ANP1106B/C Anatomy & Physiology II

Online Narrated Version Frank Feiner, PhD, MD Lecture 22. April 2, 2020
Posted April 2, 3:30 PM University of Ottawa, Ottawa, Canada

Central Nervous System, Part 2

Albert Einstein Marie Curie

(1879 – 1955) at (1867 – 1934) at
age 19 age 36
WHAT IS SAID IN THE COURSE
STAYS IN THE COURSE
DISCLOSURE: You may only access and use this
presentation for educational purposes, and may
not post it online or distribute it without the
permission of the author
SOURCE / SOURCE
SOURCE

SOURCE/ SOURCE
2
 LECTURE CONTENT
 CNS, Part 1. Professor Elbeshbishy, Ch 12
(Topic 6.2)
o Brain Anatomy & Physiology (pp 434-458)
o Protection of the Brain (pp 464-468)
o The Spinal Cord (pp 470-481)
 Central Nervous System, Part 2, Ch 12 (Topic 7.5)
o Higher Mental Function (pp 458-464)
o Homeostatic Imbalances (pp 467-470)
o Diagnostic Procedures (p 470)

Final Exam Information

3
458-459
HIGHER MENTAL FUNCTIONING
 How much do we understand?
“During the last five decades, an exciting exploration of
our ‘inner space,’ or what we commonly call the mind, has
been going on. But cognitive researchers are still
struggling to understand how the mind’s qualities spring
from living tissue and electrical impulses. Souls and
synapses are hard to reconcile!”

4
July 25, 1989 April 2, 2013
459-460
LANGUAGE
 Highly important and complex brain function
o Involves ~all of association cortex (integrates diverse
information for purposeful action) on left side of brain
o Initially, Broca’s & Wernicke’s areas considered to be
critically important. Now seen to also involve basal
nuclei/ganglia (next sl)

Figure 12.7a
Basal nuclei:
• Caudate nucleus
• Putamen
• Globus pallidus Figure 12.10a
(next slide) 5
459-460
LANGUAGE
 Highly important and complex brain function (ct’d)
o Broca’s aphasia Loss of language abilities

Expressive/n •
‘

onfluent
Can understand language, can’t speak
o Wernicke’s aphasia
aphasia’

• Can’t understand language, can speak

but nonsensical ‘word salad’ (‘fluent
aphasia’ – video)
o Clinically useful but oversimplified:
• Both areas & basal nuclei form single
language implementation system: Source

 Analyze incoming/ produce outgoing word sounds

and grammar
• Surrounding cortical areas bridge this system to
regions of cortex that hold concepts and ideas
(distributed throughout cortical association areas) 6
459-460
LANGUAGE
 Right (Non-Language-Dominant) Hemisphere
o Nonverbal emotional/affective ‘body language’
• Gestures/tone of voice: feelings communicated
• Adds understanding to what we hear

7
455-456
LANGUAGE
 Right (Non-Language-Dominant) Hemisphere
o Nonverbal emotional/affective ‘body language’
• Gestures/tone of voice: feelings communicated
• Adds understanding to what we hear
E
A F 1- aggressive
D
2- interested
3- lying
4 - menacing
5 - not open to
communicating
6 - thinks you’re
stupid

B
C 7
459-460
LANGUAGE
 Right (Non-Language-Dominant) Hemisphere
o Nonverbal emotional/affective ‘body language’
• Gestures/tone of voice: feelings communicated
• Adds understanding to what we hear
E
A F

2- interested
3- lying
4 - menacing
5 - not open to
communicating
6 - thinks you’re
stupid

B
C 7
460
MEMORY
 Storage and Retrieval of Information
o Essential for learning, incorporating experiences into
behaviour
o “Part and parcel of our consciousness”
o Different kinds of memory
• Declarative (fact)
 eg Names, faces, words, dates, etc
• Procedural (skill)
 eg Playing the piano
• Motor
 eg Riding a bike
• Emotional
 eg Fear when you hear a rattlesnake nearby
o Declarative memory storage involves 2 distinct stages:
short-term and long-term memory (see below) 8
460
MEMORY
 Short-/Long-Term (STM/LTM)
o Sensory input floods cortex
o Processed in temporary buffer
o 5% selected for transfer to STM
(working memory). Limited
capacity. Temporarily holds data
we may want to remember.
Some forgotten. Rest is lost
permanently
o Some picked for transfer to LTM.
o Limitless capacity, but ‘leaky’

Figure 12.19
9
460
MEMORY
 Long-Term Memory
o Factors influencing what gets transferred to LTM:
• Emotional state: learn best when alert/motivated etc
• Rehearsal: repeating material
• Association: tie new to old
information already in LTM
• Automatic memory: not all LTM
consciously formed
o Data transferred to LTM not
initially permanent: requires consolidation – fit new
facts into previously developed knowledge categories
o Specific pieces of each new memory (‘traces/ engrams’)
stored in brain regions where they can be quickly
associated with old, eg visual memories in occipital
cortex 10
460-461
HOMEOSTATIC IMBALANCES
 Anterograde Amnesia
o Stored memories preserved, but new memories can’t be
made
o Sufferer end up living in the here and now , eg
• No recollection of conversation even 5 minutes prior
o Can be from bilateral damage to hippocampus
o Or intended effect of [illegal] ‘date-rape’ drugs, eg
flunitrazepam (Rohypnol, ‘roofies’)
o Seen with similar benzodiazepines (eg Valium), for sleep,
pre-op, etc
 Retrograde Amnesia
o Loss of memories
formed in the past
13 11
461
BRAIN WAVE PATTERNS AND THE EEG
 Electroencephalogram
o Brain function: continuous
neuron electrical activity
o Electrodes, usually attached
to the scalp, record cerebral
cortex ‘brain wave’ activity
• Outer 2-4 mm, gray matter Figure 12.20a

o Electrodes may be inserted,

via ‘burr holes’ drilled through
the skull, deep inside the brain
to record processes of interest,
eg areas where certain seizures
can originate
12
461
BRAIN WAVE PATTERNS AND THE EEG
 Electroencephalogram (continued)
o 4 general classes of brain waves:
• Used to diagnose sleep disorders (subsequent slide)
• Also to demonstrate ‘brain death’: “flat line”

Old technique, first used almost

Alpha
a century ago (1929): “The
electrical beat of the brain.” Still
in use but very limited
Beta information on brain
structure/function

Theta

13
Delta Figure 12.20b
461
BRAIN WAVE PATTERNS AND THE EEG
 Electroencephalogram (continued)
o Use of newer brain imaging methods (eg CT, MRI, fMRI
SPECT, PET – see below) compliment/replace EEG
o EEG remains ‘gold standard’ for epilepsy diagnosis
• ~50% false negatives: normal EEG / known epilepsy

Spike wave
suggestive of
epilepsy in a
standard
20-lead EEG

14
 462
HOMEOSTATIC IMBALANCE: EPILEPSY
 Definition, Causes and Types
o A torrent of deviant electrical discharges from
groups of brain neurons
o Causes: genetic, ‘idiopathic’ [cause unknown,
20-40%], or from eg head trauma, stroke, Seizure focus
(macroscopic –
cancer, infection, etc, etc sub-microscopic)

• Originates in an (often unknown) ‘seizure focus’

o Two types:
• Generalized Seizures – involve entire brain
 Accompanied by loss of consciousness (LOC)
 Grand Mal: ‘Tonic-clonic’ convulsions – min

Tonic phase (rigid) Clonic phase (shaking)

 Absence/Petit Mal. No convulsions –

15
seconds to minutes
 462
HOMEOSTATIC IMBALANCE: EPILEPSY
Grand Mal (Tonic- Petit Mal (Absence)
Clonic) Seizure Seizure

https://www.youtube.com/watch?v=eH-eEE52F6Y
https://www.youtube.com/watch?v=q4bIyIS0eT4v

16
462
HOMEOSTATIC IMBALANCE: EPILEPSY
 Types (continued) Symptoms depend on location of focus
o Second type:
• Partial Seizures – involve only small part of brain
 Clouded consciousness (‘complex’)/no LOC (‘simple’)
 See/hear/smell/taste/feel what isn’t (hallucinate)
 Limb moves/can’t move, grimace/shrug
 Absent minded / forget words / blank out/ ‘spacey’
 False memories (déjà vu)  Out-of-body
 Exceptional mental acuity  ‘Mystical’ feeling
o Treatment:
• Antiepileptic drugs
• Surgically remove focus
• Vagus nerve / deep
brain stimulation
(VNS / DBS) 17
 462
CONSCIOUSNESS
 What Is It?
o Perception of sensations, voluntary
initiation/control of movement,
higher mental processing (logic,
memory judgement, perseverance,
creativity, love/hate, etc, etc)
o Continuum: alert  drowsy(lethargic)  stupor  coma
o Difficult to define
• More than dendrites/
axons/neurotransmitters
• Simultaneous activity large areas of cerebral
cortex
• Thought: total interconnection of entire brain, multiple
simultaneous inputs
• Superimposed on many other neuronal activities 18
 462
HOMEOSTATIC IMBALANCE
 Loss of Consciousness (LOC)
o Except during sleep, LOC always signals brain impairment
o Syncope (fainting): LOC for seconds
• Usually means inadequate cerebral blood flow from
ê BP – bleeding, med side-effect, sudden emotion
o Coma: LOC + unresponsiveness for extended period
• Brain less active, O2 consumption reduced
• Causes : head/brain stem trauma, tumor, infection
metabolic (eg ê[glucose] ), drug OD, liver/kidney
failure, prolonged brain O2 deprivation, etc, etc.
Generally not stroke.
• Damage irreparable  brain death
 Body still ‘functions’
 Withdraw life support??
19
 462-463
SLEEP
 Sleep Stages
o Sleep: partially unconscious but arousable
o Brain stem function WNL: still controls vital signs [blood
pressure (BP), heart rate(HR), respirations], some
monitoring of environment, eg alarm clock/sleep walkers
o Two major cycles alternate most of sleep cycle
 Non-rapid eye movement (NREM) sleep initially
 Gradually Stages 1  4, sleep becoming deeper
ê BP/HR. Nightmares (remember)/night terrors
(more severe, don’t remember)
 Rapid eye movement (REM) sleep follows
 Eyes moving rapidly under lids, most skeletal musc.
paralyzed (fortunately). Normal dreaming. α-Wave
on EEG. Penile/clitoral erections
 BP/HR/respiration rate é. Use of O2 by brain é é
 Are eyes following dream images? 20
 462-463
SLEEP
 Sleep Stages (continued)

Slow
wave
sleep

We do not spend any time in REM until after ~1.5 hr of sleep.

á periods
Note ing length of REM

21
Figure 12.21
463
SLEEP
 Sleep Patterns
o Alternating sleep/wake cycles: circadian (24-hr) rhythm
o Timing set by suprachiasmatic nucleus (biological clock)
which regulates preoptic nucleus (sleep-inducing centre),
both in hypothalamus
• Latter inhibits reticular activating system (RAS), puts
cerebral cortex ‘to sleep,’ but RAS still mediates sleep
o A large number of chemicals in body induce sleep, but
neurochemistry poorly understood (hypocretin)
o Before awakening, hypothalamus releases orexin protein
 RAS fires maximally, cortex ‘wakes up’
 Importance of Sleep? Possibly:
o Consolidate new memories
o Restorative: neural activity winds down
22
 463-464
HOMEOSTATIC IMBALANCES
 Narcolepsy
o Fully awake  abrupt REM sleep: no warning, x ~15 min
• Pleasurable experience (eg joke) may trigger
o Often + cataplexy: lose skeletal muscle control, like in
REM sleep, for sec-min. Conscious but can’t move
o Autoimmune destruction
of hypothalamic cells that
secrete orexin – ‘wake up
chemical’ – to RF
o Future treatments:
replacing orexins?
 Insomnia https://www.youtube.com/watch?v=palcmu2Ik-E

o Chronic inability to obtain good quality/quantity sleep

o Multiple causes: physical/psychological
o Rx: ‘sleeping pills’ – a complex clinical issue! 23
BRAIN INJURIES AND DISORDERS

24
468
TRAUMATIC BRAIN INJURIES
 Concussion
o Brain function alteration  eg dizzy, LOC
o Temporary but multiple  cumulative
 Contusion damage
o If severe  permanent bruise/neurological damage
o LOC: always if in brain stem o Hours – lifetime

 Intracranial (Subdural/Subarachnoid) Hemorrhage

o á ICP*  brain tissue compression. If herniation through
foramen magnum  HR/BP/respiration stop  death
o Rx: surgically drain
* Intracranial pressure

 Cerebral Edema
o Brain swelling Brain stem herniation
o Can be fatal 25
468-469
CEREBROVASCULAR ACCIDENTS (CVAs)
Most common neurologic disorder / 3 rd leading cause of death in
North America
 Ischemic Stroke
o Blood flow to brain blocked b/o blood clot (local/embolic
– outside brain)  tissue ischemia/death
o Sequelae: contralateral hemiplegia, aphasia (Sl 5)
o Rx: tissue plasminogen activator (TPA, ‘clot buster’)
 Hemorrhagic Stroke
o Blood flow to brain lost b/o ‘bleeding
out’ from artery
o Same symptoms/result, opposite Rx!
o Rx: drain surgically
Initial ischemia (loss of blood supply) often not disaster b/o
collateral blood flow. But O2-deprived neurons release
excitatory neurotransmitter glutamate: excitotoxin kills
surrounding neurons

 Transient Ischemic Attacks (TIAs) RX: ‘Clot- RX: Drill through

o Temporary (5-50 min) ischemia buster’ drugs,

or bore out
skull and suck out
blood (surgically)

 same symptoms
obstruction (via 26
angiogram)
469
DEGENERATIVE BRAIN DISORDERS
 Alzheimer’s Disease
o Progressive degenerative disease of brain  dementia:
memory loss, â attention, disoriented, lose language/all
skills, personality changes, combativeness, psychosis
o Seen in ~10% >65 yo. Often fatal, especially >85 yo
o Extracellular plaques: beta-

https://www.youtube.com/watch?v=7wbYEK7O14E&feature=related
amyloid peptide (from normal
membrane precursor) +
intracellular neurofibrillary
tangles of tau protein (normal
microtubule stabilizers)
• Cause or effect???
o Hippocampus, basal forebrain,
association cortex (thinking, memory) most sensitive,
but eventually spread throughout brain
o Rx: Acetylcholine boosters (almost useless!); future–anti
β-amyloid antibodies (or maybe not) 27
469-470
DEGENERATIVE BRAIN DISORDERS
Typically strikes in 50-60 yo’s
 Parkinson’s Disease
o Resting tremor, forward-bent walking, shuffling gait, stiff
facial expression, slow movements
o Degeneration of dopamine-releasing
neurons of basal ganglia
o ?? Cause: abnormal mitochondrial
proteins / protein degradation?
o RX: dopamine replacement, deep brain stimulation, gene
therapy, stem cells
Begins in
 Huntington’s Disease middle age
o Wild, jerky continuous flapping
(‘chorea’)  mental deterioration
o Fatal hereditary disorder: mutant
huntingtin protein: basal ganglia https://www.youtube.com/watch?v=JzAPh2v-SCQ

 cortical degeneration 28
DIAGNOSTIC PROCEDURES FOR
ASSESSING CNS DYSFUNCTION

29
 NEUROIMAGING
470

 Structural Studies
o All but MRI use X-rays
o Resolution (amount of detail)
and information improving
o All provide static snapshots Skull X-ray Pneumoencephalogram
of the head. No difference (1895) (1920)

of image between living and dead person, initially

Computed Tomography (CT, 1971) Magnetic Resonance Imaging (MRI, 1977) 30

 NEUROIMAGING
470

 Dynamic Studies
o Show living brain–able to study metabolism/blood flow,
brain regions in operation Complimentary technologies
o fMRI operationally simpler and better resolution than PET

31
Positron Emission Tomography (PET, 1976) Functional Magnetic Resonance Imaging (fMRI, 1995)
 NEUROIMAGING
 Human Connectome Project
o 50 billion neurons, 1,000 trillion connections

https://www.youtube.com/watch?v=2nzLxAoUuts 32
 NO MORE ANP1106 LECTURES !!

Mastering A&P Assignment # 10 (Central Nervous System)

will be posted after today’s Lecture and is due on or before
Tuesday April 21 at 11:59 PM
(All Mastering A&P Assignments # 6 - # 10 are due on or before
Tuesday April 21 at 11:59 PM)

3 Sample exam questions from today’s lecture will be posted 33

The official teaching and course evaluation period for the Winter term
will last from March 23 – April 3. Please watch your email for
instructions from the University on how you can complete the course
evaluation online.

Please take a few minutes to do this. It is a valuable opportunity to

give me feedback which may well benefit your colleagues and
classmates

36
FINAL EXAM 2: WED APR 22

* SASS students will have their extra

WHERE: ONLINE mandated time
WHEN: 9:30 AM Sharp!!! * * Multiple choice [5] questions, ~ ½
with diagrams, scrambled.
DURATION: 120 + 5 min*
10 Neuroanatomy +
CONTENT: 75 MCQs**,
no writing/fill-in-blanks 65 Neurophysiology
37