Neuroscience Week 3: Spinal Cord Lesions Flashcards Preview

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Flashcards in Neuroscience Week 3: Spinal Cord Lesions Deck (23)
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1
Q

Spinal Muscular Atrophy Clinical Features

A

Congenital degeneration of anterior horns of spinal cord

LMN lesions only, symmetric weakness

Floppy Baby with marked hypotonia (flaccid paralysis)

tongue fasciculations

Autosomal recessive inheritance of mutation in SMN1

SMA type 1 is called Werdnig-Hoffmann disease

2
Q

Spinal Muscular Atrophy

Spinal Lesion Location

A
  • LMN lesions only by degeneration of anterior horns of spinal cord
3
Q

Werdnig-Hoffmann disease AKA

A

Spinal muscular atrophy Type 1

4
Q

Amyotrophic Lateral Sclerosis Clinical Presentation & Pathophysiology

A

Combined UMN (corticobulbar/corticospinal) and LMN (medullary and spinal cord) degeneration

No sensory or bowel/bladder deficits

Can be caused by a defect in superoxide dismutase 1

LMN deficits due to anterior horn cell involvement (dysarthia, dysphagia, asymmetric limb weakness, fasciculations, atrophy)

and

UMN deficits (pseudobulbar palsy, dysarthria, dysphagia, emotional lability, spastic gait, clonus)

Fatal (COMMONLY KNOWN AS Lou Gehrig Disease)

5
Q

Amyotrophic Lateral Sclerosis Treatment

A

Riluzole

6
Q

Amyotrophic Lateral Sclerosis

Spinal lesion locations

A
  • UMN Corticobulbar/corticospinal
  • LMN (medullary and spinal cord)
  • LMN due to anterior horn cell involvement
7
Q

Complete Occlusion of anterior spinal artery Clinical Presentation & Pathophysiology

A

Spares dorsal columns and Lissauer tract

Mid-thoracic ASA territory is watershed area, as artery of Adamkiewicz supplies ASA below T8

Can be caused by aortic aneurysm repair

Presents with UMN deficit below the lesion (corticospinal tract)

LMN deficit at the level of the lesion (anterior horn),

loss of pain and temperature sensation below the lesion (spinothalamic tract)

8
Q

Complete Occlusion of anterior spinal artery

Spinal lesion location

A
  • UMN deficit below the lesion (corticospinal tract)
  • LMN deficit at the level of the lesion (anterior horn)
  • loss of pain and temperature sensation below the lesion (Spinothalamic tract)
9
Q

Tabes Dorsalis Clinical Presentation & Pathophysiology

A

Caused by 3° Syphilis

Results from degeneration (demyelination) of dorsal columns and roots → progressive sensory ataxia (impaired proprioception → poor coordination)

+ Romberg Sign and absent DTRs

Associated with Charcot joints, shooting pain, Argyll Robertson pupils

10
Q

Tabes Dorsalis

Spinal Lesion Location

A

Degeneration (demyelination) of dorsal columns and roots

11
Q

Syringomyelia Clinical Presentation & Pathophysiology

A

Syrinx expands and damages anterior white commissure of spinothalamic tract (2nd-order neurons) → bilateral symmetrical loss of pain and temperature sensation cape-like distribution

seen with Chiari I malformation

Can affect other tracts

12
Q

Syringomyelia

Spinal Lesion Location

A

anterior white commissure of spinothalamic tract (2nd-order neurons)

13
Q

Vitamin B12 Deficiency Clinical Presentation & Pathophysiology

A

Subacute combined degeneration (SCD) – demyelination of Spinocerebellar tracts, lateral Corticospinal tracts, and Dorsal Columns

Ataxic gait, paresthesia, impaired position/vibration sense

14
Q

Vitamin B12 Deficiency

Spinal Lesion Location

A
  • Spinocerebellar tracts
  • Lateral Corticospinal tracts
  • Dorsal columns
15
Q

Cauda Equina Syndrome Clinical Presentation & Pathophysiology

A

Compression of spinal roots L2 and below, often due to intervertebral disc herniation or tumor

Unilateral radicular pain, absent knee, and ankle reflex, loss of bladder and anal sphincter control, saddle anesthesia

16
Q

Cauda Equina Syndrome Treatment

A
  • emergent surgery
  • steroids
17
Q

Poliomyelitis Etiology

A
  • Caused by poliovirus (fecal-oral transmission)
  • Replicates in oropharynx and small intestine before spreading via bloodstream to CNS
  • The infection causes the destruction of cells in the anterior horn of the spinal cord (LMN death)
18
Q

Poliomyelitis Clinical Presentation

A

Signs of LMN Lesion:

  • asymmetric weakness,
  • hypotonia
  • flaccid paralysis
  • fasciculations
  • hyporeflexia
  • muscle atrophy
  • Respiratory muscle involvement leads to respiratory failure

Signs of infection: Malaise, headache, fever, nausea, etc.

19
Q

Poliomyelitis Confirmatory test findings

2 listed

A
  • CSF shows ↑ WBCs (lymphocytic pleocytosis) and slight ↑ of protein (with no change in CSF glucose)
  • Virus recovered from stool or throat
20
Q

Brown-Sequard Syndrome Hemisection of spinal cord findings

A
  1. Ipsilateral loss of all sensation at the level of the lesion
  2. Ipsilateral LMN signs (e.g. flaccid paralysis) at the level of the lesion
  3. Ipsilateral UMN signs below the level of the lesion (due to corticospinal tract damage)
  4. Ipsilateral loss of proprioception, vibration, light (2-point discrimination) touch, and tactile sense below the level of lesion (due to dorsal column damage)
  5. Contralateral loss of pain, temperature, and crude (nondiscriminative) touch below the level of lesion (due to spinothalamic tract damage)

If the lesion occurs above T1, the patient may present with ipsilateral Horner syndrome due to damage of the oculosympathetic pathway

21
Q

Friedreich Ataxia Etiology

A

Autosomal recessive trinucleotide repeat disorder (GAA) on chromosome 9 in a gene that encodes frataxin (iron-binding protein)

Leads to impairment in mitochondrial functioning

22
Q

Friedreich Ataxia Pathophysiology & Clinical Presentation

A

Degeneration of lateral corticospinal tract (spastic paralysis), spinocerebellar tract (ataxia) dorsal columns (↓ vibratory sense, proprioception), and dorsal root ganglia (loss of DTRs)

Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy (cause of death)

23
Q

Friedreich Ataxia Age of onset

A

Presents in childhood with kyphoscoliosis

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