Spinal Cord Diseases

Question 1

Corticospinal tracts:

Answer 1

control muscle strength, tone and reflexes

Question 2

Dorsal columns:

Answer 2

Vibration and position sense (proprioception)

Question 3

Anterolateral spinothalamtic tracts:

Answer 3

conduct Pain and Temperature

Question 4

Motor neurons are in the __ and lesion there cause __.

Answer 4

Anterior horns.

Weakness and atrophy.

Question 5

Decreased/absent reflexes are at the __ of the lesion and reflexes ___ below the lesion.

Answer 5

Level of lesion.

Increased below lesion.

Question 6

Dermatome level at umbilicus:

Answer 6

T10

Question 7

Dermatome level at nipples:

Answer 7

T4 (5)

Question 8

Dermatome level at thumb/fingers1,2:

Answer 8

C6

Question 9

Dermatome level at finger 3:

Answer 9

C7

Question 10

Dermatome level at fingers 4,5:

Answer 10

C8

Question 11

Achilles reflex at spinal levels:

Answer 11

S1-2

“1,2 buckle my shoe”

Question 12

Patellar reflex at spinal levels:

Answer 12

L3-4

“3,4 Kick the door”

Question 13

Biceps and brachioradialis reflexes at spinal levels:

Answer 13

C5-6

“5,6 pick up sticks”

Question 14

Triceps reflex at spinal levels:

Answer 14

C7-8

“7,8 lay them straight”

Question 15

Cord ends at __ vertebral level, spinal canal below this level contains nerve roots (cauda equina)

Answer 15

L1

Question 16

Anterior spinal artery supplies:

Answer 16

Anterior 2/3 of cord: anterior horns, spinothalamic tracts, corticospinal tracts

Question 17

Posterior spinal artery supplies:

Answer 17

Posterior 1/3 of cord: Dorsal column and dorsal horns.

Question 18

Segmental arteries from the aorta:

Answer 18

Anastomoses with spinal arteries. Example - artery of Adamkiewcz

Question 19

artery of Adamkiewicz:

Answer 19

at T10, major source of blood for lower cord.

Question 20

Brown-Sequard Syndrome = hemicord, sings:

Answer 20

• Ipsilateral Corticospinal tract signs and ipsilateral Dorsal column signs (fibers cross in medulla)
• Contralateral Spinothalamic tract (fibers cross below lesion and 1-2 segments above)
• a unilateral focal lesion (tumor, trauma)

Question 21

Lhermitte sign:

Answer 21

Electric-like sensation extending down back and/or into arms with neck flexion.
Seen with focal cervical lesions, most notably demyelinating lesions.

Question 22

Meningeal irritation:

Answer 22

With meningitis or subarachnoid hemorrhage:
Nuchal rigidity,
Kernig sign,
Brudzinski sign.

Question 23

Nuchal rigidity:

Answer 23

painful inability to flex neck

Question 24

Kernig sign:

Answer 24

painful knee extension/resistance with hips and knees flexed 90 degrees

Question 25

Brudzinski sign:

Answer 25

involuntary lifting of legs with neck flexion in spine position.

Question 26

Potential causes of acute extradural:

Answer 26

Trauma: MVA, motorcycle, sports injuries; falls in elderly—symptoms often due to fracture, infarct, hematoma.
Metastatic cancer to vertebrae: breast, lung, prostate, kidney, colon, myeloma.
Lymphoma
Abscess
Disc herniation affecting cord
AVM
Hematoma

Question 27

Acute Intradural/Extramedullary causes:

Answer 27

Primary tumor e.g. meningioma.

Meningitis with arteritis

Question 28

Acute Intradural/Intramedullary causes:

Answer 28

Inflammatory
		Transverse myelitis
		Multiple sclerosis
		Neuromyelitis optica (NMO)
		SLE
		Sjögren syndrome
		Sarcoidosis
Vascular
Infarction: arteriosclerotic versus arteritis versus aortic dissection (especially at T10—artery of Adamkiewicz)
Infectious
		HTLV1
		HIV
		Syphilis
		Tuberculosis
		Bacterial, viral and fungal lesions
Trauma: Hematomyelia
Anterior Spinal Artery Syndrome.
Posterior spinal artery syndrome.

Question 29

Acute Spinal Artery Syndrome:

Answer 29

Acute onset with initial flaccid paraplegia or quadriplegia depending on location of artery occlusion.
Followed by the flaccidity, converting to spasticity with increased reflexes and Babinski signs.
Sensory loss, with loss of pain and temperature and sparing of vibration, position sense, and partially touch. (i.e. Spare the Dorsal Columns)
Bladder and bowel function are impaired.

Question 30

Posterior Spinal Artery Syndrome:

Answer 30

Rare, and involving posterior column dysfunction and bladder and bowel symptoms.

Question 31

Chronic extradural causes:

Answer 31

Disc/osteophyte complex with chronic disc herniation and epidural extension.
Primary bone tumors e.g. chondrosarcoma, osteogenic sarcoma
Lymphoma.
Dural AVM (occasionally intramedullary) and dural AV fistula.
Lipoma.
Miscellaneous e.g. rheumatoid arthritis, Paget disease, Pott disease (TB)

Question 32

Chronic Intradural Extramedullary causes:

Answer 32

Meningioma, schwannoma, neurofibroma, AVM

Question 33

Chronic Intradural Intramedullary:

Answer 33

Syringomyelia.
Subacute combined degeneration.
Hereditary spastic paraparesis.
Friedreich ataxia.
Amyotrophic lateral sclerosis (ALS).
HTLV-1 myelopathy.
AIDS associated vacuolar myelopathy.
Poliomyelitis

Question 34

Syringomyelia:

Answer 34

Cavity within cord, at times associated with Chiari 1 malformation. Often in cervical area.
Classically, presents with pain and temperature loss in cape distribution, weakness/atrophy in arms, and, ultimately, corticospinal and dorsal column dysfunction below syrinx.

Question 35

Subacute combined degeneration:

Answer 35

Progressive involvement of corticospinal tracts and dorsal columns with increased reflexes, Babinski signs, and loss of position and vibration. A polyneuropathy is also often present.
Three most common causes are:
1. Vitamin B12 deficiency—pernicious anemia and post gastric surgery
2. Copper deficiency—post gastric surgery or excessive zinc ingestion (e.g. zinc containing dental paste) which impedes copper absorption.
3. Vitamin E deficiency—post small bowel surgery, cystic fibrosis, abetalipoproteinemia

Question 36

Hereditary spastic paraparesis:

Answer 36

Degeneration of distal corticospinal axons and dorsal column degeneration and manifested primarily by slowly progressive spastic paraparesis. Patients have spasticity, hyperactive reflexes and Babinski signs. May be inherited in autosomal dominant or recessive or X-linked fashion due to multiple potential gene abnormalities. Age of onset is variable.

Question 37

Friedreich Ataxia:

Answer 37

Autosomal recessive disorder (trinucleotide repeat expansion of the frataxin gene) causing degeneration of the dorsal columns, lateral corticospinal tract signs, spinocerebellar tracts, dorsal roots and ganglia, and peripheral nerves.
Onset is usually in childhood or adolescence and manifested by ataxia, sensory loss, dysarthria, areflexia, and Babinski signs.

Question 38

ALS:

Answer 38

Progressive disorder of upper and lower motor neurons usually beginning in adulthood and occurring sporadically most of the time but is familial in 10% of cases. It is associated with a variety of genetic abnormalities the most common of which is hexanucleotide repeat expansion of c9orf72. A merciless disease for which there is no specific treatment, life expectancy averages 5 years. Clinical features include muscle wasting and weakness beginning in the extremities or bulbar muscles, fasciculations, cramps, hyperactive reflexes, Babinski signs. As weakness progresses, reflexes may be lost. Difficulties swallowing and breathing are often late events requiring a feeding tube and respiratory assistance. Associated clinical features in a minority of patients include frontotemporal dementia and Parkinson disease.

Question 39

HTLV-1 Myelopathy

Answer 39

Progressive spastic paraparesis due to the transmission of a Type C oncovirus by semen, blood, breast milk and shared needles. It is endemic in the Caribbean and South America.

Question 40

AIDS associated vacuolar myelopathy

Answer 40

Late in the course of the systemic illness.

Major symptoms are spastic paraparesis, weakness, painless vibratory and position sense loss and sensory ataxia.

Question 41

Poliomyelitis:

Answer 41

Acute inflammatory illness affecting the motor neurons in the anterior horns.
This illness, caused by the poliovirus and characterized by flaccid weakness, has been largely eradicated but the syndrome can be caused by other enteroviruses and West Nile virus.