the higher cortical functuin

1. HIGHER CORTICAL
FUNCTIONS
Osama A. Ragab
Lecturer of Neurology
2019

2. I think; therefore I am.
I have brain activation; therefore I am.

4. introduction
 The higher cortical functions makes up the
conscious mind.
 Higher functions represent language, calculations,
spatial topography, memory, executive function,
music and creativity.
 The totality of the mental operations that comprise
human thought mean intellect.

5. Cerebral Cortex

6.  Each of the primary cortices receives signals in
only one modality (vision, hearing, or sensation)
and has connections only to association cortex
also dedicated to this modality(unimodal
association cortex) .
 Unimodal association cortices communicate with
each other via more complex connections to the
heteromodal association cortex.
Unimodal Cortex

7. Hetero-modal cortex
 The posterior heteromodal
association cortex involves the
posterior inferior parietal lobe,
especially the angular gyrus. it
perceive an analogy association
(picture of boat &word boat).
 The lateral prefrontal region ,This
region is involved with attention or
“working memory” and with
sequential processes and the
planning of motor activities
( Executive functions).

8. Supra-modal cortex
 The Orbitofrontal relates the
functions of the heteromodal
cortex regarding attention and
sequencing of responses with
intero-ceptive inputs from the
internal milieu of the body.
 The orbitofrontal area connect
with the limbic system
autonomic, and emotional
processes.

9. Neocortical Networks
 Several neocortical networks involve interactions
among different primary, unimodal, and
heteromodal association areas. These networks are
important in the following functions:
 Sensory processing and object recognition.
 Directed attention.
 Motor programming and execution.
 Language .
 Memory.

10. Sensory processing and object
recognition.

11. Visual System
 the primary visual cortex area
17,calcarine or striate cortex.
 Further processing involves
unimodal visual association
areas, namely, areas 18 and 19 .
 The dorsal stream of visual
processing involves areas in the
middle temporal and middle
superior temporal lobe and
terminates in the posterior
parietal analyzing the location
and movement of an object.
 In the ventral stream, the color
and form of an object are
analyzed in a sequentially
hierarchical fashion by neurons
located in the fusiform and
lingual gyri.

12. Auditory System
 The auditory cortex is divided into a core,a belt, and a parabelt that
participate in the sequential processing of auditory information.
 The core is the primary auditory area and contains neurons that
respond to pure tones of specific frequencies and respond primarily
to stimulation of both ears.
 The belt contains neurons that respond to complex sounds.
 The left superior temporal gyrus is critical for the acoustic
processing and extraction of the meaning of spoken language.

13. Object Recognition and Semantic Knowledge
 Object recognition is the first necessary step for
naming, using, and reacting emotionally to an
object.
 The ability of modality-specific visual,
somatosensory, or auditory information to activate
the relevant multimodal associations that lead to
face or object recognition depends on a
heteromodal network located in the left anterior
middle temporal gyrus and temporal pole.

14. Agnosia
• Agnosias are disorders of recognition.
• “normal percept stripped of its meaning.”
• Sigmund Freud originally introduced the term
agnosia in 1891 to denote disturbances in the
ability to recognize and name objects, usually
in one sensory modality in the presence of
intact primary sensation.

15. Criteria for the diagnosis of agnosia include:
(1) Failure to recognize an object.
(2) Normal perception of the object, excluding an
elementary sensory disorder.
(3) Ability to name the object once it is recognized,
excluding anomia as the principal deficit.
(4) Absence of dementia.
Agnosia

16.  The patient fails to recognize objects by sight, with
preserved ability to recognize them through touch
or hearing in the absence of impaired primary
visual perception or dementia.
 Two subtypes of visual object agnosia:
 Apperceptive visual object agnosia.
 Associative visual object agnosia.
Visual Agnosia

17. Apperceptive Visual Agnosia
 Patients with apperceptive visual
agnosia can pick out features of an
object correctly (e.g., lines, angles,
colors, movement), but they fail to
appreciate the whole object.
 The medial occipital cortex related
to appreciation of color and texture,
whereas the lateral occipital cortex
is more involved with shape
perception.

18. Associative Visual Agnosia
 Inability to connect the visual
percept with its related semantic
information stored in memory,
such as, its name, use, and
description.
 Most but not all cases of
associative visual agnosia have
involved or occipito-temporal
gyri bilaterally.

19. Optic Aphasia
 It is intermediate between agnosias and
aphasias.
 The patient cannot name objects presented
visually but can demonstrate recognition of
the objects by pantomiming or describing
their use.
 The preserved recognition of the objects
distinguishes optic aphasia from
associative visual agnosia.
 patients can name objects presented in the
auditory or tactile modalities,
distinguishing them from anomic aphasics.
 left occipital lesion

20. Prosopagnosia
 Prosopagnosia refers to the
inability to recognize faces.
 They learn to compensate by
identifying a person by voice.
 The inferior occipital lobe
and the middle fusiform
gyrus are involved in aspects
of face perception.

21. Anton syndrome
 Some patients with cortical
blindness are unaware that they
cannot see, and some even
confabulate visual descriptions or
blame their poor vision on dim
lighting or not having their
glasses (Anton syndrome).
 The thinking and language areas
of the brain are not consciously
aware of the lack of input from
visual centers.

22. Balint Syndrome
(1) ocular motor apraxia, .
(2) optic ataxia.
(3) impaired visual attention.
(4) Simultagnosia
Patients with Balint syndrome
literally cannot see the forest for the
trees.

23. Auditory agnosias can be divided into
(1) pure word deafness.
(2) pure auditory nonverbal agnosia.
(3) phonagnosia, or inability to identify
persons by their voices .
(4) pure amusia.
Patients may have one or a mixture of these
deficits.
Auditory Agnosias

24. Cortical Deafness
 Profound hearing deficits are seen in patients
with acquired bilateral lesions of the primary
auditory cortex (Heschl gyrus, Brodmann areas
41 and 42) .

25. Pure Word Deafness
 The syndrome of pure word deafness involves an
inability to comprehend spoken words, with
preserved ability to hear and recognize nonverbal
sounds.
 Pure word deafness has traditionally been
explained as a disconnection of both primary
auditory cortices from the left hemisphere
Wernicke area.

26. Auditory Nonverbal Agnosia
 Auditory nonverbal agnosia refers to patients
who have lost the ability to identify meaningful
nonverbal sounds but have preserved pure tone
hearing and language comprehension. These
cases also tend to have bilateral temporal lobe
lesions.

27. Phonagnosia
 It is a failure to recognize familiar people by their
voices.
 usually reflecting unilateral or bilateral temporal
damage, but failure to recognize a familiar voice
may involve a right parietal locus corresponding to
the specific area for recognition of faces.

28. Amusia
 Recognition of melodies
and musical tones is a
right temporal function,
whereas analysis of
pitch, rhythm, and
tempo involves the left
temporal lobe.

29. Tactile agnosia
 Lesions of the postcentral gyrus that interrrupt the
connections between the primary and unimodal
somatosensory association areas in the parietal lobe
cause tactile agnosia , or astereognosia, inability to
recognize letters or numbers written on the palm of
the hand (agraphesthesia), inability to localize
touch (atopognosia), and loss of ability to
discriminate weights (abarognosia) on the
contralateral side.

30. Attention

31. Attention
 Attention refers to being able to focus on a specific
thing without being distracted.
 Vigilance is the ability to sustain attention over
time.

32. Attention
 Neurons of the intraparietal
sulcus integrate visual,
somatosensory, and auditory
information to encode a
representation of space.
 This is forwarded to the premotor
cortex and frontal eye fields
directing gaze toward
contralateral space.
 Damage to the right parieto-
temporal region, produces
contralateral spatial neglect .

33. Spatial Attention

34. Motor programming
and execution.

35. Praxis
 Praxis involves the ability to plan and carry out a
new action when adequate cognitive and motor
skills are present.
 The components of praxis include generating an
idea of how and when to act, planning a program of
action, and execution of the action sequence.

36. All parts of the brain lobes share in production of action.
 The occipito-temporal lobe form the (what system) of vision.
 The parieto-occipital lobe form the (where system) of vision.
 The left parietal and frontal lobes contain the conceptual and
production levels of action (How system).
 The right fronto-subcortical circuits form the (When system) of action.
Praxis

37. APraxia
 Apraxia is an inability to correctly perform learned
skilled movements.
 Apraxia is essentially a cognitive deficit in motor
programming and results in errors either of the
spatiotemporal processing of the movements or in
the content of the actions.

38. Cognitive model of apraxia (Rothi et al, 1991)
Apraxia
The inferior parietal lobule contains the spatial and temporal
movement programs (praxicons or motor engrams) needed
to carry out learned skilled movements.
Multiple input modalities including visual, verbal-auditory,
and tactile can activate these movement formulas

39. Cognitive model of apraxia (Rothi et al, 1991)
Apraxia
Semantic system Non-sematic system
Sematic knowledge about object and how to use it
Sensory-motor program

40. Cognitive model of apraxia (Rothi et al, 1991)
Apraxia
object
Visual input
Auditory input
Recognition
Recognition
Sematic knowledge
Action outputSupplementary and premotor system
RT motor system
LT motor system
Corpus callosum

41. Apraxia
Conceptual Apraxia:
Can’t use object inspite recognition

42. Dissociative apraxia:
Stimulus failed to activate praxicon.
patient can’t imitate but can do action by command.
Apraxia

43. Apraxia
Ideomotor Apraxia:
These lesions result in impaired pantomime to verbal commands,
impaired imitation of gestures, and the presence of spatiotemporal
production errors.

44. Apraxia
Callosal Apraxia:
apraxia is confined to the non-dominant limb, .

45. Language

46. Language
 Language is a complex system of communicating
symbols and rules for their use.
 Aphasia is defined as a disorder of language
acquired secondary to brain damage.
 aphasia is distinguished from congenital or
developmental language disorders, called
dysphasias. (in British usage the term dysphasia
applies to partial or incomplete aphasia.)

47.  Phonemes are the smallest meaning-carrying sounds.
 Semantics refers to word meanings.
 Morphology is the use of appropriate word endings
and connector words for tenses, possessives.
 The lexicon is the internal dictionary.
 Syntax is the grammatical construction of phrases .
 Pragmatics refers to the proper use of speech and
language in a conversational setting, including
pausing while others are speaking, taking turns
properly, and responding to questions.
Language

48.  Apraxia of speech is a syndrome of misarticulation of
phonemes, especially consonant sounds.
 Clinically, speech-apraxic patients produce
inconsistent articulatory errors, usually worse on the
initial phonemes of a word and with polysyllabic
utterances.
Language

49.  Anomia, or inability to produce a specific name.
 Anomia is manifested in aphasic speech by word-
finding pauses and circumlocutions, or use of a
phrase when a single word would suffice (e.g., “the
thing you tell time with” for watch).
 Paraphasic errors are divided into literal errors
involving substitution of an incorrect sound (e.g.,
“shoon” for “spoon”) and semantic errors involving
substitution of an incorrect word (e.g., “fork” for
“spoon”).
 A pattern of paraphasic errors and neologisms is called
jargon speech.
Language

50. Relevant Neuroanatomy

51. Bedside Language Examination
1. Spontaneous speech
2. Naming
3. Auditory comprehension
4. Repetition
5. Reading
6. Writing

52.  A speech sample may be elicited by asking the patient
to describe the reason for coming to the doctor.
 Non-fluent speech is uttered in single words or short
phrases, with frequent pauses and hesitations.
 Attention should first be paid to initiation difficulty,
articulation, phonation or voice volume, rate of speech,
prosody and phrase length.
 The content analyzed for the presence of word-finding
pauses, circumlocutions, paraphasias and neologisms.
Bedside Language Examination

53.  Naming, the second part of the bedside
examination, is tested by asking the patient to name
objects, object parts, pictures, colors, or body parts to
confrontation. A few items from each category should
be tested because anomia can be specific to word
classes
 Auditory comprehension is tested first by asking the
patient to follow a series of commands of one, two,
and three steps.
 Because apraxia is difficult to exclude it is advisable
to test comprehension by tasks that do not require
a motor act, such as yes/no questions.
Bedside Language Examination

54. Broca Aphasia

55. Aphemia
 A rare variant of Broca aphasia is aphemia, a
nonfluent syndrome in which the patient initially is
mute and then becomes able to speak with
phoneme substitutions and pauses.
 All other language functions are intact,
including writing.
 This results from small lesions of the Broca area
or its subcortical white matter or of the inferior
precentral gyrus.

56. Wernicke Aphasia

57. Global Aphasia

58. Conduction Aphasia
striking deficit of repetition.
Most patients have relatively normal spontaneous
speech, although some make literal paraphasic
errors .
Naming is impaired to varying degrees, but
auditory comprehension is preserved.
The lesions of conduction aphasia usually involve
either the superior temporal or inferior parietal
region.

59. Anomic Aphasia
Anomic aphasia refers to aphasic syndromes in which
naming, or access to the internal lexicon, is the
principal deficit.
Spontaneous speech is normal except for the pauses
and circumlocutions produced by the inability to
name.
Angular gyrus as the site of lesions producing
anomic aphasia,

60. Transcortical Aphasias
 Repetition is normal.
 The lesions disrupt connections from other cortical
centers into the language circuit.
 Mixed transcortical aphasia, with large watershed
infarctions of the left hemisphere or both
hemispheres.
 Transcortical motor aphasiaoccurs with lesion is
watershed between MCA &ACA.
 transcortical sensory aphasia, lesion is watershed
between MCA &PCA.

61. Subcortical Aphasias
Left thalamic lesion frequently produce a Wernicke
like fluent aphasia with better comprehension than
in cortical Wernicke aphasia.
Basal ganglia lesion, especially those involving the
putamen, results in global or Broca like aphasia

62. Pure Alexia without Agraphia
Alexia, acquired inability
to read This ,the patients
can write but cannot read
their own writing.
On bedside examination,
speech, auditory
comprehension, and
repetition are normal.
Naming may be deficient,
especially for colors.

63. Alexia with Agraphia
acquired illiteracy in which a previously literate
patient is rendered unable to read or write.
The oral language modalities of speech, naming,
auditory comprehension, and repetition are largely
intact.
The lesions typically involve the inferior parietal
lobule, especially the angular gyrus.

64. Agraphia
writing may be affected either in isolation (pure
agraphia) or in association with aphasia
(aphasic agraphia).
Isolated agraphia has been described with left frontal
or parietal lesions

65. Language in Right Hemisphere Disorders
 left-handed patients may have right hemisphere
language dominance
Right-handed patients occasionally become aphasic
after right hemisphere strokes, a phenomenon called
crossed aphasia.
Syndromes of loss of emotional aspects of speech are
termed aprosodias.
loss of comprehension of affective language, also called
affective agnosia.
 right hemisphere–damaged patients understand what
is said, but not how it is said.

66. Memory

67. Memory
 Memory is the recording, retention, and retrieval of
knowledge.
 It accounts for all knowledge gained from
experience—facts that are known, events that are
remembered, and skills that are gained and applied.

68. Types of Memory
Memory
Declarative Non-declarative
• Episodic
• Sematic
• Procedural
• Priming

69.  Declarative memory is responsible for the learning and
remembrance of new events, facts, and materials.
 Episodic memories (remembrance of personal
experiences that took place at a particular place and
time)
 Semantic memories (knowledge of generic
information, such as the meaning of a word).
 It is the form of memory people use to recollect facts
and events consciously and intentionally and is
therefore also referred to as explicit memory.
Types of Memory

70.  Non-declarative memory are not retrieved
intentionally but reflexively or incidentally.
 Implicit forms of memory include perceptual,
motor, and cognitive skill learning(sometimes
referred to as procedural memory).
 repetition priming, which is the facilitated
processing of a stimulus, such as a word or picture,
due to prior exposure to that stimulus.
Types of Memory

71. Temporal classification.
 Immediate memory refers to the recall of
information without delay, either immediately after
presentation or after uninterrupted rehearsal. The
normal human being can retain seven digits in
active memory span.
 Working memory mediates the temporary
processing and storage of internal representations
that guide and control action.
 Information is held in working memory only as
long as it is useful for solving a problem at hand.

72.  The second stage of memory, referred to by
clinicians as short-term or recent memory,
involves the ability to register and recall specific
items such as words or events after a delay of
minutes or hours.
 Long-term memory refers to permanent and large
stores of episodic and semantic memories.
Temporal classification.

73. Anatomy of Declarative Memory

74. Anatomy of Declarative Memory
 Neocortical damage is thought to result in
domain specific memory deficits in which the
loss of old memories and the inability to gain
new memories reflect the kind of knowledge
represented in that neocortical region.
 Damage to medial temporal lobe, diencephalic,
and basal forebrain regions yields widespread,
or domain-independent, declarative memory
deficits.

75. Anatomy of Non-declarative Memory
 Each form of non-declarative memory is linked to
specific brain regions.
 For immediate auditory memory, left temporal-
parietal cortices mediate auditory verbal while right
mediate nonverbal material.
 Working memory linked to the dorso-lateral frontal
cortex and to basal ganglia and cerebellar areas .