Neuro Assessment

Glasgow Coma Scale

I. Motor Response
6: Obeys commands fully
5: Localizes to noxious stimuli
4: Withdraws from noxious stimuli
3: Abnormal flexion, i.e. decorticate posturing
2: Extensor response, i.e. decerebrate posturing
1: No response

II. Verbal Response
5: Alert and Oriented
4: Confused, yet coherent, speech
3: Inappropriate words, and jarbled phrases consisting of words
2: Incomprehensible sounds
1: No sounds

III. Eye Opening
4: Spontaneous eye opening
3: Eyes open to speech
2: Eyes open to pain
1: No eye opening

Glascow Coma Scale = add I + II + III
-Score 3-8: comatose
-Initial score of 3-4: >95% incidence of death or persistent vegetative state

Two findings on exam strongly point to a structural lesion:
1. consistent asymmetry between right and left sided responses, and
2. abnormal reflexes that point to specific areas within the brain stem.

Mental status is evaluated by observing the patient’s response to visual, auditory and noxious (i.e., painful) stimuli.
The three main maneuvers to produce a noxious stimulus in a comatose patient are:
1. press very hard with your thumb under the bony superior roof of the orbital cavity, and
2. press a pen hard on one of the patient’s fingernails.


Posturing:
-Decorticate Posturing: adduction of the upper arms, flexion of the lower arms, wrists and fingers. The lower extremities extend in decorticate posturing
-Decerebrate Posturing: adduction of the upper arms, extension and pronation of the lower arms, along with extension of the lower extremities.
-In general, patients with decorticate posturing have a better prognosis than patients who exhibit decerebrate posturing. Posturing does not have any localizing utility in humans.

Visual Acuity Testing:
Visual acuity cannot be tested in a comatose patient, but pupillary responses may be tested as usual. Visual fields may be partially evaluated by noting the patient’s response to sudden objects introduced into the patient’s visual field. Extra-ocular muscles may be evaluated by inducing eye movements via reflexes. The doll’s eyes reflex, or oculocephalic reflex, is produced by moving the patient’s head left to right or up and down. When the reflex is present, the eyes of the patient remain stationary while the head is moved, thus moving in relation to the head. Thus moving the head of a comatose patient allows extra-ocular muscle movements to be evaluated.

An alert patient does not have the doll’s eyes reflex because it is suppressed. If a comatose patient does not have a doll’s eyes reflex, then a lesion must be present in the afferent or efferent loop of this reflex arc. The afferent arc consists of the labyrinth, vestibular nerve, and neck proprioceptors. The efferent limb consists of cranial nerves III, IV and VI and the muscles they innervate. Furthermore, the pathways that connect the afferent and efferent limbs in the pons and medulla may also be disrupted and cause a lack of the doll’s eyes reflex in a comatose patient.
If the patient is being examined in the emergency department or if there is a history of potential cervical spine injury, the doll’s eyes reflex should not be elicited until after a cervical spine injury is ruled out.

Oculovestibular Reflex (Cold Calorics) :
-Technique: place the patient’s upper body and head at 30° off horizontal, and injecting 50-100cc of cold water into an ear
–Unlike the oculocephalic reflex, the oculovestibular reflex is present in awake patients

-Interpretation: The water has the same effect on the semicircular canal as if the patient’s head was turned to the opposite side of the injection. Therefore, the patient’s eyes will look towards the ear of injection. This eye deviation lasts for a sustained period of time. This is an excellent manuever to assess extra-ocular muscles in the comatose patient with possible cervical spine injury.
Both Eyes with Slow (Tonic) Phase Toward Injected Ear: coma with intact brainstem
Absent Oculocephalic Reflex (No Eye Movement): brainstem injury (lesion of pons, medulla, or less commonly the III, IV, IV or VIII nerves is present)
Slow Phase Toward Injected Ear with Fast Phase Away: psychogenic coma (patient is not comatose)
Movement on Only On Side of Stimulus: internuclear opthalmoplegia or structural brain lesion

Corneal Testing:
Cranial nerve V may be tested in the comatose patient with the corneal reflex test. Cranial nerve VII may be examined by observing facial grimicing in response to a noxious stimulus. Cranial nerves IX an X may be evaluated with the gag reflex.
The motor system is assessed by testing deep tendon reflexes, feeling the resistance of the patient’s limbs to passive movements, and testing the strength of posturing and local withdrawl movements. Local withdrawl movements may be elicited by pressing a pen hard on the patient’s fingernail and observing if the patient withdrawls the respective limb from the noxious stimulus.
Upper motor neuron lesions are characterized by spasticity. Spasticity is increased muscle tone leading to resistance of the limbs to passive manipulation. This spasticity classically results in the clasp-knife response. The clasp-knife response is when the spastic limb is passively moved with great resistance, when suddenly the limb “gives”, becoming very easy to move. The clasp knife response is most prominent in the muscle groups least affected by the upper motor lesion, e.g., flexors in the upper extremities or extensors in the lower extremities.
The sensory system can only be evaluated by observing the patient’s response, or lack of response, to noxious stimuli in different parts of the body.
In addition to withdrawing from noxious stimuli, patient’s may localize towards noxious stimuli. Localization indicates a shallower coma compared to the patient that withdraws.


Brain Death

  • Apnea Testing
    Normal Response to Apnea:
    -Expected Rise in pCO2 with Apnea: pCO2 rises 2.6-6.7 mm HG per min
    -Expected Fall in pO2 with APnea: pO2 falls 40-60 mm Hg per min

Apnea Test for Brain Death: requires lack of ventilatory response to rise in pCO2 from 40-60 mm Hg
-This would take around 5-10 min (asuming normal values above)
-Do test with 100% FIO2 preoxygenation or use “apneic oxygenation” technique

A. An apnea test may be inaccurate in patients with sleep apnea.

Coma, loss of brainstem reflexes, and apnea are the diagnostic criteria of brain death. Testing for apnea is commonly used to confirm the diagnosis. Apnea testing in patients with preexisting conditions, such as severe COPD or sleep apnea, may be inaccurate because these patients may have an abnormal hypercapnic reflex. In these patients, additional confirmatory tests are encouraged (see the following discussion).
Certain criteria should be met prior to initiation of an apnea test. A core body temperature of ≥36.5°C (97.7°F) is suggested because brainstem reflexes are blunted with hypothermia; there is no problem with apnea testing and hyperthermia, however. The patient should be hemodynamically stable and free of severe metabolic or electrolyte derangements. Additionally, drug toxicity or intoxication should be excluded. Drug classes such as sedatives, antidepressants, antiepileptics, and neuromuscular blocking agents, can confound test results.
To perform an apnea test, the patient should receive F102 of 1.0 and the oxygen saturation should be monitored continuously. The patient is then disconnected from the ventilator and observed for respiratory effort. One should be cautious about spontaneous motor responses that may mimic respiratory movements. After 8 minutes, an arterial blood gas should be obtained and the patient reconnected to the ventilator. An arterial PCO2 of 60 mm Hg or more defines the patient as apneic.

If the patient’s testing is not conclusive, there are three confirmatory tests that can provide further information:
1. Conventional angiography showing no intracerebral filling at the carotid bifurcation or in the circle of, Willis with patent external carotid
circulation; delayed filling of the superior longitudinal sinus may also be seen. Or, isotope angiography utilizing technetium-labeled albumin or
99m Tc HMPAO, followed by gamma camera scanning showing lack of intracranial isotope activity.
2. Electroencephalography demonstrating no electrical activity for at least 30 minutes.
3. Transcranial Doppler ultrasonography showing small peaks in early systole and the absence of diastolic or reverberating flow.


References

  • Guidelines for the determination of death: report of medical consultants on the diagnosis of death to the Presidents Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research. JAMA 1981; 246:2184-2186
    Report of the Quality Standards Subcommittee of the American Academy of Neurology