Seminar on Cerebral Neurolocalization.pptx

1. Neuroanatomy and
Neurolocalization of Cerebrum
Blen M.( NR-2)
Moderator Dr. Amanuel
Jan,2021

2. Content
Micro and Macro Anatomy of cerebral hemispheres
Cerebral white matter
Neuronal networks
Vascular neuroanatomy
Neurolocalization and Hemispheric specialization

3. Introduction
Clinical diagnosis in neurology requires recognition of impaired function,
the site of the nervous system affected and what the lesion is.
The pattern of structures is relatively constant from person to person
which makes localization possible
Lesion localization in the cerebral hemispheres relies on the understanding
of the function of different portions of the cerebral cortex.

4. The Cerebral Hemisphere
The paired cerebral hemispheres derive from the telencephalon
Contains approximately 20 billion neurons spread over an area of 2.5 m2
The cortex is thrown in to folds called gyri and in between are the sulci
Its thickness varies from 4.5 mm in the precentral gyrus to 1.3 mm near
the occipital pole

5. Why do women multitask better than men?
The corpus callosum is larger in women than in men and contains
more neural pathways
This is thought to make women superior in processing language,
information, emotion and cognition
The inferior-parietal lobe is larger in men and it control characteristics
that make a person more prone to mechanical and analytical thought

6. Microscopic Anatomy
Cortical Layers
1. The molecular layer: Outermost layer,
contains neuroglial cells, nerve fibers
and dendrites
2. Outer granular layer: contains small
pyramidal cells
3. Outer Pyramidal layer: contains
medium sized pyramidal cells
4. Inner granular layer: contains stellate
cells and nerve fibers.
5. Inner pyramidal (ganglionic) layer:
contains gaint pyramidal cells (Betz
cells), origin of pyramidal tract.
6. Multiform (multimorph) layer: contains
nerve fibers, neuralgia cells

8. Neocortex (new cortex) - 6 layers
a. Ideotypic cortex - 1° motor and sensory cortex
b. Homotypic cortex - association areas
Mesocortex (middle cortex) - 3-6 layers - related to limbic system
a. Cingulate gyrus
b. Para hippocampal gyrus
Allocortex (other cortex) - 3 layers
a. Archicortex - hippocampal formation
b. Paleocortex – olfactory area

9. The Gross Anatomy of the Cerebral
Hemispheres
The two hemispheres are Separated by a
longitudinal cerebral fissure
Superolateral surface are separated by two large
sulci
• Sylvian fissure
• Rolandic or central sulcus
Two imaginary lines
• From upper end of parieto-occipital sulcus to
parieto-occipital notch
• Backward continuation of the lateral sulcus
to meet the first imaginary line

10. Covered by thin grey matter (2-4mm)
Three poles
• Frontal pole anteriorly
• Occipital pole posteriorly
• Temporal pole
Surfaces
• Superolateral surface
• Medial surface
• Inferior surface

11. The four lobes are
Frontal lobe
Parietal lobe
Temporal lobe
Occipital lobe
Other, sometimes designated as a lobe
because their parts are interconnected
functionally
• Insula
• Limbic lobe

12. Broadmann’s Map
These areas were defined and
numbered by korbinian broadmann
 Based on the cortical
cytoarchitectonic organisation of
neurons
Many of the broadmann’s areas
are defined on neurological
function correlated closely to
diverse cortical functions

13. Frontal lobe
The largest of the 4 major paired
lobes of the brain, 38% of human
brain
Lateral view; central sulcus and
Sylvain fissure separates it from
adjacent lobes
Medial view; Cingulate sulcus-
separates the cingulate gyrus from
the first frontal and paracentral
gyri
Inferior view Orbital surface of the
prefrontal area

14. Frontal Lobe

15. It is divided in to 3 functional areas
• The primary motor area (area-4)
• The premotor area (areas 6, 8, 44, & 45)
• The prefrontal cortex (areas 9-12)

16. Prefrontal cortex (BA 9-12,32,45-47)
Frontal lobe anterior to premotor area
Connections: With the Hypothalamus, thalamus, limbic system, motor
areas, the temporal and occipital lobes
Has three clinically important divisions
• DLPFC(dorsolateral prefrontal cortex)
• MPC(medial prefrontal cortex)
• OFC(orbitofrontal cortex)

17. Functions
DLPFC
Organization of tasks ,execution, problem solving, personality, affect and decision
making
MPC
Important in auditory and visual associations
OFC
Connection with the limbic system, Including the amygdala
Frontal eye field control movement of the eyes to the contralateral side
Motor speech areas(Broca’s)(BA 44,45)

18. Lesions
Stimulation
• Psedoseizure like pedaling and thrusting
• Aversive seizure
Frontal eye field
• Destructive lesions cause gaze deviation ipsilaterally
• Epileptiform activity cause gaze deviation to the contralateral side
Broca’s Aphasia
Unilateral- imitation and utilization behavior

19. Frontal motor areas
1. Primary motor cortex(BA 4)
Contains large motor neurons (Betz cells)
giving tracts to
• Corticospinal
• Corticobulbar
Motor Homunculus
• Crossed and inverted representation of
the body according to the motor value

20. Function
Initiation of voluntary, fine, discrete (separate) mov´t of limbs. (eg. Hands,
fingers) on opposite side
Facilitation of stretch reflex i.e Facilitation of skeletal muscle tone and
tendon jerk
Lesions
Irritative; focal seizure
Destructive ; contralateral Flaccid paralysis
Loss of deep and cutaneous reflexes in the opposite side

21. 2. Pre motor
Receives afferents from other areas of the cortex and projects to the motor
cortex and the motor thalamus
Involved in the planning and execution of movements, particularly sequences
of movements
Some fibers descend and make up part of the extrapyramidal system
3. The SMA (Supplementary motor cortex)
consists of areas of cortex lying on the medial aspect of the hemisphere
Involved coordinating sequence of actions provided from memory

22. Lesions
Stimulation
• Tonic posturing with or without automatism
Destructive
• Increase in muscle tone & muscle spasticity than weakness
• Exaggerated tendon jerk
• Reappearance of primitive reflex
• Motor aphasia and apraxia
• Agraphia: failure of writing & drawing skills due to lesion to exner´s
center

23. Q1. Why do patients with UMNLs tend to have muscle spasticity and
increased tone?
The EPF transmit inhibitory impulses that lower muscle tone
Destruction of the secondary motor area removes the inhibitory influence,
and consequently, the muscles become spastic
Q2. What kind of plantar response do we expect with lesions in the primary
motor area
 A positive Babinski´s sign in the opposite side with only dorsiflexion of big
toe due to lesion of pyramidal fibers ( no fanning occurs in other fingers
b/c extra pyramidal tracts are intact)

24. Bilateral Frontal lobe lesions
Akinetic mutism
Gait apraxia
Incontinence
Perseveration
Lack of judgement and foresight
Aspontaneity and lability

25. Parietal lobe
The parietal lobe lies posterior to the central sulcus, anterior to the occipital lobe and
superior to the temporal lobe.
Five principal parts:
• The postcentral gyrus
• The posterior portion of the paracentral lobule
• The superior parietal lobule
• The inferior parietal lobule
• The precuneus

26. 1. The primary somatosensory cortex(S1) (BA 3, 1, 2)
 Lies between the central sulcus and the postcentral sulcus
 Granular cortex densely packed with stellate cells
 Sensations derived from skin are appreciated in anterior part of the area and
proprioceptive sensations in posterior part of the area
 If lesions occur without involving thalamus, sensations are perceived but
discriminative functions are lost
 If thalamus also affected, loss of sensations in opposite side of body

29. 2. Secondary sensory area/ SII
Situated in post central gyrus
Receives sensory impulses from primary sensory area and thalamus
Neurons in anterior part respond to touch whereas neurons in
posterior part can be excited by touch, auditory, visual and nociceptive
stimuli
3. Sensory association areas (BA 5,7,40)
• Neurons which react to passive or active rotation of a joint or joints
• Higher association area, concerned with stereognosis

30. 4. The Precuneus
• Is an area of the cortex just anterior to the occipital lobe on the medial
hemispheric surface
• Involved in visuospatial imagery, episodic memory retrieval

31. Lesions
Unilateral lesion( Either
Hemisphere)
• Loss of Cortical Sensations
• Loss fine touch more than pain
Hypotonia, muscle atrophy, and
pseudoataxia
• Lower quadrantanopia
Bilateral lesion:
• Severe Constructional Apraxia
• Optic Ataxia

32. Non-Dominant [Right]
• Unilateral anosognosia
• Amorphosynthesis: hemi-neglect,
dressing apraxia
• Visual inattention
Dominant [Left]
• Bilateral Asomatognosia
• Bilateral Astereognosis
• Tactile Agnosia
• Bilateral Ideational Apraxia
• Alexia with agraphia

33. Case-1
A 78 years old female presents with an acute onset of confusion, lately she
had a difficulty of doing her bill's with simple mathematical calculation, she
had a difficulty of reading a written language . She went to doctor and On
examination there is impaired right left orientation, arithmetic abilities and
finger identification
MRI shows severe foci of cortical and subcortical increased T2 signals the
most probable diagnosis is??

34. Gerstmann’s syndrome
Combination of the tetrads of
• Acalculia,
• Dysgraphia,
• Finger anomia and
• Right-left disorientation
Left Inferior parietal lobe damage

35. Temporal lobe
Situated inferior to the lateral fissure and anterior to the parieto-occipital sulcus
Contains three gyri, separated by two sulcus
• Superior gyrus - auditory and language functions
• Middle and inferior gyri -integration of vision
Hippocampal formation
• Learning and memory
Amygdala; emotions(fear, anger…)

36. 1. Primary auditory cortex (areas 41 and 42)
The transverse temporal gyri (of Heschl)
Buried in the Sylvain fissure at the posterior end of the superior
temporal gyrus on its dorsal surface
Hearing is bilaterally represented but there is contralateral dominance
2. The auditory association cortex(Area 22)
Found immediately adjacent to the primary auditory cortex
Differentiate and interpret sounds
3. Wernicke’s speech Area (Area 22)
Posterior superior temporal area, in the dominant hemisphere

37. Lesions
Stimulation
• Auditory hallucination, vertigo, unsteadiness and disequilibrium
• Temporal lobe epilepsy
Destructive lesions
• Wernicke's aphasia
• Geniculocalcarine pathway lesions- contralateral visual field defect
Bilateral lesions
• Partial Kluver Bucy syndrome

38. Occipital lobe
A small part of the dorsolateral surface of the
hemisphere
It rests on the tentorium cerebelli
It is separated on medial surface from parietal
lobes by parieto-occipital fissure
The lateral occipital sulcus, divides the lobe
into superior and inferior occipital gyrus
The calcarine fissure separates the medial
surface into the cuneus above and the lingual
gyrus below

39. 1. Primary visual cortex(BA 17)
At the lip of the calcarine
Receives primary visual impressions as Color, size, form, motion and illumination
Receives fibers from the temporal half of the ipsilateral retina and the nasal half of the
contralateral retina
Lesions
• Stimulation- visual hallucination, scotoma and flash of lights
• Destructives- visual field defect, usually macular sparing hemianopia
• Bilateral lesions- Cortical blindness
Bilateral hemianopia, scotoma
Anton's hallucination syndrome

40. 2. Visual Association Area – (Area18 & 19)
Recognition and identification of objects and store visual memories
Area 18- receive stimulus from the primary visual cortex
Area 19- connects with the entire cortex
Lesions- Contralateral disconnection syndrome, visual inattention
Unable to localize himself or objects in space
3. Fusiform and lingual gyri
Color vision and face recognition
Lesions- Prosopagnosia

41. The Limbic lobe
Sometimes considered a separate lobe of the brain, because of its function
than its anatomy
A ring of cortex on the medial aspect
of each cerebral hemisphere and includes
• The cingulate gyrus
• The Para hippocampal gyrus
• The hippocampus:
• The mammillary bodies (part of the hypothalamus);
• The anterior nucleus of the thalamus;

42. Functions
• This system participates in the control of autonomic function, arousal,
motivated behavior, emotion, learning, and homeostasis
Lesions
• A disturbance in this function is known as an amnestic state. And it can be
Anterograde, retrograde or global.

43. Primary Cortical Fields

44. Cerebral White Matter
• A central core of white matter that forms the bulk of the cerebrum
and represents fiber tracts
• Supported by Neuroglia, carrying information destined for the cortex
and Cortical responses to other regions of the CNS
• There are three types of fibers based on their orientation

45. Association fibers
• Connect one area of cerebral cortex with another area in the same
hemisphere
Commissural fibers,
• Connect areas of the cerebral cortex in opposite hemispheres
• Main ones are Corpus callosum, anterior commissure and the hippocampal
commissure
Projection fibers
• Project to deep structures, like the thalamus

47. Q. What is their clinical importance?
Characteristics of white matter lesions are
• Weakness
• Spasticity
• Visual field deficits
• “Pure” motor syndromes
• Urinary incontinence
Lesions cause symptoms that are referable to the cortical region giving rise
to the white matter tract involved

48. Neural networks
Five anatomically defined large-scale networks are most relevant to clinical
practice:
1. Perisylvian network for language,
2. Parietofrontal network for spatial orientation,
3. Occipitotemporal network for face and object recognition,
4. Limbic network for retentive memory, and
5. Prefrontal network for the executive control of cognition and comportment.

49. 1. The perisylvian network for language

50. Aphasia
• Aphasia is a defect in language
processing caused by damage to
any one of the neural network
component
• In ~ 90-95% of right-handers and
60-70% of left-handers, aphasia
occurs only after lesions of the left
hemisphere.

52. 1. Wernicke’s Aphasia
Markedly impaired comprehension, Impaired naming and repetition
Normal fluency, prosody, and grammatical structure.
Writing and Reading: similarly affected
Prognosis for recovery of language function is guarded
2. Broca’s Aphasia
 Intact comprehension
 Decreased fluency, Impaired repetition
 Marked naming difficulties

53. 3. Conduction Aphasias
 Normal fluency and normal comprehension, but impaired repetition
 Interruption at the arcuate fasciculus or other pathways in the vicinity of the
supramarginal gyrus that connect Wernicke’s area to Broca’s area
4. Transcortical Aphasias
Resemble Broca’s, Wernicke’s, and global aphasias, except that repetition is
spared
Classic cause: watershed infarcts
Three types; Motor (non fluent) type, Sensory (fluent) aphasia and mixed

54. 6. Global Aphasia
• The combined dysfunction of Broca’s and Wernicke’s areas
• All modalities of speech are impaired
• from strokes that involve the entire MCA distribution in the left hemisphere
6. Subcortical Aphasia
• Subcortical components of the language network including Thalamus and
Basal ganglia
• Combinations of deficits but rarely fit the specific patterns

56. Do we expect Aphasia in right hemispheric lesion???
First, right-handed patients occasionally become aphasic after right
hemisphere strokes, a phenomenon called crossed aphasia.
Second left-handed patients may have right hemisphere language dominance
Third, even right-handed persons with typical left hemisphere dominance for
language have subtly altered language function after right hemisphere
damage

57. Role of the nondominant hemisphere in language?
• Important in both the recognition and the production of the affective
elements of speech.
• Lesions: difficulty judging the intended expression imparted by a particular
tone of voice, or they may have difficulty producing emotionally
appropriate expression in their own voice.
• In lesions of the dominant hemisphere, callosal connections may allow the
nondominant hemisphere to take over some functions of the damaged
areas and to participate in at least partial recovery

58. 2. The prefrontal network for Attention &
Behavior
Prefrontal network:
• Prefrontal Cortex (motor-premotor, dorsolateral , medial , and
orbitofrontal components)
• Subcortical Structures (the head of the caudate and the dorsomedial
nucleus of the thalamus).
Important role: integration of thought with emotion & motivation.

59. Lesions
 Frontal Abulic Syndrome (DLPFC); loss of initiative, curiosity, creativity,
emotional blandness, apathy and lack of empathy.
 Frontal Disinhibition Syndrome (medial/orbitofrontal): severe
impairments of judgment, insight, foresight, and the ability to mind
rules of conduct.
 Fontal release signs (grasping, sucking)
These syndromes tend to arise almost exclusively after bilateral lesions.

60. Phineas Gage (1823–1860)
Railroad construction man,
Sustained metal injury with
accidental frontal lobectomy.
He became unreliable, with
temperament changes
hypesexuality, poor social
interaction but with preserved
intellectual function

61. 3. The Parietofrontal Network For Spatial
Orientation
Network for directed attention to extra personal
space includes:
• Cortical components
The posterior parietal lobe
Frontal eye fields
Cingulate gyrus and their connections
• Subcortical components : striatum and thalamus
Lesions
• Hemispatial neglect,
• Simultanagnosia and object finding failures.

62. Q. Why does right hemispheric lesions cause Hemineglect??
The right hemisphere directs attention within the entire extra personal
space, whereas the left hemisphere directs attention mostly within the
contralateral right hemi space

64. Case -2
A 68 years old male who had a difficulty of finding where the door is and
where the wall ends, after he wakes up from sleep. He first thought he did
not have a good night sleep he stretch out to find his telephone but couldn’t
find it out, one of his family members point it out and it was right next to
him where he left it the eye doctor told him that his vision is quite normal
despite the fact he hardly find the way out form the doctors office what is
happening to the patient ??

65. Balint’s Syndrome
Bilateral involvement of the network for spatial attention, especially its
parietal components
Components of Balint’s syndrome are:-
1. Oculomotor apraxia
2. Optic ataxia, and
3. Simultanagnosia
Etiology: CVA, hypoglycemia, sagital sinus thrombosis, Alzheimer’s disease

66. Case 3
A 65 year old male patient come to you with complaint of sudden failure to
recognize his Son by looking at his face whom he recognized later as he
conversed to him. His Ophthalmologist confirmed that he doesn’t have eye
problems. He still complains that he recognizes his son only hearing his
voice and looking his clothing.

67. 4. Occipitotemporal network
Prosopagnosia
patients are unable to recognize people by looking at their faces
The usual lesion location is the bilateral inferior occipitotemporal cortex,
also known as the fusiform gyrus
Achromatopsia
 A central disorder of color perception.
Others- Micropsia, Macropsia, Metamorphopsia, Visual reorientation:

68. 5. The Limbic Network for Memory
Includes
• Limbic and paralimbic areas
• The anterior and medial nuclei of the thalamus,
• The medial and basal parts of the striatum, and
• The hypothalamus
Function
• Memory
• Immediate (working, Short-term (recent) and Long-
term (remote) memory
Disturbance
• Amenesia
• Could be ;Retrograde amnesia, Anterograde amnesia
or Confabulation

69. VASCULAR NEUROANATOMY

70. The arterial supply is derived from the anterior circulation provided by
the bilaterally paired internal carotid arteries, as well as by the posterior
circulation provided by the bilateral vertebral arteries
These anterior and posterior circulations meet in an anastomotic ring
called the circle of Willis, from which all major cerebral vessels arise
The main arteries supplying the cerebral hemispheres are the anterior,
middle, and posterior cerebral arteries.

72. ACA
Supply – frontal to anterior
parietal lobe area
Lesions
• Contralateral weakness leg more
than the arm or face with cortical
sensory loss
• transcortical motor aphasia
• contralateral neglect
• grasp reflex, impaired judgment,
flat affect, apraxia, abulia, and
incontinence
• “alien hand syndrome”

73. MCA
Supply the dorsolateral cortex
Lesions are more common than ACA
or PCA areas
• Contralateral weakness arm and face
more than leg with cortical sensory loss
and gaze preference toward the side of
the lesion
• global aphasia, contralateral homonymous
hemianopia
• hemineglect, apraxia and anosognosia

74. PCA
Supply inferior and medial temporal
occipital lobe
Infraction typically cause a
contralateral homonymous
hemianopia
Also cause visual field defects, color
anomia and paresthesia without any
motor findings
Alexia without agraphia

75. Superficial and Deep Blood Supply to the
Cerebral Hemispheres

76. Watershed zones
Regions between cerebral arteries in both the ACA–MCA and MCA–PCA
zones
A sudden occlusion of an internal carotid artery or a drop in blood pressure
in a patient with carotid stenosis can cause an ACA–MCA watershed infarct
Infarcts can produce proximal arm and leg weakness (“man in the barrel”
syndrome), transcortical aphasia syndromes
MCA–PCA watershed infarcts can cause disturbances of higher-order visual
processing

77. VASCULAR NEUROANATOMY
VEINS
• The superficial veins drain
mainly into the superior sagittal
sinus and the cavernous sinus,
while the deep veins drain into
the great vein of Galen then
reaches the internal jugular
veins.
• Sagittal sinus thrombus and
other venous thrombus are the
common conditions

78. Principles of Cerebral Localization and
Lateralization
Q. How are cortical lesions different from sub-hemispheric lesions?
Neuroplasticity and redundant pathway
Extensive neural networks
• The result is:
 Less pronounced deficits with lesions caused a major motor or
sensory disturbance if occurs in the subcortical structures
 Single lesions may be clinically silent and become symptomatic when
additional lesions impair the function of the network

79. Cortical vs. subcortical lesions can sometimes be differentiated clinically
based on the absence or presence of so called cortical signs
These include
• Aphasia
• Neglect
• Seizures
• Homonymous visual field defects and
• Cortical sensory loss
However, each of these deficits can be seen in some cases of subcortical
lesions as well

80. Case -4
A 23-year-old woman with a 4-year history of epileptic attacks visited
her neurologist. Her families described one of her attacks. For a few seconds
before the convulsions began, the patient would complain of an unpleasant
odor, similar to that encountered in a cow shed. This was followed by a shrill
cry as she fell to the floor unconscious. Her whole body immediately became
involved in generalized tonic and clonic movements.

81. Anatomic location General characteristics of seizures
Frontal lobe
Usually occur several times per day, short in duration, during sleep.
Complex gestural automatisms is common at onset. Tonic/postural manifestation is prominent.
Occipital lobe
Usually simple partial and secondarily generalized seizures.
include visual symptoms that are contralateral to cortex:
Positive visual manifestations include sparks, flashes, and Negative visual manifestations include scotoma,
hemianopsia, and amaurosis.
Parietal lobe
Most are simple partial but can secondarily generalize.
In the dominant parietal lobe, language is often involved.
Sensory features: Positive symptoms include tingling and electric feeling.
Negative symptoms include numbness, absent body part, and asomatognosia.
Temporal lobe
Simple partial seizures: autonomic/psychic symptoms and sensory phenomena: olfactory, auditory, and
(most commonly) rising epigastric sensation. Complex partial seizures: alteration in consciousness with
behavioral arrest, often followed by oroalimentary or hand automatisms.
Postictal confusion is usually followed by amnesia of the event.
Clues to anatomic location of a seizure

82. Hemispheric Specialization
Many basic sensory and motor functions in the brain are distributed
symmetrically
For unknown reasons, however, there are marked asymmetries in
several brain functions
Cerebral dominance is related to handedness and anatomic
differences between the hemispheres

83. Handedness
• The most obvious asymmetry in cerebral function is handedness.
• Approximately 90% of the population is right-handed
• Lesions of the dominant hemisphere therefore are more commonly
associated with apraxia, a disorder of formulating skilled movements
Language
• Another well-known example of hemispheric specialization.
• The left hemisphere is dominant for language in over 95% of right-
handers, and in over 60 to 70% of left-handers

86. Anteroposterior Organization
In addition to left versus right, brain functions are also organized along the
anterior to posterior axis
More posterior regions are sensory and more anterior regions are motor
• The posterior parietal and temporal association cortex are more
involved in interpreting perceptual data and assigning meaning to
sensory information
• The anterior frontal association cortex is more important for planning,
control, and execution of actions

87. References
Dejong’s the neurologic examination, 8th
edition
W. Brazis, Localization in clinical neurology, 6th
edition
Snells clinical neuroanatomy,7th
edition
Grays the anatomic basis of clinical practice, 39th
edition
Blumenfeld Neuroanatomy through clinical cases, 2nd
edition

88. Thank you!