DOCSLIB.ORG

Narcolepsy, Idiopathic Hypersomnolence and Related Conditions

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Narcolepsy, Idiopathic Hypersomnolence and Related Conditions CMJ1103-CME_Quinnell.qxd 5/15/11 12:47 AM Page 282 CME Sleep disorders Clinical Medicine 2011, Vol 11, No 3: 282–6 coma or malingering. The weakness of Narcolepsy, idiopathic hypersomnolence cataplexy is typically bilateral and can involve the legs (‘weak at the knees’), and related conditions hands, face, neck or shoulder girdle. Frequency can range from rarely to sev- naps; if these are not possible, they can eral times a day. Ptosis may give the Timothy G Quinnell, consultant respiratory impression of unconsciousness and dis- physician; Ian E Smith, consultant have irresistible sleep episodes (‘sleep tract from the correct diagnosis but, physician and director attacks’). The identification of other fac- tors such as sleep disordered breathing apart from occasional evolution into Respiratory Support and Sleep Centre, (SDB) contributing to sleepiness should sleep, awareness is preserved. Papworth Hospital, Cambridge not discourage the pursuit of a diagnosis The differential diagnosis of cataplexy of narcolepsy if features are compelling includes periodic paralysis, myasthenia because sleep disorders can coexist.9 gravis, atonic seizures and vertebrobasilar Narcolepsy with cataplexy is primarily a insufficiency.10 The absence of cataplexy disorder of excessive daytime sleepiness can represent disease-in-evolution or so- (EDS) and episodic collapse. Despite a Cataplexy called ‘monosymptomatic narcolepsy’9 quality of life impact similar to Cataplexy is emotionally triggered but other diagnoses should be considered. Parkinson’s disease (PD)1 and significant muscle weakness and, with EDS, is individual and societal costs2 it is often essential to the diagnosis of classical Other narcoleptic symptoms overlooked. A UK survey found median narcolepsy.9–11 Symptoms usually time from first symptom to diagnosis to develop months or years after EDS but, The other symptoms of the ‘narcoleptic be 10.5 years.3 The delay in diagnosis because sleepiness can be overlooked, tetrad’ involve different facets of rapid may be because it is uncommon cataplexy is sometimes the presenting eye movement (REM) sleep invading (European prevalence 0.047%4), but is complaint. It should be considered wakefulness: no doubt exacerbated by a paucity of when patients present with apparent sleep paralysis (persistent motor sleep medicine training (median 5 min • absence episodes, unexplained collapse atonia) in UK medical undergraduate or episodic clumsiness. Prolonged or hypnogogic/hypnopompic halluci- curricula5). Narcolepsy has a variety of • intractable episodes (status cata- nations (dream-like experiences presentations which may be wrongly plecticus) may be mistaken for seizures, during sleep-wake transitions). attributed to more familiar disorders or lifestyle and there is an overlap with nor- mality. EDS is reported by up to 10% of Table 1. Causes of excessive daytime sleepiness. the general population6 and objective Insufficient sleep Time measures of sleepiness do not reliably • Quality (alcohol, caffeine) differentiate narcoleptics and normal • Both (noise, temperature) subjects.7 It is important for the acute • Other disorder Pain care physician to be aware of the features • Nocturia of, and means for, diagnosing narcolepsy • Dyspnoea so that opportunities to treat this dis- • Cough abling condition are not missed. • Medications • Daytime sedation • Nocturnal sleep disruption (diuretics, steroids, statins) Diagnosis Anxiety/depression Anyone reporting EDS warrants a Circadian rhythm disorder • Advanced sleep phase syndrome detailed sleep history. It is important to • Delayed sleep phase syndrome tease out an increased propensity to fall • Shift work disorder asleep from other symptoms reported as • Jet lag tiredness, particularly physical and emo- Sleep-disordered breathing • Obstructive sleep apnoea tional fatigue. The Epworth Sleepiness • Central sleep apnoea Scale can be a useful measure.8 • Hypoventilation Explanations for perceived sleepiness, Narcolepsy including lifestyle, mood disorders, other Restless legs syndrome/periodic limb movement during sleep medical conditions and medication, Idiopathic hypersomnia should be explored (Table 1). People with Recurrent hypersomnia narcolepsy typically need brief, refreshing 282 © Royal College of Physicians, 2011. All rights reserved. CMJ1103-CME_Quinnell.qxd 5/15/11 12:47 AM Page 283 CME Sleep disorders Automatism, poor nocturnal sleep and autoimmune condition triggered by Subjects undergo PSG-monitored nap dream enactment (REM sleep behaviour infection.19,20 opportunities at two-hourly intervals.7 disorder) can also occur.9–11 Mean sleep latency is usually less than Although not inevitable in, or exclu- Investigation eight minutes in narcolepsy (most nar- sive to, narcolepsy, when accompanying coleptics fall asleep within 5 min)7 and cataplexy and sleep attacks, it is under- Nocturnal polysomnography multiple REM sleep episodes occur standable how lack of familiarity with (Fig 3). International guidelines man- The investigation of choice for unex- these features can result in narcolepsy date a combination of these two criteria plained EDS is nocturnal polysomnog- being mistaken for seizures, psychiatric but sensitivity is only around 80% in raphy (PSG). Electroencephalogram, disorders or malingering. classical cases and they are not entirely chin electromyogram and electro-oculo- specific.9,21,22 gram enable the staging of wakefulness, Physical examination REM and non-REM sleep. Respiratory and leg monitoring allow screening for The physical examination is usually Other investigations SDB and periodic limb movement. normal. Cataplexy has characteristic Features suggestive of narcolepsy include HLA testing has only limited utility as it features, including areflexia and facial rapid sleep onset and premature entry is positive in up to 38% of non-narcolep- twitching, but episodes usually occur 18 into REM sleep (Fig 2). tics. A negative test with a classical his- only in relaxed, intimate settings and so tory may cause pause for thought. CSF 11 are rarely seen in clinic. Unless the orexin assay may be useful when PSG Multiple sleep latency test diagnosis can be confidently made and MSLT are unavailable, but the test is on clinical features alone, suspected Diurnal sleep drive is measured by the invasive and less discriminatory in cases narcolepsy and other unexplained cases multiple sleep latency test (MSLT). without cataplexy.9,14 of EDS should undergo specific investigation.9 Thalamus Pathophysiology Magnocellular basal forebrain Ventral tegmental area The discovery of the neurotransmitter (Acetylcholine) and subtana nigra orexin (hypocretin) has refined the (Dopamine) pathophysiological description of nar- colepsy as a condition of sleep-wake instability.12 Orexin stabilises wake and sleep states through widespread subcor- tical neuronal projections from the lat- eral hypothalamus (Fig 1). Cerebrospinal fluid (CSF) and brain studies have established that most people with narcolepsy and cataplexy have orexin deficiency.14–16 Up to 2% of narcoleptics have symp- Perifornical area tomatic first-degree relatives but most (Hypocren) 17 Raphe nuclei cases are sporadic. Global research has (Serotonin) yielded only one case of human nar- colepsy caused by a prepro-orexin gene Tuberomammillary nucleus mutation15 but wider genetic studies (Histamine) continue. There is a strong human Locus coeruleus leukocyte antigen (HLA) association. Pedunculoponne and (Noradrenaline) The DQB1*0602 haplotype is found in laterodorsal tegmental nuclei 88–98% of patients with non-familial (Acetylcholine) cataplexy.18 The newly discovered asso- ciation of narcolepsy with a T cell Fig 1. Hypocretin (orexin) system. The sleep-wake cycle is governed by a complex, multilevel receptor polymorphism and demonstra- neuronal system in the brainstem, thalamus, hypothalamus and basal forebrain. Hypocretin- producing neurons in the hypothalamus stabilise the activity of other key neuronal groups tion of elevated antistreptococcal anti- involved in the control of sleep and waking. These nuclei and their principal bodies in recent-onset cases support the neurotransmitters are shown here in highly schematic fashion. Reproduced with permission hypothesis of a genetically determined from BMJ Publishing Group Ltd.13 © Royal College of Physicians, 2011. All rights reserved. 283 CMJ1103-CME_Quinnell.qxd 5/15/11 12:47 AM Page 284 CME Sleep disorders Fig 2. Polysomnogram summary (hypnogram) from patient with narcolepsy. There is rapid sleep onset (blue arrow) and early rapid eye movement (REM) sleep (red arrow). There are clinically insignificant numbers of apnoeas (purple marks) and periodic limb movements (bottom trace in blue) which do not explain sleepiness in this case. Secondary narcolepsy and other weeks to years. Cognitive and behav- aetiology or diagnostic test, these are hypersomnias ioural abnormalities, classically binge- arbitrary. There is typically difficulty eating and hypersexuality, are variably waking up in the morning (sleep inertia) Rarely, other medical disorders present associated. A prolonged 24-hour sleep and EDS. Naps are more prolonged than with narcoleptic features. Those fea- time may be demonstrated if PSG is in narcolepsy and usually unrefreshing. If turing cataplexy include: achieved during an episode.9 Lithium nocturnal sleep duration allows time for • hypothalamic lesions may be useful, but evidence for its the performance of MSLT after PSG, the • paraneoplastic encephalitis effectiveness is limited.23 mean sleep
Load more

Recommended publications
  • Consciousness and Unconsciousness: Cross-Cultural Experience
    Consciousness and Unconsciousness: Cross-Cultural Experience . In the West, consciousness was a topic of considerable interest in 19th-century philosophy and the early development of psychology. The philosopher John Locke, in his Essay Concerning Human Understanding, defined consciousness as "the perception of what passes in a man's own mind." William James in The Principles of Psychology, spoke of the "stream of consciousness," emphasizing the continuous and variable nature of mental content, thus viewing consciousness as a process. James also distinguished "normal, waking" or "rational" consciousness from other types. To study consciousness, 19th-century psychologists proceeded by means of "introspection." This method, deemed unscientific and unreliable because it produced inconsistent findings, was rejected by J. B. Watson and other American psychologists of the behaviorist school in the early 1900s. Consciousness was not a topic of psychological study in the United States for more than forty years. In the 1950s diverse factors emerged in American life and science that made consciousness again a significant area of research in psychology, neurobiology, and philosophy. These factors included the development of psychoactive drugs in psychiatry and in the counterculture; experiments in psychological warfare and brainwashing as a result of the Korean War and the Cold War; studies in cybernetics and artificial intelligence; and developments in brain and sleep research, as well as interest in Eastern religions (Yoga, Zen Buddhism and others). Intensive comparative and experimental research, some under secret governmental auspices, was carried on for some years, beginning in the 1950s. This included work with hallucinogens, particularly LSD-25, also sensory deprivation, biofeedback, sleep research, etc.
    [Show full text]
  • DIAGNOSIS and TREATMENT of the NARCOLEPSY SYNDROME Analysis of Seventy-Five Case Records
    DIAGNOSIS AND TREATMENT OF THE NARCOLEPSY SYNDROME Analysis of Seventy-Five Case Records GERALD BOWLING, M.D.,* Department of Internal Medicine and NELSON G. RICHARDS, M.D. Department of Neurology HE narcolepsy syndrome is known also as Gelineau's disease, the Gelineau- Redlich syndrome, paroxysmal sleep, and sleep epilepsy. Because of the compara- tive rarity of the disease and our lack of understanding of the term narcolepsy, we recently had difficulty in diagnosing several cases of the syndrome. This report undertakes to clarify the meaning of the term, to discuss the entity, and to report an analysis of 75 case records of narcoleptics treated at the Cleveland Clinic in the last nine years. In the past it has been alleged that the sleep of the narcoleptic is paroxysmal in onset.1 Hypersomnolence has frequently been used to describe the condition in which the patient is persistently drowsy without having actual sleeping spells, or in which he falls asleep perhaps only once a day while engaged in some activity. Yoss and Daly2 recently defined narcolepsy as consisting of four components: (1) narcolepsy proper — "excessive and persistent sleepiness"; (2) cataplexy — muscular weak- ness induced by emotion; (3) sleep paralysis — transient, benign loss of muscle tone at the beginning or end of sleep; (4) hypnagogic hallucinations — usually vivid auditory or visual hallucinations or illusions occurring during day or night drowsiness, usually with sleep paralysis. We are essentially in agreement with their definition. In our 75 patients, excessive and persistent sleepiness occurred alone or in combination with other symptoms. Figure 1 illustrates the incidence of the four components of the narcolepsy syndrome in our patients.
    [Show full text]
  • The Neural Basis of the Dynamic Unconscious
    Neuropsychoanalysis, 2011, 13 (1) 5 The Neural Basis of the Dynamic Unconscious Heather A. Berlin (New York) A great deal of complex cognitive processing occurs at the unconscious level and affects how humans behave, think, and feel. Sci- entists are only now beginning to understand how this occurs on the neural level. Understanding the neural basis of consciousness requires an account of the neural mechanisms that underlie both conscious and unconscious thought, and their dynamic interac- tion. For example, how do conscious impulses, thoughts, or desires become unconscious (e.g., repression) or, conversely, how do unconscious impulses, desires, or motives become conscious (e.g., Freudian slips)? Research taking advantage of advances in technologies, like functional magnetic resonance imaging, has led to a revival and re-conceptualization of some of the key concepts of psychoanalytic theory, but steps toward understanding their neural basis have only just commenced. According to psychoanalytic theory, unconscious dynamic processes defensively remove anxiety-provoking thoughts and impulses from consciousness in re- sponse to one’s conflicting attitudes. The processes that keep unwanted thoughts from entering consciousness include repression, suppression, and dissociation. In this literature review, studies from psychology and cognitive neuroscience in both healthy and patient populations that are beginning to elucidate the neural basis of these phenomena are discussed and organized within a con- ceptual framework. Further studies in this emerging field at the intersection of psychoanalytic theory and neuroscience are needed. Keywords: unconscious; psychodynamic; repression; suppression; dissociation; neural “Nothing is so difficult as not deceiving oneself.” 1998a). Early psychodynamic theorists attempted to Ludwig Wittgenstein [1889–1951] explain phenomena observed in the clinic, but lat- er cognitive scientists used computational models of the mind to explain empirical data.
    [Show full text]
  • Disorders of Consciousness
    Disorders of Consciousness MARTIN M. MONTI Abstract Disorders of consciousness are a spectrum of neurological disorders, encom- passing coma, the vegetative state, and the minimally conscious state, in which patients acquire or develop an impairment of the two cardinal elements of consciousness–wakefulness and awareness. One of the main sources of complexity in this context is how to recognize and tell apart patients who retain some level of awareness from patients who do not. Indeed, in the absence of any direct means of assessing one’s level of awareness, we are forced to indirectly infer a patient’s state on the basis of their ability to perform behaviors that, appearing clearly voluntary, imply the presence of consciousness. In this contribution, we explore recent evidence showing how brain imaging can be harnessed to address the problem of consciousness in patients surviving severe brain injury. First, we focus on recent experiments demonstrating how neuroimaging can be used to detect the presence of voluntary “brain behavior” in otherwise non responsive patients, and to allow a rudimentary form of non muscle-dependent communication strategy based solely on voluntary brain activity. Second, we discuss recent findings concerning network activity at different levels of awareness, and the relationship between thalamo cortical circuits and consciousness. INTRODUCTION Disorders of consciousness (DOC) are a spectrum of disorders, typically acquired or developed following severe brain injury, in which an individ- ual’s consciousness is altered in a transient or permanent manner owing to severe brain injury (Monti, 2012). In this context, consciousness is (sim- plistically) conceived as encompassing two cardinal elements (Laureys, 2005): wakefulness and awareness.
    [Show full text]
  • Toxicity Associated with Carbon Monoxide Louise W
    Clin Lab Med 26 (2006) 99–125 Toxicity Associated with Carbon Monoxide Louise W. Kao, MDa,b,*, Kristine A. Nan˜ agas, MDa,b aDepartment of Emergency Medicine, Indiana University School of Medicine, Indianapolis, IN, USA bMedical Toxicology of Indiana, Indiana Poison Center, Indianapolis, IN, USA Carbon monoxide (CO) has been called a ‘‘great mimicker.’’ The clinical presentations associated with CO toxicity may be diverse and nonspecific, including syncope, new-onset seizure, flu-like illness, headache, and chest pain. Unrecognized CO exposure may lead to significant morbidity and mortality. Even when the diagnosis is certain, appropriate therapy is widely debated. Epidemiology and sources CO is a colorless, odorless, nonirritating gas produced primarily by incomplete combustion of any carbonaceous fossil fuel. CO is the leading cause of poisoning mortality in the United States [1,2] and may be responsible for more than half of all fatal poisonings worldwide [3].An estimated 5000 to 6000 people die in the United States each year as a result of CO exposure [2]. From 1968 to 1998, the Centers for Disease Control reported that non–fire-related CO poisoning caused or contributed to 116,703 deaths, 70.6% of which were due to motor vehicle exhaust and 29% of which were unintentional [4]. Although most accidental deaths are due to house fires and automobile exhaust, consumer products such as indoor heaters and stoves contribute to approximately 180 to 200 annual deaths [5]. Unintentional deaths peak in the winter months, when heating systems are being used and windows are closed [2]. Portions of this article were previously published in Holstege CP, Rusyniak DE: Medical Toxicology.
    [Show full text]
  • Management of Syncope in the Acute Care Setting
    Syncope MANAGEMENT OF SYNCOPE IN THE ACUTE CARE SETTING Maureen C. Hughes, MD Dartmouth Hitchcock Neurology BC ‘99 Disclosures None of the planners or presenters of this session have disclosed any conflict or commercial interest OBJECTIVES • Describe the assessment of syncope. • Identify appropriate testing and lab studies. • Discuss the management in the acute care setting. • Patients will present to the hospital/Emergency Room with acute syncope. This session will review the assessment and management of syncope in the acute care setting. The Patient • John Doe (JD) is the 74 yo beloved patriarch with a history of DM, HTN, CAD w stent, at his grandson’s 1 year old birthday party. • He is helping his adorable grandson blow out his candle when he passes out. • There are 45 family members at the party, 15 of them accompany him to the ED. What is our plan? • First elucidate the chief complaint to be sure the ‘spell’ is syncope using the patient history and witness history. • Syncope is a symptom, so determine type of syncope and cause of syncope. • Then determine necessary evaluation strategy and treatment plan. Syncope Syncope is a symptom of hemodynamic dysfunction and not a disease. The symptom is: An abrupt but transient loss of consciousness associated with absence of postural tone followed by a rapid and complete recovery without the need for intervention. A prodrome may be present. The Triage RN flags JD as syncope in the EMR, takes his Vital signs and he gets an EKG and directs the patient and his now 20 family members to a bed.
    [Show full text]
  • A Practical Approach to Coma Diagnosis in the Unresponsive Patient
    A practical approach to coma diagnosis in the unresponsive patient MARTIN A. SAMUELS, MD • Diagnosis of coma in the unresponsive patient can be done in a relatively short time by making key observations that will confirm disease of either the brain stem or the hemispheres, the two locations in which coma originates. Determining the location of the lesion is the primary goal in early assessment of the unresponsive patient. Examination of the patient's eyes is the single most important step in understanding coma. • INDEX TERMS: UNCONSCIOUSNESS; BRAIN STEM; EYE MANIFESTATIONS; 0 CLEVE CLIN J MED 1992; 59:257-261 IAGNOSIS OF THE unresponsive patient coma, the deepest level of unconsciousness. The varia- is a major issue in the practice of neurologi- tions in a patient's mental status along the spectrum cal medicine, internal medicine, and emer- are somewhat analogous to the conditions produced by gency medicine. If the patient is in a coma, anesthesia. The first signpost is confusion or inatten- Dthe disease is either in the ascending reticular activat- tion, the inability to maintain a coherent stream of ing system (a diffuse array of nuclei and tracts extend- thought or action. The ability to count backwards by ing from the brain stem to the thalamus), or the disease sevens from 100 (the "serial sevens" test) is a classic is bilateral and diffuse in the hemispheres. In assessing test of attention. Drugs, toxins, and metabolic en- an unconscious person, the primary goal is to deter- cephalopathy can cause inattention or confusion, mine the location of the lesion. Certain simple obser- which is the most common abnormality in mental vations made in an orderly fashion will provide the status seen in a general hospital setting.
    [Show full text]
  • Unconsciousness - First Aid: Medlineplus Medical Encyclopedia
    Unconsciousness - first aid: MedlinePlus Medical Encyclopedia U.S. National Library of Medicine GO About MedlinePlus Site Map FAQs Customer Support Health Topics Drugs & Supplements Videos & Tools Espaol Home → Medical Encyclopedia → Unconsciousness - first aid Unconsciousness - first aid Unconsciousness is when a person is unable to respond to people and activities. Doctors often call this a coma or being in a comatose state. Other changes in awareness can occur without becoming unconscious. These are called altered mental status or changed mental status. They include sudden confusion, disorientation, or stupor. Unconsciousness or any other sudden change in mental status must be treated as a medical emergency. Causes Unconsciousness can be caused by nearly any major illness or injury. It can also be caused by substance (drug) and alcohol use. Choking on an object can result in unconsciousness as well. Brief unconsciousness (or fainting) is often a result from dehydration, low blood sugar, or temporary low blood pressure. It can also be caused by serious heart or nervous system problems. A doctor will determine if the affected person needs tests. Other causes of fainting include straining during a bowel movement (vasovagal syncope), coughing very hard, or breathing very fast (hyperventilating). Symptoms The person will be unresponsive (does not respond to activity, touch, sound, or other stimulation). The following symptoms may occur after a person has been unconscious: Amnesia for (not remembering) events before, during, and even after
    [Show full text]
  • PROTOCOL 2.29: SYNCOPAL EPISODE Note: Syncope Is by Definition a Transient State of Unconsciousness from Which the Patient
    PROTOCOL 2.29: SYNCOPAL EPISODE Note: Syncope is by definition a transient state of unconsciousness from which the patient has recovered. If the patient is still unconscious, see Coma/Altered Mental Status Protocol. Emphasis should be placed on underlying cause of syncope and its treatment. Statistically, the most common cause of unconsciousness in the elderly patient in the pre-hospital setting is CVA/stroke problems. In the younger patient it is seizures. ADULT CARE 1. General Supportive Care. 2. ECG. IV NS if patient remains not alert. 3. Consider possible need for cervical spine immobilization if patient sustained fall during syncope. 4. Carefully monitor for any neurological deficits. Be aware of Medical Alert tags, breath odor, signs of drug abuse, sources of gases, potential toxins or ingestions. 5. Consider past medical history and possibility of transient dysrhythmia, hypovolemia (check for orthostatic changes in vital signs), medication side effects, glucose level abnormalities, inner ear disorders, CVA/TIA. 6. The patient that has passed out and then regained consciousness will frequently want to refuse service. Make sure patient has received full assessment (vitals, ECG, glucose check) and remind them that passing out is not normal before processing such a refusal, refer to No Transport (Refusal, Cancel) Protocol. Level II.1. None. PEDIATRIC CARE 1. General Supportive Care. 2. ECG. IV NS if patient remains not alert. 3. Consider possible need for cervical spine immobilization if patient sustained hard fall during syncope. PROTOCOL 2.29: SYNCOPAL EPISODE (cont.) PEDIATRIC CARE (cont.) 4. Carefully monitor for any neurological deficits. Be aware of Medical Alert tags, breath odor, signs of drug abuse, sources of gases, potential toxins or ingestions.
    [Show full text]
  • Syncope and Seizures*
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.12.1.25 on 1 February 1949. Downloaded from J. Neurol. Neurosurg. Psychiat., 1949, 12, 25. SYNCOPE AND SEIZURES* BY JOHN KERSHMAN From the Department of Neurology and Neurosurgery, McGill University, and the Montreal Neurological Institute, andfrom the Queen Mary Veterans' Hospital, Montreal, Canada Introduction various parts of the head being symmetrically explored with scalp-to-scalp and scalp-to-ear records. Hyper- Syncope is a clinical syndrome usually caused by ventilation was carried out for three minutes and the vasomotor, reflex, or psychogenic disturbances. record continued for two minutes after. If the record Various authors have emphasized that syncope or was on the borderline of normal, it was repeated after fainting is sometimes difficult to distinguish from hydration and pitressin, using the regime outlined by epilepsy (Weiss, 1935, 1942; Rossen, 1947), and it Penfield and Erickson (1941). In patients who had a has long been suggested that in some instances. history that alcohol was a precipitating factor in the -(Gowers, 1907; Wilson, 1928; Baxter and others, attacks, the following was frequently carried out in 1944) syncopal attacks might be the manifestation addition to the standard E.E.G. The patient was given of an epileptic disorder. In patients with syncope one ounce of whisky in a glass of sweetened fruit juice, the electro-encephidogram between attacks is and this was repeated after one and two hours. An normal, E.E.G. was started within half an hour after the last guest. Protected by copyright. (Levin and others, 1945; Sugar, 1945), although drink.
    [Show full text]
  • Evidence Report Narcolepsy (With and Without Cataplexy) and Commercial Motor Vehicle Driver Safety
    Evidence Report Narcolepsy (with and without Cataplexy) and Commercial Motor Vehicle Driver Safety Presented to The Federal Motor Carrier Safety Administration October 6, 2009 MANILA Consulting Group, Inc. 1420 Beverly Road, Suite 220 McLean, VA 22101 Evidence reports are independently reviewed by the Agency's Medical Review Board (MRB) and Medical Expert Panel (MEP). FMCSA considers MRB recommendations, MEP opinions and other data; however, all proposed changes to current standards and guidelines will be subject to public notice and comment and relevant rulemaking processes. Narcolepsy and CMV Driver Safety October 2009 Authorship Michelle Bieber-Tregear, PhD MANILA Consulting Group Jessica Roberts Williams, PhD, MSN, MPH MANILA Consulting Group Stephen Tregear, DPhil MANILA Consulting Group Policy Statement This report was prepared by MANILA Consulting Group, Inc. under contract GS-10F-0177N/DTMC75-06- F-00039 with the Department of Transportation’s Federal Motor Carrier Safety Administration. i Narcolepsy and CMV Driver Safety October 2009 Table of Contents Executive Summary ....................................................................................................................................... 1 Purpose of Evidence Report ...................................................................................................................... 1 Identification of Evidence Bases ............................................................................................................... 2 Grading the Strength of Evidence
    [Show full text]
  • Unconsciousness
    Consciousness • Vigilance • The ability to maintain attention and alertness over prolonged periods of time • Individual is fully responsive to stimuli, this is the condition of the person when awake. • Activity of ARAS (ascending reticular activating system) Unconsciousness A state of unawareness of self and environment. One shows no responsiveness to environmental stimuli but may respond to deep pain with involuntary movements. Unconsciousness • Somnolencia – ("drowsiness„) is a state of near-sleep, a strong desire for sleep, or sleeping for unusually long periods. • Sopor/stupor- is an unresponsive state from which a person can be aroused only briefly and with vigorous, repeated attempts. • Coma- is a profound state of unconsciousness. - a comatose patient cannot be awakened - fails to respond normally to pain or light - does not have sleep-wake cycles - does not take voluntary actions. - coma can last days, weeks, months, or indefinitely - the length of a coma cannot be accurately predicted or known - coma results from gross impairment of both cerebral hemispheres, and/or the ascending reticular activating system. Unconsciousness • Deep unconsciousness – absent brain stem reflexes (corneal, pupillar, pharyngeal), tendom reflexes, muscle hypotonia, spontaneous breathing is absent • Mild unconsciousness – brain stem reflexes +-, increases muscle tone, spontaneous breathing is present – different pathology Unconsciousness • Acute a/ lesion in brain stem b/ metabolic reason Unconsciousness 1. Consciousness 2. Breathing 3. Pupils 4. Position
    [Show full text]