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Question:

A 23-year-old man is found unconscious at the scene of a motor vehicle collision with an obvious left leg deformity and a large laceration of the left temporal scalp.  As the patient is being rolled onto a backboard, he regains consciousness.  He recalls no details of the collision but reports severe left leg pain, headache, and some shortness of breath.  Blood pressure is 94/60 mm Hg, pulse is 120/min, and respirations are 18/min.  Peripheral intravenous access is obtained, and 1 L of intravenous fluids is administered.  On the way to the hospital, the patient develops progressive weakness on the right side and becomes obtunded.  On arrival, blood pressure is 160/90 mm Hg, pulse is 50/min, and respirations are 10/min.  Which of the following nerves is most likely to be compromised in this patient?

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Explanation:

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This patient who sustained a head injury to the left temporal region (eg, scalp laceration) and became unresponsive after a lucid interval likely has an epidural hematoma (EH) from injury to the middle meningeal artery.  Rapid expansion of the EH can abruptly increase intracranial pressure (eg, Cushing triad of hypertension, bradycardia, and bradypnea), compress the temporal lobe, and cause herniation of the most medial portion of the temporal lobe (ie, uncus) through the tentorial notch.

When uncal herniation occurs, the following neurologic deficits are often seen:

  • Ipsilateral fixed and dilated pupil from compression of the ipsilateral oculomotor nerve (CN III) (Paralysis of the oculomotor muscles occurs later and leads to ptosis and a down-and-out position of the ipsilateral eye.)
  • Contralateral hemiparesis (eg, progressive right-sided weakness) from compression of the ipsilateral cerebral peduncle of the midbrain, which damages the descending corticospinal tracts
  • Contralateral homonymous hemianopsia with macular sparing from compression of the ipsilateral posterior cerebral artery

As worsening herniation pushes the midbrain toward the contralateral side, the contralateral cerebral peduncle may also become compressed against the tentorium, causing ipsilateral hemiparesis, a false localizing sign known as Kernohan phenomenon.

(Choice A)  Accessory nerve (CN XI) dysfunction can occur from lesions in the medulla, such as occlusion of the posterior inferior cerebellar artery, or from damage during surgical procedures involving the anterolateral neck.  Injury can cause paralysis of the ipsilateral sternocleidomastoid and trapezius muscles, with scapular winging.

(Choice B)  The facial nerve (CN VII) originates between the pons and the medulla; injuries at that level can cause a lesion of the lower motor neuron, resulting in weakness involving the whole ipsilateral face.

(Choice C)  The glossopharyngeal nerve (CN IX) originates in the medulla and is most commonly injured by compression from a nearby tumor, such as in jugular foramen syndrome (posterior fossa tumor).

(Choice E)  The vestibulocochlear nerve (CN VIII) originates between the pons and the medulla; common causes of dysfunction include compression from a vestibular schwannoma or injury within the internal acoustic canal, leading to loss of hearing and/or balance.

Educational objective:
Rapid hematoma (eg, epidural) expansion after head injury can abruptly increase intracranial pressure, compress the temporal lobe, and cause uncal herniation.  The first sign is typically an ipsilateral fixed and dilated pupil due to oculomotor nerve (CN III) compression.  Contralateral hemiparesis is often seen due to direct compression of the ipsilateral cerebral peduncle.