The neurological examination aims to determine nervous system function, localize lesions, and arrive at diagnoses and prognoses. It involves obtaining a thorough history and performing hands-off and hands-on examinations. The hands-off exam observes mental status, posture, gait, and behavior without disturbing the patient. The hands-on exam evaluates the 12 cranial nerves and identifies abnormalities to localize lesions. Key tests include menace response, pupillary light reflexes, cranial nerve function, and neurological reflexes. Abnormal findings provide clues to diagnose conditions affecting the brain, spinal cord, or peripheral nerves.
1. Neurological examination and neurological
manifestation in systemic diseases in small
animals
Submitted by:
Dr. KANWARPAL DHILLON
M.V.Sc – Medicine
GADVASU,LDH
3. The objective of the neurological examination
is….
1. To determine the presence or absence of nervous system malfunction.
2. To establish location of lesion within the nervous system.
3. To arrive at diagnoses.
4. To predict prognosis of disease.
4. History
It is very important to take a thorough history as this can give many clues in
making the most likely differential diagnoses.
species, breed, sex and age of animals.
carefully question owners about the main complaint.
The onset, evolution and course of the illness are most important for making
the most likely differential diagnoses.
5. The onset of the neurological signs should be defined as:
1. Acute (onset over minutes to hours)
2. Subacute (onset over days)
3. Chronic (onset over several days, weeks or months)
4. Episodic (the patient returns to normal between the episodes)
6. Neurological examination
The neurological examination should be performed in animals that are
not sedated, have not received any analgesia or are recovering from
seizures or general anaesthesia.
Method of examination : Hands off examination and Hands on
examination
7. Hands off examination
This part of the neurological examination can be performed while collecting
the history. The patient should be left to explore the examination room. The
clinician can observe the awareness, mental status, behaviour, posture and
gait in an undisturbed manner.
8. Mental status: Consciousness, awareness, behaviour
State of consciousness is classified in order of severity as lethargy, depression, obtundation,
stupor (semicoma) and coma.
Generally if there is an altered state of consciousness then the lesion is affecting either
diffusely both cerebral hemispheres or focally the ascending reticular activating system
(ARAS) of the brainstem.
9. Consciousness:
Normal- alert, with a normal response to environmental stimuli
Confused and delirious- responding to environmental stimuli in an
inappropriate manner
Depressed- drowsiness, inattention and less responsive to environmental
stimuli, due to cerebral cortex lesions.
10. Stuporous- state of consciousness with reduced response to external stimuli,
but can be aroused by a painful stimuli, associated with partial disconnection
of reticular formation and cerebral cortex, as in diffuse cerebral edema with
compression of the brain stem.
Coma- state of unconsciousness with absence of response to any environmental
stimuli including pain, most common cause in small animal is acute head injury
with heamorrhage in the pons and midbrain.
11. Changes in the patient’s level of awareness and behaviour include disorientation, delirium,
aggression, compulsive walking, loss of learned behaviour (e.g. in-house urination,
defecation etc.), vocalising and head pressing. Hemi-neglect or hemi-inattention syndrome is
the abnormal behaviour in animals with forebrain lesions. The lesion in the forebrain is
contralateral to the apparently “ignored” side by the animal.
13. Posture and body position
Head tilt - abnormal posture of the head when one ear is lower compared to the other one.
A head tilt indicates a vestibular disorder (central or peripheral).
Head turn - Characterized by the posture when the nose and often whole body
(pleurothotonus) are turned to one side and ears are at the same median plane. This is most
commonly associated with an ipsilateral forebrain lesion.
Ventroflexion of the head – commonly associated with a neuromuscular disorder or
spinalcord grey matter lesion.
15. Spinal curvature
a) Scolisosis (lateral deviation of the spine)
b) Lordosis (ventral curvature of the spine)
c) Kyphosis (dorsal curvature of the spine)
d) Torticollis (twisting of the neck)
16. Decerebrate rigidity - a posture when the
patient is recumbent and has extension of
all limbs and opithotonus (extension of the
neck and head). The mental status is often
stuporous or comatous and the lesion is
commonly localised in the rostral
brainstem.
17. Decerebellate posture - a posture when the
patient is recumbent, has extended thoracic
limbs and opisthotonus but the pelvic limbs
are usually flexed. The mental status is
normal and the lesion is likely to occur in the
cerebellum.
18. Schiff-Scherrington posture - observed in
animals with severe thoracic or cranial
lumbar spinal cord trauma. The animal
has extended thoracic limbs with the
normal function but has paralysis of the
pelvic limbs. This sign is present only in
acute lesions and does not have any
prognostic value.
19. Evaluation of gait
Ataxia means uncoordinated gait. Ataxia can be a consequence of peripheral nerve or spinal
cord dysfunction (general proprioceptive ataxia), vestibular system (vestibular ataxia) or
cerebellum (cerebellar ataxia).
Paresis is defined as a loss of ability to support weight or to generate the gait. Monoparesis,
paraparesis, tetraparasis,or hemiparesis.
Plegia or paralysis refers to the complete loss of a voluntary movement, whereas paresis
implies that the voluntary movements are still present.
20. Circling: circling may vary from a tendency to drift in wide circle to forced spinning in a tight
circle.
tight circle: lesion in brain stem, direction always towards the side of the lesion
Dysmetria: characterized by movements too long (hypermetria) or too short( hypometria).
‘goose-stepping’ is most common sign of dysmetria. Occur due to lesion in cerebellar and
cerebellar pathways.
21. Abnormal movements: tremor and myoclonus
Tremors- synchronous involuntary oscillating contraction of antagonistic muscle groups. Can
affect all or parts of body.
Classified as
Resting tremors
Intention tremors -occur as the animal intend to move and are exaggerated by action
oriented movements e.g. eating.
Action tremors (occur as the parts of body are maintained in certain position)
Generalized tremors are more common
22. Epileptic seizures-
clinical manifestation of excessive or hypersynchronous electrical activity in the cerebral
cortex. Can be focal or generalized
Occurs due to a fore brain disorder (may be from inside or outside of brain)
Myoclonus-
Repetitive rhythmic contraction of a group of skeletal muscles producing a quick jerking
movement of a body part.
Can be a result of encephalitis or myelitis caused by distemper virus.
23. Myotonia-
Sustained irregular contraction with delayed relaxation of a muscle or a group of muscles following
voluntary contraction.
Cataplexy-
Paroxysmal onset of flaccid paralysis with preservation of consciousness lasting for few seconds to few
minutes
Induced by excitement and can be reversed by an external stimuli
Head ‘bobbing’-
Occurs in particular breeds such as bulldog and Doberman pinscher
24. Hands on examination
Cranial nerve examination
Olfactory Nerve – (CN I)
The olfactory nerve is the sensory path for the conscious perception of the smell.
The behavioral response to a pleasurable or a noxious odor, either inferred from the
history or assessed by direct testing by Alcohol, cloves, xylol, benzol, or cat food
containing fish, appears to stimulate the olfactory nerves.
25. Letting the animal to sniff something
aromatic while blindfolded can test
the smell response.
Abnormal: Hyposomia or Ansomia
26. Optic Nerve (CN II)
Menace response is a cortically mediated blink produced by a threating gesture in front
of the visual area of the patient. Puppies will not have this response prior to 10-12 weeks
of age.
Pupillary light reflex (PLR) induces by shinning the light in each eye and observing the
pupillary constriction in both eyes.
27. The menace response is performed by
making the threating gesture at the eye. The contralateral eye
should be blinded. Care must be taken not to touch the
eyelashes or to create air current as this stimulates the CNV
and produces the palpebral or corneal reflex rather then
genuine menace response.
28.
29. Oculomotor Nerve (CN III)
This nerve innervates ipsilateral dorsal, ventral and medial recti muscles and ventral oblique
muscle. It also innervates the levator palpebrae superioris muscle which is important for
upper eyelid movement,
the oculomotor nerve plays an important role as an efferent arm of PLR. It controls the
pupillary constriction by its parasympathetic component.
30. By observing the eyeball position and movement of the eyeball by testing for
physiological nystagmus, this nerve can be easily assessed. Another observation needs
to be done by assessing the normal position of the upper eyelid. PLR of course must be
assessed.
31. An oculomotor nerve lesion results in ventrolateral strabismus and an inability to rotate
the eye dorsally, ventrally and medially. It can also produce unresponsive mydriasis and
narrowing of the palpebral fissure (ptosis of the upper eyelid).
32. Trochlear nerve (CN IV)
This is assessed by observing the position of the eyeball as well as by testing for
physiological nystagmus.
This nerve innervates contralateral dorsal oblique muscle.
Dysfunction usually results in dorsolateral strabismus of the contralateral eye.
34. Trigeminal nerve (CN V) The trigeminal nerve provides sensory innervation of the face as
well as motor innervation of the masticatory muscles. It has three major branches:
1. Ophthalmic branch – innervates medial canthus of the eye, nasal septum, cornea and
dorsum of the nose.
2. Maxillary branch – innervates lateral canthus, skin of cheeks, muzzle, palate and teeth of
the upper jaw.
3. Mandibular branch – innervates mandibular area of the oral cavity.
35.
36. The motor function is assessed by evaluating the symmetry and size of the masticatory
muscles as well as by opening the jaw.
The sensory functions assessed by corneal reflex which is done by touching the cornea with a
sterile cotton bud. The palpebral reflex tests ophthalmic and maxillary branches (afferent
arm of the reflex) by touching medial or lateral canthuses, respectively. A normal response
for corneal and palpebral reflex is the blink of the tested eye that is mediated by the facial
nerve (efferent arm of the reflex).
Other tests that can assess the trigeminal nerve are nasal stimulation and pinching of the
skin of the face that results in the ipsilateral blink or twitch of the facial muscles
38. Unilateral dysfunction of the motor part
results in unilateral masticatory muscle
wastage, whereas bilateral dysfunction
results in the dropped jaw and inability to
close the jaw voluntarily. Dysfunction of the
sensory part results in facial hypoesthesia
or anaesthesia and can also result in
decreased tear production and neurotropic
keratitis.
Unilateral wastage of the masseter and
temporal muscles
39. Abducent nerve (CN VI)
This nerve innervates
the ipsilateral lateral
rectus and retractor
bulbi muscles. The
assessment is therefore
done by observation of
the eye position.
Dysfunction results in
ipsilateral convergent
strabismus, inability of
the eye to cross the
midline when testing
physiological nystagmus
and inability to retract
the eyeball.
Ipsilateral convergent strabismus
40. Facial nerve (CN VII)
The motor function is assessed by observation of the symmetry of the face and
spontaneous blink and movement of the nostrils.
The facial nerve provides the efferent arm for palpebral reflex, corneal reflexes and
menace response and can be assessed by performing these tests.
The Schirmer tear test should be performed to assess the parasympathetic part of this
nerve.
41. Unilateral dysfunction
produces the
ipsilateral drooping of
the face, inability to
move the ear and
nostril, widened
palpebral fissure and
absent blinking
response. It can also
produce
keratoconjunctivitis
sicca by inability to
produce enough tears
by loss of
parasympathetic
innervation to the
lacrimal glands.
Right side dropping of the lips and ear
42. Vestibulocochlear nerve (CN VIII)
Observation of the gait, body and head posture can give a lot of information about the
vestibular function
Specifically physiological nystagmus can test the functional integrity of the vestibular system.
This involves moving the head from side to side and up and down. A normal response is the
involuntary “jerk” movement of both eyes to correct their position in relation to the position of
the head.
43. To assess the hearing part whistling or a handclap can be use
Dysfunction of this nerve usually results in a head tilt, falling to the side, leaning to
the side, rolling, circling, pathological (abnormal) spontaneous or positional
nystagmus, positional strabismus or asymmetrical ataxia.
44. Glossopharyngeal nerve (CN IX) and Vagus nerve (CN X)
The pharyngeal or gag reflex can assess the function of both nerves. Gently applying
pressure to the thyroid cartilages provokes swallowing in a normal animal. Observing a
patient while eating or drinking can also provide useful information about the function of
both nerves.
Dysfunction results in dysphagia, absent gag reflex, inspiratory dyspnea (due to laryngeal
paralysis), voice change and regurgitation (due to megaoesophagus).
46. Accessory nerve (CN XI)
This nerve supplies motor innervation to the trapezius, sternocephalicus and
brachiocephalicus muscles and so the dysfunction results in atrophy of these muscles and
potential deviation of the neck. However isolated lesions of this nerve are rare.
47. Hypoglossal nerve (CN XII)
Assessed by observing for symmetry of the tongue and movement of
the tongue during the eating, or licking of food. Lesions of this nerve
result in problems with prehension and mastication. Asymmetry of the
tongue and fasciculation of the musculature of the tongue can also be
seen in dysfunction of nerve.
48. nerve Diagnostic sign of
dysfunction
tests Normal responce Abnormal responce
I.Olfactory Hyposmia or
anosmia
Smell of food and
voletile oil
Food- interested or
attempt to eat,
voletile oil-sniffing
and recolling
No reaction
II. optic Hesitant walking ,
walks in to objectes,
anisocoria,
mydriasis, miosis
Sudden object
movement towards
eyes, Point source of
light in each eye
Ophthalmoscopy
examination
Avoidance and eye
blink
Direct and
consensual pupilary
constriction
Normal fundus
Absence of blink
reflex
Lack of pupillary
response
Retinal lesion found
III.Oculomotor Anisocoria,
mydriasis, miosis,
ptosis, deviation,
ventral and lateral
Light in normal eye
and light in affected
eye
Direct and
consensual reflex
present
Direct pupillary
reflex present-
consensua absent,
Direct pupillary
reflex absent-
consensua reflex
may present
49. IVTrochlear Affected eye anable
to move
ventrolaterally
Observation when
animal follows
moving objects
Follows object
ventrolaterally
Eye unable to
Follows object
ventrolaterally
V. Trigeminal Sensory-
hyperesthesia on
one side of face and
eye
Anesthesia on one
side of face and eye
Motor-weakness in
closing mouth and
unable to open
mouth
Cold object on
skin,pinprick.touch
cornea
Cold object on
skin,pinprick.touch
cornea
Test muscle
tension,palpate
tempolaris and
masseter muscle
Slight discomfort
,eye blink both side
Slight discomfort
Normal muscle
tension and normal
contour to
musculature
Intense discomfort,
recoil, may vocalize
No response
Atrophy of
temporalis and
masseter
muscle.trismus
VI. Abducens Affected eye unable
to move
laterally.medial
strabismus may
present
Observation of
movment of eye
when animal follows
moving objects
Unable to follow
laterally
50. VII. Facial Asymmetry of facial
expression. Eyelids and
lips drops.loss of ear
motion
Observation, pinprick on
the side of the
face(trigeminal is sensory
inthis test)
Retractionl
of skin eye
blink
No
retraction
no eye blink
VIII. Acoustic Cochlear nerve-deafness,
will not respond to sound
Vestibular nerve- circling,
head tilt, nystagmus, loss
of balance
Sudden loud noise, EEG
alterting response test
Observatiopn caloric test
Nystagmus No
nystagmus
IX. Glossophangeal Dificulty swallowing Touch pharynx
compression of throat
region
Gag,
deglutinatio
n, cough
No gag no
swallowing
no cough
51. X. Vagus Tachycardia? Pressure on eyeball Bradycardia
sometime
No bradycardia
XI. Spinal accessory Few sign seen. Neck
muscle
weakness.deviation
of head to one side
Palpation of
musculature
Muscle tone Lack of muscle tone
or atrophy
XII.Hypoglossal Earlydisease- tongue
deviates towords
the unaffected side
Late disease- tongue
deviates towords
the affected side or
atrophy and
corrugated
appearance
Observation pull
tongue out
Retract normaly diviates
52. Postural reactions
This part of the neurological examination is important in distinguishing neurological
disorders from diseases of other body systems.
Proprioceptive placing
This test is designed to evaluate the conscious awareness of limb position and movement in
space. It is evaluated by flexing the patient’s paw so that the dorsal surface contacts the
floor. It is important to support the patient with an arm under the abdomen if the patient is
too weak.
53. A normal response is
immediate correction
to the normal
position.
Another test involves
putting the patient’s
paw on a piece of
paper and sliding the
paper laterally. A
normal patient will
reposition its leg when
the limb reaches an
abnormal position.
Anabnormal reaction
is delayed correction
of the tested paw.
Proprioceptive placing is tested by placing
the paw in the abnormal position
54. Placing response
These are mainly used when proprioceptive positioning or hopping reaction do not confirm a
disorder.
Tactile placing-
Animal’s eyes are covered and distal part of thoracic limb is place on the edge of the table. When the
dorsal surface make contact with the edge, the animal should immediately place it’s foot on the
surface.
Visual placing-
It is performed by allowing the animal to see the table. Normal animal will reach for surface before
the paw touches the table.
56. Hopping reaction-
Hold the animal to support all it’s weight on one limb and move the animal forward or
laterally.
Each limb is tested individually and responses on left and right are compared.
Normal animals will hop on the limb while keeping the foot under their body for
support.
This is a sensitive test for subtle weakness and asymmetry.
58. Hemi-walking
Hold up the animal on
one side of the body
and move the patient
laterally. Normal
reaction is as described
for hopping reaction.
Hemi-walking
59. Wheelbarrowing-
Support the animal under
the abdomen so that the
pelvic limbs are in the air
and move the patient
forward.
Normal animal will move
with symmetrical
alternate movement of
the thoracic limbs.
This test highlights
subtle thoracic limb
weakness and ataxia.
Wheelbarrowing
60. Spinal reflexes
Spinal reflexes evaluation needs to be done in conjunction with assessment of gait and
postural reactions.
The spinal cord segmental in small animals can be divided into four regions.
1. Cranial cervical (C1-C5)
2. Cervicothoracic (C6-T2)
3. Thoracolumbar (T3-L3)
4. Lumbosacral (L4-S3)
61. If the lesion that causes spastic tetraparesis is localised in the C1-C5 region then the spinal reflexes
usually will be increased or intact.
The lesions of C6-T2 that causes tetraparesis will usually produce increased or intact reflexes in pelvic
limbs but decreased or absent in thoracic limbs.
T3-L3 lesions that cause spastic paraparesis will usually cause increased or intact reflexes in pelvic
limbs.
The lesion of L4-S3 that cause paraparesis will usually cause decreased to absent spinal reflexes of
pelvic limbs.
If the peripheral nervous system is affected then the animals will suffer flaccid tetraparesis
62. Withdrawal reflex in the pelvic limbs
This reflex evaluates the integrity of the L4-S2 spinal cord segment and sciatic and
femoral nerves. In order to perform this test the digit of the paw needs to be pinched
with the fingers. normal response results in the flexion of the hip (femoral nerve), stifle
and hock (sciatic nerve).
64. Patellar reflex
This is a monosynaptic reflex that evaluates integrity of the L4-L6 spinal cord
segment. The animal needs to be placed in to lateral recumbency with slight
stifle flexion. The limb should be held in a neutral position with the examiner’s
hand supporting the tested limb. The reflex hammer then hits the patellar
tendon and extension of the limb should be observed.
65. Patellar reflex is tested by hitting the
patellar tendon with the reflex hammer
66. Withdrawal reflex in the thoracic limbs
This reflex evaluates the integrity of the C6-T2 spinal cord segment and brachial plexus and
peripheral nerves in the thoracic limb. Pinching of the digits needs to be performed and
the flexion of all joints is considered to be a normal response.
67. Perineal reflex
This reflex is often overlooked and an important part of the neurological
examination. Stimulation of the perineum with the haemostat should result in
the contraction of the anal sphincter and flexion of the tail. This reflex tests the
integrity of the S1-Cd5 spinal cord segment and the pudendal nerve.
69. Urinary bladder palpation
Flaccid urinary bladder that is easily expressed is called lower motor neuron
bladder and suggests an S1-S3 spinal cord segment lesion, whereas the full and
turgid urinary bladder that is not easy to express and has overflow leakage of the
urine indicates an upper motor neuron disorder. The abnormal function of the
urinary bladder can as well be the result of dysfunction of the autonomic nervous
system.
71. Nociception testing
It is an important
test to do in the
cases of spinal cord
diseases because it
reflects the severity
of damage to the
spinal cord. The
noxious impulse
(squeeze of the toe
with the fingers or
haemostat) is
applied to the
tested area and the
animal must show a
behavioural
response (turning
the head, trying to
bite, vocalisation)
to say that the
nociception is
intact.
72. Cutaneous trunci reflex (panniculus)
This reflex is performed by pinching the skin of the dorso-lateral aspect of the
body between T2 and L4-L5.
A normal reaction to the pinch of the skin is a twitch of the skin (bilaterally, but
more prominent on the tested side)
73.
74. A variety of systemic disease can cause neurological signs. The cerebral cortex
and the peripheral nervous system are the parts of nervous system most
susceptible to the systemic diseases. However the white matter changes, brain
stem signs and cerebellar signs have also been documented secondary to the
systemic conditions.
75. Neurologic manifestation of systemic disease:
CNS:
1.Hypoxia:
a. Pulmonary disease
b. Cardiac diseas
infarct
hypoxia
hypertension
c. Aneasthetic accident
d. Vascular
hypertentions
coagulopathies
vasculitis
e. Hypoglycemia
insulin producing neoplasia
insulin over dose
sepsis
f. Thiamine deficiency
2.Metabolic
Hepato encephalopathy, renal encephalopathy,
hypoadrenocortism, hyperadenocortism,hypothyroidism,
hyperthyroidism
3.Electrolyte abnormalities:
Hypercalcemia,hypocalcemia, hyperkalemia, hypokalemia,
hypernatremia, hyponatremia
4.Neoplasia:
Primary, metastatic, infract, paraneoplastic syndrome
77. Hypoxia from systemic disease
Hypoxic encephalopathy is result of reduction of cerebral oxygen supply, either from decrease
arterial oxygen tension or reduced cerebral blood flow. Hypoxia can occur secondary to an
anesthetic accident, hematologic disorders (especially anemia), or cardiovascular and
respiratory failure.
Clinical sign : visual loss (most common in cats during anesthetic accidents), cytotoxic edema
in white matter
Treatment: establish normal blood flow and oxygenation in brain
Steroids are contraindicated
78. Hypertension
A rapid and sustained rise in the blood pressure cause the hypertension.
neurological signs are seizures, ataxia, stupor, and blind ness
Often occur in renal failure
Prevention by controlling seizure and neurological complication by controlling blood
pressure
79. Endocrine /metabolic cause
1. hepatic encephalopathy
Cuases: Porto systemic shunt, macrovasculature dysplasia, idiopathic non cirrhotic portal
hypertension, or other cause of liver failure.
Neurological sign: inability to learn new things and behavioral changes; head pressing,
blindness, mentation changes and seizure, generalized muscular weakness.
Treatment: decrease the production and absorption of toxin produce by bacteria in GIT.
Low protein diet, antibiotic, RL, H2 blocker
Potassium bromide: 40-60mg/kg Po once daily and gabapentin 20-60mg/kg/day divided
dose TID for controlling seizure.
80. 2. Renal encephalopathy
Toxic substance not excreted due to renal failure can cuase encephalopathic sign similar to
hepatic encephalopathy.
Increase concentration of parathyroid hormone and subsequent hypercalcemia contribute
to renal encephalopathy
Treatment: control PTH (calcitriol), Lower phosphorus level, treat hypertension.
81. 3. Hypothyroidism
Acute or chronic progressive central vestibular signs may be the sole clinical sign in dogs with
hypothyroidism
Myxedema coma is a rare but life threatening manifestation of hypothyroidism
Clinical signs: mentation changes, hypothermia without shivering, nonpitting skin edema,
bradycardia and brain edema
Treatment: adequate ventilation
Normal saline i/v, correct hypothermia, levothyroxine 5ug/kg i/v q 12h. Followed by
maintenance thyroid supplementation orally.
82. 4.Hyperthyroidism
Cats with hyperthyroidism show mild CNS signs that can include hyperactivity, change in
sleep/wake cycle, aggression or obtundation.
83. 5.hyperarenocorticism
Direct compression from a pituitary macroadenoma can cause mild to sever
neurologic sign.
Clinical sign: inappetence, mild obtundation, placing and disorientation
84. 6. Hypoglycemia
The brain since it can not synthesing glucose for normal cellular metabolism
100g/day of glucose requirement by brain
Hypoglycemia cause cellular dysfunction, vascular constriction, reduction in oxygen
supply
Hypoglycemia secondary to many condition: poor nutrition, insulinoma, liver failure,
hypoadrenocorticism, nonislet cell tumor producing insulin like growth factor, sever
polycythemia and sepsis.
85. Clinical sign: weakness, disorientation, tremors, partial or generalized seizures,
blindness, coma.
Treatment: 2-4ml/kg of 50% or 25% glucose I/V
Prednisone: to stimulate gluconeogenesis and glycogenolysis together with
frequent feeding of high protein, high fat and high complex carbohydrate diet.
86. 7. Thiamine deficiency
Essential for decarboxylation of pyruvic acid and other alfa- keto acids.
Thiamine deficiency cause poliencephalomalacia, necrosis and heamorrhage in
medial vestibular nuclei, caudal colliculi, cerebellar nodulus and the subcortical
grey matter.
87. Electrolyte abnormalities
1. Hypercalcemia:
Seizure
2.Hypocalcemia
Occur due to renal failure, hypoparathyroidism, eclampsia
Low calcium cause increase membrane excitability in both CNS and muscle.
Weakness, tetany, seizure
Treatment 0.5 – 1.5 mg/kg 10% cacium gluconate I/V over 10-20 minutes.
88. 3.Hypernatremia/Hyponatremia
Hyponatremia cause cerebral edema and life threatning diffuse encephalopathy.
Hypernatremia cause water out of the brain cells result in reduction of brain volume
which may cause rupture of cerebral vessels and focal heamorrhage.
.
89. 4. Neoplasia:
Paraneoplastic syndrome such as hypoglycemia induce by an insulin-producing tumor
and hyper calcemia secondary to lymphoma, thymoma, apocrine adenocarcinoma
directly affect the CNS.
5. Hyperthermia
The canine brain has an intrinsic thermal resistance. The origin or neurological disturbance in
dog and cats with hyperthermia usually from secondary changes such as hepatocellular
degeneration, disseminate intravascular coagulation, respiratory alkalosis.
Clinical sign: mentation changes, loss of pupillary light reflex and oculocephalic reflex as well
as tetraparesis.
90. Disease causing PNS signs
Hypoxia: aortic thromboembolism, cardiac failure or other causes
Neurologic sign: chronic exercise intolerance, with pelvic limb weakness, pelvic
ataxia, paresis or plegia signs due to ischemic myopathy, neuropathy or
myelopathy.
91. Endocrine/metabolic disorders
1.hypothyroidism:deficiency of ATP cause impairment in Na+/k+ pump reducing axonal
transport.
Neurological sign: generalized weakness, muscle atrophy, foca sign like laryngeal paralysis,
megaesophagus, facial paralysis, lameness etc
2.Hyperthyroidism
In cat cause neuromuscular weakness with ventroflection of the neck ,a plantigrade stance,
exercise intolerance.
3.Hyperadrenocorticism
Muscular weakness
92. 4.Hypoadrenocorticism
Lethargy, weakness, tremors and collapse
Treatment: glucocorticoids
5.Diabetes mellitus
Pelvic limb with plantigrade stance, difficulty jumping, postural reaction deficits,
decrease tendon reflex and muscle atrophy
6.Renal failure
Dogs and cats with chronic renal failure may have weakness associated with renal
secondary hyperparathyroidism, which cause peripheral neuropathy and myopathy.
93. Electrolyte abnormalities
1. hyperkalemia
Renal failure
Hyperkalemia alters the muscle cell resting membrane potential resulting in muscular weakness
Ventroflection of neck and generalize weakness
2.paraneoplastic syndrome
Secondry to insulinoma, adenoma, myeloma, thymoma
Thymoma is a common cause of myasthenia gravis in humans and cats and less common in
dogs.
