What's that smell? A pictorial review of the olfactory pathways and imaging assessment of the myriad pathologies that can affect them - PubMed (original) (raw)
Review
What's that smell? A pictorial review of the olfactory pathways and imaging assessment of the myriad pathologies that can affect them
Geoffrey Lie et al. Insights Imaging. 2021.
Abstract
The olfactory pathway is composed of peripheral sinonasal and central sensorineural components. The wide variety of different pathologies that can affect the olfactory pathway reflect this complex anatomical relationship. Localising olfactory pathology can present a challenge to the reporting radiologist. This imaging review will illustrate the normal anatomy of the olfactory system and describe a systematic approach to considering olfactory dysfunction. Key concepts in image interpretation will be demonstrated using examples of olfactory pathway pathologies.
Keywords: CT; MRI; Olfactory; Olfactory bulb; Olfactory tract.
Conflict of interest statement
The authors declare that they have no competing interests.
Figures
Fig. 1
Normal Anatomy. Coronal T1WI (a) and T2WI (b) MRI images of the normal location and appearances of the olfactory bulbs (OBs). These lie within the olfactory grooves (OlfGr) of the anterior cranial fossa. Notice how the olfactory bulbs are surrounded by T2 hyperintense CSF. The olfactory tracts (not shown) are a posterior continuation of the olfactory bulbs and run within the olfactory sulci (OS). The olfactory sulcus is lateral to the gyrus rectus (GR) and medial to the orbital gyrus (OG)
Fig. 2
Normal anatomy. Coronal soft tissue (a) and bone window (b) CT images at the level of the olfactory bulb, demonstrating the normal anatomy of the sinonasal compartment (SC) and anterior skull base. The olfactory nerves within the SC and olfactory recess (OR) ascend intracranially via perforations within the cribriform plate (CP). The CP is bounded laterally via the lateral lamella (LL), the crista galli (CG) is seen as a midline projection, and the fovea ethmoidalis (FE) forms the roof of the ethmoid. The position of the olfactory bulb (OB) within the olfactory groove is just discernible on the soft tissue window image (a). The gyrus rectus (GR) and orbital gyrus (OG) are separated by the olfactory sulcus (OS)
Fig. 3
Coronal T1 weighted image taken at the level of the lateral ventricles (LV) and foramina of Monroe (a), and axial T1 weighted image of the inferior frontal lobe and mesial temporal lobes (b). The olfactory tracts (not pictured) run within the olfactory sulci (OS) and transmit second-order neurones to the central olfactory regions. These are housed within the mesial temporal lobe and include the parahippocampus, the entorhinal cortex (EC), the piriform cortex (PC), and the amygdaloid body (AB). Note the other sulcal landmarks including the collateral sulcus (CS) which bounds the entorhinal cortex inferiorly, as well as the inferior temporal gyrus (ITG), and the middle temporal gyrus (MTG)
Fig. 4
Coronal bone window CT images of three different patients with sinonasal disease: 51-year-old female with 4-year history of nasal congestive symptoms and anosmia diagnosed with sinusitis (a); 70-year-old female patient presenting with bloody nasal discharge and right nasal blockage diagnosed with sinonasal carcinoma (b); and 70-year-old female presenting with nasal congestion diagnosed with malignant melanoma (c). Pansinusitis with complete opacification of the paranasal sinuses (a). The bilateral nature of the disease is a sign of benignity whilst the rarefaction and thinning of the bony architecture (arrowed) suggests a more chronic process. Conversely unilateral opacification as demonstrated in (b) and (c) is suspicious for a malignant process. Notice the bony destruction of the inferior turbinate in both cases (arrowed in b and c), which can be difficult to discern from rarefaction (arrowed, a); however, this must be assessed in the context of unilateral disease. The imaging appearances in (b) and (c) are strikingly similar on both CT and MRI (not shown) and were only distinguishable on histology, which confirmed sinonasal squamous cell carcinoma (b) and malignant melanoma (c). Incidental note is made of bilateral maxillary sinus mucus retention cysts (b), identifiable by their rounded, convex contour, and fluid density (arrowhead, b), in contrast to the concave maxillary mucosal thickening (arrowhead, c)
Fig. 5
Axial MRI images of a 66-year-old female patient with right maxillary sinus squamous cell carcinoma (SCC). She presented with symptoms of chronic rhinosinusitis for which a CT sinuses was performed (not shown) demonstrating unilateral maxillary sinus disease, suspicious for malignancy. Axial T2 weighted image (a) exhibits an isointense soft tissue lesion (white arrowhead) permeating and extending through the right maxillary sinus, which can be differentiated from the high T2 signal normal mucosa (arrow). Both the SCC (white arrowhead) and normal mucosa (arrow) are hypointense on T1W imaging (b). On T1W post-contrast imaging (c), the lesion demonstrates less enhancement (white arrowhead) compared to the adjacent hyperenhancing sinonasal mucosa (arrow) (c). Transpatial spread into the right pterygopalatine fossa is also identifiable on all sequences (black arrowheads with white outline)
Fig. 6
Transpatial spread of recurrent of sinonasal squamous cell carcinoma (SCC), in the same patient as shown in Fig. 4b. Coronal bone window CT a demonstrates the right maxillectomy. Axial bone window CT b shows a permeative process within the frontal sinus causing cortical destruction (arrowed). T1WI demonstrates recurrent SCC involving the frontal sinus (c), expanding the sinus and infiltrating the bone (long arrow) with loss of the normal fatty marrow signal (arrowhead for comparison). There is clear evidence of inner and outer table cortical breach on T1WI with loss of the normal hypointense cortical rim (short arrow) placing the patient at risk of intracranial disease. The lesion demonstrates mild enhancement (d), with associated dural thickening and enhancement (arrow) indicating transpatial spread
Fig. 7
48-year-old female with long standing nasal congestion and rhinorrhoea. Coronal (a) and axial (b) bone window CT images demonstrating extensive sinonasal polyposis with extension into the nasopharynx. Bilateral involvement is suggestive of benign disease. Note the characteristic rounded contours (arrows) which are very suggestive of polyposis. There is also complete opacification of the maxillary sinuses (MS) and ethmoid air cells (EAC)
Fig. 8
60-year-old male with neutropenic sepsis on a background of allograft bone marrow transplant for acute myeloid leukaemia. Coronal soft tissue CT a demonstrates “bubbly” aerated secretions within the maxillary sinuses and ethmoid air cells bilaterally suggestive of acute sinusitis. Hyperdense regions are indicative of inspissated secretions or fungal elements (arrowed). Axial soft tissue CT images b, c illustrate subtle abnormal soft tissue at the right orbital apex (short arrow, b) and the right pterygopalatine fossa (short arrow, c), which suggests trans-spatial spread of disease. Appearances are consistent with acute invasive fungal sinusitis. On the contralateral side, the normal fat within these spaces is preserved (long arrows in b and c). Axial T1W post-contrast (d), DWI (e), and ADC map (f) MRI sequences demonstrate a left inferior frontal lobe ring enhancing lesion with central diffusion restriction consistent with an intracranial abscess (arrowed)
Fig. 9
Axial (a) and Coronal (b) bone window CT images of a 71-year-old patient with known granulomatosis with polyangiitis (GPA) suffering from chronic nasal obstructive symptoms and nasal crusting. There is widespread mucosal thickening throughout the sinuses with evidence of “frond-like” chronic remodelling and osteitis (long arrows). On the coronal image (b), erosion of the middle turbinates and irregularity of the nasal septum can be seen (short arrow)
Fig. 10
18-year-old female presenting with no memory of ever having had a sense of smell. Coronal T2 weighted image demonstrates absence of the olfactory bulbs and olfactory tracts bilaterally (arrowed). There is additional blunting of the right olfactory sulcus (black arrowhead with white outline) whilst the left olfactory sulcus is preserved (arrowhead). The history and imaging findings are consistent with congenital anosmia
Fig. 11
51-year-old male with a history of known focal epilepsy secondary to grey matter heterotopia. Axial FLAIR sequence (a) demonstrates unilateral hypoplastic left cerebral hemisphere with focal subependymal grey matter heterotopia within the left frontal region (arrowed). Coronal T2WI (b) also demonstrates an associated ipsilateral complete absence of both the olfactory bulb and olfactory sulcus (arrowhead). In comparison, the right olfactory bulb (short arrow, b) and olfactory sulcus (long arrow, b) are preserved
Fig. 12
Olfactory neuroblastoma (Esthesioneuroblastoma) in a 41-year-old male presenting with a 2-month history of change in behaviour and anosmia. Coronal bone (a) and soft tissue window (b) CT images demonstrate a large anterior skull base mass centred upon the olfactory neuroepithelium. There is extensive bone destruction of the left and right cribriform plates and turbinates (short arrows, a), and thinning of the medial wall of the left orbit (long arrow, a). There is also inferior extension of the tumour (T) through the ethmoid air cells into the nasal cavity and extending through the left middle meatus into the maxillary sinus (arrowed, b). The soft tissue density of the tumour (T) is distinct from the left maxillary sinus fluid contents (S). Note the fluid density intracranial “capping cysts” at the left frontal lobe (arrowhead, b). Coronal T1WI with contrast (c) depicts a tumour with moderately intense contrast uptake, conforming to a “dumbbell-shape” with a “waist” at the cribriform plate (arrowed, c). Again, note the presence of T1 hypointense “capping cysts” at the intracranial margin, which are a distinguishing feature of these tumours (arrowheads, c)
Fig. 13
Olfactory groove meningioma. 51-year-old male presenting with headache. A large central intermediate intensity lesion is seen on T1W (a) and T2W imaging (b). It occupies the anterior skull base centrally crossing the midline and demonstrates grey matter immediately adjacent to the lesion (arrow, a) and a CSF cleft (arrow, b) indicative of an extra-axial location. The lesion demonstrates homogenous intense enhancement following contrast administration (short arrow, c). The coronal bone window CT (d) demonstrates hyperostosis of the underlying anterior cranial fossa (long arrows), typical for a meningioma. Despite the marked mass effect on the olfactory sulcus and intimate association with the olfactory groove (long arrow, c), the patient only complained of a mild olfactory disturbance
Fig. 14
Trauma. 67-year-old male hit by a train. 3D CT reconstruction (a) demonstrates left-sided Le Fort III fracture complex and a calvarial fracture involving the frontal bone (arrowed). Coronal bone window CT (b) demonstrates an anterior cranial fossa fracture (arrowed) placing the patient at risk of inferior frontal lobe injury. Axial soft tissue window CT (c) confirms subtle punctate haemorrhage at the inferior frontal lobe (long arrow) as well as interpeduncular and ambient cistern subarachnoid haemorrhage (short arrows). The MRI axial FLAIR sequence (d) demonstrates a corresponding area of abnormal left inferior frontal lobe signal involving the olfactory sulcus (arrowed) with microhaemorrhages on the SWI (e) sequence (long arrow). Additional microhaemorrhages within the midbrain are consistent with grade III diffuse axonal injury (short arrows), and the aforementioned cisternal subarachnoid blood is also seen. The patient unfortunately passed away from related traumatic injuries
Fig. 15
Acquired post-traumatic CSF fistulas in two different patients. Coronal bone (a) and soft tissue (b) CT images demonstrate a tiny bony defect of the right cribriform plate (arrow, a) and abnormal opacification of the right olfactory recess on the soft tissue window (arrow, b). The coronal T2WI MRI image of the same patient confirms herniation of fluid intensity CSF into the right olfactory recess consistent with a meningocele (arrow, c). For comparison, coronal T2WI MRI image of another patient (d) demonstrates herniation of both the gyrus rectus and CSF consistent with a meningoencephalocele (arrow, d)
Fig. 16
Acquired non-traumatic CSF fistula secondary to idiopathic intracranial hypertension (IIH). 43-year-old female patient diagnosed with IIH at the age of 16 but lost to follow up, presenting with nasal congestion, CSF rhinorrhoea, and blurred vision. Sequential coronal T2W sequences (a, b) demonstrate a large left meningoencephalocoele herniating through the left olfactory recess (arrow, a), extending down into the nasal cavity and obstructing the left osteomeatal complex (arrow, b). Heavily T2 weighted CISS sequence (c) demonstrates the normal olfactory tract surrounded by CSF on the right (long arrow), and the abnormal herniating brain tissue on the left (short arrow). An “empty sella” with tortuous optic nerves and dilated subarachnoid spaces around the optic nerves are consistent with IIH, which is a well-described cause of acquired CSF fistulas
Fig. 17
Fibrous Dysplasia. 24-year-old female patient with history of diabetes and café au lait spots presenting with long standing anosmia and nasal congestion, and acute left sided visual loss. Coronal CT images showing expansile multifocal osseous lesions with typical internal ground-glass matrix, involving the left cribriform plate (long arrow, a) and crista galli (short arrow, a). This is causing remodelling of the olfactory fossae and is affecting the olfactory pathway. There are similar expansile lesions affecting the anterior clinoid processes (ACP) and the sphenoid sinus (SS) which causes compromise of both optic nerve canals (OC), worse on the left—this accounts for the visual loss in the left eye. The patient was diagnosed with McCune–Albright syndrome (polyostotic fibrous dysplasia with cutaneous and endocrine abnormalities), and surgical decompression of the left optic canal was performed
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