Block 4 neuro part 2 Flashcards
(203 cards)
1
Q
positive symptoms that can be expressed in cerebral palsy
A
hypertonia, clonus, babinski sign
2
Q
clonus-
A
increased muscular contraction
3
Q
negative sympotms of cerebral palsy-
A
paresis and loss of dexterity
4
Q
spasticity-
A
velocity and direction dependent resistance to stretch in a limb
5
Q
dystonia-
A
sustained muscle contractions causing twisting repetitive movements, abnormal postures, or both
6
Q
most common CP is
A
spastic
7
Q
if a baby is full term with very low birth weight and develops CP with a combo of dystonia and spasticity, what CP does he likely have?
A
spastic quadriparesis
8
Q
if an infant had a vascular injury and developed CP, which CP does he probably have?
A
hemiparesis
9
Q
If a premature baby develops CP, which kind does he likely have?
A
spastic diplegia
10
Q
if a full term baby that is hypotonic at birth develops CP, what kind does he probably have?
A
dyskinetic CP
11
Q
main goal in treatment of CP is to treat the _______
A
lack of inhibition
12
Q
if a CP child presents with hemiplegia, what is the best treatment?
A
focal medication such as botulinum toxin
13
Q
if a CP child has spasticity and dystonia, poor underlying strength, what kind of treatment would you give her?
A
systemic treatment, such as baclofen
14
Q
baclofen is a _____ agonist
A
GABAb. enhances GABA function, relieving the spasticity affecting all the muscles
15
Q
if i child has good muscle control and strength, but suffers from spasticity, they may be a good candidate for what surgery?
A
selective dorsal rhizotomy
16
Q
if i child has good muscle control and strength, but suffers from spasticity, they may be a good candidate for what surgery?
A
selective dorsal rhizotomy
17
Q
non associative learning-
A
behavior modification based on a single stimulus
18
Q
sensitization-
A
increase in response to a stimulus following a novel, strong or noxious stimulus
19
Q
how does dishabituation/sensitization work?
A
modulatory neuron releases 5HT on habituated neuron, causing cAMP synthesis –> PKA activation–> K+ channel closure–> longer depolarization–> greater Ca++ influx–> greater NT release–> greater respone
20
Q
associative learning-
A
learning the relation between multiple stimuli
21
Q
pre-syaptic condition relies on pairing ______ with ______
A
conditioned stimulus with unconditioned stimulus
22
Q
Why does a conditioned stimulus need to be paired with an unconditioned stimulus to maximize response in presynaptic terminal?
A
Ca++-Calmodulin enhances adenylate cyclase, so if 5HT (US) binds without the conditioned stimulus, only some cAMP will be made, but if the CS also happens, Ca++ influx occurs and binds with Calmodulin, enhancing cAMP synthesis. With more cAMP, more PKA will be activated and more NT will subsequently be released
23
Q
NMDA receptors need 2 things to be activated:
A
glutamate binding and depolarization of the cell (to dislodge Mg++)
24
Q
what happens during early LTP?
A
NMDA receptors open after Mg++ is dislodged, then more AMPA receptors are inserted into postsynaptic membrane
25
what happens during late LTP?
Ca++ calmodulin binding activates CaCM kinase, which causes insertion of more NMDA receptors in the membrane, as well as other transcriptional modifications
26
what activates CREB?
cAMP
27
overall, amount of ___ entering post synaptic membrane causes LTP
Ca++
28
semantic memory-
recalling knowledge
29
______ lobe plays a critical role in declarative memory
medial temporal
30
______ lobe plays a critical role in declarative memory
medial temporal
31
encoding and retrieval of non consolidated memories occurs in ____
the MTL
32
consolidated memories reside in _____
various cortical lobes. They do not rely on the MTL
33
where are place cells located?
the hippocampus
34
the parts of the MTL include: (5)
parahippocampal cortex, perirhinal cortex, entorhinal cortex, hippocampus, and amygdala
35
describe the circuit of declarative memory in the hippocampus-
unimodal and polymodal association areas transmit to the perirhinal and parahippocampal cortices--> entorhinal cortex--> hippocampus
36
olfaction feeds directly into the _____ cortex
entorhinal
37
what serves as the gateway into the hippocampal formation?
entorhinal cortex
38
The _____ integrates information and rapidly fuses these features into a coherent memory trace retained in the cortex
hippocampus
39
left pre-frontal cortex allows for "_____" responses
remember
40
the right prefrontal cortex allows for "_____" responses
Know
| i.e. "I know X is true"
41
what 2 regions are involved retrieval of old episodic memories but are usually deactivated during episodic encoding?
posterior lateral parietal and posterior midline regions
42
priming-
change in the processing of a stimulus due to a previous encounter with the same or a related stimulus, in the absence of conscious awareness of the original encounter
43
______ cortex shows less activity in the related-word than unrelated-word condition. So its involved in distinguishing unrelated words
anterior temporal cortex
44
Causes of Alzheimer's disease include mutation in which 3 genes?
gene producing amyloid precursor protein (APP), proteins that process APP, and ApoE gene
45
4 abnormalities are observed in the brain of someone who died from AD:
neurofibrillary tangles, amyloid plaques, loss of neurons, and loss of synaptic contact
46
vascular disease of the MTL shows significant loss of ____ neurons
CA1
47
what 3 things are most heavily affected by AD and which 2 are relatively spared?
- entorhinal cortex (mostly layer 2), CA1 neurons, and subiculum
- dentate gyrus and CA3 neurons
48
TLE =
temporal lobe epilepsy
49
TLE affects what layer of the entorhinal cortex?
Layer 3
50
TLE destroys ____ and ___ neurons, as well as the _____ gyrus.
CA1, CA3, dentate
51
big difference between AD and TLE?
AD affects layer 2 of entorhinal cortex, TLE affects layer 3
52
what is the best way to keep a healthy hippocampus?
keep exercising it!
53
How do we know NMDA involved in fear conditioning?
if you block NMDA receptors in the amygdala with CPP, the animal will not learn a fear response to a stimulus.
54
stress enhances fear memory via
glucocorticoids
55
stress enhances fear memory consolidation via
glucocorticoids
56
Korsakoff Sydrome is due to damage to the-
DM nucleus of the thalamus, mammillary bodies, and disrupted circuitry to anterior cingulate gyrus
57
Symptoms of Korsakoff Syndrome
retrograde memory problems, psychiatric symptoms including apathy and story fabrication, anterograde amneisa
58
Who often gets Korsakoff Syndrome?
chronic alchoholics with vitamin B1 deficiency
59
Who often gets Korsakoff Syndrome?
chronic alchoholics with vitamin B1 deficiency
60
3 genes identified as being linked to AD
APP, PS-1, PS-2
61
what stage of AD do people begin to notice symptoms?
3
62
how do tangles contribute to AD?
they collapse and twist to destroy vital cell transport systems
63
how do beta amyloid plaques contribute to AD?
they clump together and block synapses, as well as trigger inflammation
64
What are the earliest clinical signs of AD?
olfactory loss, short term memory loss, and loss of place cells
65
Cleavage of the APP by _________ leads to formation of Abeta fragments that lead to plaques
beta and gamma secretase
66
cleavage of APP by ______ prevents the formation of Abeta fragments
alpha secretase
67
polymorphisms in the ____ gene are a prominent risk factor for AD
ApoE
68
inheritance of the ApoE4 gene _____ risk of AD, inheritance of the ApoE2 gene ______ risk of AD
- increases
| - decreases
69
AD pathophysiology: when APP is cleaved by beta or gamma secretase, it leads to the formation of ______, which aggregates into plaques
Abeta42
70
Formation of Abeta plaques alone isn't enough to cause AD. Plaque formation must be coupled with an inability to _______, for disease to occur
remove the plaques
71
Stage 3 AD symptoms can be summarized as:
cognitive problems of a wide variety that have begun to be noticed
72
Stage 4 AD symptom summary:
begin having difficulty with tasks, forgetfulness about one's own history, moody in social situations
73
Stage 5 AD symptom summary:
begin needing help with day to day activities, confusion
74
Stage 6 AD symptom summary:
very bad memory, change in sleep patterns, need help with bathroom, major personality changes
75
Stage 7 AD symptom summary:
begin to stop responding to environment and moving. May still say words
76
Where else can you find Abeta plaques?
Drusen, in age related macular degeneration
77
______ is reduced in the CA1 region of the AD brain
Neuroprotectin D1 (NPD1)
78
people with AD have a decreased ability to make what protective protein?
NPD1
79
What substance can hold back inflammation and protein misfolding in the brain, as well as help in nerve regeneration and induce neuroprotection?
DHA
80
DHA attenuates _____ secretion and enhances ______ biosynthesis
- Abeta
| - NPD1
81
DHA attenuates _____ secretion and enhances ______ biosynthesis
- Abeta
| - NPD1
82
NPD1 shifts APP processing from ______ pathway to _____ pathway
amyloidogenic to non-amyloidogenic
83
B94 is associated with ______
inflammation
84
NPD1 reduced what pro-inflammatory compounds in brain?
COX-2 and B94
85
what does PPAR gamma do?
blocks beta-secretase activity
86
neurofibrillary tangles actually accumulate in a confined manner in limbic regions including _______ and ______ as part of normal aging.
- entorhinal cortex
| - hippocampal CA1
87
the initial trigger of AD is:
Abeta aggregation
88
Decreases in CSF ____ are the first hallmark of AD and precede an in increase in CSF tau.
Abeta42
89
why does a decrease in Abeta42 indicate AD?
brain is not removing this protein fragment well enough anymore
90
if tau NF tangles are a normal process, what induces them to be pathogenic?
Abeta
91
if tau NF tangles are a normal process, what induces them to be pathogenic?
Abeta
92
why does CNS regrowth fail?
inhibitory signals from glial cells and crowding from glial cells responding to immune system mediated clearance of damaged tissue
93
order of nerve death:
nerve terminal degenerates--> distal terminal separates and degenerates--> myelin fragments--> phagocytic cells invade--> cell body swells and nucleus gets eccentric--> presynaptic terminal (dendrites of damaged nerve) retracts--> glial cells invade presynaptic terminal
94
_______ cells mediate peripheral nerve growth through secretion of signals to promote growth cone
schwann cells
95
schwann cells secrete _____, ____, _____ into ECM. These are the "bread crumbs"
laminin, fibronectin, and collagens
96
the inflammatory response to CNS nerve destruction attracts ______, which inhibit neural growth
astrocytes
97
______ factors promote axon regeneration by activating _____ receptors
- ciliary neurotrophic (CNTF)
| - GP130
98
_____ inhibits regrowth by blocking the GP130 receptors
SOCS3
99
the difference between a cut and crushed nerve regeneration:
cut nerves have to clear debris and use a growth cone to REGROW the nerve, whereas crushed nerves are REPAIRED by schwann cells secreting NGF
100
when a peripheral nerve is cut, which cell expresses growth related genes and which cell releases ECM molecules to guide regeneration?
- damaged neuron expresses growth genes
| - schwann cells
101
when a peripheral nerve is cut, which cell expresses growth related genes and which cell releases ECM molecules to guide regeneration?
- damaged neuron expresses growth genes
| - schwann cells
102
what 2 factors guide axons back to their target NMJ's?
NGF and BDNF
103
what is the necessary to reestablish a NMJ after peripheral nerve damage?
the original synapse must be maintained and the muscle health and anatomy must be maintained
104
to reinnervate the same NMJ after nerve destruction, the synapse must maintain 2 things:
synaptic specialization and AChR receptor clustering
105
this factor promotes/maintains AChR clustering
agrin
106
this transmembrane protein version of tyrosine kinase functions as an agrin receptor critical to AChR clustering
MuSK
107
responsible for transcription of AChR at post-synaptic site
Neurogulin-1
108
AChR's in damaged muscle should ______ and ______ so that the growing axon can find them
cluster and proliferate
109
do nerves have specificity for their regrowth target?
absolutely. In an experiment where C8 and T5 ganglion were transplanted then the subsequently grew to synapse on nerves of their original level. So take a C8 ganglion and put it in the superior cervical ganglion, its axons will grow towards C8 targets
110
3 main reasons CNS doesnt grow back like peripheral
1. Central damage initiates programmed cell death
2. CNS doesn't secrete ECM scaffolding to guide axons
3. CNS secretes inhibitory factors (chemorepellants)
111
Glial scars inhibit axon regrowth by secreting _____
OLIG-2
112
why does a stroke cause neuron death?
hypoxia leads to a halt in ATP production, which means it can no longer maintain electrochemical gradient and depolarizes. The depolarization causes excitotoxicity, leading to oxidative stress/necrosis. Additionally, all the glutamate spills out of this dead neuron and causes peri-infarct depolarization in neighboring neurons--> calcium overload--> mitochondrial damage--> apoptosis
113
penumbra-
region where neurons are injured but not dead
114
penumbra can be limited by neuroprotective factors such as ____
NPD-1
115
2 factors that block apoptosis-
NGF and Bcl-2
116
cytokines released in inflammatory response to nerve damage block the anti-apoptosis effect of ____
Bcl-2
117
____ is implicated in cancer, as it blocks apoptosis
Bcl-2
118
ATP is depleted in necrosis or apoptosis?
necrosis
119
which is irreversible, apoptosis or necrosis?
necrosis
120
the degree of postnatal neurogenesis decreases with increasing _________
brain complexity
121
mammals show postnatal neurogenesis in what 2 areas?
subgranular zone of the hippocampal dentate gyrus and the subventricular zone
122
subventricular zone contributes interneurons to
the olfactory bulb
123
interneurons generated in adult neurogenesis are carried to their targest by
the rostral migratory stream RMS
124
interneurons generated in adult neurogenesis are carried to their targest by
the rostral migratory stream RMS
125
what cells act as stem cells in the SVZ (subventricular zone)
astrocytes
126
the best way to augment brain development is ______, not drugs or implants
lifestyle changes
127
the major regulator of hippocampal neurogenesis is
hippocampus dependent learning
128
what can block environmentally induced neurogenesis of the hippocampus?
opioid pain killing drugs
129
rubrospinal tract sends excitatory signals to _____ in the upper extremity
flexors
130
which tract is responsible for decorticate posturing?
rubrospinal tract
131
medial vestibulospinal tract is responsible for
head-neck movement
132
lateral vestibulospinal tract is responsible for
proximal estensors for posture and balance
133
which tract is responsible for decerebrate posturing?
reticulospinal tract
134
_____ tract resonsible for head and eye movements
tectospinal
135
UMN lesion of CN VII =
flaccid paralysis on lower contra face
136
LMN lesion of CN VII =
bells palsy
137
CN X UMN lesion =
uvula deviates to same side as lesion
138
CN X LMN lesion =
uvula deviates to opposite side of lesion
139
CN XII UMN lesion =
tongue deviates to opposite side of lesion
140
CN XII LMN lesion =
tongue deviates to same side of lesion
141
CN XII LMN lesion =
tongue deviates to same side of lesion
142
pain and temperature sensory neurons terminate on cell bodies in ___________ in the dorsal horn, then secondary neurons decussate and terminate in the _____.
- rexed laminae I, II, and V
| - VPL
143
spinal trigeminal nucleus conveys
pain and temperature
144
principle sensory nucleus conveys
two point touch and vibration
145
mesencephalic nucleus conveys
proprioception
146
motor nuclei are medial to the
sulcus limitans
147
motor nuclei are medial to the
sulcus limitans
148
CN VII contributes to what 3 nuclei?
superior salivatory, facial, and solitary
149
CN VII contribution to superior salivatory nucleus is:
GVE, parasympathetic to lacrimal, submandibular, and sublingual gland
150
CN VII contribution to the facial nucleus is:
SVE, muscles of facial expression
151
CN VII contribution to the solitary nucleus (rostral portion) is:
SVA, taste
152
CN IX contributes to what 3 nuclei?
solitary, ambiguus, and salivatory
153
CN IX contribution to the rostral part of the solitary nucleus is:
SVA, taste
154
CN IX contribution to the caudal part of the solitary nucleus is:
GVA, sensory info from pharynx
155
CN IX contribution to the nucleus ambiguus is:
SVE, pharynx and larynx musculature (very small component)
156
CN IX contribution to the inferior salivatory nucleus is:
GVE, parasympathetic to the parotid gland
157
CN X contributes to what 3 nuclei?
solitary, ambiguus, and dorsal motor
158
CN X contribution to the rostral solitary nucleus is:
SVA, taste
159
CN X contribution to the caudal solitary nucleus is:
GVA, cardiorespiratory and digestive sensory info
160
CN X contribution to the nucleus ambiguus is:
SVE, pharynx and larynx musculature
161
CN X contribution to the dorsal motor nucleus is:
GVE, parasympathetics to cardiovascular and digestive systems
162
What is the only LMN that shows contralateral signs?
CN IV
163
Inferior alternating hemiplegia occurs at what level and affects what nucleus?
medulla, CN XII
164
middle alternating hemiplegia occurs at what level and affects what nerve?
pons, CN VII
165
superior alternating hemiplegia occurs at what level and affects what nerve?
midbrain, CN III
166
PICA lesion leads to ______ syndrome
wallenberg
167
what arteries supply the medulla?
ASA, PICA, and paramedian branches of vertebral
168
what 4 arteries supply the pons?
paramedian branches of basilar artery, short and long circumferential branches of the basilar artery, and AICA
169
4 arteries supplying midbrain:
PCA, SCA, quadrigeminal artery
170
4 arteries supplying midbrain:
PCA, SCA, quadrigeminal artery
171
_______ effects the pyramidal tract, medial lemniscus, hypoglossal nucleus. Produced by block of paramedian branches of and anterior spinal arteries
Medial medullary syndrome
172
___________ effects the inf. cerebellar peduncle, vestibular nu, sp. trigeminal nu., anterolateral system, nucleus ambiguus, nu. solitarius, descending sympathetic fibers. Produced by block of PICA and/or Vertebral A.
PICA/Wallenberg sydrome
173
__________ effects corticospinal and corticobulbar tracts, facial colliculus (also abducens nu, medial lemniscus). Produced by block of paramedian branches of basilar artery, ventral and dorsal territories.
Foville's syndrome
174
________ effects middle cerebellar peduncle, vestibular nu, trigeminal nu., anterolateral system, cochlear nuclei, descending sympathetic fibers
AICA syndrome
175
_________ affects oculomotor nerve or fascicles produced by block of branches of PCA and top of the basilar artery.
Weber's syndrome
176
_________ affects oculomotor nerve, red nucleus, and sup. cerebellar penduncle. Produced by block of branches of PCA and top of the basilar artery
Claude's syndrome
177
_______ affects same as above plus substantia nigra, cerebral peduncle. Same arteries blocked.
Benedikt's syndrome
178
Pt presents with aggression, refusal to eat, and no fear. Diagnosis?
bilateral loss of amygdala
179
Pt presents with pre-existing mental disorder, impairment of consciousness, and short term memory loss. Diagnosis?
unilateral hippocamal infarction
180
Pt. presents with behavior change, episode of impairment of consciousness, and progressive mental disorder (depression and psychosis)
Diagnosis?
paraneoplastic limbic encephalitis
181
Pt. presents with flu-like illness, seixures, and multiple anti-seizure drugs were unable to stop the seizures (meaning she had status epilepticus) Diagnosis?
limbic encephalitis with prefrontal involvement. She may have also had short term memory deficits from this
182
Pt presents with impaired consciousness, dream state, deja vu, picking at clothing, olfactory hallucinations. Diagnosis?
Limbic seizure
183
Pt. presents with acute episode of disorientation and memory difficulties, history of cocaine use, and short term memory deficit. Diagnosis?
Cocaine-induced hippocampi infarction
184
Pt. is being rehabbed for Acomm aneurysm and has motor deficits and memory impairment (global, short term, verbal, visual) Diagnosis?
Ischemia in Fornix (the mustache of the brain) and premotor involvement.
185
Pt. presents with confusion, short term memory loss, ocular dysfunction, gait ataxia, dysarthria, paresthesias of legs. Diagnosis?
Wernicke's Encephalopathy
186
Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?
Korsakoff's syndrome
187
Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?
Korsakoff's syndrome
188
Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?
Korsakoff's syndrome
189
Echolalia-
tendency to mimic what you hear from others. Using phrases from TV instead of independently carrying conversation
190
autistic children show insistence on sameness =
intensity on a specific object or theme at high, unusal intensity
191
how many children have some form of ASD?
1/68
192
M/F ratio of autism diagnosis
4-5 males per female
193
Neuroimaging findings of autistic children found they have above average ______ and below average number of ______ cells in the cerebellum
- head circumference
| - purkinje
194
often a diagnosis of ASD comes from both an absence of _____ and a presence of ______
typical behaviors
| atypical behaviors
195
Level 1 assesment for ASD does what?
identifies children at risk for ASD and passes them on to level 2
196
level 2 assesment for ASD does what?
determines if child meets criteria for diagnosis of ASD
197
Early signs of ASD include abnormalities in 3 things:
joint attention (moving attn. btw object and adult to share appreciation for the object), social interaction, and play
198
should a child that does not how signs of autism be screened for it anyways?
yes, you do not want to "wait and see"
199
Absolute indicators for immediate further evaluation for autism include no ____ at 12 months, no _____ at 16 months, and no ______ at 24 months
- babbling or gesturing
- single words
- two word spontaneous phrases
200
3 screenings done in level 1 autism assesment:
MCHAT, pervasive developmental disorders screening test 2, social communication questionnaire
201
2 tests done in a level 2 autism assesment
ADI-R (autism diagnostic interview) and autism diagnostic observation schedule (ADOS-2)
202
process of applying interventions based on principles of learning derived from experimental psychology to systematically change behavior-
Applied Behavioral Analysis (ABA)
203
ABA is used to generalize __________
behaviors to new environments or situations
