Brain Flashcards
Ventricular System and Hydrocephalus
The normal ventricular system consists of the:
- Third ventricle
- Intervertericular formane - connects the 3rd ventricle to the lateral ventricles
- Mesencephalic aqueduct - connect the 3rd ventrcle to the 4th ventricla
- Fourth ventricle
- Connects with the central canal
- Llateral ventricles
The third ventricle communicates with the lateral ventricles via the interventricular foramina, and the mesencephalic aqueduct connects the third and fourth ventricles. Caudally, the fourth ventricle communicates with the central canal.
Cerebrospinal fluid (CSF):
- Produced by the choroid plexus, located on the floor of the lateral ventricles and on the dorsal margins of the third and fourth ventricles.
- CSF circulates throughout the ventricular system and exits into the subarachnoid space through the lateral apertures of the fourth ventricle.
- CSF is resorbed primarily through arachnoid villi that extend into the dural venous sinuses and secondarily through lymphatic drainage of the meningeal sheaths surrounding nerve roots.
Hydrocephalus
Hydrocephalus is defined as an abnormal distension of all or part of the ventricular system with CSF. Ventricular distension is typically caused by constant or intermittent increased hydrostatic pressure. The term hydrocephalus denotes the anatomic status of the ventricular system rather than an underlying cause. Hydrocephalus can be developmental or acquired and can result from:
- Obstruction of CSF drainage
- Impaired CSF resorption
- CSF overproduction.
The latter two forms are referred to as communicating or nonobstructive hydrocephalus. Use of a related term, ventriculomegaly, may be more appropriate when passive ventricular enlargement occurs as a result of diminished brain parenchyma volume (also known as hydrocephalus ex vacuo). Normal CSF has a density near that of pure water and will therefore have a HU value of close to 0 on unenhanced CT images and will be hypoattenuating to surrounding brain parenchyma. On unenhanced MR images, normal CSF will appear T1 hypointense and T2 hyperintense to brain parenchyma and will have no or low signal on water‐nulling sequences, such as FLAIR. In patients with abnormal CSF due to hemorrhage, inflammation, or neoplasia, signal intensity may be significantly increased on T1 and pure water‐nulling sequences depending on cellular and macromolecular content.
Congenital hydrocephalus
- Congenital hydrocephalus occurs predominantly in brachycephalic and toy breeds.
- In some instances, mechanical obstruction from such entities as mesencephalic duct stenosis or Chiari malformation explains the presence of hydrocephalus; in other cases, no underlying cause is recognized.
Obstructive hydrocephalus
- Obstructive hydrocephalus may be due to intraluminal or extraluminal masses or other lesions that impair CSF flow within the ventricular system.
- The underlying causes of obstructive hydrocephalus vary widely, as do the imaging features of the ventricular system.
- Depending on the source and location of obstruction, hydrocephalus may be uniform or regional.
- Obstruction originating in or caudal to the fourth ventricle will tend to produce uniform ventricular distension, whereas obstruction in the third or lateral ventricles or in the interventricular foramina may produce asymmetrical, regional, or focal ventricular distension
Communicating (nonobstructive) hydrocephalus
Impaired CSF resorption
- Impaired CSF resorption is thought to occur with diminished resorptive capacity of the arachnoid villi.
- Postulated causes include intraventricular hemorrhage and ventriculitis with cells or debris causing obstruction of the valvular flow mechanism of individual villi.
- Chronic hydrocephalus also appears to diminish resorptive function of the villi.
Hydrocephalus from CSF overproduction
- Hydrocephalus from overproduction of CSF is thought to occasionally occur in some patients with functional choroid plexus tumors in which the abnormally high rate of CSF production exceeds the rate of resorption
Normal Ventricles (Canine)
7y FS French Bulldog.
- The normal T1 hypointense appearance of the third ventricle surrounding the interthalamic adhesion (a,b: arrows), the lateral ventricles (b: arrowheads), and the fourth ventricle (a: arrowhead).
- The mesencephalic duct is also seen as a thin, curvilinear, hypointense communication between the third and fourth ventricles (a).
- Normal cerebrospinal fluid appears hyperintense on T2 images (c) and profoundly hypointense on FLAIR images (d).
Ex vacuo Hydrocephalus (Canine)
akak “ventriculomegaly”
4y MC Maltese recovering from a penetrating head injury (dog bite) 6 months previously.
- Posttraumatic cortical atrophy of the left cerebral hemisphere results in passive expansion of the left lateral ventricle to fill the potential space.
- This dog also has evidence of more generalized ventriculomegaly.
- Discontinuity of the overlying parietal bone from previous fracture is evident on both the CT and MR images.
Hydrocephalus with Abnormal Cerebrospinal Fluid (Feline)
2y MC Domestic Shorthair with signs of a C1–C5 myelopathy.
- Bilateral lateral ventriculomegaly is seen on all MR sequences.
- Cerebrospinal fluid (CSF) is uniformly T2 hyperintense (a), but CSF in the right lateral ventricle is moderately intense compared to the low‐intensity signal within the left lateral ventricle on FLAIR (b) and T1 (c) images, indicating compartmentalization and cells or macromolecules contaminating the CSF in the right lateral ventricle.
- Thickening and intense enhancement of the right lateral ependymal lining is evident on the contrast‐enhanced T1 image (d).
A diagnosis of feline infectious peritonitis was based on cerebro- spinal fluid cytology and coronavirus titers.
Congenital Hydrocephalus (Canine)
4y MC English Bulldog with intermittent seizures.
- Marked generalized hydrocephalus is seen on all image sequences.
- Although enlargement of the lateral ventricles is most striking, third ventricular dilation is also evident, which is best appreciated on the sagittal T1 image (a: asterisk).
- Ventriculomegaly was thought to be breed related.
Obstructive Hydrocephalus (Feline)
7mo MC Domestic Shorthair with multifocal central nervous system signs.
- An obstructive mass was detected in the caudal brainstem and in the spinal cord at the level of C1 (a: arrowhead).
- Marked generalized ventriculomegaly is evident on all images, and distension of the fourth ventricle and mesencephalic duct is particularly prominent (a: arrows).
A diagnosis of feline infectious peritonitis was based on cerebrospinal fluid cytology and coronavirus titers.
Obstructive Hydrocephalus (Canine)
5y MC Labrador Retriever with hydrocephalus affecting the left lateral ventricle.
- A small contrast‐enhancing mass is present on the ventral margin of the left lateral ventricle (a,d: arrowhead).
- The left lateral ventricle is markedly distended, and there is a thin rim of hyperintensity, best seen on the FLAIR image (b: arrows), thought to represent transependymal interstitial edema.
A choroid plexus carcinoma involving the floor of the left lateral ventricle and causing partial foraminal obstruction was confirmed on postmortem examination.
Presumptive Overproduction Hydrocephalus (Canine)
6y FS Labrador Retriever with clinical signs of weakness and obtundation.
- A large, well‐defined mass is present within the third ventricle (a–d: arrow), and generalized hydrocephalus is present (a–d: arrowheads).
A solitary third ventricle choroid plexus carcinoma was confirmed on postmortem examination. There was no evidence of overt obstruction, which led to a presumptive diagnosis of overproduction hydrocephalus.
Brain Edema
Brain edema may result from a wide array of causes, which can be divided into the four principal forms listed in Table 2.2.1.1–3 Clinically, multiple forms of brain edema can occur simultaneously, and often the predominating form depends on the inciting cause as well as the time course of the disease.
Whether intracellular or extracellular, edema appears mildly to moderately hypoattenuating to normal brain parenchyma on CT images and T1 hypointense and T2 hyperintense on MR images. Because edema fluid is distributed within a microenvironment of cells and macromolecules, it will also appear hyperintense on FLAIR and other pure water‐nulling sequences.
Cytotoxic edema
- Cytotoxic edema occurs as a result of ischemia resulting in cell membrane Na/K pump dysfunction, increased intracellular fluid volume, and cell swelling.
- Because of the underlying cause and the intracellular nature of this form of edema, white and gray matter may both be affected, and the distribution of edema roughly conforms to the geographic distribution of ischemia
- In most instances, cytotoxic edema occurs in combination with vasogenic edema.
- Diffusion‐weighted imaging has been used to discriminate between the two forms following acute episodes of ischemia, with reduced apparent diffusion coefficient (ADC) intensity reflecting predominantly cytotoxic edema.
Vasogenic edema
- Vasogenic edema occurs because of a disruption of the tight junctions of the blood–brain barrier, resulting in extravasation of high‐protein fluid into the brain.
- Vasogenic edema is extracellular, so it tends to preferentially accumulate in white matter, which has a sparser cellular density and therefore more potential space for fluid distribution compared to highly cellular gray mat ter.
- Depending on the initiating cause and volume of fluid, edema can distribute widely
Interstitial or hydrocephalic edema
- Interstitial edema most often occurs in association with obstructive hydrocephalus when intraventricular pressure increases, causing transependymal CSF migration into adjacent brain parenchyma.
- As a result, hydrostatic edema preferentially occurs within periventricular parenchyma and is extracellular.
- Unlike vasogenic edema, interstitial edema fluid is a transudate containing little in the way of cells or macromolecules.
Osmotic edema
- Osmotic edema occurs rarely and is caused by reduced plasma osmolality resulting from water intoxication, hemodialysis, or metabolic disorders that reduce plasma sodium or glucose concentration.
- The imbalance in brain extracellular fluid osmolality and plasma osmolality results in a fluid shift to the brain leading to formation of extracellular edema.
Cytotoxic Edema (Canine)
3y FS Dachshund with right‐sided cerebellar infarction.
- There is a well‐circumscribed geographic region of FLAIR and T2 hyperintensity involving the right cerebellum (b,c: arrow).
- The T2 hyperintensity is due, in part, to intracellular cytotoxic edema resulting from cell hypoxia.
- The lesion distribution coincides with the tissue volume normally perfused by the right rostral cerebellar artery.
Vasogenic Edema (Canine)
3y MC Basset Hound with aspergillosis involving the frontal sinus and forebrain. This unenhanced CT image is caudal to the primary lesion.
- Marked, diffuse hypoattenuation is evident involving the white matter of the right cerebral hemisphere because of the presence of vasogenic edema.
- Although edema is recognized on CT images, it may be less conspicuous than on corresponding MR images.
Vasogenic Edema (Canine)
Adult dog of unknown age and gender with a large left frontal lobe meningioma. This image is at a level caudal to the mass.
- Marked, diffuse hyperintensity is evident involving the white matter of the left cerebral hemisphere, representing vasogenic edema.
- There is also diffuse volume expansion of the white matter associated with prominent right‐sided midline shift.
Interstitial Edema (Canine)
6y FS Toy Poodle with a caudal fossa meningioma causing obstruction of the ventricular system (a). Images b and c are at the level of the rostral horns of the lateral ventricles.
- The thin, hyperintense rim surrounding the rostral horns of the lateral ventricles on the FLAIR image (c: arrowheads) represents transependymal migration of cerebrospinal fluid to the periventricular extracellular fluid space due to increased intraventricular hydrostatic pressure.
Developmental Disorders of the Brain
Anomalous development of the brain
Brain malformation in the dog and cat can be induced by trauma, toxins, inflammatory disorders, serendipitous in utero aberrations, and genetic defects. Brain development can be broadly divided into five progressive stages:
- Dorsal induction—ventral induction
- Neuronal proliferation
- Differentiation and histogenesis
- Neuronal migration
- Myelination
Anomalies can arise during any one of these stages, and the type of anomaly will reflect the predominant development activity at the time.
Most significant anomalies are rarely imaged with CT or MRI since many patients die or are euthanized early in life. Although classification schemes for developmental brain anomalies vary widely, we have chosen to organize this section into:
- Hindbrain herniations and malformations
- Diverticulation and cleavage disorders
- Malforma tions of cortical development
- Nonneoplastic cysts
Hindbrain herniations and malformations:
Chiari-like malformation
- Chiari‐like malformation is due to reduced volume of the caudal cranial fossa, resulting in cerebellar to caudal cranial fossa volume mismatch. The disorder occurs primarily in Cavalier King Charles Spaniels, but other small and toy breed dogs can be affected. The reduced caudal fossa volume results in crowding and repositioning of the cerebellum, which may sometimes encroach on or herniate through the foramen magnum. Cerebellar crowding also causes extramural compression of the fourth ventricle and central canal, which leads to obstructive hydrocephalus and syringohydromyelia.
- Clinical signs include pain, positional pain, hyperesthesia, and neurologic deficits, but severity of clinical signs correlate poorly to imaging findings.
- On CT images, the caudal fossa will appear smaller than normal, which may be best appreciated on sagittally reformatted images. Obstructive hydrocephalus and syringohydromyelia may also be seen. Similar features will be seen on MR images, and a sagittal T2 sequence is often best for detecting ventricular and central canal distension and for recognizing cerebellar displacement and foraminal herniation
Cerebellar hypoplasia
- Cerebellar hypoplasia has been reported in cats as a sequela to in utero parvovirus infection. The disorder has also been reported in dogs, but a distinction between cerebellar hypoplasia and cerebellar atrophy from degeneration may be challenging antemortem. On MR images in people, the cerebellum is small and may appear to float in an expanded subarachnoid space. The number of folia may also be reduced. Similar gross features have been reported in domestic animals.
Cerebellar vermian hypoplasia
- Cerebellar vermian hypoplasia is a rare disorder in which the cerebellar vermis is hypoplastic or absent. In some patients, the cerebellar hemispheres and flocculus may also be involved and the caudal cranial fossa can be enlarged. The anomaly is analogous to Dandy–Walker syndrome in people.
- On unenhanced CT images, the cerebellar vermis is hypoplastic or absent, leaving a potential space filled by an expanded fourth ventricle, which is hypoattenuating compared to adjacent brain parenchyma.
- Unenhanced MR imaging features are reported to be similar, with enlargement of the fourth ventricle appearing T1 hypointense and T2 hyperintense. Concurrent hydrocephalus has been reported in one dog.
Diverticulation and cleavage disorders
- Diverticulation and cleavage disorders include complex anomalies, such as holoprosencephaly and septo‐optic dysplasia, that occur early in development and involve not only the brain but may affect the face, cranial nerves, and pituitary gland as well.
- Such anomalies are not well described in domestic animals since most affected animals likely die early in life. On both CT and MR images, these disorders will vary depending on the nature and severity of the anomaly.
Malformations of cortical development
- Malformations of cortical development represent a diverse group of developmental anomalies, including microencephaly, pachygyria–polymicrogyria, lissen cephaly, and schizencephaly.
- These anomalies may feature variable and often reduced brain volume, cortical convolution anomalies, and cortical clefts.
- On both CT and MR images, the appearance of these disorders will vary depending on the nature and severity of the anomaly, although disruption of the normal contours of the cortex is a consistent feature
Nonneoplastic cysts
Arachnoid cysts
- Intracranial arachnoid cysts arise from the arachnoid membrane surrounding the brain, do not communicate with the ventricular system, and are thought to be primarily developmental (although acquired cysts are suspected to also occur).
- Young, small‐breed brachycephalic dogs are most frequently affected, although cysts have also been reported in other canine breeds and in cats. Arachnoid cysts most commonly arise from the quadrigeminal cistern but will occasionally occur in other locations.
- Uncomplicated arachnoid cysts have a thin unicameral membrane, contain cerebrospi nal fluid, and conform to the margins of adjacent structures. Although many quadrigeminal arachnoid cysts are clinically silent, large cysts can produce cerebellar and occipital lobe compression leading to development of neurologic clinical signs. The presence of intracystic hematomas has been reported and may lend credence to the thought that some arachnoid cysts are traumatic in origin, as described in people.
- On unenhanced CT images, uncomplicated intracranial arachnoid cysts have well‐defined margins, contain fluid isoattenuating to cerebrospinal fluid, and do not contrast enhance.
- On MR images, cysts are clearly extraaxial, contain fluid isointense with CSF, and do not contrast enhance.
- Arachnoid cysts containing blood or organizing hematomas may have variable attenuation on CT and variable T1 and T2 signal intensity on MRI.
Epidermoid and dermoid cysts
- Epidermoid and dermoid cysts are rare and result from aberrant ectodermal cell migration and entrapment during neural tube closure. The most common locations are the fourth ventricle and cerebellopontine angle. Clinical signs may result from obstructive hydrocephalus.
- Epidermoid cysts consist primarily of desquamated skin cells. These masses appear hypoattenuating to adjacent brain on unenhanced CT images and are T1 hypointense and T2 hyperintense on unenhanced MR images. Epidermoid cysts would not be expected to enhance unless ruptured, producing a peripheral inflammatory response
- Dermoid cysts are more complex, containing hair follicles and sebaceous material that appear hypoattenuating on unenhanced CT images and T1 and T2 hyperintense on unenhanced MR images because of the lipid content. Fat‐suppressed T1 sequences may be used to null the lipid signal to better characterize the lesion. Similar to epidermoid cysts, dermoid cysts would not be expected to enhance unless ruptured, producing a peripheral inflammatory response.
Chiari‐like Malformation (Canine)
5y F Cavalier King Charles Spaniel with intermittent neck pain and C1–C5 myelopathy. Image c is a magnification of image b.
- Malformation of the occipital bone (a,b: arrow) results in reduced caudal cranial fossa volume.
- Mild enlargement of the third and fourth ventricles (a) and sacculated cervical syringohydromyelia (d) are evident.
- Herniation of the cerebellum through the foramen magnum is best seen on sagittal T2 images (b,c: arrowhead).
Small Cerebellum – Probable Cerebellar Hypoplasia (Canine)
3.5mo M Cocker Spaniel cross with neurologic signs referable to the cerebellum.
- The cerebellum is small, and the surface contours appear unusually well defined because of increased cerebrospinal fluid volume surrounding the cerebellar folia.
- The fourth ventricle and cerebellomedullary cistern are also larger than expected.
This diagnosis was not confirmed by biopsy or postmortem examination.
Presumptive Cerebellar Vermian Hypoplasia (Canine)
Adult dog of unknown age and unknown clinical signs. The representative transverse images are at the level of the rostral (b,d) and caudal (c,e) cerebellum.
- The volume of the caudal fossa is larger than expected, and the cerebellum is markedly reduced in size (a: arrow).
- The fluid surrounding the cerebellum within the caudal fossa is likely compartmentalized cerebrospinal fluid within a grossly distended cerebellopontine cistern.
- Both cerebellar hemispheres are hypoplastic (b–e: asterisks), and the central cleft (c: arrow) is indicative of aplasia of the caudal aspect of the cerebellar vermis.
- There is free communication (e: black double‐headed arrow) of the fourth ventricle (e: small arrow) with a markedly enlarged cerebellomedullary cistern (e: large arrow).
Although not confirmed by postmortem exam, the constellation of imaging findings is characteristic of Dandy–Walker syndrome with cerebellar vermal hypoplasia/aplasia described in people.
Lissencephaly (Canine)
Lhasa Apso of unknown age.
- The normally complex surface convolutions of the cortical gyri and sulci are absent and mild, generalized hydrocephalus is present (a–d).
- In addition, there is a striking lack of white‐matter architectural detail (c).
- This dog also has a quadrigeminal arachnoid cyst (d: arrow).
Complex Cortical Developmental Anomaly (Feline)
4mo F Domestic Shorthair with obtundation and rotary nystagmus. Representative transverse and parasagittal images reveal a complex brain anomaly that includes profound hydrocephalus and abnormal cortical and corpus callosum development (a–c). Postmortem examination documented hydrocephalus, hypoplasia of the corpus callosum, cortical gyral malformation, and pachygyria (d).
Arachnoid Cyst (Canine)
2y FS Maltese with unlocalized pain without neurologic deficits. Images a–c are representative transverse images of the brain at the level of the parietal lobes (a), occipital lobes (b), and cerebellum (c).
- Moderate, symmetrical lateral ventriculomegaly is present (a).
- A large, fluid‐attenuating arachnoid cyst (b–d: asterisk) arises from the quadrigeminal cistern and is bounded ventrally by the tectum (d: large arrow) and cerebellum (d: arrowhead), rostrally by the corpus callosum (d: small arrow), and dorsally by the tentorium cerebelli (not seen).
- The cyst is predominantly subtentorial, and it displaces and compresses the cerebellum ventrally.
Arachnoid Cyst (Canine)
MR
3y MC Shih Tzu with tetraparesis. The MR examination was performed to fully evaluate a diagnosed occipitoatlantoaxial malformation. Transverse images (a,c) are at the same level at the occipital lobes.
- A well‐defined arachnoid cyst with pure‐water signal characteristics arises from the quadrigeminal cistern (a,b: asterisk) and is bounded ventrally by the tectum (d: large arrow) and cerebellum (d: arrowhead), and rostrally by the corpus callosum (d: small arrow).
- Focal spinal cord narrowing and parenchymal T2 hyperintensity are also evident on image d, associated with the occipitoatlantoaxial malformation.
Hemorrhage
Staging Hemorrhage
The information in Table 2.4.1 is extracted from the human MRI literature, but it should approximate hemorrhage‐staging patterns in veterinary patients using unenhanced spin‐echo T1 and T2 intensities. In addition, T2* gradient echo sequences can be used to detect signal void from susceptibility of blood degradation products at most stages, though the susceptibility “bloom” sometimes overstates the actual hemorrhage volume.
Because hematoma density is greater than that of normal brain parenchyma, acute to subacute hemorrhage is hyperattenuating compared to brain parenchyma on unenhanced CT images. Density gradually reduces to become isoattenuating with brain parenchyma over many days to weeks.
Extraaxial hemorrhage
Extraaxial hemorrhage is classified as epidural, subdural, or subarachnoid, although in our experience subarachnoid hemorrhage is less frequently recognized.
Epidural hematoma
Epidural hematomas are most often traumatic in origin, arise in the potential space between the cranium and the dura mater, and typically occur from meningeal arterial hemorrhage. Epidural hematomas are described as having a characteristic biconvex or lenticular shape on cross‐sectional images. Acute epidural hematomas appear hyperattenuating to brain parenchyma on unenhanced CT images and will have variable unenhanced T1 and T2 intensity on MR images, depending on the age of the hematoma.
Subdural hematoma
Subdural hematomas are usually traumatic in origin, arise in the potential space between the dura mater and the arachnoid membrane, and typically occur as the result of venous sinus hemorrhage. Subdural hematomas are crescent shaped, conforming to the convex surface of the brain. Acute subdural hematomas will appear hyperattenuating to brain parenchyma on unenhanced CT images with a gradual reduction in density over time. They will have variable unenhanced T1 and T2 intensity on MR images, depending on the age of the hematoma.
Subarchnoid hemorrhage
Head trauma may cause bleeding into the subarachnoid space. Acute subarachnoid hemorrhage will appear hyperattenuating and will generally conform to the convolutions of the cerebral cortex and the cisterns on unenhanced CT images. Acute subarachnoid hemorrhage will appear T1 isointense and T2 and FLAIR hyperintense on MR images with a distribution similar to that seen on CT. Intensity patterns will change with chronicity.
Brain contusion and hemorrhage
Imaging features of brain contusion depend on the combination of edema and hemorrhage in the affected brain parenchyma. Edematous regions will appear hypoattenuating and focal areas of hemorrhage will appear hyperattenuating on unenhanced CT images . Edema will appear T1 hypointense and T2 hyperintense on MR images with hemorrhagic regions having a T2* signal void and an otherwise variable appearance depending on duration since trauma. Edema and hemorrhage will increase brain parenchymal volume, which can lead to:
- midline shift
- ventricular compression
- sulcal and gyral effacement
- brain herniation.
Magnetic resonance angiography, diffusion and perfusion weighted imaging, and diffusion tensor imaging can all be used to further characterize the extent of injury.
Vascular Disorders
Most infarctions are arterial in origin, and although stroke from venous thrombosis is described in people, there are few comparable reports in veterinary medicine. The rostral and middle cerebral and the striate and rostral cerebellar arteries are the most commonly involved, and infarcts involving the cerebrum, thalamus/midbrain, and cerebellum have been reported.
Infarcts are described as territorial when they involve a major intracranial vessel and lacunar when smaller penetrating vessels are obstructed. Underlying causes for stroke include:
- Atherosclerosis
- Hypertension
- Diabetes in people
**although these have not been confirmed as predisposing factors in veterinary patients.
Hematomas
Hematomas will generally appear as a hyperattenuating mass on unenhanced CT images, and there may be evidence of contrast enhancement if active bleeding (acute) or neovascularization (chronic) is present. MR imaging features will generally follow the scheme outlined in Table 2.4.1, although age can be ambiguous when multiple bleeding episodes occur over time. Secondary features of mass effect may include surrounding edema, midline shift, ventricular displacement and compression, and sulcus and gyrus effacement on both modalities.
Non-hemorrhagic infarcts
CT imaging features of nonhemorrhagic infarction may be subtle and include focal or regional hypoattenuation from edema and variable, but often minimal, mass effect.
Nonhemorrhagic infarction may appear mildly T1 hypointense and T2 hyperintense with variable mass effect involving both gray and white matter on unenhanced MR images. Due to restricted water diffusion, ischemic regions of the brain will appear hyperintense on diffusion‐weighted images and hypointense on corresponding apparent diffusion coefficient (ADC) maps. Perfusion images may define specific regions of perfusion deficit, and magnetic resonance angiographic (MRA) images can reveal relative or absolute flow deficits in affected vessels. Gradient echo T2* images will display relatively little or no susceptibility effect.
Acute Intracranial Hemorrhage
13y FS Corgi with a 1‐day history of tonic/clonic seizures and a 2‐year history of systemic hypertension.
- A well‐delineated, T1 isointense (a), T2 hypointense (b) intraaxial cerebral mass is present in the region of the right piriform lobe.
- There is moderate edema surrounding the mass (b) as well as a thin peripheral rim of contrast enhancement (c).
- There is uniform susceptibility effect within the lesion (d).
Edema will appear T1 hypointense and T2 hyperintense on MR images with hemorrhagic regions having a T2* signal void and an otherwise variable appearance depending on duration since trauma.
Edematous regions will appear hypoattenuating and focal areas of hemorrhage will appear hyperattenuating on unenhanced CT images
Subacute Intracranial Hemorrhage (Canine)
7y MC Greyhound with central nervous system deficits associated with an anesthetic recovery complication following routine dental prophylaxis performed 5 days previously.
- There is marked T1 hyperintensity (a) and mixed T2 intensity (b) involving the left cerebral hemisphere.
- The lesion involves primarily the cerebral cortex based on distribution on the T1 image, but more extensive edema involving gray and white matter is appreciated on T2 and FLAIR images (b,c), resulting in a midline shift.
- The 5‐day history of intracranial signs and imaging characteristics are consistent with subacute hemorrhage.
Chronic Intracranial Hemorrhage (Canine)
12y FS Poodle with 5‐day history of right forebrain deficits. The initial MR examination (a–c) was acquired 5 days following the onset of clinical signs. The follow‐up MR examination (d–f) was acquired approximately 6 weeks later, at which time the dog had clinically improved.
- On the initial examination, there is a large mass within the right frontal lobe that is T1 iso- to hyperintense (a) and of mixed T2 intensity (b). A prominent susceptibility effect is present on the T2* image (c). This constellation of imaging features is consistent with an acute to subacute intracranial hemorrhage, supported by the 5‐day duration of clinical signs.
- The marked reduction in lesion volume and the uniform hypointensity evident on all imaging sequences on the second examination acquired 6 weeks later are consistent with a resolving chronic hematoma (d–f).
A postmortem examination performed 1 year later for an unrelated cause of death revealed extensive neuropil loss and other chronic degenerative changes of the right frontal lobe consistent with residual effects of a healed infarct.
Acute Epidural Hemorrhage (Canine)
10y FS Labrador Retriever with lymphoplasmacytic encephalitis. The CT image was acquired immediately following CT‐guided brain biopsy.
- Epidural hemorrhage is evident involving the left parietal region.
- The biconvex shape is consistent with an epidural hemorrhage.
Although acute hemorrhage is hyperattenuating on unenhanced CT images, the increased attenuation in this patient is due, in part, to enhancement following intravenous contrast medium administration.
Subacute Subdural Hemorrhage (Canine)
5y MC Mixed Breed with head trauma 4 days previously.
- A crescent‐shaped, T1 hyperintense, right‐sided subdural hematoma is present (a: arrow).
- The hemorrhage has central hypointensity and peripheral hyperintensity on the T2 image (b: arrow), consistent with subacute hemorrhage and the 4‐day history of head trauma.
- A focal, nonenhancing, T1 hyperintense lesion is also present in the left pyriform lobe (a,b: arrowhead), associated with regional edema and consistent with subacute parenchymal hemorrhage.
- Given the location of this second lesion in relation to the subdural hematoma, it is thought to represent a contrecoup brain contusion.
Necropsy confirmed both the subdural hematoma and the brain hemorrhage.
Nonhemorrhagic Cerebellar Infarction (Canine)
13y FS Pug with central vestibular signs of 2‐day duration.
- There is a well‐delineated region of T1 hypointensity (a: arrow) and T2 hyperintensity (b,c: arrow) involving the right side of the cerebellum.
- The lesion has minimal mass effect and is not associated with other intracranial lesions.
- The focal area of hyperintensity on the B1000 diffusion image (d: arrow) and the corresponding region of hypointensity on the apparent diffusion coefficient map (e: arrow) are attributable to diffusion restriction in the ischemic tissue.
MR findings and clinical signs are consistent with nonhemorrhagic cerebellar infarction caused by right rostral cerebellar artery thrombosis.
Inherited Metabolic Disorders
Lysosomal storage disorders
Lysosomal storage disorders are a group of more than 50 rare inherited diseases characterized by failure of lysosomes to metabolize lipids or glycoproteins. Most are autosomal recessive disorders that cause a single enzyme deficiency. Although the clinical presentations associated with this spectrum of diseases vary depending on the specific defect, most include central nervous system pathology and consequent neurologic clinical signs. Comprehensive coverage of these disorders is beyond the scope of this text, but we will highlight two representative examples.
- Neuronal ceroid lipofuscinosis has been reported in many canine breeds, including Cocker Spaniels, Border Collies, American Bulldogs, Chihuahuas, Schnauzers, English Setters, Tibetan Terriers, and Polish Lowland Sheepdogs. The underlying pathology includes generalized neuronal loss with diffuse astrogliosis. Remaining neurons contain an intracytoplasmic accumulation of yellow lipopigments. Retinal cells can be similarly affected, and other organ involvement can occur. In a single case report of CT features of ceroid lipofuscinosis in a Border Collie, there was generalized cortical atrophy and ventricular dilation. MR descriptions also include cortical atrophy and ventriculomegaly. One citation describes intense enhancement of thickened meninges in a group of affected Chihuahuas, but this has not been reported elsewhere. In our experience, there is also a loss of definition of the gray–white matter interface on proton density images and possible cerebellar atrophy.
- Galactosialidosis is caused by a cathepsin A mutation that results in β‐galactosidase and neuraminidase deficiency. The disorder has three clinical variants and affects multiple organs, but the central nervous system is consistently involved. In people, neuropathologic features include atrophy of the optic nerve, thalamus, globus pallidus, lateral geniculate bodies, brainstem, and cerebellum. Microscopic findings include neuronal loss, gliosis, and abnormal lysosomal storage in remaining neurons. A lysosomal storage disorder similar to galactosialidosis has been reported in a 5‐year‐old Schipperke dog with progressive cerebellar and central vestibular signs. Enlarged and vacuolated neurons were seen on postmortem examination, which were documented to be due to the presence of glycolipid‐laden intracytoplasmic lysosomes. Imaging reports in people are lacking, but the MR features of the canine patient with a presumptive diagnosis of galactosialidosis include cerebellar atrophy and ventriculomegaly. There was diffuse cerebellar purkinje cell and granular cell loss and extensive neuronal cytoplasmic lysosomal storage in the cerebellum and hippocampus on postmortem microscopic examination.
Case findings:
2y MC Border Collie cross with 4‐month history of progressive behavior changes, ataxia, and incoordination. There is generalized reduction in cerebral and cerebellar volume with concomitant generalized ventriculomegaly and prominence of the subarachnoid space due to gyral atrophy and sulcal widening (a,c–e). There is also loss of white and gray matter definition on the proton density image (b). Postmortem examination revealed neuronal accumulation of eosinophilic granular intracytoplasmic material. The material was autofluorescent and stained positive with PAS, LFB, and Sudan black B, all of which supported the diagnosis of neuronal ceroid lipofuscinosis.
Acquired Metabolic Disorder
Thiamine deficiency
Thiamine deficiency is rare and usually results from animals being fed commercial or noncommercial diets deficient in thiamine. The disorder has also been documented in dogs and cats fed commercial pet food formulations containing sulfur dioxide as a preservative. Certain species of fish contain high levels of thiaminase, and some drugs can also induce thiamine deficiency. Clinical manifestations include:
- Neurologic
- Ocular
- Gastrointestinal
- Cardiac signs
As with other metabolic/toxic central nervous system disorders, specific regions of the brain are vulnerable, leading to symmetrical multifocal lesions on imaging studies. The lateral geniculate, dorsal cochlear, oculomotor, mammillary, and red nuclei and the caudal colliculi are most often involved. The cerebral cortex, cerebellar vermis, basal ganglia, and hippocampus can also be variably affected. Microscopic pathology includes neuronal degeneration and necrosis, myelin degeneration, and secondary vascular changes.
Lesions are usually:
- Well defined and bilaterally symmetric
- Have minimal mass‐effect
- Appear T2 and FLAIR hyperintense
- Variably T1 hypointense
- Do not typically contrast enhance
- Not all vulnerable regions are affected in every patient.
Hepatic encephalopathy
MR features of the brains of dogs and cats with portosystemic shunts include:
- T1 hyperintensity of the lentiform nuclei.
- These lesions are T2 isointense
- Do not contrast enhance
- Subside following correction of portosystemic shunt
Comparable MR lesions are described in people with chronic hepatic encephalopathy and are thought to be due to a focal accumulation of manganese, which has also been documented in dogs with the same condition.
More fulminant clinical signs and MR imaging features occur with acute hepatic encephalopathy. MR findings in people include diffusion restriction, diffuse cortical T2 and FLAIR hyperintensity, and focal T2 and FLAIR hyperintensity of thalamic nuclei without contrast enhancement. Intensity changes are due primarily to cytotoxic edema, but cortical laminar necrosis has also been described. Similar MR features have been described in a dog with fulminant hepatic encephalopathy.
Osmotic demyelination syndrome
Myelinolysis due to hypernatremia and from aggressive correction of hyponatremia has been reported in people. Myelinolysis occurs due to a high gradient between intracellular and extracellular osmolarity, which injures cells as a result of abnormal transmembrane water transit. The general term osmotic demyelination syndrome defines the underlying pathology in both clinical conditions. Hypernatremic osmotic demyelination, however, occurs both in the pons and in extrapontine locations, including white matter, corpus callosum, basal ganglia, hippocampus, cerebellum, and cortex. Clinical signs vary depending on the vulnerable tissues affected but include neurocognitive changes and motor dysfunction. MR features of acute disease include:
- Focal or multifocal, T1 hypointense
- T2 and FLAIR hyperintense lesions in the anatomic locations listed above
- Diffusion restriction on diffusion‐weighted imaging.
- Lesions typically do not enhance
Peri‐ictal encephalopathy
In people, MR imaging performed within a few days of generalized seizures reveals transient diffusion restriction, swelling, and T2 hyperintensity of cortical gray matter, subcortical white matter, and hippocampus. These changes are ascribed to seizure‐induced transient vasogenic and cytotoxic edema. MR features of peri‐ictal encephalopathy in dogs have also been reported. MR imaging features within 14 days of seizuring included variable T1 hypointensity and T2 hyperintensity of the piriform and temporal lobes. Contrast enhancement of the lesions occurred in only one dog, and lesions resolved within 10–16 weeks after the initial MR examinations. Microscopic features included edema, neovascularization, reactive astrocytosis, and acute neuronal necrosis and were similar to those reported in people. In our experience, lesion distribution may extend beyond the piriform and temporal lobes.
Case findings:
14y MC Domestic Shorthair with 2‐day history of inappetence, vomiting, and ataxia. Neurologic examination revealed multifocal neurological deficits involving the cerebellum, brainstem, and cerebrum. There are focal regions of T2 and FLAIR hyperintensity involving the lateral geniculate nuclei (a,g: arrowheads), the caudal colliculi (b,d,h: arrowheads), and vestibular nuclei (c: arrowheads). Other thalamic nuclei were similarly affected (not shown). There is also ill‐defined T2 and FLAIR hyperintensity of the axial regions of the parietal and occipital cortex (a,b,d: arrow), which enhance following contrast administration (f: arrow). These MR features are characteristic of multifocal polioencephalopathy due to thiamine deficiency. Further questioning of the owner revealed the cat had been fed an almost exclusively meat diet. Clinical signs resolved with dietary change and thiamine supplementation.
Age‐related Degeneration (Canine)
12y MC Shiba Inu with left‐sided vestibular signs.
- There is prominence of the subarachnoid space and lateral ventricles due to cortical atrophy (a,b).
- The cortical mantle is thin, and gyri are smaller than expected.
- The hippocampus also appears small with central foci of increased T2 intensity (b: arrows).
- No other abnormalities were detected on the MR examination, and clinical signs resolved after approximately 2 weeks.
Necrotizing Meningoencephalitis (Canine)
3y M Pomeranian with a recent history of seizures and circling to the left.
- There are multiple foci of marked T2 and FLAIR hyperintensity (a,d: arrowheads) and T1 hypointensity (b: arrowheads) involving the cerebral cortex and regional T2 hyperintensity of the white matter and caudate nucleus on the right (a,d: arrow).
- There is mild amorphous contrast enhancement of the right caudate nucleus (e,f: arrow) and of the meninges overlying the cerebral cortical lesions (e,f: arrowheads).
Postmortem examination revealed extensive areas of cortical necrosis and encephalomalacia, consistent with necrotizing meningoencephalitis.
Necrotizing Leukoencephalitis (Canine)
2y MC Yorkshire Terrier with acute onset of ataxia, hypermetria, and obtundation.
- There is diffuse T2 and FLAIR white matter hyperintensity in both cerebral hemispheres, consistent with vasogenic edema (b,c).
- There is focal right hemispheric subcortical T2 hyperintensity, FLAIR mixed intensity, and T1 hypointensity, consistent with a focal fluid collection (b–d: arrow).
- An additional T2 hyperintense mass is present within the pons (a: arrow).
- Following contrast administration, multiple contrast‐enhancing foci are seen in the parenchyma of the cerebrum and thalamus (e,f: arrows).
- Diffuse meningeal enhancement is also evident (e,f: arrowhead).
Postmortem examination revealed widespread multifocal lymphohistiocytic leukoencephalitis with cystic malacia and necrosis, consistent with necrotizing leukoencephalitis.
Feline infectious peritonitis meningoencephalitis
The feline infectious peritonitis (FIP) coronavirus causes systemic illness in domestic cats, with central nervous system involvement being a common component, particularly in cats with the dry or pyogranulomatous form of the disease. FIP infection causes an immune‐complex pyogranulomatous vasculitis, and in the central nervous system (CNS), it targets the:
- Leptomeninges
- Choroid plexus
- Ependymal cells
- Brain parenchyma
- Eyes
Generalized or regional obstructive hydrocephalus may be present because of ependymal and choroid inflammation. Cerebrospinal fluid (CSF) may have variable T1 and FLAIR intensity depending on cellular and macromolecular content. The brain parenchyma may appear unremarkable on unenhanced T1 MR images, although cerebellar herniation may be evident in cats with obstructive hydrocephalus. Focal or multifocal regions of parenchymal hyperintensity may be evident on T2 images, and the meninges may appear thickened and T2 hyperintense. Choroidal, ependymal, and meningeal enhancement may be marked on contrast‐enhanced T1 images
Case findings:
9mo MC Domestic Shorthair with 2‐week history of lethargy, inappetence, and reduced motor function in the pelvic limbs. The ventricular system is markedly and uniformly enlarged, indicative of obstructive hydrocephalus (a–d). The choroid plexus of the floor of the lateral ventricles is enlarged (b: arrowheads). The cerebrospinal fluid (CSF) appears abnormally hyperintense on the FLAIR image, indicating a high cellularity or macromolecular content (c: arrowheads). There is nonuniform T2 and FLAIR hyperintensity of the white matter in both hemispheres consistent with the presence of vasogenic edema. Contrast‐enhanced T1 images reveal uniform and intense enhancement of a thickened ependymal lining but no parenchymal enhancement (e–h). MR imaging findings characteristic of this disorder can be quite shocking (f,i). Based on the combination of clinical signs, MR findings, and CSF analysis, a clinical diagnosis of feline infectious peritonitis associated encephalitis and ventriculitis was made.
Intracranial Abscess
Intracranial abscesses are caused by:
- Penetrating injuries, such as migrating foreign bodies and bite wounds
- Extension of ear and nasal infections
- From bacteremia or septic emboli.
Their location within or adjacent to the brain is dependent on the initiating cause, with the brainstem most often affected by extension of otitis media/interna. Because of the inflammatory nature of the lesion and the often significant mass effect, surrounding vasogenic edema is usually pronounced. Epidural or subdural fluid collections may be present, particularly when the abscess is caused by penetrating injury. Obstructive hydrocephalus may occur, depending on abscess location.
Intracranial abscesses usually appear as solitary space‐occupying masses of variable size and with a hypoattenuating center on unenhanced CT images. Depending on the thickness of the abscess capsule, this may appear as a distinct iso‐ or mildly hyperattenuating lesion rim surrounded by relatively hypoattenuating parenchymal edema. Abscesses are generally intensely peripherally enhancing, and regional meningeal enhancement may be present in some patients.
On MR images, abscesses are centrally T1 hypointense (but higher intensity than normal CSF) and T2 hyperintense because of the presence of abscess fluid and T1 hypointense and T2 hyperintense peripheral to the mass because of vasogenic edema. Abscess contents appear hyperintense on FLAIR sequences. A distinct T1 iso‐ to hyperintense abscess capsule may also be evident. Abscesses intensely peripherally contrast enhance and regional meningeal enhancement may be seen. Diffusion weighted imaging (DWI) typically reveals high signal intensity on the DWI map and low signal on the apparent diffusion coefficient (ADC) map, indicative of restricted water diffusion (Figure 2.7.5). This may be useful for differentiating abscesses from necrotic brain lesions and mucinous intra‐axial tumors, such as oligodendroglioma.
Case findings:
16y FS Abyssinian with bilateral ceruminous gland cystadenomas and otitis media. Recent onset of intracranial neurologic signs. Nonuniformly contrast‐enhancing, soft‐tissue attenuating material is present within both tympanic bullae (a). There is a peripherally contrast‐enhancing intracranial mass, consistent with an abscess, adjacent to the internal margin of the petrous portion of the right temporal bone (a,b: arrowhead). The internal acoustic meatus can be seen (a: black arrow).
MR
2.5y FS Domestic Shorthair with acute onset ataxia and obtundation.
- T2 and T1 intensity within the left tympanic bulla is consistent with effusion (a,b).
- There is a T2 hyperintense, T1 hypointense mass adjacent to or within the left side of the brainstem (a,b: arrowhead), surrounded by a halo of T2 hyperintense edema (a).
- The mass intensely peripherally enhances following contrast administration, indicative of an abscess (c).
- Adjacent meninges also enhance and appear thickened, indicative of regional meningitis (c: arrowhead).
- The lining of the left tympanic cavity intensely enhances, consistent with otitis media (c).
Biopsy and culture of the lining of the left middle ear confirmed suppurative otitis media. The intracranial abscess and meningitis was thought to have occurred by ascending infection through the internal acoustic meatus.
Bacterial Meningitis (Canine)
9mo F Dachshund with 2‐week history of progressive weakness and lethargy. Cerebrospinal fluid analysis revealed marked suppurative inflammation and intracellular rod‐shaped bacteria.
- Meningeal and periventricular hyperintensity is evident on the FLAIR image (c).
- The cerebellum appears enlarged with loss of cerebellar folia definition (c) and ventral foraminal herniation (d: arrowhead).
- There is marked thickening and regional enhancement of the meninges in the caudal aspect of the cranial vault (d–f: arrows).
- Cerebrospinal fluid analysis also revealed large numbers of neutrophils.
A craniotomy was performed to reduce intracranial pressure. Meningeal biopsy confirmed severe suppurative meningitis.
Mycotic Granulomatous Encephalitis (Canine)
6y FS Labrador Retriever with progressive lethargy and cervical pain.
- There is a mass in the left dorsal thalamic region causing a midline shift and compression of the third and left lateral ventricles.
- The mass is characterized by T1 hypointensity (a: arrow) with heterogeneous T2 intensity (b: arrow), and there is evidence of extensive perilesional edema (b: arrowheads).
- A similar‐appearing lesion (not shown) was present in the left occipital lobe.
- The mass intensely and heterogeneously enhances following contrast administration, and mass margins are poorly defined and irregular (c: arrow).
Postmortem examination confirmed granulomatous encephalitis from systemic aspergillosis. The disease was widely disseminated with multiple organ systems affected.
Mycotic Meningoencephalitis (Feline)
4y FS Bengal cross with pelvic limb weakness.
- Multiple ill‐defined and variably sized T1 hypointense and T2 hyperintense foci are seen in the piriform lobes and parietal cortex (a,b,d,e: arrows; additional lesions not shown).
- These focal lesions heterogeneously enhance and have ill‐defined margins following contrast administration (c,f,g: arrows).
- Prominent multifocal meningeal enhancement is also seen (f,h: arrowheads).
Postmortem examination confirmed multisystemic inflammatory disease caused by Cryptococcus gattii. The chronic inflammatory response in the meninges and brain was histiocytic and lymphoplasmacytic with intralesional fungal elements.
Meningioma
Meningiomas are the most common of the primary intracranial, extraaxial neoplasms in dogs and cats. German Shepherd Dogs, Collies, Golden Retrievers, and Boxers are overrepresented. Meningiomas are derived from meningothelial cells and are divided into three grades:
- WHO grade I, benign
- WHO grade II (atypical), which have intermediate histologic features
- WHO grade III, malignant.
In a report of 112 canine meningiomas, 56% were grade I, 43% were grade II, and less than 1% were grade III.
Meningiomas in dogs most frequently impinge on the olfactory bulbs and frontal lobes and are often of a macrocystic histological subtype. Other common sites include the cerebral or cerebellar convexity and cerebellopontine, basilar, tentorial, falcine, foraminal, or intraventricular locations. Multiple meningiomas may be present simultaneously, particularly in older cats, and it is unclear whether these represent multicentric disease or metastasis from a single primary site. Meningiomas may occasionally have a mineralized, cystic, or hemorrhagic component.
Meningiomas are typically iso‐ to mildly hyperattenuating to cortical gray matter on unenhanced CT images and can produce considerable mass effect. Cystic components appear hypoattenuating, as does surrounding peritumoral edema, which can be extensive. In some patients, hyperostosis of calvarial bone adjacent to a meningioma will appear thickened and hyperattenuating.
Solid meningiomas are usually uniformly T1 isointense on unenhanced MR images but are occasionally hypo‐ or hyperintense. Approximately 70% of meningi omas are T2 hyperintense, with the remainder being isointense. Despite the relatively benign biological behavior of the majority of meningiomas, about 95% are accompanied by edema, which may be peritumoral (40%) or diffuse (50%). Edema in T2 or FLAIR images often clearly delineates the meningioma margin, confirming its extraaxial origin. Signal void of adjacent calvarial bone due to reactive hyperostosis can sometimes be seen.
On both CT and MR images, approximately 60–70% of meningiomas show marked, uniform contrast enhancement, with the remainder being heterogeneous and often associated with cystic, hemorrhagic, or mineralized com ponents. Contrast enhancement usually reveals well‐defined tumor margins; a globoid, plaque‐ like, or irregular shape; and a broad‐based superficial margin conforming to the meningeal plane. On contrast‐enhanced MR images, thickening and intense enhancement of meninges adjacent to the tumor, often referred to as a dural tail sign, is a common imaging feature of meningiomas, although not pathognomonic for the disorder. This feature may be difficult to recognize on contrast‐enhanced CT images because of the hyperattenuation of adjacent bone.
Case findings:
13y MC West Highland White Terrier with central vestibular signs. A soft‐tissue mass, which is slightly hyperattenuating compared to occipital lobe cortex, is identified in the right caudal fossa adjacent to the ventral margin of the os tentorium (a: arrow). The left side of the cerebellum is hypoattenuating, suggesting the presence of perilesional edema (a: arrowhead). The mass intensely and uniformly enhances following contrast administration and is well margined and broad based, indicating an extraaxial origin (b: arrow). Adjacent cerebellum and brainstem are displaced and compressed (b: arrowheads). Postmortem examination confirmed a diagnosis of meningioma.
Granular Cell Tumors (GCTs)
Granular cell tumors have many imaging features they have in common with meningiomas. GCTs are usually well defined and extraaxial with a plaque‐like, sessile distribution involving the meninges. They are preferentially located along the convexity of the cerebrum, the falx cerebri, or the floor of the cranial vault, and those involving the cerebrum can be quite extensive.
Peritumoral edema and mass effect associated with these tumors can be seen on both CT and MR images. Granular cell tumors are mildly hyperattenuating on unenhanced CT images and mildly T1 hyperintense and T2 iso‐ to hyperintense on MR images. Granular cell tumors intensely and uniformly enhance on both CT and MR images following contrast administration, and tumor margins are usually well defined
Case findings:
12y FS Miniature Poodle with vestibular signs. There is a thin, plaque‐like, T1 and T2 hyperintense mass involving the entire right cerebral cortex, causing a pronounced midline shift (a,b: arrowheads).The mass intensely and uniformly enhances following contrast administration (c–e: arrowheads). A gross cross‐sectional image, which correlates with MR image e, confirms the extraaxial origin of the tumor (e,f: arrowheads). The mass was histologically confirmed to be a granular cell tumor. Anwer et al 2013.19 Reproduced with permission from Wiley.
Astrocytoma
Astrocytomas are one of the most common of the intraaxial central nervous system (CNS) neoplasms. Boxers and some other brachycephalic breeds are highly predisposed. Older dogs are most frequently affected, but astrocytomas also occur in young animals. Although astrocytomas can originate from either white or gray matter, those that occur within the cerebrum appear to arise predominantly from white matter. The frontal, piriform, and temporal lobes are the most common sites.
The current human WHO classification scheme grades astrocytomas based on cytological characteristics.
- Grade I and II astrocytomas (diffuse astrocytomas) are considered the least biologically aggressive forms and consist of a uniform, well‐differentiated infiltrative cell population without mitotic activity.
- Grade III (anaplastic) astrocytomas have more nuclear atypia, a much higher cell density, and mitotic activity.
- Grade IV astrocytomas (glioblastoma multiforme) are the most malignant and infiltrative, frequently having regions of necrosis, microvascular proliferation, and sometimes intratumoral hemorrhage, which contribute heterogeneity to their MR imaging appearance in both humans and animals.
Astrocytomas may be globoid or irregularly shaped, and peritumoral edema is variable but usually minimal to moderate.
Intratumoral hemorrhage may also occur in high‐grade tumors.
MR features of gliomas and presumed cerebrovascular accidents can be similar, although gliomas tend to be distributed primarily in the cerebrum, whereas vascular lesions are more likely to be located in the cerebellum, thalamus, midbrain, and brainstem. Diffusion‐weighted imaging can be used to discriminate between these two disorders, with vascular lesions more likely to result in diffusion restriction.
Astrocytomas are generally hypoattenuating on unenhanced CT images, and mass margins may be ill defined, particularly when surrounded by peritumoral edema or when biological grade is low.
Astrocytomas typically appear mildly to moderately T1 hypointense and moderately and heterogeneously T2 hyperintense. Surrounding edema may mask tumor margins on both T1 and T2 images.
With both CT and MR, the intensity of tumor enhancement following contrast administration reflects microvascular proliferation and blood–brain barrier disruption and tends to increase with astrocytoma grade. Low‐grade astrocytomas typically do not enhance, or enhance minimally, whereas high‐grade astrocytomas are more likely to show moderate or marked, nonuni form or peripheral contrast enhancement, although the degree of enhancement is not a reliable indicator of tumor grade
Case findings:
9y MC Toy Poodle with a 3‐week history of seizures. A large, T1 hypointense, T2 and FLAIR hyperintense ovoid mass is seen in the ventral aspect of the left frontal lobe (a–c: arrow). There is mild enhancement in part of the mass following contrast administration (d,e: arrow). A more rostral contrast‐enhanced CT image reveals a hypoattenuating mass effect in the left frontal lobe inducing midline shift (f: arrow). Biopsy revealed the mass to be a grade II astrocytoma.
Oligodendroglioma
Oligodendrogliomas occur with similar frequency to astrocytomas and affect older dogs, particularly Boxers and other brachycephalic breeds.
The appearance of oligodendrogliomas on unenhanced CT images is similar to that of astrocytomas. They are typically hypoattenuating, and mass margins may be ill defined or lacking, particularly when peritumoral edema is present. Marked central hypoattenuation of some oligodendrogliomas, caused by the high water content of the mucinous core, may increase the index of suspicion for this tumor.
Oligodendrogliomas are moderately T1 hypointense and markedly T2 hyperintense, specifically when there is significant central mucinous content. Peritumoral edema ranges from minimal to moderate, although even large oligodendrogliomas may induce little edema formation.
Contrast enhancement of oligodendrogliomas on both CT and MR images is highly variable, ranging from none to marked, and when present it is often peripheral or non uniform. Focal or regional contrast enhancement is often distributed centrally or eccentrically within the greater tumor volume and may have a serpentine shape. Although high‐grade oligodendrogliomas tend to contrast enhance to a greater degree than low‐grade tumors, as with astrocytoma, this imaging feature is not a reliable indicator of biological grade
Ependymal tumors
Ependymomas are uncommon tumors that arise from the ependymal lining cells of the ventricular system and thus may occur within the ventricular system of the brain and spinal cord. Ependymomas usually affect older dogs and cats without breed predisposition. These tumors are predominantly intraventricular, although some invade the adjacent brain parenchyma, and they expand to fill the ventricular cavity in which they arise, causing distortion of the ventricle and obstructive hydrocephalus, depending on their size and location. Ependymomas may be well differentiated (WHO grade II) or anaplastic and aggressive (WHO grade III). Grossly, the tumors can be soft, lobular (papillary type), or solid (cellular subtype) and may contain cysts and/or hemorrhage. Ependymomas may be accommodated by gradual ventricular dilation, hence edema is usually absent or minimal, unless the tumor invades the periventricular brain parenchyma or hydrocephalus causes periventricular interstitial edema.
Ependymomas are typically isoattenuating on unenhanced CT images, although they can have a heterogeneous appearance.
Ependymomas appear slightly T1 hypointense to slightly hyperintense on unenhanced images and moderately to markedly T2 hyperintense.
Contrast enhancement is usually marked and may be heterogeneous, which reflects the coarse texture of the tumor parenchyma, on both CT and MR images. Heterogeneity may be even more pronounced when cysts or hemorrhage are present. Tumor margins are typically distinct, because the majority of the mass extends into a ventricular lumen
Choroid Plexus Tumors
Choroid plexus tumors (CPT) are relatively common neoplasms that arise from the choroid plexus epithelium within the lateral, third, and fourth ventricles and the lateral recesses. About 50% originate in the fourth ventricle or lateral recesses. The average age of dogs at diagnosis is 6 years, which is earlier than most other intracranial tumors. Golden Retrievers appear to be highly overrep resented. Classification of canine CPT distinguishes choroid plexus papillomas (CPP), comparable to WHO grade I and morphologically benign, from choroid plexus carcinomas (CPC), comparable to WHO grade III and histologically more abnormal and more likely to invade the brain or give rise to intraventricular or intrathecal metastases. Mild to moderate edema is present in about 45% of CPP and about 70% of CPC.
Choroid plexus tumors share many CT and MR imaging features with ependymomas. Initially, they may conform to the shape of the ventricle in which they grow, but enlargement may lead to hydrocephalus because of ventricular obstruction or, possibly, overproduction of CSF. Tumors have variable attenuation on unenhanced CT images and may be T1 hypo‐, iso‐, or hyperintense and T2 hyperintense on MR images. Choroid plexus tumors often appear heterogeneous, particularly when there is intratumoral hemorrhage.
Choroid plexus tumors usually show marked, uniform enhancement on both CT and MR images following contrast administration, which reflects the underlying papillary vascular architecture of these tumors. Intraventricular and intrathecal “drop metastases” may appear as intensely contrast‐enhancing foci in the ventricles or subarachnoid space. Choroid plexus papillomas and carcinomas cannot be reliably distinguished by CT or MR imaging, although presence of drop metastases suggests CPC.
Histiocytic Tumors
Characteristic CT features of histiocytic sarcoma have not been documented, but these tumors are T1 iso‐ to hypointense and T2 iso‐ to hyperintense on unenhanced MR images and can cause a mass effect accompanied by regional or diffuse peritumoral edema.
Contrast enhancement on both CT and MR images is moderate to marked and can be either uniform or heterogeneous. As observed with meningiomas, the margins of extraaxial histiocytic sarcomas may appear well defined on T2 and enhanced T1 images, although the degree of contrast enhancement may sometimes be less than that of meningiomas and have a fine granular pattern (Figure 2.8.18). Dural tail signs have also been reported inconsistently with these tumors.
Hemangiosarcoma
On MR images, metastatic hemangiosarcoma often appears as multiple mass lesions, although metastasis should still be considered when a solitary lesion is found. Hemangiosarcomas typically have a marked mass effect, mixed signal intensity on T1 and T2 sequences and heterogeneous intensity with susceptibility effects on T2* images because of intratumoral hemorrhage. Peritumoral edema may be marked. Contrast enhancement is variable and often peripheral (Figure 2.8.19).
Meningioma (Canine)
Adult dog of unknown gender, age, or breed.
- A mildly T1 hyperintense, T2 hyperintense broad‐ based mass is present in the right temporoparietal region causing a midline shift and compression of the right lateral ventricle (a,b: arrow).
- Adjacenct to the calvarium and the thin T2 hyperintense rim suggest an extraaxial origin of the mass.
- Diffuse surrounding T1 hypointensity and T2 hyperintensity are consistent with vasogenic edema (a,b: arrow- heads).
- The mass intensely and uniformly enhances following contrast administration, and mass margins are reasonably well defined (c,d).
- Dural tails, seen best on the dorsal plane image, confirm the mass is extraaxial (d: arrowheads).
Macrocystic Meningioma (Canine)
8y MC Golden Retriever with recent onset of seizures.
- There is a sessile T1 and T2 hyperintense mass involving the left olfactory bulb/ frontal lobe region (a,b: arrow) with an adjacent T1 hypointense, T2 hyperintense, and FLAIR‐nulling cystic component (a–c: arrowhead).
- The solid component of the mass intensely and uniformly enhances following contrast administration (d–f).
- There is a thin rim of enhancement in the cystic part, but it is otherwise unchanged.
Glioblastoma Multiforme (Canine)
10y MC Australian Shepherd with recent onset of seizures.
- There is a large ovoid mass with mixed T1, T2, and FLAIR intensity in the left cerebrum.
- Mass margins are well defined on T2 and FLAIR images, and the halo of hyperintensity surrounding the mass on these sequences is indicative of vasogenic edema.
- The mass nonuniformly enhances following contrast administration, with more intense enhancement peripherally.
Postmortem examination confirmed glioblastoma multiforme. There was extensive intratumoral hemorrhage consistent with the complex, mixed signal intensity seen on unenhanced images.
High‐grade Oligodendroglioma (Canine)
5y FS French Bulldog with inappetence, lethargy, and head tilt.
- There is a large, irregularly shaped T1 hypointense and T2 hyperintense mass in the right temporal–piriform region, resulting in midline shift and obscuration of the ventral aspect of the right lateral ventricle (a,b,d).
- Perilesional edema is conspicuously absent.
- The mass enhances nonuniformly following contrast administration, with a thin contrast rim defining the mass margins (c,e).
Postmortem examination confirmed the mass to be a grade III oligodendroglioma with extension into the right lateral ventricle (f: arrow). The high water content of the mucinous center explains the T2 hyperintensity of the tumor.
Ependymoma (Canine)
7y MC German Shorthair Pointer with 2‐week history of behavioral changes and neurologic deficits.
- There is a well‐demarcated ovoid mass within the third ventricle, which is predominantly T1, T2, and FLAIR hyperintense (a–d). The mass deforms the lateral ventricles, but there is minimal hydrocephalus and no peritumoral edema.
- The mass intensely and nonuniformly enhances following contrast administration (e,f).
Postmortem examination confirmed an ependymoma within the third ventricle (g). The granular appearance on cut surface correlates with the irregular cobblestone appearance of the tumor on MR images. An unrelated diagnosis of lymphoplasmacytic meningitis explains the meningeal contrast enhancement seen in image f.
Choroid Plexus Carcinoma (Canine)
8y MC dog of unknown breed with a recent onset of depression progressing to obtundation.
- There is a mildly T1 hypointense, FLAIR hyperintense spherical mass in the third ventricle, causing displacement of the axial margins of the lateral ventricles (a,b).
- There is focal periventricular edema dorsal to the mass (a: arrows) and nonuniform ventriculomegaly, with the mesencephalic duct and fourth ventricle disproportionately enlarged (e: arrows).
- The mass intensely and uniformly enhances following contrast administration (c,f).
Postmortem examination confirmed a choroid plexus carcinoma of the third ventricle (d). The irregular cut surface of the tumor correlates with the pattern of enhancement on MR images. The nonuniform hydrocephalus may be a result of either partial obstruction or overproduction of cerebrospinal fluid by the tumor. Westworth et al (2008).32 Reproduced with permission from Wiley.
Choroid Plexus Carcinoma with Local Metastasis (Canine)
7y MC Chow with tetraparesis.
- There is a large, T1 and T2 hyperintense ovoid mass in the left lateral recess (a,b,e: large arrow) that encroaches on the fourth ventricle, distends the contralateral lateral recess (b: arrowheads), and displaces and compresses the brainstem (a,b: small arrow) and cerebellum (a: arrowhead).
- A smaller mass is seen ventral to the brainstem (e: arrowhead).
- Both masses intensely and uniformly enhance following contrast administration (c,f: arrows).
- Distension of the third ventricle and the infundibular recess (e: small arrow) is indicative of obstructive hydrocephalus.
The large mass in the left lateral recess was confirmed to be a choroid plexus carcinoma (d: large arrow). The small mass was determined to be a local metastatic lesion (d: small arrow). The fourth ventricle and right lateral aperture were somewhat distended (d: arrowheads).
Histiocytic Sarcoma (Canine)
11y MC Shetland Sheepdog with recent onset of vestibular signs.
- There is a large T1 hypointense and T2 isointense spherical mass in the left side of the caudal fossa (a,b: arrow), causing displacement and compression of the cerebellum and brainstem.
- The T2 and FLAIR hyperintense rim surrounding the mass lends evidence that this is an extraaxial lesion (b,c: arrowheads).
- The mass enhances following contrast administration and has a subtle nonuniform “ground glass” enhancement pattern (d–f).
The mass was confirmed to be a histiocytic sarcoma on postmortem examination. Microscopically, the mass was well demarcated, but unencapsulated, and invaded adjacent brain parenchyma from a broad meningeal base.
Metastatic Hemangiosarcoma (Canine)
11y MC Pit Bull Terrier with acute onset obtundation and tetraparesis.
- There is a large left thalamic mass of T1 and T2 mixed intensity, causing ventricular compression and distortion (a,b: large arrow).
- A second, smaller mass is seen in the left endomarginal gyrus, which also has mixed T2 intensity (b: small arrow).
- There is marked susceptibility effect within both masses on the gradient echo T2* image, indicative of hemorrhage (c: arrows).
- Both masses nonuniformly and peripherally enhance following contrast administration (d,e: arrows).
Widespread hemangiosarcoma metastasis was confirmed by postmortem examination. Cut surfaces of the brain masses reveal extensive intratumoral hemorrhage, consistent with the complex intensity patterns seen on MR images (f: arrows). Anwer et al 2013.19 Reproduced with permission from Wiley.
Sellar and Parasellar region
- Normal Pituitar Gland
- Dynamic CT and MR protocols
Normal pituitary gland
The sella turcica is the osseous boundary of the pituitary gland. It is comprised of the:
- Pituitary fossa ventrally
- The rostral and caudal clinoid processes dorsally.
- The pituitary gland is located in the pituitary fossa of the basisphenoid bone.
The pituitary gland is formed of two parts:
- The vascular, glandular adenohypophysis
- The neurohypophysis
- It is suspended from the hypothalamus by the infundibulum, which courses through an incomplete dural septum covering the dorsal aspect of the fossa. The ventral aspect of the third ventricle extends centrally through the infundibulum to the proximal neurohypophysis.
The pituitary gland is perfused by branches of the internal carotid and communicating arteries of the circle of Willis, with venous drainage into the cavernous and intercavernous sinuses.
The optic chiasm is located immediately rostral to the origin of the infundibulum, and the third cranial nerves arise caudal to, and course lateral to, the pituitary fossa.
On unenhanced CT images, the pituitary gland is isoattenuating to deep gray matter and contiguous with the adjacent hypothalamus, with ventral margins well delineated by the basisphenoid bone. When the third ventricle is prominent, a relatively hypoattenuating infundibular recess may be visible extending to the proximal neurohypophysis.
On contrast‐enhanced CT and MR images, the pituitary gland markedly contrast enhances compared to brain tissue because of a rich vascular suppl.
Dynamic contrast imaging studies of the normal pituitary describe an initial central contrast blush, attributable to early enhancement of the neurohypophysis, followed by a slightly delayed peripheral enhancement of the adenohypophysis with diminished central enhancement.
On MR images, the normal pituitary gland usually has a focal T1 hyperintensity, which is thought to represent either vasopressin‐containing neurosecretory granules or glial cell lipid droplets in the neurohypophysis. T2 intensity is similar to cortical gray matter. The lipid‐rich marrow of the basisphenoid bone is hyperintense on both T1 and T2 images.
Normal canine pituitary size on CT images is approxi mately 4.5mm in height and 6mm in width. On MR images, it is reported to be 5.1±.9mm in height and 6.4±1.0mm in width, with little correlation to brain measurements or body weight.
Normal feline pituitary size has been estimated to be approximately 5mm in height and 3.5mm in width on both CT and MR imaging. While these dimensions may be useful as general guidelines, they are not particularly useful for diagnosis of microadenomas. With both imaging modalities, the presence of a prominent convexity to the dorsal pituitary margin and elevation of the dorsal margin above the sella turcica on a sagittal plane image are additional qualitative imaging features that are suggestive of a pituitary disorder.
Dynamic CT and MR protocols
Dynamic contrast CT protocols have been used to detect small (micro) hypophyseal masses. However, the current trend in human and veterinary medicine has been toward the use of MR for diagnosis and characterization of pituitary disorders. Dynamic CT and MR procedures described in the veterinary literature involve dynamic thinly collimated image acquisition through the pituitary gland every few seconds for 2–5 minutes following intra venous bolus contrast administration to detect neurohypophysis displacement by adenohypophyseal tumors
Normal Pituitary Gland (Canine)
10y FS Beagle. Images a–c are representative transverse images at the level of the pituitary fossa. Images d–e are comparable sagittal images, and image f is a magnified view of image e.
- The pituitary gland is positioned within the pituitary fossa (height=4mm, width = 6 mm) and has a relatively flat dorsal margin that does not extend above the dorsal limits of the sella turcica (d–f).
- The pituitary gland is partly T1 hyperintense because of the presence of secretory granules in the neurohyphysis that result in T1 shortening (a,d: arrow).
- The normal pituitary gland is markedly contrast enhancing as a result of the high vascular density of the gland (e,f), and the pituitary stalk is also evident (e,f: large arrow).
- Cerebrospinal fluid in the chiasmatic cistern is evident dorsolateral to the pituitary gland and is T1 hypointense and T2 hyperintense (b,c: large arrows).
- The cavernous sinus enhances on the contrast‐enhanced T1 image (c: small arrows), and circular hypointense signal voids can be seen within the sinus, representing flow voids in the internal carotid and/or communicating arteries.
- The optic chiasm is located rostral to the pituitary gland (e,f: small arrow) and can be encroached upon by expansile pituitary masses.
- Part of the mandibular branch of the left trigeminal nerve can also be seen (c: arrowhead).
Empty Sella Syndrome (Canine)
10y FS Pekinese acutely nonambulatory with neurologic deficits referable to a cerebrothalamic lesion. The dog had no clinical or clinical chemistry evidence of central endocrinopathy. Images a and b are representative transverse images at the level of the pituitary fossa. Images c–e are comparable images oriented in the sagittal plane, and image e is a magnified view of image d.
- There is diffuse brain atrophy resulting in enlargement of the ventricular system and subarachnoid space (a–e).
- The pituitary fossa is fluid filled and appears T1 hypointense and T2 hyperintense (a–d: arrow). This fluid collection appears to communicate with the third ventricle (e: asterisk) by way of the infundibular recess (e: large arrow).
- The interpeduncular (e: small arrow) and chiasmatic (e: arrowhead) cisterns are also prominent.
Pituitary Cyst (Canine)
10y FS Labrador Retriever with acute obtundation and disorientation.
- The dog had multiple meningiomas involving the right cerebrum and pons, causing the clinical signs, and the cystic pituitary gland was an incidental finding.
- Image b represents a magnified view of image a. Images c–e are representative close‐up views of the pituitary fossa in the transverse plane. The pituitary fossa contains a predominantly T1 hypointense and T2 hyperintense cyst (a–d) with a thin rim that is isointense to adjacent deep gray matter (c: arrows).
- The cyst enhances peripherally (e: arrows).
- Ill‐defined T2 hyperintense edema is present in the hypothalamus (d) because of the meningiomas.
Pituitary Hemorrhage (Apoplexy) (Canine)
10y MC Chow cross with neurologic signs consistent with increased intracranial pressure. The dog also had concurrent thrombocytopenia.
- A large, T1 and T2 hyperintense, heterogeneous mass is present involving the pituitary, hypothalamic, and thalamic regions (a,b).
- The mixed‐signal pattern is consistent with intraparenchymal hemorrhage.
- The mass moderately and heterogeneously contrast enhances (c).
Postmortem examination found that the pituitary was expanded, and in some regions obliterated, by lakes of free red blood cells and a mass composed of red blood cells, fibrin, and degenerate cells (hematoma).
Pituitary Microadenoma (Canine)
12y FS Border Terrier with confirmed pituitary‐ dependent hyperadrenocorticism. Images a and b are representative transverse images at the level of the pituitary fossa. Image d is a magnified view of image c.
- A uniformly contrast‐enhancing and symmetrical pituitary gland is evident (b–d: arrow).
- The gland is considered within normal limits for size (height = 4 mm, width = 6 mm), but the dorsal margin is convex and extends beyond the dorsal extent of the sella turcica.
Pituitary Microadenoma (Canine)
3y MC Corgi with confirmed pituitary‐dependent hyperadrenocorticism. Images a–c are representative transverse images at the level of the pituitary fossa. Image f is a magnified view of image e.
- The pituitary gland has nonuniform mixed T1 intensity and T2 signal that is isointense with that of deep gray matter.
- Although the gland measures within normal limits for size (height = 5 mm, width = 5 mm), the adenohypophysis appears prominent, displaces the more hyperintense neurohypophysis dorsally, and extends beyond the dorsal extent of the sella turcica (d: arrow).
- The adenohypophysis enhances uniformly following contrast administration (c,f: arrow).
History, clinical signs, and results of a low‐dose dexamethasone suppression test were indicative of pituitary‐dependent hyperadrenocorticism.
Idiopathic Trigeminal Neuropathy (Canine)
3y F Pug with a 6‐day history of dropped jaw. Neurologic deficits were limited to cranial nerve V motor function bilaterally.
- The mandibular branches of the fifth cranial nerves are symmetrically enlarged and are T1 and T2 isointense on unenhanced images (a,b: arrows).
- Both nerves uniformly and intensely contrast enhance, defining enlarged intracranial and distal components that exit the base of the skull through the oval foramina (c,d: arrows).
- Image d is a parasagittal view of one of the mandibular nerves.
A diagnosis of idiopathic trigeminal neuropathy was made in this patient based on the lack of any identifiable cause for the neuropathy and gradual improvement with supportive care.
Cranial Nerve II Granulomatous Meningoencephalitis (Canine)
4y MC Golden Retriever with ataxia and weakness.
- The right optic nerve is mildly enlarged and is T1 isointense and T2 hyperintense (a,b,d: arrow).
- There is also a slight bulge of the optic disc, best seen on the dorsal plane T2 image (a: arrowhead).
- The nerve moderately enhances following contrast administration (c,e: arrow).
Postmortem examination confirmed granulomatous meningoencephalitis involving the brain and the right optic nerve. The MR features of the optic nerve lesion are subtle in this patient.
Cranial Nerve II Chronic Suppurative Neuritis (Feline)
12y MC Domestic Shorthair with progressive left‐sided exophthalmos. Images a and b are to the left of midline in the parasagittal plane at the level of the optic canal. Image c is somewhat more lateral in the same plane.
- A large left retrobulbar mass (a–d: asterisk) results in rostral displacement of the ipsilateral globe.
- The mass extends caudally through the left optic canal (a,b: large arrow) and incorporates the optic chiasm (a,b: small arrow).
- Regional meningeal enhancement is also evident (c: arrow).
- The left optic nerve is not well delineated, but neural enlargement is assumed from the parasagittal images (a,b: arrowhead).
Postmortem examination revealed severe chronic suppurative optic neuritis and meningitis.
Cranial Nerve II Meningioma (Canine)
10y FS Kelpie with right exophthalmia and absent menace response of 3 week duration.
- The right optic nerve is enlarged and has a nonuniform diameter (a–c: arrow).
- The meningeal sheath intensely enhances.
- Oblique plane images were generated to approximate the path of the right (c) and left (d) optic nerves through their respective optic canals (c,d: arrow).
A right orbital exenteration was performed, and a right optic nerve meningioma was confirmed histologically.
The dog returned 2 years later with clinical signs referable to intracranial neurologic disease.
- The proximal remnant of the right optic nerve is enlarged, irregularly margined, and nonuniformly contrast enhances (e: arrow).
- The mass now includes both retrobulbar and intracranial components (e–g: arrowhead).
Cranial Nerve V Benign Peripheral Nerve Sheath Tumor (Canine)
7y MC Shetland Sheepdog with left‐sided masticatory muscle atrophy and other signs of left trigeminal nerve dysfunction.
- MR images reveal a large, well‐delineated, T1 hypointense, T2 hyperintense left‐sided extraaxial mass causing compression of the brainstem and cerebellum (a–d: arrow).
- The mass intensely and uniformly contrast enhances and extends rostrally through the trigeminal canal (d: arrowhead).
- There is also marked atrophy and T1 and T2 hyperintensity of the left masseter muscle, consistent with fatty infiltration from chronic denervation (a,b: arrowheads).
- A CT examination was performed for radiation treatment planning.
Images e and f are unenhanced and enhanced images acquired at the level of the trigeminal canal. Images h and i (next page) are more caudal, centered at the level of the mass.
- There is destruction of the temporal bone pyramid that forms the trigeminal canal (e: arrowhead).
- Note that the mass is not seen on the unenhanced CT images (h).
- The previously identified mass intensely but nonuniformly enhances (f,g,i: arrow).
- The globoid part of the mass is located in the caudal fossa (g,i: arrow) but extends rostrally through the trigeminal canal (g: arrowhead).
Postmortem examination confirmed the presence and location of the extraaxial mass (j: arrowheads). Microscopic diagnosis was left trigeminal nerve neurofibroma.
Cranial Nerve V Malignant Peripheral Nerve Sheath Tumor (Canine)
7y FS Labrador Retriever with neurologic deficits localized to the mandibular branch of the left trigeminal nerve.
- There is a large, T1 hypointense, T2 hyperintense tubular mass that arises at the origin of the left trigeminal nerve and extends rostrally through the trigeminal canal of the temporal bone (a–e: arrow).
- There is marked left temporal muscle atrophy consistent with mandibular nerve motor dysfunction, and the muscle is mildly T1 and T2 hyperintense compared to the contralateral temporal muscle as a result of fatty infiltration from chronic denervation (a,b: arrowheads).
- The mass intensely and uniformly enhances following contrast administration (c–e: arrow).
Postmortem examination confirmed a peripheral nerve sheath tumor of the origin and mandibular branch of the left trigeminal nerve (f: arrowheads).
Cranial Nerve V Lymphoma (Canine)
7y MC German Shepherd Dog with multiple cranial nerve neuropathy, including pronounced bilateral trigeminal nerve involvement.
- Prominent, well‐delineated, T1 hypointense, T2 hyperintense extraaxial masses are present on either side of the brainstem, causing axial compression bilaterally (a,b: arrows).
- The masses moderately and uniformly contrast enhance (c: arrows).
Cerebrospinal fluid analysis revealed the presence of abnormal lymphocytes. The diagnosis of lymphoma was confirmed on postmortem examination performed 6 months following the MRI examination.
Cavernous Sinus Syndrome (Canine)
8y FS Shepherd cross with cranial nerve III, IV, V, VI, and ocular sympathetic innervation deficits consistent with cavernous sinus syndrome.
- There is a large, well‐defined, T1 isointense, T2 hyperintense ovoid mass arising from the pituitary fossa (a,b: arrow).
- The carotid arteries are identified in cross‐section and appear to be surrounded by the mass (a,b: arrowheads).
- Following contrast administration, the mass uniformly and intensely enhances, and the basilar part of the mass can be seen to invade the cavernous sinus bilaterally.
Carotid arteries are confirmed to be incorporated into the mass (c: arrowheads). The cavernous sinus contains the carotid arteries, its sympathetic plexus, and the third, fourth, sixth, and some branches of the fifth cranial nerves. The invasion of the mass within the sinus explains the clinical signs.
