Chapter 8 : Lession of the Spinal Cord (2) Flashcards
Neuropathologic examination of the spinalcord reveals two lesions labeled A and B onthe illustration below. Lesion A is restrictedto five segments. Answer the following questionsrelating to this case study by selectingthe one best choice.
- The result of lesion A is best described as
(A) bilateral arm dystaxia with dysdiadochokinesia
(B) spastic paresis of the legs
(C) flaccid paralysis of the upper extremities
(D) loss of pain and temperature sensationbelow the lesion
(E) urinary and fecal incontinence
l-C. Lesion A involves degeneration of the ventral horns bilaterally at midcervical levels,resulting in flaccid paralysis in the upper extremities.
Neuropathologic examination of the spinalcord reveals two lesions labeled A and B onthe illustration below. Lesion A is restrictedto five segments. Answer the following questionsrelating to this case study by selectingthe one best choice.
- The result of lesion B is best described as
(A) dyssynergia of movements affecting botharms and legs
(B) flaccid paralysis of the upper extremities
(C) impaired two-point tactile discriminationin both arms
(D) spastic paresis affecting primarily themuscles distal to the knee joint
(E) none of the above
2-D. Lesion B involves degeneration of the lateral corticospinal tracts bilaterally, resulting in spastic paresis of the lower extremities and primarily affecting the muscles distal to the knee. Spastic paresis of the upper extremities is masked by flaccid paralysis resulting from lesion A.
Neuropathologic examination of the spinalcord reveals two lesions labeled A and B onthe illustration below. Lesion A is restrictedto five segments. Answer the following questionsrelating to this case study by selectingthe one best choice.
3. Lesions A and B result from
(A) an intramedullary tumor
(B) an extramedullary tumor
(C) thrombosis of a spinal artery
(D) multiple sclerosis
(E) amyotrophic lateral sclerosis (ALS)
3-E. Lesions A and B are the result of amyotrophic lateral sclerosis (ALS), a pure motor disease.
- All of the following statements concerningamyotrophic lateral sclerosis (ALS) are correctEXCEPT
(A) it is associated with upper motor neuron(UMN) lesions
(B) it is associated with lower motor neuron(LMN) lesions
(C) it results in sensory deficits
(D) its onset usually occurs between 50 and70 years of age
(E) it results in muscle weakness
4-C. Amyotrophic lateral sclerosis (ALS) is a motor system disease and does not involve sensory systems. Onset is usually after the age of 50 years. ALS affects the corticospinal and corticobulbar tracts [upper motor neuron (UMN) lesion] and the ventral horn cells of the spinal cord and their cranial nerve equivalents in the brainstem [lower motor neuron (LMN) lesion]
- All of the following statements concerningsyringomyelia are correct EXCEPT it
(A) is a central cavitation of the spinal cord
(B) usually is found at lumbosacral levels
(C) usually includes a lower motor neuron(LMN) lesion
(D) usually results in a bilateral loss of painand temperature sensation
(E) may result in Horner’s syndrome
5-B. Syringomyelia is a central cavitation of the cervical spinal cord and is of unknown etiology. Expansion of the syrinx typically affects the ventral white commissure, interrupting the decussating fibers of the spinothalamic tracts and resulting in a bilateral loss of pain and temperature sensation at the level of involvement. Lateral extension involves one or both of the ventral horns
and results in a lower motor neuron (LMN) lesion with muscle wasting and flaccid paralysis. Caudal extension to (C8) T1-T2 may involve the lateral horn (ciliospinal center of Budge) and produce Horner’s syndrome
- All of the following statements concerningsubacute combined degeneration are correctEXCEPT it
(A) causes demyelination of the dorsalcolumns
(B) causes demyelination of spinocerebellartracts
(C) is associated with pernicious anemia
(D) is characterized by pyramidal tract signs
(E) is characterized by lower motor neuron(LMN) symptoms
6-E. Subacute combined degeneration, associated with pernicious anemia, results in demyelination of the dorsal columns (the fasciculus gracilis more often than the fasciculus cuneatus), the spinocerebellar tracts, and the lateral corticospinal tracts. Lower motor neurons (LMNs) are not involved.
- Hemisection of the spinal cord at Tl on theleft side results in all of the following signs orsymptoms EXCEPT
(A) plantar response flexor on the left side
(B) loss of vibration sensation in the left leg
(C) leg dystaxia on the right side
(D) exaggerated knee jerk reflex on the leftside
(E) normal pain and temperature sensationon the left side
7-A. Hemisection of the spinal cord is known as Brown-Sequard syndrome. Transection of the left lateral corticospinal tract would result in an extensor plantar response on the left side (Babinski’s sign). Leg dystaxia on the right side results from interruption of the crossed ventral spinocerebellar tract.
- Upper motor neuron (UMN) lesions can befound in all of the following clinical syndromesEXCEPT
(A) amyotrophic lateral sclerosis (ALS)
(B) subacute combined degeneration
(C) syringomyelia
(D) cauda equina syndrome
(E) ventral spinal artery occlusion
8-D. Upper motor neuron (UMN) lesions by definition are lesions in which the corticospinal or corticobulbar tracts have been damaged. Amyotrophic lateral sclerosis (ALS), subacute combined degeneration, syringomyelia (with extension into the lateral funiculus), and ventral spinal artery occlusion all cause UMN lesions with spastic paresis. The cauda equina lies external to the
spinal cord; lesions of this structure do not cause UMN lesions.
- Lower motor neuron (LMN) lesions resultin all of the following deficits or signsEXCEPT
(A) loss of muscle stretch reflexes
(B) loss of superficial reflexes
(C) fasciculations
(D) muscle wasting
(E) plantar reflex extensor
9-E. Lower motor neuron (LMN) lesions result from destruction of ventral horn (or cranial nerve) motor neurons or transection of their axons. LMN lesions interrupt the final common pathway to skeletal muscles; they result in flaccid paralysis and atrophy (muscle wasting) and a loss of all reflex action (areflexia). Fasciculations (visible muscle twitching) and fibrillations (seen on an electromyogram) are signs of LMN disease. Babinski’s sign, an extensor plantar reflex, is not seen in LMN lesions.
- All of the following statements concerningpoliomyelitis are correct EXCEPT
(A) it is a viral infection
(B) it is a lower motor neuron (LMN) disease
(C) it affects dorsal root ganglion cells
(D) it affects motor cranial nerve nuclei andventral horn motor neurons
(E) it results in hypotonia
10-C. Poliomyelitis is an acute inflammatory viral infection affecting lower motor neurons
(LMNs) in the spinal cord and brainstem (bulbar paralysis) and results in flaccid paralysis, muscle
atrophy, and areflexia. There is a loss of muscle tone (atonia). The poliovirus does not attack
the sensory neurons of the dorsal root ganglia.
- All of the following statements concerningupper motor neuron (UMN) lesions arecorrect EXCEPT
(A) they are found above the pyramidaldecussation
(B) they result in the presence of Babinski’ssign
(C) they result in the absence of the kneejerk reflex
(D) they are commonly caused by cerebrovascularaccidents
(E) they frequently involve the internal capsule
11-C. Upper motor neuron (UMN) lesions result from destruction of cortical neurons (or their axons) that give rise to the corticospinal and corticobulbar tracts. UMNs are found in the cerebral cortex and in the brainstem. UMN lesions result in spastic paralysis (hyperreflexia, hypertonia,clasp-knife phenomenon, clonus, muscle weakness, and Babinski’s sign). UMN lesions are
commonly caused by cerebrovascular accidents and frequently damage the internal capsule.
- All of the following neurologic deficits areassociated with transection of the lateral corticospinal
tract EXCEPT
(A) it results in ipsilateral spastic paresisbelow the lesion
(B) it results in ipsilateral loss of vibrationsensation below the lesion
(C) it results in an ipsilateral extensor plantarreflex
(D) it results in an ipsilateral hyperreflexiabelow the lesion
(E) it results in a loss of superficial abdominalcremasteric reflexes
12-B. Transection of the lateral corticospinal tract results in an upper motor neuron (UMN) lesion. The deficits are ipsilateral and caudal to the lesion. Plantar stimulation results in extension of the great toe and abduction of the other toes—this is Babinski’s sign. Loss of vibration
sensation results from interruption of the dorsal column-medial lemniscus system.
- All of the following statements concerningHorner’s syndrome are correct EXCEPT
(A) it is seen in spinal cord lesions above Tl
(B) it is ipsilateral to the lesion
(C) it results from interruption of descendingautonomic pathways
(D) it results in mydriasis and mild ptosis
(E) it results in facial hemianhidrosis
13-D. Interruption of descending autonomic pathways found in the lateral funiculi of the spinal cord result in Horner’s syndrome. Horner’s syndrome is ipsilateral to the lesion and consists of miosis, ptosis, facial hemi anhidrosis, and apparent enophthalmos.
- Ventral spinal artery occlusion results inall of the following deficits EXCEPT
(A) areflexia at the level of the lesion
(B) loss of vibration and position sensationbelow the lesion
(C) bilateral loss of pain and temperaturesensation below the lesion
(D) bilateral spastic paralysis below thelesion
(E) urinary incontinence
14-B. The ventral (anterior) spinal artery irrigates the ventral two-thirds of the spinal cord including the ventral horns, the corticospinal tracts, and the spinothalamic tracts. Lower motor neuron (LMN) deficits (flaccid paralysis and areflexia) are seen only at the level of infarction. Bilateral destruction of the lateral spino thalamic tracts results in bilateral loss of pain and temperature sensation caudal to the lesion. Vibration and position sensation are not affected because
the dorsal columns are intact. Bilateral lesions of the anterior quadrants of the lateral funiculi interrupt corticosacral fibers that control bladder function (urinary incontinence).
- All of the following statements concerningcauda equina syndrome are correctEXCEPT
(A) its signs are frequently unilateral
(B) it may result from a herniated disk
(C) it classically involves spinal roots L3-Co
(D) it may result in profound motor deficits
(E) it may result in Babinski’s sign
15-E. Pure cauda equina syndrome involves the descending dorsal and ventral roots, classically
spinal roots L3-S5. A herniated nucleus pulposus compressing the spinal roots may cause sensory
and/or motor deficits, urinary and fecal incontinence, and impotence. Disk prolapse usually occurs unilaterally, producing symptoms on the ipsilateral side. Profound motor deficits may be seen. Babinski’s sign is seen in upper motor neuron (UMN) lesions, not in lower motor neuron (LMN) lesions.
24r-C. A neurologic manifestation of vitamin B12 deficiency is subacute combined degeneration.There is no involvement of LMNs.
25-A. Lesion A shows the territory of infarction resulting from occlusion of the ventral (anterior) spinal artery.
26-D. A spinal cord hemisection (Brown-Sequard syndrome) on the right side results in a loss of
vibration sensation on the right side and a loss of pain and temperature sensation on the left side (dissociated sensory loss).
27-A. Total occlusion of the ventral spinal artery, involving five cervical segments, results in infarction of the ventral two-thirds of the spinal cord and interrupts both lateral spinothalamic tracts. The patient would have a loss of pain and temperature sensation caudal to the lesion.
28-B. Lesion B shows a cervical syringomyelic lesion involving the ventral white commissure,both ventral horns, and the right corticospinal tract. The patient would have a bilateral loss ofpain and temperature sensation in the hands, muscle wasting in both hands, and a spastic paresis on the right side.
29-A. In lesion A, both lateral and ventral funiculi have been infarcted by arterial occlusion. Bilateral destruction of the lateral corticospinal tracts at upper cervical levels results in quadriplegia (spastic paresis in upper and lower extremities). Bilateral destruction of the ventro lateral quadrants results in urinary and fecal incontinence
30-C. In lesion C, subacute combined degeneration, there is no involvement of lower motor neurons (LMNs), hence no flaccid paralysis, muscle atrophy, or fasciculations.
31-C. In lesion C, subacute combined degeneration, there is symmetric degeneration of the white matter, both in the dorsal columns (fasciculi gracilis) and in the lateral funiculi (corticospinal tracts). In this degenerative disease, both the myelin sheaths and the axis cylinders are involved. Subacute combined degeneration is classified under nutritional diseases (in this case a
vitamin B1 2 neuropathy). In true demyelinative diseases (e.g., multiple sclerosis), the myelin sheaths are involved but the axis cylinders and nerve cells are relatively spared.
