03 August 2009

Sleep and Sleep Disorders



Sleep and Sleep Disorders
The Science of Sleep
By:Robert Averbuch, MD
Assistant Professor of Psychiatry

Lecture Outline

* Physiology of Normal Sleep
o Non-REM
o REM
o Normal patterns of sleep
* Sleep Disorders
o Dyssomnias
o Parasomnias

Physiology of Normal Sleep

2 Phases: REM and Non-REM Sleep

Non-REM Sleep

* 4 stages of progressively deeper sleep
* Normal muscle tone
* Associated with increased 5HT (serotonin)
* Decreased autonomic activity:
o Lower BP, Pulse, respirations slow

Stage One
* Brief transition between wakefulness and sleep (accounts for only 5% of sleep time)
Stage Two
* Light sleep
* Accounts for 50% of total sleep time
* ElectroEncephaloGram (EEG) shows some characteristic findings…

EEG in Stage 2
Stages 3,4

* Most restful, restorative stages of sleep
* Aka: Delta wave sleep/ slow wave sleep
* Greatest proportion is in the first 1/3 to 1/2 of night

NREM Sleep: Theories of its purpose…

* The decrease in metabolic demand on the brain during NREM allows glycogen stores to replenish
* Allows for consolidation of memories and learning

REM (dreamland)

* 10-20 min. cycles consisting of:
o Rapid Eye Movements
o ElectroEncepahaloGram shows fast activity very similar to wakeful EEG pattern
o Suppression of peripheral muscle tone
o Penile Tumescence
o Often increased autonomic tone- ie, increased blood pressure, resp, heart rate

REM (dreamland)

* Where dreaming occurs
* REM is marked by increased cholinergic activity
o Thus REM-supression seen with anti-cholinergic drugs (ex. some antidepressants)

Normal Sleep Pattern
* Sleep cycles between NREM and REM approx. 4-5 times/night
* Cycles last approx. 90min
* REM duration and frequency increase thru night
* Proportion of slow wave sleep (stages 3,4) decreases thru night

Normal Sleep Parameters
* Sleep Onset Latency- the time it takes one to fall asleep, averages 10-20min
* REM Latency- time between sleep onset and the first REM period, averages 90-120min

Normal Sleep Distribution
* REM sleep accounts for approximately 25% of total sleep time
* Non-REM sleep accounts for 75% of sleep time, with 25% of that spent in Stages 3,4 (most restful portion)

Sleep Onset
* Mediated by increased Serotonergic activity in the Dorsal Raphe Nuclei of the Pons
o Dampens activity in the ascending reticular activating system (RAS), inducing sleep
* Dopamine has opposite effect- promotes wakefulness

Age-Related Changes

* Decreases in dreaming, total sleep time, REM, and slow-wave (deep sleep)
* Increases in early morning awakening, fragmentation, daytime napping, and phase advancement-
o Ie, earlier to bed, and awaken earlier

“Measuring” Sleep
Polysomnography

The Polysomnogram

* EEG, ECG
* EOG (oculogram)
* Chin EMG (myelogram)
* Ant. Tibialis EMG
* Pulse Oxymeter
* Blood Pressure

Sleep Disorders
Sleep Disorders- 2 Divisions

* Dyssomnias- disorders of quality, timing, or amount of sleep (quantity)
* Parasomnias- abnormal behaviors associated with sleep or sleep-wake transition, that often produce arousals

Dyssomnias
* Primary Insomnia
* Narcolepsy
* Sleep Apnea
* Circadian Rhythm Sleep Disorder (jet lag, et al.)
* Restless Legs Syndrome (RLS)
* Medical/Substance related insomnia

Primary Insomnia
* “Primary”, meaning no underlying medical cause
* Onset often with stressor or disruption to sleep schedule or environment
* Results from poor sleep hygiene, along with classical conditioning-
o Faulty learning/association of sleep environment with state of arousal

INSOMNIA- an epidemic?
* Definition: “Subjective” experience of poor sleep quality or quantity that adversely affects daily functioning
* Extremely common complaint in general practice
* 30-40% adults have occasional poor sleep
* 15-20% adults have chronic insomnia

Consequences of Insomnia
* Depression
* Irritability
* Decreased cognitive functioning
* Decreased productivity
* Injuries and accidents

Narcolepsy
* A dyssomnia characterized by poor sleep quality (restless, fragmented) and dysfunction in the transitions between sleep and wakefulness
* Presents with Excessive Daytime Sedation (EDS)

Narcolepsy Tetrad

* Classic tetrad of associated findings:
o 1. Sleep attacks
o 2. Cataplexy
o 3. Sleep paralysis
o 4. Sleep hallucinations

1. Sleep Attacks
* Most common symptom of the tetrad
* Brief (10-20min) “power-naps”- refreshing and restful
* Average 10-20/wk

2. Cataplexy
* Sudden loss of muscle tone (rarely full body paralysis) caused by intrusion of REM activity into daytime wakefulness
* Triggered by heightened emotion
* Average duration: 30 seconds
* No loss of consciousness

3. Sleep Paralysis
* Brief paralysis upon waking
* Remain alert with full eye movements Can occur in the absence of Narcolepsy (ie, normal variant)

4. Sleep Hallucinations
* Hypnogogic hallucinations- occur during transition into sleep
* Hynopompic hallucinations- occur upon awakening from sleep
* Can occur in the absence of Narcolepsy (ie, normal variant)

Narcolepsy: Etiology
* CNS lesions: brain trauma, stroke, tumor, Multiple Sclerosis
* Familial/idiopathic: onset in adolescence or young adulthood

Sleep Apnea
* Dyssomnia characterized by poor sleep quality due to frequent awakenings (apneas)
* Apneas last sec-minutes- produce brief arousal
* Presents with excessive daytime sedation- EDS

Sleep Apnea: Two Types
* Obstructive Sleep Apnea: most common
* Central Sleep Apnea

Obstructive Sleep Apnea
* Classic- obese, middle-aged male with thick neck or enlarged tonsils
* Apneas- brief gasps…silence, followed by loud “resuscitative” snores, and sometimes body movements (restless)
* Usually unaware of snoring, arousals…but sleep partner is aware

Central Sleep Apnea
* Apneas- episodic cessation of central ventilation drive
o Thus snoring is less common
* More in elderly, with underlying CNS lesions- ex. tumor, stroke

Sleep Apnea: Consequences
* Depression
* Anxiety
* Morning headaches
* Cognitive dysfunction
* Hypertension

Restless Legs Syndrome
* Paresthesias and/or dysesthesias in the legs, relieved by movements
* Usually occur in transition from wakefulness to sleep

RLS Causes
* Peripheral neuropathies
* Peripheral vascular disease
* Medication side effects
* Anemia
* Pregnancy
* Renal failure

Circadian Rhythm Disorders
* Delayed Sleep Phase Syndrome
* Jet Lag
* Accelerated Sleep Phase Syndrome
* Shift Work Sleep Disorder

Insomnia from Medical Conditions
* Reflux (GERD)
* Nocturia
* Peripheral neuropathies
* Breathing problems- Asthma, COPD
* Heart Disease/Failure
* Pain conditions

Psychiatric Causes of Insomnia
* Depression
* Anxiety
* Psychosis
* Substance intoxication/withdrawal

Sleep and Sleep Disorders.ppt

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29 July 2009

Fungal Presentations



Fungal Presentations from:fungalforum.com

High Dose AmBisome Treatment: what do we know?
By:V-J Anttila, Specialist in Infectious Diseases
Helsinki University Central Hospital, Finland

INVASIVE ASPERGILLOSIS
Management with liposomal amphotericin B
By:Michael Ellis

Is invasive aspergillosis hospital or community acquired: reassessing the evidence?
By:Malcolm Richardson PhD, FIBiol, FRCPath
Department of Bacteriology & Immunology
University of Helsinki, Finland

Invasive fungal infections in immunocompetent patients Does it exists ?

Antifungal combination therapy: where are we?
By:Malcolm Richardson. University of Helsinki.

Emerging fungal pathogens: clinical usefulness of new diagnostic tools

Update on glucan detection
By:Malcolm Richardson PhD, FIBiol, FRCPath
Department of Bacteriology & Immunology
University of Helsinki

Is azole prophylaxis a double-edged sword?
By:Malcolm Richardson PhD, FRCPath
Senior Lecturer in Medical Mycology
University of Helsinki, Finland

Clinical Findings in Rare and Emerging Fungal İnfections
By:Dr. Murat Akova
Hacettepe University School of Medicine
Section of Infectious Diseases
Ankara, Turkey


Liposomal amphotericin B: 20 years of clinical experience
By:Luis Ostrosky-Zeichner, MD, FACP
Assistant Professor of Medicine and Epidemiology
University of Texas Health Science Center at Houston

Antifungal and Surgical Management of a Case of Maxillary Sinus Aspergilloma
By:Riina Rautemaa
DDS, PhD, Consultant of Oral Microbiology
Helsinki University Central Hospital Maxillofacial Clinic and Laboratory Diagnostics;
and Haartman Institute, University of Helsinki, Finland


AMPHOTERICIN B NEPHROTOXICITY
By:GILBERT DERAY
PARIS , FRANCE

Changing Epidemiology:
The Importance of Broad Spectrum Therapeutics
By:Cornelia Lass-Flörl
Innsbruck Medical University

Antifungal treatment: Past and Present
By:Malcolm Richardson, PhD, FIBiol, FRCPath
University of Helsinki

Is combination antifungal therapy a viable option for the future?
By: Brian L Jones
Glasgow Royal Infirmary, UK

Fungal infections in solid organ transplantation recipients
By:Malcolm Richardson PhD, FIBiol, FRCPath
University of Helsinki and Helsinki University Central Hospital

Ten years experience of liposomal amphotericin B, AmBisome treatment in solid organ transplant recipients (SOT)

Advances in Empirical Antifungal Therapy in Patients with Febrile Neutropenia.
By:Marc A. Boogaerts

Does azole prophylaxis confer resistance to amphotericin B and influence virulence?
By:Malcolm Richardson
Department of Bacteriology & Immunology Haartman Institute
University of Helsinki

Liposomal amphotericin B: 20 years of clinical experience
The body of knowledge and familiarity of use
By:Malcolm Richardson PhD, FIBiol, FRCPath
Associate Professor in Medical Mycology
University of Helsinki, Finland

Prophylaxis of invasive fungal infections in high risk patients with hematologic malignancies
By:Olaf Penack

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28 July 2009

Nutrition Presentation lectures



Nutrition Presentation lectures
by Dr. Scott Schaeffer
Harford Community College


Lecture notes - Unit 1

Chapter 1
Chapter 2
Chapter 3
Chapter 4

Lecture notes - Unit 2
Chapter 5
Chapter 6
Chapter 7
Chapter 8

Lecture notes - Unit 3
Chapter 9
Chapter 10
Chapter 11
Chapter 12

Lecture notes - Unit 4
Chapter 13
Chapter 14
Chapter 15
Chapter 16

Read more...
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