Monday, June 15, 2009

Case Study - 33. (Cerebral Cortex Case-1.)

A 60 year old anatomist was demonstrating a dissection when he dropped the forceps from his left hand. At the same time his speech became slurred and as he left the room he dragged his foot.

In the emergency room, he was alert and well oriented. In spite of the slurring of speech he was coherent and the content was good.

When asked to look to the left his eyes would not pass the midline. The visual exam showed a left homonymous hemianopsia. He could wrinkle his brow on both sides but in attempting to blow out his cheeks only the right side responded.

There was a spastic paresis of the left arm and leg. Pain and temperature were preserved on both sides but discriminative touch was impaired on the left and he was able to identify objects placed in the left hand.  

 
Left spastic hemiparesis suggests an upper motor neuron lesion of the corticospinals above the mid-cervical cord; weakness of the left lower face suggests a lesion of the right corticobulbar fibers ablove the mid-pons.

Loss of proprioception with sparing of pain sensation suggests a lesion of the sensory systems above the thalamus since pain can be appreciated at thalamic levels. Destruction of the right frontal eye fields, or the corticobulbar fibers e.g., genu of the internal capsule, would result in the inability to move the eyes to the left.

A left visual defect suggests a post chiasmic lesion e.g. optic radiations. The gnu and posterior limb of the internal capsule including the optic radiations are a likely site for this lesion. It is supplied by branches of the middle cerebral artery which were occluded in this patient.
 
Extended Explanation

Frontal eye fields (Area 8) of the cortex are located just anterior to the area controlling muscles of the face in area 4. Both areas project through the genu of the internal capsule.

Destructive lesions of area 9 on the right cause the eyes at rest to deviate to the right due to the activity of area 9 on the left and the eyes cannot be deviated past midline to the left upon command.

To account for facial and leg paresis might require postulating a broad lesion of the cerebral cortex including the medial side of the hemisphere (for the foot-knee paresis) and the frontal motor cortex laterally down to the lateral fissure (for facial weakness) - this would be unlikely.

However, motor and sensory fibers implicated are compacted in the genu and posterior limb of the internal capsule so this is a more reasonable site.
 
Left homonymous hemianopsia occurs with lesions of the right visual pathways behind the optic chiasm. Optic radiations form the most posterior fibers of the internal capsule; optic radiations also run deep to the cortex of the parietal and temporal lobes.

The abrupt onset of symptoms and history of high blood pressure suggested a vascular event. Neither the anterior nor posterior cerebral arteries supply all of the involved fibers implicated in this case.

However, the middle cerebral artery supplies the lateral aspects of the cerebrum and much of the deeper lying white matter, injury to which can explain all the symptoms.