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Year 4 - PAN > Neurology - Disorders of the spinal cord > Flashcards

Neurology - Disorders of the spinal cord Flashcards

1
Q

Myelopathy

A

= Spinal cord disease

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2
Q

Corticospinal tract (lateral)

A

Voluntary movement
Upper motor neurones originate from Betz cells in cerebral cortex
Decussate at the medullary pyramids - controls contralateral limb

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3
Q

Spinothalamic tract

A

Carries pain and temperature stimuli

Primary afferent neurons synapse and cross at the level they enter (or within 2 layers)

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4
Q

Posterior (dorsal) column

A

Carries proprioceptive and vibration sense

Decussates at the medial lemniscus - conveys ipsilateral information

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5
Q

What are the important clinical features of spinal cord disease?

A 
Spastic paraparesis (UMN signs in both lower limbs)
Sensory level (below which sensation is impaired, above is normal)
Bladder (not usually bowel) dysfunction
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6
Q

Does a sensory level at T10 mean the lesion is at T10?

A

No
The lesion is at or above T10
Important not to restrict images to sensory level because you can miss higher lesions

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7
Q

What sensory loss is typical of extrinsic cord lesions?

A

Extrinsic cord lesions - e.g. prolapsed disc, tumor etc - are compressive and produce saddle anaesthesia
Lamination of nerve fibres in spinothalamic tract means part of the tract carrying sensory information from lumbosacral dermatomes is closest to the surface and most vulnerable to external compression

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8
Q

Brown - Sequard syndrome

A

Hemi-section of the cord produces characteristic pattern of sensory and motor deficits
Ipsilateral loss of proprioception and vibration sense
Contralateral loss of pain and temperature
Ipsilateral UMN weakness (remember damage to anterior horn cells leads to LMN signs)

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9
Q

What is a syringomyelia?

A

= CSF filled cavity (syrinx) develops centrally in the spinal cord

Typically evolves in the lower cervical cord (though over many years it may expand to occupy most of the cord)

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10
Q

Causes of syringomyelia

A

1) Blocked CSF circulation with decreased flow from posterior fossa
- Arnold-Chiari malformation (cerebellum herniates through foramen magnum)
- Masses

2) Spina bifida
3) Secondary to cord trauma, myelitis, tumour and AVMs

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11
Q

Sensory and motor deficits in syringomyelia

A

NB Syringomyelia typically starts in the cervical cord
Spastic paraparesis in the lower limbs (due to interruption of descending corticospinal tract)
LMN signs in the upper limbs (damage to anterior horn cells)

“Dissociated sensory loss” - pain and temperature sensation lost due to interruption of the decussating pathway by the syrinx - posterior column relatively spared

Root distribution reflects syrinx location - usually upper limb and chest “cape”

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12
Q

Cardinal signs of syringomyelia

A

1) Dissociated sensory loss
2) Wasting/ weakness of hands +/- claw hand
3) Areflexia in upper limb
4) Charcot joints - shoulder and elbow

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13
Q

What is the investigation and treatment of syringomyelia?

A

Ix - MRI spine (sagittal)

Rx - Decompression at the foramen magnum or draining of the syrinx via syringostomy

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14
Q

Syringobulbia

A

Syrinx extends into the medulla

Development of bilateral lower cranial nerve palsies and Horner’s syndrome

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15
Q

What patients are at high risk of neurosyphilis?

A

Homosexual patients

Risk with HIV infection

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16
Q

Name the clinical manifestations of neurosyphilis

A

Neurosyphilis occurs in about 8% of patients with syphilis - requires 6 years (minimum) to develop
5 common presentations:
1) Asymptomatic neuropsyphilis - patient is normal but CSF tests positive for syphilis
2) Subacute meningitis - high lymphocyte, high protein, low glucose
3) Meningovascular syphilis - spirochetes attack blood vessels in brain and meninges
4) Tabes dorsalis - affects spinal cord, specifically posterior column and dorsal root
5) General paresis (of the insane)

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17
Q

Tabes dorsalis

A

Clinical manifestation of tertiary syphilis
Parenchymatous disease primarily affecting dorsal root ganglion cells of the spinal cord
Causes:
- Argyll - Robertson pupil
- Absent knee and ankle reflexes
- Sensory disturbances (e.g. Charcot joints etc)

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18
Q

How is syphilis diagnosed?

A

Serological test for syphilis - blood and CSF

CSF shows lymphocytosis, raised protein and oligoclonal bands

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19
Q

Most common cause of spinal cord disease in a) young and b) elderly (over 50) patients

A

a) MS

b) Cervical spondylosis

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20
Q

How is neurosyphilis treated? Why is steroid cover required during initial penicillin treatment?

A

IM Penicillin + Probenecid

Avoid Jarisch - Herxheimer reaction = inflammatory response to the rapid killing of spirochetes

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21
Q

Examples of intrinsic cord disease

A

“DIVINITY”

  • Degenerative - e.g. MND
  • Developmental - e.g. Friedrich’s ataxia, Hereditary spastic paraparesis
  • Infection - e.g. HIV, syphilis (tabes dorsalis)
  • Vascular - e.g. aortic dissection/ aneurysm, VTE, Vasculitis (esp PAN)
  • Inflammation - e.g. demyelination (MS), transverse myelitis
  • Neoplasia - e.g. glioma, ependymoma
  • Injury - e.g. radiation myelitis
  • Toxin/ Nutrition - e.g. B12
  • sYringomyelia
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22
Q

What is Beck’s syndrome?

A

= Anterior spinal artery infarction

Spinothalamic and corticospinal tract loss leading to bilateral loss of pain and temperature sense + spastic paraparesis

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23
Q

How do intrinsic cord diseases commonly present?

A

Painless

Early sphincter/ erectile dysfunction

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24
Q

Presentation of spinal cord compression

A

Spastic paraparesis - UMN signs below the lesion
LMN signs at the level of the lesion
Loss of sphincter control - bladder hesitancy, frequency leading to painless retention

Spinal pain is not always a consistent finding but if radicular can help lesion localisation

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25
Q

What is the most common cause of spinal cord compression?

A

Spinal cord is most commonly compressed by:
- Secondary tumours from breast, lung and prostate

  • Prolapsed intervertebral discs which usually herniate laterally causing asymmetrical signs, although central disc prolapse can occur
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26
Q

Investigations in spinal cord compression

A
  1. ) MRI - definitive imaging
  2. ) CXR/ CT chest/abdo/pelvis - exclude malignancy
  3. ) Serum electrophoresis/ Bence-Jones proteins (for myeloma)
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27
Q

Treatment of spinal cord compression

A

Neurosurgical emergency - especially if recent onset and rapid progression

Malignancy:

  • Dexamethasone IV
  • Consider chemo, radio and decompressive laminectomy

Abscesses:
- Abx, and surgical decompression

28
Q

What are the differentials to consider in spinal cord compression?

A

Other causes of spastic paraparesis:

  • MS
  • SACD
  • Transverse myelitis
  • MND
  • Anterior spinal artery stenosis
  • Parasagittal cranial meningioma
  • Copper deficiency
  • Hereditary spastic paraparesis
29
Q

How do conus/ cauda lesions differ from lesion higher up the cord?

A

These are radiculopathic
Spinal cord ends at L1 with the conus medularis
Compared with lesions higher up these lesions are flaccid and areflexic (i.e. LMN)

30
Q

Features of conus medularis lesions

A
  • Mixed UMN and LMN weakness
  • Early constipation and retention
  • Back pain
  • Sacral sensory disturbance
31
Q

Features of cauda equina lesions

A
  • Saddle anaesthesia
  • Back pain
  • Radicular pain down legs
  • Sphincter disturbance (painless retention of urine with overflow incontinence and UTIs)
  • LMN signs in legs
32
Q

Intermittent claudication of the cauda equina

A

Disturbance of blood supply to the cauda equina produces produce transient/ intermittent neurological symptoms - these are exacerbated by exercise

Can be confused with intermittent claudication but recovery is from this is more rapid and there are no sensorimotor symptoms

33
Q

Subacute combined degeneration of the cord

A

Neurological consequence of vit B12 deficiency
Patients also develop optic atrophy, peripheral neuropathy and dementia as well

Combined degeneration = demyelination of both pyramidal and posterior (dorsal) columns

34
Q

What is the common presentation of subacute combined degeneration?

A

Sensory peripheral neuropathy with numbness and paraesthesia in the feet is normal

Can present as spastic paraparesis:

  • Posterior column loss (vibration and proprioception with positive Romberg’s)
  • UMN lesion (weakness, hypertonia and hyperreflexia)
35
Q

What are the important investigations in subacute combined degeneration of the cord?

A

1) Serum B12 and folate
2) Bone marrow aspiration/ biopsy
3) Parietal cell and intrinsic factor antibodies

36
Q

How is SACD treated?

A

Vitamin B 12 (hydroxocobalamin)

NB - folic acid treatment alone may exacerbate SACD so it is crucial to measure B12 levels and replace if it is deficient in megaloblastic anaemia with any suggestion of spinal cord involvement

37
Q

Transverse myelitis

A

= Inflammatory disease localised to the middle of the spinal cord

Can be the first manifestation of MS

38
Q

Presentation of transverse myelitis

A

Acute weakness with an ascending sensory level - i.e. very similar to acute cord compression (which must be excluded by an urgent MRI)

Imaging may show a focal lesion or be normal

39
Q

What is the aetiology of transverse myelitis?

A

Proportion of patients report having a recent flu-like infection, so TM may occur as a parainfectious complication

Mycoplasma, Legionella, EBV and herpes are implicated

40
Q

What is hereditary spastic paraparesis?

A

Hereditary disease that can be autosomal dominant or recessive

Selectively affects the long motor tracts causing more spasticity than weakness

Very slowly progressive, typically presents in early adult life (although some cases may present into the fifties)

41
Q

Clinical features of copper deficiency

A

Produces a clinical picture almost identical to SACD but with normal B12 levels

Deficiency occurs as a result of general malabsorption syndrome or zinc supplementation

42
Q

Is measuring B12 levels accurate in SACD?

A

No - “low B12 levels” and a clinical picture should prompt measuring levels of methyl malonic acid and homocysteine levels which are more accurate measure of B12 levels

43
Q

Spinal shock

A

If the spinal cord is damaged suddenly by trauma, ischaemia or compression, spinal shock may occur. This is a condition where there is a temporary loss of all spinal reflexes, motor activity and sensation below the level of the lesion.

Flaccid paralysis, hyporeflexia, sensory loss and no bladder tone are cardinal features. Development of UMN signs may take several weeks.

44
Q

What is a radiculopathy?

A

= disease process affecting the nerve roots leading to:

  • Pain in the distribution of the nerve root
  • Dermatomal sensory disturbance
  • Weakness of muscle supplied by nerve
  • Reduced/ absent reflexes
45
Q

Most common cause of radiculopathy

A

Prolapsed intervertebral disc (acute disc) in the cervical (usually C5/C6 or C6/C7) or lumbar spine (usually L4/5 or L5/S1)

Normally occurs in younger patients

Nucleus pulposus herniates through the ruptured annulus fibrosus

46
Q

Less common causes of radiculopathy

A
  • Degenerative cervical or lumbar spondylotic disease (elderly)
  • Benign tumours (i.e. schwannomas and meningiomas)
  • Malignant tumours (i.e. compression from bony metastasis)
  • Inflammatory (HSV and shingles)
  • Malignant meningitis
47
Q

Summarise the anatomy of masses that compress the spinal cord

A

1) Extramedullary extradural lesions (outside the spinal cord and outside its dural covering)
- epidural abscess
- herniated disc
- epidural haematoma

2) Extramedullary intradural lesions (outside the spinal cord but inside its dural covering)
- meningioma
- neurofibroma

3) Intramedullary intradural lesions (inside the spinal cord and inside its dural covering)
- primary cord neoplasms
- syringomyelia

48
Q

Pathology of disc herniation

A

Nucleus pulposus herniates through ruptured annulus fibrosus

Lumbar discs usually herniate posterolaterally causing nerve root compression as the posterior longitudinal ligament is strongest in the midline

If the ruptured disc is large and midline, cauda equina syndrome may result

49
Q

What are the symptoms of lumbar disc prolapse?

A
  • Back pain (usually mild component)
  • Radicular pain (known as sciatica if it involves roots L5 and S1) radiating into legs and terminating in myotome of compressed root
  • Avoidance of movements
  • Weakness and sensory disturbance in nerve distribution
  • sphincter disturbance (CES)
50
Q

What are the symptoms of cervical disc prolapse?

A
  • Limitation of neck movement
  • Radicular pain (known as “brachialgia”) radiating from neck to shoulders
  • Sensory or motor symptoms
51
Q

In the lumbar spine what nerve root is affected by a herniating disc?

A

A herniated lumbar disc usually compresses the nerve root exiting the foramen below the level of herniation - i.e. L5/S1 disc prolapse will impinge upon the transiting S1 root as it passes through the lateral recess of the spinal canal before it exits below the pedicle of its corresponding vertebra

52
Q

Tests of lumbar disc prolapse

A

Lasagne’s sign (straight leg raise test) = raising affected limb by the ankle until the patient complains of pain radiating down the leg below the knee, exacerbated by ankle dorsiflexion
- Positive = pain occurring at

53
Q

Signs in L5/S1 disc prolapse

A
  • Weakness in plantar flexion (ask patient to stand on tip toes one leg at a time)
  • Depressed ankle jerk reflex
  • Reduced sensation in the lateral aspect of the foot (S1 distribution)
54
Q

What are the signs of an L4/L5 disc prolapse?

A

Impinges on L5 nerve root

  • Weakness of dorsiflexion or foot drop (ask patient to walk on their heels)
  • Extensor hallucis longus weakness
  • Sensory loss in the dorsum of the foot
55
Q

In the cervical spine what nerve root is affected by disc herniation?

A

Herniated disc compresses the nerve root exiting from the foramen at the level of the herniation as the nerve root exits above the pedicle of its corresponding vertebra - i.e. a C6/7 prolapse impinges on the C7 root (the only exception is C8 which exits below the pedicle of C7/T1)

56
Q

Signs of C6/C7 disc prolapse

A

C6/C7 disc prolapse compressing the C7 nerve root causes:

  • Reduced triceps reflex
  • Weakness of triceps (elbow extension)
  • Sensory symptoms in C7 distribution
57
Q

Signs of a C5/C6 disc prolapse

A

Impinges on C6 nerve root

  • Diminished biceps reflex
  • Weakness of biceps (elbow flexion)
  • Sensory symptoms in C7 distribution
58
Q

What imaging modality is best if lumbosacral disc prolapse is suspected? Is it always needed?

A

Majority of patients with disc herniation improve spontaneously (up to 70% within 4 weeks) so in the absence of red flag symptoms no imaging is required in the first 4 weeks

If red flags present (e.g. indicating CES) or symptoms of prolapsed disc severe enough to consider surgery persist beyond 4 weeks:

  • AP and lateral films (assess for scoliosis and spondylolisthesis, a forward “slip” of one vertebrae on the vertebrae below due to a defect in the pars interarticularis)
  • MRI
  • CT and myelography (when CT cannot be performed)
59
Q

How should lumbosacral disc prolapse be managed?

A

Majority of herniated lumbar discs improve without surgery (conservative treatment with analgesia and reduction in heavy exercise) over an average of 6wks

Surgery should be considered if symptoms persist beyond 5-8wks

Emergency surgery is indicated for CES, progressive weakness (e.g. foot drop) or severe unremitting pain despite analgesia

60
Q

How should cervical disc prolapse be managed?

A

Majority of herniated cervical discs improve without surgery

Analgesics are necessary - consider surgery if conservative treatment fails or progressive neurological deficits develop

61
Q

What are red flag symptoms for imaging?

A

Patients with lower back pain and sciatica infection, malignancy or CES should be considered and an urgent MRI:
- Signs of CES: lower back pain + bilateral sciatica + saddle anaesthesia + progressive leg weakness + bilateral absent ankle reflexes + sphincter disturbance

  • Spinal fracture: history of trauma, elderly osteoporotic patient and thoracic pain
  • Malignancy: >55 or
62
Q

What are the signs of anterior spinal artery syndrome?

A

Anterior spinal artery syndrome occurs when the anterior spinal artery is occluded. This artery supplies blood to the anterior two thirds of the spinal cord.

Occlusions results in bilateral loss of pain and temperature below the level of the lesion accompanied by weakness and bladder dysfunction. Reflexes may be hyperactive below the level of the lesion.

63
Q

What is the artery of Adamkiewicz?

A

The artery of Adamkiewicz is a major lumbar radicular artery that arises from the aorta and enters the cord between T10 and L3. It supplies the lumbar and lower thoracic segments. It forms anastomoses with the anterior spinal artery in the lower thoracic region, where the watershed area of the spinal cord is located.

64
Q

What is the micturition reflex?

A

Put simply the act of voiding is controlled by a balance between reflex actions and cortical control. Bilateral projections originating from cortical structures descend in the spinal cord just medial to the corticospinal tracts and synapse with preganglionic parasympathetic fibres in the S2, S3 and S4 regions. These fibres then travel out the ventral roots of S2, S3 and S4 to synapse at postganglionic parasympathetic fibres near the bladder to innervate the detrusor muscle. Muscle spindles located in the detrusor muscle are stretched when the bladder is filled, increasing their firing rate. This signal change increases the rate of firing of preganglionic parasympathetic fibres of S2, S3 and S4 resulting in detrusor muscle contraction and voiding of the bladder.

65
Q

What happens to micturition during spinal cord injury?

A

Following bilateral lesions to the spinal cord the bladder initially becomes flaccid (acute) and eventually becomes spastic (chronic). The reason for this is that the detrusor muscle loses its cortical input. Like deep tendon reflexes, it initially becomes flaccid resulting in urinary retention. As the bladder fills, overflow incontinence may develop because the bladder cannot hold any more urine. With time, the detrusor muscle becomes spastic. Small stretches in the muscle result in voiding. This spastic bladder results in urinary frequency and urgency.

Year 4 - PAN (43 decks)

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