This document discusses speech physiology and the centers involved in speech production and comprehension. It covers topics like: - The dominant and non-dominant hemispheres and their roles - Brain areas involved in speech like Wernicke's area, Broca's area, and their functions - Types of aphasia that can result from lesions to different speech areas - The mechanism of speech production and comprehension involving various brain areas - Other topics on neglect, dysarthria, and the lateralization of brain functions are also summarized.

1. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Dee Unglaub Silverthorn, Ph.D.
HUMAN PHYSIOLOGY
PowerPoint®
Lecture Slide Presentation by
Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University
AN INTEGRATED APPROACH
T H I R D E D I T I O N
Speech
physiology
Speech
physiology
DR. RAMADAN MOHAMED AHMED

2. The dominant & non dominant
hemisphere
The dominant & non dominant
hemisphere
The dominant hemisphere is the left hemisphere in
- 96% of the right handed person.
- 70% of the left handed persons.
In the remaining 30% of the left handed persons.
. 15% have right categorical hemisphere
. 15% showed no sign of lateralization.
►Lesions: Speech disorders and depression.
The representational hemisphere (non dominant
hemisphere)
is concerned with the visuospatial relations i.e
recognition of faces, objects by their form and
musical themes.
►Lesions; Agnosia and euphoria.

3. Brain Function: Cerebral Lateralization
• Each lobe has special functions

4. Right hemisphere functions
• Right hemisphere involved in visual-spatial and
constructional tasks, emotion and emotional intonation of
speech and music.
• Right hemisphere is often referred to as the “Minor”
Hemisphere
• Patients with injury to right cortex often exhibit neglect.

5. Neglect

6. Mechanism of speech
(1) Understanding a written word:
Written word is seen by primary visual area & understood by visual
association areas → which discharge to angular gyrus to appreciate the
meaning of
the word → which projects to the Wernicke’s area for
interpretation & formation of thoughts.
(2) Understanding a spoken word:
Spoken word is heard by primary auditory area → which discharges to
auditory association areas for understanding the meaning →
which projects to Wernicke’s area.
If the word is a name , auditory association area discharge to name area then
to Wernicke’s area.
(3) To express by written words:
Wernicke’s area → discharges to hand skill area → which form coordinated
hand movements ( with help of basal ganglia & cerebellum) → which projects
to primary motor area for hands.
(4) To express by spoken words:
Wernicke’s area → projects to Broca’s area through arcuate fasciculus →
Broca’s area formulates program for vocalization & projects to face
area in primary motor cortex.

7. Centres of speechCentres of speech
(1) Wernicke’s area
Comprehension of auditory & visual information.
(2) Broca’s area
co-ordinates vocalization & is connected to motor cortex to initiate the
appropriate movements to produce speech.
(3) Hand skills area
Lesion of this area leads to motor apraxia or agraphia.
(4) Auditory area
a. Auditory association areas.
Understanding the meaning of spoken words.
b. Area for naming objects:
(5) Visual areas
a. Visual association areas (18-19)
b. Angular gyrus;
It processes the information from the words that are read so that they
can be converted into the auditory forms of words in Wernick’s area.

8. Specialization and Integration

9. AphasiaAphasia
Types of aphasia Lesion in Person is unable
A) Reiceptive
1.Wernicke’s
aphasia
Wernicke’s area Understand the meaning of words but
talks excessively with neologism
2.Word deafness
(auditory)
auditory association area To understand the meaning of spoken
word..
3.Word
blindness
Visual association area Understand written words or letters.
4.Alexia Angular gyrus Understand meaning of written words.
B) Expressive 1) lesion in Broca’s area
Mild lesions
Speech is slow & words are hand to come.
Severe lesion
Speech is limited to 2 or 3 words which express all emotions e.g OK –NO.
2.Agraphia
lesion in Hand skill area, so Person is unable to Express thoughts by written
word
C) Global Categorical hemisphere
(extensive(
Produce or understand both
spoken & written words.

10. Dysartheria
Paralysis or Paresis of Muscles
• Flaccid: LMN problem – hypernasal, breathy
speech and imprecisely articulated consonants
• Spastic: UMN – Harsh, strained / strangled
speech with slow articulation
• Slow low volume monotonus: Basal ganglia
lesion (parkinsonism)
• Stacato speech: cerebelar lesion

11. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Dee Unglaub Silverthorn, Ph.D.
HUMAN PHYSIOLOGY
PowerPoint®
Lecture Slide Presentation by
Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University
AN INTEGRATED APPROACH
T H I R D E D I T I O N
MEMORY
physiology
MEMORY
physiology
DR. RAMADAN MOHAMED AHMED

12. Physiology of Memory
• Neurons are the basic means of information
transfer within the nervous system
• Information in the form of a stimulus is
detected by a specific type of neuron (sensory
neuron).
• The information is then passed to an adjacent
neuron (interconnecting neuron) and so on till
it gets to where it’s going in the brain
• It is an electro-chemical process that allows this
to happen

13. MEMORY
This is the ability of the brain to store and recall (i.e. reproduce) information.
MEMORY
This is the ability of the brain to store and recall (i.e. reproduce) information.
1. Short-term memory:
• This is memory that lasts a few minutes to a few hours.
The information is introduced in bits one after the other.
The capacity of the brain for this type of memory is small,
but its recall is rapid. The new information replace the
old ones.
• One aspect of short-term memory is what is called the
"working memory"(= a temporary storage of information
used to plan a future action).
2. long-term ( remote) memory :
• This is memory that lasts for long times (up to several
years). It develops from primary memory by practice or
repetition of information. The capacity of
• the brain for this type of memory is large, but its recall is
slow.
• the old information inhibits storage of new ones).

14. Duration of Memory
hours
Working memory:
seconds to minutes
•depends on attention and
avoiding other stimuli
•requires prefrontal cortex
seconds years
Short-term memory
minutes to hours
•requires motivation and attention
•impaired in confused states
•requires processing to be stored as
long-term memory
•requires temporal lobe structures
•involves changes in synaptic
strength
Long term memory
•transferred to
diffuse cortical areas
•not lost if there are
lesions to the
hippocampus

15. MECHANISMS OF MEMORYMECHANISMS OF MEMORY
(A( In short-term memory
(a) Activation of reverber-ating circuits.
(b) Short-term (post-tetanic) synaptic potentiation.
(c) Synaptic sensitization .
(d) Long-term potentiation at synapses.
(B( In long-term memory: increase in the number of
(a) The presynaptic nerve terminals
(b) The transmitter vesicles
(c) The release sites of the transmitter.

16. Reverberating loops
• Activity decays
• maintained for only a short period of time ~

17. CENTRES of memoryCENTRES of memory
@ Short-term memory
is encoded in the hippocampus.
@ Long-term memory
• are stored mostly in the neocortex, and
the amygdaloid nuclei produce the
emotional aspects
of memories only.

18. CONOLIDATION OF MEMORYCONOLIDATION OF MEMORY
DEFINITION
• This is the conversion of short-term memory
into long-term memory. It requires 5-10
minutes for minimal consolidation and about
4 hours to be complete.
MECHANISM OF CONOLIDATION OF
MEMORY
• This is produced by rehearsal of the
information in the mind . It involves new
protein synthesis in neurons.

19. AMNESIAAMNESIA
1. Retrograde amnesia
This is inability to recall memories from the past,
specially the more recent events e.g. after certain
thalamic lesions and following brain concussion.
2. Anteroqrade amnesia
This is inability to form new long­term memories
(but the already stored memories are still intact).
Its cause is commonly
lesions in the hippocampus.
3. Alzheimer disease

20. Alzheimer’ s Disease
• neurodegenerative disease
• amyloid proteins build up
and form amyloid plaques
(outside cells)
• neurofibrilllary tangles inside
cells
• leads to neuronal death
• hippocampus is one of first
areas to degenerate, leads to
anterograde amnesia
• cortex also degenerates early,
leads to retrograde amnesia
and dementia

21. Learning
A) Non associative leaning
1) habituation.
2) Sensitization.
B) Associative leaning
1) Classical conitioning
• 2) Operant conditioning

22. Reticular Formation
• Located between caudal
diencephalon & spinal
cord
• Network of Overlapping
Dendrites and Axons
• Input From
• Motor Cortex
• Basal Ganglia
• Cerebellum
• Hypothalamus
• Vestibular apparatus
• Spinothalamic tracts

23. RETICULAR
FORMATION
The Reticular Formation is the oldest part of the brain.
It forms a diffuse, multisynaptic, net­like meshwork
(reticulum) of widely interconnected neurons in the
Tegmentum. The RF is involved in nearly every aspect
of brain function including the following:
-Homeostasis
-Consciousness
-Arousal
-Pain
-Primitive motor control
-Muscle tone
-Behavioral mechanisms
RETICULAR
FORMATION

24. RETICULAR FORMATION
MID MEDULLA
PyramidPyramid

25. RETICULAR
FORMATION
VITAL
CENTERS
Vital Centers are located in the medulla and pons and control cardiovascular
respiratory, and other homeostatic mechanisms. Lesions in these centers are fatal.
Examples of RF mediated reflexes are:
-Aortic Body
-Carotid Body
-Aortic Sinus
-Carotid Sinus
-Respiratory
-Cough
-Swallowing
-Salivary
-Vomiting

26. Reticular Motor Functions
• Facilitatory Reticular Areas
• Upper Brainstem (Ascending &
descending).
• Ascending: Arousal
• Descending: Increases Muscle
Tone in Extremities
• Inhibitory Reticular Areas
• Lower and Medial Region of
Medulla
• Decreases Muscle Tone in
Extremities

27. Reticular Formation Function
• Arousal (Arousal)
• Muscle tone Modulation
• Pain Processing
• Regulation of
• Vomiting
• Coughing
• Cardiovascular Functions
• Respiration
• Speech Functions

28. Reticular Formation
Figure 12.19

29. Reticular Activating System
Maintains the conscious, alert state that makes
perception possible
 brainstem reticular formation
 ascending projection system
 non-specific thalamic nuclei
 non-specific thalamocortical projections (diffuse)
Activated by sensory information being relayed the
the cerebrum

30. RETICULAR
FORMATION
ASCENDING RETICULAR
ACTIVATING SYSTEM
(ARAS)
The midbrain RF gives rise to a tonic ascending barrage of diffuse,
non­specific sensory data called the ARAS. Acting like a battery, the
ARAS stimulates the cerebral cortex and maintains the conscious state.
Midbrain lesions of ARAS result in Coma. Incomplete lesions may result
in Stupor.

31. Reticular Activating System
• Network in brain stem
• Arousal, sleep, pain, & muscle
tone
• Ascending fiber sends signals
upward
• Arouses and activates cerebral
cortex
• Controls overall degree of
cortical alertness or level of
consciousness:
• maximum alertness
• wakefulness
• sleep
• coma

32. Reticular Activating System
Factors affecting RAS activity
►RAS is stimulated by :
1. All sensory signals especially pain & proprioceptive signals.
2. Cortical signals from: areas of emotions & Motor cortex.
3. Sympathomimetic drugs e.g catecholamines & amphetamine.
►RAS is inhibited by:
1. Withdrawal of all sensory signals.
2. Stimulation of sleep centres.
3. general anaesthetic (e.g barbiturates & ether) .
4.Damage of RAS by tumours.

33. Reticular Nuclei
• Reticularis Gigantocellular
• Pontis Oralis and Cudalis
• Lateral Reticular Nucleus
• Ventral Reticular Nucleus
• Paramedial Reticular
Nucleus
• Interstitial
• Raphe
• Ceruleus

34. Clinical considerations
• Disconnection of cortex and basal ganglia from
reticular formation
• Decerebrate Rigidity
• Extensor posturing of all Limbs
• Excessive facilitatory impulses
• Transection Below Vestibular Nucleus
• Flaccid Paralysis
• Similar to degeneration of the lower neuron

35. Electrical activity of CNS
Dr. RAMADAN MOHAMED AHMED

36. Evoked potentials
Primary evoked potential Secondary evoked potential
+ve wave followed by small –
ve wave (depolarization
followed by repolarization
of dendrites & some
neurons of cortex).
Large prolonged +ve wave,
caused by activation of
cortical neruons by signals
coming from non-specific
thalamic nuclei.
Localized to brain area at
which the sensory pathway
terminates.
Appears over most of the
cortex at the same time.
(not localized)

37. Spontaneous cortical potentials
(electro encephalogram, EEG or brain waves)
EPSPs and IPSPs on apical dendrites of
cortical pyramidal cells
Recording of EEG is done in calm room at comfortable temperature.
The subject should be fasting, in complete physical, mental rest &
unanesthiatised.
In EEG, the frequency of waves in inversely proportional to
their amplitude (Voltage).

38. Waves of EEG
1. Alpha waves
• Regular & rhythmic i.e synchronized (8-13 cycles/second).
• Recorded in adults when they are awake, relaxed & their eyes closed.
• Recorded most marked in the occipital regions.
• Produced by activity of non-specific thalamic nuclei.
2. Beta waves
• Irregular, low voltage & rapid i.e dsynchronised (18-30 c/sec.).
• Recorded during brain activity e.g when eyes are open or during
• sensory stimulation & in infants.
• Recorded at the frontal region.
• Produced by activation of RAS.

39. Waves of EEG
3. Theta waves
• Regular & rhythmic i.e synchronized (4-7 cycles/second).
• Recorded in adults when early sleep stages), children.
• Recorded most marked in the temporal & parietal regions.
• Amplitude: 100 mirovolt.
4. Delta waves
• Frequency (0.5-4 c/sec.).
• Recorded during deep sleep & in brain damage.
• Amplitude: 100 mirovolt.
• Produced by cortical neurons.

40. Brain Activity

41. Characterization of the EEG
delta (∆): deep sleep, coma.
theta (θ): sleep, childhood
alpha (α): adult, awake, relaxed, eyes closed,
especially over occipital cortex
beta (β): awake, alert, aroused, excitement
(and REM sleep) infants

42. Arousal or alerting response (Alpha block)
• Synchronized alpha waves are replaced
by beta waves by sensory stimuli or
mental concentration on opening the
eyes or when solving a problem.
• It’s due to stimulation of RAS.

43. Clinical uses of EEG recording
1- It helps in determining the sites of
tumours.
2- It helps the diagnosis of epilepsy.
3- It helps diagnosis of brain death.
4- It helps to know the stages of sleep.

44. SLEEP PHYSIOLOGY
• REM favors more fluid
thinking than NREM

45. Why Sleep?
1- Restore the biochemical and physiological
processes of the brain
2- Help brain plasticity necessary for memory
State of unconsciousness from which a person can be aroused
by sensory stimuli.
What is the Sleep?

46. Optimum Sleep Required
The bigger the animal, the less sleep needed

47. How Much Sleep?
1. Newborns : 16 to 18 hours
2. By age 1 : 13 to 14 hours
3. Teenagers : < 9 ½ hours
4. Adults : 8 hours and 20 minutes
5. Seniors : 8 hours

48. Sleep – two types
Slow-wave sleep (SWS)
REM (rapid eye movement sleep), aka
paradoxical sleep

49. Mechanism of sleep
Sleep results from depression of cerebral cortex due to Active
inhibition of RAS by: some sleep centres
a. Serotonin secreted by raphe nuclei in medulla & lower pons.
b. posterior hypothalamus increasing slow wave sleep & REM sleep.
c. discharge of cholinergic neurons in pontine reticular formation
during REM sleep.
d. discharge of noradrenergic neurons in locus ceruleus.
e. Some areas in nucleus of tractus solitarius.
F. Suprachiasmatic nucleus

50. Types of Sleep
Types of Sleep
Non rapid eye movement
(non REM sleep or slow
wave sleep)
Rapid eye movement (REM)
sleep
or paradoxical sleep.
Occurrence: at start of sleep
80%
Duration/ night’s
sleep
After 4th
stage of non REM.
20%
About 90 minutes. Duration / cycle About 20 minutes.
Eye deviate up & miosis Eye movements Rapid eye movements.
Stage1: theta waves
Stage 2: appearance of sleep spindles (light
sleep)
(alternating alpha and theta waves)
Stage 3: low frequency & High amplitude delta
waves (moderate sleep).
Stage4 : very slow large delta Waves (deep
sleep).
EEG recording Irregular fast low voltage Waves resemble
that seen in Alert state
Present Sleep talking &
walking
Absent
Absent Dreams & penile
erection
Present
Decrease HR, resp rate & ABP Increase
Decrease Ms tone Markedly decreased due to activation of
inhibitory reticular area
Low Threshold of
awaking
High

51. Coordination of Circadian Rhythms and
Sleep

52. Sleep Spindles
Spindles are caused by activity in the thalamus.
It's suspected that when spindles occur, the
thalamus is attempting to block brain signals—
prompted from external stimuli such as the
sound of a crying baby—from reaching other
areas of the brain that might disturb sleep.

53. 1 2 3 4 5 6 7 8
4
3
2
1
REM
AWAKE
SleepStages
Hours of Sleep
REM Stage
NREM
Normal Sleep Patterns in Young AdultsNormal Sleep Patterns in Young Adults

54. REM Sleep
• REM: rapid-eye movement
• lots of brain activity - EEG shows low voltage fast waves
• postural muscles are most relaxed during REM sleep
• loose associative thinking
• PGO waves - start in the pons → geniculate nucleus of thalamus →
occipital cortex

55. Metabolic theory of Sleep
Sleep-inducing endogenous chemicals:
Sleep-inducing peptide (DSIP) - >7 amino acid peptide, high
levels after sleep deprivation.

56. Thank you!

57. The Limbic System

58. Limbic System

59. Limbic system
Diencephalon

60. Limbic system Diencephalon

61. Hippocampal circuit
cortex
limbic
structure
hypothalamus
thalamus
mammillary nuclei
hippocampus
anterior nucleus
cingulate/PHG
entorhinal
fornix
Papez circuit!!
mammillo-
thalamic tract

62. Papez circuit
Hippocampus
Mammillary body
anterior nucleus of the thalamus
Cingulate Gyrus
Parahippocampal
Gyrus
Mammillothalamic tract
Fornix

63. Functions of limbic system:-
1. Olfaction perception & discrimination of olfactory
senses.
2. Control of feeding behaviour.
Lesions in anygdala → hyperphagia & amniphagia in
animals.
3. Control of sexual behviour.
Lesions in amygdala → hypersexuality in ♂ animals
Leasions in ant hypoth → abolish estrus in ♀ animals.
4. Control of maternal behaviour.
Lesions in cingulated gyrus → depress maternal
behaviour.

64. Functions of limbic system:-
5. Control of emotions i.e fear, rage & placidity.
Emotions are feelings associated with autonomic &
endocrinal responses.
Fear. Is caused by stimulation of amygdaloid
nuclei and stim of hypoth. (periventricular nuclei)
& Abolished by destruction of amygdala.
Rage = violent anger to minor stimuli. It is caused
by: Stim of ventromedial nucleus of hypoth.
(placidity area).
Bilateral destruction of amygdaloid nuclei.

65. Functions of limbic system:-
6. Motivation.
It is the force that activates a certain behavior to achieve a
goal.
Stim of the reward system → the subject is motivated to
perform tasks & has a sense of pleasure & relaxation.
Stim of the punishment system→ the subject feels fear &
displeasure & is motivated to avoid the punishment
experience. It is present in the lateral portion of the
posterior hypoth.
Dopamine is the main chemical transmitter in the reward
system. Cocaine gives the sense of the well being by ++
the dopamine.

66. The Limbic System
 Electrode
implanted in
reward center

67. Functions of limbic system:-
7. Memory.
It is important in storage & consolidation of memory.
8. Learning.
It is important in operant conditioning.