Traumatic Brain Injuries (TBI) “Concussions”

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Presentation transcript:

Traumatic Brain Injuries (TBI) “Concussions”

Meninges Collectively, support and protect brain and spinal cord Provide vascular supply and production of CSF Dura mater Arachnoid mater Pia mater

Meninges

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

Brain Blood Supply

Abnormal Postures – Think CNS/Brain Treatment???

Bony Structures Position of head Cervical vertebrae Mastoid processes 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 Pupil size 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

Special Tests Functional testing – evaluates function of CNS Memory Cognitive function Neuropsychological testing Balance and coordination Vital signs Neurological testing Cranial nerve function Nerve root evaluation

Memory Retrograde amnesia Anterograde 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

Neurological Testing Cranial nerve function Nerve root evaluation 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 Hop

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