Neuropathology Flashcards

(416 cards)

1
Q

How is the Nervous System organized?

A

CNS
PNS
Brain and Spinal cord
Somatic and Autonomic Nervous System

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2
Q

What are the two components of the CNS?

A

Brain and Spinal Cord

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3
Q

What are the two components of the peripheral nervous system?

A

Cranial nerves

Spinal Nerves

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4
Q

What are the voluntary and involuntary PNS pathways?

A

Somatic (voluntary)

Autonomic (involuntary)

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5
Q

What is the name of the sensory somatic pathways?

A

Afferent

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6
Q

What is the name of the effector somatic pathways?

A

Efferent

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7
Q

What are the two branches of the autonomic nervous system?

A

Sympathetic

Parasympathetic

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8
Q

What are the tree types of afferent information that can be transmitted to the CNS?

A

Somatic sensory
Visceral Sensory
Special Sensory

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9
Q

What are the two types of efferent responses?

A

Somatic motor

Autonomic motor

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10
Q

What are the three components of a ANS reflex?

A

Sensory
Central integrator
Motor effector

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11
Q

What are the functions of the CNS?

A

Central control center
Integrates many incoming signals and coordinates appropriate outgoing neural signals
Carry out higher mental function (memory and learning)

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12
Q

What are the functions of the PNS?

A

Connect CNS with peripheral structures
Connective tissue provides protection and support making the PNA nerves more resilient
Consists of bundles of nerve fibers, connective tissue and blood vessels

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13
Q

If injury were to occur to both the CNS and PNS which is most likely to recover and why?

A

PNS, since protective connective tissue is present

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14
Q

How are spinal nerves named?

A

Named for their site of emergence from the vertebral column

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15
Q

At what point are spinal nerves no longer considered part of the CNS?

A

Once exited from the spinal cord are now part of the PNS

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16
Q

What component of the brain is the spinal cord an extension of?

A

The Medulla Oblongata

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17
Q

What bones make up the vertebral column?

A
7 Cervical
12 Thoracic
5 Lumbar
5 Sacral
1 Coccyx (4 fused)
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18
Q

Where do the nerves of the cauda equina originate?

A

Conus Medullaris

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19
Q

What components make up the cauda equina?

A

2-5 Lumbar nerve pairs
1-5 Sacral nerve pairs
Coccygeal nerves

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20
Q

What structures does the cauda equina innervate?

A

Pelvic organs
Lower limbs
PSNS innervation to bladder and internal/external anal sphincters

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21
Q

At what level does the spinal cord typically stop?

A

T12-L2

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22
Q

What is the length of the pre-ganglionic fibers in the SNS compared to the PSNS?

A

Sympathetic short

PSNS long

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23
Q

What is the neurotransmitter of the SNS?

A

NE

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24
Q

What is the neurotransmitter of the PSNS?

A

Ach

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25
Where do SNS nerves originate?
Thoracic and Lumbar
26
Where do the PSNS nerves originate?
Cranial Sacral
27
What are the two types of cells of the nervous system?
Neurons and Supporting Cells
28
What are the components of a neuron?
Cell body Dendrite Axon
29
What name is used to describe a dense pack of cell bodies in the CNS?
Nucleus
30
What name is used to describe a dense pack of cell bodies in the PNS?
Ganglia or a Plexus
31
What is the purpose of a dendrite?
It catches impulses directed toward a cell body
32
What is the purpose of an axon?
It creates impulses away from the cell body
33
What is the name of the supporting cells in the CNS?
Neuroglial
34
What is the name of the supporting cells in the PNS?
Schwann
35
What type of cells are the majority in the brain?
Supporting cells
36
What increases the surface area for receiving incoming messages from other neurons?
Cytoplasm
37
At what point does electronic conduction occur?
Unmyelinated Axon
38
What type of conduction occurs in an myelinated axon?
Sultatory Conduction
39
What are the nodes of Ranvier?
Area of high density of VG Na channels that potentiate the AP along the axon
40
What are the benefits of Sultatory conduction?
Its fast | Energy efficient, only have Na/K ATP pumps at the nodes
41
What are the functions of the ependymal cells?
Moves CSF through the ventricles | Barrier between CSF and interstitial fluid
42
What type of cells produce myelin?
Oligodendrocytes
43
What are the functions of the astrocytes?
Regulate composition of interstitial fluid Form supportive framework for the nerve cells Provide glucose to and remove ammonia from the neurons
44
What is the equivalent to the macrophage in the CNS?
Microglia
45
What are the three layers of a nerve?
Epineurium Perineurium Endoneurium
46
How is a nerve organized?
Each axon is called a nerve fiber --> the nerve fiber aligns into a nerve bundle --> the nerve bundle runs together in a peripheral nerve
47
What can be considered a nerve fiber?
Axon or a dendrite
48
Where are nerves located?
In the peripheral nervous system, can be sensory or motor fiber
49
What terminology is used to describe a bundle of fibers in the CNS?
A nerve tract
50
What is considered the white matter of the CNS?
Composed mainly of myelinated nerve fibers which often extend the length of the spinal cord
51
What makes up the gray matter of the CNS?
Nerve cells bodies and non-myelinated nerve fibers
52
What is a tract?
Nerve fibers of the brain or spinal cord with common origin and destination (ascending or descending)
53
What type of information does an afferent neuron carry?
Conveys info from tissues and organs to CNS | Sensory receptors
54
What type of information does an efferent neuron carry?
Convey inför from he CNS out to the effector cells
55
Where are the cell bodies and dendrites of efferent neurons located?
Within the CNS, axons extend out to periphery
56
What is the purpose of an interneuron?
Connect afferent and efferent neurons within the CNS
57
Where are interneurons located?
Within the CNS
58
What factors does neuronal health, function and survival depend on?
Blood flow to the neurons Waste removal from neurons Fluid removal from the cranial vast
59
What waste needs to be removed from neurons?
Neurotransmitters need to be flushed away or dangerously high levels can accumulate
60
What consequences can occur if proper fluid removal from the cranial vault does not occur?
Increase ICP and reduce cerebral blood flow
61
What is the equation used to determine blood pressure?
delta p = Q x R --> BP = SV x HR x TPR Where CO = Q delta p = arterial pressure - venous pressure TPR = resistance
62
At what distance from a capillary will a cell receive diffusion of nutrients?
50um
63
What values represent the normal cerebral blood flow curve?
60-160 MAP is able to be regulated
64
What metabolism is the brain highly dependent upon?
glucose metabolism
65
What type of cells are able to use lactic acid as fuel?
Cardia myocytes and brain cells
66
How does ATP affect neuron volume and function?
ATP is required for activation of pumps that regulate intracellular ion concentrations and thus intracellular volume
67
What is osmotic pressure?
The pressure that must be applied to a solution to prevent the net flow of water into it
68
What term is used to describe the number of molecules in a solution?
Osmoles
69
What is the osmolality of a solution?
The osmotic concentration of a solution expressed as osmoses of solute per kg of solution
70
How does neuronal ischemia cause cell death?
Ischemia --> anaerobic metabolism --> lactic acid lactic acid accumulation/ pump dysfunction = cell swelling Neuroexcitotoxicity = cell death
71
How does lactic acid accumulation cause cell swelling?
Intracellular H ion concentration increases = pH decrease | The Na/H exchanger moves H out Na in = cell swelling
72
How does neuroexcitatoxicity occur with lactic acid accumulation?
Increased intracellular Na concentration (Na/H exchanger) causes RMP to be less negative, closer to threshold and increase AP probability
73
How do glutamate levels increase with neuroexcitatoxicity?
Elevated Na brings neurons closer to threshold causes the release of glutamate from synaptic boutons Glutamate waste accumulates due to reduced blood flow
74
What eight factors come into play with cerebral ischemia?
``` Cellular acidosis Cellular swelling Neuroexcitotoxicity Enzyme activation NO production Inflammation Apoptosis Necrosis ```
75
How does increased glutamate cause additional enzyme activation?
Glutamate causes Na/Ca influx into the cell | Ca is a powerful second messenger and activates additional enzymes
76
What enzymes are activated from neuronal ischemia?
Protease and Lipase --> digest cell inside out | Reactive oxygen species
77
Once mitochondrial injury occurs, what happens to the cell?
Mitochondrial depolarization induces apoptosis or necrosis
78
What is apoptosis?
Programmed cell death, the cell can't recover and genetic transcription stops making proteins and shrinks
79
What occurs during cell necrosis?
Lyses open and its contents leak out causing injury to other cells
80
What cells release pro-inflammatory cytokines after becoming ischemic?
Neurons, glial cells and leukocytes
81
How do leukocytes augment ischemic injury?
Cause occlusion of microcirculation | Release proteolytic enzymes and free radicles
82
Why is waste removal from neuron so important?
Higher than normal concentrations of any substance will injure brain cells --> inflammation
83
What are the waste products of neurons?
CO2, lactic acid, neurotransmitters, hormones and other secreted substances
84
What contents are in the cranial vault?
Brain 80% Blood 12% CSF 8%
85
What occurs when there is excess volume in the cranial vault?
Increased ICP
86
How is CPP calculated?
CPP = MAP - ICP
87
What are the functions of the CSF?
Protects the brain
88
Where is CFS produced?
Choroid plexus
89
Where does CSF drain into the venous circulation?
Arachnoid villi where it enters into the sagittal sinus then into the jugular and into the SVC
90
What type of cranial bleed has the highest risk of plugging the arachnoid villi?
Subarachnoid bleed
91
Why is cerebral circulation required?
Waste product removal Substrate delivery Maintaining physiological environment
92
What percentage of CO does the brain receiver?
15%
93
How does CBF rain constant?
Autoregulation and other feedback mechanisms
94
What is the average CBF in an adult?
50mL/100g/min (750mL/min)
95
What part of the brain receives more CBF?
White matter 80mL/100g/m | Gray matter 20mL/100g/m
96
How does we calculate CBF?
CPP | R
97
What occurs on an EEG when there is only 20-25mL/100g/m of CBF?
Slowing
98
What occurs on an EEG when there is only 15-20mL/100g/m of CBF?
Flat
99
What occurs on an EEG when there is only 10mL/100g/m of CBF?
Irreversible brain damage
100
What is the normal ICP?
Less than 10mmHg
101
At what ICP will CPP and CBF be compromised?
Greater than 30mmHg
102
What is a normal CPP?
80-100
103
How is CBF related to CPP?
CBF is directly proportional to CPP
104
How does CPP change is a patients CVP is greater than their ICP?
CPP = MAP - CVP
105
Which artery carries majority of the blood to the brain?
Middle cerebral artery- 80%
106
What are the two types of auto regulation?
Myogenic and Metabolic
107
How does myogenic auto regulation function?
Intrinsic response of smooth muscle in arterioles to change in MAP
108
How does metabolic auto regulation function?
Metabolic demand exceeds CBF, metabolites released cause vasodilation
109
At what MAP is the BBB disturbed?
MAPs greater than 150-160 can result in disruption of the BBB and cerebral edema/hemorrhage
110
How do changes in the CPP affect cerebral vasculature?
Decreased CPP = vasodilation | Increased CPP = vasoconstriction
111
Where do pediatric patient's MAP lie on the auto regulation curve compared to adults?
Its lower than adults making them more susceptible to changes in CBF if there is a reduction in MAP
112
How is the cerebral auto regulation curve affected by HTN?
Shifts to the right in chronic HTN, can be restored if compliant to treatment
113
Why does the changed cerebral auto regulation curve in chronic HTN patients affect anesthesia?
We drop BP with drugs, can fall below shifted auto regulation and cause issues with regulating CBF
114
How does metabolic auto regulation occur?
Too many byproducts sensed = vasodilation | Low metabolism = vasoconstriction
115
What parts of the ANS innervate the intracranial vessels?
Sympathetic fibers Parasympathetic fibers Non-cholinergic/ Non-adrenergic fibers
116
What is the relationship between CBF and PaCO2?
CBF is directly proportional to PaCO2 between 20-80mmHg
117
Below what PaO2 will vasculature and CBF be impacted?
PaO2 less than 60mmHg
118
How does body temperature affect CBF?
CBF changes by 5-7% per 1C Hypothermia decreases CBF and CMR Hyperthermia increases CBF and CMR
119
How does viscosity impact CBF?
Decreased viscosity can increase CBF
120
At what Hct is said to be optimal cerebral O2 delivery?
30%
121
How does anesthesia impact CBF?
Anesthetics increase CFB and decrease CMR (uncoupling)
122
What percentage of total body metabolism is used by the brain?
20%
123
What is the average CMRO in an adult?
3-3.8mL O2/100g/min | = 50mL/min
124
What area of the brain has the greatest CMRO?
Gray matter of the cerebral cortex
125
At what O2 partial pressure does a person become unconscious?
Less than 30mmHg, takes about 10 seconds
126
What is cerebral function dependent upon?
Continuous glucose supply, 90% glucose metabolized aerobically
127
What is the typical glucose consumption?
5mg/100g/min | =75mg/min
128
What cells form the junction between the cerebral vasculature endothelial cells which are nearly fused?
Astrocytes, responsible for BBB
129
What governs the movement of a substance past the BBB?
Size, charge, lipid solubility and protein binding
130
What is the BBB semi-permeable to ?
Electrolytes
131
What should not cross the BBB unless pathology is present?
Proteins
132
How do changes in plasma electrolyte concentrations affect the amount of fluid in the brain?
H2O moves freely across BBB, a change to plasma electrolyte concentrations produce a transient osmotic gradient between plasma and brain
133
How would hyper/hypo tonicity of the plasma affect fluid in the brain?
Hypotonicity plasma = net movement of H2O into brain | Hypertonicity plasma = net movement H2O out of brain
134
What drug can be given to brain water content?
Mannitol
135
How might a newborn develop Kernicterus?
If the child is jaundice and bile pigments enter the BBB, if untreated can cause brain damage or hearing loss
136
How do the ependymal cells move CSF through the ventricles?
They have cilia on apical surface which move CSF
137
What do the ependymal cells allow into the choroid plexus?
Allow for selective movement of water and electrolytes into the CSF
138
Where is the choroid plexus located?
3rd and 4th ventricles
139
How much CSF does a typical produce in one hour?
21mL/hr or 500mL/day
140
What is the typical CSF composition?
K Ca HCO3 and glucose are lower, Na Cl and Mg are higher Very low protein content and NO RBCs
141
What is the total volume of CSF in the cranium and spinal cord at any given time?
150mL
142
What is the normal pH and specific gravity of CSF?
SG: 1.002-1.009 pH: 7.32
143
What is the typical route of flow of CSF?
Lateral ventricles --> foramen of Monro --> 3rd ventricles --> aqueduct of Sylvius --> 4th ventricle --> enters subarachnoid space through the foramen of Magendie
144
What are the three meningeal layers around the brain and spinal cord?
Dura mater Arachnoid mater Pia mater
145
What factors affect CSF drainage?
Clogged Arachnoid villi | Increased CVP
146
If the contents of the cranial vault increase, what is the first compensatory mechanism?
Decreased CSF production and increased drainage
147
Why must an individual be laying lateral in order to get an accurate ICP measurement?
Gravity will have no affect in the lateral position
148
What is said about intracranial compliance when ICP is low?
High compliance when the ICP is low
149
What can conclusion can be made based on the ICP compliance graph?
Once we exceed a certain pressure (10mmHg) small changes in volume will elicit large changes in pressure
150
What can occur with sustained elevations in ICP?
Herniation of the brain (foramen magnum)
151
What part of the brain contains the cerebral cortex?
Forebrain
152
What are the functions of the cerebral cortex?
Participate in perception, the generation of skilled movements, reasoning, learning and memory
153
What are the major functions of the thalamus?
It is a synaptic relay station for sensory pathways on their way to the cerebral cortex Participate in skeletal muscle coordination Awareness
154
What structure of the brain is responsible for coordinated movements for posture and balance and participates in some learning?
Cerebellum
155
What are the three components of the brainstem?
Midbrain, Pons and Medulla Oblongata
156
What cranial nerves cell bodies are located in the brainstem?
III-XII
157
What type od stimulus is sensed by tactile messiness' corpuscle?
Light touch
158
What type od stimulus is sensed by Merkle's corpuscles?
Touch
159
What type od stimulus is sensed by free nerve endings?
Pain
160
What type od stimulus is sensed by pacinian corpuscle?
Vibration and deep pressure
161
What type od stimulus is sensed by ruffini corpuscle?
Warmth
162
What type of sensory stimulus crosses high?
Discriminating touch via dorsal column
163
What type of sensory stimulus crosses low?
Pain and temperature vis lateral column
164
What is the mechanism of skeletal muscle tone?
Stretch receptors send afferent information to the spinal cord (reflex) and cerebellum efferent messages are sent back. Increased rate of afferent firing increases tone Decreased rate of firing reduces motor tone
165
What is the significance of the bulboreticular area in relation to skeletal muscle tone?
Facilitates gamma motor neurons which will facilitate increased muscle tone
166
What modulates autonomic and somatic motor tone?
Sensory information
167
What are the two components of efferent motor tone?
Tonic firing and Spinal cord reflexes
168
Why is it that pain can cause ANS reflex motor responses?
Nociceptive afferent fibers from the viscera and afferents from specific somatic areas of the periphery converge on the same projection neurons in the dorsal horn
169
What path do local versus global proprioceptors take?
Local: 2nd order neuronal axons ascend ipsilateral side of spinal cord and terminate in cerebellum Global: 2nd order neuronal axons decussate in the spinal cord and ascend the contralateral side of spinal cord and terminate in the cerebellum
170
How do majority of the pyramidal tracts descend to skeletal muscle?
Decussate to the contralateral side and project via the lateral corticospinal tract
171
Where do majority of the pyramidal axons synapse?
Synapse with anterior horn motor neurons = lower motor neurons which control skilled/discrete motor functions
172
When is an axon considered extrapyramidal?
Axons descending from neuronal cell bodies in the cerebral cortex, cerebellum, reticular system and elsewhere arrive but do not pass through the medullary pyramids.
173
What are the two major extrapyramidal tracts?
Pontine Reticulospinal Tract | Vestibulospinal Tract
174
What is the final common pathway for control of basic muscle movements?
The anterior horn lower motor neurons
175
What extrapyramidal tract sends signals for gross movements?
Reticulospinal
176
What extrapyramidal tract sends signals for posture and balance?
Vestibulospinal
177
How does nociceptive pain occur?
Pain results from the direct activation of nociceptors in the skin or soft tissue in response to tissue injury
178
How does neuropathic pain occur?
Results from direct injury to nerves in the peripheral or central nervous systems and often have burning or electric sensations
179
What are the two pathways of the spinothalamic tract?
Lateral spinothalamic | Anterior spinothalamic
180
What travels down the lateral spinothalamic tract?
Pain and temperature, fast pain A-delta
181
What travels down the anterior spinothalamic tract?
Polymodal nociception, light touch, slow pain and C fibers
182
Which laminae of the grey matter in the dorsal horn receive almost all afferent neuronal activity?
The first six
183
What laminae of the grey matter are of special interest regarding pain modulation?
Substantantia gelatinosa-Laminae II and III
184
What is the infamous neurotransmitter released by pain?
Substance P
185
What areas send efferent information to the substantia gelatinosa to block transmission via IPSPs?
Periventricular Nuclei | Periaqueductal gray
186
How does the pain inhibitory complex work within the spinal cord?
Laminae where analgesia signals block the pain before it is relayed to the brain
187
What are the brain's opiate system?
Endorphins and Enkephalins
188
Where are enkephalins released?
Brain stem and spinal cord
189
Where are endorphins released?
Hypothalamus and pituitary gland
190
What spinal tract decreases pain?
The dorsolateral tract decreases pain
191
How does referred pain occur?
sensory receptors of different areas go to the spinal cord and synapse on the same second order neuron to the somatosensory cortex
192
What is the difference between upper motor neurons and lower motor neurons?
Upper motor neurons are only in the CNS that provide tonic activity and temper reflexes Lower motor neurons are in the periphery and primarily innervate skeletal muscle
193
What are the cellular processes that are dysregulated?
Excessive activation or excessive inhibition of cellular function
194
What are the two pathways cell injury can occur due to ion pump failure?
Chemical injury | Neuroexctotoxic injury
195
What is the pathological process of a chemical injury to a cell?
Damaged endothelial cells --> BBB disruption --> Increased ISF protein and pro inflammatory mediators
196
What is the pathological process of neuroexcitotoxic injury to a cell?
Increased RMP and AP --> increased glutamate --> increased Ca
197
What are the three isoforms of nitric oxide?
iNOS nNOS eNOS
198
What form of nitric oxide is beneficial in ischemia?
eNOS due to constitutively activity
199
What cause the release of iNOS and nNOS?
Ischemia
200
How does NO released during ischemia cause damage to the cell?
Combines with free radicals to damage cellular proteins, membranes and DNA
201
What are the three basic components of inflammation?
Circulatory Chemical mediator Cellular
202
What is the pathology of an ischemic stroke?
Reduction in blood flow through a major cerebral vessel, characterized by development of an infarct
203
What are the five types of cerebral edema?
``` Cytotoxic Vasogenic Hydrostatic Osmotic Interstitial ```
204
What mechanism causes cytotoxic edema?
Ion pump fails --> increased Na and Ca in neuron --> increased RMP and cell swells
205
What mechanism causes vasogenic edema?
Ion pumps fail --> damaged endothelial cells -- BBB disruption
206
What are the three types of CVAs?
Ischemic Global Hypoperfusion Hemorrhagic
207
What are typically the causes of ischemic strokes?
Thrombotic | Embolic
208
What are typically the causes of a hemorrhagic stroke?
Aneurysm rupture AVM Intracerebral bleed Subarachnoid hemorrhage
209
What are typically the causes of global hypoperfusion?
Shock | Increased ICP
210
What conditions is an intracerebral hemorrhage associated with?
``` HTN Anticoagulation therapy Drug/Alcohol abuse Neoplasia Amyloid Angiopathy Infection ```
211
What factors may suggest an ICH was from drug and alcohol abuse?
Bleed at young age (50-60) Small vessel disease etiology unknown May be associated with coagulopathy
212
What is an amyloid?
Insoluble fibrous protein aggregate
213
What components can cause an amyloid angiopathy?
Amyloid deposits in cerebral vessel wall which predispose the patient to leaky vasculature
214
What infections are especially associated with ICH?
Syphillis TB Associated with the tropics, spread along the basal meninges
215
What are some possible etiologies of aneurysm rupture?
Trauma, Inflammation, Atherosclerosis, congenital
216
What is usually the peak age of an aneurysm rupture?
35-60yrs old
217
How are aneurysms formed?
Degenerative changes in cerebral arterial wall due to turbulent blood flow at a vessel branching point
218
What are the most common locations for an aneurysm to rupture?
Bifurcation in or near the Circle of Willis | Vertebro Basilaara artery
219
What physiologic effects occur after an aneurysm has ruptured?
Increased ICP and decreased CPP Spread of blood causes inflammation Cerebral vasoconstriction Loss of autoregulation
220
What symptoms might a person have after an aneurysm has ruptured?
``` Severe headache (worst of their life) N/V Neck stiffness and photophobia HTN EKG abnormalities ```
221
What are the most common causes of morbidity and mortality in patients that have had an aneurysm rupture?
Neurologic --> ischemia, vasospasm, increased ICP Cardiopulmonary --> arrhythmias, MI, pulmonary edema Electrolyte abnormalities --> decreased Mg, K , Na
222
What causes cerebral vasoconstriction after an aneurysm has ruptured?
Post synaptic A2 receptors (vascular smooth muscle and endothelial cells)
223
Why are arrhythmias often seen after an aneurysm has ruptured?
Neurocardiogenic injury causes catecholamine surge
224
What is an arteriovenous malformation?
Tangled mass of dilated blood vessels, vascular mass center called nidus where blood flows directly from arteries to veins (no capillaries)
225
Where are majority of AVMs found in the brain?
Supratentorial
226
How does an AVM continue to grow over time?
Feeder vessels become dilated and shunt blood into malformation at the expense of surrounding tissue (steal effect)
227
How might an AVM present before the age of 40?
Headache, cerebral hemorrhage, seizure, increase ICP
228
Why is there a loss of auto regulation in AVM vessels?
Loss of elastance do not have muscles to constrict
229
What intraoperative technique can be used to help with the bleeding associated with AVM?
HoTN technique used to decrease blood loss, must consider risk of ischemia and venous thrombosis
230
What is the pathology behind an embolic stroke?
Fragments from outside the brain break off and circulate, the embolus is lodged in intracranial vessels and block blood flow to small vessels
231
What elements are possible causes of emboli formation?
Thrombi Fat Air Tumor
232
What comorbidities are associated with a thrombotic stroke?
Atherosclerosis Hypercoagulation Sickle cell disease Polycythemia vera
233
What signs may indicate an embolic stroke has occurred in broker's area?
Aphasia Expressive
234
What signs may indicate an embolic stroke has occurred in Werkicke's area?
Aphasia receptive
235
What signs may indicate an embolic stroke has occurred in the motor area?
Contralateral upper and lower extremity, face
236
What signs may indicate an embolic stroke has occurred in the somatosensory area?
Contralateral upper and lower extremity and face
237
What cardiovascular pathology predisposes a patient to an ischemic stroke?
A-fib, valve prosthesis, carotid disease, valvular surgery and bacterial endocarditis
238
What type of surgery has the highest risk for post op stroke?
CV surgery
239
How might the provider want to measure blood pressure in a patient with a previous history of a stroke?
Central monitoring BP, auto regulation may be impaired from previous stroke
240
What is a venous air embolus?
Entrainment of air or exogenously delivered gas from operative field into the venous or arterial vasculature
241
What is thought to be a fatal amount of air given to the patient that may cause a VAE?
200-300mL or 3-5mL/kg
242
What two criteria must be present to cause a VAE?
Low venous pressure | The vein must remain patent
243
How does a VAE occur?
The pressure in a vein is sub atmospheric then air could be suctioned into the vein before it collapses
244
What surgery is VAE mostly associate with?
Neurosurgery, veins in the skull may attach to cranium rudder and do not collapse during intracranial surgery
245
How does a VAE cause pulmonary edema?
Air in vasculature cause vasoconstriction, edema, leaky capillaries = pulmonary edema
246
What cardiopulmonary effects can lead to arterial hypoxemia?
Decreased right heart CO and Pulmonary edema
247
How can air move to the left side of the heart?
Inracardiac right to left shunt | Incomplete pulmonary filtering of air emboli
248
What are the cardiovascular effects of a VAE?
Chest pain Brady/tachy arrhythmias Increased filling pressure ST Changes
249
What are the pulmonary effects of a VAE?
Dyspnea, tachypnea, gasp reflex, hypercarbia and hypoxemia
250
What are the neurological effects of a VAE?
Cerebral hypo-perfusion
251
What hemodynamic changes should cause a provider to suspect a VAE?
Unexplained HoTN or sudden decrease in end tidal CO2
252
What is the most sensitive monitoring of a VAE?
TEE
253
What medical condition is contraindicated with the surgical sitting position?
Patent foramen ovale
254
What are risk factors for a subarachnoid hemorrhage?
HTN DM CAD
255
If a bleed occurs inside the brain what is another name for it?
Intra-axial bleed
256
If the bleed originates in the brain but moves to the subarachnoid space what type of bleed is it?
Extra axial bleed
257
What is a major complication associated with SAH?
Clogging of the arachnoid cilli which causes a decrease in CSF absorption = Increased ICP
258
How might secondary hydrocephalus develop after an injury to the meninges has occurred?
Scarred meninges impair reabsorption of CSF
259
How might a SAH develop?
Ruptured aneurysm or bleeding from arterial or venous vasculature in arachnoid space
260
What causes HTN, dysrhythmias and cardiac damage after a SAH?
Catecholamine surge and Increased ICP
261
How does anesthesia affect CBF?
Increases CBF and decreases CMR
262
How do barbiturates affect an ischemic brain?
Protect the brain at doses less than required to suppress EEG burst = vasoconstriction
263
How do volatile anesthetics affect an ischemic brain?
Delay but do not prevent neuronal cell death
264
How does propofol affect an ischemic brain?
Only protective for mild ischemia
265
How does etomidate affect an ischemic brain?
Increases the incidence of brain injury
266
How should anesthetic providers treat a patient with a known ischemic brain event?
Modest increases in BP NO HoTN Do not hyperventilate = vasoconstriction and increase ischemia
267
How long does it take to reestablish auto regulation after a CVA?
Autoregulation and CO2 sensitivity re-established at 4-6 weeks
268
How does DM contribute to an exacerbation of ischemic cerebral injury?
Hyperglycemia --> more substrate for glycolysis --> greater reduction in tissue pH
269
Where is the epidural space located?
Between the dura and the vertebral column
270
What are the causes of a traumatic brain injury?
Head strikes an object Trauma causes neural or glial injury Vascular injury
271
What are the three types of traumatic brain injury?
Extradural hematoma Subdural hematoma Intracerebral bleed
272
What is usually the cause of an extradural hematoma?
Usually arterial source of bleeding
273
What is usually the cause of a subdural hematoma?
Usually torn bridging vein or venous sinus
274
What is usually the cause of an intracerebral bleed?
Small vessel trauma, shearing or penetration
275
Why are children especially susceptible to TBIs?
Less myelinated tissue, larger head to body size and thinner bones that provide protection
276
Why do children have greater intracranial compliance?
Cranial bones have not fused, vaults more expandable
277
What is the goal in treating a TBI?
Preventing secondary brain injury from systemic HoTN, hypoxia, hyperglycemia Optimize CPP without increasing ICP
278
What is the best predictor of a TBI outcome?
Glasgow coma scale
279
What type of fluid should we avoid while trying to resuscitate a patient with a TBI?
Should not contain dextrose, facilitates anaerobic metabolism and inflammation
280
What are the three types of seizure disorders?
Generalized seizures Partial seizures Status Epilepticus
281
What is the most common generalized seizure?
Grand Mal
282
What are the components that make up a grand mal seizure?
Tonic: periods of intense muscle rigidity Clonic: periods of relaxation Post ictal amnesia
283
What are the most common characteristics of a seizure?
Sudden explosive disorderly discharge of cerebral neurons Transient alteration in brain function Increased cerebral O2 demand (60%) Increased cerebral ATP demand (250%)
284
What is the prodroma period of a seizure?
Hours to days before onset of seizure
285
What symptoms are associated with the prodroma period of a seizure?
Malaise and headache
286
What is an aura?
Peculiar sensation preceding onset of generalized seizure
287
What is the postictal state of a seizure?
Time period immediately following seizure activity, disorientation, confusion, fatigue and headache
288
What causes a seizure?
Epileptogenic focus (group of neurons) --> sudden changes in normal membrane potential = hyper excitable
289
What are some causes of seizures?
Hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation and sleep phases
290
What causes the RMP instability?
K conductance and Ca channel abnormalities Deficit in GABA inhibitory system Enhancement excitatory transmission
291
How can a lengthy seizure lead to a brain tissue injury?
Hypoxia from increased O2 demand, decreased pH and lactic acid build up
292
What medical conditions can predispose a patient to a seizure?
Digeorge syndrome, hypoparathyroidism and hypocalcemia
293
What metabolic conditions can predispose a patient to a seizure?
Fever, uremia, hypoxemia, hyperglycemia and hyperventilation
294
What are primarily the causes of a seizure?
Release of excitatory neurotransmitters or a decrease in inhibiting neurotransmitters and change in RMP
295
How does hyperthermia affect seizure threshold?
Increased brain glutamate release, induces respiratory alkalosis leasing to an increased pH
296
How can a sleep disorders impact the chance of a seizure?
Sleep disorders decrease seizure threshold
297
What anesthetics can precipitate a seizure?
Enflurane, Laudanosine (metabolite of NMBA), Methohexital, Ketamine and Normeperidine
298
What anesthetics can be given to increase AP seizure threshold?
Benzodiazepines Barbituates Volatile agent Acidosis
299
How can hyperventilation contribute to causing a seizure?
H+ leaves the cell --> K goes in making the RMP less negative Ca binds to proteins and instability of Na occurs
300
How can sensory stimulation alter seizure activity?
Interferes with ability to recruit brain structures that transmit paroxysmal activity to other regions
301
What is inter cranial HTN?
ICP > 20mmHg
302
How can an elevated ICP occur?
Brain edema, increased CB volume, increased intracranial CSF volume and intra, extra axial mass lesions
303
Why can't cytotoxic edema cause an increase in ICP by itself?
Simply a movement of fluid from the brain interstitium into the cell
304
What type of edema will actually cause an increased ICP?
Vasogenic, once brain interstitial fluid is reduced fluid will move from the plasma. Loss of tight junctions allows proteins to move and water to follow
305
At what PaCO2 does auto regulation occur?
20-80mmHg
306
At what PaO2 does auto regulation occur?
307
What is the pathology behind communicating hydrocephalus?
Decreased CSF absorption at the arachnoid villi
308
What is the pathology of obstructive hydrocephalus?
Obstructing to CSF circulation
309
When does hydrocephalus occur?
Excess fluid within the cranial vault or subarachnoid space | When production of CSF volume is not matched by CSF absorption
310
Why shouldn't the provider give mannitol before the cranium has been opened if a hemorrhagic event has occurred?
The increased ICP is essentially back pressure on stopping additional bleeding, give mannitol can restart the bleed
311
What are the three components of cushings triad?
HTN Bradycardia Irregular respirations
312
What cranial nerve dysfunction is associated with blurred vision?
CN II (optic)
313
What cranial nerve dysfunction is associated with inability to adduct the eye?
CN III (occulomotor)
314
What cranial nerve dysfunction is associated with inability to abduct the eye?
CN IV Trochlear
315
What is the cushing's reaction?
Initiation of CNS ischemic response due to low perfusion to the brain Results in increased arterial pressure sufficient to move blood into cranial vault
316
What interventions could the anesthetic provider implement in order to treat ICP?
``` Diuretics Hyperventilate the patient = vasoconstriction Hypothermia Normotensive Fluid restriction ```
317
How can PEEP affect ICP?
Increases ICP by generating large intrathoracic pressures which reduces venous return into the right heart Increased CVP due to back pressure in drainage from CSF from the brain
318
How does acute hydrocephalus usually occur?
Result of a head injury
319
What is the pathophysiology of hydrocephalus?
Obstructed CSF --> ventricular dilation proximal to block --> increased CSF --> atrophy of cerebral cortex = degeneration of white matter tracts
320
What two drugs are known to increase ICP?
Ketamine | Succinylcholine
321
How does a VP shunt function?
A catheter is passed into a ventricle of the brain and pump is place to direct flow to the peritoneum
322
What type of ANS dysfunction do people with Parkinson's disease have?
Gastric retention Inappropriate diaphoresis Orthostatic HoTN
323
Why do people with Parkinson;s disease have a tremor?
Basal ganglia initiate the tremor via a cerebellar circuit
324
What causes bradykinesia to occur in Parkinson;s disease?
Basal ganglia send tonic inhibitory impulses to the motor connections in the thalamus (excess GABA and decreased glutamate)
325
How can dopamine help a patient with Parkinson;s disease?
Dopamine can release the basal ganglia inhibition, dopamine initiates a motor response
326
What is the cardinal feature of Parkinson's disease?
Impaired initiation of movement
327
What occurs in Parkinson's disease that causes movements to remain inhibited?
Dopamine neurons are destroyed
328
What drugs would exacerbate the symptoms of Parkinson's disease?
Reglan Phenothiazines Butyrophenones
329
What is the role of Ach in a normal brain?
Ach interneurons modulate dopamine input to the GABA neurons
330
How does Ach affect PD?
Excess Ach can exacerbate PD due to inhibition of GABA
331
What is the role of GABA in the CNS?
Tempers the release of glutamate from the sub thalamic necleus
332
What is the purpose of the substantia Nigra pars compacta?
Group of neurons that release dopamine
333
What type of drugs would be helpful in the treatment of Parkinson's disease?
D1R agonists D2R agonists Anticholinergics NMDA antagonists
334
Why might it be beneficial to give nicotine to a patient with PD?
Nicotinic receptors located pre-synaptically on dopamine neurons activate increase release of dopamine
335
What is the pathology of Alzheimer's disease?
Neurofibrillary tangles and plaques
336
How do senile plaques affect the neurons?
Remodels the synaptic terminal
337
Where does a lot of the damage occur in AD?
Hypo campus where short term memory is converted to long term memory
338
Why do later stages of AD cause impaired motor function?
Later stages occur in the cerebral cortex
339
What genetic component contributes to the formation of AD?
Functional deficit in apolipoprotein E
340
What type of disturbances are typically seen in AD?
Memory, language, personality, motor system and intellect
341
What post op complication are patients with AD at risk for?
Emergence delirium
342
What drugs have been associated with emergence delirium?
Ketamine, Sevoflurance, Desflurane
343
If an anticholinergic was required for a patient with AD which would you use?
Glycopyrolate, it does not cross the BBB
344
What is the initiating event of cerebral palsy?
Cerebral hypoxia
345
Damage to what parts of the brain will cause dyskinetic cerebral palsy?
Basal ganglia and extrapyramidal tract damage
346
What symptoms are typically seen with dyskinetic cerebral palsy?
Fine motor coordination is poor, jerky movements
347
Damage to what part of the brain causes spastic cerebral palsy?
Cerebral cortical damage
348
What symptoms are seen with spastic cerebral palsy?
Increased muscle tone, exaggerated deep tendon reflexes, contractors, scoliosis
349
What is the pathology of MS?
T-cells attack CNS myelin protein resulting in a decrease in number of dendrites and axons in the CNS
350
What symptoms in MS may occur if brain demyelination ensues?
Seizures, spasticity, emotional lability, visual loss, dysarthria, dysphagia, congenital dysfunction
351
What symptoms are seen in patient with MS that develop spinal cord lesions?
Paresthesia, Limb weakness, bowel and bladder symptoms
352
What symptoms are seen in patients with MS that develop brain stem lesions?
ANS dysfunction | Abnormal ventilatory drive
353
What causes a relapse in MS?
Caused by focal inflammatory demyelination
354
What causes remission of MS?
When inflammation subsides and conduction is restored
355
When does permanent dysfunction of MS occur?
When axons are destroyed
356
How might anesthesia impact a patient with MS?
May worsen symptoms, especially spinal anesthesia
357
How might hyperthermia affect patients with MS?
Slows conduction and if high enough can block conduction in demyelinated fibers
358
What is the pathology of ALS?
Progressive, degenerative motor disease involving both upper and lower motor neurons
359
What crania nerves are spared in MS?
CN III, IV, and VI
360
Destruction of what neurons causes lower motor neuron symptoms?
Destruction of the ventral horn neurons (amyotrophic)
361
Destruction of what neurons causes upper motor neuron symptoms?
Scarring of lateral cortic-spinal tracts (lateral sclerosis)
362
What type of symptoms are seen with lower motor neuron demyelination?
Flaccid paralysis, muscle weakness, atrophy, hypotonia, permanent paralysis
363
What symptoms are seen with upper motor neuron demyelination?
Spastic paresis, stiff tight muscles causing weakness of movement patterns, more likely to be repaired
364
What respiratory impairments are associated with ALS?
Progressive respiratory muscle weakness Aspiration risk Difficult mechanical ventilation weaning
365
How can anesthesia affect a patient with ALS?
Subclinical autonomic dysfunction could lead to exaggerated decreases in CV function
366
What is the pathology in guillain barre syndrome?
Inflammatory/immune disorder of the peripheral nerves immune cells/AB attack the schwann cells resulting in destruction of the myelin sheath
367
What is abnormal on a spinal tap in patients with GBS?
Elevated CSF proteins
368
What hematologic complication is associated with GBS?
Thromboembolic complications
369
Why should patients with GBS be considered for enteral feeding?
Bulbar weakness
370
What is the pathology of myasthenia gravis?
Antibodies block nAchR at muscle endplate, increase their turnover flattening postsynaptic folds Antibodies damage postsynaptic membrane complement
371
What is the pathology of Lambert Eaton Myasthenic Syndrome?
There is a decreased Ach release causing muscle weakness
372
What disease process is LEM strongly correlated with?
60% association with small cell lung cancer
373
What is the pathology of muscular dystrophy?
There is a defect in the muscle fibers, absence of dystrophin protein in muscle leads to weakness
374
What population is predisposed to MD?
Males, recessive trait in X-chromosome
375
Where does the spinal cord extend?
From the base of the skull to L1
376
What does the spinal cord turn into at L1-L2?
Conus medullaris
377
What is the branching of nerves from the conus medullaris called?
Cauda equina
378
How many segments is the spinal cord divided into?
31 segments, each with a pair of ventral (motor) and dorsal (sensory) spinal nerve roots
379
What are the contents of the Grey matter?
Nerve cell bodies
380
What are the contents of the white matter?
Ascending and descending nerve tracts
381
What are majority of the causes of spinal cord injuries?
MVA and Sports in the male population
382
Where do most spinal cord injuries occur?
C1-C2 C4-C7 T1-L2 They are the most mobile portions of the vertebral column
383
What causes the secondary spinal cord injury?
Cytokine and amino acid release from injured cells leads to inflammation, free radicals formation, cellular edema, and cellular apoptosis
384
How far can spinal cord edema extend past the injury?
Two spinal cord levels above or below the injury
385
What is spinal cord shock?
Temporary loss or depression of all or most spinal reflex activity below the level of the injury = flaccid paralysis
386
When is spinal cord shock said to be resolved?
Determined by the return of somatic and autonomic reflex arcs
387
Why are patients in spinal shock unable to control their body temperature?
No sweating paired with cutaneous vasodilation
388
What is upper motor neuron syndrome?
Damage to the descending motor pathways gives rise to a set of symptoms
389
What is the pathology of upper motor neuron syndrome?
The spinal reflex circuits are suddenly deprived of input from the motor cortex and brainstem
390
What is the importance of C5-T1?
Brachial plexus
391
What is the importance of C3-C5?
Phrenic nerve
392
What is the importance of C5?
External intercostals
393
What is the importance of T1-T5?
Cardioaccelerator fibers
394
Where are the SNS fibers located?
C7-L1
395
What is the importance of S2-S4?
PSNS fibers exit
396
At what level of spinal cord injury would a patient be prone to autonomic hyperreflexia?
Above T6
397
What is scoliosis?
Lateral rotational curvature of the spine
398
What is the difference between structural and non-structural scoliosis?
Structural- is due to rotation of the spine itself | Non-structural rotation due to reasons other than spine such as posture
399
What is the pathophysiology of scoliosis?
Muscles, ligaments and soft tissue becomes shortened on the concave side of the curvature
400
What determines the degree of deformity in scoliosis?
The compressive forces
401
What does a patient with scoliosis look like?
May have rounded shoulders, prominence of one hip and rib prominences
402
What type of scoliosis can compromise alveolar ventilation?
Structural scoliosis
403
What word is used to describe a posterior and lateral spinal curvature?
Kyphoscoliosis
404
What is ankylosing spondylitis?
Chronic inflammatory joint disease
405
What structures does ankylosing spondylitis primarily affect?
Vertebral joints
406
How can ankylosing spondylitis affect pulmonary function?
Chest movements can become restricted
407
What is thought to cause ankylosing spondylitis?
Autoimmune disease that attacks antigens on cartilage
408
What is spina bifida?
Congenital disorder characterized by a defect in the closure of the neural tube
409
Where do vertebral laminae remain unfused in spina bifida?
Most often at the lumbosacral level
410
What clinical manifestation are typically seen with spina bifida?
Lower limb muscle weakness Gait abnormalities Bowel and bladder dysfunction
411
What position might impair ventilation in a patient with spina bifida?
Prone
412
What nerve pairs are associated with the cauda equina?
Lumbar 2-5 nerve pairs Sacral 1-5 nerve pairs Coccygeal nerves
413
What branch of the ANS innervates the bladder, internal and external anal sphincters?
PSNS
414
How does cauda equina syndrome occur?
Compression of nerve roots below L1 caused by spoke fracture or disk herniation
415
What type of spinal anesthetic can trigger cauda equina syndrome?
Hyperbaric LA
416
What type of LA would you want to avoid when performing a saddle block?
5% Lidocaine