Conditions Effecting the Nervous System and PharmacotherapyPart Two: Select Conditions Flashcards
Exam 3
1
Q
Traumatic Brain Injury TBI Patho: What is it usually caused by?
A
Usually caused by a sudden violent blow or jolt to the head (closed injury) or a penetrating (open injury) head wound that disrupts the normal brain function.
2
Q
Traumatic Brain Injury TBI Patho: What do TBIs do to the brain?
A
The injury can bruise the brain,
damage to axon & nerve fibers, and
cause hemorrhaging.
3
Q
Traumatic Brain Injury: How does it vary?
A
Varies from mild to severe
4
Q
Traumatic Brain Injury: Who are person’s at high risk?
A
Persons at highest risk:
males, children 0–4 years old, adolescents 15–19 years old, adults 65 years of age or older, certain military personnel, and individuals with history of substance abuse
5
Q
Traumatic Brain Injury:
What is Secondary brain injury?
A
Secondary brain injury: indirect result of primary injury, strokes, trauma.
6
Q
Traumatic Brain Injury:
What are contributing factors of Secondary brain injury?
A
Contributing factors include:
hypotension,
hypoxia,
anemia,
hyper/hypocapnia,
cerebral inflammation,
cerebral edema,
IICP,
decreased cerebral perfusion,
cerebral ischemia,
herniation
7
Q
TBI Complications: What changes?
A
Changes in thinking, sensation, language, or emotions
8
Q
TBI Complications: How do seizures occur?
A
Seizures – can occur early or up to 2-5 yrs or longer
9
Q
TBI Complications: How does Alzheimer’s occur?
A
Alzheimer’s disease – repeated brain injury, diffuse axonal injury provides the potential for tau and amyloid to develop
10
Q
TBI Complications: How does Parkinson’s disease occur?
A
Parkinson’s disease – deposits of proteins clumps build up axons & neurons
11
Q
TBI Complications: other complications include?
A
Memory decline
Depression
IICP
Death
12
Q
Types of Traumatic Brain Injuriesinclude:
A
Closed head injury
Open head injury
13
Q
Types of Traumatic Brain Injuries:
What are the types of Closed Head Injury?
A
Concussion
Contusion
Coup/Contrecoup
14
Q
Types of Traumatic Brain Injuries:
What is a Closed Head Injury?
A
Skull is not fractured, but blood vessels rupture, and brain is injured
15
Q
Types of Traumatic Brain Injuries:
What are causes of Closed Head Injury?
A
Causes: head strikes hard surface (e.g. falls, MVA) or object strikes head (e.g. baseball)
16
Q
Types of Traumatic Brain Injuries:
What occurs in closed head injury?
A
Brain lesion occurring in precise location
17
Q
Types of Traumatic Brain Injuries:
What is a Concussion:
A
momentary interruption of brain function, mild TBI
18
Q
Types of Traumatic Brain Injuries:
How many Concussions vary? What does it depend on?
A
Maybe mild (LOC < 30 min or none), mod (LOC 30 min – 6 hrs), severe (LOC >6hrs)
Depends on loss of consciousness
19
Q
Types of Traumatic Brain Injuries:
What are symptoms of concussions?
A
Sx: h/a, n/v, diff concentrating, sleeping–> permanent deficits in brain function
20
Q
Types of Traumatic Brain Injuries:
What kind of damage occurs with concussions?
A
Brainstem damage
21
Q
Types of Traumatic Brain Injuries:
Contusion (brain bruising): What is it?
A
Compression of skull
22
Q
Types of Traumatic Brain Injuries:
What occurs with Contusion (brain bruising)?
A
Blood leaking from injured vessel. Immediate loss of consciousness < 5min
23
Q
Types of Traumatic Brain Injuries:
What kind of damage occurs with Contusion (brain bruising)?
A
Edema, hemorrhage, infarction, necrosis to contused areas
24
Q
Types of Traumatic Brain Injuries:
Closed head injury: Coup/Contrecoup
What is a coup injury?
A
Coup injury: injury at site of impact
25
Types of Traumatic Brain Injuries :
Closed head injury: Coup/Contrecoup
What is a contrecoup injury? What occurs with it?
Contrecoup: injury to the opposite side of the brain from the actual impact.
Axonal sheering
26
Types of Traumatic Brain Injuries :
Closed head injury: Coup/Contrecoup
Contrecoup injury: What is the damage due to?
Damage due to the brain bouncing off the opposite side of the skull.
27
Types of Traumatic Brain Injuries :
Closed head injury: Coup/Contrecoup
Contrecoup injury: When are these injuries commonly seen?
Seen commonly in acceleration and deceleration injuries.
28
Types of Traumatic Brain Injuries:
Open head injury: What is it?
Skull is fractured and bone or other projectiles enter the brain tissue
29
Types of Traumatic Brain Injuries:
TDX & Approach to Management cont.
How is Diagnosis made?
Diagnosis:
history, physical examination (including using the Glasgow Coma scale), head computed tomography (CT), head magnetic resonance imaging (MRI), and ICP monitoring
30
Types of Traumatic Brain Injuries:
TDX & Approach to Management cont.
What treatment is done?
Treatment: rest, analgesics (specifically acetaminophen [Tylenol]), cold compresses, osmotic diuretics (e.g., mannitol), antiseizure agents, sedatives, surgery, rehabilitation (e.g., physical, speech, and occupational therapy)
31
Increased Intracranial Pressure (IICP):
Patho of IICP: What is IICP? What is it caused by?
Increased intracranial content caused by tumor, cerebral edema, excess CSF, hemorrhage.
32
Increased Intracranial Pressure (IICP):
Patho of IICP: What happens in nonexpendable compartments?
Brain, blood, & CSF in nonexpendable compartment
33
Increased Intracranial Pressure (IICP):
Compensatory mechanisms: When there is an increase in intracranial contents what happens?
What is another compensatory mech?
An increase in intracranial contents --> equal reduction of volume of other contents (blood, CSF) to maintain cerebral perfusion
Cerebral Autoregulation:
34
Increased Intracranial Pressure (IICP):
Compensatory mechanisms:
What occurs with Cerebral Autoregulation:
Compensatory alteration in the diameter of intracranial blood vessels
35
Increased Intracranial Pressure (IICP):
Compensatory mechanisms:
What occurs with Cerebral Autoregulation: What is it designed to do?
Designed to maintain a constant blood flow during changes in cerebral perfusion pressure
36
Patho of IICP:
What is IICP caused by?
Caused by disruption of blood brain barrier & loss of autoregulation by brain injury
37
Patho of IICP:
What does IICP cause?
Causes fluid shifts into brain --> cerebral edema
38
Patho of IICP: What happens to brain tissue? Why?
Increased pressure compresses brain tissue
39
Patho of IICP: What occurs with arteries?
Hypoxia, retained CO2 & acidosis dilate cerebral arteries
40
Four Stages of ICP:
Stage 1 of ICH
Compensatory mechanisms (vasoconstriction) to decrease ICP
41
Four Stages of ICP:
Stage 2 of ICH: What is it?
Cont’d expansion of intracranial contents
42
Four Stages of ICP:
Stage 2 of ICH: What occurs? Why?
Systemic arterial vasoconstriction occurs to elevate SBP to overcome IICP & maintain perfusion
43
Four Stages of ICP:
Stage 2 of ICH: What are signs and symptoms?
Subtle transient s/sx: confusion, restlessness, drowsiness
44
Four Stages of ICP:
Stage 2 of ICH: What is the most sensitive indicator?
LOC most sensitive indicator
45
Four Stages of ICP:
Stage 3 of ICH: What is it?
ICP = arterial pressure
46
Four Stages of ICP:
Stage 3 of ICH: What happens to brain tissue?
Brain tissue hypoxia, hypercapnia, condition deteriorates
47
Four Stages of ICP:
Stage 3 of ICH: What are signs and symptoms?
S/sx: decreasing LOC, abnormal breathing, widened pulse pressure, bradycardia, small sluggish pupils
48
Four Stages of ICP:
Stage 3 of ICH: What happens to compensation mechanism?
Compensation mechanism become exhausted
49
Four Stages of ICP:
Stage 3 of ICH: What is lost? What does that lead to?
Autoreg is lost --> intracranial vessels vasodilate
50
Four Stages of ICP:
Stage 3 of ICH: What happens to brain volume and ICP?
Brain volume increases, ICP rises
51
Four Stages of ICP:
Stage 4 of ICH (herniates)
What happens to brain tissue?
Brain tissue herniates to compartment of less pressure
52
Four Stages of ICP:
Stage 4 of ICH (herniates)
What happens to blood supply? What does that lead to?
Blood supply compromised --> ischemia, hypoxia in herniated tissues
53
What is a feared complication of increased ICP?
Herniation
54
What does Herniation refer to?
Refers to displacement of brain tissue
55
Herniations: Where can they occur?
Herniations can occur both above and below the tentorial membrane.
56
What are the two major groups of herniations:
1. Supratentorial:
2. Infratentorial:
57
What are the types of supratentorial herniations?
1. uncal (transtentorial);
2. central;
3. cingulate;
4. transcalvarial (external herniation through opening in skull).
58
What are the types of Infratentorial herniations?
upward herniation of cerebellum;
cerebellar tonsillar move down through foramen magnum.
59
Manifestations of IICP: What changes occur?
Changes in LOC
60
Manifestations of IICP:
Pupillary reactions
Cushing's Reflex (Cushing's Triad)
CV: late ICP sx
Other signs:
61
Manifestations of IICP: How are changes in LOC?
Decreased LOC from pressure on the brainstem & cerebral cortex
62
Manifestations of IICP: Pupillary reactions- what do they indicate?
Indicates presence & level of brainstem dysfunction
63
Manifestations of IICP: Pupillary reactions- Pinpoint pupils & midpoint reflect tell what?
Pinpoint pupils & midpoint reflect brainstem compression
64
Manifestations of IICP: Pupillary reactions- Dilated, fixed reflect what?
Dilated, fixed reflect compression of CN 3
65
Manifestations of IICP: Pupillary reactions- Dilated, Unilateral, fixed tell what?
Unilateral, fixed – compression of 1 CN 3
66
Manifestations of IICP: Cushing's Reflex (Cushings' Triad)
Respirations:
Bradycardia:
Htn:
67
Manifestations of IICP: Cushing's Reflex (Cushings' Triad): How are respirations?
Respirations: Resp shallower, irreg from brainstem compression
68
Manifestations of IICP: Cushing's Reflex (Cushings' Triad): How is bradycardia?
baroreceptor response
69
Manifestations of IICP: Cushing's Reflex (Cushings' Triad): How is htn?
Htn: ICP rises, the body increases BP to ensure adequate blood flow to the brain.
70
Manifestations of IICP: What does CV indicate?
CV: late ICP sx
71
Manifestations of IICP: What are CV symptoms?
↑ SBP, widening pulse pressure, bradycardia
72
Manifestations of IICP: What are other symptoms?
Hypothalamus: high fevers
Vomiting (projectile, results from pressure on medulla)
Decreased reflexes
Posturing
73
Posturing: What are the two types?
Decorticate: bring arms to the core
Decerebrate: Extended arms
74
Posturing: Decorticate- WHat is it?
bring arms to the core
75
Posturing: Decerebrate: - WHat is it?
Decerebrate: Extended arms
76
Posturing: Decorticate- What happens to upper extremities?
Flexion of arms, wrists, and fingers with adduction in the upper exts
77
Posturing: Decorticate- What happens to lower extremities?
External, internal rotation, and plantar flexion of feet
78
Posturing: Decorticate: bring arms to the core
Where are lesions
Lesions in hemispheres or inferomedial part of each cerebral hemisphere of the brain
79
Posturing: Decorticate: What is prognosis?
Better prognosis
80
Posturing: Decerebrate- What happens to extremities?
All four extremities in rigid extension with hyperpronation of the forearms and plantar extension of the feet
81
Posturing: Decerebrate- What is the effect on the brain?
Midbrain or upper pons damage
82
IICP: Approach to Management cont.
Respiratory support
CSF drainage
ICP monitoring
Drug Therapy:
Positioning
Temperature control
83
IICP: Approach to Management cont.
What is Respiratory support?
Mechanically ventilated
84
IICP: Approach to Management cont.
Why is CSF drainage?
Ventricular drainage to ↓ CSF volume & pressure
85
IICP: Approach to Management cont.
What is drug therapy?
Mannitol – reduce cerebral edema, produce rapid diuresis
Anticonvulsants – prevent seizures
Antacids/PPIs – prevent stress ulcers
Dexamethasone – to ↓permeability of
cerebral capillaries, ↓ cerebral edema.
Keeps capillaries from leaking plasma into brain tissue to minimize edema
86
IICP: Approach to Management cont.
What is drug therapy: Mannitol
Mannitol – reduce cerebral edema, produce rapid diuresis
87
IICP: Approach to Management cont.
What is drug therapy: Anticonvulsants –
Anticonvulsants – prevent seizures
88
IICP: Approach to Management cont.
What is drug therapy: Antacids/PPIs
Antacids/PPIs – prevent stress ulcers
89
IICP: Approach to Management cont.
What is drug therapy: Dexamethasone –
Dexamethasone – to ↓permeability of
cerebral capillaries, ↓ cerebral edema.
Keeps capillaries from leaking plasma into brain tissue to minimize edema
90
Hematomas: Patho
A collection of blood in the tissue that develops from ruptured blood vessels.
91
Hematomas: Patho- How fast do they develop?
Hematomas can develop immediately or slowly because of a TBI or surgery.
92
How are hematomas named?
Hematomas are named according to their placement in relation to the meninges, the three continuous membranes covering the brain and spinal cord.
93
Epidural hematoma: What are causes of it?
Causes: severe blow to head, MVA, falls
94
Epidural hematoma: Where does bleeding occur?
Bleeding between the dura and skull
95
Epidural hematoma: What is it usually caused by? (Specific injury not like blow to head)
Usually caused by an arterial tear to the middle meningeal artery in temporal area
96
Epidural hematoma: Accounts for what percent of head injuries?
Accounts for 1-2% of major head injuries. Venous bleed – slower – lucid for a few minutes days
97
Epidural hematoma: What occurs at injury?
Loss Of Consciousness at injury
98
Epidural hematoma: What occurs that would be considered a medical emergency?
Expands quickly….. Medical emergency requiring surgical evacuation
99
Epidural hematoma: What develops hours after injury?
Marked neurologic dysfunction that usually develops within a few hours of injury.
100
Epidural hematoma: How do symptoms start?
Decreasing responsiveness, followed by a short period of alertness if it’s a venous bleed….slower, moving to unconsciousness as hematoma expands
101
Epidural hematoma: As hematoma accumulates, what symptoms occur?
As hematoma accumulates sx: increasing h/a, vomiting, drowsiness, seizures
102
Subdural hematomas : How common?
What are causes of this?
Is more common
Cause: venous tear, trauma, anticoag tx, chronic alcohol
103
Subdural hematomas : Three types
Acute:
Sub acute:
Chronic:
104
Subdural hematomas :
Acute: Where does it develop, how fast, when are symptoms?
Acute: Develop rapidly, located top of skull, sx occur within 24 hours.
105
Subdural hematomas :
SubAcute: How long to develop? What develops?
IICP occurs over approximately 48hrs 2 weeks
106
Subdural hematomas:
Chronic: How long and who does it develop in? How does it develop?
Chronic: Weeks --> months.
Occurs in older adults - brain atrophy - more space for hematoma to develop.
107
Subdural hematomas: WHat does it lead to?
Acts like expanding mass --> IICP --> brain herniation
108
Subdural hematomas: What are symptoms?
Sx: chronic h/a, drowsiness, restless, agitation, slow cognition, confusion --> loss of consciousness, resp pattern changes, pupil dilation, visual changes
109
Subdural hematomas: How fast does it progress?
Progresses rapidly and has a high mortality.
110
Subdural hematoma: What else occurs with it?
80% have headaches, tenderness on palpation over hematoma
Dementia with rigidity
111
Subdural hematoma: What may it require?
May require clot evacuation or breakdown on its onw
112
Types of Hematomas:
Intracerebral hematoma: What does it result from?
Result from bleeding in the brain tissue itself – 2-3% of cases
113
Types of Hematomas:
Intracerebral hematoma: What are causes?
Cause: trauma, spontaneous due to AVM, htn-small vessel disease, hemorrhagic stroke
114
Types of Hematomas:
Intracerebral hematoma: What does it act like? What does it lead to?
Acts as expanding mass --> increasing ICP, compresses brain tissue
115
Types of Hematomas:
Intracerebral hematoma: When do Delayed intracerebral hematomas occur?
Delayed intracerebral hematomas may occur 3-10d after head injury
116
Types of Hematomas: symptoms?
Intracerebral hematoma
Sx: decreasing LOC, contralateral hemiplegia.
117
Types of Hematomas:
Intracerebral hematoma- delayed
symptoms?
Delayed intracerebral hematoma will present like hypertensive brain hemorrhage (sudden decreased LOC, pupillary dilation, breathing pattern changes, Babinski reflex, contralateral hemiplegia)
118
Intracerebral hematoma: What is treatment?
Tx: reduce ICP, allow hematoma to reabsorb
119
Subarachnoid hemorrhage: What is it a type of?
Type of hemorrhagic stroke
120
Subarachnoid hemorrhage: Where is the bleed?
Bleed between arachnoid mater and the pia mater from injured vessel
121
Subarachnoid hemorrhage: What is the primary cause?
What are other causes?
htn
Other causes: tumors, coag disorders, trauma, cocaine, AVM, head injury, family hx, ruptured aneurysm
122
Subarachnoid hemorrhage: Where is there traumatic bleeding?
Traumatic bleeding from the base of the brain
123
Subarachnoid hemorrhage: What occurs with bleeding?
Blood oozes from leaking vessel into subarachnoid space & coats nerve roots, impairs CSF reabsorption & obstructs passages
124
Subarachnoid hemorrhage: What does ruptured vessel cause?
Ruptured vessel causes sudden throbbing explosive headache
125
Subarachnoid hemorrhage: What are symptoms?
Other sx: n/v, visual disturbances, motor deficits, loss of consc
126
Subarachnoid hemorrhage: What are symptoms? *Major symptoms?
Meningeal irritation/inflammation: nuchal rigidity, photophobia, blurred vision, irritability, restlessness & low-grade fever
127
Subarachnoid hemorrhage: What are symptoms? *Kernig and Brudzinki?
(+) Kernig sign & (+) Brudzinki sign
128
Subarachnoid hemorrhage: What are complications?
Complications: die soon after rupture or rebleed
129
Kernig's sign
When the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended
130
Brudzinkski's sign
When patient's neck is flexed flexion of the knees and hips is produced, when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity
131
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
What does bleeding lead to?
Bleeding leads to localized pressure on nearby tissue and increases ICP.
132
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
What happens to hematomas?
The hematoma becomes encapsulated by fibroblasts, blood begins to clot and forms a more solid mass. Blood cells begin to hemolyze.
133
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
Why is more fluid pulled into the tissue?
Hemolysis creates osmotic pressure, which pulls more fluid into the tissue.
134
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
How is size and pressure of the mass?
Size and pressure of the mass increases leading to a further increase in intracranial pressure.
135
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
What does increased pressure lead to?
Increased pressure may cause the brain to herniate (move out of its current position).
136
Effects of Hematomas:
Regardless of the type of hematoma, the effects are very similar:
What occurs that leads to additional ischemia and increased damage?
Vasospasm (cerebral vasoconstriction) may also occur leading to additional ischemia and increased damage.
137
Spinal Cord Injuries:
What are causes of it?
Causes: MVAs, trauma, males (16-30), falls, violence, sports injuries, and weakening vertebral structures (e.g. RA or osteoporosis)
138
Spinal Cord Injuries:
What do they result from?
Result from direct & secondary injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels, myelin from stretching or lacerations
139
Spinal Cord Injuries:
What is a primary injury?
Primary injury - initial mechanical disruption of nerve cells,
140
Spinal Cord Injuries:
What is a secondary injury? (When does it occur?)
Secondary injury (within a few min after injury --> weeks)
141
Spinal Cord Injuries:
What occurs with secondary injury?
Hemorrhages, inflammation, cord edema
Vasospasm, occlusions, ischemia - Hypoxia
Stimulation by excitatory NTs (e.g. glutamate), intracellular calcium overload, oxidative damage, cell death
Spared neurons become damaged
Cystic cavities containing fluid, connective tissue & leukocytes form a barrier that prevents regeneration
C1-C4 cord swelling life-threatening
142
Clinical Manifestations of Spinal cord injuries:
Spinal shock: temporary loss of spinal cord function below lesion
Neurogenic shock: vasogenic shock
Autonomic Hyperreflexia
143
Clinical Manifestations of Spinal cord injuries: Spinal shock?
temporary loss of spinal cord function below lesion
144
Clinical Manifestations of Spinal cord injuries: Neurogenic shock?
vasogenic shock
145
Clinical Manifestations of Spinal cord injuries: Spinal shock- When does it develop?
Develops immediately after injury from loss of discharges from brain/stem & impulse inhibition
146
Clinical Manifestations of Spinal cord injuries: Spinal shock- What ceases? For how long?
Normal activity of spinal cord cells at & below level of injury ceases temporarily
147
Clinical Manifestations of Spinal cord injuries: Spinal shock- What is lost completely?
Complete loss of reflex function
148
Clinical Manifestations of Spinal cord injuries: Spinal shock- Complete loss of reflex function
flaccid paralysis, absence of sensation, loss of bowel & bladder control, transient hypotension, bradycardia, poor circulation, loss of thermal control b/c SNS damage – hypothalamus can’t minimize heat loss through vasoconstriction – pt assumes air temp (poikilothermia)
149
Clinical Manifestations of Spinal cord injuries: Spinal shock- How long does it last?
Lasts from 2 to 3 days --> months
150
Clinical Manifestations of Spinal cord injuries: Spinal shock- What are signs of improvement?
reflex return, spasticity, hyperreflexia, reflex emptying of bladder (can control urine), tingling sensation to legs
151
Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What can it occur with?
Occurs with cervical or upper thoracic cord injury above T6
Can occur with spinal shock
152
Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What is it a disruption of?
Disruption of autonomic pathways
153
Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What is there an absence of?
Absence of sympathetic activity & unopposed parasympathetic tone controlled by vagus nerve
154
Clinical Manifestations of Spinal cord injuries: Neurogenic shock: what are symptoms?
Sx: vasodilation, hypotension, bradycardia, failure to regulate body temp
155
Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia? What are example?
When a noxious stimulus occurs below the level of the spinal cord injury, it triggers reflex sympathetic activity.
(ex; Bladder distension from blocked catheter or urinary retentions, fecal impaction)
156
Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- How does bp increase?
Diffuse vasoconstriction, increase in BP
157
Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- How does parasympathetic response travel? What does that lead to?
Normally, the body compensates by activating the parasympathetic system, causing vasodilation and correcting BP.
However, the parasympathetic response cannot travel below the lesion site.
As a result, continued vasoconstriction leads to dangerously high blood pressure. (life threatening)
158
Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- What are symptoms?
Sx: throbbing h/a, blurred vision, sweating, pilorection
159
Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- What are pns response from the medulla?
Parasymp response from medulla: facial flushing & nasal congestion (vasodilation), bradycardia from vagal stimulation
160
Spinal Cord Injuries:
Immediate Management:
What is done to spine? What is given for swelling?
Immobilization of the spine
Corticosteroid agents to reduce swelling
Spinal traction to reduce the fracture and immobilize the spine
161
Spinal Cord Injuries:
Immediate Management:
What does surgery or removal of fluid do?
Surgical repair of vertebral fractures or surgical removal of the fluid compressing the spinal cord (decompression laminectomy)
162
Spinal Cord Injuries:
Immediate Management:
What should be managed?
Respiratory management
163
Spinal Cord Injuries:
Immediate Management:
What should be given for hypotension?
Vasopressor drugs if hypotensive
164
Patho of TIA
A temporary episode of cerebral ischemia that results in neurologic deficits
165
Spinal Cord Injuries:
Long Term Management:
Physical, occupational, and speech therapy
Mobility assistive devices
Long-term respiratory management
Meticulous skin care
Bowel and bladder training or management
Stool softeners
Antispasmodic agents to treat muscle spasms
Pain management
Nutritional support
Prompt treatment of infections
166
Patho of TIA: How long does it last?
Last less than an hour, typically deficits resolve within 24 hours
167
Patho of TIA: Why are they called mini strokes?
Also called ministrokes because these neurologic deficits mimic a cerebral vascular accident (CVA) or stroke. May occur singly or in a series
168
Patho of TIA: What are they a warning signs of?
Warning sign that a CVA may be impending; however, not all CVAs are preceded by a TIA
169
Patho of TIA: What can occur with TIA? WHy?
Ischemia can occur because of a cerebral artery occlusion (e.g., thrombus, embolus, or plaque), cerebral artery narrowing (e.g., atherosclerosis or spasms), or cerebral artery injury (e.g., inflammation or hypertension).
170
Patho of TIA: What are clinical manifestations?
Clinical manifestations: weakness, numbness, sudden confusion, loss of balance, sudden severe h/a, remains conscious, visual disturbances, or numbness and paresthesia in the face, may occur
171
Patho of TIA: What are complications?
Complications: permanent brain damage, injury from falls, and CVA.
172
TIA: DX & Approach to Management
What is Diagnosis:
history, physical examination (including a neurologic assessment and blood pressure), head CT, head CTA, head MRI, head MRA, carotid ultrasound, serum clotting studies, blood chemistry, complete blood count, erythrocyte sedimentation rate test, and serum lipids test
173
TIA: DX & Approach to Management
What is Treatment?
manage any underlying conditions, antiplatelet aggregation agents, anticoagulants, angioplasty, carotid endarterectomy, smoking cessation, minimizing dietary cholesterol/fat, anti-hyperlipidemics, increasing dietary fruits and vegetables, exercising regularly, limiting alcohol consumption, and eliminating illicit drug use
174
Cerebral Vascular Accident CVA:
AKA?
Also known as a stroke or brain attack.
175
Cerebral Vascular Accident CVA:
What is it?
An interruption of cerebral blood supply from thrombus formation, an embolus, or hypoperfusion due ↓’d blood volume or heart failure
176
Cerebral Vascular Accident CVA:
What are causes?
Causes: total vessel occlusion (e.g., thrombus, embolus, or plaque) or cerebral vessel rupture (e.g., cerebral aneurysm, arteriovenous malformation, or hypertension)
177
Cerebral Vascular Accident CVA:
What are complications?
Complications: neurologic deficits and death
178
CVA:
Who is it most common in?
Most common in African Americans and those living in the Southeast region
179
Cerebral Vascular Accident CVA:
What are modifiable risks factors?
Modifiable Risk factors: afib, physical inactivity, obesity, uncontrolled htn, smoking, hypercholesterolemia, DM, atherosclerosis, oral contraceptive usage, excessive alcohol consumption, and illicit drug use
180
CVA: Stroke Types
Thrombotic
Embolic
Lacunar
Hemorrhagic
181
CVA: Stroke Types
Thrombotic? What forms? How is onset?
Thrombus forms in arteries supplying brain/intracranial vessels
Gradual occlusion of arteries—slow onset – 20-30 yrs
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CVA: Stroke Types
Thrombotic?
Smooth stenotic area degenerates --> macrophages (foam cells), ulcerated --> platelets & fibrin adhere to damaged wall --> clot forms
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CVA: Stroke Types
Thrombotic:
What increases risk of Thrombotic?
Risk ↑: conditions causing increased coagulation or inadequate cerebral perfusion
Dehydration, hypotension, or prolonged vasoconstriction from malignant htn
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CVA: Stroke Types
Embolic: What happens?
Fragments break off from thrombus formed in heart, aorta, carotid artery
Embolus plugs vessel entirely or shatters into fragments becoming part of blood flow
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CVA: Stroke Types
Embolic: What are sources of it?
Sources: fat, air, tumor, bacterial clumps, foreign bodies
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CVA: Stroke Types
Embolic: What does it involve (What brain parts)?
Involves small brain vessels, obstructs bifurcation/narrowing
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CVA: Stroke Types
Embolic: What are risk factors?
Risk factors: afib, lt vent aneurysm, thrombus, recent MI, cardiac defects
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CVA: Stroke Types
Lacunar: What is it?
Small vessel disease, occlusion of single deep perforating artery that supplies small penetrating vessels causing ischemic lesions deep in brain
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CVA: Stroke Types
Lacunar: What does small area of infarction lead to?
Small area of infarction --> motor or sensory deficits
Pure motor & sensory deficits
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CVA: Stroke Types
Lacunar: What is it associated with?
Associated with untreated high BP
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CVA: Stroke Types
Hemorrhagic stroke: Why does it occur?
hemorrhagic stroke from bleeding into the subarachnoid space
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Patho of cerebral infarction:
What is it?
Cerebral anoxia lasting longer than 10 minutes causes cerebral infarction with irreversible changes.
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Patho of cerebral infarction:
Penumbra:
Penumbra - Core surrounded by a rim of borderline hypoxic tissue, which is not severe enough to cause structural damage – still viable!
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Patho of cerebral infarction:
What is needed to treat?
Prompt perfusion of by thrombolytic agents (TPA) promotes perfusion & may prevent necrosis & loss of neuro function
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Patho of cerebral infarction:
“Time is Brain” means?
“Time is Brain” Save the penumbra
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Patho of cerebral infarction:
What happens to the affected area hours later? (6-12hrs and 48-72 hours later)
Affected area becomes pale & softens 6-12 hrs post occlusion
Necrosis, swelling around the insult & mushy disintegration appear 48-72 hrs after
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Patho of cerebral infarction:
What infiltrates necrotic tissue?
Macrophages & phagocytes infiltrate necrotic tissue
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Patho of cerebral infarction:
When does necrosis resolve?
Necrosis resolves by 2nd wk, leaving glial scarring
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Slide 40
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Clinical Manifestations of CVA: Nervous System Dysfunction- include?
Cognitive Changes
Motor Changes
Sensory Changes
Cranial Nerve Dysfunction
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Clinical Manifestations of CVA: Nervous System Dysfunction:
Cognitive changes: What are they?
Level of consciousness
Impaired memory, judgment or problem-solving, and decision-making abilities
Proprioceptive (awareness of body position)
Aphasia (speaking)
Difficulty read, writing, recognizing things, performing simple tasks
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Clinical Manifestations of CVA: Nervous System Dysfunction:
Motor Changes
Hemiplegia/Hemiparesis
Ataxia/Hypotonia or hypertonia
Flaccid paralysis
Incontinence of bowel and bladder
Apraxia (movement/coordination)
Swallowing
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Clinical Manifestations of CVA: Nervous System Dysfunction:
Sensory Changes that occur?
Unaware of existence of paralyzed side
Amaurosis fugax (blindness in one eye)
Hemianopsia (blindness in half of the visual field)
Agnosia (problems perceiving familiar sensory info)
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Clinical Manifestations of CVA: Nervous System Dysfunction:
Cranial Nerve Dysfunction
Dysphagia (trouble swallowing)
Facial paralysis
Absent gag reflex
Impaired tongue movement
Nystagmus (involuntary movements of the eye)
Pupil constriction or dilation
Ptosis (eye lid dropping)
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
What are the types of aphasia?
Expressive (Motor)
Receptive (Sensory)
Global
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Expressive: What is the site of damage?
Broca’s area
Left frontal lobe
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Expressive: Broca's area site of damage?
Cannot speak or write fluently or appropriately.
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Expressive: Left frontal lobe
Patient is aware of deficit and may become frustrated or angry.
Patient understands what is said but cannot communicate verbally.
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Receptive (Sensory): Sites of damage
Werincke’s area
Left temporal lobe, prefrontal
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Receptive (Sensory): Werincke’s area
Unable to understand written or spoken language.
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Receptive (Sensory): Left temporal lobe, prefrontal
Patient may be able to talk, but language is often meaningless.
Neologisms (made up words) are common parts of speech.
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Global: Site of damage
Broca’s and Wernicke’s areas and connecting fibers
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Clinical Manifestations of Cerebrovascular Accident: Aphasia
Global: Broca’s and Wernicke’s areas and connecting fibers effects?
Patient cannot express self or comprehend others’ language. Reading and writing ability are equally affected.
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Evaluation & Treatment
What is eval?
History, physical examination (including a neurologic assessment), head computed tomography, head magnetic resonance imaging, carotid ultrasound, cerebral arteriogram, serum clotting studies, blood chemistry, and complete blood count
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What is treatment for CVA?
Intravenous thrombolysis:
Neurovascular interventions
Antiplatelets, anticoagulants and antihyperlipidemic long term
Anticonvulsants
Antihypertensives
Dexamethasone/Corticosteroids
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What is treatment for CVA:
Intravenous thrombolysis:
Intravenous thrombolysis: tissue-type plasminogen activator (tPA) is given within 3-4.5 hr onset of sx for ischemic strokes
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What is treatment for CVA:
Antihypertensives
- modest BP reduction, target blood pressure of 160/90 mm Hg
