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Home , Olfactory sulcus, Paleocortex

Diagnostic and Interventional Imaging (2013) 94, 985—991

. .

CONTINUING EDUCATION PROGRAM: FOCUS .

The

∗

N. Leboucq , N. Menjot de Champfleur,

S. Menjot de Champfleur, A. Bonafé

Service de neuroradiologie, hôpital Gui-de-Chauliac, CHRU de Montpellier, 80, avenue

Augustin-Fliche, 34295 Montpellier cedex 5, France

KEYWORDS Abstract Any dysfunction in olfaction requires a radiological exploration comprising the nasal

Cranial nerves; cavity, the anterior base of the skull, in particular the frontal and temporal lobes. MRI is the ref-

Nasal sinus cavities; erence examination, due to the frontal plane and the T1, T2 volume maps. In the child, aplasia of

Brain; the olfactory bulbs falls within a polymalformation (CHARGE) or endocrine (Kallman) context. In

MRI; the adult, rhino sinus disease and meningiomas are the most common etiologies. Frontal or tem-

Scanography poral impairment: tumoral or vascular and neurodegenerative disorders (Parkinson’s disease)

may accompany a loss of olfaction.

© 2013 Éditions françaises de radiologie. Published by Elsevier Masson SAS. All rights reserved.

Anatomy of the olfactory system Olfactory bulbs and tract

Neuroepithelium and The olfactory nerves come into contact with the olfactory

bulbs: ovoid structures on the cribriform plate (Fig. 1a, b, c,

The lines the roof of the nasal cav- d). They are emanations from the and contain the sec-

ity, the upper part of the nasal septum and the superior ond bipolar neurons (deutoneurons) still called mitral cells.

turbinates (Fig. 1a). It contains support cells, Bowman’s The axons of the mitral cells develop in the

glands and Schultze’s olfactory sensory neurons considered under the olfactory between the right gyri and the

as protoneurons [1]. These neurons are bipolar: their den- medial .

drites come into contact with the surface of the epithelium In front of the anterior perforated substance, the tract

while the axons group in bundles called filia. They are divides in lateral, medial and intermediate stria [2].

surrounded by a Schwann sheath. These filia, about 20 in

number on each side of the nasal cavity, form the olfac-

tory nerves that pass through the foramen of the cribriform

The olfactory cortical and subcortical areas

plate.

The medial stria [4]

They go to the septal nuclei of the (Fig. 2).

Tw o bundles leave from this area: the medullary stria that

leads to the habenula nuclei, in connection with the reticu-

∗

Corresponding author. lar formation, the salivary nuclei and the dorsal nucleus of

E-mail address: [email protected] (N. Leboucq). X, and the olfacto-hypothalamo-tegmental bundle [3].

2211-5684/$ — see front matter © 2013 Éditions françaises de radiologie. Published by Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.diii.2013.06.006

986 N. Leboucq et al.

Figure 1. Olfactory neuroepithelium, bulbs and olfactory tract: anatomy in MRI. a: front section T2: olfactory neuroepithelium under the

cribriform plate (white arrow) and olfactory bulbs (tip of white arrow); b: sagittal section T2 CISS: placed on the cribriform

plate (tip of white arrow); c: front section T2: olfactory tract (tip of white arrow) under the olfactory sulcus located between the right

and the medio-orbital gyrus; d: sagittal section T2 CISS: olfactory tract under the (tip of white arrow).

These connexions between the septal area and the The intermediate stria [2]

brain stem via the habenula and the

In the olfactory tubercles, they lead to archaic structures

are responsible for reactions of salivation or nausea,

that have disappeared in depth to leave room for the ante-

modification in the gastrointestinal peristalsis, accord-

rior perforated substance.

ing to whether the odor is recognized as agreeable or

not.

Radiological exploration of the olfactory

The lateral stria [4] system

They go to the medial side of the temporal lobes (Fig. 2). The

main cortical structures with which the lateral stria come The CT-scan

into contact are from front to rear: the pre-

With multiplane reconstructions and bone windows, the CT-

and the pre-amygdale cortex, then the and finally the

scan is indicated for the exploration of the ethmoid, nasal

para-hippocampus cortex covered by the .

cavity as well as the base of the skull.

The para-hippocampus circumvolution (area 28) communi-

cates with the hypothalamus, then with the mediodorsal

nucleus of the thalamus and beyond with the orbito-frontal The MRI

cortex and the insula. These structures and their projection

routes intervene in the characterization and memoriza- MRI is the reference examination to analyze the entire olfac-

tion of odors as well as in behavior processes as different tory system [5].

as food preferences, sexuality or even the mother—child The use of superficial antennae is classically indicated

bond. for a high-resolution study of the olfactory neuroepithelium,

The olfactory system 987

3D gradient echo sequences T1 or T2 TSE have the advan-

tage of exploring the entire olfactory system.

T1 sequences with injection are carried out with fat sat-

uration to analyze the nasal cavity, the bulbs and the base of

the skull and in 3D to explore all the endocranial olfactory

structures.

The diffusion sequence may be useful in case of infectious

or tumoral disease.

Disease of the olfactory nerves, bulbs and

olfactory tract

The congenital etiologies

The absence of olfactory lobes, called arhinencephaly, may

be isolated or associated with many anomalies involving the

face and brain. The facial anomalies are mainly hypopla-

sia or absence of nose (arrhinia), a cyst of the back of the

nose communicating with the base of the skull, a median

cleft lip and palate. The brain malformations are median:

hypoplasia or agenesia of the , impairment

Figure 2. Beginning of the lateral and medial stria in the anterior

of the hypothalamic-pituitary axis, lobar holoprosencephaly,

perforated space: anatomy in MRI. Axial view T2 CISS. The lateral

median lipoma or even fronto-naso-ethmoidal encephalo-

olfactory stria is indicated by the white tip of an arrow, the medial

olfactory stria by a white arrow. cele (Fig. 3a, b) [6].

Hypoplasia of the olfactory bulbs may be included in mul-

timalformative syndromes such as the CHARGE syndrome,

the bulbs and the tract at 1.5 Tesla. Currently, multichannel Kallmann syndrome or even craniotelencephalic dysplasia.

antennae, in particular at 3 Tesla, enable sufficient spatial The CHARGE syndrome [6] (coloboma, cardiopathy,

resolution to be free of surface antennae. choanal atresia, retarded growth and development, genital

The coronal plane is the reference plane for the analysis and ear anomalies) is secondary to a microdeletion of chro-

of the nasal cavity, the bulbs and olfactory tract. T2, T1 2D mosome 22q11.2 with mutation of gene CDH7. Hypoplasia

sequences in 2 mm coronal sections explore the olfactory of the olfactory tract should be systematically investigated.

system up to the anterior perforated space. Kallmann syndrome [6,7] associates hypogonadotropic

3D sequences of the CISS or DRIVE type, strongly weighted hypogonadism with . Several genetic mutations have

in T2 allow for fine multiplane analysis of the bulbs and been identified: KAL1 on chromosome Xp22.3 for the X

olfactory tract due to their substantial difference in signal forms, FGFR1 on chromosome 8p11.2 for the dominant auto-

with that of the LCR. somal forms. The MRI reveals an absence of olfactory sulcus

Figure 3. Down’s syndrome patient presenting ethmoido-sphenoidal meningo-encephalocele: exploration by MRI. a: front section T2:

ethmoido-sphenoidal meningo-encephalocele (tip of white arrow), right fronto-basal dysplasia, absence of olfactory bulbs; b: median

sagittal section T1: ethmoido-sphenoidal meningo-encephalocele (tip of white arrow), lipoma prolonging the terminal plate (white arrow),

hypertrophia of the chiasm, absence of pituitary gland, hypoplasia of the corpus callosum.

988 N. Leboucq et al.

and, in the severe forms or hypoplasia, not very marked atro-

phy of the frontal and temporal lobes [8], a small pituitary Boxed text 1 Main benign tumors involving the

gland. A cleft palate, dental agenesis and renal anomalies nerves, bulbs and olfactory tract.

may coexist (Fig. 4a, b).

• Meningioma

Craniotelencephalic dysplasia [6] associated with cran-

• Papilloma

iostenosis (oxycephalia, trigonocephalia), microphtalmia

• Schwannoma

with hypoplasia of the optic nerves, absence of olfactory

• Adenoma

nerves, polymicrogyria, frontal cysts, absent septum and •

Tumor of the median line (craniopharyngioma,

stenosis of the aqueduct.

pituitary gland tumor)

The exploration of an anosmia with median craniofacial

• Osteoma

anomalies should include a CT-scan of the bone windows •

Fibrous dysplasia

and a 3D reconstruction to study the bones of the nose, the •

Giant cell tumor

nasal cavity (septum, palate, posterior nasal apertures), the

base of the skull and an MRI to search for an anomaly of the

median line.

Boxed text 2 Main malignant tumors involving the

The CT-scan is indicated for the CHARGE syndrome to look

nerves, bulbs and olfactory tract.

for choanal atresia and an anomaly of the ears.

• Sthesioneuroblastoma

•

The inflammatory and infectious etiologies Squamous cell carcinoma

•

Adenoid cystic carcinoma

Acute and chronic rhinosinusitis may result in hyposmia • Rhabdomyosarcoma

by the formation of a mucous oedema preventing the • Metastases

flow of air carrying the fragrant signals from reaching the • Lymphoma

olfactory epithelium [9]. Recently, a local inflammatory • PNET

entity, characterized by opacity filling the isolated olfac-

tory cleft has recently been described, resulting in anosmia

[10]. CD57- and are derived from the glial cells of the olfactory

Granulomateous inflammatory disorders (sarcoidosis, bulbs.

Wegener’s granulomatosis) or even Sjögren’s syndrome may Malignant tumors [11] are of different origins (Boxed text

induce hyposmia. 2). Esthesioneuroblastoma (Fig. 7a, b, c) is rare. Devel-

oped from the olfactory epithelium, it crosses the cribriform

The tumoral etiologies palate to spread to the anterior cerebral fossa. The presence

of calcifications and peripheral cystic cubicles are specific

The benign tumors (Boxed text 1) [11] most often found for this tumor. It may metastasise to the cervical ganglia,

are the olfactory meningiomas (Fig. 5a, b) and those of lungs, bones and meninges. Genetic mutations have been

the small sphenoid ridge. This location may induce anosmia found on chromosomes 3p and 17q.

with a homolateral optical atrophy and a contralateral papil-

loedema (Foster-Kennedy syndrome) [3] (Fig. 6a, b). The The traumatic etiologies

schwannomas develop from olfactory nerves (amyelinic).

Tumors with OECs (olfactory ensheathing cells) [12] are Complex craniofacial fractures (Fig. 8a, b) involving the

histologically close to the schwannomas but they are nasofrontal region, the sockets and the anterior cerebral

Figure 4. Patient with Kallmann syndrome: exploration by MRI. a: front section T2: olfactory sulcus not very deep. Absence of olfactory

bulbs; b: median sagittal section: small pituitary gland.

The olfactory system 989

Figure 5. Meningioma of the olfactory groove: exploration by MRI. Front T1 (a) and axial T1 sections with contrast (b): front T2 (c) median

sub-basi-frontal extra-axial formation in hyposignal T2, with homogenous contrast enhancement.

Figure 6. Meningioma of the aliform process of the left sphenoid: exploration by MRI. Front T2 (a), front T1 with contrast (b).

Figure 7. Esthesioneuroblastoma: exploration by MRI. Front sections T2 (a) and T1 with injection (b), median sagittal section T1 with

injection (c): expansive formation developed from the olfactory neuroepithelium and transfixing the cribriform plate. Antecedents of

meatotomy and right turbinectomies.

990 N. Leboucq et al.

Figure 8. Craniofacial Lefort III disjunction. Patient victim of multiple trauma with Lefort III craniofacial disjunction, irradiating towards

the frontal and anterior cerebral cavity. CT assessment. Front (a) and sagittal (b) sections: complex bone fracture passing by the sockets,

ethmoid, cribriform plate and frontal bone.

fossa are responsible for dilacerations of the nerves, bulbs Neurodegenerative diseases

and olfactory tract [11].

Parkinson’s disease may be detected much before the

motor disorders by anosmia [15]. This hyposmia or anos-

Pathology of the olfactory cortical and mia is a good differential sign between Parkinson’s disease

and essential tremor or other Parkinsonian syndromes. It

subcortical centres

is concomitant with atrophy of the olfactory bulbs, as

Tumoral or vascular lesions [10] confirmed by morphometric studies [16]. This atrophy is

attributed to an increase in the number of dopaminergic

Tumoral or vascular lesions involving the frontal or temporal cells in the olfactory bulbs that will inhibit the olfactory

lobes, especially if on the right [13], may induce hyposmia inflow.

or anosmia. The tonsils represent the temporal zone most Alzheimer’s disease, dementia with lewy bodies may

often responsible for olfactory disorders [10]. accompany an olfactory dysfunction [17,18].

Epileptic seizures

Finally, to be complete

Epileptic seizures starting from the internal temporal, espe-

•

cially mesial scleroses (Fig. 9a, b), may begin with an Down’s syndrome (trisomia 21) (Fig. 3a, b), Klinefelter’s

olfactory aura [14]. syndrome (47 XXY);

Figure 9. Mesial sclerosis. Female patient with antecedents of pyretic convulsions in childhood presenting epilepsy with

olfactory auras: exploration by MRI. Front sections in T2 (a) and FLAIR (b): sharp hippocampus atrophy with cortico-subcortical hypersignal

especially visible in FLAIR.

The olfactory system 991

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Disclosure of interest

The authors declare that they have no conflicts of interest concerning this article.