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Neuro Lecture 3 Flashcards

1
Q

what will an EEG tell you?

A

What type of epilepsy you have

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2
Q

List the 3 main types of intracranial aneurysms

A

saccular aneurysm
fusiform aneurysm
Microaneurysms (Charcot-Bouchard)

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3
Q

what type of aneurysms is almost always a result of an inherited weakness?

A

Saccular aneurysm

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4
Q

What are some conditions that cause saccular aneurysms?

A 
Polycystic kidney disease
Marfan syndrome
Neurofibromatosis type I
Tuberous sclerosis complex
Connective tissue diseases
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5
Q

What’s an important questions to ask if someone has a saccular aneurysms?

A

Has anyone else in your family had an aneurysm?

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6
Q

What are some risks for a saccular aneurysm?

A 
Cocaine/ amphetamine use
heavy ETOH use
tobacco use
HTN
obesity
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7
Q

Are saccular aneurysms more common in males or females?

A

females

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8
Q

are saccular aneurysms common in children?

A

No, they are rare

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9
Q

Where do saccular aneurysms usually occur?

A

Circle of Willis

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10
Q

Is it common for patients with saccular aneurysms to have more than one?

A

Yes, 1/4 will have more than one

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11
Q

What are some signs of “warning leaks” of a saccular aneurysm?

A

Headaches
dizziness
eye pain and visual deficits

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12
Q

When blood hits the gray matter of the brain what can happen?

A

Seizures

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13
Q

what type hemorrhage usually happens with the rupture of saccular aneurysms?

A

Subarachnoid hemorrhage

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14
Q

What occurs when a saccular aneurysm ruptures?

A

Thunderclap headache
mental status, visual changes
N/V/ stiff neck, photophobia

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15
Q

If the rupture of a saccular aneurysm fatal?

A

Yes, 60% of people die

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16
Q

What are fusiform aneurysms usually associated with?

A

HTN and atherosclerosis

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17
Q

Where is the most common location of a fusiform aneurysm?

A

Basilar artery

second- internal carotid artery

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18
Q

Which rupture more often, fusiform or saccular aneurysms?

A

Saccular

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19
Q

what can happen with fusiform aneurysms usually by trauma?

A

Dissection

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20
Q

What is aneurysms of small blood vessels. Usually occur in basal ganglia and grey/white matter junction of the brain

A

Micro aneurysms

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21
Q

What parts of the eye are parts of the CNS?

A

Retina, optic nerves

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22
Q

who get microaneursyms?

A

chronic HTN
coccaine
diabetics

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23
Q

When intracranial aneurysms rupture, what happens?

A

Focal intraparnechymal hemorrhage

get a focal neurologic deficit

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24
Q

how are most aneurysms found?

A

Incidentally usually

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25
Q

On a CSF sample, what will you get in the sample with an aneurysm.

A

Protein will be elevated, will have blood in the sample

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26
Q

How do you test if it was a “dirty tap” or blood in the CSF?

A

collect 3 samples, if the first has most in it then it was a dirty tap

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27
Q

what do you do for the emergency treatment of a aneurysm rupture?

A

Breathing support

Reduction of ICP

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28
Q

What are three ways to treat an intracranial aneurysm?

A

Clipping
Coiling
Stenting

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29
Q

list the four types of intracranial hemorrhages?

A

Epidural
Subdural
Subarahnoid
Intracerebral

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30
Q

what 2 intracranial hemorrhages are called stroke?

A

subarachnoid

intracerebral

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31
Q

Bleeding between the dura mater and the skull?

Often due to trauma, frequently fracture

A

Epidural hemorrhage

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32
Q

what type of hemorrhage may have a lucid period followed by rapid onset of symptoms.

A

Epidural hemorrhage

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33
Q

What are some signs of an epidural hemorrhage?

A

Ipsilateral fixed and dilated pupil (CN III)

contralateral weakness, hemianopsia

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34
Q

There is a risk of what type of herniation with epidural hemorrhage?

A

uncal herniation

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35
Q

What shape will an epidural hemorrhage look like on a CT/ MRI?

A

Lens shaped

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36
Q

How do you treat epidural hemorrhages?

A

Burr hole
craniotomy
trepanning

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37
Q

Is prognosis good or bad for a epidural hemorrhage when the patient has a Glasgow Coma Score of 3?

A

Good prognosis

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38
Q

What is bruised brain tissue?

A

Concussion

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39
Q

Bleeding between the dura mater and the arachnoid mater

A

Subdural hemorrhage

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40
Q

what is more fatal, subdural hemorrhage or epidural?

A

subdural

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41
Q

what does a subdural hemorrhage look like on a CT/ MRI?

A

crescent-shaped

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42
Q

list the three types of subdural hemorrhage?

A

acute
subactue
chronic

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43
Q

List some possible symptoms of SDH?

A 
LOC at event, lucid period
sedation
headache
N/V
ipsilateral weakness
speech difficulties
seizure (blood on grey matter)
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44
Q

who is more likely to have a subdural hemorrhage?

A

Men> women
50 years of age (increases w/ age)
anticoagulation therapy or coagulopathy
intra-cranial hypotension (ex-Post LP)

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45
Q

What are some risk factors of subdural hemorrhage?

A

Chronic ETOH use (cerebral atrophy + coagulopathy)
DM
HTN
Arteriosclerosis

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46
Q

What type hemorrhage is a common finding with “shaken” baby syndrome?

A

subdural hemorrhage

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47
Q

How do you treat subdural hemorrhage?

A

watchful waiting
trepanning (bedside) or craniotomy
Rebhabilitation

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48
Q

What can you do to the skull when taking it out to keep it perfused?

A

Put it in the ommentum

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49
Q

Bleeding between the arachnoid mater and the pia mater

A

subarachnoid hemorrhage

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50
Q

is subarahnoid hemorrhage fatal?

A

Yes, 40-50% fatal

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51
Q

where does subarahnoid hemorrhage usually occur?

A

Circle of Willis

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52
Q

What is a good way to visualize a subarachnoid hemorrhage?

A

CT (hyperdense in the middle)

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53
Q

If the CT is negative and you suspect subarachnoid hemorrhage?

A

LP with 3 tubes

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54
Q

What is the most common cause of subarachnoid hemorrhage?

A

rupture of a saccular intracranial aneurysm

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55
Q

How do you treat a subarachnoid hemorrhage?

A 
Stabilize patient
address the aneurysm
CSF drain if needed for increased ICP
calcium channel blocker (vasospasm) 
Hypertension/hypervolæmia/hæmodilution
seizure prophylaxis
rehabilitation
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56
Q

If someone has a rupture saccular aneurysm what do you look for?

A

Look for more saccular aneurysm

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57
Q

How do you keep someone Hypertension/hypervolæmia/hæmodilution?

A

Pump them up with saline

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58
Q

Bleeding within the brain tissue itself

A

Intracerebral hemorrhage

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59
Q

2 sub types of intracerebral hemorrhage?

A

Intraparenchymal (inside brain tissue)

Intraventricular (inside ventricles)

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60
Q

Symptoms of an intracerebralhemorrhage?

A

Severe headache
Vomiting
Focal neurologic signs
Seizure

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61
Q

What does an intracerebral hemorrhage look like on CT?

A

A ball

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62
Q

List some risk factors of intracerebral hemorrhage

A 
HTN
DM
menopause
tobacco use
ETOH
AV malformation
rupture aneurysm
coagulopathies
African American
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63
Q

How do you treat intracerebral hemorrhage?

A 
Stabilize patient/ address underlying problem 
Surgical removal
CSF drain if needed for increase ICP
treat inflammation with steroids
seizure prophylaxis
rehabilitation
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64
Q

What type hemorrhage do you use calcium channel blockers?

A

subarachnoid hemorrhage

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65
Q

What is permanent CNS damage cause by thrombus, embolus, venous thrombus, systemic hypoperfusion, SAH or ICH?

A

stroke

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66
Q

What are some stroke symptoms?

A

imagine not having what different areas of the brain do

headache (hemorrhage stroke)

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67
Q

How do you treat a stroke?

A

Confirm last known well
Keep O2 >94%, IV isotonic saline is SBP <120
ECG (look for a-fib)
CBC platelets, BMP, INR/PT/aPTT, troponins
Neuro exam
STAT head CT w/o contrast

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68
Q

What do troponins do?

A

Give a good prognosis, how likely will we get this person rehabed?

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69
Q

If a patient has HTN what should it be brought down to?

A

<110

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70
Q

If a patient has hypotension what should it be brought up to?

A

> 120/>80

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71
Q

What is the only FDA-approved pharmacologic therapy for acute ischemic stroke?

A

Recombinant tissue plasminogen activator (rtPA)

72
Q

What criteria is used to determine eligibility for rtPA?

A

NIHSS- National Institutes of Health Stroke Scale

73
Q

How long within the last known well period can you treat with rtPA?

A

less than 4.5 hours since LKW

best results within 1.5 hours of LKW

74
Q

What are some alternatives to rtPA?

A

thrombectomy
anti-platelet (aspirin) and anticoagulation therapy (heparin/ warfarin)
hemicraniectomy (for ICP)

75
Q

What is the sequale of stroke?

A

Disability
mood disorders (depression, anxiety, panic)
sleep disturbances
seizures

76
Q

What are “mini-strokes” where symptoms resolve w/i 24 hours?

A

transient ischemic attack

77
Q

What is the area of at risk tissue around the dead tissue that is damaged but savable?

A

Peneumbra

78
Q

If you have a stroke, what are you are you more at risk for?

A

another stroke

79
Q

what does the brain tissue look like with a TIA

A

all penumbra, little necrosis

80
Q

What are ways to prevent TIAs?

A 
Smoking cessation 
nutrition (more fruits and veggies, less fat, sodium)
moderation of ETOH use
regular exercise
controlling BP and weight
81
Q

What can you do for TIA prophylaxis?

A

Antiplatelet/ anticoagulant meds

talk about preparedness

82
Q

What is the FAST algorithm?

A

Face
Arm
Speech
Time

83
Q

What can you do to look at what is causing a TIA?

A

carotid duplex- carotid stenosis
EKG (a-fib)
Echo (thrombus in heart)

84
Q

does blood show in MRI?

A

Yes, but bone doesn’t show as well

85
Q

inability to initiate movements?

A

akinesia

86
Q

slow movements

A

bradykinesia

87
Q

dystonia

A

involuntary sustained contractions

88
Q

feeling stuck in a particular position or blocked from moving for a few seconds?

A

freezing

89
Q

increased muscle tone

A

rigidity

90
Q

inability to sit still

A

akathesia

91
Q

lack of muscle coordination

A

ataxia

92
Q

slow, writhing movements

A

athetosis

93
Q

large involuntary movements

A

ballismus

94
Q

small, rapid movements flowing unpredictably from one body part to another

A

chorea

95
Q

difficulty with speech articulation

A

dysarthria

96
Q

unintentional bilateralization

A

mirror movements

97
Q

sudden, brief movement of muscle group

A

myoclonus

98
Q

compulsion/ repeated (same word over and over)

A

tic/ sterotypy

99
Q

rhythmic alternating movement of flexor/extensor, pronator/supinator, etc.

A

tremor

100
Q

what makes a physiologic tremor worse?

A

stress
fatigue
caffeine
“enhanced physiologic tremor”

101
Q

what part of the brain is involved in ataxia?

A

cerebellum

102
Q

how many people have a physiologic tremor?

A

all of us

103
Q

tremor that appears during voluntary movements (kinetic tremor/action tremor)

A

essential tremor

104
Q

What makes a essential tremor worse?

A

physical or emotional stress/ fatigue

105
Q

when does a essential tremor get more prominent?

A

with age

106
Q

Essential tremors follow what genetic pattern?

A

Autosomal dominant pattern

107
Q

If you have essential tremor you are more likely to get what?

A

Parkinson Disease

108
Q

What causes an essential tremor

A

abnormality of Purkinje cell synapses in the cerebellum, and/or of cerebello-thalamo-cortical circuits.
(similar problem caused by ETOH)

109
Q

If it is a real essential tremor, what will make it better?

A

drinking a bit of ETOH

110
Q

What makes an essential tremor temporarily worse?

A

Caffeine

111
Q

How do you medically treat essential tremor?

A 
Beta blockers (propranolol, nadolol)- gets rid of adrenaline 
anticonvulsants (PRM, GBP, TPM)
112
Q

Who is propranolol contraindicated in?

A

allergic rxn who have an epi-pen

113
Q

For severe cases of essential tremor what can you do?

A

Depp brain stimulation (DBS)

Thalamotomy

114
Q

What is a degenerative neurologic and psychiatric disorder that leads to progressive death of the dopamine-generating cells of substantia nigra in the midbrain?

A

Parkinson’s Disease

115
Q

What are the main motor symptoms of Parkinsonism?

A

Resting tremor
Cogwheel (or lead-pipe) rigidity
Bradykinesia
other motor symptoms

116
Q

Is parkinson’s disease present in sleep?

A

No

117
Q

What is very common symptom of Parkinson’s Disease?

A

Pill-rolling and voice changes

118
Q

What is cogwheel rigidity a combination of?

A

Tremor and rigidity

119
Q

What is lead pip-rigidity?

A

Arm feels like a lead pipe
Patients without tremor
asymmetric, descending

120
Q

If bradykinesia for parkinson’s disease equal for tasks?

A

No, it is unequal
Ex- can ride a bike but unable to walk
may be able to walk backward not forward

121
Q

what is difficulty initiating and executing movement?

A

Bradykinesia

122
Q

what is rapid shuffling common in PD?

A

festination

123
Q

What is typical posture with PD?

A

Flexed posture (elbows, wrists, knees, hips, spine)

124
Q

What are some PD symptoms?

A 
festination
flexed posture
dysarthria
masked facies
micrographia (write very small)
dysequilibrium/falls
125
Q

What are some neuropsychiatric symptoms of PD?

A

Cognitive disturbances (executive, attn., memory)
Mood disturbances (anxiety, depression, apathy)
Impulse control (hypersexuality, gambling…)
Dementia (2-6× risk)
Psychosis (usually iatrogenic)

126
Q

Is brain imaging helpful with PD?

A

Usually unremarkable early on

127
Q

What are some PD+ disorders?

A 
Progressive supranuclear palsy
Multiple system atrophy
Corticobasal degeneration
Pick Disease
(Alzheimer Disease)
128
Q

Do people with PD+ have a irregular resting tremor at onset?

A

No, not usually but have additional symptoms and typically poor response to dopaminergic meds

129
Q

Treatment for PD

A

Levodopa

only 5-10% crosses BBB

130
Q

What can peripheral dopamine cause?

A

Dyskinesias
naseau
stiffness

131
Q

What are some drugs you can do with levo-dopa to reduce the peripheral metabolization of levodopa. Don’t cross the BBB

A

Carbidopa

Benaserazide

132
Q

What is a drug that reduces the metabolization of dopamine that is used w/ carbidopa/ benaserazide.

A

Entacapone

133
Q

WHat can levodopa cause?

A

Dopamine dysregualtion syndrome

134
Q

What is dopamine dysregulation s yndrome

A

Compulsive use of the medication

“Punding”- compulsive fascination w/ assembling/disassembling, sorting collection

135
Q

what can happen with long term use of levodopa

A

Get “on-off” states not related to dosing/ formulation

delay use of levodopa as much as possible and keep doses low to help prevent this from happening

136
Q

what causes iatrogenic dyskinesias?

A

Levo-dopa

it is constant movement

137
Q

what are some psychiatric effects of dopamine (from levodopa)?

A

confusion, agitation, hallucinations, , irritability, panic, paranoid delusions, mental depression, dementia, mania, and psychosis

138
Q

What can dose reduction or withdrawal of levodopa lead to?

A

neuroleptic malignant-like syndrome

139
Q

What is an alternative to levodopa? Consists of selegiline and rasagiline. Makes it so receptors don’t break down dopamine.

A

Monoamine oxidase B (MAO-B) inhibitors

140
Q

What are 2 other PD treatments that are more invasive?

A

Deep Brain Stimulation (DBS)- stimulate places that tend to release dopamien (thalamus, globus pallsidus or subthalamic nucleus)

Pallidotomy- surgical destruction of the globus pallidus to control dyskinesias

141
Q

how does PD progress

A

gets worse as it goes along but doesn’t necessarily kill you

142
Q

when is the most common onset of PD?

A

60 years
higher risk with pesticide/insecticide exposure
(well water, grow up on farm, exposure to agent orange)

143
Q

What can help prevent Parkinson’s DIsease.

A

Caffeine intake
NSAID use
Tobacco use

144
Q

Disease that involves Initially restlessness, small unintentional movements, poor coordination, saccadic eye movements. Dominant inheritance pattern.

A

Huntington’s Chorea

145
Q

what are some main symptoms of HD?

A

ataxia
dysarthria
dysphagia
unstable gait

146
Q

what are some psychiatric syndromes of HD?

A 
mood
disorders
cognition (executive function)
Obsessions and compulsions
psychosis
dementia
147
Q

where is huntington protein highly concentrated?

A

nerves and testes

148
Q

What are some physical symptoms of HD?

A

testicular atrophy
muscle atrophy, osteoprossis, weight loss
impaired glucose tolerance
cardiac failure

149
Q

What is the typical onset of HD?

A

35-44 years

onset earlier with successive generations

150
Q

CAG is a CAt who’s a _______ for ______ with a really long tail.

A

Glutton

glutamine

151
Q

Huntington’s disease is a ____ repeat sequence?

A

CAG on chromosome 4

152
Q

What type of HD has chorea briefly, it at all. rigidity is the dominant symptom and seizures are common.

A

Juvenile HD

153
Q

What does a MRI of HD show?

A

atrophy of caudate nuclei or may be unremarkable

154
Q

What drug can be given for chorea?

A

Tetrabenazine

neuroleptics and benzos may be helpful

155
Q

Lifespan of HD is usually ____ years post diagnosis.

A

20 years

156
Q

An acute cognitive impaired with onset w/i a matter of hours / days. Usually fluctuates in intesity and will have attentional deficits. Confusion and decreased awareness/ orientation.

A

Delirium

157
Q

What will you find in delirium but not dementia?

A

Onset within a matter of days/ hours
Usually fluctuates
Attentional deficitis

158
Q

what are some causes of delirium

A 
Dehydration
Hypothyroidism 
Hypercalcemia
Chronic liver and kidney disease
Hypoglycemia
pernicious anemia
folate/ thiamine deficiency
159
Q

what infections can cause delirium?

A

UTI
pneumonia
skin and abdominal infections
HIV, chronic meningitis, syphillis

160
Q

what are some toxic causes of delirium?

A

ETOH/ drug abuse

ETOH/ drug withdrawal

161
Q

How do you manage delirium?

A

Identify the causing factors (there may be more than 1)

162
Q

What is a chronic cognitive impairment. Commonly becomes slowly and steadily progressive. Typically an insidious onset. Hallmarks include memory loss and language dysfunction.

A

Dementia

163
Q

Onset before ___ years is considered early onset dementia?

A

65 years

164
Q

are awareness and attention typically normal in early stages of dementia?

A

Yes

165
Q

What can you do to test for dementia?

A

MMSE
trailmaking test (connect 1 to 2 to 3 etc)
clock drawing test
questionnaires
full neuropsychometric testing (takes 10 hrs)

166
Q

what are some useful imagings for dementia?

A

SPECT and PET are more useful than head CT and MRI

167
Q

What scan is good at predicting the development of AD within the next 2 years?

A

PET scan

168
Q

Progressive dementia associated with tangles and plaques in the gray matter of the brain

A

Alzheimer Disease

169
Q

What are the tangles in AD?

A

aggregates of intraneuronal τ protein

170
Q

What are plaques in AD?

A

extracellular deposits of β amyloid

171
Q

what is often an early sign of AD?

A

difficultly remembering recent events

172
Q

Is there currently a treatment for AD?

A

No- currently no cure, or symptomatic treatment to affect the progression of the disease qWhat can be

173
Q

What can be helpful for AD?

A

Acetylcholinesterase inhibitors (mild to moderate disease)

174
Q

What drug can be helpful in moderate to severe AD?

A

Memantine (NMDA receptor agonist)

175
Q

What is the main treatment for AD?

A

Caregiving

176
Q

What needs to be provided for the caregiver of someone with AD?

A

Psychosocial support and cognitive behavioral therapy for the caregiver need to be provided.

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