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2. GETTING TO AND FROM THE CEREBRAL
CORTEX

3. THALAMUS

4. THALAMUS
 Oval, nuclear mass
 Forms 80% 0f diencephalon
 Anterior extent- interventricular foramen

5.  Superiorly- transverse cerebral fissure, floor
of lateral ventricle
 Inferiorly- hypothalamic sulcus
 Posteriorly- overlaps midbrain

13.  All sensory pathways relay in thalamus.
 Many circuits used by cerebellum, basal
nuclei and limbic system involve thalamus.
 These utilize more or less separate portions
of thalamus, which has been subdivided into
a series of nuclei.

14.  All thalamic nuclei are a mixture of projection
neurons, whose axons provide the output of
thalamus, and small inhibitory interneurons
that use GABA as a neurotransmitter

15.  Projection neurons account for 75% or more
of the neurons of the most thalamic nuclei,
though the relative proportions of projection
neurons and interneurons vary in different
nuclei

16. Thalamic nuclei
 Nuclei can be distinguished from each other
by topographical locations within thalamus
and by input/output patterns.
 divided into medial and lateral nuclear
groups by a thin curved sheet of myelinated
fibres called internal medullary lamina..

17.  It splits anteriorly to enclose a group of
nuclei, collectively called anterior nucleus,
which is close to interventricular foramen
 Medial group contains one large nucleus
called dorsomedial nucleus
 Lateral group is subdivided into a dorsal and
ventral tier

21.  Dorsal tier consists of lateral dorsal, lateral
posterior nuclei and pulvinar.
 Lateral posterior nucleus and pulvinar have
almost similar connections

22. Nuclei of ventral tier
 Ventral anterior, ventral lateral- concerned
with motor control; are connected to basal
nuclei and cerebellum
 Ventral posterior is subdivided into ventral
posterolateral[ smatosensory input from
body] and ventral posteromedial
[somatosensory input from head]

23.  Lateral and medial geniculate nuclei / bodies
are considered as posterior extensions of
ventral tier
Intralaminar nuclei
 Embedded in internal medullary lamina
 Largest of this group are centromedian and
parafascicular nuclei

25. Reticular nucleus
• Lies between lateral thalamic surface and
external medullary lamina
• developmentally not a part of thalamus.
• distinct anatomical and physiological properties.
• Considered a part of thalamus because of
location and extensive involvement in thalamic
function.

26. Midline nuclei
 Rostral continuation of periaqueductal gray
matter
 Form interthalamic adhesion [when present]

27. Role of thalamic nuclei
 Pipelines for flow of information to cerebral
cortex
 Site where decisions are implemented about
which information should reach cerebral cortex
for processing
 Any particular type of information affected by
any thalamic nucleus is a function of its input
and output connections

28. Inputs
 Specific - Regulatory
 Specific inputs convey information that a
given nucleus may pass to cerebral cortex
[and for some nuclei to additional sites].
 Examples; Medial lemniscus specifically to
VPL. Optic tract to LGB

29.  Regulatory inputs contribute to decisions
about whether or in what form information
leaves a thalamic nucleus

31. Sources
 cortical area to which the nucleus projects
 thalamic reticular nucleus
 diffuse cholinergic, noradrenergic,
serotonergic endings from brainstem
reticular formation

32. Categories of nuclei depending on
pattern of inputs
three functional groups:
1. specific or relay nuclei,
2. association nuclei
3. non-specific nuclei

33. Relay/specific nuclei
• receive well defined specific input fibres and
project to specific functional areas of cerebral
cortex
• deliver information from specific functional
systems to appropriate cortical areas
• comprise the nuclei of the ventral tier and the
geniculate bodies (nuclei).

34. Association nuclei
 project to association areas of cerebral cortex
 receive major inputs from cerebral cortex and
subcortical structures
 probably important in distribution and gating of
information between cortical areas

35.  Intralaminar and midline nuclei seem to
have special role in function of basal nuclei
and limbic system

36. Non-specific nuclei
 not specific to any one sensory modality.
 include the intralaminar and reticular nuclei.

37. Intralaminar nuclei
 contained within the internal medullary lamina
of white matter
 can be regarded as a rostral continuation of the
reticular formation of the midbrain

38.  project widely to the cerebral cortex, as well
as to the corpus striatum.
 Afferents belonging to the ascending
reticular activating system synapse in the
intralaminar nuclei

39. The thalamic reticular nucleus (TRN)
 shaped like a shield around the front and
lateral side of the thalamus
 separated from the main thalamus by the
external medullary lamina.
 All of the thalamocortical projections from
the specific thalamic nuclei pass throughTRN
and give collateral branches to it

40.  Fusiform neurons within the innermost lamina
(VI) of the cerebral cortex project to the
thalamic nuclei and also give off collaterals to
TRN.

42. SCHEME OF THALAMIC ORGANIZATION
 Every nucleus of the thalamus except the
reticular nucleus sends axons to the cerebral
cortex, either to a sharply defined area or
diffusely to a large area.
 Every part of the cortex receives afferent fibers
from the thalamus, probably from at least two
nuclei.

43. • Every thalamocortical projection is faithfully
copied by a reciprocal corticothalamic
connection.
• Thalamic nuclei receive other afferent fibers
from subcortical regions.
• Probably only one noncortical structure, the
striatum , receives afferent fibers from the
thalamus.

44.  The thalamocortical and corticothalamic axons
give collateral branches to neurons in the
reticular nucleus, whose neurons project to and
inhibit the other nuclei of the thalamus
 No connections exist between the various nuclei
of the main mass of the thalamus, although
each individual nucleus contains interneurons

45.  The synapses of the interneurons are
inhibitory, and most are dendrodendritic.
 Other synapses in the thalamus are
excitatory, with glutamate as the transmitter,
and so are thalamocortical projections

48. summary
Functional organization

49. Relay/specific nuclei
 Specific inputs from
subcortical areas[e.g.
medial lemniscus]-
project to a well
defined area of
cerebral cortex

50. Anterior
Input Output Funtions
Mamillary body Cingulate gyrus Memory

51. Ventral anterior
Input Output Functions
Pallidum [globus
pallidus]
Frontal lobe,
including premotor
and supplementary
motor areas
Motor planning and
more complex
behavior

52. Ventral lateral [anterior
division]
Input Output Functions
Pallidum [globus
pallidus]
Premotor and
supplementary
motor areas
Planning
commands to be
sent to motor
neurons

53. Ventral lateral [posterior
division]
Input Output Functions
Contralateral
cerebellar nuclei
Primary motor area Cerebellar
modulation of
commands sent to
motor neurons

54. Ventral posterolateral
Input Output Functions
Medial lemniscus,
spinal lemniscus
Primary
somatosensory area
Somatic sensation
[principal pathway,
from contralateral
body below head]

55. Ventral posteromedial
Input Output Functions
Contralateral
trigeminal sensory
nuclei
Primary
somatosensory area
Somatic sensation
[principal pathway,
from contralateral
half of head: face,
mouth, larynx,
pharynx, dura
mater]

56. Medial geniculate body
Input Output Functions
Inferior colliculus Primary auditory
cortex
Auditory pathway
[from both ears]

57. Lateral geniculate body
Input Output Functions
Ipsilateral halves of
both retinas
Primary visual
cortex
Visual pathway
[from contralateral
visual fields]

58. Association nuclei
 Major specific input
from association cortex
and project to related
association areas

59. Pulvinar
Input Output Functions
Pretectal area;
primary and all
association cortex
for vision;retinas
Parietal lobe,
anterior frontal
cortex, cingulate
gyrus, amygdala
Interpretation of
visual and other
sensory stimuli,
formation of
complex
behavioral
responses

60. Lateral dorsal
Input Output Functions
Hippocampal
formation,
pretectal
area,superior
colliculus
Cingulate
gyrus,Parietal,
temporal, and
association
cortex[visual
cortex]
Interpretation of
visual stimuli;
memory

61. Lateral posterior
Input Output Functions
Superior colliculus Parietal, temporal,
and association
cortex
Interpretation of
visual and other
sensory stimuli;
formation of
complex
behavioral
responses

62. Mediodorsal/dorsomedial
Input Output Functions
Etorhinal cortex,
amygdala
,collaterals from
spinothalamic
tract, pallidum,
substantia nigra
Prefrontal cortex Behavioral
responses that
involve decisions
based on
prediction and
incentives

63. Intralaminar and midline
nuclei/nonspecific
 Specific inputs[basal
nuclei or limbic
structures] and ptoject
to cerebral cortex,
basal nuclei, limbic
structures

64. Intralaminar nuclei
Input Output Functions
Cholinergic and
central nuclei of
reticular
formation,locus
coeruleus, collateral
branches from
spinothalamic tracts,
cerebellar nuclei,
pallidum
Extensive cortical
projections, especially
to frontal and parietal
lobes; striatum
Stimulation of cerebral
cortex in waking state
and arousal from
sleep;somatic
sensation, especially
pain [from
contralateral head
and body]; control of
movement

65. RETICULAR NUCLEUS
Input Output Functions
Collateral
branches of
thalamocortical
and
corticothalamic
axons
To each thalamic
nucleus that sends
afferents to
reticular nucleus
Inhibitory
modulation of
thalamocortical
transmission

67. Posterior group
Input Output Functions
Spinothalamic and
trigeminothalamic
tracts
Insula and nearby
temporal and parietal
cortex, including second
somatosensory srea
Visceral and other
responses to somatic
sensory stimuli

68. ‘Midline’ nuclei
Input Output Funtions
Amygdala,
hypothalamus
Hippocampal
formation and
parahippocampal
gyrus
Behavior;including
visceral and emotional
responses

70. Thalamic damage
 Vascular accidents
 Can involve adjacent structures
 Small lesion can lead to large collection of
deficits

71. THALAMIC SYNDROME[DEJERINE-ROUSSY SYNDROME]
 Damage more or less restricted to the
posterior thalamus can cause a characteristic
type of dysesthesia that is somewhat similar
to trigeminal neuralgia
 paroxysms of intense pain may be triggered
by somatosensory stimuli.

72.  The pain may spread to involve one entire
half of the body and is usually resistant to
analgesic drugs.
 In addition, those stimuli that do not cause a
pain attack may be perceived abnormally;
their intensity (and even their modality) may
be distorted, and they may seem unusually
uncomfortable or pleasant.

73.  When a threshold is reached, the sensation is
exaggerated, painful, perverted, and
exceptionally disagreeable.
 For example, the prick of a pin may be felt as
a severe burning sensation, and even music
that is ordinarily pleasing may be
disagreeable

74.  Spontaneous pain may develop in some
instances, which may become intractable to
analgesics.
 Emotional instability may also be present,
with spontaneous or forced laughing and
crying.

75.  Similar syndromes of central pain develop in
some patients after damage almost
anywhere along the anterolateral pathway;
this particular variety, because of the site of
damage, is called thalamic pain.
 The cause of thalamic pain is still not fully
understood, but lesions that cause it almost
always involveVPL/VPM.

76.  it is thought that selective damage to the
spinothalamic fibers that end inVPL/VPM,
with sparing of the spinothalamic and
spinoreticulothalamic fibers that end in other
nuclei, may result in imbalances or plastic
changes in thalamic activity.

77.  Extensive damage to the posterior thalamus
also causes total (or near total) loss of
somatic sensation in the contralateral head
and body.

78.  After a period of time, some appreciation of
painful, thermal, and gross tactile stimuli
usually returns.
 Functions customarily associated with the
medial lemniscus tend to be more severely
and permanently impaired.

79.  Discriminative tactile sensibility may be
abolished, position sense may be greatly
impaired, and a sensory type of ataxia
(resulting from the loss of proprioception)
may persist.

80.  Thalamic pain+ hemianaesthesia+sensory
ataxia contralateral to a posterior thalamic
lesion= thalamic syndrome

81.  It is often accompanied by mild and transient
paralysis (a result of damage to corticospinal
fibers in the adjacent internal capsule) and by
various types of residual involuntary
movements (a result of damage to nearby
basal ganglia).