week 2: CNS Flashcards

1
Q

most common cause of TBI
(traumatic brain injury) and how are they measured

A

MVC and falls
- measured by glasgow coma scale

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2
Q

glasgow coma scale-mild

A

GCS 13-15

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3
Q

glasgow coma scale- moderate

A

GCS 9-12

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4
Q

glasgow coma scale-severe

A

GCS 3-8

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5
Q

blunt(closed) TBI examples

A

-concussion
- epidural
- subdural
- subarachnoid
- intracerebral hemorrhage

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6
Q

penetrating (open) tbi

A

-missiles
- fractures

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7
Q

characteristics of mild concussion…LOC, GCS, amnesia, diagnostic imaging, symptoms?

A
  • no LOC or LOC of less than 30 mins
  • GCS 13-15
  • mild retrograde amnesia-less than 24 hours
  • no need for diagnostic imaging
  • headache, attention deficit, dizziness
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8
Q

characteristics of moderate concussion…LOC, amnesia, GCS, symptoms, injury to brain…

A

-LOC more than 30 mins
- amnesia 24 hours or more
- GCS 9-12
- basal skull injury…none to brain stem
- confusion, permanent deficits, vision
-transitory decerebration or decortication with unconsciousness

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9
Q

what does decerebration mean

A

abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward

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10
Q

what does decortication mean

A

they don’t wake up or respond, even with repeated efforts to rouse them

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11
Q

characteristics of severe concussion…LOC, GCS, amnesia, symptoms, what does it increase, associated with what type of injury, what happens to coordination?

A

-LOC can last more than 24 hours
- GCS 8 or less
- brain stem injury
- autonomic dysfunction
- increased icp
- badly compromised coordination

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12
Q

what demonstrates that there is a brainstem injury-severe concussion

A

pupillary reaction, cardiac and respiratory symptoms

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13
Q

what is increased ICP-severe concussion

A

-increased pressure in skull
- increased intracranial pressure

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14
Q

what does DAI stand for

A

diffuse axonal injury

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15
Q

what are DAI’s associated with

A

physical, cognitive, psychologic/behavioural and social consequences

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16
Q

what are examples of physical consequences -DAI

A

spastic paralysis, peripheral nerve injury, dysphagia, dysarthria, hearing and vision, taste and smell

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17
Q

what are examples of cognitive consequences -DAI

A

disorientation, confusion, dysphasia, poor judgement

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18
Q

what are examples of behavioural consequences -DAI

A

agitation, blunted affect, impulsiveness, social withdrawl, depression

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19
Q

symptoms of post concussive syndrome-DAI

A

headache, nervousness or anxiety, irritability, insomnia, depression, inability to concentrate, fatigability

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20
Q

for DAI’s what increased with the severity of the injury

A

decerebrate or decorticate posturing

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21
Q

how are DAI’s diagnosed

A

CT scan or MRI

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22
Q

what is the treatment for DAI

A

control seizures, fluid management

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23
Q

decorticate-where in the brain does the injury occur and abnormal what…destructive lesion of

A

higher level…upper midbrain and above (corticospinal tracts near cerebral hemisphere and basal ganglion)
- abnormal flexion

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24
Q

decerebrate…where in the brain does the injury occur and abnormal what…destructive lesion of

A

lower level…lower midbrain and below (midbrain or cephalic pons)
-abnormal extension

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25
epidural hematomas- what percent of major head injuries and what ages normally
1-2% 20-40 y/o
26
epidural hematomas- source of bleeding, what do 90% of ppl also have, where is the most common site
- artery - 90% have a skull fracture - temporal fossa
27
epidural hematomas- symptoms
loss of consciousness -> period of lucidity...includes headache, vomiting, drowsiness, seizure, hemiparesis, if temporal lobe herniation begins-ipsilateral pupillary dilation
28
epidural hematomas- how do you diagnose, prognosis good if, a medical emergency requires you to
- CT scan or MRI - prognosis good if intervention before bilateral dilation of pupils - evacuate the hematoma (surgery)
29
subdural hematomas- how many % of TBIs, what do they act as and it evolves to what
10-20% -acts as expanding masses -> ICP-> compresses the bleeding vessels
30
subdural hematomas- acute and subacute timeline
acute: within 48 hours subacute: over 48 hours- 2 weeks
31
research subarachnoid hemorrhage
32
for raised ICP
-head up - hyperventilation - hypertonic saline - medications - craniotomy
33
what medications decrease ICP
-mannitol (more blood flow to tissues) - loop diuretics (reduces sodium reabsorption) - corticosteroids (anti-inflammatory) - barbiturates (sedative-hyponotic med) - anti-seizure drugs
34
research intracerebral hemorrhage
35
TBI can be due to
coup (brain hits front of skull) contrecoup (brain hits back of skull)
36
what does SCI mean
spinal cord trauma
37
spinal cord trauma- 40% of due to, about 80% of injuries are what gender, what is the most common sport that causes this
-MVC - men - diving
38
spinal cord trauma- how do elderly get this
minor falls due to other pathology (ex. osteoporosis)
39
SCI-pathology: what type of injuries and why
vertebral injuries d/t acceleration deceleration, or deformation injuries
40
SCI- pathology: how do they injure tissues
through compression, exerting tension or traction, or shearing tissues through hyperextension, hyperflexion, vertical rotation of the spine
41
SCI-pathology: classifications
simple fracture, compressed fracture, comminuted fracture (burst or shattered) or dislocation
42
SCI- pathology: occurs mostly at
C1-2, C4-7, T1-L2
43
SCI- what happens to motor, sensory, reflex, and autonomic functions...
all the functions cease below level of transected area, may cease with concussive, contused, compressed or ischemic areas
44
SCI- what type of paralysis, what occurs slowly
-paraplegia, quadriplegia - return of spinal neuron excitability occurs slowly
45
hyperreflexia-when does it occur, why does it occur
- syndrome occurs any time after spinal shock ceases - massive uncompensated cardiovascular response to stimulation of SNS (sympathetic nervous system)
46
hyperreflexia- symptoms
hypertension, pounding headache, blurred vision, sweating above level of lesion, nasal congestion, nausea, bradycardia
47
hyperreflexia- most common causes
distended bladder or rectum
48
SCI- diagnoses
Dx. made by physical, radiologic and myelographic exam
49
SCI- treatment (tx)
- immobilize spine (surgical decompression and stabilization are possible) -corticosteroids to decrease secondary injury
50
brain tumours- 2 types
primary: intracerebral, extracerebral metastatic
51
brain tumours: primary-intracerebral
astrocytoma glioblastoma multiforme pituitary adenoma
52
brain tumours: primary- extracerebral
meningioma neurofibroma
53
brain tumours: metastatic - where?
lung breast skin kidney
54
characteristics of tumors...types, what does it cause, what causes the local effects
-primary or metastatic - cause local and generalized CM - local effects caused by destruction or compression of the brain
55
tumors: symptoms and generalized effects from
- may include seizures, visual disturbances, unstable gait and cranial nerve dysfunction - generalized effects from raised ICP, hemorrhage or cerebral edema
56
brain tumor: intracerebral: astrocytoma, rate of growth and from what
-slowly growing - arises from astrocytes
57
brain tumor: intracerebral: glioblastoma multiforme, growth rate and from what
-from more mature glial cells - very rapidly growing
58
brain tumor: intracerebral: pituitary adenoma- from what, resulting in
-pituitary cells - resulting in secreting tumor
59
brain tumor: extracerebral: meningioma-from what, and why a problem
-from arachnoid cells - problems due to location
60
brain tumor: extracerebral: neurofibroma- from what and where
- arises from schwann cells - nerve sheath
61
research metastatic disease
62
cerebrovascular accidents (CVA)...what most cause of death, leading cause of..., 5-14% have what within a year
- 3rd leading cause of death - leading cause of disability - 5-14% have a second stroke within a year
63
CVA- highest incidence in what age group, what are the most severe outcomes, classified as?
-over 65 y/o - severe outcomes are hemiplegia, coma, death - classified as ischemic or hemorrhagic
64
CVA risk factors
- arterial hypertension (increased systolic and diastolic) - smoking - diabetes - insulin resistance - polycythemia (increase in all blood cells-blood disorder) and thrombocythemia (bone marrow makes too many platelets) - impaired cardiac function - atrial fibrillation
65
ischemic (thrombotic) stroke: caused by and progressive over?
arterial occlusions due to thrombi (blood clots) in brain - progressive over hours or days
66
ischemic (thrombotic) stroke: conditions cause...that increase the risk?
inadequate cerebral perfusion (dehydration, hypotension, vasoconstriction)
67
ischemic (thrombotic) stroke: transient ischemic attacks (TIA= mini stroke)...what is it and what happens to the neurologic deficits
intermittent blockage - all neurologic deficits completely clear within 24 hours
68
ischemic (thrombotic) stroke: completed stroke means
CVA reached its max destructiveness in producing neurologic deficits
69
ischemic (thrombotic) stroke: embolic stroke involves and is often followed by
fragments of thrombi from outside the brain (or air, fat, tumors) - often followed by another embolic stroke from same source
70
hemorrahagic stroke occurs from
hypertension, ruptured aneurysms, bleeding into a tumor, bleeding disorders or anticoagulation, head trauma, illicit drug use
71
hemorrahagic stroke: 20% is
subarachnoid intracerebral
72
hemorrahagic stroke: subarachnoid...what happens
uncontrolled bleeding on surface of brain (between brain and skull)
73
diff size of hemorrhage
small: 1-2 cm in diameter massive: several cm in diameter
74
hemorrahagic stroke: intracerebral...what happens
an artery deep in brain ruptures, due to high BP
75
what does the left side of your brain control
-spoken language - reasoning - number skills - written language
76
what does the right side of your brain control
- creativity - music - spatial orientation - artistic awareness
77
CVA-patho: cerebral infarction has 2 main pathological processes
1. global process that affects neurons most susceptible to ischemia 2. focal process with a central zone of cell loss surrounded by a zone of injured cells that could survive if re-perfused in one hour
78
CVA-patho...cerebral infarction...someone can have ASK SENIOR ABOUT THESE 3 IM CONFUSED
-abrupt vascular occlusion-acute limb ischemia-sudden loss of limb perfusion - gradual vessel occlusion - partial occlusion
79
CVA patho- hemorrhagic infarctions...can be a result of, may compromise?
- result of reperfusion due to resumption of blood flow (ex from incomplete emboli) - may compromise recovery by accelerating the sequence of metabolically damaging events
80
CVA patho- cerebral hemorrhage...primary cause, bleeding precipitated by, what forms
-primary cause: hypertension - bleeding precipitated by aneurysms in smaller vessels or arteriolar necrosis(death of tissue) - mass of blood forms
81
CVA- diagnosis and when to have treatment/what is treatment
-Dx: primarily through CT and CM (physical exam) - need to start tx within 6 hours at the latest - usually done through stroke protocol with neurologist in central location
82
treatment of CVA- ischemic
- TPA (breaks up blood clot) needs to be administered within 4.5 hours - ASA (acetylsalicylic acid ex aspirin) - anticoagulant (heparin or coumadin) - BP controlled - anti-seizure meds - occasionally thrombectomy(procedure to remove blood clot)
83
why use anticoagulant for the treatment of CVA-ischemic (the source)
for cardiac or carotid source
84
treatment of CVA-hemorrhagic
- BP control (much lower than ischemic) - tranexamic acid - antiseizure meds - surgery
85
when do you use ct scans
dx tumors, internal bleeding or check for internal injuries or damage
86
what is a seizure
sudden, explosive disorderly discharge of cerebral neurons
87
what are seizures characterized by
sudden, transient alteration in brain function
88
convulsion-meaning? (seizures)
clonic-tonic movement associated with some seizures
89
what does epilepsy mean-seizures
general term for primary condition that causes seizures
90
for seizures what are conditions associated...%
20%- genetic, especially if before 20 years old 33% from a known cause or disease
91
etiologic factors associated with seizures
cerebral lesions, biochemical disorders, cerebral trauma, epilepsy
92
what can epilepsy result from-seizures
metabolic defects congenital malformation perinatal injury postnatal trauma infection brain tumor vascular disease drug or alcohol abuse
93
triggers for seizures
- hypoglycemia - fatigue - emotional or physical stress - febrile illness - excess H2O ingestion - constipation - use of stimulant drugs - withdrawal from depressant drugs - hyperventilation -environmental stimuli
94
types of seizure disorders
generalized seizures partial seizures
95
types of seizure disorders- generalized seizures...what is it, what's the onset, originates from and what happens to consciousness
-bilateral neuron involvement -general onset -originate from subcortical or deeper brain focus - impaired or lost consciousness
96
types of seizure disorders- partial seizures...what is it, what's the onset, originates from and what happens to consciousness, stimuli?
-focal seizure - unilateral neuron involvement - originate from cortical brain tissue - maintain consciousness if only unilateral but may become generalized (secondary generalization) -may not respond to outside stimuli
97
types of seizure disorders- status epilepticus
multiple seizures without regaining consciousness or seizure lasting more than 30 mins
98
types of seizure disorders- post-ictal state...meaning
time period immediately following a seizure
99
seizures patho-epileptogenic focus...what does this mean
group of neurons with more permeable plasma membranes that are hypersensitive to stimuli like hyperthermia, hypoxia and hypoglycemia
100
seizures patho-primary abnormality
-may be a membrane defect leading to instability in resting potential or other defects
101
seizures patho...what happens when neurons fire (the whole process)...watch a vid on this
- more frequency and amplitude - reaches a threshold point - goes through contralateral cortex to subcortical areas of basal ganglia, thalamus and brain stem (tonic phase) - apnea may be present for a few secs - excitement spreads down spinal cord neurons - clonic phase as inhibitory neurons in cortex, anterior thalamus and basal ganglia inhibit excitation - inhibition interrupts seizure charge, alternation becomes less frequent until it stops - epileptogenic neurons are exhausted
102
what happens in the tonic phase
muscle contraction with increased muscle tone
103
what happens in clonic phase
alternating contraction and relaxation of muscles
104
what does the maintenance of seizures activity require
250% increase in ATP 60% increase in cerebral O2 consumption 250% increase in cerebral blood flow
105
what can severe seizures cause...and it progresses to and may result in
-deficiency of ATP, phosphocreatine and glucose - secondary hypoxia, acidosis and lactate accumulation - may result in progressive brain tissue injury/destruction
106
seizures-CM: aura...what is it
partial seizure that immediately precedes a generalized seizure
107
seizures-CM: prodoma...what is it
early manifestation that can occur hours to days before a seizure
108
seizures-acute treatment
-benzodiazepines (depressant for sedation/hyponosis that reduces seizures) - phenytoin (control some types of seizures, treat and prevent) - valproic acid (treats epilepsy) - carbamazepine (manage and treat epilepsy) - phenobarbital (anti-seizure management) - levetiracetam (control certain types of seizures: myoclonic, tonic/clonic or partial)
109
for diagnosing seizures...what is most important, look for what during what, rule out, use an EEG to, why use imaging
-health history -physical exam and lab tests to look out for systemic diseases - rule out neurologic diseases - EEG to assess type of seizure and ID cause - imaging for mass lesions CT scan or MRI
110
how are benzodiazepines administered
IV, IM (intramuscular), SC (subcutaneous?)
111
how is phenytoin administered
loading dose IV
112
seizures- chronic treatment
- phenytoin - valproic acid - carbamazepine - levetiracetam - lamotrigine (controls certain seizures: partial, tonic-clonic, lennoz-gastaut syndrome) - topiramate( treat and manage epilepsy) - clonazepam (for panic disorder, epilepsy and nonconvulsive status epilepticus)
113
symptoms of meningitis
rash, stiff neck, chills
114
two most common types of meningitis
meningococcal and streptococcus
115
the main causes of meningitis
viral infection, bacteria, fungi, parasites
116
where does this occur
in CSF through subarachnoid space, starts in body and crosses blood-brain barrier
117
how do you treat meningitis
antibiotics
118
what is the age demographic more likely to get meningitis and how quickly it is over (no matter the outcome)
20-40 y/o over in 24 hours
119
what is MS, can you see in on diagnostic imaging
demyelinating disease with white matter plaques - cant see MS on CT scan
120
treatments for MS
steroids for acute interferons for chronic...this makes you feel like shit bc works on immune system
121
how do they realize that its MS
neurological findings then another neurological finding then they realize its MS
122
which hemisphere is ms more common in
northern hemisphere
123
what is myasthenia gravis
chronic autoimmune disease mediated by anti-acetylcholine receptor antibodies
124
where does myasthenia gravis occur
at neuromuscular junctions
125
what is the first sign of myasthenia gravis and how to test for it
tossus...eyelid drooping unilaterally or bilateral - tell patient to look up and eye will droop in 30secs to 1 min
126
how to test using diagnostic testing for myasthenia gravis
EMG (electromyogram)...tests muscles/measure how fast muscles are firing
127
guillain-barre syndrome....what is it
inflammatory disease that results in demyelination of peripheral nerves
128
guillain-barre syndrome symptoms and what is it preceded by
-leg paralysis then whole body - ventilation till body gets better
129
what is Alzheimer's and what is the diagnsis
progressive dementia...loss of cognitive mental function - diagnosis is clinical
130
what tests are used to see if you are testing for Alzheimers
sage test...clock drawing test(can do for short-term dementia-like delirium - quick 3 point recall...say 3 random words then say it twice more then later ask what the 3 words were -moca test -mmse
131
what treatment is used for Alzheimers
-cholinesterase inhibitors like aricept or reminyl (tries to keep the person at the level they are at...so they dont deteriorate)
132
parkinson disease...what is it and age demographic
degenerative disease of dopamine pathway in the substantia nigra (dark part of brain turns white) -usually after 40, peaking in onset around 60
133
SYMPTOMS OF PARKINSONS and type of diagnosis
resting tremor rigidity (cogwheel) bradydyskinesia postural instability -clinical diagnosis (can't see this on any imaging)
134
treatment of parkinsons
dopamine agonists