2. Caveats
• What you need to know about anatomy
– Changes with each individual case
– Involves both local and global knowledge
– Depends on your practice and referral question
• What I can give you in 90 minutes
– Conceptual understanding of organization
– Tools to think about deeper levels of analysis
– Ways of decomposing deficits
3. Key Concepts
• Functional Systems: patterns of
connectivity
• Localized damage has systemic effects
• Segregated patterns of inputs and
outputs
• Excitatory and inhibitory control
• Parallel vs. serial processing
7. • The layer of gray matter covering
the entire surface of cerebral hemisphere
• Migration of neurons from inner mantle layer of
• neural tube
• Accommodates enormous number of neurons
- Large surface area accommodates
more neurons than deep nuclei
- Gyri and sulci also increase surface area
- Laminar organization also accommodates
enormous number of neurons
Cerebral Cortex
Won Taek Lee, M.D., Ph.D.
8. Numerical Data
Total surface area: 2200 cm2 (2.5 ft2)
about 1/3 ------ surface area
about 2/3 ------ hidden in the sulci
Thickness: 1.5 mm (V I) - 4.5 mm (M I)
Generally, thickest over the crest of the
convolution and, thinnest in the depth of sulci
Weight: 600 gm (40 % of total brain weight)
180 gm --------- neurons
420 gm --------- glial cells
Cerebral Cortex
Won Taek Lee, M.D., Ph.D.
9. Numerical Data
Number of neuronal cells in cerebral cortex
neurons ----------- 10-15 billion
glial cells ---------- 50 billion
Estimation of number of cortical neurons
von Economo and Koskinas (1925) 14.0 billion
Shariff (1953) 6.9 billion
Sholl (1956) 5.0 billion
Pakkenberg (1966) 2.6 billion
Cerebral Cortex
Won Taek Lee, M.D., Ph.D.
10. Subdivision of Cerebral Cortex
Allocortex
Archicortex (hippocampal formation)
Palaeocortex (Paleopallium)
Isocortex
Neocortex (Neopallium)
Won Taek Lee, M.D., Ph.D.
11. Isocortex – typical 6 layered cortex
I. Molecular Layer
II. External Granular Layer
III. External Pyramidal Layer
IV. Internal Granular Layer
V. Internal Pyramidal Layer
VI. Polymorphic Layer
Won Taek Lee, M.D., Ph.D.
22. S I (3, 1, 2 ; postcentral gyrus)
afferents: ventrobasal complex (VPLc, VPM)
discrimination of position and intensity of sensation
S II (superior bank of lateral fissure)
Somesthetic Association Cortex (5, 7; parietal
lobe, precuneus)
afferents: S I, LP of thalamus
integration of general sensation with past experience
tactile agnosia, astereognosis
Somesthetic Area
31. Neuropsychological
Manifestations of Temporal
Lobe Lesions
Lateral (20,21,38,37)
A) Posterior: visual
recognition disturb-ances
(severity depends on whether
unilateral or bilateral
B) Anterior: anomia for
objects (left), anomia for facial
expressions (right), full-blown
anomia, retrograde memory
disturbance (bilateral)
Mesial (27,28 and limbic
structures)
Anterograde amnesia for
verbal (left) or nonverbal
(right) material; bilateral
lesions produce severe
material non-specific defect
Tranel, 1992
32. Neuropsychological
Manifestations of Occipital
Lobe Lesions
Dorsal(17,18,19,39,7)
Partial or mild Balint’s syndrome
(unilateral), severe Balint’s
syndrome (bilateral), defective
motion perception, astereopsis,
severe visuospatial disturbance,
simultanagnosia
Ventral (17,18,19)
Hemiachromatopsia (unilateral),
pure alexia (left), apperceptive
visual agnosia (unilateral, R>L),
defective imagery
Bilateral lesions produce severe
agnosia, prosopagnosia
Bilateral lesions of Area 17
produce cortical blindness (may
be transient or evolving)
Tranel, 1992
33. Neuropsychological Manifestations of
Parietal Lobe Lesions
Temporoparietal Junction (including
posterior superior temporal gyrus,
22, inferior 39,40)
A) Left: Wernicke’s aphasia
B) Right: Amusia, defective music
recognition, ‘phonagnosia’
C) Bilateral: auditory agnosia
Inferior Parietal Lobule (39,40)
A) Left: Conduction aphasia, tactile
agnosia
B) Right: neglect, anosognosia, tactile
agnosia, anosodiaphoria
C) Balint’s syndrome
Tranel, 1992
34. Neuropsychological Manifestations
of Frontal Lesions I
Frontal Operculum (44,45,47)
A) Left: Broca’s aphasia
B) Right: ‘expressive’ aprosodia
Superior Mesial (mesial 6, 24)
A) Left: akinetic mutism
B) Right: akinetic mutism
Bilateral lesions of mesial SMA (6) and
anterior cingulate (24) produce more
severe form of akinetic mutism
Tranel, 1992
35. Neuropsychological
Manifestations of Frontal Lobe
Lesions II
Inferior Mesial Region
A) Orbital Region (10, 11)
Lesions in this region produce
disinhibition, altered social
conduct, “acquired sociopathy”,
and other disturbances due to
impairment in fronto-limbic
relationships
B) Basal Forebrain (posterior
extension of inferomesial region,
including diagonal band of Broca,
nucleus accumbens, septal
nuclei, substantia innominata
Lesions here produce prominent
anterograde amnesia with
confabulation (material specificity
present, but relatively weak)
Tranel, 1992
36. Neuropsychological Manifestations
of Frontal Lobe Lesions III
Lateral Prefrontal Region (8,9,46)
Lesions in this region produce
impairment in a variety of “executive”
skills that cut across domains. Some
degree of material-specificity is
present, but relatively weak.
A) Fluency: impaired verbal fluency
(left) or design fluency (right)
B) Memory impairments: defective
recency judgment, metamemory
defects, difficulties in memory
monitoring
C) Impaired abstract concept
formation and hypothesis testing
D) Defective planning, motor
sequencing
E) Defective cognitive judgement and
estimation
Tranel, 1992
