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Veterinary Pathophysiology
Student’s Lectures, 5th Semester
PATHOPHYSIOLOGY OF THE NERVOUS
SYSTEM
Department of Internal Medicine,
Faculty of Veterinary Science
Szent István University
1
Circulation of the brain
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
2
Regulation
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.)
CBF is lost: 10 s – faint!!!
3
Anatomy
a. carotis interna (bo.: a. maxill. int.)
a. occipitalis – a. basilaris cerebri
a. vertebralis
a. spinalis ventralis
circulus arteriosus cerebri,
Circle of Willis
rete mirabile epidurale
rostrale et caudale
4
PRIMARY STRUCTURAL CHANGES
CAUSING CNS-MALFUNCTIONS
a. Inflammation of the brain and the spinal cord
causes: viruses, bacteria, parasites, fungi and toxic compounds
b. Necrosis of the tissues
causes: hypoxia, toxins, vitamin deficiency, hypoglycaemia,
effects of lipid peroxides, accumulation of some compounds
c. Atrophy of the nervous tissue
causes: neoplasma, parasites, increased intracranial pressure,
discus hernia
d. Bleeding
causes: capillary damage, embolism, trauma (epidural,
subdural, cerebral petechia or haematoma)
e. Trauma of the nervous tissue
5
PRIMARY METABOLIC CHANGES
CAUSING CNS MALFUNCTIONS 1.
a, Altered (decreased or increased) oxygen supply
Cause: brain hypoxy (Adams-Stokes syndrome), anaemia, other O2-transport disorders,
active or passive hyperaemia
Characteristics 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, death
Slow effect: cerebro-cortical necrosis (encephalomalacia)

convulsions
Hyperoxia may be as dangereous as hypoxia: ↑oxygen-radicals, ↑ LPO → regressive
changes including necrosis
6
Retinopathy, blindness due to pure
oxygen inhalation in a preterm baby
7
PRIMARY METABOLIC CHANGES
CAUSING CNS-MALFUNCTIONS 2.
b, Hyperaemia, cerebral edema
Cause: circulatory failure,
local or general disorders of the water, electrolyte and protein
metabolism, decreased outflow of CSF
increased intracranial pressure, capillary permeability
Consequence: capillary injury  decreased cranial blood supply
 unconsciousness,
 general symptoms of cerebral damage,
convulsions
8
c, Hyperthermia
Cause: 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
9
PRIMARY METABOLIC CHANGES
CAUSING CNS-MALFUNCTIONS 3.
d, Metabolic disorders
HYPOGLYCAEMIA
Causes: baby pig disease, increased blood insulin level, ketosis
Consequences: weakness, depression, unconsciousness, convulsions,
coma
HYPERGLYCAEMIA
Causes: 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, coma
HYPOCALCAEMIA
Causes: lactation, idiopathic, parathyroid gland dysfunctions
(neoplasma)
Consequences: tetany, convulsions, tremor
ACID-BASE IMBALANCES
acidosis  depression, coma
alkalosis  convulsions
10
PRIMARY METABOLIC CHANGES
CAUSING CNS-MALFUNCTIONS 4.
e, Organ-function disorders
Liver failure including PSS
Causes: 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 coma
Renal failure
Causes: organic acids, catabolised toxic compounds, changes in Ca-P
equilibrium, other electrolyte disturbances, hyperosmosis (uraemia!)
Consequences: uraemic unconsciousness, convulsions
11
PRIMARY METABOLIC CHANGES
CAUSING CNS-MALFUNCTIONS 4.
f, Effects of exogenous chemical compounds
Causes: toxins such as organic phosphate-esters, lead, drugs etc.
Consequences: general, not characteristic consequences, structural
alterations of peripherial nerves
12
CONSEQUENCES OF NERVOUS
TISSUE DAMAGE
1. Loss of functions – clinically these are the most important
a. 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 functions
c, Increased irritability of cranial and spinal nuclei
13
excitement, hyperaesthesia, convulsions
Lower and upper (motor) neurons
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.
14
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.
15
The skin area innervated by one spinal nerve is called a dermatome.
the level of lesion
b)
lumbosacral
brachial
(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)
16
- may be Horner's in CT area
- LMN signs and
LMN: the executioner
- Ipsilateral UMN signs below
the level of lesion
b)
lumbosacral
brachial
17
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
TRUNK
(myotatic
reflex), this can be NERVE
superimposed
by voluntary movements via
a)
- LMN signs and
upper motor neurons (UMN).- corresponding sensory
defects
SENSORY NERVE
ENDING
VENTRAL HORN
GREY MATTER
VENTRAL NERVE ROOT
- LMN signs only
- NO corresponding
sensory deficit
- LMN signs and
- may be Horner's in CT area
- Ipsilateral UMN signs below
the level of lesion
NEUROMUSCULAR
JUNCTION
LMN signs only
(Often diffuse and generalized)
18
MOTOR FUNCTION AND DAMAGE OF LMN-S
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!)
19
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.
20
The skin area innervated by one spinal nerve is called a dermatome.
MOTOR FUNCTION AND DAMAGE OF LMN-S
Signs of LMN-damage (LMN signs):
1. Hypotonia  weakness, flaccid paresis/paralysis
2. Hyporeflexia/areflexia  reduction in reflex activity
3. Muscle atrophy
4. 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
21
„LMN” signs might be caused by lesions
of the neuro-muscular synapsis and/or
muscle diseases too
SENSORY FUNCTION AND DAMAGE OF LMN-S
Function of sensory neurons: sensory innervation of skin, visceral
organs, information of posture of the body.
a)
NERVE TRUNK
- LMN signs and
- corresponding sensory
defects
SENSORY NERVE
ENDING
VENTRAL NERVE ROOT
- LMN signs only
NEUROMUSCULAR
JUNCTION
LMN signs only
23
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
24
Upper motor neurons (UMN)
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 movements
2. maintenance of appropriate muscle tone against gravity
(maintenace of tone in extensor muscles), coordination
3. 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
26
”UMN” is a false terminology
VENTRAL HORN
GREY MATTER
- NO corresponding
sensory deficit
(Often diffuse and generalized)
- may be Horner's in CT area
UMN:
the
judge
- Ipsilateral UMN signs below
- LMN signs and
the level of lesion
b)
lumbosacral
brachial
27
UPPER MOTOR NEURONS (UMN) 1. – con’t
1. 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-s
Function: 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, ataxia
2. Hyperreflexia  hyperactive (or normal) spinal reflexes
3. Spasticity  increased tone in extensor muscles
28
4. Abnormal reflexes
UPPER MOTOR NEURONS (UMN) 2.
B, General sensory functions of UMN
1. 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)
29
Distinguising between UMN and LMN
30
UMN and LMN: a summary
- LMN signs only
- NO corresponding
sensory deficit
LMN signs only
(Often diffuse and generalized)
VENTRAL
HORN
UMN
cell
body
is
the
judge,
making
decisions
GREY MATTER
may be Horner's
in CT branches
area
influenced
byandsensory -and
motor
i.e. defence
- LMN signs
- Ipsilateral
UMN prosecutor.
signs below
lawyer
and
LMN is the executioner
the level of lesion
b)
lumbosacral
brachial
32
General information on brain anatomy
and functions: the mental status
(video)
33
Lobes of the brain (human)
34
35
FUNCTIONS AND MALFUNCTIONS OF THE
CORTEX AND THE BASAL NUCLEI
(TELENCEPHALON) 1.
1. CORTEX
Lobus frontalis/frontal lobe
Function:
1. Pyramidal divisions  learned/skilled movements
2. Extrapyramidal divisions  not skilled, voluntary movements
3. Connection with limbic system (prefrontal area)  behaviour
(mental status! Remember “thalamocortex”)
Damage:
1. Learned and intricated movements may be lost
2. Mild paresis (contralateral hemiparesis) turning of head, wander
in large circles towards the affected side - "adverse syndrome"
3. Behavioural, mental disturbances
Cortex
cingulate
septal
Dienceph.
Thal.
Hypothal.,
hypocampus,
amygdala
Rostral part of barin stem
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…”
38
FUNCTIONS AND MALFUNCTIONS OF THE CORTEX
AND THE BASAL NUCLEI (TELENCEPHALON) 2.
1. CORTEX (con’t)
Parietal lobe
Function: (touch), pain and conscious proprioception
Damage: disorders in these sensory functions
Occipital lobe
Function: conscious perception of visual stimuli
Damage: blindness - does not affect pupillary reflex
Temporal lobe
Function: perception of hearing,
influence on behaviour
Damage: central deafness
39
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
proprioception
Damage: 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).
40
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!
41
Epilepsy
42
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)
43
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
45
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
state
These sensory/behavioural changes are frequently associated with signs
of ataxia but rarely with muscular weakness.
46
DYSFUNCTIONS OF THE BRAINSTEM 1.
DIENCEPHALON
Diencephalon is the most rostral (cranial) part of the brainstem
1. Hypothalamic dysfunctions
autonomic functional disturbances
in the regulation of:
appetite, thirst, body temperature,
endocrine organs
47
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.
48
Ascending reticular activation system - ARAS
49
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.
50
Cortex
cingulate
septal
Dienceph.
Thal.
Hypothal.,
hypocampus,
amygdala
Rostral part of barin stem
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
52
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.)
53
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 BSE
analysis
54
Cerebellum
55
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, circling
Frontal lobe damage: incoordination, stride (straddle) stand
Posterior (occipital) lobe damage: tremor
56
Cerebellar diseases - video
Malfunctions of cranial nerves
Skipped exept vestibulocohlear nerve
See Internal Medicine Diagnostics
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
60
parasympathetic fibers of CN III.)
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
61
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 3.
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 canthus
c, mandibular branch dysfunctions
 no sensation in lower jaw and cheeks
62
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 4.
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
63
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 4.
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 eye
2. Sensory dysfunctions of the tongue (taste)
64
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 5.
CN VIII. (nervus vestibulocochlearis)
1. Cochlear division dysfunctions:
 uni- or bilateral deafness
2. 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
65
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)
66
Vestibular ataxia
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 6.
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 body
Sensory dysfunctions of the caudal pharynx, larynx and viscera of the
body
Symptoms: dysphagia, megaesophagus, vocalization defects and
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tachycardia
DYSFUNCTIONS OF THE CRANIAL NERVES
(CN) 7.
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
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Spinal cord disorders
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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)
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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)
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SPINAL CORD DYSFUNCTIONS 2.
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)
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SPINAL CORD DYSFUNCTIONS 2.
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
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SPINAL CORD DYSFUNCTIONS 2.
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
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SPINAL CORD DYSFUNCTIONS 2.
Sacrococcygeal zone
(extends from S3 to Co segments; controls the tail movement)
Lesions cause:
–hypotonia/weakness of the tail
–reduced pain perception
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SPINAL CORD DYSFUNCTIONS 3.
SUMMARY 1.
Consequences of dysfunctions in afferent (sensory) tracts:
a) hypoesthesia, anesthesia
b) hyperesthesia
c) paresthesia
d) extension of the pain perception according to the dermatomes
(Head`s zones or areas)
Sir Henry Head: English neurologist, 1861-1940
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SPINAL CORD DYSFUNCTIONS 3.
SUMMARY 2.
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)
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Spinal ataxia - video
SPINAL CORD
DYSFUNCTIONS 3.
con’t
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 tail
Detrusor – n. pelvicus parasymp
Sphincter – n. pudendalis
Sympathetic innervation (L1-L4)
-receptors: increase sphincter muscle tone
-receptors: promote relaxation of the bladder wall
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SPINAL CORD DYSFUNCTIONS 3.
con’t
Cauda equina
– CES (cauda equina syndrome)
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