THALAMUS

Presented by
Mirjana Milutinovic,M.D.
Professor,
SJSM,
spring2022
Goals
To teach students functional anatomy of the thalamus as well as
main thalamic syndromes
Objectives:

At the end of this lecture, students should be able to demonstrate

the knowledge and understanding of :
 -- the fuctions, nuclei and connections of the thalamus
- the structure and importance of epithalamus:
- spatial relationships between the diencephalon and the different
components of the cerebral hemispheres (internal capsule, caudate,
putamen, globus pallidus, ventricles, etc.).
- the organization of the thalamus, relationships between different
thalamic nuclei and the subdivisions of the thalamus into nuclear
groups and positions of these groups with respect to the internal and
external medullary laminae and other landmarks.
- the details of connections and functions of individual nuclei and to
categorize them according to functional types
- the thalamic syndromes in the cases of selective damages  
Literature

Snell: Clinical neuroanatomy: p: 240-270

Gayton: p: 599-715

Recommended:
F i x: High yield neuroanatomy, relevant chapters

This presentation

Optional: Blumenfeld: NEUROANATOMY THROUGH CLINICAL CASES, relevant

chapters
61-year-old man with hypertension was seen in the
emergency department, having apparently suffered a
stroke. A neurologist was called and made a complete
examination of the patient. The patient was conscious
and was unable to feel any sensation down the right
side of his body. There was no evidence of paralysis
on either side of the body, and the reflexes were
normal. The patient was admitted to the hospital for
observation. Three days later, the patient appeared to
be improving, and there was evidence of return of
sensation to the right side of his body. The patient,
however, seemed to be excessively sensitive to testing
for sensory loss.
On light pinprick on the lateral side of the right leg, the
patient suddenly shouted out because of excruciating burning
pain,
and he asked that the examination be stopped. Although the
patient experienced very severe pain with the mildest
stimulation, the threshold for pain sensitivity was raised, and
the interval between applying the pinprick and the start of
the pain was longer than normal; also, the pain persisted after
the stimulus had been removed. Moreover,
the patient volunteered the information that the pain
appeared to be confined to the skin and did not involve
deeper structures. Later, it was found that heat and cold
stimulation excited the same degree of discomfort.
 Content

Thalamus as a part of diencephalon

Localization
Thalamic structure and nuclei
Thalamic connections
Functions of the thalamus
Symptoms Following Lesions of the Thalamus
 diencephalon

Diencephalon: thalamus,
hypothalamus, epithalamiums, sub
thalamus, optic chiasm
 Epithalamus

 Relatively small part,

located in most caudal
and dorsal region
 Lies immediately rostral
to superior colliculus
 Consists of:
 Pineal gland &
 Habenular nuclei
 Stria medullaris
 1.Pineal Gland
An endocrine organ
Synthesizes melatonin
Controls:
Sleep/awake cycle
Regulation of onset of
puberty
Includes :

• 2. Thalamic medullary
stria
connects fibers from the septal nuclei and
anterior thalamic nuclei with
habenular nuclei

• 3. Habenular nuclei
center for integration of olfactory
visceral and
somatic afferent pathways

FUNCTION: a linkage between limbic system components in the forebrain and other parts of the brain .
Localization
In horizontal coronary and sagittal section
•The thalamus is the largest structure in the diencephalon,
•Placed between the midbrain (mesencephalon) and forebrain (telencephalon).
•Sends nerve fibers out to the cerebral cortex in all directions.
•Cell station to all the main sensory systems (except the olfactory pathway – however
even olfactory signals reach the thalamus via indirect connections with the cortical
regions initially receiving the olfactory signal.).
Important STRUCTURE ABOVE
thalamus : caudate nuclei, lateral
ventricle and fornix

Below thalamus: sub thalamic

nuclei and midbrain
3 rings: stria terminalis
Stria medullaris
Fornix
Fornix
Internal capsule
The posterior limb - corticospinal fibers,
sensory fibers (including the medial lemniscus
and the anterolateral system) from the body
and a few corticobulbar fibers.
The genu contains corticobulbar fibers
The anterior limb of the internal capsule
contains:
1) frontopontine
2) thalamocortical fibers from medial
and anterior nuclei of the thalamus
.
 Thalamus - the gateway to the
cortex.
Thalamic radiation
The projection from the thalamus
to the cortex uses the internal
capsule, both the anterior and
posterior limbs. This portion of
the internal capsule is known as
the thalamic radiation.

The lateral surface of the thalamus is

separated from the lentiform nucleus by the
very important band of white matter
called the internal capsule.
Blood supply of caps. interna
Anterior limb: 
lenticulostriate branches
of middle cerebral
artery& recurrent artery of
Heubner  of the anterior
cerebral artery
Genu: 
lenticulostriate branches
of middle cerebral artery
Posterior limb: 
lenticulostriate branches
of middle cerebral
artery& anterior choroidal
artery off of the internal
carotid artery
 Thalamic structure

superior- covered with white matter-stratum zonale

lateral –external medullary lamina
internal medullary lamina divide thalamus

Stratum zonale and

external medullary
lamina
 Thalamic structure and Nuclei

internal medullary
lamina connect
nuclei

three basic types of

thalamic nuclei
 Thalamic Nuclei
Internal laminar nuclei
Intralaminar Nuclei- "nonspecific" nuclei:
centromedian nucleus involved mainly in basal
ganglia circuitry (Blumenfeld) and ascending
reticular activating systems (ARAS) to the
cortex, maintaining the alert, conscious state
The reticular nuclei the only nucleus of
the thalamus that does not project to the cortex
Other categories of
thalamic nuclei
Intralaminar Nuclei
The reticular nuclei and
The midline thalamic nuclei are
an additional thin collection of
nuclei lying adjacent to the third
ventricle, several of which are
continuous with and functionally
very similar to the intralaminar
nuclei.
Many of the intralaminar nuclei
and midline nuclei have diffuse
projections to the cortex and
have been termed "nonspecific".
These nuclei are probably mostly
involved in arousal and alertness
 Nonspecific nuclei
X midline nuclei
The midline nuclei
consist of groups of
nerve cells
adjacent to the third
ventricle
X They receive afferent
fibers from the
reticular formation,
nucleus tractus
solitarius,
Projects to the limbic
area of the cortex
included insula
Their precise
important in visceral functions functions are
unknown.
 Thalamic reticular nucleus
Reticular cells are GABAergic. Between external medullary lamina
ROLE: and internal capsule
This is the only thalamic nucleus that does not project to the
cerebral cortex, instead it modulates the information from other
nuclei in the thalamus

Input
- from the cerebral cortex and
dorsal thalamic nuclei (mostly
collaterals). (Intralaminar
nuclei)
Output: The function of this nucleus is not fully
-to dorsal thalamic nuclei, but understood, but it may be concerned
never to the cerebral cortex. with a mechanism by which the
cerebral cortex regulates thalamic
activity.
Intralaminar nuclei of thalamus-Nonspecific nuclei

Receive information from reticular

formation and spinothalamic tract
(also it give fibers to reticular
formation)
Output to all cerebral cortex

Centre median parafascicular group

centromedian nucleus:
consciousness

Attention, arousal, control of the level of cortical activity.

-Diseases: absence seizures
-Para-fascicular: The ability to perceive and orient to new information
is crucial to survival
 nucleus input output
VPL Sensory from Somatosensor
body y
and limbs cortex
VPM Sensory from Somatosensor
head y
cortex
VA/VL From BG Motor
cerebellum cortex
LGB Optic tract Primary visual
area
MGB Inf.colliculus Primary
auditory
cortex
AN Mamilothalamic Cingulate
tract gyrus
Reticular nuclei MD Memory- Wernicke korsakoff
pulvinar integration  
IL arousal  
Relay Thalamic Nuclei
 relay thalamic nuclei motor VENTRAL NUCLEI

Ventral anterior nucleus

Input: globus palidus, substantia nigra, reticular formation
Output: premotor cortex
Role: probably influence on motor cortex
 helps to function in planning movement. It initiates wanted movement and
inhibits unwanted movement.
Ventral lateral nucleus
Input: globus palidus, substantia nigra, cerebellum
Output: premotor cortex and motor cortex
relay thalamic nuclei sensory
Ventral posterior nucleus: lateral and medial
Input: lemniscus medialis and spinothalamic-VPlateral
Input: trigeminal and gustative pathway- VPmedial
Outputs:posterior limb of internal capsula-corona radiate-
-primary somatosensory cortex
MGN, LGN
The medial geniculate body forms part of the auditory
pathway and is a swelling on the posterior surface of the
thalamus beneath the pulvinar
Afferent fibers to the medial geniculate body form the inferior
brachium and come from the inferior colliculus
the inferior colliculus receives the termination of
the fibers of the lateral lemniscus
The medial geniculate body receives auditory information from
both ears but predominantly from the opposite ear
The efferent fibers leave the medial geniculate body to
form the auditory radiation, which passes to the auditory
cortex of the superior temporal gyms
The lateral geniculate body
forms part of the visual pathway and is a swelling
on the undersurface of the pulvinar of the thalamus
Input: The nucleus consists of six layers of nerve cells and is the
terminus of all but a few fibers of the optic tract (except the fibers
passing to the pretectal nucleus). The fibers are the axons of the
ganglion cell layer of the retina and come from the temporal half of the
ipsilateral eye and from the nasal half of the contralateral eye, the latter
fibers crossing the midline in the optic chiasma.
Each lateral geniculate body receives visual information from the
opposite field of vision.
The efferent fibers leave the lateral geniculate body to
form the visual radiation, which passes to the visual cortex
of the occipital lobe.
Association Thalamic Nuclei

Pulvinar
Anterior nucleus
Dorsomedial nucleus
 Association Thalamic Nuclei
Pulvinar and Lateral posterior

Pulvinar: Integration of visual, audio, somatosensory imputes

Input: thalamic nuclei, superior colliculus,
Output: parieto-temporo-occipital cortex

Lateral posterior input: thalamic nuclei, output: parietal cortex

 Pulvinar and lateral posterior
(yellow on the picture)

Thalamic reticular nuclei (white on

the picture)
Anterior nuclei of thalamus-limbic
Inputs: from mammilary bodies (mammilliothalamic) and from the subiculum via the
fornix.
Outputs: to the cingulate gyrus.

ROLE:
-modulation of
the alertness
-learning
- memory.
 Medial dorsal nucleus-limbic
Inputs:
Thiamine
-from the prefrontal deficiency in
cortex and the limbic alcoholics
system , brainstem results in
nuclei degeneration of
Outputs:
-to the pre-frontal
dorsomedial
association cortex. And nucleus
reciprocal connection of thalamus and
mamillary
A crucial role in: bodies,
attention, planning,
hippocampus
organization, abstract Medial portion
thinking, multi- and vermis of
Lateral portion
tasking and active the cerebellum
memory.

Lesions of the medial dorsal nucleus have been associated with Korsakoff's

syndrome.
 CONNECTIONS OF THE THALAMUS
1. Every thalamic nucleus (except the reticular nucleus) sends axons to
specific parts of the cerebral cortex
and every part of the cerebral cortex sends reciprocal fibers back to the
thalamic nuclei
information received by the thalamus is always shared with the cerebral
cortex and
cortex and thalamus can modify each other's activities.
2. The thalamus is an important relay station for two sensory-motor
axonal loops involving the cerebellum and
the basal nuclei:
the cerebellar-rubro-thalamic-cortical-ponto-cerebellar loop and
the corticalstriatal-pallidal-thalamic-cortical loop, both of which are
necessary
for normal voluntary movement.
Thalamic connections

THALAMIC NUCLEI
Fornix to mammillary
nuclei, from mammillary
body is mamillo thalamic
tract to anterior nucleus of
thalamus from that to
cortex- cingulate gyrus
It is papez circuit for
recent memory and it is
broken in Wernicke
Korsakov disease.
Thalamic connections
Thalamic connections
 FUNCTION OF THE
THALAMUS
The following basic principles should be committed to memory:
1. The thalamus is made up of complicated collections of nerve cells that
are centrally placed in the brain and are interconnected.
2. A vast amount of sensory information of all types (except smell)
converges on the thalamus and presumably is integrated
through the interconnections between the nuclei
3. Anatomically and functionally, the thalamus and the cerebral cortex
are closely linked.
Modes of operation of thalamic cells
in wakefulness tonic firing mode

Each thalamic projection neuron can exist in one of two basic

physiological states "tonic mode" and "burst mode."
In "tonic mode", the neurons respond like other neurons to
depolarization and hyperpolarization
Burst mode ("oscillatory mode“) is a state in this mode leading to the
rhythmic depolarization, producing a rhythm when neurons have an
intrinsic rhythmicity and when neurons are tonically hyperpolarized. A
special class of calcium channels are opened - burst of action potentials
in the thalamic projection neurons
During sleep,
most thalamic
neurons are in
burst mode.
During waking
many thalamic
neurons remain
in burst mode.
In burst mode, neurons cannot communicate specific information.
However, if a novel stimulus is presented, the sudden change from
burst to tonic mode may be a major factor in alerting the cortex.
 LESIONS OF THE THALAMUS
Sensory Loss
These lesions usually result from thrombosis or hemorrhage of one of
the arteries supplying the thalamus
Damage to the ventral posteromedial nucleus and the ventral
posterolateral nucleus will result in the loss of all forms of sensation
including light touch, tactile localization and discrimination, and muscle
joint sense from the opposite side of the body.

Usually, a thalamic lesion results in dysfunction of neighboring

structures, producing symptoms and signs that overshadow those
produced by the thalamic disease

Thalamic pain may occur as the patient is recovering from a thalamic

infarct
THALAMIC HAND
The contralateral hand is held in an abnormal posture in some patients
with thalamic lesions due to altered muscle tone in the different muscle
groups.
 http://www.youtube.com/watch?v=YAJ8A1IwI4s

electrical stimulation of the

centromedian nucleus can cause
absence seizures
General anaesthetics specifically
suppress activity in the ILN
Complete bilateral lesions
Lead to coma or vegetative
status
Symptoms Following Lesions of the Thalamus
There are two considerations that must be taken into account when attempting to
diagnose lesions of the thalamus:

1)thalamic nuclei are small so that lesions producing highly specific effects are
uncommon (although they do occur), and

2)the thalamus is immediately bounded by the internal capsule and is in close

proximity to the deep motor nuclei of the cerebral hemisphere (putamen, caudate
and globus pallidus) so that thalamic lesions frequently are accompanied by
symptoms from damage to these other structures (most commonly from hemorrhage
from the striate arteries).

3)However, since small branches of the posterior cerebral artery supply much of the
thalamus but not adjacent structures, selective thalamic lesions do occur. Occlusion
of these small branches results in a number of symptoms characteristic of the
thalamic syndrome.
Symptoms Following Lesions of the Thalamus

1) If the damage includes VPL and VPM a contralateral

hemianesthesia usually results. Typically, all somatic sensory
modalities are affected: light touch, conscious proprioception, 2-point
discrimination & vibration, and pain & temperature. This loss of all
somatic sensory modalities is an important diagnostic sign for
thalamic damage (lesions of the internal capsule or cortex that
impair somatic sensory function typically affect different modalities
to different extents, often leaving pain sensation unchanged).
2.) Sometimes seen after a period of recovery from damage to VPL and
VPM (days to months) is hyperalgesia (an exaggerated unpleasant or
painful sensation resulting from mild cutaneous stimulation) or in some
cases spontaneous pain with no apparent stimulation (causalgia). Such
pain can be severe and intractable. Hyperalgesia and spontaneous pain
do not occur with lesions confined to the cerebral hemispheres (cortex,
internal capsule, or deep nuclei). Obviously, damage to the postero-
lateral part of the thalamus also will involve other nuclei such as the
pulvinar and lateral posterior, but unilateral infarcts in these higher order
“association” nuclei typically result in no obvious deficits.
3. .) If the LGB is affected there is a contralateral homonymous
hemianopsia.
4. ) If the damage extends into the VA/VL nuclei complex movement
disorders can result. The movement disorders can be reminiscent of
cerebellar damage (ataxia and intention tremor) and/or basal ganglia
damage (choreoathetoid movements). This reflects, in part, the fact that
both the cerebellum and basal ganglia project to VA and VL. All such
problems occur contralateral to the side of the lesion.
A 45-year-old man who had suddenly developed a weakness of the
left leg 12 hours previously was admitted to a medical ward. On
examination, he was found to have paralysis of the left leg and
weakness of the muscles of the left arm. The muscles of the affected
limbs showed increased tone, and there was an exaggeration of the
tendon reflexes on the left side of the body. There was also
considerable sensory loss on the left side of the body, involving both
the superficial and deep sensations. During the examination, the
patient would exhibit spontaneous jerk ing movements of the left leg.
When asked to touch the tip of his nose with the left index finger, he
demonstrated considerable intention tremor. The same test with the
right arm showed nothing abnormal. Three days later, the patient
started to complain of agonizing pain down the left leg. The pain
would start spontaneously or be initiated by the light touch of the bed
sheet.
What is your diagnosis?
How can you explain the various signs and symptoms?
Clinical presentations of
thalamic stroke fall into 4
principal vascular syndromes
(paramedian, tuberothalamic,
inferolateral, and posterior
choroidal arteries), but there
is variation within each of
these syndromes because of
factors related to
vascular anatomy and
pathology.
Artery of Perceron
 Recovery of Function After Thalamic Infarction

- Generally regarded as being rather good compared with

lesions of the cerebral cortex or other subcortical structures,
particularly in regards to mortality and motor deficit.

- The incidence of cognitive impairment and alterations of mood

and personality after thalamic infarction are not known.

Diaschisis
Diashisis: when a lesion in one brain region produces functional
impairment in a distant, not damaged, but interconnected brain
region. This manifests not only as loss of the behavior subserved by
that circuit but also as altered metabolism on functional neuroimaging
techniques (PET or SPECT) that evaluate the integrity of the circuit.
The relief of diaschisis can sometimes be achieved through the
intervention and the brain's natural neuroplasticity.
 Human thalamic arteries show a high incidence of stroke.

A 45 y.o. woman presents to the ERwith

a headache and complains of abnormal
sensations on the right side of her body.
Sensory changes came on rapidly in the
last few hours. Her lab reports come
back normal, a spinal tap reveals normal
CSF, and her mental ability seems good.

Neurological exam: greatly reduced

sensation on the entire right side of her
body, including her face. The sensory
loss includes all modalities. The motor
exam is normal, as is her visual exam
and hearing exam.
An MRI is performed and the results are
presented:
Lacunar infarction
Questions you should answer at the end of this lecture:

Based on her neurological findings, which thalamic nuclei should be

involved in this small lesion?

Does your prediction correlate with the position of the lesion on the
MRI?

Without looking at the MRI, how could you tell this was a thalamic
lesion and not a problem with sensory cortex?

Which artery was probably involved in this lesion?

How do you know the lesion didn’t include the geniculate bodies?
A 35 yr old African American female after cardiac catheterization was difficult to
arouse . However, physical examination failed to reveal any focal neurological deficits
except for hypersomnolence. Emergent CT scan of brain failed to show any evidence of
hemorrhage or any ischemic lesions. Follow up MRI of the brain showed symmetrical
bilateral thalamic high signal intensity suggestive of acute ischemic injury.
Increased sleep requirements (> 14 hrs/day)
 Hypersomnia After Thalamic Stroke:
• Thalamus has a key role in sleep production (as well as arousal control)
• Various thalamic nuclei receive projections from certain “hypnogenic” areas (basal
forebrain, posterior hypothalamus, mesencephalic and pontine RF)
• Interruption of NE and DA activating impulses ascending from brainstem RF to
thalamus
• Diurnal sleep behavior composed of NREM stage I (drowsy) sleep; no deeper sleep
• Night sleep mechanisms preserved
• Due to proven or presumed embolic occlusion of the often unpaired thalamic-
subthalamic perforating arteries arising from top of the basilar artery

• Clinical Features:
• Increased sleep requirements (> 14 hrs/day)
• In severe cases only: vertical gaze palsy; coma
• Amnesia; confabulation; psychomotor slowing; attentional deficits; apathy; blunted
affect; lack of concern; persisting work incapacity
• Day sleep similar to night sleep, but less deep
55 y/o alcoholic is examined by the physician. The patient greets the examiner cordially as if he
knows the examiner from the past (although the examiner has never met the patient). When
asked about prior encounters, the patient tells the examiner that they met 2 weeks ago in the
hospital but does not recall exactly the topic of the conversation. The patient then proceeds to tell
the examiner that currently he is doing well and is able to give basic history about current
symptoms and uncertainty about where he will live. However, when asked about the year and the
president, the patient replies (usually without hesitation) that it is 1955 and the president is
Eisenhower. The actual year is 2005 and the president is G.W. Bush. In this case, the examiner
may not have detected any deficits until specific orientation questions are asked. Other aspect of
conversation generally lacks specificity and/or depth.

In 1881, Carl Wernicke first described an illness that consisted of paralysis of eye movements,
ataxia, and mental confusion in pts with 1. alcoholism, or 2. persistent vomiting following
sulfuric acid ingestion. Pts developed coma, and eventually died. On autopsy, Wernicke detected
punctate hemorrhages affecting the gray matter around the third and fourth ventricles and
aqueduct of Sylvius.

Related Links
Cognitive Decline
Cognitive Memory
Cognitive
Mental Aging
status changes – most interesting characteristics o W-C -
Cognitive Skills
Confabulation
Sudden Memory is Loss
classically described in Korsakoff dementia, although it may be present in
other
Memorydementias
Tests and is not necessarily present to make the diagnosis.
 Other Thalamic Strokes SYs-exampls
• Inferolateral Infarct (VP nuclear group): Sudden or
progressive onset of numbness and tingling on
opposite side of body; hemicorporeal sensory loss
with possible sparing of proprioception ; some
weakness or ataxia; Common
• Tuberothalamic Infarct (VL and DM nucleus):
Dysphasia (L); Hemineglect and impaired visuo-
spatial processing (R)
• Posterior Choroidal Artery Infarct (LGB): Partial
hemianopia; asymmetric optokinetic response
• Hypersomnia not typically associated
61-year-old man with hypertension was seen in the
emergency department, having apparently suffered a
stroke. A neurologist was called and made a complete
examination of the patient. The patient was conscious
and was unable to feel any sensation down the right
side of his body. There was no evidence of paralysis
on either side of the body, and the reflexes were
normal. The patient was admitted to the hospital for
observation. Three days later, the patient appeared to
be improving, and there was evidence of return of
sensation to the right side of his body. The patient,
however, seemed to be excessively sensitive to testing
for sensory loss.
On light pinprick on the lateral side of the right leg, the
patient suddenly shouted out because of excruciating burning
pain,
and he asked that the examination be stopped. Although the
patient experienced very severe pain with the mildest
stimulation, the threshold for pain sensitivity was raised, and
the interval between applying the pinprick and the start of
the pain was longer than normal; also, the pain persisted
after the stimulus had been removed. Moreover,
the patient volunteered the information that the pain
appeared to be confined to the skin and did not involve
deeper structures. Later, it was found that heat and cold
stimulation excited the same degree of discomfort.
exercises
 The primary afferent connection of the ventral posterolateral
thalamic nucleus is
Answer Choices:
A. Lateral lemniscus
B. Spinothalamic tract and medial lemniscus
C. Primary sensory cortex
D. Primary motor cortex
E. Dentate nucleus of the cerebellum
Imagine yourself in a microscopic ship traversing
the intricate neural networks. Your ship relies on
fiber tracts for directional navigation. You are
located in the dentate nucleus of the cerebellum.
What will be your destination in the thalamus if
you follow the efferent highway from the
dentate?
Answer Choices:
A. Anterior nucleus
B. Ventral posterolateral nucleus
C. Pulvinar
D. Dorsomedial nucleus
E. Ventrolateral nucleus
1. Structure number 1 is the:
(a) falx cerebelli
(b) anterior cerebral artery
(c) crest of frontal bone
(d) sagittal suture
(e) longitudinal fissure

2. Structure number 2 is the:

(a) genu of corpus callosum
(b) lamina terminalis (
c) septum pellucidum
(d) anterior column of fornix
(e) interthalamic connection

3. Structure number 3 is the:

(a) lentiform nucleus
(b) internal capsule
(c) putamen
(d) head of caudate nucleus
(e) globus pallidus
4. Structure number 4 is the:
(a) pineal body
(b) falx cerebri
(c) third ventricle
(d) septum pellucidum
(e) great cerebral vein
5.Structure number 5 is the:
(a) medial geniculate body
(b) thalamus
(c) choroid plexus of lateral ventricle
(d) body of caudate nucleus
(e) third ventricle

6. Structure number 6 is the(a)thalamus

(b) head of caudate nucleus
(c) internal capsule
(d) claustrum
(e) lentiform nucleus

7. Structure number 7 is the:

(a)body of lateral ventricle
(b)(b) tail of lateral ventricle
(c)(c) anterior horn of lateral ventricle
(d) (d) third ventricle
(e) (e) fourth ventricle
8. Structure number 8 is the: (a) septum pellucidum
(b) falx cerebri (c) anterior cerebral artery (d) lamina terminalis
(e) interthalamic adhesion
 Location DIENCEPHALON (in
addition to dorsal thalamus, includes
hypothalamus, epithalamus,
Location in which structure ventral/subthalamus)
Function SENSORY (CONSCIOUS)
Functio and MOTOR systems integration (e.g.
relay as well as modulation of signals)
Input Input (1) PRECORTICAL = all
sensory systems EXCEPT olfactory
system; (2) CORTICAL = cerebral
cortex
Output Output (1) CORTEX (cerebral); (2)
BASAL GANGLIA; (3)
HYPOTHALAMUS
3 types of nuclei types of nuclei (1) RELAY (receive
primary input of a specific modality);
(2) ASSOCIATION (integration
regions for other cortical output); (3)
Anterior Nucleus

Function Function Limbic system = part of

the Papez circuit of emotion
Input Input (1) ANTERIOR =
MAMMILLARY BODIES
(hypothalamic); (2) LATERAL
DORSAL = FORNIX
(hippocampal)
Output Output (1) CINGULATE GYRUS

lesion lesions Memory impairment

Dorsomedial Nucleus
Function Function (1) Limbic system =
expression of affect, emotion, and
behavior (2) Striatal system
Input Input PREFRONTAL CORTEX
Output Output PREFRONTAL CORTEX
Lesions lesions (1) Wernicke-Korsakoff
syndrome (memory loss)
Intralaminar Nuclei
2 important nuclei centromedian nucleu
Its physiological role involves attention
Role and arousal, including control of the level
of cortical activity
Connections connections
lesion It sends nerve fibres to the subthalamic
nucleus and putamen. It receives nerve
fibres from the cerebral cortex, vestibular
nuclei, globus pallidus, superior colliculus,
reticular formation, and spinothalamic
tract.
Lesion: koma
Parafascicular
Role:
The ability to perceive and orient to new
information is crucial to survival
 Ventral Anterior
Ventral tier Nuclei
are: Ventral Lateral

Ventral Posterolateral

Ventral Posteromedial
 Ventral Anterior (VA) Nucleus MOTOR;
BASAL GANGLIA (GP, SNr); input from
Ventral Anterior globus pallidus (via thalamic and lenticular
In/out fasciculi, H1 and H2) and the substantia nigra
(motor function); output to prefrontal and
orbital cortices, and to the premotor cortex
(BA6)
Ventral Lateral (VL) Nucleus MOTOR;
CEREBELLAR (D) ; input from globus
pallidus (via thalamic and lenticular fasciculi,
Ventral Lateral H1 and H2), substantia nigra, and cerebellar
In/out dentate nucleus; output to motor cortex
(BA4) and to supplementary motor area
(BA6); influences somatic motor mechanisms
via striatal motor system and cerebellum;
stereotactic destruction reduces parkinsonian
tremor
 Ventral Posterolateral (VPL) Nucleus
SOMATOSENSORY TARGET; Input from
Ventral Posterolateral spinothalamic tracts and medial lemniscus;
output to somesthetic cortex (BA 3,1,2); lesion
results in contralateral loss of pain and
temperature sensation as well as loss of tactile
discrimination in the trunk and extremities;
nucleus of termination of GSA (pain and
temperature) and SVA (taste); SENSORY
Ventral Posteromedial (VPM) Nucleus
Ventral Posteromedial SOMATOSENSORY TARGET; Input from
trigeminothalamic tracts, taste pathway via
solitary nucleus and the parabrachial nucleus;
output to somesthetic cortex (BA 3,1,2); lesions
results in contralateral loss of pain and
temperature sensation, loss of tactile
discrimination in the head, ipsilateral loss of
taste; SENSORY
 Function AUDITORY relay nucleus
Input Input via brachium of INFERIOR
Lateral Geniculate COLLICULUS (containing auditory
Body (LGB) information from both sides)
Function Output PRIMARY AUDITORY
In/out CORTEX at HESCHL'S GYRUS
(posterior portion of superior temporal
gyrus BA 41,42 via auditory radiation)

Function VISUAL relay nucleus

Medial Geniculate Input Retinal input via optic tract
Body (LGB) Output PRIMARY VISUAL CORTEX
Function (BA17, lingual gyrus, cuneus) via OPTIC
In/out RADIATION; representation of space on
the calcarine sulcus (dorsal = center FOV;
ventral = peripheral FOV; superior =
inferior FOV; via Meyer's loop to inferior
= superior FOV)
 Posterior Communicating Artery
Connects anterior and posterior
circulation; gives rise to anterior
Blood Supply thalamoperforating arteries
Posterior cerebral artery Gives
rise to the posterior choroidal
arteries and posterior
thalamoperforating arteries
Anterior Choroidal Artery
Supplies the choroid plexus
 Paraventricular nucleus and Ventral
midline nucleus Inputs from
serotinergic and catecholaminergic
Midline Nuclei nuclei in brainstem; outputs to
amygdala, NAc, Hippocampus,
Orbitofrontal cortex

Function Inhibitory/regulatory
Reticular Nuclei neurons to thalamus; potential role
in absence seizures
Input and Output Thalamic region
to thalamic region

Dejerine-Roussy cause Loss of circulation to VL and

Syndrome (Thalamic VP
or Central symptoms Hemisensory
Pain Syndrome) disturbances, minimal weakness,
minimal cognitive changes, pain