Inspire Student Journal Autumn 2023

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Case ReportVETERINARYResolution of diabetic neuropathy-associatedtetraparesis and Horner's syndrome in aLabrador Retriever: a case reportAdam MaherYear 3, Veterinary Science, University of BristolEmail: js21234@bristol.ac.ukAbstractThis case report describes a 10-year-old neutered female Labradorwith concurrent symptoms of weakness, ptosis, miosis, nictitatingmembrane prolapse, enophthalmos and diabetes mellitus. Insulintherapy initially improved the symptoms but failed to controlhyperglycaemia. The dog was subsequently diagnosed withtetraparesis and Horner's syndrome due to diabetic neuropathy.Adjustments to insulin treatment improved glycaemic control butdid not alleviate the neurological conditions. Gradual improvementwas observed over three weeks, leading to complete resolution afterfive months. The neuropathic process involves glycation, oxidativestress and neural lesions.Phenylephrine denervation hypersensitivity testing indicated apreganglionic lesion in the ocular sympathetic pathway. This casehighlights the first diagnosis of diabetic neuropathy-related bilateralHorner's syndrome in a canine, expanding our understanding ofclinical manifestations in diabetic neuropathy.KeywordsDiabetic neuropathy; Tetraparesis; Horner's syndrome; LabradorRetriever; Canine diabetes mellitus; Glycation; Insulin therapy; Neurallesions; Ocular sympathetic pathway; Case report.AbbreviationsBHS- bilateral Horner's syndromeCDM - canine diabetes mellitusOSP - ocular sympathetic pathwayClinical condition and description of clinicalpresentation 1A 10-year-old neutered female Labrador presented with generalweakness, bilateral ptosis (drooping eyelids), miosis (pupilconstriction), nictitating membrane prolapse, and enophthalmos(sunken eyes), in addition to concomitant symptoms of caninediabetes mellitus (CDM). A urinalysis confirmed CDM and daily insulintherapy commenced. Although the concomitant symptoms partiallyimproved after eight days, uncontrolled hyperglycaemia persisted.The dog was diagnosed with lower motor neuron tetraparesis(weakness of all limbs) and bilateral Horner's syndrome (BHS), bothattributed to the same diabetic neuropathy. The patient's glycaemiccontrol improved after adjusting the insulin treatment to twice daily.However, there was no improvement in tetraparesis or BHS. Afterthree weeks, there was a partial improvement in the neuropathy andcomplete resolution of tetraparesis, and BHS resolved at five months.The tetraparesis and BHS were caused by neural lesions, indicating aneuropathic process of glycation and oxidation stress. 2Glycation is a process where blood glucose binds to proteins, lipids,or nucleic acids, occurring without enzymes. In CDM, glycationis triggered by hyperglycaemia resulting from reduced insulindependency. 3 Excess glucose affects nerve tissue, impairing nervecell function and structure. 4 Over time, this process forms advancedglycation end products, accumulating systemically and causing BHSautonomic neuropathy. 5Phenylephrine was used topically for denervation hypersensitivitytesting, causing significant pupillary dilation after 30 minutes. Thisindicates a preganglionic location for the BHS-causing lesion toInspire Student Health Sciences Research Journal | Autumn 202336
the ocular sympathetic pathway. 6 BHS is a well-recognised diabeticneuropathy in humans. 7 Although commonly diagnosed in canines 8 ,this case marks the first published diagnosis of canine BHS as aclinical diabetic neuropathy.Unlike humans, dogs lack anamnesis – the ability to describesymptoms verbally. Therefore, diagnosis relies on the observationof appearance or behaviour changes. Since dogs cannot verballyconvey discomfort during physical examination, observing theirposture and response to specific stimuli is crucial. 9 Moreover, testing,such as imaging or invasive procedures, may be less practical andfeasible for dogs than humans.Relevant anatomy and physiologySympathetic nervous systemThe sympathetic nervous system in all mammals is responsible forthe "fight or flight" response, mobilising the body's energy andresources in response to a threat. 10 The ocular sympathetic pathway(OSP) originates from the hypothalamus, descends through thebrainstem, and emerges from the spinal cord at thoracic vertebrae T1-T3, synapsing at the cranial cervical ganglion. 11 The neurotransmitteracetylcholine is released by the fine terminal branches of the axon,binding to nicotinic cholinergic receptors at the postganglionic cellbody. 12 From the cavernous sinus, post-ganglionic fibres run parallelto the ophthalmic division of the trigeminal nerve before synapsingat smooth muscle targets. 6 A lesion anywhere along the OSP cancause BHS. 13 In the case discussed, the lesion was localised to thepreganglionic region. Such a localisation enables the potential fordisruption of the sympathetic nervous system further along thepathway.Canine diabetes mellitus may cause secondarybilateral Horner’s syndrome in dogs and humansDamage to the OSP by such underlying conditions as tumours,traumas, infections and neurological disorders can lead to symptomsof BHS. CDM can potentially result in diabetic neuropathy from nervefibre degeneration and blood supply disruption to specific nervestructures such as the OSP. 15 Interruption of blood flow reducesnerve function, namely mitochondrial stress, leading to increaseddysfunction. 16 Such damage in this neurological context is termeda lesion. This disruption interferes with the normal eye-relatedfunctioning of these nerves and may present as BHS. 17 Consequently,BHS could be a secondary consequence of diabetic neuropathy. 14Importantly, CDM is not the primary causal factor behind BHS.Additionally, CDM showcases a spectrum of effects and uniquelyimpacts individuals. When diagnosing BHS as an indirect result ofCDM, meticulous consideration of these two aspects is imperative. 18BHS presents similarly in humans and dogs, encompassing threeclassic signs: miosis, ptosis and enophthalmos. 19 However, the fourthsign, anhydrosis (reduced sweating), can be challenging to identify indogs. 11 Diagnosis in dogs necessitates special consideration due todifferences in communication and examination techniques.Autonomic neuropathic lesionsProlonged uncontrolled CDM can damage neurons by glycation,a process whereby the accumulation of glucose end-productmolecules leads to oxidative stress, inflammation and nervedamage. 20 Lesions can then form on nerves, disrupting function andcausing diabetic neuropathy symptoms 2 , including those observedin the above BHS case. Approximately fifteen post-ganglionic axonsexit the cranial cervical ganglion for each preganglionic axon thatenters, supplying the sympathetic nerve structures of the head andneck 21 , demonstrating how a lesion located on a preganglionic nerveof the OSP produces the varied symptoms in the above BHS case.Innervation of the eyelids and nictitatingmembranePtosis and nictitating membrane prolapse occur in this case due tothe lesion interrupting sympathetic innervation of smooth muscleassociated with their respective functions. The drooping eyelid isa result of the inability of the superior tarsal muscle to contractappropriately 6 , thereby narrowing the palpebral fissures. 22 Similarly,the smooth muscle usually responsible for holding the nictitatingmembrane in place becomes impaired, leading to prolapse. 23 Thepatient’s apparent enophthalmos results from ptosis and nictitatingmembrane prolapse. 9 True enophthalmos is caused by a loss ofvolume in the orbit or function of extraocular muscles, unaffected byimpaired sympathetic tone in this case. 24Innervation of the iris dilator muscleThe iris dilator smooth muscle plays a crucial role in regulating theamount of light that enters the eye. It is innervated by sympatheticnerves, which contract myoepithelial cells to temporarily dilatethe pupil during the "fight or flight" response. However, due to theinterruption of the sympathetic pathway via lesion damage, the irismuscle remains relaxed, and the parasympathetic tone is unopposedin activating the iris sphincter smooth muscle. 6 A lesion located onthe preganglionic OSP would interrupt the innervation of the irisdilator muscle, which presents as miosis in this case.Conclusion and treatmentAchieving control of the dog's glycaemic levels resolved the BHSsymptoms. Maintaining glycaemic levels helps alleviate diabeticneuropathy symptoms by enhancing blood flow to vessels thatsupply the OSP, promoting nerve health and function. While acomplete reversal of nerve damage may not be possible, a stableglycaemic environment can be conducive to nerve regeneration andrepair. Continued control of glycaemic levels assists in minimisingOSP dysfunction and supporting healthy mitochondrial function. 16Copyright This work is licensed under the Creative CommonsAttribution-NonCommercial-NoDerivatives 4.0 International License.To view a copy of the license, visit https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode. The copyright of all articles belongsto the author(s), and a citation should be made when any article isquoted, used or referred to in another work. All articles included inthe INSPIRE Student Health Sciences Research Journal are writtenand reviewed by students, and the Editorial Board is composed ofstudents. Thus, this journal has been created for educational purposesand all content is available for reuse by the authors in other formats,including peer-reviewed journals.References1.2.3.4.5.6.7.8.9.Holland CT. Bilateral Horner's syndrome in a dog with diabetes mellitus. TheVeterinary Record. 2007 May 12;160(19):662. Accessed: 6 September 2023Walker D, Siddique I, Anderson H, Gardiner TA, Archer DB, Boulton AJ, MalikRA. Nerve pathology in the type 1 diabetic dog: effects of treatment withsulindac. Journal of the Peripheral Nervous System. 2001 Dec;6(4):219-26.Sugimoto K, Yasujima M, Yagihashi S. Role of advanced glycation endproducts in diabetic neuropathy. Current pharmaceutical design. 2008 Apr1;14(10):953-61.Singh VP, Bali A, Singh N, Jaggi AS. Advanced glycation end products anddiabetic complications. The Korean journal of physiology & pharmacology:official journal of the Korean Physiological Society and the Korean Societyof Pharmacology. 2014 Feb;18(1):1.Ognenovski V, Buras ED. Musculoskeletal disorders associated with diabetes.InDiabetes Mellitus 2020 Jan 1 (pp. 225-248). Academic Press.Zwueste DM, Grahn BH. A review of Horner’s syndrome in small animals.The Canadian Veterinary Journal. 2019 Jan;60(1):81.Smith SA, Smith SE. Bilateral Horner’s syndrome: detection and occurrence.Journal of Neurology, Neurosurgery & Psychiatry. 1999 Jan 1;66(1):48-51.Misselbrook NG. Peripheral neuropathy in diabetic bitch. The Veterinaryrecord. 1987 Sep 19;121(12):287.Van den Broek AH. Horner's syndrome in cats and dogs: a review. Journal ofSmall Animal Practice. 1987 Oct;28(10):929-40.Inspire Student Health Sciences Research Journal | Autumn 202337
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