pISSN 2384-1095 iMRI 2021;25:59-75
https://doi.org/10.13104/imri.2021.25.2.59
eISSN 2384-1109
Review Article
Received: January 13, 2021
Revised: March 4, 2021
Accepted: March 5, 2021
Correspondence to:
Eun Ja Lee, M.D.
Department of Radiology,
Dongguk University Ilsan
Hospital, Dongguk University
College of Medicine, 27 Dongguk-
ro, Ilsandong-gu, Goyang-si,
Gyeonggi-do 10326, Korea.
Tel. +82-31-961-7827
Fax. +82-31-961-7851
E-mail: ejl1048@hanmail.net
This is an Open Access article distributed
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Attribution Non-Commercial License
(http://creativecommons.org/licenses/
by-nc/4.0/) which permits unrestricted
non-commercial use, distribution, and
reproduction in any medium, provided
the original work is properly cited.
Copyright © 2021 Korean Society
of Magnetic Resonance in
Medicine (KSMRM)
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The Fornix: Functional Anatomy,
Normal Neuroimaging, and Various
Pathological Conditions
Young Jae Choi1, Eun Ja Lee1, Jung Eun Lee2
1
Department of Radiology, Dongguk University Ilsan Hospital, Goyang-si, Korea
2
Department of Radiology, Uijongbu St. Mary's Hospital, College of Medicine, The Catholic
University of Korea, Uijongbu-si, Korea
The fornix is the major white-matter outflow tract from the hippocampus; it has a
significant role in cognitive function. It is readily imaged via magnetic resonance
imaging; its main parts are the crura, commissure, body, and columns. In this pictorial
essay, we describe and illustrate the functional and imaging anatomy of the fornix
and limbic system, as well as various disease entities involving the fornix.
Keywords: Limbic system; Fornix; Magnetic resonance imaging
INTRODUCTION
The fornix is a C-shaped, white-matter tract bundle that constitutes the limbic
system, acting as the major efferent and afferent tract of the hippocampus. It is located
on the medial side of both cerebral hemispheres, connecting the medial temporal lobes
to the hypothalamus. It has commissural fibers connecting not only the two cerebral
hemispheres but also other structures with the limbic system. It plays a critical role
in cognitive function; if any impairment occurs in it, then various type of cognitive
impairment will follow (1). With recent advances in neuroimaging techniques, more
detailed morphological evaluation of the fornix has become possible; typically, it is
clearly identified under magnetic resonance imaging. However, in clinical practice,
fornix lesions are not often emphasized, and its pathological involvement is often
overlooked. Our purpose in this article is to explain the imaging and functional anatomy
of the fornix and to present brain-imaging findings of it under diverse pathological
conditions, knowledge of which may improve evaluation of patients with memory
impairment.
Anatomy of the Limbic System and Fornix
The limbic system plays a crucial role in human memory, emotional experience,
learning, and behavior. It is composed of a complex network of cortical and subcortical
structures and is affected by many neuropathological conditions, both in isolation and
as a part of diffuse processes in connection with the rest of the brain. Anatomically,
it consists of three nesting arches: outer, middle, and inner (2) (Fig. 1). The outer arch
begins at the uncus, which is the anterior portion of the parahippocampal gyrus.
The uncus continues posteriorly to the parahippocampal gyrus. The medial aspect
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 Normal Anatomy and Pathologic Condition of Fornix | Young Jae Choi, et al.
of the posterior parahippocampal gyrus blends into the
narrow isthmus of the cingulate gyrus, which curves
superiorly and anteriorly, hugging the superior aspect of
the corpus callosum. The outer arch ends at the subcallosal
(paraolfactory) area, below the rostrum of the corpus
callosum (Fig. 1, in gray). As part of the middle arch, the
hippocampus includes both the hippocampus proper
(Ammon’s horn) and the dentate gyrus. The hippocampus
continues superiorly and anteriorly as a thin strip of
gray matter known as the indusium griseum (vestigial
supracallosal gyrus). The indusium griseum ends anteriorly
and inferiorly as the paraterminal gyrus (Fig. 1, in blue). The
inner arch is the smallest and is composed of white-matter
structures; this corresponds to the fornix (Fig. 1, in green).
The main parts of the fornix are divided into the crura,
commissure, body, and columns. The inner arch begins as
the alveus, a thin strip of white matter running along the
superior lateral surface of the hippocampus. The alveus
extends medially to form the fimbria, which continues
posteriorly and thickens to form the crus of the fornix
at the level of the posterior hippocampus. As the crura
converge at the midline, they form the commissure: a thin
sheet of fibers that bridges the opposite sides. Beyond this
Fig. 1. Schematic diagram of the three nesting arches
of the limbic system. The outer arch starts at the uncus,
proceeds backward along the parahippocampal gyrus, then
curves inward at the isthmus of cingulate gyrus, running
along the cingulate gyrus, and ends at the subcallosal area.
The middle arch starts at Ammon’s horn and the dentate
gyrus of the hippocampus, proceeds to the rear, following
the indusium griseum, and ends at the paraterminal gyrus.
Finally, the inner arch starts at the alveus, progresses to
the fimbria, and continues with the fornix crus. The entire
structure of the fornix corresponds to the inner arch.
60
convergence, the crura form the body, which is attached
to the undersurface of the septum pellucidum. At the level
of the interventricular foramen, the body separates into
the columns, which curve inferiorly toward the anterior
commissure. At that level, the columns divide into anterior
and posterior fibers, called the precommissural and
postcommissural fibers, respectively. The precommissural
fibers develop into the hippocampal pyramidal cell
layer (along with the fibers of the entorhinal cortex and
subiculum) and terminate in the basal forebrain (including
the septum), ventral striatum, and prefrontal cortex. The
postcommissural fibers arise from the subiculum of the
hippocampus and go mostly to the mamillary bodies, with
some contributions to the anterior thalamic, midbrain
tegmentum, and red nucleus of the stria terminalis (3) (Fig.
1). The postcommissural fornix facilitates communication
within an extended hippocampal network and plays a
crucial role in memory function (4). The typical anatomy of
the fornix in coronal, sagittal, and axial MRI scans is shown
in Figures 2-4.
Neurocircuit and Function of Fornix
The fornix is thought to comprise over 2,000,000 fibers in
each hemisphere, which is twice that of the pyramidal tract
(5) and the total volume is ~1000-1800 cubic millimeters
(6). The exact function of the fornix has not yet been fully
elucidated; however, it has been found to contribute to
encoding and recall of several types of memory (7, 8) with
several connections to the hippocampal formations. The
representative efferent pathway from the hippocampal
formations is well explained by the Papez circuit, a closed
neural circuit that was initially proposed by Papez in 1937
(9). A fundamental constituent of the limbic system, this
circuit consists of the hippocampus, fornix, mammillary
bodies, anterior nucleus of the thalamus, cingulate gyrus,
entorhinal cortex, and parahippocampal gyrus. Sensory
information from various association cortices converges
on the hippocampus via the cingulate gyrus (cingulum),
entorhinal cortex, and parahippocampal gyrus through
the loop around the corpus callosum. The output of the
hippocampus is transferred to the mammillary body of the
hypothalamus via the fornix. The fibers of the mammillary
body project to the anterior nucleus of the thalamus
through the mammillothalamic tract. Then the closed
circuit, and thus feedback, to the cortex are completed
via the thalamocortical fibers that pass backward to the
cingulate gyrus (1, 10) (Fig. 5).
Several case reports address Papez circuit dysfunction
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a b c

d e f
Fig. 2. (a-f) Sequential T1-weighted coronal reconstructions of a healthy fornix show the crura (arrow 1), commissure (arrow
2), and body (arrow 3) of the fornix. The body is attached to the undersurface of the septum pellucidum (d-f, arrowheads).
The fornix gives a high signal because of the high density of myelin present, in contrast to the intermediate signal from the
septum pellucidum. The alveus (d, black dashed arrow) is a thin strip of white matter that courses along the superolateral
aspect of the hippocampus and thickens medially to form the fimbria (d, dashed arrows). Note that the fimbria has a high
signal in T1-weighted images because of densely packed myelin that provides good contrast resolution with the adjacent
hippocampus. The fimbria continues posteriorly and thickens to form the crus of the fornix at the level of the posterior
hippocampus (a-c, dashed arrows). Coronal magnetic resonance imaging also shows the superoinferior orientation of the
columns of the fornix (arrow 4). The fornix bifurcates at the level of the anterior commissure (f, black arrow), with the
postcommissural fibers (arrow 5) projecting to the mammillary bodies (*). CC = corpus callosum

in various brain injuries. Using diffusion tensor imaging
(DTI), Jang and Kwon (11) reported discontinuation of the
forniceal columns as a cause for patients with decreased
memory after hypoxic damage. Chang et al. (12) reported
an injury of the thalamocingulate tract within the Papez
circuit in a patient with memory impairment following a
putaminal hemorrhage and encephalitis. Recently, several
studies have investigated the importance of the forniceal
pathway itself, which is not part of the Papez circuit, and
have revealed that fornix connectivity and robustness play
an important role in cognitive functions (13). In Fletcher
et al. (14), macroscopic and microstructural changes
were strong predictors of episodic memory performance
regardless of age or related structural pathology, and Oishi
et al. (15) concluded that fornix degeneration may precede
hippocampal dysfunction and may predict conversion
to cognitive impairment better than does hippocampal
atrophy. Some clinical and experimental data suggest a

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 Normal Anatomy and Pathologic Condition of Fornix | Young Jae Choi, et al.

Fig. 3. (a, b) Sagittal reconstructed T1-

weighted images of a healthy fornix
show the archlike configuration of
the fornix (1, anterior commisure; 2,
columns; 3, body; 4, commisure; 5,
postcommisural fibers). The fornix is
attached to the septum pellucidum,
which is attached to the inner curving
surface of the corpus callosum. The
columns of the fornix are split at the
level of the anterior commissure (arrow
a b
1) with most of the postcommissural
fibers (arrow 5) projecting to the
mammillary bodies (arrowheads).

a b c

Fig. 4. (a-e) Sequential T1-weighted

axial imaging of a healthy fornix.
The fornix is indicated with an arrow
on each image (1, crura; 2, body; 3,
columns; and 4, postcommissural
fibers). The postcommissural fibers of
the fornix (arrow 4) follows posterior
to the anterior commissure (d, dashed
arrow) and projects to the mammillary
bodies (e, arrowhead).
d e

functional distribution of the forniceal fibers: the left fornix hippocampus, which processes exteroceptive signals and
primarily carries verbal memory information, whereas integrates object recognition within a spatial context (i.e.,
the right carries visuospatial memory information. In scene learning). The lateral aspect of the fornix is presumed
addition, the medial fornix carries fibers from the caudal to carry projections from the more rostral hippocampus,

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which processes interoceptive signals for emotional and
motivational learning and memory (16). That is, several
types of injury and pathological involvement of the fornix
may cause various forms of memory impairment.
Fig. 5. Schematic diagram of the Papez circuit. The
Papez circuit consists of closed neural pathways
following this route: hippocampus, fornix, mamillary
body, mammillothalamic tract, anterior thalamic
nucleus, thalamocortical fiber, cingulate gyrus, cingulum,
parahippocampal gyrus, entorhinal cortex, hippocampus.
The solid and dotted lines represent the efferent and
afferent paths, respectively.
a b
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Various Diseases Entities Involving the Fornix
Congenital Anomaly
Congenital anomaly of the fornix is rare. A well-known
and representative congenital anomaly is the agenesis of
the fornix (Fig. 6), which is related to holoprosencephaly,
a complex developmental anomaly of the brain and skull,
characterized by hypoplasia of the most rostral portions
of the neural tube, resulting in fused cerebral hemispheres
and the absence or hypoplasia of mid-line structures,
such as the rhinencephalon, corpus callosum, and septum
pellucidum, including the fornix (17). Isolated congenital
abnormality of the structures surrounding the fornix may
also affect its development; Rosenbaum et al. (18) described
that agenesis of the mammillary body or corpus callosum
could lead to hypoplasia or agenesis of the fornix (Fig. 7).
Chun et al. (19) discussed displacements of the fornix due to
agenesis of the septum pellucidum and asserted that these
can create morbidity. Because the inferior border of the
septum pellucidum and the upper margin of the forniceal
body are connected, if there is agenesis or structural
abnormality of the former, the force supporting the latter
is insufficient, displacing the fornix downward. Moreover,
a displaced fornix can intermittently block the foramen of
Monro, which can lead to obstructive hydrocephalus. In
addition to these congenital structural defects, neonatal
damage, such as that from a hypoxic event, can cause
developmental hypoplasia of the fornix (20).
Infection
Any infection in the brain can involve the fornix. Direct or
indirect structural damage of the fornix caused by infection
Fig. 6. (a, b) Congenital absence of
the fornix in a 78-year-old female.
T2-weighted axial (a) and coronal (b)
images show congenital absence of the
fornix, with complete absence of the
septum pellucidum.
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can induce various types of cognitive impairment (Fig. 8).

Fig. 7. A hypoplastic fornix with partial agenesis of the
corpus callosum in a 2-year-old male. A sagittal T1-
weighted image shows partial agenesis of the corpus
callosum with a hypoplastic deformed fornix (arrow). Note
the complete absence of the septum pellucidum.
However, some pathogens have particular sites that are
more likely to be involved. Herpes simplex tends to involve
the mesial temporal lobe and limbic system, and thus may
often involve the fornix; such involvement can be seen
in both acute and chronic phases. Representative MRI
findings are T2 hyperintensity and diffusion restriction in
the acute phase, and atrophic change of the fornix in the
chronic phase (21) (Fig. 9). Adenovirus (22) and rotavirus
(23) infections can involve the fornix and are related
to encephalitis in pediatric patients with compromised
immunity. The MRI findings of such viral encephalitis
involving the fornix are similar to those of herpes
encephalitis, but tend to appear more infiltrating, similar to
those of rhombencephalitis. Moreover, these findings can

a b c

Fig. 8. Meningoencephalitis with forniceal involvement caused by group B

streptococcal infection in a 5-month-old boy. Diffusion-weighted magnetic
resonance imaging (a) shows focal extra-axial fluid collection over the right
temporal convexity (arrow) causing a high-signal lesion. Contrast-enhanced
fluid-attenuated inversion recovery imaging (b) shows abnormal meningeal
enhancement (arrow) of the right temporal area. Diffusion-weighted magnetic
resonance imaging (c) shows a focal high-signal lesion (arrow) in the left fornix,
with mild enhancement (arrow) on a contrast-enhanced T1-weighted image (d).
d

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a b
a b
Fig. 10. Glioblastoma in a 77-year-old man. Contrast-enhanced, axial (a), coronal (b), and sagittal (c) T1-weighted images
show an aggressive, ill-defined, infiltrating mass involving the splenium of the corpus callosum and adjacent bilateral
pericallosal and periventricular white matter with inhomogeneous enhancement. The mass also shows involvement of the
fornix (arrows).
substantially recover in follow-up.
Tumor
Tumors that spread along the white-matter tract can
involve the fornix. It is exceedingly rare that brain tumors
involve only the fornix, and tumors associated with the
fornix almost always include adjacent structures, such
as the corpus callosum. Because the fornix has crossing
fibers between the cerebral hemispheres at the level of the
commissure, tumors may spread across the midline through
it. Glioblastoma, a rapidly progressing and infiltrative
malignant brain tumor has a predilection for spreading
along the condensed white-matter tracts, such as the
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Fig. 9. Sequelae of herpes simplex
encephalitis in a 50-year-old woman.
Coronal T2-weighted MR images (a,
b), obtained three years after acute
herpes simplex encephalitis, show
severe atrophy of both fornices, more
prominent on the right side (arrows).
Note the encephalomalacic changes
in both temporal lobes, including the
hippocampus.
c
corticospinal tracts and corpus callosum, to involve the
contralateral hemisphere and be additionally spread through
the internal capsule, fornix, and anterior commissure (24,
25) (Fig. 10). Other glial tumors, such as astrocytoma, and
nonglial tumors such as lymphoma also present forniceal
involvement (26-30) (Figs. 11, 12). Although the incidence
of forniceal involvement of tumors is not known with
certainty, it is occasionally encountered in daily practice. In
many cases of tumors with forniceal involvement, patients
present symptoms related to memory; however, this may
be reversible after successful treatment (27). Blauwblomme
et al. (30) reported forniceal glioma in pediatric patients
that were treated by resection, chemotherapy and adjuvant
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a b c
Fig. 11. Presumptive diffuse glioma in a 75-year-old man. Fluid-attenuated inversion recovery images (a, b) show an
extensive, ill-defined, infiltrative, hyperintense lesion involving both areas of frontal white matter, corpus callosum, fornix
(arrows), both basal ganglia, and right thalamus. A pre-contrast sagittal T1-weighted image (c) shows forniceal involvement
with ill-defined hypointensity.

Fig. 12. Lymphoma in a 67-year-old

woman. Contrast-enhanced sagittal (a)
and coronal (b) T1-weighted images
show an ill-defined, enhancing lesion
involving the corpus callosum genu,
both inferior frontal lobes, septum
pellucidum, and fornix (arrows).
a b

radiotherapy. They had pre- and postoperative episodic
memory dysfunction, but grew well without memory
impairment.
Mesial Temporal Sclerosis
Mesial temporal sclerosis, also called hippocampal
sclerosis, is the most common underlying cause of
intractable epilepsy, which is histologically characterized
by the loss of neuronal cells, gliosis, and sclerosis. There
is controversy on the exact etiology of this condition,
but prolonged febrile seizures and limbic encephalitis are
presumed to be one of the causes (31, 32). Typical MRI
findings of mesial temporal sclerosis include hippocampal
atrophy with an increased T2 signal and loss of internal
architecture. When the sclerosis becomes severe and
chronic, it may present atrophy of the ipsilateral fornix and
mammillary body (Fig. 13). Other findings include atrophy of
the cingulate gyrus and anterior thalamic nucleus, dilation
of the temporal horn, and atrophy of collateral white matter
and the entorhinal cortex can accompany long-standing
mesial temporal sclerosis (33).
Demyelinating Disease
The fornix can be involved in a variety of demyelinating
diseases. Among them, multiple sclerosis can most often
involve the fornix. Multiple sclerosis is an autoimmune
disorder that causes demyelination of the central nerve
system, resulting in several neurological disorders. Several
studies have shown that multiple sclerosis involves the
fornix, creating pathological findings such as demyelination,

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plaque, and chronic atrophic changes. This axonal loss and
damage exhibits T2 hyperintense lesions of white matter
under MRI. Reducing fractional anisotropy (FA) of the
fornix can also be observed under DTI. In multiple sclerosis
patients, fornix involvement has clinical significance
for cognitive dysfunction (Fig. 14). Recent studies have
reported cognitive impairment in demyelinating diseases
due to degenerative changes in the fornix in the chronic
phase; there are attempts to use DTI for making predictions
using both quantitative and qualitative measurements
(34). Neuromyelitis optica (NMO) is a demyelinating
disease of the central nervous system with predominant
involvement of the optic nerves and spinal cord, associated
with anti-aquaporin-4 antibodies (NMO-IgG). These lesions
predominantly affect sites of high aquaporin-4 expression
in the brain, mainly in the periependymal region. The fornix
can often be included when NMO involve the lateral wall of
the third and lateral ventricle (35, 36) (Fig. 15).
Wernicke Encephalopathy
Wernicke encephalopathy (WE) is a neurological disease
caused by thiamine (vitamin B1) deficiency, characterized
by altered consciousness, ocular dysfunction, and gait
disturbances. MRI typically presents symmetrically increased
signal intensity in the mammillary bodies, dorsomedial
thalami, tectal plate, and periaqueductal area, and around
the third ventricle in T2-weighted images and fluid-
attenuated inversion recovery imaging (37). In addition to
the typical MRI features of WE, some patients show atypical
MRI findings involving the cranial nerve nuclei, cerebellum

a b c

Fig. 13. Mesial temporal sclerosis in a 44-year-old woman. Axial (a, b) and
coronal (c, d) T2-weighted images show severe volume reduction of the right
hippocampus (a and d, red arrows), associated with volume decreases of the
ipsilateral mammillary body (b, arrow) and fornix (c and d, arrows).
d

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Fig. 14. Chronic multiple sclerosis

in a 50-year-old woman. Axial T2-
weighted images (a, b) show multiple
nodular T2 high-signal lesions in
both the periventricular white matter
and the corpus callosum, typical of
chronic multiple sclerosis. Note the
hyperintense plaques involving both
forniceal columns (arrows) with loss of
the normal low signal intensity at these
sites.
a b

a b c
Fig. 15. Neuromyelitis optica in a 32-year-old woman. Axial fluid-attenuated inversion recovery images (a-c) show a
hyperintense lesion in the forniceal body (a, arrow), bilateral crura (b, arrows) and left forniceal column (c, arrow). Note also
multiple nodular high-signal lesions in both the periventricular white matter. The patient had T2 high-signal lesions in the
C-T spinal cord (not shown), confirmed as NMO with aquaporin-4 positive.

dentate nuclei, vermis, red nuclei, caudate nuclei, splenium,
cerebral cortex, and fornix (38, 39). As with other structures
involved in WE, forniceal involvement causes signal changes
under MRI (Fig. 16). Several cases of forniceal involvement
in WE have been reported in the literature (38-41). Borges
et al. (40) demonstrated that detecting the involvement
of the fornix in WE could be helpful in prompt clinical
assessment of cognitive function.
Infarction
The blood vessels that supply the anterior part of the
fornix are mainly branches of the proximal anterior
cerebral artery, which enter the brain through the anterior
perforated substance. Any damage to this region can affect
the fornix’s functionality. Structures supplied by these
perforating branches include not only the fornix but also
the olfactory trigone, olfactory striae, preoptic region,
anterior hypothalamus, genu of the corpus callosum,
septum, anterior commissure, and anteroinferior aspect of
the striatum. Alternatively, these branches may arise from
the anterior communicating artery by interconnection in the
Circle of Willis. Small-vessel disease is the most common

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Fig. 16. Wernicke encephalopathy in a

69-year-old man. Axial fluid-attenuated
inversion recovery images (a, b) show a
hyperintense lesion in the fornix (arrow).
Note also the symmetric high-signal
lesions in the periaqueductal gray matter,
tectal plate, and both medial thalami and
mammillary bodies, suggesting Wernicke
encephalopathy.
a b

a b c
Fig. 17. Acute infarction involving fornix in a 79-year-old woman. Diffusion-weighted images (a-c) show multifocal
diffusion-restricted lesions in both frontal lobes, the left cingulate gyrus, left corpus callosal genu, left anterior basal
ganglia, and forniceal body and columns (arrows), suggesting acute infarction in the territories of both anterior cerebral
arteries.

cause of infarction in this region, and embolism, arteritis,
and vessel injuries after removal of a tumor or ventricular
cyst can cause this. Similar infarctions can also occur
secondarily to anterior communicating artery aneurysm
rupture or embolization. Both anterograde and retrograde
amnesia are possible, with slightly more incidence of the
anterograde form. The posterior part of the fornix, which
receives blood supply from branches of the lateral posterior
choroidal artery and posterior pericallosal artery, may also
cause amnesia because of infarction (42).
The clinical symptoms of forniceal infarction are in
part reversible, but that often takes weeks to months
(43, 44). Clinical improvement might be explained by an
incomplete impairment of the fornices with preservation
of residual functions, possible because of dual vascular
supply. Another hypothesis is the recruitment of alternative
memory networks that bypass the fornix (45-47). The
most important imaging finding for detecting forniceal
infarction is diffusion restriction (Fig. 17), but diffusion
tensor tractography is a novel imaging study helpful in
predicting recovery, because it shows any insult-like edema
or Wallerian degeneration occurring in the white-matter

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tracts. After infarction, secondary degeneration caused
by destruction of neural structures comes in two types:
Wallerian degeneration and transneuronal degeneration,
either of which affect a site remote from the primary lesion
(48). Therefore, not only the infarction of the fornix itself
but also any remote degenerative change caused by the
surrounding structures is categorized pathologically as
infarction, in a broad sense.
Trauma
Penetrative and nonpenetrative trauma can also involve
the fornix. Of such injuries, diffuse axonal injury can be
important to the fornix, whose structural characteristics
make it vulnerable to acceleration-deceleration and
rotational forces. Half of the structure of the fornix is only
weakly supported by the septum pellucidum, tethered to the
dense brain parenchyma, and surrounded by cerebrospinal
fluid in the lateral and third ventricles, leaving it susceptible
to shearing forces. Diffuse axonal injury results from
axonal stretching and disruption; it appears in two forms:
ischemia or hemorrhage (Fig. 18). Memory deficits are the
most common clinical manifestation. Mild traumatic injury
of the brain may also impair episodic memory because
of the involvement of the temporal lobe structure. This
can be explained by disruption of the connectivity with
the hippocampus and limbic systems; even if there are no
obvious structural defects in the fornix on MRI, DTI can
be used to evaluate white-matter integrity in order to
assess the extent of mild traumatic brain injury. According
to Yallampalli et al. (49), decreased FA and an increased
apparent diffusion coefficient suggest a degenerative
change in white matter after such an injury, which is
considered chronic trauma encephalopathy, typically
caused by repetitive, small traumas mainly damaging the
frontal and temporal lobes, resulting in diffuse atrophy of
the hippocampus, entorhinal cortex, and amygdala, and
shrinkage of the mammillary bodies. Microscopically, tau
immunoreactivity may also cause clinical symptoms, such
as short-term memory problems or executive dysfunction, in
chronic trauma encephalopathy. However, unlike Alzheimer’s
disease or many other tauopathies, the tau immunoreactive
abnormalities tend to cluster deep in the sulci, around small
blood vessels, and in superficial cortical layers (50).
Indirect Forniceal Damage from Pathology Adjacent to
the Fornix
Mass effects caused by lesions adjacent to the fornix
can also cause structural and functional impairment in the
fornix.
a. Ventricular Pathology
The fornix is in contact with the ventricles. At the roof

a b c
Fig. 18. Diffuse axonal injury in a 63-year-old woman after a fall. Computed tomography scan (a), susceptibility-weighted
image (b), and coronal T2-weighted image (c) show the focal hemorrhage in the left forniceal crus (arrows, a-c) and the
multiple hemorrhagic foci in the cerebral subcortical regions on the susceptibility-weighted image (b), representing diffuse
axonal injury.

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of the third ventricle, the crus and body of the fornix
passes, and it also is in contact with the medial wall and
floor of the body of the lateral ventricle. The columns of
the fornix limit the anterior and lateral walls of the third
ventricle (51). Therefore increased intracranial pressure
can directly compress important structures, including the
fornix. In several reports, hydrocephalus caused by various
pathological conditions caused impairment of the fornix.
Malignant to benign intraventricular masses can also cause
forniceal impairment. Among them, colloid cysts are benign
cysts typically arising from the roof of the third ventricle in
great proximity to the fornices. Therefore, regardless of the
size, they can cause forniceal impairment and persistent
memory disturbance even when they are completely
removed (51-53).
b. Intracranial Hemorrhage (ICH)
Several studies have indicated that cognitive dysfunction
may occur after an ICH. Although the mechanism of
cognitive impairment after ICH is not fully understood,
impairment of the fornix may cause such cognitive decline
(54). When ICH occurs, compression is applied to the lateral
ventricle because of the volume effect of the hematoma,
a b
a b
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which damages the fornix adjacent to the lateral ventricle,
with chemical injury (such as that caused by free iron),
vasospasm, and cerebral ischemia also occurring. Moreover,
when resolution of the hematoma or reorganization begins,
axonal loss may occur and degenerative change, such as
atrophy, is observed (Fig. 19). Yeo et al. (55) demonstrated
forniceal injury caused by acute ICH by decreased FA and
volume one month later.
c. Brain Tumor
Brain tumors originating from other than the fornix can
affect the forniceal impairment. The mechanism is similar to
that described above, but in some reports, cases of complete
recovery are reported (56, 57).
Miscellaneous
a. Perivascular Spaces
Perivascular spaces (PVSs, also known as Virchow-Robin
spaces, are pial-lined, interstitial, fluid-filled spaces in the
brain that surround perforating vessels. Most commonly,
PVSs are located in the lower half of the basal ganglia, as
well as in the substantia nigra, dentate nucleus, subinsular
region, cingulate gyrus, corpus callosum, and fornix (Fig.
Fig. 19. Chronic changes caused by
an acute intracranial hemorrhage
of the right thalamus in a 53-year-
old man. Initial coronal T2-weighted
image (a) shows a large acute to
subacute intracranial hemorrhage
centered in the right putamen/external
capsule. Coronal T2-weighted image
(b), obtained three years after the
hemorrhage, shows the ipsilateral
atrophy of the fornix column and
mammillary body (arrows).
Fig. 20. Unusual location of PVSs in
a 63-year-old woman with headache.
Sagittal T1-weighted (a) and coronal
T2-weighted (b) images show PVSs in
the corpus callosal body (a, arrows)
and right forniceal crus (b, arrow).
71
 Normal Anatomy and Pathologic Condition of Fornix | Young Jae Choi, et al.
20); they are generally smaller than 2 mm (58, 59). PVSs
are often misidentified as pathological lesions because they
mimic several cystic brain lesions; therefore, it is important
to be familiar with typical images of normal and dilated
PVSs.
b. Normal Variation
Normal variation in the structure surrounding the fornix
can also change the form of the fornix. A cavum septi
pellucidi (CSP), a fluid-filled cavity that lies between the
two frontal horns of the lateral ventricles, has its posterior
border contacting the columns of the fornix. This causes
downward displacement of the fornix because of the
a b
a b
72
volume effect (Fig. 21). A cavum vergae, an elongated
finger-like posterior extension from the CSP that lies
between the crura of the fornix, also causes splaying and
downward movement of the fornix (60). A cavum veli
interpositi is also an anatomic variant: the dilation of the
potential space called the velum interpositum located in
front of the pineal body, below the fornix and above the tela
choroidea of the third ventricle. Because of this position,
the presence of a cavum veli interpositi may displace the
fornix upward and cause its crura to be wider than normal
(Fig. 22). CSP and cavum vergae often appear together, but
the relationship between their developmental processes has
not been revealed. Regardless, such positional changes in
Fig. 21. Cavum septum pellucidum and
vergae in a 14-year-old complaining
of headaches and dizziness. Sagittal
T1-weighted (a) and axial T2-
weighted (b) images. The fornix is
displaced downward (a, arrow) without
significant pathological change.
Fig. 22. Cavum veli interpositi in a
15-year-old female complaining of
syncope. Sagittal T1-weighted (a) and
coronal T2-weighted (b) images show
that the fornix is displaced upward (a,
arrow) without significant pathological
change.
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https://doi.org/10.13104/imri.2021.25.2.59
the fornix under these normal variants rarely cause clinically
significant symptoms.
In conclusion, the fornix is a particularly important
component of the limbic system and has a significant role
in cognitive function. Under routine imaging, the fornix
is typically not of concern and is easily overlooked, but
it should be carefully reviewed, especially when patients
complain of memory impairment. Recognition of the
involvement of the fornix could be helpful in timely clinical
assessment, treatment of cognitive function, and evaluating
the risk of permanent memory deficits.
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