CLINICAL CASE #2
A 36-year-old man presented to his family physician with weakness and sensory loss in upper
and lower extremities. He described his arms as feeling limp and his legs as feeling stiff. He
first noted the weakness and loss of sensation to temperature in the upper extremity 3 years
previously; the weakness in the lower extremity occurred recently.
The patient was awake and oriented to time and place. His speech was clear and meaningful. He
appeared older than his stated age, with noticeable muscle wasting in the upper extremity. His
heart rate, blood pressure, temperature, and respirations were normal; skin was moist and supple.
His chest was clear to auscultation and abdomen was soft to palpitation with no tenderness.
A full range of eye movements was present. Visual acuity was normal. Eyes and papillary
reflexes were present to direct and consensual light. Gag and corneal reflexes were intact and
facial movements were full. The uvula was symmetric and the tongue protruded on the midline.
Strength in the upper extremities was diminished bilaterally, especially on the left. Both
upper extremities were areflexic at the elbow and wrist and muscular fasciculations and
atrophy were present bilaterally. Strength in the lower extremities was reduced and both
legs had elevated deep tendon reflexes.
The patient lacked sensation to temperature and pinprick in a cape-like distribution over
the chest and shoulders extending throughout the upper extremity to the fingertips.
Vibratory sense, discriminative touch, and proprioception were intact throughout his chest and
upper extremities. Normal sensations were found elsewhere over the body.
Key Points:
First: is the problem in the PNS or CNS?
- The elevated deep tendon reflexes in both legs (hyperreflexia) are symptoms that
support a CNS origin to this patient’s problems.
Second: Is the problem in the spinal cord, brain stem, or cerebrum?
- The presence of muscle atrophy and fasciculation in the upper extremity along with
the absence of cranial nerve symptoms points to a spinal cord issue.
Remember:
Sign
Alpha motor neuron
lesions
Weakness
Yes
Atrophy
Yes
Fasciculations Yes
Reflexes
Decreased
Tone
Decreased
Descending motor tract lesion
Yes
No (may occur due to disuse)
No
Elevated
Elevated
Some of the inhibitory input on the reflex pathway comes from descending tract and therefore
injury to those tract lead to increased reflexes. In alpha motor neuron damage the muscle is not
innervated anymore and therefore cannot respond to reflex at all.
Third: What level in spinal cord is this lesion in?
- Lets look at the signs we want to explain:
o Motor damage to upper extremity of the alpha motor neuron type
(fasciculation and atrophy)
o Motor damage to lower extremity involving descending motor tract
o Cape like damage affecting the anterolateral system of the upper extremity
but no damage to the DCML system.
So the place where all these signs can come about is the spinal cord at the cervical level. We can
explain the bilateral absence of temperature and pain sensation to a lesion of the ventral
commissure. The cervical ventral horn is very close and can easily be affected by the same lesion
if it extended a little more ventrally. Next to the ventral horn are the corticospinal tract carrying
the descending motor commands and the same lesions can extend into the corticospinal tract
explaining the symptom of spasticity in the lower extremities.
All this can be seen in the figure below. Note the regional anatomy of the DCML system and
anterolateral system most importantly the position of the leg arm and thorax in each of the
systems.
SL
TC
CTLS
This lesion is clinically knows as central cord syndrome. One of the most common causes of
central cord syndrome is syringomyelia. It arises because of prior trauma to the spinal cord.
Patients’ develop a growing syrinx in the center of the cord that grows with time. The lesion starts
at anytime after the initial trauma and might happen as late as 30 year after the trauma. It is
sometimes rapidly progressive and in other times it stabilizes. (this information is not required
for the exam).