Neuro Flashcards
Global ischemia
Blood flow cannot meet metabolic demands (cardiac arrest, shock, asphyxiation); ischemia to the entire brain
Focal ischemia
Ischemia to one focal or specific portion of the brain (strokes)
3 types of ischemic strokes
- thrombus (disease)
- Embolism (clots)
- Hypoxia (an event)
What is a hemorrhagic stroke
primary brain bleed
What do the vertebral arteries supply?
blood to brain stem, cerebella, and occipital lobes
What do the basilar and internal carotid arteries form?
Circle of Willis
Most common of the ischemic strokes
Thrombolytic strokes
Thrombolytic stroke caused by
build up of plaque, atherosclerosis
Clot originates somewhere in the body and travels to the brain
embolic stroke (detaches from primary site)
Causes of ischemic strokes
1.Atherosclerotic/cerebrovascular disease (narrow vessels, clots pass, thromboembolic)
- Cardiogenic source (afib and other arrhythmias, embolism dislodges)
- unusual causes
Large vessel thrombotic occlusions (LVO)/Strokes
occlusions that haven’t become embolic yet (not clots yet)
Most common large vessel thrombotic occlusion (LVO)
middle cerebral artery, anterior cerebral artery
Cerebral “Small vessel disease”/ thrombotic stroke
small and deep, linked to hypertension, likely a form of atherosclerosis, “white matter disease” on x-ray
Cerebral “small vessel disease” leading cause of…
loss of function, disability, cognitive decline (dementia, strokes, motor movement issues)
Transient ischemic attack (TCA)
short lived/passing/temporary form of ischemia. warning sign for stroke
Cardiogenic sources that can cause stroke
afib, MI, endocarditis, other dysrhythmias
Other unusual causes of strokes
vasospasm after subarachnoid hemorrhage, cerebral vasoconstriction syndrome, radiation therapy, air or fat embolism, amniotic fluid following birth, tumors
Tissue penumbra
tissue at risk for infarct if reperfusion does not happen fast
allows blood to seep into and damage brain tissues
hemorrhagic stroke
process of brain hemorrhage
- rupture of blood vessel
- bleeding goes to brain
- focal hematoma
- brain swells
- brain gets compressed
- coma/death
Symptoms of hemorrhagic stroke
“thunderclap headache”, contralateral hemiplegia (weakness on opposite side), spasticity (seizures), loss of consciousness, increased cranial pressure, coma/death
Causes and risk factors for what type of stroke…
- cardiovascular disease
- uncontrolled HTN
- heart disease/atherosclerosis
- diabetes
- afib
- CAD/stenosis
- hyperlipidemia
- obesity
- eclampsia during pregnancy
Ischemic stroke
Causes and risk factors for what type of stroke…
- uncontrolled HTN
- weak vessels/no clotting
- cerebral aneurysms
- arteriovenous malformations (twist)
- head trauma
- obesity
- smoking/alcohol
- drugs that spike BP (cocaine)
- women
- post-orgasm
hemorrhagic stroke
Primary injury of hemorrhagic stroke results from
compression by hematoma, ICP (intracranial pressure)
Secondary injury of hemorrhagic stroke if not treated
inflammatory response, disruption of blood brain barrier, cerebral edema, free radical overproduction, glutamate-induced excitotoxicity, release of hemoglobin and iron from clot
Two types of hemorrhagic stroke
- intracerebral hemorrhage
- subarachnoid hemorrhage
Intracerebral hemorrhage
deep penetrating vessels, injury to brain tissue by disrupting connecting pathways and causing localized pressure injury
Subarachnoid hemorrhage
intracranial bleeding into arachnoid and pia mater
What is the most common cause of intracerebral hemorrhage
uncontrolled hypertension
Most disabling and deadly kind of stroke
Intracerebral hemorrhage
ICH process
- ruptured vessel causes bleeding
- brain tissue lacks O2 and ATP
- constriction of blood leads to further decreased blood flow
- increases cranial pressure
- brain swells
- coma
- brain herniation
- death
Subarachnoid hemorrhage characteristics
ruptured vessel is slow, thunderclap headache, bleed into subarachnoid space, related to aneurysm, found near circle of willis
If a stroke occurs in left side of brain what can be affected
difficulty understanding spoken and written language, difficulty expressing spoken and written language, changes in speech, verbal memory issues, impaired logic, sequencing difficulties
If a stroke occurs in right side of brain what can be affected
attention, left side of body control, memory, decreased awareness of deficit, loss of “big picture” thinking, altered creative or music perception
One of the most dangerous strokes
brainstem stroke
Brainstem controls what vital functions
HR, lungs, breathing, swallowing, eye movement, facial movement/sensation, hearing
Cerebellum strokes can cause
ipsilateral motor symptoms (same side), problems with balance and coordination, dizziness/vertigo, nausea/vomiting, cognitive and mood symptoms
Warning signs of stroke
(BEFAST)
Balance, Eyes, Face, Arms, Speech, Time
numbness of face, arms, legs (one sided), sudden confusion, trouble speaking or understanding, trouble seeing, trouble walking, dizziness, loss of balance, sudden severe headache with no known cause
Aphasia
absence of ability to communicate with words from damage to brain
Wernicke’s aphasia
fluent aphasia, full sentences that make no sense (word salad); reading and writing severely impaired
Broca’s aphasia
nonfluent aphasia, person understands language but has difficulty getting their own words out (expressive aphasia), may be able to read and write
global aphasia
most severe of aphasias, produce few recognizable words and understands little to no language
Primary progressive aphasia (PPA)
neurodegenerative disorder causing slow progression form of aphasia that worsens over time (alzheimers)
Abnormal pupillary responses
unilateral dilation (compression of nerve CN 3), constricted pupils, bilateral, fixed and dilated (serious brain damage)
NIH stroke scale
0 - no stroke symptoms
1-4 - minor stroke
5-15 - moderate stroke
16-20 - moderate to severe stroke
21-42 - severe stroke
Glasgow coma scale
Measures alertness
13-15 - minor
9-12 - moderate
8 or lower - severe
Stroke treatment: Ischemic
restore perfusion via Tissue plasminogen activator (t-PA), surgical intervention (thrombectomy)
Stroke treatment: Hemorrhagic
stop/control bleeding, remove hematoma, brain drain post craniotomy, burr holes, BP control, manage ICP
What does t-PA do
breaks up clot; converts plasminogen to the proteolytic enzyme plasmin, which lyses fibrin as well as fibrinogen
Window of opportunity for reperfusion for ischemic stroke
4 hours for optimal outcomes from tPA
Questions to ask before use of t-PA
confirm that the stroke is ischemic (NOT hemorrhagic), any history of cerebral hemorrhage or head trauma, recent bleeds, recent surgery, history of stomach ulcer/GI bleed, uncontrolled HTN, thrombocytopenia, seizure disorder, advanced age
CNS consists of
brain, spinal cord
PNS consists of
cranial nerves, spinal nerves
Afferent pathway
incoming sensory pathways to brain
Efferent pathway
outgoing motor pathways to body
Functioning cells of the nervous system, responsible for transport and uptake of neurotransmitters
neuron
class of cells that protects and provides developmental, physiological, and metabolic support for neurons, capable of mitosis, astrocytes, oligodendrocytes, microglia
neuroglia (glial cells)
Provide nutrients and structure for synapses, regulate ion and chemical concentrations, form blood brain barrier
astrocytes (CNS)
Myelinates CNS cells, enables fast propagation of action potentials along axons
oligodendrocytes (CNS)
critical for CSF homeostasis, brain metabolism, and clearance of waste from brain
ependymal cells (CNS)
degrade dead cells and protect the brain from invading microorganisms
microglia (CNS)
surround neuron cell bodies in PNS
satellite cells
surround all nerve fibers in PNS and form myelin sheaths around nerve fibers
Schwann cells
Carry signals from outer parts of body (periphery) into CNS, dendrites on both ends connected by long axon with cell body in middle
sensory neurons
control muscle contractions have cell body on one end, long axon in middle and dendrites on other end, carry signals from CNS to body
Motor neurons
amount of work required to separate + and - charged particles that are attracted to eachother
electrical potential
cell at “rest” before any stimulation (negative at rest)
resting potential
when membrane becomes less negative, more likely to fire
depolarization
resting potential becomes more negative, less likely to fire
hyperpolarization
temporary shift from negative to positive in neurons membrane potential caused by ions suddenly
action potential
currents that prompt one neuron to share information with next through action potential
excitatory current
level that a depolarization must reach for an action potential to occur
threshold of excitation
monroe-kellie doctrine
states that the sum of these volumes (brain, CSF, intracranial blood) should be constant, increase in one should cause a decrease in on or both remaining two
V intracranial volume = V brain. matter + V CSF + V blood
Factors that can cause increased ICP
hematoma, tumor, abscesses, infarcts, hydrocephalus, meningitis, increase in blood volume (acidosis causes increase CO2 and leads to increase cerebral blood flow), aneurysms, head trauma, venous stasis from thrombus, skull deformity, TBI
Early signs and symptoms of increased ICP
LOC, restless, pupillary changes (ovoid), headache, speech (slurring), decreased motor function, GI problems
Late signs and symptoms of increased ICP
LOC, pupillary changes (dilation, pupilledema, swelling of optic nerve), vital sign changes, abnormal reflexes, loss of brainstem reflex (sluggish then loss of corneal, cough, gag), pathologic posturing (decorticate and decerebrate)
Decorticate posture
closed hands, legs internally rotated, feet inward, arms are adducted and flexed against chest
Decerebrate posturing
head and neck arched, legs straight, toes pointed down, arms straight and extended with hands curled
Cushing’s triad
sign of cerebral swelling resulting from trauma or a space occupying lesion that is growing, posing impending fatal herniation of brain
1. change in respirations (deep and irregular)
2. widening pulse pressure (big difference in systolic and diastolic)
3. bradycardia
What happens when increased ICP is untreated
herniation of brain and death
Traumatic brain injuries (TBI)
concussion, contusion, coup contrecoup, diffuse axonal injury, chronic traumatic encephalopathy, second impact syndrome, traumatic hemorrhage, subarachnoid hemorrhage (not stroke)
Mild form of TBI, by impact to the head or whiplash
concussion
bruises on specific brain areas from impact to head
contusion
contusion present at both the site of impact and the exact opposite end of impact
coup contrecoup
shearing (tearing) of brain’s long connecting nerve fibers (axons) that happens when brain is injured as it shifts and rotates inside bony skull, usually causes coma and injury, may have normal CT
Diffuse axonal injury
brain degeneration likely caused by repeated head traumas, made only at autopsy by studying sections of brain
Chronic traumatic encephalopathy (CTE)
repetitive head injury syndrome, condition in which individual experiences a second head injury before complete recovery from initial head injury
second impact syndrome (SIS)
TBI : hematoma (bleeding outside brain or even inside that is NOT CVA) what are the two types
Epidural, subdural
arterial bleed, high pressure bleed fast, most dangerous, bleeding above dura, leads to increase ICP
characteristics of epidural hematoma
venous bleed, low pressure bleed, subdural space, leads to increase ICP
characteristics of subdural hematoma
Subarachnoid hemorrhage (SAH not stroke)
small arteries tear during initial injury, pathologic presence of blood in subarachnoid space, second most common acute injury
Sign of most severe TBI
increased ICP
TBI categorized by severity and mechanism of injury…what are these rankings
severe: unconscious, eyes dont open, LOC > 6 hrs
moderate: lethargic, open eyes to stimuli, LOC 20 min-6 hrs, brain swelling
mild: awake, eyes open, confusion, disorientation, memory loss, headache, brief LOC
Side effects of TBI physical symptoms
LOC from mins-hrs, persistent headache or headache that worsens, nausea, vomiting, convulsions or seizures, dilation of one or both pupils, clear fluids draining from nose or ears, inability to wake from sleep
Which one…Cognitive/behavioral/mental or sensory symptoms of TBI
- burred vision, ringing in ears, bad taste in mouth or changes of ability to smell, sensitivity to light or sound
sensory symptoms of TBI
Cognitive/behavioral/mental or Sensory symptoms of TBI
- LOC from secs-hrs, dazed, confused, disoriented, memory or concentration problems, mood changes or mood swings, depressed or anxious, difficulty sleeping, sleeping more
Cognitive, behavioral, mental symptoms of TBI
Frontal lobe deals with
concentration, problem solving, speech
Parietal lobe deals with
sense of touch, pain, temperature
Occipital lobe deals with
healthy vision
Temporal lobe deals with
memory, organization
Cerebellum deals with
balance and coordination
Brainstem deals with
breathing, steady heart rate
How can a TBI affect areas of the brain
Frontal: lack of focus, irritability, language difficulty
Parietal: difficulty w/reading, spatial misperception
Occipital: blind spots, blurred vision
Temporal: problems w/short term and long term memory
Cerebellum: difficulty walking
Brainstem: changes in breath, difficulty swallowing
Who is at risk for a spinal cord injury
males and ages 16-30
Impacts of SCI (spinal cord injury)
Physical dependency, morbidity/mortality, physiological stress, financial burden
Cascade of destructive events of SCI
ischemia, oxidative stress, inflammatory events, apoptotic pathways
Outcomes of spinal cord injury
incomplete quadriplegia (weakness or paralysis of all 4 limbs)
complete paraplegia (complete cut off of connection from brain and area below injury)
complete quadriplegia (neck down is affected)
incomplete paraplegia (not completely severed cords )
3 primary roles of spinal cord
send motor commands from brain to body, send sensory information from body to brain, coordinate reflexes
A spinal cord injury that disrupts conduit between body and brain and can lead to deficits in
sensation, movement, autonomic regulations, death
Where does the spinal tract begin and end
begins at brain (foramen magnum) and terminates at L1-L2
Ascending tract sends information…
sensory information to the brain
Descending tracts send information…
motor information down the cord
Complete SCI
all feeling/sensory input and all motor control/movement/function are lost below the level of injury
Incomplete SCI
some motor or sensory function loss below the affected area are preserved
Paraplegia paralysis
affects all or part of the trunk, legs, and pelvic organs (below waist), may still have movement of upper limbs
Tetraplegia/quadriplegia
arms, hands, trunk, legs, and pelvic organs are all affected by the injury (neck down)
what might happen to a person if they have a C1-C4 injury
may not be able to breathe on their own
Brown sequard syndrome
ipsilateral weakness/paralysis, contralateral sensory loss of pain and temperature below level of injury, usually puncture can be infectious or MS
Central cervical cord syndrome
impacts upper limbs more than lower, severe arm weakness, sensory deficits variable, caused by hyperextension of neck, compression, squash of spinal cord
Posterior cord syndrome
decrease in sensation of fine touch, loss of balance/coordination (+ Romberg), SCI, demyelinating disorders, compression from tumor, or degenerative disorder
Anterior cord syndrome
motor paralysis below level of lesion, loss of pain sensation below injury, SCI, severe loss of blood, trauma, affects anterior 2/3 of spinal cord
Which spinal cord syndrome causes poorest outcome
anterior cord syndrome
SCI shocks
normal activity of spinal cord cells cease at and below level of injury
Spinal shock
complete loss of reflex function, flaccid paralysis, sensory deficit, loss of bladder and rectal control, drop in BP and poor circulation, loss of thermal control, resolve when reflexes return, lower spinal cord level T7 or below
Neurogenic shock
sudden loss of sympathetic nervous system that maintains normal vascular tone, blood volume not impaired but is displaced producing hypotensive state and bradycardia, massive vasodilation, T6 and above
either in motor cortex of brain or brainstem, initiate voluntary movement throughout the body by connecting the cerebral cortex to the brain stem and spinal cord, sends nerve impulses from the brain to lower motor neuron synapses
Upper motor neurons (UMN)
neurons which travel from the spinal cord to the muscles of the body, directly responsible for communicating signals to the skeletal muscles, organs and glands, sends nerve impulses from upper motor neurons to the muscles via the lower motor neurons
Lower motor neurons (LMN)
Where are Upper motor neuron disorders located
central nervous system (CNS)
Where are the lower motor neuron disorders located
spinal cord grey matter or within the cranial nerve nuclei in the brains tem
What type of motor neuron disorders are these…
ALS, TBI, spinal cord injury, MS, CVAs (cerebrovascular accident), huntington’s disease
Upper motor neuron disorder
What type of motor neuron disorders are these…
poliomyelitis, spinal muscular atrophy SCI (spinal cord injury) can impact both
lower motor neuron disorder
What goes on in the body after an upper motor neuron lesion
spastic hyperreflexia, muscle weakness
What goes on in the body after a lower motor neuron lesion
muscular atrophy, flaccid muscle weakness, fasciculation (twitch) and hyporeflexia
Progressive and potentially disabling disease of the brain and spinal cord characterized by destruction of the myelin sheaths on the neurons of the CNS
Multiple Sclerosis
Causes of MS
largely unknown, auto immune disease, possibly environmental, genetic susceptibility
Pathogenesis of MS
T-cells attack myelin sheath as if it were a pathogen, demyelination occurs, damages action potential between axons on neurons
Neurodegenerative disorder that primarily affects the motor system and presents with progressive muscle weakness, both upper and lower motor neurons impacted
ALS (amyotrophic lateral sclerosis)
Early signs of ALS
split hand syndrome, foot drop, wasting of tongue muscle, uncontrolled laughter/crying, muscle cramps and twitches, dysphagia, slurred speech, impaired fine motor control
Late signs of ALS
diffuse severe muscle weakness, diffuse muscle atrophy, problems w/movement, dysphagia, problems speaking, impaired breathing
Generalized acetylcholine receptor (AChR) myasthenia
chronic autoimmune disease, antibodies destroy communication between nerves and muscle resulting in weakness of skeletal muscles
Neonatal myesthenis
temporary form in fetus of myasthenia gravis patient, passes acetylcholine receptor through placenta
Ocular myasthenia
muscles that move the eyes and control the eyelids are easily fatigued and weakened
Clinical manifestations of myasthenia gravis
usually affects women in 20-30 and men 50-60, drooping of eyelid (ptosis), weak eye and face muscles, impaired speech (dysarthria), dysphagia, weakness
