Nervous Dysfuntion- Priniciples and Clinical Manifestation

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Introduction to Nervous Dysfuntion- Priniciples and Clinical Manifestation:

The functions of nervous system are directed at the maintenance of body’s spatial relationship with its environment.
These functions are performed by several divison of nervous system, including the following:
- Sensorimotor system: It is responsible for maintenance of normal posture and gait
- Autonomic nervous system: It controls the activity of smooth muscle and endocrine glands and thus internal environment of the body.
- Sensory system of special senses
- Psychic system: It controls the mental state of animal.
Nervous system is reactive gear system which reacts to external and internal stimuli and translates them into activity and consciousness. This translation is dependent on integrity of both the afferent and efferent pathways.
The integrative function of nervous system with musculoskeletal system, makes difficult to determine in sick animals whether the abnormalities are present in nervous system, musculoskeletal system or acid-base, electrolyte and energy status.
Nervous system itself is dependent on other body system, mainly cardiovascular system. Inadequate oxygen delivery caused by cardiovascular disease leads to altered cerebral function because of dependence of brain on oxygen supply.

Disease in nervous system is categorized into two parts; primary disease and secondary disease. Primary disease of nervous system is largely associated with anatomy and have long-range serious consequences. Secondary disease of nervous system is more likely to be functional in early stages and are responsive to treatment.

The clinical findings that should arouse suspicion of neurologic disturbance include abnormalities in the three main functions of the system:

Posture and gait:

Animal’s ability to maintain normal posture and to walk normally depends on tone of skeletal muscle but also on efficiency of postural reflexes.
Abnormalities in posture and gait are best indicator of nervous disorder as they are largely governed by nervous system
However, its assessment in animals is of great inaccuracy because of inability to request complete voluntary relaxation by patient.

Sensory perceptivity:

Test of sensory perception in animals is only objective and never subjective as in case of human.
Any test used is heavily based on integrity of motor system.

Mental state:

Depression or enhancement of the psychic state is not difficult to judge, particularly if the animal’s owner is observant and accurate.
The difficulty usually lies in deciding whether the abnormality is caused by primary or secondary changes in the brain.

Principle of Nervous Dysfunction:

Nervous dysfunction can be broadly categorized into two forms; depressed activity and exaggerated activity.
These can be further divided into four common modes of nervous dysfunction: excitation (irritation) signs, release of inhibition signs, paresis or paralysis caused by tissue damage and nervous shock.

Excitation (irritation) signs:

Increased activity of nervous system is due to increase in number of received nerve impulse either due to excitation of neurons or because of facilitation of passage of stimuli.
Excitability of neurons can be increased by many factors such as stimulant drugs, inflammation, mild degree of those influences which in greater amount causes depression of nervous system. Ex: early or mild hypoxia may cause nervous excitation but sustained hypoxia may cause depression of function or even death of nerve cell.
Irritation phenomena may result from inflammation of nervous tissue associated with bacteria, virus, fungi, certain nerve poisons, hypoxia and edema.
The major manifestations of irritation of nervous tissue are tetany, local muscle tremor, and whole-body convulsions in the motor system and hyperesthesia and paresthesia in the sensory system.

Release of inhibition signs:

Exaggeration of normal nervous system activity occurs when lower nervous centers are released from the inhibitory effects of higher centers.
The classic example of a release mechanism is experimental decerebrate rigidity caused by transection of the brainstem between the colliculi of the midbrain. This results in an uninhibited extensor tonus of all the antigravity muscles. The head and neck are extended markedly in a posture of opisthotonus, and all four limbs in the quadruped are extended rigidly.
Cerebellar ataxia is another example of inhibitory release. In the absence of cerebellar control, combined limb movements are exaggerated in all modes of action including rate, range, force, and direction.

Paresis or paralysis caused by tissue damage:

Depression of activity can result from depression of metabolic activity of nerve cells, and the terminal stage is complete paralysis when nervous tissue is destroyed.
Such depression of activity may result from failure of supply of oxygen and other essential nutrients, either directly from their general absence or indirectly because of failure of the local circulation.
Infection of the nerve cell itself may cause initial excitation, then depression of function, and finally complete paralysis when the nerve cell dies.
Signs of paralysis are constant and are manifested by muscular paresis or paralysis when the motor system is affected and by hypoesthesia or anesthesia when the sensory system is involved.

Nervous Shock:

Acute lesion of nervous system causes damage to nerve cells in immediate area of lesion, but there may be a temporary cessation of function in parts of nervous system not directly affected. These loss of function is temporary and usually persist for only a few hours.
Stunning is obvious example. Recovery from the flaccid unconsciousness of nervous shock may reveal the presence of permanent residual signs caused by the destruction of nervous tissue
Determining type of lesion is difficult because of limited ranges of modes of reaction to injury in nervous system.
For ex: Irritation signs may be caused by bacterial or viral infection, by pressure, by vascular disturbance or general hypoxia, by poisons or hypoglycemia.
Degenerative lesions produce mainly signs of paresis or paralysis but unless there are signs of local nervous tissue injury, such as facial nerve paralysis, paraplegia, or local tremor

Clinical Manifestation of Disease of Nervous System:

The major clinical signs of nervous system dysfunction include following:

Altered mentations
Involuntary movements
Abnormal posture and gait
Paresis or paralysis
Altered sensation
Blindness
Abnormalities of autonomic nervous system

Altered mentations:

These includes excitation states, depressive state, head pressing or compulsive walking and aimless wandering.

Excitation states:

It includes mania, frenzy, and aggressive behaviour. These are the manifestation of general excitation of cerebral cortex.
The frontal lobes, temporal cortex, and limbic system which governs behaviour, intellect and individuality are highly susceptible to influences such as hypoxia and increased intracranial pressure.
Mania:
- In this form, animal acts in bizarre way and appears to be unaware of its surroundings.
- Maniacal actions include licking, chewing of foreign material, abnormal voice, constant bellowing, apparent blindess, walking into strange surroundings, drunken gait, and aggressiveness in normally docile animals.
- Mental disorientation is an obvious component of mania
- Disease characterized by mania includes:
  - Encephalitis; eg: furious form of rabies, Aujeszky’s disease in cattle
  - Degenerative disease of brain; mannosidosis, early PEM, poisoning by Astragalus sps.
  - Toxic and metabolic disease of brain; nervous ketosis, pregnancy toxemia, acute lead poisoning, poisoning with carbon tetrachloride, severe hepatic insufficiency in horse
- Frenzy:
  - It is characterized by violent activity with little regard to surroundings.
  - Animal’s movements are uncontrollable and dangerous to other animals in group and human attendants.
  - It is often accompanied by aggressive physical attacks
  - It is observed in diseases like;
    - Encephalomyelitis; Aujeszky’s disease
    - Toxic and metabolic disease of brain; hypomagnesemic tetany of cattle and sheep, poisoning with ammoniated roughages in cattle
    - Acute pain of colic in horses
    - Extreme cutaneous irritation; photosensitization in cattle

Aggressive behaviour:
- Aggression and willingness to attack other animals, human and inert object is early clinical signs of rabies, Aujeszky’s disease, postparturient hysteria in sows
- It is often difficult to differentiate between an animal with a genuine change in personality and one that is in pain or is physically handicapped
- Aggressive behaviour is also seen in cow and mare with granulosa cell tumor of ovary. It is accompanied by signs of masculinization and erratic or continuous tumors.

Depressive States:

It includes somnolence, lassitude, narcolepsy/catalepsy, syncope and coma.
These all forms are clinical manifestation of depression of cerebral cortical function in various degrees and occur as a result of those influences that depress nervous system function generally, as well as those that specifically affect behavior, probably via the limbic system.

Depression leading to coma: In all species this may result from:
- Encephalomyelitis and encephalomalacia
- Toxic and metabolic disease of brain such as uremia, hypoglycemia, hepatic insufficiency, toxemia, septicemia and most toxins that damage nervous tissue
- Hypoxia of brain
- Heat stroke
- Specific poisons that cause somnolence, including bromides, amitraz in horses, methyl alcohol, Filix mas (male fern), and kikuyu grass

Syncope:
- It is another word for sudden fainting or passing out.
- It occurs as result of following:
  - Acute circulatory and heart failure leading to acute cerebral hypoxia
  - Spontaneous cerebral hemorrhage
  - Traumatic concussion and contusion
  - Lightning strike, electrocution

Narcolepsy/Catalepsy:
- Affected animals experience episodes of uncontrollable sleep, and literally “fall” asleep.
- It is recorded in Shetland ponies and thought to be inherited in them, and in cattle.

Compulsive walking or head pressing:

Head pressing is a syndrome characterized by animal pushing its head against fixed objects and into corner of pen as well as leaning into stanchion or between fence post.
In compulsive walking, animal lower its head and walk slowly while appearing blind. If they walk into object, they lean forward and indulge in head-pressing. It should be differentiated from head pressing
It is observed in following cases:
- Toxic and metabolic brain disease, especially PEM, and hepatic encephalopathy
- Increased intracranial pressure
- Encephalomyelitis

Aimless wandering:

It is similar to compulsive walking but less severe form
There is severe mental depression, protrusion of tongue, continuous chewing movements,
Causes of this form includes:
- Toxic and metabolic disease of brain, including poisons by Helichrysum sp. and tansy mustard
- Degenerative brain disease; hydrocephalus in new born, ceroid lipofuscinosis in sheep, nigropallidal encephalomalacia in horse

Involuntary Movements:

These movements are caused by involuntary muscle contractions, which includes gradations from fasciculations, shivering and tremor to tetany, seizures, convulsions
Opisthotonus is sustained spasm of neck and limb muscles resulting in dorsal and caudal extension of head and neck with rigid extension of limbs

Tremor:

It is continuous, repetitive twitching of skeletal muscles that is usually visible and palpable.
The muscle units involved may be small and cause only local skin movement, in which case the tremor is described as fasciculations; or the muscle units may be extensive and the movement much coarser and sufficient to move the extremities, eyes, or parts of the trunk.
Tremor may become intensified when animal takes some positive action. It usually indicates cerebellar involvement.
True tremor is sufficient to cause incoordination and severe disability in gait.
Tremor may occur due to following causes:
- Diffuse disease of cerebrum, cerebellum and spinal cord
- Degenerative disease of nervous system; hypomyelinogenesis of newborn as in congenital tremor in pigs, poisoning by Swainsona sps.
- Toxic nervous disease caused by large number of poisons, especially poisonous plants and fungi, Clostridium botulinum toxin in shaker foal syndrome, early stages of hypocalcemia in cows

Tics:

These are spasmodic twitching movements made at much longer interval than in tremor
It usually lasts for few seconds and often much longer
These movements are easily visible and caused by muscles that are ordinary under voluntary control.
Rare in large animals but occurs after traumatic injury to spinal nerve.

Tetany:

It is sustained contraction of muscle without tremor.
Most common causes are Clostridium tetani intoxication following localized infection with organism.
Limbs are rigid and cannot be flexed passively (“lead pipe” rigidity)
Myoclonus is brief, intermittent tetanic contraction of skeletal muscle that results in entire body being rigid for several seconds followed by relaxation.

Convulsions:

Convulsion, seizures, fits or ictus are violent muscular contraction affecting body part or whole body.
It occurs for relatively short period of time.
These are result of abnormal electrical discharge in forebrain neurons that reach somatic and visceral motor areas, and initiate spontaneous, paroxysmal involuntary movements.
Typical convulsion has a prodromal phase, in which animal becomes restless then convulsion begins in localized part which soon spreads to whole body, when animal usually falls to ground thrashing rhythmically.
Following convulsion, there may be temporary blindness which may last for several minutes upto few hours.
Convulsion may be clonic or tonic. In clonic convulsion there is paddling movement (involuntary movement of muscle in which there is repeated muscle spasm with period of relaxation). In tonic or tetanic convulsion, there is prolonged muscular spasm without intervening period of relaxation. These type of convulsion are rare.
Convulsion can originate from disturbances anywhere in prosencephalon, including cerebrum, thalamus, or even hypothalamus alone.
Initiating cause of convulsion may be outside cranium or inside cranium, so they are divided into two types; intracranial convulsion or extracranial convulsion
Intracranial convulsion is caused by:
- Encephalomyelitis, meningitis
- Encephalomalacia
- Acute brain edema
- Brain ischemia, including increased intracranial pressure
- Local lesion caused by trauma (concussion, contusion), abscess, tumor, parasitic injury, hemorrhage
- Inherited idiopathic epilepsy
Extracranial convulsion are caused by brain hypoxia, as in acute circulatory or cardiac failure, toxic and metabolic disease of nervous system, including following:
- Hepatic encephalopathy
- Hypoglycemia
- Hypomagnesemia
- Inorganic poisons, poisonous plants, and fungi
- Congenital and inherited defects without lesions

Involuntary spastic paresis:

Involuntary, intermittent contraction of large muscle mass may result in spasmodic movement of individual limbs or part of body.
In most cases, contraction occurs when voluntary movement is attempted.
Disease in this category includes:
- Stringhalt of horses
- Inherited spastic paresis of cattle
- Inherited periodic spasticity of cattle
- Inherited congenital myotonia of cattle
- Inherited myotonia of goats

Abnormal Posture and Gait:

Posture:

It is evaluated when animal is at rest.
Abnormal posture may be adopted by animals in intermittent pains. In case of nervous disease, abnormality is usually continuous and repeatable.
Deviation of the head and neck from the axial plane or rotation of the head and neck from the horizontal plane (head tilt); drooping of the lips, eyelids, cheeks, and ears; and opisthotonus and orthotonos.
Head pressing and dog-sitting posture are also example of abnormal posture
Abnormalities in posture and gait are due to lesion in brainstem, cerebellum, all levels of spinal cord, spinal nerve, peripheral nerve, neuromuscular junction and muscles.
Clinical emphasis is on vestibular disease, cerebellar disease and spinal cord disease.
- Vestibular disease:
  - Vestibular system assist animal in maintenance of orientation in its environment with respect to gravity.
  - It helps to maintain position of eyes, trunk, limbs in relation to movement and positioning of head.
  - General signs of vestibular system dysfunction are staggering, leaning, rolling, circling, drifting sideways when walking and a head tilt, and various changes in eye position such as strabismus and nystagmus.
  - Causes of vestibular disease includes following:
    - Otitis media interna
    - Focal lesion at vestibular nucleus
    - Traumatic injury to vestibular apparatus in horse

Gait:

Gait is assessed when the animal is moving. Neurological gait abnormalities have two components; ataxia and weakness

Weakness

Weakness (paresis) is evident when animal drags its limbs, has worn hooves, or has low arc to swing phase of the stride.
When animal bears weight on affected limb, limb often trembles and animal may even collapse on that limb due to lack of support.
While circling, walking on a slope, and walking with the head elevated, an animal frequently will stumble on a weak limb and knuckle over at the fetlock.

Ataxia:

It is unconscious, proprioceptive deficit causing incoordination when animal moves.
It is manifested as swaying from side to side of the pelvis, trunk, and sometimes whole body.
Ataxia may also appears as weaving of affected limb during swing phase of stride. It results in abducted or adducted foot placement, crossing of limbs or stepping on opposite foot.
Hypermetria: It is defined as increased range of movement and seen as overreaching of limbs with excessive joint movements. Hypermetria without paresis is characteristics of spinocerebellar and cerebellar disease.
Hypometria: It is defined as decreased range of movement characterized by stiff or spastic movement of limbs with little flexion of the joints, particularly carpal and tarsal joints.
Dysmetria: It includes both hypometria and hypermetria. Goose stepping is most common sign. It is caused due to lesion in cerebellum or cerebral pathway.

Cerebellar Disease:

Ataxia is seen when there is cerebellar dysfunction or abnormality in function of cerebellum
Ataxia refers to incoordination of limbs when animal moves
In typical cerebellar disease, ataxia of limbs is common and no weakness is evident.
In true cerebellar ataxia, animal stands with legs wide apart, sways and has tendency to fall.
Ataxia of head and neck are characterized by wide, swinging, head excursions, jerky head bobbing, and nodding of head.
The fault in placement of foot is the result of poor motor coordination and not related in any way to muscle weakness or proprioceptive deficit.
Examples of cerebellar disease includes the following:
- Inherited defects of cerebellar structure
- Congenital cerebellar defects resulting from maternal virus infection such as BVD in cattle
- Dysplastic disease of cerebellum of horse
- Traumatic injury; by parasitic larvae such as Hypoderma bovis, which has cause unilateral cerebellar ataxia in cattle
- Tremorgenic mycotoxicoses and ryegrasses
- Cerebellar degeneration in cattle caused by grazing of perennial shrub Solanum bonariense
- Encephalomyelitis

Spinal Cord Disease:

Spinal cord disease causing varying degrees of weakness, and ataxia are common in large animals
Weakness is caused by damage to upper and lower motor neurons and by proprioceptive deficit by damage to ascending sensory neurons
With a mild or even moderate cervical spinal cord lesion in an adult cow or horse, signs of ataxia and weakness may be evident in the pelvic limbs only, and it can be difficult to determine whether the thoracic limbs are involved.
Ataxia caused by cerebellar dysfunction can be difficult to differentiate from the proprioceptive defects and partial motor paralysis (weakness) that occur in animals with spinal cord lesions, and it is most important that this differentiation is made.
Signs of weakness or ataxia may be elicited by gently pushing the hindquarters to one side or pulling the tail to one side as the animal is walked (the sway response).
The normal animal resists these movements or steps briskly to the side as it is pushed or pulled.
The weak animal can be easily pulled to one side and may stumble or fall and may also tend to buckle or collapse when strong pressure is applied with the hand over the withers and loin regions. The ataxic animal may sway to one side, be slow to protract a limb, cross its hindlegs, or step on its opposite limb.
The ataxic animal may abduct the outside pelvic limb too far as it is pushed to one side or moved in a small circle. The pushed or circled animal may keep a clinically affected pelvic limb planted in one position on the ground and pivot around it without moving it.
Ataxia caused by spinal cord disease includes following:
- Limited trauma to spinal cord
- Early stage of developing compression lesion in vertebral canal
- Degenerative and inflammatory disease of nervous system.
- Functional disease in toxic and metabolic disease of nervous system that are caused mainly by poisons, especially plant materials.
- Typical examples are poisoning by the fungi Claviceps paspali, Diplodia spp., Acremonium lolii, the grass Phalaris aquatic, the ferns Zamia and Xanthorrhea spp., and herbaceous plants such as Kallstroemia, Vicia, Baccharis, Solanum, Aesculus, and Ficus spp.
- Heat stress in lambs
- Nutritional deficiency especially of thiamine, occurring naturally in horse poisoned by bracken and horsetail
- Developmental defects including congenital abnormalities and abiotrophic abnormalities that develop sometime after birth

Paresis and Paralysis:

Paralysis is a physiological result in all cases of motor nerve injury. Type of paralysis often indicative of the site of lesion
A lesion of upper motor neuron causes:
- Spasticity with loss of voluntary movement
- Increased tone of limb muscles
- Increased spinal reflexes
A lesion of lower motor neuron causes:
- Paresis or paralysis with loss of voluntary movement
- Decreased tone of limb muscles
- Absence of spinal reflexes
- Wasting of affected muscles (neurogenic atrophy)
Schiff–Sherrington syndrome:
- It is special form of paralysis common in dog but rarely recorded in large animals
- It is caused by acute, severe compressive injury of thoracolumbar spinal cord
- It is manifested by extensor rigidity or hypertonia of forelimbs and hypotonic paralysis of hindlimbs.
Paresis or weakness short of paralysis can be divided into four categories:
- Animals that cannot rise or support themselves, if held up but can make purposeful movements in attempting to rise
- Animals that cannot rise but support themselves if held up
- Animals that can rise but are paretic and can move the limbs well and stumble slightly on walking
- Animals that move with difficulty and have severe incoordination and stumbling
Examples of paresis and paralysis includes the following:
- Focal inflammatory, neoplastic, traumatic lesions in the motor pathway. These lesions usually produce an asymmetric nervous deficit
- Toxic and metabolic diseases of the nervous system in their most severe form, e.g., flaccid paralysis associated with tick bite (Ixodes holocyclus, Ornithodoros sp.), poisoning, botulism, and snakebite.
- Comparable tetanic paralyses include tetanus, lactation tetany of mares, and hypomagnesemic tetany of cows and calves.

Altered Sensation:

Lesions of the sensory system are rarely diagnosed in animals, except for those affecting sight and the vestibular apparatus
The animal’s response of licking or scratching does not make it possible to decide whether the diagnosis should be paresthesia or pruritus
Lesions of the peripheral sensory neurons cause hypersensitivity or decreased sensitivity of the area supplied by the nerve
Lesions of the spinal cord may affect only motor or only sensory fiber tracts or both, or may be unilateral.
Though it is difficult to decide whether failure to respond to a normally painful stimulus is caused by failure to perceive or inability to respond, certain test gives valuable information
Test usually used is pricking the skin with a needle, or pinching the skin with forceps, and observing reaction.
The “nibbling” reaction stimulated by stroking the lumbar back of sheep affected with scrapie is a striking example of hypersensitivity.
Absence of a response to the application of a painful stimulus to the limbs (absence of the withdrawal reflex) indicates interruption of the reflex arc; absence of the reflex with persistence of central perception, as demonstrated by groaning or body movement such as looking at the site of stimulus application, indicates interruption of motor pathways and that central perception of pain persists
Increased sensitivity is described as hyperesthesia, decreased as hypoesthesia, and complete absence of sensitivity is described as
Special cutaneous reflexes include the anal reflex, in which spasmodic contraction of the anus occurs when it is touched, and the corneal reflex, in which there is closure of the eyelids on touching the cornea.
The (cutaneous trunci) panniculus reflex is valuable in that the sensory pathways, detected by the prick of a pin, enter the cord at spinal cord segments T1-L3, but the motor pathways leave the cord only at spinal cord segments C8, T1, and T2. The quick twitch of the superficial cutaneous muscle along the whole back, which is the positive response (panniculus reflex), is quite unmistakable.

Blindness:

Blindess is manifested as clinical abnormality by the animal walking into objects that it should avoid.
Vision is cerebral cortical function and evaluated using pupillary light reflex and menace response.
Pupillary light reflex:
- It is present at birth in large animals but donot need an intact cerebral cortex.
- Ruminant with thiamine-responsive polioencephalomalacia may be blind but have intact pupillary light reflex.
- In contrast, ruminant with lead poisoning and cerebral dysfunction appear blind but have depressed or absent pupillary light reflex
- Pupillary light reflex measures the integrity of retina, optic nerve and chiasm, oculomotor and pretectal nuclei in midbrain and then to descending motor pathway that includes optic nerve, ciliary ganglion, and constrictor pupillae muscle.
Menace or blink response:
- It is used to test the integrity of entire visual pathway from retina, optic nerve to occipital lobe.
- A threatening gesture of the hand (or even better by the index finger in a pointing manner) toward the eye elicits immediate closure of the eyelids.
- The finger must come close enough to the eye without touching the tactile hairs of the eyelids or creating a wind that can be felt by the animal.
- It may be necessary to alert the patient to the risk of injury by touching the eyelids first.
- The menace response is a learned response that is absent in neonates. Most foals have a menace response by 9 days after birth and most calves by 5 to 7 days after birth.
- The most definitive test is to make the animal walk an obstacle course and place objects in front of it so that it must step over the objects easily.
- A similar procedure is the only way to test for night blindness (nyctalopia). The area should be dimly lit, but the observer should be able to see the obstructions clearly.
Blindness may be central or peripheral. Animal with forebrain lesion are centrally blind with depressed menace response in one or both eyes, whereas pupillary light reflex are intact
In peripheral blindness, such as hypovitaminosis-A, menace reflex is absent, and pupillary light reflex are also absent.
Blindness may be caused by following factors:
- Disease of orbit: Keratoconjunctivitis, hypopyon, cataract, panophthalmia, idiopathic retinal degenerative disease in cattle
- Disease of retina: Retinal dysplasia in goats, lenticular cataracts caused by poisoning with hygromycin in pigs, congenital ocular malformations in calves after intrauterine infection with BVD virus
- Disease of optic nerve and chiasma: Abscess of pituitary rete mirabile, constriction of optic nerve by diet deficient in vitamin-A, tumor of pituitary gland, injury to optic nerve,
- Metabolic or ischemic lesions of the cerebral cortex as in PEM, cerebral edema, and hydrocephalus
- Localized infectious or parasitic lesions caused by abscesses or migrating larvae
- Functional blindness in which there is complete, often temporary, apparent blindness in the absence of any physical lesions is seen. Causes are acetonemia, pregnancy toxemia, and acute carbohydrate indigestion (hyperd-lactatemia) of ruminants
- Specific poisonings causing blindness include F. mas (male fern), Cheilanthes spp. (rock fern), and rape. Stypandra spp. cause a specific degeneration of the optic nerves. Lead poisoning in cattle can also cause blindness.

Abnormalities in Autonomic Nervous System:

Lesion affecting parasymphathetic nervous system causes abnormality of pupillary constriction, salivation and involuntary muscular activity in upper part of alimentary tract and respiratory tract.
Lesion affecting sympathetic nervous system interfere with normal function of heart, and alimentary tract.
Central lesions of the hypothalamus can cause abnormalities of heat exchange, manifested as neurogenic hyperthermia or hypothermia and obesity but are of minor importance in farm animals
Autonomic imbalance is described as physiologic basis for spasmodic colic of horses; grass sickness of horses is characterized by degenerative lesions in the sympathetic ganglia; and involvement of the vagus nerve in traumatic reticuloperitonitis of cattle can lead to impaired forestomach and abomasal motility as well as the development of vagus indigestion.
The sacral segments of the spinal cord are the critical ones, and loss of their function will cause incontinence of urine and loss of rectal tone.
A spinal cord lesion may cause loss of the parasympathetic control and result in urinary retention.
When the sympathetic control is removed, incontinence occurs but bladder should empty. Similar disturbance in defecation occurs.