Magnetic Resonance Imaging Findings in Metabolic and Toxic Disorders of 3 Small Ruminants

Abstract

A 2-month-old female Boer Goat with microphthal-mia since birth was referred to the Clinic for Pigs and Small Ruminants and Ambulatory Service of the University of Veterinary Medicine, Hannover, because of a 3-day period of inappetence. Physical examination revealed no abnormalities except for bilateral micro-phthalmia. During neurologic examination, apathy and pleurothotonus to the right in combination with a circling gait in the same direction were observed. Postural reactions were reduced on the left side and the goat was blind. The neuroanatomic localization of the disease was forebrain lesion on the right side. The following differential diagnoses were considered: anomaly (eg, hydrocephalus), an inflammatory disease (including parasitic infection), or a metabolic or toxic lesion. In this context and in the following reports the term metabolic disturbance refers to endogenous metabolic abnormalities and to nutritional deficiencies. Although the clinical signs were asymmetric, a metabolic or toxic lesion was included in the differential diagnosis list as in some diffuse intracranial lesions one side can be affected more severely than the other. Radiographs of the skull revealed no abnormalities. The CBC and serum biochemistry results were normal. The owners wanted to keep the goat as a pet and further investigations were carried out. The sum of thiamine monophosphate (TMP), thia-mine diphosphate (TDP), and vitamin B1 concentrations in the blood as an indicator for thiamine deficiency was 0.123 mg/L (reference range, 0.044-0.08 mg/L). Serum antibodies against caprine encephalitis arthritis virus (CAE-V) and border disease virus (BD-V) could not be detected. The goat was anesthetized with xylazine a at a dosage of 0.05 mg/kg IM and ketamine b at a dosage of 4 mg/kg IV. Cerebrospinal fluid (CSF) was collected from the cisterna magna. The CSF cell count and protein concentrations were normal. Anesthesia was maintained with isoflurane c and oxygen via a Draeger respirator d and magnetic resonance imaging (MRI) was performed after 6 days of symptomatic treatment including antibiotics, IV fluids, PO administration of rumen fluid from a healthy donor, and thiamine supplements (Thiasel, e 100 mg/kg IV). Treatment did not alleviate the neurologic signs. The MRI of all 3 patients described in this report was performed with a 1.0 Tesla scanner. f The anesthetized animal was placed in sternal recumbency with the head positioned in a head coil. The imaging protocol included a T1-weighted spin echo (SE) (repetition time [TR] in milliseconds [ms] of 330.0 ms and echo time [TE] of 12.0 ms) sequence, a T2-weighted turbo spin echo (TSE; TR: 3,458.0 ms; TE: 96.0 ms), and a fluid attenuated inversion recovery (FLAIR) sequence (TR: 9,000.0 ms; TE: 105.0 ms). These 3 sequences were performed in sagittal, transverse, and dorsal planes. Furthermore, the T1-weighted SE sequence was performed a second time at the end of the other scans after IV administration of gadolinium-dimegluminie (Magnevist, g 0.2 mmol/kg). Compared to unaffected brain tissue, the T1-weighted sequences (transverse planes) demonstrated a bilaterally symmetric hypointense area in the fronto-parietal cortex (Fig 1A). A hyperintense signal compared to normal brain parenchyma, which corresponded with the hy-pointense areas in the T1-weighted sequences, was seen in the T2-weighted sequences (Fig 1B, C). Furthermore, the T2-weighted dorsal planes (Fig 1C) demonstrated a hyperintense signal in the area between the right parietal and occipital cortex. These findings indicated a high content of fluid in the grey matter of these areas. In order to identify the character of the fluid a FLAIR-sequence was performed (Fig 1D). This protocol suppresses the signal of the CSF therefore revealing extra-and intracellular fluid because of edema. 1 The FLAIR images also disclosed a hyperintense signal in the same locations as the hyperintense areas in the T2-weighted sequences. Because of the lesion's distribution and the fact that the white matter remained unaffected, intracellular cytotoxic edema in the fronto-parietal cortex in the area between the right parietal and occipital cortex was suspected. On the postgadolinium T1-weighted sequence no contrast enhancement could be seen. These MRI findings suggest bilateral symmetric high-water-content lesions of the fronto-parietal cortex and an additional asymmetric high-water-content lesion of the right parietal and occipital cortex, probably caused by polioencephalomalacia. This diagnosis could explain the clinical presentation of the patient. Polioencephalomalacia in this location of the brain in ruminants could be due to metabolic or toxic disorders