Download University of the East Ramon Magsaysay Memorial Medical Center

University of the East Ramon Magsaysay Memorial Medical Center
Department of Clinical Neurosciences
College of Medicine
III – Medicine
Interviewer: Jorge Gabriel Ang
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Patient is a 67 year old male admitted with a complaint of sudden weakness of the left
side extremities and slurring of speech of a few minutes duration right after waking up. He was
immediately brought to the UERM for consult and admission.
Patient is a diagnosed diabetic of 20 years, taking Glipizide and Metformin with good
compliance. He also had a history of a previous stroke. He was also a smoker of unrecalled
pack years who had stopped.
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Physical examination shows blood pressure of 130/80 mmHg and harsh breath sounds on
auscultation. Cranial nerve exam shows preferential gaze drift to the right with difficulty
reaching midline and left central facial palsy. Motor examination shows loss of muscle strength
on the left upper and lower limbs with a positive Babinski reflex on the left.
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Problem I: Left Central Facial Palsy and Right Preferential Gaze
The facial nerve is the nerve that innervates the muscles of expression of the face; a facial
palsy refers to the loss of innervation of the facial muscles resulting in loss of muscle activity
and tone, observed when the patient is unable to make facial expressions such as smiling and
frowning. Central facial palsy is a specific palsy indicating loss of innervation of the lower half
of the paretic side, in this case indicating that the lesion is an upper motor neuron lesion because
the upper aspect of the face is innervated by the facial nerve bilaterally whereas the lower face is
only innervated by the contralateral nerve. A lower motor neuron lesion would cut off the nerve
entirely, causing the entire side of the face to become paretic rather than a specific quadrant,
hence differentiating it from an UMN lesion.
Preferential gazes, meaning that the eyes drifts towards a specific side rather than at
midline, occurs when the motor nerves innervating the extra-ocular muscles of one eye are lost
or reduced, causing a relative imbalance of the strength of the muscles between both eyes, thus
the drift towards the side where the innervation is stronger. In a right preferential gaze, the eyes
drift towards the right, suggesting that there is a loss of innervation of the muscles on the left eye,
specifically the left lateral rectus innervated by the abducens nerve which pulls the eye laterally.
These two conditions together suggest an upper motor neuron lesion affecting the facial
section of the motor homunculus.
Problem II: Left Sided weakness with Babinski Sign
Loss of muscle strength and a positive Babinski sign is indicative of an upper motor
neuron lesion affecting the motor homunculus governing the limbs. The Babinski sign, which is
the fanning of the toes on the affected side when the lateral plantar aspect is stimulated, occurs
due to the absence of an upper motor neuron’s inhibitory control over the primitive reflexes of
the lower motor neurons. Hence a Babinski sign is an effective tool in localizing a lesion.
Primary Diagnosis: Left Middle Cerebral Artery Embolic Infarction
The left middle cerebral artery is considered the main artery feeding the motor
homunculus on the left cerebral hemisphere, supplying the majority of the primary motor cortex
as well as the frontal and parietal lobes. Loss of blood supply to the middle cerebral artery
causes varying degrees of effects depending on the location of the lesion. The most common
causes of tissue infarction from a MCA lesion is due to a thromboembolic infarction, a
developed atherosclerotic plaque or a ruptured bleeding aneurysm.
Given that the patient has a previous history of a stroke and has risk factors for the
development of atherosclerosis such as his advanced age, previous smoking history and his type
2 diabetes mellitus, it is most likely that the patient suffered a thromboembolic infarction that
blocked the MCA segment feeding the primary motor cortex that has manifested as loss of motor
function over the left side of the body and face with a positive Babinski sign. A thromboembolic
infarction that was likely thrown off from a remote site is the likely cause due to the sudden
onset of the patient’s signs and symptoms, as opposed to a plaque or an aneurysm, which occurs
gradually or stepwise, respectively.
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Diagnostic Workup
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Cranial CT Scan
Cranial vault imaging is now the modality of choice for locating infracted sites along
the central nervous system proper, showing radioopacity changes on the site of infarction
revealing cellular degeneration of the neurons, specifically on the motor cortex along the
postcentral gyrus of the parietal lobe. A CT scan will be able to localize the location of the
bleed and help confirm the diagnosis.
Treatment Plan
I.
Tissue Plasminogen activator
In the ER setting, the drug of choice for thrombolysis in the event of a CVA is tPA, a
protein that activates plasmin and the body’s natural thrombolytic mechanism to dissolve
intravascular blood clots, and in the case of CVA dissolve the formed thrombus over the
MCA, and is considered effective when given within 3 hours of onset of symptoms. The
preferred dose is 0.9mg/kg.
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Anti-platelet Medication
COX-2 inhibitors, which inhibit the functions of platelets, are used as long term
medication for the prevention of future thromboembolic events by reducing the possibility of
the formation intravascular blood clots which can become the source of future embolic
events. Anti-platelet medications with drugs such as aspirin are considered beneficial in
preventing future vascular events.