The nervous system is composed of billions of neurons with long, interconnecting processes that form complex integrated electrochemical circuits. It is through these neuronal circuits that animals experience sensations and respond appropriately.
Neuronal processes that transmit electrical alterations to the cell body are called dendrites. Dendrites have receptor sites that receive stimulation or inhibition from outside sources. If electrical stimulation of the cell body reaches a critical threshold, an electrical discharge called an action potential develops. The action potential spontaneously travels away from the cell body along an outgoing process called an axon. When the action potential reaches the terminal branches of the axon, chemicals called neurotransmitters are released. Neurotransmitters either stimulate or inhibit receptor sites on other neurons, muscles, or glands. Although neurons may have a variety of shapes, each one has dendrites, a cell body, and an axon, and releases neurotransmitters.
Basic Sensory and Motor Functions
The peripheral nervous system (PNS) is formed by neurons of the cranial and spinal nerves. The central nervous system (CNS) is formed by neurons of the spinal cord, brain stem, cerebellum, and cerebrum.
Groups of neuronal cell bodies in the PNS are called ganglia, while those in the CNS are called nuclei. Nuclei form the CNS gray matter. Groups of axons in the CNS form the white matter and are arranged into tracts. The tracts are usually named after their site of origin and termination (eg, the spinocerebellar tract begins in the spinal cord and ends in the cerebellum).
PNS sensory or afferent neurons carry information such as nociception, proprioception, touch, temperature, taste, hearing, equilibrium, vision, and olfaction to the spinal cord or brain stem. CNS sensory neurons carry information to the cerebellum, brain stem, and cerebrum for further interpretation. Important spinal cord and brain-stem sensory tracts include several spinocerebellar, spinothalamic, and spinoreticular tract systems. The spinoreticular tracts begin in the spinal cord and terminate in the reticular formation of the medulla. The fasciculus gracilis and cuneatus of the spinal cord and the medial and lateral lemniscus of the brain stem are also important sensory tracts. In animals, these sensory tracts may carry fibers from many sensory modalities such as proprioception, nociception (pain), and touch. An alteration in sensation may be due to either CNS or PNS disease.
Reactions to sensory inputs are initiated by efferent or motor neurons in the cerebrum and brain stem called upper motor neurons (UMN). The UMN axons descend to brain stem and spinal cord segments in tracts named after their site of origination and termination.
The UMN of the reticulospinal tracts (from midbrain, pons, and medulla oblongata reticular formation) and the rubrospinal tract (from midbrain) are important for voluntary movements of skeletal muscles in domestic animals. The rubrospinal tract mainly functions to facilitate flexors of the limbs, while the pontine and medullary reticulospinal tracts have either a facilitative (pontine) or inhibitory (medullary) effect on the extensors. The corticospinal tracts (cell bodies in the cerebral cortex) are most important for voluntary movement in primates. Domestic animals with severe cerebrocortical disease may suffer only transient loss of voluntary movements because their corticospinal tract has limited influence.
The reticulospinal and vestibulospinal tracts (from vestibular nuclei of the medulla oblongata) supply extensor skeletal muscle activity used to support the body. Knowledge of location and function of sensory and motor brain stem and spinal tracts is essential for localizing nervous system lesions and determining their severity. Mild spinal cord compression affects the superficial spinal cord tracts, eg, spinocerebellar and vestibulospinal tracts, so initial signs include ataxia and extensor weakness. Important voluntary motor tracts are located in the lateral portions of the spinal cord deep to the spinocerebellar tracts, and paresis or paralysis develops with moderate spinal cord compression. Because many tracts are involved, loss of nociception from the periosteum of the toes and tail (deep pain) occurs when spinal cord lesions are bilateral and severe. This loss of nociception is also an indicator of severe cord injury because those fibers that transmit deep pain are typically nonmyelinated, slow transmitting C type fibers, which are very resistant to pressure.
Motor neurons with cell bodies in the brain stem, and spinal cord gray matter and axons that travel in the PNS cranial and spinal nerves, respectively, are referred to as lower motor neurons (LMN). Injury to either the UMN or LMN results in paresis or paralysis. Brain-stem and spinal cord reflexes are the phylogenetically oldest responses of the nervous system. When the eyelid is touched, it closes; when the toe is pinched, the limb withdraws before conscious perception intervenes. Only a sensory neuron in the PNS, a connector (internuncial) neuron in the CNS, and a LMN are necessary for a reflex to be present. In a monosynaptic reflex (eg, patellar reflex), only a sensory neuron and LMN are present. During the neurologic examination (see Nervous System Introduction: Physical and Neurologic Examinations), testing brain-stem and spinal reflexes is helpful to localize CNS and PNS lesions to specific areas. If a reflex is depressed or absent, a lesion must involve the sensory nerve, internuncial neuron, or LMN at that particular site.
The autonomic nervous system is divided into sympathetic and parasympathetic portions and controls activity in smooth and cardiac muscles and glands. Visceral afferent (sensory) neurons travel in cranial and spinal nerves and sensory spinal cord tracts to the thalamic and hypothalamic regions of the brain stem. UMN in the hypothalamus descend to LMN cell bodies of the brain-stem nuclei and to the intermedio-lateral gray matter of the spinal cord.
LMN of the sympathetic nervous system exit through thoracolumbar spinal nerves (T1 to L4) to affect smooth muscles associated with the pupils, eyelids, orbits, hair follicles, blood vessels, and thoracic and abdominal viscera. Horner's syndrome (ptosis, miosis, and enophthalmos) is a common finding associated with loss of sympathetic innervation to the eye.
LMN of the parasympathetic nervous system exit via cranial nerve (CN) III to innervate smooth muscle of the pupils and eyelids, CN VII to the lacrimal and salivary glands, CN IX to salivary glands, and CN X to cardiac muscles and glands and to smooth muscles of all the thoracic and abdominal viscera to the level of the transverse colon. LMN of the parasympathetic nervous system also exit through the sacral segments to all the viscera of the caudal abdomen, including the bladder and colon. Sacral lesions commonly result in loss of the urinary bladder (detruser) reflex.
Divisions and Effects of Lesions
Also see Nervous System Introduction: The Neurologic Evaluation. The PNS consists of 26 or more pairs of spinal nerves that correspond to each spinal cord segment and 12 pairs of cranial nerves that correspond to specific brain and brain-stem segments.
The PNS spinal nerves form the brachial plexus to the thoracic limb; the lumbosacral plexus to the pelvic limb; and the cauda equina to the bladder, anus, and tail. Brachial or lumbosacral plexus lesions cause paresis or paralysis of a thoracic or pelvic limb, respectively, with reduced or absent spinal reflexes and sensation of the limb. (see Limb Paralysis.) Cauda equina lesions result in an atonic bladder; a dilated, unresponsive anus; and a flaccid, paralyzed tail.
Lesions of all spinal nerves (eg, acute polyradiculoneuritis) result in paresis or paralysis of all 4 limbs (quadriparesis or quadriplegia, respectively) with depressed or absent spinal reflexes and altered sensation of the limbs. Lesions restricted to PNS cranial nerves result in deficits associated with dysfunction of that particular nerve and no signs of dysfunction in the limbs or other parts of the nervous system.
The spinal cord of dogs and cats is divided into 8 cervical, 13 thoracic, 7 lumbar, 3 sacral, and 5 or more caudal segments. Horses and cows have 6 lumbar and 5 sacral segments, and pigs have 6–7 lumbar and 4 sacral segments. Spinal cord lesions from T2 to L7 (L6 in horses, cattle, and pigs) produce paresis or paralysis of the pelvic limbs (paraparesis and paraplegia, respectively). Lesions from T2 to L3 cause pelvic limb ataxia, conscious proprioceptive deficits, and paresis and paralysis with normal or exaggerated spinal reflexes (UMN signs). Pelvic limb sensation caudal to the lesion may also be depressed or absent.
Spinal cord lesions from L4 to S2 cause pelvic limb ataxia, conscious proprioceptive deficits, and paresis or paralysis with depressed or absent spinal reflexes and muscle tone (LMN signs). Sensation may also be depressed or absent below the lesion.
Spinal cord lesions from C1 to C5 cause hemiparesis or hemiplegia (paresis or paralysis of the limbs on one side), or quadriparesis. Spinal reflexes in all 4 limbs are often preserved. In intramedullary spinal cord lesions extending from C6 to T2, thoracic limb spinal reflexes are depressed or absent. Severe lesions cause quadriplegia and may cause respiratory distress or arrest due to involvement of the UMN to respiratory muscles.
The brain stem is divided from caudal to rostral into 4 segments: the medulla oblongata (myelencephalon), the pons (metencephalon), the midbrain (mesencephalon), and the thalamus and hypothalamus (diencephalon).
Lesions of the medulla oblongata cause conscious proprioceptive deficits and weakness on the same side (ipsilateral) or both sides with normal or hyperactive limb reflexes similar to cervical spinal cord lesions. However, involvement of CN nuclei IX, X, XI, or XII localizes the lesion to the caudal medulla oblongata. Involvement of CN nuclei VI, VII, or VIII localizes the lesion to the rostral medulla oblongata. It is rare to have a lesion of the medulla oblongata that does not affect one or more of the cranial nerves as well as sensory and motor tracts.
Pontine lesions cause ipsilateral conscious proprioceptive deficits, hemiparesis or quadriparesis with normal or hyperactive limb reflexes, mental depression from involvement of the ascending reticular activating system (ARAS), and CN V deficits.
Midbrain (mesencephalon) lesions cause contralateral conscious proprioceptive deficits and hemiparesis. CN III nucleus involvement is present on the ipsilateral side and localizes the lesion to the midbrain. In large midbrain lesions, the ARAS is affected, and the animal will be stuporous or comatose. If the sympathetic UMN and parasympathetic LMN are both affected in the midbrain, the pupils will be midrange size and unresponsive to light.
Diencephalic lesions can be difficult to differentiate from cerebral cortical lesions, because many tracts going to and from the cerebrum pass through the diencephalon. The thalamus, hypothalamus, and subthalamus of the diencephalon have many important structures that alter feeding, drinking, sexual, sleeping, and other behaviors, as well as regulate body temperature. The pituitary gland, which controls many hormonal functions of the body, is connected to the hypothalamus. The ARAS projects through the subthalamus area, in which lesions also produce stupor or coma.
The cerebellum is part of the metencephalon and is attached to the dorsal surface of the pons and medulla by rostral, middle, and caudal cerebellar peduncles. The cerebellum coordinates all muscle activity and establishes muscle tone. The flocculonodular lobe of the cerebellum has equilibrium functions. Unilateral lesions of the cerebellum cause ipsilateral dysmetria (hypermetria or hypometria) and a contralateral (paradoxical) head tilt. Bilateral lesions of the cerebellum cause generalized incoordination of the head and limbs, head tremors, and generalized disequilibrium.
The telencephalon, also called the cerebral cortex, is divided into the neocortex, paleocortex, and archicortex. The paleocortex and archicortex include the olfactory and limbic regions, which provide smell and emotional reactions to all stimuli. The neocortex is divided into the frontal, parietal, occipital, and temporal lobes. The frontal cortex functions include intelligence and fine motor skills (corticospinal tract). Lesions in this area cause dementia, lack of recognition of the owner, difficulty in training, compulsive pacing, circling toward the lesion (adversion syndrome), and motor seizures with contralateral involuntary muscle twitching. Contralateral hopping and placing deficits are also found with frontal lobe lesions. Ascending and descending tracts to and from the frontal lobe form the internal capsule through the region of the basal nuclei and diencephalon. Lesions of the internal capsule can produce the same signs as frontal lobe lesions. The parietal lobe (somesthetic cortex) is for interpretation of general perception, nociception, temperature, and pressure.
Occipital lobe and optic radiation lesions result in blindness with pupils that respond normally to light. Unilateral occipital lobe and optic radiation lesions result in some degree of visual loss in the contralateral eye depending on the percentage of crossover of the optic nerve fibers in the optic chiasm of the species (65% in cats; 75% in dogs; 80–90% in cattle, horses, pigs, and sheep). The pupils still respond normally to light. Blindness with pupils that do not respond to light is associated with lesions of the retina, optic nerve, optic chiasm, or rostral optic tract.
Difficulty in localizing sound may occur with temporal lobe lesions, as may psychomotor seizures characterized by hysterical running. “Fly-biting” or “star gazing” hallucinations are suspected to occur with lesions in the temporal-occipital region. Aggression occurs when the pyriform area (paleocortex) of the temporal lobe and the underlying amygdaloid nucleus are affected. Aggression can also occur with hypothalamic lesions.
Lesions of the olfactory region may alter feeding or sexual behavior. Slow-growing lesions of the cerebrum and diencephalon often result in few clinical signs due to the adaptability of functions in these areas in animals.
Mechanisms of Disease
Disease processes affecting the nervous system may be congenital or familial, infectious or inflammatory, toxic, metabolic, nutritional, traumatic, vascular, degenerative, neoplastic, or idiopathic.
Congenital disorders may be obvious at birth or shortly after (eg, an enlarged head from hydrocephalus or an uncoordinated gait from an underdeveloped cerebellum). Some familial disorders (eg, lysosomal storage diseases) cause a progressive degeneration of neurons in the first year of life, while others (eg, inherited epilepsy) may not manifest for 2–3 yr. (Also see Congenital and Inherited Anomalies of the Nervous System.)
Infections of the nervous system are due to specific viruses, fungi, protozoa, bacteria, rickettsia, prions, and algae. Noninfectious inflammations such as steroid-responsive meningoencephalomyelitis and granulomatous meningoencephalomyelitis may be immune-mediated.
Toxicity of the nervous system is most frequently caused by organophosphates (see Insecticide and Acaricide (Organic) Toxicity: Organophosphates (Toxicity)), pyrethrins (see Insecticide and Acaricide (Organic) Toxicity: Insecticides Derived from Plants (Toxicity)), carbamates (see Insecticide and Acaricide (Organic) Toxicity: Carbamate Insecticides (Toxicity)), bromethalin (see Rodenticide Poisoning: Bromethalin), metaldehyde (see Metaldehyde Poisoning), ethylene glycol (see Ethylene Glycol Toxicity), metronidazole (see Antibacterial Agents: Nitroimidazoles), theobromines (see Food Hazards: Chocolate), sedatives, and anticonvulsants (eg, phenobarbital, bromide). Botulinum, tetanus, and tick toxins, as well as coral and certain other snake venom intoxications, cause neurologic signs.
Metabolic alterations of nervous system function most commonly result from hypoglycemia, hypoxia or anoxia, hepatic dysfunction, hypocalcemia, hypomagnesemia, hypernatremia, hypokalemia, and uremia. Hypothyroidism, hyperthyroidism, hypoadrenocorticism, and hyperadrenocorticism are endocrine disorders that can cause neurologic dysfunction.
Thiamine deficiency results in ataxia, stupor, and coma or seizures in dogs, cats, and cattle. Deficiency of vitamin B6 may cause seizures.
Trauma to the PNS and CNS causes focal and multifocal neurologic signs from physical damage, hemorrhage, edema, and progressive formation of oxygen-containing free radicals and nervous system destruction that is usually complete in 24–48 hr.
Vascular lesions of animals are usually due to septicemia and bacterial embolization of the CNS. Fibrocartilaginous embolization of the spinal cord is common in dogs. Arteriovenous malformations occur occasionally and cause spontaneous hemorrhages. Cerebrovascular disease from arteriosclerosis is rare in domestic animals but has been associated with hypothyroidism. Cerebrovascular disease from hypertension is rare.
Familial degeneration of neurons occurs in lysosomal storage disorders. Degeneration of intervertebral disks that subsequently herniate into the vertebral canal often produces paresis and paralysis in dogs.
Neoplasms of the CNS and PNS are most common in dogs and cats. Astrocytes, oligodendrocytes, and microglia can all become neoplastic and form astrocytomas, oligodendrogliomas, and gliomas. Ependymal cells and the choroid plexus, which line the internal cavities of the CNS and produce CSF, also can become neoplastic and form ependymomas and choroid plexus papillomas. Meningeal cells of the dura, arachnoid, and pial membranes form meningiomas, which are common in dogs and cats. Neurofibrosarcomas are common tumors of the nerve sheaths of peripheral nerves in dogs. Lymphosarcoma is a common metastatic tumor of the PNS and CNS in dogs, cats, and cattle. Hemangiosarcoma is the most common metastatic tumor of the canine CNS. (Also see Neoplasia of the Nervous System.)
The idiopathic mechanism of disease is reserved for described syndromes with characteristic clinical signs, predictable outcomes, and no known necropsy findings.
Last full review/revision July 2011 by Thomas Schubert, DVM, DACVIM, DABVP