Ataxia & Paresis Flashcards
Where does the spinal cord end in relation to the vertebral column and what fills the gap?
Spinal cord ends in most dogs around L6 and around L7 in cats
so there is no spinal cord present at the lumbosacral junction (instead it is occupied by the cauda equina)
What are the four functional segments of the spinal cord?
[divided based on their corresponding vertebrae and LMN’s]
C1-C5
C6-T2
T3-L3
L4-S3
How does the spinal cord control bladder function?
At T3-L3 is the hypogastric nerve which controls bladder relaxation and sphincter contraction
At L4-S3 is the pelvic nerve which controls bladder contraction and the Pudendal nerve which controls sphincter contraction
How can a spinal cord lesion effect the eye?
sympathetic innervation of the eye runs through the entire cervical spinal cord
What are the main clinical signs associated with spinal cord disease?
ataxia, paresis and plegia (combination of 2 or more usually)
spinal hyperaesthesia
bladder dysfunction
What is the difference in the location of lesions in the spinal cord and the presentation of ataxia vs paresis/ paraplegia?
Ataxia suggests dorsolateral lesions (white matter of spinal cord)
Paresis/ Paraplegia suggests lesions in the grey matter in the proprioceptive or sensory tracts
What does spinal hyperaesthesia suggest about a spinal cord lesion?
Not actually in the cord- spinal cord has no pain receptors- suggests damage to surrounding structures e.g. meninges, intervertebral discs
Is Urinary incontinence an upper or lower motor neuron problem?
BOTH- when lesion is in the thoracolumbar spinal cord it causes UMN bladder, increased tone (bladder increases in size and can rupture)
When lesion is localised to S1-S3 of the spinal cord it causes LMN bladder and decreased tone (urine leaks out)
What long term affects can UMN bladder cause?
Persistent atonic bladder- bladder stretches so much it struggles to retain to its original shape
How do we manage bladder issues in patients with spinal cord disease?
Empty bladder regularly either manually or insert catheter
What is Cauda Equina syndrome and what are the two we should know?
used to describe any disease that causes cauda equina dysfunction
NEED TO KNOW- Degenerative lumbosacral Stenosis (DLSS) or Distal Spondylosis
What are the clinical signs associated with Cauda Equina syndrome? (5)
Paresis without Ataxia (e.g. not unsteady but reluctant to walk)
Pelvic limb lameness
Pain on hip extension
Decreased tail tone
Urinary incontinence
[no neurological deficits]
What does a Schiff Sherrington posture indicate about the location of the lesion?
Indicates its at T3-L3 of the spinal cord
Progressive neurological deficits with acute spinal disease occurs in a specific sequence- what is this sequence?
Proprioceptive deficits > Paresis and Ataxia > Plegia > Bladder dysfunction > Tail dysfunction > Pain sensation
An intact patella reflex suggests that the lesion is NOT at which parts of the spinal cord?
What is the exception to this rule?
L4-L6
Patella reflex can be physiologically absent in older dogs or after stifle surgery
An absent or exaggerated patella suggests what about the location of the spinal lesion?
LMN lesions- reflex will be decreased or absent
UMN lesions- normal or exaggerated.
Where would we perform the cutaneous trunci reflex?
Between T2 and L4-L5 spinal cord- absent in neck and lumbosacral regions
How does lumbosacral disease cause an absent withdrawal reflex?
HINT- think about what nerve exits the spinal cord here
Sciatic nerve exits spinal cord at L7-S1 where it splits into the peroneal nerve (innervates dorsal part of limb) and the tibial nerve (innervates plantar side of limb)- damage to these parts of the spine can damage the sciatic nerve
What clinical signs will be observed in an animal with tibial nerve dysfunction? (3)
Decreased muscle tone
Dropped hock (plantigrade stance)
Overflexion of the Tarsus and loss of hock flexion
What are the clinical signs of lower motor neuron lesions?
loss of stimulation- flaccid paralysis
decreased spinal reflexes
What are the clinical signs of upper motor neuron lesions?
loss of disinhibiton- excessive stimulation/ excitation
increased muscle tone
increased spinal reflexes
