Module 11 Flashcards
1
Q
Parenchymal Unit of The Nervous System
A
The Neuron
2
Q
Afferent means…
A
Sensory
Periphery –> Brain
3
Q
Efferent means…
A
Motor
Brain –> Periphery
4
Q
2 Types of Cells for Nervous Tissue
A
Supporting Cells (Microglial, Schwan (PNS), Appendimal, etc)
Neurons
5
Q
Soma
A
Cell body of the neuron with DNA/RNA for protein synthesis in the cytoplasm
The cytoplasm extends into the dendrite and axon length
6
Q
Dendrite
A
Conducts information toward the cell body through the synaptic terminal
Communicates with axons and dendrites
7
Q
Axons
A
Long efferent processes carrying information away from the cell body
8
Q
Myelin Sheath
A
White Color - Made up of lipids
Surrounds the axons and allows for the sending of nerve impulses
The more heavily myelinated, the faster the velocity of the nerve impulse
9
Q
Multiple Sclerosis
A
Loss of myelin sheathe in the CNS in patches
10
Q
Gullain Barre Disease
A
Loss of myelin sheathe in the PNS in patches
11
Q
Nodes of Ranvier
A
Interruptions of myelin insulation at intervals across the axon allowing for saltatory conduction (Jumps of action potential) which allows rapid neuron impulse travel
12
Q
Neurons communicate via …
A
Action Potentials (Depolarization, Repolarization, Resting Membrane Potential Set by K, Na and K pump, and Threshold is set by calcium)
13
Q
Grey Matter
A
Outer layer of brain
Made up of cell bodies (soma)
14
Q
White Matter
A
Inner layer of brain
Made up of axons (white due to myelin)
15
Q
How does grey and white matter differ in the spinal cord?
A
It is backward
Instead of grey matter being outside like the brain, it is the inside
Instead of white matter being inside like the brain, it is outside
16
Q
Divisions of the Nervous System
A
NS –> CNS and Peripheral NS
CNS –> Brain and Spinal Cord
Peripheral NS –> Motor (efferent) Neurons and Sensory (Afferent) Neurons
Motor (Efferent Neurons) –> ANS and Somatic NS
ANS —> SNS and PNS
17
Q
Covering/Layers Protecting the Brain (Outward to Inward)
A
Bony Skull –> Dura Mater –> Subdural Space –> Arachnoid Membrane –> Subarachnoid Space –> Pia Mater
18
Q
Subarachnoid Space
A
Where CSF circulates to prevent brain damage / cushion
19
Q
Choroid Plexus
A
Where CSF is made
Concentrated area of ependymal cells of the CNS with a rich vascular network allowing them to make cerebral spinal fluid
20
Q
The spinal cord runs from …
A
the Lumbar to Sacral area
21
Q
What protects the spinal cord
A
Boney Vertebrae
22
Q
Dorsal Horn
A
Sensory/Afferent Information enters here and some of it will cross over while some of it stays on the same side
23
Q
Anterior/Ventral Horn
A
Efferent/Motor information will travel through the front of the spinal cord and through here
24
Q
Cervical Nerve Roots
A
lower segment (of the root)
25
Lumbar Nerve Roots
upper segment (of the root)
26
How many peripheral nerves are there?
8 Cervical
12 Thoracic
5 Lumbar
1 Coccygeal
27
What parts of the nervous system do motor neurons oversee?
ANS (SNS + PNS)
Somatic NS (Voluntary)
28
Things that Parasympathetic NS Causes
```
Constricts pupil
Stimulates Salivations
Inhibits Heart
Constricts Bronchi
Stimulates Digestive Activity
Stimulates Gallbladder
Contracts Bladder
Relaxes Rectum
```
Cholinergic (Muscarinic) Receptors - stim by acetylcholine
29
Things that the Sympathetic NS Causes
```
Dilates pupil
Inhibits Salivation
Relaxes Bronchi
Accelerates Heart
Inhibits Digestive Activity
Simulates Glucose Release by the Liver
Secretion of EP and NEP from kidney
Relaxes Bladder
Contracts Rectum
```
Adrenergic (Beta) Receptors - stim by EP and NEP
30
Anterolateral Afferent (Sensory) Tracts
Ascending cell bodies/pathways
Unmyelinated or Lightly Myelinated causing slow Conduction
Cell bodies are in the contralateral dorsal horn
31
Posterior Afferent (Sensory) Tracts
Ascending cell bodies/pathways
Large caliber axons and heavily myelinated causing Fast Conduction
Cell bodies are in the ipsilateral dorsal horn
32
Where are the anterolateral tract cell bodies?
Contralateral dorsal horn
33
Where are the posterior tract cell bodies?
Ipsilateral Dorsal Horn
34
What sort of sensation is the anterolateral tracts responsible for?
Pain
Temperature
Crude or Light Touch
Itch
Tickle
Sexual Sensation
35
What sort of sensation is the posterior tracts responsible for?
Position Sense
Discriminative Touch
Vibration Sense
Stereognosis
Graphesthesia
36
Stereognosis
Ability to recognize the form of an object/what it is when holding it
37
Graphesthesia
Can tell what someone wrote with their finger on your back/ back of hand
38
Efferent (Motor) Tracts
Descending pathways allowing for voluntary control of muscle movements
Cell bodies are in the contralateral motor cortex
Fiber crossed in the pyramidal decussation (medulla) and then synapse with ipsilateral interneurons
These tracts influence the activity of lower motor neurons (LMNs) which allow voluntary muscle control, movement, and motor function
39
Pyramidal Decussation
In the medulla oblongata
Axons crossing over and stacking up to form a pyramid shape. Allows crossing over and then ipsilateral synapsing for motor neurons
40
Frontal Lobe
Front
Higher Order thinking
Awareness, Memory, Emotion, Behavior, Skilled Movements
41
Temporal Lobe
lower area close to brainstem
42
Occipital Lobe
Back of the brain
vision and visual recognition
43
Parietal Lobe
upper part of the brain
processing sensory information
44
What lobe possesses the Motor Cortex?
frontal lobe
45
What lobe possesses Wernickes Area?
Temporal lobe
46
What lobe possesses Brocas Area?
frontal lobe
47
Motor Cortex
Area of the frontal lobe anterior to the central sulcus
Controls basic movements
next to central fissure
48
Cerebellum
part of the brainstem
the "bulb" in back of the brain
controls balance and muscle coordination
"Bella" Balance
49
Right v Left Brain Functions
Right: Reasoning, Language, Scientific Skills
Left: Insight, Spatial Awareness, Creativity
50
Cranial nerves
12 nerves connecting the CNS to various parts of the body/head
51
CN I
Olfactory Nerve
Smell
52
CN II
Optic Nerve
Vision
53
CN III
Oculomotor Nerve
Eye movements
54
CN IV
Trochlear Nerve
Eye movements
55
CN V
Trigeminal Nerve
Facial sensation and jaw movements
56
CN VI
Abducens Nerve
Lateral eye movements
57
CN VII
Facial nerve
Facial expression and taste
58
CN VIII
Acoustic (Vestibulocochlear) Nerve
Hearing and Balance
59
CN IX
Glossopharyngeal Nerve
Taste and Throat Sensations
60
CN X
Vagus nerve
Breathing, circulation and digestion
*unique as it runs throughout the whole body
61
CN XI
Spinal Accessory Nerve
Movements of neck and back muscles
62
CN XII
Hypoglossal Nerve
Tongue Movements
63
Mechanisms of Injury for the Brain
Hypoxic and Ischemic Injury
Injury from Excitatory Amino Acids
Increased Volume and Pressure
Brain Herniation
Cerebral Edema
Hydrocephalus
64
How is the brain a selfish organ?
Body is 2% of the body weight, but received > 15% of cardiac output and consumes 20% of the oxygen available to the body
This is important to know since it relates to hypoxic and ischemic injury
65
Without oxygen, how long will it take before death of brain cells occur?
4-6 minutes
66
The brain cannot do what in regard to oxygen?
cannot store oxygen or do anaerobic metabolism
67
Hypoxia
Deprivation of oxygen with maintained bloodflow
So its bloodflow w/ no oxygenation
68
What does Hypoxia do to the brain?
Depressant effect on the brain --> Euphoria, Listlessness, Drowsiness, Impaired Problem Solving ability
69
Examples of Hypoxic Injury/Situations for the brain?
Reduced Atmospheric Pressure from living at high altitude
Carbon Monoxide poisoning
Severe Anemia
Failure to oxygenate blood
70
Ischemia
Reduced or interrupted blood flow (with metabolic toxin byproduct buildup occurring as a result)
Can be focal or global
71
Hypoxia and Ischemia:
You can have ____ and no ____, but if you have ____ you do have ____
You can have hypoxia and no ischemia, but if you have ischemia you do have hypoxia
72
Focal Ischemia
when blood flow is inadequate to meet the metabolic demands of a PART OF THE BRAIN
ex: Stroke
73
What is Global Ischemia
when blood flow is inadequate to meet the metabolic demands of the ENTIRE BRAIN
ex: Cardiac arrest or circulatory shock
74
Shock
massive vasodilation and blood movement to the periphery, taking away from the brain, and leading to global ischemic injury
75
How fast does global ischemia use up brain resources?
Oxygen - used up in 10 seconds
Glucose Stores - exhausted in 2-4 minutes
Cellular ATP Stores - depleted in 4-5 minutes
76
What occurs, in regard to sodium, calcium, and potassium during global ischemia?
Excessive influx of Na and Ca occurs, with efflux of K
77
What does a large influx of sodium in neuronal cells cause?
Neuronal and Interstitial edema
*The sodium has water follow it down its concentration gradient leading to the in between cell edema (interstitial) *
78
Calcium Cascade
Excessive influx of calcium into neuronal cells (Where it does not belong)
Causes release of intracellular and nuclear enzymes causing cell destruction
79
Watershed Zones
Type of global ischemic injury
Concentrated injury occurs in anatomically vulnerable BORDER ZONES BETWEEN OVERLAPPING TEZRRITORIES supplied by major arteries
Since areas overlap, a lot of deficit, damage, and infarction occurs in junctions of two vascular territories
This type occurs due to a blockage of the cerebral vessel
*Essentially, these areas of the brain are receiving shared blood supply from multiple arteries, and those arteries get blocked meaning widespread damage occurs between areas sharing the arteries*
80
3 Major Cerebral Arteries
Middle
Anterior
Posterior
(MAP)
81
Laminar Necrosis
Type of global ischemic injury
In areas supplies by penetrating (the grey matter) arteries of the cerebral cortex (These are small penetrating arteries)
Necrosis occurs in a laminar way (along a parallel plane or layer) and is most severe in the deeper layers of the cortex
82
How is laminar necrosis like broccoli?
The grey cell bodies are like the florets
The axons are like the stems
A lot of fluid can go in and around the stems/axons during global ischemia (from Na, K, and Ca Influx and Efflux)
83
What is post-ischemic hypoperfusion?
Damage to blood vessels and CHANGES IN BLOOD FLOW as a result of [any] ischemia that prevents the return of adequate tissue perfusion despite reestablishment of circulation
84
What happens to fluid during post-ischemic hypoperfusion?
Inflammatory response launches causing fluid to move from vessels to brain tissue (leading to edema in the brain) and what is left in the capillaries clots and grows sludgy making reperfusion difficult
85
What mechanisms are involved with post-ischemic hypoperfusion?
1. Desaturation of Venous Blood
2. Capillary and Venous Clotting
3. Increased blood viscosity --> Increased flow resistance
4. Ischemic vasoconstriction
5. Increased cerebral metabolic rate and increased need for energy producing substrates
86
How and why does venous blood become desaturated during post-ischemic hypoperfusion?
VENOUS (not arterial) blood is drained of all the oxygen left in it due to the brain needing oxygenation for metabolic processes despite the capillaries being clotted with blood
This causes the venous blood to become sludgy and start clotting too
87
What does the capillary and venous clotting cause in Post-ischemic hypoperfusion?
Clotting --> Sludging of blood --> Increased blood viscosity --> Increased resistance to blood flow in the brain
88
What leads to ischemic vasoconstriction during post-ischemic hypoperfusion?
immediate vasomotor paralysis d/t extracellular acidosis
89
What causes vasomotor paralysis during post-ischemic hypo perfusion?
Acidic conditions/extracellular acidosis leads to vasomotor paralysis immediately
This becomes dangerous because they constrict and are constricted permanently which then causes vasospasm (ischemic vasoconstriction)
90
Why is hypermetabolism a part of post-ischemic hypoperfusion?
To try and rescue the brain (compensatory) EP and NEP is released and circulates which causes increased cerebral metabolic rate and increased need for energy producing substrates (hypermetabolism) which just leads to more substrates and waste products in circulation (which makes circulation even more difficult to fix)
91
Treatment for Global Ischemia
Aimed at providing oxygen and lowering metabolic needs during times when cerebral flow is not occurring as it should
92
Methods of Treatment for Global Ischemia?
Decreasing Brain Temperature
Normovolemic Hemodilution to Overcome Sludging during reperfusion
Control of blood glucose 100-200 mg/dL
93
How do they decrease brain temperature to treat global ischemia?
1. A cerebral cooling collar around the common carotids
2. Whole Body cooling (more used now) where temp is brought down while intubated during it and then carefully warmed after a few days
* Bringing down the temperature will decrease cerebral metabolic demands
94
How does normovolemic hemodilution treat global ischemia?
Normal saline is isotonic and stays in vessels
The purpose is that it overcomes sludging in the capillaries/veins during reperfusion, so fluid and flow starts going once again
95
Why do we control global ischemia patients blood glucose level at 100-200 mg/dL as treatment for global ischemia?
Giving glucose higher than the recommended need is important since the metabolic demand in the brain and tissues is high
We want to reduce the metabolic demand with cooling, but we also need to give glucose to help meet demands
96
Excitotoxicity
Injurt d/t excitatory amino acids (neurotransmitters)
Overstimulation of receptors for specific AA that act as excitatory neurotransmitters
Overproduction stimulates nervous tissue as a response to injury, and this overabundance leads to increased metabolic injury and nervous tissue damage
97
Main 2 Excitatory Neurotransmitters (AA) that can lead to excitotoxicity?
Glutamate
Aspartate
98
Glutamate
Principal Excitatory neurotransmitter in the brain involved in normal brain function
Causes calcium cascade and glutamate toxicity w/ neuronal swelling
99
How does Glutamate cause symptoms/excitotoxicity?
Injury occurs --> Extracellular glutamine accumulated --> glutamate toxicity --> Initial symptoms (w/in minutes) are neuronal swelling (d/t sodium influx w/ water following) --> Later symptoms (w/in hours) the calcium cascade influence begins
100
How does Glutamate related to the calcium cascade?
Its activity is coupled with receptor operated calcium ion channels normally --> Calcium cascade
This causes the enzyme release and tissue/cell destruction
101
Research on excitotoxicity is being directed at...
pharmacologic methods to prevent brain damage from excitatory amino acids
102
A person with excitotoxicity can do better recovery if ...
the there is a focus on prevention of the slower effects of the calcium cascade
103
Normal Intracranial Pressure (ICP)`
5-15 mmHg
104
Swelling from Sodium and Calcium Cascade leads to what?
Intracranial volume increases followed by increases in intracranial pressure
105
The skull is a confined cavity meaning it is non-expandable, so if volume increases what areas of the brain can make up for the increase be reducing?
1. Blood Volume (10%)
2. Brain Tissue (80%) (Realistically this cannot change)
3. CSF (10%)
106
Communicating versus Non-communicating Hydrocephalus
Communicating means theres too much CSF produced but theres no obstruction between ventricles
Non-communicating means theres too much fluid and an obstruction is blocking flow between ventricles
107
What things can undergo reciprocal compensation for change in ICP?
CSF and BV (Blood volume)
108
What ways does CSF amount increase?
Excess production
Decreased absorption
Obstructed Circulation
109
What ways does CSF amount decrease?
Translocation to the spinal subarachnoid space
Move some to Basal Cisterna at the bottom of the spinal column
Increased reabsorption
(This decreases volume and pressure)
110
What ways does BV amount increase?
Vasodilation of cerebral blood vessels
Obstruction of venous outflow
111
What ways does BV amount decrease?
Low pressure venous system has limited volume buffering capacity and blood flow is controlled by autoregulatory mechanisms
Basically, autoreg mechanisms like hyperventilation to decrease PCO2 will cause vasoconstriction to lower BV
112
Monroe-Kellie Hypothesis
Reciprocal Compensation
If ICP and Volume increase, CSF and BV need to decrease to compensate
113
What occurs with excessive intracranial pressure?
1. It obstructs cerebral blood flow
2. Destroys brain cells (infarction of brain tissue)
3 Herniation (displaces brain tissue)
114
What things increase cerebral volume?
Brain tumor
Cerebral edema
Bleeding into brain tissue (hematoma)
115
Cerebral Compliance
Change in Volume / Change in pressure
116
What does the pressure-volume curve show?
once compensatory mechanisms have been exceeded, even small changes in volume result in dramatic increases in pressure (only so much can vasoconstrict or go to spinal areas)
117
Normal Cerebral Perfusion Pressure (CPP)
70-100 mmHg
118
CPP Equation
MABP - ICP
*Mean Arterial Blood Pressure Minus Intracranial Pressure
119
What occurs if CPP is below 50-70 mmHg
Brain Ischemia (trouble with perfusion)
120
What occurs if ICP is greater than or equal to MABP in the CPP equation?
Inadequate tissue perfusion
cellular hypoxia
neuronal death
121
Stages of Intracranial Hypertension
1 - Compensation
2 - Increased ICP
3 - Decompensation
4 - Herniation or Loss of CPP
122
Intracranial HTN is not stair like steps/stages, they are ...
a pressure-volume curve
123
Stage 1 Intracranial HTN
Compensation:
Increase in volume in an intracranial compartment leads to decrease in one or both (CSF&BV) of the other volumes
ICP pressure remains normal due to compensation
124
Stage 2 Intracranial HTN
Increase in ICP:
Brain responds by constricting the cerebral arteries to reduce pressure but results in hypoxia, hypercarbia, and deterioration of brain function
(The constriction causes inadequate tissue perfusion, so there's a lack of O2 and buildup of CO2 leading to acidosis and deterioration)
!!!!Once O2 drops, reflex vasodilation occurs causing stage 3!!!!
125
Stage 3 Intracranial HTN
Decompensation:
Cerebral arteries respond to O2 drop with reflex vasodilation --> Increase in blood volume --> Increase further of ICP
At this point a small change in intracranial volume results in LARGE changes in ICP
126
Stage 4 Intracranial HTN
Herniation or Loss of CPP:
Swelling and Pressure increases lead to herniation
When ICP = MABP --> No cerebral perfusion is occurring
127
What are 2 important things to keep in mind when you have ICP patients?
1. Elevate the head of the bed to a maximum of 30 degrees to promote venous passive drainage from gravity (but also has minimal effect on arterial pressure)
2. Make sure head position is midline to prevent kinking of head veins
128
What is the BEST sign of increased ICP? (Test Question)
A decrease in Level of Consciousness is the earliest and most reliable sign of increased ICP
Decreased LOC --> Increased ICP
129
Cushing Reflex
A CNS ischemic response triggered by ischemia of the vasomotor center of the brain
130
What things does the Cushing Reflex cause?
1. Increased MABP (to perfuse the brain)
2. Widening Pulse Pressure (Systolic goes way higher than Diastolic)
3. Reflex Slowing of the Heart Rate (bradycardia) via efferent vagus nerve system to compensate for an increase in BP and ICP (Reflex Bradycardia)
131
What is the brain trying to do with the Cushing Reflex?
It is a "last ditch" effort to maintain cerebral circulation and stay alive, but we hope to catch things before it gets this bad (and we usually do through ICP monitoring- so this is rarely seen)
132
The cushing reflex is an important but _____ indicator of increased ICP
LATE
133
Increases in cerebral volume lead to dramatic ____ in pressure once ________ ______ are overwhelmed
increases; compensatory mechanisms
134
Cerebral Edema
Brain swelling; Increase in tissue volume d/t abnormal fluid accumulation
May or may not increase ICP
135
Way can a cerebral edema may or may not come with an increase in ICP?
It depends on whether its just a small edema and if the brains compensatory mechanisms can handle it by moving CSF or BV
136
Types of Cerebral Edema
Interstitial
Vasogenic
Cytotoxic
137
Interstitial Edema
Interstitium (spaces between cells) swells between axons, involving movement of CSF across the ventricular wall
It is associated with an increase in Sodium and Water content of the peri ventricular white matter, and it passing into it
The sodium and water movement cause ischemia, neuronal interstitial edema, and the calcium cascade
138
What condition causes interstitial edema?
Non-communicating hydrocephalus
CSF is pushed through the ventricular walls so its moving into interstitial spaces thus blocking CSF flow, causing more to move into the interstitium
139
Vasogenic Edema
Increase in Extracellular fluid (ECF) - Mainly BLOOD- surrounding brain cells
Vessels are affected
Occurs mostly in white matter since its more compliant and offers less resistance to fluid accumulation than grey matter
can make the cerebral hemisphere displace and cause herniation
140
What leads to vasogenic edema?
Brain Injury --> Blood brain barrier disrupted --> increased permeability and free diffusion of blood across capillaries that used to not allow most things to cross
141
What are some manifestations of vasogenic edema?
Focal Neurological Deficits (part of the brain, so only part of the function is affected)
Disturbances in Consciousness
Severe Intracranial HTN
*all of these things depend on how much ECF is moving
142
What are some conditions leading to vasogenic edeam?
Anything that interrupts the blood brain barrier or allows fluid into the interstitial space:
Tumors
Prolonged Ischemia
Hemorrhage
Brain Injury
Infectious processes that impair fxn of the blood brain barrier and allow transfer of water and protein into the interstitial space
143
Cellular Hypoxia
Actual swelling of brain cells from not enough O2, too much CO2 for the brain cells, so the brain enters anaerobic metabolism, has decreased ion pump function, and pre-synaptic hypo-polarization
The increased intracellular fluid primarily occurs in gray matter (since that's where the cell body is), but can also occur in white matter
Slowly progressive process
144
In cytotoxic edema, decreased blood flow leads to cellular hypoxia and then what?
1. Cellular Hypoxia --> Decreased ATP production and E stores --> Decreased ion pump function --> Water entry and cellular swelling from sodium rushing in
2. Cellular hypoxia --> Anaerobic metabolism --> Increase lactic acid and extracellular acidosis --> water entry and cellular swelling
145
What does pre-synaptic hypo-polarization in cytotoxic edema lead to?
Hypo-polarization --> Calcium Cascade from broken gates causing increased intracellular Ca --> NT like Glutamate and Aspartate is then increased in conjunction with the cascade --> There is no reuptake of calcium or NTs leading to low osmotic states, hyperpolarization, Ca channels remaining open, and loss of cellular function
146
The extra Ca and NTs from hypo-polarization in cytotoxic edema can lead to what outcomes?
1. Electrical Hyperactivity (Seizure) until exhaustion --> 2. Electrical silence (Death)
147
Potassium sets...
the resting membrane potential
148
The Na-K Pump determines ...
signals
149
Calcium sets ...
the threshold
150
What 3 things determine neuronal activity/impulses?
1. K
2. Na-K pumps
3. Calcium
151
Cytotoxic edema may be severe enough to cause what?
rupturing of cells and production of cerebral infarction with necrosis of brain tissue after
152
What sort of cells can have cytotoxic edema occur in them?
Vascular Endothelium
Smooth Muscle Cells
Astrocytes
Oligodendrocytes
Neurons
153
Manifestations of Cytotoxic Edema
Major Changes like:
Stupor
Coma
Eventual seizure
Potential brain infarction and necrosis
154
Conditions that can cause cytotoxic edema?
Hypo-osmotic states such as water intoxication
Severe ischemia that impairs the Na-K pump
Hypoxia
Acidosis
Brain Trauma
155
Cerebral edema does not necessarily disrupt brain function unless...
there is an increase in ICP
156
Ways to treat Cerebral Edema?
Localized Edema - Corticosteroids
Stabilize cell membranes and scavenge free radicals
Osmotic Diuretics
157
How are corticosteroids used to treat cerebral edema?
They are used on localized edema surrounding brain tumors
But, the use on generalized edema is controversial/does not work well
158
Why are osmotic diuretics a double edged sword for treating cerebral edema?
Diuretics like mannitol may be useful in the acute phase of vasogenic and cytotoxic edemas when hypo-osmolarity is present
But, the potent diuretics need balance because you could dierese so much volume that they cannot maintain CPP
159
Consciousness
state of awareness of self and the environment and the ability to become oriented to new stimuli
160
The most important manifestation of brain injury is...
complications with level of consciousness (LOC)
161
What are the components of consciousness?
1. Arousal and Wakefulness: State of wakefulness, ability to respond to external stimuli, mediated by RAS
2. Content and Cognition: Moods, awareness of self, awareness of environment, cognitive function, mediated by cerebral cortex in conjunction with RAS
162
What do the components of consciousness reflect?
Person
Place
Time
163
Important Levels of consciousness to consider with brain injury?
```
Confusion
Delirium
Obtundation
Stupor
Coma
```
164
Confusion
Impaired ability to think clearly
Disorientation
Inability to perceive, respond to, or remember current stimuli with customary repetition
165
Delirium
Disturbed consciousness with motor restlessness
Transient hallucinations
Disorientation and sometimes delusions
166
Obtundation
decreased alertness with psychomotor retardation
167
Stupor
not unconscious, but exhibits little or no spontaneous activity
If they were fully conscious, they would push you away or react to you pinching their skin
168
Coma
No pinching of the skin response whatsoever, unlike stupor
Unarousable and unresponsive to external stimuli or internal needs
Just because they are in a coma and are unresponsive does not mean they cannot hear you
169
What determines coma / coma level?
The glascow coma scale
170
What causes abnormal rigidity?
Brain/ Brain Stem Damage
171
Decorticate
Abnormal rigidity:
Upper arms held tightly to the sides with elbows, wrists, and fingers flexes
Legs are extended and internally rotated with feet plantar flexed
172
What causes Decorticate position?
Destructive lesion of the corticospinal tracts within or very near cerebral hemispheres
173
Decerebrate
Abnormal Rigidity
Jaws clenched and neck extended
Arms adducted and stiffly extended at the elbows, with forearms pronated and wrists and fingers flexed
Legs stiffly extended at knees with feet plantar flexed
174
What causes Decerebrate position?
Lesion in the diencephalon, midbrain, or pons
Could also be due to severe metabolic disorders like hypoxia or hypoglycemia
175
What is more dangerous: Decorticate or Decerebrate?
Decerebrate is more dangerous since it comes from brain stem lesions - a person could survive cortex issues, but not necessarily lower brain ones
176
Flaccidity
Abnormal motor response where no motor response is exhibited
If you pick up their arm it will just flop when let go
177
Purposeful Movement
Should be present, if not that is abnormal
It localizes to pain --> unconsciously attempts to remove painful stimulus
178
Complete Flexion
Should be present, if not that is abnormal
Withdraws or flexes extremity indiscriminately in response to painful stimuli
179
Focal Motor Responses that are Abnormal in Adults
Grasp Reflex
Sucking Reflex
Babinski Reflex
180
Grasp Reflex
baby should pull fingers around your finger
goes away by 6 mo old
181
Sucking Reflex
put something in babies mouth, and they suckle on it
182
Babinski Reflex
run nail across foot, under toes and across the side, and the toes should flare out
Should be gone by 2 y/o
183
Consensual Pupillary changes
When light is shined in one eye, the other pupil should constrict too and then dilate when light is removed
184
Direct pupillary changes
When light is shined in one eye, that pupil should constrict and then dilate when the light is removed
185
Pupillary Change Issues
1. Unequal or react sluggishly
2. Pinpoint or midpoint fixed
3. Dilated, fixed
4. Unilateral, fixed
186
Pupillary responses can be ___ or ___
unilateral or bilateral
187
Unequal or Sluggish Reaction of Pupillary changes is caused by ...
compression
188
Pinpoint or midpoint fixed pupillary changes is caused by ...
compression of the brainstem
189
Dilated and fixed pupillary changes is caused by ...
compression of CN III
190
Unilateral and fixed pupillary changes is caused by ...
compression of one CN III
191
Oculomotor Response means...
an intact brainstem
192
What signifies a poor prognosis (brain death) in regard to oculomotor response?
No response after > 48 hours
193
2 Oculomotor Response Tests?
1. Oculocephalic Reflex
| 2. oculovestibular Reflex
194
Oculocephalic reflex
The Doll's Eyes Reflex
Normally - when the head turns side to side the eyes rotate together to the opposite side/stay at one point
Abnormal - eyes rotate together in the same direction as the head
195
Oculovestibular Reflex
Cold or Water Caloric Test
Normally - when the ear canal is irrigated with (cold) water the eyes will turn toward the side being stimulated
Abnormal - absence of eye movement upon stimulation
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Nystagmus
Eyes working backward and forward repeatedly, back and forth, and non-voluntarily
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Important Breathing Patterns for Brain Injury Patients to watch for
1. Cheyne Stokes
2. Central neurogenic ventilation
3. Apneustic Ventilation
4. Cluster Breathing
5. Ataxic Breathing
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Cheyne-Stokes Breathing
Alternating pattern of deep and shallow breathing with periods of apnea
common with diffuse cortical injury or coma from metabolic causes
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Central neurogenic ventilation
Rapid breathing due to direct stimulation of the respiratory center
A regular hyperpneic pattern occurs (Deep and fast breathing) --> Decrease in PCO2 and Increase in pH (Alkalosis)
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What kind of breathing might a patient with diabetic ketoacidosis display?
Kussmaul breathing
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Apneustic Ventilation
Breathing in and out very slowly and prolonged
Prolonged Inspiratory cycle followed by a 2 to 3 second pause, alternating with a prolonged expiratory cycle
Found in lesions of the lower pons - which usually has conduction fibers for chewing food and manipulating the jaw during speech
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Cluster Breathing
Clusters of breaths alternating with irregular periods of apnea
indicates damage to lower pons or high medulla
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Ataxic Breathing
Chaotic respiratory effort - No pattern at all!
Chaotic
Indicates damage to the medullary respiratory control center
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Apnea
periods of 20 seconds of absolutely no breathing at all
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What are some vital signs changes that occur with brain injury?
Hypo or Hyperthermia
Cushings Triad
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How does Hypo and Hyperthermia relate to brain injury?
Hypothalamic or Pituitary injuries or head trauma can lead to inappropriate thermoregulation
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How does cushings triad effect vital sign changes in brain injury patients?
Increase in Systolic BP and Decrease in diastolic BP (Widening pulse pressure) and decreased HR alongside reflex bradycardia
Occurs with increase pressure on the lower brain stem before brain herniation
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Glascow Coma Scale
scale of 3 elements for coma patients
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3 important elements of the Glascow Coma Scale
1. E - Eye Opening
2. M - Motor Response
3. V - Verbal Response
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In the glascow coma scale what are the range of results?
3 to 15
NEVER 0
(can be +4, +6, +5 - or - +1 +1 +1)
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What vessels provide arterial blood flow in cerebral circulation?
2 Internal Carotids
2 Vertebral Arteries --> Basilar Artery
Circle of Willis
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What vessels provide venous blood flow in cerebral circulation
2 sets of veins without valves (Deep and Superficial Cerebral Vein Systems)
2 Internal Jugular Veins
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Why do the veins of the cerebral circulatory system have no valves?
because the flow depends on gravity and pressure in the venous sinuses to increase ICP
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Circle of Willis
allows for shared blood flow in the brain, and if there is a blockage of bloodflow then this allows offsetting of that issue
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Deep Cerebral Venous System
Veins that drain the inner parts of the brain
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Superficial Cerebral Venous System
Veins that drain the outer parts of the brain
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A large portion of the brain is fed by what artery, and what can occur if there is infarct for this artery?
The Middle Cerebral Artery
It supplies a lot of the brain and major damage can occur if infarct happens
*look at the slide on cerebral arteries
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Important Cerebral Arteries
```
Anterior Cerebral Artery
Middle Cerebral Artery
Posterior Cerebral Artery
Anterior Choroid Artery
Basilar Artery
```
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How much of cardiac output goes to the brain
750 mL/min (1/6 of resting CO)
15% of bloodflow goes to the brain
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What regulates cerebral blood flow?
Autoregulatory or local mechanisms that respond to metabolic needs
Examples of local mechanisms are pH and CO2 that function to trigger vasodilate or constrict to increase or decrease cerebral blood flow
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What regulates deep cerebral blood flow?
Autoregulatory mechanisms
Metabolic Factors
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What regulates superficial cerebral blood flow?
Sympathetic NS - it is responsible for vasospasm as seen in a cerebral aneurysm rupture
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Aneurysm
outpouching of the wall in the brain and potential for things to collect in that area and potentially rupture
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What sort of metabolic factors influence cerebral blood flow?
1. CO2 Concentration
2. pH
3. O2 concentration
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2x the amount of CO2 concentration means what for cerebral blood flow?
2x the cerebral blood flow
Vasodilation occurs (which can increase ICP) to prevent acidosis
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How does Hydrogen ion concentration (pH) regulate cerebral blood flow?
low pH can cause vasodilation in most cases to prevent an acidotic brain --> get more O2 and get rid of CO2
BUT, extracellular acidosis also induces vasomotor paralysis making vessels unconstrictable/dilateable past wherever they were when paralysis occurred
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How does O2 concentration regulate cerebral blood flow?
decrease in oxygen --> increase in blood flow to the brain
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Metabolic Factors regulating blood flow are all...
local factors of affecting brain blood flow
