Equine Nervous System Examination (Neuro 1) PDF
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Laura Waitt
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This document provides an overview of equine nervous system examination, focusing on objectives, information gathering, assessment of posture, and cranial nerves. It covers the neuroanatomy of horses, emphasizing the importance of assessing behavior, mentation, and posture in relation to abnormalities of gait.
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Equine nervous system: the examination (Neuro 1) Laura Waitt, DVM, DACVIM 1662 Objectives Students will demonstrate competence in performing a neurological examination on horses. With a focus on localization, personnel safety, and biosecurity Including spinal ataxia and grading schem...
Equine nervous system: the examination (Neuro 1) Laura Waitt, DVM, DACVIM 1662 Objectives Students will demonstrate competence in performing a neurological examination on horses. With a focus on localization, personnel safety, and biosecurity Including spinal ataxia and grading scheme Including cranial nerves Students will have knowledge of the pathophysiology and diagnosis of Horner’s syndrome When to perform a neurological examination Is neurological disease present? If so, where is the process localized in the nervous system? “Snapshot” of the disease vs. exams repeated over time to aid in determination of disease progression and prognosis. Limitations Subjective Subtle changes in personality or mentation may be impossible to detect Listen to your owner Range of normal Age and breed Sedatives effect results Alpha 2 agonist Information to gather Chief complaint Ie: Seizures, weakness, won’t hold up leg for farrier, cross canters behind, unexplained wounds, clumsiness Signalment Species, breed, age History Define the clinical course Treatments or diagnostics done up until this point Physical examination Systemic diseases can cause neurologic diseases Assessment of mentation and behavior Watch the animal while you are getting a history, or a video from the owner Fear, anxiety, aggression unconscious Dullness, obtundation, stupor Clinical neuroanatomy Mental awareness is a function of the higher centers in the brain Dullness < lethargy < obtundation < stupor < coma Cerebral cortex Sensory information reaches the consciousness in the cortex Voluntary movements initiated here Ascending reticular activating system (ARAS) Located throughout the medulla, midbrain and thalamus Thalamus is the most common location of progressive stupor Sensory information from the body travels via the ARAS (and other pathways) to the cortex Assessment of posture Observe the position of the head and limbs in space Heat tilt: look for strabismus and nystagmus, blindfold key Nearly always vestibular disease 1dentit as Towards the lesion in peripheral disease, and nearly all central disease cerebellum/midbrain exceptions Nystagmus “runs away from the disease” Fast phase away, slow phase towards same me Head turn Cerebral and thalamic disease It Towards the side of the lesion Assessment of posture back ofthe arching Schiff-Sherrington syndrome: forelimb extensor rigidity without opisthotonus Thoracolumbar spinal cord disease commonwithcaraccidents Opisthotonus: head and neck are in extreme extension Midbrain disease: decerebrate rigidity- all four limbs have extensor rigidity Cerebellar disease: Decerebellate rigidity- just forelimbs have extensor rigidity, intention tremors Spinal ataxia- base wide stance, knuckling, sway, dog-tracking Localize the lesion Mentation change- cerebral Intention tremors- cerebellar Ataxia with no mental change – spine Hind limbs alone – thoracolumbar/sacral spine H Front limbs and hind limbs (up to a grade worse) – cervical spine Front limbs worse than hind limbs – thoracic intumescence No limb reflexes are possible Hard to distinguish upper from lower motor neuron disease Cranial nerves 12 pairs of nerves innervate structures of the head Innervates structure on same side of head (ipsilateral) Central control of these nerve comes from the opposite cerebral cortex (contralateral) All originate from the brainstem except CN I and II Brainstem includes midbrain, pons, and medulla Review from your 1604 lecture or read Hahn paper. Numerical order Groupings by function Localizing lesions in the visual pathway Optic nerve lesions or primary eye issue (both vision and PLR abnormal) Cortical lesions (vision is affected but PLR is normal) *CAN BE BLIND WITH NORMAL PLR* Efferent arms lesions (vision is normal but PLR is abnormal) Sympathetic innervation to the eye: Responsible for dilation of the pupil, retraction of the third eyelid, retraction of the upper eyelid and rostral protrusion of the globe. Horner’s syndrome is caused by disruption of sympathetic innervation to the globe/periorbital area Clinical signs Ptosis (droopy lid)-this is most consistent Miosis (pupil constriction) Enophthalmos (globe withdrawn) Protrusion of the 3rd eyelid Sweating of the ipsilateral face and cranial aspect of the neck may be observed Horner’s syndrome Guttural pouch and cranial cervical ganglion lesions will result in sweating of the face and cranial neck (C2). Lesions involving the sympathetic trunk in the neck can causes sweating of the face and neck (C3-4). Lesions in the thoracic inlet can result in seating down to the shoulder (T1). Anisocoria: which side is normal? With no primary ocular lesion Darkened room for several minutes then expose to a dim light If both pupils dilate to equal size, then sympathetic innervation is normal The pupil that was initially more dilated is abnormal due to a CN III lesion If pupils do not dilate equally then sympathetic innervation is abnormal The eye with a smaller pupil (miosis) is abnormal, caused by Horner’s syndrome Dimlightdilationtesting on function Reflexes Many spinal reflexes can only be performed in recumbent animals (ie: Patellar reflex) Which means we often cannot tell if upper or lower motor neuron Hyper reflexive tends to be upper motor neuron Hypo reflexive tends to by lower motor neuron Panniculus or Cutaneous trunci reflex – “fly twitch” This will be absent if there is a lesion anywhere cranial to test Cervicofacial reflex Local spinal cord or facial nerve deficit Lordosis/Kyphosis response Braced indicates musculoskeletal pain Loss of balance and trouble extending after drop Perianal reflex and anal tone Pump the tail to evaluate muscular strength When the perianal area is touched/pinched the anus contracts ie: taking a temperature A deficit here indicates cauda equine or sacral disease Neck stretching This is a subjective evaluation of flexibility, stiffness, and/or pain of the neck. Abnormalities of gait Spinal ataxia Looks more normal the faster they travel Hypermetria: excessive lifting of a limb, upper motor neuron Breed standards can affect interpretation if symmetrical friesians Quarterhorses Normal Hypometria: weakness and dragging, lower motor neuron Intention tremor: most easily noted when feeding a horse Tends to be cerebellar disease Spinal ataxia Grade 0 Normal Grade 1 Extremely mildly affected, performance limiting, a professional has to perform multiple tests to determine evidence of dysfunction Grade 2 Mildly affected, easily appreciable to a professional, performance limiting Grade 3 Obvious to a layperson, abnormalities notable at rest Grade 4 Severely ataxic and could fall during the examination Dangerous to be around, advise personnel and clients appropriately Grade 5 Recumbent and unable to stand Dangerous to be around, advise personnel and clients appropriately Can only be managed appropriately at a referral facility Walking in a straight line Observe for cadence/consistency Observe for foot placement/consistency Observe for path of limb flight/consistency Walking in circles Wide circles, tight circles, and serpentines then stopping suddenly to observe for a return to a normal stance Looking for: pivoting, circumduction, low or high foot flight, toe dragging Trotting in a straight line Observe for cadence/consistency Observe for foot placement/consistency Observe for path of limb flight/consistency Cantering in a circle Normal is a cadenced 3 beat gait Neurologic horses may “bunny hop” behind or “cross canter” Note* that the faster horses go, the more normal they may appear The racetrack is a perfect example Tail pull Stand horse square Pull tail which initiates an extensor reflex A poor response suggests a lower motor lesion at L3-5. This is a subjective measure of strength While horse is walking Only pull when closest hind foot is on the ground Pull 3 times separated by a few strides Assess strength, learning, and recovery Don’t get kicked. Walking with head elevated This removes visual compensation Normal horses will just keep walking Abnormal horses will start cat walking or try to look Placements: We don’t really do it anymore Tests conscious proprioception, theoretically. Placing Hopping We don’t do hemi walking or wheel barrowing in horses You are welcome to try this, but I don’t suggest it. Obstacles- hills or curbs Measures their functional proprioception Some horses are clumsy, this is not considered as useful anymore. How we think we look… Actual footage…. Autonomous zone on This is important for horses with a single paretic limb. Radial nerve doesn’t have a consistent zone. Ei Questions? [email protected]