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Neuro 3 Flashcards

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1
Q

Hypogeusia

A

reduced sense of taste

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2
Q

Ageusia

A

loss of taste (almost never)

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3
Q

Dysgeusia

A

is a condition in which a foul, salty, rancid, or metallic taste sensation persists in the mouth
can be complication of chemo- or radiation therapy

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4
Q

Xerostomia

A

(dry mouth) can also contribute to taste disorders

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5
Q

Hyposmia

A

reduced ability to detect odors.

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6
Q

Anosmia

A

complete inability to detect odors.

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7
Q

Parosmia

A

a change in the normal perception of odors, such as when the smell of something familiar is distorted, or when something that normally smells pleasant now smells foul.

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8
Q

Phantosmia

A

the sensation of an odor that isn’t there.

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9
Q

Impaired odor identification

A

can detect odor and know its different from other but can’t label

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10
Q

causes of olfactory disorders

A

Can occur following head trauma, chemical exposure (ZnSO4), smoking, nasal passage obstruction, central neuropathology

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11
Q

Olfactory changes with neurological disorders

A 
dementia
schizophrenia
Parkinson's
PTSD
Depression
Developmental insults
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12
Q

stimulation of amygdala leads to

A

fear

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13
Q

damage to amygdala results in

A

decreased conditioned fear response

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14
Q

Hebb’s rule

A

Long-term potentiation, a cellular model of synaptic plasticity, is a leading candidate mechanism underlying associative learning.

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15
Q

Necessity of thalamo-lateral amygdala synapses

A

shown necessary for acquisition and expression of conditioned fear.

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16
Q

Kluver-Bucy syndrome cause

A

Results from bilateral destruction of amygdala.

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17
Q

Characteristics of Kluver-Bucy syndromes

A

Hypersexuality (incl. inappropriate objects)
Hyperorality (examine objects by mouth)
Docility
Hyperphagia (incl. inappropriate objects)
Visual agnosia (cannot recognize familiar objects/people)

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18
Q

prefrontal cortex does what to amygdala

A

exerts inhibitory control over amygdala and emotion

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19
Q

limbic-motor interface

A

nucleus accumbens

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20
Q

interface between emotion and cognition

A

cingulate cortex

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21
Q

Anterior cingulate receives

A

reward-related signals from the ventral tegmental dopamine cell group and fear-related signals from amygdala.

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22
Q

Electrical stimulation of dorsal AC

A

anticipation of movement

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23
Q

Electrical stimulation of ventral AC

A

intense fear or pleasure

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24
Q

Anterior cingulotomy can relieve

A

chronic intractable pain,

treatment-resistant depression, OCD

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25
bilateral removal of temporal lobes
anterograde amnesia
26
damage to hippocampus does not effect
``` perceptual learning (e.g., recognize faces, melodies) sensory-response learning (e.g., conditioned eye blink) motor learning (e.g., weaving) ```
27
damage extending into limbic cortex of medial temporal lobe
retrograde amnesia
28
Loss of ACh neurons in
Alzheimer's disease
29
neuropathology of Alzheimer's disease
Neuritic Plaques Neurofibrillary Tangles Congophilic Angiopathy Synaptic Loss
30
2 hallmarks of alzheimer's pathology
amyloid plaque | neurofibrillary tangles
31
tauopathies examples
``` alzheimer's disease fronto-temporal dimentia encephalopathy supranuclear palsy corticobasal degeneration Down's syndrome ```
32
alzheimers age of onset
familial: 65 yr
33
alzheimer's genes
presenillin 1, 2 | amyloid precursor protein (APP)
34
environmental causes of alzheimers
``` age head trauma high BO high cholesterol diabetes stroke ```
35
inherited factors of sporadic alzheimers
Apo E isoform | first degree relative
36
ApoE
colocalizes with A beta in plaques strongest genetic risk factor for sporadic AD homo- or heterozygous: 2-10X increased risk
37
small vessel disease
Ischemic white matter degeneration Lacunar infarction of structures Congophilic angiopathy
38
Binswanger's disease
Arterioles show thickened walls, infiltration with lipid and widened peri-vascular spaces. Perivascular demyelination resulting from vessel pathology
39
Lewy body dementia
Second most common form of degenerative dementia Early psychotic symptoms: visual hallucinations, delusions Parkinsonism Fluctuations/diurnal variations in attention, arousal, or behavior Orthostatic hypotension, syncope Depression Neuroleptic sensitivity REM sleep behavior disorder
40
Probable LBD
Dementia | Two or more: marked fluctuations, visual hallucinations, parkinsonism
41
Presentation of fronto-temporal lobar degeneration
Gradual and progressive change in behavior Gradual and progressive language dysfunction
42
Prion diseases
characterized by the conformational conversion of cellular prion protein (PrPc) into abnormal forms (PrPSc) that have high content of b-sheet structure and a strong tendency to aggregate and form amyloid fibrils
43
Jakob-Creutzfeld Disease
Most common prion disease; Age at onset 60yr Rapidly progressive with death
44
Clinical course of CJD
- swiftly progressing cognitive impairment - behavioral alterations - myoclonus - ataxia
45
stroke definition
Sudden focal neurological symptom, attributed to a problem with blood vessels
46
two subtypes of stroke
Ischemic (lack of blood flow) > 80% | Hemorrhagic
47
TIA definition
Transient focal neurological deficit due to ischemia Traditional Definition: Less than 24 hours (usually
48
ACA symptoms
Contralateral LE weakness and sensory loss Mental status impairment—confusion, amnesia, perseveration, personality changes, apathy Abulia (inability to make decisions or perform voluntary acts)
49
MCA symptoms
Contralateral hemiparesis and/or hemisensory loss (Face + UE > LE) Contralateral homonymous hemianopia Dominant (usually L) hemisphere: Aphasia, alexia, agraphia, or acalculia Non-dominant (R) hemisphere: Neglect, extinction, or spatial disorientation
50
VB symptoms (Vertebrobasilar)
“Crossed findings” Contralateral hemi- or quadraparesis, dysarthria Ipsilateral numbness and weakness of face Cranial nerve palsies Vertigo, nausea, ataxia, clumsiness Diplopia, nystagmus, ophthalmoplegia Diminished level of consciousness
51
PCA symptoms
Contralateral HH, cortical blindness, lack of depth perception, visual hallucinations Perseveration and dyslexia Contralateral sensory loss Pupillary dysfunction, nystagmus, loss of conjugate gaze
52
Common clinical stroke symptoms
``` Weakness Impaired language (aphasia) Vision loss Numbness Gait disturbance Slurred speech ```
53
What's missing from stroke symptoms
PAIN
54
thrombotic stroke mechanism
clot "in-residence"
55
embolic stroke mechanism
traveling clot
56
cardioembolic risk factors
``` Atrial fibrillation Recent anterior wall MI Left ventricular thrombus Left atrial thrombus Mechanical prosthetic valve Infectious endocarditis ```
57
Small vessel disease
Lacunar stroke Small infarcts involving subcortical structures of the brain: Internal capsule, basal ganglia, thalamus
58
Lacunar syndromes
``` Pure motor Pure sensory Sensorimotor Ataxic hemiparesis Clumsy hand-dysarthria Hemiballismus-hemichorea ```
59
aphasia
problem with language
60
inability to perform learned movements
apraxia
61
prosopagnosia
can't recognize faces R PCA/parietal
62
simultagnosia
can't get visual gestalt R MCA/diffuse
63
Broca's aphasia
difficulty with expression
64
Wernicke's aphasia
difficulty with receptive language
65
synesthesia
cross modal perception such as letter perceived as color
66
consciousness definition
state of full awareness of the self and one's relationship to the environment content, arousal
67
delirium definition
confusional state characterized by: rapid onset fluctuatic course impairments of many systems
68
delirium produces alterations in
``` consciousness attention sleep-wake cycles cognitive abilities memory ```
69
delirium can manifest with
hypo or hyperactivity hallucinations delusions
70
delirium is NOT
dementia
71
causes/risk factors of delirium
primary brain disorders systemic/general medical disorders substances/withdrawal related
72
delirium treatment
treat underlying cause behavioral control often necessary
73
early symptoms of DT
0-48 hours after last drink tremulousness hallucinosis seizures
74
late symptoms of DT
``` 48-72 hours after last drink fluctuating periods of confusion/clarity psychomotor agitation delusions frank hallucinations inattentiveness severe tremulousness dysautonomia (fatal) ```
75
treatment for DT
PRN diazepam is mainstay
76
alternative treatment for DT
ativan
77
medical complications of DT
dehydration, hypotension
78
Wernicke's syndrome
global confusional state opthalmoparesis gait ataxia appears over days to weeks, resulting from B1 deficiency
79
Korsakoff's dementia
anterograde and retrograde amnesia confabulation impaired insight alertness, attention, behavior preserved
80
Wernicke-Korsakoff damages which structures
maxillary bodies/hypothalamus dorsomedial and anterior thalamic nuclei
81
coma definition
state of unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli
82
coma in practice
acute, temporary no response to external stimuli eyes are closed, do not open sleep-wake cycles absent
83
3 areas of consciousness
reticular activating system bilateral thalami bilateral cortical dysfunction
84
if coma exam localizes to brainstem
likely structural lesion
85
if coma exam localizes to hemisphere
likely systemic illness
86
major elements of coma exam
Motor Response to External Stimuli Pupils Eye Movements Breathing
87
normal oculovestibular reflex
the eyes deviate slowly toward the side of the cold water. The cortex corrects the deviation and the eyes then jerk back toward midline
88
coma oculovestibular reflex
absence of the slow deviation equals brainstem dysfunction. Absence of the corrective nystagmus implies cortical dysfunction.
89
when do adults emerge from coma?
2-4 weeks
90
persistent vegetative state- timing
1 month
91
brain death
no brain function detectable on neurological exam | all brainstem reflexes absent (including respirations)
92
major goal of coma exam
distinguish between diffuse cortical dysfunction and brainstem dysfunction exclude mimics
93
diffuse cortical dysfunction
results from systemic abnormalities
94
brainstem dysfunction
structural injury
95
Gurstmen's syndrome
finger agnosia (can't name them) trouble writing trouble with math (acalculia)
96
Binswanger's disease presentation
progressive cognitive decline with hemiparesis, hemianopsia and aphasia

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