The Veterinary Journal

The Veterinary Journal 193 (2012) 367 373 Contents lists available at SciVerse ScienceDirect The Veterinary Journal journal homepage: www.elsevier.com/locate/tvjl Post-anesthetic cortical blindness in cats: Twenty cases J. Stiles a,, A.B. Weil a, R.A. Packer a,b, G.C. Lantz a a Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA b Department of Basic Medical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA article info abstract Article history: Accepted 26 January 2012 Keywords: Feline Blindness Cortical Anesthesia Cerebral ischemia Mouth gag The medical records of 20 cats with post-anesthetic cortical blindness were reviewed. Information collected included signalment and health status, reason for anesthesia, anesthetic protocols and adverse events, post-anesthetic visual and neurological abnormalities, clinical outcome, and risk factors. The vascular anatomy of the cat brain was reviewed by cadaver dissections. Thirteen cats were anaesthetised for dentistry, four for endoscopy, two for neutering procedures and one for urethral obstruction. A mouth gag was used in 16/20 cats. Three cats had had cardiac, whereas in the remaining 17 cases, no specific cause of blindness was identified. Seventeen cats (85%) had neurological deficits in addition to blindness. Fourteen of 20 cats (70%) had documented recovery of vision, whereas four (20%) remained blind. Two cats (10%) were lost to follow up while still blind. Ten of 17 cats (59%) with neurological deficits had full recovery from neurological disease, two (12%) had mild persistent deficits and one (6%) was euthanased as it failed to recover. Four cats (23%) without documented resolution of neurological signs were lost to follow up. Mouth gags were identified as a potential risk factor for cerebral ischemia and blindness in cats. Ó 2012 Elsevier Ltd. All rights reserved. Introduction Cortical blindness following general anesthesia in the cat has been infrequently reported in the literature but is anecdotally stated to occur occasionally in small animal practice. Two case reports describe blindness and other neurological signs in cats following dental cleaning (Jurk et al., 2001; Son et al., 2009). In one case the course of anesthesia was described as uneventful in a 6 year old cat, yet the animal was blind after a prolonged recovery from anesthesia (Jurk et al., 2001). Over the next 2 weeks neurological signs such as circling and head tilt progressively worsened and the cat remained blind. The cat was euthanased and on necropsy multiple areas of ischemic damage were identified in the brain, including the visual cortex. In the other case a 2 year old cat had blindness and diminished proprioceptive responses following anesthesia (Son et al., 2009). This cat recovered some vision beginning on day 2 and by day 4 had normal conscious proprioception. Walker and Rex (1958) described two cats that had cardiac during ovariohysterectomy and were resuscitated. One cat was blind for 24 h without other neurological abnormalities and then recovered vision. The other cat had decerebrate rigidity and was euthanased 4 days later. In the present study, our objectives were to review a case series of cats with immediate post-anesthetic blindness with or without other neurological signs; to document the post-anesthetic course Corresponding author. Tel.: +1 765 494 1107. E-mail address: stilesj@purdue.edu (J. Stiles). of vision as well as neurological abnormalities; and to identify risk factors for blindness following anesthesia in the cat. Materials and methods Data Medical records of cats with no clinical evidence of visual or neurological deficits before general anesthesia, and that were blind with or without other neurological abnormalities upon recovery from anesthesia, were sought from several sources. Twenty cases were identified five from Purdue University Veterinary Teaching Hospital medical records; three from a North American Veterinary School Medical Data Base search; two from a veterinary dentist; and ten from private general practitioners. Copies of medical records were obtained, and in some cases additional information from the attending veterinarian was obtained through telephone or e-mail communications. Records review Medical records were reviewed and the following information collected: signalment, health status prior to anesthesia, reason for anesthesia, anesthetic protocol, occurrence of an adverse anesthetic event, whether a mouth gag was used, body position during procedure, visual and neurological status upon anesthetic recovery, and post-anesthetic visual and neurological outcome. Adequate follow up time to evaluate vision and neurological abnormalities was considered to be 3 months. Cadaver dissection A bilateral anatomical review of the region of the maxillary artery external rete was performed in one fixed, latex injected cat specimen and two fresh cadaver cats euthanased for reasons unrelated to this study. Examination of the fresh specimens 1090-0233/$ - see front matter Ó 2012 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2012.01.028

368 J. Stiles et al. / The Veterinary Journal 193 (2012) 367 373 was performed within 30 min of euthanasia. In these two specimens, spring-held mouth gags were placed to widely open the mouth as may occur during the performance of an endoscopic or dental procedure. Results Signalment, health status, reason for anesthesia, adverse anesthetic event The age of cats ranged from 4.5 months to 18 years with a mean age of 9.7 years and a median age of 12 years. Additional signalment information is presented in Table 1. The cats were anaesthetised for the following procedures dentistry (n = 13), endoscopy (n = 4), neutering (n = 2) and treatment of urethral obstruction (n = 1; Table 1). The most common health problem identified prior to anesthesia was dental disease (n = 13), followed by chronic renal disease (n = 5), chronic gastrointestinal tract disease (n = 3), heart murmur (n = 2), diabetes mellitus (n = 1), intestinal foreign body (n = 1), and recurrent urinary tract disease (n = 1). Three cats (two for neutering, one for treatment of urethral obstruction) had cardiac under anesthesia with presumptive cerebral hypoxia/ischemia. Of the remaining 17 cats, no specific cause of potential hypoxia or cerebral ischemia was identified. All four cats that had endoscopy had a spring-held mouth gag in place for 45 60 min and were in sternal recumbency. Of the 13 cats that had dental procedures, 12 had a spring-held mouth gag in place for procedures that ranged in duration from 20 min to 5.5 h. One cat did not have a mouth gag placed. Attending veterinarians indicated that in all cats the mouth gag produced full extension. Two cats undergoing dental procedures were in dorsal recumbency and the remaining 11 were in lateral recumbency. Vision and neurological abnormalities Three of 20 cats were blind upon recovery from general anesthesia with no obvious neurological irregularities, whereas the other 17 cats were blind with additional neurological abnormalities such as circling, ataxia, head tilt, weakness, opisthotonus, decreased conscious proprioception, and abnormal mentation (Table 1). Eight cats were examined at least once by a veterinary ophthalmologist. Blindness in these eight cats was characterised as cortical based on normal size pupils, normal direct and indirect pupillary light reflexes, positive dazzle reflex, negative menace response, and lack of ocular lesions. Descriptions of the ophthalmic examinations in medical records of cats not evaluated by an ophthalmologist were also consistent with cortical blindness. Two of 20 cats were reported to be completely blind on one side, with either diminished vision (n = 1) or normal vision (n = 1) on the contralateral side. The remaining 18 cats were reported as blind bilaterally. Neurological signs were referable to the central nervous system (CNS) in all cats. In 14/20 cats (70%) vision was documented to have been recovered enough that the cats could comfortably navigate. Four cats (20%) did not recover vision and two (10%) were still blind at the last follow-up examination recorded (2 weeks for cat number 1; 11 days for cat number 13). Of the four cats that remained blind, one (number 10) was euthanased 1 month post-endoscopy due to persistent and marked neurologic deficits and blindness. A necropsy was not performed. Three cats were blind long term but adapted well. Of the 14 cats that were known to have regained vision, medical record information was available for 11 as to the first day postanesthesia that some vision was noted. The earliest time to recovery of vision was 1 day and the longest was 6 weeks. The mean interval to first evidence of vision was 4.5 days. In the three cats for which a specific day of return of some vision was not available, the medical record listed vision as present at re-examination dates of 1 month (n = 2), and 5 months (n = 1) post-anesthesia. One of the authors assessed the visual status of three cats (numbers 9, 12 and 18) on multiple occasions beginning immediately after the anesthetic episode. In all cats vision gradually improved over several months. Of the 17 cats that had neurological deficits in addition to blindness, two had persistent abnormalities including mild ataxia in one cat (number 17) and unilateral pelvic limb weakness in one cat (number 7). One cat (number 10) was euthanased after 1 month due to severe neurological deficits. Four cats (numbers 1, 4, 11 and 14) either had no information about neurological signs at the last recorded visit, or a deficit was still present but long term follow up was not available. The other 10 cats were all reported to have recovered from neurological abnormalities. It was not possible to reliably extract the time frame for resolution of neurological deficits from the medical records. The shortest recorded time was 3 days and the longest was 6 months; however there were often gaps of several months between examinations. Anesthesia The anesthetic protocols are summarised in Table 2. One cat (number 2) had cardiac following induction with ketamine and thus received no maintenance agent. One cat (number 20) was induced with propofol prior to epidural administration of a local anesthetic. This cat had cardiac immediately upon receiving the epidural injection and received no maintenance agent..hypotension, defined as a systolic arterial blood pressure (SAP) < 80 mm Hg or mean arterial blood pressure (MAP) < 60 mm Hg, (Waddell, 2000; Mazzaferro and Wagner, 2001) was documented in seven cats. Three additional cats were presumed to have had severe hypotension during cardiac, and seven cats did not have blood pressure monitoring. Three cats out of 20 did not have any recorded hypotension during the general anesthesia period. Nine cats were noted to have a prolonged recovery from anesthesia, 10 had a normal recovery time, and in one cat recovery time was not noted. An association between duration of anesthesia and severity of clinical signs was not apparent. The shortest recorded anesthetic duration was 20 min (number 3) and the longest was 5.5 h (number 14). When comparing these two cats, more severe initial clinical signs were described for cat number 3. Both cats went on to regain vision. Cat number 3 had resolution of neurological deficits while no information was available for cat number 14 regarding neurological recovery. Cadaver dissection Bilateral dissection of the maxillary artery in the region of the external maxillary rete in a latex injected cat specimen demonstrated this arterial complex lying adjacent to the skull extending from the level of the foramen rotundum to the orbital fissure and optic foramen, as previously described (McClure et al., 1973; Kamijyo and Garcia, 1975; Fig. 1). The external maxillary rete was observed to lie between the medial and lateral pterygoid muscles and the temporalis muscle. During wide opening of the mouth in the fresh cadaver specimens, the rostral aspect of the masseter and temporalis muscles were tightly stretched as assessed by digital palpation compared to the muscle tension with minimal mouth opening. An oral mucosal incision over the coronoid crest with dissection of the medial aspect of the mandibular ramus allowed subsequent identification and separation of the pterygoid and temporalis muscles with access to the ventral aspect of the skull and visualisation of the above-mentioned foramina. Without cutting the muscles, visualisation of the maxillary artery and

J. Stiles et al. / The Veterinary Journal 193 (2012) 367 373 369 Table 1 Pre- and post-anesthetic clinical information on 20 cats with cortical blindness and other neurological deficits. Cat number Signalment, (health problems identified prior to anesthesia) 1 12 year MN DSH (dental Reason for anesthesia, body position MG (Y/N) extractions dorsal 2 6 months M DSH Neuter lateral MG-N 3 14 year FS DLH cleaning lateral 4 15 year FS DSH (dental disease, chronic renal 5 18 year FS DSH (dental disease, chronic renal 6 14 year FS DSH (dental disease, chronic renal 7 11 year MN DSH (dental 8 10 year FS DSH (dental 9 12 year MN (chronic inflammatory bowel 10 14 year FS DSH (gastrointestinal lymphoma, heart murmur) 11 2 year MN DSH (dental 12 9 year MN DSH (dental 13 10 year FS DSH (inflammatory bowel 14 14 year FS DSH (dental disease, diabetic) 15 6 year MN DSH (dental disease, heart murmur) 16 15 year MN DSH (chronic renal disease, hepatobiliary cyst, intestinal foreign body) cleaning lateral Endoscopy sternal Endoscopy sternal cleaning, one extraction lateral cleaning lateral Endoscopy sternal cleaning dorsal Endoscopy, 2 days later laparotomy MG-N Post-anesthetic abnormalities Cause of brain ischemia Outcome Blind, ataxic, circling At 3 days neurologic signs improved. Still blind at 2 weeks, no additional follow up Blind, ataxic Blind, initial opisthotonus, then ataxic, circling Blind, recumbent for 24 h, ataxic, circling Cardiac At 6 weeks first sign of minimal vision, resolution of ataxia. At 4.5 year visual, good on tracking and maze testing, no menace OU At 2 days visual, at 4 days all neurologic signs had resolved At 1 month some vision, still slightly ataxic, no additional follow up Blind, weak, ataxic, circling At 2 days some vision. At 1 month vision and gait appeared normal Blind, weak At 2 days visual and able to walk. Two weeks later knuckling of pelvic limb with pain, systemic hypertension diagnosed, euthanased Blind, left thoracic and left pelvic limbs weak Blind, opisthotonus, vocalising, no postural reactions or CP, circling once ambulatory 3 days later At 7 days vision began to return, vision improved over next 2 months, but OS still had deficits. Weakness in left pelvic limb persisted At 3 days minimal vision. By 2 months vision appeared normal, resolution of neurologic abnormalities Blind, abnormal mentation At 2 days some vision, at 6 days good vision based on maze. Mentation was normal by 24 h. At 1 month visual OU, but cotton ball test weak and visual placing poor. At 3 months vision normal including placing and cotton ball Blind, unable to stand, ventroflexion of neck, limb rigidity, deaf Blind OS, visual OD, decreased CP on left side, circling At 6 days able to walk but ataxic, still blind and deaf, CP deficits. At 1 month remained blind, deaf and ataxic, euthanased, no necropsy At 9 days, still blind OS, weak CP on left side, not circling. Next exam at 4 months, normal vision, neurologic signs resolved Blind At 1 day some vision. At 1 month, good vision but with residual deficit OD. At 1.5 years no visual deficits detected Blind, abnormal mentation, ataxic Blind, circling, abnormal mentation Neurologic signs improved over 5 days but still ataxic. At 11 days still non-visual, but ataxia resolved. No further follow up At 10 days visual, no information on neurologic abnormalities Blind At 3 days visual. Six months later developed seizures and died. At necropsy encephalitis of unknown cause diagnosed Blind OD, decreased vision OS, decreased CP on right thoracic and pelvic limbs 17 4.5 months F DSH OHE MG-N Blind, initially nonambulatory, intention tremors, abnormal mentation, nystagmus 18 14 year FS DSH (dental 19 16 year MN Himalayan (dental disease, chronic renal crown amputations lateral MG-N MG-N Blind, circling, head tilt, abnormal mentation Cardiac Blind Remained blind At 5 months visual OS, blind OD. At 4 months CP normal. No information on exact time to return of vision OS Remained blind. At 5 months intention tremors, ataxic in pelvic limbs. At 14 months still slightly ataxic right pelvic limb, but no other neurologic abnormality At 10 days blind, circling, but improved mentation. At 13 days visual OS, blind OD. At 1 month still blind OD, head tilt but other neurologic signs resolved, behavior change. At 3 months some vision OD, head tilt resolved, behavior change persisted (continued on next page)

370 J. Stiles et al. / The Veterinary Journal 193 (2012) 367 373 Table 1 (continued) Cat number Signalment, (health problems identified prior to anesthesia) Reason for anesthesia, body position MG (Y/N) Post-anesthetic abnormalities Cause of brain ischemia Outcome 20 1.5 year MN DSH (recurring urinary tract Urethral obstruction MG-N Blind, ataxic Cardiac immediately after epidural Remained blind. At 2 months ataxia had resolved MN, male neutered; FS, female spayed; MG, mouth gag; Y, yes; N, no; DSH, domestic shorthair; DLH, domestic long hair; CP, conscious proprioception; OD, right eye; OS, left eye; OU, both eyes; OHE, ovariohysterectomy. Table 2 Anesthetic protocols and adverse events recorded for 20 cats with post-anesthetic cortical blindness. Cat number Premedication Induction Maintenance Duration of anesthesia 1 Oxymorphone, midazolam 2 Acepromazine, Fluid support during anesthesia Adverse event or hypotension Anesthetic recovery time Propofol Isoflurane 1 h Yes 10 ml/kg/h None Normal Ketamine NA Cardiac 2 3 min after induction Yes, during cardiac Cardiac Prolonged 3 Acepromazine, Propofol Isoflurane 20 min Yes 10 ml/kg/h No blood pressure monitoring, Normal buprenorphine pulse oximeter inoperable 4 Acepromazine, Propofol Isoflurane 50 min Yes 10 ml/kg/h No blood pressure monitoring Prolonged buprenorphine 5 Buprenorphine, Propofol Isoflurane 25 min Yes 10 ml/kg/h No blood pressure monitoring Prolonged diazepam 6 Acepromazine, Propofol Isoflurane 40 min Yes 10 ml/kg/h No blood pressure monitoring Prolonged buprenorphine 7 None used Box induction Isoflurane 2 h 50 min No No blood pressure monitoring Normal 8 Buprenorphine, Propofol, Isoflurane 3 h 15 min Yes 10 ml/kg/h None Normal diazepam 9 Midazolam, Propofol Isoflurane 1 h 40 min Yes 10 ml/kg/h Hypotensive, SAP < 80 mm Hg Prolonged for 10 min 10 Acepromazine, Propofol Isoflurane 1 h 20 min Yes 10 ml/kg/h Hypotensive, SAP < 60 mm Hg Normal for 15 min 11 Acepromazine, Propofol Isoflurane 1 h 50 min Yes 10 ml/kg/h None Normal hydromorphone 12 Acepromazine, Mask induction Isoflurane 1 h 5 min Yes 10 ml/kg/h Hypotensive, SAP = 60 mm Hg Prolonged buprenorphine, ketamine for 30 min 13 Acepromazine, Propofol Isoflurane 1 h 45 min Yes 10 ml/kg/h No blood pressure monitoring Prolonged 14 Acepromazine, Propofol Isoflurane 5 h 30 min Yes 10 ml/kg/h Hypotensive, SAP < 80 mm Hg Normal hydromorphone for three periods of 10 min each 15 Oxymorphone, midazolam Propofol Isoflurane 1 h Yes 10 ml/kg/h Hypotensive, 5 10 min MAP < 60 mm Hg Normal 16 Midazolam, oxymorphone 17 Atropine, hydromorphone 18 Acepromazine, hydromorphone, ketamine Propofol Isoflurane 1 h 30 min Yes 10 ml/kg/h and 15 ml hetastarch over 6 min Ketamine, midazolam Mask induction Hypotensive, 50 min MAP < 60 mm Hg Not reported Isoflurane Cardiac after 25 min of anesthesia Yes 10 ml/kg/h Cardiac Prolonged Isoflurane 3 h 5 min Yes 10 ml/kg/h Hypotensive, SAP < 80 mm Hg Normal for 30 min 19 None Box induction Isoflurane No No blood pressure monitoring Normal 20 None Propofol Epidural Cardiac postepidural Yes Cardiac Prolonged NA, not applicable; MAP, mean arterial blood pressure; SAP, systolic arterial blood pressure. external rete was restricted in this approach and it was not possible to determine if the vasculature was altered during the full range of mandibular motion with associated muscular tension. Discussion This is the first report of a series of cats with cortical blindness and other neurological deficits secondary to presumed cerebral ischemia, which occurred while under general anesthesia. Of 20 cats with blindness, 14 (70%) were documented to have recovery of useful vision, and two additional cats were lost to follow up during a time frame in which they could have potentially still recovered vision. For most of the 14 cats that were known to have regained vision, it was not possible to determine from the records whether vision was completely normal as detailed assessment of vision and visual field testing was not typically recorded and

J. Stiles et al. / The Veterinary Journal 193 (2012) 367 373 371 Fig. 1A. Illustration of a cat skull with the mandible removed. (a) Temporomandibular joint; (b) foramen ovale; (c) foramen rotundum; (d) orbital fissure; (e) optic foramen. Fig. 1B. Illustration of a cat skull with the mandible removed, showing the course of the maxillary artery and external maxillary rete. (a) External carotid artery; (b) caudal auricular artery; (c) parotid artery; (d) superficial temporal artery; (e) maxillary artery; (f) caudal deep temporal artery; (g) inferior alveolar artery; (h) rostral tympanic artery; (i) middle meningeal artery enters the foramen ovale; (j) branches of the maxillary rete enter the orbital fissure. may not have been evaluated. Assessment of what degree of vision constitutes normal in a cat is subjective even for experienced ophthalmologists. In the three cats examined serially over many months by one of the authors vision improved gradually over time and was not considered normal at the time the cat first had a menace response or could navigate an unfamiliar room. Resolution of other neurological abnormalities was also good for most cats. Although one cat was euthanased after 1 month for lack of improvement, 10/17 (59%) were recorded to have complete resolution of neurological signs. Two cats (10%) had permanent but mild residual deficits. Although the number of cats in our study was relatively small, the overall recovery rate for both vision and other neurological disease was encouraging. For many of the cats the clinical abnormalities in the first day or two following anesthesia were marked, potentially suggesting a poor prognosis. However, most cats began to make noticeable improvement within the first few days. In this study 17/20 cases involved either dentistry or endoscopy and in 16/17 cats a spring-held mouth gag was used. In three cats it was clear that cardiac was the cause of cerebral ischemia. In the 17 cats undergoing dentistry or endoscopy the cause of cerebral ischemia was not identifiable. Systemic hypotension was documented in seven cats and in another seven cats blood pressure was not measured. It was not clear what role hypotension may have played in cerebral ischemia. Blood supply to the feline brain is primarily via the maxillary artery, a branch off the external carotid artery (King, 1987). Maxillary artery blood is distributed to all of the brain except the caudal part of the medulla oblongata, which is supplied by the vertebral arteries. The basilar artery in the cat carries blood caudally and thus does not supply the brain. The internal carotid artery is fully functional in the new born kitten, but the extracranial portion becomes non-patent in the few weeks following birth and has no direct role in blood supply to the brain of the adult cat. The maxillary artery has an anastomosing ramus which supplies the arterial circle. This ramus has a maxillary rete, also termed a rete mirabile that has an extracranial and an intracranial portion (McClure et al., 1973; Kamijyo and Garcia, 1975; King 1987). The extracranial part of the rete extends from the level of the foramen rotundum to the optic foramen, with several large-caliber anastomotic arteries passing through the orbital fissure and into the cavernous sinus to form the intracranial portion of the maxillary rete (Fig. 1). From these vessels the cerebral arteries are formed. A small branch off the maxillary artery, the middle meningeal artery, enters the skull through the foramen ovale, along with the mandibular branch of the trigeminal nerve (Holmes et al., 1958; McClure et al., 1973; Gomes et al., 2009). The foramen ovale and foramen rotundum are approximately 5 and 6 mm respectively from the medial aspect of the temporomandibular joint, while the orbital fissure and optic foramen are within the orbit. The external maxillary rete sits adjacent to the skull with the medial and lateral pterygoid muscles ventral and the temporalis muscle dorso-lateral to the rete. The cat also receives a small contribution of arterial circle blood via the ascending pharyngeal artery, a branch off the common carotid artery (Holmes et al., 1958; Gillian, 1976). This branch enters the skull through the foramen lacerum medium, which sits just caudal to the foramen ovale (Holmes et al., 1958). It is possible that the use of a spring-held mouth gag reduces blood flow to the brain through the maxillary artery by stretching of the vasculature and/or adjacent muscles with resulting vascular compromise. We were able to demonstrate during the cadaver dissections, that wide opening of the jaw caused marked tension on the temporalis and masseter muscles. It is likely that the pterygoid muscles also develop marked tension with wide jaw opening, although due to the position of these muscles we were not able to confirm this during the cadaver dissections. The close proximity of the maxillary rete to the pterygoid and temporalis muscles would make it potentially vulnerable to compressive or stretching forces with marked tension of these muscles. It is likely that an interaction of variables may lead to blindness and neurological deficits in some cats. This may include normal variations in maxillary artery anatomy, as has been documented in humans (Anil et al., 2003; Kim et al., 2010), variations in the anatomy of other pertinent structures such as the temporomandibular joint, degree and length of time of jaw extension, and systemic blood pressure trends. In this study we were not able to prove that spring-held mouth gags compromise the maxillary artery. Additional investigation could include the use of magnetic resonance angiography (Martin-Vaquero et al., 2011) or, where available, whole-brain perfusion computed tomography scanning (Murayama et al., 2009) or positron emission tomography/single photon emission computed tomography (Lee et al., 2010; Murayama et al., 2009), in anaesthetised cats to evaluate cerebral blood flow during wide jaw extension. It is well established that certain parts of the brain are more susceptible to global ischemia than others. Cerebral cortex, hippocampus, caudal colliculi, and thalamic nuclei are the most susceptible (Summers et al., 1995; ErdemLi and Crunelli, 1998). There are two main hypotheses of the pathophysiology of ischemic injury.

372 J. Stiles et al. / The Veterinary Journal 193 (2012) 367 373 The first is that of excitotoxic injury due to increased neurotransmitter activity of glutamate (White et al., 1993a). The second hypothesis is that free radicals produced by lipid peroxidation cause neuronal injury and death (White et al., 1993a,b). Ischemic damage to the occipital cortex, the lateral geniculate nuclei, or both would result in cortical blindness, but preserve the pupillary light and dazzle reflexes, as seen in the cats in our study. It has been shown that irreversible neuronal injury can occur in cats subjected to hypoxia of durations as short as 15 30 min (Ginsberg et al., 1978). Recovery of the CNS after ischemia is complex and poorly understood. Neurons are unable to replicate and reproduce once differentiated, though where neurons survive axonal repair and/ or sprouting may allow for recovery of white matter (White et al., 1996). Clinical recovery may also occur through plasticity, in which functional development of new connections and circuits ( re-mapping ) occurs among redundant or diffuse connections already existing within the CNS (Murphy and Corbett, 2009). The majority of cats in our study showed functional recovery over time, which could be explained by the mechanism of plasticity. The role of general anesthesia in the development of blindness in the cats in this study is uncertain. General anesthetic agents can have a variable impact on cerebral blood flow and oxygen consumption, which may affect ischemic outcomes (Kirsch et al., 1996). Most of the cats in this study were anaesthetised with a combination of propofol (n = 14) and isoflurane (n = 18). Propofol has been shown to decrease cerebral blood flow, intracranial pressure, and systemic arterial pressure, and is considered to be neuroprotective (Weir et al., 1989). Isoflurane increases cerebral blood flow and intracranial pressure, while decreasing systemic arterial pressure and cerebral perfusion pressure (Kirsch et al., 1996). This is in contrast to the use of dissociative agents such as ketamine, which greatly increase cerebral blood flow and intracranial pressure without decreasing cerebral metabolism. Only four cats in this study received ketamine. Hypotension has been the most commonly reported complication of general anesthesia in dogs and cats (Gaynor et al., 1999). Autoregulation of cerebral blood flow is well controlled when MAP is between 60 and 150 mm Hg (Bagley, 2003; Harvey et al., 2007). Significant and prolonged hypotension may be a contributing factor to cerebral ischemia in the anaesthetised feline patient. However, many cats experience hypotension under general anesthesia without resulting loss of vision. In this study, cat number 19 was the only dentistry case that did not have a mouth gag utilised. This cat did not have blood pressure measured and did not receive any intravenous fluid support during anesthesia. It is possible that significant hypotension occurred in this cat leading to cerebral ischemia. Conclusions The blood supply to the feline brain is almost entirely from the maxillary artery, thus any compromise to this vessel has the potential to lead to ischemia. While the visual cortex appears to have an increased sensitivity to hypoxia in the cat, decreased perfusion to other portions of the cerebrum lead to a myriad of neurological signs in addition to blindness. This is the first clinical study to suggest that the use of spring-held mouth gags in cats may be a risk factor for decreased brain perfusion by potential compromise of the maxillary artery. Any factors that further compromise blood flow, such as systemic hypotension, may be additional risk factors for brain ischemia. The overall prognosis for cats that experienced cerebral ischemia under general anesthesia in this study was good, with recovery of useful vision occurring in 70% of the cats, while 59% of cats had full recovery from other neurologic abnormalities. Based on the findings of this study and our hypothesis of maxillary artery compromise, we recommend that spring-held mouth gags are not used in cats. Maximal opening of the jaw should be avoided for all but the briefest period. A small mouth gag can be fashioned by cutting a tuberculin syringe barrel and placing it on opposing canine teeth to hold the mouth open as minimally as needed. Conflict of interest statement None of the authors has any financial or personal relationships that could inappropriately influence or bias the content of this paper. VMDB 1 does not make any implicit or implied opinion on the subject of this paper or study. 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