A 45-year-old man is brought to the emergency department after sustaining a traumatic head injury in a motor vehicle collision. The patient was found unresponsive and had several generalized tonic-clonic seizures during transport. Medical history includes hypertension as well as alcohol and cocaine misuse. Temperature is 36.7 C (98.1 F), blood pressure is 170/96 mm Hg, pulse is 50/min, and respirations are 10/min. Pulse oximetry shows 98% on mechanical ventilation with 50% oxygen. On examination, the patient is comatose with midpositioned and fixed pupils and rigid extension of the upper and lower extremities. Noncontrast CT scan of the head is shown in the image below: Damage to which of the following structures is the most likely explanation for this patient's abnormal posturing?

Question

A 45-year-old man is brought to the emergency department after sustaining a traumatic head injury in a motor vehicle collision.  The patient was found unresponsive and had several generalized tonic-clonic seizures during transport.  Medical history includes hypertension as well as alcohol and cocaine misuse.  Temperature is 36.7 C (98.1 F), blood pressure is 170/96 mm Hg, pulse is 50/min, and respirations are 10/min.  Pulse oximetry shows 98% on mechanical ventilation with 50% oxygen.  On examination, the patient is comatose with midpositioned and fixed pupils and rigid extension of the upper and lower extremities.  Noncontrast CT scan of the head is shown in the image below:  Damage to which of the following structures is the most likely explanation for this patient's abnormal posturing?

Quizplus · Accepted Answer

11ec160b_39e2_0db1_9249_cb137569a500_MD0001_00 This patient who sustained a traumatic head injury has an extensive intraparenchymal hemorrhage that is likely complicated by brain herniation. Intracranial (eg, intraparenchymal) hemorrhage can cause significant mass effect and increase intracranial pressure, which can manifest with seizures and Cushing triad (hypertension, bradycardia, bradypnea). With further hemorrhagic expansion, horizontal shifts in midline structures or brain herniation may occur. Progressive pupillary abnormalities are common in herniation. Uncal herniation initially disrupts the ipsilateral oculomotor nerve (CN III) leading to a fixed dilated pupil; however, as the brainstem becomes inferiorly displaced (ie, central herniation), damage to the midbrain and upper pons typically results in bilateral midpositioned and fixed pupils due to loss of both sympathetic and parasympathetic innervation. Brain herniation also causes abnormal posturing from disruption of descending tracts (eg, rubrospinal, vestibulospinal) typically involved in reflexive and postural movements. The vestibulospinal tract maintains extensor tone and originates from vestibular nuclei at the pontomedullary junction. The rubrospinal tract regulates upper extremity flexor tone and originates from the red nuclei in the rostral midbrain; it is inhibited by descending cortical input from the cerebral cortex. Damage above the red nucleus (eg, cerebral hemisphere, internal capsule) typically results in decorticate (flexor) posturing due to loss of descending inhibition of the red nucleus and subsequent hyperactivity of upper limb flexors (Choices B and D). Damage below the red nucleus (eg, pons) or to the nucleus itself (eg, midbrain) often causes decerebrate (extensor) posturing due to loss of descending excitation to the upper limb flexors (via the rubrospinal tract) and extensor predominance (due to unopposed vestibulospinal tract output). (Choice A) Damage to the cerebellar vermis usually affects balance and coordination of the axial/proximal limb muscles, resulting in gait and truncal ataxia. Cerebellar vermis injury may also result in nystagmus and vertigo due to this structure's role in vestibular function. (Choice C) The cervical spinal cord is commonly damaged in the setting of closed-head injury, which may lead acutely to flaccid quadriplegia/spinal shock (ie, absence of flexor and extensor motor tone) due to loss of excitatory input from the descending motor pathways. (Choice F) Damage to the substantia nigra can result in excessive inhibition of the thalamus with subsequent decrease in excitation of the motor cortex. This leads to motor features of Parkinson disease (eg, rigidity, bradykinesia, tremor). (Choice G) The thalamus is a major relay station for motor and sensory information and also help regulate alertness and consciousness. Although bilateral damage to the thalamus may result in coma, flexor/extensor posturing is not characteristic of thalamic injury. Educational objective: Brain herniation causes abnormal posturing due to disruption of descending motor tracts (eg, rubrospinal, vestibulospinal). Damage above the level of the red nucleus (eg, cerebral hemispheres, internal capsule) typically results in decorticate (flexor) posturing. Damage at or below the red nucleus (eg, midbrain to pons) typically results in decerebrate (extensor) posturing. __________ References: Neurological assessment of coma. (http://www.ncbi.nlm.nih.gov/pubmed/11511736)

A 45-Year-Old Man Is Brought to the Emergency Department After