Large Animal Neurology. Joe Mayhew

palliative treatment of some of these disorders.^37–39

References

      1 1 Siegel JM. Clues to the functions of mammalian sleep. Nature 2005; 437(7063): 1264–1271.

      2 2 Williams DC, Holliday TA, Aleman MR, et al. Sleep in the horse: an electroencephalographic study. Am Coll Vet Int Med Forum 2002; ACVIM.

      3 3 Kryger MH, Roth DT and Dement WC. Principles and Practice of Sleep Medicine. 4th ed. Saunders, Elsevier, Philadelphia, PA. 2005; 1552.

      4 4 Dallaire A and Ruckebusch Y. Sleep patterns in the pony with observations on partial perceptual deprivation. Physiol behav 1974; 12(5): 789–796.

      5 5 Ruckebusch Y. The relevance of drowsiness in the circadian cycle of farm animals. Anim behav 1972; 20(4): 637–643.

      6 6 Ruckebusch Y, Barbey P and Guillemot P. Stages of sleep in the horse (Equus caballus). Comptes rendus des seances de la Societe de biologie et de ses filiales. 1970; 164(3): 658–665.

      7 7 Bertone JJ. Sleep deprivation not narcolepsy in horses. Proc 24th Annual Forum Am Coll Vet Int Med, Louisville KY. 2006; 24: 167–169.

      8 8 Pizza F, Antelmi E, Vandi S, et al. The distinguishing motor features of cataplexy: a study from video‐recorded attacks. Sleep 2018; 41(5): zsy026–zsy.

      9 9 Pillen S, Pizza F, Dhondt K, Scammell TE and Overeem S. Cataplexy and its mimics: clinical recognition and management. Curr Treat Options Neurol 2017; 19(6).

      10 10 Lyle CH and Keen JA. Episodic collapse in the horse. Equine Vet Educ 2010; 22(11): 576–586.

      11 11 Hughes KJ. Diagnostic challenge: lethargy and weakness in an Arabian foal with cardiac murmurs. Ventricular septal defect (VSD). Aust Vet J 2006; 84(6): 209–212.

      12 12 Lyle CH, Turley G, Blissitt KJ, et al. Retrospective evaluation of episodic collapse in the horse in a referred population: 25 cases (1995–2009). J Vet Intern Med 2010; 24(6): 1498–1502.

      13 13 Reading PJ. Update on narcolepsy. J Neurol 2019; 266(7): 1809–1815.

      14 14 Young TJ and Silber MH. Hypersomnias of central origin. Chest 2006; 130(3): 913–920.

      15 15 de Lecea L and Sutcliffe JG. The hypocretins and sleep. FEBS J 2005; 272(22): 5675–5688.

      16 16 Mignot E and Nishino S. Emerging therapies in narcolepsy‐cataplexy. Sleep 2005; 28(6): 754–763.

      17 17 Scammell TE. The neurobiology, diagnosis, and treatment of narcolepsy. Ann neurol 2003; 53(2): 154–166.

      18 18 Dauvilliers Y and Buguet A. Hypersomnia. Dialogues clin neurosci 2005; 7(4): 347–356.

      19 19 Dauvilliers Y, Challamel MJ and Touchon J. (Sleep disorders in children and adults). La Revue du praticien 2003; 53(17): 1937–1946.

      20 20 Tafti M, Maret S and Dauvilliers Y. Genes for normal sleep and sleep disorders. Ann med 2005; 37(8): 580–589.

      21 21 Black JE, Brooks SN and Nishino S. Narcolepsy and syndromes of primary excessive daytime somnolence. Semin Neurol 2004; 271–282.

      22 22 Kotagal S and Pianosi P. Sleep disorders in children and adolescents. Br Med J 2006; 332(7545): 828–832.

      23 23 ICSD‐3 AAoSM. International Classification of Sleep Disorders, 3rd ed. Buysse DJ, Ed. American Academy of Sleep Medicine, Darien, IL. 2014.

      24 24 Peyron C and Charnay Y. (Hypocretins/orexins and narcolepsy: from molecules to disease). Revue neurologique 2003; 159(11 Suppl): 6S35–6S41.

      25 25 Black JE, Brooks SN and Nishino S. Conditions of primary excessive daytime sleepiness. Neurol Clin 2005; 23(4): 1025–1044.

      26 26 Baumann CR and Bassetti CL. Hypocretins (orexins) and sleep–wake disorders. Lancet Neurol 2005; 4(10): 673–682.

      27 27 Crocker A, Espana RA, Papadopoulou M, et al. Concomitant loss of dynorphin, NARP, and orexin in narcolepsy. Neurology 2005; 65(8): 1184–1188.

      28 28 Lodi R, Tonon C, Vignatelli L, et al. in vivo evidence of neuronal loss in the hypothalamus of narcoleptic patients. Neurology 2004; 63(8): 1513–1515.

      29 29 Thannickal TC, Moore RY, Nienhuis R, et al. Reduced number of hypocretin neurons in human narcolepsy. Neuron 2000; 27(3): 469–474.

      30 30 Thannickal TC, Siegel JM, Nienhuis R and Moore RY. Pattern of hypocretin (orexin) soma and axon loss, and gliosis, in human narcolepsy. Brain Pathol 2003; 13(3): 340–351.

      31 31 Smith AJ, Jackson MW, Neufing P, McEvoy RD and Gordon TP. A functional autoantibody in narcolepsy. Lancet 2004; 364(9451): 2122–2124.

      32 32 Liblau RS. Put to sleep by immune cells. Nature 2018; 562(7725): 46–48.

      33 33 Boehmer LN, Wu MF, John J and Siegel JM. Treatment with immunosuppressive and anti‐inflammatory agents delays onset of canine genetic narcolepsy and reduces symptom severity. Exp Neurol 2004; 188(2): 292–299.

      34 34 Schatzberg SJ, Cutter‐Schatzberg K, Nydam D, et al. The effect of hypocretin replacement therapy in a 3‐year‐old Weimaraner with narcolepsy. J Vet Intern Med 2004; 18(4): 586–588.

      35 35 Toth B, Aleman M, Brosnan RJ, et al. Evaluation of squeeze‐induced somnolence in neonatal foals. Am J Vet Res 2012; 73(12): 1881–1889.

      36 36 Schiffmann C, Hoby S, Wenker C, et al. When elephants fall asleep: a literature review on elephant rest with case studies on elephant falling bouts, and practical solutions for zoo elephants. Zoo Biol 2018; 37(3):133–145.

      37 37 Klimova B, Maresova P, Novotny M and Kuca K. A global view on narcolepsy: a review study. Mini Rev Med Chem 2018; 18(5): 458–464.

      38 38 Cheung J, Ruoff CM and Mignot E. Chapter 8 – Central Nervous System Hypersomnias. Ed. Miglis M G. Sleep and Neurologic Disease. Academic Press, San Diego. 2017; 141–166.

      39 39 Evangelista E, Lopez R and Dauvilliers Y. Update on treatment for idiopathic hypersomnia. Expert Opin Investig Drugs 2018; 27(2): 187–192.

8 Coma and other altered states of consciousness

Coma (Gr: deep sleep) is a state of living nonresponsiveness. Stages of increasing levels of obtundation can be referred to as sleepiness (somnolence), semicoma (Figure 8.1) and coma, and represent a progressive lack of awareness of the environment and decreased responsiveness to physiologic and noxious stimuli. It is wise to avoid the anthropomorphic terms depression, delirium, oscitancy, torpor, stupor, lethargy, etc., because of the subjective connotation of these terms in human medicine. It is clearest to simply state what the patient is and is not aware of. Diffuse and focal lesions resulting in coma and other altered states of consciousness involve the forebrain and/or the reticular activating system (RAS) in the brainstem, particularly in the midbrain (Figure 1.7).

An alert state is maintained through multiple sensory inputs to the RAS in the rostral brainstem and subsequently to the thalamus and cerebral cortex where conscious awareness in animals presumably is attained. Diffuse cerebral disease and severe lesions involving just the thalamus, internal capsule, or frontal lobe can result in an inattentive and oblivious mental awareness in animals, often expressed as dummy syndrome. Additional signs of behavioral aberrations, seizures, and visual disturbances frequently accompany this condition. Coma can result from acute damage to these regions of the forebrain, but particularly so from lesions involving the midbrain RAS and especially the thalamus. Almost all of the diffuse inflammatory, metabolic, nutritional, toxic, traumatic, and vascular CNS diseases can ultimately result in coma prior to death.

      Mentally obtunded animals do not respond appropriately to noxious