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Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20.

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Page 1: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral Cortex: Higher Mental Functions

Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3rd Ed. Chapters 19 & 20.

Page 2: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Overview Introduction Brief overview of different neuro-investigative

techniques Functional role of cortical lobes and disorders Cerebral dominance Neurological Speech Disorders – Dysarthria

& apraxia Neurological Language Disorders - Aphasia

Page 3: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Introduction

Acute and degenerative neurological disorders frequently result in speech, language and other communication deficits. Including dysarthria, dyslexia, apraxia of speech,

and aphasia. Often, these deficits may be the first sign of a

degenerative neurological condition, and their recognition can contribute to the localization of pathologic changes and the neurologic diagnosis (Duffy, 1995).

Page 4: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Introduction Cerebral cortex – Area of about 2.5 square

feet & about 14 billion neurons. The true uniqueness of the human brain lies

in the higher mental functions such as reasoning, language, memory, speech, calculations, etc.

Page 5: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Introduction

Common investigation techniques – Imaging:

Computed Tomography (CT or CAT scan) Magnetic Resonance Imaging (MRI) Positron Emission Tomography (PET) Single Photon Emission Computed Tomography

(SPECT) Electroencephalography (EEG)

Evoked Potentials & mapping

Page 6: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

CAT Scan

MRI

PET Scan

SPECT Scan

EEG

Page 7: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Different Neuroimaging Methods

Page 8: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Introduction

Cortex is divided into – Primary areas

Areas that have direct contact to the sensors or effectors. Primary Motor areas Primary Sensory areas (for vision,

hearing, touch, smell & taste) Association areas

Unimodal association areas Also known as Secondary areas

Heteromodal association areas

Page 9: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Brodmann’s classification

Motor:Primary Area: 4 (motor cortex)Secondary Areas: 8,6, & 43

Somatosensory:Primary Area = 1, 2, 3 (somatosensory cortex)Secondary Areas = 5, 7, 39, & 40

Vision:Primary Area = 17 (visual cortex)Secondary Area = 18 & 19

Auditory:Primary Area = 41 & 42 (auditory cortex)Secondary Areas = 21 & 22

Area 44 = Broca’s or expressive/motor language areaArea 22 = Wernicke’s or receptive/sensory language

Area

Page 10: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cortical Areas Unimodal Association areas

Each of the primary sensory cortices is bordered by unimodal association areas (that is, with direct connections to only one sensory modality). These are also called secondary

areas This is where sensory information

is further processed. Premotor areas send commands

to the primary motor area.

Page 11: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cortical Areas Heteromodal association areas

These areas are – Where different modalities combineResponsible for Executive function

Refers to the process that decides which of the many incoming sensory stimuli should receive attention and in what order, and what motor responses should be activated and in what order.

Where planning, decision making, initiative, etc, occurs

Where Memory happens

Page 12: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cortical Areas Three important heteromodal association areas

Prefrontal Important for decision making (Executive function), planning

and working memory Inferior Temporal

Important for long term memory (dominant hemisphere – verbal memory; non-dominant hemisphere – pictorial memory)

Parietal-Temporal-Occipital areas Important for attention and language abilities

Page 13: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Lobes of the brain

Frontal lobe – From posterior to anterior –

Primary motor cortex (4)– Premotor or secondary motor cortex (6, 8) – Prefrontal cortex (9,10,11)

Primary motor cortex - Responsible for generating the neural impulses controlling execution of movement

Premotor cortex – Initiation and planning of skilled motor movts Broca’s area (Broadmann’s area 44) –

Anterior to the primary motor strip controlling the face area. Lesions affect voluntary speech movements

Page 14: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Frontal Lobe Prefrontal Cortex – Executive Function.

Related to abilities to differentiate among conflicting thoughts, determine good/bad, better/best, same/different, future consequences of current activities, working toward a defined goal, prediction of outcomes, expectation based on actions, and social "control"

Lesions (frontal head injury) produce disinhibition of speech & other behaviors – Frontal lobe syndrome Characterized by normal intelligence/memory but totally

changed personality, short temper, irritability, poor impulse control, antisocial personality traits, etc.

Lesions to the frontal cingulate gyrus in the medial surface may affect the Papez’s circuit (limbic lobe). Affects memory & limbic functions such as motivation &

drive

Page 15: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Frontal Lobe

Page 16: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Parietal Lobe Includes primary sensory areas (Areas 1, 2, 3), &

sensory association areas (Areas 5,7, 39, & 40). Association areas – multimodal (vision, hearing, touch)

association – involved with visuospatial functions including sterognosis & graphesthesia.

Inferior parietal lobe – Left lobe - Language especially reading, naming, & arithmetic.

Lesions may result in Gerstmann’s syndrome characterized by agraphia, acalculia, right-left confusion, & finger agnosia (loss of the ability to know which finger is which)

Right lobe – Body schema – lesions results in neglect of left side of the body & conditions such as dressing apraxia (inability to place garments correctly in relation to body parts).

Page 17: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Parietal Lobe Other dysfunctions due to a right

parietal lobe lesion include – Spatial and topographical dysfunctions

Inability to finding one’s way around & reading a map.

Deficits in Constructional skills Copying figures, drawing a clock

If left parietal lobe is not affected, speech/language are relatively preserved. However, emotional intonation is affected

Paralinguistic deficits - Cannot understand sarcasm, humor

Page 18: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Temporal Lobe Left temporal lobe

Primary Auditory Cortex (Area 41) Lesions cause central auditory processing disorders (CAPD)

Bilateral superior temporal lesions causes Pure word deafness - Inability to understand spoken words

although puretone audiometry & recognition of nonverbal sounds are preserved

Wernickes Area (Area 22) – Comprehension of verbal language.

Lesions to medial left temporal lobe – affects verbal memory Right temporal lobe – lesions may affect

appreciation of music/rhythm. Lesions to medial right temporal lobe – affects nonverbal

memory. Cerebral localization of Music – The case of Clive Wearing

Page 19: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Temporal Lobe

Temporal Lobe Epilepsy or Seizures – May result in “unusual” sensations such as déjà

vu (a feeling of familiarity), jamais vu (a feeling of unfamiliarity), or evoke some form of memories. May be auditory or gustatory such as a taste, or

olfactory. May result in dysphoric or euphoric feelings, fear,

anger, and other sensations. Are often called "auras,"

Secrets of the Mind - Video

Page 20: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Occipital Lobe Primary visual cortex (Area 17)

Unilateral lesion results in contralateral hemianopia for both eyes Bilateral damage – cortical blindness

Total loss of vision in a normal-appearing eye but response of the pupil to light is intact (Light reflex does not involve cortex).

Associated with visual hallucinations, denial of visual loss and the ability to perceive moving but not static objects

Visual Association areas (Areas 18 & 19) Involved with complex visual analysis Lesions result in visual agnosia.

Inability to make sense of or make use of some part of otherwise normal visual stimulus and the inability to recognize familiar objects or faces.

Also may result in dyslexia, impaired visual memories, and color recognition

Dr. Oliver Sacks Interview

Page 21: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specialization

Since Broca (1861), it is known that in 96% of right-handed & most left-handed people, the left hemisphere is dominant for language. Some left-handed have mixed dominance

Speech expression in the left while comprehension in the right hemisphere.

Cerebral dominance has structural correlates Longer planum temporale in the left-hemisphere Differences in blood supply (more dense for left

hemisphere)

Page 22: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specilization

Page 23: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specilization

Page 24: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specilization

Right Hemisphere Responsible for attention Functions are not as focal and isolated Cognitive Style: Holistic-gestalt-Responsible for getting the

whole picture. Map reading, sense of direction, dressing, emotional feeling

and processing Non Linear Processing, such as music and art.

Left Hemisphere Functions are more focal Cognitive Style: Analytical thinking, linear processing

(examples: Math, Language), Rule-based thinking

Page 25: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specilization

Page 26: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cerebral dominance & Functional specilization

Page 27: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20
Page 28: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20
Page 29: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Speech & Language Disorders

Motor speech disorders Dysarthria – Abnormal motor speech control

Including abnormal strength, place of articulation, timing and speed of articulatory movts, abnormal voicing & dysphagia With normal spoken and written language comprehension.

Six main types – Flaccid Spastic Ataxic Hypokinetic Hyperkinetic Mixed

Page 30: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Flaccid Dysarthria

Damage to the lower motor neurons (cranial nerves V, VII, IX, X & XII) involved in speech

Signs/symptoms Neuromuscular – Muscular weakness, lack of

normal muscle tone and reduced reflexes. Phonation - If CN X is damaged, voice will be

affected - Breathy voice Resonance - Hypernasality will occur if the

muscles involved in velar elevation have been affected.

Prosody - Monopitch and monoloudness may both result from vocal fold paralysis.

Page 31: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Flaccid Dysarthria

Signs/symptoms Associated Characteristics - Muscles affected by

flaccid paralysis may begin to atrophy or lose mass over time. Also, lack of innervation may cause fasciculations or

twitching of muscle fibers – More visible in the tongue Unilateral paralysis of the oral structures may be

noted. The affected side of the mouth may sag, causing

drooling, while it will be drawn to the unaffected side

Fasciculation's of the Tongue Normal Vocal folds Abnormal Vocal folds

Page 32: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Bilateral lesions of the motor cortex or corticobulbar tracts (UMN lesion)

Signs/symptoms Neuromuscular - Muscular weakness, exaggerated stretch

reflexes, resulting in increased muscle tone and incoordination.

Phonation - Voice quality is low pitched & harsh. Resonance - Hypernasality typically occurs Prosody – Atypical bursts of loudness during speech Articulation - Range of movement, tongue strength,

speech rate, and voice onset time for stops are reduced. Slow speaking rate & imprecise articulation

Spastic Dysarthria

Demonstration of Spastic Speech

Spastic Gait

Page 33: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Ataxic Dysarthria Damage to the cerebellar control circuit. Signs/symptoms

Neuromuscular - Inaccuracy of movement & slowness of movement.

Phonation – Harsh and loudness may vary excessively, and increased effort is evident. Ataxic speech is sometimes described as explosive

speech. Resonance – Hypernasality in some cases.

Page 34: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Ataxic Dysarthria

Signs/symptoms Prosody - Patients with ataxic dysarthria tend to

place equal and excessive stress on all syllables spoken. Known as scanning speech

Articulation – Described to be more slurred (Patients sound almost inebriated - Gait is affected in the same way). Breakdown in motor organization and control results in

slowness and inaccuracy in range, force, timing, and direction of articulatory movements.

Dysdiadokinesia

Page 35: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Hypokinetic Dysarthria

Lesion to subcortical Structures involving Basal Ganglia

Classically seen in Parkinson’s disease( lesion in the substantia nigra) However, can also result from anti-psychotic

medications, carbon monoxide poisoning & frequent blows to the head.

Signs/symptoms Neuromuscular - Slow movements & limited

range of movement Phonation – Hoarseness, reduced loudness and

pitch variability reduces intelligibility.

Parkinson’s disease - Shuffling Gait

Page 36: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Hypokinetic Dysarthria

Resonance - Hypernasality Prosody – Monopitch and monoloudness may

occur. Pallilalia, or the compulsive repetition of syllables, is

sometimes present. Articulation - Bradykinesia (reduced speed of

movt of muscles) causes difficulty in the initiation of voluntary speech. This can result in delay in starting to talk as well as

very slow speech and frequent pauses.

Sample of Parkinson's Speech

Page 37: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Hyperkinetic Dysarthria

Lesion to subcortical structures involving Basal Ganglia

Seen in chorea & related movement disorders such Huntington’s chorea

Signs/symptoms – Neuromuscular - Quick, unsustained, involuntary

movements Phonation - vocal quality may be described as harsh,

strained, or strangled. Also excessive variation in loudness and distorted vowels

Resonance - Hypernasality is common. Articulation - When voluntary speech movements are made

there is often a super-imposition of involuntary movements.

Sample of Chorea Speech

Page 38: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Mixed Dysarthrias

Combinations of any of the above 5 types Common examples include Amyotrophic Lateral

Sclerosis (ALS) and Multiple Sclerosis (MLS)

Page 39: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Apraxia of speech Is the inability to program sequences of articulatory

movements. Apraxia results from an impaired ability to generate the

motor programs for speech movements rather than from the disordered transmission of controlling messages to the speech musculature (which is dysarthria). Apraxia occurs commonly following damage to Broca's Area

and is always the result of a central nervous system lesion. It is a cortical problem, not a motor impulse transmission

problem like dysarthria. Commonly seen along with Aphasia

Page 40: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Apraxia of speech Apraxia is not dysarthria

Since apraxic problems cannot be explained by significant slowness, weakness, restricted range of movement or incoordination of the articulators.

Differences between Apraxia & Dysarthria Apraxia is a planning/programming problem, not a movement

problem like dysarthria. Apraxics have more inconsistent error patterns compared to

the consistent & predictable errors seen with dysarthria. Apraxia - There are islands of clear speech especially when

producing over-learned material or material that has become automatic.

Apraxia - Consonants are more often substituted than distorted (as in dysarthria). Apraxia - More problems with polysyllabic words and initial

consonants Verbal Apraxic Speech

Page 41: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Apraxia vs. Dysarthria

Difference between Apraxia & Dysarthria Speech rate

Dysarthria - As the rate of a dysarthric's speech increases, the intelligibility of that person's speech will decrease proportionally. Thus in order to improve intelligibility, the dysarthric must learn to

reduce speech rate by articulating complex words syllable by syllable.

Apraxia - As the rate of an apraxic's speech increases, the intelligibility of that person's speech may actually improve.

While all aspects of speech, including articulation, phonation, resonance, prosody, rate and respiration, may be affected by dysarthria, apraxia is mainly a disorder of articulation.

Page 42: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Apraxia vs. Dysarthria

Difference between Apraxia & Dysarthria Associated problems

Dysarthria – May be accompanied with changes in muscle tone and movements of the soft palate, lips, tongue and jaw may be impaired not only during speech, but also in the context of vegetative functions such as chewing and swallowing. Dysarthria and dysphagia often co-occur.

Apraxia - Do not usually see changes in muscle tone & may occur without concomitant swallowing problems. The movement of the velum, lips, tongue and jaw will only

be impaired during speech.

Page 43: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Aphasia

Typically refers to acquired disorders of language processing secondary to brain disease. Intelligence is not affected In contrast to congenital or developmental language

problems (dysphasia), motor speech disorders (dysarthria, dysphonia, apraxia), or impaired thought processes (dementia, schizophrenia).

Five major types: Broca’s Wernicke’s Global Conduction Anomia

Oliver Sach’s Interview (25 min – Aphasia)

Page 44: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Cortical areas important for speech

Structures numbered represent pathway for a spoken description of an object or scene

Page 45: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Broca’s Aphasia Broca’s area

Inferior third frontal gyrus in the hemisphere that is dominant for language.

Is involved in the coordination or programming of motor movements for the production of speech sounds. While it is essential for the execution of the motor

movements involved in speech, it does not directly cause movement to occur (function of neurons in the primary motor strip)

The neurons in Broca's area generate motor programming patterns when they fire.

Lesion to the Broca’s area of the dominant hemisphere– Broca’s Aphasia Also known as Expressive aphasia or Anterior aphasia

Page 46: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Broca’s Aphasia

Signs/symptoms - Spontaneous speech is nonfluent and

agrammatical. Speech becomes slow and labored. It may sound telegraphic, with function words like

articles, conjunctions, and prepositions missing but responses generally makes sense.

Speech articulation is slurred. Comprehension is not seriously affected. If writing is involved, spontaneous writing is

usually poor, but reading comprehension is better. Repetition is affected Broca’s Aphasic Speech

sample

Page 47: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Wernicke’s Aphasia Wernicke’s area – Posterior 2/3rd of the left superior

temporal gyrus. Wernicke’s area is primarily responsible for relating

auditory experiences to present situations, Is an auditory association area. Wernicke’s area is also primarily responsible for speech

recognition. Wernicke’s area is also responsible for comprehension of

written language and for visual recognition of written language.

Lesion to the Wernicke’s area of the dominant hemisphere– Wernicke’s Aphasia Also known as Fluent aphasia, Sensory aphasia or Posterior

aphasia

Page 48: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Wernicke’s Aphasia

Signs/symptoms - Auditory comprehension is impaired. Sentences are spoken fluently and with normal

inflections. But lacking in meaning. Words are often inappropriate, if not sheer nonsense

(neologistic paraphasia). Paraphasia refers to the production of unintended

syllables, words, or phrases during the effort to speak Repetition is impaired. Spontaneous writing shows well formed letters,

but reading comprehension is poor.

Wernicke’s Aphasic Speech Sample

Page 49: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Global Aphasia

Sum of Broca’s & Wernicke’s aphasia. Typically the result of a large blockage of the

middle cerebral artery. Signs/symptoms –

Typically nonfluent or mute & exhibit impaired comprehension

All language aspects (speech, naming, comprehension, repetition, reading & writing) are severely impaired.

Page 50: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Conduction Aphasia

Caused by damage to the nerve fibres in the arcuate fasciculus, which connects Wernicke's and Broca's areas.

Patients with conduction aphasia show the following characteristics: Speech is fluent Comprehension remains good Oral reading is poor Repetition is poor

Page 51: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Conduction Aphasia

Transpositions of sounds within a word ("television" → "velitision") are common - Sounds are combined in wrong sequences. ‘Stop’ may come out ‘pots’, ‘tops’, ‘post’. Hearing word repeated correctly does not improve

performance. Patient is aware of these errors and makes efforts

at self-correction.

Page 52: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Anomic Aphasia

In this type of aphasia, patient has difficulty remembering or recognizing names which the subject should know well. The patient speaks fluently, grammatically, has

normal comprehension Only deficit is trouble with "word finding,“ Often use circumlocutions (speaking in a

roundabout way) in order to express a certain word

Often know the purpose/use of an object, but still not be able to give a name to the object.

Page 53: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Anomic Aphasia

For example, show a subject an orange, and ask what it's called. The same subject may be well aware that the object can be peeled and eaten, and may be able to demonstrate this by actions or even verbal responses.

Anomia is caused by isolated damages to various parts of the parietal lobe or the temporal lobe.

Page 54: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Language features of common types of Aphasia

Page 55: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Other Types of Aphasias

Transcortical aphasia – Lesions that do not directly affect the primary language areas or the circuit between the Broca’s and Wernicke’s area, but to other areas that project to the language cortex.

Three types - Transcortical motor aphasia Transcortical sensory aphasia Transcortical mixed aphasia

Preserved repetition skill is a defining quality of all transcortical aphasias

Page 56: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Transcortical Motor Aphasia Typically due to an injury to the anterior superior

frontal lobe. The area of insult is sometimes referred to as a watershed

region, a region surrounding Broca's area. Characteristics –

Less common impairment than Broca's aphasia. Good comprehension since Wernicke's area is usually not

affected. Are non-fluent (halting and effortful) speech and their

utterances are typically only one or two words long. However retain the ability to repeat words, phrases or

sentences since the arcuate fasciculus is intact. Writing ability parallels speaking ability

Page 57: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Transcortical Sensory Aphasia

Typically associated with lesions to the left posterior temporo-occipital lobe sparing the Wernicke’s region. Is also seen in patients with Alzeimer’s disease.

Characteristics – Speech is fluent but paraphasic & auditory comprehension

is severly affected (like Wernicke’s aphasia) However ability to repeat phrases & sentences is

preserved. Reading comprehension & writing are impaired.

Page 58: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Transcortical Mixed Aphasia

Is the transcortical equivalent of Global aphasia In this rare condition, Broca's area, Wernicke’s area,

and the arcuate fasciculus are intact but the watershed region around them is damaged. This damage isolates these areas from the rest of the brain

Characteristics – Cannot speak fluently, comprehend spoken language,

name objects, read or write. However can repeat fluently

Page 59: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20
Page 60: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20

Aphasia Types & Lesions

Page 61: Cerebral Cortex: Higher Mental Functions Bhatnagar (2008) Neuroscience for the Study of Communicative Disorders, 3 rd Ed. Chapters 19 & 20