1. What aspects of this patient’s head injury history are concerning?
The patient was not wearing a helmet.
She struck the right temporal-parietal area of her skull.
2. What was her Glasgow Coma Scale (GCS) upon arrival to the ED?
E4M6V5 = 15 (see slide #1)
3. What was her Glasgow Coma Scale (GCS) at the time of neurological evaluation?
E2M4V2 = 8 (see slide #1)
4. Is the weakness on the right side of the face of the upper motor neuron or lower motor neuron type?
Upper motor neuron (UMN)
5. Is the weakness on the right side of the body of the upper motor neuron or lower motor neuron type?
Upper motor neuron (UMN)
6. Indicate the specific structures involved by the pathologic process to produce each of the signs and symptoms experienced by this patient.
a. Diminished level of consciousness
This suggests some degree of involvement of both cerebral hemispheres and/or thalami, plus or minus involvement of the ascending reticular activating system (ARAS), probably at the midbrain level.
b. Ptosis, fixed/dilated pupil, impaired adduction, elevation, and depression involving the right eye with exotropia of that eye in primary gaze
The right oculomotor nerve (III), with involvement of both the
parasympathetic (GVE) fibers supplying the sphincter pupillae muscle (via a synapse in the ciliary ganglion) and the somatic efferent (SE) fibers supplying the levator palpebrae superioris muscle, the superior, inferior, and medial rectus muscles, and the inferior oblique muscle. The eyeball is deviated laterally at rest (exotropia) due to the intact lateral rectus (and superior oblique) muscle
c. Right facial weakness and weakness of the right upper and lower limbs
Left corticonuclear (corticobulbar) and corticospinal tracts.
d. Increased muscle tone, increased deep tendon reflexes, and an extensor plantar reflex on the right side
Left corticospinal tract and other UMN descending pathways.
7. Indicate the level of the neurologic lesion in this case and the pathophysiological process producing the above signs and symptoms.
The main level of the neurological lesion is at the upper midbrain region of the brain stem, involving the right oculomotor nerve (III) and UMN fibers in the (left) corticonuclear and corticospinal tracts.
The pathophysiologic process underlying the patient’s signs and symptoms is right transtentorial (uncal) herniation (Early third nerve stage), which compresses and exerts traction on the ipsilateral oculomotor nerve (see slide #6).
As uncal herniation progresses, the medial temporal lobe usually compresses the ipsilateral crus cerebri of the midbrain and causes a contralateral hemiparesis. Occasionally, a “false-lateralizing” phenomenon occurs, as in this patient (see question #9).
8. What is the term describing the patient’s level of consciousness between the initial head injury and her subsequent deterioration in the ED? What pathologic process is often associated with this phenomenon? What is the vascular source for this lesion?
A “lucent interval” is defined as a period of time after the initial head injury and loss of consciousness during which the patient is neurologically normal prior to suddenly becoming unresponsive. This patient did not lose consciousness initially; although she was “dazed”.
Lucent intervals are most often seen in patients with acute epidural hematomas; although they may also be seen occasionally in patients with acute subdural hematomas (see references #2 and 3).
Epidural hematomas are usually caused by tearing of the middle meningeal artery due to a fracture of the squamous part of the temporal bone.
9. Explain why the eye findings and the weakness of the limbs are on the same side. What is the term for this phenomenon?
Occasionally, the herniating medial temporal lobe (including the uncus) causes compression of the contralateral crus cerebri against the free edge of the tentorium cerebelli forming the tentorial notch. This results in dysfunction of the contralateral corticonuclear and corticospinal tracts; thereby producing a “paradoxical false-lateralizing” ipsilateral UMN facial palsy and hemiparesis. This was what occurred in the patient described in this case.
This phenomenon is called a “Kernohan Notch” or, more properly, a “Kernohan-Woltman Notch”; since the phenomenon was first described by both authors (see reference #1).
10. What diagnostic procedure(s) would you undertake at this point?
References:
1. Kernohan JW, Woltman HW. Arch Neurol Psychiatry 1929;21:274-287.
2. Kole MK, Hysell SE. Neurology 2000;55:1751.
3. Codd PJ, et al. JAMA Neurology 2013;70:1194-1195.
4. Posner JB, Saper CB, Schiff ND, Plum F. Plum and Posner’s Diagnosis of Stupor and Coma, 4th edition. New York: Oxford University Press, Inc, 2007.
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