Spinal Cord and Root Disease Flashcards
- A 57-year-old woman began having weakness and trouble walking 1 year ago. Current exam findings include weak, wasted muscles with spasticity, fasciculations, extensor plantar responses, and hyperreflexia. This case is most suggestive of
a. Dorsal spinal root disease
b. Ventral spinal root disease
c. Arcuate fasciculus damage
d. Motor neuron disease
e. Purkinje cell damage
D
(Rowland, pp 708–713.) Motor neuron disease in the anterior horns of the spinal cord and damage to the corticospinal tracts or motor neurons contributing axons to the corticospinal tracts would account for these neurologic signs. Damage to the dorsal spinal root would be expected to produce sensory, rather than motor, deficits and would produce areflexia, rather than hyperreflexia, at the level of the injury. Damage to the ventral spinal roots would produce weakness and wasting, but no spasticity or hyperreflexia would develop. Purkinje cell damage would be expected to produce ataxia without substantial weakness. The arcuate fasciculus connects elements of the cerebral cortex not involved in the regulation of strength or motor tone.
- A 36-year-old man is being evaluated for left hand weakness. On examination, it is readily apparent the he has atrophy of the first dorsal interosseous muscle. This may indicate damage to spinal roots
a. C5 and C6
b. C6 and C7
c. C7 and C8
d. C8 and T1
e. T1 and T2
D
(Rowland, pp 424–429.) The first dorsal interosseous muscle is innervated by the ulnar nerve. The fibers of the ulnar nerve reaching this muscle originate at the C8 and T1 roots. If the ulnar nerve itself is the neural element injured, it is usually because of damage at the elbow, where the ulnar nerve runs superficially in the groove over the ulnar condyle. All the interosseous muscles of the hand are supplied by the ulnar nerve: complete transection of that nerve will produce interosseous wasting and impaired finger adduction and abduction. Although the lumbrical muscles are situated alongside the interosseous muscles of the hand, only two lumbricals—those on the ulnar metacarpals—are innervated by the ulnar nerve. The other two lumbricals are innervated by the median nerve. All four lumbricals insert on the extensor sheaths of the fingers and participate in extension of the digits.
- A 35-year-old woman falls 12 ft off of a ladder and fractures her c-spine, causing damage at the C4 level. She is initially a flaccid quadriplegic with areflexia. This areflexia and flaccidity usually evolve into hyperreflexia and spasticity within
a. 2 to 4 months
b. 1 to 2 months
c. 3 days to 3 weeks
d. 1 to 3 h
e. 5 to 25 min
C
(Victor, p 56.) Spinal shock is a transient phenomenon that occurs with damage to fibers from upper motor neurons. The spasticity that usually develops within a few days of the spinal cord injury is presumed to represent exaggeration of the normal stretch reflexes in the limbs disconnected from upper motor neuron control. The evolution from spinal shock to spasticity is much more typical of spinal cord injuries than it is of cerebrocortical injuries, but even with cerebrocortical injuries there is usually an interval of hours to days during which limbs that eventually become hyperreflexic and spastic are hyporeflexic and flaccid.
- After biopsy resection of a lymph node in her neck, a 23-year-old woman notices instability of her shoulder. Neurologic examination reveals winging of the scapula on the side of the surgery. During surgery, she probably suffered damage to the
a. Deltoid muscle
b. Long thoracic nerve
c. Serratus anterior muscle
d. Suprascapular nerve
e. Axillary nerve
B
(Victor, p 1432.)Winging of the scapula most often occurs with weakness of the serratus anterior muscle. This is innervated by the long thoracic nerve, whose course starts high enough and runs superficially enough to allow injury to the nerve with deep dissection into the root of the neck. The long thoracic nerve is derived from C5, C6, and C7. Winging is elicited by having the patient push against a wall with the hands at shoulder level. With this maneuver, the scapula with the weak serratus anterior will be pulled away from the back and the vertical margin of the scapula will stick out from the back. Injuries to the long thoracic nerve are usually unilateral and are often due to trauma or surgical manipulation.
- A 25-year-old woman is involved in a motor vehicle accident. Among her injuries is a lumbar vertebral body fracture. Which of the following most likely contributed to this injury?
a. Flexion
b. Extension
c. Torsion
d. Spondylolisthesis
e. Subluxation
A
(Victor, p 213.) Extreme flexion of the lumbar spine is likely in automobile accidents and in falls where the person is upright. Fracture of a lumbar vertebral body may be seen in vehicular accidents when the victim is restrained during a high-speed impact by a seat belt without a shoulder harness. The rapid and extreme forward flexion of the lumbar spine may produce a variety of spinal injuries, ranging from fractures to dislocations. Fractures suffered during falls in which the person is upright, such as may occur when someone jumps off a building, are usually compression fractures of the vertebral body. Fracture of the vertebral body will usually produce pain coincidental with the injury. Patients with fractures of the vertebral body that occur without trauma or with inconsequential trauma must be investigated for malignant processes, such as metastatic carcinoma, multiple myeloma, and unsuspected osteomyelitis.
35-year-old man injured his thoracic spine in a motor vehicle accident 2 years ago. Initially he had a bilateral spastic paraparesis and urinary urgency, but this has improved. He still has pain and thermal sensation loss on part of his left body and proprioception loss in his right foot. There is still a paralysis of the right lower extremity as well.
- This patient has which spinal cord condition?
a. Brown-Séquard (hemisection) syndrome
b. Complete transection
c. Posterior column syndrome
d. Syringomyelic syndrome
e. Tabetic syndrome
A
(Victor, p 170.) Hemisection of the spinal cord results in a contralateral loss of pain and thermal sensation due to spinothalamic damage, and ipsilateral loss of proprioception due to posterior column damage. There is also an ipsilateral motor paralysis due to destruction of the corticospinal and rubrospinal tracts as well as motor neurons. Complete transection of the spinal cord would cause a bilateral spastic paralysis, and there would be no conscious appreciation of any cutaneous or deep sensation in the area below the transection. Posterior column syndrome would result in a bilateral loss of proprioception below the lesion, with relative preservation of pain and temperature sensation. Syringomyelic syndrome results from a lesion of the central gray matter. Pain and temperature fibers that cross at the anterior commissure are affected, which may result in bilateral loss of these sensations over several dermatomes. However, tactile sensation is spared. The most common cause of this type of syndrome is syringomyelia. Trauma, hemorrhage, or tumors are other possible etiologies. If the lesion becomes large enough, then other spinal cord systems become affected as well. Tabetic syndrome results from damage to proprioceptive and other dorsal root fibers. It is classically caused by syphilis. Symptoms include paresthesias, pain, and abnormalities of gait. Vibration sense is most affected.
A 35-year-old man injured his thoracic spine in a motor vehicle accident 2 years ago. Initially he had a bilateral spastic paraparesis and urinary urgency, but this has improved. He still has pain and thermal sensation loss on part of his left body and proprioception loss in his right foot. There is still a paralysis of the right lower extremity as well.
- In this patient, where would you expect the pain and temperature abnormalities to begin?
a. Exactly at the level of the lesion
b. Four or five segments above the lesion
c. Four or five segments below the lesion
d. One or two segments above the lesion
e. One or two segments below the lesion
E
(Victor, p 170.) The spinothalamic system is responsible for pain and temperature sensation. It enters the spinal cord through the dorsal root ganglion. The second-order neurons then ascend one or two levels as they cross in the anterior gray commissure. Thus a lesion of the right spinothalamic tract at the T8 spinal cord level would result in a contralateral loss of pain and temperature on the left body beginning at approximately the T9–10 dermatome.
A 35-year-old man injured his thoracic spine in a motor vehicle accident 2 years ago. Initially he had a bilateral spastic paraparesis and urinary urgency, but this has improved. He still has pain and thermal sensation loss on part of his left body and proprioception loss in his right foot. There is still a paralysis of the right lower extremity as well.
- The posterior column neurons decussate at what level?
a. At the medulla
b. At the midbrain
c. At the pons
d. At the thalamus
e. Within one or two levels after entering the spinal cord
A
(Victor, pp 160–162.) After the primary sensory fiber enters the spinal cord, the ascending branch enters the dorsal columns and travels to the medulla. The fibers from the legs and trunk travel medially in the fasciculus gracilis, while those from the arm and neck travel laterally in the fasciculus cuneatus. These first-order neurons synapse in the medulla, and then the second-order neurons decussate as the internal arcuate fibers and ascend in the medial lemniscus. The second-order fibers synapse in the ventroposterolateral nucleus of the thalamus, which then synapses on the somatosensory cortex.
A 35-year-old man injured his thoracic spine in a motor vehicle accident 2 years ago. Initially he had a bilateral spastic paraparesis and urinary urgency, but this has improved. He still has pain and thermal sensation loss on part of his left body and proprioception loss in his right foot. There is still a paralysis of the right lower extremity as well.
- The lateral corticospinal tract decussates at what level?
a. At the junction of the medulla and the spinal cord
b. At the junction of the midbrain and the medulla
c. At the junction of the pons and the medulla
d. At the thalamus
e. Within one or two levels after entering the spinal cord
A
(Victor, p 51.) The lateral corticospinal tract originates primarily in the precentral gyrus (primary motor cortex). These axons then travel in the posterior limb of the internal capsule, and then the middle section of the cerebral peduncle. They enter the basal pons and continue as the pyramids in the medulla. At the decussation of the pyramids, the lateral corticospinal tract crosses and then continues down the spinal cord.
A 61-year-old man, who smokes five packs of cigarettes per day and has hypertension, had an abdominal aortic aneurysm repair 8 h ago. The surgery went very well, and there were no reported perioperative complications. Now the patient is unable to move his legs and states that they are “numb.” On examination, he has a flaccid paresis of both lower extremities and has impaired pinprick sensation to a T9 level bilaterally. Joint proprio-ception is normal.
- The most likely diagnosis in this case is
a. Cerebral stroke
b. Conversion disorder
c. Multiple sclerosis
d. Spinal cord compression
e. Spinal cord infarct
E
(Victor, pp 171, 1317–1318.) This patient probably has a spinal cord infarction from an anterior spinal artery occlusion. The posterior cord may be spared, preserving joint proprioception. Bilateral lower extremity deficits without cranial nerve or mental status findings would be an exceedingly unusual cerebral stroke presentation. There is no information, such as psychological stressors or a non-physiologic exam, to suggest a conversion disorder in this case. Multiple sclerosis causes neurological deficits over space and time. In this case we have a single deficit at a single point in time. History of metastatic cancer or trauma might make the physician suspect spinal cord compression.
A 61-year-old man, who smokes five packs of cigarettes per day and has hypertension, had an abdominal aortic aneurysm repair 8 h ago. The surgery went very well, and there were no reported perioperative complications. Now the patient is unable to move his legs and states that they are “numb.” On examination, he has a flaccid paresis of both lower extremities and has impaired pinprick sensation to a T9 level bilaterally. Joint proprio-ception is normal.
- The arteria radicularis magna (artery of Adamkiewicz) enters at approximately what level?
a. C2–C5
b. C5–C8
c. T2–T8
d. T10–L1
e. L4–S4
D
(Victor, p 1315.) The artery of Adamkiewicz is a major anterior radicular artery and may supply the lower two-thirds of the spinal cord. It is at risk of occlusion during abdominal aortic aneurysm repair. Other branches off of the aorta or internal iliac arteries may also supply the thoracic and lumbar cord. The upper segments of the spinal cord are usually supplied off the vertebral arteries.
A 61-year-old man, who smokes five packs of cigarettes per day and has hypertension, had an abdominal aortic aneurysm repair 8 h ago. The surgery went very well, and there were no reported perioperative complications. Now the patient is unable to move his legs and states that they are “numb.” On examination, he has a flaccid paresis of both lower extremities and has impaired pinprick sensation to a T9 level bilaterally. Joint proprioeption is normal.
- Which of the following would you expect to find in this patient 6 months from now?
a. Fasciculations
b. Fibrillations
c. Flaccid paralysis
d. Hyporeflexia
e. Spastic paralysis
E
(Victor, pp 55–58.) This patient has an upper motor neuron lesion. The damage has been done proximal to the synapse of the anterior horn of the spinal cord. He will therefore develop a spastic paralysis. Fasciculations, fibrillations, flaccid paralysis, and hyporeflexia are all found following lower motor neuron lesions (at the anterior horn cell or more distally).
A 61-year-old man, who smokes five packs of cigarettes per day and has hypertension, had an abdominal aortic aneurysm repair 8 h ago. The surgery went very well, and there were no reported perioperative complications. Now the patient is unable to move his legs and states that they are “numb.” On examination, he has a flaccid paresis of both lower extremities and has impaired pinprick sensation to a T9 level bilaterally. Joint proprioeption is normal.
- The periumbilical area is innervated by which sensory dermatome?
a. C6
b. T2
c. T5
d. T10
e. S3
D
(Victor, p 160.) There can be some interindividual variation; however, T10 is clearly the best choice.
- This patient noticed ulcers on the fingers of both of his hands. They were associated with no pain and appeared to be the residua of burns. The probable site of damage responsible for this defect is the
a. Posterior column
b. Anterior horn
c. Clarke’s column
d. Spinothalamic tract
e. Spinocerebellar tract
D
(Patten, pp 256–257.) There is a cystic lesion in the spinal cord of this patient. It has probably destroyed the anterior decussation of the spinothalamic tract at the upper thoracic and cervical cord levels. There has probably been damage to additional components of the cervical spinal cord, but this may not become symptomatic until the spinal cord is much more compromised.
- Examination of this patient might reveal which of the following abnormalities?
a. Third-nerve palsy
b. Calf atrophy
c. Charcot joints
d. Atrophy of the intrinsic hand muscles
e. Grasp reflexes
D
(Patten, pp 256–257.) As the lesion in this region of the spinal cord increases in size, it may also affect the lower motor neuron in the anterior horn of the spinal cord, producing weakness in the distribution of the affected motor neurons. Because it is a lower motor neuron lesion, reflexes will be lost rather than increased in the upper extremities, which may at first seem counterintuitive in a spinal cord lesion. The more laterally placed corticospinal tract may be spared, leaving leg function and reflexes relatively normal.
- The most likely cause of the spinal cord abnormality evident on this T1-weighted magnetic resonance image (MRI) is
a. Neoplasia
b. Syrinx
c. Infarction
d. Hemorrhage
e. Abscess
B
(Patten, p 256.) The sausage-shaped structure in the spinal canal is a syrinx extending from C2 down into the thoracic spinal cord. This is filled with a fluid that appears similar to CSF on MRI. That this patient has syringomyelia independent of neoplasia, infarction, or intraspinal hemorrhage is suggested by the protrusion of cerebellar structures below the foramen magnum. The combination of a low-lying vermis or cerebellar tonsils and syringomyelia points to a Chiari malformation. Although it is inapparent on this MRI scan, the posterior fossa would be expected to be abnormally small and the tentorium cerebelli would insert relatively low on the cranium. Other spinal or spinal cord problems, such as spina bifida and tethered spinal cord, would not be unusual features in association with a Chiari malformation. Even an imperforate anus might be found in the infant with a Chiari malformation, but damage to the cord sufficient to produce paraplegia is most likely with a lumbosacral myelomeningocele. With this lesion, there is a defect in the dorsal aspect of the spinal column with an attendant outpouching of meninges and neural elements from the spinal cord. Potential treatment modalities of syrinxes include laminectomy (to reduce damage to the spinal cord from pressure that develops between the intraspinal cyst and the vertebrae), cyst aspiration, marsupialization (slicing open and leaving open the cyst), and shunting.
- This type of lesion is most likely to evolve after neck trauma if there has been intraspinal
a. Hyperthermia
b. Hypothermia
c. Transient ischemia
d. Contusion
e. Demyelination
D
(Patten, p 256.) After cervical cord contusion, cyst formation may occur as damaged tissue is removed. This is especially likely if there has been extensive intraspinal hemorrhage. Ischemic damage may produce similar changes, but the ischemia must be substantial and persistent enough to produce infarction of spinal cord tissue. Demyelination does not lead to syringomyelia, even in cases with extensive intraspinal demyelination.
