Spinal cord clinical correlations

Question 1

Lesions of a dorsal root may result in…

Epicritic pain fibers?

atonic bladder?

Answer 1

1. anesthesia of the corresponding sensory dermatome.
2. diminished muscle tone and reflex.
3. compromised in the meningovascular infection associated with tabes dorsalis.
4. lesion in dorsal root results in the “atonic bladder” (S2-4)

Question 2

1. lesions in the dorsal roots

Answer 2

1. Ipsilateral sensory dermatomal anesthesia
2. Ipsilateral diminished muscle tone/reflex, if reflex arc to muscle is impaired

Question 3

Lesions in the posterior columns

Answer 3

Ipsilateral loss of proprioceptive/2-point discrimination below level of lesion

Question 4

Lateral funiculus lesions

Answer 4

Ipsilateral UMN paralysis/paresis below level of lesion

Question 5

Anterior funiculus lesions (3 listed)

Answer 5

1. LSTT: Contralateral loss of pain and temperature below the level of lesion
2. Anterior Horn Cells: Ipsilateral lower motor paralysis at the level of lesion
3. Bladder: IF the lesion is bilateral, volitional control of bladder and bowel is lost

Question 6

The receptors for this system are free nerve endings, peritrichial nerve endings, and Merkel’s tactile disks

Answer 6

Ventral Spinothalamic Pathway

The Ventral Spinothalamic Pathway (VSTT) system conveys light (passive) touch, crude tactile sensations and pressure.

The receptors for this system are free nerve endings, peritrichial nerve endings, and Merkel’s tactile disks.

The receptors are innervated by the peripheral processes of pseudounipolar neurons whose cell bodies are located in the dorsal root (spinal) ganglia. These are the primary neurons in this sensory pathway

Question 7

A unilateral lesion of the spinal lemniscus results

Answer 7

results in a contralateral hemianalgesia and thermal hemianesthesia. The loss of passive touch may be masked by the intact posterior column/medial lemniscal system.

Question 8

unilateral lesions of the VSTT

Answer 8

Clinically, may be difficult to lose crude touch sensations, because fibers ascend in both the posterior (primary fibers) and anterolateral funiculi (secondary fibers). This separation of information provides the system with a degree of bilaterality. Also, deficits associated with discrete lesions of the VSTT may be “masked” if the posterior column/medial lemniscal system is intact.

Question 9

Unilateral lesions of the spinal lemniscus result in

Answer 9

Unilateral lesions of the spinal lemniscus result in a contralateral hemianalgesia and thermal hemianesthesia

Question 10

Unilateral Lesions of the lateral spinothalamic tract

Answer 10

result in a contralateral loss of pain and temperature sensation two sensory dermatomal segments below the level of the lesion.

Question 11

unilateral lesions of the spinoreticular fibers

Answer 11

1. do not result in significant sensory deficits.
2. indirect spino-reticulo-thalamic pathway is too bilateral and diffuse to be affected by unilateral lesions.
3. This is part of the neuroanatomical basis of persistent or intractable pain. Bilateral lesions such as spinal cord transections may eliminate crude pain sensations along with other sensations as well.

Question 12

Unilateral lesions of the ACST

Answer 12

Unilateral lesions of the ACST have minimal clinical effect.

Question 13

Unilateral lesions of the CST

Answer 13

Unilateral lesions of the CST result in contralateral spastic hemiplegia or spastic hemiparesis.

Question 14

Unilateral lesions of the LCST

Answer 14

Unilateral lesions of the LCST result in

ipsilateral paralysis or paresis of the distal limb musculature innervated by those spinal segments below the level of the lesion.

spastic paralysis, hyperreflexia, hypertonia, Babinski sign, clonus, and disuse atrophy.

Question 15

LMN lesions

Answer 15

1. Flaccid paralysis. Muscle is completely “limp” and there is no resistance to passive movement.
2. Areflexia. The loss of the efferent component of the reflex arc to a muscle results in the an absence of the associated muscle reflex
3. Atonia. Destruction of gamma motor neurons or their axons results in the absence of muscle tone
4. Atrophy. Denervated muscle atrophies due to the loss of stimulation from the motor neurons
5. Fasciculations or twitching of the denervated muscle, probably due to hypersensitivity of the motor end plate

Question 16

Lesions above T1

Answer 16

Horner’s syndrome

Lesions of the reticulospinal fibers descending to the intermediolateral (preganglionic sympathetic) cell column at T1 will result in a transient Horner’s syndrome.

Question 17

Lesions above T2

Answer 17

1. Above T2
2. Sweating & vasomotor disturbances of the body

Question 18

Lesions @ C1-C4

Answer 18

Trauma to the upper cervical cord may disrupt the phrenic nucleus and result in respiratory depression or arrest

Question 19

Lesions @ C5-T6

Answer 19

“Rocking horse” type of respiration. High thoracic or low cervical damage may disrupt the descending fibers to the MMCC. The resultant paralysis does not allow the intercostal muscles to assist in breathing, and the patient mimics this particular movement.

Question 20

Lesiosn @ S2

Answer 20

reflex bladder

Lesions of the cord above the level of S2 may result in a reflex or spastic bladder. Although there is no voluntary bladder control, distention of the bladder wall results in a reflex (usually incomplete) voiding of the bladder.

Question 21

Lesions @ S3-5

Answer 21

Incontinence

Lesions in this region result in flaccid anal sphincter tone with bowel incontinence.

Question 22

Lateral reticulospinal tract (LRST) lesion

Answer 22

Transection of the spinal cord above S2 interrupts the lateral reticulospinal tracts to the sacral autonomic nucleus, and the patient is unable to voluntarily void his bladder, i.e., there is urinary retention.

After spinal shock, the bladder reflex may return without voluntary control, and the patient will have automatic reflex voiding or a reflex bladder.

Question 23

Lateral funiculus lesions

Answer 23

Lateral funiculus

3. LCST: Ipsilateral UMN paralysis/paresis below level of lesion

Question 24

Anterior funiculus lesion

Answer 24

Anterior funiculus:

1. LSTT: Contralateral loss of pain and temperature 2 levels below lesion
2. Anterior White Commissure: bilateral loss pain/temp
3. Anterior Horn: Ipsilateral lower motor paralysis at the level of lesion
4. LRST: IF the lesion is bilateral, volitional control of bladder and bowel

Question 25

Tabes Dorsalis: causes and symptoms

Answer 25

1. Meningovascular inflammation of the blood vessels as they pierce the pia mater at the junction between the posterior columns and the dorsal rootlets
2. results as a result of tertiary syphilus
3. symptoms: charcot joints, rheumatic/lightening pains, slapping gait, +romberg’s test, atonic bladder/incomplete voiding, painless retention of urine, argyl roberts pupil

Question 26

Polio symptoms

Answer 26

The symptoms may subside and the patient completely recovers (nonparalytic poliomyelitis), or it may result in varying degrees of paresis or paralysis (paralytic poliomyelitis).

Question 27

Paralytic poliomyelitis

Answer 27

may involve damage to the nucleus ambiguus, phrenic nucleus, or medial motor cell column with resultant paralysis of the pharyngeal, laryngeal, diaphragm, or intercostal muscles.

associated problems of airway obstruction and clearance and pulmonary ventilation are potentially life-threatening conditions.

Question 28

Transection of the spinal cord between the levels of C5-6

Answer 28

1. results in bilateral paralysis of the upper and the lower extremities or quadriplegia

Question 29

Transection of the spinal cord between the levels of T1-L2

Answer 29

1. Transection of the spinal cord between the levels of T1-L2
2. results in bilateral paralysis of the lower extremities or paraplegia

Question 30

three phases of physical events following Spinal Cord Injury (SCI): first phase

Answer 30

First phase

Spinal Shock: Immediately following transection there is complete suppression of the spinal reflex arcs distal to the lesion.

spinal shock period lasts between 4 days to 6 weeks

average of about 2-3 weeks (complete time of first phase)

Loss of all sensations, reflex activities

Bilateral flaccid paralysis of involved extremities
Loss of voluntary control of a spastic urinary bladder
Loss in sexual potency in the male
Various visceral deficits (loss of thermoregulation (cool, dry, skin with no sweating) Transient Horner’s syndrome, if the lesion is above T2

Question 31

three phases of physical events following Spinal Cord Injury (SCI): second phase

Answer 31

1. Second Phase: appearance of any spinal reflex activity distal to the lesion.
2. eturn of basic spinal reflexes indicates the patient’s recovery from spinal shock.
3. results in variable and overlapping changes in reflexes and spasticity
4. The reflexes are due to a reactivation of the intrinsic circuits of the spinal cord distal to the lesion.
5. patient displays some degree of spastic paresis of the axial and proximal limb musculature in addition to some degree of spastic paralysis of the distal limb musculature, especially the upper extremity.

Question 32

three phases of physical events following Spinal Cord Injury (SCI): 3rd phase

Answer 32

After an interval of 1-2 years (Third Phase), the affected muscle groups will exhibit tonic muscle spasms of the extensors (67%), or flexors (13%), or remain flaccid (<20%).

Question 33

Brown-Séquard Syndrome: cause and symptoms

Answer 33

1. unilateral transverse lesion or hemisection of the spinal cord usually due to a knife or bullet wound, or a tumor such as a meningioma pressing upon the cord. It is a relatively common trauma. It is characterized by the following signs and symptoms:
   
   1. Ipsilateral loss of proprioception and vibratory sensations from the body below the level of the lesion due to interruption of the posterior columns
   2. Ipsilateral spastic paralysis below the level of the lesion due to the destruction of the descending motor tracts.
   3. Contralateral loss of pain and temperature sensations from the body 2 sensory dermatomal segments below the level of the lesion, due to the destruction of the LSTT.

Question 34

Syringomyelia

Answer 34

1. syringomyelia is defined as a gross cavitation and gliosis of the central canal usually occurring in the cervical regions of the spinal cord.
   
   1. As syrinx enlarges neurological deficits progressively worsen over a period of months or years.
   2. The etiology is unknown.
   3. may occur secondary to central cord syndrome (CCS).
2. CCS results in an abrupt onset of neurological deficits.

Question 35

Enlargement of the syrinx results in…

Answer 35

results in:

1. Destruction of the anterior white commissure with a bilateral loss of pain and temperature sensations to the upper extremities (“yoke-like” anesthesia).
2. Asymmetrical (unilateral or bilateral destruction of the lateral corticospinal tracts (UMN)
   
   1. spastic paralysis, hyperreflexia, and hypertonia of the lower extremity.
3. The anterior horns (LMN) may be destroyed unilaterally or bilaterally,
4. Some part of the posterior columns may also be affected, and result in an ipsilateral anesthesia (proprioceptive and 2-point

Question 36

Amyotrophic Lateral Sclerosis (ALS)

Answer 36

1. Although the cause of ALS (Lou Gehrig’s disease) is basically unknown, it may be due to a defect in glutamate metabolism.
2. average age of onset is 66.
3. Death is due to bulbar paralysis, i.e., the vital respiratory centers, within an average of four years of onset. The most common form of ALS involves a combination of following structures:
   
   1. LMNs
      
      1. Anterior Horn Cells
      2. Hypoglossal Nucleus
      3. Nucleus Ambiguus
      4. Facial Motor Nucleus
4. UMNs
   
   1. Chronic, progressive degeneration of the Corticospinal Tracts

Question 37

ALS leads to:

Answer 37

ALS leads to:

1. LMN paresis and atrophy of the intrinsic muscles of the hands followed later by the arms and shoulder musculature.
2. Patients may develop dysarthria, dysphagia and paresis of the tongue.
3. Involvement of UMN (corticospinal tract) leads to spastic paralysis, hyperreflexia and a Babinski sign.
4. There are NO SENSORY DEFICITS.