above for narco lepsy, but in the typical form naps are unrefreshing. In most sleep disorders clinics with experience in this area, approxi mately one-third of hypersomnia cases are diagnosed with this condition (Aldrich, 1996). In contrast, the prevalence of idiopathic hypersomnia without prolonged sleep time may be more substantial, as most patients are likely not diagnosed (Arand et al. Recurrent hypersomnia is periodic either in synchrony with menstrua tion (menstruation-linked periodic hypersomnia) or without any associa tion and mostly in males with Klein-Levin syndrome (Billiard and Cadilhac, 1988; Arnulf et al. Klein-Levin syndrome is characterized by re current episodes of dramatic hypersomnia lasting from 2 days to several weeks. These episodes are associated with behavioral and cognitive abnor malities, binge eating or hypersexuality, and alternate with long asymptom atic periods that last months or years (Arnulf et al. The prevalence of narcolepsy with definite cataplexy has been documented in adults by numerous population-based studies and occurs in 0. In contrast, very little is known about the prevalence of narcolepsy without cataplexy. Secondary cases of narcolepsy or hypersomnia are also common, but the overall prevalence is not known (Table 3-3). These can occur in the context of psychiatric disorders, for example depression; central nervous system tumors, most notably in the hypothalamus; neurodegenerative dis orders, such as Parkinson’s disease; inflammatory disorders, such as mul tiple sclerosis or paraneoplastic syndromes; traumatic disorders, such as head trauma; vascular disorders, such as those that are attributed to median thalamic stroke; and genetic disorders, including myotonic dystrophy or Prader-Willi syndrome (Billiard et al. Etiology and Risk Factors Similar to other sleep disorders, little is known about the pathophysiol ogy and risk factors for narcolepsy and hypersomnia. Most of the knowl edge in this area pertains to narcolepsy with cataplexy, which affects males and females equally. Many contributing factors influence an individual’s susceptibility, including both genetic and environmental factors (Mignot, 1998, 2001). Approxi mately 70, 000 hypothalamic neurons that are responsible for producing the neuropeptide hypocretin (orexin) are lost in individuals with narcolepsy with cataplexy (Thannickal et al. Hypocretin is an excitatory neuropeptide that regulates the activity of other sleep regula tory networks. An unknown portion may be caused by partial or complete hypocretin deficiency (Kanbayashi et al. When the disorder is associated with prolonged sleep time, it typically starts during adolescence and is lifelong. It is essential to exclude secondary causes, such as head trauma or hypersomnia owing to depression (Roth, 1976; Billiard and Dauvilliers, 2001). Some cases with prolonged sleep times have been reported to be familial, suggesting a genetic origin. Even in the case of narcolepsy in which the disorder is caused by hypocretin deficiency, current treatment does not aim at improving the defective neurotransmis sion (Mignot et al. Behavioral measures, such as napping, support groups, and work arrange ments are helpful but rarely sufficient. In most cases, pharmacological treat ment is needed (Nishino and Mignot, 1997; Lammers and Overeem, 2003). However, as with other pharmaceuticals designed to treat sleep problems, large-scale clinical trails have not examined the efficacy and safety of drugs to treat narcolepsy in children and adolescents.
Dur ing deployment they were exposed to anxiety 5-htp cheap fluvoxamine on line war zone stressors as such as enemy fre anxiety vs stress trusted 50mg fluvoxamine, armed combat anxiety emoji buy fluvoxamine online pills, and seeing seriously injured fellow soldiers and civilians anxiety problems 100 mg fluvoxamine for sale. All participants were medically healthy male and were free from psychotropic medication and alcohol or drugs dependence in the past six months. Sleep registrations with simultaneous blood sampling Sleep registrations during two consecutive nights were conducted in the sleep laboratory of the Central Military Hospital in Utrecht, the Netherlands. We adjusted the 8 hour sleep period to the habitual times of participants, with a time of lights out between 2200h and 0000h, and lights on between 0600h and 0800h. From now on, we will only refer to the normalized times: by defnition, “2300h” is time of lights out and “0700h” is time of lights on. This allowed us to collect venous blood samples without disturbing subjects’ sleep. Blood samples were drawn every 20 minutes, immediately put on ice, and centrifuged within four hours. Participants were instructed to refrain from alcohol on the day prior to sleep registration, and to refrain from caffeine containing beverages after 1600h on the day prior to sleep registration. Fifteen neutral one syllable words were visually presented on a computer screen, and repeated three times. A free delayed recall was assessed the next morning between 30 – 45 minutes after awakening. Patients were unaware of the delayed recall task the next morning to prevent rehearsal. A nonparametric Kruskal Wallis test for group differences was used for variables that were not normally distributed after log transformation. No group differences were present in age, daily coffee intake and weekly alcohol intake. This is in line with a previ ous study that found decreased hippocampal activation and decreased performance after a night of experimentally induced sleep fragmentation (van der Werf et al. To the best of our knowledge, this is the frst study that found a relationship between spontaneous sleep fragmentation in the frst half of the night and decreased memory performance. The time between encoding and delayed recall was longer in our study, as we tested memory consolidation in the morning following sleep. It is unlikely that they contributed unequally to the difference with controls, as the mean of the medication naive patients was still much lower than controls. To rule out a confounding group-effect, we performed a sub analyses in all three groups separately. We used only one declarative memory task to assess sleep de pendent memory consolidation. To address this limitation a larger and preferably longitudinal study is warranted to replicate our preliminary fndings. Sleep-dependent surges in growth hormone do not contribute to sleep-dependent memory consolidation. Sleep pathophysiology in posttraumatic stress disorder and idio pathic nightmare sufferers. Neuropsychological performance is related to current social and occupational functioning in veterans with post traumatic stress disorder. Magnetic resonance imaging study of hippocampal volume in chronic, combat-related posttraumatic stress disorder. An ultra short episode of sleep is suffcient to promote declarative memory performance. Growth hormone/insulin like growth factor-I axis in obstructive sleep apnea syndrome: an update. Circulating neurotransmitters during the different wake-sleep stages in normal sub jects. Trauma exposure rather than posttraumatic stress disorder is associated with reduced baseline plasma neuropeptide-Y levels. The effect of growth hormone substitution on cognitive performance in adult patients with hypopituitarism. Two formulas for com putation of the area under the curve represent measures of total hormone concentration versus time-dependent change. A manual of Standardized Terminology, Techniques and Scor ing System for Sleep Stages of Human Subjects. Low cerebrospinal fuid neuropeptide Y concentrations in posttraumatic stress disorder. Shift from hippocampal to neocortical centered retrieval network with consolidation. Chapter 6 Pharmacotherapy for disordered Sleep in Post traumatic Stress disorder: a Systematic review Saskia van Liempt1, eric vermetten1, 2, elbert Geuze1, 2, herman G. From this database English-language, human subject, data driven papers published after 1980 were selected. Open-label and case studies suggest effcacy for some antidepressants, anticonvulsants and atypical antipsychotics. They show promising results for the atypical antipsychotic olanzapine, and the 1-adrenoceptor antagonist prazosin. However, randomized controlled trials with larger popu lations need to be conducted. In clinical presentation of symptoms, sleep complaints are frequently reported (Geuze and Vermetten, 2004). A number of studies describe other alterations in sleep with unclear clinical importance. These alterations include less movement time, especially in patients with nightmares or co-morbid panic disorder (Woodward et al. Trauma-related nightmares were also associated with more wake after sleep time, whereas non-trauma related nightmares were not (Woodward et al. Moreover, noradrenaline promotes wakefulness under stressful conditions (Hunsley and Palmiter, 2004). Agents inhibiting noradrenergic activity in the brain may thus alleviate sleep complaints. Articles were excluded if sleep was not evaluated and explicitly mentioned as a separate outcome measure. One small trial compared imipramine and chloral hydrate in the treatment of 25 pediatric burn patients with acute stress disorder (Robert et al. Eighty percent of all patients treated with imipramine for 1 week experienced symptom relief compared to 45% of patients treated with chloral hydrate. Eight of the responders no longer had nightmares, and a small sample of nine ex perienced signifcant relief of insomnia. Remarkably, patients stopped having nightmares after 5 days to 1 month of medication. Sleep disturbances and frequency of trauma-related nightmares decreased signifcantly. Each patient received clonazepam and placebo for 2 weeks, with no effect on sleep complaints during clonazepam treatment. Four case reports demonstrated that temazepam improved symptoms of acute stress, including disturbed sleep (Mellman et al. A subsequent placebo-controlled trial with temazepam in the acute aftermath of trauma revealed that subjective sleep improved in the temazepam group, but this effect was not maintained when treatment was discontinued after 7 days (Mellman et al. However, only limited studies have evaluated improvement of sleep complaints as a primary outcome measure. This was confrmed in a pooled analysis of three placebo-controlled studies (Stein et al. A placebo-controlled trial showed a signifcant decrease in ‘trouble sleeping’ after fuoxetine treatment, as measured by a self administered questionnaire. However, the improvement was not signifcant as measured by a structured interview. Fluoxetine did not have an effect on nightmares in this study (Meltzer-Brody et al.
However anxiety symptoms 97 fluvoxamine 100mg, the condition is common anxiety symptoms treatment and prevention buy fluvoxamine without prescription, serious anxiety 7dpo cheap fluvoxamine 100 mg amex, and a cause of serious microvascular and macrovascular health complications anxiety xanax forums purchase fluvoxamine 50mg mastercard. Selective testing of high-risk individuals can reduce the costs compared to universal testing. Relevant Resources: Casagrande, 2013; Colosia, 2013; Waugh, 2013; Ackermann, 2011; Li, 2008; Gregg, 2004 Return to Algorithm Return to Table of Contents 1. Some patients may have increased testing and treatment without benefit, and having the diagnosis of diabetes could potentially have negative psychosocial and economic ramifications for individuals. Relevant Resources: Casagrande, 2013; Colosia, 2013; Waugh, 2013; Rahman, 2012; Ackermann, 2011; American Diabetes Association, 2010; Li, 2008; U. Preventive Services Task Force, 2008 Return to Algorithm Return to Table of Contents Quality of Evidence: Low Strength of Recommendation: Strong Benefits: Universal screening incurs substantial costs for initial screening procedures, and many individuals would need to undergo additional testing procedures to confirm or refute the initial screening test, leading to both testing costs and economic costs, such as time away from work or other productive activities. Two randomized trials failed to show a benefit of screening for diabetes on overall mortality. One of these trials found little evidence of benefits from screening on clinical measures of diabetic complications, cardiovascular health, medication use or functional status. In this trial, screening for diabetes appeared to shorten the time to diagnosis of diabetes by only about three years. Harms: Universal screening would be expected to maximize the number of people diagnosed with diabetes early in their disease process. This would allow for early implementation of therapeutic measures to control hyperglycemia, resulting in a hopefully cost-effective intervention to reduce the incidence of later diabetes-related complications. A randomized trial of screening for diabetes found no evidence of adverse effects of screening on physical or emotional health of screened compared to unscreened individuals. Benefits-Harms Assessment: the absence of clinical benefit as shown in data from randomized trials and increase in costs would argue against a recommendation for universal screening in unselected populations or populations judged to be at low risk for diabetes. Preventive Services Task Force, 2008 Return to Algorithm Return to Table of Contents 1. Additionally, if a patient has symptoms of hyperglycemia and casual plasma glucose 200 mg/dL, diabetes may be Strength of Recommendation: Strong diagnosed. There may also be racial or ethnic differences in the relationship between glycemia and A1c levels, and these could result in false-negatives or false-positives. Benefits-Harms Assessment: the general acceptance of all three testing methods and the specific thresholds are well established. Providing a choice of testing methods is likely to increase the likelihood that appropriate patients are tested for diabetes, minimize cost and inconvenience, and allow clinicians to individualize test selection based on individual patient characteristics. If both tests meet diagnostic criteria for diabetes, a diagnosis of diabetes can be made. If it is again above the diagnostic threshold on repeat testing, a diagnosis of diabetes can be assigned. Diagnosis of prediabetes is made when an individual meets one or more of the following criteria: • A1c 5. Intensive lifestyle change or programs have been proven effective in delaying or preventing the onset of diabetes by about 50-58%. Effective lifestyle changes include setting achievable goals, obtaining weight loss when needed (between 5-10% of total body weight is recommended), and increasing physical activity to a minimum of 150 minutes per week (Tuomilehto, 2001). Patients who respond to lifestyle interventions: • Annual follow-up and reassessment of risks for developing diabetes (American Diabetes Associa tion, 2014; Chiasson, 2002; Heart Outcomes Prevention Evaluation Study Investigators, The, 2002; Kelley, 2002; Eriksson, 1999) Patients who are high risk and not responding to lifestyle interventions: • Intensify education and counseling on lifestyle interventions. Health care clinicians should follow patients diagnosed with prediabetes on an annual basis to monitor his/ her progress and review treatment goals (American Diabetes Association, 2014). Inpatient Diabetes Management Inpatient care may be appropriate in the following situations (American Diabetes Association, 2004a): • Elderly patients with infection or illness, weight loss, dehydration, polyuria or polydipsia • Life-threatening acute metabolic complications of diabetes: Hyperglycemic hyperosmolar state with impaired mental status, elevated plasma osmolaity that includes plasma glucose greater than 600 mg/dL Diabetic ketoacidosis with a plasma glucose greater than 250 mg/dL, arterial pH less than 7. These negative outcomes are observed more frequently in hospitalized patients with newly discovered hyperglycemia. Hyperglycemia is an independent marker of inpatient mortality in patients with undiagnosed diabetes (Umpierrez, 2002). Hyperglycemia has been associated with increased infection rates and poorer short-term and long-term outcomes in critically ill patients in the intensive care unit, post-myocardial infarction and post-surgical settings. Earlier studies supported that aggressive glucose management in medical and surgical patients improves outcomes (Van den Berghe, 2001). Types of Insulin Based on outpatient studies, consider insulin Glargine or Detemir as the basal insulin (there are limited inpatient studies to date). Initial studies comparing rapid-acting insulin with human regular insulin show rapid-acting insulins to be more effective at reducing the peak postprandial glucose concentration (Reynolds, 2004). They may also lower the demand for endogenous insulin, provide superior postprandial glycemic control, and cause fewer hypoglycemic episodes requiring medical intervention (Rave, 2006; Pettitt, 2003; Gerich, 2002). Insulin lispro, glulisine and aspart have similar pharmacokinetics; they have an earlier onset and peak of action than regular insulin. Peak action usually occurs at one hour with a duration of three to four hours, while regular insulin has a peak action of two to four hours and a duration of six to eight hours. Lispro, glulisine and aspart may then reduce the occurrence of late postprandial hypoglycemia compared to regular insulin (Guerci, 2005; John, 2004). Insulin Dosing Schedule Insulin dosing schedules must be individualized based on a variety of factors, including the severity of diabetes, oral intake, severity of illness and other concurrent diabetic medication. It is not feasible to design a single algorithm for determining an insulin regimen in every patient. The following information provides general guidance in determining initial insulin doses. Approximately 50% of this insulin is secreted as basal insulin and 50% as postprandial boluses following meals (Polonsky, 1988b). Fifty percent of subjects were receiving between 23 and 53 units of insulin per day. The average weight of subjects was 75 kg, so the "average" daily insulin requirement was about 0. Therefore, in initiating subcutaneous insulin in a hospitalized patient who is eating meals, a total daily insulin dose of 0. Hospital length-of-stay or incidences of hypoglycemia did not differ between the basal/prandial insulin regimen or the sliding scale insulin regimen (Umpierrez, 2007). Basal insulin Typical approach is to give 40-50% of the estimated total daily insulin dose as the basal insulin component. Prandial insulin For patients eating meals, several approaches have been suggested to initiate a prandial insulin regimen: • Divide 50% of the estimated daily insulin requirement into three equal insulin doses given before the three meals. Typical insulin requirements using this last approach are one to two units of insulin per carbohydrate unit (Clement, 2004). It is recommended that prandial insulin be given as a rapid-acting insulin analog within 0-15 minutes of the meal (Clement, 2004). Prandial insulin replacement has its main effect on peripheral glucose disposal into muscle. Also referred to as "bolus" or "mealtime" insulin, prandial insulin is usually administered before eating. There are occasional situations when this insulin may be injected immediately after eating, such as when it is unclear how much food will be eaten. In such situations, the quantity of carbohydrates taken can be counted and an appropriate amount of rapid-acting analog can be injected (Clement, 2004). Patients who are not eating meals will not typically require a prandial insulin component, although they may need periodic correction insulin. For patients eating meals, it is typically given with meals by simply increasing the rapid acting insulin dose by an additional amount based on the correction schedule. If rapid-acting insulin is used in this situation, an every-four-hour schedule may be optimal. A typical assumption is that one unit of insulin will lower the blood glucose 50 mg/dL (Hirsch, 2002). An empiric "Rule of 1, 700" has been proposed as one way of estimating the insulin correction requirement. The "Low, " "Medium" and "High" correction schedules included on the order set assume that one unit of insulin will lower the blood glucose by approximately 50, 25 and 15 mg/dL, respectively. There does not appear to be a consensus whether correction insulin should be given at bedtime. Some experts argue against bedtime correction insulin due to a fear of nocturnal hypoglycemia with short or rapid-acting insulin given at bedtime (Hirsch, 1995).
Cross References Anosognosia; Confabulation; Macula sparing anxiety scale 0-10 generic fluvoxamine 100 mg with visa, Macula splitting; Optokinetic nystagmus anxiety uti generic fluvoxamine 100mg without a prescription, Optokinetic response; Prosopagnosia; Pupillary reexes; Visual agnosia Cotard’s Syndrome A delusional syndrome anxiety symptoms for hiv order cheap fluvoxamine on line, rst described in the 1890s anxiety 6 months after giving birth purchase generic fluvoxamine canada, characterized by the patient’s denial of their own existence, or of part of their body. The patient may assert that they are dead and able to smell rotten esh or feel worms crawling over their skin. Although this may occur in the context of psychiatric disease, especially depression and schizophrenia, it may also occur in association with organic brain abnormalities, specically lesions of the non-dominant temporoparietal cortex, or migraine. Some envisage Cotard’s syndrome as a more pervasive form of the Capgras syndrome, originating similarly as a consequence of Geschwindian disconnection between the limbic system and all sensory areas, leading to a loss of emotional contact with the world. Cross References Capgras syndrome; Delusion; Disconnection syndromes Coup de Poignard Coup de poignard, or dagger thrust, refers to a sudden precordial pain, as may occur in myocardial infarction or aortic dissection, also described with spinal subarachnoid haemorrhage. Subarachnoid haemorrhage presenting as acute chest pain: a variant of le coup de poignard. Coup de Sabre Coup de sabre is a localized form of scleroderma manifest as a linear, atrophic lesion on the forehead which may be mistaken for a scar. This lesion may be associated with hemifacial atrophy and epilepsy, and neuroimaging may 95 C Cover Tests show hemiatrophy and intracranial calcication. Whether these changes reect inammation or a neurocutaneous syndrome is not known. Cross Reference Hemifacial atrophy Cover Tests the simple cover and cover–uncover tests may be used to demonstrate manifest and latent strabismus (heterotropia and heterophoria), respectively. The cover test demonstrates tropias: the uncovered eye is forced to adopt xation; any movement therefore represents a manifest strabismus (heterotropia). The cover–uncover test demonstrates phorias: any movement of the cov ered eye to re-establish xation as it is uncovered represents a latent strabismus (heterophoria). The alternate cover or cross-cover test, in which the hand or occluder moves back and forth between the eyes, repeatedly breaking and re-establishing xa tion, is more dissociating, preventing binocular viewing, and therefore helpful in demonstrating whether or not there is strabismus. It should be performed in the nine cardinal positions of gaze to determine the direction that elicits maxi mal deviation. However, it does not distinguish between tropias and phorias, for which the cover and cover–uncover tests are required. Cross References Heterophoria; Heterotropia Cramp Cramps are dened as involuntary contractions of a number of muscle units which results in a hardening of the muscle with pain due to a local lactic aci dosis. Cramps are not uncommon in normal individuals but in a minority of cases they are associated with an underlying neurological or metabolic disorder. Recognized associations of cramp include • Normal individuals: Especially during periods of dehydration with salt loss; pregnancy. Symptomatic treatment of cramps may include use of quinine sulphate, vitamin B, naftidrofuryl, and calcium channel antagonists such as diltiazem; carba mazepine, phenytoin, and procainamide have also been tried. Assessment: symptomatic treatment for muscle cramps (an evidence-based review): report of the Therapeutics and Technology Subcommittee of the American Academy of Neurology. Cross References Fasciculation; Myokymia; Neuromyotonia; Spasm; Stiffness Cremasteric Reex the cremasteric reex is a supercial or cutaneous reex consisting of con traction of the cremaster muscle causing elevation of the testicle, following stimulation of the skin of the upper inner aspect of the thigh from above downwards. The cremasteric reex is lost when the corticospinal pathways are damaged above T12 or following lesions of the genitofemoral nerve. It may also be absent in elderly men or with local pathology such as hydrocele, varicocele, orchitis, or epididymitis. Cross References Abdominal reexes; Reexes Crocodile Tears Crocodile tears, gustatory epiphora, or Bogorad’s syndrome reect inappropri ate unilateral lacrimation during eating, such that tears may spill down the face (epiphora). Cross References Bell’s palsy; Epiphora; Synkinesia, Synkinesis Crossed Adductor Reex Contralateral adductor muscle contraction in response to a tap on the adductor tendon may be found with a pyramidal lesion above L2, although it is a normal nding in infants. Cross Reference Reexes 97 C Crossed Aphasia Crossed Aphasia Aphasia from a right-sided lesion in a right-handed patient, crossed aphasia, is rare, presumably a reection of crossed or mixed cerebral dominance. Cross Reference Aphasia Crossed Apraxia A name given to apraxia in right-handed patients with right-sided lesions; apraxia is more commonly associated with left-sided brain injury. Cross Reference Lid retraction Dazzle Dazzle is a painless intolerance of the eyes to bright light (cf. It may be peripheral in origin (retinal disease; opacities within cornea, lens, vitreous); or central (lesions anywhere from optic nerve to occipitotemporal region). Cross Reference Photophobia Decerebrate Rigidity Decerebrate rigidity is a posture observed in comatose patients in which there is extension and pronation of the upper extremities, extension of the legs, and plantar exion of the feet (= extensor posturing), which is taken to be an exagger ation of the normal standing position. Painful stimuli may induce opisthotonos, hyperextension, and hyperpronation of the upper limbs. Decerebrate rigidity occurs in severe metabolic disorders of the upper brain stem (anoxia/ischaemia, trauma, structural lesions, drug intoxication). A similar picture was rst observed by Sherrington (1898) following section of the brain stem of cats at the collicular level, below the red nuclei, such that the vestibular nuclei were intact. The action of the vestibular nuclei, unchecked by higher centres, may be responsible for the profound extensor tone. Decerebrate rigidity indicates a deeper level of coma than decorticate rigid ity; the transition from the latter to the former is associated with a worsening of prognosis. The lesion responsible for decorticate rigidity is higher in the neuraxis than that causing decerebrate rigidity, often being diffuse cerebral hemisphere or diencephalic disease, although, despite the name, it may occur with upper brainstem lesions. Cross References Coma; Decerebrate rigidity Deja Entendu A sensation of familiarity akin to deja vu but referring to auditory rather than visual experiences. However, since the term has passed into the vernacular, not every patient complaining of ‘deja vu’ has a pathological problem. Recurrent hallucinations or vivid dream-like imagery may also enter the differential diagnosis. A phenomenon of slight con fusion in which all is not clear although it is familiar has sometimes been labelled ‘presque vu’. Epileptic deja vu may last longer and be more frequent and may be associated with other features such as depersonalization and derealization, strong emotion such as fear, epigastric aura, or olfactory hallucinations. Epileptic deja vu is a complex aura of focal onset epilepsy; specically, it is indicative of temporal lobe onset of seizures and is said by some authors to be the only epileptic aura of reli able lateralizing signicance (right). Deja vecu (‘already lived’) has been used to denote a broader experience than deja vu but the clinical implications are similar. Deja vu has also been reported to occur in several psychiatric disorders, such as anxiety, depression, and schizophrenia. Cross References Aura; Hallucination; Jamais vu Delirium Delirium, also sometimes known as acute confusional state, acute organic reaction, acute brain syndrome, or toxic-metabolic encephalopathy, is a neurobe havioural syndrome of which the cardinal feature is a decit of attention, the ability to focus on specic stimuli. Diagnostic criteria also require a concurrent 102 Delirium D alteration in level of awareness, which may range from lethargy to hypervigilance, although delirium is not primarily a disorder of arousal or alertness (cf. Other features commonly observed in delirium include • impaired cognitive function: disorientation in time and place; • perceptual disorders: illusions, hallucinations; • behavioural disturbances: agitation, restlessness, aggression, wandering, which may occur as a consequence of perceptual problems (hyperalert type); or unresponsiveness, withdrawal (hypoalert or quiet type); • language: rambling incoherent speech, logorrhoea; • altered sleep–wake cycle: ‘sundowning’ (restlessness and confusion at night); • tendency to marked uctuations in alertness/activity, with occasional lucid intervals; • delusions: often persecutory. Subtypes or variants are described, one characterized by hyperactivity (‘agitated’), the other by withdrawal and apathy (‘quiet’). The course of delirium is usually brief (seldom more than a few days, often only hours). On recovery the patient may have no recollection of events, although islands of recall may be preserved, corresponding with lucid intervals (a useful, if retrospective, diagnostic feature). Delirium is often contrasted with dementia, a ‘chronic brain syndrome’, in which attention is relatively preserved, the onset is insidious rather than acute, the course is stable over the day rather than uctuating, and which generally lasts months to years. However, it should be noted that in the elderly delirium is often superimposed on dementia, which is a predisposing factor for the development of delirium, perhaps reecting impaired cerebral reserve. Risk factors for the development of delirium may be categorized as either predisposing or precipitating. It is suggested that optimal nursing of delirious patients should aim at envi ronmental modulation to avoid both understimulation and overstimulation; a side room is probably best (if possible). However, if the patient poses a risk to him/herself, other patients, or staff which cannot be addressed by other means, regular low-dose oral haloperidol may be used, probably in preference to atypical neuroleptics, benzodiazepines (lorazepam), or cholinesterase inhibitors. Cross References Agraphia; Attention; Coma; Delusion; Dementia; Hallucination; Illusion; Logorrhoea; Obtundation; Stupor; ‘Sundowning’ Delusion A delusion is a xed false belief, not amenable to reason. There are a number of common forms of delusion, including • persecutory (paranoia); • reference: important events or people being inuenced by patient’s thoughts, ideas; • grandiose/expansive: occur particularly in mania; • guilt/worthlessness: occur particularly in depression; • hypochondria; • thought broadcast and thought insertion; • control by an external agency. Specic, named, delusional syndromes are those of: • Capgras: the ‘delusion of doubles’, a familiar person or place is thought to be an impostor, or double; this resembles the reduplicative paramnesia described in neurological disorders such as Alzheimer’s disease. Delusions are not only a feature of primary psychiatric disease (psychoses such as schizophrenia; neuroses such as depression), but may also be encountered in neurological disease with secondary psychiatric features (‘organic psychiatry’). Cross References Delirium; Dementia; Hallucination; Illusion; Intermetamorphosis; Misidentication syndromes; Reduplicative paramnesia Dementia Dementia is a syndrome characterized by loss of intellectual (cognitive) func tions sufficient to interfere with social and occupational functioning. Cognition encompasses multiple functions including language, memory, perception, praxis, attentional mechanisms, and executive function (planning, reasoning).
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