Transcript Case Presentation Neuroradiology Block

Case Presentation
Neuroradiology Block
A. Swartbooi
Diag Rad
UFS
Patient Information
16 yr old female patient
Day 4 post partum
Referred from Manapo Hospital
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Presented with persistant convulsions
Severe headache
N&V
Treated for Eclampsia
No response to RX
Admitted 12 June at Universitas Neurology for
further management
Clinical Presentation
Patient acutely ill
Vitals normal
JACCOL NAD
Disorientated
No Neck Stiffness
Left hemiplegia
CVS, RESP, GIT Exam – NAD
Lab Results
U&E
FBC
N
HB 12.2
Platelets 291
WCC N
HIV
(-)
Virology NAD (Herpes, Syphillis)
Imaging
Computed Tomography
Imaging
Computed Tomography
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Computed Tomography
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Computed Tomography
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Computed Tomography
Imaging
Computed Tomography
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Oedema (R) Temporoparietal lobe
No Haemorrhage
No Venous sinus Thrombosis
Patient basal cisternae
Lumbar Puncture done
– NAD
Imaging
Magnetic Resonance Imaging
Imaging
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Magnetic Resonance Imaging
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Magnetic Resonance Imaging
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Magnetic Resonance Imaging
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Magnetic Resonance Imaging
Imaging
MRI
– High Signal intensity right occipital lobe and right
temporal lobe
– No other cerebral parenchymal abnormalities
– No SSS Thrombosis
– Right transverse and Sigmoid sinuses normal
– Left tranverse and Sigmoid sinuses not visualized
– No secondary signs of thrombosis noted
– Lesion of low signal on T1 and of high signal intensity on
T2 and FLAIR sequences in the splenium of corpus
callosum
Discussion
Venous Sinus Thrombosis
– Causes
Diverse, with over 100 causes identified
Trauma
Tumors
Infections
Dehydration
Behcet disease
Coagulopathies related to systemic disease
Congenital coagulation disorders
Pregnancy
Post-partum period
Use of oral contraceptives
Cause unknown in 20-25 % of cases
Discussion
Venous Sinus Thrombosis
– CT Findings
Noncontrast CT scan, the classic finding is the delta sign, which is
observed as a dense triangle (from hyperdense thrombus) within
the superior sagittal sinus
On contrast-enhanced CT scan, the reverse delta sign (ie, empty
triangle sign) can be observed in the superior sagittal sinus from
enhancement of the dural leaves surrounding the comparatively
less dense thrombosed sinus.
The presence of both the delta and reverse delta signs increases
the likelihood of the diagnosis.
Axial non-contrast CT shows high density in the
right transverse sinus, consistent with acute
thrombus
Discussion
Venous Sinus Thrombosis
– CT Findings
infarctions in a nonarterial distribution in the white matter and/or
cortical white matter junction, often associated with hemorrhage,
should suggest the possible diagnosis of venous thrombosis
Bilateral cerebral involvement can occur, including the superior
cerebral white matter of the convexities from superior sagittal
sinus thrombosis, or the basal ganglia and thalami from internal
cerebral vein thrombosis in which the internal cerebral veins
appear hyperdense in the noncontrast scan
Discussion
Venous Sinus Thrombosis
– Indirect CT Findings
Focal cerebral cortical ischemia with gyral enhancement
Small ventricles compressed by cerebral edema
Intense tentorial enhancement
Occasionally the transcerebral medullary cortical veins can be
observed
Discussion
Venous Sinus Thrombosis
– CT Limitations
Characteristic CT scan appearances and signs strongly suggest
cerebral venous thrombosis, but CT scans are seldom conclusively
diagnostic
Because of the subtlety of the findings, the prospective diagnosis
of venous thrombosis may not be made unless a high index of
suspicion is maintained during interpretation of the CT study
A false-positive delta sign may occur in a trauma setting because
of an adjacent subdural hematoma
Discussion
Venous Sinus Thrombosis
– MRI Findings
In most patients, MRI brain scan with MRV is recommended to
establish the CT diagnosis
Parenchymal regions of T2-hyperintense signal abnormality in the
distribution of the draining sinus is often observed
Frequent parenchymal MRI finding is thalamic edema
Restricted diffusion may or may not be seen in cerebral venous
thrombosis
Dilated venous collaterals, such as transcortical medullary veins,
provide indirect evidence of venous thrombosis
Discussion
Venous Sinus Thrombosis
– MRI Findings
The diagnosis usually can be made without intravenous contrast,
although contrast enhancement can aid in confirming the diagnosis
A thrombus can be directly visualized within a vessel
Secondary venous infarctions and foci of hemorrhage can be seen
with gradient-echo images
Discussion
Venous Sinus Thrombosis
– MRI Limitations
Hypoplasia or severe attenuation of a transverse sinus, which are
normal anatomic variants, may simulate venous sinus thrombosis
In-plane flow-induced signal loss in 2D TOF MRV also can mimic
intravenous thrombus
Prominent arachnoid granulations may simulate thrombus
Discussion
– Hyperintense signal in the thrombosed superior sagittal
sinus
– MRV – TOF revealed absence of a signal in the superior sagittal sinus
Discussion
Venous Sinus Thrombosis
– Angiography Findings
Cerebral catheter arteriography and venography was used
before the advent of MRI to confirm the diagnosis
Classic findings
– Filling defects from thrombus within the venous sinus
– Occlusion of a draining sinus
Discussion
Venous Sinus Thrombosis
– Angiography Findings
Secondary indirect angiographic findings are as follows:
– Decreased focal venous circulation around a thrombosed
venous sinus
– Visualization of collateral circulation
– Narrowing of arteries in the involved region
– Prolonged contrast blush in the brain parenchyma
– Tortuous vessels in the capillary and venous phases
– Collateral flow in dilated anastomotic vessels
Discussion
– Large part of the superior
sagittal sinus and some
cortical veins do not fill
with contrast material
Discussion
Diagnosis
– No Venous Sinus Thrombosis
Absent / Hypoplastic Left Transverse Venous Sinus
– Posterior Reversible Encephalopathy Syndrome
Discussion
PRES
– Classically characterized as symmetric parietooccipital
edema but may occur in other distributions with varying
imaging appearances
– Usually reversible neurologic syndrome with a variety of
presenting symptoms ranging from headache, altered
mental status, seizures, and vision loss to loss of
consciousness
Discussion
PRES
– Causes
Hypertension
Eclampsia and preeclampsia
Immunosuppressive medications such as cyclosporine
Various antineoplastic agents
Severe hypercalcemia
Thrombocytopenic syndromes
Henoch-Schönlein purpura
Hemolytic uremic syndrome
Amyloid angiopathy
Systemic lupus erythematosus
Various causes of renal failure
Discussion
PRES
– Mechanism is not entirely understood but is thought to
be related to a hyperperfusion state, with blood–brain
barrier breakthrough, extravasation of fluid potentially
containing blood or macromolecules, and resulting
cortical or subcortical edema
– It has also been proposed that vasospasm may
precipitate the reversible edema, leading to cytotoxic
edema if left untreated
Discussion
PRES
– Typical imaging findings of PRES are most apparent as
hyperintensity on FLAIR images in the parietooccipital
and posterior frontal cortical and subcortical white
matter
– Less commonly, the brainstem, basal ganglia, and
cerebellum are involved
Discussion
PRES
– Blood pressure may even be normal in some cases of
PRES
Chemotherapy
Immunosuppressive therapy
Sepsis
– Insult from raised blood pressure could persist for days
after the onset of symptoms
– Radiologists should be aware that PRES may
occasionally present with minimal or no detectable
parietooccipital edema
Imaging
Incidental Finding
– Lesion in the Splenium of the Corpus Callosum
Imaging
Incidental Finding
– Lesion in the Splenium of the Corpus Callosum
Discussion
Corpus Callosum Lesions
– Often reversible changes due to:
Vasogenic edema following a seizure
Withdrawal of an antiepileptic drug
Reversible demyyelination due to Antiepileptic drug toxicity
Trauma
Infarct
High altitude cerebral oedema
Neoplasm
Adrenoleukodystrophy and other leukodystrophies
AIDS dementia complex
Marchiafava–Bignami disease
Childhood-onset anorexia nervosa
Multiple sclerosis
– Non-specefic end point of different disease processes
leading to vasogenic oedema
Patient Outcome
Clinical dx – Transverse sinus Thrombosis
Treated as follows:
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Therapeutic LP
Diamox
Tramal and Dolorol
Epilim
Clexane
Warfarin
Recovered remarkably regaining full power and
higher functions
Discharged 23 July
– Stable condition
– No Neurological deficit
References
Intracranial MR Venography in Children: Normal
Anatomy and Variations; AJNR 2004 25: 1557-1562
Thrombosis of the Cerebral Veins and Sinuses;NEJM
352;17 2005
Posterior Reversible Encephalopathy Syndrome:
Incidence of Atypical Regions of Involvement and
Imaging Findings; AJR 2007; 189:904–912
Focal lesion in the splenium of the corpus callosum in
epileptic patients: Antiepileptic drug toxicity? AJNR
Neuroradiol. 1999;20:125–9