Neurologic Disorders Flashcards
(343 cards)
1
Q
What are the lobes of the cerebellum?
A
- anterior
- posterior
- flocculonodular (in-between anterior/posterior)
2
Q
What does the cerebellum do and what does it control?
A
- regulates muscle tone & coordinates muscle groups
- controls stance, gait & posture
3
Q
What are two possible clinical presentations will you see in a pt who has a lesion or damage to the cerebellum?
A
- ataxia (due to a dec. in motor activities)
- dysmetria (overshoot/undershoot of voluntary motor activity)
4
Q
What is ataxia?
A
uncoordinated gait
5
Q
Describe the presentation of a pt with ataxia:
A
wide stance, flinging arms/legs out
(“drunk”)
6
Q
Polyglutamine ataxia is a genetic mutation that causes dysfunction of the cerebellum. Why does this occur?
A
genetic mutation causes excess glutamine
7
Q
T/F the pathway of excess glutamine in polyglutamine ataxia is known:
A
FALSE - it is unknown
8
Q
Tentorium cerebelli is the fold of what meningeal layer?
A
fold of the dura mater
9
Q
In tentorium cerebelli, where does the fold of dura mater occur in the brain?
A
in the fold separating the cerebellum from inferior part of occipital lobe
10
Q
Supratentorial lesions develop where?
A
superior to the tentorium
11
Q
Is the manifestations of supratentorial lesions narrow or widespread?
A
narrow (very localized)
12
Q
If a pt has a supratentorial lesion, what sx are they most likely to have?
A
paresthesias in fingers of one hand (localized)
13
Q
Infratentorial lesions develop where?
A
below the tentorium
14
Q
Is the manifestations of infratentorial lesions narrow or widespread?
A
widespread
15
Q
If a pt has a infratentorial lesions this can also affect what part of the brain?
A
brain stem
16
Q
What are 3 motor neuron diseases?
A
- UMN disease
- LMN disease
- ALS (amyotrophic lateral sclerosis)
17
Q
The corticospinal pathway contains what primary tract?
A
the primary voluntary motor tract
18
Q
The corticospinal tract extends from where to where?
A
cortex to spine
19
Q
Is the corticospinal pathway longer or shorter than the corticobulbar pathway?
A
longer (goes to spine!)
20
Q
The corticobulbar tract extends from where to where?
A
cortex to medulla
21
Q
Is the corticobulbar pathway longer or shorter than the corticospinal pathway?
A
shorter (stops at medulla!)
22
Q
The upper motor neurons contain what two tracts?
A
- corticospinal
- corticobulbar
23
Q
If a pt has damage or a lesion to the upper motor neurons, what sx will they present?
A
- weakness
- paralysis
- hyperreflexia
- spastic paralysis
24
Q
Damage or lesions to the upper motor neurons may cause paralysis. Is this paralysis ipsilateral or contralateral?
A
contralateral paralysis = UMN
25
What is hyperreflexia?
increase in muscle tone + reflexes
26
Why does hyperreflexia occur if there's damage or lesions to the upper motor neurons?
spinal cord is still carrying out reflexes, no inhibition from cortex
27
Damage to the lower motor neurons in the anterior horns of the spinal cord causes what?
- weakness or paralysis on same side at or below lesion
- hyporeflexia
- flaccid paralysis
28
Does paralysis occur on the same side or contralateral side of a lesion in upper motor neuron disease?
contralateral
29
Damage or lesions to the lower motor neurons may cause weakness and paralysis. Is this paralysis ipsilateral or contralateral?
ipsilateral or below lesion = LMN
30
A pt with ataxia may not always have a lesion or damage to the cerebellum. Polyglutamine ataxia is one etiology that can cause dysfunction of the cerebellum due to degeneration. Why does this happen?
cerebellum is degenerating bc of xs glutamine = ataxia
31
What is hyporeflexia?
no muscle tone/little to no reflexes
32
What does ALS stand for and what's another name for ALS?
ALS = amyotrophic lateral sclerosis
ALS = Lou Gehrig's disease
33
What does amyotrophic mean? (hint: ALS)
amyotrophic = muscle atrophy
34
What does "lateral sclerosis" in ALS mean?
sclerosis or 'hardening' of the lateral corticospinal tracts
35
T/F ALS is the most common form of motor neuron degenerative disease:
TRUE
36
T/F ALS affect upper and lower motor neurons:
TRUE
37
ALS involves problems with two tracts, what are they?
corticospinal & corticobulbar
38
ALS involves the bulbar muscles. What are these muscles and what function is affected?
- muscles of mouth, neck, throat
- affects speech/swallowing
39
In ALS, death usually occurs 3-5 years after diagnosis due to what?
respiratory failure
40
ALS primarily affects who?
men 40-60 y/o
41
Why did Dr. Stephen Hawking live so long with ALS?
possibly due to sheer determination and early diagnosis
42
What is the cause of ALS?
unknown but possibly due to glutamate pathway
43
What percent of ALS cases are familial?
10%
44
What type of neurotransmitter is glutamate?
excitatory
45
Describe the mechanism of glutamate (hint: how does glutamate release calcium?)
1. released from presynaptic terminal
2. activates ion channels or PLC
3. uses IP3 as second messenger
4. causes release of calcium from cytoplasmic reticulum
46
Increased glutamate causes increased calcium. What does this cause?
death of muscle cells
47
Glutamate should be removed by transport proteins on ______.
astrocytes
48
What happens when astrocytes don't remove glutamate?
- increase in glutamate
- glutamate remains in environment
- neurons begin to die
49
What is the function of neurofilaments in large motor neurons?
structure & transport
50
What degenerates in ALS?
neurofilaments in large motor neurons
51
Large motor neurons have neurofilaments that degenerate in ALS. What happens as a cause of this? (hint: 4 steps)
1. decrease transport of factors necessary for motor neuron survival
2. plaques/scleroses develop due to neuron degeneration
3. neurons can't innervate muscles
4. muscle begins to atrophy including respiratory muscles
52
T/F in ALS cognitive function and the body decline:
FALSE - no cognitive decline while body is declining
53
What are some clinical presentation in ALS?
- hyperreflexia + spastic paralysis (UMN)
- hyporeflexia + flaccid paralysis (LMN)
- fasciculations = muscle twitch
54
ALS has no cure but what medication can be given to slow the progression of this disease?
Rilutek - riluzole (glutamate inhibitor)
55
What can cause ICP?
trauma, infection, hemorrhage, tumors
56
Will ICP cause an increase or decrease in blood flow?
decrease
57
What will the body do to decrease pressure in the skull?
shunt CSF down into the spinal cord
58
In an effort to decrease ICP, will the body increase or decrease venous return?
increase
59
What is autoregulation?
where every organ's blood vessels will take care of own organ
(body will restrict or dilate for own organ)
60
If a pt has ICP and no medical intervention is taken, brain tissue will eventually start to die. When this happens, the body's last attempt is to bring more O2 to the brain. What happens to the blood vessels and what does this cause?
- body brings more O2 to brain and blood vessels DILATE
- dilation increases ICP
61
How does the body compensate for ICP in an effort to shunt blood to the brain?
systemic vasoconstriction
62
Explain systemic vasoconstriction due to ICP:
- increase BP = increase pulse pressure
- decrease HR
- decrease CO2 in blood
- chemo receptors detect decrease in blood CO2
- causing a decrease in respiratory rate (less CO2)
63
If the body cannot compensate for ICP, ischemia can occur. What brain center does this damage?
respiratory center in medulla
64
Some pt's with increased ICP will develop Cheyenne-Stokes respiration. Explain this:
pt's will breathe deeply, then breathe fast, then breathe slow, then stop
65
What is it called when a pt stops breathing for a period of time?
apnea
66
What is pulse pressure?
systolic - diastolic = pulse pressure
67
What are the first signs of ICP?
- lethargy
- papilledema
- headaches + vomiting
68
If you suspect a pt has ICP, what quick exam can you do to check for this?
eye exam - you'll see edema of optic nerve from light of ophthalmoscope (papilledema)
69
Why do some pt's with increased ICP present with emesis?
pressure on brain increases pressure on medulla oblongata (emetic center)
70
ICP can affect which cranial nerve? What can this lead to?
- CN 3 (oculomotor)
- ptosis & pupil constriction
(affected eye will be ipsilateral to lesion)
71
How can you measure CSF?
manometer
72
What is an abnormal ICP level? What is normal? (hint: mmHg)
abnormal = >20 mmHg
normal = 9-14 mmHg
73
What does cloudy, pink, and yellow/light green CSF indicate?
cloudy = many WBC
pink = many RBC
yellow/light green = infection
74
What is Parkinson's disease and what does it affect?
= progressive degenerative disorder
affects motor branch of nervous system & extrapyramidal neurons
75
What part of the brain is degenerating in Parkinson's?
basal ganglia
76
Parkinson's is known as the disease of _______.
bradykinesia (slow movement)
77
Parkinson's is caused by what?
a decrease in dopamine from the substantia nigra
78
What percent of neurons are lost in the substantia nigra in Parkinson's?
50-70% of neurons
79
What type of neurotransmitter is dopamine?
inhibitory
80
In Parkinson's dopamine is decreased. What does this do to muscle?
increases muscle tone & muscle activity
81
What are the clinical presentations of a pt with Parkinson's disease?
resting tremors, muscle rigidity & instability
(dec. dopa = inc. muscle tone/activity = sx)
82
What nerves will eventually be affected in Parkinson's?
corticospinal nerves
(cortex won't be able to inhibit impulses from spine)
83
Who does primary Parkinson's disease affect?
male & female >60 y/o
84
What percent of primary Parkinson's is familial?
5%
85
T/F Parkinson's disease is multifactorial:
TRUE but not proven
86
What are some causes of secondary Parkinson's disease?
trauma & drugs
(happens in young people - Michael J. Fox)
87
What is found scattered in neurons of pt's with Parkinson's?
Lewy bodies
88
What are Lewy bodies composed of?
α-synuclein & other proteins
89
Lewy bodies are also found in what other disease?
Lewy body dementia
90
How is Lewy body dementia diagnosed?
autopsy
91
Failure of what system is a theory of Parkinson's?
failure of UPS (ubiquitin-proteasome system)
92
What should the ubiquitin-proteasome system (UPS) be doing, but fails to do in Parkinson's?
should be removing damaged/misfolded proteins & amino acids that haven't folded into proteins
93
Failure of the ubiquitin-proteasome system (UPS) causes what?
aggregation of neurons in brain
94
What are the sx of Parkinson's?
- weakness
- muscle aches
- facial expressions change
- tremors in hand
- pill rolling movement of fingers
- festination (short shuffling steps)
95
Festination is seen in pt's with Parkinson's disease. Describe this:
festination = short shuffling steps that accelerate as pt goes on
96
Facial expressions change in Parkinson's disorder. This is known as "Parkinson's mask". Describe this:
Parkinson's mask = pt can't smile/frown bc voluntary motion is lost
97
Pt's with Parkinson's will present with tremors in hands. What does this look like?
tremors at rest, tremor stops when reaching for something
98
There is no cure for Parkinson's disease but there are several treatments available. What medication is a precursor of dopamine that you can give to pt's with Parkinson's?
Levodopa (L-dopa) = dopamine precursor
99
If pt's with Parkinson's need dopamine, why can't we just give them dopamine?
dopamine can't cross the BBB
100
What are three medications you can give pt's with Parkinson's to treat their sx?
- Levodopa (L-dopa)
- dopamine agonists
- MOA-B inhibitors (monoamine oxidase)
101
T/F L-dopa can cross the BBB and treat pt's with Parkinson's disease:
TRUE
102
What does L-dopa metabolize to when it crosses the BBB?
dopamine
103
Dopamine agonists are one of the treatments available for pt's with Parkinson's. What does a dopamine agonist do?
stimulates dopamine receptors
104
What does the enzyme 'MAO' stand for and what does it do?
MAO = monoamine oxidase
breaks down dopamine
105
MAO-B inhibitors are used for the treatment of Parkinson's disease and prevents the degradation of what neurotransmitter?
dopamine (keeps dopamine off receptors longer)
106
Pt's with Parkinson's will benefit from what two kinds of therapies?
physical & occupational therapy
107
Name two MAO inhibitors and their function:
Selegiline & Rasagiline
(keeps dopamine off receptors longer)
108
What is the most common cause of ICP
brain tumors (benign or malignant)
109
What is the most common malignant brain tumor that causes ICP?
gliomas
110
Gliomas are developed from what type of brain cell?
glial cell (NOT neurons)
111
Gliomas are classified as what type of glial tumor?
astrocytoma
112
What is the function of glial cells?
they are supporting cells
113
What is the most abundant and largest glial cell?
astrocyte
114
You are doing an autopsy on a pt who died of a brain tumor and notice flattening of the gyri. What tumor does the pt have?
astrocytoma
115
A tumor that develops from the meninges is called a what?
meningioma
116
What are the meninges?
pia mater, arachnoid mater, dura mater
117
What is an adenoma?
a tumor developed from a gland
(e.g. pituitary gland)
118
What is a secondary brain tumor and give an example:
a brain tumor that developed as a RESULT of cancer elsewhere in the body
e.g. = lung/breast cancer that metastasized to brain
119
The growth of a brain tumor can cause ICP. What can happen to the brain as a result of this pressure?
can herniate through foramen magnum due to pressure
120
What are the two most common brain tumors in children?
brain stem & cerebellar
121
T/F brain tumors in adults are most common than brain tumors in children:
FALSE - children are affected the same % as adults
122
What is the most common brain tumor in adults?
cerebral
123
What are the S&S of a brain tumor?
- headaches
- lethargy
- unexplained nausea/vomiting
- vision problems
- problems with gait
124
Name 3 ways to treat a brain tumor:
1. chemo
2. radiation
3. drugs to dec. blood to tumor (not many cross BBB)
125
What is Myasthenia Gravis?
an autoimmune disease where the body produces IgG antibodies against own acetylcholine receptors
126
What is the only neurotransmitter for skeletal muscles?
acetylcholine
127
If your body is destroying Ach receptors, like in pt's with Myasthenia Gravis, what else is it destroying as a result?
skeletal muscles
128
Pt's with Myasthenia Gravis have muscle weakness that ______ with exercise/movement and _______ with rest.
increases, decreases
129
What muscles are affected the most in pt's with Myasthenia Gravis?
muscles with small motor units
130
What is the first sx of Myasthenia Gravis?
problems involving the ocular muscles
(e.g. ptosis)
131
What muscle can be affected in severe cases of Myasthenia Gravis and lead to death?
diaphragm (muscle of primary inspiration)
132
In Myasthenia Gravis, receptors on postsynaptic muscle membranes are decrease by how much?
70-90%
133
T/F pt's with Myasthenia Gravis have enough acetylcholine:
TRUE - Ach is not affected, ONLY Ach receptors
134
T/F acetylcholine and acetylcholine receptors are destroyed in Myasthenia Gravis:
FALSE - ONLY Ach receptors
135
90% of pt's with Myasthenia Gravis have antibodies against what?
Ach receptors
136
Who does Myasthenia Gravis affect and what is the onset?
women more than men (onset = 20-30 y/o)
137
What are some sx of Myasthenia Gravis?
- ptosis
- weakness of skeletal muscles
138
5% of pt's with Myasthenia Gravis seem to have multiple autoimmune antibodies. Why is this happening?
pts are not only producing Abs against acetylcholine receptors but against other organs too
139
5% of pt's with Myasthenia Gravis produce antibodies against other organs. What two sx can be a result of this?
hyperthyroidism & hyperplasia of thymus
140
What are two tests to diagnose Myasthenia Gravis and what are they checking for?
1. blood tests (check for autoimmune Abs)
2. EMG's (check how strong skeletal muscles are)
141
What are two treatments for Myasthenia Gravis?
1. anti-cholinesterase inhibitors
2. immunosuppressives
142
What is an anti-cholinesterase inhibitor used for the treatment of Myasthenia Gravis? What does it do?
Prostigmin - neostigmine
(keeps Ach on receptors for longer)
143
Vascular disorders can be 4 things. What are they?
- hemorrhagic
- ischemic
- focal (one part of brain)
- general (septic shock or MI)
144
What is a TIA and is it permanent?
TIA = transient ischemic attack = mini stroke
NOT permanent
145
T/F a TIA can happen in one area of the brain or multiple areas of the brain:
TRUE
146
What is the main cause of a TIA and what are two other causes?
main cause = atherosclerosis
other causes = small embolus/vascular spasms
147
Why is it important to treat the underlying cause of a TIA?
bc pt could have a major stroke later on
148
What are the S&S of a TIA?
- blurred vision or partial loss
- weakness in 1 limb
- numbness/paresthesia's on face
- confusion
- aphasia (difficulty speaking)
149
How long will the sx of a TIA last?
few min - hours
150
What is a CVA?
cerebrovascular accident = MAJOR stroke
151
What are two characteristics of a CVA?
- sudden, localized neurologic defect for 24 hrs+
- problem with cerebral circulation
152
What 4 things are going to help you determine if a pt had a TIA or a CVA? (mini stroke vs major stroke)
- cholesterol levels
- atherosclerosis
- which blood vessel is clotted or bleeding
- collateral blood flow
153
Occlusions int eh brain occur more often in large blood vessels. Name 3 large blood vessels in the brain:
internal carotid, middle cerebral, basilar arteries
154
What are lacunar infractions?
multiple little areas of affects in an ischemic stroke
155
What can happen if a pt loses 5 or more minutes of blood flow to the brain?
irreversible damage
156
List 3 categories of strokes:
1. atherosclerosis
2. embolism
3. hemorrhagic
157
What is an atherosclerotic stroke?
stroke of the large artery like the carotids
158
What develops in an atherosclerotic stroke?
atheromas/plaques in arteries
159
What is the cause of an atherosclerotic stroke?
unsure but possibly due to prior damage to blood vessel
160
What is the new theory of the cause of atherosclerotic strokes?
prior endothelial damage to blood vessels possibly from high BP
161
How does high BP cause damage to the blood vessels?
- inflammation and WBCs attach to area
- fibroblasts & smooth muscle cells multiply
- circulating lips attach
- start of lipid attachment causes plaque to stick
- plaque dec. diameter of blood vessels
- blood flow is decreased
- ischemia
162
What is an embolic stroke?
a thromus/clot that break away and flows in blood to brain = stroke
163
Atherosclerotic and embolic are classified as what type of stroke?
ischemic stroke
164
What is a hemorrhagic stroke?
intracerebral hemorrhage due to rupture of cerebral artery/blood vessel
165
A ruptured blood vessel in a hemorrhagic stroke is most likely the cause of what?
HTN & ICP
166
Besides a ruptured blood vessel, what else could cause a hemorrhagic stroke?
trauma
167
What do you need to do in the first 24-48 hours of your pt having a hemorrhagic stroke?
take care of the inflammation and pressure ASAP
(if not taken care of, more damage is done)
168
Why do you need to treat a hemorrhagic stroke quickly?
CNS neurons don't regenerate
- as brain tissue dies, neurons can't regenerate
- fibrous tissue comes in and causes scar tissue
- connective tissue regenerates and leaves cyst openings in brain
169
What are risk factors for ALL strokes?
- HTN
- atherosclerosis
- high cholest.
- diabetes
- systemic lupus
- young women - smoking + oral contraceptives
170
Strokes are the ___ leading cause of death in the US:
3rd
171
What are sx for an occlusion of the larger arteries?
aphasia, hemiparesis. coma, death
172
What are sx for an occlusion of the anterior cerebral artery in the frontal lobe:
contralateral weakness + sensory loss
173
What are sx for an occlusion in the posterior cerebral occipital lobe?
loss or partial loss of vision
174
In some pt's having a stroke you'll see flaccid paralysis. What will develop in the next few weeks?
spastic paralysis
175
What is the treatment for a stroke?
depends on the cause
for mini stroke = TPA = tissue plasminogen activator (Alteplase IV)
176
TPA is given intravenously for pt's having a mini stroke. What is the name of this medication and when should it be administered?
Alteplase IV - must be given within 3 hours of TIA
177
What percentage of stroke are ischemic?
87%
178
What is the treatment for an ischemic stroke?
endovascular procedure/medical thrombectomy
179
Explain the process of a medical thrombectomy?
- thread a catheter in blood vessel of groin up to brain
- grab clot, pit in "wire basket", pull clot out
180
When should a medical thrombectomy be done for pt's having an ischemic stroke?
within 6 hours of onset
181
What is the treatment for a hemorrhagic stroke?
surgery to do thrombectomy
(can't give TPA bc it will cause more bleeding)
182
Why can't you give TPA to pt's having a hemorrhagic stroke?
causes more bleeding
183
What does F.A.S.T. stand for? (hint: act FAST)
F- facial drooping
A- arm weakness
S- speech changes
T- time
184
What is an aneurysm?
weakness of a vessel wall (localized dilation)
185
Are aneurysms asymptomatic?
they can be until they get large
186
T/F pt's having an aneurysm don't lose consciousness
FALSE - they can lose consciousness
187
What is the most common cause of a subarachnoid hemorrhage?
rupture of blood vessel
188
The rupture of a 'berry' aneurysm will cause what?
ICP
189
Chronic HTN can result in multiple little aneurysms called what?
Charcot-Bouchard aneurysms
190
What are the sx of an aneurysms?
- HA
- photophobia
- nuchal rigidity
- confusion = small leak
- emesis
- seizures
- LOC = rupture of blood vessel (can lead to death)
191
What is the treatment for an aneurysm? (hint: old & new method)
old = surgical clipping
new = endovascular coiling
192
What is the endovascular coiling treatment for a stroke?
metal coil through groin to brain = seal blood vessels
193
What is epilepsy?
uncontrolled, abnormal depolarization of cortical neurons
194
If neurons have a lower threshold are the depolarizing faster or slower?
faster
195
What percent of epilepsy is idiopathic?
75%
196
What percent of epilepsy is due to trauma, infection, or brain tumors?
25%
197
T/F not all seizures are epilepsy;
TRUE
198
Describe the presentation of a pt having an epileptic seizure:
last a few seconds without loss of posture (pt stares for a while)
199
If you are newly diagnosing a pt with epilepsy, what do you need to find out?
if there is a trigger
200
What are a few things that could trigger a pt to have an epileptic seizure?
stress, hypoglycemia, loud noises
201
What are two types of seizures?
partial/focal or generalized
202
When talking about seizures, what does 'generalized' mean?
location on both side of brain
203
Do absence, or petit mal, seizures primarily occur in adulthood or childhood?
childhood
204
Will children who have absence/petit mal seizures suffer from seizure in adulthood?
no
205
Describe what it would look like if a child was having a absence/petit mal seizure:
lasts a few seconds, doesn't lose posture, staring straight ahead then resumes regular activity
206
An absence/petit mal seizure can be an autosomal dominant trait with incomplete ______.
penetrance
207
What are two types of generalized seizures?
absence/petit mal & tonic-clonic
208
Tonic-clonic, or grand mal, seizures occur in who?
children and adults
209
Tonic-clonic seizures follow a prodromal sign. What does this mean?
prodromal sign = follows a pattern
210
What are some prodromal signs pt's will have before a tonic-clonic, or grand mal, seizure?
- auditory sensation
- nausea
- muscle twitching (hrs before seizures)
- an aura before LOC
211
What are two phases of loss of consciousness in tonic-clonic seizures?
tonic phase (or ictal phase)
clonic phase
212
Explain the tonic, or ictal phase, of a tonic-clonic seizure:
powerful muscle contractions
(arch back and extends limbs 10-30 sec)
213
How long does the tonic phase last in tonic-clonic seizures?
10-30 sec
214
Explain the clonic phase of a tonic-clonic seizure:
jerking of limbs (1-several min)
215
How long does the clonic phase last in tonic-clonic seizures?
1 to several minutes
216
What is the phase called after a pt has a tonic-clonic seizure?
postictal phase
217
After a pt has a grand mal seizure, they enter a poetical phase. Describe this phase:
when pt regains consciousness after seizure - they are very tired/confused and want to sleep
218
Partial or focal seizures affect how many areas of the brain?
one area of the brain
219
Describe the presentation of a pt having a partial or focal seizure:
- one arm jerking
- head/neck jerking
- VERY localized
- pt is conscious
220
How do you treat a pt with seizure disorder?
- try to identify triggers
- anticonvulsant drugs
221
What is the most common anticonvulsant drug?
Dilantin
222
Dilantin is a common anticonvulsant drug that may give pt's what kind of gun disease?
gingival hyperplasia
223
What does Dilantin, an anticonvulsant, do?
raises threshold for neurostimualtion
224
What are some side effects of anticonvulsant drugs?
dec WBCs, platelets, clotting factors
225
T/F meningococcus in the nasopharynx can cross the mucus membranes:
TRUE
226
If meningococcus enters the nasopharynx and crosses the mucus membranes, what can happen?
can affect choroid plexus (produced CSF) and can lead to ICP
227
What is the choroid plexus?
network of capillaries that produce CSF
228
What are two etiologies of meningitis in children and your adults?
Neissseria meningitides
Haemophilus influenzae
229
What is the etiology of meningitis in elderly and very young people?
Streptococcus pneumoniae
230
What are 3 sx of meningitis?
HA, photophobia, nuchal rigidity
231
What are two physical exams to test for meningitis and explain them:
1. Kernig's sign - flex hips + knees at right angles and try to extend leg (pain = positive)
2. Brudzinski's sign - pt is supine, flex head to neck, pt flexes knees = positive
232
How do you confirm meningitis?
test CSF for pathogens
233
What is the treatment for meningitis?
antibiotics
234
What are 3 ways a pt could develop a brain abscess
1. ear infection
2. nose/throat infection
3. bacterial endocarditis via teeth cleaning in vulnerable pts
235
Encephalitis is the infection of what?
connectie tissue + membranes of CNS
236
What are the signs of encephalitis?
stiff neck, lethargy, HA, fever
237
T/F encephalitis is bacterial:
FALSE - it's viral
238
Who contracts Western equine encephalitis and how?
children via mosquitos
239
Who does St. Louis encephalitis primarily affect?
in elderly people across the US
240
What are sx of West Nile encephalitis:
flu like sx, HA, fever, can get into nervous system
241
West Nile encephalitis is widespread across what two countries and how is it transmitted?
US/Canada via mosquitos
242
What is another name for Lyme disease and what is the bacteria called that is transferred from ticks?
Lyme disease = neuroborreliosis
bacteria = Borrelia burgdorferi
243
What are sx of Lyme disease and what is the hallmark sign?
sx = flu-like, pain and paresthesia's on face, severe arthritis
hallmark sign = bulls eye lesion (red lesion w central area)
244
How do you treat Lyme disease?
with tetracyclines (doxycycline = Monodox)
MONTHS of antibiotics
245
What nerve can herpes simplex encephalitis (HSV1) travel through?
trigeminal nerve - CN 5
246
How do you treat herpes simplex encephalitis (HSV1)?
acyclovir (Zovirax)
247
What are some infections that can also affect the nervous system?
- meningitis
- brain abscess
- encephalitis
- Lyme disease
- herpes simplex encephalitis
248
What are some other infections that can affect the nervous system?
rabies, tetanus, poliomyelitis
249
Rabies enters the PNS and travels to the CNS and affects what two brain structure?
brain stem + basal ganglia
250
Tetanus is also called what? What does it cause?
lockjaw - Clostridium tetani (causes muscle stiffness)
251
What is the treatment for tetanus and what's the mortality rate?
antitoxin (mortality = 50%)
252
Poliomyelitis is a virus that multiplies in what tissue that travels to the CNS? What does it cause?
lymphoid tissue (causes severe paralysis)
253
Describe what shingles looks like:
erythematous vesicular linear rash
254
T/F shingles affects 1 cranial nerve or 1 dermatome on 1 side of the body
TRUE
255
What are two vaccines for herpes zoster?
zostrix (65+) & shingrix (2 doses)
256
Pt's with Guillian-Barre syndrome will have post-infectious ______.
polyneuritis
257
Guillian-Barre syndrome is a viral infection that produces what?
abnormal immune responses
258
Why do pt's with Gillian-Barre syndrome get decreased nerve conduction of the legs?
because of demyelination of the nerves
(inflammation = axons are destroyed)
259
In Guillian-Barre syndrome, loss of nerve conduction starts where? Which direction does it travel?
starts = ankles + feet, knees, legs, diaphragm = fatal
MOVES UPWARDS
260
In Gullian-Barre syndrome, inflammation of the PNS resolves in what direction?
opposite direction as it starts (legs, knees, feet + ankles)
261
What is dementia?
acquired, progressive, chronic disease of cortical degeneration
262
What are the sx of dementia?
- loss of motor coordination
- loss of short term and long term memory over time
- personality changes
263
How many defective genes are found in Alzheimer's disease?
4
264
What do we think causes Alzheimer's disease?
- dec. Ach
- plaques & neurofibrillary tangles
265
What do the plaque proteins contain in Alzheimer's disease?
amyloid B-peptide
266
Neurofibrillary tangles in Alzheimer's disease is a defect in what protein?
tau protein
267
What is the treatment for Alzheimer's disease? What does it inhibit?
Aricept (donzepezil) = anticholinesterase inhibitor
268
What are some causes of brain injuries?
skill fx, hemorrhage, edema, etc.
269
What is another name for a concussion?
mild traumatic brain injury
270
What is a concussion?
mild injury to head (movement of brain within skull)
271
Describe some S&S of a concussion. Does permanent brain damage occur?
- temporary amnesia
- LOC
- HA
- no permanent damage (recovery in 24 hrs)
272
What is a countercoup brain injury?
where brain bounces from back to front
273
What is an open head injury?
skull fx or penetration of brain (ex: bullet wound)
274
What is a basilar skull fracture? What can it cause?
fx at base of skull (causes CSF to leak out of brain)
275
What is a head injury due to trauma in babies is called what?
shaken baby syndrome
276
List some brain injury sx:
- ICP sx + seizures
- ottorhea (CSF leaking from ears)
- otorrhagia (blood leaking from ears)
- rhinorrhea (CSF leaking from nose)
277
Name one treatment for brain injuries. What does it decrease?
steroid medications (dexomethazon) - decreases edema
278
What is a contusion?
bruising of brain w rupture of small blood vessels
279
What is the difference between a concussion and a concussion?
concussion = mild injury to head where brain moves w/in skull
contusion = bruising of brain w small blood vessel rupture
280
What type of head injury can a concussion and contusion be classified as?
closed head injury
281
What is a primary brain injury?
direct injury to brain tissue, blood vessels, nerves, etc.
282
Pt's with a primary brain injury will present with 3 things that start with "I", what are they?
inflammation, ICP, ischemia
283
What is a secondary brain injury?
effects of something else causing brain injury
(what is the effect of edema, hemorrhage, hematoma, etc)
(what is happening from that effect?)
284
Where would you see an epidural hematoma in the brain?
hemorrhage is between dura & skull
(usually by meningeal artery)
285
Where would you see a subdural hematoma?
between dura and arachnoid (cortical veins bleeding into space)
286
What is a common cause of a subarachnoid hemorrhage?
rupture of aneurysm
287
Will you see a hematoma on an MRI of a pt who has a subarachnoid hemorrhage?
no hematoma bc blood is mixing with CSF
288
What is an intracerebral hematoma
a hematoma within brain itself
289
What type of injury can cause vertebrae damage?
spinal cord injury
290
What can rip the spinal cord and its ligaments?
hyperextension nd hypoflexion
291
How can the spinal cord be damaged?
- penetrating wounds
- dislocated vertebrae
- compression fx (fall from height)
- severing the s.c.
292
What will happen if the spinal cord is severed at T10?
irreversible loss of sensory and motor functions inferior to the injury
293
What is spina bifida and what region does it usually occur?
defects in the formation of the spine and spinal cord
= common in lumbar region
294
What category of defects does spina bifida fall under?
neural tube defects
295
What week of life does the neural tube open into anterior and posterior ends?
4th week
296
T/F your entire nervous system is developed from the neural tube
TRUE
297
Name 3 types of spina bifida:
1. spina bifida occulta (hidden)
2. meningocele
3. myelomeningocele (worst case)
298
What happens in spina bifida occulta? Is there neurological damage?
some posterior spinous processed don't fuse
(no neurological damage)
299
What happens in meningocele spina bifida?
meninges herniate through area taking CSF w it
300
In meningocele spina bifida, what does not fuse to form a sac?
the vertebrae
301
Within how many days can you do surgery to repair the meninges in meningocele spina bifida? Will there be neurological damage?
3 days (neurological damage will be low)
302
What is the worst case of spina bifida?
myelomeningocele
303
Describe myelomeningocele spina bifida:
open, with meninges - CSF & spinal nerves herniated through unfused vertebrae
304
In myelomeningocele, the spinal process of the vertebra lack fusion. What happens to the spinal nerves in this case?
it takes nerves out of vertebrae with it
305
Pt's with myelomeningocele will experience what sx? Can surgery help this type of spina bifida?
- muscle weakness, possible paralysis, incontinence
- surgery doesn't have much benefit (very controversial)
306
The risk of spina bifida increases in babies if the pregnant mother has what deficiency?
folic acid
307
Besides mothers with a folic acid deficiency, what other risk factors can cause spina bifida?
- women with uncontrolled diabetes
- women on anti seizure medication
- AFP (a-fetoprotein)
308
High levels of AFP (a-fetoprotein) in a mom can cause the baby to develop what?
neural tube defects
309
High levels of AFP (a-fetoprotein) in a mom can cause the baby to develop a neural tube defect. How does this happen?
produced by fetus's liver and some enter's mother's blood
310
What is cerebral palsy?
a non-progressive neurological disorder
311
What is cerebral palsy a result of?
genetic mutations that leads to abnormal brain development
312
Cerebral palsy is a result of a generic mutation. How is this genetic mutation caused?
possible infectious process of mother
(germinal/rubella, herpes simplex, lack of o2 during delivery)
313
The level of severity of cerebral palsy I can be determined how?
if the entire brain is affected or if its just small areas of the brain
314
Cerebral palsy is classified according to what?
according to motor disability
315
What are 3 classifications of motor disabilities in cerebral palsy?
1. spastic paralysis
2. dyskinetic disease
3. ataxic cerebral palsy
316
What fraction of people who have cerebral palsy have normal cognitive abilities and why?
1/3 bc disease is NONPROGRESSIVE
317
What motor disability is most commonly seen in pt's with cerebral palsy?
spastic paralysis
318
What is spastic paralysis and how do pt's with cerebral plays walk if they have spastic paralysis?
- damage to motor cortex or corticospinal tracts (hyperreflexia)
- walk on toes and scissors type of gate
319
Dyskinetic disease is a motor disability in pt's with cerebral palsy. What does dyskinetic disease damage?
basal nuclei (or extrapyramidal tracts)
320
You'll see choreiform movements in pt's with cerebral palsy. What are chloreiform movements?
rapid jerky involuntary movements
321
You'll see athetoid movements in pt's with cerebral palsy. Wha are athetoid movements?
snake moving, facial expression = grimace or frown
322
Some pt's with cerebral palsy will have dyskinetic motor disease. What are two types of movements that you may see in these pt's?
- choreiform movements
- athetoid movements
323
Ataxic cerebral palsy is a result of damage to the cerebellum in pt's with cerebral palsy. What other sx may you see if a pt has ataxic CP?
seizures, visual problems, hearing problems
324
What is the treatment for cerebral palsy? (hint: not a medication)
PT/OT, supportive care
325
What is multiple sclerosis?
a progressive neurological disorder
326
Multiple sclerosis is caused by what?
myelination of brain and spinal cord neurons
327
Multiple sclerosis is a possibly autoimmune disease of what type of cell?
T cells
328
How do T cells in multiple sclerosis begin to degree myelin on nerves?
T cells cross BBB in MS
329
How do T cells get through the BBB in multiple sclerosis?
an infectious process made BBB more permeable
330
In MS, as nerves are destroyed, myelin develops lesions known as what?
plaques or scleroses
331
What virus could be a possible cause of multiple sclerosis?
EBV (Epstein-Barr virus)
332
Who does MS affect and at what age?
women 2x as much as men (20-40 y/o)
333
What are early S&S of MS?
- blurred vision
- muscle weakness
- paresthesia (depends where CNS is being attacked)
- periods of remission (end up in wheelchair as pt becomes paralyzed)
334
What are two treatments for MS?
- interferon beta-1b (Betaseron - immunosuppressive)
- steroids (prednisone to decrease inflammation)
335
Huntington's disease is also known as what?
huntingtons chorea
336
What does chorea refer to in Huntington's chorea?
chorea = choreiform movements = rapid jerky involuntary motions
337
Is Huntington's disease autosomal dominant or autosomal recessive?
autosomal dominant
338
Huntington's disease is a genetic disease carried on what chromosome?
chromosome 4
339
When does Huntington's disease manifest?
in adulthood
340
What causes the brain to progressively atrophy in Huntington's disease?
aggregation of proteins
341
What two structures of the brain are affected in Huntington's chorea?
basal ganglia + frontal lobe
342
What two neurotransmitters are decreased in Huntington's disease and what is a result of this?
- decrease in Ach/GABA
- increased motor function & decreased cognitive function
343
What is the treatment for Huntington's disease? What does it do? Is this treatment a cure?
Tetrabenazine = decreases chorea/rapid movements
NO CURE
