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426 Cards in this Set
- Front
- Back
Components of a motor unit:
|
Lower motor neuron
Peripheral nerves NM Junction Skeletal muscle fibers Sensory nerves |
|
Clinical signs associated with motor unit disease:
|
Weak or ineffective movement (paralysis or paresis)
RAPID loss of muscle tone and bulk Altered sensation if sensory nerves affected DIMINISHED or absent spinal reflexes |
|
Rapid loss of muscle tone and bulk is associated with UMN or LMN disease?
|
LMN
|
|
Diminished or absent spinal reflexes is associated with UMN or LMN disease?
|
UMN
|
|
Causes of motor unit (LMN) disease:
|
Loss of single nerve
Loss of group of nerves (i.e. plexus) Generalized loss of nerves, NM junction or skeletal muscle |
|
What is a spinal reflex?
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An unconscious response to stimulation
|
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What is required for a spinal reflex?
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Receptor
Afferent neuron Efferent neuron NM junction Skeletal muscle |
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True/false: A spinal reflex does not require higher centers.
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True
|
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Which of these is not required for a spinal reflex:
Afferent Neuron Skeletal Muscle Sensory nerves Efferent neuron NM junction |
Sensory nerves
|
|
What are the thoracic limb spinal reflexes?
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Triceps reflex
Biceps reflex Extensor carpi radialis reponse Withdrawl |
|
By percussing the triceps tendon, which nerve are you evaluating?
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Radial nerve
|
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The radial nerve is evaluated by the triceps reflex. This corresponds to which spinal cord segments?
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C7-T1
|
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Percussion of the biceps tendon evaluates which nerve?
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Musculocutaneous
|
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The musculocutaneous nerve is evaluated with the biceps reflex. Which spinal cord segments does this correspond to?
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C6-C8
|
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Evaluation of the extensor carpi radialis muscle evaluates which nerve?
|
Radial nerve
|
|
Evaluation of the extensor carpi radialis evaluates the radial nerve at which spinal cord segments?
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C7-T2
|
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With withdrawl response in the thoracic limb, the efferent response is mediated by what?
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Axillary, musculocutaneous, median and ulnar nerves (at C6-T2 spinal cord segments)
|
|
What reflexes are involved in the pelvic limb?
|
Patellar reflex
Cranial tibial reflex Gastrocnemius reflex Sciatic reflex Perineal reflex Withdrawal |
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The patellar reflex evaluates which nerve?
|
Femoral nerve (L4-S2)
|
|
The cranial tibial reflex evaluates which nerve?
|
Peroneal branch of sciatic nerve (L6-S2)
|
|
Percussion of the achilles tendon evaluates which nerve?
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Tibial branch of sciatic nerve (L6-S2)
|
|
Efferent response associated with withdrawl in the pelvic limb is mediated by which nerves?
|
Sciatic nerve
Cranial and caudal gluteal (L6-S3) |
|
When you percuss the sciatic notch, which nerve are you testing?
|
Sciatic
L6-S2/3 |
|
How do you test for the perineal reflex?
|
Stimulate the perineum
|
|
Normal response of the perineum when stimulated is:
|
Contraction of the external anal sphincter
|
|
Stimulation of the perineum evaluates which nerve?
|
Pudendal
S1-S3 |
|
What is contained within the gray matter of the spinal cord?
|
LMN (motor units)
Interneurons |
|
What is contained within the white matter of the spinal cord?
|
Axons from sensory neurons that are relaying information to the brain from peripheral sensory receptors
Motor axons from UMN |
|
Upper motor neurons are collections of motor neurons located primarily where?
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In the brain stem
|
|
What regulates LMNs?
|
UMNs
|
|
What are the clinical signs associated with UMN injury?
|
Weak or ineffective movement (paresis to paralysis)
Gradual loss of muscle tone and bulk (due to disuse rather than denervation) Altered sensation if sensory tracts in spinal cord are severed EXAGGERATED and abnormal spinal reflexes |
|
Why are spinal reflexes exaggerated and abnormal with UMN injury?
|
Because without the UMN, there is no coordination of the LMN
|
|
Do you get exaggerated and abnormal spinal reflexes with UMN injury or LMN injury?
|
UMN injury
|
|
What are two examples of abnormal spinal reflexes associated with UMN injury?
|
Crossed extensor
Babinski |
|
How do you perform a Babinski?
|
Apply moderate pressure to the plantar surface of the hock in sweeping motion away from the digits. Positive response is extension of the digits
|
|
True/false: Clinical signs associated with spinal cord injury vary with location.
|
True
|
|
Are spinal cord segments the same as vertebral segments?
|
NO
|
|
What are the clinical signs of injury to spinal cord segments L4-S3?
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Weakness/paralysis of rear limbs
Rear limb atrophy, hypotonia Changes in sensation if injury is severe Diminished or absent spinal reflexes in rear limbs No changes in thoracic limbs |
|
What are the clinical signs of injury to spinal cord segments T2-L4?
|
Weakness/paralysis of rear limbs
Rear limb muscle atrophy in chronic cases (disuse) Sensation altered w/ severe spinal cord injury Exaggerated spinal reflexes Panniculus reflex absent in segments caudal to injury Thoracic limbs normal |
|
The panniculus reflex is AKA:
|
Cutaneous trunci reflex
|
|
What are the clinical signs of injury to spinal cord segments C6-T2?
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Weakness/paralysis in all four limbs
Rear limb changes indistinguishable from T2-L4 injury Muscle atrophy, hypotonia in front limbs Changes in sensation if injury is severe Spinal reflexes diminished/absent in front limbs, exaggerated in rear limbs Absent panniculus reflex Horners syndrome |
|
What causes Horner's syndrome?
|
Loss of sympathetic innervation to the eye causing miosis, ptosis and enophthalmus
|
|
What is ptosis?
|
Palpebral fissure is narrowed
|
|
What is miosis?
|
Contriscted pupil
|
|
Why does Horner's syndrome arise with injury to spinal cord segments C6-T2?
|
The presynaptic neuron that provides sympathetic innervation to the face arises from neurons located at T1-2 and exits with the brachial plexus
|
|
What are the clinical signs of injury to spinal cord segments C1-C6?
|
Weakness/paralysis in all four limbs
Muscle atrophy only in chronic cases All limbs retain some tone Changes in sensation only if injury is severe Spinal reflexes exaggerated in all four limbs Respiratory muscles may be affected |
|
What does the postural reaction test?
|
Whether the animal can recognize its foot is in an abnormal position to bear weight
Evaluates both UMN and LMN |
|
With spinal cord lesions, postural reaction deficits are worse on the same or opposite side of the lesion?
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Same side
|
|
Postural reactions can't tell you if it is an UMN or LMN injury. How can you tell?
|
Do spinal reflexes
|
|
How do you test for conscious proprioception?
|
Knuckle foot over on dorsum and let go
|
|
What are the postural reaction tests?
|
Conscious proprioception
Wheelbarrowing Hopping Extensor postural thurst Hemistanding, Hemiwalking Placing reaction |
|
Ascending sensory and descending motor pathways from the brain are most easily evaluated how?
|
With postural reaction
|
|
Injury to ascending sensory and descending motor pathways in the midbrain or rostral (diencephalon, cerebrum) will create postural deficits on the ipsilateral or contralateral side?
|
Contralateral
|
|
Injury to the ascending sensory and descending motor pathways in the midbrain, pons and medulla (as well as spinal cord and peripheral nerve) will cause ipsilateral or contralateral postural deficits?
|
Ipsalateral
|
|
Which cranial nerve is actually an extension of the brain?
|
CN II; the other cranial nerves are nothing more than peripheral nerves
|
|
The reticular formation extends from:
|
Caudal diencephalon to the medulla
|
|
What is the job of the reticular formation?
|
Receives sensory input and sends output to many areas of nervous system
Centers control inspiration, expiration, normal breathing rhythm, HR, BP |
|
CN I is associated with which portion of the brain?
|
Telencephalon
|
|
CN II is associated with which portion of the brain?
|
Diencephalon (thalamus/hypothalamus)
|
|
CN III and IV are associated with which portion of the brain?
|
Mesencephalon (midbrain)
|
|
Another name for mesencephalon:
|
Midbrain
|
|
Another name for diencephalon and telencephalon?
|
Forebrain
|
|
CN V - XII are found in which portion of the brain?
|
Metencephalon
Myelencephalon |
|
True/false: CN I is not routinely evaluated
|
True
|
|
How is vision evaluated (and thus CN II)?
|
Observing movement and ability to follow objects - if in doubt, throw a cotton ball
|
|
What does the menace response test?
|
Vision
|
|
True/false: In most animals, information from the optic nerve crosses the optic chiams to the contralateral lateral geniculate ganglion.
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True
|
|
The right eye projects primarily to the left or right visual cortex?
|
Left visual cortex
|
|
Light entering the eye stimulates what?
|
Retina
|
|
Describe the pathway for pupillary light reflexes.
|
Light stimulates retina
Impulse transmitted via optic nerve to optic chiasm Afferent neuron passes through lateral geniculate ganglion to pretectal nucleus in the midbrain and back to the opposite side (same side as stimulus). Parasympathetic nucleus of CN III initiates efferent resopnse to constrict pupil. |
|
How does consensual PLR occur?
|
Crossover at the paraympathetic nucleus of CN III, so the opposite eye is stimulated to contract as well. The consensual response is never as strong as the direct response.
|
|
Motor (efferent) control of the pupil is controlled by:
|
Constriction = Cell bodies located in parasympathetic nucleus exit brainstem w/ CN III
Dilation = sympathetic innervation via pretectal nucleus. Neurons in the midbrain respond to lack of light and thus dilate the pupil |
|
How do you evaluate the parasympathetic component of CN III?
|
PLR
|
|
If you see ptosis of the upper eyelid, ventrolateral strabismus and a dilated pupil, what cranial nerve is affected?
|
CN III
|
|
If you see rotational deviation of the globe, what CN is affected?
|
CN IV (trochlear)
|
|
CN IV =
|
Trochlear
|
|
Which three cranial nerves are evaluated together by observing eye movement?
|
CN III, IV, VI
|
|
Cranial nerve VI =
|
Abducens
|
|
If you see ventromedial strabismus (inability to move the eye laterally), which CN is affected?
|
CN VI
|
|
Injury to CN III, IV, VI together cause complete paralysis of the globe, AKA:
|
Ophthalmalplegia
|
|
CN V is evaluated with what other cranial nerve?
|
VII
|
|
Which cranial nerve supplies sensation to the face?
|
CN V
|
|
Which cranial nerve supplies motor to muscles of facial expression?
|
CN VII
|
|
How do you test CN V and VII together?
|
Gently touch, pinch or stroke hairs of face to see if animal response with facial movement, blink, lip retraction
|
|
Which cranial nerve supplies parasympathetic innervation to the lacrimal glands?
|
CN VII
|
|
Which cranial nerve supplies motor to muscles of mastication?
|
CN V
|
|
Injury to what cranial nerve causes ptosis of the upper lid, loss of ability to close the eye, loss of ability to retract the lip, loss of tear production, and loss of taste to the anterior 2/3 of the tongue?
|
CN VII
|
|
CN VIII is AKA:
|
Vestibulocochlear
|
|
How do you evaluate an animal's vestibular function?
|
Observe body posture (head tilt?), gait (ataxic?) and eye movement
|
|
What are the two hallmarks of vestibular disease?
|
Nystagmus and Strabismus
|
|
Injury to inner ear structures would be a peripheral or central vestibular lesion?
|
Peripheral
|
|
Injury to the central nervous system structures related to CN VIII would cause peripheral or central vestibular disease?
|
Central
|
|
What is the most reliable way to distinguish peripheral vs. central vestibular lesion?
|
Postrual reactions
Normal w/ peripheral, decreased on the side of the lesion w/ central |
|
Which often is associated with Horner's syndrome - a peripheral vestibular lesion or central?
|
Peripheral
|
|
What other cranial nerve deficit is sometimes associated with a peripheral vestibular lesion?
|
CN VII
|
|
True/false: With central vestibular disease, the direction or character of nystagmus varies in different head positions
|
True
|
|
True/false: With peripheral vestibular disease, a head tilt is away from the side of the lesion
|
False - toward the side of the lesion
|
|
How do we test CN IX, X, XI?
|
Test pharyngeal sensation and motor function with a gag response
|
|
Lesions in CN IX, X, XI will cause what?
|
Inability to swallow, weak gag response
|
|
CN XII is responsible for what?
|
Tongue movement
|
|
True/false: With central vestibular disease, the direction or character of nystagmus varies in different head positions
|
True
|
|
True/false: With peripheral vestibular disease, a head tilt is away from the side of the lesion
|
False - toward the side of the lesion
|
|
How do we test CN IX, X, XI?
|
Test pharyngeal sensation and motor function with a gag response
|
|
Lesions in CN IX, X, XI will cause what?
|
Inability to swallow, weak gag response
|
|
CN XII is responsible for what?
|
Tongue movement
|
|
What clinical signs will you notice with a lesion in CN XII?
|
Tongue deviates to normal side initially but chronicity the tongue atrophies on affected side
|
|
The pons and medulla make up what part of the brain?
|
Metencephalon and Myelencephalon
|
|
The cerebrum makes up what part of the brain?
|
Telencephalon
|
|
The thalamus and hypothalamus make up what part of the brain?
|
Diencephalon
|
|
Clinical signs of injury to the pons and medulla:
|
Gait and postural reaction ipsalateral to the lesion
Deficits in CN V - XII Head tilt to side of lesion Abnormal respiration, HR and levels of arousal with severe injury |
|
What is the role of the cerebellum?
|
Receives input from all motor centers and projects to all motor centers.
Regulates rate, range and force of movement Tone and posture Controls fine motor skills Functions in balance and equilibrium |
|
UMNs coordinate LMN. What coordinates the UMN?
|
Cerebellum
|
|
What part of the brain functions in balance and equilibrium and controls fine motor skills via regulation of UMNs?
|
Cerebellum
|
|
Clinical signs of injury to the cerebellum:
|
Ataxia, spastic gait and postural reactions
Tremors that are goal oriented Central vestibular dysfunction |
|
Why might you lose your menace response with injury to the cerebellum?
|
Because ALL reflex movement is facilitated by the cerebellum
|
|
Clinical signs of midbrain injury:
|
Gait and postural reaction deficits - ipsilateral or contralateral to lesion
Changes w/ CN III, IV Head tilt |
|
What structures are located in the diencephalon?
|
Thalamus
Hypothalamus CN II |
|
What clinical signs are associated with diencephalon injury?
|
Behavioral changes
Autonomic dysfunction Endocrine imbalances Seizures Head tilt/circling to side of lesion Gait and postural reactoin deficits CONTRALATERAL to injury CN II deficits - blindness, PLR |
|
What are the prominent structures in the telencephalon?
|
Cerebral cortex
Basal nuclei |
|
What are the clinical signs associated with injury to the telencephalon?
|
Behavioral changes
Seizures Normal gait w/ contralateral postural deficits Pacing, circling to side of lesion |
|
True seizures arise in what part of the brain?
|
Diencephalon
Telencephalon |
|
What does paresis mean?
|
Weakness
|
|
What does plegia mean?
|
Paralysis
|
|
Monoparesis is most commonly caused by what?
|
A disease affecting one or more peripheral nerves in close proximity
|
|
True/false: motor unit disease either affects 1 limb or all 4 limbs
|
True
|
|
Generalized motor unit disorders are characterized by:
|
Generalized weakness with diminished or absent spinal reflexes
|
|
Can you distinguish clinicall btween polyneuropathy, polymyopathy and junctionopathy?
|
No
|
|
What is polyneuropathy?
|
Diffuse peripheral nerve dysfunction
|
|
What is polymyopathy?
|
Diffuse skeletal muscle dysfunction
|
|
What is junctionopathy?
|
Disorder of neuromuscular transmission
|
|
Most common causes of monoparesis or monoplegia:
|
Trauma or neoplasia
|
|
What are some ways the sciatic nerve might be typically damaged?
|
IM injection
Pelvic fracture Lumbosacral fracture IM pinning of femur |
|
Peripheral nerve trauma is divided into 5 separate classes based on:
|
Severity of injury
|
|
What is neuropraxia?
|
Nerve conduction is temporarily impaired usually by crush injury. Complete recovery occurs within hours
|
|
Does recovery occur with neuropraxia?
|
Yes
|
|
What type of nerve injury causes nerve conduction to be temporarily impaired, usually by a crush injury?
|
Neuropraxia
|
|
What is axonotmesis?
|
Axons are interrupted, but the supporting connective tissue remains intact. Most common form is a nerve stretch injury
|
|
Describe Wallerian degeneration.
|
Occurs distal to the site of injury, but regeneration is usually effective since regenerating axons can be guided back to the appropriate targets
|
|
What is neurotomesis?
|
Nerve is severed
|
|
What are the clinical signs associated with monoparesis due to peripheral nerve trauma?
|
Usually acute
Non-progressive loss of function Specific clinical signs vary with nerve affected |
|
What might you notice on PE with an animal who is presented with monoparesis due to peripheral nerve trauma?
|
Muscle atrophy and weakness
|
|
How do you diagnose a monoparetic lesion?
|
Clinical signs, including motor loss, loss of cutaneous sensation, distribution of muscle atrophy
|
|
What ancillary aid can you use to aid in diagnosis of a monoparetic lesion?
|
EMG may confirm area of denervation. Motor and sensory nerve conduction velocity may help ascertain if injury is complete
|
|
How do you treat a dog with monoparesis due to peripheral nerve injury?
|
Peripheral axons regenerate at a rate of 1-2 mm/day. Surgical repair has been attempted
|
|
What is the prognosis for an animal who presents with a peripheral nerve injury causing monoparesis?
|
Depends on class of injury and length axons must regrow to reach target. Prognosis much better if supportive structures remain intact and provide directional guidance for regenerating axons
|
|
You are presented with a dog who has peripheral nerve damage and subsequent monoparalysis. How long should you wait to give a prognosis?
|
Wait a few wks to 2 months - give it time to regrow
|
|
What is the primary nerve that determines if the thoracic limb is functional?
|
Radial
|
|
Why does the radial nerve primarily determine if the thoracic limb is functional?
|
Functions to extend the elbow, carpus and digits - without it you have loss of weight bearing, unable to fix limb in extension
|
|
True/false: The injury to the suprascapular nerve causes little gait abnormality.
|
True
|
|
Where does the radial nerve come off the spinal cord?
|
C6-T2
|
|
Which nerves function to flex the carpus and digits?
|
Median and ulnar
|
|
What is the function of the axillary nerve?
|
Flexion of shoulder
|
|
Which nerve serves to flex the shoulder?
|
Axillary
|
|
Which nerve serve to extend the shoulder?
|
Suprascapular
|
|
Which nerve serves to flex the elbow?
|
Musculocutaneous
|
|
Which nerves serve to flex the carpus and digits?
|
Median and ulnar
|
|
With injury to the axillary, median or ulnar nerves, you get little gait abnormality and incomplete what?
|
Withdrawal reflex
|
|
If a dog has lost sensation to the central dorsal part of the front paw, which nerve has been damaged?
|
Radial
|
|
If a dog loses sensation to the palmar surface of the paw and the caudal forelimb which nerve(s) are damaged?
|
Median and ulnar
|
|
If a dog loses sensation to the medial portion of the leg only, which nerve is most likely injured?
|
Musculocutaneous
|
|
What are the two nerves in the pelvic limb that we worry about injury and gait abnormality?
|
Femoral and Sciatic
|
|
What is the function of the femoral nerve?
|
Extension of the stifle
|
|
What is the function of the sciatic nerve?
|
Flexion and extension of the hip
|
|
Which nerve serves to adduct the pelvic limb?
|
Obturator
|
|
If you have damage to the obturator nerve, what sign of dysfunction might you see?
|
Little gait abnormality - limb may slide laterally on slick floor
|
|
Which nerve serves to flex the hock and extend digits?
|
Peroneal
|
|
If you have damage to the peroneal nerve, what are the signs of dysfunction?
|
Cannot extend paw therefore knuckles on dorsum, poor hock flexion
|
|
If you have damage to the tibial nerve, what is the result?
|
Unable to fix hock in extension
|
|
Which nerve serves to extend the hock and flex the paw?
|
Tibial
|
|
What is the cutaneous distribution for the tibial nerve?
|
Plantar surface of paw
|
|
Which of the nerves in the pelvic plexus does not have a cutaneous distribution?
|
Obturator
|
|
If you have loss of sensation to the medial portion of the thigh and medial digit of the hind limb, which nerve is injured?
|
Femoral
|
|
If you have loss of sensation to the caudal and lateral surfaces of the hind limb, which nerve is injured?
|
Sciatic
|
|
If you have loss of sensation to the dorsal aspect of the hind paw, which nerve is injured?
|
Peroneal
|
|
What are the 6 nerves of the brachial plexus?
|
Suprascapular
Axillary Radial Musculocutaneous Median and ulnar |
|
If you have an inability to extend the stifle, which nerve is damaged?
|
Femoral
|
|
What are the 5 nerves of the pelvic plexus?
|
Obturator
Femoral Sciatic Peroneal Tibial |
|
What branch of the femoral nerve supplies the medial thigh and digit?
|
Saphenous
|
|
With brachial plexus avulsion, why are the nerve rootlets near the intervertebral foramen the weakest point of the plexus?
|
They are vulnerable to stretch injury b/c the perineurium has not formed completely in this transitional zone
|
|
Common ways to cause a brachial plexus avulsion:
|
Severe adduction or abduction - like when an animal falls; nerves will tear right at the intervertebral foramen
|
|
True/false: The radial nerve is almost always affected with brachial plexus avulsion.
|
True
|
|
What might some of your clinical findings be with a brachial plexus avulsion?
|
Distribution of analgesia of the limb
Horner's syndrome Ipsilateral panniculus reflex may be lost |
|
What are some ancillary tests that can be used to confirm the extent of a brachial plexus avulsion?
|
EMG
NCV |
|
How do you treat a brachial plexus avulsion?
|
Give it time - about a month (b/c of axonotmesis or neuropraxia)
Physical therapy Amputation |
|
What is the prognosis for brachial plexus avulsion?
|
Usually poor for return to function
|
|
Why is analgesia associated with a complete brachial plexus avulsion distal to the elbow?
|
b/c proximal to the elbow sensory innervation is supplied by nerves originating outside the brachial plexus
|
|
Which is more common, primary or secondary nerve root tumors?
|
Primary
|
|
What is the difference between primary and secondary nerve root tumors?
|
Primary = neoplastic transformation within peripheral nerves
Secondary = peripheral nerves are invaded by neoplastic hemolyphatic cells or are entrapped by nearby carcinomas or sarcomas |
|
True/false: With malignant nerve sheath tumors they rarely invade surrounding tissue and metastasis is rare.
|
True
|
|
Neurologic signs associated with malignant nerve sheath tumors are created by:
|
Compression of peripheral axons, spinal cord or brainstem by expanding neoplastic mass
|
|
Nerve sheath tumors are more common in dogs or cats?
|
Dogs
|
|
What history is associated with an animal with a malignant nerve sheath tumor?
|
Chronic progressive lameness
|
|
What might you notice on PE with an animal who has a nerve sheath tumor associated with the brachial plexus?
|
Lameness and muscle atrophy are prominent
Pain may be elicited by deep palpation of the plexus |
|
What ancillary aid is helpful to distinguish neurogenic atrophy of a leg from disuse atrophy?
|
EMG
|
|
What ancillary aids are useful to help diagnose a malignant nerve sheath tumor?
|
EMG
CT, MRI Myelography to help determine if the mass has reached the spinal canal |
|
What is the treatment for a brachial plexus associated nerve sheath tumor?
|
Amputation
|
|
What is the prognosis for a brachial plexus nerve sheath tumor?
|
Poor b/c it is difficult to remove all neoplastic cells; often there is regrowth even with resection and amputation
|
|
Why doesn't a nerve sheath tumor respond to chemo?
|
Its of mesenchymal origin
|
|
What are some ways to help narrow down the location of generalized motor unit disease?
|
CK - if elevated muscle more likely
Eletrophysiology Muscle biopsy |
|
When an animal takes short choppy steps, this is what type of gait?
|
Paretic
|
|
What are the most common causes of acute onset generalized polyneuropathy or junctionopathy?
|
Coonhound paralysis
Saddle thrombus (cats) Botulism Tick paralysis |
|
What are the most common reasons for chronic and progressive onset of generalized polyneuropathy or junctionopathy?
|
Metabolic diseases
Paraneoplastic disease Myasthenia gravis Demyelinating neuropathy |
|
What do you have to remember about inherited peripheral nerve diseases in dogs and cats?
|
That there is a huge list - consider this as an option with any young animal that presents with generalized LMN signs
|
|
What are the top 3 metabolic disorders that can cause polyneuropathy?
|
Hypothyroidism
Hypoglycemia/Insulinoma Diabetes Mellitus |
|
Coonhound paralysis is AKA:
|
Acute polyradiculoneuritis
|
|
Acute polyradiculoneuritis is AKA:
|
Coonhound paralysis
|
|
What is coonhound paralysis?
|
Acute, inflammatory demyelination of peripheral nerves and ventral nerve roots
|
|
An acute, inflammatory demyelination of peripheral nerves and ventral nerve roots is AKA:
|
Coonhound paralysis
|
|
How would a dog acquire coonhound paralysis?
|
Clinical signs begin 7-12 days after raccoon bite, but there are some cases where the dog had no exposure to raccoons
|
|
Describe the clinical signs associated with coonhound paralysis.
|
Ascending generalized LMN disease that progresses over 2-10 days - includes complete quadriplegia w/ variable crnial nerve weakness and respiratory paralysis. Often animal maintains the ability to wag its tail.
|
|
What is the treatment for coonhound paralysis?
|
Time really - many animals begin to show spontaneous remission; complete recovery can take a few wks to a few months
|
|
What is the etiology of coonhound paralysis?
|
Unknown - Possibly autoimmune. Possibly something antigenically similar to peripheral nerve myelin in the raccoon saliva and thus initiates an autoimmune reaction against myelin
|
|
How do you diagnose coonhound paralysis?
|
Based on hx, cs and exlusion of other rapidly progressive motor unit diseases.
EMG, MNCV, CSF |
|
With coonhound paralysis, what do you expect the results of a MNCV test to be?
|
Slowed with reduced and dispersed evoked action potential due to demyelination of peripheral nerves
|
|
With coonhound paralysis, what do you expect the results of an EMG to show?
|
Diffuse spontaneous activity
|
|
Which disease is characterized by a deficiency in acetylcholine receptors and is destribed in Springers, Jack Russells, and Dachshunds?
|
Myasthenia gravis - congenital form
|
|
Which is rare - the congenital form or acquired form of myasthenia gravis?
|
Congenital
|
|
Which dog breed is especially susceptible to myasthenia gravis?
|
Akita
|
|
What is the pathophysiology of the acquired form of myasthenia gravis?
|
Results from immune reaction in which antibodies bind to acetylcholine receptor
|
|
Clinically, myasthenia gravis most often results in:
|
Exercise-induced weakness
|
|
What two other conditions are often associated with myasthenia gravis?
|
Megaesophagus and pharyngeal paralysis
|
|
Very severe forms of generalized myasthenia gravis are AKA:
|
Acute Fulminant myasthenia gravis
|
|
Which type of myasthenia gravis is due to a lack of acetylcholine receptors?
|
Congenital
|
|
When only esophageal motility is affected by myasthenia gravis, this is AKA:
|
Focal myasthenia gravis
|
|
Evidence supports an association between geriatric myasthenia gravis and what?
|
Occult neoplasia
|
|
What are the clinical signs associated with myasthenia gravis?
|
Weakness that worsens w/ exercise and improves with rest
Dysphagia Facia muscle weakness Megaesophagus |
|
True/false: Limb weakness associated with myasthenia gravis often looks worse in the hind limbs
|
True
|
|
What are some ancillary aids to help diagnose myasthenia gravis?
|
Radiographs of esophagus
EMG, NCV -->usually normal Tensilon test |
|
What is the Tensilon test?
|
Administer edrophonium chloride (a short acting anti-cholinesterase) IV to collapsed dog with myasthenia gravis. Within 2-3 minutes normal strength should return for 10-15 minutes
|
|
Which AchE inhibitors can you use to treat megaesophagus?
|
None - they won't work
|
|
What are some drugs that can be used to treat myasthenia gravis?
|
Pyridostigmine bromide
Neostigmine bromide Prenisolone |
|
What is the prognosis for a dog with myasthenia gravis?
|
Varies. About 50% die within a few weeks of diagnosis from aspiration pneumonia. When antibody titers fall, esophageal motility improves. Spontaneous remission occurs
|
|
How can we decrease antibody titers with myasthenia gravis?
|
Stabilize patient on AchE inhibitors first
Start w/ anti-inflammatory dose of pred and gradually increase to an immunosuppressive dose |
|
How can you diagnose chronic inflammatory (demyelinating) neuropathy?
|
EMG -->normal or shows patchy areas of spontaneous activity
MNCV -->slowed suggesting a primary demyelinating condition Histology -->demyelination |
|
The majority of patients with chronic inflammatory (demyelinating) neuropathy respond to what treatment?
|
Steroids (prednisolone) and therapy can be gradually tapered and withdrawn in some
|
|
What is the most likely etiology of chronic inflammatory (demyelinating) neuropathy?
|
Immune mediated
|
|
Describe the type of neuropathy associated with toxic exposures.
|
Chronic and progressive diabilities due to chronic low level intoxication; can appear acutely as well - depending on the toxicant
|
|
How do you diagnose a toxic neuropathy?
|
History, demonstration of toxic substance in serum or tissues and response to removal
|
|
What is the etiology of tick paralysis?
|
Female Dermacentor ticks secrete a neurotoxin that blocks the release of Ach from axon terminal
|
|
Which two female ticks can cause tick paralysis?
|
Dermacentor variabilis
Dermacentor andersoni |
|
What are the clinical signs associated with tick paralysis?
|
Acute (possibly ascending) flaccid paralysis that can affect respiration and cranial nerves
|
|
How do you diagnose tick paralysis?
|
Based on CS and reponse to tick removal. EMG --> normal; MNCV --> normal but muscles response may be weak or absent; SNCV --> normal
|
|
If a dog has tick paralysis and you remove all of the ticks, how soon do clinical signs resolve?
|
12 hours
|
|
How many neurotoxins can C. botulinum produce and what do they do?
|
8 --> They block the release of ACh from nerve terminal
|
|
How do animals usually get botulism?
|
Toxin ingested from spoiled food
|
|
What are the clinical signs of botulism?
|
Acute onset of generalized LMN quadriparesis; cranial nerves often severely affected with mydriasis; decreased jaw tone and gag reflex, poor facial muscle tone
|
|
What is mydriasis?
|
Pupillary dilation
|
|
How do you diagnose botulism?
|
Demonstration of toxin in foodstuffs, stomach contents, feces
Eletrophysiologic changes similar to tick paralysis |
|
How do you treat botulism?
|
Antitoxin; however, antitoxin does not affect toxin that has already bound to nerve terminals, therefore therapy is largely supportive.
|
|
What is the prognosis for botulism?
|
Depends on severity of signs. Remission occurs within 4 wks and is attributed to regrowth of peripheral nerve terminals
|
|
Which produces an irreversible binding of toxin to nerve terminals, botulism or tick paralysis?
|
Botulism
|
|
Muscular dystrophy (or inherited myopathies) are characterized by what?
|
Progressive degeneration of skeletal muscles
|
|
Which animal gets Type II Myofiber deficiency?
|
Labs
|
|
How are muscular dystrophies best diagnosed?
|
Muscle biopsy
|
|
What signalment is typical for an animal presenting with a potential muscular dystrophy?
|
Young
Pure-bred |
|
Which cat breed is particularly vulnerable to hypokalemic myopathy (periodic paralysis) and why?
|
Burmese cats - b/c they have an inherited renal disease that causes them to lose K via the kidneys
|
|
True/false: Only Burmese cats are susceptible to hypokalemic myopathy.
|
False - all cats are susceptible
|
|
What are the clinical signs associated with hypokalemic myopathy in cats?
|
Acute onset of appendicular weakness and marked ventro-flexion of the neck
|
|
How do you diagnose hypokalemic myopathy in cats?
|
Low serum potassium levels
Elevated CK Evidence of renal dysfunction Metabolic acidosis |
|
How do you treat hypokalemic myopathy in cats?
|
Potassium replacement. Oral treatment recommended unless swallowing deficits. If respiratory paralysis is imminent, give IV
|
|
The maximum rate of potassium infusion should never exceed what?
|
0.5 mEq/kg/hr
|
|
Hyperadrenocorticism is AKA:
|
Cushings Disease
|
|
What are teh two forms of muscle disease associated with Cushings?
|
Atrophic myopathy
Pseudomyotonia |
|
Atrophic myopathy associated with Cushings disease preferentially affects what?
|
Proximal appendicular muscles
|
|
Which form of muscle disease associated with Cushings is more common?
|
Atrophic myopathy
|
|
Hypoadrenocorticism is AKA:
|
Addison's disease
|
|
Describe the myopathy associated with Addison's disease.
|
Generalized muscle weakness, often with pharyngeal and esophageal weakness
|
|
True/false: with Cushings and Addison's disease associated myopathies, correcting hte underlying disease corrects the myopathy.
|
True
|
|
Are both hypothyroidism and hyperthyroidism associated with myopathies? If not, which one is?
|
Both
|
|
Why are hypo and hypoer parathyroidism associated with myopathies?
|
Because any significant alteration in serum Ca or K will cause muscle weakness
|
|
Which two protozoal parasites can cause myopathies?
|
Toxoplasma gondii
Neospora caninum |
|
What clinical signs are seen in puppies <4 months old who have a T. gondii or N. caninum infection?
|
Hyperextension of both rear limbs (stiff stifle syndrome)
|
|
Typically, how do clinical signs present in adult dogs who have T. gondii or N. caninum infections?
|
Multi-focal neurologic diseases with various degrees of encephalitis, myelitis, polyradiculoneuritis and myositis
|
|
How do you diagnose T. gondii or N. caninum as a cause of myopathy?
|
Rising titers and demonstration of organism within biopsy
|
|
How do you treat T. gondii or N. caninum infections that cause myopathies?
|
Pyrimethamine and sulfadiazine or clindamycin
|
|
What is the prognosis for myopathies associated with T. gondii and N. caninum?
|
Depends on extent of CNS involvement. Extensor rigidity is NOT reversible
|
|
Why is it that sometimes muscles of mastication are preferentially affected by myopathies?
|
They have a different isoform of myosin and sometimes the body attacks it
|
|
Masticatory muscle myopathy occurs in which animal?
|
Dog - at any age, sex or breed
|
|
What are the clinical signs of masticatory muscle myopathy?
|
Acute - inflammatory condition causing swelling over temporal region and pain on opening jaw
Chronic - Progressive atrophic condition in which damaged muscle fibers are slowly replaced by fibrous CT |
|
How do you diagnose masticatory muscle myopathy?
|
Type II M antibody titer
Biopsy of temporal muscles |
|
How do you treat masticatory muscle myopathy?
|
Supress immune response w/ steroids
Physical therapy to gradually stretch and improve flexibility of remaining muscle tissue |
|
What is the prognosis for masticatory muscle myopathy?
|
Good to guarded depending on the degree of fibrosis
|
|
What are the clinical signs associated with immune mediated generalized polymyositis?
|
Generalized, poorly localized pain; muscle cramping and exercise associated weakness are generally less obvious; looks like they are walking on eggshells
|
|
How do you diagnose immune mediated generalized polymyositis?
|
CK, EMG, muscle biopsy. R/O infectious causes of inflammatory myositis and other possible causes
|
|
How do you treat immune mediated generalized polymyositis?
|
Immunosuppressive drugs and analgesics - Pred, Azathioprine, Cyclosporine, etc
|
|
What is the prognosis for immune mediated generalized polymyositis?
|
Guarded
|
|
This is an autosomal dominant condition that commonly occurs in Greyhounds and is characterized by intermittent episodes of intense skeletal muscle contracture:
|
Malignant hyperthermia
|
|
What is the etiology of malignant hyperthermia?
|
Defect in intracellular muscle calcium homeostasis
|
|
When are episodes of malignant hyperthermia seen?
|
Stress
Anesthetic agents (esp Halothane) |
|
What are the clinical signs associated with malignant hyperthermia?
|
Muscle cramps
Hemoconcentration Hyperthermia |
|
How do you diagnose malignant hyperthermia?
|
Halothane test
|
|
How do you treat malignant hyperthermia?
|
Dantroline - a skeletal muscle relaxant can reverse the episode if given IV
|
|
Which animal gets exercise associated myopathy?
|
Lab
|
|
What signalment is associated with dogs affected by exercise associated myopathy?
|
Labs from field trial lineages
7 mos - 2 yo |
|
Describe the clinical signs associated with exercise associated myopathy in labs.
|
Dogs normal at rest and during mild exercise; 5-15 mins after strenuous exercise they develop weakness and collapse; normal after 10-20 mins rest
|
|
How do you diagnose exercise associated myopathy in labs?
|
No test yet
|
|
How do you treat exercise associated myopathy in labs?
|
Don't have them do field trials anymore - the dog is now a couch potato
|
|
All vertebral bodies are separated by intervertebral disks, except:
|
C1-2
|
|
What makes up an intervertebral disk?
|
Annulus fibrosis
Nucleus pulposis |
|
Most common spinal disease:
|
IVD disease
|
|
With age, the nucleus pulposis can under what two changes?
|
Chondroid metaplasia
Fibrinoid metaplasia |
|
Which type of nucleus pulposus metaplasia more frequently becomes calcified?
|
Chondroid
|
|
Hansen divided degenerative disk disease into two categories - what are they?
|
Type I - disk material extruded from annulus
Type II - disk material remains within annulus but protrudes dorsally into spinal canal |
|
Disks that undergo chondroid metaplasia more frequently cause what type of disk disease?
|
Type I
|
|
Disks that undergo fibrinoid metaplasia more commonly cause which type of disk disease?
|
Type II
|
|
Type I disk disease occurs most commonly with what signalment?
|
Chondrodystrophoid breeds of dogs (Dachsund, etc)
3 yo + |
|
What is the typical signalment associated with fibrinoid metaplasia?
|
Large, nonchondrodystrophoid breeds
5 yo+ |
|
What are the clinical signs associated with Type I disk disease?
|
Acute onset
Spinal cord compression and trauma with associated vascular changes |
|
What are the clinical signs associated with Type II disk disease?
|
Insidious and progressive onset
|
|
How do you diagnose IVD?
|
Radiography
Myelography |
|
How would you treat a dog with a score of 1 or 2 for IVD?
|
Cage rest for 2-4 wks
NSAIDS |
|
If a dog has a score of 3-5 for IVD, how do you treat it?
|
Surgical decompression and removal of herniated disc material
|
|
How would you treat a cervical disk extrusion?
|
Ventral slot procedure
|
|
How would you treat a T-L disk extrusion?
|
Hemilaminectomy
Modified dorsal laminectomy |
|
The only definitive treatment for type II disk protrusion:
|
Surgical decompression w/ removal of protruding mass
|
|
True/false: Chronic spinal cord compression does not respond to surgery as readily as acute spinal cord compression and warrants a more guarded prognosis.
|
True
|
|
Cervical vertebral stenosis is AKA:
|
Wobbler's
|
|
Cervical vertebral stenosis is characterized by:
|
Chronic progressive spinal cord compression secondary to type II disk protrusion, hypertrophy of dorsal longitudinal ligament, hypertrophy of ligamentum flavum, etc
|
|
Which vertebrae are most commonly affected by cervical vertebral stenosis?
|
Caudal cervical - C5, C6, C7
|
|
Which dogs are usually affected by cervical vertebral stenosis?
|
Dobies (3-9 yo)
Great Danes (<2 yo) |
|
What are the most striking clinical signs associated with cervical vertebral stenosis?
|
Pelvic limb ataxia and cervical pain
Extensor rigidity of thoracic limbs Eventual quadriparesis |
|
What ancillary aids can you use to diagnose cervical vertebral stenosis?
|
EMG - mild denervation of cervical paraspinal muscles and shoulder muscles
Radiographs - may be normal or show narrowing of affected disk spaces and spondylosis Myelogram |
|
What ancillary aid is REQUIRED to identify cervical vertebral stenosis and determine whether the compressive material is dorsal or ventral to the spinal cord?
|
Myelogram
|
|
How do you treat cervical vertebral stenosis?
|
Can try medical therapy (like prednisolone and restricted neck movement), but usually lesions are too far along for this. Surgical intervention is indicated if significant compression is seen w/ rads. Ventral decompression w/ type II dis protrusion. Fusion of disks can be done.
|
|
What is the prognosis for an animal with cervical vertebral stenosis?
|
Varis w/ duration and severity of spinal cord compression, as well as type of compression and ability to relieve it surgically.
|
|
What is spinal canal stenosis?
|
Any type of narrowing of the spinal canal or intervertebral foramina or both
|
|
What are some processes that cause lumbosacral stenosis?
|
Congenital vertebral malformations
Type II disk protrusion Hypertrophy/hyperplasia of interarcuate ligament Proliferation of articular facets Subluxation of lubosacral junction |
|
What are the two distinct subtypes of lumbosacral stenosis?
|
Congenital
Acquired |
|
Although convertebral malformation with congenital lumbosacral stenosis is present at birth, why do signs not appear until middle to old age in small to medium sized dogs?
|
Because additional narrowing of the spinal canal occurs secondary to degenerative disk disease and ligamentous hypertrophy
|
|
Which is more common, congenital or acquired lumbosacral stenosis?
|
Acquired
|
|
What is the signalment associated with acquired lumbosacral stenosis?
|
Large breed dogs
Males more comomonly affected German Shepherds predisposed Usually mature adult (avg 7 yo) |
|
What are the clinical signs associated with lumbosacral stenosis?
|
Gradual in onset and progressive
Compression of L7- coccygeal spinal nerve roots, so LMN signs to tail, perineum and sciatic nerves Muscle atrophy in caudal thigh and distal limb, paraparesis, tail weakness, urinary and anal sphincter distrubances Can be asymmetrical Sensory disturbances due to nerve root compression (pain to parasthesias) |
|
How do you diagnose lumbosacral stenosis?
|
Radiographs usually show spondylosis at LS junction
Myelography is rarely of benefit b/c the subarachnoid space does not extend to LS junction EMG |
|
How do you treat lumbosacral stenosis?
|
Strict confinement and restricted leash walks w/ corticosteroids
Clinical signs often return Decompressive laminectomy of L7-S1 Fusion of LS joint if there is instability |
|
Why might a dog with lumbosacral stenosis have a poor prognosis?
|
B/c of bladder atony and fecal incontinence
|
|
What is degenerative myelopathy?
|
Chronic, progressive, degenerative condition affecting spinal cord white matter tracts and occasionally nerve roots
|
|
What is the signalment associated with degenerative myelopathy?
|
Large breed dogs, esp. G. Shepherds
5-14 yo |
|
What are the clinical signs associated with degenerative myelopathy?
|
Begin with mild paraparesis and ataxia; most animals paralyzed within 6 mos to a year
Asymmetric postural reaction deficits in pelvic limbs /w exaggerated rear limb reflexes ad no evidence of thoracolumbar hyperpathia |
|
How can you diagnose degenerative myelopathy?
|
Suspect this in any older large breed dog w/ chronic progressive paraparesis. Can only confirm diagnosis w/ histopathology. R/O other causes of progressive myelopathy w/ rads, CSF analysis and myelography
|
|
What are some treatments you can try for degenerative myelopathy?
|
Nothing to resolve the histologic changes; can try exercise, diet, herbs, vitamins, etc
|
|
Congenital vertebral and spinal cord abnormalities may be divided into two categories based largely on embryological origins of tissues:
|
Ventral compartment
Dorsal compartment |
|
The ventral compartment associated with the vertebrae and spinal cord consists of what/
|
Vertebral body and IVD
|
|
The dorsal compartment associated with the vertebrae and spinal cord consists of what?
|
Vertebral arch and spinal cord
|
|
True/false: the spinal cord is usually normal with ventral compartment abnormalities unless the vertebrae are sufficiently misshapen to cause secondary spinal cord compression.
|
True
|
|
What are disorders associated with ventral compartment malformations?
|
Hemivertebrae
Block vertebrae Butterfly vertebrae |
|
What are block vertebrae?
|
Appear radiographically as fushion of two vertebrae - may involve vertebral bodies, vertebral arches, or entire vertebrae
Note, the sacrum is a form of block vertebrae |
|
Block vertebrae is a form of ventral or dorsal compartment malformation?
|
Ventral
|
|
Butterfly vertebrae are a form of ventral or dorsal compartment malformation?
|
Ventral
|
|
Which type of vertebral malformation appears radiographically as a dorsal-ventral cleft in the vertebral body that results from incomplete fusion of the right and left halves of the vertebral bodies?
|
Butterfly (cleft) vertebrae
|
|
When vertebrae are shortened and wedge shaped and frequently result in significant curvature of the spine in either a dorsal (kyphosis) or ventral (lordosis) or lateral (scoliosis) plane:
|
Hemivertibrae
|
|
What is the signalment associated with ventral compartment malformations?
|
Brachycephalic breeds bred for 'screw-tailed' conformation
German Short-Haired Pointers |
|
What are the clinical signs associated with ventral compartment abnormalities?
|
Usually incidental findings; can cause spinal cord compression in rare instances - gradual progressive deterioration of spinal cord function results in para or quadriparesis
|
|
How do you diagnose ventral compartment spinal abnormalities?
|
Survey radiographs; may need myelogram to determine whether spinal cord is being compressed by the anomaly
|
|
How do you treat ventral compartment spinal abnormalities?
|
Surgical decompression w/ stabilization if necessary
|
|
What disorders result in dorsal compartment malformation?
|
Spina Bifida
Spinal dysraphism |
|
What condition is associated with vertebral arches that fail to fuse resulting in a bony defect in the dorsal portions of the vertebrae?
|
Spina bifida
|
|
Any open dysraphic disorder that results in potential communication between the nervous system and the environment may be referred to as:
|
Spina bifida aperta
|
|
What signalment is associated with spina bifida?
|
Bulldogs and Max cats - likely related to the genetic selection for kinked or absent tails in these breeds
|
|
When spina bifida occurs alone, this is AKA:
|
Spina bifida occulta
|
|
Which type of spina bifida usually produces no neurologic deficits?
|
Spina bifida occulta
|
|
How do you diagnose spina bifida?
|
Survey rads
Myelography to outline associated neural or meningeal abnormalities |
|
How do you treat spina bifida?
|
Surigcal correction in selected cases; unfortunately there are usually other neural defects not radiographically apparent
|
|
What is the prognosis for dorsal compartment malformations?
|
Guarded to grave
|
|
Which carries a worse prognosis, ventral or dorsal compartment malformations?
|
Dorsal compartment
|
|
What is spinal dysraphism?
|
Spinal cord defect tha tresults from failure of fusion of the neural tube - this creates a dorsal sagittal defect in the spinal cord
|
|
What signalment is associated with spinal dysraphism?
|
Weimeraner dogs
|
|
What are the clinical signs associated with spinal dysraphism?
|
Different degrees of paraparesis. Symmetrical hopping gait, hindlimb abduction and slow postural reactions in pelvic limbs. Withdrawal reflex produces flexion of both pelvic limbs. May also have misshapen thorax, odd length to extremities and body, and abnormal hair patterns along dorsal trunk.
|
|
How do you diagnose spinal dysraphism?
|
CT and MRI; clinical signs usually sufficient for a tentative diagnosis
|
|
How do you traet spinal dysraphism?
|
No treatment; clinical signs rarely progress beyond a few months of life. Prognosis varies w/ severity of deficits
|
|
How are the first two vertebrae joined?
|
Series of ligaments, most of which attach to a prominent rostral projection from the body of C2 - the dens, to either occipital bone or C1.
|
|
Malformation of the dens results in:
|
Instability between the first two cervical vertebrae and subsequent subluxation
|
|
Why does malformation of the dens occur?
|
Because it has a separate ossification center
|
|
What is the signalment associated with atlanto-axial subluxation?
|
Congenital absence of dens i nminiature and toy breeds of dogs
<1 yo |
|
What are the clinical signs associated with atlanto-axial subluxation?
|
Instability between atlas and axis. Vertebral subluxation results in compression of the cervical spinal cord. May have intermittent pain to complete transection of the cervical spinal cord and death. Could have ataxia and head tile b/c edema extends up into the brain stem
|
|
How do you diagnose atlanto-axial subluxation?
|
Survey radiographs - best w/ VD or oblique lateral views
|
|
What do you have to remember when radiographing for probably atlanto-axial subluxation?
|
Not to flex the neck in these patients - you don't want to cause further spinal cord trauma
|
|
How do you treat atlanto-axial subluxation?
|
Stabilize the joint with external support, surgical stabilization w/ either dorsal or ventral approach (pins)
|
|
The most common type of neoplastic process in the spinal cord:
|
Extradural
|
|
These tumors develop outside the dura and include vertebral tumors and metastatic soft tissue tumors:
|
Extradural
|
|
_________ is the most common metastatic tumor and can cause meningeal, nerve root, or spinal cord infiltration or extradural mass lesions.
|
Lymphosarcoma
|
|
How might you diagnose an extradural neoplastic lesion?
|
Radiographs identify bony lysis
Myelography to outline spinal cord compression |
|
Long term prognosis is ____ for all types of spinal cord neoplasia.
|
Poor
|
|
These tumors develop inside the dura, but outside the spinal cord itself:
|
Intradural/extramedullary
|
|
Most common intradural/extramedullary tumors:
|
Meningiomas and nerve root tumors
|
|
How do you treat an intradural/extramedullary meningioma or nerve root tumor?
|
Surgical removal, but many cases reoccur b/c of incomplete removal of all neoplastic cells
|
|
Which type of spinal cord neoplastic process presents with the 'golf tee' sign?
|
Intradural/extramedullary
|
|
These tumors develop within the spinal cord parenchyma:
|
Intramedullary
|
|
What signalment is associated with intramedullary spinal cord tumors?
|
Boxers and Bostons
Any age |
|
Pain is usually absent with which type of spinal cord neoplasia?
|
Intramedullary
|
|
Intradural/extramedullary and intramedullary neoplasms of the spinal cord are diagnosed via:
|
Myelography to outline the mass
|
|
Two ways in which neoplastic spinal cord processes could present:
|
Chronic and progressive
Acute |
|
Infection of the IVD w/ concurrent osteomyelitis of contiguous vertebrae is AKA:
|
Diskospondylitis
|
|
What other conditions may be present concurrently with diskospondylitis?
|
Cystitis or bacteremia; diskospondylitis often occurs secondarily to one of these primary foci of infection
|
|
Which bacteria is most frequently isolated from diskospondylitis?
|
S. intermedius
|
|
What signalment is associated with diskospondylitis?
|
Adult
Large breed dogs Males 2x more likely |
|
What are the clinical signs associated with diskospondylitis?
|
Variable. Stiff gait, pain, hyperesthesia are most common. Neurologic deficits may develop later either due to spinal cord compression or extension of infection into spinal canal
|
|
Which ancillary aids are helpful for diagnosis of diskospondylitis?
|
CBC and U/A, blood culture
Radiographs |
|
How do you treat diskospondylitis?
|
Antibiotics in cases of bacterial etiology - usually start out with broad spectrum impirical ABs for 4-6 wks
|
|
What is the prognosis for diskospondylitis?
|
Good w/ bacterial etiologies except Brucella. Poor w/ fungal etiologies
|
|
Inflammation of the meninges is AKA:
|
Meningitis
|
|
Inflammation of the spinal cord is AKA:
|
Myelitis
|
|
What is meningiomyelitis?
|
Inflammation of the meninges and spinal cord
|
|
Two non-infectious causes of meningomyelitis:
|
Canine granulomatous meningomyelitis
Feline polioencephalomyelitis |
|
What is a steroid responsive meningitis?
|
Suppurative meningitis for which an infectious cause cannot be identified; antimicrobials not effective but most dogs respond to steroids
|
|
What signalment is associated with steroid responsive meningitis?
|
Beagles, large breed dogs
< 2yo |
|
What are the clinical signs associated with steroid responsive meningitis?
|
Cervical pain is most consistent. Fever, lethargy, anorexia.
|
|
How do you diagnose steroid responsive meningitis?
|
CBC and CSF - both with leukocytosis, non degenerate neutrophils. Absence of an identifiable organism and unresponsive to antibiotics; rapid response to steroids
|
|
How do you treat steroid responsive meningitis?
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Prednisolone; neurologic deficits should improve in next couple wks. Can usually taper and then discontinue therapy after 2-6 mos. Some have complete resolution.
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True/false: Spinal cord trauma occurs with any rapid deformation of the cord.
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True
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What are the two phases of spinal cord trauma?
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1. Immediate effect/primary
2. Delayed effect/secondary |
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Describe the immediate effect/primary injury associated with spinal cord trauma.
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Primary injury can vary in severity. It initiates a series of biochemical events that result in additional neurologic injury referred to as secondary/delayed injury.
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Describe the delayed effect or secondary injury associated with spinal cord trauma.
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Generation of unstable free radicals, which in turn cause further membrane damage and perpetuate the cycle. If severe enough, this phase can create a self perpetuating hemorrhagic necrosis of the cord - hematomyelia or myelomalacia which can extend caudally and cranially from the injury until the animal dies from respiratory failure
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What is the Schiff-Sherrington syndrome?
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With spinal cord trauma to the TL spinal cord, you will see flaccid paralysis of the rear limbs and involuntary extension of the thoracic limbs. Postural reactions are intact in the front limbs despite the rigidity.
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The presenc eof Schiff-Sherrington syndrome indicates waht?
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Severe but not irreversible injury to the spinal cord
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How do you treat spinal cord trauma?
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Methylprednisolone as soon as possible after the injury if the animal is seen w/in 8 hrs of the trauma
Surgical decompression/stabilization |
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What drug should you never use to treat spinal cord trauma?
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Dexamethasone
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With spinal cord trauma, what warrants a poor prognosis?
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Absence of deep pain perception after 24 hrs
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What is a fibrocartilaginous infarct?
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Material similar to the nucleus pulposus enters the arterial and/or venous blood suppl to the spinal cord at any level and causes ischemic or hemorrhagic necrosis of the cord tissue
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Describe the progression of disease associated with a fibrocartilaginous infarct.
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Onset is acute and signs progress over few hours to 1-2 days. Signs usually asymmetrical and nonpainful.
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Why are fibrocartilaginous infarcts not painful?
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B/c the spinal cord has no pain fibers
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Are fibrocartilaginous infarcts associated with herniated disks?
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NO
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What are the clinical signs associated with fibrocartilaginous infarcts?
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Acute quadriplegia, hemiplegia, paraplegia or monoplegia. Dog may have cried out and suddenly developed signs
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If you have a fibrocartilaginous infarct on the left side of the caudal cervical area, what signs might you see on NE?
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Flaccid paralysis of the thoracic limb and spastic paralysis of the ipsilateral pelvic limb; pain perception may or may not be present in the most involved thoracic limb; Horners syndrome may be seen on the involved side
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What ancillary aids can help diagnose fibrocartilaginous infarcts?
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CSF
MRI |
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What is the treatment for fibrocartilaginous infarcts?
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Time and physical therapy
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What is the prognosis for fibrocartilaginous infarcts?
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If LMN signs are present prognosis isn't as good as for UMN signs. If no deep apin, prognosis is poor
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