NEURO_PHASE_III

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soren101
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NEURO_PHASE_III
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2011-05-10 15:49:18
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neuro phase III
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  1. List the three major functions the vestibular system serves in man
    ·Primary organ of equilibrium – subjective sensation of motion and spatial orientation

    ·Vestibular input to posture control system – adjustments of muscles to prevent falling

    ·Vestibular influence on eye movement – stabilize eyes in space while moving head
  2. List the three major sources of sensory information used by the brain in the maintenance of equilibrium
    • · Visual
    • cues (MOST IMPORTANT!!)

    • · Proprioception
    • info from neck and leg muscles

    • · Vestibular
    • impulses
  3. Explain what is meant by polarization of a hair cell
    • ·
    • The
    • hair cells have stereocilia that are gradually longer, ending in the largest –
    • the kinocilium

    ·











    • Depending on which way the
    • moving endolymph bends them the cell will either depolarize (towards
    • kinocilium) or hyperpolarize (away from kinocilium)
  4. Describe a stimulus that would increase the firing
    in the left horizontal canal to a maximum and on that would decrease the firing
    to a minimum
    • ·
    • Increase
    • to maximum: Head
    • tilted 30º forward and rotating to the left

    • ·
    • Decrease
    • to a minimum:
    • Head tilted 30º forward and rotating to the right
  5. Describe
    the functions of the utricle and saccule
    They respond to linear acceleration like gravity (ex: plane turbulence, head tilt)

    • ·
    • Utricle: positional reflexes (placement
    • of eyes and body), correcting reflexes

    Saccule: function unknown
  6. Explain the effective stimuli for the otolith organs
    • · When head is moved with respect to gravity the
    • otoliths are displaced with respect to the endolymph

    • ·Hair
    • cells in utricle are oriented with respect to the striola, which bisects
    • the macula. It’s sensitive to a variety of head positions & linear
    • movements

    • · The
    • kinocilia are always facing the striola

    • · Thus
    • there are 2 groups of hair cells on each macula that will respond oppositely to
    • the same stimulus (functional pair)
  7. Explain the relationship between the vestibular
    complex and the cerebellum
    Vestibular system must bring information into cerebellum about posture so that the cerebellum can compute whether something needs to be changed.
  8. Explain nystagmus and the use of the mnemonics COWS
    • Nystagmus:
    • o Fast return phase of eye movement
    • as a response to rotation.
    • o In the same direction as the
    • rotation (as opposed to the slow compensatory movement of eyes in the opposite
    • direction which serves to keep image stationary)

    o Bárány’s caloric test:

    • o Putting cold water/air in the ear
    • will cause the endolymph to move down à causing sensation of rotation in
    • the opposite ear’s direction.

    • o Normally, nystagmus will occur
    • and it will be in the opposite direction of the ear:

    Cold– Opposite



    • o Putting hot water/air in the ear
    • will cause the endolymph to move up à causing sensation of rotation in
    • that ear’s direction.

    • o Normally, nystagmus will occur
    • and it will be in the same direction Warn Same

    o --> COWS (Cold-Opposite Warm-Same)
  9. List the tests for vestibular function
    • Bárány’s
    • chair:

    • o Rotation on chair in one
    • direction elicits feeling of rotation at first but when the endolymph catches
    • up with the rotation the sensation of rotation ceases. (Nystagmus will begin in
    • the same direction of rotation but will stop when adaptation occurs)

    • o When chair is stopped, the
    • endolymph will keep moving and will cause sensation of rotation in the opposite
    • direction (same with nystagmus, which will reappear in the opposite direction
    • than before)

    • ·
    • Balance
    • Test:

    • o Close eyes and stand perfectly
    • still

    • o If equilibrium system is non
    • function, patient will fall to the side

    • ·
    • Bárány’s
    • caloric test:
  10. List the rules to understand directionality with
    respect to the vestibular system
    • NORMAL
    • · Stimulation
    • of horizontal semicircular canal on one side leads to stimulation of medial
    • rectus of ipsilateral eye and the lateral rectus of the contralateral eye

    • ·
    • If
    • rotate someone counterclockwise, eye movements (slow ones) will be clockwise,
    • whereas nystagmus (fast, returning ones) will be counterclockwise.

    • ABNORMAL
    • · Direction
    • of spontaneous nystagmus is away from diseased side

    • ·
    • Direction
    • of falling and past pointing is toward lesion

    • ·
    • If
    • the lesion is in the vestibular apparatus itself, caloric testing won’t elicit
    • correct response on diseased side; if the lesion is central, caloric test will
    • give past pointing and falling, but no nystagmus

    • ·
    • Slow
    • component of nystagmus is due to vestibular and brainstem vestibular apparatus
    • and motor system

    • ·
    • Fast
    • component of nystagmus is due to the cerebral hemisphere opposite the direction
    • of movement

    • ·
    • Vertigo
    • is in the direction of the slow component

    • ·
    • Spontaneous
    • cerebellar nystagmus isn’t altered by changes in head movement

    • ·
    • Lesions
    • of vestibular apparatus often involve hearing problems
  11. Define or explain all new terms and key words for vestibular system
    • Labyrinth:
    • inner ear auditory apparatus and adjacent structures responsible for
    • posture and equilibrium maintenance

    • · Statokinetic labyrinth:
    • vestibular apparatus
    • o Bony labyrinth:
    • 3 semicircular canals, hollow
    • o Membranous labyrinth: 3 semicircular ducts
    • o Endolymph:
    • in membranous labyrinth, + charge, high K & low Na
    • o Perilymph: bt membranous & bony, low K
    • & high Na

    • ·
    • Ampulla: dilation of semicircular ducts
    • as they join the utricle
    • o Contains sensory epithelium -->
    • o Crista ampullaris (aka crista
    • acustica): neuroepithelial ridge (saddle)

    • ·
    • Cupola:
    • dome shaped mucilaginous body where stereocilia project
    • o Forms fluid tight partition with
    • ampulla
    • o Pushed with movement

    • ·
    • Dizziness: vague term used to describe
    • many abnormal sensations which may include light-headedness or faintness,
    • nausea or unsteadiness on one’s feet in addition to true vertigo

    • ·
    • Type
    • I hair cell: pear shaped, flat surface facing
    • endolymphatic spaces; bottom has chalice-like nerve ending from
    • Vestibular/Scarpa’s g.

    • ·
    • Type
    • II hair cell: cylindrical; innervated by small terminals

    • ·
    • Kinocilium & stereocilia:
    • bending causes generation of activity in vestibular nerve

    • ·
    • Otoliths or Otoconia: Ca Carbonate crystals in gelatinous covering
    • into which sterocilia extend; more dense than endolymph

    • ·
    • Vertigo: false sensation that the person
    • or his surroundings are whirling around him

    • ·
    • Optokinetic
    • Nystagmus:
    • o Paper with vertical lines moved
    • horizontally in front of patient
    • o Nystagmus of visual activity only
    • o This is cortical nystagmus
    • (brainstem has nothing to do with this)
  12. Describe
    the descending pathways from the hypothalamus
  13. 1.
    Know the centers for and the working of the
    hypothalamic centers involved in central temperature regulation and fever
    reduction
    • Heat
    • Loss center - anterior hypothalamic area (preoptic)

    • o Increased firing in the low
    • threshold receptors that turn off heat production by inhibiting neurons in the
    • posterior hypothalamus

    • o Increased firing in high
    • threshold receptors that give rise to a heat loss response (vasodilation and
    • sweating)



    • ·
    • Heat
    • Generation center - posterior hypothalamus

    • o Decreased inhibition from
    • anterior hypothalamus

    • o Vasoconstriction and inhibition
    • of sweating

    • o Heat generation (shiver &
    • increase BMR)
  14. Define
    what pyrogens are and the theory on how they elevate body temperature
    Pyrogens = lipopolysaccharides (LPS)

    Isolated from various bacteria and viruses

    • Formed
    • by WBCs in tissue damage and infection

    • IL-1
    • and prostaglandins cross BBB (Blood Brain barrier) at organum vasculosum
    • of lamina terminalis
    • o
    • Act
    • on hypothalamic neurons that interpret the body temp as too low and resets the
    • set point higher
    • o
    • Fever
    • inducing
    • o
    • Peripheral
    • constriction and shivering
  15. 1.
    Define heat stroke and know the body temperatures
    that are life threatening
    • o
    • High
    • environmental temp causes a decrease or disappearance of sweating, indicates a
    • breakdown in hypothalamic thermoregulatory mechanisms

    • o
    • 104
    • - Life threatening

    • o
    • 106
    • - Brain death begins

    • o
    • 113
    • - Death nearly certain

    • o
    • Signs:
    • coma, confusion, convulsions, vomiting
  16. 1.
    Identify some factors responsible for heat stroke
    • o
    • High
    • environmental temp with humidity

    • o
    • Young
    • age (left in closed car)

    • o
    • Social
    • circumstance

    • o
    • Other

    • o
    • Excessive
    • heat exposure

    • o
    • Dehydration

    • o
    • Exercise
  17. 1.
    Discuss the factors involved in the regulation of
    water balance
    • Excretion (vasopressin aka
    • ADH)

    • Water intake/thirst
    • (angiotensin & dryness of oropharyngeal membranes)
  18. 1.
    Discuss the control of the release of ADH and its
    role in the control of excretion
    • ADH synthesized in
    • paraventricular and supraoptic nuclei

    • Stored in posterior
    • pituitary

    • Signal to paraventricular
    • and supraoptic nuclei generates AP that stimulates release from pituitary

    • Acts on kidneys to decrease
    • water excretion

    • Stimuli that release ADH:
    • Increase in osmotic
    • pressure

    • Increase in circulating
    • angiotensin II

    • Decrease in BP and blood
    • volume

    Pain and emotions

    • Morphine, nicotine and
    • barbiturates

    • **ethanol inhibits release
    • of ADH!**
  19. 1.
    Know the definition of diabetes insipidus
    Loss of water

    Unbearable thirst

    • Lesion of supraoptic and
    • paraventricular nuclei
  20. 1.
    Discuss the mechanisms of thirst
    • Osmoreceptors are stimulated
    • by an increased osmotic pressure of body fluids

    Decreased ECF volume

    Hemorrhage

    • Dryness of pharyngeal mucous
    • membranes
  21. Discuss
    and be able to draw a normal cystometrogram and its various phases
    • 1st
    • desire: 175ml
    • ·
    • Fullness:
    • 400ml
    • ·
    • Voiding:
    • 400-500ml

    • ·
    • Continence
    • = ability of bladder to retain urine

    • ·
    • Micturition/urination=
    • act of emptying

    • ·
    • Can
    • be altered by hormones
  22. 1.
    Describe in detail the innervations of the bladder
    • Detrusor
    • muscle excited by parasympathetic fibers in pelvic splanchnics (S2-S4)

    • Sympathetics
    • relax detrusor (T11-L2)
    • -Beta adrenergicAlpha adrenergic (inhibit parasymp)
    • -Sympathetics
    • ---excite trigoneAlpha adrenergic
    • -External
    • sphincter is striated muscle, voluntary control
    • -Bladder
    • filling detected by stretch receptors in bladder wall from afferents in pelvic splanchnics
  23. 1.
    Discuss the voiding reflex and higher centers of its
    control
    • Urine propelled by peristalsis
    • in ureters from kidneys to bladder

    • Filling conditions
    • -Primarily sympathetic
    • control
    • -Tonic activity mediates
    • constriction of external anal sphincter

    • Pressure on bladder wall
    • activates tension receptors to a threshold

    • Reflex arc to micturation
    • center in Pons - supraspinal stimulation
    • -Inhibits symp
    • -Stimulates parasymp
    • -Inhibits efferents to
    • external sphincter

    • Spinal level reflex arc –
    • role is uncertain

    • Once begun, process
    • accelerates explosively
    • -Positive feedback
    • -Reflex activation and
    • blocking

    • Higher centers of control
    • -PRF – powerful facilitatory
    • center
    • -Pre-optic area of
    • hypothalamus --> powerful bladder
    • contraction when stimulated
    • -Lateral reticulospinal
    • (medulla)
    • -Medial reticulospinal
    • (pons)
  24. 1.
    List factors that are involved in urinary
    incontinence
    Bladder hyperactivity

    Sphincter incompetence

    Both

    • TREATMENTS:
    • -Anticholinergic drugs help
    • with hyperactivity by increasing threshold volume
    • -Beta agonists relax detrusor
    • -CNS drugs can suppress
    • hyperreflexia
  25. 1.
    Discuss the neuronal control of bowel evacuation
    • Sympathetic and
    • parasympathetic sacral innervation

    • Internal and external
    • sphincters

    • Tonic contraction of
    • external sphincter maintained by spinal reflex
    • -striated muscle (S2-S4
    • pudendal nerve)

    • Relaxation of internal
    • sphincter is a reflex response to filling of rectum (external contracted)

    • Supraspinal (cortical)
    • mechanisms make a large contribution to continence by exciting motor
    • neurons to external anal sphincter and inhibiting parasymp spinal reflexes

    Defecation is voluntary

    • Spinal parasympathetic
    • reflex actions cause colon/rectum contraction

    Sphincters relax

    • Rise in intra-abdominal
    • pressure
  26. 1.
    Discuss the effects of transection of spinal cord on
    urination and defecation
    • Reflexes eliminated by
    • destruction of sacral spinal cord

    • Transection of cord above
    • sacral level loses voluntary motor control
  27. 1.
    The major
    control centers in the hypothalamus that regulate hunger and satiety
    • Tuberal region: ventromedial nucleus (VMH) -
    • Satietyincreased stimulation = decreased feeding

    Lateral zone (LH): feeding/hunger centerincreased stimulation = increased feeding
  28. GLP HORMONE (HYPO)
    • GLP
    • (Glucagon-like peptide):
    • Stimulated by food ingestion
    • Causes:
    • ↑ glucose-dependent insulin secretion
    • ↓ GCN secretion
    • ↓ gastric emptyingMeal-to-meal satiety
  29. GHRELIN (HYPO)
    • Stimulated by fasting/weight loss
    • Inhibited by meal/obesity
    • Casues:
    • GH secretion
    • ↑contraction and emptying
    • Hunger (--> initiates eating)
    • ↑ appetite
    • ↓ energy expenditure
  30. INSULIN (HYPO)
    • Stimulated by meal and rise in plasma glucose
    • Causes:
    • Lowering of plasma glucose
    • Store glucose
    • Intake of AA into cells
    • Store glucose as fat
    • ↓ appetite
    • ↑ energy expenditure
  31. LEPTIN (HYPO)
    • Stimulated by various things
    • Causes:
    • ↓ appetite
    • ↑ energy expenditure
  32. NEUROPEPTIDE Y (HYPO)
    • Stimulated by
    • ghrelin

    Inhibited by insulin/leptin

    • Causes:
    • Regulation of blood flow and of gut motility
    • ↑ appetite
    • ↓ energy expenditure
  33. ALPHA MELANOCYTE STIMULATING HORMONE (HYPO)
    Stimulated by insulin/leptin

    • Causes:
    • ↓ appetite
    • ↑ energy expenditure
  34. AMYLIN (HYPO)
    Stimulated by meal and rise in plasma glucose

    • Causes:
    • ↓ appetite
    • ↓ post-prandial glucagon secretion
    • ↓ gastric emptying
  35. 1.
    Definition
    of obesity as defined by BMI
    • BMI 30-40
    • Morbid >40
  36. 1.
    Types of
    obesity
    • Primary
    • -Possibly due to leptin resistance
    • -2/3 of variability in weight is genetic

    • Secondary
    • -Cushing’s
    • -Hypothyroidism
    • -Hypogonadism
    • -Binge eating
    • -Genetic
    • -Trauma
  37. MAJOR EATING DISORDERS
    • Anorexia
    • nervosa

    • Refusal to maintain healthy weight
    • Excessive concern with gain
    • Distorted body image

    • Bulimia Nervosa
    • Recurrent binge eating and neutralizing
    • Purging subtype
    • Non-purging subtype
    • --neutralizing behavior: exercise, temporary food
    • restriction

    • EDNOS (eating Disorder not Otherwise Specified)
    • Different patterns
  38. 1.
    Identify the hypothalamic nuclear groups which
    relate to the function of the anterior pituitary gland
    • Supraoptic nucleus (SON):
    • regulation of water intake and urine formation (ADH)

    • Medial hypothalamic nuclei:
    • regulate secretion from anterior and posterior pituitary

    • Medial forebrain bundle
    • --Multi-synaptic
    • --Non-myelinated
    • --Info from central tegmemtum to nucleus accumbens
    • --Pleasure/reward center
  39. 1.
    Explain the functional significance of the
    hypothalamo-hypophyseal portal system in relation to neuroendocrine physiology
    • Allows hypothalamus hormones
    • to flow to the anterior pituitary

    • Thalamo-hypothalmic pathway
    • modulates release of ant. Pituitary hormones

    • Tuberoinfundibular tract
    • arises from monoaminergic neurons in arcuate n.
    • --Axons flow into primary
    • portal plexus to secondary portal plexus
    • --Release hormones act on
    • target cells in ant. Pituitary
  40. 1.
    Distinguish between the various fiber tracts in the
    hypothalamus which are concerned with neuroendocrine function
    Supraopticohypohyseal: to post. Pituitary (ADH & oxytocin), derived from SON & PVN

    Medial preoptic

    Mammalothalamic tract

    • Tuberoinfundibular tract:
    • from monoaminergic neurons in arcuate n.
    • --Releases hormones on ant. Pituitary

    • Thalamohypothalamic:
    • modulates release of ant .pituitary hormones
  41. 1.
    List the hypothalamic regulatory hormones and
    explain their significance to specific anterior pituitary hormones
    • Corticotropin releasing
    • factor (ACTH release)

    LH releasing factor

    • Prolactin inhibiting factor=
    • Dopamine

    • GH Inhibiting Factor=
    • somatostatin

    GH releasing factor

    Prolactin releasing factor

    • Thyrotropin releasing
    • hormone
  42. 1.
    List the anatomical connections between the retina
    and the pineal gland
    • Neurons in both central and
    • peripheral sympathetic nervous system

    • Rods & cones =
    • photoreceptive cells in retina
    • --sub serve vision cells

    • Ganglion cells =
    • photoreceptive
    • --sub serve non-visual
    • functions

    • Retino-hypothalamic tract
    • --Dark stimulates SCN --> fibers to PVN--> through DLF to spinal cord and out sympathetics to Sup. Cervical g. --> release NE on pinealocytes
    • --Increased CAMP --> increased protein
    • synthesis --> increased melatonin
  43. 1.
    Explain the metabolic conversion of tryptophan in
    the pineal gland
    • Serotonin is the precursor
    • to melatonin

    • Derived from tryptophan
    • --Tryptophan hydroxylase

    • In pineal gland, serotonin
    • is acetylated then methylated to give melatonin
    • --N-acetyltransferase and 5-hydroxyindole-O-methyltransferase
  44. 1.
    Describe the nuroendocrine control of melatonin
    production and secretion
    • N-ganglion cells in retina
    • have melanopsin
    • --Travels through retinohypothalamic tract to stimulate serotonin to become melatonin

    Not regulated by hormones

    Don’t need sight to work

    • 470-475nm most inhibits
    • melatonin
  45. 1.
    Understand the association between variations in the
    circadian melatonin rhythm and certain disease states that involve free
    radicals
    Melatonin directly reduces many toxic oxygen and nitrogen based reactants

    Preserves functional integrity of other antioxidants

    Ischemia/reperfusion injury

    Toxic drug exposure

    Bacterial toxin exposure

    Alzheimer’s or Parkinson’s

    Neonatal sepsis

    Disease states believed to involve free radical damage

    Melatonin levels correlate with total antioxidant capacity of serum

    Melatonin is 60-70 times more effective at reducing DNA damage than either vit C or E

    Melatonin reduces uptake of growth factor by cancer cells

    • Melatonin inhibits telomerase activity in cancer
    • cells
  46. SYMP/PARA FOR EYE, HEART, AND VESSLES
    • Eye
    • - Symp: alpha;
    • dilates pupil, contracts eyelid
    • - Para: constricts
    • pupil, contracts ciliary muscle

    • Heart
    • - Symp: beta1;
    • decreased refractory period & duration of AP= pump more blood
    • - Para: decrease
    • refractory period & duration of AP

    • Vessels
    • -Symp: contraction
    • and dilation
    • o alpha 1 & 2
    • constrict with NE
    • o Beta dilates with
    • Epi
  47. SYMP/PARA LUNGS, GI, AND KIDNEY
    • Lungs
    • -
    • Symp: Beta2
    • bronchodilates, alpha1 decreases gland secretion
    • -
    • Para:
    • bronchoconstricts and increases gland secretion

    • GI
    • -
    • Symp: alpha2
    • decreases secretion, constricts sphincters, relaxes smooth muscle
    • -
    • Para: increases
    • secretion, relax sphincters, contract smooth muscle

    • Kidneys
    • -
    • Symp: beta1
    • secretes rennin, alpha1 increases salt & fluid absorption
  48. SYMP/PARA BLOOD, UT, SWEAT GLANDS
    • Blood
    • -
    • alpha2 increases
    • platelet aggregation

    • Urinary Tract
    • -
    • alpha1 constricts
    • trigone
    • -
    • Para: sustains
    • erection with NO

    • Sweat Glands
    • -
    • Symp only, Ach
    • receptors
  49. SYMP/PARA LIVER, SKEL, AND FAT
    • Liver
    • -
    • Beta2 increase
    • glycogenolysis and gluconeogenesis

    • Skeletal Muscle
    • -
    • beta2 increase
    • glycogenolysis and contractility

    • Fat
    • --Beta1 increases lipolysis
  50. SYMP/PARA PANCREAS AND SALIVARY GLANDS
    • Pancreas
    • -
    • alpha2 decreases
    • insulin secretion

    • Salivary Glands
    • -
    • symp: alpha1,
    • thick viscous mucous
    • -
    • para: Ach, watery
    • amylase filled saliva
  51. 1.
    Describe the anatomy of the brain stem reticular
    formation
    • Precerebellar reticular
    • nuclei:
    • modulate stretch reflexes and muscle tone

    • Raphe system: modulates ascending
    • sensory signals and influences the state of consciousness

    • Central and Lateral groups
    • of nuclei:
    • --Central: main ascending
    • RAS, modulates info to thalamic nuclei and is relayed to cerebral cortex
    • --Lateral: control of
    • movement, taste, and limbic system

    • Catecholamine pathways -
    • locus ceruleus:
    • modulate synapses and contact contractile cells of vasomotor system
  52. 3 LONGITUDINAL ZONES OF RETICULAR FORMATION NUCLEI IN THE BRAINSTEM
    1) RAPHE NUC -- THIN PLATES OF NEURONS NEXT TO MIDSAGITAL PLANE, NT 5-HT

    2) MEDIAL ZONE -- LONG DESCENDING AND ASCENDING PROJECTIONS, INCLUDING GIGANTOCELLULAR RETICULAR NUCLEUS OF THE ROSTRAL MEDULLA.

    3) LATERAL ZONE -- ROSTRAL MEDULLA AND CAUDAL PONS. CRANIAL NERVE REFLEXES AND VISCERAL FUNCTIONS
  53. 4 GENERAL FUNCTIONS OF RETICULAR FORMATION
    MOTOR CONTROL

    SENSORY CONTROL

    VISCERAL CONTROL

    CONTROL OF CONSCIOUSNESS
  54. MOTOR CONTROL IN RETICULAR FORMATION
    TO CEREBELLUM:

    • 1) LATERAL RET NUC (MEDULLA)
    • 2) PARAMEDIAN RET NUC (MEDULLA)
    • 3) RET TEGMENTAL NUC (PONS)

    TO SPINAL TRACTS (RET-SPINAL)

    1) CAUDAL & ORAL PONTINE RET NUC --> MEDIAL RET-SPINAL TRACT --> EXCITATORY SPINAL CORD

    2) GIGANTOCELLULAR (MEDULLA) --> LATERAL RET-SPINAL TRACT --> INHIBITORY SPINAL CORD

    BOTH GROUPS RECIEVE DESC. CORT-RET AND ASC SPINO-RET FIBERS. MAINTAIN POSTURE AND MOD MUSCLE TONE
  55. SENSORY CONTROL IN RETICULAR FORMATION
    CONTROLLING ACCESS OF SENSORY INFO TO ASC PATHWAYS

    NUC RAPHE MAGNUS --> DORSAL HORN --> INH PAIN TRANSMISSION BY INTERNEURONS. RELEASE 5-HT AND ENKEPHALINS
  56. VISCERLA CONTROL IN RETICULAR FORMATION
    CARDIO AND RESP FUNCTIONS IN VENTROLATERAL MEDULLA

    VASOPRESSOR CENTER --> IMLCC FOR CARDIO --> INC PERIPH VASC RESISTANCE AND CARDIAC OUTPUT

    VENTRAL RESP COLUMN -- COUPLED OSCILLATOR NUCLEI FOR INSP AND EXP INCLUDING NUC AMBIGUOUS: CENTRAL APNEA OR ONDINE'S CURSE -- RESP ONLY WITH CONSCIOUS VOLUNTARY ACTION

    • TONSILAR HERNIATION: POST CRANIAL FOSSA; DAMAGE TO VENTROLAT RET AREA:
    • 1) CHEYNE-STROKES -- RESP WITH INTERMITTENT APNEA
    • 2) HYPERTENSION
    • 3) HYPERVENTINLATION
    • 4) DEC CONSCIOUSNESS
  57. RETICULAR CONTROL OF CONSCIOUSNESS
    MIDBRAIN RETICULAR FORMATION

    I- VESTIBULAR NUC, ASC PAIN PATHWAYS INCLUDING SPINORET, SPINOTHAL AND SPINALTRIGEMINAL

    O- PEDUNCULOPONTINE AND LATERODORSAL TEGMENTAL NUC (BOTH CHOLINERGIC) --> THAL (INTRALAMINAR, MIDLINE NUC, NUC RETICULARIS) --> CORTEX.

    DAMAGE = COMA

    TUBEROMAMMILLARY NUC IN HYPOTHAL ALSO MODS WAKEFULNESS --> HISTAMINE --> MAKES YOU DROWSY

    LOCUS CERULEUS NEAR FLOOR OF 4TH VENT IN ROSTRAL PON --> NORMELANIN AND NOREPI --> CENTRAL TEGMENTAL TRACT --> CORTEX --> REG OVERALL EXCITABILITY
  58. 1.
    Identify the monoaminergic systems of the reticular
    formation
    • Catecholamine Pathways
    • -Locus ceruleus: noradrenergic tracts to forebrain and cerebellum
    • ---Mainly inhibitory
    • ---Axons in CFF, DLF, and
    • medial forebrain bundle
    • ---Sleep stages, depression,
    • etc
    • ---Focus attention

    • Histamine Pathways
    • -Tuberomammillary n.
    • ---enhance arousal mechanisms and wakefulness
  59. 1.
    Describe the sleep stages
    • Stages 1-4, Non-REM
    • --EEG: slow waves with high
    • amplitude
    • --Motor: relaxed muscles with
    • frequent position changes
    • --EMG: slow resting
    • --Autonomics: parasymp = decreased BP, HR, respirations & increased GI motility
    • --Dreaming minimal
    • --Neurotransmitter: pontine raphe neuron decreased

    • REM
    • --EEG: low voltage, fast desynchronizing
    • --Motor tone decreases, EMG
    • silent
    • --EOG: rapid eye movements,
    • middle ear muscles contract
    • --Autonomics: symp= increased BP, HR, resp & decreased GI motility
  60. 1.
    Identify some of the reticular areas affecting sleep
    • Raphe
    • System Nuclei

    • raphespinal
    • raphe cerebellar
    • raphe brainstem
    • raphe cerebral
  61. 1.
    Describe some of the problems associated with sleep
    • Narcolepsy
    • o excessive daytime sleepiness,
    • severe= sleep attacks
    • o Cataplexy: sudden loss of muscle tone with
    • consciousness
    • o Sleep paralysis = loss of muscle
    • control in period bt sleep and awake
    • o Hypnagogic hallucinations= false
    • visual or auditory perceptions as a person falls asleep

    • Sleep Apnea
    • o Stop breathing

    • REM sleep behavior disorder
    • o Act out dreams

    Coma: state of extended unconsciousness from which a patient can’t be aroused

    • Concussion: brief loss of
    • consciousness

    • Syncope (fainting):
    • transient loss of consciousness due to widespread neuronal ischemia

    • Stupor: moderate spontaneous
    • movement, can be aroused

    • Obtundation: alertness mildly or
    • moderately depressed, if undisturbed fall asleep

    Somnolence: patient easily aroused showing appropriate verbal and motor responses to stimuli, falls asleep with no stimuli

    • Delirium: agitated/confused with
    • possible illusions, hallucinations, delusions

    • Akinetic mutism: awake and tracking but no
    • response to commands

    • Abulia: sit passively, may respond
    • to commands after long delay (frontal lobe lesions)

    • Locked in Syndrome:
    • awake with eyes open but can’t respond
    • --Bilateral pontine lesions
    • --Blinking only
  62. Causes
    of diminished olfaction
    • Blockage
    • ·
    • Chronic
    • infections (olfactory epithelium replaced with respiratory)

    • ·
    • Receptor
    • destruction

    • ·
    • Trauma

    • ·
    • Intracranial
    • lesions

    • ·
    • Old
    • age

    • ·
    • Disease
    • states (Alzheimer’s, Parkinson’s, Huntington’s)

    • ·
    • Kallmann’s
    • Syndrome (males)

    • o
    • Inherited

    • o
    • Can’t
    • smell, no development due to failed migration

    • o
    • Underdeveloped
    • gonadal function

    • ·
    • Cocaine
    • use
  63. 1.
    Know the type of cells in the olfactory mucosa and
    bulb and their primary connections
    Types of Cells in Olfactory Mucosa

    • Sustentacular
    • cell: pigment
    • ·
    • Receptor
    • cell: cilia contain receptor proteins
    • o can
    • generate ever 60 days
    • o may
    • be direct route for viruses and bacteria to the brain
    • ·
    • Nasal
    • binding protein: absorb excess odorants or deliver odorants to epithelium
    • o secreted
    • from lateral nasal gland
    • ·
    • Fila olfactoria: olfactory nerves passing through cribiform plate

    • Olfactory Bulb Cells
    • ·
    • Mitral
    • cell: terminate in glomerulus (synapse) to form the lateral, intermediate, and
    • medial olfactory stria (all of which secrete Glutamate) -->
    • o Anterior
    • Olfactory n.
    • o
    • Anterior
    • perforated substance
    • o
    • Septal
    • area
    • o
    • Amygdala
    • o
    • Primary
    • olfactory core
    • ·
    • Tufted
    • cell: release glutamate
    • o Cross
    • in anterior commissure
    • o Don’t
    • project centrally
    • ·
    • External
    • granule cell: inhibitory (GABA) between glomeruli
    • ·
    • Internal
    • granule cell: GABA
    • o No
    • axons
    • o Inhibit
    • mitral cell synapses on basal dendrites
    • ·
    • Noradrenergic
    • input from locus ceruleus
    • ·
    • Serotoninergic
    • input from raphe nuclei
  64. 1.
    Know the anatomy of the amygdala and its connections
    • Corticomedial
    • group - olfaction
    • ·
    • Central
    • group - olfaction

    • ·
    • Basolateral
    • group - extensive interaction with cortex

    • Inputs
    • to Corticomedial group
    • ·
    • Olfactory
    • ·
    • Food
    • intake
    • ·
    • Dorsomedial
    • n. of thalamus
    • ·
    • Brainstem
    • taste areas
    • o
    • Nucleus
    • solitarius
    • o
    • Medial
    • parabrachial n.

    • Outputs from corticomedial group (via stria terminalis) ® predatory aggression, no vocal
    • ·
    • Hypothalamus
    • ·
    • Nucleus
    • accumbens
    • ·
    • Septal
    • area

    • ¨
    • Basolateral projections (amygdalofugal) ® affective aggression with vocalizations and posturing

    • ¨
    • Lateral amygdale = fear, violent aggression, attention, fear anxiety
    • ¨
    • Learned
    • fear: emotional context to memories
    • --Central n. --> hypothalamus (autonomic response), periaqueductal gray (behavioral), cerebral cortex (emotional experience)
  65. 1.
    Anatomy of hippocampal formation to include
    afferent, efferents, and internal connections
    Considered part of the limbic system in core of the brain

    • Hippocampal formation
    • --Dentate gyrus
    • -----Molecular layer
    • -----Granule cell layer form mossy fibers that synapse on CA3 pyramidal neurons- excitatory (Glu)
    • -----Polymorphic layer
    • -----Basket cells= inhibitory (GABA) interneurons

    • Hippocampus Proper
    • Molecular layerPyramidal cells layer
    • -
    • Pyramidal cells have apical and basal dendrites- excite

    Polymorphic layer

    Basket Cells

    • Four Regions:
    • Cornu ammon 1:
    • o Pyramidal cells (smaller than CA3)
    • o Axonsto subiculum and entorhinal cortex
    • o Glutamate receptors
    • CA 3
    • o Giant pyramidal cells w/large dendritic tree
    • o Axons in alveus --> fimbria --> fornix to septal nuclei and mammillary bodies
    • o Collaterals to CA 1

    • Subiculum
    • Molecular layer
    • Pyramidal layer - Excitatory
    • Polymorphic layer
  66. 1.
    Functional activity through the circuitry of
    hippocampus
    Major input: entorhinal cortex

    Serial circuit: processing projected in sequential steps

    Parallel circuit: entorhinal info projects directly to each component

    • Trisynaptic Serial circuitry
    • ---Perforant path fibers: entorhinal cortex® dentate granule cells (excite)®Mossy fibers ® CA3 pyramidal cells (excite)® Schaffer collaterals ® CA1 pyramidals (excite)

    • Output Neurons
    • ---Pyramidal neurons form alveus® exit via fimbria and then fornix® other subcortical structures

    • ---Subiculum and hippocampus proper ® entorhinal cortex ® prefrontal cortex, orbitofrontal cortex, parahippocampal gyrus, cingulated cortex, insular
    • cortex

    • Cholinergic inputs:
    • From basal forebrain
    • --N. Basalis of Meynert ® cerebral cortex
    • --Medial septal nucleus and n. of diagonal band of Broca ® hippocampus

    Generally facilitatory

    Rhythmic oscillation: hippocampal theta rhythm

    Dopaminergic inputs: From ventral tegmental area

    • Norepi inputs
    • 1) To entire forebrain
    • 2) From locus ceruleus and lateral tegmental area

    • Serotonergic inputs
    • 1) To entire forebrain and medial temporal lobe
    • 2) From rostral raphe nuclei
  67. 1.
    Functional (behavioral) aspects of hippocampal
    circuitry
    Can influence virtually all associate areas of the temporal, parietal, and frontal lobes

    Long term consolidation of information

    Info from higher order associate areas of cerebral hemisphere is next processed in limbic association cortex of medial temporal lobe (perirhinal, parahippocampal, entorhinal) then to Hippocampal formation which creates a memory representation

    • Hippocampal formation:
    • --Integrates info
    • --Learning and memory
    • --Spatial location
    • --Affective/emotional
    • --Homeostasis

    • Long Term Potentiation
    • --High frequency electrical stimulation at a synapse produces a long lasting increase in synaptic strength between the neurons
    • --Seen in Schaffer collateral-CA1 synapses
    • --CA3 to CA1 has most LTP
    • ----Most NMDA channels and CA1 neurons
    • ----Most sensitive to oxygen loss
  68. 1.
    Pathology and disease states associated with the
    hippocampus
    CA1 pyramidal neurons are susceptible to ischemia due to large # NMDA channels (glutamate receptors)

    • Epilepsy
    • --Loss of neurons in hippocampus associated with temporal lobe epilepsy in CA1, CA3, dentate gyrus,
    • subiculum
    • --Circuit abnormalities
    • --Partial temporal lobe seizures
    • ----Aura
    • ----Unresponsive/unaware
    • ----Repetitive movements

    • Alzheimer’s
    • --Dramatic cell loss in CA1, subiculum, & entorhinal cortex
    • --Neurofibrillary tangles in pyramidal neurons
    • ----Paired helical filament with altered Tau protein
    • --Neuritic (senile) plaques have insoluble core of amyloid fibrils
    • --Hypothesized that it’s due to a loss of cholinergic innervation
  69. SEIZURES, EPILEPSY, AND AURAS
    • Seizure: abrupt change in behavior with electrical discharge
    • o
    • Synchronizes a large population of neurons
    • o
    • Typically begins in neocortex

    • Epilepsy: occurrence of more than one unprovoked seizure
    • ·
    • Auras can help with localization of a seizure
    • o
    • Nausea or
    • tachycardia (insula)
    • o
    • Déjà vu (amygdala)
    • o
    • Visual (occipital lobe)
  70. PARTIAL AND GENERALIZED SEIZURES
    Partial Seizures

    • Simple partial seizures: consciousness not impaired
    • --Motor signs
    • --Sensory symptoms
    • --Autonomic signs/symptoms
    • --Psychic symptoms
    • Complex partial seizures: consciousness is impaired
    • --Impairment of consciousness can develop after
    • simple partial onset or occur from beginning
    • --Unconscious repetition of simple activities

    • Generalized Seizures:
    • --Absence seizures: interruption to consciousness
    • where the person is vacant and unresponsive for a short time
    • --Myoclonic: extremely brief (<0.1s) muscle contraction that can result in a jerky movement
    • --Clonic: myoclonus that repeat at a rate of 2-3/second
    • --Tonic-clonic: initial contraction of muscles (tonic) followed by rhythmic contractions
    • (clonic)
    • --Atonic: loss of muscle tone, person falls to ground

    • Partial seizure can be indicative of an impending
    • generalized seizure (aura)

    • EEG detects interictal spike and wave discharges
    • --Generated by membrane potentials, surface
    • negativity/positivity
    • --Regional differences in potentials over time
    • --Due to conductance of Na+, Ca2+, Cl-, K+

    • Focal epileptic discharge
    • --Paroxysmal depolarizing shift
    • --Absence of stimulation of CA4 basket cells
    • (inhibits)
    • --Granule cell hyperexcitability
  71. ASSOCIATION FIBERS
    • Connect different regions of the same hemisphere
    • --Short Association: arcuate fibers (aka U-fibers) connecting
    • --Long association: connect cortical regions in
    • different lobes
    • §
    • Superior longitudinal fasciculus:
    • --Frontal-parietal-occipital
    • --Superior to the arcuate fasciculus
    • § Superior occipitofrontal fasciculus
    • § Arcuate fasciculus
    • --Connects the superior and middle frontal gyri with temporal lobe—important in speech.
    • § Uncinate fasciculus:
    • --Orbitofrontal-mid/inf
    • frontal- anterior temporal
    • --Connect the orbital frontal gyri and parts of the inferior and middle frontal gyri with anterior portion of the temporal lobe particularly the amygdala.
    • § Inferior longitudinal fasciculus:
    • --Occipital-frontal
    • --Connects occipital gyri with all the temporal gyri
    • § Inferior occipito frontal fasciculus:
    • --Frontal-occipital
    • --Deeper than the uncinate and connects frontal
    • lobe with occipital lobe.
    • § Cingulum:
    • --Connects frontal, parietal and occipital lobes
    • with cingulated and parahippocampal gyri.
    • § Extreme capsule:
    • --Connects fibers from the insula with frontal and
    • temporal cortex. Some fibers from parietal and temporal cortex also use this.

    • Arcuate fasciculus: connects Broca’s and Wernicke’s speech areas
    • o Lesion=conduction aphasia (impaired repetition)

    Parahippocampal commissure/commissure of the fornix: connects hippocampal and dentate gyri
  72. COMMUSSURAL AND PROJECTION FIBERS
    Commissural Fibers : connect corresponding parts of the 2 hemispheres

    • Corpus callosum
    • o Rostrum
    • o Genu—connects rostral parts of frontal lobe
    • o Body—connects some frontal lobe and parietal lobe areas
    • o Splenium—connects temporal and occipital lobe areas

    • Anterior commissure:
    • -- A small anterior portion connects olfactory structures in frontal and mid/inf temporal
    • o Larger posterior portion connects regions of the middle and inferior temporal gyri

    • Hippocampal commissure:
    • o Connects 2 fornices

    Projection Fibers: connect cortex with subcortical structures

    Corona radiata - radiating fibers which converge toward the brain stem to form a compact band - internal capsule

    External capsule - axons from area 4 and from supplemental motor areas destined for the midbrain

    Fornix
  73. ANT NUC (THAL)
    I-Mammillary body
  74. O-Cingulate gyrus
  75. F-Limbic
  76. VA NUC (THAL)
    • I-GLOB PAL
    • O-PREMOTOR CORTEX
    • F-MOTOR
  77. VL NUC (THAL)
    • I-DENTATE OF CEREBELLUM
    • O-MOT/PREMOT CORTEX
    • F-MOTOR
  78. VPL (THAL)
    • I-MED LEM & SPINOTHAL
    • O-SOMATIC SENSORY CORTEX
    • F-SOMATIC SENSATION OF BODY
  79. VPM (THAL)
    • I-SENSORY NUC OF V
    • O-SOMATIC SENSORY CORTEX
    • F-SOMATIC SENSATION OF FACE
  80. MGN (THAL)
    • I-INF COLLICULUS
    • O-AUD CORTEX
    • F-HEARING
  81. LGN (THAL)
    • I-RETINAL GANG CELLS
    • O-VISUAL CORTEX
    • F-VISION
  82. LD (THAL)
    • I-CINGULATE
    • O-CINGULATE
    • F-EMOTIONAL EXPRESSION
  83. LP (THAL)
    • I-PARIETAL LOBE
    • O-PARIETAL LOBE
    • F- INTEGRATION OF SENSORY INFO
  84. PULVINAR
    I-SUP COLLICULUS, PRIM VIS CORT, TEMP, PARIETAL, OCC

    O-TEMP, PARIETAL, OCC

    F-INTEGRATION OF SENSORY INFORMATION
  85. DM (THAL)
    • I-AMYG, OLF, HYPO
    • O-PREFRONTAL CORT
    • F-LIMBIC
  86. CM (THAL)
    • I-RET, GP, CORTICAL AREAS
    • O-BG
    • F-MOD OF MOTOR SYSTEMS
  87. CL (THAL)
    • I-SPINOTHAL
    • O-SOMATOSENSORY PARIETAL CORT
    • F- MOD OF PAIN
  88. RETICULAR NUC (THAL)
    • I-CEREBRAL CORT AND THAL NUC
    • O-THAL NUC
    • F-MOD OF THAL ACTIVITY
  89. MIDLINE NUC (THAL)
    • I-RETICULAR FORMATION, HYPO
    • O-BASAL FOREBRAIN
    • F-LIMBIC
  90. THAL NUCs INVOLVED IN LIMBIC SYSTEM
    • AN
    • DM
    • MIDLINE NUC
  91. THAL NUCs INVOLVED IN MOTOR
    • VA
    • VL
    • CM (MOD)
  92. PAPEZ CIRCUIT
    • CING
    • HIPPO
    • FORNIX
    • MAM
    • THAL (AN)

    CING -- CINGULUM -- HIPPO -- FORNIX (POST COMM FIBERS) -- MAM -- MAMTHAL TRACT -- THAL AN -- THALCORT FIBERS -- CING
  93. BOUNDARIES OF LIMBIC SYSTEM
    • CING
    • HIPPO
    • FORNIX
    • MAM
    • THAL (AN)
    • AMYG
    • PARAHIPPO
    • HYPO
    • PITUITARY
    • DENTATE
    • ENTORHINAL CORTEX
  94. 1.
    Relate given structures in the limbic system to
    specific neural deficits
    • Lesion in hippocampus – become very aggressive
    • ·
    • Lesion in mammillary bodies – become non reactive emotionally
    • ·
    • Lesion in dorsomedial thalamus – spontaneous laughing or crying (uncontrolled)

    • Lesion in cingulate gyrus – become un-reactive to
    • emotional stimuli
  95. Kluver
    Bucy syndrome:
    • Bitemporal lobectomy (amygdala, hippocampus and
    • adjacent temporal lobe)
    • o Was done on monkeys and experimentally on a very very aggressive human patient.

    • Psychic blindness:
    • o Unable to recognize objects based on sight alone.
    • o Put object in their mouth to identify, whether dangerous or not.
    • o Human was able to recognize mother as a female, but not as his mother.
    • o Was able to distinguish between females and males but not within the category.

    • Oral and vocal tendencies:
    • o Exam things with mouth
    • o Vocalizations that have a sexual overtone.
    • o Monotonous talking
    • o Can spell but can’t put letters into sequence and read the word aloud

    • Hypermetamorphosis (akathesia):
    • o Hyperactivity - easily distracted, usually by visual stimuli

    Emotional changes

    • Hypersexuality:
    • o Hetero, homo, auto - all types of sexual behavior

    • Docility:
    • o Very relaxed, can’t even be provoked into bad behaviour
  96. GILASTIC FITS
    LIMBIC



    • ·
    • Spontaneous uncontrolled laughing/crying
    • (inappropriate)

    • ·
    • Altered state of consciousness

    • ·
    • Individuals are unaware

    • ·
    • May be evil-type laughter

    • ·
    • Frequencyàroughly one episode per
    • week

    • ·
    • Treated medically or surgically (psychosurgery)
  97. ANOREXIA NERVOSA
    LIMBIC


    • ·
    • Refusal to keep weight above minimally normal
    • weight

    • ·
    • Intense, irrational fear of weight gain

    • ·
    • Misperception of weight and shape of one’s bodyàstarve,
    • if do eat, work out LOTS

    • ·
    • Delayed menarche and altered menstrual cyclesàyellow
    • skin, drawn features, often wear big clothing

    • ·
    • Age 12-21

    • ·
    • 1% of adolescent females—up to 10% dieàstarve
    • to death
  98. Bulimia
    Nervosa
    • ·
    • binge eatingàintense eating
    • behavior, then purge

    • ·
    • feeling of being out of control

    • ·
    • Frequency of binges—roughly one binge/month

    • ·
    • Purging—get so good at purging, can’t hear them.

    • ·
    • Molars are discolored due to bile acids
  99. Binge
    eating disorders
    LIMBIC

    • ·
    • Recurrent binge eating

    • ·
    • No appropriate compensatory measures: purging,
    • exercise, laxatives

    • ·
    • Noticeable distress over binges

    • ·
    • 2% of adultsàmore in males than in
    • females

    • ·
    • Most are obese
  100. Tourette’s
    Syndrome
    • LIMBIC
    • ·
    • Onset during adolescence
    • ·
    • Vocalization of motor tics --> coprolalia—vulgar
    • phrases, echolalia—repeating everything said, paloalia—repeating everything they say themselves.
    • ·
    • Barking/gruntingàtry to disguise their
    • grunting/barking
    • ·
    • Hysterical personality
    • ·
    • Spontaneous jerking—extreme muscular jerking
    • ·
    • Facial grimacing
    • ·
    • Forceful protrusion of tongue—shrugging
    • shoulders, blinking
    • ·
    • Can be controlled with drugs
    • ·
    • More common in males
  101. Seasonal
    affective disorder (winter subtype)
    LIMBIC


    • ·
    • Associated with short winter days

    • ·
    • Socially withdrawn

    • ·
    • Carbohydrate cravingàweight gain

    • ·
    • Depression; can be very severeàsuicide
    • attempts

    • ·
    • Latitudinal distribution

    • ·
    • Treatment: phototherapy (1/2 hr. of bright light
    • treatment, adjust biological clock)
  102. Korsokoff’s
    psychosis
    LIMBIC


    • ·
    • Usually occurs in alcoholics; thiamine
    • deficiency caused by malnutrition

    • ·
    • Degenerative changes in mammillary nuclei and
    • dorsomedial nuclei of thalamus

    • ·
    • Antherograde and retrograde amnesia

    • ·
    • Confabulation—to cover up memory impairments

    • ·
    • Reduced speech

    Generalized apathy
  103. ENGRAM
    • physical
    • representation or location of a memory in the brain

    • Widely distributed among the connections that
    • link neurons

    • May result/reside in same neurons involved in
    • perception of stimulus
  104. LIST SYNDROMES OF LIMBIC SYSTEM
    • GILASTIC FIT
    • ANOREXIA NERVOSA
    • BULIMIA NERVOSA
    • BINGE EATING
    • TOURETTE'S
    • SEASONAL AFFECTIVE DISORDER
    • KORSOKOFF'S PSYCHOSIS
  105. DECLARATIVE AND NONDECLARATIVE MEMORY
    • Nondeclarative Memory: info on how to perform
    • something
    • ·
    • Recalled unconsciously
    • ·
    • Training reflexive motor or perceptual skills
    • ·
    • Simple Forms:
    • 1) Nonassociative learning: subject learns about properties of a single stimulus
    • ---Habituation: ability to ignore a benign stimulus when presented repeatedly
    • ---Sensitization: enhanced response to a noxious stimulus
    • 2) Associative learning: subject learns about
    • relationship between 2 stimuli or between stimulus and behavior
    • --Classical conditioning= pairing of 2 stimuli, when CS follows US, CS will begin to elicit a response
    • ----Conditioned stimulus- produces no response
    • ----Unconditioned stimulus- produces strong consistent response

    • Complex Forms:
    • 1) Priming: improvement in the ability to detect or identify words or objects after recent experience with them
    • --Unconscious

    • 2) Perceptual learning: improvement in the ability to discriminate different simple perceptual attributes
    • --Memory in sensory cortical areas responsible for detection

    • 3) Emotional learning: prior experiences influence the way we feel about the information processed
    • --Unconscious
    • --Amygdala: Lesion= no emotional responses during fear conditioning. Integration of storage supports nondeclarative

    • 4) Motor skills: embedded in procedures
    • --Expressed unconsciously through performance
    • --Sensorimotor cortices and neostriatum

    • 5) Habit learning: acquire a procedure for operating in the world
    • --Neostriatum

    • 6) Conditioning: stimulus precedes a biologically significant stimulus such as food or shock
    • --Pairing 2 stimuli so the response that is normally elicited to the biological stimulus is elicited by the neutral stimulus
    • --Delay conditioning
    • --Cerebellar cortex and interpositus deep cerebellar nuclei

    Declarative Memory

    Semantic: general knowledge of facts and concepts that isn’t linked to any particular time and place (naming object, verbal fluency)

    • Episodic: explicit recollection of incidents that
    • occurred at a particular time and place in one’s personal past
  106. 1.
    Memories have stages: short-term and long-term memory
    Short Term

    • Immediate memory: held actively in the mined the moment it is received.
    • --Limited capacity
    • --30 seconds
    • --stored in regions responsible for higher order
    • analysis of the perceived stimulus

    • Working memory: info in immediate memory
    • is rehearsed and retained for many minutes in working memory
    • --Phonological loop concerns language and
    • temporarily stores spoken words
    • --Visuospatial sketch pad stores images such as
    • faces and spatial layouts
    • --Prefrontal cortex, sensory cortices and higher
    • order association cortices

    Long Term

    Stored in same distributed set of neurons that perceive, process, and analyze what is to be remembered

    • Semantic memory: built up through
    • association over time
    • --Interconnections between areas
    • --Not stored in a single region
    • --Lesions: Posterior parietal cortex- associative visual agnosia. Cannot name objects but can identify and draw. Visual association areas in occipital lobe and
    • surrounding temporal- apperceptive visual agnosia, Can name but can’t draw. Inferior temporal cortex- prosopagnosia, Can’t recognize faces or learn new ones

    • --Episodic Memory: recall of where and when an event happened.
    • ----Frontal lobes
    • ----Lesion - source of amnesia, can remember facts without recognition of events involving people

    • Short to Long Term:
    • --Medial temporal lobe. Damage impairs consolidation of all declarative memory
    • --Hippocampal formation for shorter term
    • declarative memory recall
  107. Memory has 5 distinct processes
    • encoding, consolidating, storage, retrieval and
    • forgetting

    • Encoding: process by which newly learned info is
    • attended to and processed when first encounteredFor good memory, info must be associated with
    • well established knowledge

    • Consolidating: process that alters newly
    • acquired info to make it more stable

    Storing: mechanism and sites of storage by which memory is retained over time

    • Retrieving: processes that permit the recall and use
    • of stored information. Most effective when in same context in which info was acquired

    Forgetting: memories weaken over time. Best at generalizing, abstracting, and assembling general knowledge
  108. 1.
    Various forms of declarative and non-declarative
    memories and to identify brain locations involved in their storage
    • Long term declarative memory
    • · Stored in the same distributed set of neurons that perceive, process and analyze the info to be remembered

    • Semantic memory:
    • Built up through association over time.

    Accomplished by interconnections between association areas used to store the information

    Ability to recall depends on how well these associations have organized the information to be retained

    Storage spreads across higher order association areas of cerebral cortex

    Posterior Parietal Cortex. If lesioned, patients can’t name objects but can identify the object by selecting the correct drawing and can reproduce a detailed drawing of the objects --> associative visual agnosia

    • Ventral association areas. In occipital lobe and surrounding temporal lobe. If lesioned, patients can’t draw objects but can name them --> appreciative
    • visual agnosia

    Inferior temporal cortex. If lesioned, patient unable to recognize faces or learn new ones (all other aspects of visual recognition remain intact --> prosopagnosia

    • Episodic memory
    • Stored in association areas of frontal lobe

    • They work with other association areas of neocortex
    • to allow recall of where and when an event happened

    If frontal lobe damage – tend to forget how information was acquired --> source amnesia

    Still have ability to recall large amount of factual (semantic) information
  109. 1.
    Amnesia and possible causes of memory loss
    Amnesia: Loss of memory or ability to learn

    • Damage to medial temporal lobe or related
    • areas.

    Alzheimer’s: degenerative disease that affects consolidation and storage of declarative memory. Early pathological changes seen in entorhinal cortex.

    Transient global amnesia: short period of amnesia with sudden onset of anterograde amnesia lasting from minutes to days in combination with retrograde amnesia for recent events
  110. Neural plasticity
    • Process of altering synaptic pathways in response
    • to continual stimulation

    • Represents the biological basis of learning and
    • memory

    LTP (long-term potentiation): if 2 neurons are active at the same time, the connection between them may be strengthened: "fire together wire together”
  111. Activity Dependent
    Facilitation of Synaptic Transmission
    • Neural habituation:
    • --Response to a novel stimulus
    • --If repeated stimuli prove neither harmful or
    • helpful, subsequent stimuli may be ignored
    • --Decreased glutamate releasenon-NMDA receptor activation only
    • --Sensitization is an increasingly more vigorous
    • response to repeated stimuli

    • Neural sensitization
    • --Complex response to harmful stimuli
    • --Increased responsiveness
    • --Both non-NMDA and NMDA receptor activation
  112. Mechanism for Long Term
    Potentiation (LTP)
    • Early LTP (single train of AP)
    • Presynaptic release of glutamate, activates
    • non-NMDA receptors (NMDA blocked by Mg2+)

    • Repeated stimulation of post-synaptic non-NMDA
    • (Na+ influx)

    Depolarization

    Mg2+ expelled from NMDA receptors

    Ca2+ influx through NMDAs

    • Activates NO synthase (enhances presynaptic
    • glutamate release)

    • Late LTP (repetitive train of AP)
    • Activates calcium calmodulin dependent kinase II
    • (CAMKII)

    • CaMKII phosphorylates AMPA receptors, more
    • sensitive to Na+ inflow and depolarization (can increase the number of receptors at synapse)

    • Activates camp dependent PKA: translocated into
    • nucleus where it phosphorylates camp response element binding protein (CREB-1)

    • CREB-1 binds to camp response elements: enhanced
    • gene expression for proteins involved in growth of new synaptic connections

    • End result of LTP
    • Enhanced synaptic transmission both at receptor level and through an increase in the # of axodendritic synapses
  113. DYSARTHRIA AND APRAXIA DEFINITION
    • Dysarthia: neuromuscular speech disorders with abnormal muscle movement, muscle, condition, or both.
    • --Muscles are affected for all movements, reflexive, volitional, and automatic.
    • --Dysarthria is a disorder of execution not programming

    Apraxia: phonetic-motor disorder of speech production caused by inefficiencies in the translation
  114. FLACCID PARALYSIS
    • Lower Motor Neuron
    • Fasciculation
    • Fibrillation
    • Flaccid condition
    • Hypotonia
    • Hyporeflexia
    • Atrophy

    • SX
    • Short Phrase Length
    • Reduced Loudness
    • Breathy Voice
    • Hypernasality
    • Articulatory
    • Imprecision
  115. SPASTICITY (SPEECH)
    • Upper Motor Neuron
    • Hypertonia
    • Hyper and abnormal reflexia
    • Clonus

    • SX
    • Hypernasality
    • Short Phrases
    • Harsh Voice
    • Low Pitch
    • Slow Rate
    • Strained Voice
    • Breathy Voice
  116. HYPOKINESIA
    • Basal Ganglia (substantia nigra)
    • Bradykinesia
    • Rigidity
    • Cogwheeling
    • Resting tremor
    • Pill rolling

    • SX
    • Reduced Loudness
    • Monopitch
    • Inappropriate Silences
    • Short Rushes of Speech
    • Variable Rate
    • Imprecise Articulation
  117. ATAXIA - CEREBELLUM (SPEECH)
    • Impaired synergy
    • Hyper-and hypo-metria
    • Impaired diadochokinesis
    • Action or intention tremor

    • SX
    • Equal/Excess Stress
    • Irregular
    • Articulatory
    • Breakdown
    • Distorted Vowels
    • Excess Loudness Variation
    • Prolonged Phonemes
  118. HYPERKINESIA - BG (SPEECH)
    • Chorea
    • Athetosis
    • Dystonia

    • SX
    • Palilalia
    • Prolonged Intervals
    • Sudden Forced Insp/Exsp
    • Intermittent
    • Hypernasality
    • Coprolalia
  119. APRAXIA - LEFT FRONTAL (BG?)
    • PROGRAMMING
    • GMPs, PARAMETERS

    • SX
    • Poor SMRs
    • SMRs (pataka)
    • Articulatory Groping
    • Distortions of Sounds
    • Equal Stress
    • Segmentation of Speech
    • Inconsistent Errors
  120. Differential Diagnosis
    AOS vs. Dysarthria
    • AOS: Variable and often inconsistent
    • Dysarthria: Consistent and often invariant

    • AOS affected by automaticity
    • Dysarthria less affected by automaticity

    • AOS affected by utterance length
    • Dysarthria less affected by utterance length

    • AOS-complications of target phonemes with additions, simplifications, substitutions, distortions, and prolongations
    • Dysarthria-simplification of target
    • phonemes and predominance of distortions

    • AOS-trial and error, effort groping
    • Dysarthria—no groping

    • AOS-SMR < AMR
    • Dysarthria-SMR=AMR
  121. APHASIA
    • Phonology
    • Syntax/Morphology
    • Semantics
    • Affects linguistic rule system

    • Etiology
    • Typically left hemisphere stroke
    • Perisylvian Region (frontal, parietal, temporal)
    • Middle Cerebral Artery

    • Symptoms
    • Aphasia affects all language modalities
    • Oral Production
    • Auditory Comprehension
    • Reading
    • Writing
  122. BROCAs WERNICKEs
    • Broca’s Aphasia: Lesion- BA44- -Frontal Lobe
    • Non-Fluent Agrammatic output
    • Poor repetition of speech
    • Impaired comprehension (better than output)
    • Effortful speech
    • Impaired Naming

    • Wernicke’s Aphasia: Lesion, BA22, Temporal Lobe
    • Fluent
    • Paragrammatic Speech
    • Jargon
    • Impaired Naming
    • Impaired Auditory Comprehension
    • Reading and writing impaired

    Global Aphasia: Large perisylvian lesion Frontal, Temporal, Parietal

    • All areas of language severely impaired
    • Non-Fluent
    • Often a single stereotypical utterance (ooo-by)



    • Right Hemisphere Language Symptoms
    • Pragmatic impairment (use of language in social contexts)

    • Impaired humor
    • Impaired prosody (speech melody)
    • Impaired Insight
  123. FRONTAL SYSTEMS
    prefrontal lobes and white matter links to various association cortices/limbic area and to subcortical areas like basal ganglia and thalamus

    · Responsible for intention: developing and executing plans
  124. Dorsolateral
    Prefrontal Cortex
    · Brodmans 9-12, 45, 46, part of 47

    · Analyze external criteria of new task and develop a motor plan for execution

    · Role in working memory

    · Heavily connected to sensory association cortices

    · Blood supply= middle cerebral

    · Lesion: dysexecutive function syndrome
  125. Orbitofrontal
    cortex
    · Uses internal criteria for developing plans and decision making concerning novel situations

    · Dependent on previous memories and primitive limbic urges

    · Planning associated with expectation, reward, punishment

    · Personality

    · Lesions: inappropriate social behavior, lack sense of responsibility
  126. Dorsomedial
    Cortex and Anterior Cingulate Cortex
    · Initiating and sustaining behavior

    · Reward anticipation, decision-making, anticipation, motivation, empathy

    · M3 motor cortex here

    · Anterior cingulated gyrus has some autonomic control possibly because of emotional connection

    • · Anterior cingulated cortex activated by tasks that elicit some form of conflict for the individual
    • --Stroop test- word colors
  127. TESTS FOR FRONTAL SYSTEMS
    • Utilization behavior = action with object requires no thought in execution
    • --Prefrontal lobe damage: actions executed at improper time/place

    • Thurstone Word Fluency Test= list words beginning with specific letter
    • --Failure indicates inability to develop and execute a strategy to search memory

    • Trailmaking Test= connect line between numbers and letters
    • -- Failure: can’t resist natural tendency to go in order rather than alternate between numbers and letters
    • -- Dorsolateral prefrontal lobe damage

    • Abulia: Lost will or motivation to perform
    • normal daily functions
    • -- Stroke damaging frontal lobe

    • Mental Status Exam:
    • Orientation and memory

    Attention- working memory (repeat #s, World backwards)

    Judgment and abstract reasoning (scenario and response, how 2 objects are like, proverb interpretation)

    Set generation (word fluency test)

    Receptive language (follow directions, read and do)

    Expressive language (describe picture, write sentence about pic, read a paragraph and recall info about it, name objects and function, repeat sentence)

    Praxis (perform skilled motor tasks with no nonverbal prompting, face the limbs, imitate actions or pretend like doing an action)

    Gnosis: ability to recognize objects perceived by senses (close eyes and recognize an object in hand, write # in palm)
  128. The basic anatomical pathway by which we direct our
    attention or selectively engage objects in our environment or cause us to seek out the source of distractions by sounds, tactile and visual stimuli
  129. 1.
    The clinical model of attention
    • Sohlberg and Mateer hierarchical model
    • o Focused attention: ability to respond discretely to specific stimuli
    • o Sustained attention: ability to maintain a consistent behavioral response during continuous and repetitive activity
    • o Selective attention: ability to maintain a consistent behavioral response while ignoring distracting stimuli
    • o Alternating attention: capacity for mental flexibility that allows individual to move between tasks with differing cognitive requirements
    • o Divided attention: respond simultaneously to multiple demands
  130. 1.
    Inattentional blindness
    · Perceptual blindness

    · Not being able to see things that are actually there

    · No internal frame of reference or result of lack of focus and distraction
  131. 1.
    Visual search, feature search and conjunction search
    • Visual Search
    • · Active scan of visual environment for a particular object or feature among other objects or features
    • · With or without eye movements

    • Feature Search
    • · Searching for targets with a unique set of features
    • · Usually efficient

    • Conjunctional Search
    • · Target stimulus is defined by a combination of features, not one
    • - Typically inefficient
  132. 1.
    Spotlight theory
    · Attention is like a moveable spotlight that is directed towards intended targets, focusing in a serial manner

    · When info is attended to, processing is more efficient

    · Shift of spatial attention shifts attention to next attended location
  133. 1.
    Understand how genes and environment may play a role in attention
    deficit/hyperactivity disorder (AD/HD)
    · Smaller brains

    · Catecholamine rich fronto-subcortical systems: disruption could be causing problem

    • · Executive function impairments
    • o Working memory and recall
    • o Activation, arousal, effort
    • o Emotion control
    • o Internalizing language
    • o Complex problem solving

    · Problems with attention, impulsivity, over activity

    · Genetic component though not well defined

    • Progressive supranuclear palsy: difficult to exert voluntary eye movements, particularly vertical ones
    • o damage in midbrain and associated cortical areas
    • o still able to shift attention covertly

    Overt attention: change in spatial attention with eyes moving

    Covert attention: change in attention with eyes remaining fixed

    Mind wandering: attention shifts to matters unrelated to the external environment (spontaneous thought)

    • Executive Function: frontal cortex that controls our thoughts and actions to produce coherent behavior
    • o maintaining behavioral goals and using goals as a basis for choosing what aspects of the environment to attend to

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