Second Impact Syndrome
Tanvir Choudhri, MD
Assistant Professor of Neurosurgery
Ichan School of Medcine at Mount Sinai
Department of Neurosurgery
SIS: What is it?
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When repeat injury is
sustained before
symptoms of previous
head injury have been
resolved
Rare, often fatal,
traumatic brain injury occurs
(Weinstein et al., 2013)
Department of Neurosurgery
SIS: What is it?
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Saunders RL, Harbaugh RE
The second impact in
catastrophic contact-sports
head trauma
JAMA 252:538-539, 1984
Department of Neurosurgery
SIS: How often does it occur?
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Exact incidence unknown
Less than 20 documented SIS cases
in world literature
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(Randolph et al., 2009, Arch Clin Neuropsychol)
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1 possible SIS for every 205,000
player seasons
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Annual participation rate: 1.8 million high school/collegiate
subjects
(McCrory, et al., 2012, Current sports medicine reports)
Department of Neurosurgery
SIS: What are the risk factors?
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Males 16-23 years old (Mori et al., 2006, Acta
Neurochirugica Supplementum)
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Most brain fatalities occurred during
games (Boden et al., 2013. Am J Sports Med)
Fatal injury sustained most frequently
either tackling or being tackled (Cantu & Mueller,
2003, Neurosurgery)
 History of 3+ concussions
3x more likely to sustain
incident concussion
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(Guskiewicz et al., 2003, JAMA)
Department of Neurosurgery
SIS: How does it occur?
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Within vulnerable period from previous injury
(Weinstein et al., 2013, J Neurosurg)
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Impairment of cellular energetic metabolism
Loss of autoregulation of cerebral blood flow
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Subsequent vascular engorgement
Increased intracranial pressure
Eventual herniation
Subdural hematoma
Brain Swelling
Department of Neurosurgery
SIS: Effects of 2nd Impact
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Loss of autoregulation
Rapid onset massive cerebral edema
Transtentorial brain herniation
Raised intracranial pressure
Death can be as early as 2-5 min (Zollman,
2011, Demos Medical Publishing)
Department of Neurosurgery
SIS: Pathophysiology
Functional injury
 Reinjury to neuronal cells within vulnerable
period from previous injury (Weinstein et al., 2013, J
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Neurosurg Pediatrics)
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Dysautoregulation 
 hyperemic brain swelling
 Increased intracranial pressure
 Herniation
 Brainstem compression
Department of Neurosurgery
Concussion: Pathophysiology
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Neurometabolic cascade (Marshall, 2012, J Can
Chiropr Assoc)
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 Mechanical stretching/shearing of
neurons
 Disrupts ion channels
 Excitation phase
 Neuronal suppression
Net result = neuronal ion imbalance, cellular
dysfunction, cerebral energy deficit
Requires max function of Na+/K+ pump to
restore homeostasis
Department of Neurosurgery
Concussion: Pathophysiology
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http://www.youtube.com/watch?v=KrvC2UUEJ8
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http://www.youtube.com/watch?v=uEGXcNNyzp
Y
Mount Sinai / Presentation Slide / December 5, 2012
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SIS: How to recognize it?
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2nd injury generally not severe
Remains standing - appears dazed
Sec-min after 2nd blow collapses to
ground
Semicomatose, dilating pupils, loss of
eye movement, respiratory failure (Cantu &
Gean, 2010, Journal of neurotrauma)
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Death can be as early as 2-5 min of 2nd
impact (Zollman, 2011, Demos Medical Publishing)
Department of Neurosurgery
SIS: Symptoms
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Headache most commonly reported
Dizziness
Neck pain
Nausea and vomitting
Light/Noise sensitivity
Sleep pattern changes
Memory/Concentration problems
Fatigue
Respiratory arrest
Aniscoria
Coma
Department of Neurosurgery
SIS: Evaluation and Management
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Hyperemic swelling
Brain Herniation
Post-herniation ischemia
CT (Cantu & Gean, 2010, Journal of Neurotrauma)
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Engorged cerebral hemisphere
Abnormal mass effect
Midline shift
MRI (McCrory et al., 2012, Current sports medicine
reports)
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Metabolic change up to 15 d
after concussive injury
Department of Neurosurgery
SIS: Neurosurgeon’s role
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Neurosurgical consult in case of anatomic
abnormality (Bey & Ostick, 2009, Western Journal of Emergency
Medicine)
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Attention for potential c-spine injury
Patient immediately stabilized
Airway management
Rapid intubation
Mannitol to minimize morbidity
Surgery generally not effective for treatment
of impaired autoregulation
Department of Neurosurgery
Case
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(Weinstein et al., 2013, J Neurosurg Pediatrics)
Previously healthy 17 yo M
Helmet to helmet hit
Felt dizzy, played immediately after
Reported H/A after game from hit
Resumed typical activities
c/o fatigue and persistent H/A
Department of Neurosurgery
Case
(Weinstein et al., 2013, J Neurosurg Pediatrics)
- Normal evaluation/neurological exam with PCP 4d after game
- Head CT: WNL
Department of Neurosurgery
Case
(Weinstein et al., 2013, J Neurosurg Pediatrics)
- Persistent H/A, difficulty with concentration
- 5 days after initial injury participated in practic (including
hitting drills)
- After a hit on fourth drill: slow to get up “OK” but H/A
- Several plays later  down on one knee  dizziness and
headache  couldn't feel legs  unresponsive 
generalized seizure activity
- Local ER: intubated, treated with lidocaine, mannitol,
fosphenytoin, fentanyl, midazolam
- Air transport to trauma/NS center
- 143/79, HR 93, GCS 7T, 3mm sluggish pupils, ICP 25-30
- Coagulation studies normal, Utox neg
Department of Neurosurgery
Case
(Con’t)
- Brain/cervical spine MRI:
mild downward transtentorial herniation,
bilateral subdural hematomas,
abnormal T2 signal
restricted diffusion in medial left
thalamus
- Midline structures displaced caudally
(thalamus hypothalamus)
Department of Neurosurgery
Case
(Con’t)
Hospital course:
Episode of hypotension, severe metabolic acidosis and renal failure,
Sepsis, ventilator-assoc. pneumonia with empyema, disseminated
intravascular coagulation, cardiac arrest
Later resolution of subdural hematomas and areas of
encephalomalacia
At time of discharge (day 98) nonverbal and nonambulatory
Department of Neurosurgery
Case
(Con’t)
3+ years after injury living at home
regained limited verbal, motor, cognitive skills
Department of Neurosurgery
SIS
http://www.youtube.com/watch?v=V12Z
qmd3Btc
Department of Neurosurgery
Traumatic Subdural Hematoma
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Bleeding into the space between the dura
mater and the brain
From venous hemorrhage
12-30% of patients with severe head injury
36-79% mortality
Often requires surgical
intervention
Department of Neurosurgery
Traumatic Epidural Hematoma
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Bleeding into the space between the dura
mater and the skull
From arterial laceration
Typically from disruption of middle
meningeal artery
Arterial bleeding 
increased intracranial
pressure  cell lesion
& brain damage
~20% mortality
Department of Neurosurgery
Post Concussion Syndrome
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Persistent post-concussion symptoms
3+ months
Increased risk of depression
Working memory and Info processing speed
impairments in mild TBI and persistent PCS
(Dean & Sterr, 2013, Frontiers in Human Neuroscience)
Department of Neurosurgery
Chronic Traumatic Encephalopathy
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Repetitive brain trauma necessary for development
of CTE
Progressive neurodegenerative disease
Symptoms present years after trauma (Stern et al., 2011,
American Academy of Physical Medicine and Rehabilitation)
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Decline of memory/cognition
Depression
Suicidal behavior
Poor impulse control
Aggressiveness
Parkinsonism
Dementia
Generalized atrophy
Department of Neurosurgery
Conclusions
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Vulnerable window following TBI
Second impact before resolution of
symptoms can result in catastrophic brain
injury/ fatality
Highlights importance of return-to-play
decisions
PCS and CTE represent long-term
consequences of repetitive head impacts
Department of Neurosurgery
Future Directions
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Better identification of concussions
X2 Helmet
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Better protocols (sideline, ER, etc)
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Increased awareness
Department of Neurosurgery
Acknowledgements
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Alexa Dessy, BA
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Jonathan Rasouli, MD
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Mount Sinai PLAYSAFE team
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Alex Gometz, DPT, CIC (Concussion Management of New York)
Department of Neurosurgery