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Flashcards in Neuro 3 Deck (96):
1

Hypogeusia

reduced sense of taste

2

Ageusia

loss of taste (almost never)

3

Dysgeusia

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

4

Xerostomia

(dry mouth) can also contribute to taste disorders

5

Hyposmia

reduced ability to detect odors.

6

Anosmia

complete inability to detect odors.

7

Parosmia

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.

8

Phantosmia

the sensation of an odor that isn’t there.

9

Impaired odor identification

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

10

causes of olfactory disorders

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

11

Olfactory changes with neurological disorders

dementia
schizophrenia
Parkinson's
PTSD
Depression
Developmental insults

12

stimulation of amygdala leads to

fear

13

damage to amygdala results in

decreased conditioned fear response

14

Hebb's rule

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

15

Necessity of thalamo-lateral amygdala synapses

shown necessary for acquisition and expression of conditioned fear.

16

Kluver-Bucy syndrome cause

Results from bilateral destruction of amygdala.

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Characteristics of Kluver-Bucy syndromes

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

18

prefrontal cortex does what to amygdala

exerts inhibitory control over amygdala and emotion

19

limbic-motor interface

nucleus accumbens

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interface between emotion and cognition

cingulate cortex

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Anterior cingulate receives

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

22

Electrical stimulation of dorsal AC

anticipation of movement

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Electrical stimulation of ventral AC

intense fear or pleasure

24

Anterior cingulotomy can relieve

chronic intractable pain,
treatment-resistant depression, OCD

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

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thrombotic stroke mechanism

clot "in-residence"

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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

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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