COVID-19 Acute Necrotizing Encephalopathy

Case report: COVID-19 associated acute necrotizine hemorrhagic encephalopathy – ANE – associated iwth other viral infections.  Female, late 50s, 3-day cough, fever, altered mental status.

Work-up NEG for influenza, nasopharyngeal swab (+) coronavirus, CSF limited – traumatic LP, CSF bacterial culture NG, HSV HSV 1 and 2, varicella, WNV NEG; unable to test CSF for SARSCoV-2.

CT head:   symmetric hypoattenuation within the bilateral medial thalami with a normal CT angiogram and CT venogram

MRI: hemorrhagic rim enhancing lesions within the bilateral thalami, medial temporal lobes, and subinsular regions

Acute necrotizing encephalopathy

  • rare complication of influenza / viral infections
  • related to intracranial cytokine storms –> BBB breakdown
  • no direct viral invasion or parainfecitous demyelination
  • reported mostly in pediatric population but occurs in adults as well

Imaging Features

  • symmetric, multifocal lesions with invariable thalamic involvement
  • Other commonly involved locations include the brain stem, cerebral white matter, and cerebellum
  • hypoattenuating on CT
  • MRI shows T2 FLAIR hyperintense signal with internal hemorrhage
  • Postcontrast images may demonstrate a ring of contrast enhancement

 

Capture

Image from noncontrast head CT demonstrates symmetric hypoattenuation within the bilateral medial thalami (arrows). B, Axial CT venogram demonstrates patency of the cerebral venous vasculature, including the internal cerebral veins (arrows). C, Coronal reformat of aCT angiogram demonstrates normal appearance of the basilar artery and proximal posterior cerebral arteries.

Capture2

MRI images demonstrate T2 FLAIR hyperintensity within the bilateral medial
temporal lobes and thalami (A, B, E, F) with evidence of hemorrhage indicated by hypointense signal intensity on susceptibility-weighted images (C, G) and rim enhancement on postcontrast
images (D, H).

 

Reference:

Poyiadji, N., Shahin, G., Noujaim, D., Stone, M., Patel, S., & Griffith, B. (2020). COVID-19–associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI Features. Radiology, 201187. doi: 10.1148/radiol.2020201187

Mt. Fuji Sign

The Mt. Fuji sign is a radiologic finding seen in tension pneumocephalus.  Bilateral hypoattenuating collections are seen in the frontal subdural space, which causes compression and separation of the frontal lobes.

 

1.jpg

2.jpg

Notice the widening of the interhemispheric space between the tips of the frontal lobes which resembles the silhouette of Mt. Fuji.  

 

In tension pneumocephalus, air enters into the cranial vault through disruption of the skull or skull base.  Air pressure increases within the subdural space due to a ball-valve mechanism, where air enters into subdural space but egress of air is blocked by an obstruction.

Tension pneumocephalus may occur after surgical evacuation of SDH (2.5-16%), skull base surgery, paranasal sinus surgery, posterior fossa surgery in sitting position, or head trauma.

To diagnose tension pneumocehpalus, CT findings should correlate with clinical signs of deterioration.

Peaking sign” (compression of frontal lobes without separation of frontal lobes) has also been linked to tension pneumocephalus.

Treatment includes:

  1. emergent decompression to alleviate pressure
    1. drilling burr holes
    2. craniotomy
    3. needle aspiration
    4. EVD placement
  2. administration of 100% oxygen
  3. closure of dural defects
  4. careful monitoring for clinical signs of deterioration
  5. serial CT scanning of brain

This is Mt. Fuji in Japan

3.jpg

 

Reference

Michel, Steven J. “The Mount Fuji Sign.” Radiology 232.2 (2004): 449-450.

 

Digital atlas of MCA territory infarction

The color refers to the frequency of infarction at each voxel. The highest frequency of infarct occurrence is in the centrum semiovale and striatocapsular and insular regions.

 

This slideshow requires JavaScript.

 

Reference:

Phan, T. G. et al. “A Digital Map Of Middle Cerebral Artery Infarcts Associated With Middle Cerebral Artery Trunk And Branch Occlusion”. Stroke 36.5 (2005): 986-991.

Hydrocephalus CT Findings

KEY FINDINGS of HCP on neuroimaging:

  • expansion of the temporal horns
  • convexity of the third ventricular walls
  • rounding of the frontal horns
  • effacement of sulci
  • enlargement of ventricles out of proportion to sulcal dilatation

 

Reference:

Dupont, Stefan and Alejandro A Rabinstein. “CT Evaluation Of Lateral Ventricular Dilatation After Subarachnoid Hemorrhage: Baseline Bicaudate Index Balues”. Neurological Research 35.2 (2013): 103-106.

Patterns of Contrast Enhancement in Brain CT/MRI

7 Patterns of Contrast Enhancement seen in CT / MRI of the Brain:

  • Dural-based enhancement (meningioma)
  • Dura-arachnoid enhancement / pachymeningeal enhancement.
  • Pia-arachnoid or subarachnoid enhancement (bacterial meningitis or carcinomatous meningitis)
  • Gyral gray matter enhancement
  • Ring lesions – A. smooth ring (abscess)  B.  irregular ring, shaggy inner margin (necrosis, high-grade neoplasm)
  • Fluid-secreting neoplasms and demyelination
    • cerebellar “cyst with nodule” (pilocytic astrocytoma)
    • classic “open-ring” sign (tumefactive demyelinating lesions)
    • fluid secreting “cyst with nodule”
  • Periventricular enhancement
    • thin linear rim of enhancement – ependymitis (CMV infection)
    • mass / thick irregular rind surrounding ventricle (periventricular lymphoma, primary B cell lymphoma)

 

Capture.JPG

 

 

 

  1.  Dura-arachnoid enhancement / pachymeningeal enhancement.

2. Dural-based enhancement   (typical for meningioma)

3. pia-arachnoid or subarachnoid enhancement (bacterial meningitis or carcinomatous meningitis)
4.  gyral gray matter enhancement
5.  ring lesions – A. smooth ring (abscess)  B.  irregular ring, shaggy inner margin (necrosis, high-grade neoplasm)
6.  Fluid-secreting neoplasms and demyelination
a. cerebellar “cyst with nodule” (pilocytic astrocytoma)
b. classic “open-ring” sign (tumefactive demyelinating lesions)
c.  fluid secreting “cyst with nodule”
7.  periventricular enhancement
a.  thin linear rim of enhancement – ependymitis (CMV infection)
b.  mass / thick irregular rind surrounding ventricle (periventricular lymphoma, primary B cell lymphoma)

 

 

<click here to access powerpoint file>

Reference:

Naidich, Thomas P et al. Imaging Of The Brain. Ch 5 Patterns of Contrast Enhancement.  1st ed. Print. pp. 79-95.

 

Bicaudate Index

Diagram showing the method for measuring the bicaudate index (A / B). A = the width of the frontal horns at the level of the caudate nuclei; B = the diameter of the brain at the same level.

 

Capture.PNG

 

 

The bicaudate index is a commonly used linear measure of the lateral ventricles. To account for the natural changes in the size of ventricles with aging, BCI is then divided by the upper limits of ‘normal’ for age to calculate the relative bicaudate index.

Diagnosis of hydrocephalus is established when RBCI is >1. Normative values determined from subjects without neurological disease, in the mid to late 1970s.

 

Divide the width of the frontal horns, at the level of the caudate nuclei, by the corresponding diameter of the brain. Perform measurement on the cut which included the Foramen of Monro.  If the foramen of Monroe is in between two cute, use mean value for of the two cuts.

 

Bicaudate index plotted against age. The density ellipsoid includes 95% of the data points.

Capture.JPG

 

Normal BCI values, stratified by age group, in a cohort of SAH patients without co-existing hydrocephalus.

Capture.JPG

 

References:

Gijn, Jan van et al. “Acute Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage”. Journal of Neurosurgery 63.3 (1985): 355-362.

Dupont, Stefan and Alejandro A Rabinstein. “CT Evaluation Of Lateral Ventricular Dilatation After Subarachnoid Hemorrhage: Baseline Bicaudate Index Balues”. Neurological Research 35.2 (2013): 103-106.

 

Collateral Circulation of the Brain

2 Sources of Collateral Circulation of the brain

  1. extracranial source
  2. intracranial route

 

EXTRACRANIAL:

F1.medium.gif

  • a=facial a. with ophthalmic a.
  • b= maxillary a. with ophthalmic a.
  • c = middle meningeal a.with ophthalmic a.
  • d=  middle meningeal with dural artery
  • e= occipital with dural artery through mastoid foramen
  • f=occipital with dural artery through parietal foramen

 

 

INTRACRANIAL:

ab.JPG

  • a=pcomm a.
  • b=ACA and MCA (leptomeningeal anastomoses)
  • c=PCA and SCA (leptomeningeal anastomoses)
  • d=tectal plexus (PCA and SCA)
  • e=anastomoses of distal cerebellar arteries
  • f=acomm a.

 

bd.JPG

  • a=pcomm a.
  • b=ACA and MCA (leptomeningeal anastomoses)
  • c=PCA and SCA (leptomeningeal anastomoses)
  • d=tectal plexus (PCA and SCA)
  • e=anastomoses of distal cerebellar arteries
  • f=acomm a.

 

 

*divided into primary or secondary collateral pathways

 

Primary collaterals = arterial segments of circle of Willis

  • Anterior COW
    • interhemispheric blood flow across Acomm
    • reversal of flow in proximal ACA
  • PComm supply either direction (ant / post)
  • Proximal PCA at posterior COW

 

Secondary collaterals = ophthalmic artery and leptomeningeal vessels

  • reversal of blood flow within ophthalmic artery
  • anastomoses between distal major cerebral arteries
    • between ACA and MCA
    • between MCA and PCA
    • between PCA and ACA
  • distal branches of cerebellar arteries (links vertebral and basilar segments)
  • leptomeningeal and dural arteriolar anastomoses with cortical vessels

 

Other collaterals less commonly encountered:

  • tectal plexus (supratentorial branches of PCA with infratent branches of SCA)
  • orbital plexus (ophthalmic artery with facial, middle meningeal, maxillary and ethmoidal arteries)
  • rete mirabile caroticum (ICA and ECA)

 

 

F3.large.jpg

  • a=pterygoid plexus
  • b=deep middle cerebral vein
  • c=inferior petrosal sinus and basilar plexus
  • d=superior petrosal sinus
  • e=anastomotic vein of Trolard
  • f=anastomotic vein of Labbé
  • g=condyloid emissary vein
  • h=mastoid emissary vein
  • i=parietal emissary vein
  • j=occipital emissary vein

 

 

Reference:

Liebeskind, D. S. “Collateral Circulation”. Stroke 34.9 (2003): 2279-2284. Web.