A known case of right frontal tuberculoma, on treatment, had seizures, went into status and had to be intubated. Later, patient was found to have bradycardia and non reacting pupils. A CT scan was done.

CT showed swollen brain, loss of gray white differentiation, compression of CSF spaces. And most strikingly, sulcal and cisternal hyperdensity. Looks like SAH!. But it is not. Look at the dural sinuses, they are hyperdense as well. This is a case of ‘pseudo SAH’ appearance due to stagnant flow in the arteries and veins.

A 38 years old female presented with increasing fatigue, weight gain, hyperpigmentation and increasing hairs since 9 months.

She had hypercortisolism.

MR brain showed a 12 mm sized adenoma on right side of anterior pituitary.

CT abdomen shows a large cystic pancreatic mass with specks of wall calcification.

PET (not shown) had shown a ‘Hot spot’ in duodenum.

Dexamethasone suppression test was inconclusive (suppressed with high dose, not suppressed with low dose).

She was hence taken up for inferior petrosal sinus(IPS) sampling.

Right ICA injection AP and Lateral views did not show filing of right IPS. In fact the cavernous sinus also is minimally seen.

Left ICA injection  AP and lateral views did show the left IPS.

Now there was a dilemma…

the adenoma was on the right side, and the right IPS was not seen….so what to do?

A vertebral artery injection was taken which did show both IPS. Sometimes the IPS drainage does get disconnected from the cerebral hemispheres and drains the posterior fossa via the petrosal vein.

A 5F catheter was navigated into the jugular vein and thence into the left IPS.

Venogram showed well the left IPS, left cavernous sinus. And as expected, a moderately forceful injection also filled the opposite cavernous sinus and with good reflux down the right IPS. What luck!

So we navigated another catheter (4F this time) into the right IPS and took samples as required.

three pairs of simultaneously drawn samples were sent to the laboratory along with a peripheral venous sample and a right femoral vein sample.

And as expected, ACTH values from right IPS were > 3 times of the left IPS.

The patient was sent for pituitary adenoma surgery.

A common understanding among physicians, radiologists, surgeons and interventionists is that contrast enhancing tumours on MRI are hyper vascularity as opposed to non enhancing or mildly enhancing ones.

This, however is only partially correct, enhancing tumours not necessarily being hyper vascular.

Visual assessment of contrast enhancement of tumours as seen on MRI depends on many things..

e.g..

1. Amount of contrast given
2. Delay between contrast injection and image acquisition
3. presence of abnormal ‘leaky’ intratumoral vessels
4. presence of contrast ‘pools’ in the tumour
5. presence on intratumoral AV shunts
6. type of sequence and various parameters utilised

etc.

A case below illustrates our facts;

This was a female patient with two episodes of epistaxis. Nasal examination found a left sided polyp.

An MRI was done and showed an enhancing tumour.

A biopsy was done which showed spindle cell tumour probably angioleiomyoma

Prior to surgery, the ENT surgeon asked for embolization, considering the MRI and the biopsy report.

However, angiogram showed only a mild vascularity, with very small feeders from left internal maxillary artery. Hence, embolizaation was abandoned; the patient was operated upon and near total tumour removal achieved with mild and easily controllable blood loss.

Fig 1: Coronal T1WI and fat sat axial T2WI show left nasal tumor, iso –hypointense on t1 and apparently hyperintense on the t2WI

Fig 2: Coronal fat sat post gad T1WI show enhancement of the tumour – apparently considered hyper vascular

Fig 3: Histopathology slides  (microscopy and IHC) and reports

Fig. 4: left ECA angiogram shows the mildly vascular tumor

Fig 6: coronal fat sat t2WI shows that the tumor is isointense to gray matter

Two important sequences are: t2Wi and DWI;

t2 hyperintensse images tend to have high vascularity and tumors with high difusivity also tend to have higher vascularity.

The lesion in our case was wrongly interpreted as hyperintense on t2Wi as only fat sat images were done…and no comparision with cortex was done probably.

DWI is a sequence most MRI centers still do not perform for PNS lesions, though it has shown its utility beyond doubt.

A 65 years old male patient had vision problems following head injury. Examination suggested a cortical type involvement and was confirmed on MRI as right PCA  territory infarct

Fig 1: CT head and MRI T2WI showing chronic right PCA territory infarct

Fig 2: Axial and Coronal CT orbit does not show any definite e/o fracture

The patient was managed on conservative lines.

After  a year he had sudden development of left orbital swelling and proptosis

Fig 3: Axial T2W MRI images showing left proptosis; note the prominent superior ophthalmic veins which prompted for a DSA

Fig 4: DSA showing direct type of RIGHT CCF. Prominent intercavernous venous channels connect to the ipsilateral cavernous sinus to the opposite side from which the LEFT ophthalmic veins fill retrogradely and produce the proptosis. Ipsilateral cavenous sinus also fills but to smaller extent. Also note the reflux into the deep venous system which makes this fistula a dangerous one.

Such findings are not uncommon although most patients will also have clinical manifestations on same side also.

What is rare is the fact that this patient came after a year with proptosis, probably a small aneurysm had developed and ruptured later on.

Case: A 48 years old female patient, previously healthy, presented with right hemiparesis which improved rapidly over two days with some residual weakness. She was found to have left perforator infarct on CT, and a doppler study showed absence of bilateral ICA flow.

Fig1: CECT (actually source image of CTA) showing left gangliocapsular infarct

CT Angiogram was done which confirmed bilateral ICA occlusion.

Fig 2: CTA; 3D color SSD images; AP and oblique views; both internal carotids are completely occluded – right one from origin while on the left side a small stump is seen, right vertebral artery is dominat, left vertebral artery is hypoplastic, entire brain in almost dependent upon a solitary vessel –right vertebral, patent circle of Willis saving the patient from any major catastrophe with supratentorial parenchyma being supplied via posterior and anterior communicating arteries.

Discussion:

Spontaneous ICA dissection is an uncommon but increasingly recognized entity, with the increased awareness among physicians and the advent of modern imaging technologies, especially USG (and doppler) which is fast, ubiquitous and cheap.

Cervicocephalic dissections may occur spontaneously or secondary trauma which may be major but many patients have only minor trauma, something like playing cricket, yogasana, hiccups etc, while many housewives don't exactly recollect even trivial injuries. In some patients, they are associated with an underlying arteriopathy like

• Fibromuscular dysplasia, vessel tortuosity , Marfan syndrome , Ehlers-Danlos syndrome, Alpha-1-antitrypsin deficiency, Cystic medial necrosis, Type 1 collagen point mutation, Other connective tissue disorders
• In many, no cause of spontaneous dissection is found.
• systemic infections, hypertension,  elevated homocysteine, alcohol, OCP have also been associated..

The cervical internal carotid artery is affected in 75% of patients (usually approximately 2 cm distal to the bifurcation) and the extracranial vertebral artery in 15%. The remaining cases usually involve the intracranial internal carotid artery, intracranial vertebral artery, middle cerebral artery, or basilar artery. Anterior cerebral arteries have been traditionally considered resistant, however modern imaging esp. DSA has found dissections in them too.

15% of cases are bilateral, and one half of these occur in patients with underlying fibromuscular dysplasia.

Age/Sex: Females> males, young- middle aged; cervicocephalic dissections are responsible for 1-2.5% of ischemic strokes in the general population and for 5-20% of strokes in individuals younger than 45 years.

Clinical features: commonest-focal unilateral headache; common- focal cerebral ischemic symptoms, oculosympathetic paresis, bruits, light-headedness, and neck pain; less common- syncope, amaurosis fugax, scalp tenderness, swelling in the neck, and dysgeusia

*Cephalic pain is frequent and often inaugural in carotid dissection; its recognition is important for early diagnosis and treatment, many also have painful Horner’s syndorme.

Cerebral ischemia occurs in at least 75% of reported cases (TIAs in 30%, infarcts in 45-50%).

Imaging: fat sat axial T1WI on MR very well show the dissected artery with hematoma and thrombus

Puppy sign in bilateral ICA dissection

 J Neurol Neurosurg Psychiatry2007;78:1055 doi:10.1136/jnnp.2007.115857

However, sometimes MRI, MRA and Doppler will miss the dissections, and DSA is still the best for diagnosing as well as planning treatment.

Further reading:

1. Mokri Bahram et al. Spontaneous dissection of the cervical internal carotid artery. Annals of Neurology. http://dx.doi.org/10.1002/ana.410190204
   
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3. Lucas C, Moulin T, Deplanque D, Tatu L, Chavot D. Stroke patterns of internal carotid artery dissection in 40 patients. Stroke 1998;29: 2646-8. [PubMed]
4. Bradley Scott Townend, Laura Traves, Denis Crimmins, Bilateral spontaneous carotid artery dissection, Journal of Clinical Neuroscience, Volume 12, Issue 5, June 2005, Pages 592-594, ISSN 0967-5868, DOI: 10.1016/j.jocn.2004.08.020. (http://www.sciencedirect.com/science/article/B6WHP-4G1PKN8-8/2/c30c4ff302aaca48e64cc69e26ee967e)