Neuroimaging Flashcards
Ventricular Anatomy

Cerobrospinal Fluid (CSF) (Ventricular Anatomy)
The ventricular system consists of two lateral ventricles and midline third and fourth ventricles.
The foramen of Monro connects the lateral ventricles with the third ventricle.
The cerebral aqueduct (of Sylvius) connects the third ventricle with the fourth ventricle.
The fourth ventricle continues inferiorly as the central canal of the spinal cord. The fourth ventricle also drains into the subarachnoid space and basal cisterns via three foramina:
Paired foramina of Luschka (Luschka is lateral).
Single foramen of Magendie (Magendie is medial).
CSF Dynamics
Cerebrospinal fluid is produced by the choroid plexus, which is located in specific locations throughout the ventricular system: Body and temporal horn of each lateral ventricle. Roof of the third ventricle. Roof of the fourth ventricle. There is NO choroid plexus in the cerebral aqueduct or occipital or frontal horns of the lateral ventricles.
The ventricular volume is approximately 25 mL. The volume of the subarachnoid space is approximately 125 mL, for a total CSF volume of approximately 150 mL.
CSF production is 500 mL/day, which completely replenishes the total CSF volume 3-4 times per day.
CSF is absorbed primarily by the arachnoid granulations (leptomeningeal evaginations extending into the dural venous sinuses) and to a lesser extent by the lymphatic system and cerebral veins.
Cerebral Edema
Edema within the brain can be caused by cell death, altered capillary permeability, or hemodynamic forces.
Cytotoxic Edema
Cytotoxic edema is cell swelling caused by damaged molecular sodium-potassium ATPase ion pumps. It can affect both gray and white matter.
Cytotoxic edema is caused by cell death, mot commonly due to infarct. Water ions trapped inside swollen cells feature reduced diffusivity.
Vasogenic Edema
Vasogenic edema is interstitial edema caused by increased capillary permeability. It is seen primarily in the white matter, as there is more interstitial space.
Vasogenic edema is caused most commonly by neoplasm, infection, or infarct.
Interstitial Edema
Interstitial edema is caused by imbalances in CSF flow, most commonly due to obstructive hydrocephalus.
Interstitial edema presents on imaging as periventricular fluid, often called “transependymal flow of CSF”, even though it is unlikely that the CSF actually flows across the ependymal cells lining the ventricles.
Herniation
The total volume in the skull is fixed. Increases in intracranial pressure may lead to herniation across a dural fold.
Herniation may be due to a mass lesion (such as a neoplasm or hematoma) or may be due to edema secondary to a large stroke. Because the volume of the posterior fossa is especially limited, cerebellar infarcts are prone to herniation.

Subfalcine Herniation
Subfalcine herniation is seen when the cingulate gyrus slides underneath the falx.
Subfalcine herniation may rarely cause compression of the anterior cerebral artery (ACA) against the falx, resulting in infarction.
Contralateral hydrocephalus may result from foramen of Monro obstruction, resulting in ventricular entrapment.
Transtentorial (uncal) herniation
Downward transtentorial herniation results in inferomedial displacement of the medial temporal lobe (uncus) through the tentorial notch, causing compression on the brainstem and adjacent structures.
The ipsilateral cranial nerve III (oculomotor nerve) may be compressed, leading to pupillary dilation and CN III palsy (eye is “down and out”).
Compression of the ipsilateral posterior cerebral artery (PCA) may cause medial temporal/occipital infarct.
Upper brainstem Duret hemorrhages are caused by shearing of perforating vessls due to downward force on the brainstem.
Compression of the contralateral cerebral peduncle against Kernohan’s notch causes a hemiparesis ipsilateral to the herniated side.
Upward transtentorial herniation is superior transtentorial herniation of the cerebellar vermis due to posterior fossa mass effect. The main complication of upward transtentorial herniation is obstructive hydrocephalus from aqueductual compression.
Cerebellar tonsillar herniation
Downward displacement of the cerebellar tonsils through foramen magnum causes compression of the medulla.
Compression of medullary respiratory centers is often fatal.
Hydrocephalus
Communicating hydrocephalus is ventricular enlargement without an obstructing lesion.
Subarachnoid hemorrhage can cause communicating hydrocephalus by impeding arachnoid granulation reabsorption of CSF.
Normal pressure hydrocephalus (NPH) is a form of communicating hydrocephalus characterized by normal mean CSF pressure and the clinical triad of dementia, ataxia, and incontinence. NPH is an important diagnosis as it is a treatable and potentially reversible cause of dementia. Imaging typically shows enlargement of the lateral and third ventricles.
Noncommunicating hydrocephalus is hydrocephalus due to an obstructing lesion, such as a thrid ventricular colloid cyst or a posterior fossa mass obstructing the fourth ventricle.
Intra-axial and extra-axial compartments
An intra-axial lesion is within the brain parenchyma itself, underneath the pial membrane.
An extra-axial lesion is external to the pial membrane. The meninges and subarachnoid space are extra-axial.
Basal cisterns
The basal cisterns, also known as the perimesencephalic cisterns, are CSF–filled spaces surrouding the midbrain and pons.
Compression or effacement of the basal cisterns may be a sign of the impending or actual herniation.
MRI in Neuroradiology
As discussed in the physics section, inherent tissue T1 and T2 characteristics depend on the longitudinal recovery/relaxation (T1) and transverse relaxation (T2) times of the protons in that tissue. Any tissue signal abnormality is produced by alterations (prolongation or shortening) of the transverse or longitudinal relaxation.
T1 shortening is hyperintense (bright) on T1-weighted images and T1 prolongation is hypointense (dark). Conversely, T2 shortening is hypointense on T2-weighted images and T2 prolongation is hyperintense.
It is technically incorrect to refer to image signal abnormality as “T2 hypo/hyperintense” or “T1 hypo/hyperintense” as it is the MRI image that may exhibit signal abnormalities, rather than the proton relaxation times. Correct terminology would include, “a esion is hyperintense on T2-weighted images” or “a lesion demonstrates T2 prolongation.”
Conventional spin-echo T1
Most brain lesions are hypointense on T1-weighted images due to pathologic prolongation of the longitudinal recovery. The presence of hyperintensity on T1-weighted images (caused by T1 shortening) can be an important clue leading to a specific diagnosis.
Causes of T1 shortening (hyperintensity) include:
Most commonly: Gadolinium, fat, and proteinaceous substance.
Some paramagnetic stages of blood (both intra- and extracellular methemoglobin).
Melanin.
Mineralization (copper, iron, manganese).
Slowly-flowing blood.
Calcium (rarely; when dispersed, not in bone). It is much more common for calcium to be hypointense.
Conventional spin-echo T2
Most brain lesions are hyperintense on T2-weighted images. Water has a very long T2 relaxation constant (water is very “bright” on T2-weighted images). Edema is a hallmark of many pathologic processes and causes T2 prolongation.
Since most pathologic lesions are hyperintense on T2-weighted images, the clue to a specific diagnosis may be obtained when a lesion is hypointense.
Causes of hypointensity on T2-weighted images include:
Most paramagnetic stages of blood (exceput hyperacute blood and extracellular methemoglobin).
Calcification
Fibrous lesion.
Highly cellular tumors with a high nucleus; cytoplasm ratio producing low lesional water content (for instance, lymphoma and medulloblastoma).
Vascular flow-void.
Mucin. Desiccated mucin, as seen in desiccated sinus secretions, is hypointense on T2-weighted images. Conversely, mucinous lesions in the pelvis tend to be hydrated and thus hyperintense.
Fluid attenuation inversion recovery (FLAIR)
The FLAIR sequence is the workhorse of neuroradiology. FLAIR is a T2-weighted image with suppresion of water signal based on water’s T1 characteristics.
A normal FLAIR image may appear similar to a T1-weighted image since the CSF is dark on both. However, the signal intensities of the gray and white matter are different.
T1: Normal white matter is brighter than gray matter because the fatty myelinated white matter has a shorter T1 time.
FLAIR: White matter is darker than gray matter.
Conventional spin-echo proton density (PD)
Proton denisty (PD) images are not used in many neuroradiology MRI protocols, but they do have the highest signal to noise ratio of any MRI sequence.
PD sequences are useful in the evaluation of multiple sclerosis (MS), especially for visualization of demyelinating plaques in the posterior fossa.
Diffusion weighted images and apparent diffusion coefficient (DWI and ADC)
Diffusion MRI is based on the principal that the Brownian motion of water protons can be imaged. Signal is lost with increasing Brownian motion. Free water (CSF) experiences the most signal attenuation, while many pathologic processes (primarily ischemia) cause reduced diffusivity and less signal loss.
Diffusion MRI consists of two separate sequences - DWI (diffusion weighted imaging) and ADC (apparent diffusion coefficient), which are interpreted together to evaluate the diffusion characteristics of tissue.
Diffusion imaging has revolutionized evaluation of cerebral infarct and is approximately 95% sensitive and specific for infarct within minutes of symptom onset. In the setting of stroke imaging, diffusion restricted tissue represents infarction.
DWI is an inherently T2-weighted sequence (obtained with an echo-planar technique). On DWI, reduced diffusivity will be hyperintense (less Brownian motion -> less loss of signal) and lesions are very conspicuous.
The ADC map shows pure diffusion information without any T2 weighting. In contrast to DWI, reduced diffusivity is hypointnese on the ADC map. Because studies have shown that readers are less sensitive to detecting reduced diffusivity using the ADC map alone, DWI is the primary sequence used to detect diffusion abnormalities.
An important pitfall to be aware of is the phenomenon of T2 shine through. Because DWI images are T2-weighted, lesions that are inherently hyperintense on T2-weighted images may also be hyperintense on DWI even without restricted diffusion. This phenomenon is call T2 shine through. Correlation with the ADC map for a corresponding dark spot is essential before cocnluding that diffusion is restricted.
In the brain, diffusion images are obtained in three orthogonal gradient planes to account for the inherent anisotropy of large white matter tracts. Anisotropy is the tendency of water molecules to diffuse dircetionally along white matter tracts.
The b-value is an important concept that affects the sensitivity for detecting diffusion abnormalities. The higher the b-value, the more contrast the image will provide for detecting reduced diffusivity. The downside to increasing the b-value is a decrease in the signal to noise ratio, unless scan time is proportionally increased for additional acquisitions. The previously described ADC map is calculated from a set of at least two different b-value images.
Although diffusion MRI is most commonly used to evaluate for infarct, the differential diagnosis for reduced diffusion includes: Acute stroke, Bacterial abscess, Cellular tumors (lymphoma and medulloblastoma), Epidermoid cyst, Herpes encepalitis, Creutzfeldt-Jakob disease.
Gradient recal echo
Gradient recall echo (GRE) captures the T2* signal. Because the 180-degree rephasing pulse is omitted, GRE images are susceptible to signal loss from magnetic field inhomogeneities.
Hemosiderin and calcium produce inhomogeneities in the magnetic field, which creates blooming artifacts on GRE and makes even small lesions conspicous.
The differential diagnosis of multiple dark spots on GRE includes:
Hypertensive microbleeds (dark spots are primarily in the basal ganglia, thalami, cerebellum, and pons)
Cerebral amyloid angiopathy (dark spots are in the subcortical white matter, most commonly the parietal and occipital lobes).
Familial cerebral cavernous malformations (an inherited form of multiple carvernous malformations).
Axonal shear injury.
Multiple hemorrhagic metastases.
Magnetic resonance spectroscopy
MR spectroscopy describes the chemical composition of a brain region. In some circumstances, spectroscopy may help distinguish between glioblastoma and metastasis. (Glioblastoma is an infiltrative tumor that features a gradual transition from abnormal to normal spectroscopy. In contrast, a metastasis would be expected to have a more abrupt transition.)
The ratioes of specific compounds may be altered in various disease states. N-acetylaspartate (NAA) is a normal marker of neuronal viability that decreases in most abnormalities. In tumors, NAA decreases and choline increases, although this pattern is nonspecific. Creatine provides information about cellular energy stores. The peaks of the three principle compounds analyzed occur in alphabetical order: Choline (cho), creatine (cr), and NAA. (Canavan disease is a dysmyelinating disorder known for being one of the few disorder with elevated NAA.)
A lactate “doublet” may be seen in high-grade tumors indicating anaerobic metabolism.
“Hunter’s angle” is a quick way to see if a spectrum is close to normal. A line connecting the tallest peaks should point up like a plane taking off.
Blood Brain Barrier (BBB) and enhancement
Micro or macro disruption of the blood brain barrier (BBB) produces parenchymal enhancement after contrast administration, which may be secondary to infection, inflammation, neoplasm, trauma, and vascular etiologies.
The BBB is formed by astrocytic foot processes of brain capillary endothelial cells and prevents direct communication between the systemic capillaries and the protected extracellular fluid of the brain.
Several CNS regions do not have a blood brain barrier, and therefore normally enhance: Choroid plexus, Pituitary and pineal glands, Tuber cinereum (controls circadian rhythm, located in the inferior hypothalamus). Area postrema (controls vomiting, located at inferior aspect of 4th ventricle).
The dura also lacks a blood brain barrier, but does not normally enhance. This phenomenon is subsequently explened in the section on pachymeningeal (dural) enhancement.
Vascular enhancement is due to a localized increase in blood flow, which may be secondary to vasodilation, hyperemia, neovascularity, or arteriovenous shunting. On CT, the arterial phase of contrast injection (for instance a CT angiogram) mostly shows intravascular enhancement. Parenchymal enhancement, including the dural folds of the falx and tentorium, is best seen several minutes after the initial contrast bolus.
On MRI, routine contrast-enhanced sequences are obtained in the parenchymal phase, several minutes after injection. Most intracranial vascular MRI imaging is performed with a noncontrast time of flight technique.
Intracranial enhancementmay be intra- or extra-axial. Extra-axial structures that may enhance in pathologic conditions include the dura (pachymeninges) and arachnoid (leptomeninges).
Perfusion
Perfusion MR is an advanced technique where the brain is imaged repeatedly as a bolus of gadolinium contrast is injected. The principle of perfusion MR is based on the theory that gadolinium causes a magnetic field disturbance, which (counterintuitively) transiently decreases the image intensity. Perfusion images are echo-planar T2* images, which can be acquired very quickly.
Perfusion MR may be used for evaluation of stroke and tumors.























