anatomy and physiology Flashcards

1
Q

signal transmitting cells fo the nervous system

A

neurons

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2
Q

permanent cells in the brain

A

nuerons

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3
Q

dendrites?

A

receive info

have nissl bodies

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4
Q

axons?

A

give away info

no nissle bodies

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5
Q

what happens when an axon is injured

A

wallerian degeneration
degeneration distal to injuery and axonal retraction proximally
allows for potential regeneration of the axon !@ the pNS (Schwann cells)

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6
Q

what happens to the astrocytes in neuronal injury

A

reactive gliosis

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7
Q

GFAP?

A

astrocytes

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8
Q

function fo astrocytes

A
physical support
repair
K metabolis
removal of excess neurotransmitter
glycogen fue reserve buffer
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9
Q

where astrocytes come from

A

neuroectoderm

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10
Q

what is the role fo microglia

A

phagocytic scavenger cells fo the CNS

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11
Q

what happens to microglia in response to tissue damage

A

microglia

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12
Q

does nissl stain the microglia

A

noppers

rer - not really a protein maker, the microglia

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13
Q

how does HIV affect the microglia

A

HIV infected microglia fuse to form multinucleated giant cells in the CNS

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14
Q

who cares about myelin

A

increases conduction velocity of signals transmitted down axons

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15
Q

what happes at the nodes fo ranvier

A

salutatory conduction fo the ap - high concentration of Na - inward current

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16
Q

what makes myelin in the CNS and the PNS

A

CNS - oligodendrocytes

PNS - shcwann cells

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17
Q

how does myelin increase rate of conduction

A

by wrapping and insulating the axon, myelin increase the space constant (distance before ap dissipates), and increase conduction velocity

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18
Q

how many axons does the schwann cell myelinate

A

only 1

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19
Q

role fo schwann cell please

A

myeliante sPNS axon and promotes axonal regeneration

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20
Q

what disease hurts schwann cells

A

guillina barrer

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21
Q

what is an acoustic neuroma

A

type of schwanooma in the internal acoustic meatus = affects CNVIII

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22
Q

bilateral schwanommas you think

A

neurofibromatous II

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23
Q

hows an oligodendrocyte diff from schwann cells

A

oligos - mor ethan one axon, from neuroectoderm and no regenerative properties

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24
Q

you see a fried egg on histology you think of

A

oligodendrocytes

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25
what hurts oligodendrocytes
multiple sclerosis progressive multifocal luekoencephathy leukodystrophies
26
what is the predominant glial cell type in white matter
oligos
27
describe the fibres of: free nerve endings
c - slow unmyelinated | A delta - fast myelinated
28
describe the fibres of: miessner corpuscles
large meylinated fibres | adapt quickly
29
describe the fibres of: pacinian corpusles
large myelinated fibres | adapt quicly
30
describe the fibres of: merkel discs
larege myelinated fibres | adapt sloqly
31
describe the fibres of: ruffini corpuscles
dendritic endings with capsul | adapt slolwy
32
which sensory receptors adapt quickly
meissnuer and pacinain
33
which sensory receptors adapt slowly
merkel discs and ruffini corpuscles
34
location of: free nerve endings
all skin epidermis some viscera
35
location of: meissner corpuscles
glabrous/hairless skin
36
location of: pacinain cortpscules
deep skin layers ligaments joints
37
location of: merkel discs
finger tipes | superficial skin
38
location of: ruffini corpuscles
finger tips | joints
39
sensory receptors in joints please
pacinian and ruffini
40
superficial sensory receptors in skin pelase
free nerve endings meissner corpuscles meckel discs
41
receptors for: pain and temperature
free nerve endings
42
receptors for: dynamic, dine/light toucn/position sense
meissners
43
receptors for: pressure, deep static touch (shapes and edges), position sense
mekels discs
44
receptors for: vibration and pressure
pacinian
45
receptors for: pressure, dlippage of objects along surface of skin and joing angle change
ruffinin corpuscles
46
what do the messiner copruscles sense
light tough dynamic position sense
47
what do the meckels disc sense
pressure deep static touch position sense shapes/edges
48
what do ruffini corpuscles sense
pressure slippage of objects joint position sense
49
what do pacinian corpuscles sense
vibration | poressure
50
list the layers of a peripheral nerve
nerve - endoneurium - perineurm - ectoneurium
51
which layer of a peripheral nerve needs to be connected in microsergry for limb reattachment
peripneurium
52
what part of nerve affected at guilliarn barre
endoneurium - inflammatory infiltrate
53
synthesis of Ne occurs at?
locus coreuleus at the ponts
54
where is DA made?
substnatia nigra pars compacta in midbrain | ventral tegmentum
55
where is 5-HT made
raphe nuclei @ pons, midbrain and medulla
56
where is ACh made
basal nucles of meynert
57
what is GABA made
nucleus accumbens
58
what is the locus ceruleus responsible for
stress and panic | NE
59
what is the nucleus accumbens and septal nucles responsible for?
GABA | reward centre, pleasure, addiction, fear
60
list the changes in NE seen in different pathos
NE increased in anxiety | NE decreased in depression
61
list the changes in DA seen in different pathos
DA decreased in Parkinson DA increased in Huntington DA decreased in depression
62
list the changes in 5-HT in different pathos
decreased in depression | increasedin depression
63
list the changes in Ach in different pathos
increased in Parkinson decreased in Alzheimer decreased in huntington
64
list the changes seen in GABA
decreased in anxiety | increasedin huntington
65
neurotransmitter changes: anxiety
anxiety - increased Ne, decreased 5HT, decreased DA
66
neurotransmitter changes: depression
depression - decreased Ne, decreased 5HT, decreased DA
67
neurotransmitter changes: huntington
Huntington- increased DA, decreased GABA, decreased ACh
68
neurotransmitter changes: parkinson
Parkinson - decreased DA, increased Ach
69
neurotransmitter changes: alzheimer
decreased Ach )Ach decreased in elderly brains natural course too)
70
what are the three strucutres that form the BBB
tight junctions between nonfenestrated capillary endotheial cells basement membrane astrocyte foot processes vrs GFR ;)
71
how are glucose and amino acids transported across the BBB
carrier mediated transport | SLOW
72
how are lipid molecules transported across the BBB
diffusion | FASTER
73
whats the point of having no BBB in certain areas in the brain
molecules in blood can affect brain function and neurosecretory products enter circulation
74
list some locations where there is no BBB and what the point of them is pelase
OVLT: senses osmotic stuffs area postrema: vomit needed neurohypohysis: Secretion of hypothalamix to circulation
75
what can cause damage to the endothelial cells of the BBB
infarction and or neoplasm detrosy endothelila cell tight junctions
76
whats the result of infarction or neoplasm on the endothelial cells of the BBB
disrupts tight junctions -- VASOGENIC OEDEMA
77
where are other notable barriers besides the BBB located in the body
blood-testis barrier | maternal-fetal blood barrier of the placenta
78
what is the hypothalamus responsible for
``` TAN HATS thermoregulation adenohypophysis neurohypophysis hunger autonomic regulation thirst and water balance sexy urges ```
79
what are the inputs to the hypothalamus
no BBB = OVLT for osmolarity monitoring and the area postrema for response to emetics as well as the supraoptic nucleus for ADh and the paraventricular nucleus for oxytocin.
80
where are ADh and oxytocin sotred
the posterioir pituitary
81
what part of the hypothalamus drives hunger
lateral
82
what part of the hypothalamus drives satiety
ventromedial
83
what happens if knock out lateral hypothalmaus
responsible for eating - so get skinny
84
what happens if you knock out the ventromedial hypothalamus
tells you that you are full - so get bigger
85
what is the role of leptin on the lateral hypothalamus
leoin from fat cells wants to make you not eat | so will inhibit the lateral hypothalamus that is telling you to get lat/fat
86
what is the role of leptin on the ventromedial hypothapamus
leptin from adipose wants to make you not eat | so will stimulate the ventromedial hypothalmaust that is telling you already that you are satieated
87
whats the rold of the anterior hypothalamsu
cools you down like A/C (anterior/cools)
88
whats the role of the posterior hypothalamus
heast you up
89
what happens if you lesion out the anterior hypothalamus
cant cool down
90
what happens if you lesion out the posterior hypothalamus
cant heat up
91
whats the role of the suprachiasmatic nucleus
circadian rhythm
92
what regulates sleep
the suprachiastmatic nucleus via circadian rhythm
93
describe the molecular regulation of sleep
circadian thrythm - nortuncl relase of ACTH, prolactin, melatonin, NE the SCN --> norepinephrine release - pineal gland - melatonin
94
what regulates the SCN
light :) always thought this was romantic | light controls our dreams
95
what hormones are under circadian ctonrol
ATCH prolactin melatonin NE
96
what do ATCH, prolaction, melatonin and NE have in common
circadian control
97
what stage of sleep has EOM movements
REM
98
what causes the rapid eye movemenst in rem
PPRF activity paramedian pontine reticular formation ie the conjugate gaze centre
99
how often does REM occur
every 90 minutes | increases in duration through the nigth
100
what causes decreased REM sleep
alcohol benzodiazepines barbiturates NE
101
what causes decreased delta sleep
NE
102
effect of OH, benzos, barbituates on sleep
decreased REM sleep
103
effect of NE on sleep
decreased REM sleep and decreased delta waves
104
how do you treat sleep enuresis
oral desmopression an ADH analogue (also vWF and Hemophilia VIII)
105
how else can you treat bedwetting?
desmopression > imipramine
106
how do you treat night terros and sleepwalking
benzodiazepines
107
when do night terrors occur
nonREM
108
describe brain activity when awake with eyes open
beta waves - highest frequency and lowest amplitude
109
describebrain activity when awak with eyes closed
alpha waves
110
describe brain activity in nonREM I
theta waves
111
describe brain acitivty in nonREM II
K complexes | sleep spindles
112
describe brain activity in nonREM III
delta waves | lowest frequency, highest amplitude
113
describe REM brain activity
beta waves highest frequency lowest amplitude
114
when does bruxism?
during deepr sleep with sleep spindles and K complexes | nonREM II
115
what is bruxism?
teeth grinding
116
what is the deepest non REM sleep?
stage nonREM III delta waves lowest frequency and highest amplitude
117
what happens in N3 sleep?
delta waves sleep walking night terrors bedwetting
118
when does sleepwalking, night terrors, and bedwetting occur?
nonREM III | delta waves
119
brain activity in light sleep
theta
120
brain activity in deep sleep
delta waves
121
describe what happens in REM sleep
``` loss of motoro tone increased brain O 2 use increased and variable puls and blood pressure dreaming penile clitoral tumescence memory processing function BETA WAVES ```
122
name sleep state: night terrors
N3 with delta waves
123
name sleep state: bruxism
N2 with k complexes and sleep spindles
124
name sleep state: memory consolidation
REM with beta waves
125
name sleep state: dreaming
REM with beta waves
126
name sleep state: sleep walking
N3 with delta waves
127
name sleep sate: bed wetting
N3 with delta waves
128
name sleep state: penile/clitoral stuffs
same as dreaming | REM
129
alpha waves
awake with eyes close
130
delta waves
N3
131
theta waves
N1
132
K spikes | sleep spindles
N2 - teeth grnding
133
what stage of sleep si most time spent in
45% N2 - k spikes and sleep spindles
134
what is second most common stage ot sleep
REM (memory, dreams, night mares bp and pulse, motor O2 use e, beta) and N3 (delta waves, sleep walking, bed wetting, night terrors) are tied with 25%
135
what is the least amount of time spent in sleep
n1 - tehta waves - 5%
136
rank time for each stage of sleep from most to least
N2 > N3=REM > N1
137
whats the point of the thalamus
major relay for all ascending sensory information except olfaction
138
what is the only ascending sensory pathway that bypasses the thalamus
olfactory
139
what is the input for the VPL
spinothalamic and dorsal colomns/medial lemniscus
140
what info does the VPL receive
spinothalamic - pain and temp | dorsal colomns/medial lemniscus - vibration, proprioception, touch, pressure
141
where does the VPL send information
primary somatosensory cortex
142
what is the input to the VPM
ma face! | trigeminal and gustatory pathway
143
what info does the VPM receive
face sensation and taste
144
what part of thalamus does taste go through?
VPM with face sensation
145
where does VPM send information
primary somatosensory cortex
146
Makeup goes on the face
face and taste to VPM
147
what info goes to the LGN
vision | L is for Light and LGN
148
what is the input to the LGN
CN II
149
where does the LGN send information
visual information to the calcarine sulcus
150
what is the input to the MGN
superior olive and inferior colliculus of tectum | Music at the MGN
151
what information goes to the MGN
auditory
152
where does the MGN send information
to the auditory cortex of the temporal lobe
153
what input goes to the VL
basal ganglia and the cerebellum
154
what info goes to the VL
motor
155
where does the VL send its info
motor cortex
156
describe the thalamus and pain, temp, pressure, touch, vibration and proprioception
input via the spinothalamic and dorsal colomns/medial lemniscus to the VPL to the primary somatosensory cortex
157
describe the thalamus and facial sensation and taste
input via the trigeminal and gustatory pathway to the VPM to the primary somatosensory cortex
158
describe the thalamus and vision
input via CN II to the LGN to the occipital cortex
159
describe the thalamus and auditory
superior olive and inferior colliculus to the MGN to the auditory cortex in the temporal lobe
160
describe the thamalus and motor
input via the basal ganglia and cerebellum to the VL to the motor cortex
161
what is the limbic system
a collection of neural structures involved in emotion, long term memory olfaction and behaviour modulation
162
olfactory doesn't go through the thalamus, it goes through
the limbic system
163
function of the limbic ystem
``` emotion long term memory olfaction behavioural modulation ANS function feed, feel, flee, fight, sex ```
164
what structures make up the limbic system
``` acfm amygdala cingulate gyrus fornix mammillary bodies ACFM ```
165
``` acute paralysis - cant move dysarthria - cant speak dysphagia - cant swallow diplopia - cant see loss of consciousness ```
osmotic demyelination syndrome | central pontine myelinolysis
166
symptoms of osmotic demyelination syndrome/central pontine myelinolysis
``` acute paralysis loss of consciousness diplopia dysphagia dysarthria ```
167
what is the pathophys of osmotic demyelination syndrome/central pontine myelinolysis
massive asocan ldemyelination in pontine white matter secondary to osmotic changes
168
what causes osmotic demyelination syndrome/central pontine myelinolysis
rapid correction of hyponatremia
169
what happens when hyponatremia is rapidly corrected
osmotic demyelination syndrome/central pontine myelinolysis: loss fo consciousness, acute paralysis, diplopia, dysphagia, dysparhtira
170
what happens hypernatremia is rapidly corrected?
cerebral edema/herniation
171
from low to high?
your pons will die: acute paralysis, loss of consciousness, diplopia, dysarthria, dysphagia
172
from high to low?
your brain will blow - cerebral edema, and herniation
173
what is the function of the cerebellum
modulates movement | aids in coordination and balance
174
what is the input to the cerebellum
contralateral cortex ia middle cerebellar peduncle | inpsilateral proprioceptive information via inferior cerebellar peduncle from spinal cord
175
inferior cerebellar peduncle
ipsilateral proprioceptive information from spinal cord
176
middle cerebellar peduncle
contralateral input form cortex
177
what is output of the cerebellum
info to the contralateral cortex to mosulate movement.
178
desribce the output nerves of the cerebellum
purkinje cells - deep nuclei of cerebellum - contralateral cortex via superior cerebellar peduncle
179
superior cerebellar peduncle
purkinje cells - deep nuclei of cerebellum - contralateral cortex out via superior cerebellar peduncle
180
what are the deep nuclei of the cerebellum
dentate - emboliform - globose - fastigial
181
DONT EAT GREASY FOODS
dentate - emboliform - globose - fatigial | lateral to medial deep nuclei of the cerebellum
182
lateral lesions present as
propensity to fall to ispilatera sides as lesions
183
what is lateral cerebellum responsible for
voluntary movements of extremities
184
what are the midline structures
fastigial nucles and verma cortex and of the flocculonodular lobe
185
what happens when the fastigial nucleus/veris cortex and or the flocculonodular lobe
trnucal ataxia - wide based cerebellar gait nystagmus head tilting
186
wide based cerebellar gait nystagmus head tiliting
midline cerebellar lesion gastigial nucleus vermis flocculonodular lobe
187
midline lesions of cerebellum usually result in?
bilateral motor deficits affecting axial and procimal limb musculature wide based cereberllar gait - truncal ataia nystagmus and head tilting
188
what are the basal ganglia good for
important I voluntary movements and making postural adjustments
189
where does the basal ganglia receive its input from
cortical input
190
what is putput of the basla ganglia
negative feedback to the cortex via the VL of the thalamus
191
what is the striatum
putamen (motor) and caudate (cognitive)
192
what is the lentiform
putamen and globus pallidus
193
describe the direct pathway in the basal ganglia
substantia nigra pars compacta receives stimulatory input from the motor cortex - sends out DA to the putamen - inhibits the globus pallidus interna -- inhibits the thalamus -- stimulates the cortex --. when activated results in increased motion
194
describe the indirect pathway in the basal ganglia
cortex stimulates the substanstia nigra pars compacta - DA sent out to putamen and inhibits it - sends out inhibitor to globus pallidus externa - inhibits the subthalamic nucleus - stimulates the thalamus - inhibits the cortex - results in decreased motion
195
what is the inhibitor neurotransmitter used in the direct pathway
GABA
196
what is the pedunculopontine nucleus?
from cortex to the spinal cord
197
athetosis
slow writhing movements especially in fingers
198
writhing, snake like movement
athetosis
199
where is athetosis seen?
huntington
200
damage to the ? causes athetosis
basal ganglia
201
what is chorea
sudden, jerky, purposeless movements
202
''dancing''
chorea - sudden jerky purposeless movements
203
damage to the ? causes chorea
basal gangial
204
huntingotn movement disorders observed
athetosis: slow, writhing movements esp in fingers AND chorea: sudden jjerky purposeless movements both due to damage at the basal ganglia
205
what is dystonia
sustained, involuntary muscle contractions
206
sustained, involuntary muscle contractions
dystonia
207
what type of movement disorder is writers cramp
dystonia - sustained involuntary muscle contractions
208
what type of movement disorder is blepharospams
dystonia - involuntary muscle contractions - sustained eylid twtiches
209
exampls of dystonia
writers cramp and blepharospasm
210
what is an essential tremor
high frequency remor with sustained posture | worse with movement or when anxious
211
tremor self medicated with EtOH = ?
essential tremor | decreases tremor amplitude
212
how do you treat essential tremors
beta blockers and PRIMIDONE
213
beta blockers and primidone treatment for
essential tremor - high frequency tremor with sustained postire, worse with movement or when anxious - why can treat with beta blocker
214
what is hemiballismus
sudden wild flailing fo one arm with or wtihotu ipsilateral leg
215
where is the lesion with sudden wild flailing of one arm with or without ipsilateral leg
contralateral subthalamic nucleus
216
lesion in subthalamic nucleus
hemiballisumus ie sudden wild flailing of one arm with or without ipsilateral leg
217
what type of stroke can cause hemiballismus
lacunar stroke
218
movement disorder associated with lacunar stroke
subthalamic nucleus infarction - contralateral subthalamic nucleus
219
what is an intention tremor
slow sizsax motion with pointing ot extending towars a target
220
what causes an intention tremor
cerebellar lesion
221
what is myoclonus
sudden, brief, uncontrolled muscle contraction
222
examples of myoclonus
jerks hiccups common in metabolic abnormalities such as renal and liver dailure
223
sudden brief, uncontrolled muscle contractions you suspect
metabolic abnormalities ie RENAL and LVIER failure
224
what is a resting tremor
uncontrolled movement of DISTAL appendages - mostly in hands | tremor alleviated by intestinal movement (vrs essential that is worse with movement)
225
where do you see a resting tremor
Parkinson | occurs at rest
226
pill rolling tremor
uncontrolled movement of distal appendanges mostly inhands that is alleviated by intestinal movement
227
uncontrolled movement of distal appendanges mostly in hands that is alleviated by intentional movement
pill rolling tremor
228
lewy bodies
Parkinson disease | composed of alpha synucleni - intracellular eosinophilc inculsions
229
``` pill rolling remor at rest cogwheel rigidity akinesia postural instability shuffling gait ```
``` Parkinson disease lewy bodies alpha synuclein loss of da ercig nerus in substantia nigra pars compacta increased Ach and decreased DA ```
230
describe Huntington disease
AD trinucleotide of CAG chromosome 4
231
wen do symptoms manifest in hunting ton
between twenty and fity
232
choreiform movements aggression depression dementia
hntington disease
233
presentation of Huntington please
``` choreiform movements aggression depression dementia sometimes initially mistaken for substance abuse ```
234
neurotransmitter changes in huntingotn disease
decreased Ach increased DA decreased GABA
235
what causes the neuronal death in Huntington disease
cia NMDA receptor bidngin an dGLUTAMATE TOXICTY
236
MRI of huntingotn disease
atrophy of caudate nuclei with ex vacuo dilatation of frontal horns
237
atrophy of caudate nuclei with ex vacuo dilatation of fronal horns
``` Huntington depression aggression dementia choreiform ```
238
CAG - caudate loses Ach and GABA
glutamate toxo and NMDA receptor binding
239
define aphasia please
higher order inability to speak
240
what is dysarthria
motor inability to speak via movement deficit
241
what is a non fluent aphasia
cant speak
242
fluent aphasia
speak
243
where is brocas area
inferior frontal gyrus of frontal lobe
244
inferior frontal gyrus of frontal lobe damage
brocas aphasia
245
what are symptoms of brocas aphasia
nonfluent aphasia inctact comphrehension inability to repeat
246
where is wernickes area
superior temporal gyrus of temporal lobe
247
superior temporal gyrus of temporal lobe damage
wernickes aphasia
248
fluent aphasia, impaired concentration, impaired repitition
wernickes aphasia
249
describe sxs of wernickes aphasia
fluent apadia imapried comprehension impaired repetition
250
whats the purpose do the arcuate fasciculus
connets brocas to wernickes
251
conduction aphasia
damage to the arcuate fasciculus
252
fluent speech intact comphrehension impaired repetition
conduction aphasia | impaired arcuate fasciculus
253
sxs of conduction aphasia
fluent speech intact comprehension imapreid repetition
254
nonfluent aphasia intact comprehension intact repetition
transcortical motor aphasia
255
sxs of transcortical motor aphasia
``` nonfluent aphasia intact comprehension intact repetition (brocas except with repetition is good) ```
256
fluent aphasia impaired comprehension intact repetition
transcortical sensory aphasia
257
sxs of transcortical sensory aphasia
fluent aphasia impaired comprehension intact repetition wernickes only with godo repeittion
258
nonfluent speech impaired comprehension intact repetition
mixed transcortical aphasia
259
sxs of mixed transcortical aphasia
nonfluent speech impaired comprehension intact repetition
260
what areas are damage in mixed transcortical aphasia
brocas and wernicks | arcuate fasciculs not involved (or else would lose repetition)
261
what is damaged in global aphasia
broas, wernickes, arcuate fasciculs
262
nonfluent aphasia impaired comprehension impaired repetition
global aphasia
263
where is the extrapyramidal circuit
premotor areas in the frontal cortex
264
disinhibited behaviour hyperphagia hypersexuality hyperorality
amygdala damage | KLUVER BUCY SYNDROME
265
sxs of kluver bucy syndrome
amygdala damage hyperphagia hyperoralitiy hypersexuailtiy
266
what virus is associated with kluver bucy syndrome
HSV-1 | bad news for its spread
267
disinhibtion and deficits in concentration, orientation, judgement,
frontal lobe
268
brain lesion associated with re-emergence of primitive reflexes
frontal lobe | deficits in concentration, orientation ,judgement
269
nondominant parietal temporal cortex
hemispatial neglect syndrome | agnosia of the contralateral side fo the world
270
dominant parietal temporal cortex
agraphia acalculi finger agnosia left right disorientation
271
what is gerstmann syndrome
``` dominant parietal temporal lobe lesion agraphia acalculi finger agnosia left right disorientation ```
272
lesion of reticular activating system/midbrain
reduce levesl or arousal and wakefulness
273
bilateral mammillary bodies damage
Wernicke: confusion, ataxia, ophthalmoplegia Korsakoff: personality changes, confabulation, memory loss (antero and retrograde)
274
what is mamilliary bodies bilateral lesions associated with
B1 deficiency | excessive EtOH
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what can worsen a) confusion, ataxia, opthalmoplegia and b) confabulation, personality changes and memory loss
glucose infusion without B1
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lesion of basal ganglia
tremor at rest chorea athethosis
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what disease are associated with basal ganglia lesion
Parkinson disease | Huntington disease
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lesions to the cerebellar hemispheres
``` LATERAL intention tremor limb ataxia loss of balance IPSILATERAL DEFICINTS fall to same side ```
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lesion to the cerebellar vermis
MEDIAL truncal ataxia and dysarthria nystagmus head tilting
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damage to subthalamic nucleus
hemiballsimus on contral ateral side | lacunar infarcts
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hippocampus bilateral lesion
anterograde amnesia
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paramedian pontine reticular formation
eyes look away from side of lesion
283
frontal eye field lesion
eyes look toward the lesion