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Clinical Neurology > Diseases of the Spine, PNS, NMJ and Muscle in the Dog and Cat > Flashcards

Diseases of the Spine, PNS, NMJ and Muscle in the Dog and Cat Flashcards

1
Q

What are the DDx for Spinal Pain?

A

D: Intervertebral disk disease, or Lumbosacral stenosis
A: Atlantoaxial subluxation, Chiari-like malformations, Caudal cervical malformation/ Malarticulation
M:
N: Primary vs Secondary Neoplasia of the vertebrae, nerve root or intracranial
I: Discopondylitis, Meningitis, polymyositis or polyarthritis
T: Vertebral Fracture
V:

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2
Q

What is Steroid-responsive meningitis-arteritis (SRMA)?

A

A noninfectious inflammatory disease of the meninges

Suspected to be immune-mediated in origin, with an overrepresentation in certain breeds: Bernese Mt Dog, Pointer and Beagle
(Medium to large breed dogs 8-18 months of age)

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3
Q

What are the clinical signs associated with Steroid-responsive meningitis-arteritis (SRMA)?

A
  • Pain in the cervical region
  • Fever
  • Depression
    +/- waxing and waning

and usually no neurological deficits
Meanwhile neurological deficits are common with Meningoencephalitis of unknown origin (MUO) or GME

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4
Q

How can Steroid-responsive meningitis-arteritis (SRMA) be diagnosed?

A
  • CSF tap + analysis: will see marked neutrophilic pleocytosis
    +/- neutrophilia on hematology
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5
Q

How can Steroid-responsive meningitis-arteritis (SRMA) be treated/ managed?

A
  • Immunosuppressive doses of corticosteroids
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6
Q

What is syringomyelia?

What is hydromyelia?

A

Syringomyelia is the development of a CSF-filled cavity (syrinx) within the parenchyma of the spinal cord

Hydromyelia is the accumulation of excessive CSF within a dilated central canal

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7
Q

Why does syringomyelia or hydromyelia develop?

A

These can develop as a result of:

  • Altered CSF pressures within the spinal canal
  • A loss of spinal cord parenchyma
  • Secondary to obstructed CSF flow caused by congenital malformations, trauma, or inflammatory/ neoplastic disorders
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8
Q

What is Chiari-like malformation and why might it lead to syringomyelia or hydromyelia?

A

Chiari-like malformation is a congenital malformation of the skull in Cavalier King Charles Spaniels

The malformation of the skull reduces the volume of the caudal fossa and displaces the cerebellum and brainstem into the foramen magnum, thus obstructing CSF movement

The CSF, which normally flows through the foramen magnum during systole becomes turbulent at the craniocervical junction, leading to syrinx formation

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9
Q

How can Chiari-like malformation be confirmed/ diagnosed in the CKCS?

A
  • 95% of CKCS have some degree of CM, 50% of those will have syringomyelia, and 35% of those affected show clinical signs
  • Clinical signs: cervical pain (can be intermittent), may resent having their ears, limbs, face or neck touched. Some dogs will phantom scratch (scratch at their neck without making contact with the skin). Can also see neurological deficits
  • MRI: see a decreased caudal fossa due to congenital hypoplasia of the occipital bone, leading to herniation of cerebellum + compression of the craniocervical dural/ fibrous band
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10
Q

How can clinically affected CKCS with Chiari-like malformation be treated/ managed?

A

Medical:

  • Analgesia: Gabapentin for neuropathic pain
  • Drugs to decrease CSF production: Omeprazole, acetazolamide or prednisone

if medical management does not work, then surgical should be considered
- Dorsal laminectomy +/- durotomy

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11
Q

What are the DDx for Ataxia?

A

D: Intervertebral disk disease, degenerative myelopathy
A: Atlantoaxial subluxation, caudal cervical malformation/ malarticulation
M:
N: Primary vs secondary neoplasia
I: Discospondylitis, Meningomyelitis
T: Trauma
V:

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12
Q

What is Degenerative Myelopathy?

A

A degenerative disorder of the spinal cord white matter, characterized by widespread myelin and axon loss with no evidence of cord compression or inflammation, usually most severe in the mid to caudal thoracic spinal cord.
Cause is unknown but a mutation in the Superoxidase Dismutase 1 gene (SOD1) has been identified as a necessary condition for the development of this disease

Overrepresentation in certain breeds: GSD and Boxers (6-12 years old) and other medium and large breeds

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13
Q

What are the clinical signs associated with Degenerative Myelopathy in dogs?

A

Insidious onset of signs

  • Mild proprioceptive pelvic limb ataxia and paresis leading to limb knuckling, and wearing of the dorsal nail surface, chronic cases can result in complete paresis until non-ambulatory
  • Normal or increased rear limb reflexes
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14
Q

How can Degenerative Myelopathy be diagnosed in the dog?

A

Diagnosis is of exclusion:
- Clinical signs + breed and age of onset: must be differentiated from spinal cord neoplasia, spinal cord compression by articular cysts and type II disk protrusion

  • Rads: will be normal
  • CSF analysis: will be normal +/- slight protein increase
  • Myelography or MRI: to rule out spinal cord compression or neoplasia

Definitive diagnosis: PM findings of axonal degeneration, demyelination, and astroglial proliferation in the lateral funiculus and dorsal columns of the thoracic spinal cord

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15
Q

How can Degenerative Myelopathy be treated/ managed in dogs?

A

Treatment: none
Do NOT give steroids as they can cause muscle wasting and exacerbate muscle weakness

Management:

  • Vitamin E, Vitamin B complex, Vitamin C + omega-3 FAs and antioxidants may help
  • Exercise + intensive targeted physiotherapy may help in slowing disease progression
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16
Q

What are the DDx for Tetraparesis/ tetraplegia or Hemiparesis/ hemiplegia?

A

D: Intervertebral disk disease, diskospondylitis
A: Atlantoaxial subluxation, caudal cervical malformation/ malarticulation, Chiari-like malformation, Myasthenia gravis
N: neoplasia can cause this if hemorrhage, ischemia or fracture occurs as a result
I: viral, bacterial, fungal, parasitic infection, meningomyelitis, tick paralysis, acute polyradiculoneuritis
T: Trauma, Botulism, snake envenomation, aminoglycoside intoxication
V: hemorrhage, fibrocartilagenous embolism

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17
Q

What is the definition of Tetraparesis?

A

Weakness in all 4 limbs with some voluntary movement maintained

Mild: weak but ambulatory
Moderate: weak, non-ambulatory + sternal recumbency
Severe: weak, non-ambulatory + lateral recumbency

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18
Q

What is the definition of Tetraplegia?

A

Loss of voluntary movements in all 4 limbs

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19
Q

What is a Fibrocartilaginous Embolism and why does it occur?

A

A fibrocartilage piece breaks off, likely from the nucleus pulposus of a degenerating IVD and becomes trapped in a very small artery or vein that supplies the spinal cord, parenchyma and leptomeninges, leading to infarction

The reason for this to occur is unknown, but there is a genetic predisposition for young large breeds and Mini Schnauzers

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20
Q

What are the clinical features associated with a Fibrocartilagenous Embolism?

A
  • Acute onset of neurological signs
  • 50% of cases will have clinical signs after a minor trauma or during exertion
  • Deficits will depend on the region of the spinal cord affected and the severity of the cord involvement
  • Neurological dysfunction may be mild or severe, usually the thoracolumbar or lumbosacral are affected, with only about 10% of cases having cervical spinal signs
  • Common for dogs to be painful at first and then present to the vet NON-painful (even with manipulation of the spine) and show asymmetrical signs
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21
Q

How can a Fibrocartilagenous Emboli be diagnosed?

A

Diagnosis of exclusion

Suspicion is based on:
- Signalment, history, recognition of peracute, nonprogressive, nonpainful spinal cord dysfunction

  • Rads: will be normal, but help rule out diskospondylitis, fractures, lytic vertebral neoplasia and IVDD
  • CSF analysis: will be normal, +/- increased protein
  • Myelography or Spinal CT: rule out compressive lesions of the spinal cord due to fractures, disk extrusion and neoplasia
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22
Q

If a Fibrocartilagenous Emboli is diagnosed or suspected, what is the treatment/ management?

A
  • Nonsupportive measures, nursing care and physiotherapy
  • Cage rest is NOT required, in fact early intervention with physiotherapy may help speed recovery

Note: most clinical improvements take place in the first 7-10 days, but it can take 6-8 weeks for complete return of function
If no improvement is seen in the first 21 days, then it is unlikely the animal will improve

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23
Q

What is Acute Canine Polyradiculoneuritis (Coonhound paralysis)?

A

The only acute-onset polyneuropathy commonly diagnosed in dogs

  • Clinically and histologically similar to the human Guillain Barre Syndrome: an autoimmune allergic neuritis thought to be caused by exposure to a triggering antigen
  • This triggering antigen is unknown and could be anything
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24
Q

What clinical features are associated with Acute Canine Polyradiculoneuritis (Coonhound paralysis)?

A
  • Inflammation of the axons and myelin sheaths at the level of the ventral nerve roots causes an acute, rapidly progressive LMN paresis or paralysis. A stilted, short-strided, weak rear limb gait progresses rapidly over a few days to tetraparesis, with most affected dogs tetraplegic within 5 to 10 days of onset.
  • Hyperaesthesia: hyperreactive to pinching toes or muscle palpation is a feature of ACP that does not occur in NMJ disorders like tick paralysis or botulism
  • Despite severe paralysis or paresis, dogs with ACP are BAR, eat and drink and can wag their tails
  • Bladder and rectum functions remain normal
  • Most have NO cranial nerve involvement, some may have bilateral facial paralysis or a hoarse bark

Caution: respiratory paralysis can occur in a few dogs and can lead to death or require mechanical ventilation

25
Q

How can Acute Canine Polyradiculoneuritis (Coonhound paralysis) be diagnosed?

A
  • Historical, clinical and neurological findings are important
  • Must differentiate from NMJ disorders that can also cause acute LMN tetraparesis: tick paralysis, botulism, acute fulminating myasthenia gravis. Do this by testing for hyperaesthesia in the limb by pinching toes and manipulating the muscles, and can use Electromyography (will reveal diffuse denervation with fibrillation potentials and positive sharp waves, which are not expected in NMJ disorders)
  • If no history of raccoon exposure or recent vaccination, then test for Toxoplasma and Neospora
  • Definitive diagnosis requires a nerve biopsy, but this is rarely necessary
26
Q

What is the treatment/ management for Acute Canine Polyradiculoneuritis (Coonhound paralysis)?

A
  • Non-specific treatment: monitoring respiratory compromise is vital to ensure the animal does not reach pulmonary paralysis
  • Signs usually stabilize in 5-10 days, they may require support to eat and drink at home and should be kept on an air mattress, waterbed or lounge chair and turned periodically to prevent lung atelectasis and pressure sores
  • Glucocorticoid treatment is NOT beneficial and may slow recovery
  • Most dogs will improve after the first week, and fully recover in 3-4 weeks. Some may never recover
27
Q

Does Botulism cause a rigid or flaccid paresis/ paralysis?

A

Flaccid
The toxin blocks the release of ACh at the NMJ, resulting in complete presynaptic neuromuscular blockade and LMN paralysis

Tetanus causes a rigid paralysis

28
Q

How can Botulism be diagnosed?

A
  • Clinical signs: acute flaccid tetraparesis
  • CN involvement: hoarse bark, dysphagia, megaesophagus, facial paresis, decreased jaw tone, dilated pupils and absent Pupillary Light Reflex
  • Decreased or absent Spinal Reflexes
  • Hx: of eating raw meat or a dead animal e.g. roadkill
  • Definitive diagnosis: demonstration of botulinum toxin in blood, vomitus, feces or stomach contents
29
Q

How can Botulism be treated?

A
  • Before clinical signs: if suspected, the anti-toxin can be given
  • Once signs develop: supportive care, ventilator if breathing stops, eye lube, placement of a NG tube + manual expression of bladder or placement of a urinary catheter

With proper supportive care, the signs will gradually resolve in 1-4 weeks

30
Q

What are the most common neoplasias that affect the spinal cord in the dog and cat?

A

Dog:
Extradural arising from the vertebral body = osteosarcoma, chondrosarcoma, fibrosarcoma, myeloma

Extradural soft tissue tumors that metastasize: hemangiosarcoma, carcinoma, liposarcoma, lymphoma

Intradural extramedullary (spinal cord but within the dural sheath) = meningiomas, neuroepithelioma, peripheral nerve sheath tumor

Cat: Lymphoma

31
Q

What is a common presentation for a dog or cat with a spinal neoplasia?

A
  • Chronic, insidious onset
  • Progressive lameness and pain on limb manipulation
  • Paraparesis/ tetraparesis

DDx: other disorders that cause slow progressive neurological dysfunction, including type II disk protrusion and degenerative myelopathy (DM)

32
Q

How can a spinal neoplasm be diagnosed?

A
  • Physical and Neurological exam
  • Palpation + cytology aspirated of lymph nodes
  • Rads and US
  • CBC + Biochem
  • Myelography
  • MRI
33
Q

What are the clinical signs associated with muscle diseases?

A
  • Generalized weakness
  • Exercise intolerance
  • Stiff, stilted gait
  • Localized or generalized muscle atrophy
  • Generalized muscle hypertrophy
  • Dimple contracture
  • Muscle pain on palpation = myalgia is common
  • Limited joint movement
  • Normal mentation and sensation
  • Normal proprioception/ postural reactions if the animal is supported
34
Q

What are the 3 classifications of muscle diseases?

A
  • Inflammatory
  • Non-inflammatory
  • Metabolic myopathy: Primary vs Secondary
35
Q

What are the Primary and Secondary Metabolic myopathies?

A

Primary:

  • Mitochondrial myopathies
  • Lipid storage myopathies
  • Glycogen storage diseases
  • Malignant hyperthermia

Secondary:

  • Hyperadrenocorticism
  • Hypokalemia
36
Q

You suspect a muscle disease in an animal, what are the steps to approaching a case like this?

A
  • Signalment + Hx
  • Physical exam
  • Hematology, biochemistry: CK and electrolytes, and urinalysis
  • Thoracic rads
  • Abdominal US
  • Endocrine evaluation
  • ACh receptor antibodies
  • Electro-diagnostic testing: electromyography, nerve conduction velocity
  • Muscle biopsy
37
Q

What are the Inflammatory muscle diseases?

A
  • Immune-mediated polymyositis
  • Masticatory muscle myositis
  • Infectious
38
Q

What are the non-inflammatory myopathies?

A

Often these are breed-related abnormalities in components of the muscle, such as Dystrophin

  • Myotonia congenita: abnormality of the ion channels
  • Muscular dystrophy: multiple breeds affected including the Golden
  • Centronuclear myopathy: myopathy of labs
  • Lab Retriever Episodic Exercise-Induced Collapse

Use genetic tests to confirm these

39
Q

What is Masticatory Myositis?

A

This is a focal autoimmune myositis affecting the muscles of mastication (temporalis, masseter and digastricus)

The body produces antibodies against the muscle fibers of the masticatory muscles (which are unique to limb musculature)

40
Q

What breeds are most commonly affected by Masticatory Myositis?

A

Is the most common form of myositis in dogs, and has not been reported in cats

  • Young large-breed dogs are overrepresented, especially the GSD
41
Q

What clinical signs are associated with Masticatory Myositis?

A
  • Inability to open the mouth (trismus)
  • Swelling and or pain of the masticatory muscles
  • Severe muscle atrophy
  • Fever, depression, weight loss, dysphagia, dysphonia and exophthalmos from swelling of the pterygoid muscles
42
Q

How can Masticatory Myositis be diagnosed?

A
  • Clinical signs
  • Presence of antibodies against the type 2M fibers: specificity of nearly 100%, sensitivity of 80%
  • Muscle biopsy: if dog tests negative for antibody test
  • Creatine Kinase test may help but isn’t always elevated
  • Electrodiagnostic tests: presence of fibrillation potentials and positive sharp waves
43
Q

How can Masticatory Myositis be treated/ managed?

A
  • Immunosuppressive doses of corticosteroids: prednisone
  • Can also add azathioprine
    Once clinical signs reside, gradually taper the dose over several months

Caution: never force the jaw open: can fracture, damage or luxate the TMJ

44
Q

What is Polymyositis?

A

Polymyositis is characterized by a multifocal or diffuse infiltration of skeletal muscle by lymphocytes and negative serology for infectious disease

Although most cases are primary autoimmune, paraneoplastic immune-mediated myositis may be associated with malignancies such as lymphoma (particularly in Boxers)

45
Q

What breeds are most affected by Polymyositis?

A

Young large-breed dogs, and boxers, Newfoundlands and Vizlas are overrepresented

This is considered uncommon in dogs, and rare in cats

46
Q

What clinical signs are associated with Polymyositis?

A
  • Generalized weakness that worsens with exercise and a characteristic stiff gait
  • Cervical ventriflexion may occur
  • Pain on palpation of affected muscles
  • Dysphagia, generalized muscle atrophy, dysphonia , tongue atrophy and fever may be present
47
Q

How can Polymyositis be diagnosed?

A
  • Clinical signs
  • Elevated CK on biochem
  • Electrophysiologic testing
  • Serology testing for infectious causes to rule out infectious sources: Toxoplasma gondii, Neospora caninum, Borrelia burgdorferi, Clostridia, Ehrlichia canis, Rickettsia rickettsii, Hepatozoon americanum, Leishmania and Leptospirosis
  • Muscle biopsy can be definitive
48
Q

How can Polymyositis be treated?

A

Similar to Masticatory Myositis:
- Immunosuppressive doses of corticosteroids: prednisone
- Can also add azathioprine
Once clinical signs reside, gradually taper the dose over several months

49
Q

Why can Disorders of the Neuromuscular Junction lead to generalized LMN paresis or paralysis, and loss of reflexes?

A

Prevention of ACh release into the NMJ, thus inability initiate movement of the musculature

50
Q

What is Tick Paralysis and why does it occur?

A

This is a rapidly ascending flaccid motor paralysis, that is caused by a salivary neurotoxin which interferes with ACh release at the NMJ, causing presynaptic neuromuscular blockade

Only certain strains of tick are known to have this neurotoxin: Dermacentor andersoni and D. variabilis

51
Q

What are the clinical features associated with Tick paralysis?

A
  • Rapidly progressing ascending flaccid paralysis 4-9 days after the tick attaches, when the tick is engorged
  • Signs begin in the pelvic limbs and progress rapidly to LMN tetraplegia
  • Muscles are flaccid, spinal reflexes decreased
  • Usually CN’s are not affected but can get facial weakness, dysphagia, decreased jaw tone
52
Q

How can Tick Paralysis be diagnosed?

A

Often confused with other causes of acute tetraparesis such as acute polyradiculoneuritis, botulism, and acute fulminating Myasthenia gravis

  • Clinical signs, Hx and knowledge of geographic region
  • Sometimes a tick can be found, and diagnosis can be confirmed by documenting rapid improvement after tick removal
53
Q

What is the treatment for Tick Paralysis?

A
  • Removal of the tick, or dipping the animal in an insecticidal solution
    Should see rapid recovery in 24-72 hours
54
Q

What is the difference between Congenital and Acquired forms of Myasthenia gravis?

A

Congenital: rare group of hereditary disorders of neuromuscular transmission caused by structural or functional defects of the neuromuscular junction

Acquired: common immune-mediated disorder in which antibodies are directed against a portion of the nicotinic AChRs of skeletal muscle. Antibodies bind to the receptors, reducing sensitivity of the postsynaptic membrane to ACh. When nerve stimulation occurs and ACh is released into the synapse, there are less successful interactions between ACh and AChRs, causing smaller muscle end-plate potentials and failure to reliably generate a muscle action potential, resulting in weakness. Weakness is compounded during exercise when some of the functional AChRs are already bound by ACh

55
Q

What are the clinical features associated with Acquired Myasthenia Gravis?

A
  • Muscle weakness in the limbs, that worsens with exercise but improves with rest
  • Excessive salivation and regurgitation are common, caused by megaesophagus
    +/- Dysphagia, hoarse bark or meow, persistent dilated pupils, and facial muscle weakness

Note: can get focal MG causing megaesophagus with no limb weakness (25-40% of dogs), thus always consider MG if megaesophagus is seen

56
Q

What is Acute Fulminating Myasthenia Gravis?

A

Sudden Onset and rapid progression of severe limb muscle weakness that does NOT improve with rest
- Non-ambulatory and in lateral recumbency with profound weakness but preserved reflexes

Occurs in 5%-15% of dogs and cats with acquired MG

Weakness can cause megaesophagus, pharyngeal and laryngeal muscle weakness, aspiration pneumonia, respiratory fail and death

57
Q

How can Myasthenia Gravis be diagnosed?

A
  • Definitive: demonstrate antibodies against the AChR’s by immunoprecipitation radioimmunoassay
  • Can also support diagnosis with the administration of a short-acting anticholinesterase: Neostigmine methylsulfate
    Atropine is given too to minimize the muscarinic effects

No response may be seen in focal MG, and 50% of dogs with acute fulminating MG will have no response because of the marked antibody-mediated destruction of AChRs
- Negative test does not exclude MG

  • Rads: to assess megaesophagus, aspiration pneumonia or thymoma
  • Electrodiagnostic testing

note: Concurrent immune-mediated disorders are common in dogs with MG: hypothyroidism, immune-mediated thrombocytopenia, immune-mediated hemolytic anemia, hypoadrenocorticism, polymyositis and SLE

58
Q

What is the treatment for Myasthenia Gravis?

A
  • Supportive care: feed and water in an upright position in animals with megaesophagus
  • Anticholinesterase drugs (neostigmine or pyridostigmine bromide)
    +/- immunosuppressive agents

Caution: AVOID antibiotics that impair neuromuscular transmission e.g. ampicillin or aminoglycosides

Clinical Neurology (17 decks)

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