Brain sag, AKA intracranial hypotension
- postural headache is the most common presenting symptom – displacement of pain-sensitive dural structures, or caused by subdural collections
- changes in mental status (drowsiness, decreased GCS)
- cranial nerve deficits – result from nerve traction
- VI nerve palsy, transient visual obscurations, binasal visual field deficits – result from nerve traction
- roaring tinnitus – result from pressure gradients across cochlear aqueduct leading from the subarachnoid space to the perilyphatic system of the inner ear
- anisocoria, hyperacusis, vertigo, nausea
- decerebrate posturing
- epidural hematoma / spontaneous subdural hematoma or hygromas
- diffuse meningeal enhancement
- descent of the brain, optic chiasm and brainstem
- downward migration of splenium
- brainstem infarction
- elongated or oval-shaped pons or midbrain
- effaced cisterns
- narrowing of interpeduncular and prepontine cisterns
- more vertical direction of the anterior wall of the 4th
- Arnold-Chiari malformation
- low-lying cerebellar tonsils
- enlarged dural sinuses
- enlargement of the pituitary gland
Dural enhancement is due to decreased CSF volume resulting in expansion of the intracranial venous volume. Dura is engorged, enabling contrast to readily diffuse through the dura because its endothelial cells are outside the blood-brain barrier and lack tight junctions.
Mnemonic: SEEPS = (s)ubdural fluid collections, pachymeningial (e)nhancement, (e)ngorgement of venous structures, (p)ituitary hyperemia and (s)agging of the brain
SPOT THE DIFFERENCE:
Above images: Image (a) is a T1 MRI of a patient with brain sag and image (B) is a normal brain MRI for comparison. The labelled numbers correspond to: 1.) oval-shaped pons, 2.) downward migrating splenium, 3.) vertical shaped anterior wall of IV ventricle, and 4.) narrowing of the interpeduncular and prepontine cisterns.
Diagnostic Criteria (Komotar, 2005 & 2006)
- clinical signs fo transtentorial herniation (decline in mental status, pupillary asymmetry or nonreactivity, flexor or extensor posturing
- head CT revealing effacement of basal cisterns with an oblong brainstem (“oblong” meant rostrocaudal dimension of brainstem > maximum bipeduncular dimensions)
- clinical improvement after clamping of lumbar drain or using Trendelenburg position at -15 to -30 degrees relative to the horizontal
*all 3 criteria must be fulfilled
- Trial of Trendelenburg
- CT / MRI
- isotopic cisternography of whole neuraxis
- MRI to search for a morphological spinal nerve root abnormality
- Basilar artery apex displaced inferiorly with respect to the posterior clinoid process – creates a noticeable kink in the basilar artery “cobra sign”
- Foreshortening or kinking of the intracranial vertebral artery
- PCAs are displaced medially and inferiorly
- *Reversal of angiographic features after resolution of brain sag
Below are cerebral angiograms of the vertebrobasilar artery system with anteroposterior views (left panels) and lateral views (right panels). A & B shows normal arterial anatomy at baseline. C and D are angiograms taken at the time of brain sag.
Not the following features in the above angiogram:
- curved arrow – descent of the PCAs (down and inward)
- arrowhead – descent of basilar tip
- small arrow – kinking of the basilar artery
- large arrow – kinking of the vertebral artery
The figure below (by Christa Wellman) illustrates how the blood vessels are displaced during brain sag (in black), in relation to the original configuration (in gray):
- divide maximal AP distance by the maximal bipeduncular distance of midbrain
- normal sag ratio ~0.9 (in brain sag ~1.18)
- a=maximal AP diameter (midbrain level)
- b=maximal bipeduncular diameter
- mild symptoms:
- conservative treatment (up to 2 weeks) may be the first step
- bed rest without head elevation; adequate hydration, analgesics
- epidural blood patch (large volume, autologous, lumbar)
- inject 20-30 mL of blood with head lowered 30° x 5 minutes then bed rest x several days (to allow movement of blood from lumbar space to cervical region)
- one article had better experience with higher volumes of blood injected (20-40 mL) in L3-L4 or L4-L5 spaces, supine x2 hours, no strenuous exercises x 3 weeks
- visualize epidural blood deposition by alternating injections of contrast material and blood, inject large amounts of blood (30ml up to 100ml)
- CT myelography immediately followed by targeted blood patch
- Possible complications:
- bowel and bladder dysfunction
- intracranial hypertension
- epidural fibrin patch
- inject 1 ml fibrin glue
- ascertain fibrin glue depositino around 1/2 of circumference of thecal sac
- if above measures fail:
- find source of CSF leak by ancillary studies
- detailed MRI of spine, must be reviewed by an experienced neuroradiologist
- isotope cisternography (find intracranial leak or identify focal collection of extradural CSF)
- myelography (may be done with lumbar intrathecal infusion of preservative-free saline infusion)
- exploratory surgery for persistent CSF leaks
- ligation of meningeal diverticulae (sealing likely ineffective) by suture or aneursym clips, sutural dural tears packing epidural space with gelfoam or fibrin glue
- nonsurgical treatments usually achieve cure in ~75% of cases
- saline intrathecal perfusion
- can temporarily restore CSF volume until leak repaired in patients requiring urgent treatment
Alaraj, Ali et al. “Angiographic Features Of “Brain Sag””. Journal of Neurosurgery 115.3 (2011): 586-591.
Berroir, S. et al. “Early Epidural Blood Patch In Spontaneous Intracranial Hypotension”. Neurology63.10 (2004): 1950-1951.
Kim, You-Sub et al. “Brain Stem Herniation Secondary To Cerebrospinal Fluid Drainage In Ruptured Aneurysm Surgery: A Case Report”. SpringerPlus 5.1 (2016): n. pag.
Komotar, Ricardo J. et al. “Herniation Secondary To Critical Postcraniotomy Cerebrospinal Fluid Hypovolemia”. Neurosurgery 57.2 (2005): 286-292.
Pleasure, S. J. et al. “Spontaneous Intracranial Hypotension Resulting In Stupor Caused By Diencephalic Compression”. Neurology 50.6 (1998): 1854-1857.
Wiesemann, Elke et al. “Spontaneous Intracranial Hypotension: Correlation Of Imaging Findings With Clinical Features”. European Neurology 56.4 (2006): 204-210.
Hedna, Vishnumurthy Shushrutha et al. “Intracranial Hypotension Masquerading As Nonconvulsive Status Epilepticus”. Journal of Neurosurgery 120.3 (2014): 624-627.