Consciousness Case File

Consciousness Case File

EUGENE C.TOY, MD, RAHUL JANDIAL, MD, PhD, EVAN YALE SNYDER, MD, PhD, MARTIN T. PAUKERT, MD

CASE 48

A 19-year-old male, who suffers an accident on his dirt bike, is brought into the emergency department (ED) by paramedics. He cannot recall the crash, but says he was not wearing a helmet. Currently he is alert and oriented, complaining of nausea, vomiting, and has a left-sided scalp contusion, laceration, and an underlying bony step-off. You send the patient for a CT scan of the head and call for an urgent neurosurgery consult. As you are waiting for the operating room, the patient becomes more difficult to arouse and confused. Based on the patient’s presentation, you make a diagnosis of an epidural hematoma (EDH).

• Which artery is likely to be affected leading to EDH?
• What is the most likely explanation for the patient’s symptoms?
• What is the CT scan of the patient’s head likely to reveal?

ANSWERS TO CASE 48: CONSCIOUSNESS

Summary: A 19-year-old male status post unhelmeted motorcycle accident, presents with head trauma and decreasing level of consciousness. He is amnesic of the accident, has a lucid interval, then following CT scan becomes obtunded. The CT scan reveals an EDH.

• Artery affected: The middle meningeal artery runs on the surface of the dura, and a rupture of this artery leads to trapping of blood between the dura and the skull, also known as an EDH.
• Most likely cause of this patient’s symptoms: Although not experienced by all patients with an EDH (<20%), he has a classic lucency window, where the patient is alert, but then deteriorates rapidly.
• The CT scan of the patient’s head likely to reveal: Image of an EDH, with a depressed open skull fracture. The classic finding of an EDH is an extraaxial, homogeneous, biconvex, or lenticular lesion, generally confined by suture lines. This is in contrast to a subdural hematoma, which follows the convexity of the brain.

CLINICAL CORRELATION

Traumatic brain injury and resulting increases in intracranial pressure (ICP) may lead to changes in a patient’s level of consciousness. With EDH as with other supratentorial space-occupying lesions, pressure is placed on the brain, leading to midline shift. EDH commonly results from laceration of the middle meningeal artery. Should the ICP continue to increase, contralateral hemiparesis and ipsilateral dilated pupil (secondary to subfalcine herniation and compression of the third cranial nerve) occurs. Without intervention, this may progress to flexor and then extensor posturing and patients may exhibit a Cushing response: hypertension, bradycardia, widened pulse pressure. The outcome of EDHs such as mortality can range from 5% to 50% depending upon the patient’s presentation (Glasgow coma scale, GCS), progression, and other factors, including age, location (eg, posterior fossa vs. temporal), and size of the lesion. An excellent recovery is predicted for preoperative patients without normal level of consciousness, and the mortality increases for obtunded (10%) and comatose patients (20%).

APPROACH TO CONSCIOUSNESS

Objectives

1. Know the definition of consciousness.
2. Know how to evaluate consciousness.
3. Understand the neuroanatomical relationship between increased ICP and decreased level of consciousness.

Definitions

Consciousness: Awareness (content) of self and the environment and arousal (level).

Obtunded: Dulled or blunted.

Stupor: Reduced sense or sensibility.

Persistent vegetative state: Wakefulness without awareness, intact sleep/wake cycles.

Coma: Unarousable, either by external stimuli or inner needs, absent sleep/ wake cycles.

Locked-in syndrome: Paralysis of voluntary muscles except for ocular movements, no disturbance of awareness.

Oculocephalic reflex (doll’s eye reflex): Conjugate eye movement opposite to head movement in order to maintain forward gaze during neck rotation. Brain stem lesions lead to absent or asymmetric eye movement.

Calorics: Ice water is placed in the external auditory meatus, leading to a slow, ipsilateral, conjugate eye deviation.

Ocular bobbing: Conjugate, bilateral fast downward jerk followed by slow return to mid-position.

DISCUSSION

Consciousness involves the ability to be awake, alert, and aware. Like awareness, arousal is not an all-or-nothing concept, but rather it ranges from inattentiveness, to stupor and obtundation. Consciousness is a complex process, centered around the reticular activating system (RAS). The RAS is a portion of the rostral pons (paramedian tegmental zone), continuous caudally with the spinal cord and rostrally with the subthalamus, hypothalamus, and thalamic nuclei. Consciousness depends on intact diencephalic connections with the RAS. The ascending acetylcholinergic neurons from the RAS that project to the thalamus act as an on-off switch, determining if ascending information arrives at the cortex, and if descending information is likewise transmitted. The acetylcholine pathways sensitize the thalamic neurons, allowing sensory input. This leads to an “awake” state.

Disturbances of consciousness have multiple etiologies, including traumatic injury, metabolic disturbances, psychiatric, infarction/hemorrhage, brain stem disorders, neoplastic, and toxins. Coma requires damage of the bilateral cerebral hemispheres, bilateral thalamic/hypothalamic lesions, and/or the RAS. As described in the case, increases in ICP can lead to tentorial herniation and compression of the brain stem RAS. Comas are generally caused by lesions rostral to the level of the pons.

The Glasgow Coma Scale (GCS) score is a validated physical examination scoring system to evaluate level of consciousness, shown to be predictive of certain outcomes following neurological injury. It is determined by three categories: eye, verbal, and motor. They are scored as follows, with a maximum of 15 and a minimum of 3: eye: open spontaneously 4, open to sound 3, open to pain 2, do not open 1; verbal: responsive and appropriate 5, confused 4, unintelligible 3, moans to pain 2, no noise 1; motor: follows commands 6, localizes 5, withdraws 4, decorticate (flexor) 3, decerebrate (extensor posturing) 2, no movement 1. The GCS < 6 arbitrarily defines coma as a failure to open eyes in response to verbal command (E2), perform no better than weak flexion (M4), and utter only unrecognizable sounds in response to pain (V2).

The eye examination provides important insight into the origin of the decrease in consciousness. In an insult to the bilateral hemispheres, the papillary examination and oculocephalic response is normal. As was mentioned in the case, supratentorial mass lesions lead to secondary brain stem compression and a blown pupil on the same side as the lesion. Brain stem lesions lead to abnormal oculocephalic responses. Patients with metabolic disturbances have normal pupils. An intact pontine reticular formation allows the patient to blink, either spontaneously or in reaction to stimuli. If the oculocephalic response is absent, progress to the calorics evaluation. Roving eye movements occur with intact third nerve nuclei and connection, meaning the insult is likely toxic/metabolic or bihemispheric. Seizures lead to contralateral conjugate eye deviation. Acute pontine lesions lead to ocular bobbing.

The red nucleus is important for the localization of a lesion affecting consciousness. Output from the red nucleus reinforces antigravity flexion of the upper extremity. When this is lost, unregulated reticulospinal and vestibulospinal tract output reinforces the extension tone of the extremities. If the patient has an upper motor neuron lesion above the red nucleus, the patient will have flexor or decorticate posturing. Upon receipt of painful stimulus, the patient will have upper limb flexion with pronation of the forearm, and lower limb extension with foot inversion. Below the level of the red nucleus but above the level of the vestibulospinal and reticulospinal nuclei, decerebrate posturing will occur. Decerebrate posturing is the extension and pronation of the upper extremities with extension of the lower extremities. With a lesion of the medulla, descending corticospinal tract is disrupted, leading to acute flaccidity.

COMPREHENSION QUESTIONS

[48.1] A 32-year-old woman is brought into the ED by the paramedics following a rollover motor vehicle accident in which she was trapped in the car and had to be extricated with the jaws of life. On arrival to the ED, she is noted to be completely unresponsive and has a GCS of 4. What normal CNS structure(s) is (are) required for the maintenance of consciousness?

A. Cerebral cortex

B. RAS

C. Spinal cord

D. Both the cerebral cortex and the RAS

[48.2] You are examining a patient who is comatose in the ICU. Your first item of examination is to check basic brainstem reflexes, and you start with the pupillary reflexes. Shining your light into either of the patient’s eyes results in equal direct and consensual pupillary constriction. Based on this finding alone, where would you localize the lesion causing the coma?

A. Diffuse cortical damage

B. Midbrain damage

C. Pontine damage

D. Medullary damage

[48.3] You are examining an unresponsive patient, brought into the ED by EMS. When presented with a painful stimulus, the patient responds by flexing all of his extremities (decorticate posturing, score 2 on the motor section of the GCS). This response indicates motor output directed by what level of the nervous system?

A. Cerebral cortex

B. Red nucleus

C. Pontine reticular formation

D. Vestibular nuclei

Answers

[48.1] D. Consciousness depends on the interaction between the intact cerebral cortex and the RAS, and damage to either or both of these structures or the communications between them can cause lack of consciousness, or coma. The RAS serves as a gate which determines whether or not sensory input is relayed to the cortex, so without it, no information reaches the cortex, making it unable to interact with the outside world. Diffuse injury to the cortex can also cause coma, because although information can reach it (the RAS is intact) there is no cortex available to process.

[48.2] A. Because of the variety in this patient’s symptoms, there seems to be multiple lesions accounting for diffuse cortical damage. Intact pupillary reflexes indicate intact and functioning midbrain and lower. The reflex depends on intact structures in the superior colliculus and the oculomotor complex, both of which reside in the midbrain. In a patient like this diffuse cortical dysfunction is the likely cause, possibly from hypoxic-ischemic injury to the cortex or a metabolic encephalopathy.

[48.3] B. Motor outflow from the red nucleus, through the rubrospinal tract stimulates antigravity flexion of the extremities. Interruption of descending motor control between the cortex and red nucleus leaves it as the primary motor outflow, resulting in decorticate (flexor) posturing. Interruption of motor control below the level of the red nucleus results in motor outflow being driven by the reticulospinal and vestibulospinal tracts, which stimulate extensors, resulting in decerebrate (extensor) posturing.

NEUROSCIENCE PEARLS ❖ A portion of the rostral pons, the RAS plays a key role in consciousness, acting as an on-off switch between the spinal cord and thalamus. ❖ GCS is a validated assessment of consciousness and neurological function in patients with brain injury. ❖ Lesions either rostral or caudal to the red nucleus lead to decerebrate or decorticate posturing.

REFERENCES

Bateman DE. Neurological assessment of coma. J Neurol Neurosurg Psychiatry. September 2001;71(suppl 1):i13-i17.

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