Neuroscience Week 3: Spinal Cord Disorders Flashcards
Patient presents with a few-month course of trunk and lower limb sensory dysesthesias.
Exam reveals:
hyperreflexia throughout except for absent ankle jerks;
pathologic (ie, positive) Babinski’s;
loss of vibration/ proprioception sensation in the lower extremities with preserved pain/temperature sensation;
and mild, diffuse lower extremity weakness.
- Show that the loss of vibration/proprioception sensation with preserved pain/temperature sensation suggests posterior column involvement.
- Then, show that the diffuse motor weakness is due to corticospinal tract involvement.
Indicate that this combination of deficits is often found in subacute combined degeneration due to vitamin B12 deficiency.
Subacute combined degeneration affects the posterior and lateral columns.
Although not mentioned, gait ataxia is often present in this disorder and may be due to the profound vibration/proprioception sensory loss or due to posterior spinocerebellar tract involvement from lateral column pathology.
B12 deficiency also often causes a superimposed neuropathy, which explains the absent ankle jerks.
Patient presents with an abrupt onset of interscapular pain, lower extremity weakness, sensory disturbance, and bowel and bladder incontinence.
Exam reveals:
areflexia of the lower extremities;
paraparesis;
loss of pain/temperature sensation with preserved vibration/proprioception sensation in the lower extremities;
anal sphincter atonia;
and a normal motor, sensory, and reflex exam in the upper extremities.
Show that the sudden weakness and areflexia suggests bilateral anterior motor horn cell involvement.
The longitudinal loss of pain/temperature sensation suggests the involvement of the anterolateral system with preservation of the posterior columns.
Indicate that this constellation of deficits suggests anterior spinal artery ischemia, in which the anterior two-thirds of the spinal cord are affected.
Note that this syndrome variably affects the lateral corticospinal tracts.
The most common site of anterior spinal artery ischemia is at the T4 level.
Patient presents with sudden weakness on the right side of the body and sensory disturbance.
Exam reveals:
right side weakness,
right-side loss of vibration/proprioception sensation,
and left -side loss of pain/temperature sensation.
reflexes are absent on the right side and normal on the left.
Show that the right-side hemi-body weakness suggests right-side corticospinal tract involvement.
The right-side loss of vibration/proprioception suggests right-side posterior column tract involvement.
The left-side loss of pain/temperature sensation suggests right-side anterolateral system involvement.
The right-side areflexia suggests right-side lower motor neuron involvement, which could occur from either anterior horn injury or posterior horn injury.
Indicate that this constellation of deficits suggests a hemi-cord syndrome involving the right half of the spinal cord, called Brown-Séquard syndrome.
Patient presents with a few-month course of progressive burning pain across the shoulders.
Exam reveals:
the weakness of the upper extremities;
absent biceps reflexes with hyperreflexia of lower extremities;
pathologic (ie, positive) Babinski’s;
absent pain/temperature sensation across the upper chest and limbs with preserved vibration/proprioception sensation.
Show that the dissociation of loss of pain/temperature sensation with preserved vibration/proprioception sensation in a suspended sensory level suggests damage to the crossing anterolateral system fibers.
Show that the loss of strength and areflexia of the upper limbs in that same segment suggests bilateral anterior motor horn damage.
Indicate that this constellation of deficits suggests a central cord syndrome, often a syringomyelia.
Syringomyelia is a fluid-filled cavity within the spinal cord, which may be limited to a dilatation of the central canal, may extend outside of the central canal, or may be separate from the central canal, entirely.
It causes lower motor neuron signs at the level of the lesion, impaired pain/temperature sensation but preserved vibration/proprioception in a segmental distribution (classically, in a cape-like distribution across the arms and upper trunk): a so-called suspended sensory level, and upper motor neuron signs below the level of the lesion.
Patient presents with a several-month course of weakness that began in the left arm and has since spread to both arms and legs.
Exam reveals:
asymmetric but diffuse upper and lower extremity weakness;
mixed hyperreflexia and areflexia throughout the bilateral upper and lower extremities;
bilateral pathologic (ie, positive) Babinski’s;
sensory exam is normal.
Show that the presence of motor weakness in conjunction with mixed hyperreflexia and areflexia with bilateral pathologic Babinski’s and a normal sensory exam suggests both corticospinal tract and anterior motor horn involvement.
Indicate that this constellation of deficits is often found in amyotrophic lateral sclerosis (aka ALS or Lou Gehrig’s disease).
Patient presents with years of progressive “lightning-like” pain in the lower extremities.
Exam reveals:
profound lower extremity loss of vibration/proprioception sensation with preserved pain/temperature sensation;
preserved strength in the lower extremities;
areflexia in the lower extremities;
upper extremities are normal.
Show that the loss of vibration/proprioception sensation with preserved pain/temperature sensation and preserved motor function suggests posterior column spinal cord involvement.
The lower extremity areflexia suggests lower motor neuron involvement, so also show that there is dorsal root involvement.
The dorsal root involvement causes the lancinating pain — presumably from irritation of the pain/temperature fibers.
Indicate that this constellation of deficits is often found in amyotrophic lateral sclerosis (aka ALS or Lou Gehrig’s disease).
Patient presents with muscle pains and slowly progressive muscle wasting.
Exam reveals:
asymmetric lower extremity weakness;
hyporeflexia in the lower extremities;
the absence of pathologic Babinski’s (ie, negative Babinski’s);
and normal sensation.
Show that the weakness in conjunction with hyporeflexia and a normal sensory exam suggests anterior motor horn involvement, only.
Many illnesses cause select anterior horn cell loss. Indicate that two common illnesses that cause this pathology are spinal muscular atrophy and Polio syndrome.
Patient presents with a several-month course of weakness that began in the left arm and has since spread to both arms and legs.
Exam reveals:
asymmetric but diffuse upper and lower extremity weakness;
mixed hyperreflexia and areflexia throughout the bilateral upper and lower extremities;
bilateral pathologic (ie, positive) Babinski’s;
sensory exam is normal.
Show that the weakness in conjunction with spasticity, hyperreflexia, bilateral pathologic Babinski’s, and a normal sensory exam suggests corticospinal tract involvement.
Indicate that select corticospinal tract involvement suggests a diagnosis of primary lateral sclerosis.
Patient presents with longstanding gait disturbance and weakness.
Exam shows:
lower extremity areflexia with preserved upper extremity reflexes;
pathologic (ie, positive Babinski’s);
profound ataxia;
vibration/proprioception sensory loss out of proportion to pain/temperature sensory loss;
and motor weakness of the upper and lower extremities.
Show that the mixed reflex pattern in the presence of pathologic Babinski’s suggests a mixed upper and lower motor neuron disease pattern with the pathology of the dorsal nerve roots and dorsal horns.
Then, show that the vibration/proprioception sensory loss with preserved pain/temperature sensation suggests posterior column involvement.
Next, show that the profound ataxia suggests spinocerebellar tract involvement.
And finally, indicate that the motor weakness suggests corticospinal tract involvement.
Indicate that this constellation of deficits is found in Friedreich’s ataxia, an inherited progressive ataxia with pathology that first appears in the dorsal roots.
Spinocerebellar tract involvement is an important distinguishing feature of this disorder.
