CNS trauma

Question 1

2. Know the peak age groups in which head injuries occur and the mechanisms whereby these injuries are received

Answer 1

The peak age range is 24-35 with small peaks at 0-4 years for child abuse and over 65 years for falls at home. Males > females. Major causes include traffic/transport (highest- 20-50%), violence (20-40%) assaults, homicides, suicides and falls.

Question 2

Forces responsible for traumatic brain injury

Answer 2

1. contact: object striking head leading to fractures, epidural hematomas, cerebral contusions. 2. acceleration/deceleration: shear, tensile and compressive strains. 3. penetrating (knives, etc). 4. secondary injury (hypoxia, hypotension)

Question 3

Linear skull fractures

Answer 3

Linear skull fractures of the calvarium are identified by radiologic studies and by themselves portend no independent prognosis other than to suggest a high-impact injury

Question 4

depressed skull fracturs

Answer 4

Depressed skull fractures consist of comminuted bone fragments that may or may not be driven into the brain. Occasionally these injuries require surgical intervention to prevent infection or correct a cosmetic defect.

Question 5

Basilar skull fracturs

Answer 5

Basilar skull fractures are common with high-velocity blunt injuries. may extend through the cribiform plate or petrous bone and result in CSF leaks (otorrhea or rhinorrhea) that may lead to meningitis

Question 6

Signs of skull base fracture

Answer 6

CSF rhinorrhoea, Bilateral periorbital haematomas (Racoon eyes), Subconjunctival haemorrhage, Bleeding from external auditory meatus, CSF otorrhoea, Battle’s sign (blood accumulation behind ear, occurs 12 hrs later), Facial nerve palsy

Question 7

diastatic skull fractures

Answer 7

Diastatic fractures are traumatic separations of the skull at suture lines and have the same significance as linear fractures.

Question 8

growing skull fractures

Answer 8

Growing fractures of infancy (0-18 months of age) result from dural tears and herniation of the arachnoid into the fracture site. CSF pulsations then cause bone loss over months, often requiring surgical correction

Question 9

Epidural hematoma cause, location, presentation, treatment, mortality

Answer 9

Epidural hematomas typically result from intracranial, extradural arterial bleeding from skull fractures in the distribution of the middle meningeal artery. Classically they present after an impact injury with a “lucid interval: prior to progressive obtundation and coma as the hematoma expands. Treatment is timely surgical removal of the mass lesion and the prognosis principally depends on the time from injury to evacuation. Mortality is less than 20% with evacuation in less than one hour.

Question 10

Subdural hematoma cause, location, treatment, mortality

Answer 10

Subdural hematomas result from translational acceleration from high velocity mechanisms. Hemorrhage into the subdural space results from rupture of the bridging veins that connect the cortical surface of the brain with the sagittal sinus. This injury is often associated with underlying cerebral contusions. Associated with elevated intracranial pressure and distant secondary cerebral injury. Treatment includes prompt surgical removal of the blood clot, control of the intracranial pressure, and restoration of adequate cerebral blood flow. Mortality from subdural hematomas is between 40-60%.

Question 11

cerebral contusion cause, location, presentation, treatment, mortality

Answer 11

High velocity translational and impact injuries result in superficial hemorrhagic contusions of the brain. Characteristic locations include those brain surfaces in contact with the rough bony surface of the anterior cranial fossa (frontal lobe) and the sharp edge of the greater wing of the sphenoid (temporal lobe). Hemorrhage into areas of damaged brain results in mass effect and herniation with secondary brain injury. Treatment involves medical management to prevent brain swelling and occasional surgical evacuation of large hematomas. Mortality is less than 20%.

Question 12

Coup vs contrecoup

Answer 12

coup: injury at the front of the brain. Contrecoup: injury at the back of the brain

Question 13

Diffuse Axonal Injury cause, presentation, MRI results, mortality

Answer 13

Diffuse axonal injury results from high velocity rotational acceleration/deceleration injury. The exact pathophysiology remains controversial. Shearing of axons is thought to result in pathologically identifiable “retraction balls” or axonal spheroids on microscopic examination. Clinically the patient is rendered unconscious from the moment of injury, without significant anatomical correlation of injury on CT. MRI studies often show punctuate hemorrhages in large white matter tracts such as the corpus callosum. Patients typically remain in a chronic vegetative state without significant recovery. Mortality is as high as 80%.

Question 14

Axonal spheroids- when do they appear, how are they detected, where are they most common, how long do they last

Answer 14

Appear when coma exceeds 6hrs. Detectable with light microscopy after 24 hrs. Most common in corpus callosum and brainstem. Last days to weeks. Invisible on CT/MRI

Question 15

primary vs secondary injury

Answer 15

primary: occurs at the moment of impact, and is largely irreversible injury. Secondary injury: inadequate resuscitation. Mechanisms include hypoxia, altered cerebral blood flow (dysautoregulation), and release of free radical mediators

Question 16

How do free radials mediate CNS injury

Answer 16

free radical mediators break down the blood brain barrier and result in interstitial (vasogenic) edema. The combination of events results in brain swelling, elevated intracranial pressure (ICP), further hypoxia, dysautoregulation, and herniation

Question 17

Monroe-Kellie doctrine

Answer 17

CSF volume + cerebral arterial blood volume + cerebral venous blood volume + brain volume + volume of intracranial mass lesion must equal constant volume ( volume of intracranial compartment). An increase in size of mass must be compensated by decrease in volume of another compartment, otherwise compression results.

Question 18

What is the point of decompensation/critical point on volume pressure curve for brain

Answer 18

The volume of mass where even a small increase in compression results in a large increase in pressure.

Question 19

Herniation syndromes

Answer 19

forcible displacement of brain tissue across the falx, tentorium, or foramen magnum due to elevated intracranial pressure and mass effect

Question 20

Common characteristic of most herniation syndromes

Answer 20

progressive lethargy and poor responsiveness (obtundation) - hallmark of acute rise in intracranial pressure and should be recognized as an emergency. Manifest as abrubt changes

Question 21

Subfalcine herniation

Answer 21

the cingulate gyrus is pushed away from the expanding mass and herniates beneath the falx cerebri. In the process, the anterior cerebral artery is often kinked, and a stroke in the distribution of this vessel is not uncommon

Question 22

Central herniation

Answer 22

Occurs when there is downward pressure centrally, and can result in bilateral uncal herniation.

Question 23

Transtentorial (Uncal) herniation

Answer 23

the uncus, a part of the medial temporal lobe, herniates across the tentorial edge, and downward into the posterior fossa. It compresses the midbrain and its ipsilateral cerebral peduncle, usually producing an ipsilateral third nerve palsy and a contralateral hemiparesis or hemiplegia.

Question 24

Kernohans notch

Answer 24

Rarely, uncal herniation can compress the opposite cerebral peduncle against the tentorial edge, resulting in a hemiparesis that is ipsilateral to the mass lesion and herniated uncus.

Question 25

Duret hemorrhage

Answer 25

Hemorrhage produced by uncal herniation which which produces devastating neurologic consequences, because of disruption of the ascending reticular activating system

Question 26

Tonsillar herniation

Answer 26

cerebellar tonsils herniate downward into the foramen magnum, a process also referred to as “coning”. The medulla is compressed, and this can produce abnormal cardiac and respiratory responses, including Cushing’s reflex, which consists of bradycardia and hypertension in the setting of high intracranial pressure. Tonsillar herniation most commonly is encountered in the setting of a mass lesion in the posterior fossa.

Question 27

Lumbar puncture in setting of intracranial mass lesion?

Answer 27

can precipitate a herniation syndrome, because of the differential pressures this creates between the cranial and spinal subarachnoid space

Question 28

pathophysiology of traumatic brain injury

Answer 28

Spike in extracellular K,cytotoxic edema, Excitotoxicity, vasogenic edema, increased intracranial pressure causes ischemia

Question 29

Describe excitotoxicity and vasogenic edema leading to TBI

Answer 29

Excitotoxicity: mechanical forces cause massive neuronal depolarization, with massive neurotransmitter release. Overactivation of NMDA and AMPA receptors by glutamate allows high levels of Ca to enter cell, activating phospholipases, endonucleases and proteases (calpain) which damage cell structures, then damage blood brain barrier. Vasogenic edema results from increased permeability

Question 30

Describe extracellular K levels and cytotoxic edema leading to TBI

Answer 30

widespread simultaneous neuronal depolarization results in an immediate spike in extracellular K. This causes reversal of glutamate transporters on astrocytes and adds to glutamate toxicity. Also, influx of K into astrocyte causes cell to swell, causing cytotoxic edema and contributing to brain edema. Swelling of astrocyte foot processes causes increased capillary resistance and decreased cerebral blood flow.

Question 31

Ischemia and TBI

Answer 31

The increased ICP from cytotoxic and vasogenic edema reduces the perfusion of the brain, and the resultant ischemia causes further failure of energy dependent ATPases, further depolarization of neurons (who depend on sodium potassium ATPases to maintain hyperpolarization)

Question 32

Basic componenets of treatment of elevated intracranial pressure

Answer 32

Minimize ICP and maximize oxygen/metabolite delivery by manipulating the three intracranial compartments: 1) the intravascular space 2) the brain parenchyma, and 3) the cerebrospinal fluid space.

Question 33

Steps for unconcious patient care

Answer 33

Endotracheal intubation > Controlled ventilation to pCO2 of 35mmHg then reduced to 25mmHg with resultant decrease in blood volume (vasoconstriction) and ICP > elvate head (prevent venous congestion) > IV osmotic diuretics (ie mannitol) reduce interstitial brain edema > ventricular cathether to drain hydrocephalus > drug induced coma w/ barbituates to decrease metabolism and scavenge free radicals

Question 34

Glasgow coma scale components

Answer 34

1. eye opening: spontaneous (4), to speech (3), to pain (2), none (1). 2. BEST motor response: Obeys commands (6), localizes pain (5), flexion (4), abnormal flexion (3), extension (2), none (1). 3. Verbal response: Oriented (5), confused (4), inappropriate words (3), incomprehensible sounds (2), none (1)

Question 35

Risk of operable intracranial mass lesion in head injured patient using glasgow coma scale

Answer 35

15: 1 in 3615 risk. 9-14: 1 in 51 risk. 3-8: 1 in 7 risk.

Question 36

Brainstem reflexes used to test location of TBI

Answer 36

Pupillar reflex (CN 2, 3, midbrain), corneal blink reflex (CN 5,7 pons), cold caloric testing “dolls eyes” (CN 8,6,3 pons to midbrain), gag reflex (CN9,10 medulla)

Question 37

Outcomes 1 year after head injury using glasgow coma scale

Answer 37

Mild severity (GCS 13-15): most have good outcome. Moderate severity (GCS 9-12): Most (38%) have good outcome but 16% are dead/vegetative. Severe (GCS 3-8): most (38%) are dead or vegetative

Question 38

ranges of ICP pressures

Answer 38

Normal: -3 - 15 mm Hg. Slight increase: 16 - 20, Moderate increase: 21 - 40. Severe increase:> 40

Question 39

Cerebral perfusion pressure equation

Answer 39

CPP: MAP- ICP. Normal is around 70

Question 40

Define concussion and its hallmarks

Answer 40

alteration in mental status caused by biomechanical forces which may or may not cause loss of consciousness. The hallmarks of concussion are confusion and amnesia

Question 41

Common symptoms of concussion

Answer 41

headache, dizziness, poor attention, inability to concentrate, memory problems, fatigue, irritability, depressed mood, intolerance of bright light or loud noise, and sleep disturbance

Question 42

Post concussive syndrome symptoms

Answer 42

persistent headache, lightheadedness, decreased attention and concentration, poor memory, easy fatigability, irritability, anxiety or depressed, sleep disturbance

Question 43

signs of concussion

Answer 43

vacant stare, delayed response, inattention, disorientation, slurred or incoherent speech, incoordination, inapropriate emotionality, memory problems, loss of conciousness

Question 44

definition of of mild loss of consiousness

Answer 44

less than 30 minutes

Question 45

Pathophys of concussion

Answer 45

differ from that of severe TBI only in degree, and the regions of the brain affected tend to be confined to the junction of the grey and white matter immediately beneath the cortex where gradient echo MRI often detects shearing lesions of DAI

Question 46

glasgow coma scale for concussions

Answer 46

Mild severity (GCS 13-15)

Question 47

Which brain lobes are most affected during concussions

Answer 47

frontal and temporal

Question 48

Which types of forces are more damaging

Answer 48

rotational (angular) are more damaging than translational (linear)

Question 49

Which forces cause contrecoup contusions

Answer 49

linear (translational) forces will cause contusion on the side opposite of the original injury

Question 50

Colorado Concussion grading scale

Answer 50

Grade 1 – Confusion without amnesia or LOC. Grade 2 – Confusion and amnesia. Grade 3 – LOC

Question 51

Second Impact Syndrome

Answer 51

rare but usually fatal consequence of a second concussion while still suffering the effects of an earlier one. Loss of autoregulation of CNS vasculature, cerebral vessels become congested , ICP rises, cerebral perfusion decreases leading to ischemia and vasogenic edema

Question 52

How long should someone with a concussion be observed closely following the incident?

Answer 52

24 hrs- It is not usually necessary to have the patient awakened multiple times during the night following an acute event unless there had been prolonged amnesia or unconsciousness

Question 53

When is CT scan indicated for concussions

Answer 53

CT scanning for intracranial bleeding is indicated acutely for anyone with witnessed LOC.

Question 54

Sleep disturbance and concussions

Answer 54

Sleep disturbance is very common a few days after a concussion and should be treated promptly to avoid the prolongation of symptoms

Question 55

Recommended treatment for aches/pains from concussion

Answer 55

Acetaminophen should be offered for headaches and associated bodily pain, such as whiplash neck pain, and is considered safe in the acute phase of the injury.