Trauma Neurological Exam

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Continuing Education Activity

The nervous system coordinates and regulates all bodily functions, from basic physiological processes to complex behaviors and cognition. The presence of focal neurologic findings or mental status changes following a traumatic event is predictive of complications, some of which may be long-term or even fatal. Thus, quick identification of the neurological impact of physical trauma is essential to diagnostic and management decisions. A systematic approach can help ensure thoroughness while attempting to complete the neurologic examination expeditiously.

This activity for healthcare professionals is designed to enhance learners' competence in performing a neurological examination in patients with physical trauma. Valuable insights will be gained that will equip learners to collaborate effectively with an interprofessional team caring for affected individuals.

Objectives:

  • Identify the basic parts of the neurological examination in acute trauma settings.

  • Apply the proper neurological examination techniques in the setting of acute physical trauma.

  • Differentiate normal and abnormal neurological findings when evaluating patients with acute physical trauma.

  • Communicate effectively with an interprofessional team when analyzing and relaying the neurological findings in a patient with acute physical trauma.

Introduction

The nervous system consists of vital organs inside and outside the skull and axial skeleton. This manner of organization confers various levels of protection to neuronal tissues and their supporting elements. Physical trauma can have profound and multifaceted effects on the nervous system, ranging from mild, immediate injuries to severe, long-term neurologic and psychological sequelae. Prompt recognition, appropriate management, and comprehensive rehabilitation are essential for optimizing outcomes and promoting recovery in individuals affected by trauma.

A systematic approach to the neurologic examination ensures that all relevant aspects of neurologic function are thoroughly evaluated, leaving less room for oversight or omission of significant findings. Consistency in assessment techniques helps ensure that the examination is performed accurately and consistently across different healthcare providers and clinical settings.

Anatomy and Physiology

The nervous system is divided into central and peripheral organs. The central nervous system (CNS) consists of the vital organs, the brain and spinal cord. Meanwhile, the peripheral nervous system (PNS) comprises cell bodies and nerves conducting impulses to and from the CNS. The neuron is the nervous system's structural and functional unit specialized for rapid information transmission. Chemically and electrically mediated neuronal communication occurs between nerve cell bodies and their dendrites and axons. Lipid-rich myelin surrounding some axons enables fast signaling in specific nerve types, such as motor neurons. Neuroglia are nonneuronal cells supporting the nervous tissues, including oligodendria, astrocytes, ependymal cells, and microglia. The ependymal cells produce cerebrospinal fluid (CSF).

CNS nuclei form from nerve cell body groups. Nervous tracts arise from nerve fibers formed by axons. The gray matter contains nerve cell bodies. The white matter bears the nerve fiber tracts. The meninges protect the CNS structures and are divided into the dura, arachnoid, and pia mater. The brain is organized into the forebrain, midbrain, and hindbrain. Parts of the forebrain include the cerebral cortex, thalamus, limbic system, and basal ganglia. The midbrain occupies the brainstem region between the forebrain and the pons. The pons, cerebellum, and medulla oblongata constitute the hindbrain. The cranial nerves emanate from different brain levels but are often considered part of the PNS.

The spinal cord continues from the medulla oblongata, extending from the occipital bone's foramen magnum to the L2 vertebra. The medullary cone is the spinal cord's tapering end that may terminate between the T12 and L3 vertebrae. The spinal cord regions innervating the limbs are prominently enlarged. The cervical enlargement gives rise to the brachial plexus and runs from spinal levels C4 to T1. The lumbosacral enlargement transits from T11 to L1, forming the lumbar and sacral nerve plexuses supplying the lower extremities. The cauda equina arises from the lumbosacral spinal nerve roots and medullary cone.

A spinal nerve consists of dorsal and ventral roots. The spinal nerve dorsal roots contain afferent (sensory) fibers from the limbs, trunk, abdomen, and viscera. Their ventral counterparts have efferent (motor) and presynaptic autonomic nerves. The ventral gray horns contain the ventral roots' cell bodies, while the spinal ganglia (dorsal root ganglia) have the cell bodies of the dorsal roots. The spinal nerves divide into dorsal and ventral primary rami upon exiting the vertebral canal. The filum terminale is the spinal cord's caudal vestigial portion, anchoring the dural sac to the vertebrae distal to the medullary cone.

The PNS is composed of nerves connecting the CNS with peripheral structures. The PNS is organized into the somatic (SNS) and autonomic nervous system (ANS). The SNS is comprised of the sensorimotor nerves in all parts of the body except the viscerae. The ANS comprises motor nerves to involuntary smooth muscles, cardiac muscles, glands, and visceral sensory nerves.

The ANS has 2 divisions: sympathetic and parasympathetic. The sympathetic division arises from the cell bodies in the spinal cord's intermediolateral columns from nerves T1 to L2 or L3. The paravertebral ganglia comprise the sympathetic ganglionic chains on both sides of the spinal column. The prevertebral ganglia are cell body collections near the abdominal aorta. Postsynaptic sympathetic fibers transit from the paravertebral ganglia to their destinations in the neck, body wall, and limbs through the gray rami communicantes and ventral rami.

The parasympathetic nervous system arises from the cranial nerve nuclei in the brain and S2 to S4 spinal cord segments. The parasympathetic ganglia in the head are the ciliary, pterygopalatine, submandibular, and otic ganglia. Presynaptic parasympathetic fibers elsewhere synapse with postsynaptic bodies in the target organ.[20]

Dermatomes are specific skin areas supplied by sensory fibers arising from a single spinal nerve root. These nerve fibers transmit sensory information, such as touch, temperature, and pain, from the skin to the spinal cord and brain. Dermatomes can be clinically assessed by testing for sensation in specific areas of skin using various stimuli, such as light touch, pinprick, or temperature sensation. Testing multiple dermatomes can help localize sensory deficits and identify the level of spinal cord or nerve root involvement in patients with neurological symptoms or injuries.

Understanding the nervous system's organization helps localize neurologic lesions. Proficiency in performing a complete and accurate neurologic examination without diagnostic tests is crucial in prehospital settings and during patient monitoring.

Indications

Indications for performing a neurologic examination in a patient who sustained physical trauma include the following:

  • Mechanisms with a high neurologic damage risk, such as high-speed motor vehicle collisions, falls from significant heights, or penetrating injuries
  • Altered level of consciousness
  • Head, spine, or extremity trauma
  • Signs and symptoms of focal neurologic deficits reported after a trauma incident, whether transient or persistent
  • Progressive symptoms following trauma
  • Presence of multiple injuries

A neurologic examination must be performed in patients with trauma based on clinical indications, including the nature and mechanism of injury, presenting symptoms, and potential risk factors for neurologic involvement.

Equipment

Standard neurologic examination equipment includes the items listed below. These tools can help conduct the neurologic examination, but clinical judgment and patient interaction remain crucial for obtaining accurate findings. Additionally, the specific equipment needed may vary depending on the clinical setting, patient population, and presenting symptoms.

  • Snellen card or chart
  • Ophthalmoscope
  • Tongue depressor
  • Small flashlight
  • Reflex hammer
  • Disposable safety pin
  • Small cotton wool pledget
  • 128- and 256-Hz tuning forks 
  • Samples of coffee or mint
  • Paper and pen
  • Compass with 2 blunt tips
  • Coins
  • Small common objects like screws

Technique or Treatment

Neurological examinations are most clinically useful in unsedated patients who are well-oxygenated, normotensive, and normoglycemic. Sedation, hypoxia, hypotension, and hypoglycemia can depress nerve function and render the assessment inaccurate.[1]

Parts of the neurologic examination crucial in trauma settings include the patient's mental status, cranial nerves (CNs), sensory exam, motor exam, and reflexes. A full neurologic examination often cannot be performed in uncooperative and unconscious individuals. However, careful observation may still provide clues about some aspects of these patients' neurologic condition, such as mental status, some cranial nerve functions, and motor strength. Reflex testing may be conducted in patients in a comatose state.

Glasgow Coma Scale

The Glasgow Coma Scale (GCS) is a commonly used system for assessing a patient's level of consciousness. GCS assessment helps determine the severity of traumatic brain injury (TBI) and may be performed by relatively inexperienced care providers in pre- and in-hospital settings. The grading scale, detailed in Table 1, is based on the degree of response in 3 domains: eye opening and verbal and motor function. The latest terminologies are also given in parentheses.[2]

Table 1. Glasgow Coma Scale Domains and Scoring

Eye opening (Scored 1-4)

  • Spontaneous – 4
  • To speech (To sound) – 3
  • To noxious stimulation (To pain) – 2
  • No response (None) – 1 

Verbal function (Scored 1-5)

  • Alert and Oriented (Oriented) – 5
  • Confused/Disoriented (Confused) – 4 
  • Inappropriate Words (Words) – 3
  • Incomprehensible Sounds (Sounds) – 2
  • No Response (None) or in intubated patients – 1

Motor function (Scored 1-6)

  • Obeys commands – 6
  • Localizes to noxious stimuli (Localizing) – 5
  • Withdraws from pain – 4
  • Decorticate posture (Abnormal flexion) – 3
  • Decerebrate posture (Abnormal extension) – 2
  • No Response (None) – 1 

The combined GCS score ranges from 3 to 15, with a lower score suggesting more severe neurologic dysfunction. Some clinicians may prefer reporting each category's score rather than the total score to provide more information about an individual's mental state. For example, a patient with head trauma with spontaneous eye opening but who is confused and does not follow commands has a GCS score of E4V4M5. Meanwhile, alcohol drinking, common in assault cases, may result in disorientation and eye opening to speech without affecting a person's ability to grip the examiner's hand on command. The GCS score, in this case, is E3V4M6. Note that the total GCS score in both instances is 13. 

Factors that can hinder the assessment of one of the GCS domains include orbital trauma and the presence of an endotracheal tube. For intubated patients, a score of 1 should be assigned to the verbal function, with the total score followed by a "T" to signify that the patient is intubated. For example, an intubated patient with no response in all 3 domains has a GCS score of 3T. Serial or repeat GCS scores should be performed to identify changes in neurologic function in the immediate aftermath of a traumatic injury.[3]

The GCS Pupils Score (GCS-P) includes consciousness and pupil reaction gauges, which can help assess both cortical and brainstem functions.[4] The Pupil Reactivity Score (PRS) needs to be determined initially according to the following system:

  • PRS 0: both pupils react to light
  • PRS 1: only 1 pupil reacts to light
  • PRS 2: neither pupil is reactive

The GCS-P is calculated by subtracting the PRS from the GCS total score: GCS-P = GCS - PRS. The value serves as an index of the severity of a patient's clinical state and prognosis.[5]

Mental Status

The mental status examination assesses the consciousness or alertness level, which can help determine if a more detailed cognitive function assessment may be performed. Consciousness refers to awareness of the internal and external environments. An individual with normal consciousness is "awake" or can be easily awakened, "alert" or responds appropriately to visual or verbal cues, and "oriented" or knows their identity, location, and situation and can state at least the approximate date and time. Abnormal or depressed consciousness exists on a continuum, ranging from mild sleepiness to an unarousable state termed "comatose" or "coma."[6][7]

For patients with significantly depressed consciousness, proper description is crucial. Examples are the following:

  • The patient opens their eyes and turns toward the voice but does not obey verbal commands.
  • The patient responds only to noxious sternal rub by moving the right arm and grimacing.
  • The patient is unresponsive to voice and sternal rub.

Alert and conscious individuals can subsequently be assessed for cognitive function, which involves complex activities in various cortical and subcortical regions. Language and memory may be initially evaluated while obtaining a description of the traumatic events during history taking. The memory may be tested with the examiner naming 3 objects, eg, house, plane, and apple, and asking the patient to recall them 5 minutes later. The cortical function can be assessed by asking the patient to subtract 7 serially from 100, eg, 100, 93, 86, 79, and so on. Alternatively, the patient may be asked to spell a simple word, eg, world, both forward and reverse.

Any overt speech or language disorder should be evident during conversation and initial evaluation. Significant head trauma may present with a peculiar, flat affect, where patients appear devoid of emotion and speak in a slow, monotonous voice.  

Cranial Nerves

CN examination provides crucial information about potential brainstem dysfunction in the setting of acute trauma. Of the 12 CNs, only the olfactory nerve (CN I) is not routinely tested as part of the trauma neurologic assessment. Central lesions manifest with contralateral CN weakness. Peripheral lesions, ie, damage along the cranial nerve, manifest with ipsilateral weakness.

The optic nerve (CN II) can be assessed in comatose patients using the "blink-to-threat" test. Rapid hand movement toward the eyes from different directions normally makes a person blink in response. The lack of a blinking response is an abnormal finding.

A Snellen eye chart may be used to assess visual acuity in cooperative patients. The visual field may be evaluated in these individuals by asking them to fixate on an object in the anterior midline and report when a finger can be seen moving in each of the 4 visual quadrants. The eyes must be examined separately.

The normal pupillary response is evidence of normal optic and oculomotor (CN III) nerve function. In patients with impaired consciousness, pupillary responses can help determine brain injury severity. Pupil size and shape at rest must be noted before proceeding with the examination. A light is then directed toward each eye twice. The first light stimulation assesses the illuminated pupil's direct response, while the second evaluates the non-illuminated pupil's consensual response. The normal response is bilateral pupillary constriction to the light stimulus.

The oculomotor (CN III), trochlear (CN IV), and abducens (CN VI) nerves may be assessed in an alert patient by having them close one eye and focus on a moving finger in their visual field. The patient then follows the moving finger in all directions—horizontally, vertically, and diagonally—from a central point. Testing the eyes separately can help identify abnormal movements in each eye or fixed deviation in a particular direction. Testing the eyes together can help determine whether abnormal eye movements are unilateral or bilateral. A conjugate gaze is when the eyes move in the same direction. A dysconjugate gaze is when the eyes do not move in the same direction. Nystagmus is a condition notable for repetitive, uncontrolled eye movements.

Meanwhile, CNs III, IV, and VI may be examined in comatose patients by testing the oculocephalic reflex circuit. The test is performed by holding the patient's eyes open and rotating the head from side to side or up and down. The normal response is eye movement opposite the head's direction, resembling a doll's eye movements. Thus, the oculocephalic reflex is also called the "doll's eye reflex." These maneuvers should not be performed if a cervical spinal injury is suspected or confirmed by imaging.

The corneal reflex test can help detect trigeminal (CN V) or facial (CN VII) nerve dysfunction in the comatose patient. Each cornea is touched gently with a cotton wisp to stimulate bilateral blinking. A lack of response is an abnormal finding. Vigorously rubbing the area anterior to the ear or the supraorbital ridge can also help evaluate the same CNs. The normal response is facial grimacing to the painful stimulus. 

Testing CN V in responsive patients may be accomplished by assessing mastication muscle tone and facial skin sensation symmetry. CN VII may be assessed in these individuals by asking them to make facial expressions, such as smiling and frowning. Asymmetry in any of these actions is abnormal.

Appropriate responses while verbally conversing, eg, during history-taking, may indicate an intact vestibulocochlear nerve (CN VIII) in responsive individuals. Further testing may be performed by rubbing the fingers together adjacent to the patient's ears. The sound intensity in both ears should be perceived as equal. Tuning fork tests can help determine if hearing impairment is central or peripheral.

A bilaterally intact gag reflex is evidence of glossopharyngeal (CN IX) and vagus (CN X) nerve function and may be elicited in a responsive or unconscious patient. A cotton swab is used to touch the posterior pharynx or tongue base on each side. The gag reflex may also be appreciated in intubated patients. Symmetric uvula elevation in response to a tactile stimulus is also a sign of CN IX and X function.

The accessory nerve (CN XI) may be assessed in a responsive individual by asking them to shrug their shoulders upward or rotating the head side to side against resistance. Normal tongue movement and strength and absence of lateral deviation are signs of an intact hypoglossal nerve (CN XII).

Sensory Examination

The somatosensory examination may be performed in both unconscious and conscious patients, though not all aspects of this examination may be conducted in unconscious individuals. 

In cooperative patients, light touch, sharp and dull pain, 2-point discrimination, joint position, temperature, and vibration may all be tested. Light touch sensation is assessed by applying a light stimulus, such as a cotton swab or finger, on the skin. Sharp pain sensation may be examined by lightly pricking the skin with a clean, disposable pin. Dull pain sensation may be tested using a blunt object. Two-point discrimination applies sharp pain stimulus at 2 distinct points on the skin close to each other.  

Joint position sense may be tested by grasping the sides of a finger or toe's distal phalanx and slightly displacing the digit's joint up or down. Temperature and vibration sensations are not urgently tested in most trauma situations but can be examined using a metal tuning fork, which can conduct heat and vibrate.

Somatosensory tests may be approached in a dermatomal fashion. The patient's sensation may be assessed by asking if they can feel, locate, and describe the stimulus. In unconscious patients, painful stimuli may elicit a motor response, such as wincing or attempting to remove the stimulus source.

Motor Examination

The motor examination has several components, including inspection, palpation, and functional (tone and strength) testing of individual muscle groups. This part of the neurologic exam requires that injuries that can be aggravated by extremity manipulation are ruled out first. Afterward, the muscles are inspected visually and palpated for shape and size abnormalities, tenderness, and the presence of involuntary movements.

The pronator drift is the abnormal inward rotation or downward drift of a hand when the arms are stretched upward for several seconds. This finding may indicate upper motor neuron injury.[8]

Muscle tone is gauged by palpating the limb muscles and passively moving the joints. Weak resistance to passive joint movements signifies a reduced muscular tone characteristic of lower motor neuron abnormalities. Increased tone or passive resistance to joint movement may indicate the presence of an upper motor neuron lesion.

Muscle strength should be examined in the extremities, neck, and trunk. Muscle strength examination in a cooperative patient is performed by providing resistance to muscle movement in various directions and observing for weakness against the applied resistance. Neck strength should be deferred until cervical spine injuries have been excluded. 

The following scale is widely used to describe muscle group strength, rated on a scale of 0 to 5 out of 5, as follows:

  • 0/5 – No contraction
  • 1/5 – Muscle flicker, but no movement
  • 2/5 – Movement possible, but not against gravity (contraction in the horizontal plane)
  • 3/5 – Movement possible against gravity, but not resistance
  • 4/5 – Movement possible against some resistance
  • 5/5 – Normal (full) strength

The muscle groups must be tested bilaterally and compared to gauge symmetry. In unconscious patients, motor function may be reported in relation to pain response.

Reflex Testing

The deep tendon reflexes (DTRs) can help assess spinal nerve motor and sensory functions. A reflex hammer is used to tap the distal insertion tendon of the tested muscle. A normal response is elicited when the muscle contracts, but the intensity of the response must also be assessed. The DTR intensity should be rated as follows:

  • 0: Absent reflex
  • 1+: Trace response
  • 2+: Normal response
  • 3+: Brisk response
  • 4+: Non-sustained clonus (repetitive vibratory movements)
  • 5+: Sustained clonus

The right- and left-side DTRs should be compared to determine symmetry. Reflex responses to stimuli can be described as normal (normoreflexia), less reactive (hyporeflexia), or more reactive (hyperreflexia). The commonly tested reflexes are listed in Table 2.  

Table 2. Commonly Tested DTRs

Name of Reflex Spinal Nerved Being Tested How to Elicit the DTR
Biceps reflex C5-C6 Hold the patient's elbow flexed at a right angle with their palm facing upward. The examiner places a thumb on the biceps tendon on the medial side. The examiner then strikes the thumb, which transmits the force to the patient's biceps tendon, and observes for elbow flexion (see Media. Biceps Deep Tendon Reflex Clinical Examination).
Triceps reflex C7 The patient's elbow is supported by the examiner's hand while letting the forearm hang downward at a right angle. The examiner then strikes the triceps tendon just above the elbow's bony prominence. A slight arm extension should be noted (see Media. Triceps Deep Tendon Reflex Clinical Examination).
Knee (patellar) reflex L2-L4 The patient sits on the edge of the examiner's table with legs hanging loosely. The examiner then strikes the patellar tendon with the percussion hammer. A slight knee extension should be noted (see Media. Patellar Deep Tendon Reflex Clinical Examination). 
Ankle reflex S1

The patient may be in a sitting, supine, or prone position. The examiner grasps the patient's foot and strikes the Achilles tendon. A slight plantarflexion should be noted (see Media. Ankle Deep Tendon Reflex Clinical Examination). 

The patient positions described in Table 2 apply only if the patient is cooperative. DTR testing is still possible in unconscious patients by positioning the limb so that sufficient muscle stretch is present at the tendon being tested.

Coordination and Gait

Injuries restricting weight-bearing must be ruled out before examining a patient's gait. After ruling out such injuries, the patient's posture, gait, coordinated automatic movements (swinging arms), and ability to walk in a straight line must be observed. Any abnormal motions or asymmetric movements should be noted. 

The Romberg test helps assess proprioception. The test is conducted with the patient standing with heels and toes together and eyes closed.[9] The examiner should stand beside the patient and be prepared to catch them. Swaying or failing to maintain posture with closed eyes is a positive Romberg sign.

In the finger-to-nose test, the patient places the tip of a finger on their nose and then touches the examiner's finger, which is placed at an arm's length away from the patient. A lower-extremity equivalent of this test is the heel-to-shin test. In this test, the patient places one heel on the opposite knee and then moves the heel up and down along the shin. The extremities are tested separately when conducting these tests.

General Physical Examination Findings Associated with Neurologic Damage

Other areas of the general physical examination may provide clues to a possible neurologic injury and include those listed below. Finding these signs should prompt a detailed neurological assessment in patients with trauma.

  • Papilledema: swollen or blurred optic disc that may signify increased intracranial pressure
  • Subhyaloid hemorrhage: intraocular collection of blood, suggestive of a subarachnoid hemorrhage
  • Irregular breathing patterns: associated with brainstem damage; the abnormal pattern may provide a clue regarding which brainstem region is affected
  • Bony step-off: palpable skull discontinuity arising from a displaced fracture; facial bones should also be examined for fractures; associated nerve damage depends on the location and severity of the skull injury
  • CSF rhinorrhea: CSF drainage from the nose due to a possible break in the anterior cranial fossa, which may have associated forebrain or CN lesions
  • CSF otorrhea: CSF drainage from the ear likely from a temporal bone fracture, which may have associated brainstem or CN damage
  • Hemotympanum: dark blood visible behind the tympanic membrane (eardrum), which may indicate brainstem or CN damage
  • Battle sign: dark bruising visible in the skin overlying the mastoid process, which may have associated brainstem or CN injury
  • Raccoon eyes: dark bruising visible in the skin around the eyes; may have associated forebrain or CN injuries [10][11]
  • Internal carotid artery or eye globe bruit: auscultation findings that may suggest carotid dissection or carotid-cavernous fistula; the carotid artery supplies the brain's anterior circulation
  • Posterior midline tenderness: may suggest a vertebral fracture with associated spinal cord injury
  • Pain, pallor, and pulselessness in a muscle compartment: signs of compartment syndrome together with paralysis and paresthesia; can lead to limb loss from neurovascular compromise

Clinical Significance

Mental Status

  • Unconsciousness can arise from brainstem damage, which may be confounded by toxic and metabolic factors, eg, alcohol intake and hypoglycemia. Thus, toxic or metabolic encephalopathy must be ruled out in patients with trauma presenting with altered sensorium.
  • - Severe: GCS less than 9; mortality 40% [12]
  • - Moderate: GCS 9 to 12; mortality 10%
  • - Mild or minor: GCS 13 to 15; mortality 0.1%
  • TBI is classified as follows:
    • The term “concussion,” which may also refer to mild or minor TBI, is defined as a reversible neurologic impairment following a head injury. Clinical features of this condition include loss of consciousness during the traumatic injury, “seeing stars” (visual changes), and other symptoms such as headache, dizziness, nausea, and vomiting.[13] A concussion can result in a transient change in mental status, while a severe TBI may lead to coma or even death. Notably, mild TBI can result in postconcussive syndrome, with symptoms such as headaches, lethargy, mental dullness, and sleep disturbance that can persist for several months post-injury.[14][15]
    • TBI is a nonspecific term for brain injury arising from various mechanisms, such as blunt, penetrating, and blast injuries. TBI may be classified as mild, moderate, or severe based on the GCS score.
    • A single GCS assessment is of limited value. Meanwhile, serial GCS assessments are more useful prognostically. Persistently low or declining GCS scores are associated with poorer outcomes than consistently high or improving GCS scores. Thus, a single high GCS score does not eliminate the possibility of severe intracranial injury. 
    • Frontal lobe trauma may present with flat affect. Standard motor and sensory examinations cannot test this area of the brain.[16] 

Cranial Nerves

  • Visual field defects suggest damage to the complex visual pathways.
  • Pupil reactivity relies on an intact retina and the unimpaired neural pathway starting from CN II and going to the midbrain and CN III, which innervates the pupillary sphincter muscle. Lack of pupillary response may be due to damage anywhere along this pathway, localizable by a good neurologic examination. Brainstem damage can also cause abnormal pupillary responses.
  • CNs III, IV, and VI determine baseline eye position and extraocular muscle movements. The absence of the oculocephalic reflex in the comatose patient suggests brainstem dysfunction, though this finding can be normal in the awake patient. Abnormal horizontal eye movements may indicate damage to CN III or VI or the pons. Abnormal vertical eye movements may signify damage to CN III, CN IV, or the midbrain. An abducens nerve palsy may result from a clivus fracture or may be a false localizing sign due to elevated intracranial pressure. 
  • The lack of a corneal reflex on either side suggests damage to CN V or CN VII.
  • Hearing loss may suggest damage to CN VIII or crucial middle or inner ear structures. 
  • An absent or asymmetric gag reflex may signify damage to either CN IX or X. Lack of any gag reflex may indicate an injury to CN IX, the afferent portion of the reflex. An asymmetric uvula elevation suggests damage to 1 of the 2 efferent portions of the reflex, the left or right vagus nerve.
  • Significant muscle weakness or asymmetry during CN XI and CN XII testing may suggest damage to these nerves. 

Sensory, Motor, and Reflexes

  • Somatic sensorimotor testing, done systematically by dermatomal approach, can help localize and assess the extent of SNS injury.[17] 
  • Spinal shock is a condition that may arise from traumatic spinal cord injury. The symptoms include flaccid paralysis below the level of spinal cord damage, loss of DTRs, decreased sympathetic outflow, and absent sphincter reflexes or tone.[18] The decreased sympathetic outflow leads to vascular smooth muscle relaxation and blood vessel dilation, producing hypotension.[19] Bradycardia also results from reduced sympathetic stimulation. Spinal shock may resolve over weeks to months. Afterward, spastic paralysis and hyperreflexia below the injured spinal nerve's level manifest. Some sphincter and erectile reflexes may return, often without voluntary control. 

Enhancing Healthcare Team Outcomes

An interprofessional approach in patients with trauma helps improve outcomes. Emergency medical services provide initial evaluation and treatment in the prehospital setting. Emergency medicine physicians perform a more thorough examination, stabilize the patient, and activate trauma protocols.

The neurological examination in patients with trauma is often initially performed by the trauma service. Abnormal findings warrant a referral to the neurologist or neurosurgeon as indicated. Once admitted, the neurotrauma nurse monitors the patient's vital signs, GCS score, and neurologic indicators like the pupillary reflex. Other specialists, such as intensivists, pulmonologists, and cardiologists, may also be involved if the patient requires intensive care or develops organ-specific sequelae. A mental health specialist may be involved if the patient develops psychiatric complications.

Pharmacists can help manage medication administration. Respiratory therapists may be involved if the patient requires oxygenation and mechanical ventilation. Patients with mild to moderate TBI may benefit from early referral to physical and occupational therapists.

The prognosis of neurotrauma patients depends on TBI severity, the presence of a neurological deficit on admission, comorbidity, age, and the need for immediate surgery. The prognosis is good for patients with mild TBI (GCS 13-15), but the recovery can be prolonged. Patients with severe TBI (GCS less than 9) usually have a guarded prognosis, and many are left with residual neuropsychiatric deficiencies.



<p>Contributed by Dr. Raju S. Menon (https://www.youtube.com/watch?v=62jADalpDaI)</p>

<p>Contributed by Dr. Raju S. Menon (https://www.youtube.com/watch?v=62jADalpDaI)</p>

<p>Contributed by Dr. Raju S. Menon (https://www.youtube.com/watch?v=62jADalpDaI)</p>

<p>Contributed by Dr. Raju S. Menon (https://www.youtube.com/watch?v=62jADalpDaI)</p>
Details

Author

Andrew Clark

Author

Joe M. Das

Updated:

2/24/2024 6:33:06 PM

References


[1]

Milligan TA. Diagnosis in Neurologic Disease. The Medical clinics of North America. 2019 Mar:103(2):173-190. doi: 10.1016/j.mcna.2018.10.011. Epub 2018 Dec 17     [PubMed PMID: 30704675]


[2]

Jain S, Iverson LM. Glasgow Coma Scale. StatPearls. 2024 Jan:():     [PubMed PMID: 30020670]


[3]

Novick D, Wallace R, DiGiacomo JC, Kumar A, Lev S, George Angus LD. The cervical spine can be cleared without MRI after blunt trauma:A retrospective review of a single level 1 trauma center experience over 8 years. American journal of surgery. 2018 Sep:216(3):427-430. doi: 10.1016/j.amjsurg.2018.03.003. Epub 2018 Mar 6     [PubMed PMID: 29530277]

Level 2 (mid-level) evidence

[4]

Ambesi V, Miller C, Fitzgerald MC, Mitra B. The GCS-Pupils (GCS-P) score to assess outcomes after traumatic brain injury: a retrospective study. British journal of neurosurgery. 2024 Jan 23:():1-4. doi: 10.1080/02688697.2023.2301071. Epub 2024 Jan 23     [PubMed PMID: 38259200]

Level 2 (mid-level) evidence

[5]

Brennan PM, Murray GD, Teasdale GM. Simplifying the use of prognostic information in traumatic brain injury. Part 1: The GCS-Pupils score: an extended index of clinical severity. Journal of neurosurgery. 2018 Jun:128(6):1612-1620. doi: 10.3171/2017.12.JNS172780. Epub 2018 Apr 10     [PubMed PMID: 29631516]


[6]

McClenathan BM, Thakor NV, Hoesch RE. Pathophysiology of acute coma and disorders of consciousness: considerations for diagnosis and management. Seminars in neurology. 2013 Apr:33(2):91-109. doi: 10.1055/s-0033-1348964. Epub 2013 Jul 25     [PubMed PMID: 23888394]


[7]

Rabinstein AA. Coma and Brain Death. Continuum (Minneapolis, Minn.). 2018 Dec:24(6):1708-1731. doi: 10.1212/CON.0000000000000666. Epub     [PubMed PMID: 30516602]


[8]

Weaver DF. Rotator drift: A sign of upper motor neuron leg weakness. Clinical neurology and neurosurgery. 2020 Oct:197():106084. doi: 10.1016/j.clineuro.2020.106084. Epub 2020 Jul 13     [PubMed PMID: 32683196]


[9]

Forbes J, Munakomi S, Cronovich H. Romberg Test. StatPearls. 2022 Jan:():     [PubMed PMID: 33085334]


[10]

M Das J, Munakomi S. Raccoon Sign. StatPearls. 2024 Jan:():     [PubMed PMID: 31194384]


[11]

Becker A, Metheny H, Trotter B. Battle Sign. StatPearls. 2024 Jan:():     [PubMed PMID: 30725789]


[12]

Mollayeva T, Mollayeva S, Pacheco N, D'Souza A, Colantonio A. The course and prognostic factors of cognitive outcomes after traumatic brain injury: A systematic review and meta-analysis. Neuroscience and biobehavioral reviews. 2019 Apr:99():198-250. doi: 10.1016/j.neubiorev.2019.01.011. Epub 2019 Jan 11     [PubMed PMID: 30641116]

Level 1 (high-level) evidence

[13]

Jackson WT, Starling AJ. Concussion Evaluation and Management. The Medical clinics of North America. 2019 Mar:103(2):251-261. doi: 10.1016/j.mcna.2018.10.005. Epub 2018 Dec 3     [PubMed PMID: 30704680]


[14]

Permenter CM, Fernández-de Thomas RJ, Sherman AL. Postconcussive Syndrome. StatPearls. 2024 Jan:():     [PubMed PMID: 30521207]


[15]

Skjeldal OH, Skandsen T, Kinge E, Glott T, Solbakk AK. Long-term post-concussion symptoms. Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke. 2022 Sep 6:142(12):. doi: 10.4045/tidsskr.21.0713. Epub 2022 Aug 17     [PubMed PMID: 36066235]


[16]

Weber E, Spirou A, Chiaravalloti N, Lengenfelder J. Impact of frontal neurobehavioral symptoms on employment in individuals with TBI. Rehabilitation psychology. 2018 Aug:63(3):383-391. doi: 10.1037/rep0000208. Epub 2018 Jul 19     [PubMed PMID: 30024202]


[17]

Assir MZK, M Das J. How to Localize Neurologic Lesions by Physical Examination. StatPearls. 2024 Jan:():     [PubMed PMID: 29630211]


[18]

Ruiz IA, Squair JW, Phillips AA, Lukac CD, Huang D, Oxciano P, Yan D, Krassioukov AV. Incidence and Natural Progression of Neurogenic Shock after Traumatic Spinal Cord Injury. Journal of neurotrauma. 2018 Feb 1:35(3):461-466. doi: 10.1089/neu.2016.4947. Epub 2017 Dec 18     [PubMed PMID: 29141498]


[19]

Rabinstein AA. Traumatic Spinal Cord Injury. Continuum (Minneapolis, Minn.). 2018 Apr:24(2, Spinal Cord Disorders):551-566. doi: 10.1212/CON.0000000000000581. Epub     [PubMed PMID: 29613899]