Cerebellar Infarcts in Two Dogs Diagnosed With Magnetic Resonance Imaging
Two dogs presented with severe, peracute-onset, neurological signs. Neuroanatomical localization was cerebellovestibular. Magnetic resonance imaging (MRI) was performed and revealed focal, wedge-shaped lesions in the cerebellum. Diagnosis of cerebellar infarctions was made based on peracute-onset, clinical signs, MRI, and outcome as well as ancillary diagnostic information. Both dogs recovered completely. Cerebellar infarction should be included in the differential of any dog with peracute-onset, central cerebellovestibular signs regardless of severity of clinical signs. Outcome was excellent in these dogs.
Introduction
Cerebellar infarcts represent approximately 3% of all brain infarcts in humans.1 No statistics are known for veterinary patients. There have been only two reported cerebellar infarcts in dogs, and none have been described based on magnetic resonance imaging (MRI) findings.2 In this report, the authors describe MRI findings of two dogs with cerebellar infarcts.
Case Reports
Case No. 1
A 10-year-old, spayed female golden retriever was presented to the local emergency hospital for a peracute onset of unilateral imbalance, a left head tilt, and two episodes of vomiting. The event occurred while the clients observed the dog playing outdoors. No trauma was noted prior to clinical signs. The dog was on monthly heartworm preventative and was current on vaccines. The owners described an isolated event 2 years previously, which was consistent with a grand mal seizure. No other prior health problems were noted.
On presentation to the emergency hospital, the dog was unable to stand. Heart rate (68 beats per minute [bpm]), respiratory rate (20 breaths per minute), and temperature (101°F) were all within reference ranges. A neurological examination was not performed at this time. The dog was treated with prednisolone sodium succinate (18 mg/kg body weight, intravenously [IV]) approximately 3 hours after clinical signs began. The dog was placed on lactated Ringer’s solution (2.8 mL/kg body weight per hour, IV) and was given ampicillin (22 mg/kg body weight, IV q 8 hours). An electrocardiogram (EKG), blood pressure, complete blood count (CBC), urinalysis, serum biochemical profile, blood gas analysis, and thoracic and abdominal radiographs were performed on admission. The EKG revealed a normal sinus arrhythmia with normal complexes. The blood pressure was normal at 150/90 mm Hg (reference range, 80/60 to 180/100 mm Hg). All other tests were within reference ranges. The dog was monitored overnight and transferred to the primary care veterinarian in the morning.
The dog was subsequently referred for evaluation approximately 26 hours after clinical signs were noted. On presentation, the physical examination was normal. Neurological examination revealed an alert and mentally appropriate dog. Cranial nerve examination revealed a left head tilt, right menace deficit, and right nasal hypesthesia. A positional ventrolateral vestibular strabismus of the left eye was noted on dorsal flexion of the head. No other cranial nerve abnormalities were noted, including pathological nystagmus (spontaneous or positional). The dog was nonambulatory and preferred sternal or right lateral recumbency. When supported to stand, she would lean and fall to the left. Postural reactions were difficult to elicit because of the dog’s imbalance. Conscious proprioception was decreased in the right thoracic and pelvic limbs. Crossed extensor reflex from left to right in the thoracic limbs and increased tone in the right thoracic limb were noted. No sensory deficits were noted. The neurological examination supported a right paradoxical vestibular lesion. Differential diagnosis included vascular disorders (e.g., coagulopathy, infarction, emboli, vasculitis, vasculopathy, thrombopathia, arteriovenous malformation, hypertension, and hypothyroidism-related atherosclerosis), primary or metastatic neoplasia, infectious encephalitis (e.g., Rocky Mountain Spotted Fever, ehrlichiosis, bacterial), granulomatous meningoencephalomyelitis, parasitic migration (Cuterebra), and trauma. Serum total and free thyroxine, canine thyroid-stimulating hormone, and thyroglobulin autoantibody tests were within reference ranges. A systolic blood pressure was repeated with a Doppler and was found to be 150 mm Hg.
After all preliminary tests were negative, an MRI and collection of cerebrospinal fluid (CSF) were performed 78 hours after initial clinical signs. The dog was anesthetized with diazepam (0.25 mg/kg body weight, IV) and propofol (4 mg/kg body weight, IV) and maintained on isoflurane through a nonrebreathing system. An MRI was performed.a Pulse sequences performed were axial T2-weighted images [Figure 1], axial proton density-weighted images, axial T1-weighted precontrast images, axial T1-weighted postcontrast (i.e., gadolinium-DTPA) images [Figure 2], and sagittal T2-weighted images [Figure 3]. On T2- and proton density-weighted axial images, a hyperintense (relative to the normal brain parenchyma), wedge-shaped lesion was evident in the right cerebellar hemisphere. It was broadest at the dorsal cerebellar meningeal surface, and it extended ventrally into the medulla oblongata and medially to the vermis and two-thirds of the way to the lateral cerebellar surface. Axial T1-weighted postcontrast images revealed scant uptake and blushing, with contrast mainly at the periphery of this lesion. On sagittal T2-weighted images, a focal, clearly delineated, hyperintense lesion in the right rostral cerebellar hemisphere was noted. Sagittal, precontrast T1-weighted images revealed no significant abnormalities. The lesion observed was most consistent with focal ischemia resulting from acute infarction.3 Cerebrospinal fluid was acquired from the cerebellomedullary cistern, and analysis revealed an increased white blood cell (WBC) count of 12 per mm3 (reference range, <5 mm3), composed of a mononuclear pleocytosis and increased protein content of 31.8 mg/dL (reference range, <25 mg/dL). These CSF results were consistent with a diagnosis of central nervous system (CNS) infarction with necrosis. A cerebellar infarct of the right rostral cerebellar artery was the leading differential based on peracute onset of clinical signs, location, shape, and features of the lesion seen on MRI. No further medical treatment was instituted. Physical and vestibular rehabilitation therapies were recommended and performed three times daily. These exercises included passive range of motion exercises, massage, and walking as far and often as possible.4 Meclizineb (an antivertiginous antihistamine) was not initiated, because the dog was able to eat without vomiting and the drug has been shown to slow vestibular rehabilitation in humans.5 Over the ensuing 3 days, the dog improved to the point of being able to walk despite moderate listing and falling to the left greater than the right, truncal ataxia, and subtle intention tremors of the head. Over the next 1 to 2 weeks, the dog improved, and the owners reported her normal 5 weeks after the initial incident.
Case No. 2
A 10-year-old, spayed female basset hound presented to the referring veterinarian for peracute onset of collapse. Past medical history was confined to recurrent otitis externa. Vaccinations were up to date. On physical examination by the referring veterinarian, the dog was noted to be dull, have a left torticollis and horizontal nystagmus (fast phase not noted), and a subtle left nasal hypesthesia. Proliferative ear canals with severe waxy discharge were noted bilaterally. No additional abnormalities were reported on the referring physical and neurological examinations. A CBC, serum biochemical profile, and EKG were performed and found to be within reference ranges. Dexamethasone sodium phosphate (0.75 mg/kg body weight, IV) was administered on admission to the referring veterinarian’s hospital. The dog was also treated with lactated Ringer’s solution (3.25 mL/kg body weight per hour, IV), cefazolin (22 mg/kg body weight, IV tid), and an otic preparation with enrofloxacin (three drops in both ears, bid) for the next 3 days. Minimal improvement was noted, and the dog was referred on day 4. On neurological examination, she was mentally dull. Cranial nerve examination revealed a left head tilt and torticollis, a decreased left menace response, and a sustained positional vertical nystagmus. The dog was nonambulatory and would fall and roll to the left when supported to stand. Proprioception was normal in the forelimbs and difficult to assess in the rear limbs because of her inability to balance. The remaining neurological examination was normal. Physical examination was normal except for the aforementioned proliferative external ear canals. A left-sided central vestibular lesion was diagnosed. Differentials were as forwarded for case no. 1. Preanesthetic thoracic radiographs were normal. Systolic blood pressure was repeatable at 190 mm Hg using a Doppler. Anesthesia and an MRI were performed as for case no. 1. Results revealed a similar, focal, wedge-shaped lesion (as in case no. 1) in the left rostral cerebellar hemisphere, which was hyperintense on T2-weighted images (relative to the normal parenchyma), isointense on T1-weighted images, and only blushed with enhancement at the periphery on T1-weighted, postcontrast images. A diagnosis of left rostral cerebellar infarct in the territory of the rostral cerebellar artery was made based on clinical and MRI findings. Spinal fluid analysis was not performed. The following day, a repeat blood pressure via Doppler revealed persistent hypertension (220 mm Hg). A thyroid panel, echocardiogram, and abdominal ultrasound were recommended to investigate the etiology of the hypertension, but the owner declined because of financial reasons. The dog was discharged with amlodipine (0.17 mg/kg body weight, q 24 hours), recommendations to repeat the blood pressure in 2 weeks, and the same rehabilitation instructions as for case no. 1. Five days after discharge, the owner reported significant improvement, including the dog walking voluntarily but with residual imbalance and veering to the left. The referring veterinarian rechecked the blood pressure 2 weeks later, and the hypertension persisted (210 mm Hg) and the amlodipine was increased (0.35 mg/kg body weight, q 24 hours). The dog was reported to be ambulating well with only occasional imbalance. Two weeks later, the blood pressure was reported to be normal (140 mm Hg), and the dog was clinically normal on the referring veterinarian’s neurological examination. Amlodipine was continued at the current dose.
Discussion
Neuroanatomically, a pure cerebellar lesion cannot explain the unilateral loss of conscious proprioception seen in case no. 1, because the cerebellum regulates only rate, range, and force of motion.6 There are no direct conscious proprioceptive fiber connections within the cerebellum.6 In humans, the rostral cerebellar artery has branches that supply areas of the pons and medulla where conscious proprioception fibers are located.7 The extent of the lesion appears to incorporate at least part of the dorsolateral medulla oblongata. Associated edema, mass effect compression, or both would explain the ipsilateral conscious proprioception loss (i.e., interarcuate fibers and medial lemniscal system) and hypesthesia (i.e., sensory nucleus of the trigeminal nerve).6
Common clinical signs and symptoms noted in humans with cerebellar infarcts include dizziness, headache, vomiting, gait difficulty, nystagmus, intention tremor, tinnitus, vertigo, and dysarthria.7 Many of these signs but not symptoms were noted in the dogs of this report, including nystagmus, torticollis, head tilt, intention tremor, gait difficulty, and vomiting.
Cerebrovascular disease is the third leading cause of death and the number one cause of adult disability in the United States.1 Strokes are broadly classified as ischemic or hemorrhagic.1 Eighty-five percent of strokes are ischemic in humans.1 Ischemic strokes are then subdivided into cardioembolic, lacunar, atherosclerotic, and idiopathic categories.1 Causes of hemorrhagic stroke include intracerebral hemorrhage and aneurismal subarachnoid hemorrhage.1 Hemorrhagic infarction is a term reserved for ischemic infarcts that become hemorrhagic when perfusion to the ischemic area is restored.1 Cerebellar infarcts in humans are also classified according to location and etiology.1 Three arteries supply the cerebellum in humans: the superior cerebellar artery, the posterior inferior cerebellar artery, and the anterior inferior cerebellar artery. In dogs, the cerebellum’s blood supply originates from the basilar and caudal cerebral arteries.8 The basilar artery is formed through the union of the two vertebral arteries that arise from the subclavian arteries. Penetrating, short and long circumferential branches of the basilar artery supply areas of the midbrain, pons, and medulla oblongata. The rostral cerebellar arteries arise from the caudal cerebral arteries. These supply the different areas of the rostral cerebellum and dorsolateral brain stem. The basilar artery gives rise to the caudal cerebellar artery, which supplies the caudal and ventral cerebellum and lateral medulla. Infarcts in the territories supplied by the three cerebellar arteries in humans produce specific clinical syndromes.7 No information is available for differences in clinical signs in animals.
Predisposing factors for brain infarction in humans and presumably animals include cardiac disease (e.g., arrhythmias, atrial fibrillation, dilated cardiomyopathy, bacterial endocarditis, atrial myxomas, valvular disease, rheumatic heart disease, myocardial infarcts), hypercoagulable states, diabetes mellitus, chronic hypertension, hyperlipidemia, obesity, alcoholism, and tobacco use.9 Another cause in the elderly is cerebral amyloid angiopathy.10 Similar changes have been identified in old dogs, but no correlation with cerebrovascular disease has yet been detected.11 Hypothyroidism, diabetes mellitus, hyperadrenocorticism, and hereditary hypercholesterolemia are the major causes of atherosclerotic disease in veterinary patients, which could predispose to ischemic infarcts.12 The pathophysiology of infarcts secondary to atherosclerosis is either artery-to-artery embolism or hypoperfusion.1 Case no. 1 had no predisposing factors that could be identified. Although an echocardiogram was not performed, there were no clinical indications of heart disease, and the thoracic radiographs and EKG were normal. The etiology of the hypertension in case no. 2 could not be identified because of financial constraints.
Initial management in humans with suspected stroke include performing a blood glucose, blood pressure, EKG, noncontrast computed tomography (CT) scan, and laboratory profiles to include coagulation profile, platelet counts, hematocrit, serum biochemical profiles, and oxygen saturation measurements.1 Computed tomography is virtually 100% specific for intracranial hemorrhage, but for acute ischemia many have normal CT findings within the first 24 hours.1 Magnetic resonance imaging is more sensitive in these early stages.1
Cerebrovascular disease has infrequently been reported in the veterinary medical literature, with only sporadic case reports and one large case series reported.13–20 The most commonly reported cerebrovascular disorder, feline ischemic encephalopathy, has recently been attributed to migration of Cuterebra larva.21 Cerebellar infarcts are less often reported, but they do occur. Specifically, the authors have had seven necropsy-confirmed cerebellar infarcts in dogs and cats in the past 5 years. Previously limited availability of advanced diagnostic imaging modalities such as MRI and CT, financial restraints, low clinical suspicion, and lack of primary atherosclerotic disease in small animals are possible reasons for under-diagnosis.
The imaging modality of choice for early ischemia is MRI.3 Since water accumulates during the first few hours of ischemia and each water molecule contains two hydrogen ions, MRI has improved the ability to detect infarction earlier than CT imaging.1 Relaxation times on both T2- and T1-weighted images are prolonged because of the water accumulation secondary to the disruption of the blood-brain barrier.22 Prolongation of T1-weighted images will show low intensity within the area of ischemia.22 High intensity in the same region will be shown by T2-weighted images because of the slow decay of signal based on prolonged T2 relaxation.22 The T2-weighted images are more sensitive to infarction.22 The blushing seen on postcontrast T1 images is due to leakage through the disrupted blood-brain barrier.22 Depending on time of infarction to imaging, the degree of enhancement varies and is directly dependent on the amount of concurrent vasogenic edema and mass effect which presumably compromises the microvasculature.22 An MRI is extremely important when considering caudal fossa disorders, which are much more difficult to visualize on CT because of bone-hardening artifact in this region.23 Computed tomography is utilized as an initial screening tool for intracranial hemorrhage in human medicine.1 If negative, then an MRI is indicated.1
Treatments for infarcts are mainly supportive in veterinary medicine. Fibrinolytic therapy has been used for vascular occlusion but has not been used to treat stroke in veterinary patients.24 Diagnosis needs to be confirmed with either CT or MRI to eliminate hemorrhagic infarcts before treatment is initiated in humans.1 Tissue plasminogen activator is the drug of choice in human medicine, and the golden period to initiate treatment is within 3 hours of onset of clinical signs.25 In humans, the only indication for use of heparin IV is acute ischemic stroke with a proven cardiac source of embolus, such as atrial fibrillation or dilated cardiomyopathy.1 Proof of the effectiveness of anticoagulant therapy other than for cardioembolism is not established in human medicine.1 Volume expansion therapy has not proven useful in ischemic strokes, but some patients may benefit from hydration if they are volume depleted.1 Corti-costeroids are ineffective for treating patients with intracranial hemorrhage.1 Hyperventilation and hyperosmotic diuretics such as mannitol are effective in lowering intracranial pressure, but they can lead to reduced cerebral perfusion and should only be used in cases of severe edema and brain stem compression.1
Hypertension should not be treated acutely because of the inability of the autoregulatory mechanisms of the brain in ischemic areas to provide adequate oxygenation; thus, these regions are primarily reliant on cardiac output and systemic blood pressure.25 Other therapies such as methyl-prednisolone sodium succinate have not been shown in human or veterinary medicine to be of benefit with cerebral infarction.26
Reasons for progression of clinical signs include expansion of a hematoma or edema.7 Rarely cerebellar infarcts can initiate a cascade of edema, brain stem compression, and obstructive hydrocephalus that can lead to death.7 This has been seen by the authors in one case of a necropsy-confirmed, cerebellar infarct. Cerebellar swelling generally occurs 2 to 4 days after infarction.7 Surgical extirpation of cerebellar infarcts in this category has been shown to be of life-saving benefit in humans.7
Conclusion
Prognosis for isolated cerebellar infarcts in humans is generally excellent, and recovery is similar to what was seen in the patients of this report. Acute-onset, lateralizing, nonprogressive neurological signs should alert the clinician to the possibility of cerebrovascular disease in veterinary patients. The initial severity of clinical signs does not always correlate with outcome and should not be reason for a poor prognosis without identifying the etiology. Cost, availability of CT or MRI, and presentation related to time of onset are limiting factors to the medical interventional treatments of cerebrovascular disease in veterinary patients. If MRI or CT capabilities are accessible, quick diagnosis and possibly fibrinolytic therapy could change the treatment of infarcts in veterinary patients in the future. Larger case studies are required to better define ideal treatment protocols.
1.5T GE Signa MRI; General Electric Medical Systems, Milwaukee, WI
Meclizine; Geneva Pharmaceuticals, Broomfield, CO
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390203
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390203
Citation: Journal of the American Animal Hospital Association 39, 2; 10.5326/0390203
A magnetic resonance image (MRI) demonstrating the location of a cerebellar infarct in a 10-year-old dog with peracute onset of vestibular signs. A hyperintense, wedge-shaped lesion is visible in the right cerebellum (T2-weighted, fast spin-echo, axial image).
