NHB FINAL

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jrcoben
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NHB FINAL
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2011-04-19 16:55:38
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  1. Describe the James-Lange theory 1887
    Theory that emotions are direct result of autonomic arousal.
  2. Cannon- Bard theory 1929
    Emotions and physiological responses are independent, activated separetly by brain
  3. Schachter's cognitive theory 1975
    Emotions result from the interaction between physiologic response and cognitive interpretation
  4. What represents "afferent feeback" and influences cognitive processes in decision making
    Somatic markers
  5. Limbic lobe components
    Cingulate gyrus, uncus, parahippocampal gyrus
  6. Papez Circuit
    • Hippocampus
    • Mammillary body
    • Anterior thalamic nucleus
    • Cingulate gyrus
  7. Sham rage
    Surgical removal of the cerebral cortex, causes emotional behavior provoked by ordinary stimuli
  8. No "Sham rage"
    Disconnecting hypothalamus and brainstem abolishes emotional behavior.
  9. Uvea components
    Iris, Ciliary body and choroid
  10. Aqueous Humor contents
    H/Cl, Ascorbate, Low HCO3, No protein
  11. Aq. humour secretion
    2-2.5 microliters/min
  12. Open Angle Glaucoma
    • Blockage in trabecular meshwork, causes increased intraocular pressure > 21mmHg
    • Trabeculotomy - surgery if needed
  13. Closed Angle Glaucoma
    • Iris scars and adheres to lens, causing increased intraocular pressure
    • Laser Iridotomy- surgical treatment
  14. Drugs to decrease production of Aq. humour
    • Alpha Agonists
    • Beta-blockers
    • Carbonic Annhydrase Inhibitors
    • (ABC)
  15. Drugs to increase outflow of Aq. Humour
    • Alpha Agonist
    • Cholinergics
    • Prostaglandins
  16. Beta Blocker for Glaucoma
    Timolol
  17. Alpha Agonist for Glaucoma
    Brimonidine
  18. Prostaglandin analogues for Glaucoma
    Latanoprost
  19. Carbonic annhydrase inhibitor
    Dorzolamide
  20. Cholinergics for Glaucoma
    Pilocarpine
  21. Foveola- center of fovea
    • Avascular area .5mm
    • Cones only
  22. Most common cause of blindness
    Degenerative process involving choroid-retina interface
    (Basal laminar deposits, atrophy of RPE, loss of photoreceptors, Neovascularity)
    Macular Degeneration
  23. RPE
    Rods, cones
    OLM
    ONL
    OPL
    INL
    IPL
    GCL
    NFL
    ILM
    Name layers of retina
  24. Name the 4 types of photoreceptors
    • Red, blue and green cones
    • rod
  25. 11-cis retinal to all-trans-retinal to Activated G protein which activates cGMP phosphodiesterase which hydrolyzes cGMP, diminishing it and closing NA channels, hyperpolazing membrane
    Light's action on phototransduction
  26. Dark effects on rods
    Depolarization because cGMP holds Na channels open, causes depolarization and glutamate release
  27. Degeneration of photoceptors
    Waxy pallor, arteriolar attenuation, bony spicules
    Retinitis pigmentosa
  28. part of blood-retinal barrier
    phagocytoses junk from photoceptors
    stores vit A
    absorbs light minimizing scattering
    Connects to photoceptors
    Functions of RPE
  29. •Jelly like substance
    •Made of collagen II
    •Mostly water
    •Salts, sugars, and GAG (HA)
    •Only attaches to two areas
    –ON
    -Ora Serrata
    Vitreous Humor
  30. •Magnocellular layers 1&2
  31. –Responds to contrast & mvmt
  32. –Responds to color, form, & detail
  33. •Parvocellular layers 3-6
  34. •Projections are either ipsi or contra
  35. –1,4, & 6 are contra
    –2,3, & 5 are ipsi
  36. –Composed of 1.2 million nerve fibers
    –Diameter of 1.5 mm
    –Runs through of Annulus of Zinn (origin of rectus muscle) and enters optic canal
  37. •Optic nerve
  38. –10 mm above pituitary gland
    –55% of fibers decussation
  39. •Optic chiasm
  40. –Part of thalamus
    –Crossed & uncrossed synapse
    –Magnocellular neurons
    •Motion detection, stereoacuity, and contrast sensitivity
    –Parvocellular neurons
    •Spatial resolution, color vision
    –Koniocellular neurons
  41. •Lateral geniculate body
  42. –Connects LGB to cortex
    –Meyer’s loop (inf ret fibers) travel around vent. system in temporal lobe à ”PIE in SKY”
    –Superior retinal fibers go through parietal cortex à “PIE in FLOOR”
    Optic Radiations
  43. –Brodmann’s area 17
    –Divided horizontally by calcarine fissure (Superior retinal fibers go inferiorly and vice versa)
    –Macula fibers are on posterior VC
    –Peripheral VF are ANT VC
    –Temporal crescent on VF (55-100 degrees)
    Primary visual cortex
  44. Nerve à Chiasm à Optic tract
    Posterior 1/3 of optic tract
    Travel in brachium of superior colliculus to midbrain (pretectal nucleus)
    Synapse
    2 Edinger-Westphal nucleus
    Afferent Visual Pthwy
  45. Edinger-Westphal nucleus
    Pregang parasymp fiber travel with inferior division of CN III
    Ciliary ganglion synapse
    Sympathetic & Sensory pass
    Postgang parasym fibers (short ciliary nerves) enter globe Innervate sphincter & ciliary m.
    Efferent Visual Pathway
  46. •Disruption in CNS
    •Light-Near Dissociation
    •If one sided
    –Limited direct response
    –Good consensual response
    –Normal near response
    •Reason:
    –Fibers for near response approach EW from ventral position bypass affected midbrain area.Frontal eye fields & efferent system intact
    Argyll-Robertson Pupil
  47. •Sympathetic pathway
    •Interruption = Horner
    •Hypothalamus (IMLCC)
    •Ciliospinal center of SC
    •Superior cervical ganglion
    •Postgang via ICA
    •Cavernous sinus
    •Travel with V1 into orbit
    –Ciliary ganglion – Short to choroidal blood vessel
    –Long to iris dilator and ciliary muscle
    Pupillary Dilation Pathway
  48. –SCG to Iris dilator muscle
    –Etiology: ICA Dissection
    3rd order Horners
  49. –Spinal cord to SCG
    –Etiology: Mediastinal or Apical lung tumors
    –Most common: Neuroblastoma, Pancoast tumors
    Second Order Horners
  50. –Hypothalamus to spinal cord
    –Etiology: Brainstem lesions (MB, Pons, Med)
    –Most common: Strokes like PICA (AKA?)
  51. •First Order = Central Horner’s
  52. •Nucleus in midbrain
    •Red nucleus and CST in cerebral peduncles
    •Passes through SCA & PCA
    •Then lateral to Post comm artery – IMP !
    •Enters cavernous sinus
    •Receives sympathetics from ICA
    •Passes through SOF and divides into sup & inf
    •Innervates all EOM EXCEPT SO & LR
    CN III
  53. •Nucleus in caudal mesencephalon
    •Passes between PCA and SCA
    •Lateral wall of cavernous sinus
    •Enters orbit via superior orbital fissure outside annulus of Zinn
    •Innervates SO muscleONLY nerve that leaves dorsal aspect of CNS
    CN IV
  54. •Nucleus in dorsal pons
    •Medial to CN VII
    •Through pyramidal tract
    •Exit lower pons
    •Climbs over the clivus over petrous ridge along skull base
    •Enters cavernous sinus
    •SOFSupplies LR
    CN VI
  55. •CN III
    •CN IV
    •CN V1
    •CN V2
    •CN VI
    •So whenever multiple cranial nerves, ALWAYS rule out CS lesion
    Cavernous sinus contents
  56. •Right MLF turns eyes to right
    •Left MLF turns eyes to left
    •Lesion of MLF = ipsilateral INO
    Medial Longitudinal Fasciculus
  57. –Nasal fibers = Temporal loss
    –Infero-nasal & Infero-temporal fibers = Ipsi Temporal lobe = Contra Pie in sky
    –Supero-nasal & Supero-temporal = Ipsi Parietal lobe = Contra Pie in floor
    –Optic tract = Contra homonymous hemianopsia
    –Occipital lobe = Contra homonymous hemianopsia with macular sparing
    Summary slide
  58. CN 3,4, V1, V2, 6
    cavernous sinus syndrome
  59. •9th leading cause all ages
    •3rd leading cause age 15 -24
    •30,000/year, 12/100,000 in US
    •1 million word wide
    suicide epidemiology
  60. •1 : 23
    •1 : 200 female adolescents
    •1 : 4 persons over age 64
    •50% had a prior attempt
    •1:100 will complete, 10% die in 10 years
    Completed suicide
  61. mental illness + psychosocial stressor + (intoxication + impulsivity + means) =
    suicide
  62. Depressed people have higher risk of suicide when?
    Depressed
  63. Schizophrenia have high risk of suicide when?
    non-pyschotic + demoralized
  64. Decreased serotonin metabolite 5-HIAA in what areas of suicide victims?
    Brainstem, subcortical nuclei and CSF
  65. Frontal cortex of suicide victims has
    • Decreased serotonin binding
    • Increased 5HT2 post synaptic binding
  66. Decreased 5-HIAA in what pts?
    • Aggressive
    • impuslive
    • suicide attempters
  67. Increased NE (4-hydroxyphenylglycol), causes
    Decreased Serotonin and Increased NE
  68. Dopamine aka homovanillic acid levels in suicide
    Decreased
  69. • serum cholesterol
    •Abnormalities in urine breakdown products
    • 5 HT 2 platelet receptors
    Suicide victims
  70. Methods of Suicide
  71. •55-60% Firearms
    • •14% Hanging
    • •11% Ingestion and poison
    • •9% Gas
  72. Common Method for suicide in General Hospital
    Jumping from a window
  73. Common method in Psych ward
    Hanging
  74. •60% told spouse
    •50% told relatives
    •18% told therapist
    Pts who committed suicide
  75. •Responsibility to family
    (minors at home)
    •Fear of killing oneself
    •Fear of the unknown
    •Religious beliefs
    •Future plans
    •Help seeking
    Suicide preventers
  76. •How bad do you feel?
    •Do you wish you were dead?
    •Thoughts of ending your life?
    •Thoughts about a particular way to end your life?
    •How close have you come in doing anything?
    Suicide Questions, last one most important
  77. Assessing Suicide Attempts from Pt
  78. •Isolation and timing
    • •Precautions against intervention
    • •Lethality
    • •Acting to get help
    • •Prior final acts (e.g. will)
    • •Suicide note
    • •Prior communication of attempt
  79. Pts report of Attempted suicide
  80. •Alleged purpose of the attempt
    • •Expectations of fatality
    • •Expectations of interventions
  81. •False sense of security
    •Significant if refused
    •No research support
    •More than ½ of inpatient suicides had them in place
    No-suicide contracts
  82. papez circuit + amygdala
    + dorsomedial thalamus, + basal forebrain nuclei
    + prefrontal cortex (orbital and medial)
    Limbic System
  83. Placidity- emotional blunting
    Psychic blindness- prosopagnosia
    Hypersexuality
    Hyperorality
    Cause- lesions of medial temporal lobe structures, requires lesion of amygdala
    Kluver-Bucy syndrome
  84. basal forebrain components
    • Nucleus Basalis of Meynert
    • Ventral Pallidum
    • Ventral Striatum (nucleus accumbens)
    • Septal Nuclei
  85. Medial temporal lobe parts
    Hippocampus + amygdala
  86. Limbic Cortex parts
    • Cingulate gyrus
    • parahippocampal gyrus
    • Uncus
    • Prefrontal cortex (medial + orbital)
  87. cholinergic neurons
    “pleasure center”
    Septal Nuclei
  88. Nucleus Accumbens
    Ventral pallidum
    • GABAergic neurons
    • reward, addiction
  89. Nucleus Basalis of Meynert
    cholinergic neurons, cognition, AD
  90. Fornix pathway
    • Hippocampus to hypothalamus
    • septal nuclei and prefontal cortex to hippocampus
  91. MTT pathway
    Hypothalamus (MB) to thalamus, anterior nucleus
  92. Cingulum pathway
    Cingulate gyrus to parahippocampal gyrus, bidrectional
  93. Stria terminalis
    Amygdala to Hypothalamu and Septal nuclei (bidirectional)
  94. Ventral Amygdaloid Pathway
    Amygdala to Brainstem, hypothalamus, basal forebrain (septal nucleus, etc), thalamus (dorsomedial), limbic (prefrontal) cortex
  95. MFB projections include
    • Dopaminergic-(VTA) motivation, reward, cognition (addiction, schizophrenia)
    • Serotonergic projectiosn (Raphe nucleus)- arousal, emotions, mood (anxiety, depression, addiction)
    • Noradrenergic projections (Locus Coreulues) - Attention, vigilance - anxiety, depression
  96. Regions of the hypothalamus
    • preoptic
    • Anterior
    • Tuberal
    • Posterior
  97. Preoptic Nuclei
    Sleep promoting, regulation of temperature and water balance
  98. Suprachiasmatic nucleus
    Circadian rhythm, master clock
  99. Supraoptic and paraventricular (magnocellular neurons)
    Hormone secreting ADH and oxytocin
  100. Arcuate and paraventricular (parvocellular neurons)
    Releasing factors (for pituitary hormones)
  101. Arcuate
    feeding behavior
  102. medial tuberal
    satiety center
  103. lateral tuberal
    feeding center
  104. Hypothalamus -Autonomic control
    Input?
    To what hypothalamic nuclei?
    • Visceral input to solitary tract nucleus (7,9, 10) cardio and respiratory info
    • Somatosensory input from spinal cord dorsal horn neurons
    • Thalamic nuclei- Ventromedial, paraventricular nuclei
  105. Hypothalamic Autonomic Control (Output) Efferent projections
    • From Lateral and Paraventricular nuclei
    • to autonomic ctrs in brainstem and spinal cord via DLF and descending sympathetics
    • Parasympathetics - dorsal motor nucleus of vagus and nucleus ambiguus
    • Sympathetic preganglionic neurons
    • IML of spinal cord
  106. Increased HR--Baroreceptor afferents--solitary tract nucleus--VM and PV
    Afferent Input
  107. Hypothalamus (PV and Lateral Nuc) to Nucleus ambiguus and Dorsal motor nucleus of X, which are parasympathetic and slow HR, also IML gets inhibited to decrease sympathetics
    Efferent Output
  108. PV and Arcuate nuclei (parvocellular) releasing factors to portal vein- to ant. pituitary hormones to general circulation
    Parvocellular endocrine control
  109. PV and SO (magnocellular) release Hormones with go down Supraoptic hypophyseal tract to post pituitary to general circulation
    magnocell release
  110. •Memory impairment (anterograde memory deficit)
    •Disruption of Papez circuit:
    hippocampus ® fornix ® MB ® MTT ® anterior thal. ® cingulate cortex
    •Also: gait ataxia (vermis) and problems with gaze (III)
    Bilateral lesions of MB / MTT can lead to
  111. Wernicke-Korsakoff’s syndrome (amnestic confabulatory syndrome)
  112. Miosis small pupil (partial constriction)
    Ptosis drooping eyelid
    Anhydrosis flushing and lack of sweating
    in ipsilateral skin of the face
    (red, dry skin i.l. face)
    Enophthalmus recession of eyeball
    Horner syndrome
  113. nInterface between limbic system and neocortex
    ÞCognitive and memory functions
    nMajor role in memory formation: consolidation (transfer of information from short-term to long-term memory)
    nInvolved mainly in explicit (declarative) and contextual and spatial memory processes
    nDysfunctions-disorders:
    qTemporal lobe epilepsy
    qAmnesia (anterograde)
    qAlzheimer’s disease
    qSchizophrenia
    Hippocampus
  114. •Molecular layer
    • Granule cell layer
    • Polymorphic layer
    Dentate gyrus
  115. • Molecular layer
    • Pyramidal cell layer
    • Polymorphic layer
    Cornu ammonis
  116. Transition zone from 3-layered cortex of hippocampus proper to 6-layered neocortex
    Subiculum
  117. q“psychomotor epilepsy” Complex partial seizures (seizure spreads to involve both temporal lobes) Hippocampal sclerosis (cell loss in CA1, CA3 and dentate) is the most common pathologic finding
    Temporal Lobe Epilepsy
  118. •Bilateral medial temporal lobe resection for untreatable temporal lobe seizures (1953)
    •Anterograde amnesia (inability to form new memories)
    •Impaired memory consolidation (> minutes)
    •Intact working memory (seconds)
    •Intact long-term memory (childhood, adolescence)
    •Partial retrograde amnesia (few years before surgery)
    •Intact learning of motor skills (procedural memory)
    H.M.
  119. qGeneral brain atrophy (atrophic gyri and widened sulci)
    particularly prominent in the limbic cortex
    qNeurofibrillary tangles and senile plaques
    predominantly in the parahippocampal gyrus:
    hippocampus and amygdala
    Neuropathology of Alzheimer Dz
  120. qDementia
    qMemory loss (starting with short-term memory)
    qLoss of judgment; disorientation
    qEmotional changes (depression and/or aggressiveness)
    Alz Dz- cognitive and affective deficits
  121. nAttaching emotional significance to a stimulus
    nEmotional (associative) learning and (implicit) memory
    nTriggering emotional responses (emotional behavior)Reward mechanisms
    Amygdala normal functions
  122. Urbach-Wiethe syndrome
    • Selective bilateral destruction (calcification) of the amygdala
    • but not hippocampus
    • S.M. failed to recognize facial expressions of fear

    • qImpaired storage and recall of emotional memories (visual and verbal),
    • Buchanan, Tranel, Adolphs (2005) J Neurosci 25:3151-3160
    • qImpaired recognition of negative emotional expressions (fear) in human faces
    • Impaired storage and recall of emotional memories
    • -Indifference to pain
  123. Areas of increased blood flow (PET scan) in the left amygdala and the prefrontal cortex of patients with ? relative to normal control patients.
    Major depressive disorder
  124. qConscious experience of emotions
    qCognitive interpretation of emotional situations
    qAttention
    qAnticipation of an upcoming (aversive) stimulus (e.g., pain)
    (this may involve other areas of the medial prefrontal cortex)
    Cingulate Cortex
  125. Bilateral radiofrequency cingulotomy lesion for the treatment of chronic pain
    Often releiced the suffering of intractable pain w/o destroying sensory awareness
  126. nExecutive functions
    nConscious experience - subjective feelings
    nCognitive component of emotions (evaluation)
    nEmotion-driven and reward-based decision-making
    nCognitive control of limbic functions (emotions)
    qSham rage experiment:
    Decortication precipitates emotional behavior
    qPhineas Gage case Emotional instabilityFear and fear extinction
    Medial Prefrontal cortex function
  127. Case of Phineas Gage
  128. Orbital and medial
    • prefrontal cortex lesion
    • Þ Personality change
    • qdisinhibition
    • qirritability
    • qemotional lability (“moody”)
    • qshallow emotions
    • qimpaired judgment
    • qsocial withdrawal
    • qapathy (diminished spontaneity)
    • qakinesis (diminished motor behavior)
    • qmutism (diminished verbal output)
  129. Prefrontal control of emotions
    Prefrontal cortex activates amygdala to increase or decrease fear, prefrontal control of amygdala may be important for PTSD
  130. •bipolar sensory neurons
    • with G-protein coupled receptors
    • unmyelinated axons collect into olfactory fila
    • form olfactory nerve CN I
    • penetrate cribriform plate
    • terminate in glomeruli
    • synapse on dendrites of mitral cells
    Olfactory Receptors
  131. nBenign tumor; does not invade brain tissue
    nGrows along the olfactory tract
    nPrincipal symptoms:
    qLoss of smell (anosmia)
    qHeadache (DD frontal sinusitis, migraine and neuralgia)
    nOther symptoms:
    qCompression of the optic nerve(s)
    ØVisual deficits (visual field deficits or even blindness if tumor grows large enough)
    nCan grow to a large size prior to being diagnosed because changes in the sense of smell are difficult to detect routinelyTx: Surgical excision only if symptomatic or enlarging
    Olfactory Groove Meningioma
  132. nManifestation of temporal lobe epilepsy
    nOriginate in the vicinity of the uncus
    nBegin with “olfactory” hallucinations (illusion of smell or taste) along with chewing movements of lips and tongue
    n“Uncus”:
    qmedial protuberance from the anterior end of the parahippocampal gyrus caused by the underlying amygdala
    qsite of the primary olfactory cortex
    nPrimary olfactory cortex includes:
    qpiriform cortex
    qperiamygdaloid cortex
    q(anterior) entorhinal cortex
    Uncinate seizures
  133. Deccorticate shame rage
    Korsakoff's syndrome
    Hypothalmus (MB)
  134. Horner syndrome
    Hypothalamus- sympathetics
  135. Memory loss (amnesia)
    hippocampus
  136. Alzheimers Disease structures involved
    hippocampus, amygdala, n. basalis of Meynert
  137. Temporal lobe epilepsy "limbic seizures"
    hippocampus, amygdala
  138. Kluver-Bucy sundrome
    Urbach-Wiethe syndrome
    amygdala
  139. Fear-Anxiety
    Depression
    Amygdala, prefrontal cortex
  140. Schizophrenia
    MFB-mesolimbic-mesocortical
  141. Reward-addiction
    MFB-basal forebrain-prefrontal cortex
  142. Acquired disorder, isolated loss of spoken or written language, different types
    Aphasia
  143. Defect in articulation with intact mental function, comprehension and word memory
    Anarthria
  144. Dysarthria
    Difficulty in articulation
  145. Aphonia
    loss of voice due to disorder of larynx
  146. Wernicke's area
    • Comprehension of language, posterior aspect of superior temporal lobe at interface between occipital, parietal and temporal lobes
    • Area 22
  147. Area 44,45
    Motor function of speech
    Broca's area
  148. non-fluent aphasia, expressive, motor- loss of fluency, some improvement from time of initial insult- not much recovery after 4-6 months
    Broca's aphasia
  149. Fluent aphasia, receptive, sensory,
    Wernickes aphasia
  150. disconnection b/w Wernickes and Brocas areas, --disturbed repitition
    Conduction aphasia
  151. transcortical disturbance
    due to disruption of cortico-cortical connections that associate closely together with Broca's or Wernickes
  152. Global loss of languag functions
    injury to several language regions
  153. Anterior lesions cause loss of ?
    Fluency
  154. Lesions b/w Wernickes and Brocas cause loss of ?
    Repitition
  155. Posterior lesions cause loss of ?
    Comprehension- in most people on the lesfft, in a very few, on the right.
  156. Crossed Wernickes Aphasia
    Wernickes area in right hemisphere, so a right sided degeneration== loss of comprehension
  157. Input from visual cortices converges on angular gyrus which projects to Wernickes area, output from Wernickes area reaches Brocas area through the arcuate fasciculus, output from Broca's projects to the laryngeal representation in the primary motor cortex
    Speaking a Written Word Pathway
  158. Input from primary auditory cortex reaches Wernickes, output from Wernickes reaches Brocas area by means of arcuate fasciculus, brocas area projects to laryngeal representation in the primary motor cortex.
    Speaking a Heard Word
  159. Classic type of M.S.
    Charcot
  160. Neuomyelitic optica
    Devic
  161. Acute fulminant type of MS
    Marburg
  162. Concentric rings of demyelinated/myelinated white matter, variant form of MS
    Balo
  163. Large, usually symmetric, hemispheric plaques, MS variant
    Schilder
  164. Chromosome 22
    • NF2 gene- Nuerofibromatosis
    • Meningioma
  165. Oligodendrogliomas genetic basis
    Loss of hetoerozygosity at 1p and 19 q on chromosome 19
  166. NF1 genetic basis
    Chromosome 17
  167. Hemangioblastoma genetic basis
    chromosome 3
  168. Best Verbal Response
    • None-1
    • Incomprehensible-2
    • Inappropriate words-3
    • Confused-4
    • Oriented-5
  169. Best Motor Response 1-6
    • None-1
    • Abnormal Extensor-2
    • Abnormal Flexor-3
    • Withdraws-4
    • Localizes-5
    • Obeys-6
  170. Eye Opening 1-4
    • None-1
    • To pain-2
    • To speech-3
    • Spontaneously-4
  171. GCS- 50% mortality when?
    Less than or equal to 8 for 6 hours
  172. Over 9 GCS
    Not in coma
  173. Causes of Coma
    • Diffuse or bilateral cerebral injury-destroys content
    • Reticular activating system injury
    • Physical lesions or metabolic alterations
  174. Lateral 2/3s of RF
    receive afferents from somatic and special sensor pathways, cortex
  175. Medial 1/3 of Rf
    Large neurons with long ascending and descending projections. Damage will alter consciousness.
  176. Vegetative state
    No cerebral function, some brain stem function.
  177. Akinetic mutism
    can't move or speak, patient not aware. Not locked-in syndrome where patient is fully aware.
  178. Cheyne-Stokes respiration
    Supratentorial lesions- diffuse lesions in cerebral hemispheres. Breathing decreases and then increases
  179. Central neurogenic hyperventilation
    lesion in midbrain, rapid but regular breathing
  180. Apneusis
    lesion in pons, slow deep rhythmic breathing, large respirations
  181. Cluster breathing
    lesion in lower pons, cycles of hyperpnea leading to periods of apnea
  182. Ataxic breathing
    lesion in caudal pons or medulla, chaotic breathing with irregular pauses and increasing periods of apnea
  183. Dural Venous Sinus Pressue + (CSF fromation X Resistance for CSF Absorption) = ?
    Static Intracranial Pressure
  184. 0-5lymphocytes/ul, 45-85 glucose mg/dl, 15-45 proteins mg/dl, 70-180mmH2O
    Normal CSF values
  185. Neonates 0-2 mo acute meningitis organisms
    • 1. Streptococcus alagactiae (group B)
    • 2. E. coli
    • 3. Klebsiella
    • 4. Enterobacter
  186. 3 mo- 50 years
    • 1. Strep pneumoniae
    • 2. Niesseria meningitidis
    • 3. Haemophilus influenzae
  187. > 50 years
    • 1. Streptococcus pneumoniae
    • 2. Neisseria Meningitidis
    • 3. Gram - bacilli
  188. Similarities of major agents in acute meningitis
    • 1. Colonize respiratory surfaces= resist local immunity
    • 2. Multiply extracellularly
    • 3. Polysacharide capsule- evade phagocytosis
    • 4. Autolyitc- induce inflam response
  189. Increased Pressure, Increased WBC (esp nuetrophils), Decreased Glucose, Increased Protein
    Acute Bacterial meningitis
  190. Chronic meningitis- TB
    • Hematogenous dissem occurs soon after initial infxn.
    • Rich focus in CNS may be present for yrs.
    • Presents as subacute/chronic meningitis w symptoms for 1-3 weeks.
  191. Meningeal infiltrate on basilar surface
    Granuloma and few mycobacteria in immunocompetent, but sheets of macrophages and lots of mycobacteria in immunocompromised
    Arteritis in what artery?
    • TB Meningitis
    • Middle Cerebral Artery- leads to infarcts in basal ganglia
  192. Hyponatremia in blood
    CSF- increased lymphocytes, increased protein, decreased glucose
    Definitive test?
    • PCR for nucleic acids- of mycobacteria
    • LAb Findings for TB meningitis
  193. Decreased glucose, increased protien, mildly increased lymphocytes, yeast in gram stain prep india ink or mucin stain prep
    soap bubbles in perivascular spaces
    Cryptococcal Meningitis Findings
  194. Acute presentation in AIDs
    Subacute/chronic in immunocompetent
    papilledema in 1/3, nerve palsies in 1/5
    Pulminary infx often clears before meningitis shows.
    brain abscess also common
    Cryptococcal Meningitis
  195. EEG- periodic high voltage discharges in one or both temporal lobes in a background of general slowing
    HSV-1 EEG
  196. CT/MRI findings in HSV-1 encephalitis
    involvement of medial temporal lobe, subfrontal and insular area with sparing of occipital parietal and cerebellar areas.
  197. Increased Protein, Slightly elevated lymphocytes, normal glucose
    CSF
    HSV-1 encephalitis findings
  198. False negatives first couple days or after 10-14 days, takes 6-8 hrs, procedure of choice for definitive diagnosis of HSV-1 encephalties
    PCR for herpes in CSF
  199. 1) Spread along olfactory nerve fibers
    2) Reactivation of latent virus in trigeminal ganglion and axonal spread to fibers innervating dura
    Possible mechanisms of HSV-1 encephalitis
  200. Acyclovir treatment = 20% mortality, with 50% experiencing sequelae
    Basal/medial temporal lobe often shows hemorrhagic necrosis
    see viral inclusion bodies histologically
    HSV-1 treatment and sequelae
  201. Agents that cause Brain Abscess
    • 1) streptococci
    • 2) Bacteriodies/Prevotella
    • 3) Enterobacteriaceae
    • 4) Staph aureus
    • 5)Fungi
    • * 30-60% of cases are mixed infxns
  202. 50%- spread from infection (otitis media, dental/facial abscess)
    25%- hematogenous spread (endocarditis)
    Cryptogenic (20%)
    Penetrating trauma
    Pathogenesis of Abscess
  203. Stages of Abscess formation (4)
    Once abscess is walled off, have to have surgery
    • 1. Focal suppurative encephalitis days 1-3
    • 2. Focal suppurative encephalitis with central necrosis days 4-9
    • 3. Early encapsulation days 10-13
    • 4. Late encapsulation day 14
  204. Delta- slow wave sleep 0-3Hz
    Theta- drowsiness, arousal 4-7Hz
    Alpha- relaxed wakefulness 8-13 Hz
    Beta- intense mental activity > 14 Hz
    Brain Waves
  205. Part of hypothalamus controlling circadian rhythm and temperature, melatonin, and cortisol levels
    Suprachiasmatic nucleus
  206. SCN projects to?
    forebrain, thalamus which then project to VLPO and LC.
  207. Time givers synchronizing agents
    Light, Physical Activity, Melatonin
  208. -promotes wakefulness
    -receives light via retinohypothalmic tract
    -receives non-photic info via serotonergic pathway from dorsal raphe nucleus
    -regulates indirect pathwy from sup cervical ganglion to pineal gland
    SCN
  209. VLPO
    Promotes sleep
  210. Stage 4 sleep
    Over 50% of page has high voltage delta activity
  211. Stage 3 Sleep
    20-50% of page has high voltage delta activity
  212. Low voltage 2-7 hz activity mixed with rapid eye movements and reduced chin activity
    REM
  213. Less than 20% delta activity with K complexes and spindles
    Stage 2
  214. less than 50% alpha and then 50% 2-7 Hz mixed activity
    Stage 1
  215. Greater than 50% is alpha activity 8-13 hz or low voltage 2-7 Hz mixed activity
    Waking state
  216. (ARAS), the midbrain reticular formation (ACh), posterior hypothalamus (histamine),Lateral Hypothalamus(Hypocretin/orexin) and the nucleus basalis of Meynert (ACh).
    Wakefulness is initiated and maintained by?
  217. bind to GABA-A receptors; decrease sleep latency and the number of awakenings, while improving sleep duration and sleep quality; dependency
    Benzodiazepines (estazolam, temazepam
  218. newer hypnotics; non-BZD structure but act similar to GABA agonist, binding to the BZD site; relatively low side effects (growing concern about this) and risk of dependency
    Eszopiclone (Lunesta), Zaleplon(Sonata)-Zolpidem tartrate (Ambien)
  219. Melatonin agonist acting at melatonin receptors in SCN. Good for sleep initiation (short half-life), low abuse potential, minimal side effects
    Ramelteon (Rozerem)—
  220. Orexin A and Orexin B are Nt's released by lateral thalamus that stabilize wakefulness and inhibit REM sleep. They increase transmission of LC and Raphe Nuclei, tuberomammillary nucleus.
    Narcoleptics lack these 2 transmitters
  221. stimulants (Modafinil; pemoline, amphetamines, e.g. Adderall) for sleepiness
    REM suppressors (tricyclic antidepressants or MAOIs) for cataplexy. Not entirely adequate; some have serious side effects (e.g., pemoline/liver).
    Narcolepsy Tx
  222. Repeated interruptions in breathing (for more than 10 s at a time) during a PSG (both REM and NREM); >5 interruptions/hour
    Sleep Apnea
  223. vObesity
    vMale sex
    vAge
    vAdenotonsillar hypertrophy, particularly in children and young adults
    vAlcohol use
    vCraniofacial skeletal abnormalities, particularly in nonobese adults and children
    vFamily history: Risk increases with each additional close family relative with OSAHS
    Risk Factors for Sleep Apnea
  224. diaphragm does not contract
    due to CNS abnormality.
    Central Apnea
  225. collapsed upper airway (usually obese people).
    Upper Airway Apnea
  226. Mixed Apnea
    Central apnea followed by upper airway apnea
  227. Best treatments for Cataplexy Now
    SSRIs like zoloft or Paxel, now SNRI, venlafaxine
  228. association b/w two stimuli
    Classical conditioning
  229. association b/w stimuli and behavior
    • operant conditioning
    • B.F. Skinner
  230. Apply a positive stimulus = strengthen behavior
    positive reinforcement
  231. Apply a negative stimulus = decrease behavior
    Punishment
  232. Remove a Negative stimulus = increase behavior
    Negative reinforcement
  233. Remove a positive stimulus = decrease behavior
    Extinction
  234. Social Cognitive Theory
    -Bandura
    -motivational factors involved in behavior
    Imitated learning requires
    • 1. Attention
    • 2. Retention
    • 3. Reproduction
    • 4. Motivation
  235. Birth to 2
    learn through motor and reflexes
    thought from sensation, movement
    learns she is seperate from environment
    Sensorimotor operations
  236. language to 7 years
    assumes everyone sees things like them
    oriented to present, but can think about things not immed present
    thinking influenced by fantasy
    can use symbols to represent objects
    Preoperational Operations
  237. 7 to early adolescence
    can think abstractly and make rational judgements about concrete phenomena w/o manipulating physically
    Concrete Operations
  238. Adolescence
    can make rational judgments, no longer a req to have concrete objectscan take another's views
    can hypothetical and deductively reason
    Formal operations
  239. id-
    ego-
    superego-
    • id-instinct
    • ego- seat of reason
    • superego- seat of morality (self-criticism)
  240. Unconscious
    Defense mechanisms
    Hypnosis
    Talking dialog for therapy
    Freuds contributions
  241. Prefrontal cortex
    ex. hearing sequence of numbers and repeating them
    Required to encode and recall explicit memory
    Short-term (working memory)
  242. Visuospatial sketchpad
    • part of short-term/working memory
    • visual properties and spatial location of objects
    • posterior association cortices
  243. Articulatory loop
    • short-term/working memory
    • stores rapdily decay memory traces for words, numbers, subvocal articulations
    • involves posterior assoc cortices
  244. Implicit memory structures
    cerebellum, striatum and/or neocortex
  245. Explicit memory structures
    medial temporal lobe
  246. Emotional memories
    amygdala and its connections
  247. Automatic recall
    limbic cortex/neocortex
  248. Active recall
    frontal lobes
  249. Non associative learning
    • learning from a single type of stimulus
    • requires cerebellum
    • habituation, sensitization, imitation
  250. habituation
    decreased response to a stimulus following repeated exposure
  251. Sensitization
    increased response to a stimulus following repeat exposure
  252. Amygdala lesions
    cannot recognize frightening cues
  253. Hippocampus is important for acquisition of spatial memory in rats, but not its storage
  254. Perforant pathway
    Inflow of entorhinal synaptic inputs to dentate granule cells
  255. Mossy fiber pathway
    dentate granule cells connect to hippocampal pyramidal cells in CA3
  256. Schaffer collateral pathway
    CA3 collaterals connect to pyramidal cells in CA1 of hippocampus, CA1 cells then send output back to subiculum and entorhinal cortex
  257. Snail gill withdrawal reflex
    • Strong stimulation of the tail sensitizes the reflex such that a larger EPSP occurs in motorneuron
    • If tail and siphon are paired w/ classical conditioning, reflex becomes even stronger, more long-lasting
  258. Stronger 5-HT input causes long term changes -
    more cAMP, more PKA, and MAPK and CREB, which go to nmore cAMP, more PKA, and MAPK and CREB, which go to nucleus to code for proteins that enhance synaptic strength.
  259. ? phosphorylates K channels closing them, decreasing thershold and increasing excitability of membrane
    PKA effects on LTP
  260. disturbance of consciousness
    reduced ability in attention
    change in cognition, not from preexisting condition
    Acute
    quiet or loud
    prevalent in hospitals 10-25%, 3 month mortality rate
    Delirium
  261. delirium risk factors
    • Over 65
    • comorbid dementia
    • post-op
    • bone fracture
    • infxn
    • narcotic use
    • drug,alc w/drawak
  262. Haloperidol (anti-psychotic), treats?
    Delirium
  263. memory impairment + decline in executive functioning + 4 A's? = what disease
    • Alzheimers
    • Amnesia
    • Aphasia
    • Apraxia- difficulty executing complex behavior (dressing)
    • Agnosia- can't recognize things even tho can see
  264. Workup for treatable causes of Dementia
    • HIV, syphillis
    • thyroid panel- hypothyroidism
    • B12- foalte levels, myelin or neuronal deg
    • CT/MRI- tumor or stroke
    • Urinalysis- diabetes, drug toxicities
    • Serum chemistries
    • CBC infections
  265. Statins and Alzheimers DZ
    • current users have half the risk of developing AD
    • former users have increased risk than controls
  266. Treats Amyloid toxicity in Alzheimers by preventing its deposition, delay nursing care for 1 yr
    Bapineuzumab, Statins
  267. Cholinesterase inhibitors for tx of Alz DZ
    donepezil, galantamine, rivastagmine
  268. Tx inflammatory process in Alz, but usefulness does not offset GI bleeding risks
    NSAIDS, estrogen, prednisone
  269. Free radical toxicity tx for Alz
    • Vitamin E better than
    • Vitamin E + Selegeline
    • Vitamin C
  270. Treats glutamate toxicity in Alz dz. An NMDA receptor antagonist
    • Memantine
    • combo of cholinesterase + memantine may be effective
    • also, neramexane
  271. Treats nerve growth deficiency in Alz Dz. Mimics a naturally occuring growth factor, helps to generate new cells, may prevent death
    Cerebrolysin
  272. Other Alz tx possibilities
    • Antihypertensives
    • DHA (omega 3) not shown to slow progression of Alz,
    • Gingko biloba- not proven
  273. 1) tight junctions between Müller cells and inner segments of photoreceptors
    Outer Limiting Membrane
  274. Nuclei/cell bodies of photoreceptors
    Ouer nuclear layer
  275. synapses b/w bipolar cells and photoreceptors (includes horizontal cells)
    Outer plexiform layer
  276. bipolar, horizontal, amacrine cell nuclei
    Inner nuclear layer
  277. bipolar and amacrine synapses with ganglion cells
    Inner plexiform layer
  278. Axons from ganglion cells form optic nerve
    Nerve fiber layer
  279. thin basal lamina
    Inner limiting membrane
  280. At foveal pit, these layers are pushed aside to minimize number of layers light has to penetrate to get to photoreceptors
    INL, IPL, and ganglion cell layer
  281. Retina à Optic nerve à Optic chiasm à Optic tract à
    Lateral Geniculate Nucleus of the thalamus à Optic radiation
    à Primary visual cortex
    Basic visual pathway
  282. magnocellular, form the
    M channel and are responsible for movement
    and contrast
    Layers 1 and 2 of Lateral Geniculate
  283. · are parvocellular, form the P channel and are responsible for color and form
    Layers 3-6 of lateral geniculate
  284. o Pupillary constriction to change the depth of focus
    o Prevents diverging light rays from hitting the periphery of the retina and resulting in a blurred image
    o Requires cerebral cortex participation
    Near Reflex
  285. ·





    Area 19





    Magnocellular Projection
    (movement, stereopsis)
    Deficit in this area leads to loss of movement so moving cars look frozen





    Parvocellular Projection
    (inferotemporal Ctx, form& color)
    Deficit in this area would result in a black&white worldMagnocellular projection (movement, stereopsis – depth perception)
    · Parvocellular projection in inferotemporal ctx (form, color)
    · Damage in these areas results in odd deficits, such as loss
    of form but not color, or being unable to see movement.
    Assoc Visual Cortex 18,19
  286. 1) entire left field loss with macular sparing
    Lesion of BOTH cuneus and lingual gyrus on right
  287. 1) left upper quadrantanopsia (upper, outer quadrant).
    • Could be caused by tumors in temporal lobe
    • Lesion of Meyer’s loop on right
  288. Medications to treat alcholism
    Disulfiram, Acamprosate, Naltrexone, Topiramate
  289. Medications to treat opiate addiction
    Buprenorphine (Suboxone), Methadone
  290. Medications to treat Nicotine addiction
    Buproprion, Varencicline (Chantax)
  291. Methohexitol
    Anesthetic agent in ECT
  292. SIG E CAPS = Major depressive episode
    • Sleep disturbance
    • Loss of Interest
    • Guilt or Feelings of worthlesness
    • Loss of Energy
    • Loss of Concentration
    • Appetite/weight changes
    • Psychomotor retardation or agitation
    • Suicidal ideation
    • depressed mood
  293. Manic Episode= DIG FAST
    • Distractability
    • Irresponsibility
    • grandiosity
    • Flight of Ideas
    • Increase in goal-directed Activity/psychomotor Agitation
    • Decreased need for Sleep
    • Talkativeness or pressured speech
  294. Unacceptable feelings and thoughts are expressed through actions
    (Immature)
    ex: tantrums
    Acting Out
  295. Temporary, drastic changes in personality, memory, consciousness, or motor behavior to avoid emotional stress.
    Ex: multiple personality disorder
    Dissociation (immature)
  296. Avoidance of awareness of some painful reality.
    Ex: common in newly diagnosed AIDs patients
    Denial (immature)
  297. Partially remaining on a more childish level of development
    ex: men fixating on sports games
    Fixation (immature)
  298. Modeling behavior after another person who is more powerful (although not necessarily admired)
    ex: abused child identifies himself as abuser
    Identification
  299. An unacceptable internal impusle is attributed to an external source
    ex: man who wants another woman thinks his wife is cheating.
    Projection (immature)
  300. process where a warded-off idea or feeling is replaced by an (unconsciously derived) emphasis on its opposite
    ex: a patient with immoral thoughts enters monastery
    Reaction formation (immature)
  301. Turning back the maturational clock and going back to earlier modes of dealing with the world
    ex. children under stress bedwet
    Regression (immature)
  302. involuntary withholding of an idea or feeling from conscious awareness
    ex: not remembering a traumatic experience
    Reperssion (immature)
  303. People are all good or all bad due to intolerance to ambiguity.
    Splitting (immature) seen in borderline personality disorder
  304. guilty feelings alleviated by unsolicited generosity toward others
    Altruism (mature)
  305. Appreciating the amusing nature of an anxiety-provoking situation
    Humor
  306. Process whereby one replaces an unacceptable wish with a course of action that is similar to the wish but does not conflict with ones values.
    sublimation (mature)
  307. voluntary withholding of an idea or feeling from conscious awareness
    choosing not to think about car wreck till after big exam
    suppression (mature)
  308. Mature women wear a SASH
    • S-sublimation
    • A-altruism
    • S-suppression
    • H-humor
  309. ADHD brain structures involved
    • Prefrontal cortex
    • hippocampus
    • N. accumbens and striatum
    • Sensory organs and parietal lobe
    • limbic system
  310. In ADHD, name effect on frontostriatal regions
    decreasein NE and Dopamine activity
  311. decreased sleep
    decreased appetite
    tics
    Side effects of amphetamines and methylphenidate in tx od ADHD
  312. Amphetamines and Methylphenidate MOA
    block catecholamine reuptake transporter, increase release of NE and dopamine, midly inhibit MAO.
  313. ADHD with tiny laser drilled hole so efficacy for 12 hours
    concerta (methylphenidate)
  314. Alpha 2 agonists for treatment of ADHD
    clonidine, guanfacine
  315. good for control of impulsivity and inattention, debatable for hyperactivity.Watch for BP drops, sedative
    clonidine, guanfacine
  316. Antidepressants to treat ADHD
    imipramine, buproprion, atomoxetine
  317. Anger associated with what 3 brain structures
    • Left orbitofrontal cortex
    • Right anterior cingulate cortex
    • Bilateral anterior temporal lobes
  318. PET study of murderers found NGRI showed reduced glucose metabolism in what structures, and saw assymetric activity in what structures
    • Prefrontal cortex
    • Superior parietal gyrus
    • left angular gyrus
    • corpus callosum
    • assymetry in amygdala, thalamus and right medial temporal lobe
  319. Nuerological findings in aggressive people
    • Head injuries
    • EEG abnormalities-difficulty processing info
    • Seizure disorders- aggressive behavior may occur during a seizure
    • Neurological soft signs- synkinesis
  320. In 10 IED subjects had abnormal response to facial expressions
    • Left amygdala overreacts to angry, happy, neutral faces, but underreacts to surprised or sad.
    • orbitofrontal cortex showed diminished response
  321. Low serotonin in CNS and aggression
    Causes impuslive aggression which is worsened by elevations in peripheral aggression during heated moment.
  322. GABA and aggression
    Inhibitory effect on aggression
  323. Low NE and aggression
    impulsive and episodic aggresion
  324. ACH and aggression
    predatory, premeditated aggression
  325. Reduced serotonin
    Increased dopamine, NE
    • Cortical lesion
    • decreased cortical volume
    • orbitofrontal/cingulate cortex processing inefficiency
  326. Reduced GABA
    Increased glutamate and ACH
    • Hyperactivity of amygdala, limbic system
    • Reduced amygdalar volume
    • Emotional hypersensitivity
    • Kindling
  327. MAOA-L volume reduced in what structures
    bilateral amygdala, supragenual anterior cingulate, and subgenual anterior cingulate cortex
  328. MAO-L males show increased volume in what structures compated to MAO-H males
    lateral orbitofrontal volume bilaterally
  329. 5-HTTLPR (Serotonin Transport Linked Promoter Region plymorphism in rhesus monkeys
    • Short allele= increased aggresiion in peer raised
    • Long allele- good socialization in peer or mom raised
  330. No-Go experiment
    In aggressive subjects, less efficient processing, impuslive, over-reactive, delayed response.
  331. NO-GO anteriro cingulae gyrus
    lo MAO males have decreased activity in anterior cingulate gyrus during response inhibition than controls
  332. psychostimulants, hallucinogens, sedative hypnotics, opiates, anticholinergics, steroids
    Drugs that increase aggression
  333. Top-down regulation on aggression
    • orbital frontal cortex
    • anterior cingulate gyrus
    • (suppression-regulation)
  334. Bottom-up "drive" on aggression
    signal,trigger
    amygdala, insula
  335. Tx for aggression by decreasing limbic activation, increasing prefrontal control. Esp for organic impairment or psychotic thought processes
    Neuroleptics (haloperidol, clozapine)
  336. Tx for acutely aggressive, Helps calm patients. In some can cause disinhibition, increasing aggression
    Benzodiazepines (diazepam)
  337. Tx for those with compulsive aggression.
    Anticonvulsants- valproate, phenytoin
  338. Tx for aggression, esp in those iwth organic impairment of MR. Requries large doses
    B-adrenergic blockers, propanolol
  339. Not as helpful as initially hoped in tx aggression
    SSRIs- sertraline
  340. Improves aggression in ADHD patients.
    Psychostimulants, methylphenidate
  341. Primary olfactory cortex
    (uncus) components
    • Piriform cortex
    • Periamygdaloid cortex
    • Entorhinal cortex

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