A 7-day-old female Alpaca cria was examined at the University of Wisconsin Veterinary Medical Teaching Hospital because of anorexia and ataxia of 1 day's duration. It was accompanied by its dam and a clinically normal twin cria. Parturition had been assisted, but both crias appeared clinically normal in the first 5 days after parturition. The affected cria developed anorexia and hypermetric ataxia and paresis the day prior to examination. The ataxia and paresis had been rapidly progressive and was grade 4 of 5 (modified Mayhew neurologic scale1) on examination. The cria had no affinity for the dam and was unable to locate the udder but did have a suckle reflex. On physical examination, the rectal temperature was 38.3°C (101.0°F), heart rate was 200 beats/min, and respiratory rate was 60 breaths/min. A 1-cm reducible umbilical hernia was present. The cria was small (5.4 kg [11.88 lb]) for 7 days of age but was in good body condition. The small size was attributed to being a twin. On neurologic examination, the cria was obtunded, had a head tilt to the right, and had a compulsive, mildly hypermetric, ataxic gait. The results of postural reaction testing and the finding that the cria had a tendency to lean to the right were suggestive of a right-sided anatomic localization. The lesion was localized to the right cerebrum, brainstem, and cerebellum. The compulsive behavior was consistent with a lesion in the cerebrum or thalamus, whereas the ataxia, head tilt, and hypermetria were consistent with a lesion in the vestibular system and cerebellum. The obtundation may have been the result of a lesion in the brainstem or cerebrum. The results of a CBC and serum biochemical panel were within reference limits. An IV polyurethane catheter was placed in a jugular vein,a and a lumbar CSF sample was collected. There was mild blood contamination of the CSF sample, but no cytologic abnormalities were noted and the total protein concentration was within reference limits. An infectious etiology was considered unlikely because of the results of CBC and CSF analysis and serum protein concentration, which suggested adequacy of passive immunoglobulin transfer. Given the age of the cria, hypoxic ischemic encephalopathy was also considered unlikely. An indwelling nasoesophageal tube was placed to facilitate feeding. Treatment was initiated with vitamin E (30 U, PO, q 24 h), thiamine (10 mg/kg [4.5 mg/lb], IV, q 24 h), flunixin meglumine (0.5 mg/kg [0.23 mg/lb], IV, q 12 h), ceftiofur sodium (5 mg/kg [2.3 mg/lb], IV, q 12 h), and polyionic fluids (50 mL/kg/d [22.7 mL/lb/d]). The cria was fed 10% of its body weight in alpaca milk replacer/d over 12 feedings via the nasoesophageal feeding tube. Over the following 12 hours, the patient's neurologic status notably worsened. The cria became stuporous, with persistent vertical nystagmus, a right-sided head tilt, and anisocoria with mydriasis of the left and miosis of the right pupil. A pupillary light response was present but sluggish in the mydriatic left pupil. A commercial hypertonic saline (7.2% NaCl) solutionb (4 mL/kg [1.82 mg/lb], IV) was administered as a bolus for treatment of possible increased intracranial pressure, and the cria was anesthetized for diagnostic imaging. Premedication was performed with midazolam sodium (2 mg, IV) and butorphanol tartrate (1 mg, IV) followed by induction of anesthesia with propofol (120 mg, IV), endotracheal intubation, and maintenance of anesthesia via isoflurane in oxygen. Computed tomography of the skull and cranial portion of the vertebral column showed a large fluid-attenuating non–contrast-enhancing lesion that displaced the cerebral hemispheres laterally, ventrally, and caudally (Figure 1). The lesion was located within the longitudinal cerebral fissure, extending from the rostral portion of the frontal bone rostrally along slightly over one-half the length of the fissure, with an estimated volume of 35 mL. No communication could be demonstrated between the lesion and the ventricular system. In addition, there were multiple, small, non–contrast-enhancing regions of hypoattenuation within the cranial cervical portion of the spinal cord. A diagnosis of an intracranial cyst with marked cerebral compression with secondary syringohydromelia or cervical spinal cord edema was made. Cerebellar herniation was not demonstrated on CT; however, this was suspected on the basis of the degree of mass effect and the rapid clinical deterioration of the patient.
An emergency trephination and drainage of the cyst was performed with the cria in sternal recumbency under continued general anesthesia and the head and neck secured with a cushionc and towels under the neck to prevent jugular vein compression. After standard sterile preparation and draping, a 3-cm incision was made centered over the vertex of the skull. The periosteum was elevated from the parietal bone with an osteotome. Hemorrhage was controlled with electrocautery. A hole was drilled with a handheld drill in the parietal bone on the right side 1 cm from the vertex. Hemorrhage was controlled with bone wax. The dura was penetrated with an 18-gauge needle, and 25 mL of cyst fluid was aspirated. The fluid protein concentration was 341.4 mg/dL, and there were no nucleated cells. The bone defect was sealed with a small piece of bone wax. The periosteum and subcutaneous tissues were closed with 3–0 polyglyconate synthetic absorbable sutured in a simple continuous pattern. The skin was closed routinely. Following decompression, the patient's neurologic deficits notably improved. The cria was able to nurse from the dam but remained grade 2 of 5 ataxic and paretic. The head tilt, anisocoria, and nystagmus had resolved. Intravenous fluid administration was discontinued, and esophageal tube feedings were reduced to 5% of body weight/d and then discontinued 2 days after surgery because the cria continued to nurse aggressively. Preoperative treatment with vitamin E, thiamine, flunixin meglumine, and ceftiofur were continued.
Three days following the emergency craniotomy, MRI was performed under propofol and isoflurane anaesthesia as before (Figure 2). A large T2-hyperintense, T1-isointense lesion was identified slightly to the right of midline, causing displacement of the cerebral hemispheres laterally, ventrally, and caudally and occupying the dorsal one-half to two-thirds of the dorsal portion of the cranial cavity. The cerebellum did not appear herniated into the foramen magnum. The mass only partially suppressed on FLAIR sequences, which was consistent with the proteinaceous nature of the cystic fluid removed at surgery. The intracranial cyst was smaller than identified by CT, with an estimated volume of 17 mL. The subjective increase in volume, compared with that calculated to be present following trephination, was believed to demonstrate the continued production of cystic fluid because the difference was greater than could be explained by innate errors in volume calculation. No communication between the ventricular system and the cyst could be identified. A 1.4 × 0.36-cm curvilinear T2-hypointense, T1-isointense, non–contrast-enhancing region that created a signal void on gradient echo sequences was located along the caudodorsal margin of the cyst. Because no similar hyperattenuating region was present on the CT images, this lesion was determined to be an intracystic hematoma that had formed secondary to the emergency craniotomy. Contrast enhancement of the cyst lining as well as the meninges was present and likely represented sterile meningitis from the previous craniotomy. Additional MR findings included T2-hyperintense, T1-hypointense linear regions on either side of the central canal within the dorsal cervical portion of the spinal cord. This was consistent with spinal cord edema or syringomyelia as suspected on the CT scan. Furthermore, a 1.2 × 1.1 × 0.8-cm, T2-hyperintense, mildly T1-hypointense, well-defined, contrast-enhancing triangular region consistent with infarction was identified in the right occipital lobe immediately caudal to the intracranial cyst. A diagnosis of an intracranial cyst, possibly subarachnoid in location, was made.
The cria's neurologic status continued to improve, and by day 7 of hospitalization, 6 days following surgery, no neurologic deficits were appreciated. Flunixin meglumine and thiamine administration were discontinued on day 5 of hospitalization, but antimicrobial treatment was continued as before. However, 10 days after trephination and drainage, acute deterioration in the patient's status was noted. The cria had become grade 3 of 5 ataxic and paretic, obtunded, and unable to nurse. The cria was again anesthetized as previously and placed in sternal recumbency. A 3-cm incision was made lateral to the previous incision centered over the vertex of the skull. The bone wax was removed from the previously drilled hole. The dura was penetrated with an 18-gauge needle, and 30 mL of cyst fluid was aspirated. The fluid was blood tinged. The bone defect was again sealed with a small piece of bone wax. The periosteum, subcutaneous tissues, and skin were closed as previously described. Again, the cria responded well to decompression, with notable improvement in neurologic deficits upon recovery from anesthesia.
On day 13 of hospitalization, 2 days following the second surgical decompression, the cria was again anesthetized for craniotomy and attempted removal of the cyst lining. The cria was anesthetized and prepared for surgery as previously described. The incision from the second surgery was reopened and extended rostrally to the level of the medial canthus of the eyes and caudally to the nuchal crest. Cutaneous hemorrhage was controlled by electrocautery. The periosteum was elevated from the parietal bone with an osteotome. An approximately 2 × 3-cm bone window was created with a variable-speed bone drille within the parietal bone over the parietal lobe on the right side. An osteotome was used to remove the bone flap to expose the underlying dura mater. The dura mater was incised over the cyst. A high-frequency (18-mHz) ultrasound probef placed over the cyst failed to identify a connection or thin membrane between the cyst and the lateral ventricles. The lining of the cyst was carefully removed. Hemorrhage was controlled with bipolar cautery. Because of moderate blood loss during surgery, a whole blood transfusion was administered. Thirty-six milliliters of the dam's blood was administered without complication. Following excision of the cyst lining, a small piece of temporalis muscle fascia was harvested to use as a graft to close the dural defect. The dura was closed with 4–0 polyglyconate synthetic absorbable suturesd in a simple interrupted pattern. Holes were drilled in the skull around the defect and also in the removed bone flap. The bone flap was secured to the skull with 3–0 nylon suturesg placed through the holes. The periosteum and subcutaneous tissues were closed in a simple continuous pattern with 3–0 polyglyconate synthetic absorbable suture.d The skin was closed with a subcuticular layer of 3–0 polyglyconate synthetic absorbable sutured and skin staples. Flunixin meglumine (0.5 mg/kg, IV, q 12 h) was given immediately prior to and for 48 hours following this surgery, and antimicrobial treatment was continued as before. The cria recovered uneventfully from anesthesia. Immediately following surgery, the ataxia and pareis persisted (grade 2/5) but mentation was normal and the cria interacted with the twin and the dam normally and was able to nurse effectively. Over the following 4 days, the ataxia and paresis improved to grade 1 of 5. The cria gained weight at an expected rate (500 g/d) during this time. Antimicrobial treatment was discontinued 3 days following the third surgery, and the cria was discharged 24 hours later.
The cria was examined 161 days following the final surgery. Results of the physical examination were normal, body weight and body condition score were appropriate, and no neurologic deficits were appreciated. The owners reported that the cria behaved normally in the herd. The cria was anesthetized and MRI was repeated (Figure 3). The intracranial cyst was reduced in size to 5.3 mL and was only mildly displacing the cerebral hemispheres laterally, caudally, and ventrally. The intracystic hematoma was no longer present. An additional small (0.4 mL) region with similar MRI signal characteristics was present within the right cerebrum ventrolateral to the original cyst and corresponded to a parenchymal cistern identified at surgery. No communication could be identified between these 2 lesions. Meningeal enhancement was no longer identified. There was mild compensatory dilation of the lateral ventricles secondary to cerebral atrophy. The right lateral ventricle was slightly larger than the left lateral ventricle. The parietal bone at the level of the craniotomy had reduced medullary signal intensity and was thicker than previously, indicating hyperostosis. The spinal cord edema had resolved. The previously described infarct in the right occipital lobe was smaller than previously described and was now T2-hyperintense, T1-hypointense to -isointense, and non–contrast-enhancing, consistent with a chronic infarct.
Fluid-attenuated inversion recovery
Mila International Inc, Erlanger, Ky.
Hypertonic saline (7.2% NaCl) solution, Phoenix Pharmaceutical, St Joseph, Mo.
Olympic Vac-Pac, Olympic Medical, Seattle, Wash.
Maxon, Syneture-Tyco Healthcare LP, Norwalk, Conn.
Surgairtome Two Drill, Zimmer Corp, Carpinteria, Calif.
Esaote MyLab70, Genova, Italy.
Monosof, Syneture-Tyco Healthcare LP, Norwalk, Conn.
1. de Lahunta A. Large animal spinal cord disease in veterinary neuroanatomy and clinical neurology. 3rd ed. St Louis: Saunders/Elsevier, 2009;285–318.
2. Hill FI, Mirams CH. Intracranial teratoma in an alpaca (Vicugna pacos) in New Zealand. Vet Rec 2008; 162:188–189.
3. Talbot CE, Mueller K, Granger N, et al. Diagnosis and surgical removal of brain abscesses in a juvenile alpaca. J Am Vet Med Assoc 2007; 231:1558–1561.
4. Miyagami M, Tsubokawa T. Histological and ultrastructural findings of benign intracranial cysts. Noshuyo Byori 1993; 10:151–160.
5. Rengachary SS, Watanabe I. Ultrastructure and pathogenesis of intracranial arachnoid cysts. J Neuropathol Exp Neurol 1981; 40:61–83.
7. Weber R, Voit T, Lumenta C, et al. Spontaneous regression of a temporal arachnoid cyst. Childs Nerv Syst 1991; 7:414–415.
9. Vernau KM, Kortz GD, Koblik PD, et al. Magnetic resonance imaging and computed tomography characteristics of intracranial intra-arachnoid cysts in 6 dogs. Vet Radiol Ultrasound 1997; 38:171–176.
10. Vernau KM, LeCouteur RA, Sturges BK, et al. Intracranial intra-arachnoid cyst with intracystic hemorrhage in two dogs. Vet Radiol Ultrasound 2002; 43:449–454.
11. Lowrie M, Wessmann A, Gunn-Moore D, et al. Quadrigeminal cyst management by cystoperitoneal shunt in a 4-year-old Persian cat. J Feline Med Surg 2009; 11:711–713.
12. Saito M, Olby NJ, Spaulding K. Identification of arachnoid cysts in the quadrigeminal cistern using ultrasonography. Vet Radiol Ultrasound 2001; 42:435–439.
13. Kitagawa M, Kanayama K, Sakai T. Quadrigeminal cisterna arachnoid cyst diagnosed by MRI in five dogs. Aust Vet J 2003; 81:340–343.
14. Duque C, Parent J, Brisson B, et al. Intracranial arachnoid cysts: are they clinically significant? J Vet Intern Med 2005; 19:772–774.