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Mahidol University Faculty of Veterinary Science

From Equine Surgery (Third Edition)

Clinical Clerkship in Equine Nattapol Seehawat 5016007 VSVM/B

Development and organization of the nervous system • The Cranium, The Vertebral Column, Cerebrospinal Fluid, Physiology of neurotransmission

Clinical neuroanatomy • Whole brain • Level of consciousness, Upper motor neuron system • Forebrain • Behavior, Seizures, Perception of pain, Smell, Vision • Midbrain • Pupillary light response, Pupil size • Hindbrain • Mastication, Facial expression and movement , Balance and equilibrium, • Cerebellum • Spinal cord • Upper motor neuron, Lower motor neuron and spinal cord reflexes, Proprioception, Urination, Defecation, Sensation

The nomenclature relating to embryologic, medical, and common description of the parts of the brain is inconsistently applied and can be confusing.

The nervous system derives from a specialized strip of ectoderm, the neural plate, which runs along the dorsal midline of the developing embryo. Ventral to the neural crest is the primordial vertebral organ, the notochord, which develops in concert with the central nervous system (CNS). The sides of the neural crest fold upward and medially to meet in the midline and form the neural tube.

Hemispheres of the cerebrum Thalamus and Hypothalamus

Pons and Cerebellum Spinal cord Medulla oblongata

Third ventricle and Cerebrum (lateral ventricles)

The rostral part of the neural tube buds large vesicles laterally on either side

Cranial nerves I and II arise from the forebrain Cranial nerves III and IV arise from the midbrain Cranial nerve V arise from the pons Cranial nerve VI to XII arise from the medulla

Naming Systems for Principal Parts of the Brain Primary Segments Prosencephalon (forebrain) Mesencephalon (midbrain) Rhombencephalon (hindbrain)

Secondary Segments Telencephalon Diencephalon Mesencephalon Metencephalon


Principal Divisions

Common Usage


Cerebrum Thalamus Hypothalamus Midbrain Cerebellum Pons Medulla oblongata

Brain Brain stem

Lateral ventricle 3rd ventricle

Brain stem Brain stem

Mesencephalic aqueduct

Brain stem Brain stem

4th ventricle

The cranium is made up of - The occipital bone - The spheniod bone - The ethmoid bone - The interparietal bone - The parietal bone - The frontal bone - The temporal bone Volume of approximately 650 ml in an adult horse


Adult horses

• Cervical stenotic myelopathy with ataxia of the limbs and trunk

• Cranial part of cervical vertebrae fracture or injury

Envelops, bathes, and protects the CNS Produced at a high rate by the choroid plexuses

Ventricular system of the horse

More generally by the meninges and ependyma CNS homeostasis Modified transudate Lower K+ and Ca++

Lateral view showing direction of flow of cerebrospinal fluid

Higher Cl-, Na+ and Mg++ (Compare with plasma)

The blood–brain barrier reportedly allows passage of therapeutic amounts of sulfonamide-trimethoprim, chloramphenicol, enrofloxacin, and ceftriaxone into the CNS of horses.

The nervous system functions through propagation of electrical signals via changes in cell membrane potential 1) Resting 2) Excitatory

Neurochemical pathways in the CNS can be divided into two main groups • Relay systems include the long sensory and motor pathways that connect neurons of peripheral nerves to centers in the brain. • Diffuse projection systems modulate brain function by distributing signals from individual nuclei to multiple other (usually higher) areas of the brain.

Level of Consciousness The ascending reticular activating system (ARAS) at brain stem • Awake state • Maintenance the sleep

Lesions anywhere in the brain stem, whether they are focal or extensive, may reduce the level of consciousness • Cortical injury must be diffuse to cause noticeable obtundation • Sleep disorders • Narcolepsy • Cataplexy

Upper Motor Neuron System (Voluntary Movement) Initiation of voluntary movement Regulation of posture through support against gravity Modulation of the antigravity myotactic reflexes of the limbs The component of the UMN system • Originating in the hypothalamus is responsible for the control of muscular activity associated with visceral functions (respiratory, cardiovascular, urinary)

Damage of the caudal midbrain, hindbrain, or spinal cord • Increases extensor tonus and may result in limb spasticity • With UMN injury there are also limb weakness hyperactive extensor reflexes, and crossed extensor reflexes all in the ipsilateral limbs.

Behavior (Limbic System, Temporal Lobes)

Limbic system

• Controlling intrinsic behavior

Temporal lobes

• Thought that controlling behavior based on conditioning and experience (i.e., learning)

Structural, metabolic, or psychological disturbances affecting these areas may result in behavioral abnormalities Dementia Encephalitis, Head trauma, Space-occupying lesion, Malformation, Infarct, Metabolic disorders, Rabies, Eastern equine encephalomyelitis (EEE), Leukoencephalomalacia, Neonatal encephalopathy, Cerebral abscess, Cholesterol granuloma, Frontal/parietal trauma, Postseizure encephalopathy, Hepatic encephalopathy, Hyperammonemia, Hydrocephalus

Seizures Seizures frequently originate in the frontal (motor) cortex and involve muscle fasciculation and tremors around the head or abnormal movements of the jaws and tongue Seizures manifest as sudden recumbency

• With a brief phase of extensor tonus, followed by clonic movements of the legs, loss of consciousness, sweating, urination, defecation, pupillary dilation Mild motor seizures are often accompanied by behavioral signs such as Obtundation • Compulsive walking • Hyperresponsiveness to stimuli Seizure foci in the forebrain may occur at sites of previous or current trauma or inflammation

• Examples include skull trauma, equine protozoal myeloencephalitis (EPM), EEE, intracranial neoplasia, and aberrant parasite migration Causes external to the brain include

• Hyperammonemia, hyponatremia, hyperthermia, and hepatic or renal failure

Causes of Seizures in Horses

Perception of Pain (Parietal Cortex, Cranial Nerve V)

Terminate at thalamus Conscious perception of pain

Multisynaptic spinothalamic tract

Smell (Olfactory Bulbs, Cranial Nerve I) Information on smell is relayed through the thalamus to centers in • Conscious cerebrum • Unconscious (limbic system)

Vision (Thalamus, Occipital Cortex, Cranial Nerve II) Visual perception is evaluated by • Obstacle tests (with and without blindfolding of one eye) • Menace response • Requires the central visual pathway just described plus normal facial nerve function and Integrity of the cerebellar cortex • It is important to note that the menace response does not develop in foals until they are 1 to 2 weeks old.

Disease that causes diffuse, severe cerebral dysfunction is likely to cause blindness • EEE, postseizure encephalopathy, hyperammonemia, leukoencephalomalacia, and frontal/parietal trauma. • Asymmetric frontal/parietal skull trauma, EPM, cerebral abscess, and cholesterol granuloma are diseases that may cause unilateral visual deficits by affecting the forebrain on the opposite side.

Pupillary light response, Pupil size (Midbrain, Cranial Nerves II, III) Pupil size reflects • The balance of sympathetic (dilator) and parasympathetic (constrictor) influences on the smooth muscle of the iris.

Horner’s syndrome • Miosis of the pupil, enophthalmos, ptosis, and spontaneous sweating and vasodilatation over the side of the face

Pupillary Light Reflex (PLR) This system is responsive to the amount of light received by each eye. The afferent part of the pupillary light reflex passes via the optic nerves and optic tracts, past the thalamus, to terminate in the midbrain. There is extensive decussation of these tracts in both the chiasm and the midbrain, so light directed into one eye causes reflex pupillary constriction in both eyes.

Mastication (Pons, Cranial Nerve V) Sensory trigeminal neurons and are distributed to the muscles of mastication: masseters, pterygoids, temporals, and rostral digastricus With unilateral damage to the trigeminal nucleus (or nerve), there is deviation of the lower jaw toward the normal side By 2 weeks after injury, there is obvious muscular atrophy.

Bilateral severe involvement of the trigeminal nuclei (or nerves) causes a dropped jaw, weak jaw tone, slight tongue protrusion, and inability to prehend or chew feed. Damage to the nucleus of V, either unilaterally or bilaterally, is found in some horses with EPM

Facial Expression and Movement (Medulla, Cranial Nerve VII) Normal facial tone, expression, and movements are dependent on the integrity of the facial nerves The effects of interruption of this motor pathway depend on the site of damage • Drooping of the ear and lip, ptosis, and collapse of the nostril, and the muzzle is pulled toward the normal side. Saliva often drools from the affected side of the mouth, and the horse has difficulty prehending food, especially grain. There may be exposure keratitis secondary to eyelid paralysis.

Balance and Equilibrium, Hearing (Medulla, Cranial Nerve VIII)

The vestibular system showing afferent input from the inner ear via cranial nerve VIII to the vestibular nuclei in the hindbrain

There is complex integrated output to the cranial nerves controlling extraocular muscles (III, IV, and VI), the cerebellum, and the trunk and limbs (vestibulospinal tracts)

The cerebellum regulates and smoothes motor activity initiated by the UMN system Maintain equilibrium and appropriate body posture during rest and motion Cerebellar disease is usually diffuse and manifests as symmetric ataxia without weakness Limbs may appear spastic with excessive (hypermetric) or inadequate (hypometric) flexion during protraction

With diffuse cerebellar cortical disease, the menace response is absent, although vision is normal

Upper Motor Neuron (Muscle Tone and Voluntary Movement) Interruption of UMN tracts in the spinal cord causes signs of ipsilateral weakness of the trunk and limbs Signs of paresis range in severity from slight toe-dragging and delayed protraction, to recumbency and inability to rise UMN disease (in the spinal cord) include • EPM, equine degenerative myeloencephalopathy, spinal cord abscess or tumor, and aberrant parasite migration

In keeping with the basic principles of neuroanatomic localization • UMN lesions from C1 to T2 (inclusive) • May cause neurologic signs in all four limbs • lesions from T3 to S2 • Only affect the pelvic limbs • Lesions caudal to S2 • Do not directly affect gait • With external compression of the cervical spinal cord (as in CSM) • Signs are typically worse in the pelvic limbs than in the thoracic limbs

Lower Motor Neuron and Spinal Cord Reflexes Abnormalities of LMN (in gray matter, ventral root, peripheral nerve, or neuromuscular junction) manifest as • Flaccid muscle weakness (paresis, paralysis) with hypotonia and hyporeflexia. • Within 1 to 2 weeks, muscle atrophy is noticeable • Neurogenic muscle atrophy progresses rapidly

Note that neurogenic atrophy is a consequence only of LMN disease UMN involvement results in weakness without atrophy Examples of conditions that affect the LMN in horses are • Botulism (neuromuscular junction), trauma, ischemia associated with recumbency, neuritis of the cauda equina/polyneuritis equi, EPM, postanesthetic myelomalacia, and equine motor neuron disease.

Proprioception Proprioceptive pathways

Spinocerebellar tracts  Cerebellum

Regulating posture, muscle tone, locomotion, and equilibrium

Somesthetic sensory cortex  Midbrain and thalamus

Interruption of spinal cord proprioceptive pathways interferes with recognition by the brain of the positions in space of the body and limbs • Ataxia (incoordination)

Signs of proprioceptive deficit in the horse include • Base-wide or base-narrow limb placement • Swaying of the trunk and torso during walking (but not usually at rest) • Overstriding, especially in the pelvic limbs

Urination Parasympathetic LMNs to the bladder’s smooth muscle (detrusor) • Supplies autonomic innervation to the smooth muscle of the bladder and rectum

Sympathetic LMNs to the bladder • Supplies smooth muscle in the body and neck of the bladder and proximal urethra

Centers in the midbrain and hindbrain receive sensory information from the bladder andmodulate reflex activity via UMNs Forebrain influence on these centers is responsible for initiation of voluntary voiding

In horses with severe spinal cord disease cranial to S2, there may be loss of voluntary control of urination

Defecation The smooth muscle of the rectum and anus is innervated by postganglionic parasympathetic neurons in a way that parallels that described for the bladder Innervation of striated muscle of the anus is provided by the pudendal nerve Spinal cord lesions cranial to S2 are unlikely to affect defecation

Involvement of the sacral segments results in rectal obstipation and may cause colic

Sensation Sensory information from pain, thermal, and touch receptors is conveyed to the spinal cord by peripheral nerves, spinal nerves, and dorsal roots Branches pass several segments both cranially and caudally from the site of spinal cord penetration and terminate on spinothalamic neurons or interneurons involved in spinal reflexes The flexor (withdrawal) reflexes require only sensory nerves, contiguous spinal cord segments, and LMNs

The nervous system of a horse

The relationship between sensory, relay and motor neurons



























Anatomy and physiology of the nervous system  
Anatomy and physiology of the nervous system