Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs
Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs
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DOI：
10.1892/0891-6640(2006)20
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发表时间：
2006-03-01
影响因子：
2.6
通讯作者：
Schatzberg, SJ
中科院分区：
文献类型：
--
作者：
Garosi, L;McConnell, JF;Schatzberg, SJ
本文回顾了40只犬的磁共振成像(MRI)诊断急性起病、非进展性、颅内功能障碍的临床资料。脑梗塞部位：端脑11例，丘脑/中脑8例，小脑18例，多灶性3例。在大脑中动脉(4/11)、大脑嘴动脉(2/11)和纹状动脉(5/11)的区域内可见端脑。丘脑/中脑梗塞发生在穿支动脉或丘脑尾侧部分和脑干吻侧部分(8/8)。所有小脑梗塞(18/38)均位于小脑嘴动脉或其一个分支的范围内。所有的梗塞都是非出血性的，在38例中只有3例观察到显著的对比增强，所有这些都是在出现神经功能障碍的迹象后7天以上进行成像的。6只狗的弥散加权成像(DWI)序列均在出现神经功能障碍迹象的5天内进行成像。可疑梗塞在DWI序列上呈高信号，在表观弥散系数图上呈低信号。端脑梗塞导致精神状态异常、对侧姿势反应障碍、对侧鼻痛觉减退、对侧威胁障碍和同侧旋转。丘脑/中脑梗塞导致对侧或同侧姿势反应障碍、对侧威胁障碍、同侧头部倾斜或转向、眼球震颤、腹外斜视和眼球不对称。小脑梗塞导致同侧非对称性小脑质量共济失调、头部倾斜、间歇性视功能不全、眼球震颤和同侧视力明显正常的威胁缺陷。
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 in farcts 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 or the caudal portion of the thalamus and rostral portion of the brain stein (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 (logs, 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 oil 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 opistliotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.