Advanced Patho Final - Neuro I (Acute)

Front 1

What is neuro system analogous to?

Back 1

Web: one neuron might synapse with multiple others which communicate with multiple others, vast web of signaling and response, neuro networks/pathways

Front 2

What is consciousness? In order to have consciousness what two things do you need?

Back 2

Consciousness is a state of awareness of oneself and the environment

Two components:
1) Arousal
2)Awareness

Front 3

Closer look at arousal
What is it?
What does it involve?
What are alterations?

Back 3

Arousal-1 of 2 components of consciousness

Arousal is state of awakeness
-Involves RAS (reticular activating system) and HTO
-Alterations: coma, brain death, seizure

Front 4

Closer look at awareness..
What is it?
What is an alteration?

Back 4

Awareness- 1 of 2 components of consciousness

-Awareness is content of thought
-Alteration is dementia

Front 5

What else does arousal involve?

Back 5

RAS:
1) HTO
2) thalamus
3) epithalamus
4) subthalamus

Front 6

What else does awareness entail?

Back 6

1) superior colliculi
2) pulvinar of thalamus
3) right parietal lobe

Front 7

What is a coma? What are some possible reasons?

Back 7

Coma is alteration of arousal caused by metabolic or structural changes
-metabolic: i.e. hypoglycemia, hypoxia
-structures: i.e. damage to RAS, brainstem, lesions/masses, disjoint b/w neurons

Front 8

******What is the GCS?

Back 8

Glascow Coma Scale
The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.
-lowest score-3; highest-15
-3 categories: eye opening, motor response, verbal response

Front 9

What are other measures of brain functions?

Back 9

respiratory pattern
pupillary changes
positioning
oculocephalic reflex
oculovestibular reflex
pathologic reflexes
--rooting reflexes, in infants, not adults, if so-pathological situation, reflexes may also indicate decline/change in brain function

Front 10

What is a TBI?

Back 10

Traumatic Brain Injury
-a traumatic insult to the brain and possible producing physical, intellectual, emotional, social, and vocational changes

Front 11

What are the two main mechanisms of injury?

Back 11

Blunt vs. Open
Focal vs. Diffuse

Front 12

Closer look at blunt vs. open

Back 12

Blunt (closed, nonmissle) trauma
dura intact
focal or diffuse injury ie head to steering wheel

Open (penetrating, missle) trauma
break in dura
focal injury in brain ie GSW

Front 13

Closer look at focal or diffuse

Back 13

Focal:
Coup/Contrecoup Injury
-usually closed
Bone fractures
-open or closed
Basilar skull fracture
-cervical vertebrae pushes upwards into base of skull
focal-you can see, can happen with penetrating or blunt, basilar skull fx-base of skull on spine, compression down, pushes spine up into brain from bottom

Diffuse
Injury to axons of the nerve cells
-injury to a lot of the nerve cell axons, axon can be short or long, depends on what cell it is and where it is, axons can be close to be each other, pull/stretch on axons can cause injury
-shaken baby syndrome-diffuse, brain jostled in skull, axons have shearing, can cause axon damage and brain damage, severity of injury depends on force axons move with

Front 14

What is coup/contrecoup injury?

Back 14

coup/contrecoup-brain not fixed in skull-exists in CSF and can move around, if hit brain on one side impacts that side of skull but will move on other side and hit again, first injury-coup, opposing side of skull-contrecoup, on steering wheel coup then back contrecoup additional injury

Front 15

What kind of axon damage occurs?

Back 15

axon damage-twist, stretch, tear a little bit, can end up w/ microscopic tears, can cause changes in permeability in cell membrane-movement of Ca channels dysrupted-elevation Ca can cause cell edema, neuro firing, cell's ability to function changes
- phospholipid bilayer can be damaged, changes in ability for cell to synthesize/break down proteins, all these can be altered if enough cells are altered

Front 16

What are some results of injury?

Back 16

-Observal brain lesion-laceration
-Contusions
-Hematomas (extradural/epidural hemorrhages or hematomas); subdural; intracerebral
-increased ICP
-concussion
-diffuse axonal injury

Front 17

What is a contusion?

Back 17

-like a "bruise", brain gets bumped
-severity depends on force of impact of brain on skull
-may have temporary loss of consciousness
-clinical manifestations depend on location

Front 18

What are the 3 types of hematomas?

Back 18

1) Extradural (epidural) hematoma-hematoma is above the dura
2) Subdural hematoma-hematoma is under the dura, late, 2 weeks later
3) Intracerebral hematoma-hematoma is in cerebral tissue

Front 19

Closer look at extradural hematoma..

Back 19

epidural/extradural-bleeding above dura matter, blood trapped b/w dura mater and skull, MVA most common cause, typically bleeding is f/ artery, often have fx of skull, as it grows or more blood-increase in HA, vomiting, drowsiness, confusion, may have seizure, may have one sided hemiperisis, ipsilateral pupil dilation (same side as injury), may be unconscious at time of injury, regain, then lose it again

Front 20

********Closer look at subdural hematoma..

Back 20

subdural-below dura but above brain tissue, often commonly caused by MVA, about half associated w/ skull fx, usually f/ venous source, can be very acute rapidly after injury or slow hematoma-2 days-2 wks after injury, so monitor LOC, HA, behavior after an injury, restlessness, changes in cognition, confusion

Front 21

**Closer look at Intracerebral hematoma..

Back 21

Hematoma is in cerebral tissue
-bleeding inside cerebrum tissue, MVA again, also with falls, may have contusions w/ brain, a lot of shearing forces on brain on axons and vessels can lead to bleeding and intracerebral hematoma, all of these have increased ICP risk but this one is higher, may have coma if so, can occur 3-10 days after injury

Front 22

What is intracranial pressure?

Back 22

pressure exerted by incompressible tissue (skull) and fluid volumes
-interstitial fluid
-blood
-CSF

Increases with increased intracranial content
-edema
-hemorrhage
-excess CSF

Front 23

How do you initially compensate for increased ICP?

Back 23

ie f/ hematoma-body compensates-decreases CSF around brain, some venous constriction for less blood flow, balances out so brain pressure doesn't become so great, works for a while, but once you reach certain point body can't compensate (only so much CSF and constriction can take place), b/c skull is so fixed ICP rises very quickly

Front 24

*****What are early signs of increased ICP?

Back 24

-decreased O2
-transient confusion, drowsiness, slight pupillary and breathing changes

Front 25

**What are some later signs of ICP?

Back 25

-hypoxia, acidosis
-decreased arousal, respiratory changes, sluggish and dilated pupils, bradycardia
-herniation

Front 26

What is a herniation?

Back 26

part of brain actually shifts, tissue that is edematous causes tissue to shift to area of lower pressure, diff types of herniation
-bad b/c injury to tissue on other side of brain, chances of recovering are lowered b/c more brain is damaged, if you hit area that's not vital have better change, brain can adapt other noninjured areas can learn esp in children

Front 27

What is a concussion?

Back 27

temporary axonal disturbances causing varying degrees of attention deficits, memory deficits, and loss of consciousness
-Graded I-IV

Front 28

*******What are the different grades of concussions? Which is "classic"

Back 28

can be contusion-hits skull, or axon sheathing, can be mild impact to severe impact, no loss of consciousness, transient, or longer unconsciousness

I-III: considered mild, and no loss of consciousness
I: confusion, disorientation, and momentary amnesia
II: momentary confusion and retrograde amnesia
III: confusion with retrograde and anterograde amnesia

****Grade IV: classic cerebral concussion

Front 29

Closer look at Grade IV Concussion

Back 29

Classic Cerebral Concussion: disconnect of function and signaling
-disconnection of cerebral systems from the brain system and reticular activating system
-physiologic disruption: brief vital sign changes: lowered respiration and BP
Neurologic disruption:
********-loss of consciousness (<6 hours)
-Anterograde and retrograde amnesia
-confusion

Front 30

WHat is a diffuse axonal injury?

Back 30

produces a traumatic coma lasting more than 6 hours b/c of axonal disruption

Front 31

What are first two types of diffuse axonal injury?

Back 31

Mild:
-6-24 hours of coma
-decebrate or decorticate posturing

Moderate:
>24 hours of coma
-actual tearing of some axons
-GCS: 4-8 progressing 6-8 by 24 hours
-decebrate or decorticate posturing
-confusion with waking
-retrograde and anterograde amnesia
-permanent neuro changes

Front 32

******What is the third type of diffuse axonal injury?

Back 32

*****Severe:
-severe mechanical disruption of axons
-GSC: 3-8
-immediate autonomic dysfuntion
-permanent neuro changes

Front 33

********What is an aneurysm? What causes it?

Back 33

Pressure inside vessel > strength of vessel wall

Causes:
-HTN
-thin endothelial layer
-internal elastic lamina altered
-missing muscularis layer
-atherosclerotic changes-watch cholesterol changes

-may be asymptomatic
-sx associated with structure aneurysm is compressing
-concern-rupture

Front 34

What are the 3 types of strokes? Just list..

Back 34

Stroke-closely associated with aneurysm

1) Thrombolytic Stroke
2) Embolic Stroke
3) Hemorrhagic Stroke

Front 35

********Closer look at thrombotic strok

Back 35

Thrombotic stroke
-arterial occlusions caused by thrombi formed in arteries supplying the brain or in the intracranial vessels
-*****Transient Ischemic Attack (TIA)

Front 36

******Closer look at hemorrhagic stroke

Back 36

Hemorrhagic Stroke
-bleeding occurs
-ruptured aneurysm, vascular malformation, bleeding disorders
-HTN --> vessel rupture

-Cerebral Hemorrhage
-increased hematoma leads to increased ICP
-damage to adjacent tissue
-decreased cerebral blood flow in vasculature leads to ischemia
-disruption of blood brain barrier

Front 37

Thrombotic Stroke & Embolic Stroke patho

Back 37

With both (not hemorrhagic):
area of ischemia, blood supply blocked b/c vessels too narrow or emboli has come f/ somewhere else and cause block-ischemia and low oxygen-can cause depletion of ATP, ATP needed in neurons to keep membrane potential, lose ATP and can lose membrane potential and changes in polarization-can lead to influx of Ca (see previously discussed assoc problem), also can have lactic acid buildup f/ ischemia which can lead to cell damage/death, brain is aerobic doesn't like anaerobic situations

In sum:
-calcium accumulation
-increased lactic acid
-lead to cellular damage and death

Front 38

What are manifestations of stroke?

Back 38

all of a sudden can't perform neurologically, visually, sensory, personality, motor, bad HA

Front 39

What are long term results of brain injury?

Back 39

Depends on area of brain injured
-personality changes
-memory changes
-comprehension
-speech/language changes
-motor changes
-coordination changes
-frontal lobe: nice to mean or mean to nice

Front 40

What is a spinal cord injury?

Back 40

Traumatic injury of vertebral and neural tissues due to compressing, pulling, or shearing forces

Front 41

Type of spinal cord injuries?

Back 41

-Most commonly occurs during or b/c of vertebral injuries:
-hyperflexion
-hyperextension
-rotation
-fracture of vertebrae
-compression

Front 42

********What are some results of injury?

Back 42

*****Spinal shock
-temporary cessation of normal activity (including reflex function) of the spinal cord at and below the level of injury
-may resolve completely or with partial complications=para/quadriplegia

paraplegia
quadriplegia
remaiing and lost function depends on level of injury

Autonomic dysreflexia

Front 43

*******What is autonomic dysreflexia?

Back 43

autonomic hyperreflexia/dysreflexia:
-massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system

Front 44

Autonomic dysreflexia: what is mechanism of normal spine?

Back 44

1) stimulus
2a) signal to brain
2b) signal to reflex arc
3) brain responds to organs

-normal-stimulation-ie full bladder, cause signaling up spine and up ganglion of Sympathetic NS, might involve reflex arc or communication up and down link
-full bladder-need BR, brain recognizes and emptying occurs, under motor control, need all of these working for nml response to stimuli

Front 45

Autonomic dysreflexia: what happens in this?

Back 45

1) stimulus
2) Sympathetic NS responds
3) medulla cannot control other SNS symptoms b/c lesion blocks the signal
4) vasodilation until level of lesion: flushing HA, sweating

normal signal flow; stimulus-travels up spine and can't travel anymore, signals can't reach brain, SNS picks it up and get a sympathetic response, HTN, pallor, goosebumps, so that signal is not traveling up but symp response, brain can response to sympathetic changes, but can't send signal back down to correct sympathetic changes, b/c ganglion doesn't run the whole way down, ie control heart and SA node but not others, disaray of going on and body is confused, chaos in this, brain can't send signal down correction of stimuli, also has autonomic

Front 46

************what is a seizure?

Back 46

sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons
-often resulting in convulsions (clonic-tonic) but not always
-can be caused by trauma, fever esp in kids, brain injury, can also be chronic ie epilepsy

Front 47

******What is an epileptogenic focus?

Back 47

Group of neurons that are hypersenstivive to paroxysmal depolarization

epileptogenic focus-neurons hypersensitive to depolarization, like to depolarize easily, random firing of neurons, normally excitation = inhibition
- seizure-lots more excitation and not enough inhibition, some has to do with lack of membrane stability-movement of K, Na, Ca across cell membrane abnormally which fires more, also inc in glutamate (neurotransmitter) can cause excitation of neurons; gamma-inhibitory, slows down K/Ca channels so harder to get membrane potential to occur w/ neuron, if you lose gaba (animobyturic acid) lose some inhibition, balance off and can have firing of neuron, all about balance-want factors that cause excitation of neuron = inhibition

-EXCITATION > inhibition
-cell membrane instability
-increased glutamate
-aminobyturic acid

Front 48

What is the patho of seizures?

Back 48

1) Epileptogetic neuron firing: (Ca channels open: calcium influx; Na channels open; action potential fires)

leading to..
2) Spread to interhemispheric tracks to contralateral cortex

leads to..
3) subcortical basal ganglia thalamus brain stem spinal cord

Front 49

Seizures-when do they begin and end?

Back 49

Begin:
have trigger typically-can be easy to ID or not-sleep deprivation, lights, stress, a smell, end up w/ firing of epileptogenic-see slide, end up with movement of signaling and firing of neurons across hemisphere b/c brain is so compact, inc firing of basal ganglia f/ movement, also thalamus, brain stem, spinal cord, etc. leading to convulsion

End: will resolve when nerves/muscle can no longer generate action potential-out of glucose, oxygen, resources to make membrane potential gone..

Front 50

What are some different types of seizures?

Back 50

1) generalized seizure-tonic (contraction) then clonic movement, afterwards-tired and wants to sleep, can also lose contents of urine and consciousness which can help dx

2) partial (focal) seizures-isolated to a part of body, not the whole grand mal, b/c epileg focus remains isolated to one part of brain, doesn't travel and recruit more parts of brain as with grand mal, can be arm movement, hearing change, kids have absence seizure where they just stare space out

Front 51

***********What is meningitis?

Back 51

Meningitis (infection of the meninges) may be caused by bacteria, viruses, fungi, parasites, or other toxins.

Front 52

*********Clinical manifestations of meningitis?

Back 52

-inflammation and irration-generalized meningeal signs-throbbing HA that gets worse, photophobia gets worse, nuchal rigidity, Kernig sign, Brudzinski sign
-local tissue dysfunction-hemiparesis/hemiplegia, ataxia, and seizures
-mass effect-decreased LOC, n/v, inc ICP
-vascular compromise

Front 53

What is encephalitis?

Back 53

an acute febrile illness, usually of viral origin, with nervous system invovement
-most common by arthropod/mosquito borne virusses and herpes simplex
-fever, confusion