Neuroradiology #44

March 25, 2026March 31, 2026 ~ EDiR Holders ~ 1 Comment

Clinical Data

70-year-old male patient:

Status post:

Intracranial hypertensive right basal ganglia bleed a year ago, resulting in mild left-sided hemiparesis.
Small left cerebellar ischemic infarction half a year ago.

Now presents with worsening of left-sided hemiparesis (left-sided facial droop, severe weakness of the upper/moderate lower limbs) and aphasia. Onset of symptoms two hours ago.

The patient had similar transient neurologic episodes in the preceding week, which improved spontaneously, then presumed to represent transient ischemic attacks (TIAs).

A non-contrast head CT, CT angiogram (CTA) of the cervical and intracranial arteries and CT perfusion (CTP) were performed (code stroke).

What do you see?

No signs of acute/hyperacute ischaemic infarction in the right (or left) cerebral hemisphere.
No signs of acute intracranial haemorrhage.
Stripe of encephalomalacia/gliosis in the region of right basal ganglia, external capsule and corona radiata – location of the old intracranial hemorrhage.
Volume loss of the crus of right mesencephalon following Wallerian degeneration.
Old infarction in the left cerebellum.

The perfusion maps show a large area supratentorially on the right with changes of the perfusion parameters, consistent with hypoperfusion (decreased CBV and CBF values, increased TTP and Tmax values).

CBV: cerebral blood volume
CBF: cerebral blood flow
TTP: time to peak
Tmax: time to maximum

Is the patient a candidate for intravenous thrombolysis, mechanical clot retrieval, both, or neither of the two treatment methods?

Neither of the two treatment options, somewhat surprisingly.

Based on the CTP maps, which arterial territory/territories are involved? Which arteries do you think are occluded?

The perfusion abnormalities span the majority of the right cerebral hemisphere, sparing only the region of the right basal ganglia. It seems that the regions of both the anterior and posterior circulation are involved.

Speaking in terms of vascular territories, we would expect such abnormalities if the anterior cerebral artery (ACA), M2 medial cerebral artery (MCA) segment, and the posterior cerebral artery (PCA) on the right were simultaneously occluded.

Internal cerebral artery (ICA) occlusions also cause abnormalities in the ACA and MCA territories, yet an ICA occlusion would also cause abnormalities in the M1 segment of the MCA (the region of the basal ganglia, which is not involved in our case).

The PCA can be supplied by the ICA through a prominent posterior communicating artery, yet in the majority of the cases it gets blood supply mostly from the basilar artery (which is supplied by the vertebral arteries).

So we have an odd situation, where we would be able to explain the perfusion abnormalities by the simultaneous occlusion of an artery of posterior circulation (PCA) and two arteries of the anterior circulation – ACA and part of the MCA. The sparing of the basal ganglia regions argues against proximal ICA occlusion.

Another explanation might be that we are not dealing strictly with a vascular problem.

Is it important to review the CTA image?

Yes, absolutely!

Showing CTA – intracranial arteries, VRT’s (Coronal and oblique/lateral)

CTA: parasagittal MIP’s, right and left carotid bulb

The CTA images demonstrate patent carotid and intracranial arteries (including all of the extra- and intracranial arteries on the right).

What is the diagnosis?

Seizure-related perfusion changes in a patient with postictal paralysis and post-stroke epilepsy.

Stroke is a term used to describe a sudden onset of focal neurological deficit/deficits of presumed vascular origin. It is most commonly caused by arterial occlusion (ischaemic stroke) or an intracerebral haemorrhage (haemorrhagic stroke).

If done promptly enough, arterial occlusions in ischaemic stroke might be resolved by administering i.v. thrombolysis. Occlusions of larger/more proximal arteries might be treated endovascularly by mechanical clot retrieval.

Although stroke is fundamentally a clinical diagnosis, radiology plays an important role in the management of patients, especially in selecting the subgroup who might benefit from the two treatment methods mentioned above.

Stroke is not the only entity causing a sudden onset of focal neurological deficits. Stroke mimics are nonischaemic conditions with clinical presentations similar to stroke. Because of their non-vascular pathophysiology, treating them with i.v. thrombolysis or mechanical clot retrieval is not indicated, as these treatment methods carry the risk of causing intracerebral haemorrhage.

The two of the most common stroke mimics are seizures with postictal paralysis and migraines.

Seizures are transient neurological events characterized by signs/symptoms caused by abnormal increased and synchronous activity of the neurons in the brain. They are common, often single events, and can be provoked by drugs, sleep deprivation or fever. Seizures might cause transient focal neurological deficits after they subside and thus mimic stroke – a term known as postictal/Todd paralysis.

If unprovoked seizures keep recurring in an individual, the term epilepsy is used. Epilepsy might be associated with structural brain lesions of various etiologies, which serve as an epileptogenic focus.

Damaged brain tissue from old ischaemic or haemorrhagic infarcts might also represent an epileptogenic focus and a subset of patients after stroke suffer from post-stroke epilepsy. Re-infarctions and seizures are two main differential diagnoses in post-stroke patients, presenting with worsening of their neurological status.

CT perfusion plays an important role in hyperacute and acute ischaemic stroke imaging. If medial or large vessels are occluded (MeVO and LVO), perfusion parameters are changed in the corresponding brain regions supplied by these arteries, i.e., the perfusion changes in the respective vascular territories. CTP most commonly demonstrates areas of hypoperfusion in the affected regions with increased TTP and TMax values, decreased CBF values and variable CBV values (decreased in ischaemic core and normal/ increased in the ischaemic penumbra).

Stroke mimics might not only cause clinical findings imitating stroke, but also cause CTP changes that can mistakenly be attributed to ischaemic stroke.

CTP changes related to seizures are most often explained by the concept of neurovascular coupling, which states that increased neuronal activity leads to a proportionate increase in blood flow and vice versa. We would expect that imaging a patient at the moment of seizure (ictal phase) would show areas of hyperperfusion in the corresponding part of the seizing brain, owing to the increased neuronal firing. Imaging after the seizure (post-ictal phase) would show signs of hypoperfusion because of the neuronal exhaustion and decreased activity. There is however some overlap between the findings of hypo- and hyperperfusion in clinical practice and CTP cannot be reliably used to differentiate the ictal and post-ictal phases of seizures.

The hypoperfusion pattern is especially important, as the changes in CTP parameters are similar to those observed in stroke. The involved regions in seizure-related changes however do not follow the vascular territories. The described patterns include changes in the whole hemisphere (holohemispheric pattern), lobar, multilobar, and cortical patterns. Correlation with CTA is of utmost importance in these cases, as the examination shows patent arteries in post-seizure-related changes.

Our case revisited

The CTP study showed a holohemispheric pattern of hypoperfusion in the region of the right cerebral hemisphere – changes are not consistent with a vascular distribution. The patency of the vessels was also confirmed by the CTA examination. It was suggested that the CTP findings might be post-seizure related and the neurological deterioration could be a manifestation of postictal paralysis.

The patient did not receive i.v. thrombolysis and also mechanical thrombectomy wasn’t attempted. His neurological symptoms improved spontaneously in the following hours after the CT examination.

After obtaining additional history, it became clear that the patient experienced similar transient neurological episodes in the preceding three months. They were also preceded by twitching of the muscles in his left upper extremity – retrospectively representing seizures.

On the basis of the clinical, imaging and subsequent EEG findings, a diagnosis of post-stroke epilepsy was made. The region of the older haemorrhagic infarction was presumed to represent the epileptogenic focus. The patient was discharged from the hospital on an antiepileptic medication.

References

Prodi, E., Danieli, L., Manno, C., Pagnamenta, A., Pravatà, E., Roccatagliata, L., Städler, C., Cereda, C., & Cianfoni, A. (2021). Stroke mimics in the acute setting: Role of multimodal CT protocol. American Journal of Neuroradiology, 43(2), 216–222. https://doi.org/10.3174/ajnr.a7379
Tranvinh, E., Lanzman, B., Provenzale, J., & Wintermark, M. (2018). Imaging evaluation of the adult presenting with New-Onset seizure. American Journal of Roentgenology, 212(1), 15–25. https://doi.org/10.2214/ajr.18.20202
Phillips, A. A., Chan, F. H., Zheng, M. M. Z., Krassioukov, A. V., & Ainslie, P. N. (2015). Neurovascular coupling in humans: Physiology, methodological advances and clinical implications. Journal of Cerebral Blood Flow & Metabolism, 36(4), 647–664. https://doi.org/10.1177/0271678×15617954
Van Cauwenberge, M. G., Dekeyzer, S., Nikoubashman, O., Dafotakis, M., & Wiesmann, M. (2018). Can perfusion CT unmask postictal stroke mimics? Neurology, 91(20). https://doi.org/10.1212/wnl.0000000000006501
Adams, M., & Sharma, R. (2017). Todd paralysis. Radiopaedia.org. https://doi.org/10.53347/rid-57248
De Cocker, L., D’Arco, F., Demaerel, P., & Smithuis, R. (2012, September 1). Epilepsy – Role of MRI. The Radiology Assistant. Retrieved June 25, 2025, from https://radiologyassistant.nl/neuroradiology/epilepsy/role-of-mri

Neuroradiology #43

February 25, 2026November 5, 2025 ~ EDiR Holders ~ Leave a comment

Clinical Data

2-year-old male:

Presented with enlarged skull and suspected hydrocephalus

Indicate the abnormality:

Description:

Mild symmetrical dilatation of the supra & infratentorial ventricular system. Crowded foramen magnum with an inferior location of the cerebellar tonsils below the margins of the foramen magnum.

Which of the following statements are correct?

Chiari I malformation characterized by a caudal descent of the cerebellar tonsils through the foramen magnum
Treatment with posterior decompression is usually reserved for symptomatic patients or those with a syrinx
Chiari I malformations may be seen in association with cervical cord syrinx or hydrocephalus
Becoming symptomatic is proportional to the degree of descent of the tonsils
Abnormal skull base , cervical segmentation anomalies, small cranial vault, and posterior fossa could be resembling Chiari I malformation
Excessive brain tissue could represent acquired Chiari malformation

Come back next week to see the answer. In the meantime, check our social networks to leave your guesses!

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Neuroradiology #42

January 7, 2026January 14, 2026 ~ EDiR Holders ~ Leave a comment

Clinical Data

97-year-old polymorbid female:

Acute onset left hemiplegia (Time of last known well two hours ago)
Code stroke activated
Imaging in our institution constituted of:

Non-contrast head CT
CTA of aortocervical and intracranial vessels
CT perfusion

Non-contrast head CT:

CT perfusion revealed a large ischemic core compared with the penumbra (approximately 2:1)

Based on the CTA and non-contrast head CT, which arteries were occluded?

The CTP shows perfusion changes in the vascular territories of both the right MCA and ACA.
We know that the MCA is also most certainly occluded because of the dense MCA sign.
Based on this, there is either a simultaneous occlusion of both the MCA and the ACA or the occlusion is even more proximal – ICA.

CTA shows occlusion of the M1 segment of the right MCA, and the terminal segment of the ICA is patent

However, more proximal intracranial segments of the right ICA were not opacified with contrast

The cervical ICA segments were also not opacified with contrast.(ECA and vertebral artery on the right, no ICA)

Modified sagittal reformation of the bifurcation

Given the CTA appearance of the right ICA, which of the following are the reasonable differentials?

Occlusion of the right carotid bulb with near total distal ICA occlusion
ICA dissection
ICA pseudo-occlusion

Solution:

Occlusion of the right carotid bulb with near total distal ICA occlusion – FALSE
ICA dissection – TRUE
ICA pseudo-occlusion – TRUE

Explanation:

The carotid bulb is patent and contrast opacification stops 1 to 2 centimeters after the bulb. If the bulb would be really occluded, contrast opacification would stop (almost) at the level of the bulb and the atherosclerotic changes of the bulb would be more extensive.
The sagittal images nicely show the gradual tapering of contrast opacification in the proximal cervical ICA, which is known as the flame sign.
The flame sign can be seen in carotid artery dissections and pseudo-occlusions.

How would you differentiate a pseudo-occlusion from a real dissection or ICA occlusion, while the patient is still lying in the CT scanner?

Obtain a delayed CTA scan of the arteries.
In other words, repeat the CTA scan at a later time point. Preferably tell the technician at the moment you see the flame sign on the console to just fire the CTA scan again (additional contrast application is not needed).
(In our case, the clinical context might also have helped. Spontaneous carotid artery dissections are the leading cause of stroke in younger/middle-aged patients. Our patient was almost 100 years old, which made dissection not the most probable diagnosis.)

Normal vs delayed CTA: the unopacified parts of the ACI are now opacified:

Carotid artery pseudo-occlusion:

A slightly confusing term, as the carotid artery is still occluded, just not in the extent you might think!
Carotid artery pseudo-occlusion is seen, when there is an occlusion of a distal segment (usually one of the intracranial ones) of the ICA. This occlusion makes it harder for the contrast bolus to flow through the normal ICA – as the cervical ICA segment has no branches. So, using normal timings for the CTA bolus, the cervical segment might still be unopacifed, compared with the normal side. If we wait a little bit and obtain a delayed scan, we give the ICA time to fill up and can assess the extent of the occlusion more accurately. This can be achieved with a delayed CTA scan and is also easily identified with DSA (today mostly performed as the first part of mechanical thrombectomy).

The cavernous segment was unopacified in both the normal and delayed CTA – representing the true level of the occlusion

What are the final diagnoses?

Right MCA and right cavernous segment ICA occlusion with resultant ischemic stroke
Pseudo-occlusion of the proximal (mostly cervical) parts of the ICA

Neuroradiology #41

December 24, 2025December 29, 2025 ~ EDiR Holders ~ 1 Comment

Clinical Data

38-year-old female (outpatient setting):

Appointed for a non-contrast brain MRI
Requested card information:

Vertigo
Unsteady gait
Headache
Chronic onset of symptoms that appeared approximately three years ago and got worse in the preceding weeks

T2-weighted axial image:

The MRI sequences demonstrated no signs of acute or chronic ischaemic lesions, also no mass lesions were detected.
The signal of the white and grey matter was also otherwise normal.
Supratentorially, no abnormalities were detected.

T2-weighted axial image:

Infratentorially, however, the brainstem appeared compressed anteriorly by the dens.

An additional sagittal T2-weighted image was obtained to clarify the anatomy and the cause of obstruction.

The sagittal slices demonstrated several congenital abnormalities.

Which of the congenital abnormalities contributes the most to the patient’s symptoms?

Basilar invagination (in combination with mild retroflexion of the dens).
The high riding dens causes compression of the brainstem at the pontomedullary junction.

What other congenital anomaly is basilar invagination commonly associated with?

Platybasia

Definition of terminology:

Congenital basilar invagination and platybasia are often seen together.

Basilar invagination:

A congenital or acquired condition, where the dens protrudes more cranially than it should be, typically above the foramen magnum.
If the dens causes compression of the brainstem, symptoms might ensue.

Platybasia:

A congenital or acquired condition, denoting abnormal flattening of the skull base, formally described as an increased base of skull angle. A simple way to think about it is also a shape of the base of the skull, where the clivus lies more horizontally than it should be (the clivus normally has a downward sloping shape, as clivus is a latin word for slope/hill).
Translated directly from Greek, platybasia means “flat base” (of skull). And platypus means “flat foot”, just in the case you are wondering.
Platybasia does not cause symptoms on its own.

The sagittal slices demonstrated several congenital abnormalities:

In addition to basilar impression, platybasia and dens retroflexion, several other anomalies were seen or suspected on the sagittal slices.
The most obvious additional anomaly was a hypoplastic clivus/basioccipital hypoplasia.
What seemed to be the tip of the clivus also seemed oddly very sclerotic.

A CT of the cervical spine and base of skull was recommended to further evaluate the relationship of the bones:

Basilar impression, platybasia and clivus hypoplasia were redemonstrated.

CT also showed an additional ossicle/unfused bone immediately superior to the tip of the dens/posterior to the clivus – in the same place as the structure, that appeared to be the sclerotic tip of the dens.

Sagittal and axial reformats:

The reformats demonstrated a bony arch, which were isolated from the rest of the occipital bone, representing the very rare variant called prebasioccipital arch.

Sagittal and axial reformats, what would we expect in a normal examination from a different patient?

We are still not finished (Part 1):

Hypoplasia of the occipital condyles, which appear flattened. They are commonly observed together with the aforementioned anomalies.
Oblique sagittal reformats right and left occipital condyle.

Condylar hypoplasia, oblique coronal reformat.

Oblique right sagittal and coronal reformats, what we would expect (normal examination from a different patient)?

The normal occipital condyles are convex.

We are still not finished (Part 2):

Additionally, the angle of the foramen magnum and the plane of the atlas were tilted cranially and posteriorly, resulting in a so-called “lordotic angulation”. The atlas was also noted to be hypoplastic.

Sagittal reformat, what we would expect (normal examination from a different patient)?

Wait a minute! The dens doesn’t actually protrude through the foramen magnum, as the foramen itself is tilted. So…

Are we still dealing with a case of basilar invagination?

Yes, we are.

Although the usual definition of basilar invagination says that the dens should protrude through the foramen magnum, the condition might be defined by several craniometric lineas and measurements. They also take into account conditions, where the foramen magnum itself is abnormally positioned, as in our case.

On sagittal images, they include the McRae, McGregor and Chamberlain lines. On coronal images, the digastric and bimastoid line.

The following Radiopaedia link has them all covered for you: https://radiopaedia.org/cases/basilar-invagination-measurements

In our case, we used the Chamberlain line. It is a line connecting the posterior edge of the bony hard palate to the opisthion (the midline point of the posterior edge of the foramen magnum). If the tip of the dens lies more than 3 mm above this line, we are dealing with basilar invagination.

Chamberlain line; our case and a normal CT of the cervical spine. Basilar invagination is defined, if the tip of the dens lies more than 3 mm above this line (the measurement in our case was 22 mm).

Platybasia measurements

Platybasia is also defined by a craniometric measurement, namely by an abnormally high base of skull angle (>143°).

On CT and MRI, it is defined as angle between the line drawn from the bottom of the anterior cranial fossa (or the nasion) and the tuberculum sellae, and the line drawn from the tuberculum sellae down the posterior margin of the clivus.

Base of skull angle, our case and a normal CT of the cervical spine.

An angle measuring more than 143° defines platybasia. The measurements of the angle were 146° and 67°, respectively.

Conclusion:

When confronted with a congenital anomaly, always be on the lookout, as they are often not isolated.

In the region of the craniocervical junction, congenital basilar invagination and platybasia often occur together.

It is important though to try to put emphasis on the most clinically relevant anomalies. In our case, among the many findings, basilar invagination was the most important one, causing symptoms by exerting pressure on infratentorial structures. Severe cases of basilar invagination can be treated by neurosurgical operative decompression.

Congenital anomalies of the craniocervical junction represent a complex topic. When confronted with difficult or ambiguous cases, looking up and reviewing many craniometric lines and measurements might be helpful.

Neuroradiology #40

October 29, 2025November 5, 2025 ~ EDiR Holders ~ 2 Comments

Clinical Data

19-year-old female presents to the neuro-emergency department with:

Right-sided hypesthesias and sensorimotor aphasia
Subacute onset: the symptoms did not develop extremely quickly as we would expect in a stroke
Unremarkable past medical history (mild gastroesophageal reflux)
Non-contrast CT was ordered

Describe the findings:

An ill-defined hypodense lesion primarily located in the deep white matter of the left parietal lobe.

MRI was performed:

FLAIR / T1 FFE / DWI / ADC / T2 / T1 FFE post-contrast AX / SAG / COR

MRI was performed (superior slices):

What are the top 3 differential diagnoses for lesions involving the corpus callosum?

Glioblastoma (formerly known as glioblastoma multiforme/GBM).
Primary CNS lymphoma.
Demyelinating disorders (multiple sclerosis…).

Did the MRI help in narrowing your differential?

A T2/FLAIR hyperintense lesion with enhancement was seen in the mentioned location and it was reported as representing either lymphoma or GBM in the conclusion of the MRI by the neuroradiologist.

Imagen axial T2-weighted: [Describir hallazgos, ej. 'lesión hiperintensa en región X'] — T2WI Axial

Imagen axial T1-weighted post-contraste: [Describir realce o anatomía relevante] — T1WI Post-Contrast

Does the lesion have a complete or incomplete rim of enhancement?

The lesion has an incomplete rim of enhancement.

What type of enhancement would you expect in the top 3 differential diagnoses?

Glioblastoma: complete ring, irregular enhancement.
Primary CNS lymphoma: homogeneous enhancement. (In immunocompetent patients)
Demyelinating disease: incomplete ring enhancement.

A small digression:

A well-known mnemonic for remembering ring-enhancing CNS lesions is…

MAGICAL DR

M = Metastasis
A = Abscess
G = Glioblastoma (or other high-grade gliomas)
I = Infarct (subacute phase may show enhancement)/Infections (others – non-pyogenic pathogens: Mycobacteria, Toxoplasmosis, Cysticercosis, Cryptococcus)
C = Contusion and resolving hematomas
A = AIDS related: again, non-pyogenic infections (Cysticercosis, Cryptococcus)
L = Lymphoma
D = Demyelinating disease
R = Radiation necrosis

Can demyelinating disease simulate CNS tumors?

These lesions can closely resemble CNS tumors, and in such cases, they are referred to as tumefactive demyelinating lesions.

Back to our case:

Another odd thing was overlooked.

Do you notice it on the T2-weighted image?
Does it additionally help narrowing the differential?

We see concentric rings at the periphery of the lesion.
Alternating hyper- and hypo-intense bands. Resembling the layers of an onion bulb.

Meanwhile:

The patient was admitted to neurosurgery.
Thinking it was a tumor, the neurosurgeons resected most of the lesion.
The histological diagnosis was not consistent with GBM or lymphoma. It mentioned a focus of leukoencephalitis with fiber destruction.
While ad definitive diagnosis was not provided by the pathologists: it was presumed, however, that the lesion represented “some sort of demyelinating disease or MS”.

The bands were seen on multiple MRIs

2 weeks after the initial MRI, before surgery (performed as part of pre-op MR tractography).
T1 GRE sag and ax, without contrast.

After surgery (2 days after the previous MRI).
T2WI sag and ax.

1 year after the first presentation, after surgery.
T2WI ax and FLAIR cube sag.

The bands are quite obvious on all MRI examinations.

The alternating bands are characteristic of what disease?

The “onion bulb” or “bullseye” appearance is characteristic of Baló concentric sclerosis.

This is a case of Baló concentric sclerosis, a rare demyelinating disease, often considered a variant of multiple sclerosis (MS).
Unlike conventional MS, the clinical course of Baló’s sclerosis is typically monophasic, with more severe symptoms during a single episode of demyelination. Our patient has not developed additional focal neurological deficits or new lesions outside of the previously operated area.
The hallmark MRI findings are the “onion bulb” or “bullseye” appearance, most clearly seen on pre-contrast T1- and T2-weighted images. Similar to other demyelinating disease, contrast enhancement usually appears as an incomplete open ring. DWI might show diffusion restriction during the episode of active demyelination (representing in most part intramyelinic edema).
This case serves as a reminder thta, when faced with a complex diagnosis, it‘s important to pause,reflext and ask key questions.
Asking the right questions at the right time might help you to narrow the list of your differential diagnoses and rule out other possibilities.
In our case, if the possibility of tumefactive demyelination had been considered based on the pre-operative imaging, the extensive surgery could have been avoided.
The three most common tumor or tumor-like lesions of the corpus callosum are glioblastoma, primary CNS lymphoma and demyelinating disorders. Corpus callosum is composed of dense white matter tracts, that make it hard for hematogenous metastases to deposit in that area, so they are rarely seen in this region and not on the top of your differentials. The abundance of white matter tracts probably explains, however, why predominantly white matter diseases affect this region – namely glioblastoma and demyelinating diseases. CNS lymphoma has a predilection for periventricular regions, corpus callosum being one of those regions.
Enhancement can help in differentiating the three entities, with classically glioblastoma having irregular ring enhancement or heterogeneous enhancement, lymphoma having homogenous enhancement and demyelinating diseases having the open ring enhancement.
Knowing the epidemiology can also be helpful. Glioblastoma and CNS lymphoma are seen in slightly older/older patients (>40 years), with a slight male predominance. Tumefactive demyelinating lesions have, similar to other demyelinating disorders, a younger age of onset (<40 years) with a female predominance. Our patient was a female in her late teens.

Reference:

Neuroradiology #39

September 3, 2025September 25, 2025 ~ EDiR Holders ~ 3 Comments

Clinical Data

40-year-old female presents with:

Fever
Progressive headache
Confusion in the last two days
Previous medical history was unremarkable
CT brain without contrast was performed in the emergency department

CT images:

What are the most important findings on CT?

Subtle hypodensity in the medial temporal lobe on the right side.
Sparing of the basal nuclei on the right side.

What are your next steps?

Immediately call the ordering physician to communicate that the imaging (and clinical) findings are suggestive of Herpes Simplex Encephalitis.
- This will prompt the clinician to directly start with an antiretroviral agent (acyclovir) if not started already and to perform a lumbar puncture to confirm HSV in CSF.

MRI was performed:

What are the findings on MRI?

T2 hyperintense regions with swelling/oedema and involvement of both white matter and cortex centered around the right sylvian fissure with involvement of the right temporal, frontal and insular region. Subtle patchy and leptomeningeal enhancement in the right temporal lobe can be seen.

What is the most likely diagnosis?

Herpes Simplex Encephalitis

The clinical picture is already highly suggestive of this diagnosis with supporting imaging findings. The diagnosis was confirmed with positive PCR for HSV-1 in CSF.
Typical imaging findings of herpes encephalitis are T2(/FLAIR) hyperintense swollen areas of cortex and white matter with bilateral but asymmetrical involvement of the fronto-temporo-insular regions. Characteristic is sparing of the lentiform nuclei, which distinguishes it from ischemia due to vessel occlusion. Diffusion restriction and hemorrhage can be present.
This is a radiological emergency and the phone must be picked up directly to alert the clinician and to prevent significant mortality and morbidity.

Reference:

Frazier. Herpes Simplex Encephalitis. RadioGraphicsVol. 37, No. 1
https://radiopaedia.org/articles/herpes-simplex-encephalitis?lang=us

Neuroradiology #38

June 18, 2025June 25, 2025 ~ EDiR Holders ~ 2 Comments

Clinical Data

35-year-old male presents with:

Progressive headache and ataxia
Previous medical history was unremarkable
MRI brain was performed

What do you see?

Cystic lesion with an enhancing lesion in the posterior fossa on the left side. No enhancement of the cystic wall. Discrete flow voids in the solid nodule.
Relevant mass effect with compression on the 4th ventricle and obstructing supratentorial hydrocephalus.

What is your differential diagnosis?

The differential diagnosis of a cyst with an enhancing mural nodule in the posterior fossa includes hemangioblastoma, pilocytic astrocytoma, ganglioglioma and cystic metastasis.

What are the most likely diagnoses?

When a cystic lesion with a mural nodule is encountered in the posterior fossa, the most likely diagnosis is hemangioblastoma in an adult in the absence of a primary tumor elsewhere. The imaging findings support hemangioblastoma, since the mural nodule shows flow voids on T2 and no enhancing cystic wall. Typically, the cystic wall of hemangioblastoma does not enhance, while a subtle enhancing wall can be discerned in pilocytic astrocytomas.
The majority of hemangioblastomas occur spontaneously. In case of multiple hemangioblastomas, think about Von Hippel-Lindau syndrome.

Reference:

Raz et al. Cyst with a mural nodule tumor of the brain. Cancer Imaging. 2012 Aug 10;12(1):237–244. doi: 10.1102/1470-7330.2012.0028

Neuroradiology #37

May 31, 2023December 2, 2022 ~ EDiR Holders ~ 1 Comment

Clinical Data

40-year-old female presents with acute severe headache at the emergency department.
The neurologist wants to rule out an intracranial haemorrhage and orders a CT brain.

Showing images CT without contrast

More images: MRI

What do you see?

CT shows
* low attenuating suprasellar lesion (fat density) with rim calcification.
* multiple scattered smaller similar subarachnoid lesions supra and infratentorial.
* enlarged supratentorial ventricles.

MRI shows
* the suprasellar lesion shows T1 heterogenous and T2-hyperintense signal,
* multiple scattered T1-hyperintense foci subarachnoid and intraventricular in the left frontal horn (arrows).
* no enhancement.
* no diffusion restriction (not shown).

What is the most likely diagnosis?

Ruptured suprasellar dermoid cyst.

Ruptured intracranial dermoid cyst

Intracranial dermoid cysts are often incidental findings and most do not cause symptoms. Both dermoid and epidermoid cysts are ectodermal in origin and lined by stratified squamous epithelium. In addition, dermoid cysts contain epidermal appendages such as sebaceous glands which secrete sebum, an oily substance.

Symptoms occur due to mass effect or rupture. In case of rupture, dermoid material (sebum droplets) can leak into the subarachnoid space which can lead to chemical meningitis and cause symptoms such as headaches, seizures, and vasospasms.
CT shows
-hypoattenuating primary lesion (fat density due to sebum).
-typically, not exclusively, in midline location.
-sometimes rim calcification of the primary lesion.
-smaller similar hypoattenuating lesions in the subarachnoid space in case of rupture.

MRI shows
-generally T1-hyperintense signal (sebum).
-scattered T1-hyperintense droplets in the subarachnoid space and intraventricular. Fat-fluid level within the ventricles.
-variable T2 signal.
-generally no enhancement of the lesion. Leptomeningeal enhancement in case of chemical meningitis.

References

https://radiopaedia.org/articles/intracranial-dermoid-cyst-1

Neuroradiology #36

April 19, 2023December 2, 2022 ~ EDiR Holders ~ 1 Comment

Clinical Information

A young adult male presents with progressive limb numbness and gait disturbances. Medical history was unremarkable.
MRI brain was performed and showed no intracranial abnormalities.
The neurologist ordered an MRI scan of the cervical spinal cord.

Showing MRI images:

What do you see?

A long segment T2-hyperintense lesion in the posterior part of the cervical myelum, specifically in the dorsal columns (‘inverted V-sign’). There is no perilesional oedema, mass effect, or enhancement.

What is the differential diagnosis based on the MRI findings?

Subacute Combined Degeneration due to Vitamin B12 deficiency or inactivation
Intrathecal MTX-induced myelopathy
Vitamin E deficiency
Copper deficiency
Tabes dorsalis (neurosyphilis)
HIV vacuolar myelopathy

More information
The laboratory values of Vitamine B12 were normal, as well as Copper and Vitamin E values.
HIV and Syphilis screening were negative.

The patient finally confirmed recreational (ab)use of nitrous oxide.

What is the most likely diagnosis?

Subacute Combined Degeneration due to nitrous oxide-induced Vitamin B12 inactivation.

Subacute Combined Degeneration

SCD is a neurological complication of vitamin B12 deficiency or inactivation. Several drugs can inactivate vitamin B12 such as metformin and nitrous oxide. Abuse of nitrous oxide inactivates vitamin B12 by oxidizing Cobalt-ion. In case of nitrous oxide abuse, vitamin B12 serum levels can appear normal.
Clinical symptoms include loss of vibration and proprioception in hands and feet and sensory gait ataxia. In severe cases, muscle weakness especially in the distal extremities can be seen.
MRI shows bilateral T2 high signal in the dorsal columns (inverted V sign) which explain the sensory deficits (paraesthesia, propriocepsis, and fine touch). In severe or untreated cases, the lateral columns may be involved leading to motor deficits such as limb weakness, spasticity, and paraplegia. The lesions typically involve a long segment in the cervical and higher thoracic spinal cord and show no enhancement or cord expansion.
It is crucial to promptly identify this disease and treat the vitamin B12 deficiency and/or discontinue the inactivating drug to prevent serious complications.

Neuroradiology #35

December 2, 2022April 5, 2023 ~ EDiR Holders ~ 1 Comment

What do you see in the following images?

Click here to see the answer

Polymicrogyria
Bilateral cortical thickening with numerous small gyri with signal characteristics similar to normal grey matter.
Dilated bilateral perivascular spaces in the subjacent white matter.