Neurologic disorders are often dreaded by field practitioners, in part due to unfamiliarity with the neurologic exam and difficulty obtaining CSF for diagnostic analysis. Here we will discuss clinical approaches to neurologic horses with a focus on the neurologic exam and CSF collection.

The Neurologic Examination

A competent neurologic examination can be compared to evaluation of lameness—a systematic approach involving an initial passive examination followed by the assessment of the gait. The only equipment needed is a transilluminator (or smartphone flashlight) and hemostat. The neuro exam is used to localize a lesion or lesions, and serves as the basis for formulation of a differential list and diagnostic plan. In this discussion, all potential abnormal findings are interpreted in the context of a neurologic explanation; however, in a clinical setting, full general physical and lameness examinations should also be performed to assess possible involvement of other body systems.

Cranial nerves

Mayhew’s grading scale for ataxia

Mentation and Behavior

Assess level of consciousness or alertness on a continuous scale from normal (i.e., bright and alert) to comatose. Progressive levels of obtundation are termed lethargy, stupor, semi-coma, and coma. Abnormalities of behavior are termed dementia. Behavior is assessed from history and general observation in the course of the examination. Typical abnormal behaviors resulting from CNS disease include self-mutilation, head-pressing, compulsive walking (often in a circle), yawning, aggression (including unprovoked biting or kicking), timidity, loss of affinity of a foal for its dam, and loss of learned behaviors and skills.

Examination of the Head

Head Orientation

Evaluate the orientation of the head from directly in front. Asymmetric disease of the vestibular system (CN VIII, brainstem), causes the head to tilt, whereas asymmetric cerebral disease may cause the head and neck to turn without tilting. Carefully blindfold the horse and observe the effect on head position. Blindfolding removes visual input to head position and exacerbates abnormalities caused by either vestibular or cerebral disease. Because of the close proximity of cranial nerves VII and VIII, facial paralysis is often seen in horses with vestibular disease. Offer feed or a treat to the horse and observe the way in which the horse moves its head in response. Coarse or fine head bobbing, especially intentional, indicates diffuse cerebellar dysfunction.

Facial Expression, Sensation, and Muscle Symmetry

Examine the head carefully for symmetry of facial expression, particularly with respect to the ears, eyes, and muzzle. With unilateral facial paralysis (CN VII), there is drooping of the ear, and lower lip and immobility, narrowing, and lengthening of the affected external nare. The muzzle is deviated away from the affected side and saliva may drool from the mouth. In some horses, there also is mild ptosis.

Evaluate sensory branches of the trigeminal nerve (CN V) and facial nerve motor function by testing “flick” reflexes on each side of the face. Each of these reflexes requires intact trigeminal sensory branches, central connections in the hindbrain, as well as functioning facial nerves. To test these reflexes, touch in turn the commissure of the lips, the medial and lateral canthi of the eye, the supraorbital fossa, and the ear. Appropriate responses are retraction of the commissure of the lip, blinking of the eye (medial and lateral canthi and supraorbital fossa), and flick of the ear, respectively. It is helpful to have the handler cover the ipsilateral eye during testing of the lip and ear. Further assess the sensory branches of the trigeminal nerve (CN V) by firmly poking the nasal septum. The normal response to this noxious stimulus is vigorous movement of the head away from the side of the stimulus. Compare the intensity of responses on each side. Trigeminal nerve dysfunction results in ipsilateral deficits in both motor and/or sensation, while horses with unilateral forebrain disease may lose sensation to the contralateral side of the face.

Menace Response

Stand in front of the horse, hold the halter noseband with one hand, and use the palm of the other hand to make a threatening gesture toward the eye. Test from both temporal and nasal directions on each side. Stimulate the horse just before each menace gesture by tapping the skin below the eye. A normal menace response is blinking of the eye.

The menace response can be interrupted anywhere in its pathway from the eye via the optic nerve (CN II) to the contralateral optic tract, diencephalon, internal capsule and visual cortex. From the visual cortex, the menace response pathway continues to the facial nucleus and nerve (CN VII) on the side being tested probably after passage through the ipsilateral cerebellum. Normal neonates and horses with cerebellar cortical disease may lack menace responses despite having normal vision. In these settings, vigorous threatening gestures toward the eye may cause evasive movements of the head without blinking of the eye.

Pupil Size and Pupillary Light Reflex

First examine the eyes in neutral light conditions and determine whether or not the pupils are of equal size and if the diameter of each pupil is appropriate for the conditions. Unequal pupillary size is termed anisocoria, a constricted pupil is miotic, and a dilated pupil is mydriatic. Next, examine the eyes in subdued or dim light so that the pupils are large enough to easily allow appreciation of reflex constriction. Aim the light at the skin below one eye. Redirect the beam directly into the eye. This strong light should elicit both a dazzle reflex in the ipsilateral eye and pupillary light reflexes (PLR) in both eyes. The dazzle response is an avoidance reaction to bright light. There is blinking, retraction of the eyeball, and movement of the head away from the light. A normal pupillary light reflex is immediate equal constriction of the pupils of both eyes in response to light directed into one eye. If the direct (i.e., ipsilateral) pupillary light reflexes are normal on both sides, no further testing is necessary. If one is abnormal, then consensual (indirect) reflexes should be tested. To perform the consensual reflex, watch the pupil in one eye while an assistant shines the light into the opposite eye.

Position and Movement of the Eyeballs

While continuing to stand in front of the horse, observe the position and size of the pupils while the head is held level (i.e., a line through the center of each eyeball is parallel to the ground). While keeping the head level, lift the chin slowly. The eyeballs should remain stationary while the chin moves upward; thus, the eyes rotate ventrally relative to the long axis of the head. In horses with vestibular disease (CN VIII), abnormal eye positions are exaggerated by this maneuver.

In horses with strabismus the eyeball may be rotated medially or laterally, clockwise or counterclockwise. If the pupils are in abnormal positions, try to position the head in such a way (usually by rotation) that the pupils are normally oriented relative to the transverse axis of the head. For example, a horse with vestibular disease usually has ventral deviation of the eyeball on the side of the lesion and dorsal deviation on the opposite side. In horses with vestibular strabismus, eye position can be normalized relative to the axis of the head simply by rotating the head in the direction of the ventrally deviated eye. True strabismus is eye deviation that can’t be corrected by repositioning the head and usually reflects dysfunction of nerves to the extraocular muscles (i.e., oculomotor, trochlear, or abducens nerves [CNs III, IV, VI]).

Move the horse’s head in a horizontal arc from side to side and observe the movements of the eyeballs. Signs of physiologic nystagmus should normally be elicited—namely, a series of horizontal movements of the eyeballs consisting of a rapid phase in the direction of head movement followed by a slow phase in the opposite direction. Each fast phase is accompanied by an eyelid blink. Physiologic nystagmus is normal and should be distinguished from eye movements characteristic of vestibular disease: spontaneous nystagmus, which occurs when the head is stationary and in a neutral position, and positional nystagmus, which only occurs when the head is moved to certain positions. In horses with asymmetric vestibular disease, physiologic nystagmus often is abnormal or absent when the head is moved toward the side of the lesion. With peripheral vestibular disease, there often is spontaneous horizontal or arc-shaped nystagmus with the fast phase directed away from the side of the lesion. In horses with involvement of the central components of the vestibular system, there may be horizontal or vertical nystagmus.

Assess abducens nerve (CN VI) function by performing a modified corneal reflex. Hold the eyelids closed and, through the eyelid, push the eyeball medially. The normal response to this maneuver is retraction of the eyeball. This reflex requires intact sensory branches of the trigeminal nerve (CN V), central connections in the hindbrain, and motor fibers of the abducens nerve (CN VI).

Swallowing

It is difficult to assess competence for swallowing during a physical examination. On the basis of history and observation, note whether feed, water, or saliva return through the nose, especially when the horse eats or drinks. Dysphagic horses often cough when eating or drinking, and may be initially misdiagnosed as chokes. Pass a nasogastric tube into the pharynx and assess effectiveness of swallowing movements as the horse attempts to move the tube into the esophagus. Involvement of the nucleus ambiguous in the hindbrain, or peripheral parts of the glossopharyngeal (CN IX) and/or vagus (CN X) nerves can cause dysphagia. These nerves are particularly vulnerable to damage as they pass in folds of the guttural pouches.

Tongue

Pull the jaws slightly apart and observe the movements of the unrestrained tongue. With acute unilateral weakness, the tongue curls toward the unaffected side. Grasp the tongue from one side after inserting the hand through the interdental space. Note resistance of the tongue to being stretched and look for atrophy and muscular fasciculations (CN XII). Gently pinch the side of the tongue with a hemostat and look for reflex retraction (CN V). Pull the tongue out one side of the mouth, release it, and look for retraction of the tongue back into the mouth. In normal horses, one or two chewing movements occur as the tongue is quickly retracted. Delayed or absent retraction of the tongue back into the mouth can occur with hypoglossal nerve (CN XII) dysfunction, neuromuscular weakness (especially botulism), or obtundation from cerebral disease.

General Examination of the Neck, Trunk, and Limbs

Examination

With the horse standing squarely, assess muscle mass, paying particular attention to asymmetries. Note any circumscribed or asymmetric areas of sweating. Firmly press the cranial edge of each of the cervical transverse processes from C3 to C6 on each side to test for a pain response. Put pressure on the C6-C7 intervertebral joints by pushing medial to the deep pectoral muscle in front of the shoulder on each side. Test lateral neck flexion by enticing the horse to move its head toward feed held at the point of the elbow, and then the point of the hip. Neck pain revealed by palpation or reluctance to turn laterally may follow any neck trauma but usually reflects arthritis of intervertebral joints. Press down firmly on each section of the thoracic and lumbar epaxial muscles to evaluate for back pain.

Severe or rapidly developing muscle atrophy indicates denervation and is a localizing sign. Neurogenic muscle atrophy is caused by damage to the lower motor neuron in the ventral column of the gray matter, nerve roots, or peripheral nerves supplying that muscle. Neurogenic atrophy of thoracic limb musculature results from lesions of the C6-T2 spinal cord segments or roots, brachial plexus, or peripheral nerves, while atrophy of pelvic limb muscles reflects involvement of L3-S2. Anesthesia of a strip of skin is caused by loss of the segmental sensory nerve, dorsal nerve root, or connections in the spinal cord. Because sympathetic fibers are distributed with spinal nerves, spontaneous sweating may occur over denervated skin.

Cervicofacial Reflex

Place the left index and middle fingers at the commissure of the left lip, then strike the skin over the brachiocephalic us muscle with the closed tip of the hemostat. Begin at the cranial end of the neck and continue back to the shoulder. The expected response is facial contraction, detected as retraction of the commissure of the lip, and contraction of the brachiocephalic us and cutaneous colli, observed as shrugging of the shoulder, lateral jerking of the head, and twitching of the skin of the neck. This reflex typically is reduced at the level of a cervical spinal cord lesion, but is normal cranial and caudal to the lesion.

Slap (Thoracolaryngeal) Test

While standing on the left side, reach under the horse’s neck and hook the index and middle fingers of the left hand over the highest palpable point of the larynx—the muscular process of the arytenoid. Have the handler move the head slightly to the left of midline, then gently strike the horse behind the withers several times with the palm of the right hand. The expected response is slight palpable movement (adduction) of the arytenoid in response to each slap. Repeat the procedure from the right side.

Sensory input to this reflex is the sensory nerves and roots under the area that is slapped (approximately T7-T11). Central pathways are thought to cross to the other side at this level, pass rostrally to the nucleus ambiguus in the white matter of the spinal cord, then efferent fibers pass out in the vagus nerve via the recurrent laryngeal nerve to innervate the contralateral laryngeal adductor muscles. Severe cervical spinal cord disease often affects this test bilaterally, and the vagus and recurrent laryngeal nerves may be affected at the guttural pouch or within the jugular groove.

Cutaneous Trunci Reflex (Panniculus)

To elicit the panniculus reflex, use the thumb to firmly prod the lateral thoracic wall, beginning cranially just behind the shoulder and extending caudally to the last intercostal space. Check every intercostal space both ventrally and dorsally. For safety, firmly grasp the back of the mane with the left hand and face backwards when testing the reflex, because horses that resent this test will try to kick the examiner. Repeat on both sides of the horse. A normal response is twitching of the skin, with or without indication of conscious perception of the stimulus.

The reflex pathway is input from sensory thoracic nerves to the ipsilateral spinal cord, where it courses rostrally via interneurons to end in the C8 and T1 segments, and thence via the brachial plexus to the lateral thoracic nerve and the cutaneous trunci muscle. Interruption of this pathway in the spinal cord white matter results in loss of the reflex from approximately the point of the lesion caudally. A lesion of the sensory nerve will only affect the reflex within the same dermatome (skin strip) while loss of lateral thoracic nerve function ablates the entire ipsilateral reflex. Horses with botulism may display a generalized loss of panniculus reflex bilaterally.

Back Reflexes

Make sure that the pelvic limbs are positioned equally and squarely, then stroke the closed tip of the hemostat caudally along the skin over the longissimus dorsi muscle, from mid-thorax caudally to the level of the tuber coxae. For safety, hold the back part of the mane with the other hand. The expected response is brisk extension of the back and pelvis without disengagement of the stay apparatus of the pelvic limb followed quickly by return to normal posture. Next, stroke the hemostat caudally along the skin over the gluteal muscles. This should elicit spinal flexion, followed by relaxation of the lumbar spine and pelvis, again without release of the patella from the medial femoral trochlear ridge. Common abnormal reactions to these tests include (1) partial collapse in the pelvic limbs, (2) wobbling of the pelvis from side to side, and (3) no response; all of which may be observed in horses with truncal and pelvic limb weakness and/or ataxia caused by spinal cord disease.

Tail and Anus

Assess tail strength by lifting (extending) the tail. Prod or pinch the skin adjacent to the anus and observe the anal contraction and tail-clamp reflexes.

If these reflexes are abnormal or if the history suggests possible cauda equina syndrome, perform a rectal examination to assess rectal tone and bladder size and tone. Assess muscular symmetry of the tail and test cutaneous sensation over the tail and caudal structures.

Anesthesia and areflexia of the tail, penis, and perineum and paralysis of the anus, rectum, bladder, and penis are signs of cauda equina syndrome. Lesions of the spinal cord or nerve roots caudal to the S2 spinal cord segment cause some to all of the signs of cauda equina syndrome.

Gait Evaluation

Examination

Have the handler walk the horse in straight lines while keeping the horse’s head and neck as straight as possible during walking. Follow directly behind the horse. From this vantage point evaluate leg position and stride symmetry. Also, watch for excessive (1) side to side (wobbling) movement of the pelvis, (2) up-and-down movement of the tuber coxae (pelvic roll), and (3) side-to-side rotation of an imaginary line from the tailhead to the tuber sacrale (pelvic yaw). Next, watch the gait from the side while walking in stride with the pelvic and then thoracic limbs. Note any toe-dragging, knuckling, stride-length asymmetries, and abnormal protractive movements such as hyperflexion, stiffness (hypometria), or excessive range of movement (hypermetria). Often, these signs are most obvious as the horse transitions from standing still to walking. Repeat this part of the examination with the horse’s chin lifted and with the horse walking up and down a modest slope. These maneuvers exacerbate most gait abnormalities, especially stiffness of the thoracic limbs. Take extreme caution when walking ataxic horses up and down slopes, as they are more likely to stumble or fall on uneven ground.

Back the horse briskly, observing for limb coordination and willingness to move backward. Normal horses should readily back in a straight line in 2-beat fashion, with diagonal limb-pairs moving in synchrony (e.g., left thoracic and right pelvic limbs). A horse with spinal cord disease may sag backwards before moving and slide its hooves along the ground rather than picking them up and placing them.

Take the horse in hand for the next part of the examination. Hold the lead rope with the left hand and, by walking backwards, lead the horse in counterclockwise circles. It is very important that the horse is always walking forward in these circles. Vary the diameter, making the circles alternately small and large. Observe carefully the motion of the right (outside) pelvic limb by looking under the horse’s torso. This limb will often arc out widely on the outside of the circle (i.e., circumduction) in horses with spinal cord disease. In mirror-image fashion, lead the horse from the right side in clockwise circles.

Next, pull the horse sideways in tight circles in either direction. To do this, position yourself slightly behind the shoulder and walk backward while pulling the lead rope caudally and downward. The goal is to ask the horse to pivot around its center of gravity, with the forelimbs coming toward you and the hind limbs moving away. If done correctly in normal horses, the opposite thoracic limb should cross in front of the supporting limb and the pelvic limbs should move reciprocally causing the horse to pivot around a point midway between the thoracic and pelvic limbs. Horses that are weak and ataxic tend to sag backwards in the hindquarters before they start to move, then pivot the front part of the body around one or both pelvic limbs. There is often also interference between or otherwise inappropriate placement of thoracic limbs. Horses with caudal neck pain will often display reluctance or refusal to cross one forelimb over the other.

Signs of limb weakness and ataxia suggest spinal cord (or, rarely, peripheral nerve) damage at or cranial to the affected limb. If there is obvious ataxia and weakness in thoracic and pelvic limbs, there likely is at least one lesion in the spinal cord somewhere between the front of the C1 and back of the T2 spinal cord segments. In cases where the signs are caused by external compression of the cervical spinal cord (e.g., CVSM), signs in the pelvic limbs are usually worse than those in the thoracic limbs. When, in such cases, the pelvic limb signs are mild, thoracic limbs may appear normal. In contrast, when thoracic limbs are normal but there is moderate or severe ataxia and weakness in the pelvic limbs, there likely is at least one lesion caudal to T2 and cranial to S3. If one or both thoracic limbs are abnormal in a horse that has normal pelvic-limb gait, the gray matter of the C6-T2 spinal cord segments (without white matter involvement), the roots or nerves of the brachial plexus, or the peripheral nerves to the limbs are likely affected. Asymmetric lesions in the spinal cord cause signs that are more severe on the side of the lesion. Occasionally, there are signs of weakness without ataxia (e.g., botulism, equine motor neuron disease) or ataxia without weakness (e.g., cerebellar abiotrophy, peripheral vestibular disease, equine degenerative myelopathy). Additional signs such as defective reflexes (cervicofacial, slap, or cutaneous trunci), neurogenic muscle atrophy, or cutaneous anesthesia, often help to localize the spinal cord lesion.

Tail Pull

The tail-pull test is done both at rest and while the horse is walking in a straight line. With the horse standing squarely, take the tail and pull sideways with gradually increasing force. After initial slight movement in the direction of pull, normal horses usually cannot be moved sideways, even with strong pressure. Next, pull sideways on the tail while the horse is walking in a straight line. Normal horses of 450-kg bodyweight can only be moved slightly to the side. Perform the test in mirror-image fashion from the right side (i.e., with the horse being led from the right side).

If a full-sized adult horse can easily be pulled sideways at rest, there is likely a lesion located either in the ventral gray matter or roots (L3-L5) that form the femoral nerve or in the femoral nerve itself. The much more common finding is lack of resistance to tail-pull only during walking, and is often observed with ipsilateral spinal cord lesions affecting descending upper motor neurons anywhere from C1 to S2.

Hopping

The hopping test evaluates both proprioceptive function (spinocerebellar tracts, cerebellum) and limb strength. From the left side, hold the halter with the left hand. Pick up the left leg then push the head toward the right side while leaning against the left shoulder. Normal horses use the right limb to hop briskly around a circle centered on the pelvic limbs. With limb weakness, the response may be delayed so that the horse leans markedly before hopping or the limb may buckle after landing.

Cerebrospinal Fluid Collection (CSF)

Lumbosacral (LS Tap)

Collection of CSF from the lumbosacral (L6-S1) space is performed in the standing, sedated horse and yields 10–20 cc of CSF. Restraint in stocks is recommended, as some horses react to the spinal needle puncturing the dura. Due to the cranial-to-caudal flow pattern of CSF, lumbosacral collection may be diagnostically advantageous for conditions affecting the spinal cord.

Procedure

The horse is placed in stocks and sedated with detomidine and butorphanol (moderate to heavy sedation is required). A 6-inch square area is clipped on the dorsal midline between the last lumbar and first sacral vertebrae. The LS space can be palpated in thin horses as a depression just caudal to the last lumbar vertebra. Alternatively, the space can be located by drawing an imaginary line between the caudal border of the tuber coxae and the dorsal midline. The LS space is where the line crosses midline. The clipped area is sterilely prepped and a nose twitch applied. The site is blocked with 1–2 ml of 2% lidocaine followed by a stab incision through the skin using a #15 scalpel blade. An 18–20 gauge 15–20 cm spinal needle is inserted through the skin and carefully advanced. The needle is advanced through the dura mater, often denoted by a ‘popping’ sensation, and the stylet removed. A 6 cc or 10 cc syringe is attached and CSF is collected with slow, gentle suction. A depth of 12–14 cm is frequently required. If no CSF is obtained, replace the stylet and advance the needle a few millimeters at a time, checking by removing the stylet and aspirating often. If multiple syringes are obtained, latter samples often contain the least amount of contamination. Following sample collection, the needle is removed with syringe attached.

Note: It is essential that the needle is placed on midline and remains perpendicular to the spinal column. It is often helpful to have an assistant stand behind the horse (at a safe distance) and confirm that the needle remains straight throughout the procedure. If bone is felt at the end of the needle, or blood is obtained, the needle is likely not directly on midline or not straight. In this case, retract the spinal needle nearly all the way out and redirect.

Arrow pointing to location for lumbosacral CSF collection in the standing horse. The ‘X’ denotes the point of the tuber coxae

Standing Atlantoaxial (C1-C2 Tap)

Collection of CSF from the atlantoaxial (C1-C2) space is performed with ultrasound guidance in the standing, sedated horse, and yields up to 10–20 cc of CSF. Due to the proximity of the needle to the spinal cord, this procedure requires the most precision of any of the techniques performed in this lab, and it is recommended to practice on cadavers prior to performing it in patients. An excellent description of this procedure is described by Pease et al. (see additional reading references below), and the reader is encouraged to review this manuscript for additional details

Procedure

The horse is placed in stocks and sedated with detomidine (moderate to heavy sedation is required). Butorphanol should be avoided, as it produces twitching movements in many horses. After the horse displays adequate levels of sedation, 30 mg of morphine is slowly administered intravenously.

Note: The use of morphine is critical, as it anesthetizes the dura and prevents the horse from reacting to the needle passing through the dura into the subarachnoid space.

A 6-inch square area is clipped on the proximal neck over the C1-C2 articulation, behind the ear and just lateral to the mane. This procedure may be performed on either side of the neck. The area is rough prepped and the subarachnoid space between C1 and C2 is located using a curvilinear or microconvex ultrasound probe. The area is then sterilely prepped and the ultrasound probe is placed within a sterile glove or probe cover. At this time, our practice applies a nose twitch to most horses to assist in control of the head and prevent movement. The horse’s head and neck should be held in a neutral, straight position.

Using ultrasound guidance, an 18 g, 3.5-inch spinal needle is introduced ventral to the ultrasound probe and guided horizontally to the dura mater. The needle is advanced through the dura mater and the stylet removed. A 10cc or 20cc syringe is attached and CSF is collected with slow, gentle suction. Following sample collection, the needle is removed with syringe attached.

Proper position of ultrasound probe and needle for C1-C2 tap

Ultrasound image corresponding to ultrasound probe position shown in figure on left

Note round spinal cord (SC) and axis (C2). The needle is introduced below the probe and courses toward the spinal cord, denoted by the arrow.

Atlanto-occipital (AO Tap)

This collection method is performed on an anesthetized horse positioned in lateral recumbency (xylazine-ketamine ± diazepam is commonly used). While this method is the least technical of the CSF collection options, clinicians must weigh the risk of anesthetizing and then recovering a neurologically impaired horse.

Procedure

The anesthetized horse is positioned in lateral recumbency and a 15 cm square rectangular area beginning just caudal to the forelock on the dorsal midline is clipped and sterilely prepped. The horse’s head is flexed to an angle of 90°.

The wing of the atlas is located, and an atlanto-occipital (AO) cisternal puncture is performed with an 18-gauge, 8.3-cm (3.5 in) needle inserted at the intersection of lines running along the front of the atlas and along the dorsal midline and directed toward the middle of the lower jaw. A popping sensation and the flow of CSF will confirm proper positioning. Connect an extension set to the needle and withdraw up to 50 ml of CSF.

Location of AO CSF collection from an anesthetized horse

CSF Sample Handling

Normal cerebrospinal fluid is clear and colorless. Samples for cytology should be placed into EDTA (purple top tube) and be accompanied by several air-dried, non-stained slide preps. Creating a ‘cytospin’ slide by first centrifuging the sample and using only the concentrated cell pellet can helpful for quantifying cell populations in low density samples.

Samples may be placed in routine culture media (Amies Transport Media) for bacterial culture. If available, blood culture media vials likely result in enhanced growth and pathogen yield. Aliquots may also be placed in red top tubes for specific serologic and/or antigen detection assays. All samples should be shipped chilled, with the exception of slides, which should be protected and maintained at room temp to prevent condensation and cellular artifact.

Normal CSF Cytologic Values

• Appearance: clear, colorless
• Total nucleated cells: 0–5/μL (should be all mononuclear cells)
• Total protein: 40–90 mg/dL

References

1.  Johnson, A. Nervous system: diagnostic and therapeutic procedures. In: Equine Emergencies, 4th edition. Divers, TJ; Orsini JA, eds. Elsevier. 2014;339–342.

2.  Pease A, Behan A, Bohart G. Ultrasound-guided cervical centesis to obtain cerebrospinal fluid in the standing horse. Vet Radiol Ultrasound. 2011;53(1):92–5.