Concussion

Question 1

Mild Traumatic brain injury (TBI)

S/SX

Answer 1

Confusion
Amnesia
Sometimes loss of consciousness
Headache
Dizziness
Nausea/vomiting

Question 2

Mild TBI

Neurologic assessment

Answer 2

• History with as much detail as possible
  Include before and after recollections
• Mental status exam
  Short term memory
  Attention and concentration
• Neurologic exam
  Cranial nerve exam
  Limb strength and reflexes
  Coordination and Gait

Question 3

Pathophysiology of TBI

Answer 3

Axon stretch due to injury
Excitatory neurotransmitters released
K+ efflux and Ca++ influx

This leads to metabolic changes
Hyperglycolysis
Lactate accumulation
Mitocondrial dysfunction/oxidative phosphorylation
Increased energy need/decreased energy production

Globally:
Axonal swelling
Apptosis
Decreased cerebral blood flow
Inflammation

Question 4

Question 5

Concussion Recovery Rate

Answer 5

Brain Metabolism
30 days
Concussive Symptoms
15 days
Ion Imbalance
4 days

Question 6

Second Impact Syndrome

Answer 6

Diffuse cerebral swelling in setting of second concussion
Rare, but can be fatal
May be due to disorder of cerebral autoregulation that causes
Cerebrovascular congestion
Cerebral edema
Increased intracranial pressure

Careful consideration for “return to play”

Question 7

Post Concussion Syndrome

General

Answer 7

Common sequela of TBI
30-80% of patient with mild/moderate TBI will experience some type of symptom
Female and increased age are risk factors

Question 8

Post Concussive Syndrome

S/Sx

Answer 8

Headaches
Tension
Migraine
Other
TMJ, occipital neuralgia, trigeminal nerve injury
Dizziness
Lightheadedness, vertigo
Sleep Disturbances
Insomnia usually
Psychological and cognitive symptoms (50% of patients)
Personality change, irritability, anxiety, depression

Question 9

SKull fracture

most common fracture and causes

Answer 9

Most fractured-> parietal bone, followed by the temporal, occipital, and frontal bones.

Most common fracture-> linear, followed by depressed and basilar skull fractures.

Each year, approximately 2.8 million people suffer head injuries in the US alone.

Most common causes-> Falls, assaults, motor vehicle collisions, penetrating missiles

Question 10

skull fracture

After injury

Answer 10

-You should assume a skull fracture exists in a any patient who has sustained a significant head injury or other major trauma.

-High kinetic injury is needed to cause injury

-Important to maintain immobilization of the cervical and thoracic spine

-A dressing held in place by a circumferential head bandage
is often not sufficient

Question 11

skull fracture

patient arrives to the ER..

Answer 11

Identify and stabilize life threatening injuries

Protect and stabilize airway

Note: bleeding wounds from skull fractures can be profuse. Use Direct pressure for approximately 15 minutes as initial treatment

After stabilization, assess for: altered mental status, focal neurologic deficits, scalp lacerations, bony step-off of the skull, or periorbital or retroauricular ecchymosis.

Do NOT probe scalp wounds…

Question 12

skull fracture

Dx

Answer 12

Non-contrasted CT is the imaging study of choice
There is a specialized study but not much research on it

If there is evidence suggestive of basilar fracture, reasonable to obtain CT angiography to assess for vascular injury
There is little evidence supporting use of CTA for skull fracture. Chat with radiologist to determine next best steps.

MRI is useful if evaluating vascular or ligament injury BUT CT is main choice

No benefit with skull x-rays
If that is the only option depending on practice location, 2 views should be performed

Negative plain radiographs in low risk situation (minor mechanism of injury, normal neuro eval) are reassuring however, they cannot completely rule out injury

Question 13

skull fracture

don’t miss on Dx

Answer 13

You may need to keep looking.. Per Up to Date 5-15% of patients with skull fracture also suffer fracture of cervical spine.

Essential to perform careful assessment for concurrent injuries
In addition to imaging, may need to consider tox screen if altered mental status

Question 14

Types of skull frcatures

Answer 14

Linear

Depressed

Basilar

Question 15

Linear skull frcature

General

Answer 15

A single fracture that often extends through the entire thickness of the skull
Location: most often involving the temporoparietal, frontal, and occipital regions
Fortunately, the majority of linear skull fractures have minimal or no clinical significance

Question 16

linear skull fracture

There is always a catch…..

Answer 16

If the linear fracture crosses the middle meningeal groove in temporal bone or major venous dural sinuses- could cause significant extra axial bleeding (beneath the skull but outside the brain parenchyma.

Question 17

linear skull fracture

Presentation

Answer 17

Presentation- if simple and closed- usually no neurologic symptoms.
There may be swelling over fracture site
A minority who develop ICH can have depressed mental status, headache, vomiting, cranial nerve deficit

Question 18

Depressed Skull Fracture

general

Answer 18

Occur when trauma drives a segment of skull below the level of the adjacent skull
Ex: direct trauma from a bat or a club

Often involve injury to the brain parenchyma
Increased risk of CNS infection, seizures, and death if not early ID and managed appropriately
Mortality is high among patients with depressed fractures with a significant decline in mental status

Closed or Open - majority are open, assume any depressed fracture is open until proven otherwise

Question 19

depressed skull fracture

Presentation

Answer 19

They can present with report of loss of consciousness

CAREFULLY palpate but this is often limited due to swelling
Bone fragments can easily lacerate adjacent structures such as the dura mater —-which can lead to CNS infection
DO NOT blindly probe wound itself

Question 20

Basilar skull fracture

general

Answer 20

Involve at least one of the 5 bones that make up the skull base
Cribiform plate of ethmoid bone, orbital plate of the frontal bone, petrous and squamous portion of the temporal bone, and sphenoid and occipital bones.

Most commonly occur through temporal bone, so high risk for extra-axial (outside of the brain but beneath the skull) hematomas
The temporal bone is relatively weak and is right by the middle meningeal artery and vein

Question 21

basilar skull fractures

Clinical signs

Answer 21

Periorbital ecchymosis– Racoon eyes
Retroauricular ecchymosis (mastoid)- Battle’s sign
These appear 1-3 days later than initial injury

Otorrhea- CSF leak from ear

Rhinorrhea- CSF leak from nose
20% of patients display this. Within hours or up to several days after trauma

Hemotympanum- blood behind the tympanic membrane
Common
Generally appears within hours of injury

Neurologic presentation depends on degree of brain tissue and cranial nerve injury
If close to brainstem, N/V due to vestibular centers

Oculomotor deficits from injury to CN III,IV, or VI as may facial nerve palsies or hearing loss due to injury of CN VII and VIII.

Question 22

basilar skull fracture

CSF leak

Answer 22

CSF leak occurred in approximately 11-45% of these fractures as noted prior
Most traumatic CSF leaks resolve spontaneously within 7 days but in rare cases, can persist for as long as several months.
lab to check if CSF- Beta 2 transferrin

Question 23

Elevated skull fracture

Answer 23

Uncommon
Occur when the fracture fragment is elevated above the underlying skull
Impact usually tangential rather than perpendicular
Tangential skull fracutres- gun shot wounds- hemorrhage likely to be noted
Often affect frontal skull
Limited literature but associated with significant intracranial injury

Question 24

Penetrating skull fracture

Answer 24

Result of gun shot, stab wounds, and blast injuries
Significant brain injury and hemorrhage
Emergent neurosurgical consult

Question 25

Linear fractures

Tx

Answer 25

No specific intervention is necessary if CT reveals no underlying brain injury or depressed fracture
Emergency neurosurgical consultation ordered for intracranial hemorrhage
Can be admitted for observation for any suspicion or evidence of brain injury
Neuro checks
Patients can also be observed in ER (if no evidence of ICH) for 4-6 hours to detect delated complications.
Confirm adequate supervision for the next 24 hours and clear discharge instructions to return to ER

Question 26

depressed skull fracture

Tx

Answer 26

Increased risk of infection and seizures—need prophylactic measures
Tetanus status determined
Prophylactic abx for 5-7 days
Anticonvulsants often given to reduce risk of seizures-consult with neurosurgeon or neurologist
Usually admitted to neurosurgery
If depressed more than the thickness of the skull, to OR for elevation (usually any greater than 5mm below adjacent structure)
If open and depressed but NO evidence of dural penetration or complications on CT…can be managed non operatively. Similar is recommended for uncomplicated, closed, depressed skull fractures.

Question 27

Basilar fracture

Tx

Answer 27

Surgical emergency if ICH
ALL basilar skull fracture patients require admission for observation even if no surgical indications
Be suspicious of epidural hematoma if temporal bone involved…close neuro monitoring
If any noticeable change in neuro status, STAT non contrasted CT of the head should be ordered
CSF can be distinguished from local nasal secretions with beta-2 transferrin

The majority of CSF leaks resolve spontaneously in one week
Recent studies did not support prophylactic antibiotics- consult with neurosurgeon and ID to determine next steps
Incidence of bacterial meningitis rises substantially if leak lasts over 7 days

Question 28

basilar fractures

Tx for cranial nerve palsy if develops

Answer 28

If cranial nerve palsies develop (usually delated to 2-3 days after injury) can treat with glucocorticoids
If facial nerve palsy appears acutely, poor prognosis of recovery of nerve function. Likely due to transection.

Question 29

skull fractures

Anticoagulated patients

Answer 29

high risk of ICH
Symptoms of neurologic deterioration may not appear for up to 6 hours following injury
Risk greater in elderly population that are anticoagulated
All patients who are anticoagulated with a skull fracture should be admitted to unit equipped for close neurologic monitoring
Any sign of neuro deterioration -> STAT non contrasted CT of the head (why non contrasted…..??)
Can consider reversal of excess warfarin or DOACs (apixaban, rivaroxaban)

Another random tid-bit for extra fun- idarucizumab for dabigatranreversaland and exanet alfa for apixaban and rivaroxaban reversal

Question 30

ICH intracranial hemorrhage

general

Answer 30

-Intracerebral hemorrhage is the second most common cause of stroke after ischemic stroke per Up To Date
-Spontaneous or traumatic
-Enlargement of hemorrhage is associated with neurologic decline, increased intracranial pressure
-Edema around focus of hematoma can delay perfusion due to mass effect, local neuronal ischemia, or accumulation or cytotoxic factors
-This can impair cerebral autoregulation and cause acute blood pressure changes-this can then contribute to further ischemia
-Most common causes are hypertension, amyloid angiopathy, and rupture AV malformation
-Also neoplasms, coagulopathy, illicit drugs

Question 31

ICH

RF

Answer 31

HTN, Non compliance, Smoking, ETOH
Male>female
DOACs
NSAIDs
drugs
trauma

Question 32

ICH

Presentation

Answer 32

Varies on type of hemorrhage but if sudden and maximal onset of headache= subarachnoid hemorrhage

Can then become obtunded
Blood is an irritant when in the “wrong” place. Due to taking up some space, irritation can be due to traction on meningeal pain fibers, increased ICP in general, or just the blood being present where it should not be.
Elevation of BP
Focal neurologic deficit on exam
Vomiting
If complaining on stiff neck, blood is interventricular and circulating in CSF- meningismus
Nuchal rigidity, photophobia, headache
Stupor or coma are often ominous signs
Seizures may accompany acute ICH
Cardiac abnormalities are commonly associated with spontaneous ICH
EKG prolonged QT interval and ST-T wave changes
May be due to catecholamine-induced cardiac injury that is central mediated release of this due to stress of pressure and autonomic disturbance

Question 33

ICH

work up

Answer 33

Stable???? Does the patient need intubation and mechanical ventilation, anticoagulation reversal? BP control, neurosurgical consult for intracranial pressure monitoring?
Elevate head of bed >30 degrees
Non contrasted CT of the head is first choice for imaging- mandatory to confirm.
Labs- CBC, CMP, PT, INR, troponin, toxicology screen, urinalysis, pregnancy test
EEG? Later on.
Serial non contrasted CT is warranted to monitor
MRI brain with contrast can help identify the underlying cause of ICH for most patients- ischemia/structural change
Cerebral angiography is gold standard for pre op eval to determine source of bleeding
Can consider LP to assess for presence of blood

Question 34

Subarachnoid hemorrhage

S/Sx

Answer 34

Thunder clap headache
“The WORST headache of my life!”
Nausea/vomiting
Decreased level of consciousness
Nuchal rigidity
Seizures

Question 35

SAH

aneurysm

Answer 35

Major cause is rupture of arterial aneurysm
Other causes: AVM, bleeding disorders, trauma, illicit drug use.
With other causes- bleeding is less abrupt and may continue over a longer period of time
Risk factors for aneurysm: smoking, HTN, ETOH, family history of SAH or connective tissue disorder (Marfan’s), or personal previous SAH

Question 36

Cerebral Amyloid Angiopathy

general

Answer 36

Involves the deposition of amyloid beta-peptide within the cerebral vasculature
Not well understood what leads to this. Genetic factors-autosomal dominant
Can lead to hemorrhage due to deposition in the vascular wall leading to concentric splitting of the vascular wall
Most common clinical manifestation of CAA is acute lobar intracerebral hemorrhage
Lobar = location in cortex and subcortical white matter of a hemispheric lobe of the brain.
Interestingly enough, the depositions favor cortical vessels
Crossing into stroke territory as these lobar hemorrhages can cause hemiparesis and so on

Question 37

Subdural hematoma

general

Answer 37

Bleeding between the dura and arachnoid membranes
Occurs when bridging vessels between membranes tear during trauma

Question 38

subdural hematoma

Dx and Tx

Answer 38

conCAVE lesions on CT brain
Can present with headache or confusion
Weightlifter picked up barbell-got headache
Surgical management in severe cases
Can monitor with serial CT scans
Supportive care

Question 39

Epidural hematoma

General
Dx and Tx

Answer 39

RARE
Occurs when blood pools between dura matter and the skull
conVEX lesions on CT brain
Management similar to subdural hematoma
Surgical if severe
Supportive care and monitoring

Question 40

ICH

Tx recap

Answer 40

In general, examine patient and obtain history
* Stabilize-intubation, BP management, etc
* CT to determine cause
-If AV malformation- can obliterate these via surgery-neurointerventionalist/vascular
-Treat hydrocephalus and increased ICP-neurosurgery
* Vasospasm after intervention
-Volume expansion and HTN-promotes cerebral perfusion after aneurysm has been obliterated
-CCB of choice by surgeon can be used to dilate vessels and prevent vasospasm. Nimodipine.