REVIEW

CURRENT
OPINION Anesthesia and the brain after concussion
Jeffrey J. Pasternak and Arnoley S. Abcejo

Purpose of review
To provide an overview of acute and chronic repeated concussion. We address epidemiology,
pathophysiology, anesthetic utilization, and provide some broad-based care recommendations.
Recent findings
Acute concussion is associated with altered cerebral hemodynamics. These aberrations can persist despite
resolution of signs and symptoms. Multiple repeated concussions can cause chronic traumatic
Downloaded from http://journals.lww.com/co-anesthesiology by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 12/07/2020

encephalopathy, a disorder associated with pathologic findings similar to some organic dementias.
Anesthetic utilization is common following concussion, especially soon after injury, a time when the brain
may be most vulnerable to secondary injury.
Summary
Brain physiology may be abnormal following concussion and these abnormalities may persist despite
resolutions of clinical manifestations. Those with recent concussion or chronic repeated concussion
may be susceptible to secondary injury in the perioperative period. Clinicians should suspect
concussion in any patient with recent trauma and strive to maintain cerebral homeostasis in the
perianesthetic period.
Keywords
anesthesia, chronic traumatic encephalopathy, concussion, traumatic brain injury

INTRODUCTION the head as patients with concussion may or may

Although public awareness of concussion has
recently increased, our understanding of the
pathophysiology of both acute and chronic
repeated concussion is still limited. Aberrations
in systemic physiology, such as those commonly
encountered in the perianesthetic period, may
serve as a source of secondary injury to the poten-
tially vulnerable concussed brain. We provide a
brief synopsis of epidemiology, pathophysiology,
and anesthetic utilization in patients with concus-
sion along with broad-based suggestions for the
perianesthetic care of patients with concussion.
DEFINITION AND EPIDEMIOLOGY
The American Academy of Neurology defines con-
cussion as a trauma-induced alteration in mental
status that may or may not involve a loss of con-
sciousness [1]. However, the term ‘concussion’ is
frequently used to describe the clinical manifesta-
tions that occur following a mild traumatic brain
injury (i.e., those with a Glasgow Coma Score of 13–
15 following restoration of consciousness). The
diagnosis of concussion is independent of radio-
graphic findings on computerized tomography of
not have intracerebral contusion, hemorrhage, or
diffuse axonal injury.
The true incidence of concussion is difficult to
ascertain as many patients do not seek medical care
following injury. The Centers for Disease Control
and Prevention estimates that 2.2–2.7 million mild
traumatic brain injuries occur in the United States
annually [2]. This estimate does not include indi-
viduals who either did not seek medical care or those
who sought care at a clinic. When considering only
sports-related concussions, Daneshvar et al. [3] esti-
mate 1.8–3.6 million occur annually in the United
States; this estimate does not include concussions
that result from other mechanisms such as falls,
motor vehicle accidents, assaults, or injuries
encountered by the military.
Department of Anesthesiology and Perioperative Medicine, Mayo Clinic
College of Medicine, Rochester, Minnesota, USA
Correspondence to Jeffrey J. Pasternak, MD, Department of Anesthesi-
ology and Perioperative Medicine, Mayo Clinic College of Medicine, 200
First St. SW, Rochester, MN 55905, USA. Tel: +1 507 255 4235;
fax: +1 507 255 6463; e-mail: Pasternak.jeffrey@mayo.edu
Curr Opin Anesthesiol 2020, 33:639–645
DOI:10.1097/ACO.0000000000000906

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Neuroanesthesia

concussion although further study is required to

KEY POINTS determine if electroencephalography has an role
 Brain physiology is not normal following a concussion in diagnosis or stratifying prognosis in those with
and resolution of clinical manifestations may not concussion [8]. There is a paucity of data describing
indicate a return to normal physiology. a role for standard frontal near-infrared (IR) spec-
troscopy in those with concussion. However, func-
 Repeated concussion can predispose to deposition of b-
tional near-IR spectroscopy was associated with an
amyloid, hyperphosphorylated tau, and a-synuclein
protein in the brain; pathologic findings similar to other attenuation of oxyhemoglobin response while per-
organic dementias. forming cognitive tasks and reduced interhemi-
spheric motor coherence [9,10]. In 2018, the
 Patients with concussion commonly require anesthesia United States Food and Drug Administration
to facilitate diagnostic tests and procedures that may or
approved a blood test for concussion based on an
may not be associated with the trauma that resulted
in concussion. increase in two serum biomarkers: ubiquitin car-
boxy-terminal hydrolase-L1 and glial fibrillary
 The need for anesthesia is greatest soon after acidic protein [11]. This test, the Brain Trauma
concussion – a time when brain physiology is likely Indicator, had a sensitivity and specificity of pre-
most disrupted.
dicting abnormal findings on computerized tomo-
graphic imaging of the head of 97.5 and 99.6%,
respectively. However, the utility of the Brain
MANIFESTATIONS AND DIAGNOSIS OF Trauma Indicator test as well as other serum bio-
CONCUSSION markers in the diagnosis of concussion in those
Immediately following concussive injury, patients without abnormal imaging findings is unclear and
may suffer from confusion, amnesia, or even loss of a topic of ongoing research [12].
consciousness. In the days to weeks following con-
cussion, the prevalence of signs and symptoms of PATHOPHYSIOLOGY OF ACUTE
concussion are summarized in Table 1 [4,5]. Typi- CONCUSSION
cally, most manifestations resolve within 1 week but
may persist longer in those with more severe injury During acute concussion, injury to the brain can
or in those with a prior history of head injury [6]. occur as a result of the brain forcefully contacting
Many screening tests for concussion are avail- the inner calvarium as well as due to stretching of
able that rely on a combination Glasgow Coma inelastic axons. Immediately following injury, there
Score, presence of classic signs and symptoms, is a significant increase in cerebral metabolic rate
and ability to perform executive functions [7]. that may account for alterations in mental status
Electroencephalographic slowing, with increases and level of consciousness [13]. In the minutes to
in theta and delta power, can occur following hours after concussion, the brain enters a hypome-
tabolic state that occurs in the setting of increased
cerebral blood flow that may last for days to weeks
Table 1. Prevalence of symptoms in athletes with recent [14–16]. This excess in cerebral perfusion may
concussion account for typical clinical manifestations. Stephens
et al. [15] showed that patients with persistent clini-
Symptom Prevalence of symptoms (%) cal manifestations at 6 weeks following injury had a
Headache 93 tendency to have increased cerebral blood flow
Unsteadiness 75
compared with those without manifestations as
illustrated in Fig. 1. However, there are no reliable
Difficulty concentrating 67
data to indicate that the resolution of clinical man-
Confusion 46
ifestations following concussion is associated with
Sensitivity to light 38
normalization of cerebral blood flow or metabolism.
Nausea 29 &&
Churchill et al. [17 ] also found an increase in
Drowsiness 27 cerebral blood flow in the periconcussion period
Amnesia 24 but reduced cerebral blood flow 1 year after athletes
Sensitivity to noise 19 returned to sport.
Tinnitus 11 The ability of the brain to autoregulate blood
Irritability 9 flow may be impaired following acute concussion.
Hyperexcitability 2 Vavilala et al. [18] showed that, despite a normal
Glasgow Coma Score, five of six individuals less than
Adapted with permission [5]. 18 years of age had impaired autoregulation or frank

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1.30
P=0.058
Left Dorsal ACC Relative CBF (mL/100g/min)
1.10
1.10
1.00
0.90
0.80
Physical Symptoms
Present
FIGURE 1. Regional cerebral blood flow in the left dorsal
anterior cingulate cortex at approximately 6 weeks following
concussion (white boxes) stratified based on the presence or
absence of symptoms. Controls were similar patients without
concussion. Adapted from [15] with permission.
autoregulatory failure. Moir et al. [19] also found
attenuation of autoregulation soon after concussion
that may be persistent for more than 12 weeks
despite resolution of clinical manifestations.
Responsiveness of the cerebral vasculature to hyper-
capnia may also be impaired following concussion
with both hyporesponsiveness and hyperrespon-
siveness being described [20,21]. This discrepancy
may be due to multiple factors including differences
in timing of testing following injury and differences
in injury severity. Using functional MRI, Jantzen
et al. [22] measured changes in regional cerebral
blood flow that accompany performance of cogni-
tive tasks. Despite no difference in the ability to
perform complex tasks, those with recent concus-
sion had exaggerated increases in regional cerebral
blood flow compared with those without concus-
sion.
Microstructural changes can also occur follow-
ing concussion. The directionality of water move-
ment within the brain, specifically within axonal
tracts, can be measured with diffusion tensor MRI.
Following concussion, the direction of axonal water
flow becomes less unidirectional, manifested by
decreased fractional anisotropy and increased radial
diffusivity – indicating loss of integrity of axonal
membranes. This may be due in part to stretching of
axons during the concussion event when the brain
moves quickly within the calvarium [23]. These
changes can be detected soon after injury and can
last for at least weeks to months, especially in those
with persistent clinical manifestations [24–26].
Collectively, the physiological and microstruc-
tural changes in the brain that accompany
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Anesthesia and the brain after concussion Pasternak and Abcejo
concussion may persist despite resolution of clinical
P=0.002
signs and symptoms. Thus, the absence of clinical
P=0.679 manifestations may not be a reliable indicator that
physiological and microstructural changes of the
brain have also resolved. The changes in the brain
that follow concussion may potentially increase
vulnerability of the brain to insults such as changes
in systemic blood pressure (BP).
REPEATED CONCUSSION
Chronic traumatic encephalopathy (CTE) is a neuro-
degenerative disorder that occurs in individuals who
Physical Symptoms Controls
have sustained multiple concussions. CTE is associ-
Absent ated with significant micropathologic changes first
described in the brains of two American football
players [27,28]. Significant findings included wide-
spread deposition of both b-amyloid protein and
neurofibrillary tangles comprised of hyperphos-
phorylated tau protein. These pathologic findings
are also described in those with Alzheimer’s demen-
tia. Grossly, there is significant brain atrophy. The
diagnosis of CTE can currently be only made at
autopsy. However, it can be suspected in those with
a history of multiple concussions who exhibit vari-
ous signs and symptoms including problems with
memory, performance of executive functions, and
psychiatric changes such as changes in behavior
and depression.
The Concussion Legacy Foundation has
founded a Global Brain Bank for the study of
CTE [29]. Mez et al. [30] reported data from next
of kin and neuropathological findings from 202
brains donated to the Global Brain Bank by Amer-
ican football players. CTE was identified based on
the presence of deposits of hyperphosphorylated
tau protein and was identified in 21%, 91%, and
99% of brains donated from individuals who
played American football only though high
school, only through college, and as a profession,
respectively. The authors stratified the severity of
CTE based on the amount of deposition of hyper-
phosphorylated tau. Those with mild CTE had
isolated epicenters of deposition, whereas those
with severe CTE had more widespread deposition.
Increased severity of CTE was associated with
increased deposition of b – amyloid protein and
insoluble deposits of a-synuclein, the protein that
comprises Lewy bodies. The cerebellum is often
less affected than supratentorial regions of the
brain. A comparison of patient characteristics
among those with mild versus severe CTE is pro-
vided in Table 2. Although cognitive changes,
behavior, and mood problems, and substance
abuse were common in both groups, dementia
and motor manifestations such as ataxia,
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Neuroanesthesia
Table 2. Characteristic of subjects who played American football stratified by the severity of chronic traumatic
encephalopathy
Median age at death (IQR)
Most common cause of death
Sport duration
Cognitive symptoms
Behavior and mood problems
History of substance abuse
Dementia
Motor disorders
CTE, chronic traumatic encephalopathy; IQR, interquartile range. Adapted from [27].
discoordination, and tremor, were more common
in those with severe CTE. There are currently
significant efforts being made to identify findings
on brain imaging that can be used to diagnose CTE
&
in the living patient [31 ]. On the contrary, there
is a paucity of data describing cerebral hemody-
namic changes associated with CTE.
CONCUSSION IN THE PERIPROCEDURAL
PERIOD
As described earlier, the normal homeostasis and
physiology of the brain are disrupted following
concussion. Head trauma rarely occurs in isolation
and patients may have concurrent bone fractures,
spinal cord injury, intrathoracic, and intra-abdomi-
nal injuries that can lead to blood loss, hypovole-
mia, hypotension, and shock impairing perfusion
and oxygen delivery to the brain and other vital
organs. Hypoxia resulting from pulmonary contu-
sion or aspiration as well as hyperglycemia second-
ary to trauma-related sympathetic nervous system
activation can be a source of secondary injury to a
vulnerable brain [32,33].
Cardiophysiologic disturbances, such as auto-
nomic dysfunction and cardiovascular instability,
have been well described after severe traumatic
&
brain injury [34 ,35,36]. Cardiovascular and auto-
nomic dysfunction can has been recently described
in patients following concussion often manifest as
altered heart rate variability [37,38]. These cardio-
vascular changes, occurring simultaneously with
changes in cerebrovascular physiology, may hasten
cognitive recovery following concussion [39 ].
Surgery and anesthesia are also associated with
disruptions of systemic homeostasis that could
potentially adversely impact a vulnerable brain.
These include but are not limited to changes in
systemic BP, arterial tensions of oxygen and carbon
dioxide, activation of the inflammatory cascade,
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Mild CTE Severe CTE
44 years (29–64 years) 71 years (64–79 years)
Suicide Neurodegenerative diseases
Mostly high school and college Mostly college and professional
85% 95%
96% 89%
67% 49%
33% 85%
48% 75%
and effects of various drugs used in the perioperative
period on cerebral physiology. Thus, given the
changes in brain physiology that occur following
concussion, the concussed brain may be vulnerable
to secondary injury from changes in systemic phys-
iology that occur in the perioperative period.
Abcejo et al. [40] retrospectively quantified uti-
lization of anesthesia in patients with concussion at
a single institution. During a 10-year period, of 7699
patients identified with concussion, 1038 (13.8%)
received at least one general or regional anesthetic
or monitored anesthesia care to facilitate a surgical
or diagnostic procedure within 1 year of injury.
Demographics and tabulation of anesthetic cases
are stratified by injury type and summarized in
Table 3. Most concussions were due to motor vehicle
accidents and falls. Patients with sport-related inju-
ries were younger, and those who sustained a con-
cussion due to a fall were older than those who
sustained a motor vehicle accident or assault. Most
sports-related concussions were evaluated in the
outpatient setting, those due to assaults and falls
were most often evaluated and dismissed from the
emergency room, and those due to motor vehicle
accidents are often admitted from the emergency
room. Collectively, 93% of patients had a formal
diagnosis of concussion documented within 1 week
of injury. However, the time of greatest need for
anesthesia services is soon after injury with 30% and
45% of all anesthetics occurring within 1 week and
1 month of injury respectively, a time when cerebral
homeostasis is most disrupted. Motor vehicle acci-
dents account for the greatest utilization of anesthe-
&&
sia per patient (2.4 anesthetics per year per patient).
The fraction of patients receiving anesthesia for
unrelated procedures within 1 year of injury ranged
from 20 to 80% in those with concussions due to
motor vehicle accidents and sports injuries, respec-
tively. Twenty-nine of 554 (5.2%) anesthetics
administered within 1 week of injury were to
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 Anesthesia and the brain after concussion Pasternak and Abcejo

Table 3. Characteristic of patients who required anesthesia within 1 year of concussion stratified by injury type

Motor vehicle accident Sports injury Fall Assault

Number of patients 375 209 367 87

Age (years), mean  SD 39  21 20  14 50  24 36  20
Male sex, n (%) 236 (63%) 141 (67%) 176 (48%) 56 (64%)
Disposition, n (%)
Outpatient clinic, n (%) 18 (5%) 91 (44%) 64 (17%) 13 (15%)
Dismissed from ER, n (%) 33 (9%) 86 (41%) 178 (49%) 49 (56%)
Admitted from ER, n (%) 324 (86%) 32 (15%) 125 (34%) 25 (29%)
Diagnosis within 1 week of injury, n (%) 349 (93%) 194 (93%) 341 (93%) 81 (93%)
No. of anesthetics within 1 year of concussion 892 244 571 113
Anesthetics for procedures unrelated to injury, n (%) 182 (20%) 194 (80%) 428 (75%) 70 (62%)

ER, emergency room. Adapted from [37].

facilitate procedures that were deemed elective and
unrelated to the injury that resulted in concussion.
Taken collectively, patients who sustained a concus-
sion frequently require anesthesia to facilitate pro-
cedures that may or may not be related to their
injury, they may not have a formal diagnosis of
concussion at the time of their procedure, and the
greatest utilization of anesthesia occurs soon follow-
ing concussion injury.
Currently, it is unclear how long elective proce-
dures requiring anesthesia should be delayed follow-
ing concussion injury. As noted earlier, resolution of
clinical manifestations may not reliably indicate
normalization of cerebral physiology. There are also
currently no data (ND) to support whether or not
abnormalities in the brain following concussion
lead to increased risk for adverse outcomes in those
requiring anesthesia soon following concussion.
&
D’Souza et al. [41 ] retrospectively matched 60
patients requiring anesthesia within 90 days of
injury with 178 similar patients who also required
anesthesia for similar procedures but did not sustain
concussion. There were no differences in physio-
logic variables either during surgery or in the post-
anesthesia recovery room between groups. On
univariate analysis those with concussion having
anesthesia within 30 day of injury had significantly
higher rates of visual analog pain scores at least 7 out
of 10 in the postanesthesia recovery room (21%) and
higher rates of complaints of headaches within
90 days of anesthesia (24%) versus those without
concussion [15% (P ¼ 0.02) and 7% (P ¼ 0.01) for
pain score at least 7 and headache within 90 days,
respectfully]. Also on univariate analysis, those with
concussion having anesthesia between 31 and
60 days following injury had lower mean Richmond
Agitation-Sedation Scale score in the recovery room
(1.61  1.29) compared with those without
concussion (0.2  0.45; P ¼ 0.002) indicated
greater sedation in those with concussion. However,
when corrected for potential confounders and for
multiple comparisons, no significant differences
between groups were identified. These findings do
not necessarily support the notion that there is no
need to delay elective anesthetics following concus-
sion as this small retrospective study may have had
limited power and precision to identify differences.
We may require investigation of other outcome
variables, such as cognitive skills, that are assessed
prospectively.
Currently, there are no standard guidelines spe-
cific to the management of patients with concus-
sion in the periprocedural period. With the current
available data, the following points are worth con-
sidering:
(1) Anesthesia personnel should suspect concus-
sion in any patient who recently sustained a
traumatic injury.
(2) Resolution of clinical manifestations of concus-
sion do not reliably indicate a normalization of
cerebral pathophysiology.
(3) As of now, there are ND to guide delay of elec-
tive procedures but delay of completely elective
procedures until resolution of clinical manifes-
tations seems reasonable.
(4) Those who have likely sustained multiple con-
cussions (i.e., American football players,
boxers), may represent a group of patients with
a vulnerable brain in the perianesthetic period.
(5) Although the Brain Trauma Foundation Guide-
lines [42] are not specific to the care of patients
with concussion, anesthesia personnel should
be familiar with these guidelines and may be
helpful to guide periprocedural management of
patients with concussion:

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Neuroanesthesia
(a) Avoidance of unnecessary hyperventila-
tion.
(b) Maintaining SBP more than 100 mmHg in
patients 50–69 years old and more than
110 mmHg in those less than 50 and more
than 69 years old.
(c) Minimizing hypoxia (PaO2 < 90 mmHg and
SaO2 < 90%).
(d) Avoiding the unnecessary use of corticoste-
roids.
CONCLUSION
Concussion results in disruption of normal cerebral
physiology and axonal microstructure. Repeated
concussion can result in CTE that is associated with
cerebral atrophy and pathologic changes similar to
those encountered in other forms of organic demen-
tia. Changes in the brain following both acute and
chronic repeated concussion may make the brain
vulnerable to secondary injuries as may be encoun-
tered in the periprocedural period. Further research
is needed to better understand the risks of anesthesia
in the concussed brain and to determine how risk
can be minimized in the patient with concussion
who require anesthesia to facilitate surgical and
diagnostic procedures.
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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