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17 HIPPOCAMPAL FORMATION AND FORNIX

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Brain



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Interventricular foramen

Corpus callosum (cut)

Cut edge of tela choroidea of 3rd ventricle

3rd ventricle

Choroid plexus

Internal cerebral vein

Superior thalamostriate vein

(vena terminalis)



Head of caudate nucleus

Septum pellucidum

Columns of fornix

Anterior tubercle

Stria terminalis

Interthalamic adhesion



Pes hippocampi

Inferior horn of lateral ventricle

Dentate gyrus

Collateral eminence

Hippocampus

Fimbria of hippocampus



Lamina affixa

Stria medullaris

Habenular trigone

Pulvinar (lifted)

Lateral geniculate body

Medial geniculate body

Brachium of superior colliculus



Posterior commissure

Brachium of inferior colliculus

Habenular commissure

Pineal gland



Superior colliculus

Inferior colliculus



Collateral trigone

Cerebellum

Calcar avis

Posterior horn of lateral ventricle



Calcarine sulcus (fissure)



3.18  THALAMIC ANATOMY

The thalamus is viewed from above. The entire right side of the

brain, just lateral to the thalamus, has been removed, the head

of the caudate nucleus has been sectioned, the corpus callosum

and all tissue dorsal to the thalamus have been removed, and

the third ventricle has been opened from its dorsal surface.

The pineal gland is present in the midline, just caudal to the

third ventricle; it produces melatonin, a hormone that helps

regulate circadian rhythms, sleep, and immune � responses.



The superior and inferior colliculi are shown, depicting the

dorsal surface of the midbrain. On the left, the temporal horn

of the lateral ventricle, with the hippocampal formation, has

been exposed to show the relationship of these structures to

the thalamus. The terminal vein and choroid plexus accompany the stria terminalis along the lateral margin of the thalamus. The stria medullaris runs along the medial surface of the

dorsal thalamus.



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Overview of the Nervous System



3rd ventricle

Interthalamic adhesion

Internal medullary lamina



MD



LP



Mi



rnal



Inte

M



n



dli



Intralaminar

nuclei



)



l

dia

Me

llary

edu



ina



ian



ed



m

e(



l am



Pulvinar



a



lamin



m



VA



LD



LP



VPL



VL



3rd ventricle



CM



VI



VP



M



VP

M



VP



Reticular nucleus

of thalamus



L



VP



External medullary lamina



Pulvinar

Lateral geniculate body

Thalamic nuclei



Midline (median) nuclei



Schematic section through thalamus

(at level of broken line shown in

figure at right)



CM

LD

LP

M

MD

VA

VI

VL

VP

VPL

VPM



Centromedian

Lateral dorsal

Lateral posterior

Medial group

Medial dorsal

Ventral anterior

Ventral intermedial

Ventral lateral

Ventral posterior (ventrodorsal)

Ventral posterolateral

Ventral posteromedial



3.19  THALAMIC NUCLEI

The thalamus is subdivided into nuclear groups (medial,

lateral, and anterior) that are separated by medullary (white

matter) lamina. Many of these thalamic nuclei are “specific”

thalamic nuclei that are reciprocally connected with discrete

regions of the cerebral cortex. Some nuclei, such as those embedded within the internal medullary lamina (intralaminar

nuclei such as the centromedian and parafascicular nuclei)

and the outer, lateral shell nucleus (reticular nucleus of the

thalamus), have very diffuse, nonspecific associations with the

cerebral cortex.



Medial geniculate body



Schematic representation of thalamus



(external medullary lamina and reticular nuclei removed)



Lateral cell mass

Medial cell mass

Anterior cell mass



CLINICAL POINT

Thalamic syndrome (posterolateral thalamic syndrome, or Dejerine-Roussy syndrome) results from obstruction of the thalamo�

geniculate arterial supply to the region of the thalamus where the

�ventroposterolateral nucleus is located. Initially, all sensation is lost

in the contralateral body, epicritic more completely than protopathic.

Commonly, severe spontaneous pain occurs contralaterally, described

as stabbing, burning, or tearing pain; it is diffuse and persistent. Even

light stimulation can evoke such pain (hyperpathia), and other �sensory

stimuli or emotionally charged situations can result in these painful

sensations. Even when the threshold for pain and temperature sensation (protopathic sensations) is elevated, the thalamic pain may be

present; it is called analgesic dolorosa. If the vascular lesion includes

the subthalamic nucleus or associated basal ganglia circuitry, the patient may also experience hemiballismus (or choreoform or athetoid)

movements in addition to the sensory deficits.



4



BRAIN STEM AND

CEREBELLUM



4.1



Brain Stem Surface Anatomy: Posterolateral View



4.2



Brain Stem Surface Anatomy: Anterior View



4.3



Cerebellar Anatomy: External Features



4.4



Cerebellar Anatomy: Internal Features



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54



Overview of the Nervous System



Posterolateral View

Thalamus



Pulvinar



Optic tract

Pineal gland



Lateral geniculate body

Medial geniculate body



Brachia of superior and inferior colliculi



Cerebral peduncle

Trochlear (IV) nerve



Superior colliculi



Pons



Inferior colliculi



Trigeminal (V) nerve

Superior cerebellar peduncle



Superior medullary velum



Middle cerebellar peduncle

Vestibulocochlear (VIII) nerve



Medial eminence



Facial (VII) nerve

Inferior cerebellar peduncle



Rhomboid fossa of 4th ventricle



Vestibular area

Facial colliculus

Cuneate tubercle

Gracile tubercle

Dorsal roots of 1st spinal nerve (C1)

Fasciculus cuneatus



Olive

Hypoglossal (XII) nerve

Glossopharyngeal (IX) and vagus (X) nerves

Hypoglossal trigone

Vagal trigone

Accessory (XI) nerve



Fasciculus gracilis



4.1  BRAIN STEM SURFACE ANATOMY:

�POSTEROLATERAL VIEW

The entire telencephalon, most of the diencephalon, and the

cerebellum are removed to reveal the dorsal surface of the brain

stem. The three cerebellar peduncles (superior, middle, and inferior) are sectioned and the cerebellum removed. The dorsal

roots provide input into the spinal cord, and the cranial nerves

provide input into and receive output from the brain stem. The

fourth nerve (trochlear) is the only cranial nerve to exit �dorsally

from the brain stem. The tubercles and trigones on the floor of

the fourth ventricle are named for nuclei just beneath them.

The superior and inferior colliculi form the dorsal surface of

the midbrain, and the medial and lateral geniculate nuclei (associated with auditory and visual processing, respectively) are

shown at the caudalmost region of the diencephalon.



CLINICAL POINT

The facial colliculus is an elevation on the floor of the fourth ventricle in the pons under which is located the abducens nucleus (cranial

nerve VI) and the axons of the facial nerve nucleus (VII), which arc

around the abducens nucleus. A tumor or other lesion on one side

of the floor of the fourth ventricle may induce symptoms related to

cranial nerves VI and VII, including ipsilateral paralysis of lateral gaze

(lateral rectus) and medial gaze (resulting from damage to nerve VI’s

interneurons, which ascend to the nucleus of CN III via the medial

longitudinal fasciculus) as well as ipsilateral facial palsy.

The cerebellar peduncles convey the cerebellar afferent and efferent fibers. The superior peduncle conveys the major efferents to

the red nucleus and thalamus (especially the ventrolateral nucleus),

whereas the inferior peduncle conveys the major efferents to the vestibular and reticular nuclei. The middle peduncle conveys the corticoponto-�cerebellar fibers. Afferents enter the cerebellum especially

through the inferior peduncle but also through the superior peduncle.

Damage to the lateral hemisphere of the cerebellum or its associated

peduncles can result in ipsilateral symptoms, including limb ataxia,

mild hypotonia, dysmetria (misjudgment of distance), decomposition of movement (especially movement involving several joints),

intention tremor (with movement), dysdiadochokinesia (inability

to � perform rapid alternating movements), and inability to dampen

movements appropriately (rebound phenomena).



Brain Stem and Cerebellum



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Insula

Olfactory tract



Anterior View



Anterior perforated substance



Optic chiasm

Infundibular stalk

Tuber cinereum

Optic tract

Cerebral peduncle



Mammillary body

Temporal lobe

Oculomotor (III) nerve

Trochlear (IV) nerve

Pons



Posterior perforated substance

in interpeduncular fossa



Trigeminal (V) nerve



Lateral geniculate body



Facial (VII) nerve



Abducens (VI) nerve



Vestibulocochlear (VIII) nerve

Basilar groove



Flocculus



Middle cerebellar peduncle

Olive

Pyramid

Ventral roots of 1st spinal nerve (C1)

Pyramidal decussation



4.2  BRAIN STEM SURFACE ANATOMY:

�ANTERIOR VIEW

The left temporal lobe is dissected to show the anterior ―ventral)

surface of the brain stem. The cerebral peduncles, direct caudal

extensions of the posterior limb of the internal capsules, carry

corticospinal and corticobulbar fibers from the internal capsule to the spinal cord and brain stem, respectively. The decussation of the pyramids marks the boundary between the caudal

medulla and the cervical spinal cord. Cranial nerve XI (accessory) is associated with the lateral margin of the upper cervical

spinal cord. Cranial nerves XII (hypoglossal), X (vagus), and

IX (glossopharyngeal) emerge from the ventrolateral margin

of the medulla. Cranial nerves VI (abducens), VII (facial),

and VIII (vestibulocochlear) emerge from the boundary between the medulla and the pons. Cranial nerve V (trigeminal)

emerges from the lateral margin of the upper pons. Cranial

nerve III (oculomotor) emerges from the interpeduncular

fossa in the medial portion of the caudal midbrain. The optic

nerve, chiasm, and tract (cranial nerve II) and the olfactory

tract (cranial nerve I) are not peripheral nerves; they are central nervous system tracts that were mistakenly called cranial

nerves by anatomists in centuries past.

CLINICAL POINT

The oculomotor nerve (III) emerges from the ventral surface of the

brain stem in the interpeduncular fossa, at the medial edge of the



Choroid plexus of 4th ventricle

at foramen of Luschka

Glossopharyngeal (IX) nerve

Vagus (X) nerve

Hypoglossal (XII) nerve

Accessory (XI) nerve



cerebral peduncle. In conditions of increased intracranial pressure in

the anterior and middle cranial fossa, such as that caused by a tumor,

edema from injury, or other space-occupying lesions, the brain stem

can herniate through the tentorium cerebelli, a rigid wing of dura. The

resultant transtentorial herniation can compress the third nerve on

one side (ipsilateral fixed and dilatated pupil resulting from parasympathetic disruption and paralysis of medial gaze resulting from motor

fiber disruption) and compress the cerebral peduncle on that same

side, resulting in contralateral hemiparesis.

The medullary pyramids contain the descending corticospinal tract

fibers from the ipsilateral cerebral cortex, particularly from the motor

and premotor cortex. The major crossing of the corticospinal tract

takes place in the decussation of the pyramids (80%), producing the

crossed, descending, lateral corticospinal tract in the spinal cord. An

infarct in the upper reaches of the anterior spinal artery or the paramedian branches of the vertebral artery can result in damage to the ipsilateral pyramid (contralateral hemiparesis); to the ipsilateral medial

lemniscus (contralateral loss of epicritic somatosensory sensations

such as fine, discriminative touch, vibratory sensation, and joint position sense); and the ipsilateral hypoglossal nerve (cranial nerve XII;

paralysis of the ipsilateral tongue, which deviates toward the weak side

when protruded). This condition is called Dejerine’s syndrome. The

hemiparesis is not spastic and is characterized by mild loss of tone, loss

of fine hand movements, and a plantar extensor response (Babinski’s

sign). It appears that isolated damage to the pyramids does not result

in spasticity. Damage to other descending systems, from either the

�motor-related cortices or the upper motor neurons, must accompany

pyramidal tract damage to produce spasticity. Thus, the term pyramidal tract syndrome, when used to describe spastic hemiplegia, is a misnomer and is anatomically incorrect.



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