The purpose of this talk is to discuss what MR can and cannot image, review the basic neurologic diseases imaged with MR,
and ultimately know when to recommend MRI to your patients. First of all why do we use MRI? It has superior spatial resolution,
which is the ability to distinguish two distinct objects when separated by a small distance. MRI allows definition of actual
tissue characteristics (i.e. extracellular fluid, oxyhemoglobin, and methemoglobin). By comparison CT defines tissue by its
x-ray beam attenuation and cannot differentiate between CSF and extracellular fluid. Another reason we use MRI is multiplanar
image acquisition. We can obtain in sagittal, axial, and dorsal planes with MRI, while CT acquires in one plane and then requires
reconstruction. Also with MRI, there are no artifacts in the caudal fossa of the brain, a common problem with CT images through
this region. There are however several times/ instances that MRI not useful. Any tissues that lack hydrogen (i.e. lungs, dense
cortical bone, fibrous tissue, calcification, rapidly flowing blood) and any time that a study needs to be performed quickly
due to movement (i.e. lungs, abdomen).
First let's review the imaging planes. Transverse (also known as axial) is at a right angle to the hard palate. Sagittal is
aligned with the median plane of the brain. And dorsal (called coronal in people) is parallel to the base of the brain.
Next let's touch on some imaging sequences used in MRI. Different sequences are designed to optimize signal from a particular
tissue. T1 weighting is excellent for anatomy. T1 with contrast enhancement identified breaks in the blood brain barrier.
T2 weighting detects increased fluid in tissues (i.e. edema, CSF, hemorrhage – sometimes, and bone marrow). T2 is often called
a "pathology" scan. Fluid attenuation (FLAIR) is used occasionally to null signal from CSF while all other fluids remain bright.
This helps to identify periventricular lesions in the brain. Fat attenuation (STIR) series nulls signal from fat and helps
to differentiate bone marrow in skull from other pathology. STIR can also be useful to identify peripheral nerve sheath tumors
in the brachial plexus. And lastly gradient echo (GE) identifies blood.
In radiology we use opacity to describe the blackness or whiteness of a structure. In ultrasound we use echogenicity. In MRI
we use intensity. Tissues with high signal appear white and are called bright or hyperintense. Tissues with low signal appear
black and are called dark or hypointense.
Let's review basic brain anatomy/ associated neurologic signs with disease in each area. The brain can be grossly subdivided
into forebrain, brain stem, and cerebellum. Abnormalities in each of these areas can produce different neurologic signs. In
forebrain lesions, behavioral abnormalities, changes in appetite or thirst, constant pacing or circling, decreased awareness
and vision on one side of the body, some animals act as if they are in pain, and the big one - SEIZURES!!!! If a lesion is
in the brain stem, vestibular signs (i.e. loss of balance, head tilt, leaning and falling, ataxia, circling) as well as circling,
weakness on one side of the body, difficulty swallowing, inability to move eyes, and voice change can be seen. Neurologic
signs noted with cerebellar lesions include hypermetria, head tremors, wide based stance, and all of these are present with
normal strength present.
Now we can begin a review of abnormalities in the cerebrum and cerebellum. Initially we can break them down categorically
into non-neoplastic (i.e. congenital/ developmental, inflammatory/ infectious, vascular) and neoplastic. This list is important,
as it makes us realize that not all problems in the brain are cancer. Congenital/ developmental disorders include hydrocephalus,
Chiari malformations, caudal occipital malformation syndrome, intra-arachnoid cysts, and uncommonly lissencephaly. Hydrocephalus
means dilated ventricular system in the brain. This can be idiopathic/ congenital or caused by altered CSF flow. Chiari malformations
are a congenital anomaly of the caudal occipital region of the skull which leads to overcrowding of the caudal fossa with
compression and or herniation of the cerebellum through the foramen magnum. CSF flow dynamics are altered, resulting in increased
CSF pressures, and ultimately dilation of the central canal in the spinal cord (syringohydromyelia). ALMOST ALL AFFECTED DOGS
HAVE BEEN CAVALIER KING CHARLES SPANIELS though have been seen in Pomeranians too. Clinical signs with Chiari malformations
can include persistent scratching activity directed toward the head, neck, and shoulder regions, cervical myelopathy, seizures,
and facial nerve deficits. MRI shows obliteration of the dorsal subarachnoid space at the cervicomedullary junction, rostral
displacement of the caudal cerebellum by the occipital bone with (or without) concurrent 1.5 – 5.1mm herniation of the ventral
cerebellum through the foramen magnum, syringohydromyelia in the cervical spine usually from C2 caudally. Other abnormalities
commonly seen concurrently include enlarged lateral ventricles, intra-arachnoid cysts, and intervertebral disc protrusion/
extrusion in the cervical spine. Intra-arachnoid cysts are the second intracerebral disease to discuss. They are accumulations
of CSF within the arachnoid membrane because of splitting or duplication of the structure. They are common supra-tentorially
(i.e. dorsal to the osseous tentorium). Arachnoid cysts can be congenital/ developmental or acquired due to post inflammatory
loculation of subarachnoid space caused by head injury, intracranial infection, and hemorrhage. Lissencephaly is uncommon
and appears as a paucity of gyral formation with thickening of cerebral cortex. It is seen in Lhasa Apsos and they present
with forebrain signs such as seizures, behavioral abnormalities and visual deficits. Next we'll discuss infectious diseases
(which include rabies, distemper, parvovirus encephalomalacia, FIP, protozoal, bacterial, and mycotic) and inflammatory disorders
such as granulomatous meningoencephalitis (GME), steroid responsive meningitis, and necrotizing meningoencephalitis. With
these disorders the MRI findings are multifocal or diffuse and hyperintense on T2 weighted series. However 24% had normal
MRI. In this category of diseases CSF is the single most useful diagnostic test. The cause of GME is unknown. It is suspected
to be auto-immune however. GME affects middle aged small breed dogs (i.e. poodles and terriers). They can present with cervical
pain, fever, vomiting, and hyperesthesia. MRI findings are two distinct varieties. Focal, with a single round mass like granuloma
detected, and diffuse with diffuse meningeal enhancement. The granuloma with focal GME looks just like a tumor, as it creates
contrast enhancing mass. Can differentiate between neoplasia via CSF analysis. Necrotizing encephalitis is seen most commonly
in middle aged Yorkies, Pugs, and Maltese. They show forebrain signs of seizures and/or behavioral changes. The CSF analysis
shows non-suppurative inflammatory disease. The underlying etiology of necrotizing meningoencephalitis is not known. Vascular
disruptions include infarction and hemorrhage. STROKE as we know it in people is a sudden onset focal brain dysfunction and
can be caused by either infarction or hemorrhage. An infarction is a vascular occlusion by embolus or thrombus. These can
be due to hypothyroidism, septic thromboemboli, or neoplasia. Hemorrhage may be due to coagulopathy, hypertension, aneurysm
rupture, or a blood clot creating an infarct. Vascular lesions on MRI are wedge shaped and can involve both gray and white
matter. There is minimal to no mass effect and minimal contrast enhancement.