Traumatic Brain Injury Flashcards
(121 cards)
1
Q
What is the leading cause of
morbidity and mortality in
Americans between 1 and 45
years of age?
A
TBI
2
Q
According to the Traumatic
Coma Data Bank (TCDB) what is
the outcome for severe TBI?
A
- Death: 30 to 36%
- Persistent vegetative state: <5%
- Severe disability: 15%
- Moderate disability: 14 to 20%
- Good outcome: 25%
3
Q
What are the three components
of the Glasgow Coma Scale
(GCS)?
A
- Eyes (scores of 1–4)
- Motor (scores of 1–6)
- Verbal (scores of 1–5)
4
Q
Categorize the head trauma
severity based on the GCS.
A
Mild: GCS 14 or GCS 15 and LOC and impaired alertness or memory Moderate: GCS 9–13 Severe: GCS 5–8 Critical: GCS 3–4
5
Q
What are the two main reasons
for the increase in brain injuries
in the elderly?
A
- The growing ranks of the elderly.
- The concurrent growth in the number of elderly
patients taking anticoagulation or antiplatelet
drugs.
6
Q
What are the two types of forces
in brain injury?
A
Contact: produces focal injuries (fractures,
contusions, hematomas)
Inertial: the brain undergoes acceleration and
deceleration (translational, rotational, or both),
which can occur without head impact:
• Translational: leads to focal injuries
• Rotational: common with high-speed motor
vehicle accidents, causes diff use injuries
7
Q
What is concussion?
A
A mild TBI, with or without LOC.
Alteration of consciousness as a result of closed
head injury.
Negative fi nding on computed tomography (CT).
8
Q
Is there evidence of microscopic
changes in concussion?
A
No, but there is a transient disturbance in
neuronal function. Levels of glutamate increase
and the brain enters a hyperglycolytic/
hypermetabolic state up to 7 to 10 days after
injury.
9
Q
What is a cerebral contusion?
A
Intraparenchymal lesion due to closed head injury,
aka hemorrhagic contusion
10
Q
Where are the most common
locations for cerebral contusion?
A
Areas where sudden head deceleration causes the
brain to impact on bony prominences (inferior
frontal cortex and anterior temporal lobe)
11
Q
What is a contrecoup injury?
A
After TBI, the force imparted to the head may cause
the brain to be thrust against the skull directly
opposite the blow.
12
Q
What is DAI?
A
Diffuse axonal injury.
• Result from the disparate densities of the gray and
white matter and the consequent diff erence in
centripetal force associated with a rotational
vector of injury
• Most often occurs in high-speed motor vehicle
accident
• Present in 50% of all severe TBIs
13
Q
What lesions can be seen in
DAI?
A
Hemorrhagic lesions seen most frequently in corpus
callosum and dorsolateral rostral brainstem
14
Q
What are the microscopic
fi ndings in DAI?
A
Under microscope, axonal retraction balls, microglial
stars, and degeneration of white matter fi ber
tracts can be seen.
Fragmentation of axons and axonal swelling
appear 24 to 48 hours after trauma.
15
Q
What is important about the
development of DAI?
A
Axotomy may not be complete immediately after
trauma.
16
Q
Explain secondary axotomy.
A
Secondary axotomy begins with an impairment of
axoplasmic transport, cytoskeletal collapse, and
secondary disconnection
17
Q
What are the three levels of
severity of DAI?
A
• Mild DAI: coma of 6- to 24-hour duration
• Moderate DAI: coma of more than 24 hours
without decerebrate posturing
• Severe DAI: coma of more than 24 hours with
decerebrate posturing and fl accidity
18
Q
What is the mortality of severe
DAI?
A
50%
19
Q
What would you include in the initial general physical exam in the ER in addition to the neurological exam (neuro-oriented assessment)?
A
Evidence of basal skull fracture: • Raccoon’s eyes: periorbital ecchymoses • Battle’s sign: postauricular ecchymoses • CSF rhinorrhea/otorrhea • Check for facial fractures • Physical signs of spine trauma
20
Q
And what would you include in
your neuro exam (focused and
concise)?
A
• Level of consciousness (on the GCS)
• Pupils (size and reaction)
• Motor exam: (1) if patient cooperative, check
motor strength in all four extremities; (2) if not,
check for movement of all four extremities
• Sensation exam: (1) if patient cooperative, check
pinprick and touch in major dermatomes; (2) if
not, check for central response to noxious stimulus
• Brainstem refl exes: evaluate corneal, gag, and
cough refl exes, and if the patient is breathing over
ventilator.
• Muscle stretch refl exes
• Anal sphincter tone and Babinski reflex
• Gait and coordination if conscious and cooperative
21
Q
What is the GCS in a patient who, after TBI, is intubated, localizing to pain on the right side, and opens eyes to pain stimuli?
A
GCS: 8T = M:5, E:2, V:1T
22
Q
What is delayed deterioration?
Describe its possible etiologies.
A
Referred as “talk and deterioration” or “talk and die,” seen in 15% of patients who do not initially exhibit signs or symptoms4,5 Possible etiologies: • 75% exhibit intracranial hematoma • Diff use cerebral edema • Hydrocephalus • Tension pneumocephalus • Seizures • Vascular events (dural sinus thrombosis, major artery dissection, SAH, embolism) • Meningitis
23
Q
What is the minimum radiographic
evaluation needed in
TBI?
A
Noncontrast CT of head and cervical x-ray series
24
Q
Which TBI patients get a CT?
A
GCS <14, unresponsiveness, depressed level of
consciousness, focal defi cit, amnesia for injury,
altered mental status, seizures, and those with
physical fi ndings with moderate risk for intracranial
injury.
25
Who is at moderate risk for
| intracranial injury?
* Loss of consciousness (LOC)
* Progressive headache (HA)
* Alcohol (ETOH) or drug intoxication
* Age <2 years or suspected child abuse
* Unreliable history
* Signs of basal or calvarial skull fractures
* Serious facial injury
* Signifi cant subgaleal swelling
26
What is the most common type
| of skull fracture?
Linear fractures typically over the lateral convexities
27
What are the criteria to elevate
(surgically) depressed skull
fracture?
```
• >8–10 mm depression (or greater than thickness
of skull)
• Defi cit related to underlying brain
• CSF leak
• Compound fracture (open)
• Cosmetic region
```
28
What is the exception for
repairing a depressed skull
fracture that meets the above
criteria?
Depressed skull fracture overlying and depressing
one of the dural sinuses
Alternative: craniotomy technique with proximal
and distal venous control
29
What is the best radiographic
study to diagnose a basal skull
fracture?
CT with thin cuts and coronal images
30
What is the most common
location for basilar skull
fractures?
Anterior skull base, often involves the cribriform
| plate, disrupting the olfactory nerve
31
What structures can be damage
in posterior basilar skull
fracture?
Posterior basilar skull fractures may extend through
petrous bone and internal auditory canal damaging
cranial nerves VII and VIII.
32
Which basal skull fractures may
| require specifi c management?
• Persistent CSF rhinorrhea
• When fracture extends into air sinuses and is
causing meningitis or brain abscess (may occur
years after)
• Cosmetic deformities
• Optic nerve or extraocular muscle entrapment
33
What are the types of temporal
| bone fractures?
Longitudinal fracture and transverse fracture
34
What is the most common type
| of temporal bone fracture?
Longitudinal fracture (70–90%): through petrosquamosal
suture, usually passes between cochlea
and semicircular canals, sparing VII and VIII, but
may disrupt ossicular chain
35
Why does a transverse fracture
of the temporal bone have the
worst prognosis?
```
Transverse fracture: perpendicular to external
auditory canal (EAC) through cochlea and stretch
on geniculate ganglion, damaging VII and VIII
```
36
Why does a transverse fracture
of the temporal bone have the
worst prognosis?
```
Transverse fracture: perpendicular to external
auditory canal (EAC) through cochlea and stretch
on geniculate ganglion, damaging VII and VIII
```
37
Are steroids indicated for
| posttraumatic facial palsy?
Often utilized but effi cacy unproven. If patient is not
improving, then surgical repair may be indicated,
but it is not done emergently (40 to 75% will
recover).
38
Do all frontal sinus fractures
| need to be repaired?
No, only fractures that disrupt the posterior wall
with nasofrontal outfl ow obstructions require
surgical repair to prevent intracranial infections.
39
What is a Ping-Pong ball
| fracture?
Caving in of a focal area of the skull, seen only in the
| newborn
40
What is the treatment for a
| Ping-Pong ball fracture?
• Observation
• Repair only if the fracture is on the frontal area
for cosmesis purposes
41
What is a growing skull
| fracture?
It is a fracture line that widens with time, usually
asymptomatic. Requires widely separated fracture
and dural tear; 90% occur in patients before age
3 years
42
What is the other name for
| growing skull fracture?
Posttraumatic leptomeningeal cyst
43
What is the most common
| fi nding in CT after TBI?
Subarachnoid hemorrhage, which may be associated
| with an increased risk of posttraumatic vasospasm
44
What is the strongest predictor
for enlargement of hemorrhagic
contusion?
The presence of traumatic SAH on CT. The second
important predictors are the size of the contusion
and the presence of SDH.
45
What are the indications for
surgical management in
traumatic intracerebral
lesions?
• Signs of progressive neurological deterioration,
medically refractory intracranial hypertension,
or signs of mass eff ect on CT
• GCS score of 6 to 8 with frontal or temporal
contusions >20 cm3 with midline shift >5 mm
and/or cisternal compression
• Any lesion >50 cm3
46
```
What are the treatment options
for patients with refractory
intracranial hypertension
(IC-HTN) and diff use parenchymal
injury for impeding
transtentorial herniation?
```
Decompressive procedures:
• Subtemporal decompression
• Temporal lobectomy
• Hemispheric decompressive craniectomy
47
Bifrontal decompressive
craniectomy is a treatment
option in which scenario?
Patients with diffuse, medically refractory
| posttraumatic cerebral edema and IC-HTN
48
What are the factors that
determine outcome in intracerebral
hematomas?
* GCS score
* Hematoma volume
* Occurrence of hypoxia
49
What is a Duret’s hemorrhage?
Hemorrhage into the base of the pons or midbrain,
result from disruption of the perforating arteries at
the time of uncal herniation; high morbidity and
mortality
50
What is DTICH?
Delayed traumatic intracerebral hemorrhage12
• Incidence of 1 to 8% in patients with severe TBI
• Occurs most frequently within 72 hours of the
trauma in the frontotemporal region as a
“countercoup” from parietoccipital trauma.13
• Contributing factors are coagulopathy, hemorrhage
into an area of necrotic brain, and loss of
tamponade eff ect after evacuation of extraaxial
hematomas.
• Risk factors: diabetes, alcohol use, and advanced
age13
• Mortality 50% or higher in most series13
51
In which population is it rare to
| see epidural hematomas (EDH)?
Before 2 years of age and after age 60; dura is more
| adherent to the inner table in this group
52
Is the source of bleeding of the
| EDH always arterial?
No; 85% arterial bleeding (middle meningeal
artery), and the remainder from bleeding from
the middle meningeal vein and dural sinus
53
What is the most common
| location of EDH?
75% laterally over the hemisphere with the
epicenter at the pterion. The rest in the frontal,
occipital, and posterior fossae.
54
What is Kernohan’s
| phenomenon?
Shift of the brainstem away from a mass (due to
mass eff ect), which may compress the opposite
cerebral peduncle on the tentorial edge, causing
hemiparesis ipsilateral to the side of the mass lesion
(which is a false localizing sign)
55
What is the classic CT appearance
| of EDH?
85% of EDHs are hyperdense biconvex (lenticular)
adjacent to skull; in 10% the side against the skull is
convex and the side along the brain is straight; in 5%
it is crescent shaped.
56
What are the indications for
| surgical evacuation of an EDH?
• Any symptomatic EDH
• Asymptomatic but >1 cm in its thickest measurement
(diffi cult for the brain to reabsorb)
• In pediatrics, threshold for surgery should be very
low
57
What are the risk factors of a
| delayed EDH?
• Lowering ICP medically or surgically (evacuating
contralateral hematoma)
• Coagulopathies
• Rapidly correcting shock
58
What is important about
| posterior fossa EDH?
85% have an occipital fracture, most commonly
from a dural sinus tear, and surgeon should have
low threshold for surgical evacuation.
59
What is important about
hematomas that compress the
temporal lobe?
They can rapidly cause uncal herniation with
minimal enlargement and with no elevation in ICP.
Surgeon must have a low threshold for evacuation.
60
Why is a subdural hematoma
| (SDH) more lethal than an EDH?
The magnitude of impact damage is much higher;
there is always associated injury to underlying brain
parenchyma and cerebral edema.
61
How often is an underlying
cerebral contusion seen in
SDH?
Up to 67% of patients with SDH have an underlying
| contusion.
62
What are the biochemical
fi ndings on the brain tissue
underlying an evacuated SDH,
and what do they indicate?
The biochemical pattern of increased lactate and
pyruvate and decreased partial pressure of
oxygen in brain tissue (PbtO2) may indicate
evolving injury in the brain tissue that was
previously compressed by the SDH.
63
What is the classic CT appearance
| of acute SDH?
Hyperdense crescentic mass of increased attenuation
adjacent to inner table; usually on convexity
but may be interhemispheric, along tentorium, or in
posterior fossa
64
Why can acute SDH be hypodense
| on CT?
Because of the low hemoglobin content, seen in up
| to 10%
65
What is diff erent between SDH
| and EDH on CT
SDH is more diffuse, concave over brain surface, and
| often less dense (mixed with CSF)
66
What are the indications for
| surgery in SDH?
• Any symptomatic SDH
• SDH greater than 1 cm at the thickest point (5 mm
in pediatrics) with >5 mm of midline shift
67
What is the mortality of
patients with surgically
evacuated acute subdural
hematomas?
• 40 to 60% depending on the series19,20; if initial
GCS score is 3, mortality approaches 100%.
• Functional recovery occurs in approximately 38%.
68
What factors may increase
hospital mortality following
traumatic SDH in the elderly?
* Initial GCS ≤7
* Age >80
* Acute subdural hematoma
* Patient who required craniotomy
69
What actions may improve
outcome in traumatic subdural
hematoma?
• Early management of ICP
• Early surgical evacuation in those patients who
meet criteria
70
What are the CT fi ndings
| predictive of outcome?
• Hematoma thickness
• Midline shift
• Presence of underlying brain swelling or
contusion
71
Is the source of bleeding of the
| SDH always venous?
No, SDH can result from arterial ruptures (usually
| cortical arteries).
72
How can we diff erentiate an
SDH resulting from arterial
rupture from those resulting
from venous rupture?
SDH resulting from arterial rupture are generally
located in the temporoparietal region, and those
caused by bridging vein rupture are in the
frontoparietal parasagittal region.
73
Is the shape of the hematoma
the same between arterial and
venous SDH?
No, venous SDH tends to have a homogeneous
width, whereas arterial SDH tends to have a more
pronounced thickening in the middle third.
74
What is the positive displacement
| factor?
When the midline shift exceeds the hematoma
thickness; the prognosis has been found to be
poorer. Also termed shift out of proportion.
75
What is the definition of “early”
| vs. “late” surgery?
* Early: within 4 hours of injury
| * Late: after 4 hours of injury
76
What are the advantages of large
craniotomy for acute SDH
(ASDH)?
• Gain access to potential sources of bleeding:
• Large draining veins close to superior sagittal
sinus
• Contused tissue in the subtemporal and
sub frontal areas and temporal and frontal poles
77
What is the exception to the
general practice of using large
fl aps for ASDH?
In coagulopathic patients with relatively focal
| subdural hematomas
78
During opening, brisk epidural
bleeding may be encountered.
What options does the surgeon
have to achieve hemostasis?
• Place numerous, closely spaced epidural tack-up
sutures
• Place small amount of absorbable hemostasis
agent (Gelfoam or Surgicel)
79
What are the advantages of
opening the dura in a cruciate
fashion?
• Evacuation of the clot from all four quadrants
• If the brain begins to swell and the intradural
bleeding has stopped, dura can be closed quickly.
80
Why should the dura be open in
a slow, controlled manner,
according to experienced
neurotraumatologists?
Because it enables a more gradual reduction of
the pressure on the cerebral cortex, reducing the
likelihood of sudden, massive herniation of brain
through the craniotomy opening
81
What is the eff ectiveness of
| decompressive craniectomy?
• Decompressive craniotomy eff ectively reduces ICP
in most (85%) patients with refractory IC HTN.
• Brain oxygenation measured by tissue PO2 and
blood fl ow improve with decompressive
craniotomy.
• There are no results from randomized control
trials (RCTs).
• Rescue ICP and DEcompressive CRAniectomy
(DECRA) are two ongoing RCTs.
82
Why is important to have the
head as parallel to the fl oor as
possible during decompressive
craniectomy?
Because it allows access to the posterior and inferior
regions of the cranial vault, which are often not well
decompressed even by a standard large fl ap
83
What is the goal of taking the
decompression to the fl oor of
the temporal fossa during
decompressive craniectomy?
To achieve optimal decompression of the perimesencephalic
| cisterns
84
What are the disadvantages of
small craniectomies or dural
openings?
Herniation of swollen brain tissue through causing
| strangulation, infarction, additional brain swelling
85
What surgical technique can be
used to enlarge a previous
craniotomy into a large
decompressive craniotomy?
T-incision technique: Begin at the posterosuperior
part of the existing incision and curve gently
toward the inion; the scalp on the two sides can be
refl ected and bone can be removed as a separate
piece.
86
When is the ideal time to make
preparations for subsequent
replacement of the bone fl ap?
During the closing of the decompressive craniotomy,
with the placement of another sheet of dural
substitute to prevent adhesions between dura and
scalp
87
When should a bone fl ap be
| replaced?
• ASAP
• The determining factor is the cerebral edema
(may require weeks).
• Usually 4 to 6 weeks after the initial craniectomy
88
What are potential problems
occurring after decompressive
craniectomy?
• Postoperative EDH and subgaleal hematomas
• Fluid accumulation remote from the craniotomy
site
• Brain injury at the edges of the craniotomy
• Lack of brain protection
• Impairment of cerebral metabolism from lack of
overlying cranium (syndrome of the trephined)
• Hydrocephalus
89
What is the RESCUEicp trial?
Randomized Evaluation of Surgery with Craniectomy
for Uncontrolled Elevation of IntraCranial
Pressure, the only prospected randomized study (to
date) that is evaluating the effi cacy of decompressive
craniectomy for refractory intracranial
hypertension
90
What are the risk factors for
chronic subdural hematomas
(CSDH)?
Elderly, alcoholism, seizures, CSF shunt,
| coagulopathies, and patient at risk for falls
91
What is the pathophysiology of
| CSDH?
Most cases start out as an acute SDH evoking an
infl ammatory response, fi broblasts invade the clot,
membranes are formed on the inner (brain) and
outer (dura) surfaces, followed by growth of
neocapillaries and liquefaction of blood.
92
How long does it take for the
| membrane to form?
3 weeks following initial presence of the blood
93
How does CSDH present?
Patients may deny history of trauma, which often is
mild and often not remembered. Pseudodementia,
gait ataxia, focal weakness, headaches, and strokelike
symptoms are some of the most frequent
forms of presentation; less frequently seizure or
meningismus.
94
What is the management of
| CSDH?
In patients with coagulation anomalies or medicated
with aspirin, clopidogrel, warfarin, or similar
medication, reversal of anticoagulation with
vitamin K and fresh frozen plasma is paramount.
Surgery should be performed on symptomatic
lesions or CSH with maximum thickness >1 cm
with >5 mm of midline shift.
95
What is important to remember
about chronic subdural
hematomas?
• Its frequent recurrence
• The lack of consensus regarding surgical techniques,
perioperative management, and medical
approach to nonsurgical cases
96
What are the surgical options
| for CSDH?
• Two burr holes and irrigating through and through
• Single large burr hole with irrigation and
aspiration
• Single large burr hole drainage and placement of a
subdural drain
• Twist drill craniostomy
• Formal craniotomy with membranectomy; DO
NOT attempt to remove the deep membrane
adherent to the pia.
97
What else can be done to
promote continued drainage of
CSDH?
• Use closed-system drainage.
• Keep the patient on bedrest with head of bed
(HOB) fl at (for 24 hours, according to most
authors).
98
What are some of the risks that
| augment the recurrence rate?
• Advanced age
• Bilateral SDHs with poor reexpansion
• Postoperative air accumulation
• Alcohol use
• Bleeding tendency
• Diabetes (due to increased blood viscosity,
osmotic pressure, and platelet aggregation)
99
List the technical pearls to
| prevent recurrence in CSDH.
• Use copious irrigation.
• Use closed-system drainage.
• Use bipolar coagulation of the edge of the dura
and subdural membrane back to the full width of
the bony opening.
• Place a piece of Gelfoam over the opening to help
prevent fl esh blood oozing into the opening.
• Use the suggested postoperative posture: recent
studies indicate that the supine position may
decrease recurrence.
100
What is a subdural drain?
• A ventriculostomy-type catheter placed underneath
the dura, connected to a closed system. The
draining bag is maintained 60 to 80 cm below the
level of the head.
• During the operation such a catheter may be used
for cross-irrigation between holes when two burr
holes are used.
101
Which patients have a better
| outcome with CSDH?
Patients who have high subdural fl uid pressure tend
to have more rapid brain expansion and clinical
improvement.
102
Is clinical improvement only
achieved if the CT shows
resolution of the CSDH?
Clinical improvement does not require complete
resolution of the fl uid collection on CT. DO NOT treat
persistent fl uid collection based only on CT.
103
What are some of the complications
of surgical treatment of
the CSDH?
* Need for recurrent surgical intervention
* Seizures
* Intracerebral hemorrhage
* Failure of the brain to reexpand
* Tension pneumocephalus
* Wound infection or subdural empyema
* CSF leak
104
What can be done to treat a
persistent recurrent chronic
subdural hematoma?
• Implantation of an Ommaya reservoir in the sub -
dural cavity29 with subsequent serial aspiration
• Shunting of the subdural space
105
What are the possible etiologies
of a spontaneous subdural
hematoma?
* Vascular abnormalities
* Neoplasm
* Infection (meningitis, tuberculosis)
* Connective tissue disease
* Alcoholism
* Coagulopathies
106
What is a hygroma?
• A collection of CSF in the subdural space
• It may be spontaneous or traumatic in origin. Its
management is similar to the subdural hematoma.
On imaging, the fl uid collection has a density
identical to that of CSF, as opposed to subdural
hematomas.
107
What is the pathogenesis of
| traumatic subdural hygroma?
The pathogenesis likely involves a tear in the
arachnoid membrane, with resultant CSF leakage
into the subdural space. It most commonly occurs
in the sylvian fi ssure and chiasmatic cistern.
It may be under pressure and may increase in
size.
108
What are the main diff erences
between adult and pediatric
head injury?
• Lower chances of surgical lesions
• Better outcome
• Peculiar and age-specifi c injuries (birth injuries,
walker injuries, child abuse, cephalohematoma,
Ping-Pong fracture [discussed earlier])
109
What are the two types of
| cephalohematoma?
Subgaleal and subperiosteal
110
Describe the subgaleal type of
| cephalohematoma.
Bleeding into the soft tissue, between periosteum
and galea, crosses sutures, does not calcify, and
may have signifi cant blood loss.
111
Describe the subperiosteal type
| of cephalohematoma.
It is seen in newborns; hematoma may elevate
periosteum, does not cross sutures, scalp moves
freely over the mass, 80% reabsorb by themselves,
and may calcify.
112
What is the treatment for
| cephalohematoma?
• Avoid the temptation of percutaneous aspiration.
• Follow hemoglobin and hematocrit.
• If calcifi ed, surgery is performed for cosmetic
reasons, but typically normal contour returns in
3 to 6 months.
113
What are some of the factors
that raise the index of suspicion
for child abuse?
• Retinal hemorrhage
• Bilateral CSDH in children <2 years of age
• Multiple skull fractures
• Signifi cant neurological injury with minimal signs
of external injury
• Rib fractures and pulmonary contusions
114
What are some of the late
| complications of head injury?
* Posttraumatic seizures
* Communicating hydrocephalus (4%)
* Posttraumatic (postconcussive) syndrome
* Hypogonadotropic hypogonadism
115
How does posttraumatic
hydrocephalus (PTH) typically
present?
* Failure to thrive
* Headaches in the awake patient
* Behavioral changes
116
What is the incidence of
| symptomatic PTH?
• 10 to 40% following decompressive craniectomy31
• 0.7 to 30% overall; incidence of asymptomatic
ventriculomegally is higher
117
What are the advantages of
programmable valves for these
patients?
The valve setting can be increased to a higher
pressure 2 days prior to a cranioplasty operation if
the fl ap is signifi cantly sunken, to better defi ne the
anatomical planes and avoid postoperative dead
space.
118
Defi ne postconcussion
| syndrome.
Cluster of symptoms (organic and/or psychological):
• Headache, dizziness, visual disturbances, anosmia,
hearing diffi culties
• Diffi culty concentrating, dementia
• Emotional diffi culties, personality changes, loss of
libido, insomnia, intolerance to light and noise
119
What is chronic traumatic
| encephalopathy (CTE)?
Also called dementia pugilistica since it was
described in retired boxers, although it is common
in all contact sports including American football).
It includes:
• Cognitive symptoms: mental and memory defi cits
• Personality changes: explosive behavior, paranoia
• Motor symptoms: cerebellar dysfunction,
Parkinson-like signs and symptoms
120
What are the neuroimaging
| findings of CTE?
• Atrophy
• Increased incidence of anterior cerebral artery
(ACA) circulation aneurysms
121
What are the pathological
| findings of CTE?
* Cerebral and cerebellar atrophy
* Neurofibrillary degeneration
* β-amyloid deposits
