Chapter 17: Sleep and Sleep-Wake disorders Sleep Regulation Sleep is necessary for: § Organization and memory storing of wake-time information § Restoration of mental and physical function- cardiovascular health § People with less sleep have higher risk of cardiovascular incidents - Controlled by the thalamus & cerebral cortex -Melatonin: § Synthesized and released by pineal gland § Regulated by hypothalamus § Causes shifts in circadian rhythm à 24-hour sleep-wake pattern, regulated by hypothalamus response to light-dark stimuli Sleep Stages • Alternating periods of REM and NON-REM REM: Complete loss of muscle activity, increased cerebral activity, increased heart rate, increased BP, increased temperature, rapid eye movements, decrease in cerebral blood flow and metabolism, last about 1-5 mins. NON-REM: makes up about 80% of your sleep cycle, made up of the 4 sleep stages, slowed autonomic responses, decreased cerebral activity, slow rolling eye movement, moderate movement Stage 1: Period between sleep • 1-7 mins • Easily arousable • Hypnic jerks Stage 2: Deeper than stage one • Last 10-25 mins Stage 3 & 4: Deep sleep • • • Brief stage 3 Stage 4 last 20-40mins, muscles are pretty relaxed but not completely inactive Little bit of muscle activity INSOMNIA VS. NARCOLEPSY Insomnia • Most common sleep disorder, happens more in older age Clinical manifestations: -impaired ability to initiate or maintain sleep -daytime fatigue, sleepiness, irritability, decreased attention & memory -can be chronic (long lasting, last entire life) or acute (phases, happens some night) Treatment: -sleep hygiene: not having screens in bedroom, regular schedule, no caffeine -behavioral therapy: what is that cause? -address the cause -meds: short term use only, people can become dependent, can lead to crazy dreams, BE CAREFUL Narcolepsy • Hypersomnolence Peaks between ages of 15-35yrs Clinical manifestations: -daytime sleepiness -sleep paralysis -hypnagogic hallucinations: zoning out -type one: cataplexy (muscle weakness in response to emotional reactions) example- fainting goats -type two: no cataplexy Diagnosis: -day and night sleep studies Treatment: -no cure -sleep hygiene education -educate about driving risks -stimulant meds MOVEMENT DISORDERS: RESTLESS LEG SYNDROME 70% of people experience it once in their life Primary vs. Secondary Primary: probably genetic Secondary: iron deficiency, neurologic disorders, pregnancy, meds, uremia Clinical manifestations: -motor restlessness, pacing -symptoms worse at rest & in evening -usually in stage 2 of sleep Treatment: -iron if FE is low -dopaminergic meds -anti seizure meds -ambulation and stretching OBSTRUCTIVE SLEEP APNEA • • • Cessations of breathing for 10+ seconds Partial or full collapse of upper airway Can occur 300-500 episodes each night Risk Factors: -older age -genetics -obesity -ETOH & drugs -large neck girth -postmenopausal women Clinical manifestations: -snoring -alternating between labored breathing and apnea (Period of silence) -daytime symptoms -chronic problems -waking up multiple times a night Diagnosis: -history -sleep studies Treatment: -lifestyle modifications (reduce alcohol usage) -CPAP -surgery (adenoid extraction) AGE RELATED SLEEP CHANGES Children -newborns sleep 16-20hrs per day -circadian rhythm established around 2-4 months, not usually developed naturally. Must have a schedule set by parent Sleep disorders: • Sleep terrors- nightmares on steroids, kid doesn’t remember it once awoken • Confusional arousal’s- kid wakes up and they’re confused • Sleepwalking- more common in children Older Adults -high prevalence of insomnia -more sleep-wake pattern changes -spend less time in deep sleep Etiology: • • • • • Primary or secondary sleep disorders Lack of exercise- can affect sleep Medications Stress Co-morbidities- prosthetic hyperplasia, nighttime urination Treatment: -treat underlying cause -sleep hygiene -avoid ETOH and stimulants CHAPTER 18: DISORDERS OF MEMORY, THOUGHT, AND EMOTION UNDERSTANDING PSYCHIATRIC DISORDERS Stress-Diasthesis Theory says that it’s a combination of genetics and environment that cause psychiatric disorders • Genetics + Environment -Adverse childhood experiences: positive correlation of adverse childhood experiences and mental health disorders -2x more susceptible for cardiovascular disorders -can alter DNA if experienced at a young age -Sexual abused people= 3x more likely to have mental health disorders than people who haven’t been abused. -Trauma vs stress Trauma: an event that leaves a person helpless Stress: a burden response to outside stressors/stimuli, doesn’t normally leave a person “helpless” Neuroplasticity: the ability of nervous system to change structure and function in response to stress/stimuli - If there’s not a healthy response, it can lead to psychiatric disorders NEUROCHEMICALS • Activate or inhibit genes Neurohormones: 1. corticotropin-releasing hormone (CRH): stimulates the release of ACTH from the pituitary, releases cortisol in response to stress 2. serotonin: responsible for self-esteem, also a sleep chemical 3. oxytocin- feelings of love and trust, without this you can have attachment disorders 4. melatonin- rest and relaxation 5. norepinephrine- feelings of excitement 6. phenylethylamine- bliss and infatuation 7. dopamine- reward chemical 8. endorphins- pain killers 9. acetylcholine- alertness. Releases cortisol SCHIZOPHRENIA • • • • Onset 16-30 years, males > females until after age 50 Genetics + environment Studies show that only about 50% of identical twin studies are showing that both twins have it- so there’s definitely an environmental link Happens in 1% of population Risk factors: -age -adverse childhood events/experiences -malnutrition, low vitamin D -long term cannabis or methamphetamine usage -older age fathers (not sure why) -migrant status -exposure to retro virus’ (HIV) -malnourished while you’re in utero -living in poverty Neurophysiology: -dysregulation of dopamine and serotonin -lower production of gabba -loss of grey matter -cortical thinning -changes to your neuron (front lobe) Clinical manifestations: -positive symptoms: incomprehensible speech, hallucinations, delusions, disorganized or cationic behavior -negative symptoms: abnormal social behavior, disorganized behaviors *More difficult to treat than positive symptoms* Treatment: -negative signs are difficult to treat -meds: typical and atypical, antipsychotic for positive signs; atypical antipsychotics for negative signs -psychosocial support: for person, and caregivers/family MOOD DISORDERS: DEPRESSION: one of most common • • • Females > Males, age of onset mid-30’s (decreasing now, starting as young as 18-25 on average) Depression in older adults can signal neurocognitive disorder Many different types -there’s a spectrum. *in this class we are mainly focusing on major depressive* Treatment: usually a combo of these -Antidepressants -Electric shock therapy: it’s been made safer -Phototherapy: used for seasonal depression -Therapy Major depressive disorder • Loss of interest in activities • lack of energy • recurrent suicidal thoughts • decreased appetite • impaired decision making and concentration • feelings of worthlessness • insomnia or hypersomnolence • *SYMPTOMS MUST BE PRESENT NEARLY EVERYDAY FOR 2 WEEKS* PHQ-2 scale used to determine if they’re at risk for depression MOOD DISORDERS: BIPOLAR DISORDER • • • Cardinal components: MDD + Bipolar mania Age of onset= 25 years More common in Females> males Pathophysiology: -impaired neuroplasticity (not making proper neuro connections) -genetic + neuroendocrine, autonomic, immune dysregulation -prefrontal cortex abnormalities Clinical manifestations: Bipolar 1: 1+ manic episodes alternating with depressive episodes, mood swings, rage, interference with school/work Bipolar 2: depression + at least one hypomanic episode (a less severe mania in bipolar1) Cyclothymia: similar to bipolar 1, but less severe Rapid cycling: 4+ manic episodes for 2+ weeks a year Treatment: -psychosocial interventions for depression -Meds for manic episodes to regulate neurochemical & neuroelectric Meds: antipsychotics, anticonvulsive, lithium (not used as much, has a narrow therapeutic index) MOOD DISORDERS: GENERALIZED ANXIETY DISORDER • Diagnosed between ages 45-59, females > males Neurophysiology: -altered neuroplasticity + genetics -neurochemicals dysregulation (decreased gabba, increased norepinephrine, decrease serotonin, increase dopamine, increase corticosteroid and glutamine) Clinical manifestations: -chronic, intense, excessive fear or worry without precipitating event -autonomic hyperactivity -interferes with activities/relationships -may lead to fatigue, sleep disruptions, difficulty concentrating -depression is a common co-morbidity Treatment: -Meds: 1st line defense (long term): anti-depressants, SSRI’s, 5HT agonists 2nd line of defense: benzodiazepines, valium, Ativan -behavior and psychosocial therapies MOOD DISORDERS: SUBSTANCE USE DISORDERS • Includes dependence or abuse of substances • 40% have co-occurring mental illness • Can alter brain development if onset is at or <20 years of age Neurophysiology: -genetics + environment -50% have a parent with substance abuse problem -increased dopamine Criteria for Diagnosis: -giving up important things in order to spend more time with substance -continued use even with adverse effects (continuing to drink even though you lost your job and have liver failure) Treatment: -physiological alterations in the brain cause relapse -treat psychiatric co-morbidities -combo therapy (it should NEVER be just medications) -some meds available for ETOH, tobacco, and opioid cessation MEMORY AND COGNITITION REVIEW Classifications of memory: 1. Immediate- seconds to minutes 2. Recent- minutes to days 3. Remote- years ago Implicit vs. Explicit Memory Implicit- responsible for unconscious, somatic, emotional and procedural memories (Ex: remembering the day your dad changed your tire) Explicit-responsible for processing factual knowledge (Ex: how to change a tire) Normal changes in aging: • Slow, progressive decline of memory • New learning is slower • Decreased executive functioning • Conceptual reasoning and processing decline Brain structures involved in memory -Amygdala -Hippocampus: explicit memory, reality testing, amygdala inhibition à decreased in people w/ trauma -Cerebral cortex: 1. prefrontal cortex- information processing, planning, problem solving 2. frontal lobe- language formation 3. temporal lobe- language comprehension -Cerebellum: allows for rapid efficient shifts in attention NEUROCOGNITIVE DISORDERS: DEMENTIA VS. DELIRIUM *very different conditions* Delirium: commonly a symptom of another condition Dementia: tends to be an actual diagnosis ALZHEIMERS DISEASE- form of dementia • • • Cortical atrophy, loss of neurons in parietal and temporal lobes 6th leading cause of death in the US Half of people over 85 will get it. Usually will be females since they live longer Neurophysiology: - Cortical atrophy, loss of neurons in parietal and temporal lobes Etiology: -? Disruption of neurotransmitters, oxidative distress, neuroinflammation -impaired cholinergic transmission -smaller cortex -neurofibrillary tangles and amyloid plaques -genetics Hallmark symptoms: -loss of short-term memory -language difficulty: understanding and remembering words -behavior changes: frustration, irritability Diagnosis: -cerebral autopsy/biopsy -based on clinical findings when alive Treatment: -maintain socialization, lots of caregiver support -adjustments to environment (alarm on door, latches higher up), redirection, music therapy -meds Stages of Alzheimer’s: HUNTINGTON DISEASE • Autosomal dominant disorder- If your parent has it, there’s a great likelihood of child having it • Progressive, terminal disease • Death is usually 10-15 years after onset of symptoms Clinical manifestations: -memory deficits -frontal lobe deterioration -motor disturbances- difficulty swallowing, chorea -cause of death = usually infection, secondary to the ability to swallow Treatment: no cure -supportive care CHAPTER 19: DISORDERS OF VISUAL FUNCTION Anatomy review: 12 cranial nerves 6 responsible for control of vision: -Optic -Oculomotor -Trochlear -Trigeminal -Abducens -Facial DISORDERS OF THE EYELID • • • • Ptosis: drooping of the eyelid Blepharitis: bilateral inflammation of the lashes/lid margins Hordeolum (stye): infection of the meibomian gland (oil gland on eye lid) -drainage -pain Chalazion- obstruction/blockage of the meibomian gland (usually on upper eyelid) -usually painless -firm lump CONJUNCTIVITIS • Allergic- bilateral, itchy, redness, watery/stringy discharge Tx: cold compress, antihistamines • Bacterial (commonly pink eye) - burning, thick/goopy drainage, starts out unilaterally, most likely spreads bilaterally Tx: antibiotics, eye drops • Viral- watery discharge, unilateral (herpes can cause it) Tx: cold compress, artificial tears DISORDERS OF THE EYE: CORNEA • KERATITIS- inflammation of the cornea HSV keratitis: usually hsv1, vertical transmission of hsv2 is possible during birth -leading cause of corneal scars/ blindness -primary or recurrent Symptoms: -irritation -photophobia -tearing -reduction of vision -corneal opacities Treatment: -topical anti-viral -avoid topical corticosteroids • VARICELLA ZOSTER OPTHALMICUS- shingles on your face -reactivation of latent herpes zoster virus -shingles activated in the trigeminal cranial nerve -prodromal period (fever, headaches, periorbital itching) -acute state: vesicular rash, pustular rash, crusting *Medical emergency*- can cause blindness! Treatment: -high dose oral antivirals GLAUCOMA • • Increase in intraocular pressure from aqueous humor (what makes your eyeball wet/squishy) Temporary or permanent vision impairments 1. Open Angle - Chronically increased IOP without obstruction - Usually asymptomatic - Risks: >40 years old, genetics, black, myopia, DM II, hyperthyroidism, OSA Treatment: -Meds or surgery 2. Closed Angle - anatomic defect with narrowing of anterior chamber angle - acute attack: sudden intermittent ocular pressure, pain, blurred vision, unilateral vision *Medical emergency! * -Risks: older age, Asian or Inuit descent Treatment: -Meds -Laser iridotomy (taking out the iris) REFRACTION AND CATARACTS Refractive Disorders: Hyperopia (farsightedness)- blurred vision to things close up Myopia (nearsightedness)- blurred vision to things far away Astigmatism- cornea is bowed like an almond, you can’t see anything at all, very blurry *can have a combo of these refractive disorders* Tx: -corrective lenses - laser surgery Cataracts: • Lens opacity- interferes with light transmission • Very common in older age, many different causes Clinical manifestations: -bilateral or unilateral -visual acuity decreases -pupil dilation in dim light improves vision -glare in visual field Treatment: -eyeglasses -surgery RETINAL DISORDERS Anatomy: Rods- light detection Cones- color detection Macula- acute & detailed vision Vascular Retinopathies • Microaneurysms in the retinal vasculature Diabetic Retinopathy: most common -non-proliferative: contained to the retina, tiny hemorrhage’s, leads to glare -proliferative: severe, new fragile blood vessels, pulls retina apart, leads to retinal detachment Treatment: early treatment of laser photocoagulation, prevents complications Macular Degeneration • Degenerative changes in macula cause loss of central vision • Common in people >50 yrs • More common in females, white folks, smokers • Will have a blind spot in central vision Treatment: laser therapy, steroid injections Retinoblastoma: intraocular malignancy • Occurs in kids <2 years old • Can be fatal if untreated • Commonly caught by taking a pic of baby with flash- sees a white spot • Causes tearing, redness, cross eyed, vision loss Clinical manifestations: -unilateral leukocoria (white reflex) Treatment: -laser therapy -cryotherapy -chemotherapy -surgical removal of the eye DISORDERS OF EYE MOVEMENT Strabismus • Loss of binocular vision from misalignment of the eyes- caused from abnormalities in neurons or muscles • Can be paralytic or non-paralytic (more common) Types: -esotropia: one eye looks towards the middle -exotropia: one eye looks more laterally -hypertropia: eye rolls upwards -hypotropia: eye rolls downwards Treatment: -surgery (last effort) -glasses, eye patch -eye exercises (first effort) Amblyopia • “lazy eye” • Unilateral decrease in visual activity • Eyes are correctly aligned, but unable to focus together Treatment: -correct underlying cause -alternate eye patching
