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Neuro > Neuro 3 > Flashcards

Neuro 3 Flashcards

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
Q

bilateral removal of temporal lobes

A

anterograde amnesia

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26
Q

damage to hippocampus does not effect

A 
perceptual learning (e.g., recognize faces, melodies)
sensory-response learning (e.g., conditioned eye blink)
motor learning (e.g., weaving)
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27
Q

damage extending into limbic cortex of medial temporal lobe

A

retrograde amnesia

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28
Q

Loss of ACh neurons in

A

Alzheimer’s disease

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29
Q

neuropathology of Alzheimer’s disease

A

Neuritic Plaques
Neurofibrillary Tangles
Congophilic Angiopathy
Synaptic Loss

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30
Q

2 hallmarks of alzheimer’s pathology

A

amyloid plaque

neurofibrillary tangles

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31
Q

tauopathies examples

A 
alzheimer's disease
fronto-temporal dimentia
encephalopathy
supranuclear palsy
corticobasal degeneration
Down's syndrome
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32
Q

alzheimers age of onset

A

familial: 65 yr

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33
Q

alzheimer’s genes

A

presenillin 1, 2

amyloid precursor protein (APP)

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34
Q

environmental causes of alzheimers

A 
age 
head trauma
high BO
high cholesterol
diabetes 
stroke
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35
Q

inherited factors of sporadic alzheimers

A

Apo E isoform

first degree relative

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36
Q

ApoE

A

colocalizes with A beta in plaques

strongest genetic risk factor for sporadic AD

homo- or heterozygous: 2-10X increased risk

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37
Q

small vessel disease

A

Ischemic white matter degeneration
Lacunar infarction of structures
Congophilic angiopathy

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38
Q

Binswanger’s disease

A

Arterioles show thickened walls, infiltration with lipid and widened peri-vascular spaces.

Perivascular demyelination resulting from vessel pathology

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39
Q

Lewy body dementia

A

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
Q

Probable LBD

A

Dementia

Two or more: marked fluctuations, visual hallucinations, parkinsonism

41
Q

Presentation of fronto-temporal lobar degeneration

A

Gradual and progressive change in behavior

Gradual and progressive language dysfunction

42
Q

Prion diseases

A

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
Q

Jakob-Creutzfeld Disease

A

Most common prion disease;

Age at onset 60yr
Rapidly progressive with death

44
Q

Clinical course of CJD

A
  • swiftly progressing cognitive impairment
  • behavioral alterations
  • myoclonus
  • ataxia
45
Q

stroke definition

A

Sudden focal neurological symptom, attributed to a problem with blood vessels

46
Q

two subtypes of stroke

A

Ischemic (lack of blood flow) > 80%

Hemorrhagic

47
Q

TIA definition

A

Transient focal neurological deficit due to ischemia

Traditional Definition:
Less than 24 hours (usually

48
Q

ACA symptoms

A

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
Q

MCA symptoms

A

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
Q

VB symptoms (Vertebrobasilar)

A

“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
Q

PCA symptoms

A

Contralateral HH, cortical blindness, lack of depth perception, visual hallucinations

Perseveration and dyslexia

Contralateral sensory loss

Pupillary dysfunction, nystagmus, loss of conjugate gaze

52
Q

Common clinical stroke symptoms

A 
Weakness
Impaired language (aphasia)
Vision loss
Numbness
Gait disturbance
Slurred speech
53
Q

What’s missing from stroke symptoms

A

PAIN

54
Q

thrombotic stroke mechanism

A

clot “in-residence”

55
Q

embolic stroke mechanism

A

traveling clot

56
Q

cardioembolic risk factors

A 
Atrial fibrillation
Recent anterior wall MI
Left ventricular thrombus
Left atrial thrombus
Mechanical prosthetic valve
Infectious endocarditis
57
Q

Small vessel disease

A

Lacunar stroke

Small infarcts involving subcortical structures of the brain:
Internal capsule, basal ganglia, thalamus

58
Q

Lacunar syndromes

A 
Pure motor
Pure sensory
Sensorimotor
Ataxic hemiparesis
Clumsy hand-dysarthria
Hemiballismus-hemichorea
59
Q

aphasia

A

problem with language

60
Q

inability to perform learned movements

A

apraxia

61
Q

prosopagnosia

A

can’t recognize faces

R PCA/parietal

62
Q

simultagnosia

A

can’t get visual gestalt

R MCA/diffuse

63
Q

Broca’s aphasia

A

difficulty with expression

64
Q

Wernicke’s aphasia

A

difficulty with receptive language

65
Q

synesthesia

A

cross modal perception such as letter perceived as color

66
Q

consciousness definition

A

state of full awareness of the self and one’s relationship to the environment

content, arousal

67
Q

delirium definition

A

confusional state characterized by:
rapid onset
fluctuatic course
impairments of many systems

68
Q

delirium produces alterations in

A 
consciousness
attention
sleep-wake cycles
cognitive abilities
memory
69
Q

delirium can manifest with

A

hypo or hyperactivity
hallucinations
delusions

70
Q

delirium is NOT

A

dementia

71
Q

causes/risk factors of delirium

A

primary brain disorders
systemic/general medical disorders
substances/withdrawal related

72
Q

delirium treatment

A

treat underlying cause

behavioral control often necessary

73
Q

early symptoms of DT

A

0-48 hours after last drink
tremulousness
hallucinosis
seizures

74
Q

late symptoms of DT

A 
48-72 hours after last drink
fluctuating periods of confusion/clarity
psychomotor agitation
delusions
frank hallucinations
inattentiveness
severe tremulousness
dysautonomia (fatal)
75
Q

treatment for DT

A

PRN diazepam is mainstay

76
Q

alternative treatment for DT

A

ativan

77
Q

medical complications of DT

A

dehydration, hypotension

78
Q

Wernicke’s syndrome

A

global confusional state
opthalmoparesis
gait ataxia

appears over days to weeks, resulting from B1 deficiency

79
Q

Korsakoff’s dementia

A

anterograde and retrograde amnesia
confabulation
impaired insight
alertness, attention, behavior preserved

80
Q

Wernicke-Korsakoff damages which structures

A

maxillary bodies/hypothalamus

dorsomedial and anterior thalamic nuclei

81
Q

coma definition

A

state of unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli

82
Q

coma in practice

A

acute, temporary
no response to external stimuli
eyes are closed, do not open
sleep-wake cycles absent

83
Q

3 areas of consciousness

A

reticular activating system
bilateral thalami
bilateral cortical dysfunction

84
Q

if coma exam localizes to brainstem

A

likely structural lesion

85
Q

if coma exam localizes to hemisphere

A

likely systemic illness

86
Q

major elements of coma exam

A

Motor Response to External Stimuli
Pupils
Eye Movements
Breathing

87
Q

normal oculovestibular reflex

A

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
Q

coma oculovestibular reflex

A

absence of the slow deviation equals brainstem dysfunction. Absence of the corrective nystagmus implies cortical dysfunction.

89
Q

when do adults emerge from coma?

A

2-4 weeks

90
Q

persistent vegetative state- timing

A

1 month

91
Q

brain death

A

no brain function detectable on neurological exam

all brainstem reflexes absent (including respirations)

92
Q

major goal of coma exam

A

distinguish between diffuse cortical dysfunction and brainstem dysfunction

exclude mimics

93
Q

diffuse cortical dysfunction

A

results from systemic abnormalities

94
Q

brainstem dysfunction

A

structural injury

95
Q

Gurstmen’s syndrome

A

finger agnosia (can’t name them)
trouble writing
trouble with math (acalculia)

96
Q

Binswanger’s disease presentation

A

progressive cognitive decline with hemiparesis, hemianopsia and aphasia

Neuro (15 decks)

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