Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.
Medical records of 33 dogs presented for acute onset, nonprogressive, intracranial dysfunction that had a magnetic resonance imaging diagnosis of brain infarction were reviewed. Postmortem confirmation of brain infarction was available in 10 dogs. All dogs were evaluated by CBC, serum biochemistry, thyroid and adrenal testing, urinalysis, thoracic and abdominal imaging, and cerebrospinal fluid analysis. Results of coagulation profile and arterial blood pressure were available in 32/33 and 28/33 dogs, respectively. On the basis of the imaging findings, infarcts were classified depending on their type (territorial or lacunar) and location within the brain (telencephalic, 10/33; thalamic/midbrain, 8/33; cerebellar, 15/33). No marked associations among location or type of infarct and patient age and sex, occurrence of systemic hypertension, and the presence or absence of a concurrent medical condition were identified. Small breed dogs (< or =15 kg) were significantly more likely to have territorial cerebellar infarcts, whereas large breed dogs (>15 kg) were significantly more likely to have lacunar thalamic or midbrain infarcts. A concurrent medical condition was detected in 18/33 dogs with brain infarcts, with chronic kidney disease (8/33) and hyperadrenocorticism (6/ 33) being most commonly encountered. Of 33 dogs, 10 were euthanized because of the severity and lack of improvement of their neurologic status or the severity of their concurrent medical condition. No association was identified between type or location of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts.
Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.
A method for foramen magnum decompression (FMD) in dogs with caudal occipital malformation syndrome (COMS) and results for 16 dogs are described. In brief, a dorsal approach to the caudal portion of the occiput and arch of the atlas was made, and a high-speed drill was used to remove a portion of the occiput in the region of the foramen magnum and the dorsal aspect of C1. The meninges that were exposed were removed or marsupialized to surrounding tissues. Foramen magnum decompression was performed in 16 dogs. No intraoperative complications occurred, and postoperative complications occurred in only 2 dogs after initial surgery and in 1 of these dogs after follow-up surgery. In both dogs, postoperative complications after the initial surgery resolved without additional treatment. One dog was nonambulatory tetraparetic after follow-up surgery and died of a suspected ruptured viscus 9 days after surgery. Four dogs developed evidence of scar formation at the surgery site and required additional surgery. Overall, 14 dogs survived, 1 died, and 1 was euthanatized. Clinical signs resolved in 7 of the 14 dogs that survived, improved in 6, and did not change in 1. Results suggest that FMD may be an effective treatment for dogs with COMS, especially if performed early in the course of the disease.
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