Telencephalon

Lecturer: Dr. Lara | June 25,2021

Trans by: Zingapan, Dumelod, Matila, Calaycay

OUTLINE ▪ Vibration sense.

▪ Sense of position and sense of movements
I. Telencephalon A. Amygdala and
A. Anatomy and Emotion → Posterior parietal cortex: integrates somatosensory,
Physiology III. Hippocampal formation visual, auditory information for visuospatial attention and
B. Lobes of the Brain IV. Olfactory system control of motor function.
C. Histology A. Clinical correlation • Temporal lobe
D. Laminar structure of B. Neocortical network → Primary auditory cortex; its lateral aspect includes
the Neocortex C. Sensory processing and auditory and association areas required for object
E. Columnar Organization object recognition recognition and naming
of the Cerebral Cortex V. Visual system → Inferior aspect: critical for visual recognition of objects
F. Hierarchical processing VI. Auditory system and faces.
of information in the A. Auditory cortex
• Occipital lobe
cerebral cortex VII. Object recognition and
G. Parallel Processing of semantic knowledge → Contains the visual areas in the calcarine cortex and
Information VIII. Spatial attention surrounding cortex.
H. Reciprocal Interactions IX. Motor programming and → The dominant (usually, left) hemisphere is involved with
in the Cerebral Cortex execution language and calculation, and the right hemisphere is
I. Distributed Networks of X. Neocortical networks involved with visuospatial functions.
the Cerebral Cortex XI. Control of behavior and • Insular lobe
J. Cortical Plasticity executive function → Involved in pain, visceral, and taste sensation.
K. Connections through XII. Clinical syndromes of the
C. Histology
the subcortical white cerebral cortex
1. Pyramidal cells
matter A. Diffuse disorders
L. Anatomy and basic B. Focal disorders → constitute the majority of neurons in the cerebral cortex.
connectivity of the C. Visual field defect → excitatory projection neurons that have L-glutamate as the
basal ganglia D. Frontal lobe syndromes neurotransmitter.
M. Parallel cortical-basal E. Parietal lobe syndromes → Typically, they have an apical dendrite and basal dendrites,
ganglia-thalamocortical F. Temporal lobe all with dendritic spines.
circuits syndromes 2. Local interneurons
II. Limbic System Network G. Occipital lobe syndromes → inhibitory and have ℽ-aminobutyric acid (GABA) as a
XIII. Subcortical lesions neurotransmitter.
XIV. Evaluation of cortical
→ control the excitability of the pyramidal cells in the different
disorders
layers of the cerebral cortex.
I. Telencephalon
A. Anatomy and Physiology
• The supratentorial level consists of two main anatomical
regions: the diencephalon and the telencephalon.
• Telencephalon: Arises from lateral evaginations of the most
rostral portion of embryonic neural tube- prosencephalon
• It forms the cerebral hemispheres, which consist of the cerebral
cortex, basal ganglia, and subcortical white matter tracts

B. Lobes of the Brain

• Frontal lobe
→ Has executive and motor functions
→ Prefrontal cortex: involved in attention, decision making, and
control of affective behavior, and the premotor and motor
areas, which are involved with the programming and
execution of limb movements, control of gaze, and speech
production
→ Precentral gyrus: Responsible for control of voluntary
muscles
→ Broca’s area: Speech control and expression of language
vocally
• Parietal lobe
→ Post central gyrus: somatosensory cortex
→ It receives the following sensations:
Post central gyrus: somatosensory cortex
→ It receives the following sensations:
▪ Fine touch (tactile localization, tactile
discrimination, etc.).
▪ Fine grades of temperature.
i. Pyramidal cells receive excitatory glutamatergic input from
other pyramidal cells (corticocortical projections) and the
thalamus (thalamocortical projections).
ii. Excitatory inputs terminate on dendritic spines.
iii. Pyramidal cells receive inhibitory GABAergic input from
different types of local interneurons, which do not synapse on
spines.
iv. Ascending projections from structures of the consciousness
system, including neurons producing acetylcholine (ACh),
norepinephrine (NE), dopamine (DA), serotonin (5-HT), and
histamine (HA), modulate the response of pyramidal cells to
excitatory and inhibitory inputs.

Trans # 13 Telencephalon 1 of 17

D. Laminar structure of the Neocortex
1. Layer I, the superficial layer, contains the apical
dendrites of pyramidal cells as well as local interneurons
and receives projections from thalamic and brainstem
neurons.
2. Layer II, the external (outer) granular layer,contains local
interneurons and pyramidal cells that project to
contralateral cerebral cortex (commissural fibers).
3. Layer III, external (outer) pyramidal layer,contains
pyramidal cells that give rise to commissural or
association fibers.
4. Layer IV, the internal (inner) granular layer,has closely
packed spiny stellate cells that receive input from
thalamocortical fibers and project to pyramidal
neurons.This layer is highly developed in primary
sensory cortical areas; the cortex in these regions is
called granular cortex.
5. Layer V, the internal (inner) pyramidal layer,contains the
large pyramidal cells that project to the basal ganglia,
brainstem, and spinal cord.
6. Layer VI,or multiform layer,contains pyramidal neurons
that project to the thalamus.
E. Columnar Organization of the Cerebral Cortex
• Column
→ functional unit of the cerebral cortex
→ vertical cylinder of cortical tissue that includes all 6 layers
→ where recurrent excitatory interactions between
pyramidal cells of deep layers and superficial layers
occur
→ its activation is associated with inhibition of the
surrounding columns
F. Hierarchical processing of information in the
cerebral cortex
G. Parallel Processing of Information
→ occurs in two parallel streams involving the parietal and
temporal lobes.
→ Characterized best for the visual system
→ Input from primary visual cortex is processed in a:
Trans # 13 Telencephalon
-DORSAL STREAM involving neurons in the unimodal visual
association cortex of the posterior parietal lobe that respond
to object in location and motion.
-VENTRAL STREAM involving neurons in the unimodal
visual visual association cortex of the inferior
occipitotemporal region that respond to object shape and
color and allow identification
→ Sensory processing occurs in a dorsal(parietal) stream involved
with object location and a ventral (temporal) stream involved with
object identification.
→ Information from the ventral stream is processed in the premotor
cortex for visual guidance of eye and limb movement, and
information from the ventral stream is used for object recognition,
naming, emotional response, and memory.
H. Reciprocal Interactions in the Cerebral Cortex
→ Reciprocal input from the limbic system to the paralimbic and
then heteromodal cortex provides emotional bias to sensory
processing and contributes to recognition of the object.
→ Feedback projections from the prefrontal and posterior parietal
cortices to the unimodal sensory areas are critical for attention.
I. Distributed Networks of the Cerebral Cortex
→ Every cortical function depends on the parallel and simultaneous
processing of information by anatomically separate networks that
involve widespread areas of neocortex, paralimbic cortex,and
limbic cortex that interact through their specific cortical and
subcortical connections.
→ Cortical activity involves the simultaneous interaction of
widespread, distributed, but temporally linked cortical networks.
J. Cortical Plasticity
→ The ability of the cerebral cortex to undergo anatomical and
functional change in response to environmental circumstances
→ This phenomenon is essential for establishing connections
during development of the nervous system,but it also occurs in
the cerebral cortex throughout life.
→ Cortical plasticity may explain recovery of function after a large
hemispheric lesion.
K. Connections through the subcortical white matter
1. Projection Fibers
→ The projection fibers that connect subcortical and cortical
areas form a compact group of axons called the internal
capsule - a broad band flanked medially by the thalamus and
caudate nucleus and laterally by the globus pallidus and
putamen.
i. AFFERENT PROJECTION FIBERS
✓ arise largely from the thalamus and are called thalamic
radiations
✓ The optic radiations are in the retrolenticular portion of
the internal capsule,and the auditory radiations are in the
sublenticular portion
✓ As the axons spread out from the internal capsule to
reach all areas of the cortex,they form the corona radiata.
ii. EFFERENT PROJECTION FIBERS
✓ pass through the corona radiata into the internal capsule
en route to the thalamus, basal ganglia, hypothalamus,
red nucleus, and brainstem reticular formation
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2. Commissural fibers
→ Commissural fibers connect homologous areas in the two
hemispheres, integrating the activity of the two sides.
- Most of these axons pass through the corpus callosum,
which is the large bundle of fibers that forms the roof of
the lateral ventricles.
3. Association Fibers
→ Fiber tracts known as association pathways run
longitudinally within a hemisphere, correlating the activity of
different lobes. These include the:
- superior longitudinal fasciculus
- inferior longitudinal fasciculus, which connect the
posterior parietotemporo-occipital regions with the frontal
lobe,
- uncinate fasciculus, which interconnects the temporal
and frontal lobes, and the cingulum, which interconnects
the medial surface of the frontal, parietal, and temporal
lobes.
→ Short association fibers that connect adjacent gyri are
called arcuate, or U, fibers.
L. Anatomy and basic connectivity of the basal
ganglia
→ The basal ganglia include the striatum and globus pallidus.
→ Striatum includes the caudate nucleus, putamen,and nucleus
accumbens.
→ The caudate and the putamen are separated by the internal
capsule.The caudate consists of a head,body,and tail and is
intimately related to the walls of the lateral ventricle.The
nucleus accumbens,or limbic striatum,is located in the M. Parallel cortical-basal ganglia-thalamocortical
ventral portion of the striatum and forms part of the basal circuits
forebrain. → The cerebral cortex and the basal ganglia are involved in
→ The globus pallidus (“pale”) is separated from both the different parallel reentrant cortical-basal ganglia-
thalamus and the substantia nigra by the internal capsule. thalamocortical circuits.These circuits involve different
→ The globus pallidus consists of external and internal portions of the frontal lobe,striatum,globus
pallidus,subthalamic nucleus,and thalamus.
segments.
→ The motor circuit involves the motor and supplementary
→ The globus pallidus and putamen together are referred to as
the lenticular nucleus because of the shape.However,the two motor cortices,putamen,specific portions of the globus
pallidus and subthalamic nucleus, and the ventral oralis
nuclei have different connections and functions.The basal
nucleus of the thalamus,which projects back to the
ganglia circuits include two functionally related structures:the
supplementary motor area.
subthalamic nucleus and substantia nigra.
→ The ocular motor circuit involves the frontal eye
→ The basal ganglia circuits have a basic pattern of
fields,caudate nucleus,and substantia nigra pars reticulata
connectivity.
(which is functionally homologous to the internal segment of
→ The cerebral cortex,particularly the frontal lobe- sends
the globus pallidus) and,through the superior
excitatory input to the striatum.
colliculus,controls saccadic eye movements.
→ The striatum contains GABAergic inhibitory neurons that
→ The cognitive, or association circuit involves the prefrontal
project to both the external and internal segments of the
cortex,head of the caudate nucleus,substantia nigra pars
globus pallidus.
reticulata, and dorsomedial nucleus of the thalamus.This
→ The internal segment sends a GABAergic inhibitory
circuit is involved in executive functions,including planning
projection to the thalamic nuclei that project to different
and monitoring behavior.
portions of the frontal lobe.
→ The limbic circuit involves the orbitofrontal and anterior
→ The subthalamic nucleus contains excitatory neurons that
cingulate cortices, nucleus accumbens,and ventral
also project to both segments of the globus pallidus.The
pallidum.This circuit is important in controlling emotional and
subthalamic nucleus receives a direct excitatory projection
motivated behavior.
from the cerebral cortex and a reciprocal inhibitory projection
from the external segment of the globus pallidus.
II .Limbic system

A. Amygdala and Emotion

• Anatomy
→ Afferent Fibers:
▪ BASOLATERAL: Receive input from:
- Dorsal thalamus, Prefrontal cortex, Cingulate,
Parahippocampal gyri, Temporal lobe, Insular cortex,
Subiculum
▪ CENTROMEDIAL: Receive input from:

Trans # 13 Telencephalon 3 of 17
 - Olfact ory, Hypothalamus, Dorsomedial & Medial nuclei A. Anatomy
of the dorsal thalamus • Hippocampal formation
• Efferent Fibers: → Subiculum
→ STRIA TERMINALIS: Distributes to: → Hippocampus
→ Dentate gyrus
- Hypothalamus, Nucleus accumbens, Septal nuclei,
Caudate nucleus, Putamen

→ VENTRAL AMYGDALOFUNGAL: Distributes to:

- Hypothalamus, Septal area
• Afferent Fibers:

• Afferent Fibers
• Efferent Fibers: → PERFORANT PATHWAY:
▪ Entorhinal cortex → Granule cells of Dentate gyrus → Area
CA3 → Area CA1 → Subiculum

• Physiology

→ Emotional or associative memory (conditioned responses)

→ Anterior cingulate cortex - motor responses

→ Orbitomedial prefrontal cortex → Amygdala - inhibiting

emotional responses.

III. HIPPOCAMPAL FORMATION: LEARNING AND

DECLARATIVE MEMORY
Trans # 13 Telencephalon 4 of 17
 • Papez Circuit
→ Hippocampus (Subiculum) → Fornix → Mamillothalamic tract
• Efferent Fibers → Anterior nucleus of the thalamus → Cingulate gyrus
→ Subiculum → Alveus → Fimbria of the Hippocampus → Fornix
→ Postcommisural fornix and Precommisural fornix →
Mammillary body

B. Physiology: Declarative memory

• Consolidation of long-term memories from immediate and short-
term memories.
• Declarative memory (Explicit memory):
→ Learn, store, and retrieve information about the
autobiographic events, facts and names, and places.

C. Clinical correlations
• AMNESIA
→ Loss of declarative memory
→ Usually is due to bilateral damage of the medial temporal
cortex, which impairs the ability to learn and store new
information.
→ Typical of Alzheimer disease
▪ Most common degenerative dementia.
▪ The memory impairment in this disorder reflects
involvement of the entorhinal and perirhinal cortices,

Trans # 13 Telencephalon 5 of 17
 followed by that of the hippocampus and the loss of the • Motor programming and execution
cholinergic neurons in the basal forebrain • Language
▪ Early stage – remote memory is preserved • Control of behavior
• Selectively impaired learning and declarative memory
→ Acute and subacute lesions affecting the medial temporal lobe C. Sensory processing and object recognition
or its connection • Somatosensory, visual, and auditory information reach the cortex
→ Diencephalic amnesia through specific relay nuclei that receive input from the specific
▪ Korsakoff Syndrome: sensory pathways
− Thiamine deficiency • Dorsal (parietal) stream
• Memory Disturbances • Ventral stream
→ Anterograde amnesia
▪ Inability to form new memories or to learn new information Somatosensory system
beginning at the time of the injury • Primary somatosensory
→ Retrograde amnesia → Areas 3a,3b,1,and 2 - areas of the primary somatosensory
▪ Inability to recall events that occurred before an injury cortex contain separate somatotopic representations of the
→ Transient global amnesia contralateral body
▪ Reversible (within 24 hours) inability to learn new → 3a - primary area for proprioception
information → 3b - area for tactile representation
→ Confabulations: → 1 and 2 - integrate input from both modalities
▪ Recurrent seizure activity → Stegnosis - tactile information from the fingers during active
IV. OLFACTORY SYSTEM touch is important for recognizing the shape of an object.
→ Information from areas 1 and 2 is processed in a dorsal stream
• Smell → Olfactory nerves → Cribriform plate → Olfactory bulb → that involves areas 5 and 7 of the posterior parietal cortex
Olfactory tract → The posterior parietal cortex integrates this information with
visual information to guide reaching and grasping movements.
• Secondary somatosensory
→ A ventral stream through the second somatosensory cortex
and insular cortex,connects the somatosensory areas and
heteromodal areas required for the tactile recognition of object
V. VISUAL SYSTEM
Right and left visual hemifields
• Primary visual cortex - calcarine fissure on the medial aspect
and pole of the occipital lobe.
• Dominance columns

A. Clinical correlations
• Complex partial seizures
→ Associated with transient loss of awareness
→ Symptoms: Superior and inferior visual fields
▪ Olfactory hallucinations
▪ Oromandibular automatism
▪ Fear or other affective symptoms
▪ Déjà-vu or jamais vu reflect disturbances of episodic
memory
• Olfactory bulb is involved early in some neurodegenerative
diseases
• Mass lesion on the orbital surface of the brain (olfactory
groove meningioma) affects the olfactory tract

B. Neocortical networks
• Magnocellular pathway / Dorsal stream
• Sensory processing and object recognition
• Parvocellular pathway / Ventral stream
• Directed attention
• Koniocellular pathway

Trans # 13 Telencephalon 6 of 17
 → 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 anterior middle
temporal gyrus and temporal pole.

A. Clinical correlations: Agnosias

• Agnosia
→ Inability to identify an object despite being able to perceive.
→ Lesions in the unimodal sensory association areas and can
involve any of the sensory modalities.
• Astereognosia
→ Unable to identify an object by palpating it
→ Associated with cortical sensory loss
▪ Loss of twopoint discrimination
▪ Agraphesthesia
▪ Atopognosia
▪ Abarognosia
• Lesions of primary visual cortex
→ Produce homonymous hemianopsia
• Monocular blindness • Lesions of unimodal visual association cortex
• Bilateral hemianopia → Akinetopsia
• Left hemianopia → Hemiachromatopsia
• Left homonymous hemianopia → Visual agnosia
• Left Inferior Quadrantanopia • Contralateral hemiachromatopsia.
• Left Superior Quadrantanopia • Visual agnosia
→ Prosopagnosia
→ Object agnosia

• Prosopagnosia
→ Inability to identify familiar faces
→ Bilateral lesions of the mid to anterior part of the lingual and
fusiform gyri of the inferior occipitotemporal cortex
• Visual object agnosia
→ Inability to recognize or name an object or to describe its use

VI. AUDITORY SYSTEM

• The auditory cortex is located in the transverse temporal gyri of • Lesions of primary auditory cortex
Heschl, which lie on the dorsal surface of the superior temporal • Lesions in unimodal auditory association cortex or its
gyrus. connections
• The middle part (area 41) is the primary auditory receptive → Cortical deafness
area. → Auditory agnosia
• The remaining parts of the transverse gyrus and the adjacent → Pure word deafness
parts of the superior temporal area (area 42) are auditory • Lesions in the anterior middle temporal or temporopolar
association areas. cortex
→ Particularly of the left hemisphere, lead to loss of semantic
A. Auditory cortex knowledge of the world
• Core - primary auditory area; pure tones of specific frequencies
and responds primarily to stimulation of both ears.
• Belt - complex sounds
VIII. SPATIAL ATTENTION
• Parabelt - white noise
A. Anatomy
VII. OBJECT RECOGNITION AND SEMANTIC KNOWLEDGE
• Semantic memory
→ Recognition of objects,including faces.
• Object recognition
Trans # 13 Telencephalon 7 of 17
 → Supplementary eye fields - anterior to the supplementary
motor area
→ Parietal eyefields - intraparietal sulcus

C. Physiology
• Neurons of the intraparietal sulcus of the posterior parietal cortex
respond to different combinations of
visual,somatosensory,auditory, and vestibular input to produce a
representation of space.
• Motor programs for limb movements initiated in response to
visual stimuli are generated by neurons in the intraparietal
sulcus
• Supplementary motor area (medial area 6)
• Presupplementary motor area
• Primary motor cortex

B. Physiology
• 2 separate networks for attention:
→ Bilateral network
▪ Intraparietal sulcus and the frontal eye fields
▪ Orientation toward contralateral space
▪ Binding the different features of an object or scene into a
single percept
→ Ventral frontoparietal network
▪ Directing attention to behaviorally relevant and unexpected
sensory stimuli

C. Clinical Correlations
• Damage to the parietotemporal region C. Clinical correlations: Apraxias
→ Contralateral spatial neglect • Apraxia:
→ Fail to orientate toward or to detect items on their left → Inability to perform learned,skilled,purposeful movements in
side,including people or large objects - Constructional the absence of an attentional disorder, weakness,sensory
apraxia abnormality, or incoordination.
• Right parietal lesions • Ideamotor apraxia:
→ Neglect own contralateral body parts, failing to use or show → Know what to do but not how to do it.
any interest in them • Ideational apraxia:
▪ Dressing apraxia → Do not know what to do.
▪ Anosognosia X. NEOCORTICAL NETWORKS

• Balint Syndrome - Bilateral lesions of the superior parietal

lobule of the posterior parietal cortex (angular gyrus) A. LANGUAGE
→ Simultagnosia
→ Oculomotor apraxia
→ Optic ataxia

IX. MOTOR PROGRAMMING AND EXECUTION

A. Anatomy
• The motor regions of the frontal lobe
→ Primary motor area in the precentral gyrus (area 4)
→ Lateral premotor area (lateral area 6)
→ Supplementary motor area on the medial aspect of the
FIGURE 1: A, the perisylvian language network, located in the left hemisphere of
hemisphere (medial area 6) all right-handed and most lefthanded persons. B, Typical location of lesions
→ Regions of the anterior cingulate gyrus producing classic aphasic syndromes. However, in most cases, left hemisphere
• Oculomotor control lesions produce aphasia with mixed features.
→ Frontal eye fields - anterior to the lateral premotor area from
the limbs) ANATOMY AND PHYSIOLOGY

Trans # 13 Telencephalon 8 of 17
• Language depends on the activity of a distributed neocortical
network located around the sylvian fissure.
• The left cerebral hemisphere is dominant for language in almost
all right-handed persons and in more than two-thirds of left-
handed persons.
• 2 epicenters of the perisylvian language network:
1. Wernicke area
→ Posterior epicenter
→ located in the posterior part of the superior temporal
gyrus (area 22), superior temporal sulcus, and the
adjacent areas of the supramarginal (area 40) and
angular (area 39) gyri.
→ receives input from heteromodal association areas
of the left temporal lobe devoted to object
recognition (semantic knowledge).
→ Wernicke area is anatomically and functionally
heterogeneous.
→ functions in the recognition, comprehension, and
retrieval of words and renders words in a precise
form for the production of spoken or written
language.
2. Broca area
→ Anterior epicenter
→ located in the inferior frontal gyrus and including
areas 44,45, and surrounding areas 46 and 47.
→ Broca area receives input from the prefrontal and
anterior cingulate cortices.
→ Broca area contains separate regions in the left
inferior frontal gyrus involved in different aspects of
expressive language, including semantic
processing, syntax, and processing of phonemes.
(the arrangement of words and phrases to create
well-formed sentences in a language "the syntax of
English “)
→ These patients do not have paralysis of the speech
apparatus but have great difficulty translating
thoughts and concepts into coherent sentences.
Broca aphasia is also called expressive Aphasia.
• These two epicenters are interconnected by the arcuate
fasciculus in the inferior parietal lobe.
• Perisylvian language network (also referred to as the arcuate
fasciculus) comprising of three white matter fibre tracts: the long
segment running dorsally from the frontal lobe (“Broca's territory”)
to temporal structures comprising Wernicke's area, the anterior
segment connecting.
• Anterior insula is the area critical for speech production
(articulation).
• Lateral prefrontal cortex participates in high-level control of
• sentence production.
• Anterior cingulate cortex provides the behavioral drive for the
initiation of speech.
• Right hemisphere has an important role in language
comprehension in normal subjects; it participates in processes
such as prosody, figurative language, metaphor, and connotative
meaning.
CLINICAL CORRELATIONS
• 3 types of Disturbances of language and speech:
1. Aphasia- disorders of central language processing
2. Apraxia of speech- disorders of motor programming of
language symbols
3. Dysarthrias- disorders of mechanism of speech
• Aphasia and apraxia of speech are disorders of the supratentorial
level.
• In contrast, dysarthria may occur with disorders of the
corticobulbar pathway, basal ganglia, cerebellar control system,
or lower motor neurons in the brainstem or disorders at the level
of the peripheral nerve, neuromuscular junction, or muscle.
Trans # 13 Telencephalon
1. APHASIA
→ is a disorder of the language network or its connections
(usually) in the left hemisphere that impair comprehension,
repetition, production, or expression of words or other symbols
for communication (including sign language).
→ Different types of aphasia have been characterized on the
basis of fluency, content, comprehension, and repetition
of words
▪ Lesions involving Wernicke area produce fluent
aphasia.
− These patients produce excessive volume of well-
articulated words, but speech conveys little meaning.
− Lesions in Wernicke area impair the comprehension of
spoken or written language.
− The speech may be unintelligible because of errors in
phoneme and word choice, causing paraphasia and
jargon speech
▪ Lesions of Broca area or its subcortical connections
produce nonfluent aphasia, Broca aphasia.
− characterized by loss of speech fluency, agrammatism
(inability to organize words into sentences), and
telegraphic speech (the nonfluent use of content words
without connecting words).
− Although the patients have normal reception of
language, they cannot convert thoughts into meaningful
language.
− These patients may also have hemiparesis of the
contralateral face and upper extremity.
▪ Lesions in subcortical white matter of the inferior
parietal lobe, including the arcuate fasciculus, that interrupt
the connections between Wernicke and Broca areas,
produce Conduction aphasia.
− This disconnection syndrome is characterized by a
major deficit in repetition.
− Patients with this type of aphasia can produce intelligible
speech and comprehend sentences.
▪ Features of Wernicke aphasia and Broca aphasia are
combined in Global aphasia, which is associated
commonly with a dense contralateral hemiplegia.
▪ Perisylvian aphasias
• due to infarctions in the territory of the left middle cerebral artery,
but they may also be an early manifestation of a neoplastic,
inflammatory, or degenerative disorder.
▪ Transcortical aphasia
→ Infarctions in the arterial border zones.
→ These lesions interrupt the connections between the
perisylvian language areas and either the prefrontal
cortex or lateral temporal cortex
→ Repetition is spared
▪ Anomia
→ All aphasias are associated with word-finding difficulties
and difficulty naming objects, a deficit called anomia.
→ pure anomia may also occur with lesions in areas of the
left lateral temporal lobe, including the anterior pole,
which are involved in the integration of sensory
information for knowledge of the world
▪ Semantic paraphasia- particularly common after a left
temporal or large left frontal lesion.
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 TABLE 1: Features of the Main Types of Aphasia [Mayo Clinic]
• Aphasia should be distinguished from other disorders of speech
production, including speech apraxia, mutism, and dysarthria.
2. APRAXIA OF SPEECH (MOTOR SPEECH APRAXIA)
→ It is a manifestation of lesions restricted to the left insular
region in Broca area.
→ This consists of the partial or complete inability to form
the articulatory movements of the lips, tongue, and lower
jaw for producing individual sounds that make up words.
→ The patient knows what he or she wants to say but is
unable to execute the motor aspects of speech.
• Mutism
→ lack of speech production due to impaired behavioral drive
to initiate speech.
→ It results from bilateral lesions of the prefrontal cortex and
anterior cingulate gyrus
• Two syndromes are characterized by the inability to read words,
called alexia:
1. Alexia with agraphia
→ it is a deficit in both reading and writing and is associated
with damage of the left angular gyrus.
2. Pure alexia or alexia without agraphia
→ patients have a relatively preserved ability to write but
are unable to read what they have written.
→ The classic lesion involves the left calcarine cortex or
optic radiation (producing a right hemianopia) and the
splenium of the corpus callosum, interrupting the
connections from the right to the left occipital association
cortex, which provides access to Wernicke area.
→ The splenium of the corpus callosum connects the
posterior cortices with fibers varying in size from thin
late-myelinating axons in the anterior part,
predominantly connecting parietal and temporal areas,
to thick early-myelinating fibers in the posterior part,
linking primary and secondary visual areas.
*** Those who suffer from "alexia" and "dyslexia" can have
similar difficulties, however, "alexia" refers to an acquired
reading disability, where reading ability had previously been
developed, usually occurring in adulthood conditions, while
"dyslexia" refers to developmental reading disability. ***
Trans # 13 Telencephalon
FIGURE 2: Manifestations of lesions affecting the left inferior parietal lobule
(supramarginal and angular gyri) [Mayo Clinic]
• Gerstmann syndrome - Lesions of the left inferior parietal lobule
produce agraphia in association with acalculia (inability to
perform calculations), finger agnosia (inability to recognize the
fingers), and left-right disorientation.
LANGUAGE: KEY POINTS!!
• The language network is located in the perisylvian region of the
dominant (generally left) hemisphere and includes Wernicke area
(involved in word comprehension), Broca area (involved in word
production), and their connections.
• Disorders of central language processing produce aphasia.
• Lesions in Wernicke area produce fluent aphasia and impair
the comprehension of language.
• Lesions in Broca area produce nonfluent aphasia and impair
the expression of language.
• Conduction aphasia selectively impairs repetition of words.
• Most patients with aphasia have mixed features because of the
interruption of the language network.
• Anomia occurs in all types of aphasia and, in its pure form, is
associated with lesions in the left lateral temporal lobe and
temporal pole.
• Disorders of motor programming of language symbols produce
apraxia of speech.
• Disorders of the mechanism of speech produce dysarthrias.
• Alexia is the inability to read; alexia with agraphia (inability to
write) results from lesions in the left angular gyrus, whereas pure
alexia is commonly the result of combined lesions of the left
occipital lobe and the splenium of the corpus callosum.
• Lesions of the left inferior parietal lobule produce agraphia,
acalculia, left-right disorientation, and finger agnosia
(Gerstmann syndrome)
XI. Control of behavior and executive function
ANATOMY AND PHYSIOLOGY
• The prefrontal cortex, anterior to the premotor and motor areas,
is the largest region of the frontal lobe.
• Prefrontal cortex has connections with association and
paralimbic areas, amygdala, caudate nucleus, dorsomedial
nucleus of the thalamus, and midbrain dopaminergic neurons.
• Prefrontal cortex is the site of the confluence of two functional
networks:
1. Dorsolateral prefrontal cortex
− is involved in attention and executive function
− The lateral prefrontal cortex is involved in goal-directed
attention and working memory, which is the
temporary, online holding of information and its mental
manipulation to guide behavior.
− Working memory involves retaining information for a
short time, for example, looking up a telephone number
and remembering it briefly while dialing it.
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 − The lateral prefrontal cortex has a central role in
attention, which includes the ability to prevent
interference from distracting stimuli. It also is necessary
for abstraction, retrieval of stored information to guide
behavior, novelty seeking, response choice, and
behavioral flexibility. All these are referred to as
executive functions.
− They are required for stimulus selection and for
planning, initiating, maintaining, monitoring, and
modifying behavior according to the goal and
environmental context.
2. Orbitomedial prefrontal cortex
− involved in decision making and the control of
affective behavior.
− through its connections with the amygdala and
hypothalamus, has an essential role in the
modulation of emotional responses to behaviorally
significant events.
− It links emotional responses related to previous
experience or outcomes with selected decisions and
behaviors.
FIGURE 3: The Theory of Mind
• The anterior cingulate cortex,
− interconnected with the orbitofrontal cortex, is
involved in behavioral drive and the evaluation of the
outcomes of the behavior.
− allow the person to infer what another person might
think or feel in response to specific events or actions,
the theory of mind.
− This ability is critical for social interaction.
FIGURE 4: Functions of the heteromodal dorsolateral prefrontal cortex (salmon
area) (A) and paralimbic orbitomedial prefrontal cortex (blue area) (B). Lesions
(gray area) of dorsolateral prefrontal cortex produce a dysexecutive syndrome (C),
Trans # 13 Telencephalon
and those of the orbitomedial prefrontal cortex impair decision making and social
behavior (D). [MayoClinic]
CLINICAL CORRELATIONS
• Lesions of the prefrontal cortex change cognition and
behavior. Because these changes, or abnormalities, occur in the
absence of impaired memory, language, motor, or sensory
function, they are frequently misinterpreted as a psychiatric
illness and may be misdiagnosed until an imaging study is
performed.
• Thus, any marked change in personality or behavior should
always raise the suspicion of a prefrontal lobe lesion.
• Dysexecutive Syndrome
→ produced by Lateral prefrontal lesions
→ characterized by a deficit of attention, working memory,
planning, and response selection.
→ Abulia
▪ a condition where the patients may lack initiative and
spontaneity
→ They are easily distracted, cannot maintain a train of thought
or complete a given task,have little concern for either the past
or the future, and have the tendency to spontaneously repeat
verbal or motor behaviors despite instructions not to do so,
which is called perseveration.
→ Patients may develop an external stimulus–bound state in
which thinking becomes concrete and behavior is guided by
events in the environment.
→ For example, a patient may imitate the gestures of the
examiner (imitation behavior) or pick up and use objects
placed in front of him or her without being asked to do so
(utilization behavior).
→ This severe lateral prefrontal syndrome most commonly
occurs after bilateral damage, for example, from an infiltrating
tumor, multiple infarcts, or certain degenerative disorders.
• Lesions of the orbitomedial prefrontal cortex affect decision
making, personality, and social behavior.
• The patients are unable to organize future activities and to hold
employment; they have an unrealistic favorable view of
themselves, diminished capacity to respond to punishment, and
a tendency for inappropriate social conduct.
• They may have either a jocular or humorless attitude, sexually
disinhibited humor, inappropriate self-indulgence, perseverative
impulse to seek immediate gratification, emotional lability, poor
tolerance of frustration, and lack of empathy or concern for
others. This is referred to as acquired sociopathy.
• Orbitofrontal Syndrome
→ is often the consequence of a traumatic head injury, a tumor
in the olfactory groove, or a focal degenerative disorder, but
it may also occur with a vascular or inflammatory condition.
COMPARISON OF MEMORY SYSTEMS
TABLE 2: Comparison of Memory Systems
• From the description of the different functions of supratentorial
networks and effects of lesions, it can be deduced that memory
is a complex function with many different components and
anatomical substrates
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 → Working memory is the ability to hold for relatively short
periods information to be used for actions planned in the
near future. This is the basis of attention, and it depends
on the lateral prefrontal cortex
→ Declarative memory is the ability to learn and store
information about autobiographical events (episodic
memory), facts (semantic memory), names, and places;
it depends on structures in the medial temporal lobe
→ Associative (or emotional) memory consists of
conditioned responses to emotionally relevant stimuli and
involves the amygdala
→ Procedural memory (also called implicit memory) is the
learning of habits (such as riding a bicycle) and involves
motor circuits of the caudate nucleus and dentate nucleus
of the cerebellum.

XII. CLINICAL SYNDROMES OF THE CEREBRAL CORTEX

FIGURE 6: Electroencephalographic accompaniment of a generalized tonic-

clonic seizure. Segments of the recording during different phases of the seizure
are shown. Interictal is before the seizure; tonic phase (body stiff) shows repetitive
spikes; clonic phase (body jerking) shows spike-and-wave discharges; and
postictal phase (after the seizure) shows
suppression of activity.

FIGURE 5: Cerebral Hemispheres Disorders

• Disorders of the cerebral hemispheres may be diffuse or focal

and may be expressed as either loss of function (deficit) or
excessive activity (seizures).
• Diffuse disorders may consist of altered cognition and behavior,
bilateral motor abnormalities, or generalized seizures.

A. DIFFUSE DISORDERS
• Important causes of diffuse disorders at the supratentorial level
include inflammatory and infectious conditions (e.g.
Encephalitis), degenerative disorders, toxic or metabolic
disorders, and developmental disorders.
• Their manifestations depend on the location of the lesion FIGURE 7: Electroencephalographic accompaniment during a typical absence
(cerebral cortex, basal ganglia, or both) and the underlying seizure consisting of a 3-Hz spikeand- wave pattern, during which the patient
lesion. was unresponsive.
• They include generalized seizures, confusion, dementia, mental
• Status Epilepticus.
retardation, and movement disorders.
→ Repeated seizures
GENERALIZED SEIZURES → This is defined by the presence of repeat seizures without
recovery of consciousness in between episodes.
• diffuse hyperexcitability of the cerebral cortex and paroxysmal
→ Status epilepticus may be convulsive or nonconvulsive. It
synchronization through corticothalamocortical loops
constitutes a neurologic emergency.
produces the widespread discharges.
→ Prolonged seizure activity leads to neuronal death from
• Tonic-Clonic (Grand Mal) • Absence (Petit Mal) excitotoxicity.
➢ Abrupt loss of consciousness ➢ Abrupt cessation of
CONFUSIONAL STATE
→ tonic body stiffening → activity,
symmetrical clonic jerking → unresponsiveness, but • is a state of decreased awareness of the environment that
urinary incontinence, tongue with minimal movement typically reflects deficits in attention.
biting, apnea ➢ Lasts for 5 to 30 secs; • It may be associated with perceptual disturbances (illusions or
➢ Lasts 1 to 2 minutes; slow quick return to normal hallucinations), increased or decreased psychomotor activity,
return of consciousness (10 alertness incoherent speech, and disturbances of the sleep-wake cycle.
to 30 min) • Commonly develops over a period of hours to days, tends to
fluctuate during the day, may be reversed if caused by a treatable
condition.
• Confusional state is a potentially reversible state of impaired
attention and awareness that may result from a metabolic, toxic,

Trans # 13 Telencephalon 12 of 17
 vascular, or inflammatory process diffusely affecting the cerebral
hemispheres. *
DEMENTIA (DELIRIUM)
FIGURE 8: Dementia
1. Dementia is an acquired condition involving a change in cognitive
function in an alert person, from a previous level of performance
to the point that social and occupational functions are impaired.
2. Most dementias are progressive and caused by degenerative
disorders of the cerebral cortex.
3. Although degenerative dementias reflect diffuse or bilateral
involvement of the cerebral cortex, the initial clinical features may
reflect specific involvement of specific cortical areas.
• Alzheimer disease
→ most common degenerative dementia
→ medial temporal lobe structures → impairment of
declarative memory, particularly the learning of new
information about recent events and facts → neocortical
association areas → agnosia and apraxia develop
FIGURE 8: Coronal T1-weighted magnetic resonance
image of the brain of a patient withAlzheimer disease.Note
the severe generalized atrophy, involving predominantly
the medial temporal and parietotemporal regions.
Trans # 13 Telencephalon
FIGURE 9: Axial T1-weighted magnetic resonance
image of the brain of a patient with frontotemporal
dementia. Note the severe atrophy of the frontal lobes,
with relative preservation of other cortical areas.
Other common types of degenerative dementia:
• Dementia with Lewy bodies
→ profound impairment of visuospatial function, fluctuations in
cognitive function, and visual hallucinations
● Frontotemporal dementia
→ the second most common dementia (<65 yo)
→ prefrontal cortex involvement → present with dysexecutive
syndrome, changes in personality and behavior, particularly
loss of personal and social awareness, blunting of affect,and
loss of insight.
→ Memory is relatively spared, in contrast to Alzheimer disease.
→ Primary progressive aphasia → left fronto-temporal
perisylvian region
→ Semantic dementia → lateral and anterior temporal cortex,
particularly on the left side.
→ Posterior cortical atrophy → visuospatial attention
impairment
• Chronic, focal, progressive disorders are most frequently the
result of a mass lesion (neoplasm), they may also be a
manifestation of a focal degenerative disorder.
• However, this degenerative process eventually affects other
areas of the cerebral cortex.
• Some dementias are potentially treatable, most commonly ones
due to inflammatory (immune or infectious) or toxic-metabolic
disorders.
MENTAL RETARDATION
• is a failure to develop normal intelligence and can result from
congenital or acquired disorders.
• Presence of cortical neurons with immature dendrites, reduced
dendritic arborization, fewer dendritic spines
• Chromosomal abnormalities:
a. Down syndrome - triplication of a gene on chromosome 21
encoding for the amyloid precursor protein
b. Fragile X syndromes- second most common genetically
determined form of mental retardation; due to a trinucleotide
repeat expansion in a gene on chromosome X encoding for a
ribonucleoprotein.
• Genetic biochemical defects:
a. Tay-Sachs disease - inherited autosomal recessive disorder
characterized by an excessive accumulation of the lipid
ganglioside in neurons of the central nervous system
- hexosaminidase A
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 b. Phenylketonuria - inherited autosomal recessive disorder in
which phenylalanine cannot be converted to tyrosine because of
an enzymatic defect.
- phenylalanine hydroxylase
• Exogenous causes: Trauma, Anoxia, Drugs, Toxins, Infections.
• Important examples are maternal exposure to alcohol during
pregnancy or congenital infections with cytomegalovirus or
human immunodeficiency virus.
B. FOCAL DISORDERS
FIGURE 10: Cerebral Hemispheres Disorders
• ETIOLOGY
→ Focal lesions may be:
a. nonprogressive (nonmass) ex. Infarct
b. progressive (mass lesions) ex. Hematoma, abscess, or
neoplasm
→ Vascular and neoplastic lesions - most common focal
lesions
→ The most common neoplasms are astrocytomas,
meningiomas, and metastases.
→ Mass lesions may be vascular (hematoma), inflammatory
(abscess), or neoplastic
→ An important example of a focal, progressive, inflammatory
lesion is herpes simplex encephalitis, which preferentially
affects the temporal lobes
→ Focal lesions produce focal disorders that differ in their clinical
effects depending on the location of the lesion.
→ These effects include excessive cortical activity (focal or
partial seizures), visual field defects, and deficits in motor,
sensory, cognitive, or behavioral functions.
FIGURE 12: Coronal T1-weighted magnetic resonance image showing areas of
acute hemorrhage (arrows) in both temporal lobes and left insular cortex. This Is
typical of herpes simplex encephalitis.
PARTIAL SEIZURES
• Seizures arising from a localized area of the cortex are called
partial seizures.
Trans # 13 Telencephalon
• Complex partial seizures are associated with an alteration of
awareness.
• Simple partial seizure - awareness is preserved
• The symptoms of partial seizures depend on the site of
discharge.
→ Precentral gyrus of the frontal lobe - clonic movements of
the contralateral side of the face or the contralateral
extremities
→ Postcentral gyrus - paresthesisas or dysesthesias
contralateral side of the face or contralateral extremities
→ Occipital lobe - impaired vision
• Seizures arising from the temporal lobes are the most common
partial seizures and may impair awareness, constituting
complex partial seizures.
TABLE 4: Features of Partial (Focal) Seizures
C. VISUAL FIELD DEFECTS
• defects have localizing value at the supratentorial level.
• Lesions of the optic tract, the lateral geniculate body, or optic
radiation on one side produce homonymous defects in the
opposite visual field.
• Complete destruction of the optic tract or optic radiation on one
side produces a complete homonymous hemianopia.
• Incongruous homonymous field defect happens because of
the divergent course of axons in the optic radiation.
• inferior quadrantic field defect- A lesion in the parietal
lobe destroys the superior optic radiations
• superior quadrantic field defect (“a pie in the sky”)- A lesion in
the temporal lobe on one side destroys the fibers in the lower
portion of the optic radiation.
• Lesions at the level of the calcarine fissure produce a
homonymous hemianopia in the contralateral visual field.
• Two features may help distinguish homonymous hemianopia due
to occipital lesions.
1. the defect tends to be similar in both halves of the affected
visual field (congruent).
2. because of the dual vascular supply of the pole of the occipital
lobe (by branches of the posterior and medial cerebral arteries),
the representation of the macula may be spared. This is called
macular sparing.
D. FRONTAL LOBE SYNDROMES
• The frontal lobe includes the primary motor cortex, premotor
area, supplementary motor area, medial motor area, frontal eye
fields, Broca area, lateral prefrontal cortex, and orbitofrontal
cortex.
• Lesions restricted to primary motor cortex impair the ability to
perform contralateral fine
• finger movements or produce paralysis or, in the case of lesions
in the paracentral lobule, leg weakness.
• Lesions involving the lateral premotor cortex and supplementary
motor area produce hyperreflexia and disinhibition of primitive
reflexes, including forced grasping.
14 of 17
• Acute, bilateral lesions of the anterior cingulate gyrus and - Simple visual hallucinations, such as flashing or
supplementary motor area produce akinetic mutism twinkling lights, lines, or angles, can be manifestations of
• Lesions of the frontal eye fields impair voluntary and visually occipital lobe seizures.
guided contralateral saccades. - typical with occipital lobe involvement in dementia
• Lesions of the motor speech (Broca) area may produce with Lewy bodies.
nonfluent aphasia or apraxia of speech. Seizures arising in this
region result in transient speech arrest.
• When the lesion affects the neighboring olfactory structures, the
sense of smell is lost (anosmia).
E. PARIETAL LOBE SYNDROMES
• The parietal lobe includes the primary somatosensory cortex in
the postcentral gyrus, the unimodal somatosensory association
area, and the multimodal cortex of the posterior parietal lobe.
• Lesions of primary somatosensory cortex produce
contralateral cortical sensory loss characterized by impaired
tactile discrimination, touch localization (topognosis), two-point
discrimination, weight discrimination (barognosis), recognition of
a number written on the hand (graphesthesia),and joint position
sense.
• Patients with seizures in primary somatosensory cortex present
with transient symptoms of numbness or tingling sensation
of the contralateral face or body
• Lesions of the left inferior parietal lobule may produce a
combination of deficits that includes agraphia, acalculia, finger
agnosia, and right-left disorientation (Gerstmann syndrome)
as well as ideomotor apraxia.
• Lesions of the dorsal(superior) portion of the optic radiation at
TABLE 5. Focal Lobular Syndrome
the level of the parietal lobe produces a contralateral inferior
quadrantanopia.
XIII. SUBCORTICAL LESIONS
F. TEMPORAL LOBE SYNDROME
• The subcortical white matter and the basal ganglia may be
• The temporal lobe includes primary auditory cortex (Heschl affected by focal or diffuse lesions of the cerebral hemispheres.
gyrus), unimodal auditory and visual association cortices,
• These lesions interrupt one or several of the cortical- basal
paralimbic cortex, and limbic cortex.
ganglia-thalamocortical circuits.
• Damage of Wernicke area in the posterior part of the superior
temporal gyrus in the dominant hemisphere produces fluent A. SUBCORTICAL WHITE MATTER
aphasia characterized by a comprehension deficit for all
modalities. • The subcortical white matter is commonly affected in vascular,
demyelinating, and some toxic-metabolic conditions.
• Bilateral lesions of this area produce pure word deafness;
patients react to environmental noise (i.e., they are not deaf) and • Important examples include small-vessel disease due to
recognize written language but cannot understand or repeat hypertension or amyloid angiopathy, demyelinating disease such
spoken language. as multiple sclerosis, progressive multifocal
• Focal lesions of the temporal lobe are frequently associated with leukoencephalopathy (a viral disease caused by the JC virus in
immunosuppressed patients) and HIV related dementia,
contralateral superior quadrantanopia, from the interruption of
radiation-induced leukoencephalopathy, and hereditary
the ventral (inferior) component of the optic radiation.
metabolic disorders (leukodystrophies).
• Complex partial seizures arising in the medial temporal lobe are
• Important manifestations of these disorders include
the most common form of partial seizures.
disturbances of gait and bladder function, spasticity,
• The most common cause is mesial temporal sclerosis.
• dementia, and visual impairment.
G. OCCIPITAL LOBE SUNDROME • Lesions of the subcortical white matter of the frontal lobe may
• The occipital lobe includes the primary visual area in the banks severely impair the automatic control of axial muscles, gait
of the calcarine fissure on the medial surface of the occipital lobe initiation, and automatic gait.
(area 17) and visual association areas 18 and 19 (peristriate • Interruption of the inhibitory cortical input to the pontine
cortex). micturition center produces an uninhibited bladder, characterized
• A lesion of visual cortex of one occipital lobe produces by urinary urgency and incontinence.
homonymous loss of vision in the contralateral visual field.
Bilateral lesions of the occipital lobes produces cortical
blindness.
• Patients may retain some perception of movement despite the
inability to perceive the object. This phenomenon, called
blindsight, is mediated by the visual pathway from the superior
colliculus to the pulvinar to the posterior parietal cortex.
• Disorders of occipital cortex can also be associated with
subjective transient anomalies of vision such as scintillating
scotomata, visual hallucinations, and illusions.
a. scintillating scotomata FIGURE 13: Axial fluid-attenuated inversion recovery (FLAIR) images of the brain
- Sensations of flashing lights in the field of vision showing severe subcortical white matter involvement by small-vessel disease.
b. visual illusion
- Distorted perceptions of external visual stimuli. B. BASAL GANGLIA
c. visual hallucinations
- Perceptions of visual images for which there is no • Clinical manifestations:
external stimulus.
Trans # 13 Telencephalon 15 of 17
 → motor, oculomotor, cognitive, and behavioral changes in
various combinations, depending on the main location of the
lesion.
• main motor dysfunctions associated with basal ganglia circuit
disorders are parkinsonism and several hyperkinetic syndromes,
including chorea, hemiballismus, and dystonia
• Parkinsonism
→ Parkinson’s disease results from the loss of dopaminergic
neurons in the substantia nigra pars compacta that synapse
in the striatum
→ characterized by hypokinesia, bradykinesia, tremor at rest,
and postural instability
• Hyperkinetic disorders
→ Huntington disease
- characterized by chorea resulting from atrophy of the
caudate nucleus and, to a lesser extent, the putamen
• Wilson disease
→ parkinsonism and dystonia in combination with
abnormalities of cognition and behavior
• Creutzfeldt-Jakob disease.
→ An important cause of rapidly progressive dementia
associated with both cortical and basal ganglia dysfunction (as
well as ataxia)
XIV. EVALUATION OF CORTICAL DISORDERS
• Bedside Mental Status Examination
→ an essential component of the neurologic examination.
• Important considerations while taking the history include:
→ level of education
→ whether the patient is right- or left-handed.
→ Level of alertness
→ Attention and language
A. LEVEL OF CONSCIOUSNESS
● evaluated by testing the patient’s arousal and awareness of (or
response to) the external environment.
→ Arousal is tested by assessing the intensity of responses
to verbal, visual, tactile, and painful stimuli.
B. ORIENTATION
• The patient is asked to give the his or her full name and address,
current location (building, city, and state), and the date (day of
the week, month, and year).
C. ATTENTION
• The overall ability of the patient to attend to environmental stimuli
can be tested by assessing attention span, which is a reflection
of working memory function.
• This can be tested by forward and backward digit spans. The
examiner reads to the patient a list of random digits at 1-second
intervals, usually starting with a span of 4 digits and then
increasing the number of digits. The patient is asked to reproduce
exactly the span forward and backward.
• Normally, patients can repeat up to 7 digits forward and 5 digits
backward.
• Other measures of attention include resistance to perseverance
(eg, recitation of the months of the year or days of the week
forward and backward).
• Directed attention also tests the function of the parietal lobe. It
is tested, for example, by double simultaneous stimulation of
tactile, visual, or auditory sensation.
D. LANGUAGE
• The 4 modalities of central language processing:
→ Listening
→ Speaking
→ Reading
→ Writing
• Examination of language should assess fluency, comprehension,
naming, and repetition.
• Fluency
Trans # 13 Telencephalon
→ the rate of production and accuracy of words.
→ assessed by asking the patient to give common nouns that
start with the letter A, F, or S, or to name, in a span of 60
seconds, all animals, vegetables, or fruits the patient can think
of. The patient is asked to look at a picture, describe it orally,
and write a few sentences about it. This will disclose word-
finding difficulties, production of an incorrect word instead of a
target word (paraphasia), prosody, and articulation.
• Auditory comprehension is assessed by asking the patient to
perform a series of maneuvers of increased complexity (eg,
“Open your mouth,” or “First look at the ceiling and then point to
the floor”).
• Naming is assessed by asking patients to identify common
pictures.
• Repetition is assessed by asking the patient to repeat sentences
(eg, “No if’s, and’s, or but’s”).
• Reading should be evaluated by having the patient read a
paragraph silently and explain the content of the paragraph or, if
speech is significantly impaired, point to words and sentences on
the printed page spoken by the examiner.
• Writing can be tested by having the patient write something from
dictation or copy a written message. Reading and writing are
impaired in aphasia. However, impairment of reading (alexia) or
writing (agraphia), or both, also may occur without aphasia.
E. MEMORY
→ acquisition (learning)
→ retention (recall after a delayed interval
→ retrieval
• The patient is instructed to learn, retain, and recall 4 unrelated
words, such as apple, Mr. Johnson, charity, and tunnel
• After the patient is given the 4 words, the patient is asked to
repeat them immediately (to assess learning) and to repeat them
after approximately 5 minutes (to assess retention)
• If the patient cannot recall the words, the examiner may provide
cues or prompts, and if this fails, the patient is asked to select a
word from a list (recognition test).
• Similar tests are used for nonverbal material (eg, pictures).
F. CALCULATION
• Calculation can be assessed by asking the patient to multiply
5 times 13, subtract 7 from 65, divide 58 by 2, and add 11 to
29. More complex arithmetic problems can be used.
G. CONSTRUCTION
• Constructional tasks depend on perceptual abilities and
skilled motor functions.
• The patient is asked to draw the face of a clock showing
11:10 and to copy a 3- dimensional cube.
H. ABSTRACT REASONING
• These tasks depend on complex higher cortical functions
integrated at the level of the prefrontal cortex.
• The patient is required to draw on acquired knowledge and
to apply it to a task in an unfamiliar fashion.
• This function can be assessed by interpreting similarities in
word pairs, such as orange and banana, horse and dog, and
table and bookcase.
• Other tasks involve the interpretation of proverbs, such as
“People who live in glass houses should not throw stones.”
I. INFORMATION
• General knowledge of the world, including the name and use of
objects and facts, constitutes semantic memory.
• The general fund of information should be tested in the context
of the patient’s intellectual level, cultural background, and
geographic origin.
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• To assess this function, the patient can be asked to state the
name of the current president of the United States, the name of
the first president of the United States, the number of weeks in a
year, and the definition of island.
J. CORTICAL SENSORY PROCESSING
• Disorders of high-level sensory processing include the inability to
recognize an object (ie, agnosia: patient cannot name the object
or describe its use.).
• Tests of somatosensory processing include asking the patient to
recognize objects placed on the hand and to recognize a part of
the body.
• In astereognosis, patients are not able to identify objects by
touch despite being able to describe its shape.
• Finger agnosia can be assessed by telling the patient, “Show
me your thumb,” or “Touch your left ear with your right thumb.”
• To test visual processing, the patient can be asked to identify
and name pictures or objects. If the patient cannot name the
object, recognition can be tested by asking the patient to
demonstrate the use of the object.
• Auditory processing is assessed by asking the patient to
identify a particular sound.
→ used to detect abnormalities of cerebral function and to
indicate whether the disturbance is focal or generalized.
→ particularly helpful in evaluating patients with seizures,
altered states of consciousness, and focal cortical lesions
4. Other Testing
→ All patients with cortical dysfunction should be tested for
metabolic disorders, particularly vitamin B12 deficiency.
→ Patients with rapidly progressive dementia or
encephalopathy should also be tested for autoantibodies
against nervous system antigens.
→ Cerebrospinal fluid examination is indicated to
investigate suspected infectious or autoimmune causes,
to assess neuronal damage in prion disorders (14-3-3
protein), or, in selected cases, to evaluate biomarkers for
Alzheimer disease (Aβ42 to phosphorylated tau ratio).
V. REFERENCES
• Reporter’s Presentation
• Mayo Clinic Medical Neuroscience

K. CORTICAL MOTOR FUNCTION

• The ability to perform learned skilled motor acts is called praxis,
and it can be assessed by asking the patient to perform various
tasks on command.
• This includes demonstrating a gesture (such as a kiss; a salute;
use of a toothbrush, hammer, and nail; or combing the hair).
• If the patient is unable to perform these tasks, the examiner
demonstrates the task and asks the patient to imitate the motion.
• If the patient is still unable to do so, an actual object such as a
comb or key may be given to the patient. The patient may be
asked to perform a sequential task, such as hang a picture on a
wall or find a number in the telephone book and make a
telephone call.

L. OLFACTION
• Testing for olfaction may be useful in cases of traumatic brain
injury, orbitofrontal dysfunction, or suspected Parkinson disease.
• Olfaction is tested by having the patient sniff a substance that
has an identifiable odor (eg, camphor, coffee, or wintergreen)
with each nostril separately, while the other nostril is occluded.
• Intranasal disease is a common cause of impaired olfactory
sensation and must be excluded before making the diagnosis of
neurogenic anosmia.
M. LABORATORY ASSESSMENT OF CORTICAL FUNCTION
1. Neuropsychological Assessment
→ involves the administration of a standardized battery of
tests of learning, memory, attention, language,
visuospatial skills, and executive or reasoning functions.
2. Imaging Studies
→ fundamental importance to evaluate cortical disorders, as
shown in several examples throughout this chapter.
→ MRI
- allows detecting focal lesions, cortical atrophy, white
matter changes, hydrocephalus, iron accumulation related
to microhemorrhages, hydrocephalus, and other structural
lesions.
- assess the resting state activity of cortical networks and
mapping to detect tau deposition in the brain are being
developed in experimental settings
→ 18Ffludeoxyglucose positron emission tomography
(PET)
- assess focal metabolic activity in the cortex and allow
detection of neurodegenerative disorders even in the
absence of abnormalities in structural imaging.
→ Amyloid imaging with PET- helpful to detect early Alzheimer
disease pathology.
3. Electroencephalogram

Trans # 13 Telencephalon 17 of 17