Encephalon
The equine brain weighs approximately 600-700 grams; relatively small compared to the horse's 450-500 kg body mass (brain:body ratio ~1:700). The cerebellum is proportionally large, reflecting the critical importance of balance, coordination, and proprioception for a large, fast-moving quadruped. The cerebral cortex is moderately convoluted (gyrencephalic). The brainstem controls vital functions (respiration, cardiovascular regulation) and houses the nuclei of the 12 cranial nerves. The blood-brain barrier limits drug penetration, complicating treatment of CNS infections.
A thorough neurological examination assesses mentation, cranial nerves (I-XII), gait (ataxia graded 0-5 on the Mayhew scale), postural reactions (tail pull, circling, backing), and cervical flexibility. Cerebrospinal fluid (CSF) analysis from the atlantooccipital or lumbosacral space aids diagnosis. MRI is increasingly available for equine brain imaging. Core vaccinations (EEE/WEE/WNV/tetanus) are essential neuroprotection.
Equine Protozoal Myeloencephalitis (EPM) is a progressive neurologic disease caused by infection of the central nervous system with the protozoan parasite *Sarcocystis neurona*. It can cause a wide ra
Mosquito-borne flavivirus infection causing nonsuppurative encephalomyelitis. Polioencephalomyelitis preferentially affects the gray matter of the brainstem and spinal cord ventral horns.
Mosquito-borne alphavirus infections. EEE has the highest mortality (~90%) of any equine encephalitis. Both are core vaccinations recommended by AAEP.
Wobbler syndrome, also known as cervical vertebral stenotic myelopathy, is a neurologic condition caused by compression of the spinal cord in the neck. It leads to progressive incoordination (ataxia),
Injury from falls, kicks, rearing and flipping backward, or collision with fixed objects. Basilar skull fractures may involve the petrous temporal bone. Horses that flip over may fracture the basisphe
Neuropathogenic strains of EHV-1 cause vasculitis in the CNS, leading to ischemic damage to the spinal cord and brain. The D752 mutation in the DNA polymerase gene is associated with neuropathogenicit
Equine Protozoal Myeloencephalitis (EPM) is a progressive neurologic disease caused by infection of the central nervous system with the protozoan parasite *Sarcocystis neurona*. It can cause a wide range of neurologic deficits and is one of the most common infectious neurologic diseases of horses in the Americas. ## What it is Horses become infected by ingesting sporocysts of *Sarcocystis neurona* shed in the feces of opossums, the definitive host. The parasite migrates to the central nervous system, where it causes inflammation and damage to the brain and spinal cord. The disease is highly variable in its presentation because the parasite can affect any part of the CNS. Clinical signs depend on the location and severity of the lesions. EPM is not contagious between horses. Opossums are the main source of infection, and horses are considered dead-end hosts. ## Signs and symptoms - Asymmetric incoordination (ataxia), often worse in the hind limbs - Muscle atrophy, especially of the gluteal or shoulder muscles - Head tilt, facial nerve paralysis, or difficulty swallowing - Weakness, stumbling, or toe dragging - Behavioral changes or lethargy - In severe cases, recumbency or seizures - Signs can be acute or slowly progressive ## Causes and risk factors EPM is caused by *Sarcocystis neurona*. Risk factors include exposure to opossum feces (contaminated feed, water, or pasture), stress, immunosuppression, and young age. The disease is more commonly diagnosed in horses in the eastern and central United States but can occur anywhere opossums are present. ## How it is diagnosed Diagnosis is based on clinical signs, neurologic examination, and laboratory testing. The most common tests are serum and cerebrospinal fluid (CSF) antibody tests (IFAT or ELISA) to detect exposure and evidence of central nervous system infection. Ruling out other neurologic diseases is important. Advanced imaging (MRI) can help identify lesions in some cases. ## Treatment and management Treatment involves prolonged courses of antiprotozoal medications, most commonly ponazuril or diclazuril, often combined with anti-inflammatory drugs such as flunixin meglumine or dexamethasone in the early stages. Supportive care, including rest, physical therapy, and nutritional support, is important. Treatment duration is typically 1 to 3 months or longer, and response varies. Some horses recover well, while others have permanent neurologic deficits. ## When to call the vet Contact your veterinarian immediately if your horse shows any signs of incoordination, muscle atrophy, head tilt, or other neurologic abnormalities. EPM can progress rapidly, and early treatment improves the chance of a favorable outcome. ## Prevention Prevention focuses on reducing exposure to opossum feces. Keep feed and water sources covered and clean, control opossum populations around barns when possible, and avoid feeding hay or grain that may have been contaminated. Stress reduction and good overall health management may help lower susceptibility. ## Frequently asked questions **Is EPM contagious between horses?** No. Horses cannot transmit EPM to each other. Opossums are the definitive host that sheds the infective stage. **Can a horse fully recover from EPM?** Some horses make a full recovery with early and aggressive treatment. Others are left with permanent neurologic deficits depending on the extent of damage. **How long does treatment for EPM take?** Treatment typically lasts 1 to 3 months or longer, with regular monitoring of clinical response and antibody levels. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Asymmetric incoordination (ataxia), often worse in the hind limbs; muscle atrophy, especially of the gluteal or shoulder muscles; head tilt, facial nerve paralysis, or difficulty swallowing; weakness, stumbling, or toe dragging; behavioral changes or lethargy; in severe cases, recumbency or seizures; signs can be acute or slowly progressive
Mosquito-borne flavivirus infection causing nonsuppurative encephalomyelitis. Polioencephalomyelitis preferentially affects the gray matter of the brainstem and spinal cord ventral horns. Signs include: Fever; muscle tremors; stumbling; hypersensitivity to touch and sound; recumbency in severe cases; muscle fasciculations (especially face and muzzle); ataxia; hindlimb weakness; hyperesthesia; behavioral changes; 30-40% mortality without treatment
Mosquito-borne alphavirus infections. EEE has the highest mortality (~90%) of any equine encephalitis. Both are core vaccinations recommended by AAEP. Signs include: High fever; depression; circling; head pressing; blindness; seizures; death within 2-3 days of neurological signs; EEE: High fever, severe depression, head pressing, circling, blindness, seizures, rapid death (2-3 days). WEE: Similar but less severe, ~30-50% mortality
Wobbler syndrome, also known as cervical vertebral stenotic myelopathy, is a neurologic condition caused by compression of the spinal cord in the neck. It leads to progressive incoordination (ataxia), primarily in the hind limbs. There are two main forms: Type I (dynamic compression in young horses) and Type II (static compression in older horses due to osteoarthritis). ## What it is In Type I wobbler syndrome, developmental abnormalities of the cervical vertebrae cause narrowing of the vertebral canal and dynamic compression of the spinal cord during neck movement. It typically affects horses between 1 and 4 years of age, most commonly at C3 to C5. Type II wobbler involves static compression from osteoarthritic enlargement of the articular facets, usually affecting older horses at C5 to C7. Both forms result in damage to the spinal cord, leading to proprioceptive deficits and ataxia that is usually worse in the hind limbs. ## Signs and symptoms - Progressive hindlimb incoordination and ataxia - Wide-based stance and stumbling, especially when turning or going downhill - Toe dragging and difficulty backing - Neck stiffness or pain in some cases - In severe cases, weakness or falling - Symmetric or slightly asymmetric ataxia that is worse in the hind limbs than forelimbs - Positive cervical flexion test in many cases ## Causes and risk factors Type I wobbler is developmental and linked to rapid growth, genetic factors, and nutritional imbalances (especially copper deficiency or excess protein/calcium in young horses). Type II is associated with chronic wear and osteoarthritis of the cervical facet joints. Risk factors include large body size, rapid growth rates in young horses, and conformational issues that place abnormal stress on the neck. ## How it is diagnosed Diagnosis is based on clinical neurologic examination and confirmed with radiographs and myelography or MRI. Standing or recumbent radiographs can show vertebral canal narrowing or facet joint changes. Myelography or MRI provides the most accurate assessment of spinal cord compression. A neurologic grading system helps quantify the severity of ataxia. ## Treatment and management Treatment depends on the type, severity, and age of the horse. Conservative management includes stall rest, anti-inflammatory medication, and controlled exercise. For young horses with Type I, dietary management and restricted growth may help. Surgical options (ventral interbody fusion or dorsal laminectomy) are available for selected cases and can improve neurologic function in many horses. Prognosis varies widely depending on the severity and duration of compression before treatment. ## When to call the vet Contact your veterinarian promptly if your horse shows incoordination, stumbling, or difficulty backing or turning. Early diagnosis improves the chance of successful management or surgical intervention. ## Prevention For Type I wobbler in young horses, prevention focuses on balanced nutrition (avoiding excessive protein and calcium while ensuring adequate copper and other minerals) and avoiding overly rapid growth rates. Regular monitoring of at-risk young horses can help with early detection. ## Frequently asked questions **Can a horse with wobbler syndrome be ridden?** Many horses with mild to moderate signs can be ridden carefully after treatment, but those with severe ataxia are usually retired for safety reasons. **Is surgery always successful for wobbler syndrome?** Surgical success rates are good in appropriately selected cases, but results vary depending on the severity and chronicity of spinal cord damage. **Is wobbler syndrome hereditary?** There is a genetic component, especially in Type I. Breeding horses with wobbler syndrome or from lines with high incidence is generally discouraged. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Progressive hindlimb incoordination and ataxia; wide-based stance and stumbling, especially when turning or going downhill; toe dragging and difficulty backing; neck stiffness or pain in some cases; in severe cases, weakness or falling; symmetric or slightly asymmetric ataxia worse in hind limbs; positive cervical flexion test in many cases
Injury from falls, kicks, rearing and flipping backward, or collision with fixed objects. Basilar skull fractures may involve the petrous temporal bone. Horses that flip over may fracture the basisphenoid bone. Signs include: Altered consciousness; unequal pupils; head tilt; bleeding from ears/nose; seizures; Altered mentation (obtunded to comatose); anisocoria (unequal pupils); nystagmus; vestibular signs; hemorrhage from ears/nose; recumbency
Neuropathogenic strains of EHV-1 cause vasculitis in the CNS, leading to ischemic damage to the spinal cord and brain. The D752 mutation in the DNA polymerase gene is associated with neuropathogenicity. Signs include: Acute onset hindlimb ataxia and weakness following fever; urinary incontinence and bladder distension; perineal and tail hypalgesia; dog-sitting posture; may progress rapidly to recumbency; Fever followed 6-10 days later by acute hindlimb ataxia and weakness; urinary incontinence; perineal hypalgesia; may progress to recumbency; outbreaks common
A thorough neurological examination assesses mentation, cranial nerves (I-XII), gait (ataxia graded 0-5 on the Mayhew scale), postural reactions (tail pull, circling, backing), and cervical flexibility. Cerebrospinal fluid (CSF) analysis from the atlantooccipital or lumbosacral space aids diagnosis. MRI is increasingly available for equine brain imaging. Core vaccinations (EEE/WEE/WNV/tetanus) are essential neuroprotection.
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