Introduction
A 1-year-old 20-kg castrated male goat was referred because of anorexia, signs of depression, and stiff gait of all 4 limbs over a 48-hour period. Despite initial treatment with tolfenamic acid, propionic acid, strychnos nux vomica, and ivermectin, the goat’s clinical signs worsened. The goat was not vaccinated, had no previous medical history, and was fed hay and grass. It was living with another goat that remained healthy. The owners reported a possible ingestion of plastic tarpaulins 1 week before development of clinical signs.
Clinical evaluation revealed tachycardia (100 beats/min) and tachypnea (32 breaths /min). The rest of the examination findings were normal. Neurologic examination revealed altered consciousness (signs of depression to stupor) and lateral recumbency with opisthotonus and seizures. To stabilize the goat’s condition, treatment with diazepam (0.15 mg/kg, IV), isotonic solution (lactated Ringer solution, 2.5 mL/kg/h, IV), dexamethasone (0.2 mg/kg, IV), and thiamine hydrochloride (9 mg/kg, IV) was administered as well as tetanus antitoxin (30 U/kg, SC). Subsequently, the goat’s condition improved. The goat became ambulatory but remained mentally depressed and developed head pressing, circling, ataxia, and spastic tetraparesis. The goat also had a bilateral lack of menace response and stargazing, decreased pupillary light responses, and lingual paralysis.
Neurologic examination
Assessment
Anatomic diagnosis
| Problem | Rule out location |
|---|---|
| Depressed mental status or stupor | Forebrain (thalamus) or brainstem (midbrain) |
| Opisthotonus | Brainstem (midbrain) or cerebellum |
| Seizures | Forebrain (cerebrum or thalamus) |
| Circling and head pressing | Forebrain (cerebrum) or brainstem (midbrain) |
| Ataxia and tetraparesis | Brainstem (pons or medulla oblongata) or cerebellum or cervical spinal cord segments (C1-T2) |
| Blindness (no menace response and stargazing) | Forebrain (cerebrum or thalamus) or cranial nerve II |
| Decreased pupil response | Brainstem (midbrain) or cranial nerve II or III |
| Flaccid tongue and decreased gag reflex | Brainstem (medulla oblongata) or cranial nerve IX, X, XI, or XII |
Likely location of 1 lesion
Multifocal to diffuse disease affecting the forebrain and the brainstem was suspected.
Etiologic diagnosis—Differential diagnoses included inflammatory and infectious diseases (listeriosis, caprine arthritis encephalitis, parasitic infections, or brain abscesses), toxicosis (lead or copper), metabolic diseases (hypoglycemia, polioencephalomalacia [PEM {secondary to thiamine deficiency}], sulfur intoxication, hypernatremia, or hepatic encephalopathy) as well as developmental, traumatic, neoplastic, or vascular disorders. The planned diagnostic processes included a CBC, serum and plasma biochemical analyses, and CSF analysis to rule out infectious or inflammatory disease and some metabolic and toxic disorders, radiography to exclude traumatism, abdominal ultrasonography to rule out obvious hepatic or urinary diseases, and MRI of the brain to investigate other anomalies.
Diagnostic test findings—The history of the goat excluded exposure to toxic agents, and its age (as well as the absence of progressive signs) made a diagnosis of caprine arthritis encephalitis unlikely. On day 1, skull radiography and abdominal ultrasonography revealed no abnormalities. Results of a CBC were consistent with mild neutrophilic leukocytosis (WBC count, 16,700 WBCs/µL [reference range, 4,000 to 14,000 WBCs/μL] and neutrophil count, 9,700 neutrophils/µL [reference range, 1,200 to 7,200 neutrophils/μL]) and mildly high RBC count (24.3 X 106 RBCs/μL; reference range, 8 X 106 to 18 X 106 RBCs/μL). Serum biochemical analysis revealed hyperglycemia (163 mg/dL; reference range, 50 to 90 mg/dL), mild hypernatremia (162 mmol/L; reference range, 142 to 155 mmol/L), mild hypokalemia (3 mmol/L; reference range, 3.5 to 6.7 mmol/L); plasma alkaline phosphatase activity was high (938 U/L; reference range, 93 to 387 U/L). Other biochemical variables were within reference limits. Urinalysis revealed glycosuria secondary to hyperglycemia (renal threshold for glucose, 140 mg/dL). These findings were considered to be of little clinical relevance and not the cause of the goat’s clinical signs and were attributed to mild dehydration and anorexia.
On day 3, the goat was anesthetized and underwent MRI of the brain, performed with a 1.5-Tesla scanner (Magnetom Essenza 1.5 T; Siemens Medical Solutions). The protocol included acquisition of T1- and T2-weighted turbo spin echo images in 3 planes (T1-weighted images were obtained before and after contrast medium administration), transverse FLAIR images, and transverse T2-weighted gradient echo images. The T2-weighted sequences revealed a bilateral symmetric hyperintense signal in cortical gray matter in the frontal, parietal, and occipital lobes and in the dorsal portion of the hippocampus, corresponding to edema within the gray matter (Figure 1). Obliteration of the cortical sulci in these areas as a result of thickening of the gyri was also evident. The FLAIR sequence confirmed these lesions, which were consistent with cytotoxic edema that spared the white matter. On postcontrast images, mild meningeal enhancement surrounding frontal and parietal lobes was seen. No lesion was observed in the brainstem and cerebellum, and no anomaly was seen in the T2-weighted gradient echo images.
Dorsal T2-weighted MRI image of the brain of a 1-year-old goat that was evaluated because of anorexia, signs of depression, and stiff gait of all 4 limbs. Subsequently, the goat developed altered consciousness and became laterally recumbent with opisthotonus and seizures. The images were obtained after stabilization of the goat’s condition. Notice the bilateral symmetric hyperintense signal in the cortical gray matter of the frontal and parietal lobes that corresponded to edema and the obliteration of the cortical sulci in these areas because of thickening of the gyri. These findings are consistent with polioencephalomalacia.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
Dorsal T2-weighted MRI image of the brain of a 1-year-old goat that was evaluated because of anorexia, signs of depression, and stiff gait of all 4 limbs. Subsequently, the goat developed altered consciousness and became laterally recumbent with opisthotonus and seizures. The images were obtained after stabilization of the goat’s condition. Notice the bilateral symmetric hyperintense signal in the cortical gray matter of the frontal and parietal lobes that corresponded to edema and the obliteration of the cortical sulci in these areas because of thickening of the gyri. These findings are consistent with polioencephalomalacia.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
Dorsal T2-weighted MRI image of the brain of a 1-year-old goat that was evaluated because of anorexia, signs of depression, and stiff gait of all 4 limbs. Subsequently, the goat developed altered consciousness and became laterally recumbent with opisthotonus and seizures. The images were obtained after stabilization of the goat’s condition. Notice the bilateral symmetric hyperintense signal in the cortical gray matter of the frontal and parietal lobes that corresponded to edema and the obliteration of the cortical sulci in these areas because of thickening of the gyri. These findings are consistent with polioencephalomalacia.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
After MRI, a CSF sample was collected by lumbar puncture. Analysis of the CSF sample revealed high numbers of nucleated cells (3,200 cells/µL; reference range, 0 to 7 cells/µL) and RBCs (790 X 103 RBCs/µL; reference range, 0 to 558 RBCs/µL), high creatine kinase activity (54 U/L; reference range, 2 to 48 U/L), and high protein concentration (42 mg/dL; reference range, 0 to 40 mg/dL). However, blood contamination of the sample had occurred during its collection, making these results difficult to interpret. Cytologic examination of the CSF sample ruled out severe inflammatory and infectious diseases and the MRI findings ruled out developmental, infectious, neoplastic, and vascular lesions. The nature and distribution of lesions detected by MRI were consistent with PEM associated with toxic or metabolic diseases, among which thiamine deficiency or excess dietary sulfur (or both) was considered the principal cause of the goat’s clinical signs.
Administration of supplemental thiamine was continued at a dosage of 9 mg/kg (IV, q 3 h for 24 hours; then IV, q 6 h for 5 days; and then IM, q 12 h for 8 days). The goat was hospitalized for several days to resolve its state of dehydration and electrolyte imbalance by IV administration of isotonic fluids complemented with glucose and potassium. The goat also received corticosteroids DMSO, and mannitol IV to reduce intracranial pressure and brain edema. The neurologic status of the goat progressively improved and on day 4, it was no longer circling and head pressing. A week after admission, the goat was discharged to the owner, who was instructed to administer thiamine hydrochloride (9 mg/kg/d, PO, for 15 days), corticosteroids (IM, tapered dosage over 10 days), and strychnos nux vomica (PO, [to support of rumen function] for 7 days). At the time of hospital discharge, the goat’s neurologic signs were completely resolved except for remaining blindness and lingual paresis.
Two months later, the goat was reexamined to assess the cortical lesions. Night blindness persisted, and findings of a neurologic examination were considered normal with the exception of mild bilateral decreased menace responses. Repeated MRI revealed marked improvement in the previously observed abnormalities. The MRI images showed an enlargement of the subarachnoid space with a signal similar to CSF in all sequences of the frontal, parietal and occipital lobes (Figure 2). Atrophy of the cortical gyri was evident where the edema had been previously. A remaining focal cortical hypersignal consistent with residual edema was observed at the periphery of the occipital lobes. Lateral ventricles were sparingly enlarged, compared with their appearance at the first MRI examination. The MRI findings were indicative of resolution of PEM but with secondary cortical atrophy and residual occipital edema. Several months after this examination, the goat was reported to have had no neurologic relapse.
Dorsal T2-weighted MRI image obtained from the goat 2 months after the initial examination and following treatment with supplemental thiamine. Neurologic signs were completely resolved at the time of this examination except for night blindness. There is evidence of resolution of the lesions of edema of the gray matter with secondary cortical atrophy of the frontal and parietal lobes and opposing enlargement of the subarachnoid space.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
Dorsal T2-weighted MRI image obtained from the goat 2 months after the initial examination and following treatment with supplemental thiamine. Neurologic signs were completely resolved at the time of this examination except for night blindness. There is evidence of resolution of the lesions of edema of the gray matter with secondary cortical atrophy of the frontal and parietal lobes and opposing enlargement of the subarachnoid space.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
Dorsal T2-weighted MRI image obtained from the goat 2 months after the initial examination and following treatment with supplemental thiamine. Neurologic signs were completely resolved at the time of this examination except for night blindness. There is evidence of resolution of the lesions of edema of the gray matter with secondary cortical atrophy of the frontal and parietal lobes and opposing enlargement of the subarachnoid space.
Citation: Journal of the American Veterinary Medical Association 259, 11; 10.2460/javma.20.07.0392
Comments
In goats, toxic, metabolic, and infectious diseases are more frequent causes of brain lesions than are neoplastic or vascular diseases, and the prevalence of encephalitis, meningitis, and PEM in that species are high.1 Indeed, the main causes of seizures in goats and sheep are structural or metabolic, and the most common cause is PEM.2
Polioencephalomalacia is a neurologic disorder associated with toxic or metabolic disease in ruminants and characterized by necrosis of the cortical gray matter. It is usually associated with altered thiamine status, high sulfur intake, water deprivation- sodium ion toxicosis, and lead poisoning.1 Few cases of PEM in goats are reported in the veterinary medical literature. Clinical signs are inappetence, apathy or excitability, obtundation, opisthotonus, tremor, circling, ataxia, lack of menace response and seizures consistent with forebrain and brainstem disease.2,3,4,5
Determination of the cause of neurologic disorders is often not possible on the basis of history and clinical findings; thus, performance of accurate diagnostic tests is necessary. A CBC, serum biochemical analysis, CSF analysis, and serologic tests are useful to evaluate inflammatory and infectious diseases but in the case of metabolic or toxic disorders, anomalies could be encountered because of cellular reaction to neuronal damage.4 Magnetic resonance imaging provides additional information, and MRI has diagnostic value for evaluation of metabolic diseases by providing evidence of intra-axial and symmetric distribution of lesions.4
In cases of PEM, selective changes in forebrain gray matter are present, such as a high water-content signal consistent with cytotoxic edema. The specificity of this pattern is useful to differentiate PEM from inflammatory or infectious diseases that result in asymmetric lesions.3,4,6
The forebrain is the most affected part in animals with PEM, but the cerebellar cortex and thalamus can be involved.4,6,7
The treatment of PEM depends on the cause. In cases of sodium toxicosis or lead poisoning, removal of the source of intoxication is easily completed. The relationship of thiamine deficiency with PEM remains unclear. In contrast, the association of PEM with excessive ruminal sulfide production has been demonstrated.8 Results of a recent survey9 of cattle suggest that the pathogenesis of sulfur-induced PEM is associated with reduced activity of thiamine-dependent and cytochrome c oxidases in the cerebral cortex. Because the pathogenesis of thiamine- or sulfur-related PEM is unknown, treatment is based on administration of large amounts of thiamine and management of cerebral edema or removal of sulfur sources from the affected animal’s environment.10 For the goat of the present report, emergency treatment was administered before treatment with thiamine was commenced; therefore, the cause of PEM remained unknown. On the other hand, a source of sulfur in the goat’s (water or forage) was not identified.
Regarding MRI follow-up of small ruminants with PEM, there is no information in the veterinary medical literature, to our knowledge. However, findings of MRI follow-up could be beneficial, especially because sequelae of cortical atrophy and residual edema may cause neurologic deficits. Indeed, persistent neurologic signs, such as night blindness, and MRI findings (secondary cortical atrophy and residual occipital edema) for the goat of the present report could be suggestive of an active process that might require prolonged treatment.
References
- 1. ↑
Allen AL, Goupil BA, Valentine BA. A retrospective study of brain lesion in goats submitted to three veterinary diagnostic laboratories. J Vet Diagn Invest. 2013;25(4):482–489.
- 2. ↑
Chigerwe M, Aleman M. Seizure disorders in goats and sheep. J Vet Intern Med. 2016;30(5):1752–1757.
- 3. ↑
Ertelt K, Oevermann A, Precht C, Lauper J, Henke D, Gorgas D. Magnetic resonance imaging findings in small ruminants with brain disease. Vet Radiol Ultrasound. 2016;57(2):162–169.
- 4. ↑
Schenk HC, Ganter M, Seehusen F, et al. Magnetic resonance imaging findings in metabolic and toxic disorders of 3 small ruminants. J Vet Intern Med. 2007;21(4):865–871.
- 5. ↑
Chapter 5. Nervous system. In: Smith MC, Sherman DM, eds. Goat Medicine. 2nd ed. Wiley-Blackwell; 2009:222–226.
- 6. ↑
Tsuka T, Taura Y, Okamura S, et al. Imaging diagnosis—polioencephalomalacia in a calf. Vet Radiol Ultrasound. 2008;49(2):149–151.
- 7. ↑
Garosi LS, Dennis R, Platt SR, Corletto F, de Lahunta A, Jakobs C. Thiamine deficiency in a dog: clinical, clinicopathologic, and magnetic resonance imaging findings. J Vet Intern Med. 2003;17(5):719–723.
- 8. ↑
Apley MD. Consideration of evidence for therapeutic interventions in bovine polioencephalomalacia. Vet Clin North Am Food Anim Pract. 2015;31(1):151–161.
- 9. ↑
Amat S, Hendrick S, Moshynskyy I, Simko E. Reduce activities of thiamine-dependent and cytochrome c oxydase enzymes in cerebral cortex of cattle affected by sulfur-induced polioencephalomalacia. Can J Vet Res. 2017;81(4):242–248.
- 10. ↑
Niles GA, Morgan SE, Edwards WC. The relationship between sulfur, thiamine and polioencephalomacia. A review. Bov Pract (Stillwater). 2002;36:93–99.
