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SA Neurology > Spinal cord disorders > Flashcards

Spinal cord disorders Flashcards

1
Q

Segments of the spinal cord

A

8 cervical
13 thoracic
7 lumbar
3 sacral
At least 2 caudal

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2
Q

Four functional regions of the spina cord

A

Cranial cervical (C1-C5)
Cervicothoracic (C6-T2)
Thoracolumbar (T3-L3)
Lumbosacral (L4-S3)

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3
Q

Lower motor neurons

A

Efferent neurons connecting the central nervous system to an effector organ

Cell bodies located within grey matter of cervicothoracic intumescence (C6-T2) for the thoracic limbs, and lumbosacral intumescence (L4-S3) for the pelvic limbs

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4
Q

UMN weakness

A

Refers to a lesion that interrupts the descending motor pathways from supraspinal neurons that converge on the LMN pool.

Clinical signs of UMN weakenss manifest as paresis and/or plegia with normal to increased spinal reflexes (hyperreflexia) and muscle hypertonia.

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5
Q

LMN weakness

A

Refers to a lesion of the ventral spinal cord grey matter and its axon coursing to the muscle through the spinal nerve roots and peripheral nerve.

Clinically manifests as paresis and/or plegia, decreased to absent spinal reflexes (hyporeflexia to areflexia), decreased muscle tone and muscle atrophy that is severe and rapid in onset.

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6
Q

C1-C5 lesions

A

Neck pain

Tetraparesis/plegia, ipsilateral hemiparesis/plegia, ataxia
- postural reaction deficits in all 4 limbs or in ipsilateral thoracic and pelvic limbs
- normal to increased spinal reflexes in all 4 limbs
- normal to increased tone in all 4 limbs

Ipsilateral Horner’s syndrome

Respiratory difficulty

Urinary retention

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7
Q

C6-T2 lesion

A

Neck pain

Tetraparesis/plegia, ipsilateral hemiparesis/plegia, ataxia
- postural reaction deficits in all 4 limbs or in ipsilateral thoracic and pelvic limbs
- decreased to absent reflexes in thoracic limbs, normal to increased reflexes in hind limbs
- decreased to absent tone in thoracic limbs, normal to increased tone in pelvic limbs
- muscle atrophy in thoracic limbs

Ipsilateral Horner’s syndrome

Respiratory difficulty

Urinary retention

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8
Q

T3-L3 lesions

A

Back pain

Paraparesis/plegia, ipsilateral monoparesis/plegia, ataxia
- postureal reaction deficits in both ot one pelvic limbs
- normal to increased spinal reflexes in pelvic limbs
- normal to increased tone in pelvic limbs

Schiff sherrington phenomenon possible in acute and severe lesion

Absent trunci reflex caudal to the level of the last in tact dermatome

Urinary retention (UMN bladder)

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9
Q

L4-S3 lesions

A

Back pain

Paraparesis/plegia, ipsilateral monoparesis/plegia, ataxia
- postural reaction deficits in both ot one pelvic limb
- decreased to absent spinal reflexes in hind limbs
- decreased to absent tone in pelvic limbs
- muscle atrophy in pelvic limbs

Urinary incontinence (LMN bladder)

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10
Q

Ataxia

A

Loss of proprioception, incoordination

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11
Q

Paresis

A

Reduced voluntary motor funtion

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12
Q

Paralysis

A

Absence of voluntary motor function

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13
Q

Schiff-sherrington posture

A

Lesion in thoracolumbar spinal cord segments alters the ascending inhibitory pathways from the border cells in the lumbar grey matter (L2-L4).

Axons of these cells ascend and terminate in the cervical intumescence.

Loss of this ascending inhibition to the thoracic limbs results in extension.

In spite of this increased in extensor tone the thoracic limbs are normal neurologically with respect to neuro function.

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14
Q

Vascular spinal diseases

A

Fibrocartilaginous embolic myelopathy

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15
Q

Infectious causes of spinal disease

A

Infectious meningo(encephalo)myelitis

Discospondylitis

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16
Q

Inflammatory causes of spinal disease

A

Steroid responsive meningitis

Meningo(encephalo)myelitis of unknown origin (MUO)

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17
Q

Idiopathic causes of spinal disease

A

(Sub)arachnoid diverticulum (SAD)

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18
Q

Traumatic causes of spinal disease

A

Vertebral fracture,

(sub)luxation

Spinal cord contusion

Haemorrhage

Traumatic disc herniation (Acute non-compressive neucleus pulposus extrusion - ANNPE)

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19
Q

Anomalous causes of spinal disease

A

Atlanto-axial instability

Vertebral and spinal cord anomalies

Syringohydromyelia

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20
Q

Neoplastic causes of spinal disease

A

Spinal tumours (extradural, extramedullary, intramedullary)

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21
Q

Nutritional causes of spinal disease

A

Hypervitaminosis A in cats

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22
Q

Degenerative causes of spinal disease

A

Inherited neurodegenerative diseases (storage diseases)

Intervertebral disc disease

Wobbler’s syndrome

Degenerative myelopathy

Lumbosacral stenosis

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23
Q

Spinal pain

A

Tissue damage or inflammation produces pain through stimulation of nociceptors

Most CNS parenchyma doesn’t have nociceptors - damage to grey and white matter is not painful

Meninges have a high density of nociceptors

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24
Q

What are the pain sensitive structures of the spine?

A

Periosteum of the vertebrae
Blood vessels
Meninges
Nerve roots
Intervertebral discs

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25
Q

Neurodiagnostic investigation of the spine

A

Haematology, serum biochemistry, urinalysis

Chest x-rays, abdominal U/S

Survey spinal radiographs

CSF (cell count, cytology, protein conc.)

Myelography, CT, or MRI

Culture, serology, PCR

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26
Q

Prognosis of spinal diseases

A

Progressive compressive extradural spinal cord disease - order of losses

  1. concious proprioception
  2. motor function
  3. bladder function
  4. deep pain perception

Assessment of pelvic limb pain sensation in paraplegic animals good prognosticator

Tetraplegic animals at risk of respiratory failure due to paresis of intercostal muscles and diaphragm, atelectasis as a result of recumbency

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27
Q

Pathogenesis of Fibrocartilaginous embolic myelopathy (FCE)

A

Fibrocartilage identical to the nucleus pulposus, embolises to the spinal cord vasculature, producing an area of ischaemic necrosis centred on the spinal cord grey matter.

Signs are often lateralised, as the embolus usually lodges in one branch of the ventral spinal artery

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28
Q

Epidemiology of Fibrocartilaginous embolic myelopathy (FCE)

A

Young and non-chondrodystrophic breeds

Rare in cats

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29
Q

Clinical signs of Fibrocartilaginous embolic myelopathy (FCE)

A
  1. per-acute onset, excersise at onset
  2. non-painful
  3. lateralised neurological herniation
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30
Q

Differential diagnoses of Fibrocartilaginous embolic myelopathy (FCE)

A

Traumatic disc (acute non-compressive nucleus pulposus extrucrion, ANNPE)

Acute disc herniation

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31
Q

Diagnosis of Fibrocartilaginous embolic myelopathy (FCE)

A

X-ray and myelogram show no evidence of compression (diagnosis by exclusion)

Infarcted are is visible on MRI (hyperintense on T2 weighted images)

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32
Q

Prognosis of Fibrocartilaginous embolic myelopathy (FCE)

A

Depends on extent of injury

GOod prognosis when preservation of deep pain perception

Guarded prognosis in absence of deep pain sensation

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33
Q

Treatment of Fibrocartilaginous embolic myelopathy (FCE)

A

Rehabilitation, improvement can be dramatic over the first 7 days and will continue for 1-3 months after injury

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34
Q

Pathogenesis of Discospondylitis

A

Infection of the intervertebral disc and adjacent vertebrae by
1. haematogenous spread from distant foci of infection
2. penetrating wounds or plant material
3. iatrogenic (surgery)

Immunosuppression is considered a predisposing cause

Staphylococcus intermedius is the most common aetiolgical agent of canine discospondylitis

35
Q

Epidemiology of Discospondylitis

A

Multifocal in the vertebral column

Most frequently in large male intact middle aged dogs, less common in cats

Most commonly affected site in L7-S1

36
Q

Clinical signs of Discospondylitis

A

Spinal pain (+++)

Fever - systemic signs 30% (fever, weight loss, endocarditis)

Combination of neurological deficits regarding the spinal cord segment affected

37
Q

Diagnosis of Discospondylitis

A

Leucocytosis

Blood and urine culture

Spinal radiographs
- narrowing or enlarged disc space
- may not be evident in first 2-4 weeks
- entire spine should be radiographed as can be multifocal

Scintigraphy

Myelogram/CT/MRI

MRI with contrast

Abdominal/cardiac U/S

Thoracic radiographs

38
Q

Prognosis of Discospondylitis

A

Very good unless fungal aetiology

39
Q

Treatment of Discospondylitis

A

Antibiotics (cephalosporins, amoxicillin) for min 2 months

Cage rest

Analgesics (NSAIDs)

(Surgical decompression)

40
Q

Pathogenesis of Steroid-responsive meningitis-arteritis

A

Suspected immunological cause, resulting in vasculitis and meningitis

41
Q

Epidemiology of Steroid-responsive meningitis-arteritis

A

Predisposition in Beagles, Bernese Mountain Dogs, Boxers (BBB), other breeds

Young adults (<2 years)

42
Q

Clinical signs of Steroid-responsive meningitis-arteritis

A

Acute form: febrile, anorexia, neck pain

Chronic form (rare): neurological deficits - meningomyelitis

50% concurrent polyarthritis (IMPA, immune mediated polyarthritis)

43
Q

Diagnosis of Steroid-responsive meningitis-arteritis

A

Neutrophilia (left shift)

High CRP in serum

CSF: neutrophilic pleocytosis and protein elevation

High IgA levels in serum and CSF

44
Q

Prognosis of Steroid-responsive meningitis-arteritis

A

Good if treated early and aggressively

45
Q

Treatment of Steroid-responsive meningitis-arteritis

A

Long term (4-6 months) tapering immunosuppressive doses of corticosteroids

46
Q

Pathogenesis of traumatic intervertebral disc disease

A

ANNPE: acute non-compressive nucleus pulposus extrusion

HNPE: Hydrated nucleus pulposus extrusion

47
Q

ANNPE

A

Acute non-compressive nucleus pulposus extrusion

Intervertebral discs are mainly healthy or only mild/early signs of degeneration

There is traumatic rupture of the annulus fibrosus with acute extrusion of fluid healthy nucleus pulposus into the vertebral canal

Causes per-acute contusive but non-compressive myelopathy

48
Q

HNPE

A

Hydrated nucleus pulposus extrusion

Gelatinous to liquid, histologically only partially degenerated nucleus pulposus extrudes causing contusive and compressive myelopathy

Unknown spontaneous cause, rarely to be associated with exercise or trauma

49
Q

Epidemiology of traumatic intervertebral disc disease

A

ANNPE: classically in large breed dogs, non-chondrodystrophic, also in cats. Older adults (mean 7yr)

HNPE: any breed, and cats. Adults (5-12 yrs, median 9yrs)

50
Q

Clinical signs of traumatic intervertebral disc disease

A

Common localisation at C1-C5

ANNPE: common to be lateralised and painful in the first 24 hrs, vocalisation at onset. Signs tend to stabilise or improve after 24-48hrs

HNPE: symmetric non-lateralised signs; spinal pain rarely detected

51
Q

Diagnosis of traumatic intervertebral disc disease

A

MRI of the neuroanatomical localisation distinguishes ANNPE from HNPE and other myelopathies

Differentials are FCE, disc herniation

52
Q

Treatment of traumatic intervertebral disc disease

A

ANNPE: supportive, it is mainly a spinal cord contusive injury

HNPE: supportive when mild to moderate signs or improving. Decompressive surgery can be attempted on non-improving severe cases

53
Q

Prognosis of traumatic intervertebral disc disease

A

ANNPE and HNPE: good prognosis if deep pain is preserved

HNPE: unsuccessful if tetraplegia with respiration compromise (remember C1C5)

54
Q

Pathogenesis of atlanto-axial instability

A

Subluxation of the atlantoaxial junction is a relatively common problem and usually results from a failure of ligamentous support and/or congenital absence or hypoplasia of the dens

55
Q

Epidemiology of atlanto-axial instability

A

Classically young toy and small breeds

<2 years

Traumatic fracture of the dens and rupture of the ligaments can occur in any dog or cat

56
Q

Clinical signs of atlanto-axial instability

A

Neck pain (do not flex head!)

Neurological deficits for C1C5

57
Q

Diagnosis of atlanto-axial instability

A

Survey radiographs of the cervical spine (extreme care if sedated or anaesthetised, flexion of the neck can cause iatrogenic spinal cord damage)
- Lateral view: increased space between dorsal lamina of atlas and dorsal spinous process of the axis
- Ventrodorsal view: reduced size or absence of the dens

58
Q

Treatment of atlanto-axial instability

A

Conservative: external splint/bandage from ears to shoulders minimum 2-3 months, plus strict rest

Surgical: reduction of subluxation and stabilisation with K wires, screws, and polymethacrylate

59
Q

Prognosis of atlanto-axial instability

A

Conservative: often effective on short term, long term deficiency doubtful but possible

Surgical: excellent if mild neurological deficits, worse if severe and chronic neurological deficits. Risk of resp arrest and death in 48-hour post-operative period (20%)

60
Q

Pathogenesis of spinal cord tumours

A

Primary:
- Extradural: verterbral tumours (sarcomas, multiple myeloma), lymphoma
- Intradural-extramedullary: meningiomas, nerve sheath tumours, nephroblastoma, lymphoma
- Intramedullary: ependymomas, gliomas, lymphoma

Secondary: metastatic

61
Q

Epidemiology of spinal tumours

A

Older dogs and cats

Extradural lymphoma is the most common spinal tumours in cats. Most affected cats are <2yrs of age. FeLV has been associated.

62
Q

Clinical signs of spinal tumours

A

Spinal hyperaesthesia (extradural or intradural-extramedullary)

Neurological deficits depending on localisation

Pathological fractures of vertebral body results in acute onset of neurological deficits

63
Q

Diagnosis of spinal tumours

A

Survey radiographs: vertebral tumours: lysis, pathological fractures

Abdominal U/S, chest radiographs

CT/MRI

Fluoroscopic-guided needle aspiration or surgical biopsy

Scintigraphy: vertebral tumours - metastasis

Bone marrow biopsy (myeloma, lymphoma)

Monoclonal gammopathy in serum and urine, Bence Jones proteinuria (myeloma)

64
Q

Treatment of spinal tumours

A

Palliative, combination of surgery, irridation +/- chemotherapy

65
Q

Prognosis of spinal tumours

A

Guarded to poor - depends on type of tumour, localisation, staging, and tumour size

66
Q

Pathogenesis of degenerative intervertebral disc disease

A

Type 1 = extrusion
- central nuclear material of disc ruptured through dorsal fibrous structures into the vertebral canal
- nucleus pulposus ages prematurely in chondrodystrophic breeds so nucleus matrix degenerates and mineralises making them prone

Type 2 = protrusion
- disc ‘bulging’ into vertebral canal
- fibroid degeneration involves a progressive thickening of the dorsal annulus fibrosus and loss of elasticity

67
Q

Epidemiology of degenerative intervertebral disc disease

A

One of the most common neurological disorders in dogs, less common in cats

Type 1: small breed dogs, unusual in dogs <2yrs

Type 2: large breed dogs, 5yrs or older, most commonly cervical and thoracolumbar region

68
Q

Clinical signs of degenerative intervertebral disc disease

A

Type 1: acute, minutes-days
Type 2: chronic, slowly progressive (weeks-months)

Depends on localisation

69
Q

Diagnosis of degenerative intervertebral disc disease

A

Survey spinal radiographs
- type 1: narrowing of intervertebral disc space, narrowing of the intervertebral foramen and presence of mineralised material within the vertebral foramen and mineralised material within canal and discc space
- type 2: spondylosis

Myelography, CT, or MRI

70
Q

Treatment of degenerative intervertebral disc disease

A

Conservative:
- if first time with spinal pain, only mild-moderate paresis
- any time if still ambulatory
- if finacial restrictions
- Strict cage rest, then restricted exercise
- mandatory to support healthy micturition - bladder needs to be manually expressed 3-4x a day

Surgical
- spinal decompressive surgery
- removal of disc materal by ventral slot if cervical or hemilaminectomy if thoracolumbar

71
Q

Prognosis of degenerative intervertebral disc disease

A

Depends on clinical signs good if ambulatory or non ambulatory paraparesis but gets worse if paraplegic and without deep pain response

72
Q

Lumbosacral stenosis

A

Stenosis of vertebral canal or foramina and compression of the cauda equina

IV disc herniation (type II>type I)

Ventral subluxation of S1/instability/malalignment

Vertebral anomalies

Soft tissue proliferation

Osteophytosis

Osteochondrosis

73
Q

Pathogenesis of degenerative myelopathy

A

progressive neurodegenerative disease in dogs with both upper and motor neuron involvement

Has been associated with a variation of the gene SODI with a missense mutation

74
Q

Epidemiology of degenerative myelopathy

A

Severeal dog breeds, including GSD, boxer, chesapeake bay retriever

Usually 8yrs or older

75
Q

Clinical signs of degenerative myelopathy

A

Insidious, progressive ataxia and paresis of the pelvic limbs (UMN) ascending to tetraparesis (LMN)

Control of urination or defecation may be affected late in the disease process

76
Q

Differential diagnosis of degenerative myelopathy

A

Intervertebral disc disease or degenerative lumbosacral stenosis

Degenerative myelopathy is not painful!

77
Q

Diagnosis of degenerative myelopathy

A

Ruling out other diseases causing progressive myelopathy

Genetic test: mutation in the SODI gene is a risk factor

Post mortem

78
Q

Prognosis of degenerative myelopathy

A

Poor, dogs often lose the ability to ambulate within 6 months of diagnosis

79
Q

Treatment of degenerative myelopathy

A

Regular exercise

Physiotherapy may improve the dogs quality of life

80
Q

Disc associated cervical spondylomyopathy

A

Multifactorial/unknown aetiology

Large breed dogs

Middle-older age

C5-C7 (more caudal)

Mild pain - moderate (tetraparesis/’2-engine gait’/C6T2)

81
Q

Osseous associated cervical spondylomyopathy

A

Multifactorial/unknown aetiology

Giant breed dogs

Young age

C3-C6 (more cranial)

Mild pain - moderate (tetraparesis/C1C5/C6T2)

82
Q

Conservative mangement of cervical spondylomyopathy

A

Exercise restriction/rest
Anti-inflammatories (preds)
Physiotherapy

83
Q

Surgical treatment of cervical spondylomyopathy

A

Severe progressive/relapses
Direct decompression
Indirect decompression

SA Neurology (11 decks)

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