Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
www.ivis.org
Proceedings of the
47th British Equine Veterinary
Association Congress
BEVA
Sep. 10 – 13, 2008
Liverpool, United Kingdom
Next Congress:
Reprinted in IVIS with the permission of the British Equine Veterinary Association – BEVA
http://www.ivis.org/
Thursday H1A.qxp 1/4/09 15:23 Page 43
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
13.45–15.00
Over the last 5 years or so we have learnt much about existing and new disorders in horses from documentation of careful
clinical observations and interventions and from painstaking pathological studies with special emphasis on clinicopathological
correlates. Some of these disorders will be discussed elsewhere in this conference and this paper will highlight a few of
these disorders through which we have added to our understanding of anatomy, physiology and clinicopathological correlates
- the building-blocks for advancing equine neurology.
Figure 1: A continuous lesion in the dorsal grey column in the neck (star) causes a segmental interruption of the postural regulation of the
muscle tone in epaxial muscles, resulting in scoliosis of the neck. In addition, it interrupts the proprioceptive and general somatic afferent
input to higher centres resulting in ataxia and hypalgesia. If adjacent white matter is affected, ataxia in pelvic limbs may result.
43
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 44
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
Figure 2: The spinovestibular pathway processes special proprioceptive input from the neck to the cauda vestibular nuclei in the medulla
oblongata. Interruption to this system can result in vestibular disease without there being damage to the brain stem.
the C1–3 dorsal spinal nerve roots to ascend the spinal cord via the spinovestibular tract (Figure 2) to the caudal vestibular
nuclei. These nuclei receive no other afferent inputs. Lesions involving these cranial cervical nerves or the vestibulospinal
input to the vestibular apparatus can result in signs of vestibular disease. This certainly can be seen with symmetric lesions
of the dorsal nerve roots of C1–3 when loss of balance, eye deviation and head tilt have been seen.
44
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 45
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
Table 1: Proportion of major clinical signs recorded for 104 cases of EMND (34, 39).
Definitive diagnosis is dependent on the post mortem demonstration of degeneration and loss of cell bodies in the ventral
horn of the spinal cord and in motor nuclei in the brain stem with the exception of those supplying cranial nerves III, IV and
VI. In experimental cases and in naturally-occurring cases of EMND in North America and in Europe, vitamin E deficiency
has been the only consistent nutritional or toxic-related abnormality determined34. Further studies are necessary to explain
the development of hypovitaminosis E and EMND in horses that have adequate access to pasture. Genetic factors for
alterations in amount or activity of the alpha-tocopherol transfer protein, such as the 744 del A mutation of the alpha-TTP
gene operative in some forms of human hypovitaminosis E44,45, will need exploration in this regard.
45
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 46
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
Exercise intolerance associated with mild to moderate muscle stiffness may be the only initial clinical sign. This may easily
be attributed to a primary myopathy, with pain on muscle palpation, although serum muscle enzyme concentrations remain
in the normal range. Components of the syndrome bear resemblance to such disorders as tetanus, equine motor neuron
disease, hyperkalaemic periodic paralysis, exertional myopathies and especially the acquired channelopathies associated
with the mycotoxicoses such as perennial ryegrass staggers.
The most useful diagnostic test is detection of antibodies against GAD in serum and cerebrospinal fluid and, although
some cases have had high anti-GAD titres, several strongly suspected cases have been negative on this test.
The overall message really is that with the array of enigmatic movement and postural disorders encountered in equine
neurology that appear to be variations on the themes of stringhalt, shivering and claudication72–74, a broad approach to
delving into possible aetiological mechanisms should be taken that includes the possibility of immune associated
neurotransmitter derangements such as SPS.
GRASS SICKNESS
Grass sickness or equine dysautonomia has been described since the early 20th century and since then has had quite a
devastating effect on equine populations in parts of Western Europe75–78.
Per-acute colic with gastrointestinal stasis and rupture, anorexia with mild signs of colic and ileus, to chronic cachexia
covers the general spectrum of syndromes seen with this very unusual disease. Moderate tachycardia, indifference to food,
difficulty swallowing, excessive salivation, depressed gastrointestinal sounds, abdominal distension and usually mild colic are
very often present to varying degrees. Muscular tremor and patchy sweating may be primary signs or may reflect the
dehydration, electrolyte imbalances and colic that occur. Posturing with all feet close together as a weak patient does, ptosis
and especially rhinitis sica are very distinctive signs when present.
No definitive clinical diagnostic test exists. As the clinical signs of Horner’s syndrome are symmetric, ptosis can be
difficult to detect. However, a recently described aid to clinical diagnosis is the observance of a rapid reversal of ptosis with
0.5 ml of 0.5% phenylephrine eye drops89. The resulting marked difference in degree of ptosis and particularly in eye lash
angle can be spectacular.
ATYPICAL MYOPATHY
Several hundred cases of highly fatal, atypical myopathy or myoglobinuria have been reported in young, adult, grazing
horses mostly from Europe but also North America and Australasia90–93. Horses may be found dead or more often
showing various signs of reluctance to move, stiff and short strides, apparent sedation and fine muscle tremors. They
quickly become laterally recumbent and urine becomes dark with myoglobin staining although more sub-acute cases do
occur90. Plant, bacterial and fungal toxins have all been considered as possibilities but the cause or causes remain
completely unknown90. Clinicians suspecting cases are urged to log on to the atypical myopathy alert site and complete
the appropriate forms in an effort to unravel the epidemiology of this dastard disease: (dominique.votion@ulg.ac.be);
(http://www.ivis.org/reviews/rev/votion/chapter.asp?LA=1#forms).
FLUPHENAZINE TOXICITY
The long acting phenothiazine drugs perphenazine and fluphenazine have caused an interesting syndrome of fluctuant
somnolence and compulsive activity that can consist of adopting abnormal postures and displaying incredibly frantic,
repetitive movements99–103. Thus an affected horse may stand fixated by an object and appear to watch unapparent
images move, stand with the forelimbs placed well forward and the head flexed between the knees, and perform tonic
repetitive movements such as incessant pawing with one limb, head swinging and pseudo-rubbing on objects. Recumbency
without somnolence and seizure-like activity also occurs. Anticonvulsant and narcotic drugs are indicated to help control the
signs102 and possibly anticholinergic drugs such as benztropine and diphenhydramine can be considered100,103.
46
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 47
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
disease, eosinophilic granulomatous disease, equine sarcoidosis, multisystem granulomatosis, systemic granulomatous
disease and equine histiocytic dermatitis; the former definition being preferable for many reasons104–108. In one case of
idiopathic systemic granulomatous disease in an aged mare, there was a multifocal granulomatous encephalomeningitis, and
neurological signs consisted of a rapid progression of somnolence, head pressing, excitement, seizures and recumbency109.
Subacute leukoencephalitis and necrosis was accompanied by necrotising vasculitis and large perivascular accumulations of
lymphocytes, macrophages, some neutrophils and multinucleated giant cells. Several other very similar isolated cases have
been seen in horses by the author and have been documented110.
In general, it is accepted that equine idiopathic generalised granulomatous disease is a programmed immune response
to chronic environmental antigens107,111. On the other hand, with further cytological specification some of the apparently
inflammatory meningoencephalitides may more closely resemble diffuse lymphoma, meningeal sarcoma or
microglioma111, 112. Drawing a likeness between this idiopathic generalised granulomatous disease in horses to Vicia
villosa (hairy vetch, fodder vetch) toxicity113–116 is enticing. This is particularly so as firstly these plants contain numerous
phytolectins that bind lymphocytes117 and secondly nonsuppurative, granulomatous leukoencephalitis has been detected
histologically in one horse with this disease114.
SCLEROSING PANENCEPHALITIS
Sclerosing panencephalitis occurs in at least 2 specific diseases in man, namely subacute sclerosing panencephalitis
associated with modified measles virus DNA and progressive multifocal leukoencephalopathy associated with a papovavirus.
A novel case of sclerosing panencephalitis has been documented in a mature horse showing progressive multifocal
asymmetric signs including blindness, hypermetric ataxia and multiple asymmetric cranial nerve dysfunction over
approximately 12 weeks118. Lymphocytic encephalitis, necrosis, demyelination and prominent fibrillary and gemistocytic
astrogliosis dominated the lesions widespread throughout the neuropil and meninges of the brain. Although a diffuse
astrocytoma could result in some of the cellular characteristics it was concluded that this was primarily a panencephalitis.
A search for viral DNA in future cases is warranted.
47
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 48
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
for the movement disorder with abnormal input via the 1a-afferent fibres to the α-efferent neurons resulting in inappropriate
firing of lateral digital extensor and other muscles.
Although palliative, removing a section of the myotendinous region of the lateral digital extensor muscle relieves the
syndrome quite spectacularly in many cases128,129.
TEMPOROHYOID OSTEOARTHROPATHY
Temporohyoid osteoarthropathy (THO) with proliferative osteopathy involving the temporal bone, temporohyoid joint and hyoid
bone, is reported only in adult horses and may be sub-clinical or may result in evidence of difficulty chewing or more often
neurological syndromes, notably various combinations of facial and vestibulochoclear nerve dysfunction. Some of the cases
have bilateral disease as determined by endoscopic and radioimaging studies, although the clinical signs are most often
unilateral130–134.
The cause of temporohyoid osteoarthropathy is unclear although to this author a traumatic origin is most plausible in
most cases135 with chronic otitis media/interna accounting for a select few cases. Regardless of the aetiology of the
osteoarthritis, clinical signs can occur from either the osteoarthritis itself or from fractures of the adjacent temporal bone
and rarely basilar bones, due to partial or complete fusion of the joint.
Physical examination findings may include difficulty chewing, pain on external palpation of the parotid area, head shaking
and behavioural problems especially when being ridden131,132,134,136. Once the joint is partly fused, sudden forced head
jerking, falling, teeth floating, nasogastric intubation and sudden prolonged vocalisation can cause periarticular fractures of
the petrous temporal bone resulting in combinations of an abrupt onset of facial and vestibular nerve dysfunction.
Endoscopic examination of the guttural pouch is probably superior to plain radiographic imaging in confirming the presence
of the disease by revealing enlargement of the proximal stylohyoid bone due to osteoarthritis when compared to the opposite
side. In acute or progressive cases having ill-defined endoscopic and plain radiographic imaging findings, gamma scintigraphy
should be considered as a diagnostic aid. Monitoring brain stem auditory evoked potential recordings is a very noninvasive
procedure that may assist in refining the prognosis in individual cases137 and following progress of the disease.
Several cases have improved with the passage of time only to show further signs relative to facial and vestibular nerve
dysfunction in weeks to months time. These would seem to be ideal candidates for unilateral surgical disunion of the hyoid
apparatus. Initial surgical disunion of the hyoid apparatus was performed by removal of a mid-shaft portion of the stylohyoid
bone138. To reduce the temporary difficulties in swallowing encountered and to reduce the possibility of other real and
potential complications of this surgery the technique of ceratohyoidectomy was proposed and used with success135,136.
Except with major cranial fractures and if eye problems cannot be resolved135, the outlook for survival with residual
neurological deficits is quite good. Of 33 cases of temporohyoid osteoarthropathy132, 20 cases survived for which there
were longer term follow-up details. Of these, 70% returned to previous level of use although more than 50% of the 20
horses still had evidence of facial nerve deficits and/or vestibular dysfunction. Thus, in spite of some optimistic suggestions,
if full athletic performance without neurological dysfunction is required then the prognosis with or without surgical
intervention has to be fair to guarded for these cases.
Cases of THO have given us a better insight into the ability of horses to accommodate to vestibular dysfunction and to
survive with degrees of facial paralysis.
CONCLUDING COMMENTS
Being a biology watcher does have its rewards in equine neurology. Over the last 5–10 years by making accurate
observations, recording of findings and publishing clinical results we have a better insight into the pathophysiology of
diseases, the application of better therapy and improved accuracy of diagnosis and prognosis. Hopefully this discourse on
some of the interesting aspects of several equine neurological diseases will stimulate others to share their experiences.
48
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 49
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
49
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 50
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
37. Riis, R.C., Jackson, C., Rebhun, W., Katz, M.L., Loew, E., Summers, B., Cummings, J., de Lahunta, A., Divers, T. and Mohammed, H. (1999)
Ocular manifestations of equine motor neuron disease. Equine vet. J. 31, 99-110.
38. Verhulst, D., Barnett, K.C. and Mayhew, I.G. (2001) Equine motor neuron disease and retinal degeneration. Equine vet. Educ. 13, 59-67.
39. McGorum, B.C., Mayhew, I.G., Amory, H., Deprez, P., Gillies, L., Green, K., Mair, T.S., Nollet, H., Wijnberg, I.D. and Hahn, C.N. (2006) Horses
on pasture may be affected by equine motor neuron disease. Equine vet. J. 38, 47-51.
40. Valentine, B.A., de Lahunta, A., George, C., Summers, B.A., Cummings, J.F., Divers, T.J. and Mohammed, H.O. (1994) Acquired equine motor
neuron disease. Vet. Pathol. 31, 130-138.
41. Gruys, E., Beynen, A.C., Binkhorst, G.J., Van Dijk, S., Koeman, J.P. and Stolk, P. (1994) Neurodegenerative disorders of the central nervous
system in horses. Tijdschr Diergeneeskd 119, 561-567.
42. Furuoka, H., Hasegawa, M., Kobayashi, Y. and Matsui, T. (1999) Peripheral nerve lesions in a case of equine motor neuron disease. J. vet.
med. Sci. 61, 557-560.
43. Weber Polack, E., King, J.M., Cummings, J.F., de Lahunta, A., Divers, T.J. and Mohammed, H.O. (1998) Quantitative assessment of motor
neuron loss in equine motor neuron disease (EMND). Equine vet. J. 30, 256-259.
44. Eggermont, E. (2006) Recent advances in vitamin E metabolism and deficiency. Eur. J. Pediatr. 165, 429-434.
45. Marzouki, N., Benomar, A., Yahyaoui, M., Birouk, N., Elouazzani, M., Chkili, T. and Benlemlih, M. (2005) Vitamin E deficiency ataxia with (744
del A) mutation on alpha-TTP gene: genetic and clinical peculiarities in Moroccan patients. Eur. J. Med. Genet. 48, 21-28.
46. Valberg, S.J., Macleay, J.M., Billstrom, J.A., Hower-Moritz, M.A. and Mickelson, J.R. (1999) Skeletal muscle metabolic response to exercise
in horses with ‘tying-up’ due to polysaccharide storage myopathy. Equine vet. J. 31, 43-47.
47. Valberg, S.J., Cardinet, G.H.3rd, Carlson, G.P. and DiMauro, S. (1992) Polysaccharide storage myopathy associated with recurrent exertional
rhabdomyolysis in horses. Neuromuscul. Disord. 2, 351-359.
48. Valentine, B.A. (2003) Equine polysaccharide storage myopathy. Equine vet. Educ. 15, 254-262.
49. Piercy, R.J. and Rivero, J.L. (2004) Muscle diseases of equine athletes. In: Equine Sports Medicine and Surgery, Eds: K.W. Hinchcliff, R.J. Geor
and A.J. Kaneps, W.B. Saunders Co.
50. Firshman, A.M., Valberg, S.J., Bender, J.B. and Finno, C.J. (2003) Epidemiologic characteristics and management of polysaccharide storage
myopathy in Quarter Horses. Am. J. vet. Res. 64, 1319-1327.
51. Firshman, A.M., Baird, J.D. and Valberg, S.J. (2005) Prevalences and clinical signs of polysaccharide storage myopathy and shivers in Belgian
draft horses. J. Am. vet. med. Ass. 227, 1958-1964.
52. Valberg, S. and Mickelson, J.R. (2007) The interplay of genetics, exercise and nutrition in polysaccharide storage myopathy. In: American College
of Veterinary Internal Medicine, ACVIM, Seattle, Washington.
53. Valberg, S.J., Mickelson, J.R., Gallant, E.M., MacLeay, J.M., Lentz, L. and de la Corte, F. (1999) Exertional rhabdomyolysis in quarter horses
and thoroughbreds: one syndrome, multiple aetiologies. Equine vet. J., Suppl. 30, 533-538.
54. Valentine, B.A., Habecker, P.L., Patterson, J.S., Njaa, B.L., Shapiro, J., Holshuh, H.J., Bildfell, R.J. and Bird, K.E. (2001) Incidence of
polysaccharide storage myopathy in draft horse-related breeds: a necropsy study of 37 horses and a mule. J. vet. diag. Invest. 13, 63-68.
55. Valentine, B.A. and Cooper, B.J. (2005) Incidence of polysaccharide storage myopathy: necropsy study of 225 horses. Vet. Pathol. 42, 823-827.
56. Firshman, A.M., Valberg, S.J., Bender, J.B., Annandale, E.J. and Hayden, D.W. (2006) Comparison of histopathologic criteria and skeletal
muscle fixation techniques for the diagnosis of polysaccharide storage myopathy in horses. Vet. Pathol. 43, 257-269.
57. McKenzie, E.C., Valberg, S.J., Godden, S.M., Pagan, J.D., MacLeay, J.M., Geor, R.J. and Carlson, G.P. (2003) Effect of dietary starch, fat, and
bicarbonate content on exercise responses and serum creatine kinase activity in equine recurrent exertional rhabdomyolysis. J. vet. int. Med.
17, 693-701.
58. Ribeiro, W.P., Valberg, S.J., Pagan, J.D. and Gustavsson, B.E. (2004) The effect of varying dietary starch and fat content on serum creatine
kinase activity and substrate availability in equine polysaccharide storage myopathy. J. vet. int. Med. 18, 887-894.
59. Edwards, J.G.T., Newton, J.R., Ramzan, P.H.L., Pilsworth, R.C. and Shepherd, M.C. (2003) The efficacy of dantrolene sodium in controlling
exertional rhabdomyolysis in the Thoroughbred racehorse. Equine vet. J. 35, 707-711.
60. McKenzie, E.C., Valberg, S.J., Godden, S.M., Finno, C.J. and Murphy, M.J. (2004) Effect of oral administration of dantrolene sodium on serum
creatine kinase activity after exercise in horses with recurrent exertional rhabdomyolysis. Am. J. vet. Res. 65, 74-79.
61. Meyer, T.S., Fedde, M.R., Cox, J.H. and Erickson, H.H. (1999) Hyperkalaemic periodic paralysis in horses: a review. Equine vet. J. 31, 362-367.
62. Carr, E.A., Spier, S.J., Kortz, G.D. and Hoffman, E.P. (1996) Laryngeal and pharyngeal dysfunction in horses homozygous for hyperkalemic
periodic paralysis. J. Am. vet. med. Ass. 209, 798-803.
63. Bailey, J.E., Pablo, L. and Hubbell, J.A. (1996) Hyperkalemic periodic paralysis episode during halothane anesthesia in a horse. J. Am. vet.
med. Ass. 208, 1859-1865.
64. Rudolph, J.A., Spier, S.J., Byrns, G., Rojas, C.V., Bernoco, D. and Hoffman, E.P. (1992) Periodic paralysis in quarter horses: a sodium channel
mutation disseminated by selective breeding. Nat. Genet. 2, 144-147.
65. Laboratory, V.G. Services and Research. http://www.vgl.ucdavis.edu/
66. Van Haeringen. Van Haeringen Laboratorium bv. http://www.vhlgenetics.com/vhl/index.html
67. Bowling, A.T., Byrns, G. and Spier, S. (1996) Evidence for a single pedigree source of the hyperkalemic periodic paralysis susceptibility gene in
quarter horses. Anim. Genet. 27, 279-281.
68. Naylor, J.M. (1994) Selection of quarter horses affected with hyperkalemic periodic paralysis by show judges. J. Am. vet. med. Ass. 204, 926-928.
69. Murinson, B.B. (2004) Stiff-person syndrome. Neurologist 10, 131-137.
70. Hassin-Baer, S., Kirson, E.D., Shulman, L., Buchman, A.S., Bin, H., Hindiyeh, M., Markevich, L. and Mendelson, E. (2004) Stiff-person
syndrome following West Nile fever. Arch. Neurol. 61, 938-941.
71. Nollet, H., Vanderstraeten, G., Sustronck, B., Van Ham, L., Ziegler, M. and Deprez, P. (2000) Suspected case of stiff-horse syndrome. Vet. Rec.
146, 282-284.
72. Davies, P.C. (2000) Shivering in a thoroughbred mare. Can. vet. J. 41, 128-129.
73. Mitchell, W.M. (1930) Some further observations on pathological changes found in horses affected with Shivering and their significance. Vet. Rec.
10, 535-537.
50
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 51
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
74. Deen, T. (1984) Shivering, a rare equine lameness. A case report. Equine Pract. 6, 19-21.
75. Pirie, R.S. (2006) Grass sickness. Clin. Tech. equine Pract. 5, 30-36.
76. Timoney, P.J. and Wernery, U. (2003) International conference on equine grass sickness, Dubai, United Arab Emirates September 22-23,
2001. Vet. J. 165, 7-10.
77. McCarthy, H.E., Proudman, C.J. and French, N.P. (2001) Epidemiology of equine grass sickness: a literature review (1909-1999). Vet. Rec.
149, 293-300.
78. Gilmour, J. and Jolly, G.M. (1974) Some aspects of the epidemiology of equine grass sickness. Vet. Rec. 95, 77-81.
79. Hahn, C.N., Whitwell, K.E. and Mayhew, I.G. (2005) Neuropathological lesions resembling equine grass sickness in rabbits. Vet. Rec. 156,
778-779.
80. Cottrell, D.F., McGorum, B.C. and Pearson, G.T. (1999) The neurology and enterology of equine grass sickness: a review of basic mechanisms.
Neurogastroenterol. Mot. 11, 79-92.
81. Ashton, D.G., Jones, D.M. and Gilmour, J.S. (1977) Grass sickness in two non-domestic equines. Vet. Rec. 100, 406-407.
82. Wales, A.D., Blunden, A.S. and Hosegood, O.M. (2001) Grass sickness with atypical presentation in a young zebra. Vet. Rec. 148, 818-819.
83. Middleton, J.R., Johnson, G.C., Pardo, I., Chigerwe, M. and O’Brien, D.P. (2006) Dysautonomia and salmonellosis in an 11-year-old female llama
(Lama glama). J vet. int. Med. 20, 213-216.
84. Griffiths, I.R. and Whitwell, K.E. (1993) Leporine dysautonomia: further evidence that hares suffer from grass sickness. Vet. Rec. 132, 376-377.
85. Vörös, K., Bakos, Z., Albert, M., Barátossy, G. and Fejér, B. (2003) Occurrence of grass sickness in Hungary (Hungarian). Magyar Allatorvosok
Lapja. 125, 67-74.
86. Araya, O., Vits, L., Paredes, E. and Ildefonso, R. (2002) Grass sickness in horses in southern Chile. Vet. Rec. 150, 695-697.
87. Johnson, P.J. (2003) Equine grass sickness in a horse from Missouri.
88. Uzal, F.A. and Robles, C.A. (1993) Mal seco, a grass sickness-like syndrome of horses in Argentina. Vet. Res. Comm. 17, 449-457.
89. Hahn, C.N. and Mayhew, I.G. (2000) Phenylephrine eyedrops as a diagnostic test in equine grass sickness. Vet. Rec. 147, 603-606.
90. Finno, C.J., Valberg, S.J., Wunschmann, A. and Murphy, M.J. (2006) Seasonal pasture myopathy in horses in the midwestern United States:
14 cases (1998-2005). J. Am. vet. med. Ass. 229, 1134-1141.
91. Votion, D.M., Amory, H., Demoulin, V., Desmecht, D., Rollin, F., Thiry, E., Baise, E., Cassart, D., Delguste, C., Piat, E., Sandersen, C. and
Linden, A. Atypical Myopathy (Atypical Myoglobinuria) www.ivis.org. http://www.ivis.org/reviews/rev/votion/chapter.asp?LA=1
92. Votion, D.M., Delguste, C., Baise, E. and Al, E. (2003) Diagnostic différentiel en cas de présomption de myopathie atypique des équidés:
illustration au travers de cas référés ą la Faculté de Médecine Vétérinaire de l’Université de LiŹge au cours du printemps 2003. Ann. Méd. Vét.
147, 183-193.
93. Whitwell, K.E., Harris, P. and Farrington, P.G. (1988) Atypical myoglobinuria: an acute myopathy in grazing horses. Equine vet. J. 20, 357-363.
94. Gerber, V., Straub, R. and Frey, J. (2006) Equine botulism and acute pasture myodystrophy: new soil-borne emerging diseases in Switzerland?
Schweiz Arch Tierheilkd. 148, 553-559.
95. Birklein, F. (2005) Complex regional pain syndrome. J. Neurol. 252, 131-138.
96. Scadding, J. (2003) Neuropathic pain. Adv. Clin. Neurosci Rehab. 3, 8-14.
97. McMahon, S. and Koltzenburg, M. (2005) Wall and Melzack’s Textbook of Pain. 5th edn. Churchill Livingstone.
98. Collins, N.M., Keen, J.A., Barakzai, S.Z., Mayhew, I.G. and McGorum, B.C. (2006) Suspected complex regional pain syndrome in 2 horses.
J. vet. int. Med. 20, 1014-1017.
99. McCrindle, C.M., Ebedes, H. and Swan, G.E. (1989) The use of long-acting neuroleptics, perphenazine enanthate and pipothiazine palmitate in
two horses. J. S. Afr. vet. Ass. 60, 208-209.
100. Kauffman, V.G., Soma, L., Divers, T.J. and Perkons, S.Z. (1989) Extrapyramidal side effects caused by fluphenazine decanoate in a horse.
J. Am. vet. med. Ass. 195, 1128-1130.
101. Brewer, B.D., Hines, M.T., Stewart, J.T. and Langlois, J.F. (1990) Fluphenazine induced Parkinson-like syndrome in a horse. Equine vet. J. 22,
136-137.
102. Brashier, M. (2006) Fluphenazine-induced extrapyramidal side effects in a horse. Vet. Clin. N. Am.: Equine Pract. 22, 37-45.
103. Baird, J.D., Arroyo, L.G., Vengust, M., McGurrin, M.K.J., Rodriguez-Palacios, A., Kenney, D.G., Aravagiri, M. and Maylin, G.A. (2006) Adverse
extrapyramidal effects in four horse given fluphenazine decanoate. J. Am. vet. med. Ass. 229, 104-110.
104. Latimer, K.S., Bounous, D.I., Colatos, C., Carmichael, K.P. and Howerth, E.W. (1996) Extreme eosinophilia with disseminated eosinophilic
granulomatous disease in a horse. Vet. clin. Pathol. 25, 23-26.
105. Axon, J.E., Robinson, P. and Lucas, J. (2004) Generalised granulomatous disease in a horse. Aust. vet. J. 82, 48-51.
106. Pusterla, N., Pesavento, P.A., Smith, P., Durando, M.M., Magdesian, K.G. and Wilson, W.D. (2003) Idiopathic granulomatous pneumonia in
seven horses. Vet. Rec. 153, 653-355.
107. Sellers, R.S., Toribio, R.E. and Blomme, E.A. (2001) Idiopathic systemic granulomatous disease and macrophage expression of PTHrP in a
miniature pony. J. comp. Pathol. 125, 214-218.
108. Heath, S.E., Bell, R.J., Clark, E.G. and Haines, D.M. (1990) Idiopathic granulomatous disease involving the skin in a horse. J. Am. vet. med. Ass.
197, 1033-1036.
109. Peters, M., Graf, G. and Pohlenz, J. (2003) Idiopathic systemic granulomatous disease with encephalitis in a horse. J. vet. med. A. Physiol.
Pathol. Clin. Med. 50, 108-112.
110. Summers, B.A., Cummings, J.F. and de Lahunta, A. (1995) Veterinary Neuropathology, Mosby. p 527.
111. Peters, J., McDonough, S., de Lahunta, A., Hahn, C.N. and Summers, B. (2002) Equine CNS lymphoma and meningovascular amyloidosis:
connection or coincidence? In: Proceedings of the 53rd Annual Meeting of the American College of Veterinary Pathology.
112. Fankhauser, R., Luginbuhl, H. and McGrath, J.T. (1974) Tumours of the nervous system. Bull. World Health Org. 50, 53-69.
113. Anderson, C.A. and Divers, T.J. (1983) Systemic granulomatous inflammation in a horse grazing hairy vetch. J. Am. vet. med. Ass. 183, 569-570.
114. Woods, L.W., Johnson, B., Hietala, S.K., Galey, F.D. and Gillen, D. (1992) Systemic granulomatous disease in a horse grazing pasture
containing vetch (Vicia sp.). J. vet. diag. Invest. 4, 356-360.
51
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom
Thursday H1A.qxp 1/4/09 15:23 Page 52
Reprinted in IVIS with the permission of BEVA Close this window to return to IVIS
Thursday Hall 1A
115. Fighera, R.A. and Barros, C.S. (2004) Systemic granulomatous disease in Brazilian cattle grazing pasture containing vetch (Vicia spp).
Vet. Hum. Toxicol. 46, 62-66.
116. Johnson, B., Moore, J., Woods, L.W. and Galey, F.D. (1992) Systemic granulomatous disease in cattle in California associated with grazing
hairy vetch (Vicia villosa). J. vet. diag. Invest. 4, 360-362.
117. Grubhoffer, L., Ticha, M. and Kocourek, J. (1981) Isolation and properties of a lectin from the seeds of hairy vetch (Vicia villosa Roth). Biochem. J.
195, 623-626.
118. Swain, J.M., Hudson, N.P., Rhind, S.M., Baird, P.M. and Mayhew, I.G. (2005) A novel, progressive, sclerosing panencephalitis in a horse. Equine
vet. J. 37, 276-280.
119. McCann, J.L., Dixon, P.M. and Mayhew, I.G. (2004) Clinical anatomy of the equine sphenopalatine sinus. Equine vet. J. 36, 466-472.
120. Huntington, P.J., Jeffcott, L.B., Friend, S.C., Luff, A.R., Finkelstein, D.I. and Flynn, R.J. (1989) Australian Stringhalt--epidemiological, clinical and
neurological investigations. Equine vet. J. 21, 266-273.
121. Cahill, J.I., Goulden, B.E. and Pearce, H.G. (1985) A review and some observations on stringhalt. N. Z. vet. J. 33, 101-104.
122. Gardner, SY., Cook, A.G., Jortner, B.S., Troan, B.V., Sharp, N.J.H., Campbell, N.B. and Brownie, C.F. (2005) Stringhalt associated with a
pasture infested with Hypochoeris radicata. Equine vet. Educ. 17, 118-122.
123. Gay, C.C., Fransen, S., Richards, J. and Holler, S. (1993) Hypochoeris-associated stringhalt in North America. Equine vet. J. 25, 456-457.
124. Araya, O., Krause, A. and Solis de Ovando, M. (1998) Outbreaks of stringhalt in southern Chile. Vet. Rec. 142, 462-463.
125. Takahashi, T., Kitamura, M., Endo, Y., Eto, D., Aoki, O., Kusunose, R., Yoshihara, T. and Kai, M. (2002) An outbreak of stringhalt resembling
Australian stringhalt in Japan. J. equine Sci. 13, 93-100.
126. Slocombe, R.F., Huntington, P.J., Friend, S.C., Jeffcott, L.B., Luff, A.R. and Finkelstein, D.K. (1992) Pathological aspects of Australian
Stringhalt. Equine vet. J. 24, 174-183.
127. Cahill, J.I., Goulden, B.E. and Jolly, R.D. (1986) Stringhalt in horses: a distal axonopathy. Neuropathol. Appl. Neurobiol. 12, 459-475.
128. Torre, F. (2003) Clinical diagnosis and results of surgical treatment of 11 cases of acquired bilateral stringhalt (1991-2002). In: Proceedings
of the Annual Scientific Meeting of the European College of Veterinary Surgeons.
129. Torre, F. (2005) Clinical diagnosis and results of surgical treatment of 13 cases of acquired bilateral stringhalt (1991-2003). Equine vet. J. 37,
181-183.
130. Power, H.T., Watrous, B.J. and de Lahunta, A. (1983) Facial and vestibulocochlear nerve disease in six horses. J. Am. vet. med. Ass. 183,
1076-1080.
131. Johnson, P.J. and Kellam, L.L. (2001) The vestibular system. Part II: Differential diagnosis. Equine vet. Educ. 13, 141-149.
132. Walker, A.M., Sellon, D.C., Cornelisse, C.J., Hines, M.T., Ragle, C.A., Cohen, N. and Schott, H.C. 2nd. (2002) Temporohyoid osteoarthropathy
in 33 horses (1993-2000). J. vet. int. Med. 16, 697-703.
133. Blythe, L.L., Watrous, B.J., Schmitz, J.A. and Kaneps, A.J. (1984) Vestibular syndrome associated with temporohyoid joint fusion and temporal
bone fracture in three horses. J. Am. vet. med. Ass. 185, 775-781.
134. Blythe, L.L. (1997) Otitis media and interna and temporohyoid osteoarthropathy. Vet. Clin. N. Am.: Equine Pract. 13, 21-42.
135. Divers, T.J., de Lahunta, A., Ducharme, N.G., Irby, N.L. and Scrivani, P.V. (2006) Temporohyoid osteoarthropathy. Clin. Tech. equine Pract. 5,
17-23.
136. Pease, A.P., van Biervliet, J., Dykes, N.L., Divers, T.J. and Ducharme, N.G. (2004) Complication of partial stylohyoidectomy for treatment of
temporohyoid osteoarthropathy and an alternative surgical technique in three cases. Equine vet. J. 36, 546-550.
137. Mayhew, I.G. (2003) The clinical utility of brainstem auditory evoked response testing in horses. Equine vet. Educ. 15, 27-33.
138. Blythe, L.L., Watrous, B.J., Shires, G.M.H. and Kaneps, A.J. (1994) Prophylactic partial stylohyoidostectomy for horses with osteoarthropathy
of the temporohyoid joint. J. equine Sci. 14, 32-37.
139. McKay, J.S., Forest, T.W., Senior, M., Kelly, D.F., Jones, R.S., de LA and Summers, B.A. (2002) Postanaesthetic cerebral necrosis in five
horses. Vet. Rec. 150, 70-74.
140. Spadavecchia, C., Jaggy, A., Fatzer, R. and Schatzmann, U. (2001) Postanaesthetic cerebral necrosis in a horse. Equine vet. J. 33, 621-624.
141. Hewetson, M. (2002) Cerebral Syndrome: Equine Neurology Course, University of Liverpool.
142. Ripoll, S., Clarke, K.W., Borer, K., Neiger-Aeschbacher, G., Hammond, R., Alibhai, H.I., Taylor, P.M., Bennett, R.C., Walsh, C.M., Bilbrough,
G.E., Waterman, A., Brearley, J.C., Hall, L.W., Clutton, R.E., Flaherty, D. and Johnston, G.M. (2002) Postanaesthetic cerebral necrosis in five
horses. Vet. Rec. 150, 387-388.
52
Proceedings of the 47th British Equine Veterinary Association Congress 2008 - Liverpool, United Kingdom