KIN 191B – Advanced Assessment of Upper

Extremity InjuriesHead Anatomy, Evaluation and

Injuries

Anatomy

• Bony anatomy

• Brain

• Meninges

• Cerebrospinal fluid

• Circulatory anatomy

Bony Anatomy

• Skull– Provides protection for brain– Reduces forces transmitted to brain (thickness and shape)

• Occipital bone– Inion – “bump of knowledge”

• Parietal bones• Frontal bone• Temporal bones• Sphenoid bones

Bony Anatomy

Brain

• Cerebrum

• Cerebellum

• Diencephalon

• Brainstem

Brain

Cerebrum• Anatomy

– Two hemispheres separated by longitudinal fissure– Each hemisphere has frontal, parietal, temporal and occipital lobes– Sulci and fissures form contours

• Function– Controls primary motor functions

• Gross and sequenced, coordinated movements– Processes sensory information

• Temp, touch, pain, pressure, proprioception, vision, hearing, smell, taste– Cognitive function

• Spatial relationships, behavior, memory

Cerebrum

Cerebellum

• Located at posterior and inferior aspect of brain

• Two hemispheres separated by fissure

• Processing center for incoming and outgoing information relative to maintaining balance and coordination– Quick link to cerebrum for processing sensory information– Quick link to musculoskeletal system to carry out proper

muscular contractions and joint movements

Diencephalon• Formed by thalamus and hypothalamus– processing

center for conscious and unconscious brain input

• Thalamus– “gatekeeper”, routes sensory info to appropriate area of

brain

• Hypothalamus– Center of autonomic nervous system (sympathetic and

parasympathetic nervous systems)• Body temperature, GI activity, hunger, emotions

– Regulates some of body’s hormones

Diencephalon

Brainstem• Relays info to and from central nervous system and

controls involuntary systems

• Medulla oblongata– Links cerebrum to brainstem and spinal cord– Regulates heart and respiratory rates, vascular changes,

coughing, vomiting

• Pons (“bridge”)– Links cerebellum to brainstem and spinal cord– Regulates respiratory rate

Brainstem

Meninges

• Collectively, support and protect brain and spinal cord

• Provide vascular supply and production of CSF

• Dura mater• Arachnoid mater• Pia mater

Meninges

Dura Mater• “hard/tough mother”• Outermost meningeal layer - is periosteum for skulls

inner aspect• Falx cerebri and falx cerebelli – folds between

cerebral and cerebellar hemispheres• Contains meningeal arteries which provide blood

supply to bones of skull• Venous sinuses– Dura separates into two layers at various points– Space between layers are venous sinuses– Route venous blood from skull to jugular veins of neck

Arachnoid Mater

• Middle meningeal layer

• Layer has similar appearance to cobweb

• Separated from dura mater by subdural space

• Beneath arachnoid mater is subarachnoid space which contains cerebrospinal fluid

Pia Mater

• “tender/little mother”

• Innermost meningeal layer

• “Attaches”/adjacent to brain and spinal cord tissue, including following contour into fissures and sulci

Cerebrospinal Fluid

• Originates in choroid plexuses deep within brain

• Circulates around entire CNS– Ventricle system

• Allows CNS to “float” in subarachnoid space– Protects against injury

CSF Circulation

Circulatory Anatomy• Internal carotid arteries branch into anterior and

middle cerebral arteries

• Vertebral arteries unite at level of pons and become basilar artery, which then branches into posterior cerebral arteries

• Circle of Willis– Posterior communicating arteries connect posterior and

middle cerebral arteries– Anterior communicating arteries connect anterior cerebral

arteries

Brain Blood Supply

Primary Survey

• Stabilize cervical spine• A – Airway– Ensure that airway is clear (mouthpiece, tongue, etc.)

• B – Breathing– Look, listen and feel

• C – Circulation– Evaluate for presence carotid pulse

• D – Disorientation/Dysfunction– Conscious vs. unconscious

Position and Posture• Position– Ideal circumstances have athlete supine– If prone or side laying, will eventually need to be rolled to

supine position

• Posture– Decerebrate posture – indicative of brainstem injury

• Extension of extremities, retraction of head– Decorticate posture – injury above brainstem

• Flexion of elbows/wrists, clenched fists, extension of LEs– Flexion contracture – spinal cord injury at C5-C6 level

• Arms flexed across chest

Abnormal Postures

Unconscious Athlete

• Activate EMS• Must assume that athlete has head and/or

cervical spine injury• If ABCs not intact, must initiate rescue

breathing or CPR• If ABCs intact:– Establish and monitor vital signs– Evaluate pupillary response (PEARL)– Palpate skull and c-spine for deformity, swelling,

etc.

Equipment Considerations• Consensus that helmet should not be removed

during pre-hospital care of head/c-spine injury– Facemask removal allows for access to airway

• Shoulder pads should not be removed during pre-hospital care of head/c-spine injury– Straps and laces are cut to expose chest for auscultation

and/or chest compressions• Justifiable reasons for removing helmet and shoulder

pads– Necessity or likelihood of defibrillation– Inability to remove facemask to access airway– If remove one, must remove other to avoid imbalance

Conscious Athlete – Secondary Survey

• Assumes ABCs intact – establish and monitor vital signs• History

– Loss of consciousness, mechanism of injury, symptoms (pain, numbness/tingling, etc.)

– Orientation x 4 (self, others, place, time)• Inspection

– Skull/c-spine alignment• Palpation

– For bony deformity, swelling, muscle spasm (guarding)• Neurological screening

– Sensory testing (dermatomes) compared bilaterally– Motor testing not performed clinically – if all other symptoms

negative, may ask to wiggle fingers and toes to establish distal motor function

Clinical Scenario• Assumes that all field scenario evaluations are

benign and it’s determined to be safe to allow the athlete to leave the field for further evaluation on sideline or in clinical environment – continuous monitoring of athlete occurs (vital signs, level of orientation, etc.)

• History• Inspection• Palpation• Special Tests– Functional testing– Neurological testing

History• Location of symptoms

• Mechanism of injury/etiology– Head vs. cervical spine

• Loss of consciousness

• Prior history of head injury

• Complaints of weakness

Location of Symptoms

• Cervical pain or muscle spasm– More concerning if accompanied by numbness,

tingling, burning sensations and/or radiating pain

• Head pain– If localized, may indicate contusion, skull fracture

and/or intracranial bleeding– Most common complaint is headache

Mechanism of Injury• Head injuries

– Coup – stationary skull struck by high velocity object, results in trauma at site of impact

– Contrecoup – moving skull strikes a non-moving object, brain “floats” and strikes skull opposite impact causing trauma

– Repeated subconcussive forces – cumulative neurological deficits– Rotational or shear forces – sudden acceleration/deceleration forces,

can disrupt CNS activity and result in concussive symptoms

• Cervical spine injuries– May involve any ROM (flexion, extension, lateral flexion and/or

rotation – may be combined)– If flexed ~30 degrees, lordotic curve is lost and cervical spine most

susceptible to axial load injury (unable to dissipate forces)

Other Historical Elements

• Loss of consciousness– Component of memory evaluation– Can athlete or others establish whether there was or was

not momentary loss of consciousness

• History of concussion– Recent history of prior concussion increases risk of second

impact syndrome

• Complaints of weakness– Reports of weakness in extremities may indicate brain,

spinal cord and/or nerve root injury

Inspection

• Bony structures

• Eyes

• Nose and ears

Bony Structures

• Position of head– Should be centered - if rotated/laterally flexed, may

indicate cervical dislocation • Cervical vertebrae– Observe spinous processes for normal alignment - if

displaced or rotated, may indicated cervical dislocation• Mastoid processes– Ecchymosis indicative of basilar skull fracture - “Battle’s

sign”• Skull and scalp– Evaluate for deformity, swelling and bleeding

Bony Injuries

Eyes• Dazed stare may indicate abnormal function• Nystagmus– Presence of involuntary flutter and/or eye movements– May indicate cranial nerve and/or inner ear injury

• Pupil size– Unilaterally dilated pupil indicative of intracranial bleeding– Must be aware of anisocoria – “normal” unequal pupils

• Pupils reaction to light– Should be ipsilateral and contralateral constriction with

exposure to light– Absence may indicate cranial nerve injury

Pupil Reaction

Nose and Ears

• Bleeding from nose may indicate nasal and/or skull fracture

• Bleeding from ears may indicate skull fracture– Halo test – gauze placed in ear to absorb leaking fluids, if

“halo” forms around sample it indicates leakage of CSF = skull fracture

• Ecchymosis around eyes (“raccoon’s eyes”) may indicate nasal and/or skull fracture

Eye Ecchymosis

Palpation of Bony Structures

• Skull– Palpate all cranial bones for pain and deformity

• Spinous processes– Palpate cervical spinous processes for pain and crepitus

associated with fracture

• Transverse processes– Can only directly palpate C1, but palpate area over

remaining transverse processes for pain and crepitus

Palpation of Soft Tissues

• Musculature– Palpate sternomastoid and upper trapezius

muscles for spasm secondary to strain, sprain, fracture and/or dislocation

• Throat– Palpate thyroid cartilage, cricoid cartilages and

hyoid bone to rule out larynx and tracheal injury

Special Tests• Functional testing – evaluates function of CNS– Memory– Cognitive function– Neuropsychological testing (computer based also)– Balance and coordination– Standardized Assessment of Concussion (SAC)– Vital signs

• Neurological testing– Cranial nerve function– Nerve root evaluation

Memory• Retrograde amnesia– Difficulty or inability to remember events preceding the

injury – more severe if can’t remember events of day before as opposed to more recent events

– Some assessed with orientation x 4, pre-game meal?, who played last game?

• Anterograde amnesia– Difficulty or inability to remember events after the onset

of injury– Athlete given verbal list of items and asked to repeat them

serially over time

Cognitive Function• Brain injury can present as abnormal behavior, personality

changes, inability to process information accurately

• Behavior– May become violent, belligerent, etc. - abnormal

• Analytical ability– Typically assessed with serial number repetitions

• Information processing– Cannot follow simple instructions

Neuropsychological Testing• Multiple neuropsychological test methods (six in text – not

responsible for exam)– Hopkins Verbal Learning Test (HVLT)– Wechsler Digit Span Test (WDST)– Controlled Oral Word Association Test (COWAT)

• Used to objectively quantify amount of dysfunction demonstrated by athlete

• More and more common to see these tests employed during PPE as baseline upon which to compare results after head injuries and for return to play considerations

Computerized Neuropsychological Testing

• Limited applications due to financial constraints and personnel to implement the recommended models (pre- and post-injury testing and comparisons)

• Most computerized testing takes 20-30 minutes per athlete – can be done in group format (all at computers at same time) for efficiency

• Allows for more precise measurement of subtle deficits associated with concussion including reaction time, cognitive processing speed, and response latency– Essential benefits to research on concussions and return to play

criteria– Also allows for easy storage/access of data

Computerized Neuropsychological Testing

• HeadMinder Concussion Resolution Index (CRI) - 1999– Internet-based neuropsychological test to compare post-concussion

performance to pre-injury baseline– Measures memory, reaction time, speed of decision making and

speed of information processing

• University of Pittsburgh Medical Center Immediate Post-concussion Assessment and Cognitive Testing (ImPact) – mid-1990’s– Software includes Self-Report Symptom Questionnaire, a Concussion

History Form and tests to evaluate the elements listed below– Measures attention span, working memory, sustained attention,

selective attention, non-verbal problem solving, reaction time, visual and verbal memory, and response variability

Balance and Coordination• Evaluation for possible cerebellar injury affecting muscle

coordination (ataxia)– Romberg test – single leg stance with shoulders abducted 90 degrees,

eyes closed and head back– Tandem walking – heel to toe walking forward and backward along

straight line

• Balance Error Scoring System (BESS)– Double leg, single leg, and tandem leg stance on firm and then foam

surfaces with eyes closed and hands on hips– Attempt to hold for 20 seconds, points for errors– Scores can be used as baseline for comparison following head injuries

and for return to play considerations

Standardized Assessment of Concussion

• Standardized Assessment of Concussion (SAC)– Quick (5 minutes) screening instrument to

administer and assess four domains of cognition• Orientation• Immediate Memory• Concentration• Delayed Recall

– Composite score is identified to provide index of cognitive impairment and injury severity

Vital Signs

• Pulse rate, respiratory rate, blood pressure taken early in evaluation process to establish baseline and repeated serially for comparison

Neurological Testing

• Cranial nerve function– Serial evaluations must be performed initially to evaluate

for changes– Cranial nerves arise from brain and are susceptible to

impairment secondary to intracranial bleeding and resulting pressure

• Nerve root evaluation– Sensory (dermatome), motor (myotome) and reflex testing

necessary to rule out or identify level of spinal cord injury

Cranial Nerve Evaluation• Olfactory• Optic• Oculomotor• Trochlear• Trigeminal• Abducens• Facial• Acoustic/Vestibulocochlear• Glossopharyngeal• Vagus• Accessory (spinal)• Hypoglossal

• On• Old• Olympus• Towering• Top• A• Fin• And• German• Viewed• A• Hop

Cranial Nerve Evaluation

• I – Olfactory– Sense of smell

• II – Optic– Visual acuity

• III – Oculomotor– Pupillary size and reaction– Eye adduction and downward rolling– Elevation of upper eyelid (blink)

Cranial Nerve Evaluation

• IV – Trochlear– Upward eye rolling

• V – Trigeminal– Muscles of mastication (chewing)– Facial sensation

• VI – Abducens– Lateral eye movements

Cranial Nerve Evaluation

• VII – Facial– Taste– Facial expressions

• VIII – Acoustic/Vestibulocochlear– Hearing– Equillibrium/balance

• IX – Glossopharyngeal– Taste– Swallowing

Cranial Nerve Evaluation

• X – Vagus– Gag reflex– Swallowing– Involved in heart rate, respirations, digestion, etc.

• XI – Accessory– Shrug shoulders and rotate cervical spine

• XII – Hypoglossal– Symmetrical stick out of tongue

Injuries• Head injuries– Concussion– Post-concussion syndrome– Second impact syndrome– Intracranial hemorrhage

• Epidural hematoma• Subdural hemtoma

– Skull fracture

• Cervical spinal cord injuries– Cervical spine fracture/dislocation– Quadraplegia

Concussion• Cerebral concussion = mild/traumatic brain injury (M/TBI)

• Hallmark symptoms include mental confusion, altered mental status, amnesia and potential loss of consciousness

• Multiple occurrences may produce cumulative degenerative effects

• Ultimate assessment based upon duration of loss of consciousness (if any) and neuropsychological findings

Concussion• Additional symptoms of concussion may include but

are not limited to:– Dizziness– Tinnitus– Nausea/vomiting– Motor impairment– Memory loss

• Glasgow coma scale– Allows for objective evaluation of symptoms of brain injury– Normal score is 15 – scores >11 likely to recover

Classification of Concussions

• Concussion rating systems– Injury graded at time of injury based upon existing signs/symptoms

within 15 minutes of injury• American Academy of Neurology Concussion Grading Scale

– Injury graded after all signs/symptoms have resolved• Cantu Evidence-Based Grading Scale

• Recommendations from 2001 & 2004 Vienna Conference on Concussion in Sport– Individual’s recovery attended to based upon symptoms,

neuropsychological tests and postural stability tests

Concussion Rating Systems

• Guidelines for identifying concussion severity and determining return to play timeline – often considered conservative for athletic population

• Significant differences between scales – be consistent with scale utilized – more than 16 rating systems have been identified

• American Academy of Neurology Concussion Grading Scale• Cantu Evidence-Based Grading Scale

Vienna Conference Recommendations

• Simple vs. complex concussions

• Simple concussions– Most common concussion but most difficult to

recognize

• Complex concussions– Involves persistent symptoms and also individuals

suffering multiple concussions over time

Simple Concussions

• Signs & symptoms– No LOC– Only neurological deficit is brief post-traumatic

confusion and/or post-traumatic amnesia– Symptoms typically resolve within 30 minutes – if

persist for more than 30 minutes, a more serious (complex) concussion exists

Simple Concussions• Management

– Removed from activity with serial evaluations following initial evaluation at ~5 minute intervals until asymptomatic

– Once asymptomatic, introduce exertion – if exertion exacerbates symptoms, disqualify from activity

– If asymptomatic for 15 minutes at rest and with exertion, can return to activity

– Second episode during same activity session disqualifies individual from further activity that day

– If symptoms progress – ultimate progression of evaluation for return to activity is; at rest, with exertion, with sport-specific activities, return to full activity

Complex Concussions

• Signs & symptoms– Persistent symptoms (with and/or without

exertion), specific sequelae (prolonged LOC), or prolonged cognitive impairment

– Also includes those with multiple concussions over time

– Protracted post-traumatic amnesia is typical, usually lasting 30 minutes – 24 hours

Complex Concussions

• Management– Removed from activity that day– Serial evaluations to identify or rule out potential

development of intracranial pathology – may require referral to physician for special test evaluation (CT/MRI)

– Formal neuropsychological testing should be considered – performance utilized to make decisions regarding return to activity (return to baseline – ideally pre-injury baseline is available)

Return to Play Criteria

• Multiple factors to consider include whether or not loss of consciousness occurred, duration of symptoms, total number of concussive episodes, exertional testing

• Universal agreement that individual who lost consciousness for any period of time should not be allowed to return to activity on the same day even if all symptoms have resolved

Post-Concussion Syndrome

• Individuals may present with concussion symptoms long after “normal” resolution would have occurred

• Common symptoms include– Decreased attention span– Difficulty concentrating– Memory impairment– Prolonged headaches– Balance impairments– Decreased cognitive function

Second Impact Syndrome• Defined as symptoms resulting from second concussive

episode before symptoms of first concussive episode have resolved– Entirely preventable, return to play considerations

• Second trauma typically not as violent as initial injury – thought to affect brain blood supply causing increased intracranial pressure which impacts brainstem function

• Quick progression from mild concussive symptoms to comatose state

• Even if treated appropriately, has ~50% mortality rate

Intracranial Hemorrhage

• Named for location relative to meningeal layers

• Caused by injury to blood vessels supplying brain blood supply

• Increased pressure from bleeding in confined space compresses neural tissue

• Onset of symptoms associated with nature of bleeding – venous vs. arterial (lucid interval)

• Epidural hematoma• Subdural hematoma

Epidural Hematoma

• Arterial bleeding between skull and dura mater• Initially may present with concussive symptoms• Short lucid interval (typically <48 hours)–

individual appears “OK”– Due to arterial nature of bleeding

• Subsequently may c/o disorientation, confusion, drowsiness, increasing headache intensity, signs of cranial nerve changes (esp. pupil changes)

• If untreated, can be fatal

Epidural Hematoma

Subdural Hematoma• Venous bleeding between brain and dura mater• May not present with symptoms of concussion• Longer lucid interval – may be hours, days or weeks

before symptoms present– Due to venous nature of bleeding

• Subsequent development of headaches, confusion, changes in cognitive/motor abilities, cranial nerve changes

• More likely to cause death due to lack of recognition of nature/source of symptoms and delay in subsequent treatment

Subdural Hematoma

Skull Fractures• Minimal risk with head protection, but may still

suffer bony injury• May cause CSF leakage from nose/ear, may have

residual/secondary ecchymosis• Linear– Hairline fractures in bone

• Comminuted– Multiple fracture fragments

• Depressed– Easier to identify on evaluation – gross deformity– Potential for fragments to injure meninges/brain

Skull Fractures

Cervical Spinal Cord Injuries• Risk minimized with rules and coaching emphasis

changes• Spinal cord injury caused by– Impingement/laceration from bony displacement– Compression from bleeding, swelling, ischemia to cord

• Mechanism of injury is key to decisions on management – must assume worst case scenario until proven otherwise

• Trauma at spinal cord level affects function distal to level of injury– At or above C4 level – death is likely due to impact on

brainstem and vital functions

Cervical Fracture/Dislocation

• Spinal cord injury typically secondary to actual bony injury from swelling, bony fragment displacement, etc.

• With dislocation, diameter of canal for spinal cord is impacted and can compress spinal cord

• Must differentiate between spinal cord symptoms and brachial plexus injury symptoms (longer duration vs. transient symptoms)

• Often treat with steroid injections to limit swelling and subsequent pressure on spinal cord with these injuries

Quadriplegia

• Transient quadriplegia often results from cervical hyperextension, hyperflexion and/or axial loading

• Several predisposing factors– Cervical stenosis– Cervical spine instability– Posterior arch abnormalities of cervical spine

• If truly transient, symptoms often resolve within 48 hours