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SLIDE 20
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A
SLIDE 12
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B
D
E
F
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SLIDE 18
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SLIDE 19
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SLIDE 23
B
A
E
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D
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SLIDE 24
G
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SLIDE 26
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B
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D
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SLIDE 30
C
B
A
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Drawings by Neglect Patients
Extinction?
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7. Which of the following statements is FALSE? A.
coma follows central herniation involving the
diencephalon B. there can be pupillary and eye
movement problems following central herniation C.
a lesion of the spinal cord does not result in
coma D. locked in syndrome results from
bilateral damage to descending corticospinal and
corticobulbar pathways within the basilar
(ventral) pons E. the ARAS is involved in the
locked in syndrome
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17. Which of the following associations is/are
correct regarding the four different stages of
damage shown here? A. in A there are normal
calorics B. in B there is
decerebrate rigidity C. in C the pupils are
meiotic D. in D pupils are dilated E. in A the
pupils are constricted8
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3. Partial seizures that impair consciousness A.
are called a complex partial seizure
B. patient remembers what they do during
seizure C. never evolve to tonic-clonic D. do not
involve the limbic system E. none of the above
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21. The human circadian pacemaker is located in
the A. supraoptic nucleus B. pineal C. pons D.
pituitary E. suprachiasmatic nucleus
2. Which of the following nuclei are
GABA-ergic? A. LC B. dorsal raphe C. LTD
LDT D. PPT E. none of the above
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• Epilepsy Reading
• child space out  go into a trance, roll his eyes
  back in his head had hundreds of seizures daily
• child had cortical dysplasia an area of grey in
  the frontal lobe  was up to five times as thick
  as normal
• medication/drugs successfully controlled the
  seizures
• the operation removed significant portion of the
  child's frontal lobe.  Thus, while the seizures
  were alleviated, the child's future prospects are
  poor

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LITTLE ALBERT done by John B. Watson was
afraid of loud noises (US)-conditioned with a
nice white rat- and other neutral things like a
Santa Clause maskDREAMING during dreamingareas
of brainareas areas responsible for emotions,
fears and memories are activated---in contrast,
areas notably for their role in logic seem to
excuse themselves from the party CARTOONS
activate VTA-Accumbens-the same reward circuits
in the brain that are tickled by cocaineBRITISH
ACCENT some stroke don't recover their normal
speech and when they only have very, very
residual effects left its heard as an accent
LEPTIN-is released by fat cells and tells the
brain how much fat is on the body ECSTACY
release of serotonin, blocks its reuptake, and
depletes amount in brain
17

beta-awake-18-25 cps-10-30 microvolts desynchronou
slow amp.- high freq.
.

alpha-relaxed-eyes closed-8-13 cps-relaxed adult
stage 1-theta4-8 cps-dreamlike hypnic jerks

stage 212-14 cps-sleep spindles K complexes-
stage 3/41-4 cps-slow wavedeltaorthodoxres--ti
ve in infants-
REM-like stage 1-paradoxicalactive in infants
deltasynchronoushigh amp.- low freq.
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WAKING-AROUSED
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GABA TIME
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DR and LC were firing in NR
DREAM TIME
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• REM Sleep-phasic (episodic) tonic (persistant)
• rapid eye movements flaccid paralysis
• muscle twitches
• variable heart rate

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• acetylcholinekeeps you awake
• nicotine Ach agonistkeeps you awake for those
  all- nighters
• histamine from caudal hypothal.wakefullness
• antihistaminesedation
• DA and NEwakefulness via amphetamines and
  cocaine
• cortisol and CRH result in arousal

.
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• age is major determinant of how we sleep
• newborn sleeps 16-18 hours a day widely
  distributed in the 24 hours

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• Organization of Sleep
• 5-7 in Stage 1
• 50 Stage 2
• 7 Stage 3
• 11 Stage 4
• 20-25 REM
• cycles of REMNREMeach 90-110 minutes
• stages 3 and 4 most prominent early
• REM-lengthens later in nightmore intense dreams

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• ELDERLY
• approximately same REM (25) but more napping
• less (or absent) stage 3-4 (the good, delta
  stuff!)-replaced by Stages 1 and 2
• major sleep problem is insomnia
• more napping
• total hours of sleep same
• sleep apnea (cessation of breathing) and
  noctural myclonus (periodic leg movements)

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Suprachiasmatic nucleuscircadian _at_ a day
lesion SCN arrhythmic but AMOUNT OF SLEEP DOES
NOT CHANGE light most impt. for entrainment of
biol. clock

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live in cave circadian (about a day) rhythms
persist (core temp., hormone secretions) no
entrainment from normal environment
(Zeitgebers) no clues to tell him/her the
time does things when one feels like it innate
circadian oscillation takes over free running
period of between 24.5 and 25.5 hrs. cave
person goes to bed one hour later each
night core temp. lowest when he/she goes to sleep
because greatest propensity for sleep is at
coolest time (try getting up at 5AM)
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• Neuroendocrine
• thyroid stimulating hormone peaks prior to sleep
  onset its secretion is inhibited by sleep
• growth hormone (GH)-early part of the sleep and
  its secretion is enhanced by SWS
• prolactin secretion during the middle of the
  night may increase REM sleep maximal levels
  early AM
• cortisol levels rise at the end of the sleep or
  right after waking upmorning arousalsleep onset
  is inhibitiory
• melatonin from pineal gland-released at night,
  even if wakeful nocturnal melatonin release
  inhibited by light
• sleep in the day no release

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• Thermoregulation
• brain and body temperature are down-regulated
  during NREM sleep, particularly SWS--go to sleep
  feeling somewhat cold and wake up several hours
  hot
• during REM sleepdecreased ability to regulate
  body temperature through sweating and shivering.

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SOME SLEEP DISORDERS

• NARCOLEPSY

• CATAPLEXY sudden attacks of REM sleep than can
  last 5-30 min.
• due to emotional stimulus, patient falls (loss of
  muscle tone
• exhibit sleep paralysis with hypnagogic
  hallucinations
• hypocretin/orexin-hypothalamus (around peri
  fornix) excite ARAS cellsnarcolepsyfall asleep
• 2. PERIODIC LIMB MOVEMENTS
• Babinski-like response common cause of insomnia
• 3. RESTLESS LEG SYNDROME
• creepy-crawly sensations in legs around bed time
• irresistible urge to move legs

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• process S-longer one stays awake, greater
  propensity
• to sleep
• process C-circadiantied to time of day like
  clock
• and does not need to be reset
• sleep onsetgreatest separation between S and C
• S occurs around 10-11 PM (for me) and C later
  in night

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• A. diffuse cortical-thalamic damage patient
  exhibits contralateral flexion of arms and
  extension of legs DECORTICATE RIGIDITY
• small pupils-Hornerspressure on hypothalamus
  (cells project toT1-L2) pupils reactive as CN 3s
  are OK, but arent very big to start with
• calorics OK as vestibulo-ocular reflex is
  fine- as CN 8 gets info. to vestibular nuc.-get
  DOLLS EYES-no snap back-lack of cortical input

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DOLLS EYES
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B. focal cerebral lesion with central mass effect
(pushes on deeper structures) decorticate
rigidity flexion/arms and extension/legs
pupils mid-sized and unreactivebilateral
interruption of the descending autonomics and
stretching of CN IIIs. Calorics/VOR
affected-right ear with warm watermovement of
the left eye (right vestibular apparatus, right
vestibular nuclei, left PPRF and left LR6 are
fine). However, the right medial rectus does NOT
contract as CN III is shot. No DOLLS EYES.

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C. Lesion lies between superior and inferior
colliculi bilateral extension of upper and
lower limbs DECEREBRATE RIGIDITY large,
un-reactive pupils-CN 3s are shot and descending
autonomics headed for T1-L2-pupils are
midposition (makes sense if both inputs lost)
Calorics/VOR affected-right ear with warm
watermovement of the left eye (right vestibular
apparatus, right vestibular nuclei, left PPRF and
left LR6 are fine). However, the right medial
rectus does NOT contract as CN iii is shot. No
DOLLS EYES


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D. Lesion in medulla (yeah level 3!!) kind of
wash motor-wise pupils are still in midposition
(descending autonomics and CN III are shot!) and
fixed (remember, the lesion now runs the length
of the brainstem). Since the vestibular
nerves/nuclei are now damaged, the VOR does not
work.

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left cortical mass develops fast and kills CST
fibers immediately. Cortical swelling pushes
left uncus through tent, resulting a left dilated
pupil and right hemipl/Bab (contra to dead CST
cells also can smash left CP). Then opposite
cerebral peduncle pushed against free border of
tentbilateral hemipl/Bab.
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locked inrespiration, sleep cycles, and EEG
are fine
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(No Transcript)
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EPILEPSY THREE SLIDES TO GO!!! (well,
maybe not.have you been sleeping?)
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child space out  go into a trance, roll his eyes
back in his head had hundreds of seizures
dailychild had cortical dysplasia an area of
grey in the frontal lobe  was up to five times
as thick as normalmedication/drugs
unsuccessfully controlled the seizures the
operation removed significant portion of the
child's frontal lobe while the seizures were
alleviated, the child's future prospects are good
42

• Partial Seizure- if EEG and behavioral evidence
  indicate that they begin in a part of the brain
  limited to one hemisphere
• simple partial no alteration in awareness-can
  progress to
• complex partial alteration in awareness (2-3
  minutes)
• simple partial and complex partial can progress
  to secondarily generalized seizure

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• Generalized Seizure- when EEG and behavioral
  evidence indicate they begin bilaterally-always
  an alteration of consciousness
• tonic muscle rigidity-either flexion or
  extension
• tonic clonic (1-2 minutes) grand mal
• clonic
• atonic
• absence (petite mal few seconds)-petit mal