Higher cortical functions final

the higher cortical functuin

1. Higher cortical functions Osama A. Ragab Lecturer of Neurology 2019

2. Which is true?! I think; therefore I am. I have brain activation; therefore I am.

3. introduction T he 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 .

4. Cerebral Cortex

5. 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

6. 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 ).

7. 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.

8. 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. M otor programming and execution. Language . Memory.

9. S ensory processing and object recognition.

10. 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 .

11. 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.

12. 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.

13. 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.

14. 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

15. 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

16. 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.

17. 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.

18. 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

19. 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.

20. 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.

21. 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.

22. 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

23. 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) .

24. 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.

25. 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.

26. 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.

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

28. 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.

29. Attention

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

31. 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 .

32. Spatial Attention

33. Motor programming and execution.

34. 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.

35. 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

36. 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.

37. 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

38. 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

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

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

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

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

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

44. Language

45. 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.)

46. 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

47. 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

48. 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

49. Relevant Neuroanatomy

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

51. 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

52. 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

53. Broca Aphasia

54. 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 .

55. Wernicke Aphasia

56. Global Aphasia

57. 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.

58. 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,

59. 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.

60. 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

61. 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 .

62. 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 .

63. 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

64. 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.

65. Memory

66. 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.

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

68. 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

69. 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

70.   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.

71. 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 .

72. Anatomy of Declarative Memory

73. 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.

74. 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 .