Veterinary Pathophysiology Student’s Lectures, 5th Semester

1

Veterinary PathophysiologyStudent’s Lectures, 5th Semester

Department of Internal Medicine,Faculty of Veterinary Science

Szent István University

PATHOPHYSIOLOGY OF THE NERVOUS SYSTEM

2

The brain comprises only 2% of the body's weight but receives 20% of the blood supply (cardiac output).Cerebral blood flow (CBF) = 50 ml / 100 g of brain / minute

CBF = CPP / CVR (cerebral perfusion pressure=CPP, cerebrovascular resistance=CVR)

cerebral blood flow (CBF)cerebral blood volume (CBV)cerebral energy metabolism (CEM)measured as cerebral metabolic rate of oxygen (CMRO2) measured as cerebral metabolic rate of glucose (CMRglu)

grey matter > white matter

CBF is the same between Part: 60 - 160 mmHg

Circulation of the brain

3

1. Metabolic control (or 'metabolic autoregulation') (pH, Pco2 adenosine, glycolytic intermediates, and extracellular potassium)

2. Pressure autoregulation 3. Chemical control (by arterial pCO2 and pO2) 4. Neural control (These neurons contain norepinephrine (NE)

and neuropeptide-Y (NPY), which are both vasoconstrictors. A second system consists of parasympathetic neurons in the sphenopalatine and otic ganglia. which contain acetylcholine (ACh) and often coexpress vasoactive intestinal peptide (VIP). The third consists of sensory fibers originating in the trigeminal ganglion. These contain substance P (SP) and calcitonin generelated peptide (CGRP), both of which are vasodilators.)

Regulation

CBF is lost: 10 s – faint!!!

4

Anatomy

circulus arteriosus cerebri,Circle of Willis

rete mirabile epidurale rostrale et caudale

a. carotis interna (bo.: a. maxill. int.)a. occipitalis – a. basilaris cerebri

a. vertebralisa. spinalis ventralis

5

PRIMARY STRUCTURAL CHANGES CAUSING CNS-MALFUNCTIONS

a. Inflammation of the brain and the spinal cordcauses: viruses, bacteria, parasites, fungi and toxic compounds

b. Necrosis of the tissuescauses: hypoxia, toxins, vitamin deficiency, hypoglycaemia, effects of lipid peroxides, accumulation of some compounds

c. Atrophy of the nervous tissuecauses: neoplasma, parasites, increased intracranial pressure, discus hernia

d. Bleedingcauses: capillary damage, embolism, trauma (epidural, subdural, cerebral petechia or haematoma)

e. Trauma of the nervous tissue

6

PRIMARY METABOLIC CHANGES CAUSING CNS MALFUNCTIONS 1.

a, Altered (decreased or increased) oxygen supplyCause: brain hypoxy (Adams-Stokes syndrome), anaemia, other O2-transport

disorders, active or passive hyperaemiaCharacteristics of blood supply:

– lack of anastomoses, presence of own reflex regulation (sinus caroticus: baroreceptors; glomus caroticus: chemoreceptors)

– pCO2 local vasodilation– rich in collateral network

Consequences: unconsciousness after 7-8 sec of total cortical anoxia, death after 15 minutes

The sensitivity to the decreased O2 supply of the central nervous system increases from a caudal to cranial direction.Fast effect: cerebro-cortical necrosis, unconsciousness, deathSlow effect: cerebro-cortical necrosis (encephalomalacia)

convulsions

Hyperoxia may be as dangereous as hypoxia: ↑oxygen-radicals, ↑ LPO → regressive changes including necrosis

7

Retinopathy, blindness due to pure oxygen inhalation in a preterm baby

8

b, Hyperaemia, cerebral edema

Cause: circulatory failure,local or general disorders of the water, electrolyte and protein metabolism, decreased outflow of CSFincreased intracranial pressure, capillary permeability

Consequence: capillary injury decreased cranial blood supply unconsciousness, general symptoms of cerebral

damage, convulsions

PRIMARY METABOLIC CHANGES CAUSING CNS-MALFUNCTIONS 2.

9

c, HyperthermiaCause: thermoregulatory disturbance due to increased external heat or decreased heat loss. Body temperature is > 40-42 °C (heat stroke)Consequences: cerebral hyperaemia, -edema, capillary damage,unconsciousness, convulsions, damage of the respiratory and the circulatory centre

10

d, Metabolic disordersHYPOGLYCAEMIA

Causes: baby pig disease, increased blood insulin level, ketosisConsequences: weakness, depression, unconsciousness, convulsions, coma

HYPERGLYCAEMIACauses: hyperosmolarity of the blood due to diabetes mellitus,

iatrogenic glucose overload (similar effects develop during saline toxicosis or uraemia) cerebral dehydration cerebrocortical necrosis

Consequences: depression, comaHYPOCALCAEMIA

Causes: lactation, idiopathic, parathyroid gland dysfunctions (neoplasma)Consequences: tetany, convulsions, tremor

ACID-BASE IMBALANCESacidosis depression, coma alkalosis convulsions


11

e, Organ-function disordersLiver failure including PSSCauses: NH3, mercaptane, indol, short chain fatty acids, toxins (due to

their decreased catabolism), false neurotransmitters (synaptic effect)Consequences: "Hepato-cerebral syndrome” or hepatic encephalopathy,

hepatic comaRenal failureCauses: organic acids, catabolised toxic compounds, changes in Ca-P

equilibrium, other electrolyte disturbances, hyperosmosis (uraemia!)Consequences: uraemic unconsciousness, convulsions


12

f, Effects of exogenous chemical compoundsCauses: toxins such as organic phosphate-esters, lead, drugs etc.Consequences: general, not characteristic consequences, structural

alterations of peripherial nerves


13

CONSEQUENCES OF NERVOUS TISSUE DAMAGE

1. Loss of functions – clinically these are the most importanta. Damages of the brain and spinal cord nuclei (cell bodies)

- dysfunction of the activatory and/or inhibitory functions ( motor function disorders),

- disturbances of consciousness changes in behaviour- disturbances of some sensory pathways decreased sensory functions (hypoaesthesia)

b. Damages of stimulatory fibers and tracts• decreased reflex-movements, decreased irritability, loss in

activatory and/or inhibitory function• motor function disorders (m. weakness: paresis, paralysis)

2. Increased functionsc, Increased irritability of cranial and spinal nucleiexcitement, hyperaesthesia, convulsions

14

The term "upper or lower motor neuron" is actually misleading because these motor neurons are not really motor neurons.

Lower motor neurons (a type of second-order neuron) are cranial and spinal nerves. The cell bodies of these neurons are located in the CNS (brain or spinal cord), but their axons can leave the CNS and synapse with the muscles of the body

Upper motor neurons are a type of first-order neuron. They never leave the CNS.

Lower and upper (motor) neurons

15

LOWER MOTOR NEURONS (LMN)

1. Efferent motor neurons: connecting the central nervous system (CNS) and peripherial muscles or glands

cell body: in all spinal segments in the intermediate and ventral horns of the gray matter and in the nuclei of the cranial nerves.

The muscle or group of muscles innervated by one spinal nerve is called a myotome.

Each spinal nerve has a dorsal (sensory) and a ventral (motor) root.

2. Afferent sensory neurons: connecting CNS to skin and visceral organs

cell body: in the ganglia of the dorsal roots along the spinal cord and in the ganglia of some cranial nerves with the exception of olfaction, vision, hearing and balance.

The skin area innervated by one spinal nerve is called a dermatome.

16

(b) Schematic representation of the nervous system. UMN pathways are shown descending through the spinal cord to synapse with the LMN cell bodies in the gray matter of the brachial and lumbosacral intumescenses. (Robinson and Huxtable, 1988)

17

LMN: the executioner

18

MOTOR FUNCTION AND DAMAGE OF LMN-S

Function of motor neurons: maintaining muscle tone, proprioception.LMN forms the motor arm (alpha motor neuron) of the stretch reflex (myotatic reflex), this can be superimposed by voluntary movements via upper motor neurons (UMN).

19


Effects of LMN-damage: so called ”LMN-signs”a, Loss of normal, resting (involuntary) muscle tone (hypotony of

muscles, flaccid paresis/paralysis) due to interruption of the myotatic reflex arc.

b, Loss of voluntary muscle movement too, as the "final common pathway" is non-functional and the reflex arc for tendon reflexes is disrupted. (The UMN is not effected!)

20

LOWER MOTOR NEURONS (LMN)

1. Efferent motor neurons: connecting the central nervous system (CNS) and peripherial muscles or glands

cell body: in all spinal segments in the intermediate and ventral horns of the gray matter and in the nuclei of the cranial nerves.

The muscle or group of muscles innervated by one spinal nerve is called a myotome.

Each spinal nerve has a dorsal (sensory) and a ventral (motor) root.

2. Afferent sensory neurons: connecting CNS to skin and visceral organs

cell body: in the ganglia of the dorsal roots along the spinal cord and in the ganglia of some cranial nerves with the exception of olfaction, vision, hearing and balance.

The skin area innervated by one spinal nerve is called a dermatome.

21


Signs of LMN-damage (LMN signs):1. Hypotonia weakness, flaccid paresis/paralysis 2. Hyporeflexia/areflexia reduction in reflex activity3. Muscle atrophy4. Electromyographic (EMG) changes after 5-7 days.5. Contracture and fibrosis of the muscles after weeks

If the sensory nerve is not affected, superficial pain perception disappears but deep pain perception is retarded

„LMN” signs might be caused by lesions of the neuro-muscular synapsis and/or

muscle diseases too

23

SENSORY FUNCTION AND DAMAGE OF LMN-S

Function of sensory neurons: sensory innervation of skin, visceral organs, information of posture of the body.

24

SENSORY FUNCTION AND DAMAGE OF LMN-S

Damage of sensory neurons:

1.Anesthesia (complete, most severe consequence)2.Hypoesthesia or decreased pain sensation (partial lesion)3.Hyperesthesia or increased sensation or pain (irritative

lesion)4.Loss of reflexes (hypo-, areflexia)5.Virtual loss of motor functions (LMN signs)

Damage of sensory peripherial nerves influences both superficial and deep pain perceptions

Upper motor neurons (UMN)

26

UPPER MOTOR NEURONS (UMN) 1.

Mainly motor systems within the CNS. A false terminology too.Cell bodies: in the cerebral cortex, basal nuclei (brainstem). Neurons do

not leave CNS.A, General motor function:

1. initiation and continuation of voluntary movements2. maintenance of appropriate muscle tone against gravity

(maintenace of tone in extensor muscles), coordination3. regulation of posture (UMN modulates muscle tone activity by its

control over the myotactic reflex arc /stretch receptor, muscle spindles/ by inhibitory interneurons)

UMN is divided into pyramidal and extrapyramidal systems. Ascending sensory pathways are also parts of this system. This is the reason why ”UMN” is a false terminology

27

UMN: the judge

28

UPPER MOTOR NEURONS (UMN) 1. – con’t1. Extrapyramidal system:

Several groups of interconnected and related structures that form a series of neurons in a multisynaptic pathway from the brain to the LMN-sFunction: perform basis of voluntary movements

2. Pyramidal (corticospinal) system:Monosynaptic system, axons descend directly via the pyramids of the

medulla to the spinal cord.Function: finely skilled movements

Inhibitory effects of UMN are limiting/controlling the extensor muscle tone (inhibitory tracts: reticulospinal-, rubrospinal tract)

Motor function damage of UMN (UMN signs)1. Poor performance of postural rections, ataxia2. Hyperreflexia hyperactive (or normal) spinal reflexes3. Spasticity increased tone in extensor muscles4. Abnormal reflexes

29

UPPER MOTOR NEURONS (UMN) 2.

B, General sensory functions of UMN1. Responsible for proprioception (sensation of position/posture of

the body via fasciculus cuneatus & f. gracilis)2. Responsible for superficial and deep pain

Sensory-function damage of UMN(Especially following compression of the spinal cord)1. Deficit in reflex-proprioception ( tractus spinocerebellaris)2. (Conscious) proprioceptive deficit (fasciculus cuneatus, f. gracilis)3. Loss of superficial pain (at the same time as the lost of voluntary

motor activity)4. Loss of deep pain (last clinically useful sign)

30

Distinguising between UMN and LMN

UMN and LMN: a summary

32

UMN cell body is the judge, making decisions influenced by sensory and motor branches i.e. defence

lawyer and prosecutor. LMN is the executioner

33

General information on brain anatomy and functions: the mental status

(video)

34

Lobes of the brain (human)

35

FUNCTIONS AND MALFUNCTIONS OF THE CORTEX AND THE BASAL NUCLEI

(TELENCEPHALON) 1.1. CORTEXLobus frontalis/frontal lobeFunction:

1. Pyramidal divisions learned/skilled movements2. Extrapyramidal divisions not skilled, voluntary movements3. Connection with limbic system (prefrontal area) behaviour

(mental status! Remember “thalamocortex”)

Damage:1. Learned and intricated movements may be lost2. Mild paresis (contralateral hemiparesis) turning of head, wander

in large circles towards the affected side - "adverse syndrome"3. Behavioural, mental disturbances

Rostral part of barin stem

Dienceph.Thal.Hypothal., hypocampus, amygdala

Cortexcingulateseptal

38

Frontal lobe – essential part of mental status & behaviour

PHINEAS GAGE (1823-1860)

„On 13th September, 1848, 25-year-old Gage and his crew were working on the Rutland and Burlington Railroad near Cavendish in Vermont…”

39

FUNCTIONS AND MALFUNCTIONS OF THE CORTEX AND THE BASAL NUCLEI (TELENCEPHALON) 2.

1. CORTEX (con’t)

Parietal lobe Function: (touch), pain and conscious proprioceptionDamage: disorders in these sensory functions

Occipital lobeFunction: conscious perception of visual stimuliDamage: blindness - does not affect pupillary reflex

Temporal lobeFunction: perception of hearing,

influence on behaviourDamage: central deafness

40

FUNCTIONS AND MALFUNCTIONS OF THE CORTEX AND THE BASAL NUCLEI

(TELENCEPHALON) 3.

2. BASAL NUCLEI or BASAL GANGLIA

included: caudate nucleus, putamen and globus pallidus. These are parts of the extrapyramidal UMN system.Function: control of muscle tone, voluntary movements and proprioceptionDamage: contralateral weakness, UMN signs (in humans: Parkinsonism and Huntington’s disease/chorea)

Paralysis:Here: Loss of voluntary muscle control resulting in partial or complete loss of movement. (Other forms of paralysis such as muscular, synaptic etc. are also known).

Paresis:Here: Muscular weakness of neural origin (less severe than paralysis).

41

DISTURBANCES IN CORTICAL MOTOR FUNCTION 1.

1, SEIZURE (FIT)Paroxismal, transient disturbance of consciousness, usually accompanied

by abnormal somatic and visceral motor activity. Sudden onset, cease spontaneously, tend to occur repeatedly often in "clusters".

Originate as bursts of activity from neurons in the cerebrum, diencephalon or in the reticular formation (ARAS) of the brainstem, and may be associated with organic lesions (neoplasms, abscesses) or induced by metabolic disturbances (NH3 toxicosis, hypoglycemia) and emotional effects.

Phases: prodromal stage, aurea, ictus, postictus (interictus: time between seizures)Widely known form: epileptoform seizure, epilepsy (narcolepsy is also known). For details see Internal Medicine!

42

Epilepsy

43

Narcolepsy

Transient status; a sudden fall in sleep (REM /rapid eye movement/phase). A neurological sleep disorder.More common in humans; in dogs rarely occurs.

Orexin-mediator releasing disorder (in humans) or orexin-mediator binding disorder (in dog)

45

DISTURBANCES IN CORTICAL MOTOR FUNCTION 2.

2, INCOORDINATION OF MOVEMENT WITHOUT SEIZURES

The control of body movement involves the complex interaction of several parts of CNS (cerebrum, midbrain, brainstem, cerebellum, vestibular system, spinal cord).

A disturbance in control of voluntary movement means: skilled/learned movements– ataxia (unsteady or irregular gait, incoordination):

CEREBRAL/CORTICAL/PROPRIOCEPTIVE ATAXIA (often together with behavioural changes i.e. apathy, depression)

– muscular weakness– involuntary movements, tendency to walk in large circles– no head tilt

46

CORTICAL SENSORY AND BEHAVIOURAL DISTURBANCES

1. Decreased olfactory, visual, hearing, touching sensation and conscious proprioception (centers are located in the cortex)

2. Behavioural disorders (thalamocortex!):• excitament, agressivity, hypersexuality;• loss of learned habits (i.e. in house-trained pets)• depression, dementia• disturbances in consciousness: semi-comatose and comatose

stateThese sensory/behavioural changes are frequently associated with signs

of ataxia but rarely with muscular weakness.

47

DYSFUNCTIONS OF THE BRAINSTEM 1. DIENCEPHALON

Diencephalon is the most rostral (cranial) part of the brainstem

1. Hypothalamic dysfunctionsautonomic functional disturbances

in the regulation of: appetite, thirst, body temperature, endocrine organs

48

DYSFUNCTIONS OF THE BRAINSTEM 1. DIENCEPHALON - con’t

2. Dysfunctions of thalamus – The relay center, “Thalamocortex”–contralateral deficits in sensory functions: vision, proprioception, pain–motor dysfunctions (thalamus relays motor information from the

cerebellum and extrapyramidal nuclei to the cortex: contralateral dysmetria

–disturbances of consciousness (thalamus is a part of the ascending reticular activating system, ARAS): loss of consciousness, convulsions

–behavioural changes (thalamus is connected to the limbic system*): emotional and behavioral abnormalities

* The limbic system has hypothalamic connections, hypothalamus has regulative function in the visceral components of the emotional reactions.

49

Ascending reticular activation system - ARAS

50

DYSFUNCTIONS OF THE BRAINSTEM 1. DIENCEPHALON - con’t

2. Dysfunctions of thalamus – The relay center, “Thalamocortex”–contralateral deficits in sensory functions: vision, proprioception, pain–motor dysfunctions (thalamus relays motor information from the

cerebellum and extrapyramidal nuclei to the cortex: contralateral dysmetria

–disturbances of consciousness (thalamus is a part of the ascending reticular activating system, ARAS): loss of consciousness, convulsions

–behavioural changes (thalamus is connected to the limbic system*): emotional and behavioral abnormalities

* The limbic system has hypothalamic connections, hypothalamus has regulative function in the visceral components of the emotional reactions.

Rostral part of barin stem

Dienceph.Thal.Hypothal., hypocampus, amygdala

Cortexcingulateseptal

52

DYSFUNCTION OF THE BRAINSTEM 2.MIDBRAIN (MESENCEPHALON) DYSFUNCTIONS

1. Disturbances in the function of ARAS (reticular formation, functions to stimulate the cerebral cortexx)

damage causes: unconsciousness, semi-comatose/comatose state

2. Disturbances in the function of oculomotor nucleus with the connections of the pontine and the medullary (medulla oblongata) reticular formation

3. Formatio reticularis pontine reticular formation: stimalator of the extensor muscle tone medullary reticular formation : inhibitory influence of extensor muscle tone

53

Severe damage:may develop when intracranial pressure increases and causes

unconsciousness (ARAS), opisthotonus (UMN-signs), ventrolateral strabismus with fixed dilated pupils (Oculomotor nucl.)

Less severe damage:Depression (ARAS) spastic tetra- or hemiparesis (causes milder UMN

signs); pupils are asymmetrical or bilaterally miotic (Oculomotor nucl.)

http://veterinaryanswers.files.wordpress.com/2008/03/figure-32-3.jpg

54

DYSFUNCTIONS OF THE PONS AND THE MEDULLA OBLONGATA

• Lesions of motor neurons of this area cause UMN signs (ataxia, spastic paresis, hyperreflexia) of all four limbs (BSE!) - ipsilateral signs if unilateral lesion exists

• Simultaneous deficits of cranial motor nerves V to XII (LMN signs – flaccid paresis/paralysis!)

• As medullary and pontine areas control vital centres for respiration, blood pressure and heart rate, ARAS - damage of these areas causes life-threatening consequences

A sample cut for BSEanalysis

http://www.pref.iwate.jp/~hp1310/picture%20for%20hp/03%20medulla%20oblongata.jpg

55

Cerebellum

http://www.newmanveterinary.com/images/Brain-Cortex%20and%20Cerebellum.gif

56

CEREBELLAR DYSFUNCTIONS

The cerebellum regulates and coordinates voluntary movements, monitors information from various parts of CNS concerning body position and movement.

Damage of the cerebellum causes: ataxia without weakness (hypermetria, truncal ataxia, tremor,

opisthotonus, - exaggeration of movements) – ipsilateral!! vestibular signs (loss of equilibrium, abnormal nystagmus) intention(al) tremor (a tremor that occurs when a voluntary

movementv is attempted) Absence of menace response (with vision!!!!!)

Symptoms due to the damage of different cerebellar regions:Vermix damage: ataxia, circlingFrontal lobe damage: incoordination, stride (straddle) standPosterior (occipital) lobe damage: tremor

Cerebellar diseases - video

Malfunctions of cranial nerves

Skipped exept vestibulocohlear nerveSee Internal Medicine Diagnostics

60

DYSFUNCTIONS OF THE CRANIAL NERVES (CN) 1.

CN I. (nervus olfactorius/olfactory nerve)Anosomia (absence of the sense of smell)

CN II. (nervus opticus/optical nerve)This nerve is the sensory path for vision and the pupillary light reflexes no menace response (eye blink and averted head as a result of a threatening gesture) no direct and indirect pupillary light reflex (as a result of light there is a pupillary constriction (miosis) - due to parasympathetic fibers of CN III.)

61

DYSFUNCTIONS OF THE CRANIAL NERVES 2.

CN III. (nervus oculomotorius)Decreased function of:

1. parasympathetic motor fibers for pupillary constriction pupil is constantly dilated (mydriasis)

2. general somatic efferent fibers for motor control of the extraocular muscles - dorsal, medial, ventral recti and ventral oblique; motor pathway of m. levator palpebrae

fixed ventrolateral strabismus, dropping of the upper eyelid (ptosis)

CN IV. (nervus trochlearis/trochlear nerbe)Decreased function of:motor pathway to the dorsal oblique muscle of eye,

which normally rotates the dorsal pole of the eye towards the midline - outward rotation of the dorsal pole of the eye

62


CN V. (nervus trigeminus/trigeminal nerve)1. motor division dysfunctions:

mandibular, masseter, temporal, rostral digastric, pterygoid, and mylohyoid muscles dropped jaw, drooling saliva, inability to prehend and chew

2. sensory division dysfunctions:a, ophtalmic branch dysfunction absence of the palpebral reflex (blink response by touching the eyelid, medial canthus) no corneal reflex (by gently touching the cornea the eyeball retracts, third eyelid flicks across)b, maxillary branch dysfunction- no palpebral reflex by touching the lateral canthusc, mandibular branch dysfunctions no sensation in lower jaw and cheeks

63


CN VI. (nervus abducens/abducens nerve)Dysfunction of the lateral rectus and retractor bulbi muscles

medial deviation of the eyeball (strabismus convergens) suppression of the corneal reflex exophtalmus

64


CN VII. (nervus facialis/facial nerve)1. Dysfunction of the motor pathway of the facial muscles (facial

expression), (hemi)paresis of facial muscles (mimetic muscles) dropped eyelid, ear, (in case of hemiparesis the nose and upper lip

will be drown towards the normal side) menace and palpebral reflex deficiencies involuntary retraction of the eyeball which serves to bring the third

eyelid across the eye2. Sensory dysfunctions of the tongue (taste)

65


CN VIII. (nervus vestibulocochlearis)1. Cochlear division dysfunctions:

uni- or bilateral deafness2. Vestibular division dysfunctions:

a) Disorders in maintening the position of the eyes, trunk, limbs imbalance, disorientation

(vestibular sensory pathway: receptor cells /inner ear/ - CN. VIII - vestibular nuclei of the medulla oblongata or cerebellum)Connections with the vestibular nuclei:

1. spinal cord (vestibulospinal tract)2. brainstem (medial longitudinal fasciculus)3. cerebellum

a) Disorders of the vomiting center

66

Consequences of unilateral vestibular disease

- VESTIBULAR ATAXIA without weakness, due to loss of equilibrium- circling, rolling toward the side of the lesion (ipsilateral)- head tilt, postural abnormalities (ipsilateral)- hypertonia of muscles, hyperreflexia on the side opposite of the lesion

(i.e. contralateral, due to removal of the inhibitory contralateral UMN vestibulospinal influence)

- vestibular nystagmus (involuntary rhythmic oscillation of the eyeball whenever head moves normally)

- abnormal nystagmus: spontaneous and positional nystagmus that occurs while the head is not moving

- vestibular strabismus (ventral deviation of the eyeball on the affected side)

Vestibular ataxia

68


CN IX. (nervus glossopharyngeus/glossopharingeal nerve)Dysfunctions of the motor pathway of the pharynx, zygomatic and parotid glands, sensory difficulties at the caudal one-third of the tongue and pharyngeal mucosa loss of gag reflex, loss of taste and

dryness of tongue pharyngeal asymmetry

CN X. (nervus vagus/vagal nerve)Dysfunctions of the motor pathway of the pharynx, larynx, palate, and parasympathetic motor pathways to the viscera of the bodySensory dysfunctions of the caudal pharynx, larynx and viscera of the body

Symptoms: dysphagia, megaesophagus, vocalization defects and tachycardia

69


CN XI. (nervus accessorius/accessory nerve)Dysfunction of the motor pathway of the trapezius, sternocephalicus and brachiocephalicus muscles - no typical signs

CN XII (nervus hypoglossus/hypoglossal nerve)Dysfunction of the intrinsic and extrinsic muscles of tongue.- paralysis, atrophy

70

Spinal cord disorders

71

SPINAL CORD DYSFUNCTIONS 1.Upper cervical zone

(comprises cord segment C1 to C4, which is at the anterior level to the brachial plexus)Lesion causes:– UMN signs of all four limbs (spastic tetraparesis/paralysis)– ataxia, hypertonia, hyperreflexia, weakness (tetraparesis), – reduced conscious proprioception, respiratory failure– (ataxia is more severe in the hindlimbs: wobbler-syndrome,

CVI=cervical vertebral instability)

72

SPINAL CORD DYSFUNCTIONS 1.

Cervicothoracic zone(extends from C5 to T2; includes the origin of the brachial plexus)Lesion causes:– LMN signs in the forelegs/-limbs, UMN signs in the hindlegs Pain sensation (hypo-/anaesthesia)

73

Thoracolumbar zone(extends from T3 to L3; includes no major peripherial nerves)

Lesion causes:• UMN signs in the hindlegs, suppression of pain perception• (forelimbs are not affected, except Schiff-Sherrington

phenomenon)


74

Thoracolumbar zone (in fact upper thoracic region damagae)(in the L2 – L4 segment there are „border neuron cells”)

Lesion causes:

Schiff-Sherrington phenomenon UMN signs in the forelegs/-limbs, LMN signs in the hindlimbs


75

Lumbosacral zone(extends from L4 to S2; origin of the major nerves of hindlimbs, perineum and pelvic viscera)Lesions cause: cauda equina complex (CEC or CES)

• LMN signs in the hindlimbs, perineum and adversely affected bladder function

• increased pain sensation (hyperaesthesia) of pelvic limbs, tail and perineum


76

Sacrococcygeal zone(extends from S3 to Co segments; controls the tail movement)

Lesions cause: –hypotonia/weakness of the tail–reduced pain perception


77

Consequences of dysfunctions in afferent (sensory) tracts:a) hypoesthesia, anesthesiab) hyperesthesiac) paresthesiad) extension of the pain perception according to the dermatomes

(Head`s zones or areas)

Sir Henry Head: English neurologist, 1861-1940

SPINAL CORD DYSFUNCTIONS 3.SUMMARY 1.

78

Consequences of dysfunctions in efferent (motor) tracts:a, mainly LMN signs: flaccid paresis (paralysis), areflexia, reduced

muscular tone b, UMN signs: hyperreflexia, increased muscular tone (spastic

paralysis)ATAXIA IS ALSO COMMON (SPINAL ATAXIA)

SPINAL CORD DYSFUNCTIONS 3.SUMMARY 2.

Spinal ataxia - video

80

DISTURBANCES IN URINATION (MICTURITION) AND DEFECATION

a) UMN signs: loss of cortical and supracortical effects incontinence, abnormal positioning/posture during urination

b) LMN signs: decreased muscular tone of the urinary bladder, anal muscles, and tailDetrusor – n. pelvicus parasympSphincter – n. pudendalisSympathetic innervation (L1-L4)

-receptors: increase sphincter muscle tone -receptors: promote relaxation of the bladder wall


con’t

81

SPINAL CORD DYSFUNCTIONS 3.con’t

Cauda equina – CES (cauda equina syndrome)

Documents

Veterinary Pathophysiology Student’s Lectures, 5th Semester