Spinal Cord/Lesions

Question 1

Dorsal Column (what it carries, path)

Answer 1

Ascending pressure, vibration, fine touch, proprioception`
Sensory nerve ending to cell body in DRG, enters SC and ascends as fasciculus gracilis (medial, lower body) or cuneatus (lateral, upper body/arms) and synapses at ipsilateral nucleus gracilis/cuneatus in medulla
Decussates in medulla and ascends contralaterally in medial lemniscus
Synapses at VPL in thalamus then goes to sensory cortex

Question 2

Spinothalamic tract (what it carries, path)

Answer 2

Ascending lateral: pain, temperature. Anterior: crude touch, pressure
Sensory nerve ending (Adelta and C fibers) cell body in DRG then enters SC via Lissauer’s tract. Rise in ipsilateral gray matter 1-2 levels, synapse, then decussate at anterior white commissure and ascend contralaterally in spinothalamic tracts.
Synapse at VPL in thalamus and go to sensory cortex

Question 3

Lateral corticospinal tract (what it carries, path)

Answer 3

Descending voluntary movement of contralateral limbs
UMN: cell body in primary motor cortex, descends ipsilaterally through internal capsule, most fibers decussate at caudal medulla (pyramidal decussation) and descend contralaterally (legs lateral, arms medial here)
Decussate in cell body of anterior horn in spinal cord and leave as LMN, then synapse at NMJ

Question 4

Poliomyelitis (transmission, what it causes, CSF)

Answer 4

Fecal oral, replicates in oropharynx and SI before spreading to bloodstream/CNS
Destruction of cells in anterior horn of spinal cord so LMN death and signs - weakness, hypotonia, flaccid paralysis, fasciculations, hyporeflexia, atrophy
CSF has lymphocytes and slight protein increase but normal glucose

Question 5

Werdnig-Hoffman Disease (what it is, inheritance, what it causes)

Answer 5

AR Congenital degeneratio of anterior horns of spinal cord so LMN lesion. “Floppy baby” at birth with tongue fasciculations, die soon

Question 6

Friedreich Ataxia (genetics, what it is, what it causes, presentation)

Answer 6

AR trinucleotide repeat disorder (GAA) on Ch 9 that encodes fratanxin (Fe binding prot). Impairment in mt function that degenerates multiple spinal tracts, lose some senses, staggering gait, frequent falling, hypertrophic cardiomyopathy (cause of death). Presents with kyphoscoliosis in childhood

Question 7

Brown-Sequard Syndrome

Answer 7

Hemisection of Spinal Cord. Findings:
Ipsilateral UMN signs below level of lesion (corticospinal tract damage)
Ipsilateral loss of tactile, vibration, proprioception sense below level of lesion (dorsal column damage)
Contralateral pain and temperature loss starting like 1-2 levels below level of lesion (due to spinothalamic tract damage)
Ipsilateral loss of all sensation at level of lesion
Ipsilateral LMN signs (flaccid paralysis) at level of lesion

Question 8

Charcot’s Triad of MS

Answer 8

Scanning speech, intention tremor, nystagmus

Question 9

ALS Location, Enzyme Defect, and Treatment

Answer 9

Anterior horn (LMN) and lateral corticospinal (UMN), so both of those but no sensory deficits
Can be caused by defect in superoxide dismutase I
Riluzole somewhat increases survival but decreasing presynaptic glutamate release

Question 10

Tabes Dorsalis

Answer 10

Tertiary syphilis, get degeneration/demyelination of dorsal columns so get impaired sensation and proprioception, so get Positive Romberg sign

Question 11

Argyll Robertson pupils

Answer 11

Accomodation but no reaction to light, in tabes dorsalis

Question 12

Anterior Spinal Artery Occlusion

Answer 12

Kinda opposite of tabes dorsalis, gets everything but dorsal columns and Lissauer tract. So have touch/proprio but lose pain/temp and UMN and LMN

Question 13

Vitamin B12 Deficiency

Answer 13

Subacute combined degeneration - demyelination of dorsal columns, lateral corticospinal tract, and spinocerebellar tracts

Question 14

Syringomyelia

Answer 14

Syrnix expands and damages anterior white commissure of spinothalamic tract (2nd order neurons) so get bilateral loss of pain and temperature sensation, often “cape like” distribution in upper extremities. Often seen in Chiari I malformation