Flashcards for USMLE STEP 1 Neurology

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The notochord induces what to differentiate into what?
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Induces overlying ECTODERM to differentiate into NEUROECTODERM and form NUERAL PLATE
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Neural plate then gives rise to?
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Neural tube and neural crest cells
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Notochord becomes what?
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Nucleus pulposus of the intervertebral disks in adults
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Alar Plate
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Dorsal [Sensory] Same orientation as spinal cord
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Basal Plate
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Ventral [Motor] Same orientation as the spinal cord
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How does FGF affect chordin and noggin?
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FGF regulates chordin and noggin to down regulate BMP which leads to neural plate induction
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Three Primary Vesicles
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1. Forebrain [Prosencephalon] 2. Midbrain [Mesencephalon] 3. Hindbrain [Rhombencphaln]
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The Forebrain gives rise to:
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1. Telencephalon [Cerebral hemispheres, lateral ventricles] 2. Diencephalon [Thalamus, Third Ventricle]
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The Midbrain gives rise to:
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1. Mesencephalon [Midbrain, aqueduct]
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The Hindbrain gives rise to:
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1. Metencephalon [Pons, cerebellum, upper part of the fourth ventricle] 2. Myelencephalon [Medulla, Lower part of the fourth ventricle]
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CNS/PNS Origins
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Neuroectoderm = CNS neurons, ependymal cell [Inner lining of ventricles, makes CSF], oligodendrocytes, astrocytes Neural crest cells = PNS, schwann cells Mesoderm = Microglia [Like Macrophages, originate from Mesoderm]
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Neural tube defects
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NEUROPORES fail to fuse [4th week] ? Persistent connection between amniotic cavity and spinal canal Associated with: 1. Low folate levels before conception and during pregnancy 2. ? a-fetoprotein levels [AFP] in amniotic and maternal serum 3. ? AChE in amniotic fluid [Helpful confirmatory test] -- Fetal AChe in CSF transudates across defect into amniotic fluid
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Spina bifida occulta
Spina bifida occulta
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Failure of bony spinal canal to close, NO STRUCTURAL HERNIATION Usually seen at lower vertebral levels DURA INTACT Associated w/ tuft of hair or skin dimple at level of bony defect NORMAL AFP
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Meningocele
Meningocele
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Meninges [BUT NO NEURAL TISSUES] herniates through bony defect
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Meningomyelocele
Meningomyelocele
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Meninges and neural tissue herniate through bony defect Associated w/ Arnold-Chiari Type II Malformation
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Anencephaly
Anencephaly
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Malformation of the ANTERIOR NEURAL TUBE ? 1. No forebrain 2. Open calvarium Clinical Findings: 1. ? a-fetoprotein levels [AFP] 2. Polyhydramnios [No swallowing center in brain] 3. Associated w/ MATERNAL TYPE I DIABETES 4. Maternal folate supplementation ? risk
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Holoprosencephaly
Holoprosencephaly
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Failure of LEFT AND RIGHT HEMISPHERES TO SEPARATE Usually occurs during the 5th and 6th week May be related to mutations in the SONIC HEDGEHOG signaling pathway Moderate form = Cleft lip/palate Severe form = Cyclopia Seen in: 1. PATAU SYNDROME 2. FETAL ALCOHOL SYNDROME
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Chiari Type II Malformation
Chiari Type II Malformation
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Posterior fossa malformation Significant HERNIATION of the CEREBELLAR TONSILS and VERMIS through FORAMEN MAGNUM with AQUEDUCTAL STENOSIS and HYDROCEPHALUS Patients often present w/: 1. Lumbosacral meningomyelocele 2. Paralysis below the defect
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Dandy-Walker Malformation
Dandy-Walker Malformation
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AGENESIS of CEREBELLAR VERMIS with CYSTIC ENLARGEMENT of the 4th ventricle Fills enlarged posterior fossa Associated w/: 1. Hydrocephalus 2. Spina bifida
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Syringomyelia
Syringomyelia
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Cystic cavity [Syrinx] within SPINAL CORD If central canal = Hydromyelia Crossing anterior spinal commissural fibers are typically damaged CAPE-LIKE BILATERAL LOSS OF PAIN and TEMPERATURE in the UPPER EXTREMITIES Fine touch sensation is preserved Associated w/: 1. Arnold Chiari malformation 2. Trauma 3. Tumor Most common C8-T1 [CERVICAL ENLARGEMENT]
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Arnold Chiari Type I Malformation
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CEREBELLAR TONSILLAR ECTOPIA > 3-5 mm Congenital Usually asymptomatic in childhood Manifests w/ HEADACHE and CEREBELLAR SYMPTOMS
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Which arches form the anterior 2/3rds of the tongue
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1st and 2nd brachial arches -- Sensation via CN V -- Taste via CN VII
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Which arches form the posterior 1/3rd of the tongue
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3rd and 4th brachial arches --Sensation and taste via CN IX -- Extreme posterior vagus
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Motor innervation of the tongue
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CN XII [Hypoglossal nerve] to: 1. Hyoglossus = Retracts and depresses tongue 2. Genioglossus = Protrudes tongue 3. Styloglossus = Draws sides of tongue upward to create a trough for swallowing CN X [Vagus] to: 1. Palatoglossus = Elevates posterior tongue during swallowing
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Neurons
Neurons
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Signal-transmitting cells of the nervous system Permanent cells = DO NOT DIVIDE IN ADULTHOOD Signal relaying cells w/ dendrites [Receive input], cell bodies, and axons [Send output] CELL BODIES AND DENDRITES CAN BE SEEN ON NISSLE STAINING [Stains RER] RER is not present in an axon
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Loss of Nissle substance indicates
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Irreversible hypoxic damage = Red neuron
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Injury to axon results in what?
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Wallerian degeneration ? 1. Degeneration distal to the injury 2. Axonal retraction proximally 3. Allows for regeneration of axon [If in PNS]
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Astrocytes
Astrocytes
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Functions: 1. Physical support 2. Repair 3. K+ metabolism 4. Removal of excess neurotransmitter 5. Component of the blood brain barrier via foot process interaction w/ perivascular space 6. Glycogen fuel reserve buffer 7. Reactive gliosis in response to neural injury 8. DERIVED FROM NEUROECTODERM
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Astrocyte Marker
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GFAP
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Microglia
Microglia
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Phagocytic scavenger cells of CNS [Mesodermal, mononuclear origin] Activated in response to tissue damage NOT READILY DISCERNIBLE BY NISSL stain HIV-INFECTED MICROGLIA FUSE TO FORM MULTINUCLEATED GIANT CELLS IN CNS
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Myelin
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? Conduction velocity of signals transmitted down axons ? Saltatory conduction of action potential at nodes of Ranvier [HIGH CONCENTRATIONS of Na+ channels] CNS = Oligodendrocyte [Single sheath, 50 axons] PNS = Schwann cells [Single sheath, single axon] Wraps and insulates axons ? Space constant and ? Conduction velocity
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Schwann cells
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Each Schwann cells myelinates only 1 PNS aon Also promotes axonal regeneration Derived from NEURAL CREST ? Conduction velocity of signals transmitted down axons ? Saltatory conduction of action potential at nodes of Ranvier [HIGH CONCENTRATIONS of Na+ channels] May be INJURED IN GUILLAIN-BARRE SYNDROME
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Acoustic Schwannoma
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Typically located in the internal acoustic meatus [CN VIII] If BILATERAL, strongly associated with NEUROFIBROMATOSIS TYPE 2
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Oligodendroglia
Oligodendroglia
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Myelinated axons of neurons in CNS Each oligodendrocyte can myelinate ~30 axons PREDOMINANT TYPE OF GLIAL CELL IN WHITE MATTER Derived from NEUROECTODERM FRIED EGG appearance histologically Injured in: 1. Multiple Sclerosis 2. Multifocal progressive leukoencephalopathy [PML] 3. Leukodystrophies
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Free nerve endings
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C = Slow, unmyelinated fibers A? = Fast, myelinated fibers Location: All skin, epidermis, some viscera Sense: Pain, temperature
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Meissner Corpuscles
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Large myelinated fibers, adapt quickly Location: Glabrous [Hairless] skin Senses: Dynamic, light touch/position sense
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Pacinian Corpuscles
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Large, myelinated fibers, adapt quickly Location: Deep skin layers, ligaments, joints Senses: Vibration, pressure
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Merkel Discs
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Large, myelinated fibers, adapt quickly Location: Fingertips, superficial skin Senses: Pressure, deep static touch [Shapes, edges], position sense
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Ruffini Corpuscles
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Dendritic endings w/ CAPSULE ADAPT SLOWLY Location: Fingertips and joints Senses: Pressure, slippage of objects along surface of skin, joint angle change
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Endoneurium
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Invests single nerve fiber layers [INFLAMMATORY INFILTRATE IN GUILLAIN BARRE SYNDROME] Inner
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Perineurium
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PERMEABILITY BARRIER Surrounds fascicle of nerve fibers MUST BE REJOINED IN MICROSURGERY FOR LIMB REATTACHMENT Around
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Epineurium
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Dense connective tissue that surrounds entire nerve [Fascicles and blood vessels] Epi = Outer
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Norepinephrine
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? Anxiety ? Depression Location: Locus coeruleus [Pons] = Stress and Panic
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Dopamine
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? Huntington's Disease ? Parkinson's Disease ? Depression Location: Ventral tegmentum and substantia nigra pars compacta [Midbrain]
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5-HT [Serotonin]
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? Anxiety ? Depression Location: Raphe nuclei [Pons, medulla, midbrain]
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ACh
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? Parkinson's Disease ? Alzheimer's Disease ? Huntington's disease Location: Basal nucleus of Meynert
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GABA
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? Anxiety ? Huntington Disease Location: Nucleus Accumbens = Reward center, pleasure, addiction, fear
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Blood brain barrier
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Prevents circulating substances [Bacteria and blood] from reaching the CSF/CNS Formed by 3 structures: 1. Tight Junctions between nonfenestrated capillary endothelial cells 2. Basement membrane 3. Astrocyte foot processes Glucose and amino acids cross slowly by CARRIER-MEDIATED transport mechanisms NONPOLAR/LIPID-Soluble cross rapidly via diffusion
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Specialized brain regions w/ fenestrated capillaries and no blood brain barrier
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Allow molecules in blood to affect brain function 1. Area postrema = Vomiting after chemo 2. OVLT = Osmotic sensing Or neurosecretory products to enter circulation 1. Neurohypophysis = ADH release
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Infarction and/or neoplas destroys what to cause vasogenic edema?
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Endothelial tight junction ? vasogenic edema
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Blood barriers:
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1. Blood brain barrier 2. Blood testis barrier 3. Maternal-fetal blood barrier of placenta
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Hypothalamus
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Wears TAN HATS 1. Thirst and water balance 2. Adenohypophysis control [Regulates anterior pituitary] 3. Neurohypophysis [Releases hormones in hypothalamus] 4. Hunger 5. Autonomic regulation 6. Temperature 7. Sexual urges Inputs [AREAS NOT PROTECTED BY BBB] 1. OVLT = Organum vasculosum of the lamina terminalis -- Senses changes in osmolality 2. Area Postrema [Responds to emetics]
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Vasopressin [ADH] is produced where?
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Supraoptic nucleus of the hypothalamus
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Oxytocin is produced where?
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Paraventricular nucleus
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Lateral Area of the Hypothalamus
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1. Hunger 2. Destruction ? Anorexia, failure to thrive 3. INHIBITED BY LEPTIN If you zap your lateral, you shrink laterally
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Ventromedial Area of the Hypothalamus
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1. Satiety 2. Destruction [Craniopharyngioma] ? Hyperphagia 3. STIMULATED BY LEPTIN
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Anterior Hypothalamus
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Cooling, parasympathetic A/C = Anterior, cooling
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Posterior Hypothalamus
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Heating, sympathetic If you zap your Posterior hypothalamus, you become a Poikilothermic [Cold-blooded, like a snake]
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Suprachiasmatic Nucleus
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CIRCADIAN RHYTHMS You sleep to be charismatic
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Sleep cycle is regulated by what?
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Sleep cycle is regulated by the circadian rhythm [Driven by the suprachiasmatic nucleus of the hypothalamus] SCN is regulated by the environment [Light]
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Circadian rhythms control nocturnal release of what?
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1. ACTH 2. Prolactin 3. Melatonin 4. Norepinephrine SCN ? Norepinephrine release ? Pineal Gland ? Melatonin
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Two Stages of Sleep:
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1. Rapid-eye movement [REM] and non-REM -- Extraocular movements during REM sleep due to activity of the PPRF [Paramedian pontine reticular formation/conjugate gaze center] -- Occurs every 90 minutes, duration ? throughout the night At night, BATS, Drink Blood Awake [Eyes open] = Beta Awake [Eyes closed] = Alpha Non-REM N1 =Theta Non-REM N2 = Spindle and K complex Non-REM N3 = Delta REM = Beta
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What is associated w/ ? REM sleep and delta wave sleep?
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1. Alcohol 2. Benzodiazepines 3. Barbiturates 4. Norepinephrine
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Treatment for bedwetting [Enuresis]
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Oral desmopressin [ADH analog] Preferred over imipramine [Due to adverse effects]
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Treatment for night terrors and sleep-walking
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Benzodiazepine
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Awake [Eye's open]
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Alert, active mental concentration Beta [Highest frequency, lowest amplitude]
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Awake [Eye's closed]
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Alpha waves
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Non-REM Sleep: Stage N1 [5%]
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Light sleep Theta waves
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Non-REM Sleep: Stage N2 [45%]
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Deeper sleep, when bruxism occurs Sleep spindles and K complexes
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Non-REM Sleep: Stage N3 [25%]
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Deepest non-REM sleep [Slow-wave sleep] When: 1. Sleepwalking 2. Night Terrors 3. Bedwetting occurs Delta wave [Lowest frequency, highest amplitude]
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REM Sleep [25%]
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1. LOSS OF MOTOR TONE 2. ? Brain O2 use 3. ? Variable pulse and pressure 4. When dreaming and penile/clitoral tumescence occurs 5. May serve memory processing function Beta wave
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Thalamus
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Major relay for all ascending sensory information [EXCEPT OLFACTION]
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VPL of Thalamus
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1. Spinothalamic and dorsal columns/medial lemniscus INFO: Pain, temperature, touch, vibration, proprioception Destination: 1° Somatosensory cortex
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VPM of Thalamus
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1. Trigeminal and gustatory pathway INFO: Face sensation, taste Destination: 1° somatosensory cortex Notes: Makeup goes on the face
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LGN of Thalamus
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1. CN II INFO: Vision Destination: Calcarine sulcus Lateral = Light
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MGN of Thalamus
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1. Superior olive and inferior colliculus of tectum INFO: Hearing Destination: Auditory cortex of temporal lobe Medial = Music
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VL of Thalamus
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1. Basal ganglia, cerebellum INFO: Motor Destination: Motor cortex
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Limbic System
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Collection of neural structures involved in 1. Emotion 2. Long-term memory 3. Olfactory 4. Behavior modification 5. ANS function STRUCTURES: 1. Hippocampus 2. Amygdala 3. Fornix 4. Mammillary bodies 5. Cingulate gyrus RESPONSIBLE FOR [5 F's]: 1. Feeding 2. Fleeing 3. Fightin 4. Feeling 5. Sex
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Osmotic Demyelination Syndrome [Central pontine myelinolysis]
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Clinical Manifestations: 1. Acute paralysis 2. Dysarthria 3. Dysphagia 4. Diplopia 5. LOC 6. Can cause locked-in syndrome MASSIVE AXONAL DEMYELINATION IN PONTINE WHITE MATTER 2° to osmotic changes [Commonly iatrogenic, can be due to overly rapid correction of hyponatremia] -- Results in cerebral edema/herniation Correcting serum Na+ too fast: 1. From low to high, your pons will die! [Osmotic Demyelination Syndrome] 2. From high to low, your brains will blow! [Cerebral edema/herniation]
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Cerebellum
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Modulates movement, aids in coordination and balance Input: 1. Contralateral cortex via middle cerebellar peduncle 2. Ipsilateral proprIoceptive Information via Inferior cerebellar peduncle from spInal cord Output: 1. Sends information to the contralateral cortex to modulate movement -- Output nerves = Purkinje cells ? Deep nuclei of the cerebellum ? Contralateral cortex via superior cerebellar peduncle Deep nuclei [Lateral to medial] = Don't Eat Greasy Foods 1. Dentate 2. Emboliform 3. Globose 4. Fastigial
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Lateral Lesions to the Cerebellum
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Voluntary movement of extremities PROPENSITY TO FALL TOWARD IPSILATERAL SIDE
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Medial Lesions to the Cerebellum
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Lesions involving midline structures [Vermal cortex, fastigial nuclei] and/or flocculonodular lobe ? 1. Truncal ataxia [Wide-based cerebellar gait] 2. Nystagmus 3. Head tilting 4. Generally, midline lesions result in BILATERAL MOTOR DEFICITS affect AXIAL and PROXIMAL LIMB MUSCULATURE
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Basal Ganglia
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Important in voluntary movements and making postural adjustments Receives cortical input, provides negative feedback to cortex to modulate movement Striatum = Putamen [Motor] + Caudate [Cognitive] Lentiform = Putamen + Globus pallidus D1 receptor = DIrect pathway Indirect = Inhibitory
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Excitatory pathway in the basal ganglia
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Cortical inputs stimulate striatum, stimulating release of GABA [Disinhibits the thalamus via the GPi/SNr] = ? Motion
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Inhibitory pathway in the basal ganglia
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Cortical inputs stimulate the striatum [Disinhibits STN via GPe, STN stimulates GPi/SNr to inhibit thalamus] = ? Motion
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Dopamine binds to what in the basal ganglia
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D1 receptors stimulating the excitatory [Direct pathways] D2 inhibiting the inhibitory pathway ? ? Motion
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Athetosis
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Slow, writhing movements, ESPECIALLY SEEN IN FINGERS Locations of Lesion: Basal ganglia [Huntington] WRITHING, SNAKE-LIKE MOVEMENT
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Chorea
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Sudden, jerky, purposeless movements Location of Lesion: Basal ganglia [Huntington] CHOREA = Dance-like
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Dystonia
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Sudden, involuntary muscle contractions Example: Writer's cramp Blepharospasm [Sustained eye twitch]
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Essential Tremor
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HIGH-FREQUENCY tremor w/ SUSTAINED POSTURE [Outstretched arms], WORSENED w/ MOVEMENT Often familial Patient's often self-mediate w/ EtOH = ? Tremor amplitude Treatment: B-blockers, Primidone
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Hemiballismus
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Sudden, wild flingin of 1 arm +/- IPSILATERAL LEG Location: CONTRALATERAL subthalamic nucleus [Lacunar stroke]
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Intention Tremor
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Slow zigzag motion when pointing/extending toward target Location: Cerebral dysfunction
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Myoclonus
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Sudden, brief, uncontrolled muscle contraction JERK HICCUPS common in metabolic abnormalities such as renal and liver failure
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Resting tremor
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Uncontrolled movement of distal appendages [Most appreciable in hands] Tumor ALLEVIATED BY INTENTIONAL MOVEMENT Example: Parkinson's disease [Pill-rolling tremor]
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Parkinson's Disease
Parkinson's Disease
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Degenerative disorder of CNS associated w/ LEWY BODIES [Composed of a-synuclein = Intracellular eosinophilic inclusions] and LOSS OF DOPAMINERGIC NEURONS [Depigmentation] of substantia nigra pars compacta Parkinson TRAPS your body: 1. Tremor [Pill-rolling tremor at rest 2. Rigidity 3. Akinesia [or bradykinesia] 4. Postural instability 5. Shuffling gait
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Huntington's Disease
Huntington's Disease
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AUTOSOMAL DOMINANT Trinucleotide repeat on chromosome 4 [CAG repeats] -- Caudate loses ACh and GABA Symptoms manifest between ages 20-50 Clinical Manifestations: 1. Choreiform movements 2. Aggression 3. Depression 4. Dementia [Sometimes mistaken for substance abuse] Labs: 1. ? Dopamine 2. ? ACh 3. ? GABA Neuronal cell death via NMDA-R binding and GLUTAMATE TOXICITY ATROPHY OF CAUDATE NUCLEI w/ ex vacuo DILATION OF FRONTAL HORNS
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Aphasia
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Higher-order inability to speak [Language deficit]
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Dysarthria
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Motor inability to speak [Movement deficit]
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Broca's Area
Broca's Area
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NONFLUENT aphasia Intact comprehension with IMPAIRED REPETITION INFERIOR FRONTAL GYRUS OF FRONTAL LOBE
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Wernicke' Area
Wernicke' Area
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FLUENT aphasia with IMPAIRED COMPREHENSION and REPETITION SUPERIOR TEMPORAL GYRUS OF TEMPORAL LOBE Wernick is Wordy but makes no sense
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Conduction Aphasia
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Poor repetition but fluent speech, INTACT COMPREHENSION Caused by damage to the arcuate fasciculus Can't repeat phrases like "NO, IFS, ANDS, or BUTS"
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Global
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NONFLUENT APHASIA WITH IMPAIRED COMPREHENSION Arcuate fasciculus, Broca's, and Wernicke's areas affected
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Transcortical motor
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Nonfluent aphasia with good comprehension and intact repetition
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Transcortical sensory
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Poor comprehension with fluent speech and intact repetition
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Mixed transcortical
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Nonfluent speech, poor comprehension, INTACT REPEPTITON
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Amygdala Lesion [Bilateral]
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Kluver-Bucy Syndrome = Disinhibited behavior [Hyperphagia, hypersexuality, hyperorality] Associated w/ HSV-1
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Frontal lobe Lesion
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Disinhibition and deficits in concentration, orientation, judgement May have a reemergence of primitive reflexes
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Nondominant parietal-temporal cortex Lesion
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HEMISPATIAL NEGLECT [Agnosia of the contralateral side of the world]
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Dominant parietal-temporal cortex Lesion
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1. Agraphia 2. Acalculia 3. Finger agnosia 4. Left-right disorientation GESTERMANN SYNDROME
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Reticular Activating System [Midbrain] Lesion
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Reduced levels of arousal and wakefulness [Coma]
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Mammillary Bodies [Bilateral] Lesion
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Wernicke-Korsakoff Syndrome 1. Confusion 2. Ophthalmoplegia 3. Ataxia 4. Memory loss [Anterograde and retrograde amnesia] 5. Confabulation 6. Personality changes Associated w/ B1 [Thiamine] Deficiency and excessive EtOH use Can be precipitated by GLUCOSE w/out B1 to a B1-deficient patient Wernicke problems in a can of beer: 1. Confusion 2. Ataxia 3. Nystagmus
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Basal Ganglia Lesion
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May result in a tremor at rest, chorea, athetosis Parkinson's Disease Huntington's Disease
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Cerebellar Hemisphere Lesion
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1. Intention tremor 2. Limb ataxia 3. Loss of balance 4. Damage to cerebellum ? Ipsilateral deficits FALL TOWARD THE SIDE OF THE LESION Cerebellar hemispheres are LATERALLY LOCATED and affect the LATERAL LIMBS
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Cerebellar Vermis Lesion
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1. Truncal ataxia 2. Dysarthria Vermis is CENTRALLY LOCATION affects the CENTRAL LIMBs
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Subthalamic Nucleus Lesion
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CONTRALATERAL hemiballismus
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Hippocampus [Bilateral]
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Anterograde amnesia = Inability to make new memories
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Paramedian Pontine Reticular Formation
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Eyes look away from the side of lesion
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Frontal Eye fields
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Eyes look toward the side of the lesion
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Watershed Zones
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Between 1. Anterior/middle cerebral 2. Posterior/Middle cerebral DAMAGE IN SEVERE HYPOTENSION 1. Upper arm/leg weakness 2. Defects in higher-order visual processing
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Homunculus
Homunculus
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Topographic representation of motor and sensory areas in cerebral cortex Distorted image is due to certain body regions being more richly innervated and thus having ? cortical representations
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Regulation of cerebral perfusion
Regulation of cerebral perfusion
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Brain perfusion relies on tight autoregulation Cerebral perfusion is mostly driven by PCO2 [PO2 modulates perfusion in severe hypoxia] Therapeutic hyperventilation [? PCO2], helps ? ICP in cases of 1. Acute cerebral edema [Stroke, trauma] via vasoconstriction Fainting in panic attacks due to ? perfusion
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Hypoxemia and cerebral perfusion
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? cerebral perfusion pressure only when PO2 ; 5o mmHg
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Cerebral perfusion pressure is proportional to what
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Cerebral perfusion pressure is proportional to PCO2 until PCO2 ; 90 mmHg
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Cerebral perfusion and blood pressure
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Cerebral perfusion lies on pressure gradient between mean arterial pressure [MAP] and ICP ? blood pressure or ? ICP ? ? Cerebral perfusion pressure [CPP] CPP = MAP - ICP If CPP = 0, there is not cerebral perfusion ? Brain death
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MCA Lesion
MCA Lesion
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1. Motor cortex = Upper limb and face [Contralateral paralysis] 2. Sensory cortex = Upper limb and face [Contralateral loss of sensation] 3. Temporal lobe = Wernicke Area 4. Frontal lobe = Broca's Area APHASIA IF IN DOMINANT [Usually left hemisphere] HEMINEGLECT IF IN NONDOMINANT [Usually right hemisphere]
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ACA Lesion
ACA Lesion
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1. Motor cortex = Lower limb [Contralateral paralysis] 2. Sensory cortex = Lower limb [Contralateral loss of sensation]
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Lenticulostriate Artery Lesion
Lenticulostriate Artery Lesion
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Striatum [Putamen = Motor, Caudate = Cognitive, Internal capsule Contralateral hemiparesis/hemiplegia COMMON LOCATION OF LACUNAR INFARCTS, 2° to unmanaged hypertension
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Anterior Spinal [ASA]
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1. Lateral corticospinal tract = Contralateral hemiparesis [Upper and lower limbs] 2. Medial lemniscus = ? Contralateral proprioception 3. Caudal medulla = Hypoglossal nerve [Ipsilateral hypoglossal dysfunction = Tongue licks the lesion] STROKE COMMONLY BILATERAL
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Medial Medullary Syndrome
Medial Medullary Syndrome
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Caused by infarct of paramedian branches of ASA and vertebral arteries
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PICA Lesion
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1. Lateral medulla -- Vestibular Nuclei -- Lateral Spinothalamic tract -- Spinal trigeminal nucleus -- Nucleus ambiguus -- Sympathetic fibers -- Inferior cerebellar peduncle [Proprioceptive information] Clinical Manifestations: 1. Vomiting 2. Vertigo 3. Nystagmus 4. ? Pain and temperature sensation from IPSILATERAL FACE and CONTRALATERAL BODY 5. DYSPHAGIA 6. HOARSENESS 7. ? Gag reflex 8. Ipsilateral horner syndrome 9. Ataxia 10. Dysmetria
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Lateral Medullary [Wallenberg Syndrome] Lesion
Lateral Medullary [Wallenberg Syndrome] Lesion
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Nucleus ambiguus effects are SPECIFIC TO PICA lesion "Don't PICA Horse [Hoarseness] that can't eat [Dysphasia]
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ACA
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LATERAL PONS 1. Cranial facial nerve 2. Vestibular nuclei 3. Facial nuclei 4. Spinal trigeminal nuclei 5. Cochlear nuclei 6. Sympathetic fibers MIDDLE AND INFERIOR CEREBELLAR PEDUNCLES 1. Ataxia 2. Dysmetria Clinical Manifestations: 1. Vomiting 2. Vertigo 3. Nystagmus 4. PARALYSIS OF FACE 5. ? Lacrimation, salivation 6. ? Taste from anterior 2/3rd of tongue 7. IPSILATERAL ? pain and temperature 8. CONTRALATERAL ? pain and temperature
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Lateral Pontine Syndrome
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Facial nucleus effects are specific to AICA lesions FACIAL DROOP means AICA's pooped
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PCA
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1. Occipital cortex 2. Visual cortex [CONTRALATERAL hemianopia w/ macular sparing]
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Basilar Artery
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1. Pons 2. Medulla 3. Lower Midbrain 4. Corticospinal and corticobulbar tracts 5. Ocular cranial nerve nuclei 6. Paramedian pontine reticular formation Clinical Manifestation [LOCKED IN SYNDROME]: 1. Preserved consciousness and blinking 2. Quadriplegia 3. Loss of voluntary facial, mouth, and tongue movement 4. Locked-in syndrome
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Anterior Communicating Artery [ACom]
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Most common lesion is ANEURYSM Can lead to STROKE SACCULAR [BERRY] aneurysm can impinge cranial nerves VISUAL FIELD DEFECTS [Due to compression of the optic chiasm] LESIONS ARE TYPICALLY ANEURYSMS, not strokes
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Posterior Communicating Artery [PCom]
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Common site of saccular aneurysm CN III palsy = EYES DOWN AND OUT [Ptosis and mydriasis] LESIONS ARE TYPICALLY ANEURYSMS NOT STROKES
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Saccular [Berry] Aneurysm
Saccular [Berry] Aneurysm
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Occurs at bifurcations in the CIRCLE OF WILLIS Most common site is JUNCTION OF ANTERIOR COMMUNICATING and ANTERIOR CEREBRAL Rupture [Most common complication] ? Subarachnoid hemorrhage *** WORST HEADACHE OF MY LIFE Can also lead to hemorrhagic stroke Can cause: 1. Bitemporal hemianopia via compression of optic chiasm Associated with: 1. ADPKD 2. Ehlers-Danlos Syndrome 3. Advanced age 4. HTN 5. Smoking 6. ? Risk in black
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Charcot-Bouchard Microaneurysm
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Chronic HTN Affects small vessels [Basal ganglia, thalamus]
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Central Post-Stroke Pain Syndrome
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Neuropathic pain due to THALAMIC LESIONS Initial paresthesia followed in WEEKS TO MONTHS by 1. Allodynia [Ordinarily painless stimuli cause pain] 2. Dysesthesia OCCURS IN 10% of STROKE PATIENTS
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Epidural hematoma
Epidural hematoma
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Rupture of MIDDLE MENINGEAL ARTERY [Branch of the MAXILLARY] Often 2° to fracture of temporal bone LUCID INTERVAL Rapid expansion under systemic arterial pressure ? TRANSTENTORIAL herniation, CN III Palsy CT show BICONVEX [Lentiform], Hyperdense blood collection NOT CROSSING SUTURE LINES Can cross FALX and TENTORIUM
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Subdural hematoma
Subdural hematoma
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Rupture of BRIDGING VEINS SLOW VENOUS BLEED [Less pressure =Hematoma develops over time] Seen in: 1. Elderly 2. Alcoholics 3. Blunt trauma 4. SHAKEN BABY SYNDROME [Predisposing factors = Brain atrophy, shaking, whiplash] CRESCENT-SHAPED hemorrhage that CROSSES SUTURE LINES MIDLINE SHIFT Cannot cross falx, tentorium
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Subarachnoid hemorrhage
Subarachnoid hemorrhage
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Rupture of ANEURYSM [Berry/saccular aneurysm in Ehlers-Danlos and ADPKD] or ARTERIOVENOUS MALFORMATION Rapid time course WORST HEADACHE OF MY LIFE Bloody or yellow spinal tap [Xanthochromia] 2-3 days afterward, risk of vasospasm due to blood breakdown [Not visible on CT, treat w/ NIMODIPINE] and rebleed [Visible on CT]
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Intraparenchymal [Hypertensive] Hemorrhage
Intraparenchymal [Hypertensive] Hemorrhage
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Commonly caused by SYSTEMIC HTN Also seen w/ 1. AMYLOID ANGIOPATHY [Recurrent lobar hemorrhagic stroke in elderly 2. Vasculitis 3. Neoplasm Typically occurs in BASAL GANGLIA, INTERNAL CAPSULE [Charcot-Bouchard Aneurysm of lenticulostriate vessels]
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Ischemic Brain Disease/Stroke
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Irreversible damage begins after 5 minutes of hypoxia [Due to glucose dependence] Most vulnerable: 1. Hippocampus 2. Neocortex 3. Cerebellum 4. Watershed areas Ischemic HYPOxia = HYPOcampus most vulnerable
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Stroke Imaging
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Noncontrast CT to exclude hemorrhage [Before tPA can be given] CT detects changes in 6-24 hours Diffusion weighed MRI can detect ischemia w/in 3-30 minutes
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Time since ischemia event and histologic factors
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12-48 hours = Red neurons 48-72 hours = Necrosis + neutrophils 3-5 days = Macrophages [Microglia] 1-2 weeks = Reactive gliosis + vascular proliferation ; 2 weeks = Glial scar
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Hemorrhagic Stroke [15%]
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Intracerebral bleeding, often due to: 1. HTN 2. Anticoagulation 3. Cancer [Abnormal vessels can bleed] May be 2° to ischemic stroke followed by reperfusion [? Vessel fragility] BASAL GANGLIA ARE THE MOST COMMON SITE OF INTRACRANIAL HEMORRHAGE
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Ischemic Stroke [85%]
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Acute blockage of vessels ? Disruption of blood flow and subsequent ischemia ? LIQUEFACTIVE NECROSIS Three Types 1. Thrombotic = Clot forms directly at site of infarction [Commonly MCA] 2. Embolic = Embolus from another part of the body obstructs vessel -- Can affect multiple vascular territories -- Examples: Atrial fibrillation, DVT w/ patent foramen ovale 3. Hypoxic = Hypoperfusion or hypoxemia -- Common during CARDIOVASCULAR SURGERIES -- TENDS TO AFFECT WATERSHED AREAS Treatment: tPA [If w/in 3-4.5 hours of onset and no hemorrhage/risk of hemorrhage] Reduce risk w/ medical therapy: 1. Aspirin 2. Clopidogrel 3. Optimum control of BP, blood sugars, lipids 4. Treat conditions that ? atrial fibrillation
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Transient Ischemic Attack [TIA]
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Brief, reversible episode of focal neurologic dysfunction without acute infarction [- MRI] Majority resolves in ; 15 minutes, deficits due to FOCAL ISCHEMIA
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Dural Venous Sinuses
Dural Venous Sinuses
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Large venous channels that run through the dura Drain blood from cerebral veins and receive CSF from arachnoid granulation EMPTIES INTO JUGULAR VEINS
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Ventricular System
Ventricular System
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Lateral ventricle ? 3rd ventricle via right and left interventricular foramen of Monro 3rd ventricle ? 4th ventricle via cerebral aqueduct [of Sylvius] 4th ventricle ? Subarachnoid space via 1. Formina of Luschka [Lateral] 2. Foramina of Magendie [Medial]
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CSF
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Is made from the ependymal cells of the choroid plexus Reabsorbed in by subarchnoid granulation and then drains into the dural venous sinuses
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Idiopathic Intracranial Hypertension [Pseudotumor cerebri]
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? ICP with no apparent cause on imaging [No hydrocephalus, obstruction of CSF outflow] Patients present w/: 1. Headaches 2. Diplopia [Usually from CN VI palsy] 3. Non mental status alterations 4. Papilledema [Seen on exam] Risk factors: 1. Being a woman of child-bearing years 2. Vitamin A excess 3. DANAZOL [Synthetic steroid suppresses GnRH] Lumbar Puncture reveals ? opening pressure and provides headache relief Treatment: 1. Weight loss 2. Acetazolamide [Carbonic anhydrase inhibitor] 3. Topiramate [Anticonvulsant] 4. Invasive procedures for refractory cases [Repeat lumbar puncture, CSF shunt placement, nerve fenestration surgery]
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Communicating Hydrocephalus
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? CSF absorption by arachnoid granulations ? ? ICP, papilledema, herniation [Arachnoid scarring post-meningitis + chronic subdural hematomas]
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Normal Pressure Hydrocephalus
Normal Pressure Hydrocephalus
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AFFECTS ELDERLY, idiopathic CSF pressure elevated only EPISODICALLY Does not result in ? subarchnoid space volume EXPANSION OF VENTRICLES distorts the fibers of the CORONA RADIATA ? Triad: 1. Urinary Incontinence = Wet 2. Ataxia = Wobbly 3. Cognitive Dysfunction [Sometimes reversible] = Wacky
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Noncommunicating hydrocepahlus
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Caused by STRUCTURAL BLOCKAGE of CSF circulation through the ventricular system [Stenosis of aqueduct of Sylvius, Colloid cyst blocking foramen of Monro]
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Ex vacuo ventriculomegaly
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Appearance of ? CSF on imaging is due to DECREASED BRAIN TISSUE [Neuronal atrophy] 1. Alzheimer's disease 2. Advanced HIV 3. PICK DISEASE ICP is NORMAL, Triad is not seen
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Spinal Nerves
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There are 31 pairs of spinal nerves in total: 1. 8 cervical 2. 12 thoracic 3. 5 Lumbar 4. 5 Sacral 5. 2 coccygeal Nerves C1-C7 exit ABOVE the corresponding vertebrae C8 spinal nerve exits BELOW C7 and above T1 All other spinal nerves exit BELOW
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Vertebral disk herniation
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Nucleus pulposus [Soft central disk] herniates through annulus fibrosus [Outer ring] Usually POSTEROLATERALLY at L4-L5, L5-S1
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Spinal Cord - Lower Extent
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In adults, the spinal cord extends to the lower border of L1-L2 Subarachnoid space [Which contains CSF] extends to lower border of S2 vertebrae Lumbar puncture is usually performed at L3/L4 or L4/L5 [Level of the cauda equina]
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Goal of lumbar puncture
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To obtain a sample of CSF w/out damaging spinal cord To keep the cord alive, go in between L3-L5
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Spinal Cord Mnemonics
Spinal Cord Mnemonics
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Legs [Lumbosacral] are Lateral in Lateral Corticospinal tract Dorsal columns are organized as you are, hands at side, arms out side legs [Cuneatus outside of gracilis]
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Ascending Tracts
Ascending Tracts
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1. Dorsal Column [Pressure, vibration, touch, proprioception] 2. Fasciculus gracilis [Lower body, legs] 3. Fasciculus cuneatus [Upper body, arms] 4. Lateral spinothalamic tract [Pain and temperature] 5. Anterior spinothalamic tract [Touch, pressure] ASCENDING TRACTS SYNAPSE THEN CROSS
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Descending Tracts of Spinal Cord
Descending Tracts of Spinal Cord
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1. Lateral corticospinal tract [Voluntary motor] 2. Anterior corticospinal tract [Voluntary motor]
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Dorsal Column
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Ascending pressure, vibration, fine touch, proprioception 1st Order Neuron = -- Sensory nerve endings ? Cell body in dorsal root ganglion -- Enters spinal cord, SYNAPSES IN IPSILATERAL NUCLEUS CUNEATUS OR GRACILIS ? ascends ipsilaterally in dorsal column 2nd Order Neuron -- Decussates in medulla ? Ascends CONTRALATERALLY in MEDIAL LEMNISCAL ? Synapses in the VPL [Thalamus] 3rd Order Neuron Sensory cortex
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Spinothalamic Tract
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Ascending [Lateral] pain and temperature, [Anterior] Crude touch and pressure 1st Order Neuron = -- Sensory nerve endings [A? and C Fibers]? Cell body in dorsal root ganglion -- Enters spinal cord, SYNAPSES IN IPSILATERAL GRAY MATTER [Spinal cord] ? 2nd Order Neuron -- Decussates at ANTERIOR WHITE COMMISSURE ? Ascends CONTRALATERALLY ? Synapses in the VPL [Thalamus] 3rd Order Neuron Sensory cortex
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Lateral Corticospinal Tract
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Descending, Voluntary movement of contralateral limbs UMN: Cell body in 1° motor cortex ? Descends ipsilaterally through INTERNAL CAPSULE, most fibers decussate at CAUDAL MEDULLA [Pyramidal decussation] ? Descends CONTRALATERALLY 1st Synapse: 1. Cell body of ANTERIOR HORN LMN: Leaves spinal cord Synapse II: NMJ
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UMN Lesions Signs
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Clinical Manifestations: 1. Weakness 2. Hyperreflexia 3. Hypertonia 4. Positive Babinski [Normal in infants] 5. SPASTIC paralysis 6. CLASP KNIFE SPASTICITY Upper MN = Everything up [Tone, DTR, toes]
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LMN Lesion Signs
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Clinical Manifestations: 1. Weakness 2. Hyporeflexia 3. Hypotonia 4. Atrophy 5. Fasciculations [Muscle twitching] 6. FLACCID paralysis Lower MN = Everything lowered [Tone, DTR, toes]
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Werdnig Hoffman Disease
Werdnig Hoffman Disease
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Poliomyelitis and spinal muscular atrophy LMN lesions only [Due to destruction of anterior horns] FLACCID PARALYSIS
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Multiple Sclerosis
Multiple Sclerosis
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Due to demyelination MOSTLY WHITE MATTER OF CERVICAL REGION Random and ASYMMETRIC lesions due to demyelination Clinical Manifestations: 1. Scanning speech 2. Intention tremor 3. Nystagmus
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Amyotrophic Lateral Sclerosis [ALS]
Amyotrophic Lateral Sclerosis [ALS]
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Combined UMN and LMN deficits with NO SENSORY LOSS or oculomotor deficits Can be caused by SUPEROXIDE DISMUTASE 1 defect Clinical Manifestations: 1. Commonly presents as fasciculations with eventual ATROPHY AND WEAKNESS OF HANDS 2. Fatal 3. Riluzole treatment modestly ? survival by ? presynaptic glutamate release Lou Gehrig disease = Give RiLOUzole [Glutamate antagonist]
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Complete Occlusion of Anterior Spinal Artery
Complete Occlusion of Anterior Spinal Artery
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SPARES DORSAL COLUMN and LISSAUER TRACT Upper thoracic ASA territory is WATERSHED AREA Artery of Adamkiewicz supplies ASA below T8
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Tabes Dorsalis
Tabes Dorsalis
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Caused by 3° Syphilis Results from degeneration [Demyelination] of DORSAL COLUMNS and roots ? 1. Impaired sensation and proprioception 2. Progressive sensory ataxia [Inability to sense or feel legs ? poor coordination] Associated w/ 1. Charcot joints 2. Shooting pain 3. Argyll Robertson pupil 4. ABSENCE OF DTRs and + Romberg Sign
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Syringomyelia
Syringomyelia
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Sprinx expands and damages ANTERIOR WHITE COMMISSURE of SPINOTHALAMIC TRACT [2nd order neurons] 1. Bilateral loss of pain and temperature [C8-T1] 2. Seen in Chiari Type I Malformation 3. Can expand and affect other tracts
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Vitamin B12 Deficiency
Vitamin B12 Deficiency
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Subacute Combine Degeneration Demyelination of DORSAL COLUMNS, LATERAL CORTICOSPINAL TRACTS, and SPINOCEREBELLAR TRACTS 1. Gait ataxia 2. Paresthesia 3. Impaired position and vibration sense
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Poliomyelitis
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Caused by poliovirus [Fecal-oral transmission] Replicates in OROPHARYNX and SMALL INTESTINE before spreading via bloodstream to CNS Infection causes destruction of cells in ANTERIOR HORN of spinal cord [LMN] Symptoms [LMN Signs] 1. Weakness 2. Hypotonia 3. Flaccid paralysis 4. Fasciculations 5. Hyporeflexia 6. Muscle atrophy 7. Signs of infection [Malaise, headache, fever, nausea] Findings: 1. CSF w/ ? WBC and slight ? protein [NO CHANGE IN CSF GLUCOSE] 2. Virus recovered from throat or stool
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Spinal Muscular Atrophy [Werdnig-Hoffman Disease]
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Congential degeneration of anterior horns of spinal cord ? LMN FLOPPY BABY w/ marked hypotonia and TONGUE FASCICULATIONS Infantile type has median age of death at 7 months AUTOSOMAL RECESSIVE INHERITANCE
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Friedrich Ataxia
Friedrich Ataxia
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AUTOSOMAL RECESSIVE Trinucleotide repeat [GAA] on chromosome 9 in the gene that encodes FRATAXIN [Iron binding protein] Leads to MITOCHONDRIAL DYSFUNCTION Degeneration of multiple spinal tracts 1. Muscle weakness 2. Loss of DTRs, vibratory sense, proprioception 3. STAGGERING GAIT 4. FREQUENT FALLING 5. Nystagmus 6. Dysarthria 7. Pes Cavus 8. Hammer toes 9. DIABETES MELLITUS, HYPERTROPHIC CARDIOMYOPATHY [Cause of death] 10. Presents in childhood w/ KYPHOSCOLIOSIS
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Brown-Sequard Syndrome
Brown-Sequard Syndrome
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Hemisection of spinal cord Findings: 1. Ipsilateral UMN signs BELOW level of lesion 2. Ipsilateral loss of tactile, vibration, proprioception sense BELOW level of lesion [Due to dorsal column damage] 3. CONTRALATERAL pain and temperature loss below level of lesion [Loss of spinothalamic] 4. Ipsilateral loss of ALL SENSATION AT LEVEL OF LESION 5. Ipsilateral LMN signs IF lesion occurs ABOVE T1 = PATIENT WILL PRESENT WITH HORNER SYNDROME [Due to damage of the oculosympathetic pathway]
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Landmark Dermatomes: C2
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Posterior half of skull [ca]
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Landmark Dermatome: C3
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High turtleneck shirt
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Landmark Dermatome: C4
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Low collar shirt
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Landmark Dermatome: T4
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At the nippel [The Teat pore]
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Landmark Dermatome: T7
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Xiphoid Process
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Landmark Dermatome: T10
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At the umbilicus [Important for early appendicitis pain referral] T10 at the belly butTEN
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Landmark Dermatome: L1
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Inguinal ligament LI =Inguinal Ligament
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Landmark Dermatome: L4
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Included kneecap Down on ALL 4's
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S2, S3, S4
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Erection and sensation of the penis S2, S3, S4 Keeps the penis off the floor
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S1, S2
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Buckle my shoe [Achilles tendon reflex]
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L3. L4
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Kick the door [Patellar reflex]
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C5, C6
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Pick up sticks [Biceps reflex]
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C7, C8
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Lay them straight [Triceps reflex]
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L1, L2
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Testicles move [Cremaster reflex]
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S3, S4
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Winks galore [Anal wink reflex]
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Primitive Reflexes
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CNS reflexes that are present in healthy infant, but are absent in neurologically intact adult Normally disappear w/in the first year of life Primitive reflexes are inhibited by a mature developing frontal lobe May reemerge in an adult following FRONTAL LOBE LESIONS ? Of inhibition of this reflex
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Moro Reflex
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"Hanging on for life" Reflex = Abduct/Extend when startled, then draw together
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Rooting Reflex
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Movement of head toward side of cheek if mouth or cheek is stroked [Nipple seeking]
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Suckling Reflex
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Sucking response when roof of mouth is touched
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Palmar Reflex
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Curling of fingers if palms are stroked
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Plantar Reflex
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DORSIFLEXION of large toe and FANNING OF OTHER TOES upon plantar stimulation Babinski sign - Presence of this reflex in an adult, may signify an UML
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Galant Reflex
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Stroking along one side of the spine while newborn is in a ventral position [Face down] causes LATERAL FLEXION OF LOWER BODY TOWARD STIMULATED SIDE
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CN nuclei that lie medially
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III, IV, VI, XII "Factors of 12, except 1 and 2"
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Dorsal View of Brainstem
Dorsal View of Brainstem
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Pineal Gland = Melatonin secretion, circadian rhythms Superior Colliculi = Conjugate vertical gaze center Inferior Colliculus = Auditory Your EYES are ABOVE your EARS
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Parinaud Syndrome
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Paralysis of the conjugate vertical gaze due to lesion in SUPERIOR COLLICULUS [Stroke, hydrocephalus, pinealoma]
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Cranial Nerve Nuclei
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Located in the tegmentum portion of brain stem [Between dorsal and ventral portions] Midbrain = Nuclei CN III, IV Pons = Nuclei CN V, VI, VII, VIII Medulla = Nuclei CN IX, X, XII Spinal Cord = Nucleus of CN XI Lateral Nuclei = Sensory [aLar plate] --- Sulcus limitans Medial Nuclei = Motor [Basal Plate]
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Cranial Nerve and Vessel Pathways: Cribriform plate
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CN I
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Cranial Nerve and Vessel Pathways: Middle Cranial Fossa
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CN II-IV [Through sphenoid bone] 1. Optic canal = CN II, ophthalmic artery, central retinal vein 2. Superior Orbital Fissure = CN III, IV, V1, VI, ophthalmic vein, sympathetic fibers 3. Foramen Rotundum [CN V2] 4. Foramen Ovale [CN V3] 5. Foramen Spinosum [Middle Meningeal Artery]
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Cranial Nerve and Vessel Pathways: Internal Auditory Meatus
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CN VII, VIII
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Jugular Foramen
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CN IX, X, XI, jugular vein
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Hypoglossal canal
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CN XII
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Foramen Magnum
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Spinal roots of XI, brain stem, vertebral arteries
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Olfactory Nerve
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CN I Smell [ONLY CN WITHOUT THALAMIC RELAY TO CORTEX] Sensory
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Optic Nerve
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CN II Sight Sensory
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Oculomotor
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CN III 1. Eye movement [SR, IR, MR, IO] 2. Pupillary constriction -- Sphincter pupillae = Edinger-Westphal nucleus, muscarinic receptors 3. Accomodation 4. Eyelid opening [Levator palpebrae MOTOR
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Trochlear
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CN IV Eye movement [SO] Motor
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Trigeminal
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CN V 1. Mastication 2. Facial sensation [Ophthalmic, Maxillary, Mandibular divisions 3. Somatosensation from anterior 2/3 of tongue BOTH
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Abducens
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CN VI Eye movement [LR] MOTOR
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Facial
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CN VII 1. Facial movements 2. Taste from anterior 2/3rd of tongue 3. Lacrimation, salivation [Submandibular, Sublingual glands] 4. Eye closing [Orbicularis oculi] 5. Stapedius muscle in ear [Nerve courses through parotid gland but does not innervate it]
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Vestibulocochlear
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CN VIII Hearing and balance Sensory
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Glossopharyngeal
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1. Taste and somatosensation from posterior 2/3 of tongue 2. Swallowing 3. Salivation [Parotid gland] 4. Monitoring carotid body and sinus chemo- and baroreceptors 5. Stylopharyngeus [Elevates pharynx, larynx] BOTH
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Vagus
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CN X 1. Taste from epiglottic region 2. Swallowing 3. Soft palate elevation 4. Midline uvula 5. Talking 6. Coughing 7. Thoracoabdominal viscera 8. Monitoring aortic arch chemo- and baroreceptors BOTH
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Accessory
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CN XI 1. Head turning, shoulder shrugging [SCM, trapezius] MOTOR
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Hypoglossal
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CN XII Tongue movement MOTOR
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Mnemonic for Cranial Nerves
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Some Say Marry Money But My Brother Says Big Brains Matter Most
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Nucleus Solitarius
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Visceral SENSORY information [Taste baroreceptors, gut distension] CN VII, IX, X
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Nucleus aMbiguus
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MOTOR innervation of pharynx, larynx, upper esophagus [Swallowing, palate deviation] IX, X, XI [Cranial portion]
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Dorsal Motor Nucleus
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Sends autonomic [Parasympathetic] fibers to: 1. Heart 2. Lungs 3. Upper GI CN X
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Cranial Nerve Reflex; Corneal
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AFFERENT: V1 [Ophthalmic nasociliary branch] EFFERENT: VII [Temporal branch, orbicularis oculi]
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Cranial Nerve Reflex: Lacrimation
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AFFERENT: V1 [Loss of reflex does not preclude emotional tears] EFFERENT: VII
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Jaw Jerk Reflex
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AFFERENT: V3 [Sensory - Muscle spindle from masseter] EFFERENT: V3 [Motor - Masseter]
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Pupillary Reflex
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AFFERENT: CN II EFFERENT: CN III
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Gag Reflex
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AFFERENT: CN IX EFFERENT: CN X
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CN V Motor Lesion
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Jaw deviates TOWARD SIDE OF LESION, due to unopposed force from opposite pterygoid muscle
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CN X Lesion
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Uvula deviates AWAY FROM SIDE OF LESION Weak side collapses and uvula points away
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CN XI LEsion
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Weakness turning head to CONTRALATERAL side of lesion [SCM] Shoulder droop ON SIDE OF LESION [Trapezius] The left SCM contracts to help turn head to the right
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CN XII Lesion [LMN]
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Tongue deviates TOWARD SIDE of lesion [TONGUE LICKS THE LESION] due to weakened tongue muscles on affected side
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Cavernosus Sinus
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Collection of venous sinuses ON EITHER SIDE OF THE PITUITARY Blood from eye and superficial cortex ? Cavernous sinus ? Internal jugular vein 1. CN III. IV, V1, VI and occasionally V2 plus postganglionic sympathetic pupillary fibers en route to orbit all pass through the cavernous sinus 2. Nerves that control extraocular muscles V1 and V2 CAVERNOUS PORTION OF INTERNAL CAROTID ARTERY is also here
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Cavernous Sinus Syndrome
Cavernous Sinus Syndrome
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Present w/ 1. Variable ophthalmoplegia 2. ? Corneal sensation 3. Horner Syndrome 4. Occasional ? maxillary sensation 5. 2° pituitary mass effect 6. Carotid-cavernous fistula 7. Cavernous sinus thrombosis related to infection CN VI is most susceptible to injury
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Outer Ear
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Visible portion of ear [Pinna], includes auditory canal and eardrum TRANSFERS sound waves via vibration of eardrum
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Middle Ear
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AIR-FILLED SPACE with three bones called the ossicles 1. Malleus 2. Incus 3. Stapedius CONDUCT AND AMPLIFY SOUND from eardrum to inner ear
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Inner Ear
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SNAIL-SHAPED, fluid-filled cochlea Contains basilar membrane that vibrates 2° to sound waves Vibrations are transduced via specialized hair cells ? Auditory nerve signaling ? brain stem Each frequency leads to a vibration at specific locations on the basilar membrane [Tonotopy] 1. Low frequency sounds heard at apex near helicotrema [Wide and flexible] 2. High frequency heard best at base of cochlea [Thin and rigid]
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Conductive Hearing Loss
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Abnormal [Bone ; Air] = Localizes to affected ear
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Sensorineural Hearing Loss
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Normal [Air ; Bone] = Localizes to unaffected ear
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Noise induced
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Damage to STEREOCILIATED CELLS in ORGAN OF CORTI Loss of HIGH-FREQUENCY hearing 1st Sudden extremely loud noises can produce hearing loss due to TYMPANIC MEMBRANE RUPTURE
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Cholesteatoma
Cholesteatoma
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Overgrowth of DESQUAMATED KERATIN DEBRIS within MIDDLE EAR SPACE May erode ossicles, mastoid air cells ? CONDUCTIVE hearing loss
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UMN Facial Lesion
UMN Facial Lesion
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Lesion of the motor cortex or connection between cortex and facial nucleus Contralateral paralysis of lower face FOREHEAD SPARED DUE TO BILATERAL UMN LESION
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LMN Facial Lesion
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IPSILATERAL paralysis of the upper and lower face
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Facial Nerve Palsy
Facial Nerve Palsy
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Complete destruction of the facial nucleus itself or its branchial efferent fibers [Facial nerve proper] Peripheral ipsilateral facial paralysis [ABSENT FOREHEAD CREASES and DROOPING SMILE] with inability to close eye on involved side Can occur idiopathically [Bell's palsy], gradual recover in most cases Can be associated with: 1. Lyme Disease 2. Herpes Simplex [Less common] 3. Herpes Zoster [Ramsey Hunt Syndrome] 4. Sarcoidosis 5. Tumors 6. Diabetes TREAT W/ CORTICOSTEROIDS
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Mastication muscles
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3 muscles close jaw [Masseter, Temporalis, Medial Pterygoid] 1 muscle opens [Lateral Pterygoid] All are innervated by CN V, V3 [Trigeminal nerve] M's Much L Lowers "It takes more to keep your mouth shut"
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Refractive Errors
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Common cause of impaired vision, correctable with glasses
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Hyperopia
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Eye too SHORT for refractive power of cornea and lens ? Light focused BEHIND RETINA
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Myopia
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Eye too LONG for refractive power of cornea and lens ? Light focused in FRONT of the retina
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Astigmatism
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Abnormal CURVATURE of the cornea ? Different refractive power at different axises
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Presbyopia
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AGE-RELATED impaired ACCOMMODATION [Focusing on near objects] possibly due to ? LENS ELASTICITY Often necessitates reading glasses
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Cataract
Cataract
answer
Painless, OFTEN BILATERAL opacification of lens ? 1. ? Vision Risk factors: 1. ? Age 2. Smoking 3. Ethanol 4. Excessive sunlight 5. Prolonged CORTICOSTEROID USE 6. CLASSIC GALACTOSEMIA 7. GALACTOKINASE DEFICIENCY 8. Diabetes mellitus [Sorbitol] 9. Trauma 10. Infection
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Glaucoma
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OPTIC DISK ATROPHY with characteristic CUPPING [Thinning of outer rim of optic nerve head] Usually w/ ? IOP [Intraocular pressure] and PROGRESSIVE PERIPHERAL FIELD LOSS
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Open Angle
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Associated with: 1. ? Age 2. African American 3. Family hx PAINLESS, more common in US Primary = Cause unclear Secondary = BLOCKED TRABECULAR MESHWORK FROM WBCS [uveitis], RBCs [Vitreous hemorrhage], retinal elements [Retinal detachment]
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Closed/Narrow Angle
Closed/Narrow Angle
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Primary = ENLARGEMENT of FORWARD MOVEMENT OF LENS against central iris [Pupil margin] ? 1. OBSTRUCTION OF NORMAL AQUEOUS FLOW THROUGH THE PUPIL 2. Fluid builds up behind iris [Pushing peripheral iris against the cornea] 3. Impedes through through trabecular network Secondary = HYPOXIA from retinal disease [Diabetes mellitus, vein occlusion] -- Induces vasoproliferation in iris that contracts angle
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Chronic Close/Narrow Angle Closure
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Often asymptomatic with damage to optic nerve and peripheral vision
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Acute Closed/Narrow Angle Closure
Acute Closed/Narrow Angle Closure
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TRUE OPHTHALMIC EMERGENCY ? IOP pushes iris forward = Angle closes abruptly 1. Very PAINFUL 2. RED EYE 3. SUDDEN VISION LOSS 4. HALOS around lights 5. Rock-hard eye 6. FRONTAL HEADACHE Do not given epinephrine b/c of its mydriatic effects
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Uveitis
Uveitis
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Inflammation of the uvea [Anterior uveitis, choroiditis/posterior uveitis] May have 1. Hypopyon [Accumulation of pus in the anterior chamber] 2. Conjunctival redness Associated w/ systemic inflammatory disorders: 1. Sarcoidosis 2. RA 3. Juvenile idiopathic arthritis 4. HLA-B27-associated conditions
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Age-Related Macular Degeneration
Age-Related Macular Degeneration
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Degeneration of macula [Central area of retina] Causes: 1. Distortion [Metamorphopsia] and eventual LOSS OF CENTRAL VISION [Scotomas] DRY [NONEXUDATIVE] 1. 80% of cases 2. Deposition of yellowish extracellular material in and beneath Bruch membrane and retinal pigment epithelium [Drusen] w/ gradual ? in vision 3. Prevent w/ MULTIVITAMIN and ANTIOXIDANT SUPPLEMENTS WET [Exudative] 1. 10-15% 2. Rapid vision loss due to bleeding 2° to choroidal neovascularization 3. Treat w/ anti-VEGF injections [Ranibizumab] or laser
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Diabetic Retinopathy
Diabetic Retinopathy
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RETINAL DAMAGE due to chronic hyperglycemia Two Types: 1. NONPROLIFERATIVE --. Damaged capillaries leak blood ? Lipids and fluids seep into retina -- Hemorrhages and macular edema -- Treatment - Blood-sugar control, macular laser 2. PROLIFERATIVE -- Chronic hypoxia ? New blood vessel formation with resultant traction on retina -- Treatment: Peripheral retinal photocoagulation, anti-VEGF [Bevacizumab]
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Retinal Vein Occlusion
Retinal Vein Occlusion
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Blockage of central or branch retinal vein due to COMPRESSION from nearby ARTERIAL ATHEROSCLEROSIS Retinal hemorrhages and venous engorgement Edema in affected areas
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Retinal Detachment
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Separation of NEUROSENSORY layer of retina [Photoreceptor layer w/ RODS AND CONES] from outermost pigmented epithelium [Normally shields excess light, supports retina] Degeneration of photoreceptors ? Vision loss May be 2° to: 1. Retinal breaks 2. Diabetic traction 3. Inflammatory effusions Visualized on fundoscopy by the splaying and paucity of retinal vessels Correlation with cross-sectional optical ultrasound BREAKS MORE COMMON IN PATIENTS W/ HIGH MYOPIA -- Often preceded by posterior vitreous detachment [FLASHES and FLOATERS] and eventual monocular loss of vision LIKE A CURTAIN BEING DRAWN DOWN SURGICAL EMERGENCY
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Central Retinal Artery Occlusion
Central Retinal Artery Occlusion
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Acute, PAINLESS, monocular vision loss Retina CLOUDY with attenuated vessels and CHERRY RED spot on fovea [Center of macula]
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Retinitis Pigmentosa
Retinitis Pigmentosa
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INHERITED RETINAL DEGENERATION Painless, progressive, vision loss beginning w/ NIGHTBLINDNESS [Rods affected first] Bone spicule-shaped deposits around macula
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Retinitis
Retinitis
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Retinal edema and necrosis leading to scar OFTEN VIRAL [CMV, HSV, HZV] Associated w/ IMMUNOSUPPRESSION
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Papilledema
Papilledema
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Optic disk swelling [Usually BILATERAL] due to ? ICP [2° to mass effect] Enlarged BLIND SPOT and ELEVATED OPTIC DISC w/ BLURRED MARGINS
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Miosis
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Constriction, PARASYMPATHETIC 1. 1st neuron = Edinger-Westphal nucleus to ciliary ganglion via CN III 2. 2nd neuron = Short ciliary nerves to pupillary sphincter muscles
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Pupillary Light Reflex
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Light in either retina sends a signal via CN II to pretectal nuclei in MIDBRAIN that activates bilateral EDINGER-WESTPHAL NUCLEI Pupils constrict bilaterally [Consensual reflex] Resul: Illumination in one eye ? Bilateral pupillary constriction
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Mydriasis
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DILATION, SYMPATHETIC 1st neuron: Hypothalamus to ciliospinal center of Budge [C8-T2] 2nd neuron: Exit at T1 to superior cervical ganglion [Travels along the cervical sympathetic chain near lung apex, subclavian vessels] 3rd neuron = Plexus along internal carotid, through cavernous sinus, enter orbit as LONG CILIARY NERVE to pupillary dilator muscles SYMPATHETIC fibers also innervate SMOOTH MUSCLE OF EYELID [Minor retractors] and SWEAT GLANDS OF FOREHEAD AND FACE
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Marcus Gunn Pupil
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AFFERENT pupillary defect Due to OPTIC NERVE DAMAGE or SEVERE RETINAL INJURY ? Bilateral pupillary constriction when light is shone in the eye relative to unaffected Test w/ SWINGING FLASHLIGHT TEST
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Horner Syndrome
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SYMPATHETIC DENERVATION OF FACE 1. Ptosis [Slight drooping of eyelid = Superior tarsal muscle] 2. Anhidrosis [Absence of sweating] and flushing [Rubor] of affected side of face 3. Miosis [Pupil constriction] Associated w/ lesion of spinal cord ABOVE T1 1. Pancoast tumor 2. Brown-Sequard syndrome [Cord hemisection] 3. Late stage syringomyelia ANY INTERRUPTION RESULTS IN HORNERS PAM is Horny
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CN VI
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Lateral Rectus
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CN IV
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Superior oblique LR6SO4 Abducts, intorts, and depresses while abducted
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CN III
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Innervates all eye muscles except [LR, SO]
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Obliques
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go OPPOSITE [Left SO and IO tested with patients looking to the right] IOU: IO tested looking up
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CN III Damage
CN III Damage
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CN III has both motor [Central] and parasympathetic [Peripheral] components Motor output to ocular muscles = Affected primarily by VASCULAR DISEASE [Diabetes mellitus: Glucose ? Sorbitol] -- Due to ? diffusion of oxygen and nutrients to interior fibers from compromised vasculature that resides on outside of nerves DOWN AND OUT Parasympathetic output = Fibers on periphery are 1st affected by compression [PICA aneurysm, uncal herniation] -- Diminished or absent pupillary reflex -- Blown pupil often w/ down and out gaze
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CN IV Damage
CN IV Damage
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Eyes move upward, particularly with CONTRALATERAL gaze HEAD TILT TOWARD SIDE OF LESION Problems going down stairs, may present w/ compensatory head tilt in opposite direction
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CN VI Damage
CN VI Damage
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MEDIALLY directed eye that cannot abduct
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Visual Field Defects: Bitemporal hemianopsia
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Pituitary lesion, chiasm
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Visual Field Defects: Left upper quadrant anopia
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Right temporal lesion, MCA
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Visual Field Defects: Left lower quadrant anopia
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Right parietal lesion, MCA
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Visual Field Defects: Left hemianopia w/ macular sparing
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PCA infarct
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Visual Field Defects: Central scotoma
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Macular degeneration
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Meyer Loop
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Inferior retina, loops around inferior horn of lateral ventricle
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Dorsal Optic Radiation
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Superior retina, takes SHORTEST PATH via INTERNAL CAPSULE
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When an image hits the 1° Visual cortex, it is
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Upside down, left-right reversed
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Internuclear Ophthalmoplegia
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Medial longitudinal fasciculus [MLF] = Pair of tracts that allow for crosstalk between CN VI and CN III nuclei Coordinates both eyes to move in the same horizontal direction HIGHLY MYELINATED [Must communicated quickly to move at the same time] Lesions may be unilateral or bilateral [Seen in MS]
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Lesion in MLF
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Internuclear ophthalmoplegia [INO] results in conjugate horizontal gaze palsy Lack of communication does not stimulate CN III to stimulate medial rectus to fire when CN VI nucleus activates Abducting eye gets NYSTAGMUS [CN VI overfires to stimulate CN III] CONVERGENCE NORMAL Direction term [right INO, left INO] refers to which eye is paralyzed
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Alzheimer Disease
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Most common cause of DEMENTIA in elderly DOWN SYNDROME patients have ? risk of developing Alzheimer's [Typically before age 40] Familial Form [10%] associated with: 1. ApoE2 ? risk 2. ApoE4 ? risk 3. APP, presenilin-1, presenilin-2, = ? Risk of early onset WIDESPREAD CORTICAL ATROPHY -- Narrowing of gyri, widening of sulci -- ? ACh SENILE PLAQUES IN GRAY MATTER = Extracellular B-amyloid core [May cause amyloid angiopathy ? intracranial hemorrhage] AB [Amyloid B] synthesized by cleaving amyloid precursor APP NEUROFIBRILLARY TANGLE = Intracellular, hyperphosphorylated tau protein INSOLUBLE cytoskeletal elements NUMBER OF TANGLES CORRELATED w/ DEGREE OF DEMENTIA
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Dementia
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A ? in cognitive ability, memory, or function with intact conciousness
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Frontotemporal Dementia [Pick Disease]
Frontotemporal Dementia [Pick Disease]
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Clinical Manifestations: 1. Dementia 2. Aphasia 3. Parkinsonian effects 4. Change in personality SPARES PARIETAL LOBE and POSTERIOR 2/3 of superior temporal gyrus PICK BODIES = Silver staining spherical tau protein aggregates
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Lewy Body Dementia
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Initially dementia and hallucinations [haLEWYcinations] followed by parkinsonian features a-synuclein defect [Lewy bodies primarily cortical]
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Creutzfeldt Jakob Disease
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Rapidly progressive [Weeks to months] dementia with MYOCLONUS Spongiform cortex [Associated w/ prions] Prions [PrPc ? PrPsc] B-pleated sheet are resistant to proteases
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Multi-infarct Dementia [Vascular dementia]
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2nd most common cause of DEMENTIA IN ELDERLY
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Other Causes of Dementia
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1. Syphilis 2. HIV [Associated w/ foamy macrophages and multinucleated giant cells, prominent endothelial cells] 3. Vitamins B1, B3, or B12 deficiency 4. Wilson disease 5. Normal pressure hydrocephalus [Wet, Wacky, Wobbly]
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Multiple Sclerosis
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AUTOIMMUNE INFLAMMATION and DEMYELINATION of CNS [Brain and spinal cord] Patients can present with: 1. Optic neuritis [Sudden loss of vision resulting in Marcus Gun pupil] 2. INO 3. Hemiparesis 4. Hemisensory symptoms 5. BLADDER AND BOWEL INCONTINENCE Relapsing and remitting course Most often affects women in their 20-30s Charcot Classic Triad [SIN]: 1. Scanning speech 2. Intention tremor [Also Incontinence and INO] 3. Nystagmus
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Findings in MS
Findings in MS
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1. ? Protein [IgG] in CSF 2. Oligoclonal bands are diagnostic 3. MRI is gold standard 4. PERIVENTRICULAR PLAQUES [Areas of oligodendrocyte loss and reactive gliosis] with destruction of axons 5. Multiple white matter lesions separated in time and space
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Treatment
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Slow progression of disease with DMARDs [B-interferon, natalizumab] Treat acute flares w/ IV STEROID Symptomatic treatment for Neurogenic bladder: 1. Catheterization 2. Muscarinic antagonists SPASTICITY 1. Baclofen 2. GABAB receptor agonist PAIN = OPIOIDS
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Acute Inflammatory Demyelinating Polyradiculopathy
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Common common subtype of GUILLIAN BARRE Autoimmune condition that destroys SCHWANN CELLS ? Inflammation and demyelination of peripheral nerves and motor fibers SYMMETRIC ASCENDING muscle weakness/paralysis beginning in lower extremities FACIAL paralysis [50% of cases] May see autonomic dysregulation: 1. Cardiac irregularities 2. Hypertension or hypotension 3. Sensory abnormalities Almost all patients survive, majority recover completely after weeks to months Findings: 1. ? CSF protein with NORMAL CELL COUNT [Albuminocytologic dissociation] 2. ? Protein may cause papilledema Associated with: 1. Campylobacter jejuni infection [Autoimmune attack of peripheral myelin due to MOLECULAR MIMICRY and STRESS] RESPIRATORY SUPPORT IS CRITICAL UNTIL RECOVERY Treatment: 1. Plasmapheresis 2. IV Immunoglobulins
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Acute Disseminated [Postinfectious] Encephalomyelitis
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Multifocal PERIVENTRICULAR inflammation and demyelination after infection [Measles, VZV] or vaccinations [Rabies, smallpox]
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Charcot-Marie-Tooth
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Hereditary Motor and Sensory Neuropathy [HMSN] Group of progressive disorders related to: 1. Defective production of proteins involved in structure and function of peripheral nerves or the myelin sheath AUTOSOMAL DOMINANT Associated with: 1. Scoliosis 2. Foot deformities [High or flat arches]
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Krabbe Disease
Krabbe Disease
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AUTOSOMAL RECESSIVE LYSOSOMAL STORAGE DISEASE Due to deficiency of GALACTOCEREBROSIDASE Buildup of galactocerebroside and psychosine destroys myelin Findings: 1. Peripheral neuropathy 2. Developmental delay 3. Optic atrophy 4. GLOBOID CELLS
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Metachromatic Leukodystrophy
Metachromatic Leukodystrophy
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AUTOSOMAL RECESSIVE LYSOSOMAL STORAGE DISEASE Most commonly due to ARYLSULFATASE A deficiency Buildup of sulfatides ? Impaired production and destruction of myelin sheath Findings: 1. Central and peripheral demyelination 2. Ataxia 3. Dementia
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Progressive Multifocal Leukoencephalopathy
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Demyelination of CNS due to DESTRUCTION OF OLIGODENDROCYTES Associated w/ JC virus Seen in 2-4% of AIDS patients [Reactivation of latent virus] Rapidly progressive, usually fatal ? Risk associated w/ Natalizumab, Rituximab
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Adrenoleukodystrophy
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X-LINKED genetic disorder Typically affecting MALES Disrupts metabolism of VERY LONG CHAIN FATTY ACIDS ? 1. Excessive build-up in CNS, adrenal glands, testes 2. Progressive disease that can lead to long-term coma/death 3. ADRENAL GLAND CRISIS
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Seizures
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Characterized by synchronized, high-frequency neuronal firing. Variety of forms
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Partial [Focal] Seizure
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AFFECTS SINGLE AREA OF BRAIN Most commonly in MEDIAL TEMPORAL LOBE Often preceded by seizure AURA, can secondarily generalize
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Simple Partial Seizure
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Consciousness intact Motor, sensory, autonomic, psychic
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Complex Partial Seizure
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Impaired Consciousness
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Generalized Absence Seizure [Petit mal]
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3 Hz, NO POSTICTAL confusion, blank stare
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Generalized Myoclonic Seizure
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Quick, repetitive jerks
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Generalized Tonic-Clonic Seizure [Grand Mal]
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Alternating stiffening and movement
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Generalized Tonic Seizure
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Stiffening
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Generalized Atonic Seizures
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Drop seizures [Falls to floor], commonly mistaken for fainting Typically starts in childhood [6 months - 5 years]
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Epilepsy
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Disorder of recurrent seizures [Febrile seizures are not epilepsy]
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Status epilepticus
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Continuous or recurring seizures that may result in brain injury Variably defined as > 10-30 minutes
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Causes of Seizure by Age 1. Children 2. Adults 3. Elderly
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CHILDREN 1. Genetic 2. Infection [Febrile] 3. Trauma 4. Congenital 5. Metabolic ADULTS 1. Tumor 2. Trauma 3. Stroke 4. Infarction ELDERLY 1. Stroke 2. Tumor 3. Trauma 4. Metabolic 5. Infection
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Cluster Headache
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Unilateral Duration: 15 min- 3 hours, repetitive REPETITIVE BRIEF HEADACHES Excruciating, PERIORBITAL pain w/ LACRIMATION and RHINORRHEA May induce horner's syndrome More common in MALES Treatment: 100% O2
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Tension Headache
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BILATERAL Duration: ; 30 minutes [Typically 4-6 hours], Constant STEADY PAIN Treatment: Analgesics, NSAIDs, Acetaminophen, Amitriptyline for chronic pain
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Migraine
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Unilateral Duration: 4-72 hours Clinical Manifestation [POUND] 1. Pounding/Pulsatile 2. One-day duration 3. Unilateral 4. Nausea and vomiting 5. Disabling 6. PHOTOPHOBIA or PHONOPHOBIA 7. May have aura Due to irritation of CN V, meninges, blood vessels [Release of substance P, calcitonin gene-related peptide, vasoactive peptide] Treatment: 1. Abortive therapies [Triptans, NSAIDs] 2. Prophylaxis [Propranolol, Topiramate, Ca2+ channel blockers]
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Other causes of headaches:
answer
1. Subarachnoid Hemorrhage 2. Meningitis 3. Hydrocephalus 4. Neoplasia 5. Arteritis
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Trigeminal Neuralgia
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REPETITIVE SHOOTING PAIN in the distribution of CN V Typically lasts for ; 1 minute
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Vertigo
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Sensation of spinning while actually stationary Subtype of dizziness, but distinct from light-headedness
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Peripheral vertigo
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MORE COMMON INNER EAR ETIOLOGY 1. Semicircular debris 2. Vestibular nerve infection 3. Meniere Disease Positional testing ? DELAYED HORIZONTAL NYSTAGMUS
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Central vertigo
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BRAIN STEM or CEREBELLAR lesion STROKE affecting VESTIBULAR or POSTERIOR FOSSA TUMOR Findings: 1. Direction change of nystagmus 2. Skew deviation 3. Diplopia 4. Dysmetria Positional testing ? Immediate nystagmus in any direction, may change directions FOCAL NEUROLOGIC FINDINGS
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Sturge-Weber Syndrome
Sturge-Weber Syndrome
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Congenital, non-inherited [Somatic] developmental anomaly of NEURAL CREST DERIVATIVES [Mesoderm/Ectoderm] 1. Due to activating mutation of GNAQ 2. Affects small [Capillary-sized] blood vessels ? Port wine stain of face 2. Nevus flammeus = Non-neoplastic birthmark in CN V1/V2 distribution 3. Ipsilateral leptomeningeal angioma 4. Seizures/epilepsy 5. Intellectual disability 6. Episcleral hemangioma 7. ? IOP ? Early onset GLAUCOMA STURGE-Weber 1. Sporadic, port-wine stain 2. Tram track calcifications 3. Unilateral 4. Retardation [Intellectual disability] 5. Glaucoma, GNAQ 6. Epilepsy
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Tuberous Sclerosis
Tuberous Sclerosis
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HAMARTOMAS 1. Hamartomas in CNS 2. Angiofibromas 3. MITRAL REGURGITATION 4. Ash-leaf spots 5. Cardiac RHABDOMYOMA 6. Autosomal dOminant 7. Mental retardation [Intellectual disability] 8. Renal Angiomyolipoma 9. Seizures, Shagreen patches ? Incidence in subependymal astrocytomas and ungual fibromas
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Neurofibromatosis Type I [Von Recklinghausen Disease]
Neurofibromatosis Type I [Von Recklinghausen Disease]
answer
1. Cafe-au-lait spots 2. Lisch nodules [Pigmented iris hamartomas] 3. Cutaneous neurofibromas 4. Optic gliomas 5. Pheochromocytomas Mutated NF1 TUMOR SUPPRESSOR GENE [Neurofibromin = Negative regulator of RAS] on chromosome 17 Skin tumors of NF-1 are derived from neural crest cells
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von Hippel-Lindau Disease
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X-Linked Recessive HEMANGIOBLASTOMAS [High vascularity w/ HYPERCHROMATIC NUCLEI] in: 1. Retina 2. Brainstem 3. Cerebellum 4. Spine Angiomatosis = Cavernous hemangiomas in skin, mucosa, organs BILATERAL RENAL CELL CARCINOMAS Pheochromocytomas
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Glioblastoma Multiforme [Grade IV Astrocytoma]
Glioblastoma Multiforme [Grade IV Astrocytoma]
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Common, HIGHLY MALIGNANT 1° brain tumor with ~ 1 year survival Found in CEREBRAL HEMISPHERES CAN CROSS CORPUS CALLOSUM [Butterfly glioma] Stain astrocytes for GFAP Histology: 1. Pseudopalisading 2. Pleomorphic tumor cells 3. Border CENTRAL AREAS OF NECROSIS and hemorrhage
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Meningioma
Meningioma
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Common, typically BENIGN 1° brain tumor Most often occurs in CONVEXITIES of hemispheres near surfaces of the brain and PARASAGITTAL SINUS Arises from ARACHNOID CELLs EXTRA-AXIAL [External to brain parenchyma] May have a DURAL ATTACHMENT [Tail] Often asymptomatic, may present w/: 1. Seizures 2. Focal neurologic signs Treatment = Resection or radiosurgery Histology: 1. SPINDLE cells concentrically arranged in WHORLED PATTERN 2. PSAMMOMA BODIES [Laminated calcifications]
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Hemangioblastoma
Hemangioblastoma
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Most often CEREBELLAR Associated w/ von-Hippel-Lindau syndrome Found with RETINAL ANGIOMAS Can produce ERYTHROPOIETIN ? 2° Polycythemia Histology: 1. Closely arranged, thin-walled capillaries with minimally intervening parenchyma
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Schwannoma
Schwannoma
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Classically at CEREBELLOPONTINE ANGLE, but can be anywhere along peripheral nerve Schwann cell origin [S-100] Often LOCALIZED TO CN VIII ? Vestibular schwannoma Resectable or treatable w/ stereotactic radiosurgery BILATERAL VESTIBULAR SCHWANNOMA = NF2
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Oligodendroglioma
Oligodendroglioma
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Relatively rare, slow growing Most often in FRONTAL LOBES CHICKEN-WIRE capillary pattern Histology: 1. Oligodendrocytes = FRIED EGG cells [Round nuclei with clear cytoplasm] OFTEN CALCIFIED
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Pituitary Adenoma
Pituitary Adenoma
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Most commonly prolactinoma Bitemporal hemianopia [Normal visual fields above] due to pressure on the Optic Chiasm
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Pilocytic [Low-Grade] Astrocytoma
Pilocytic [Low-Grade] Astrocytoma
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Usually well-circumscribed In CHILDREN Found in the POSTERIOR FOSSA [Cerebellum] May be supratentorial GFAP + Benign, good prognosis ROSENTHAL FIBERS = Eosinophilic, corkscrew fibers CYSTIC + SOLID
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Medulloblastoma
Medulloblastoma
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HIGHLY MALIGNANT CEREBELLAR tumor A form of primitive NEUROECTODERM Can compress 4th ventricle causing hydrocephalus Can send DROP METASTASES to spinal cord HOMER-WRIGHT ROSETTE Solid, SMALL BLUE CELLS
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Ependymoma
Ependymoma
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Ependymal cells most commonly found in the 4th ventricle Can cause hydrocephalus POOR PROGNOSIS Characteristic perivascular rosettes Rod-Shaped Blepharoplasts [Basal ciliary bodies] found near nucleus
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Craniopharyngioma
Craniopharyngioma
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Benign CHILDHOOD tumor Can cause bitemporal hemianopia MOST COMMON CHILDHOOD SUPRATENTORIAL tumor Derived from remnants of Rathke's pouch Calcification common
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Cingulate [Subfalcine] Herniation under Falx Cerebri
Cingulate [Subfalcine] Herniation under Falx Cerebri
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Can compress anterior cerebral artery
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Downward Transtentorial [Central] Herniation
Downward Transtentorial [Central] Herniation
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Caudal displacement of brain stem ? Rupture of PARAMEDIAN BASILAR ARTERY BRANCHES ? Duret's hemorrahges
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Uncal Herniation
Uncal Herniation
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Uncus = Medial Temporal lobe 1. Compresses Ipsilateral CN III [Blown pupil, down and out] 2. Ipsilateral PCA [Contralateral homonymous hemianopia] 3. Contralateral Crus cerebri at the Kernohan notch [Ipsilateral paresis = False localization sign]
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Cerebellar Tonsillar Herniation into the Foramen Magnum
Cerebellar Tonsillar Herniation into the Foramen Magnum
answer
Coma and death result when the herniations compress the brain stem
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Glaucoma Drugs
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? IOP via ? Amount of aqueous humor [Inhibits synthesis/secretion of ? drainage]
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a-agonists
answer
Drugs: Epinephrine [a1], Brimonidine [a2] MOA: 1. ? Aqueous humor synthesis via vasoconstriction 2. ? Aqueous humor synthesis Side Effects: 1. Mydriasis [a1] = Do not use in CLOSED-ANGLE glaucoma 2. Blurry vision 3. Ocular hyperemia 4. Foreign body sensation 5. Ocular allergic rxns 6. Ocular pruritus
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B-blockers
answer
Timolol, Betaxolol, Carteolol MOA: ? Aqueous humor synthesis
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Acetazolamide
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MOA: ? Aqueous humor synthesis via inhibition of carbonic anhydrase
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Direct Cholinomimetics [Pilocarpine, Carbachol] Indirect Cholinomimetics [Physostigmine, Echothiophate]
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MOA: ? Outflow of aqueous humor via CONTRACTION OF CILIARY MUSCLE and OPENING OF TRABECULAR NETWORK Use pilocarpine in emergencies = Very effective at opening meshwork into canal of Schlemm Adverse Effects: Miosis and cytoplasm [Contraction of ciliary muscle]
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Latanoprost [PGF2a]
answer
? Outflow of aqueous humor Adverse Effect: Darkens color of iris [Browning]
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Opioid Analgesics
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Drugs: Morphine, Fentanyl, Codeine, Loperamide, Methadone, Meperidine, Dextromethorphan, Diphenoxylate, Pentazocine MOA: Acts as agonists at opioid receptors [? = Morphine, ? = Enkephalin, ? = dynorphin] to modulate synaptic transmission Opens K+ channels, closes Ca2+ channels ? ? Synaptic transmission Inhibits release of 1. ACh 2. Norepinephrine 3. 5-HT 4. Glutamate 5. Substance P
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Clinical Use of Opioids
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1. Pain 2. Cough suppression [Dextromethorphan] 3. Diarrhea [Loperamide, diphenoxylate] 4. Acute pulmonary edema 5. Maintenance programs for heroin addicts [Methadone, buprenorphine + Naloxone]
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Toxicity of Opioids
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1. Addiction 2. Respiratory depression 3. Constipation 4. Miosis [Pinpoint pupils] 5. Addictive 6. CNS depression w/ other drugs TOLERANCE DOES NOT DEVELOP TO MIOSIS AND CONSTIPATION Toxicity treated w/ Naloxone or Naltrexone [Opioid receptor antagonist]
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Butorphanol
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MOA: ?-opioid receptor agonist and ? partial agonist Produces analgesia Clinical Use: 1. Severe pain [Migraine, labor] 2. Causes less respiratory depression than full opioid agonists Adverse Effects: 1. Can cause opioid withdrawal symptoms if a patient is also taking full opioid agonist [Competition for opioid receptors] 2. Overdose not easily reversed with naloxone
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Tramadol
answer
MOA: Very weak opioid agonist Also inhibits 5-HT and Norepi REUPTAKE [Works on multiple neurotransmitters -Tram it all w/ TRAMADOL] Clinical Use: 1. Chronic pain Toxicity: 1. Similar to opioid 2. DECREASES SEIZURE THRESHOLD 3. SEROTONIN SYNDROME
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Ethosuximide [Epilepsy]
answer
ABSENCE SEIZURES MOA: Blocks thalamic T-Type Ca2+ Channels Side Effects [EFGHIJ]: 1. Fatigue 2. GI upset 3. Headache 4. Itching 5. SJS
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Benzodiazepines [Epilepsy]
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FIRST LINE TREATMENT IN STATUS EPILEPTICUS 1. Diazepam, Lorazepam, Clonazepam MOA: ? GABAA action Side effects 1. Sedation 2. Tolerance 3. Dependence 4. Respiratory depression and hypotension
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Phenytoin, Fosphenytoin [Parenteral]
answer
MOA: ? Na channel inactivation, zero order kinetics Side Effects: 1. Nystagmus, diplopia 2. Ataxia 3. Sedation 4. GINGIVAL HYPERPLASIA 5. Hirsutism 6. Peripheral neuropathy 5. MEGALOBLASTIC ANEMIA 6. Teratogenic [Fetal hydantoin syndrome] 7. SJS 8. Osteopenia
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Carbamazepine [Epileptic]
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1st LINE FOR TRIGEMINAL NEURALGIA MOA: ? Na channel inactivation, potentiates K+ efflux Side Effects: 1. Diplopia 2. Ataxia 3. Blood dyscrasias [AGRANULOCYTOSIS, APLASTIC ANEMIA] 4. Liver toxicity 5. SIADH 7. SJS 8. Osteopenia
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Valproic acid [Epileptic]
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USED FOR MYOCLONIC SEIZURES, BIPOLAR DISORDER MOA: ? Na channel inactivation, ? GABA concentration by inhibiting GABA transaminase Side Effects: 1. FATAL hepatotoxicity [Check LFTs] 2. Neural tube defects [Spina bifida] 3. Tremor 4. Weight gain 5. Contraindicated in pregnancy
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Gabapentin [Epileptic]
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MOA: Primarily inhibits high-voltage-activated Ca2+ channels, designed as GABA analog Side Effects: 1. Sedation 2. Ataxia
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Phenobarbital [Epileptic]
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FIRST LINE IN NEONATES MOA: ? GABAA action Side Effects: 1. Sedation 2. Tolerance 3. Dependence 4. Cardiorespiratory depression
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Topiramate [Epileptic]
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Also used for migraine prevention MOA: Blocks Na channels, ? GABA action Side Effects: 1. Sedation 2. Mental dulling 3. Kidney stones 4. Weight loss
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Lamotrigine [Epileptic]
answer
MOA: Blocks voltage-gated Na channels, blocks glutamate release Side Effects: 1. SJS
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Levetiracetam [Epileptic]
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MOA: Unknown, may modulate GABA and glutamate release
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Tiagabine [Epileptic]
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MOA: ? GABA by inhibiting reuptake
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Vigabatrin [Epileptic]
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MOA: ? GABA by irreversibly inhibiting GABA Transaminase
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SJS
answer
Prodrome of fever, malaise followed by rapid onset of erythematous/pruritic macules [Oral, ocular, genital]. Skin lesions progress to epidermal necrosis and sloughing
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Barbiturates
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Drugs: Phenobarbital, Pentobarbital, Thiopental, Secobarbital MOA: Facilitate GABAA action by ? DURATION of Cl- channel opening ? ? Neuron firing CONTRAINDICATED IN PORPHYRIA Clinical Use: 1. Sedative for anxiety 2. Seizures 3. Insomnia 4. Induction of anesthesia [Thiopental] Adverse Effects: 1. Respiratory and cardiovascular depression [Can be fatal] 2. CNS depression [Can be exacerbated by EtOH use] 3. Dependence 4. Drug interactions [Induces CYP450] Treatment of OD = Supportive [Assist respirations, maintain BP]
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Benzodiazepines
answer
Drugs: Diazepam, lorazepam [Anticonvulsants], Triazolam [Insomnia], Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam MOA: Facilitate GABAA action by ? FREQUENCY of Cl- channel opening ? REM sleep Most have long half-lives and active metabolites, exceptions [ATOM = High addictive potential]: 1. Alprazolam 2. Triazolam 3. Oxazepam 4. Midazolam
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What binds GABAA
answer
Benzos, Barbs, EtOH
question
Clinical Use of Benzodiazepines
answer
1. Anxiety 2. Spasticity 3. Status epilepticus [Diazepam, Lorazepam] 4. Detoxification [Especially alcohol withdrawal] 5. Night terrors, sleepwalking 6. General anesthetic [Amnesia, muscle relaxant] 7. Hypnotic [Insomnia]
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Benzodiazepine Toxicity
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1. Dependence 2. Addictive CNS depression effects w/ alcohol 3. Less risk of respiratory depression and coma than with barbiturates Treat overdose with: Flumazenil [Competitive antagonist at GABA benzodiazepine receptor]
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Nonbenzodiazepine Hypnotics
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Drugs: Zolpidem, Zaleplon, eZopiclone [All ZZZs put you to sleep] MOA: Act via the BZI subtype of GABA receptor Effects reversed by Flumazenil Clinical use: 1. Insomnia Adverse Effects: 1. Ataxia 2. Headaches 3. Confusion Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and a few amnestic effects ? Dependence risk compared to benzos
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Anesthetics - General Principles
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1. CNS drugs must be lipid soluble [Cross the BBB] or be actively transported 2. Drugs w/ ? solubility in blood = Rapid induction and recovery time 3. Drugs w/ ? solubility in lipid = ? Potency = 1/MAC
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Minimal Alveolar Concentration [MAC]
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Inhaled anesthetic = Required to prevent 50% of subjects from moving in response to noxious stimulant [skin incision] Examples: Nitric oxide [N2O] has ? solubility in blood and ? lipid solubility = Fast induction and low potency Halothane = ? Lipid and blood solubility, high potency and slow induction
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Inhaled anesthetics
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Drugs: Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O Effects: 1. Myocardial depression 2. Respiratory depression 3. Nausea/emesis 4. ? Cerebral blood flow [? Cerebral metabolic demand] Adverse Effects: 1. Hepatotoxicity [Halothane] 2. Nephrotoxicity [Methoxyflurane] 3. Proconvulsant [Enflurane] 34. Expansion of trapped gas in the body [N2O]
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Malignant Hyperthermia
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Rare. life-threatening hereditary condition in which inhaled anesthetics [N2O] and succinylcholine induce FEVER and SEVERE MUSCLE CONTRACTIONS Treatment = Dantrolene
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Intravenous Anesthetics: Barbiturates
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Thiopental HIGH POTENCY, HIGH SOLUBILITY Rapid re-entry into brain Used for induction of anesthesia and short surgical procedures Effect terminated by rapid redistribution into tissue [skeletal muscle] and fat ? Cerebral flow
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Intravenous Anesthetics: Benzodiazepines
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Midazolam most commonly used for ENDOSCOPY Used adjunctively with gaseous anesthetics and narcotics May cause SEVERE POST-OPERATIVE RESPIRATORY DEPRESSION ANTEROGRADE AMNESIA ? BlP Treat OD: Flumazenil
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Arylcyclohexylamines [Ketamine]
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PCP analogs that act as dissociated anesthetics Block NMDA receptors CARDIOVASCULAR STIMULANTS Cause: 1. Disorientation 2. Hallucination 3. Bad dream 4. ? Cerebral blood flow
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Opioids
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Morphine, fentanyl Used with other CNS depressants during general anesthesia
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Propofol
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Used for sedation in the ICU, rapid anesthesia induction, short procedures LESS POST-OPERATIVE NAUSEA than thiopental Potentiates GABAA
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Local Anesthetics
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Esters = Procaine, cocaine, tetracaine Amides = Lidocaine, Mepivacaine, Bupivacaine [Amides have two I's] MOA: Binds Na+ channels by binding to specific receptor on inner portion of channel Preferentially binds to ACTIVATED NA+ CHANNELS [Most effective in firing neurons] 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form
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Principle of Local Anesthetics
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Can be given with vasoconstrictors [Usually epinephrine] to enhance local action ? ? Bleeding, ? anesthesia by ? systemic concentration In infected [Acidic] tissue ALKALINE anesthetics are CHARGED and CANNOT PENETRATE MEMBRANE effectively ? Need more anesthetic
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Order of Nerve Blockade for Local Anesthetics
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Small-diameter > Large Diameter Myelinated fibers > Unmyelinated fibers SIZE PREDOMINATES OVER MYELINATION such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers Order of Loss: 1. Pain 2. Temperature 3. Touch 4. Pressure
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Toxicity of Local Anesthetics
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1. CNS excitation 2. Severe cardiovascular toxicity [Bupivacaine] 3. Hypertension/Hypotension 4. Arrhythmias [Cocaine] 5. Methemoglobinemia [Benzocaine]
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Neuromuscular Blocking Drugs
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Muscle paralysis in surgery or mechanical ventilation Selective for motor [vs. autonomic] nicotinic receptors
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Depolarizing Neuromuscular Blocking Agents
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Drug: Succinylcholine MOA: Strong ACh receptor agonist, produces SUSTAINED DEPOLARIZATION and PREVENTS MUSCLE CONTRACTION Reversal of Blockade: 1. Phase I [Prolonge depolarization] = No antidote -- Block potentiated by cholinesterase inhibitors 2. Phase II [Repolarized but blocked] = ACh receptors are available but desensitized Antidote = Cholinesterase Inhibitors Complications: 1. Hypercalcemia 2. Hyperkalemia 3. Malignant hyperthermia
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Nondepolarizing Neuromuscular Blocking Agents
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Drugs: Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium MOA: Competitive antagonist, compete w/ ACh receptors Reversal of blockade: 1. NEOSTIGMINE [Must be given with atropine to prevent muscarinic effects = Bradycardia] 2. Edrophonium 3. Other cholinesterase inhibitors
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Dantrolene
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MOA: Prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle Clinical Use: 1. Malignant hyperthermia 2. Neuroleptic malignant syndrome [Toxicity of antipsychotic drugs]
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Baclofen
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MOA: Inhibits GABAB receptors at spinal cord, inducing skeletal muscle relaxation Clinical Use: Muscle spasms
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Cyclobenzaprine
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MOA: Centrally acting skeletal muscle relaxant Structurally related to TCAs Similar anticholinergic side effects Clinical Use: Muscle spasms
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Dopamine Agonists
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Ergot = Bromocriptine Non-ergot [Preferred] = Pramipexole, Ropinirole
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? Dopamine Availability
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Amantadine ? Dopamine release and ? Dopamine Reuptake Also used as an antiviral against influenza A and rubella Toxicity 1. Ataxia 2. Livedo Reticularis
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? L-dopa availability
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Agents prevent peripheral [pre-BBB] L-dopa degradation ? ? L-dopa entering CNS ? ? Central L-dopa available for conversion to dopamine Levodopa [L-dopa]/Carbidopa = Carbidopa block peripheral conversion of L-Dopa to dopamine by inhibiting DOPA decarboxylase Also reduces side effects of peripheral L-dopa conversion into dopamine [Nausea and Vomiting] Entacapone, Tolcapone = Prevent peripheral L-dopa degradation to 3-O-methyldopa [3-OMD] by inhibiting COMT
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Prevent dopamine breakdown
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Agents act centrally [post-BBB] to block break down of dopamine ? ? Available Dopamine 1. Selegiline = Blocks conversion of dopamine into 3-MT by selectively inhibiting MOA-B 2. Tolcapone = Blocks conversion of dopamine by DOPAC by inhibiting central COMT
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Curb Excess Cholinergic Activity
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Benztropine [Antimuscarinic, improves TREMOR and RIGIDITY, but has little effect on BRADYKINESIA]
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L-Dopa
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Drug: Levodopa/Carbidopa MOA: ? LEvel of dopamine in the brain Unlike dopamine, L-dopa can cross the BBB and is converted by dopa decarboxylase in the CNS to dopamine Carbidopa [Peripheral dopa decarboxylase inhibitor] is given with L-dopa to ? the bioavailability of L-dopa in the brain and limit peripheral side effects Clinical Use: Parkinson's Disease Adverse Effects: Arrhythmias from ? peripheral formation of catecholamines Long-term use can lead to dyskinesia following administration [on-off phenomenon] Akinesia between doses
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Selegiline
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Selectively inhibits MOA-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, ? availability of dopamine Clinical Use: Adjunctive agent to L-dopa in treatment of PArkinson Disease Toxicity: May enhance adverse effects of L-dopa
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Alzheimer drugs [Memantine]
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Drug: Memantine MOA: NMDA receptor antagonist, helps prevent excitotoxicity [Mediated by Ca2+] Toxicity: Dizziness, confusion, hallucination
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Alzheimer drugs [Donepezil, Galantamine, Rivastigmine, Tacrine]
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MOA: AChE inhibitors Toxicity: Nausea, dizziness, insomnia
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Huntington Disease Drugs
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Neurotransmitter changes in Huntington Disease [? GABA, ? ACh, ? Dopamine] Treatments: 1. Tetrabenazine and Reserpine = Inhibit vesicular monoamine transporter [VMAT] -- Limits DOPAMINE VESICLE PACKAGE AND RELEASE 2. Haloperidol = D2 receptor antagonist
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Triptans
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Sumatriptan MOA: 5-HT 1B/1D agonist -- INHIBITS TRIGEMINAL NERVE ACTIVATION -- Prevents vasoactive peptide release -- Induces vasoconstriction Clinical Use: Acute migraine, cluster headache attacks Adverse Effects: 1. Coronary vasospasm [Contraindicated in patients w/ CAD or Prinzmetal angina] Mild paresthesia
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