Neurological System Flashcards
Major Division of Nervous System
Central nervous system (CNS)
a) Brain
b) Spinal cord
And
Peripheral nervous system (PNS)
Composed of
Autonomic nervous system (ANS)
Further divided into..
a) Sympathetic nervous system
b) Parasympathetic nervous system
What is a neuron and describe the 2 types
Basic unit of the nervous system
Transmits impulses (“messages”)
>Motor neurons (efferent): Carry impulses from CNS to PNS
> Sensory neurons (afferent): Carry impulses from PNS towards CNS
Axons can be covered by myelin sheath
> White fat/lipid covering = white matter
> Non-myelinated axons = gray matter
3 Main Areas of Brain and basic function
Forebrain: largest portion and and most advanced in function
> further broke down into diencephalon (thalamus, subthalamus, hypothalamus, epithalamus), cerebrum, and cerebral cortex
Cerebellum: voluntary/involuntary muscle coordination
Brainstem: vital functions (RR, HR, BP)
Diencephalon function and components
Thalamus, subthalamus, hypothalamus, pineal gland (epithalamus)
Regulates hormones and metabolic function
Cerebrum function and components
Largest
Divided into 2 hemispheres
Control muscle functions and also control speech, thought, emotions, reading, writing, and learning.
Cerebral cortex function and components
Grey matter of cerebrum
Highest function: thought/information processing
Composed of frontal, parietal, occipital, and temporal lobes
Frontal lobe function
voluntary movement, expressive language and for managing higher level executive functions. Executive functions refer to a collection of cognitive skills including the capacity to plan, organise, initiate, self-monitor and control one’s responses in order to achieve a goal.
Parietal lobe function
receiving and processing sensory input such as touch, pressure, heat, cold, and pain
Occipital lobe function
visuospatial processing, distance and depth perception, color determination, object and face recognition, and memory formation.
Temporal lobe function
processing auditory information and with the encoding of memory. The temporal lobes are also believed to play an important role in processing affect/emotions, language, and certain aspects of visual perception.
Function of and bones composing the skull
Formed by cranial bones:
* frontal
* ethmoid
* sphenoid
* occipital
* parietal
* temporal &
* Facial bones
Protects cranial vault contents
Overall thick (up to 6mm)
Non-flexible
> No absorptive capacity with brain movement
Internal surface of skull base: rough and irregular
> Movement within vault can cause injury within itself
Describe the layers of the meninges
Protective covering of brain & spinal cord
1. Pia mater
> Inner most layer; firmly attaches to brain and spinal cord
> Subarachnoid space: between pia and arachnoid; where CSF circulates
2. Arachnoid membrane
> Subdural space; between arachnoid and dura
> Between…
3. Dura mater
> Epidural space– between dura and skull
> Extends down spinal cord
> Adheres to skull
Where/how much CSF is produced, where does it circulate and what does it contain?
- Produced by choroid plexus in the brain ventricles
> 125-150 ml at any one time – constantly produced and reabsorbed
> About 650 ml produced every day - Circulates in subarachnoid space (beneath arachnoid membrane) and through central canal of spinal cord
- Contains water, protein, glucose**, ions (Na, Cl, K)
What substances does the blood brain barrier allow to enter?
- Oxygen
- Glucose
- CO2
- ETOH
- Anesthetics
- Water
What substances does the blood brain barrier prevent from entry?
large molecules
* albumin
* substances bound to albumin
* many drugs – antibiotics
can cause issues with certain treatments
Where arteries supply the brain?
- R/L internal carotid (anterior circulation)
- R/L vertebral arteries (posterior circulation)
The R/L internal carotid arteries branch in to
- ophthalmic: eyes
- middle (MCA): hearing + upper body motor sensory
- Anterior (ACA): lower body motor/sensory
The R/L verebral arteries branch into
The basilar artery
- occipital
- brainstem
- cerebellum
What protective mechanism exists in the blood supply in the brain in case of blockage?
Eventually these arteries: anterior, middle, and posterior arteries join form ring at base of brain
= Circle of Willis
Protective mechanism; if there is a blockage, blood can travel around circle and still perfuse (minimally)
Where are the middle meningeal arteries located + what does injury to them result in?
above dura mater
* Most superficial
* Injury: epidural hematoma
Where are the bridging veins located + what does injury to them result in?
beneath dura mater
* Injury: subdural hematoma
Where do the large arteries in the brain enter and what does injury to them result in?
enter skull in subarachnoid space
* Where carotids enter
* Injury: subarachnoid hematoma
How is blood drained from the brain?
Only source of drainage: venous blood drains via jugular veins
Something blocking the only output = backup of pressure into brain
What system controls the ANS?
Controlled by reticular system in brainstem
What does the ANS regulate and control?
Regulates cardiac and smooth muscle and glands
Controls homeostasis
12 Functions SNS
- Speeding up ( metabolism)
- Fight or flight
- Increased HR, CO
- Decreases urine output
- Vasoconstricts vasculature
- Increased mental alertness
- Diaphoresis
- Dilated pupils
- Vasodilated coronary arteries
- Bronchodilation
- Decreased intestinal peristalsis
- Increased releases of glucose by liver
12 Functions PNS
- Slowing down ( metabolism)
- Storage and maintenance of organs during rest periods
- Slows HR, CO
- Increased urine output
- Vasodilation of vasculature
- Decreased mental alertness
- Increased GI fluid secretion (stimulates GI system)
- Vasoconstriction of coronary arteries
- Bronchoconstriction
- Increased intestinal peristalsis
- Decreased release of glucose by liver
Explain the theory of cerebral autoregulation
Because brain does not have ability to store nutrients, their acquisition is completely dependent on cerebral blood flow.
cerebral arteries can alter their own blood flow to maintain a constant pressure
Cerebral blood flow (CBF) matches cerebral metabolic demand
> Vasodilation/vasoconstriction based upon brain’s needs
In what range must the MAP to allow for cerebral autoregulation
between 60-140 mmHg
> When too low/high; brain is no longer able to autoregulate
> Cerebral blood flow matches metabolic need of brain
What is the autoregulation of cerebral blood flow based on?
Blood Pressure and Acid Level
Factor that vasodilate the cerebral arteries ________ blood flow to the brain
Increase blood flow to brain
- hypotension
- acidosis (CO2 is a potent vasodilator)
Factors that can vasoconstrict cerebral arteries ________ blood flow to the brain
Decrease blood blow to brain
- hypertension
- alkalosis (sedation, low RR)
Effects of high CO2 on vasculature
Increase CO2: Increase Diameter to increase oxygen (Hypoventilation – retaining CO2)
Effects of low CO2 on vasculature
Decrease CO2: Decrease Diameter to decrease oxygen (Hyperventilation – blowing off CO2)
What is the munroe-kellie doctrine?
Intracranial vault will not expand or contract. Composed of:
* Brain
* Cerebral blood volume
* Cerebrospinal fluid
“As the volume of one component of the cranial vault triad expands, the volume of one or both of the other components must decrease to maintain a constant ICP”
> Increased ICP = Decreased Blood Flow = Ischemia
What is ICP + normal/abnormal values
The pressure exerted by the CSF within the ventricles of the brain
* Measured in the CSF– many ways to monitor ICP, commonly in ICU
> Normal ICP: 0-15 mmHg
> Need for treatment begins at = sustained ICP of 22 mmHg
- Brain is ischemic at this threshold
Causes of increased ICP (6)
anything taking up extra space in brain:
- Cerebral edema (swelling of cells/tissues)
- Hemorrhage/hematoma/mass
- Excess CSF (hydrocephalus)
- Increased cerebral blood flow (hypertensive states)
- Increased intrathoracic pressure
- Reduced cerebral venous drainage (blockages in jugulars)
If ICP is rising, what should the body do to attempt to maintain perfusion to the brain?
> Brain – not much can be done about actual tissue
Blood – if outside parameters cannot be autoregulated
> First response: CSF regulation
- shunted from cranial vault into spinal cord
- rate of ventricular absorption increased
- lessens protective mechanism of CSF; less ability to absorb force
- only accounts for 10% of cerebral pressures – protective mechanism has minimal effect
Signs of increasing ICP
- Headache
- Nausea & vomiting
- Amnesia
- Behavioral changes: restlessness, irritability, and confusion, impaired judgement
- Decreased level of consciousness (LOC), drowsiness
- Aphasia, changes in speech pattern/dysarthria
- Cranial nerve dysfunction
- Seizures
Late/terminal signs of increasing ICP
- Cushing triad – lack of brainstem function
- Widening pulse pressure: Increased difference between SBP and DBP
- Bradycardia
- Irregular respirations: cheyne-stokes; slow, deep breathes followed by periods of apnea - Abnormal motor posturing : Decerebrate (extensor); Decorticate (flexor)
- Unilateral or bilateral pupillary reactivity (“fixed”)
- Unilateral or bilateral pupillary dilatation
* Dilated and Fixed = blown pupil
What is CPP and normal value?
Cerebral Perfusion Pressure
Pressure gradient necessary to supply adequate amounts of blood to the brain
> Measure of adequacy of cerebral blood flow
Normal 60-100mmHg
What does a CPP < 60mmHg mean?
< 60 mmHg means arterial pressure can’t overcome increased pressure gradient to deliver O2 and nutrients to brain
What is permissive hypertension?
With increased ICP… MAP may need to be higher to maintain CPP
High intracranial pressure means higher blood pressure is needed to get oxygen and nutrients into the brain
How do you calculate CPP?
CPP = MAP - ICP
MAP = SBP + 2xDBP/3
When autoregulation in the brain fails, perfusion becomes dependent on:
Mean arterial pressure
7 Core Components of CNS Assessment
- LOC
- Vitals
- Language/Speech
- Cranial nerve status
5, Pupils - Grip strength/movement
- Sensation
Describe GCS
Used to quantify consciousness & severity of head injury
**LOC #1 assessment in head injury
Score: 3-15
EVM - 456
Eye opening:
* 4: spontaneous
* 3: to sound
* 2: to pain
* 1: never
Verbal Response
* 5: oriented
* 4: confused conversation
* 3: inappropriate words
* 2: incomprehensible
* 1: none
Motor response
* 6: obeys commands
* 5: localizes pain
* 4: normal flexion/withdrawal
* 3: abnormal flexion
* 2: extension
* 1: none
Describe assessment of pupils and difference findings
Assess: shape, size, reactivity, symmetry
Pinpoint: narcotics/pons damage
Dilated: stimulants/epinephrine
Bilateral dilated and fixed: increased ICP
Unilateral dilated and fixed: compressed cranial nerve 3
Sluggish reactivity/moderate: changes/grey area/increasing ICP
Describe assessment of posturing
- Decorticate: abnormal flexion - bad
- Decerebrate: abnormal extension - worse
6 Age Related Changes to the Brain
- Brain tissue atrophy
> Stretching of bridging veins, predisposing them to tearing
> Additional space in cranial vault due to shrinkage/atrophy substantial bleeding before onset of symptoms - Increased likelihood of anticoagulant/antiplatelet meds
> Increased risk of bleeding from brain injury - Mobility changes > slower movement and response times
- Decreased sensory perception increased risk for falls
- Altered balance; decreased coordination
- Slower cognitive processing time
Define TBI and causes
Damage to the brain from an external mechanical force (direct or indirect) not caused by neurodegenerative or congenital conditions
- Blunt Injury
* Falls**: most common cause of TBI
* MVCs
* Sports-related
* Recreation and recreational vehicle related - Penetrating Injury
* Firearms
* Exploding objects
* Projectiles
Risk factors for TBI
- on Anticoagulants
- Ages: > 75, 0-14, 15-19
- substances causing delayed response (alcohol, sedatives, etc)
- previous head injury
Primary Brain Injury and categories
Result from DIRECT transfer of energy caused by blunt or penetrating force
* Occurs at time of injury
* Skull and craniofacial #
Categorized:
o Focal (limited to one spot) or diffuse (widespread impact)
o Open (to air - penetrating) or closed (within vault)
o Mild, moderate, or severe
Secondary Brain Injury and 6 causes
Any processes that occur after initial injury and worsen or negatively influence outcomes
Increase extent of injury and/or cause additional damage
Caused by pathophysiological changes that are an extension of the primary injury, including:
1. Hypotension: inadequate perfusion
2. Hypoxemia: inadequate delivery
3. Cerebral edema: increasing pressure, decreasing perfusion
4. Increased ICP: increasing pressure, decreasing perfusion
5. Decreased CPP: increasing pressure, decreasing perfusion
6. Cerebral ischemia: increasing pressure, decreasing perfusion
Mild TBI GCS, description and symptoms
13-15
Blow to the head, transient confusion or feeling dazed or disoriented,
AND 1 or more of:
(1) possible LOC for up to 30min,
(2) loss of memory for events immediately before or after, and
(3) focal neurologic deficit(s) that may or not be transient
No evidence of brain damage on a CT or MRI
Vary: from headache and dizziness to changes in behavior
Symptoms usually resolve within 72hrs; may persist (post-concussion syndrome)
Moderate TBI GCS, description, and symptoms
9-12
Loss of consciousness for 30mins- 6hrs
Often (not always) brain injury can be seen with CT or MRI
Posttraumatic amnesia may last up to 24 hours
May occur with either closed or open brain injury
short stay may be needed for close monitoring and to prevent secondary injury
Severe TBI GCS, description, symptoms
< 8
Loss of consciousness for > 6hrs
Focal and diffuse damage to the brain, cerebrovascular vessels, and/or ventricles is common
Injury can be focal or diffuse
CT and MRI can capture images of tissue damage quite early
ICU, including hemodynamic, neurologic, and ICP monitoring
High risk for secondary injury
GCS < 8 = intubate (impaired airway protection)
Acceleration Injury
When the stationary brain is suddenly moved rapidly in one direction along a linear path
Causes injury at site of impact
* Ex: Assault with fist or object
Deceleration Injury
When the brain stops rapidly in the cranial vault
As the skull stops moving, the brain continues to move until it hits the skull
Causes injury at site of impact with the skull
* Ex: Fall
Coup-Countrecoup Injury
Following initial acceleration (coup) injury the brain rebounds and sustains additional deceleration (contrecoup) injury
Most common for acceleration/deceleration to occur together
Rotational Injury
When a force impacting the head transfers energy to the brain in a non-linear fashion resulting in shearing forces being exerted throughout brain tearing of axons
Head twists really fast, brain doesn’t move at same time causing stretching of tissue
* Ex: Boxing
Blast Injury
Creates pressure wave and diffuse contused tissue
Penetrating Injury
When a foreign object invades the brain
* Ex: Bullet, knife, falling object
Linear skull fracture
non-displaced # through entire thickness of skull
Depressed skull fracture
pieces of #’d bone extend below the surface of the skull; may cause dura mater laceration and brain tissue injury
Basilar Skull fracture
of any of the 5 bones in the base of the skull; bottom bones
Associated with considerable amount of force
Can result in punctures/lacerations to brain tissue, CNs, and CSF leakage
Leakage indicated torn meninges (protective areas)
Often occur concurrently with facial #’s; usually mandibular
Raccoon Eyes and Battle Signs also indicative of basilar
How to test is fluid leakage from ear/nose is CSF
use BGM - normal BG or a bit lower
Halo Test: put fluid on clean gauze and centre will be red/pinkish ring if CSF
Do not pack areas that have CSF leakage; increases ICP and provides area for CSF growth
4 Types of Focal Brain Injuries
Localized to One Specific Area of Brain
- Cerebral contusion
- Intracerebral hematoma
- Epidural hematoma
- Subdural hematoma (acute and chronic)
Cerebral Contusion
Bruised or damaged soft brain tissue
Capillaries in brain tissue are damage > localized hemorrhage, infarction, necrosis and edema
Significant contusions with swelling can cause midline shift over 2-3 days
Can lead to intracranial hematomas developing
Most common type of brain injury
Often located in frontal and temporal lobes
Can also occur in tissue beneath a depressed skull #
Commonly caused by blunt trauma
Epidural Hematoma and causes
ARTERIAL bleeding into space between dura mater and skull
- Often caused by temporal bone # that lacerate the middle meningeal artery
- ARTERIAL = FASTER loss of blood - rapid ICP increase = secondary brain injury
Large vs Small Epidural Hematoma Treatment
Large = immediate surgical evacuation – drains, burr holes
Small = nonoperative with frequent neuro assessments & repeat CTs
Cues of Epidural Hematoma
- CLASSIC: Transient loss of consciousness followed by a “lucid interval” (minutes-hours), then rapid deterioration in neuro status
- Headache, dizziness, nausea, vomiting
- Pupil changes (ipsilateral (same side) unilateral fixed and dilated pupil)
- Contralateral (other side) hemiparesis, hemiplegia, or abnormal motor posturing
Subdural Hematoma
Accumulation of blood between the dura and the arachnoid layers of the meninges
- Usually due to acceleration, deceleration, or combined forces
- Most often from tearing of the bridging veins and associated direct injury to the underlying brain tissue
> Age related changing: atrophy of bridging veins
VENOUS bleeding occurs slower = SLOW onset of symptoms
Management of subdural hematoma
Highest mortality rate: often unrecognized until presents with severe neuro compromise
Management:
* Surgical evacuation of hematoma
* LOC, neurologic assessments
Acute presentation of subdural hematoma
(within 48hrs)
* Headache
* Nausea, vomiting
* Change in level of consciousness (drowsiness, confusion, slowed thinking, agitation)
* Ipsilateral dilated or nonreactive pupil
* Unilateral weakness or hemiparesis
Chronic presentation of subdural hematoma
(2 weeks- several months)
Accumulates slowly, over longer period
Differences in finer details like memory, speech, cognition (as compared to epidural/more acute where you are seeing the bigger S+S)
Often confused with TIA symptoms
Primarily seen in elderly patients due to tearing of bridging, more space for blood to accumulate and anti-coagulation
Cues:
> Worsening headache** key to watch
> Alteration in cognitive abilities
> Decline in level of consciousness (confusion to coma)
> Loss of memory or altered reasoning
> Motor deficit (contralateral hemiparesis, hemiplegia, or abnormal motor posturing or ataxia)
> Slurred speech, difficulty with word finding
> Ipsilateral unilateral fixed and dilated pupil
> Incontinence
> Seizure
What is an intracerebral hematoma/hemorrhage
What do they result from, cues, management?
Hemorrhagic Stroke
Accumulation of blood in the parenchyma of brain tissue caused by tearing of small arteries and veins in the subcortical white matter
Result from:
* Uncontrolled HTN
* Ruptured aneurysm
* Trauma with a high-impact blow
Cues:
* Headache
* Progressive and often rapid decline in LOC
* Signs of increased ICP
* Dilation of one pupil
* Contralateral hemiparesis, hemiplegia, or abnormal motor posturing
Management
* Evacuation usually not possible; too deep – IN tissue
* Management of ICP and CPP
4 Types of Diffuse Injuries
Often sports related and not seen on diagnostic imaging
- Concussion
- Post-concussive Syndrome
- Diffuse Axonal Injury
- Subarachnoid hemorrhage
What is a concussion?
Mild TBI
Often from blunt injury to head or neck, or acceleration/deceleration
Pathophysiological changes at cellular level– axonal disruption, neurochemical disruption
NO BLEEDING, NO TEARS, NO BRUISING
* Most have no CT findings
Cues of concussion
GCS 13-15 (must be done at least 30 mins post-injury)
Confusion, disorientation
Headache, dizziness, nausea, vomiting
Poor concentration, anxiety, irritability
Post-traumatic amnesia for <24hrs
Photophobia/phonophobia
Post-Concussive Syndrome
Prevention and Cues
Most common secondary injury from mild TBI
Non-resolution of concussive symptoms
Continuations of manifestations days to months after the head trauma
Prevention: return to play/work after full resolution of symptoms
Cues
* Dizziness, persistent headache
* Nausea
* Irritability, depression, anxiety, emotional lability
* Insomnia/sleep disturbance
* Difficulty concentrating or amnesia, impaired judgement
* Reduced ETOH tolerance
* Noise and light oversensitivity
Diffuse Axonal Injury
Widespread microscopic damage, primarily to axons results in diffuse, microscopic hemorrhagic lesions and cerebral edema
Diffuse shearing, tearing, or compressive stress from rotational or acceleration/deceleration MOI
Can follow hypoxic or ischemic insult from initial trauma
What structures are most at risk in DAI and what is the result?
Deeper structures (brain stem – VITAL FUNCTIONS COMPROMISED - reticular activating system) most at risk for injury > prolonged coma
Graded I-III based on location and severity of injury
Mild: coma may last from hours to days and may be followed by recovery with minimal effects; resolution of swelling to brainstem
Severe: prognosis is poor and may include prolonged coma or death
Cues for DAI
- Unconsciousness – coma for some duration of time r/t brainstem involvement
- Increased ICP
- Abnormal motor posturing
- Hyperthermia (>40 C)
- Excessive sweating
- Mild to severe memory loss; cognitive, behavioral, intellectual deficits
Subarachnoid Hemorrhage
Accumulation of blood between the arachnoid layer and the pia (in the subarachnoid space)
2nd type of hemorrhagic stroke
Can be focal with little consequence or massive and diffuse (usually diffuse)
Cues:
* Acute neuro deficits
* Nuchal rigidity – neck stiffness
* Blood may leak into CSF
* CSF is usually contained in subarachnoid space
* Sudden, severe headache
3 TBI Priorities
ABC’s!
Maintain adequate perfusion to the brain
Prevent secondary injury (hypoxia, increased ICP, increased CSF, hypotension)
Maintenance of oxygenation/ventilation in TBI Patient
Consider early intubation and mechanical ventilation
Suction for less than 10 seconds at a time
Sp02 > 95%
Obtain ABG early so that targets can be obtained
o PaO2 > 60 mmHg
o PaCO2 35-45 mmHg
Prevention of secondary injury to hypoxia/hypotension in TBI
Maintain SBP > 100mmHg for patients 50-69 years old
Maintain SBP > 110mmHg for patients 15-49 and >70 years old
Maintain CPP > 60 mmHg (MAP [60-100] – ICP [0-15])
- Administer IV fluids/blood products to treat hypotension
- Administer vasopressors
- Monitor for pulmonary edema
- May need arterial line for continuous BP monitoring
Temperature control in TBI
Maintain normal body temperature
- Hyperthermia increases ICP and cerebral metabolic rate
- Shivering increase cerebral metabolic rate
- Prevent inflammation
Utilizes more oxygen
Prevention of seizure in TBI
Compromise brain oxygen supply
Monitoring
Prophylactic Medications
Maintenance of ICP < 20 in TBI
Consider inserting ICP monitoring device for severe TBI or high risk for worsening
Positioning to facilitate drainage CSF and CBF
> keep head midline (neutral alignment) to facilitate drainage
once C-spine cleared, elevate HOB 30-45 if tolerated
Sedation – (decrease oxygen needs)
Manage nausea/vomiting, pain, anxiety, and agitation (prevents spikes in ICP)
Ventilation
> hyperventilate: cause vasoconstriction in brain – decrease CO2
External ventricular drain (EVD), craniotomy to allow for brain expansion
Do NOT pack ears/nose if CSF leak suspected
What type of fluids are used in TBI management?
Hyperosmolar Fluids: draw fluids out of cells
> Mannitol – osmotic diuretic; not only pull fluid out of brain cells put also pee it out
> Do not give to hypovolemic patients
> Hypertonic saline
What medications are key in management of TBI patients?
- hyperosmoloar fluids
- sedatives to decrease metabolic demand (propfol, midazolam, fentanyl)
- anticoagulant reversals if bleed (vit k and protamine sulfate)
- paralytics: lower metabolic demands (rocuonium)
- anticonvulants: seizure prophylaxis (phenytoin, lorazepam, levetiracetam)
Which patients need a CT and repeat CT?
Adult Trauma:
- altered/depressed mental status
- loss of consciousness or
- significant post-trauma amnesia
Repeat:
- If on anti-coagulants: even if initial negative
- No change or worsening
Diabetes Insipidus Definition and Treatment
Damage to the pituitary gland results in loss of ADH secretion
Decreased reabsorption of water = urine dilute
Polyuria & polydipsia
Hypovolemia
Hypernatremia
Treatment
* Fluid replacement
* ADH replacement (desmopressin- DDAVP)
Cerebral Salt Wasting Definition and Treatment
Not well understood but excess loss of sodium in urine (hyponatremia) causes water to follow = hypovolemia
Normal or low ADH
Polyuria
Usually resolves in weeks to months
Treatment
- Isotonic or hypertonic saline
SIADH
Excess ADH secretion as result of pituitary gland injury = water retention
Hyponatremia
Euvolemia
Usually transient
Treatment
* Fluid restriction
* Hypertonic saline
* Salt tablets
Seizures are due to:
a) increased ICP
b) hypoxia
c) increased metabolic demand
d) secondary injury
Priorities for seizures
a) ABCs
b) Safety
c) anticonvulsants
Brain Herniation Definition, Causes, and Symptoms
Caused by increased ICP
a) Decreased space in cranial vault shifting of brain tissue from normal location
b) Brain presses on medulla (basic functions to sustain life)
Causes drastic neurological deterioration – progress to death; brain forced into brainstem
a) Pupils unequal & sluggish or fixed blown
b) Abnormal posturing
c) Cushing’s Triad
