It's a no brainer...magnetic resonance imaging of the nervous system (Proceedings)

Article

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.

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.

Brain neoplasia can be subdivided into two categories, extra-axial (i.e. meningiomas, choroid plexus papilloma, and pituitary – either adenoma or carcinoma) and intra-axial (i.e. gliomas – astrocytoma or oligodendroglioma) or metastases. It is relatively easy to differentiate primary brain neoplasia from metastatic neoplasia (similar to on thoracic radiographs). Primary neoplasia is usually a single lesion resulting in a mass effect that is contrast enhancing to some degree. Boxers are more commonly affected with primary brain neoplasia than other breeds.

Each of the following brain tumors has specific imaging findings. Meningiomas are broad based along the skull and there is commonly a dural tail sign, intense diffuse contrast enhancement, and adjacent hyperostosis of calvarium can be visualized. IN cats meningiomas can be multiple.

Pituitary macroadenoma are greater than 10mm in height in humans, located in the sella turcica in the ventral brain, with diffuse contrast enhancement. There is no apparent relationship to presence of a pituitary tumor and development of neurologic signs as a recent study noted that 20% dogs with tumor showed no neurologic signs while 56% with neurologic signs had no detectable tumor. Vague neurologic signs (such as lethargy, mental dullness and inappetence) were more likely associated with a pituitary macroadenoma than more specific neurologic signs (such as seizures). Intra-axial gliomas are located in middle of brain parenchyma, have variable amounts of contrast enhancement (depends on aggressiveness) and there is often lots of peritumoral edema.

We know that seizures alone can also create changes detectable on MRI. In people, there is increased signal on T2 images without a mass effect which resolves without therapy. These can occur in multiple locations but are seen commonly in the piriform lobes. Histologically these are confirmed to be edema. Time to reversal of lesions is unknown in both people and pets, but known by at least 10 weeks.

Why do we do MRI of the brain? Because even if it is cancer there are many treatment for our patients these days which improve both quality and quantity of life. Treatment options for brain neoplasia include palliative chemotherapy with steroids, seizure treatment with phenobarbital/ KBr, surgery – especially frontal lobe meningiomas, radiation therapy – metastatic disease, pituitary tumors, lymphosarcoma, meningiomas. Survival times of up to 12 months can be achieved in patients with pituitary macroadenomas treated with radiation therapy. As for chemotherapy, some cross the blood brain barrier, and may also play a role in treatment.

Extracranial diseases (such as nasal adenocarcinoma or fungal rhinitis, cranial nerve neoplasia or neuritis, and ocular/ear neoplasia/ infection) can extend into the brain parenchyma. Nasal adenocarcinoma often presents with epistaxis. MRI shows mass involving the ethomoturbinates which invades the olfactory lobe of the rostral cerebrum causing a shift in the longitudinal cerebral fissure. Trigeminal nerve neoplasia is identified as a mass effect that distorts the brain stem with bulbous expansion of the trigeminal canal, unilateral masticatory muscle atrophy with increased muscle intensity. By comparison trigeminal neuritis reveals an enlarged cranial nerve 5 sometimes with a mass that distorts the brain stem. There is masticatory muscle atrophy and increased muscle intensity which is similar in appearance to neoplasia. Bacterial meningoencephalitis is a result of otitis interna or penetrating skull lesion.

MRI can also be useful in imaging spinal abnormalities. There are numerous non-neoplastic diseases of the spine as well as a few cancers. Non-neoplastic diseases include cervical stenotic myelopathy, spinal arachnoid cysts, intervertebral disc disease, cartilaginous exostoses, vascular disorders, lumbar stenotic myelopathy, and intraspinal facet cysts. Neoplastic diseases in the spine are less common than in the brain and include meningiomas, nerve sheath tumors, and tumors affecting the vertebral bodies that impinge on the spine.

"Wobblers" has also been called cervical vertebral instability, cervical spondylopathy, cervical spondylomyelopathy, cervical spondylolithesis, and cervical vertebral malformation-malarticulation. Cervical stenotic myelopathy is preferred terminology by some. Young (majority less than 2 years old) male Great Danes show degenerative disease of the articular processes which compress the spinal cord. Doberman Pinschers are usually middle to older age when affected. They have type II Hansen disc protrusion present as well. MRI shows ventral compression of the spinal cord/canal due to dorsal vertebral "tipping" or misshapen vertebral bodies, intervertebral disc protrusion, and hypertrophy of the dorsal longitudinal ligament (which is located in the ventral spinal canal). Dorsal and lateral compression of the spinal cord/ canal due to hypertrophy of the interarcuate ligaments and joint capsule of the articular processes as well as osteoarthrosis of the articular processes with excessive soft tissue proliferation and synovial cysts. The compression of the spinal cord results in intramedullary edema which is hyperintense on T2 series. Spinal arachnoid cysts are fluid filled regions of the subarachnoid space which cause compression of the spinal cord as they enlarge. Reportedly most common in the dorsal cervical spine. Rottweilers are commonly affected. The etiology of spinal arachnoid cysts are many. They may be congenital or acquired due to trauma, hemorrhage, and inflammation. They can be incidental findings, as the patient may be asymptomatic at the time of diagnosis, but clinical signs can progress. The hypothesis is that gradual expansion of the cyst occurs due to a valvular mechanism associated with pulsatile CSF flow. MRI findings include a fluid filled structure usually in the dorsal subarachnoid space with secondary compression of the spinal cord, dilation of the central canal (syringomyelia) caudal to the cyst can occur due to altered CSF flow. Intervertebral disc disease is the most common spinal malady. MRI findings include decreased intensity of the nucleus pulposus (jelly-like central portion of the disc), narrowing of the disc space, abnormal shape of the disc space (wedging), hyperintense signal in the spinal cord (due to malacia, edema, or hemorrhage), narrowing of the spinal cord by a mass effect in the ventral vertebral canal, and obliteration of the perineural epidural fat signal. This is common in canine's and uncommon in cats. The most common site of disc extrusion in a cat is at C2-3 and is often traumatic in etiology. Vascular diseases such as infarcts and hemorrhage occur in the spine and are similar in appearance on MRI as seen in the brain. Cartilagenous exostoses can be single or multiple. They are cartilage capped bone growths that arise from metaphyseal or juxta-epiphyseal regions of axial and appendicular skeleton. Historically they are reported to parallel growth of the skeleton, with cartilage cap being converted to bone at the time of skeletal maturity. They are caused by abnormal differentiation of cartilage cells. Malignant transformation to chondrosarcoma and osteosarcoma can occur. Lumbosacral stenosis is an abnormal narrowing of the spinal column resulting in compression of the cauda equina nerve roots or blood vessels. Other concurrent findings include intervertebral disc degeneration, bone proliferation on the vertebral endplates and articular facets, vertebral subluxation, and hypertrophy of the surrounding ligaments and joint capsules (similar to cervical spondylomyelopathy). It affects male large breed dogs primarily. It can be either congenital (as with spina bifida or lumbosacral malformation) or acquired/ degenerative (lumbosacral transitional vertebrae predispose GSD to cauda equina syndrome, sacral OCD, and lumbosacral instability). Sagittal T1 allows evaluation of multiple intervertebral disc spaces. The dorsal longitudinal ligament (runs along ventral vertebral canal) is visualized on T1 and will be displaced with disc rupture. MRI is also able to visualize nerve root compression as well as mass of disc in lumbosacral canal. Transverse T1 allows evaluation of the bilateral diathrodial joint articulations and periradicular fat in the intervertebral canals. Degenerative myelopathy shows no MRI changes and therefore is diagnosed by ruling out other causes of rear end weakness. Intraspinal facet cysts develop secondary to degenerative joint disease in the spinal diarthrodial joints. Cysts are located immediately adjacent to a degenerated articular process. These can be either synovial cysts or ganglion cysts, but differentiation between the two is not possible on MRI.

Neoplasia affecting the spine include intradural cancer (such as meningiomas and nerve sheath tumors), extradural lesions of the bone (osteosarcoma, chondrosarcoma, and hemangiosarcoma), and intramedullary gliomas. These appear similar to neoplastic lesions in the brain. Nerve sheath tumors are either neurofibromas or schwanomas and are most common in the brachial plexus. Chronic forelimb lameness, unilateral thoracic limb atrophy, Horners syndrome - if T1 and T2 nerve roots affected (miosis, ptosis, enopthalmus, and third eye prolapse). Bone neoplasia impinging on the spinal cord may be best evaluated with CT, as it is superior for bone detail. Though fat suppression (STIR) and T2 weighted gradient echo may help with vertebral evaluation in MRI.

References

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