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Diagnosing Incoordination (Ataxia) and Weakness in Horses
including ataxia, spasticity, and hypermetria
   by Robert N. Oglesby DVM

Introduction
Coordination and strength requires the proper integration of the brain (cerebrum, cerebellum, and brainstem), spinal cord, peripheral nerves, and muscles. Failure at any point causes signs of incoordination and/or weakness. The nature and location of the symptoms helps localize the disease to which structure or structures is diseased. By localizing the diseases structures you can generate a list of probable diseases or focus your diagnostic efforts accurately. This article describes the different forms that weakness and incoordination take and how to localize the disease. From the localization a list of rule outs is provided with links to articles on specific diseases for further research.

If your horse is also showing changes in alertness or behavior along with the incoordination he have have a disorder of the brain, for which there is a separate article...for more information.

Labeling Symptoms Accurately

The nervous system can be grouped into functional regions that correspond with anatomical structures. The first step in diagnosing dieseases of the nervous system is defining the functional disorder which leads to an anatomical location of the disease. Once a anatomical location is identified a list of diseases that commonly effect that location can be generated and either further diagnostic work or therapy can be planned. The main functional disorders and definitions are:
  • Dementia: behavorial changes including depression, semicoma, aimless wandering or circling, seizure, delirium, and blindness...for more information.
  • Spastic Ataxia: spasticity is a stiff and stilted (tin-soldier) gait, with a short stride and lack of joint flexion. Most often spasticity is seen in combination with other signs of brain disease, like cranial nerve involvement. When a horse displays primary signs of spasticity with dementia or cranial nerve signs usually the brain stem is involved...for more information.
  • Hypermetric Ataxia: seen as increased or exaggerated joint flexion. When hypermetria presents as the primary sign frequently accompanied by tremors during voluntary movement (intention tremors) the lesion may localize to the cerebellum. Primary cerebellar disease is seen most often in foals...for more information.
  • Propioceptive Ataxia: seen as increased swaying of the trunk, prolonged pelvic limb stride, waving of the limb in the air before placement, abduction of the limb during forward movement, crossing the limb under the body, and stepping on the opposite limb. The primary sign of spinal cord disease is ataxia (incoordination) and not weakness, though exceptions exist. The reason is the way the muscles and reflexes work. Even without the innervation of the upper motor neuron in the spinal cord muscles maintain tone. This is mainly do to the peripheral nerves (also known as the lower motor neuron) and their spinal reflexes. So if communication is lost futher up the spinal cord, the leg still has strength but loses its ability to coordinate with other limbs and be controlled by the brain, ie ataxia.
  • Weakness or paresis: seen as knuckling, stumbling, dragging of the limb, and dipping of trunk during weight bearing. Weakness occurs when the peripheral nerve, neuromuscular junction, or muscle is dysfunctional. The exception is if the lesion in the cord happens to be where the spinal cord is effected where the peripheral nerve communicates with it. Careful consideration of the symptoms is sometimes needed to distinguish ataxia and weakness. For instance stumbling and swaying of the body occurs with both conditions: did it occur because the horse was unable to coordinate it's movements or because of an inability to move and support the limb because the muscle was not strong enough. Sometimes you must look at other signs to differentiate them and occasionally they happen together.

Gait changes may also be seen as a result of unusual conformation or shoeing. Some horses can show excessive flexion, pronounced external rotation (winging out), circumduction, or decreased action at normal gaits. The owner, trainer, or handler may help provide valuable information to help distinguish between normal and abnormal behavior and gait for that individual horse. Once a behavioral or gait problem is recognized, regardless of its severity, it must be defined in its simplest form and a problem list must be generated. In addition, horses with musculoskeletal disease can show signs of weakness when painful limbs are passively lifted off the ground or spasticity when they use painful joints (reluctance to flex).

Many lesions affecting the nervous system can be localized to a single focus but when such localization is not possible, a diffuse or multifocal disease of the nervous system should be considered. Accurately labeling and listing of symptoms seen will help lead to accurate localization.

Neurological Examination for Ataxia and Weakness

Disease of the spinal cord is seen as three main symptoms with incoordination (ataxia) being the predominant one. Stiffness (spasticity) and paresis (weakness) may also be present. The location and severity of the symptoms of disease of the spinal cord is less effected by the cause of the disease and more by it's location. The spinal cord is ensheathed in the vertebral column which is then buried deep in the muscle masses of the neck and back direct examination is impossible. As a result it is often possible to know where the disease is but harder to know what is causing the disease.Without specific evaluation for spinal cord disease mild problems may be overlooked. The following procedures will help determine whether there is the presence of spinal cord disease:

  • Symmetry of neck, trunk, and limbs
  • External thoracolaryngeal (slap) reflex
  • Cutaneous reflexes and sensitivity
  • Abnormal sweating
  • Tail and anal tone
  • Anal reflex
  • Examination of rectum and bladder
  • Postures adopted at rest
  • Gait at walk and trot and canter and while during turning
  • Gait while cantering in circles

The ??Slap Test??
The thoracolaryngeal response (??slap test??) is a useful part of the complete neurological examination of horses suspected to have involvement of the vagal or recurrent laryngeal nerves or cervicothoracic spinal cord. The test can be performed in cooperative horses by palpating the dorsal and lateral laryngeal musculature while simultaneously slapping the contralateral dorsolateral thoracic (saddle) region, from the cranial withers to near the last rib. The hand slap should be performed during expiration and examiners may find it easier to perform a double slap, palpating for a double movement of the laryngeal musculature and/or cartilages. If there is difficulty in interpretation of this test, observing the larynx via an endoscope while performing the test may be necessary.

This response is not consistently absent in horses with cervical vertebral malformation or other forms of cervical spinal cord disease (wobblers) and may inexplicably be absent in some apparently normal horses. Depression or absence of the reflex on the left side must be taken as strong evidence for the presence of recurrent laryngeal neuropathy or prior laryngeal surgery. Exercising the horse will be necessary to confirm any clinical problem arising from laryngeal paralysis. Bilateral absence of the palpable response in the absence of other signs of laryngeal or cervicomedullary disease must be interpreted cautiously particularly in excitable horses.

Cervical Reflexes
The local cervical and cervicofacial reflexes can be useful to help confirm the presence and sometimes the location of a cervical lesion. The former is the contraction of the cutaneous coli (neck) muscle in response to tapping the neck with a blunt probe. The sensory input for this reflex is segmental but the motor output from the CNS is not completely clear but includes ventral spinal nerve roots, especially C6.

The second of these reflexes is twitching of all facial muscles including the cutaneous facei (facial subcuticular) muscle in response to the same cervical stimulus as for the first reflex. The same segmental cervical sensory input likely applies to this reflex. However, both the sensory and motor pathways may be more complex as there is an anastomotic connection from the C2 nerve (and subsequently the first six cervical nerves via the transverse cervical nerve) and a cervical branch of the facial (cranial nerve VII) nerve. The fact that this anastomosis could contain sensory or motor or both types of fibers makes accurate interpretation of this reflex enigmatic.

Finding depressed and particularly asymmetrical local cervical and cervicofacial reflexes can be useful in localizing a cervical spinal cord lesion. Because of the incomplete understanding of these reflexes interpretation may need to be as imprecise as "consistent with a caudal cervical lesion" or "consistent with a cranial cervical lesion."

Cutaneous Trunci Reflex and Cutaneous Sensation
The cutaneous trunci reflex (incorrectly referred to as the panniculus reflex) is a robust reflex in horses. It consists of contraction of the cutaneous trunci muscle in response to tapping the lateral trunk with a blunt probe. The sensory input is segmental through dorsal thoracic nerve roots passing cranially through the spinal cord to reach the motor neurons in the cranial thoracic gray matter to reach the cutaneous trunci muscle via the lateral thoracic nerve. This reflex can be useful in delineating the cranial extent of a thoracic spinal cord lesion particularly when such a lesion is asymmetrical. Rarely, a degree of hypalgesia can be detected caudal to the cranial extent of a region of cutaneous trunci hyporeflexia. This is seen only with severe thoracic spinal cord disease.

Evaluating for hypalgesia over the trunk, as elsewhere, should be performed with a two-pinch test. This is performed by pinching the skin into a fold, inserting the fold into the jaws of a strong hemostat or needle holder and after the patient has settled to this, a brief, sharp squeeze is applied to elicit a behavioral response.

Neck pain
It is difficult to interpret an apparent reluctance of a patient to move the neck passively or actively in any direction as indicating neck pain or stiffness. On the other hand, a horse that will not lower its head to eat usually is quite evidently compromised, usually because of mechanical or painful disruption to flexion of the caudal cervical vertebrae or extension of the atlantooccipital and/or the atlantoaxial joints.

Sweating
Identifying the presence of well-delineated regions of cervical and thoracic sweating can be useful in localizing a spinal cord lesion. Such areas can represent focal sympathetic denervation (decentralization) of the vasculature in the skin, resulting in increased circulating epinephrin stimulating sweat glands. However, care must be taken in interpreting patchy sweating that is not well delineated. Very asymmetrical patchy sweating can occur in horses that are excited or distressed, particularly when in a draughty trailer or stall, without a sympathetic lesion being present.

Gait and Posture
Neurological gait abnormalities involve degrees of weakness and ataxia. Weakness may predominantly involve flexor or extensor muscle groups and ataxia can be characterized as having components of decreased range of joint movement (hypometria or spasticity), and increased range of joint movement (hypermetria or high striding).

Extensor weakness in a limb is best evaluated by observing for muscle trembling, buckling on a limb when turning and the ease in which the patient can be pulled to the side by the tail, both while standing still and while moving. Flexor weakness may be more evident as dragging of a toe and a low foot flight, particularly while turning. Subtle degrees of weakness in the thoracic limbs may be accentuated by performing a hopping test wherein one forelimb is held up and the horse made to hop laterally away from the examiner on the other forelimb. A horse with extensor weakness often will buckle on an affected limb. Pelvic limb and/or thoracic limb weakness can be detected by attempting to pull on the halter and tail at the same time. This is particularly useful if there is asymmetry in the degree of weakness. Normal alert horses resist such pulling whereas a weak animal is easy to pull to the side.

Mild degrees of ataxia can be detected by performing additional postural maneuvers. Considerable time usually is spent in performing serpentine maneuvers, circling wide and tight, elevating the head while walking the patient on a flat and on a sloped surface, turning tightly upon stopping abruptly from a trot and backing. These maneuvers alter visual, gravitational, vestibular and proprioceptive input to the nervous system such that any subtle sensory or motor deficit can become more clearly expressed. The overall severity of any gait abnormality in each of the four limbs can be graded one through four, as subtle, mild, moderate or severe.

Rather than manually placing limbs in abnormal positions to evaluate conscious proprioception, it appears more reliable to maneuver the horse rapidly (say in a circle) and stop the maneuver abruptly. This often results in an initial awkward placement of a limb and then the examiner can determine how long the horse leaves the limb in such an abnormal posture to determine the presence or not of a conscious proprioceptive deficit.

To determine the presence of weakness in the limbs of a horse suffering from spinal cord disease the three most useful tests are the tail pull, the tail and halter pull and thoracic limb hopping (Fig. 10). Pulling the tail while the patient remains static initiates, an extensor (patellar or quadriceps) reflex. This reflex is poor with lower motor neuron disease at the level of L3 - 4 and the patient will demonstrate weakness while standing still (hypotonia) as well as voluntary extensor weakness while moving. In contrast, a horse with an upper motor neuron lesion (wobbler) will have good resting muscle tone and be difficult to pull to the side in a singular movement while standing still. However, such a patient will be easily pulled to the side while walking. This demonstrates voluntary extensor weakness but the presence of intact or even hyperactive extensor reflexes in the pelvic limb.

Pulling on a lead rope and the tail simultaneously while circling the horse around the examiner is a postural reaction that also evaluates voluntary extensor strength and in addition can exaggerate a patient?s tendency to pivot on a hind limb and to maneuver limbs in an ataxic fashion. Flexor weakness leads to the patient not flexing the affected limb well and thus dragging the toe on the ground. A worn toe will result. Some neurologically normal horses will "toe drag"; many of these will have orthopedic disease.

A horse that has extensor weakness in a thoracic limb often will tend to tremble on the limb while the opposite thoracic limb is held up on initiation of the hopping test. It also will have difficulty in hopping to the side when pushed with the examiner's shoulder.

Evaluation of horses while being walked across curbs has not proven to be a useful test of proprioceptive dysfunction. Normal horses, particularly if distracted, often will stumble and those that are quite weak and ataxic but moving cautiously often can maneuver such obstacles. In the author?s experience blindfolding a horse suspected of suffering from spinal cord disease usually has not added anything substantial to the neurological evaluation. Normal horses react in different ways, from extremes of excitement to calmness and the subsequent movements they make depends on this behavioral response.

Signs of dysmetric ataxia and loss of balance will be markedly exacerbated when a blindfold is applied to a horse suffering from vestibular or occasionally from spinocerebellar disease.

Equine practitioners do find cases for which there is some indication of spinal cord involvement but no definitive proof. These cases usually are suspected of suffering from a painful musculoskeletal disorder, a peripheral neuromuscular spastic disorder, a behavioral problem (belligerency), laziness or back disease. Such patients may show one or more of the signs listed in Table 4. Other forms of frantic behavior have been associated with a strong suspicion of exposure to nettles or poison ants, but in these situations the signs usually abate with time. With horses that demonstrate a mild or unusual gait or postural abnormality, emphasis often will be on detecting evidence of spinal cord, peripheral nerve and muscle disease and distinguishing such evidence from signs resulting from primary orthopedic disorders.

Syndromes Wherein an Organic Spinal Cord or Vertebral Column Lesion May Be Suspected but Usually Not Proved

  • Prominent toe dragging
  • Shivering Intermittent
  • unusual lameness
  • Stringhaltlike movements
  • Prominent sinking with dorsal lumbar pressure
  • Other spastic movements
  • Throwing to the ground when a saddle is applied
  • Extreme difficulty in getting up
  • Rearing violently when first ridden
  • Lying down a lot

Localizing Lesions of the Spinal Cord

After the precise type of gait abnormality present has been determined, the most likely site of an acute spinal cord lesion and the pathways involved frequently can be accurately defined, with some exceptions. With peracute lesions, particularly those of an inflammatory nature and those with soft tissues compressing the spinal cord (such as with caudal cervical synovial cyst formation), resulting signs can wax and wane quite dramatically over periods of hours to days. Such signs usually stabilize with subacute to chronic lesions.

On the other hand, a horse with chronic spinal cord disease may show quite different neurological signs. For example a horse that has suffered a single insult of cervical spinal cord compression a year before examination may have an unusual, perhaps hypermetric, mild ataxia in the pelvic limbs with no evidence of weakness. There may be no signs in the thoracic limbs save for a questionable response to hopping.

Functional Sections of the Equire Spinal Cord
Key: Cervical vertebrae (C), Thoracic (T), Lumbar (L)

  • Upper neck (C1 - C5): Characteristically injury results in both front and rear limb ataxia with rear worse than the front.
    • Damage to the nerves going into the first three cervical vertebrae can result in incoordination that is similar to disease of the vestibular system.
  • Lower neck (C6 - T2): Characteristically injury results in both front and rear limb ataxia with front limbs worse with weakness than the rear.
  • Withers and Back (T3 - L3): Characteristically injury results in mild to moderate rear limb ataxia.
    • An interesting involvement of spinal afferent fibers in respiratory control has been shown in ponies. One month after spinal lesions in the lumbar area, mainly sectioning the dorsal spinocerebellar tracts, there was a change in the CO2 levels during exercise. It is thus possible that minor spinal lesions may influence performance through effects on respiration.
  • Loin and Croup (L4 - S4): Characteristically injury results in moderate to severe rear limb ataxia and weakness.
  • Croup to the Tail (S5 - Ca1): Tail paralysis, bladder atony, loss of feeling around the perineal area.

Prominent Gait and Postural Abnormalities Present with Neurologic Lesions at Different Locations

Lesion Location (tracts and sites) Postural Deficits Paresis Ataxia Hypometria Hypermetria
Spinal cord—UMN ++ ++ 0 ++ ++
Vestibulospinal +++ 0 ++ +++ 0
Spinocerebellar ++ 0 +++ ++ +++
Spinal cord—LMN ++ +++ 0 ++ (due to weakness) 0
Musculoskeletal + ++ 0 0 (May be mechanical) 0
NOTE. Characteristics of many musculoskeletal disorders are included for comparison.
UMN, upper motor neuron; LMN, lower motor neuron; 0, not usually expected; +, mild if present; ++, usually present; +++, quite characteristically present.

With the neurological examination completed the examiner may be able to decide if and where any possible lesions exist. If this is not clear then it is often worthwhile returning to the patient and performing an even more critical evaluation. With a very fractious or a very excited horse suspected of having a neurological abnormality involving the limbs, exercise such as lunging or running on very soft going for 20 minutes can be undertaken and then a reevaluation made.

When lameness is present or is suspected, possibly interfering with interpretation of a horse’s gait and posture, then appropriate regional analgesia or short acting systemic analgesia (e.g. using synthetic opioids), may be used. In more chronic cases, nonsteroidal anti-inflammatory drugs may be given at a relatively high dose for several days (or weeks) and then the horse’s gait can be reevaluated, when lameness often will be reduced.

Neurological Examination of Foals
The neurological evaluation of foals is very similar to that of adults but several developmental landmarks should be borne in mind. The spinal reflexes are hyperactive in newborn foals and the patellar reflex, cranial tibial and gastrocnemius tendon reflexes are performed easily. Up to one month of age there are normal, strong, crossed extensor reflexes in the thoracic and pelvic limbs. In addition, an extensor thrust reflex is obtained, at least in very young foals, by rapidly overextending the animal’s toe while the limb is already in extension. This results in forceful extension of the limb. Refusing to eat from the ground, or consistently adopting a very abnormal posture (as shown) can be quite good evidence of neck pain. Newborn foals have very active spinal reflexes for the first few days to weeks of life. These can include a crossed extensor reflex, as shown with flexion of the limb being tested, and reflex extension of the other limb. The more active the foal, the sooner these hyperactive reflexes return to normal (adult like). Brainstem auditory evoked responses are very robust waveforms but do vary somewhat from horse to horse. They are very repeatable in the same horse

In addition to the evaluation of gait and reflexes in non recumbent adults, other postural reactions can be performed in foals and are of most benefit in detecting subtle proprioceptive and motor pathway lesions when the gait is normal. These include wheelbarrowing the patient to make it walk on just the thoracic limbs, hopping it laterally while supporting weight on just the left then the right thoracic limb in turn and hemistanding and hemiwalking the patient by making it stand and then move laterally on both left, then both right limbs. Spinal cord lesions cause postural reaction deficits on the same side as the lesions. Lesions involving the proprioceptive and motor pathways to the limbs result in an extremely slow or absent hopping response in that limb.

Objective Neurophysiologic Testing
Neurological examinations in horses have tended to be primarily subjective, however recent publications addressing the use of objective electrodiagnostic measurements in the horse are available. These include the evaluation of the thoracolaryngeal reflex, recurrent laryngeal nerve conduction velocities and latencies, auditory brain stem evoked potentials, magnetic motor evoked potentials, and sensory nerve conduction velocities. Needle electromyography can be a useful diagnostic adjunct in defining the extent of any denervation but probably should be delayed for 3–4 weeks when repeatable denervation potentials will be recordable.

Diseases of the Spinal Cord

Other conditions such as injection-site abscesses can occur, but less frequently. A history of previous cervical injection can be helpful in making the diagnosis.

Cervical vertebral malformations

  • Atlanto- occipital malformation is rare and occurs in Arabian and Arabian-cross foals. The occipital bone, atlas, and axis are malformed and exhibit different anatomic features. Problems characteristic of cranial cervical spinal cord compression from atlanto-occipital malformation can occur within the first few months of life. However, in some cases, no neurologic signs are seen, just restricted movement of the neck.
  • Cervical stenotic myelopathy (CSM) (spinal ataxia, cervical vertebral instability, wobbler syndrome) can lead to cervical spinal cord compression. Problems usually develop between 6 and 30 months of age and can progress very rapidly or remain static. Large, rapidly growing Thoroughbred, Quarter Horse, and warmblood youngsters seem predisposed to CSM, whereas other breeds such as Standardbreds, Tennessee Walking Horses, and Arabians may be less predisposed. Frequently these horses present with some history of trauma and symmetric gait deficits, but they may present with asymmetric gait deficits. For example, a young racehorse may present initially for a unilateral hindlimb lameness, but the signs may progress to be a more symmetric presentation of obvious neurologic origin...for more information.

Equine Degenerative Myelopathy (EDM)

  • Progressive symmetric ataxia, weakness, and spasticity of the pelvic limbs in horses less than 3 years of age suggest EDM. Clinically it looks much like CSM discussed above though there may be a history of low vitamin E intake, low vitamin E blood levels, and distinctive changes on the retinae of the eye...for more information.

Spinal cord trauma

  • Commonly occurs when horses fall or collide with a relatively immovable object. Foals appear to be more susceptible to vertebral trauma than adult horses and frequently suffer fractures of the cranial cervical (C 1-C 5) and caudal thoracic vertebrae. Hyperflexion injuries result in fracture and luxation of the dens, and hyperextention injuries result in vertebral epiphyseal fractures. Adult horses are more susceptible to injury of the caudal cervical (C 5-C 7) and caudal thoracic vertebrae.
  • Profound weakness and hyporeflexia in the front limbs with hyperreflexia to normoreflexia in the rear limbs can be localized to the cranial intumescence (C 6-T 2). Lesions in this region are usually traumatic, although malformations of the thoracic vertebrae, fibrocartilaginous infarcts, and inflammatory diseases also occur. Normal front limb signs with mild ataxia and weakness in the rear limbs can be localized to the thoracolumbar spinal cord (T 3-L 3).

Paresis and Weakness, without pronounced ataxia

Weakness, limb hyporeflexia, muscle hypotonicity, rapid muscle atrophy, and decreased pain sensation in any or all four limbs can be anatomically localized to the peripheral nerve, neuromuscular junction, or muscle itself. Weakness or paresis can be observed as muscle trembling, knuckling, stumbling, dragging of the limb, and dipping of trunk during weight bearing. When the horse does not stumble, foot flight and placement are usually normal. Weakness can be exacerbated by observing for buckling on a limb when turning and the ease in which the patient can be pulled to the side by the tail, both while standing still and while moving. Muscle atrophy is common with these diseases. Diseases of the peripheral nerves can be divided into several categories, depending on their anatomic location along the motor unit ( peripheral nerve, neuromuscular junction, and muscle):
  • Diseases of the ventral horn cells of the spinal cord and ventral root:
  • Diseases of the peripheral nerves:
  • Neuromuscular junction diseases include equine botulism (forage poisoning, shaker foal syndrome) and myasthenia-like syndrome. Dysphagia, decreased eyelid tone, delayed palpebral response, delayed PLR, and weakness in all four limbs suggest equine botulism. Normally horses displaying these symptoms respond to the examiner but appear depressed, weak, and listless. Horses with botulism usually progress to recumbency and may die of respiratory failure. Ileus, constipation, and urinary incontinence can occur in horses with botulism...for more information.
  • Unclassified disorders of the peripheral nerves include:
    • Equine Motor Neuron Disease (EMND) (amyotrophic lateral sclerosis) is a degenerative neuropathy that affects the motor neurons and ventral roots in the spinal cord. Horses with this disease present with progressive trembling, weakness, and muscle wasting. Horses have a very short anterior stride without loss of proprioception. The disease stabilizes after 1-2 months and may remain static for up to 3 years...for more information.

Multifocal Diseases: Ataxia and Dementia Together

Dementia, cranial nerve signs, ataxia, and weakness in one or several limbs in an unequal distribution are problems that cannot be localized to a single focus and thus are considered diffuse or multifocal. Subtle differences in the clinical problems exist between these conditions, which may help in their differentiation:
  • Polyneuritis equi:
    This is the newer term for cauda equina neuritis and preferred because of the frequent involvement of other peripheral nerves those of the cauda equina. Progressive symmetric weakness of the rear limbs, analgesia of the tail, anus, and perineum, and cranial nerve signs may suggest polyneuritis equi. Fecal incontinence, paraphimosis, urine scalding, and bacterial cystitis may also be observed. The owner may mistake bilateral gluteal muscle atrophy and facial muscle atrophy for weight loss. The cause of polyneuritis equi is unknown, but bacterial, viral, and immune-mediated mechanisms have been proposed. Antimyelin antibodies have been detected in some cases....for more information
  • EPM:
    Progressive asymmetric ataxia, weakness, muscle atrophy, and cranial nerve signs suggest EPM. This disease usually occurs in horses of racing and performance age. Obscure hindlimb lameness, lateral digital extensor tenectomy, and medial patellar desmotomy are often part of the history. Sarcocystis neurona is thought to be the causative agent. These protozoal organisms randomly invade the gray and white matter of the spinal cord, resulting in multifocal upper- and lower-motor neuron disease....for more information
  • Viral Encephalotides:
  • Often knowledge of the diseases that occur locally, clinical course and history can lead you to a likely diagnosis.
    • EEE, WEE, VEE:
      Rapid onset of fever, depression, and ataxia that progress to recubency during mosquito season...for more information.
    • West Nile Virus:
      Variable fever with hyperesthesia to touching during mosquito season...for more information.
    • Equine herpesvirus (EHV) 1:
      Acute onset and rapidly stabilizing (within 24-48 hours) symmetric ataxia, bladder atony, urinary incontinence, and hypotonus of the tail and anus with or without cranial nerve signs suggest EHV 1 encephalomyelitis. This condition may occur 7-10 days after an outbreak of respiratory disease or abortion. EHV 1 causes vasculitis and thrombosis, which lead to infarction and necrosis of the nervous tissue. The vasculitis is thought to be an immunocomplex disease...for more information.

Conclusion

Variations in number and shape of vertebrae as well as prominent performance related and ageing changes in vertebrae need to be understood to interpret disease states more accurately. More objective measurement of vertebral canal and myelographic diameters in different sized horses will definitely improve identification of spinal cord compression. The roll of cranial cervical afferent input to the vestibular system and the clinical syndromes seen with lesions to cranial cervical nerves need to be better understood. Finally, critical documentation of localizing signs such as hypalgesia, hyporeflexia and sweating over the neck and trunk is often difficult but can be extremely useful in localizing spinal cord disease.

Scientific Reports

Vet Q 2001 Jan;23(1):49-50
Neurological signs in a horse due to metastases of an intestinal adenocarcinoma.

Spoormakers TJ, IJzer J, Sloet van Oldruitenborgh-Oosterbaan MM

Department of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.

A 22-year-old Dutch Warmblood mare was referred to Utrecht University with progressive left hind limb paresis and hyporeflexia. The preliminary clinical diagnosis was the neurological form of equine herpes virus (EHV-1) infection. Within 1 day of admission, the mare became recumbent and deteriorated rapidly. Postmortem examination revealed an adenocarcinoma of the caecum, with metastases in all regional lymph nodes and extending from the lumbar nodes into the vertebral canal, causing spinal cord compression and destruction of the left 4th and 5th lumbar nerves.

      ~Word Count: 5068 words (The average magazine page contains about 600 words);
      ~Last Updated: April 17, 2011;

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