Brain Herniation - Axial CT or MR
Brain Herniation - Axial CT or MR
Search Pattern Assist ?Exam
Purpose
2. Recognize that subfalcine shift not only affects the mid and low convexity midline cerebrum, but also (if sufficient )the subfalcine shift pulls the mesencephalon in the same direction. Be aware that this can result in compression of the opposite side cerebral peduncle against the opposite side free tentorial free margin. When this happens the opposite side ambient & crural cisterns are effaced, the cerebral peduncle can be damaged, and the opposite side 3rd nerve can be compressed resulting in paradoxical localizing signs and symptoms.
3. Recognize the normal topographic relationships of mesial structures (both supratentorial, infratentorial), and those structures located within the tentorial hiatus. The tentorial hiatus refers to the actual space defined by the free margins of the tentoria. The incisura refers to the structures and cisterns within the free margins of the tentoria. The plane of the incisura is an estimate of the relative position of the free tentorial margins. By defining the plane of the incisura we are able to detect when structures adjacent to the plane of the incisura are shifted downward into the incisura from above the incisural plane (i.e. downward transtentorial herniation) or when infratentorial structures are shifted upward from below the plane of the incisura (i.e. upward transtentorial herniation). We can also determine what has happened to both the mesencephalon and the circummesencephalic cisterns dependent on the direction(s) of the transtentorial displacements.
4. Note that transtentorial herniations affect the incisural cisterns differently depending on direction. Downward transtentorial herniation involves mesial and/or downward displacement of predominantly ventral structures (uncus, parahippocampal gyrus, & lower 3rd ventricle); such herniation affects (effaces) mainly ventral CSF spaces namely the suprasellar cistern and the ventral circummesencephalic cisterns. Upward herniation involves upward displacement of predominantly the mesial subtentorial cerebellar parenchyma & the superior vermis not the incisura from below. Hence, it affects (effaces) mainly dorsal incisural cisterns, namely the quadrigeminal plate cistern, the vein of Galen cistern, & the superior cerebellar cisterns.
5. Recognize the normal topographic relationships of caudal posterior fossa structures (i.e. the caudal vermis, the caudal suboccipital cerebellum and the cerebellar tonsils to 1. the rigid bone the foramen magnum, 2. the cisterna magna and its upward extension (the vallecula which separates the cerebellar tonsils), and 3. the cervicomedullary cord. The plane of the foramen magnum defines the position of the osseous margins of the foramen magnum. Structures above the plane of the foramen magnum (mainly the cerebellar tonsils) are downwardly displaceable initially toward plane of the foramen magnum and then passed it into the upper cervical canal. Once passed the plane of the foramen magnum the displaced cerebellar tonsils can compress the cervicomedullary core and block the central canal producing hydromyelia. This process is referred to as "downward tonsillar herniation". There is no upward herniation in the foramen area.
6. Recognize the structures forming the suprasellar space and ventral circummesencephalic cisternal spaces (interpeduncular space, crural and ambient cisterns), and which structures are affected by uncal herniation and which by posterior parahippocampal gyrus herniation.
7. Recognize that nonlateralized, or global mass effects (usually HIE, viral encephalitis, cytokine storm, or acute toxic encephalopathy) can produce central herniation. Central herniation can be upward or downward or concurrent in which case there is no net shift, but the combination compresses the mesencephalon, which is seldom a survivable state if prolonged.
8. Recognize that intracranial hypotension typically exhibits both downward incisural herniation & downward tonsillar herniation concurrently. This distinguishes it from Chiari malformations, which have tonsillar herniation often compressing the cervicomedullary cord, possibly with hydromyelia, but no incisural displacement. Developmental tonsillar ectopia is common. It exhibits only minimally low tonsillar displacement (< 6mms shift) and no cervicomedullary cord compression.
9. Recognize the normal topographic relationships of the anterior temporal fossa, which is formed by the greater wing of the sphenoid. Structures include the anterior temporal pole, the anterior temporal cisterns, the basifrontal cortices and their sulci, the uncinate fasciculus (interconnecting the frontal and temporal lobes), the superior sylvian vein/sphenoparietal dural sinus, and the proximal M1 and M2 MCA arterial segments. Rostral shift of the anterior temporal lobe, or caudal shift of the ventral basifrontal lobe impact these parenchymal structures upon the relative sharp edge of the greater sphenoid wing. This state is referred to as "trans-sphenoidal herniation". Trans-sphenoidal shifts can be associated with both arterial and venous problems, but importantly, injury to the uncinate fasciculus can result in personality changes later.
10. Recognize that all brain herniations can have secondary arterial occlusive complications. Significant subfalcine shifts can result in ICA buckling (and possible occlusion) over the interclinoid ligament, or buckling/thrombosis of the ACA (mainly its' marginal or pericallosal branches) against the free margin of the falx. Incisural herniation can buckle (and/or occlude) the P4-PCA segment, as it crosses the tentorial free margin. And finally, PICA arteries can originate from the C1 level, and therefore, can potentially be compressed or occluded on the osseous foramen margins in the context of downward tonsillar herniation.
11. Recognize that mass lesion(s) located in the pineal region, or within the mesencephalon surrounding the cerebral aqueduct can compress or stenose the cerebral aqueduct. Since this obstruction may be gradual, the degree of dilatation of the lateral and 3rd ventricle can be subtle (initially). Later, if the early stages are not detected, the ventriculomegaly will become significant, ultimately producing global central downward transtentorial herniation.
12. Recognize the with enough subfalcine shift, the 3rd ventricle and/or the foramen of Monroe on the opposite side can be compressed resulting in bilateral or unilateral (opposite side) hydrocephalus; the ipsilateral lateral ventricle is usually compressed in this circumstance. Sequestered ventricles can create very unusual types of brain herniations.
13. Recognize that any significant compression of the mesencephalon can present as depressed level of consciousness. In addition, upon resolution of the mass effect, there can be reperfusion hemorrhage into the central mesencephalon (i.e. "Duret' hemorrhage").
14. There is measurable subfalcine (midline) herniation in the mid convexity the extent of which can be calculated by the interval distance the plane of the falx to the septum pellucidum.
15. There is evidence of actual displacement (bending) of the falcine dura indicating significant mass effect.
16. There is evidence of downward, transtentorial, uncal herniation related to anterior temporal mass effect.
17. There is evidence of downward, transtentorial, posterior parahippocampal gyrus herniation related to posterior temporal mass effect.
18. There is supratentorial global pressure effects (i.e. global cerebral swelling, hydrocephalus, or bilateral extraaxial mass effect) producing a central downward transtentorial (or incisural) herniation.
19. There is evidence of downward incisural displacement originating from mass effect in the pineal gland or splenium (corpus callosum).
20. There is evidence of focal anterior temporal fossa or latero-ventral frontal regional mass effect resulting in "trans-sphenoidal herniation". This can produce thrombosis of the superior sylvian vein complex.
21. There is evidence of unilateral (asymmetric) mass effect, or bilateral (central) mass effect producing upward transtentorial herniation.
22. There is evidence of 4th ventricular side to side displacement, or intraventricular, or periaqueductal lesion present which change the appearance of the 4th ventricle and cause hydrocephalus.
23. There is evidence of compressive effacement of the vallecular cistern and downward tonsillar herniation into the foramen magnum.
24. There is evidence of global brain swelling with both upward and downward transtentorial herniation plus downward tonsillar herniation.
25. There is evidence of focal arterial compression (ACA beneath falx, PCA over tent, ICA for interclinoid ligament, PICA over foramen magnum.
26. There is evidence of subfrontal contusion related midline shift over the crista galli.
27. There is a post compressive reperfusion hemorrhage (i.e." Duret hemorrhage") after transtentorial herniation.
28. There is compression of the 3rd ventricle, cerebral aqueduct or 4th ventricle with secondary internal hydrocephalus. Or, in the case or tonsillar herniation/ectopia, there is secondary hydromyelia.
29. There is evidence of subfrontal midline shift with lesions in the anterior basifrontal mesial cerebrum.
30. There is more mass effect with more midline shift than can be explained by the observed hematoma. This can occur with post traumatic dysautoregulation expanding the venocapillary pool, which adds regional mass effect without altering the parenchymal intensity.
31. There is evidence of midline shift of the 3rd ventricle related to unilateral mass effects usually arising primarily in the low convexity mesial cerebrum.
32. There is evidence of focal arterial compression (ACA beneath falx, PCA over tent, ICA for interclinoid ligament, PICA over foramen magnum.
33. There is evidence of focal anterior temporal fossa or latero-ventral frontal regional mass effect resulting in "trans-sphenoidal herniation". This can produce thrombosis of the superior sylvian vein complex, therefore correlate for perisylvian area edema.
34. There is evidence of downward incisural displacement originating from mass effect in the pineal gland or splenium (corpus callosum).
35. There is compression of the 3rd ventricle (or cerebral aqueduct) can result in internal hydrocephalus with significant dilatation of the lateral & 3rd ventricles producing downward transtentorial herniation.
36. There is evidence of upward transtentorial herniation producing upward shift of the superior vermis and subtentorial cerebellar cortex.
37. There is evidence of upward transtentorial herniation producing upward shift of the entire brain stem and rostral cerebellum
38. There is evidence of 4th ventricular side to side displacement, or intraventricular, or periaqueductal lesion present, which change the appearance (conformation) of the 4th ventricle or obliterate it altogether with resultant internal hydrocephalus.
39. There is evidence of compressive effacement of the vallecular cistern, downward tonsillar herniation into the foramen magnum.
40. There is evidence of intracranial hypotension with both downward incisural & downward tonsillar herniation.
41. There is evidence of unilateral (asymmetric) posterior fossa mass effect, or bilateral (central) mass effect producing upward transtentorial herniation.
42. There is evidence of lateralized displacement of the 4th ventricle and vallecula (vallecular extension of the cisterna magna). Note: the 4th ventricle and the vallecula are the best indicators of the midline in the posterior fossa.
43. There is evidence of downward tonsillar herniation into the foramen magnum.
44. There is evidence of intracranial hypotension with both downward incisural & downward tonsillar herniation.
45. There is a post compressive reperfusion hemorrhage (i.e." Duret hemorrhage") after transtentorial herniation.
Findings
Axial head CT or MR
There is evidence of one or more focal or regional supratentorial, intraaxial, masses (tumor, bleed, abscess, asymmetric vent size, etc.) producing or contributing to subfalcine shift (crossing the plane of the falx cerebri), and/or lateralized downward uncal and/or parahippocampal brain herniation (crossing the plane of the incisura from above), and/or an ipsilateral trans-sphenoidal herniation. [Yes/No]
There is evidence of one or more focal or regional supratentorial, extraaxial, masses (dural-based tumor, bleed, empyema, etc.) producing or contributing to a lateralized subfalcine shift (crossing the plane of the falx cerebri from one side to the other), and/or lateralized downward incisural herniation (crossing the plane of the incisura from one side), and/or an ipsilateral trans-sphenoidal herniation. [Yes/No]
There is evidence of bilateral, symmetric, counter-balancing mass effects (intraaxial, ventricular, extraaxial or admixture) producing little or no midline shift but causing centralized, downward, incisural herniation. Common lesions include hydrocephalus (dilated bilateral lateral vent and/or 3rd ventricular enlargement), and/or bilateral intraaxial (usually global edema), or concurrent, extraaxial, similar-sized, lesions (usually bilateral subdurals), or enough subfalcine herniation from unilateral mass obstructing the contralateral foramen of Monroe causing contralateral (counter-balancing) hydrocephalus. [Yes/No]
There is of transcranial brain herniation through diastatic fractures or craniotomy defects. [Yes/No]
There is evidence of mesial and/or downward, transtentorial, uncal herniation related to mid temporal mass effect. [Yes/No]
There is evidence of downward, transtentorial, posterior parahippocampal gyrus herniation related to posterior temporal mass effect. [Yes/No]
There is evidence of focal anterior temporal fossa or latero-ventral frontal regional mass effect resulting in trans-sphenoidal herniation. [Yes/No]
There is evidence of downward incisural displacement originating from mass effect in the caudal 3rd ventricle, or pineal gland or splenium (corpus callosum). [Yes/No]
There is evidence of one or more focal or regional infratentorial, intraaxial, masses (tumor, bleed, abscess) producing enough mass effect to shift midline structures and to result in an asymmetric (lateralized) upward transtentorial herniation and/or unilateral cerebellar tonsillar herniation. [Yes/No]
There is evidence of one or more focal or regional infratentorial, extraaxial, masses (tumor, bleed, abscess) producing enough mass effect to shift midline structures and to result in an asymmetric (lateralized) upward transtentorial herniation and/or unilateral cerebellar tonsillar herniation. [Yes/No]
There is evidence of bilateral intra of extraaxial posterior fossa mass effect(s) to produce symmetric downward cerebellar tonsillar displacement approaching or crossing the plane of the foramen magnum, and/or central upward transtentorial herniation, and compressing but not shifting midline structures (i.e. the 4th ventricle and vallecula). [Yes/No]
There is unexplained symmetric or lateralized cerebellar tonsillar ectopia into the cisterna magna, or less than 6mms below the plane of the foramen magnum without effacement of cisterns and without downward incisural herniation. This likely reflects developmental variation and not tonsillar herniation. [Yes/No]
There is unexplained symmetric or lateralized cerebellar tonsillar downward displacement into the cisterna magna, greater than 6mms below the plane of the foramen magnum usually with effacement of cisterns and possible hydromyelia, but without any concurrent downward incisural herniation. This likely reflects developmental Chiari malformation. [Yes/No]
There is evidence of concurrent downward central transtentorial and bilateral downward tonsillar herniation without evidence of any apparent cause other than intracranial hypotension with acquired Chiari-like tonsillar features. [Yes/No]
Does the overall mass effect(s) match the degree and direction of the herniation or not? [Yes/No]
No other concurrent significant abnormality is present. [Yes/No]
