Feline Ischemic Encephalopathy
Feline ischemic encephalopathy (FIE) results in cerebral ischemic necrosis. Feline ischemic encephalopathy occurs in male and female cats of all ages and is more prevalent in the summer months. The cause of FIE is uncertain. Preliminary evidence suggests Cuterebra infection as a potential cause in some cases.
Clinical pathology is usually unremarkable. Cerebrospinal fluid (CSF) analysis may be normal or have mildly elevated protein levels and a mild to moderate pleocytosis. An increased proportion of large foamy macrophages have been observed in the CSF from 2 to 7 months after the onset of seizures. Suspected diagnosis can be made by T2 weighted MRI. In one study of six cats with FIE, MRI findings included mild to marked asymmetry of the cerebral hemispheres and bilateral asymmetric enlargement of the subarachnoid space.
Gross lesions are usually unilateral and may involve up to 75% of one cerebral or cerebellar hemisphere (or both). Hemispheres may appear atrophic and ridged with wide sulci. Histopathologic findings have included parenchymal atrophy and cystic degeneration, gliosis, and phagocytic macrophage infiltration. Perivascular lymphocytic cuffing of small capillaries and vascular occlusive lesions including thrombosis and vasculitis has been reported. Infarction of the middle cerebral artery represents the most common distribution.
Clinical signs are typically acute in onset, nonprogressive, and suggestive of unilateral cerebral or brainstem involvement. Seizures are the most common historical or presenting clinical sign. Other clinical signs may include depression, head tilt, anisocoria, circling, seizures, and behavior changes.
Treatment is limited to supportive care, and the prognosis is generally favorable. Clinical improvement typically occurs over several days to weeks. Multiple episodes can occur. Behavior changes and uncontrollable seizures can persist.
Fibrocartilaginous embolization (FCE) is associated with ischemic necrosis of the spinal cord parenchyma. The pathogenic mechanism is not resolved. Spinal cord arteries and veins become occluded with fibrocartilage originating from the nucleus pulposus of the intervertebral disc. Trauma may be a predisposing factor in a large percentage of affected cases. Fibrocartilaginous embolization can occur at any age but is most common in adult non-chondrodystrophoid breeds. Young Irish wolfhounds and miniature schnauzers are particularly prone to the disease. Fibrocartilaginous embolization has been reported less commonly in cats.
Clinical signs of myelopathy vary depending on the location and severity of the spinal cord ischemic injury. Deficits are often asymmetrical, and the clinical signs are not progressive. Affected animals do not typically show evidence of pain, although brief painful periods have been described just prior to the onset of clinical signs.
Diagnosis of FCE is based on excluding other causes of acute myelopathy. Results of plain radiographs are normal. CSF evaluation may be normal or show nonspecific abnormalities including mild protein elevations, mild pleocytosis, and xanthochromia. Myelography is typically normal, or mild spinal cord swelling is seen. MRI may reveal spinal cord edema on T2 weight images.
Treatment is primarily supportive care and physical therapy. Evidence for the use of glucocorticoid therapy is lacking, if treatment is attempted, methylprednisolone succinate (MPS) should be given within the first 6 to 8 hours after the onset of neurologic signs. Prognosis for recovery is variable depending on the location and extent of the lesion. Poor prognostic indicators include lower motor neuron (LMN) signs and size of the animal because of the inherent difficulties of performing physical therapy on large breed dogs.
An arterial aneurysm is a circumscribed dilation of an arterial wall or a blood-containing swelling connecting directly with the lumen of an artery. Arterial aneurysms are rare in dogs and cats and only isolated cases have been reported. Aneurysms can be categorized based on their shape (saccular or fusiform), cause (atherosclerotic, mycotic, inflammatory, arteritis, traumatic, congenital, dissecting), or their histologic appearance Two major histologic classes of aneurysms are (1) true aneurysms (aneurysma verum) and (2) false aneurysms (aneurysma spurium).
True Aneurysm A true aneurysm is a vascular dilatation caused by a weakened arterial or venous wall with subsequent widening of the vascular lumen. Histologically, true aneurysms involve the entire arterial wall and contain three microscopic arterial layers. Aneurysms may result from destruction of the media or the elastic fibers of large arteries (or destruction of both) by inflammatory or degenerative processes. Traumatic aneurysms can be true aneurysms or pseudoaneurysms, depending on their cause and histologic appearance. Aneurysms have been found in the aorta of dogs that were caused by migrating larvae of Spirocerca sanguinolenta (formerly S. lupi). Aneurysms can also result from turbulent blood flow with arteriovenous (AV) fistulas.
Dissecting aneurysm (aortic dissection) involves a hematoma associated with a defect in the aortic intima. Blood within the aortic lumen is forced through the intimal tear into the outer and middle layers of the aortic media, forming a second or false lumen. The dissection can then propagate proximally or distally along the aorta. A report of a dissecting aortic aneurysm was reported in a dog with clinical and histologic findings similar to that reported in humans. Dissecting aortic aneurysm has also been reported in two cats: one with CHF, severe aortic insufficiency and systemic hypertension and a second cat with signs of weakness, lethargy, and cardiogenic shock.
Peripheral aneurysms appear as soft, warm, pulsating bulges. Occasionally, a “machinery” murmur can be auscultated over these areas (see Arteriovenous Fistulas). Clinical signs are frequently absent or vague. If spontaneous vascular rupture occurs, pain, signs of anemia and shock, and pleural or mediastinal effusion may be present. Exsanguination resulting from aneurysmal rupture is possible.
Spurious (Pseudo) Aneurysm Spurious aneurysms, also known as pseudoaneurysms, are caused by localized disruption of the native artery. Their histologic appearance includes arterial wall architecture that is formed by fibrous tissue One cause of spurious aneurysms is a hematoma that communicates with an arterial lumen resulting from venipuncture.S Traumatic spurious aneurysms are probably more common than is usually realized. Clinical signs may include lameness, persistent pain, and deep muscular swelling unresponsive to local therapeutic measures, antibiotics, or glucocorticoids. Pitting peripheral edema may be present, and neither blood nor pus can be aspirated from the swelling. The diagnosis of spurious aneurysms may be suspected from physical examination. Survey radiographs may indicate soft tissue swelling. Diagnostic confirmation has classically relied on arteriography, which illustrates a nodular exudation of contrast medium at the arterial defect. Doppler echocardiography, especially color flow Doppler imaging, aids in identification by depicting blood flow and turbulence. Additional diagnostic tests include computed tomography (CT), radionuclide angiography, and surgical exploration. The differential diagnosis includes chronic infection, obstruction of a deep vein, or abscessation. With a spurious aneurysm, however, pyrexia and neutrophilia are not encountered. The prognosis is favorable if surgical vascular repair can be accomplished.
Arteriosclerosis is defined as chronic arterial wall remodeling consisting of hardening, loss of elasticity, and luminal narrowing. These changes result from proliferation of connective tissue and hyaline degeneration of media and intima. Proliferation and thickening of the intima with the deposition of ground substances leads to progressive fibrosis and vascular stenosis. Inflammation is not a feature of arteriosclerosis. Arteriosclerotic lesions are commonly detected in old dogs and cats and may comprise part of the normal aging process. These changes are typically mild and usually unimportant to health and survival. Thrombosis is rarely a complication of such microscopic lesions, and their functional significance is not known. In other instances, arteriosclerosis may be severe and associated with substantial reduction in intraluminal diameter (often referred to as small vessel disease). Lesions of this nature are also common in feline myocardial diseases, particularly hypertrophic cardiomyopathy, and may be detected in canine aortic stenosis as well. Arteriosclerotic changes may also occur in aorta and cerebral, renal, spinal, and sinoatrial node artery. Intramural coronary arterial narrowing commonly occurs in association with chronic degenerative valve disease as well. Arterial lesions may have been associated with small regions of myocardial necrosis and fibrosis. Intramural coronary arteriosclerosis was found in 26.4% of old dogs undergoing necropsy. Extensive nonthrombotic, nonatherogenic stenosis of extramural coronary arteries was described in two adult male Labrador retriever dogs with congestive heart failure. Disease of extramural arteries is less common. Endothelial aortic plaque formation associated with arteriosclerosis was detected in 77.8% of 58 dogs brought to a small animal clinic in Helsinki for euthanasia. Spontaneous arteriosclerosis, with a predilection for renal vasculature, has been demonstrated in young (<2 years old) greyhounds. The severity of the lesions was correlated with increased renal vascular tortuosity and high shear stress. Clinical consequences of these lesions have not been determined.