Comatose Patient: Neurologic Examination

Neurologic Examination of the Unconscious or Comatose Patient

• Performing a neurologic examination on an unconscious or comatose patient is vital
• Evaluating a comatose patient for possible brain death is critical

General Physical Exam

• Inspection of the head may reveal signs of basilar skull fracture
• Basilar skull fracture signs include raccoon eyes (periorbital ecchymoses) and Battle sign (swelling and discoloration of the mastoid bone)
• Hemotympanum can be indicative of basilar skull fracture
• CSF rhinorrhea or otorrhea may be also be apparent
• High-resolution scanning is required for localization of CSF leak
• A depressed skull fracture may be found by palpating the head
• Swelling of soft tissues at the trauma site can also be indicative of basilar skull fracture
• Elevated blood pressure in a comatose patient may reflect long-standing hypertension, predisposing to intracerebral hemorrhage or stroke
• Hypertensive encephalopathy is rare, but when present blood pressure exceeds 250/150 mm Hg in chronically hypertensive patients
• Blood pressure may be lower in children or after acute elevation of blood pressure in previously normotensive patients
• Elevated blood pressure may be a result of a condition causing coma, such as intracerebral/subarachnoid hemorrhage or brainstem stroke
• Hypothermia in coma occurs in ethanol/sedative drug intoxication, hypoglycemia, Wernicke encephalopathy, hepatic encephalopathy, myxedema, and exposure
• Hyperthermia is seen in heat stroke, status epilepticus, malignant hyperthermia related to inhalational anesthetics, anticholinergic drug intoxication, pontine hemorrhage, and certain hypothalamic lesions
• Meningeal irritation (e.g., nuchal rigidity, Brudzinski sign) may indicate meningitis or subarachnoid hemorrhage
• Signs of meningeal irritation are typically lost during deep coma
• Examination of optic fundi helps reveal underlying conditions like papilledema or retinal hemorrhages due to chronic/acute hypertension
• Subhyaloid hemorrhages strongly suggest subarachnoid hemorrhage in adults

Neurologic Exam

• A neurologic examination is critical for diagnosis
• Pupillary size and reactivity should be checked
• Reflex eye movements must be tested
• The motor response to pain should be evaluated in detail

Pupils

• Normal pupils are typically 3-4 mm in diameter (larger in children, smaller in the elderly), equal, and constrict briskly and symmetrically in response to light
• Normally reactive pupils in a comatose patient are characteristic of a metabolic cause
• Slightly smaller (~2 mm) reactive pupils are present in early stages of thalamic (diencephalic) compression from mass lesions, from interruption of descending sympathetic pathways
• Fixed, dilated pupils are greater than 7 mm in diameter and fixed (unreactive to light), usually result from oculomotor nerve compression
• Fixed, dilated pupils may be seen also in anticholinergic or sympathomimetic drug intoxication
• Transtentorial herniation, medial temporal lobe from a supratentorial mass is the common cause of fixed, dilated pupils in comatose patients
• Fixed, midsized pupils fixed measure approximately 5 mm, and is a result brainstem damage at the midbrain level, which interrupts both sympathetic, pupillodilator and parasympathetic, pupilloconstrictor nerve fibers
• Pinpoint pupils measure 1-1.5 mm and usually indicate opioid overdose or a focal structural lesion in the pons with associated defects in horizontal eye movements
• Check with magnifying glass, pupils may appear unreactive to light
• Structural versus opioid causes can be distinguished via naloxone administration, pinpoint pupils caused by organophosphate poisoning, miotic eye drops, or neurosyphilis (Argyll-Robertson pupils)
• Pupil asymmetry (anisocoria) of ≤1 mm is normal in 20% of people
• Physiologic anisocoria sees each pupil constricting to same degree in response to light, and extraocular movements unimpaired
• A pupil that constricts less rapidly or to a lesser extent than its fellow pupil typically indicates a lesion affecting the midbrain, oculomotor nerve, or eye

Eye Movements

• Eye movement pathways begin at pontomedullary junction, traverse through the brainstem reticular activating system, arriving to the contralateral midbrain

Methods of Testing Eye Movement

• Eye movements are tested in the comatose patient by stimulating the vestibular system by passive head rotation (oculocephalic reflex/doll's eye maneuver)
• Use ice-water irrigation against the tympanic membrane (oculovestibular reflex/cold-water caloric testing) for stronger stimulus

Doll's Eye Reflex (Oculocephalic) or Maneuver

• Rotate head horizontally to elicit horizontal, and vertically to elicit vertical eye movements; eyes move opposite to the rotation direction
• An inadequate stimulus for eye movements, reflex may be overridden in conscious patients

Cold-Water Caloric (Oculovestibular) Stimulation

• A more potent stimulus. Irrigating one tympanic membrane with ice water
• Otoscopic examination should be undertaken before this maneuver is attempted to confirm membrane isn't perforated
• In conscious patients: unilateral cold water irrigation produces nystagmus with fast phase directed away from irrigated side
• In comatose patients with intact brainstem function: unilateral ice water irrigation results in tonic deviation of eyes toward irrigated side
• An absent/impaired response to caloric stimulation with 50 mL of ice water suggests peripheral vestibular disease, a structural lesion in the posterior fossa (cerebellum/brainstem), or sedation intoxication

Normal/Abnormal Eye Movements

• Normal movements exhibits full conjugate horizontal eye movements
• With a structural lesion of brainstem the cause of coma, eye movement cannot be achieved, suggesting nonstructural cause/bilateral hemispheric lesions
• Affecting the oculomotor (III) nerve like hemispheric masses: cold-water caloric testing fails to produce adduction of the contralateral eye, ipsilateral eye abducts normally
• Complete unresponsiveness to cold-water caloric testing signals a structural lesion of brainstem affecting the pons or metabolic disorder affecting the brainstem like sedative drug intoxication
• Sedative drug intoxication is also indicated by downward deviation of one or both eyes to unilateral cold-water caloric testing

Motor Response to Pain

• Strong pressure on the supraorbital ridge, sternum, or nail beds is applied to assess motor response to pain
• Evaluating whether the condition affecting the brain is symmetrical (like metabolic and diffuse disorders) or asymmetrical with unilateral structural lesions will help diagnosis
• This helps to localize cerebral dysfunction and assess coma depth
• Cerebral dysfunction of moderate is indicated if patient's localize an offending stimulus by reaching towards stimulus site; limb abduction is typically not reflective of reflex movements
• Decorticate response to pain (flexion of the arm at the elbow, adduction at the shoulder, and extension and internal rotation of the leg and ankle) is classically associated with lesions involving the thalamus directly or large hemispheric masses that compress the thalamus
• Decerebrate response (extension at the elbow, internal rotation at the shoulder/forearm, and leg extension) typically occurs when brain dysfunction has descended to the midbrain; decerebrate posturing implies more severe brain dysfunction than decorticate posturing
• Imprecise in localizing dysfunction site regardless
• Bilateral symmetric posturing may be seen in structural or metabolic disorders
• Unilateral or asymmetric posturing suggests structural disease in the contralateral cerebral hemisphere/brainstem
• No response to pain in pontine/medullary lesions, but knee flexion is spinal reflex

Glasgow Coma Scale

• Glasgow Coma Scale turns pupillary, eye movement, and motor responses described earlier to numerical scale
• Glasgow Coma Scale translate changes in examination may be more easily noticed over time and compared between different examiners.

Findings Associated with Specific Lesions

• Supratentorial, infratentorial, metabolic, or diffuse lesions produce characteristic symptoms

Supratentorial Structural Lesions

• Unilateral lesions can cause coma if acute (disrupting the contralateral cerebral hemisphere) or cause significant lateral brain displacement
• Downward brain displacement and rostrocaudal brainstem dysfunction with transtentorial herniation: reticular activating system is interrupted
• Respirations may progress from Cheyne-Stokes to hyperventilation to ataxic breathing to apnea
• Decorticate posturing may progress to decerebrate posturing and then to unresponsiveness
• Unilateral oculomotor palsy progresses to ophthalmoplegia and pupillary unreactivity, circulatory collapse and death eventually
• Lesions causing transtentorial herniation: trauma (epidural, subdural, or intraparenchymal hemorrhage), stroke (ischemic or hemorrhagic), infection, and neoplasm (primary or metastatic)

Infratentorial Structural Lesions

• Can cause downward herniation through the foramen magnum with compression of the medulla, apnea, and circulatory collapse
• Primary infratentorial structural lesions: bilateral weakness or sensory loss, crossed cranial nerve and long-tract signs, miosis, dysconjugate gaze, ophthalmoplegia, or ataxic breathing

Metabolic or Diffuse Lesions

• Mental/respiratory abnormalities early
• Tremor, asterixis, multifocal myoclonus may be apparent
• The pupils remain reactive
• Focal seizures/lateralizing neurologic signs can be due to metabolic disease

Brain Death Evaluation

• Absence of clinically detectable brain functions when the proximate cause is known/demonstrably irreversible
• Neuroimaging may be necessary
• The clinical diagnosis requires the absence of potentially confounding factors like neuromuscular blocking agents, deep sedation, severe metabolic disturbances, and hypothermia
• Severe injury to the entire brain leads to irreversible whole brain destruction
  • This includes traumatic brain injury, hypoxic-ischemic injury, stroke (hemorrhagic, malignant hemisphere infarction), or intracranial infection like encephalitis or meingitis

Clinical Features of Brain Death

• Coma without cerebral motor response to pain
• Absent pupillary response to bright light
• No oculocephalic/oculovestibular reflexes
• Absent corneal reflexes, jaw jerk reflex, grimace to noxious stimuli, Absent pharyngeal reflexes, and Apnea must be confirmed by formal testing
• During apnea testing core temperature must be ≥36°C, systolic BP≥100 mmHg, normal PO2, pre-oxygenate with 100% O2 for at least 10 minutes
• A pulse oximeter must be connected and ventilator support paused
• Supplemental oxygen may be administered through a cannula inserted through the endotracheal tube and placed at the level of the carina
• Arterial blood must be drawn after 8-15 minutes to assess if respiratory movements are observed while visually monitor the chest
• Reconnect the ventilator, if arterial PCO2 is >60 mmHg or up by 20 mmHG then diagnosis for neurologic death can occur

Other Clinical Observations:

• Clinical observations are compatible, but not mistreated as evidence of brainstem function: spontaneous extremity movement
  • Shoulder elevation/adduction, back arching, intercostal expansion
  • Autonomic responses like sweating/blushing/tachycardia, hemodynamic stability without pharmacologic support, absence of diabetes insipidus, up-going plantar responses

Diagnosis

• The protocol for determining brain death may vary
• Some can diagnose death by neurologic criteria like repeated assessments after intervals

Established Ancillary Tests for Brain Death Confirmation

• Conventional catheter-based cerebral angiography: showing absent intracranial flow above the skull base
• Radionuclide brain imaging: showing absent brain blood flow
• Transcranial Doppler ultrasound: showing oscillating flow/short systolic spikes in both hemispheres and across the foramen magnum
• EEG: electrocerebral silence (no cerebral activity over 2 µV from symmetrically placed electrode pairs at least 10 cm apart), deep sedation may also produce electrocerebral silence
• Continuous and open communication with family is important, maintain emotional support, notify of organ procurement protocols
• Advocacy needs to be maintained, decision to donate organs from pt