Equine Central Nervous System Trauma – NAVLE Study Guide

Overview and Clinical Importance

Central nervous system (CNS) trauma in horses encompasses injuries to the brain and spinal cord and represents a significant cause of morbidity and mortality, particularly in young horses. Traumatic brain injury (TBI) and spinal cord trauma are common sequelae of accidents during halter training, trailer loading, falls during exercise, and kicks from other horses. Understanding the pathophysiology, clinical presentation, and management of CNS trauma is essential for the NAVLE, as prompt recognition and treatment can significantly improve outcomes.

The prognosis for horses with CNS trauma has historically been considered poor; however, recent studies demonstrate that with appropriate medical management, approximately 62% of horses with traumatic brain injury survive to hospital discharge. Key prognostic factors include the presence of basilar skull fractures and duration of recumbency, making early and accurate assessment critical for clinical decision-making.

Relevant Anatomy

Equine Skull Anatomy

The equine skull consists of 34 bones that form a complex protective structure around the brain. The calvarium (brain box) is composed of six bones that directly encase the brain. Understanding skull anatomy is crucial because approximately three-quarters of the skull protects the nasal passages and oral structures, with a relatively small area dedicated to brain protection.

Key Anatomical Structures

Basisphenoid and Basioccipital Bones: These bones form the base of the skull and are critically important in poll injuries. The suture between these bones remains open until 2-5 years of age, making young horses particularly susceptible to basilar skull fractures.

Rectus Capitis Ventralis Muscle: The largest flexor muscle of the neck inserts on the basisphenoid bone. During poll trauma with hyperextension, traction forces from this muscle can cause avulsion fractures of the basilar bones.

Guttural Pouches: Located adjacent to the basilar bones and contain important neurovascular structures. Hemorrhage into the guttural pouches from basilar fractures can be detected via endoscopy.

Foramen Magnum: The circular opening in the base of the skull through which the spinal cord exits. Cerebellar herniation through this opening is a life-threatening complication of severe intracranial hypertension.

Cervical Spine Anatomy

The horse has seven cervical vertebrae (C1-C7). The first two vertebrae, the atlas (C1) and axis (C2), are morphologically specialized for head movement. The cervical spine contains the spinal cord, which transmits motor and sensory information between the brain and body. The vertebral canal houses the spinal cord, and the intervertebral foramina allow exit of spinal nerve roots.

Etiology and Pathophysiology

Mechanisms of Injury

Traumatic brain injury in horses occurs in three main clinical settings:

• Poll impact: Most commonly occurs when horses flip over backwards, striking the poll on the ground. This mechanism is responsible for basilar skull fractures and brainstem injury.
• Frontal/parietal impact: Occurs when horses run into fixed objects (fences, trailers, walls). Results in cerebral contusion and potential frontal bone fractures.
• Kick injuries: Direct blows from other horses can cause skull fractures and underlying brain injury, often affecting the temporal region.

Common Activities Associated with CNS Trauma

Primary vs Secondary Brain Injury

Understanding the distinction between primary and secondary brain injury is fundamental to managing CNS trauma. Primary injury occurs at the moment of impact; secondary injury is preventable through appropriate medical management.

Clinical Signs and Diagnosis

Clinical Presentation of Traumatic Brain Injury

Clinical signs depend on the location and severity of brain injury. Horses may present with signs immediately after trauma or develop progressive neurological deterioration over 12-48 hours as edema increases.

Pupillary Signs and Prognostic Significance

Bilateral miosis: Indicates rostral midbrain swelling

Bilateral mydriasis (fixed, dilated pupils): Indicates midbrain compression or herniation - POOR PROGNOSTIC INDICATOR

Abnormal respiratory patterns: Consistent with cerebellar herniation through the foramen magnum

Signs Specific to Basilar Skull Fracture

Basilar skull fractures carry a significantly worse prognosis. Horses with basilar fractures are 7.5 times more likely to die than horses without this type of fracture.

• Bilateral epistaxis (blood from both nostrils)
• Blood from external ear canal (petrous temporal bone fracture)
• CSF leakage from nostrils or ears
• Loss of consciousness at time of injury
• Vestibular dysfunction and facial nerve paralysis
• Tetraparesis
• Hemorrhage visible in guttural pouch on endoscopy

Modified Mayhew Ataxia Scale

The Modified Mayhew Scale is the standard grading system for assessing neurological deficits in horses. It is used for general proprioceptive (spinal) ataxia only, not for cerebellar or vestibular ataxia.

Diagnostic Imaging

Treatment

Emergency Stabilization

Initial management focuses on preventing secondary brain injury by addressing systemic abnormalities. The mnemonic "ABC + D" applies: Airway, Breathing, Circulation + Disability (neurological status).

Immediate Priorities

• Ensure safety: Prevent further trauma; move to padded stall if possible
• Establish IV access: 14-gauge catheter for fluid administration
• Address hypotension: Target MAP greater than or equal to 80 mmHg (normal: 120/70 mmHg)
• Provide oxygen: Nasal insufflation at 10-15 L/min; target SpO2 greater than 96% or PaO2 greater than 80 mmHg
• Control seizures: Diazepam or midazolam immediately if seizing
• Control temperature: Cool hyperthermic patients; hypothermia may be neuroprotective

Pharmacological Treatment

Fluid Therapy Considerations

Fluid therapy in TBI patients requires careful balance. The goal is to maintain euvolemia and normotension while avoiding fluid overload that could worsen cerebral edema.

• NEVER restrict fluids in head trauma patients - hypotension worsens secondary brain injury
• AVOID hypotonic fluids (5% dextrose, 0.45% saline) - lowers plasma osmolarity and worsens cerebral edema
• Preferred fluids: Isotonic crystalloids (LRS, Normosol-R) or hypertonic saline/colloid combinations
• Avoid hyperglycemia: Do not supplement glucose unless patient is hypoglycemic

Prognosis

Prognosis for horses with TBI is more favorable than historically believed. Key studies report an overall survival rate of approximately 62% for horses that receive appropriate treatment.

Prognostic Factors

Board Tip - Key Statistics to Remember: Survival rate approximately 62%. Recumbency greater than 4 hours = 18x increased mortality. Basilar fracture = 7.5x increased mortality. Even severely affected horses can recover dramatically "as long as there are no compound or markedly displaced fractures."

Cervical Spinal Cord Trauma

Cervical spinal cord trauma may occur independently or concurrently with brain injury. Common causes include falls, kicks, and trailer accidents. The clinical presentation depends on the level and severity of spinal cord damage.

Localization of Cervical Lesions

Cervical Vertebral Fractures

Cervical vertebral fractures can occur at any level but are often associated with severe neurological deficits. Management depends on fracture stability and neurological status.

Clinical Signs: Neck pain and stiffness, reluctance to move head, abnormal neck posture, tetraparesis (all four limbs affected), ataxia of varying severity

Diagnosis: Cervical radiographs may identify fractures but sensitivity is limited. CT provides superior fracture detail and is the imaging modality of choice when available.

Treatment: Stable fractures without neurological deficits may be managed conservatively with stall rest and anti-inflammatory therapy. Unstable fractures or those with severe neurological signs carry a grave prognosis.