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MRCPsych Part A - Al-Rashid Hospital > Applied Neuroscience > Flashcards

Applied Neuroscience Flashcards

1
Q

Name some frontal tests

A 
Similarities
Lexical fluency
Luria motor test
Go/on go test
Cognitive estimates test
Trail making test
Alternative pyramids
Proverb interpretation
Frontal release signs
Digit span
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2
Q

What is the similarities test?

A

Comparing two objects to test the ability of categorisation and not a description of common parts.
This tests abstract ability.

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3
Q

What does the similarities test.. test?

A

Frontal lobe

Abstract ability

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4
Q

What is the lexical fluency test?

A

Naming items such as animals - category fluency or

generation of words starting with letters FAS (word fluency).

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5
Q

What does lexical fluency test?

A

Speed and accuracy
Ability to shift from one set of objects to the next
Frontal lobe

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6
Q

What is the luria motor test?

A

Fist palm edge.

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7
Q

What does Luria motor test.. test?

A

Motor planning
Exectition
Error correction
Frontal lobe

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8
Q

What does the go/on go test.. test?

A

Response inhibition
Absence of perseveration
Resistance to interference

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9
Q

What is the cognitive estimates test?

A

E.g. How tall is an average English woman?

Uses questions that need abstract not mere factual thinking.

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10
Q

Give examples of tests that test abstract ability

A

Similarities Test

Cognitive estimates test

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11
Q

What is the trail making test?

A

Firstly, simple number sequence used to join dots.

Secondly, use alternating numbers and letters - more sensitive to frontal lobe dysfunction.

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12
Q

What does trail making test?

A 
Frontal lobe
Visuomotor tracing
Attention
Conceptualisation
Set shifitng
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13
Q

Name some parietal tests

A 
Copying shapes
Identifying fingers
Calculation ability
Graphesthesia
Right Left orientation
Stereognosis
Two point discrimination
Visual inattention
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14
Q

Describe the copying shapes test.

A

Ability to draw shapes and construct geometrical patterns.

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15
Q

Describe the identifying fingers test.

A

Test the ability to recognise the touched finger when eyes are closed.
Test ability to correctly show ones index, middle and ring fingers.
Interlocking fingers test - ability to copy examiners interlocking fingers.

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16
Q

What does identifying fingers test.. test?

A

Dominane parietal damage causes finger agnosia as part of Gerstmann syndrome.

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17
Q

What is the calculation ability test?

A

Tests simple mathematical function.

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18
Q

What if often intact in calculation ability even if parietal dysfunction?

A

Recognition and use of numbers - arithmetic ability.

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19
Q

What does calculation ability test.. test?

A

Dominant parietal damage can cause acalculia as part of Gerstmann syndrome.

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20
Q

Describe Right left orientation test

A

Test for ability to touch right ear lobe with left index finger when eyes closed.

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21
Q

What does Right left orientation test.. test?

A

Dominant parietal damage can cause right-left disorientation as part of Gerstmann syndrome.

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22
Q

What is the stereognosis test?

A

Ability to recognise objects by palpation, without visual inspection.

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23
Q

What does stereognosis test?

A

Bilateral parietal function - somatosensory cortices.

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24
Q

What does the two point discrimination test.. test?

A

Cortical sensation

Bilateral somatosensory cortical function

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25
Q

Describe the visual inattention test

A

Letter or star cancellation task
Line bisection test
Draw a person/tree tasks

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26
Q

What are you looking for in the visual inattention test?

A

Hemineglect - feature of parietal lesions.

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27
Q

Signs and symptoms of unilateral front lobe lesion

A

Contralateral spastic hemiplegia
Elevation of mood, increased talkativeness, tendency to joke inappropriately (Witzelsuch)
Frontal release signs (grap/suck reflexes)
Anosmia

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28
Q

Signs and symptoms of left frontal lobe lesion

A

Motor speech disorder with agraphia with or without oro-buccal apraxia
Loss of verbal fluency with persevaration

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29
Q

Signs and symptoms of bilateral frontal lobe lesions

A

Bilateral hemiplegia
Spastic bulbar palsy
Abulia (indecisiveness, lack of drive)
Decomposition of gait and sphincter incontinence
Combination of grasping, sucking, obligate imitative movements, ulitization behaviour

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30
Q

Specific frontal syndromes?

A

Pseudo depressive
Dysexecutive
Pseudo psychopathic

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31
Q

What is a gelastic seizure?

A

Epileptic fit of incessant laughter, from left prefrontal seizure

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32
Q

Signs and symptoms of unilateral parietal lobe lesion

A

Corticosensory syndrome and sensory extinction
Mild hemiparesis
Homonymous hemianopia or inferior quadrantanopia

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33
Q

Sign of right parietal lobe lesion

A

Neglect of opposite side of external space

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34
Q

Sign of left parietal lobe lesion

A

Gerstmann syndrome

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35
Q

What is Gerstmann syndrome?

A

Dysgraphia
Dyscalculia
Finger agnosia
Right-left confusion

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36
Q

What causes Gerstmann syndrome?

A

Lesion in left parietal lobe

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37
Q

Signs and symptoms of bilateral parietal lobe lesions

A

Spatial disorientation and visual spatial defects
Bilateral ideomotor and ideational apraxia
Tactile agnosia
Balint syndrome

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38
Q

Signs of unilateral temporal lobe lesion

A 
Homonymous upper quadrantanopia
Wernickes aphasia
Degrees of amusia and/or visual agnosia
Dysnomia
IMpairment auditory verbal learning
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39
Q

Signs of bilateral temporal lobe lesions

A 
Hallucinations
Dreamy states with uncinate seizures
Emotional and behavioural changes
Disturbance of time perception
Korsakoff amnesic defect (hippocampaal formations)
Apathy and placidity
Hypermetamorphospia - compulsion to attend to all visual stimuli
Kluver-Bucy syndrome
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40
Q

Signs of Kluver-Busy syndrome

A

Hyperorality
Hypersexuality
Blunted emotional reactivity

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41
Q

Where is the lesion in homonymous upper quadrantanopia?

A

Unilateral temporal lobe

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42
Q

What is Geschwind syndrome?

A

Personality change reported in all epilepsy patients.

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43
Q

Pathology underlying Geschwind syndrome?

A

Due to lost connectivity among cerebral areas.

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44
Q

Symptoms of Geschwind syndrome?

A 
Hypergraphia
Circumstantiality
Interpersonal viscosity
Hyperreligiosity
Hyposexuality
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45
Q

What is the most common aura in epilepsy?

A

Autonomic

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46
Q

Give e.g. of autonomic auras

A

Salivation

Vertigo

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47
Q

What is a forced thinking aura?

A

Individual has a compulsion to think on a certain restricted topic

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48
Q

What is evocation of thought aura?

A

Intrusion of stereotyped words or thoughts

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49
Q

Name auras of temporal lobe epilepsy

A 
Autonomic sensations
Forced thinking
Evocation of thought
Sudden obstruction to thought flow
Panoramic memory
Psychic seizures
Uncinate crises
Transient dysphagia
Strong affective experiences
Dostoevsky's epilepsy
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50
Q

What is Doestoevsky’s epilepsy?

A

Temporal lobe aura - ecstatic content

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51
Q

Common emotions in strong affective experiences aura?

A

Fear and anxiety

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52
Q

What is the uncinate crises aura?

A

Hallucinations of taste and smell associated with dream like reminiscence and altered consciousness

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53
Q

What is psychic seizures aura?

A

Isolated auras with hallucinations, depersonalisations, micropsia or macropsia, deja vu/jamais vu

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54
Q

What is panoramic memory aura?

A

Recall of expansive memories in incredible detail

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55
Q

Signs of unilateral occipital lobe lesions

A

Contralateral homonymous hemianopia - central/peripheral
Elementary (unformed) hallucinations
Visual object agnosia
Visual illusions - metamorphosis and hallucinations

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56
Q

What are elementary hallucinations often due to?

A

Irritative unilateral occipital lobe lesions

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57
Q

Which sign is more common right right-sided occipital lobe lesion?

A

Visual hallucinations

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58
Q

Which signs are common in unilateral occipital lobe lesion involving deep white matter or splenium of corpus callosum?

A

Alexia

Color-naming defect

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59
Q

Signs of bilateral occipital lobe lesions

A 
Cortical blindness (pupils reactive)
Anton syndrome
Achromatopsia - loss of perception of colour
Prosopagnosia
Simultanagnosia
Balint syndrome
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60
Q

What is Anton syndrome?

A

Denial of cortical blindness

Visual anosognosia

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61
Q

What signs are more common in parieto-occipital lesions?

A

Simultanagnosia

Balint syndrome

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62
Q

What sign is more common in temporo-occipital lesion?

A

Prosopagnosia

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63
Q

What is the most widely used intelligence test in clinical practice?

A

Wechsler Adult Intelligence Scale

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64
Q

Age range for Wechsler Adult Intelligence scale?

A

16-89 y/o

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65
Q

What age is Wechsler Preschool and Primary scale used for?

A

4-6.5 years of age

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66
Q

What is the Wechsler Adult intelligence scale composed of?

A

11 subtests:
6 verbal
5 performance
Lead to verbal, performance and combined IQ

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67
Q

What are the verbal tests in the Wechsler Adult intelligence scale?

A 
Similarities
Arithmetic
Digit span
Vocabulary
Information
Comprehension
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68
Q

What are the performance tests Wechsler Adult intelligence scale?

A 
Picture arrangement
Block design
Picture completion
Digit symbol
Matrix reasoning
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69
Q

What are hold tests in Wechsler Adult intelligence scale?

A

Resistant to age-related decline. May be sensitive for organic brain damage.

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70
Q

What are the hold tests in Wechsler Adult intelligence scale?

A

Vocabulary
Information
Picture completion
Object assembly/matrix test

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71
Q

What are the non-hold tests in Wechsler Adult intelligence scale?

A

Block design
Digit span
Similarities
Digit symbol

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72
Q

How are the scores from hold and non-hold tests derived in Wechsler Adult intelligence scale?

A

Using a deterioration quotient

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73
Q

What is the Raven’s progressive matrix?

A

IQ test that is independent of education of cultural influences.

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74
Q

What tasks are used in Raven’s progressive matrix?

A

Visuospatial problem-solving (Performance IQ)

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75
Q

What ability is resistant to organic brain damage?

A

Reading

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76
Q

What is used to estimate premorbid IQ?

A

National adult reading test

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77
Q

What does the National adult reading test.. test?

A

Previous word knowledge prior to becoming ill

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78
Q

What is the stroop test?

A

Measures set shifting abilities and response inhibition

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79
Q

What does the stroop test.. test?

A

Frontal function

Ability to pay selective attention

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80
Q

What does the Wisconsin Card Sorting Test.. test?

A

Abnormal in people with frontal lobe damage/caudate and some schizophrenics

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81
Q

Method of Wisconsin Card Sorting test

A

Stimulus of cards of different colour, form and number.

Present to patients to sort into groups according to principle e.g. sort by colour, ignore form and number.

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82
Q

Which four tests.. test set-shifting ability and thereby executive functioning?

A

Trail Making Test
Wisconsin Card Sort Test
Hayling Test (sentence completion)
Bixton task

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83
Q

What is the most widely used memory test battery for adults?

A

Wechsler Memory Scale-Revised

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84
Q

What does the Wechsler Memory Scale-Revised test for?

A

Yields a memory quotient which is corrected for age and approximates the WAIS IQ.
In amnesic conditions, a disproportionately low MQ but preserved IQ is seen.

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85
Q

What does the Wechsler Memory Scale-Revised consist of?

A 
Verbal paired associate
Paragraph retention
Visual memory for designs
Orientation
Digit span
Rote recall of alphabet
Counting backwards
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86
Q

What is the Benton Visual Retention Test?

A

Short term visual memory test

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87
Q

What does the Benton Visual Retention Test consist of?

A

Presentation of geometric figure for 1- seconds, after which patient attempts to draw figure from memory.

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88
Q

What does the Bender Visual Motor Gestalt Test.. test?

A

Visuomotor coordination - both adults and children

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89
Q

What did Halstead and Reitan create?

A

Battery of tests to determine location of specific brain lesions.

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90
Q

Name the tests created by Halstead and Reitan.

A 
Category Test
Tactual performance test
Rhythm test
Finger-oscillation test
Speech-sounds perception test
Trail making test A and B
Critical flicker frequency
Time sense test
Aphasia screening test
Sensory-perceptual test
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91
Q

What are the components of consciousness?

A

Arousal - wakefulness

Awareness - attentional processing

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92
Q

What does arousal depend on?

A

ARAS - Ascending Reticular activatinv system

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93
Q

What does the ARAS do?

A

Via thalamic intralaminar nuclei, synchronises rhythmical bursts of neuronal activity (20-40Hz) from the thalamocortical connections.
arousal is proportional to these.

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94
Q

What is required for maintenance of attention?

A

Intact right frontal lobe

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95
Q

What can lesions in ARAS lead to?

A

Small lesions of ARAS = stuporous state

Large bilateral lesions at cortical level = depression in altertness

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96
Q

What is the pathology in most patients in stupor?

A

Diffuse organic cerebral dysfunction

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97
Q

Describe stupor in a patient

A

Appear to be asleep but when vigorously stimulated, will manifest alertness by ocular movement.

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98
Q

What happens if you do caloric testing in organic stupor?

A

Reveal tonic deviation

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99
Q

What happens if you do caloric testing in psychiatric stupor?

A

Ocular nystagmus

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100
Q

What damage leads to akinetic mutism?

A

Diencephalic or bilateral anterior cingulate damage.

Lesion that interferes with reticular/cortical integration but spares corticospinal pathways.

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101
Q

Signs of akinetic mutism?

A

Immobility
Eye closure
Little or no vocalisation
Absence of spastcity and rigidity

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102
Q

What pathology results in vegetative state?

A

Isolated actions of ARAS and thalamus in absence of higher cortical influence due to extensive cortical damage.

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103
Q

Signs of vegetative state

A

Spasticity and rigidity of limbs.

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104
Q

Pathology of Locked in syndrome

A

Total paralysis below level of third nerve nuclei.
Due to infarction of ventral pons, pontine tumours, pontine haemorrhage, central pontine myelinolysis, HI or brain stem encephalitis.

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105
Q

Signs of locked in syndrome

A

Patients open eyes and elevate and depress eyes on command, but horizontal eye movements lost.
No other voluntary movement possible.

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106
Q

Clinical tests for attention

A

Serial 7s
Digit span
Spelling ‘world’ backwards
Recite months of year/days of week in reverse order.

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107
Q

Why is reverse-order mont of year measure of sustained attention?

A

Highly over-learned sequence

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108
Q

What does digit span depend upon?

A

Working memory

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109
Q

What conditions is digit span impaired in?

A

Delirium
Focal left frontal damage
Aphasia
Moderate to severe dementia

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110
Q

What is normal digit span?

A

7+/-2
Varies with age and general intelligence.
5 is normal in elderly.

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111
Q

What is considered normal time orientation?

A

Being inaccurate by 2 days or less

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112
Q

What is included in person orientation?

A

Name
Age
DOB

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113
Q

When is disorientation to ones own name seen?

A

Psychogenic amnesia

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114
Q

What is orientation to place affected?

A

Reduplicative paramnesia, seen in delirium

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115
Q

What does executive function include?

A 
Planning
initiation
Sequencing
Coordinating
Error detection/correction
Set shifting
Termination
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116
Q

What does executive function depend upon?

A

Dorsolateral frontal lobe

Intact frontal-subcortical circuits

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117
Q

What is impulsivity a result of?

A

Response inhibition - seen in inferior frontal pathology.

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118
Q

How can impulsivity be tested?

A

Go-No-Go task.

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119
Q

Describe the Go-No-Go task.

A

Examiner instructs patient to tap once in response to single tap and withhold a response for two taps.

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120
Q

When asking a patient to copy a short sequence of alternating squares and triangles, what are you testing?

A

Ability to switch task

Inhibition of appropriate or persevative responses

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121
Q

What does the cognitive estimates test.. test?

A

Will result in bizarre/improbable responses in patients with frontal or executive dysfunction.

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122
Q

What does questioning the similarity between two conceptually similar objects assess?

A

INferential reasoning

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123
Q

How does information go from the visual cortex towards the temporal or parietal cortex?

A

Dorsal (‘where’) stream

Ventral (‘what’) stream

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124
Q

What does the dorsal stream link?

A

Visual information with spatial position and orientation in parietal lobe

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125
Q

What does the ventral stream link?

A

Visual information to store of semantic knowledge in temporal lobes

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126
Q

What are disorders of visuospatial function?

A

Neglect

Constructional apraxia

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127
Q

What results in neglect?

A

Lesions in right hemisphere - usually inferior parietal or prefrontal

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128
Q

What results in left sided personal/extrapersonal neglect?

A

Damage to right parietal lobe

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129
Q

Which parietal lobe damage rarely results in neglect?

A

Left-sided

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130
Q

Which visuospatial side gets bilateral parietal lobe representation?

A

Right

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131
Q

How can neglect be discovered?

A

Simultaneous bilateral sensory or visual stimulation
Having patient bisect lines of variable lengths
Letter and star cancellation tasks

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132
Q

What is anosognosia?

A

Extreme form of neglect - patient will deny they are hemiplegic or that the affected limb belongs to them

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133
Q

What are apraxias?

A

Deficits in dressing and constructional ability

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134
Q

What do copying 3D shapes/clock test?

A

Constructional ability - will also highlight neglect

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135
Q

How to test dressing apraxia?

A

Ask patient to put on clothing that has been turned inside out

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136
Q

Classification of memory according to duration?

A

Immediate - seconds
Recent - minutes/days
Remote - months/years

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137
Q

Classification of memory according to encoding?

A

Explicit - semantic/episodic

Implicit

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138
Q

What is implicit memory?

A

Includes skills and procedures

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139
Q

What is semantic memory?

A

Memory for word meanings and general knowledge.

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140
Q

What is episodic memory?

A

Events

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141
Q

What does episodic memory depend on?

A

Hippocampal-diencephalic system

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142
Q

What is episodic memory important for?

A

Personal memories

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143
Q

What type of memories are anterograde and retrograde memories?

A

Episodic

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144
Q

What is working memory?

A

Limited capacity that allows us to retain information for a few seconds.

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145
Q

What is the working memory made up of?

A

Central executive system and 2 buffer systems.

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146
Q

What is the central executive system of working memory made up of?

A

Attention system

Dorsolateral prefrontal

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147
Q

What are the 2 buffer systems in working memory?

A

Visuospatial sketchpad

Phonological loop

148
Q

What does the visuospatial sketchpad depend on?

A

Right hemisphere

149
Q

What does the phonological loop depend on?

A

Left hemisphere

150
Q

What is left hippocampus important for in memory?

A

Encoding declarative verbal memories

151
Q

What is right hippocampus important for in memory?

A

Encoding non-verbal memories

152
Q

Where is navigational memory?

A

Hippocampus

153
Q

What is the hippocampal place code?

A

Pattern of cellular activation in hippocampus that corresponds to animals location in space

154
Q

Does unilateral hippocampal lesion affect memory?

A

Rarely - hippocampus is able to compensate

155
Q

Relevance of amygdala in memory?

A

Rates emotional importance of experience and regulates level of hippocampal activity accordingly.
Emotional memory and emotional face processing.
Helps in memory consolidatino depending on emotional input.

156
Q

What does amygdalar damage result in?

A

Loss of fear conditions in monkeys and loss of maternal behaviour

157
Q

What structures are associated with new learning?

A

Diencephalic structures such as dorsal medial nucleus of thalamus and mamillary bodies

158
Q

Give e.g. of diencephalic amnesia (when diencephalic structures are damaged)

A

Korsakoff syndrome

159
Q

Which type of memory stays in tact in most types of memory loss?

A

Procedural

160
Q

E.g. of disease in which procedural memory is lost but declarative memory is intact

A

Parkinsons

161
Q

What structures are thought to be involved in non-declarative procedural memory storage?

A

Cerebellum
Striatum
Amygdala
Motor area of neocortex

162
Q

What is the key area for semantic memory?

A

Anterior temporal lobe

163
Q

What is long-term potentiation?

A

Strengthening connection between two neurons on repeated communication

164
Q

What is the neuronal basis of memory?

A

Long-term potentiation

165
Q

What mediates long-term potentiation?

A

NMDA mediated calcium entry in glutamate neurons

166
Q

What does learning result in, on a microscopic level?

A

Increases branching and synapse formation

Influences neurogenesis

167
Q

Define anterograde amnesia

A

Forgetting newly encountered information from time of lesion

168
Q

Define retrograde amnesia

A

Loss of memory of past events that happened before lesion was sustained

169
Q

How does anterograde amnesia present

A

Forgetting appointments, losing items at home, inability remember conversations leading to repeated questions.

170
Q

How does retrograde amnesia present?

A

Forgetting past events such as jobs, holidays, unable to remember a route and getting lost

171
Q

E.g. of damage resulting in pure anterograde amnesia

A

Hippocampal damage:
herpes simplex encephalitis
Focal temporal lobe tumours or infarction

172
Q

Characteristics of transient global amnesia

A

Pronounced anterograde and variable retrograde amnesia

173
Q

Characteristics of memory lacunes

A

Repeated brief episodes of memory loss

174
Q

What is Ribots law of retrograde amnesia?

A

Dissolution of memory is inversely related to recency of event.
i.e. recent memories are more likely to be lost than more remote in organic amnesia

175
Q

What is semantic dementia?

A

Variant of frontotemporal dementia

176
Q

How does semantic dementia present?

A

Patients complain of loss of words.
Vocabulary diminishes and patients use words such as ‘thing’ instead.
Parallel impairment in appreciating meaning of individual words.

177
Q

What pathology is semantic dementia associated with?

A

Atrophy of anterior temporal lobe, usually left

178
Q

How can working memory deficits present?

A

Lapses in concentration and attention e.g. losing ones train of thought, inability to process complex task as copmonents not retained long enough to be processed.

179
Q

Pathology in which structures leads to working memory deficits?

A

Basal ganglia

White matter diseas

180
Q

Characteristics of dissociative amnesia

A

Memory of important recent events that is partial, patchy and selective.
Episodic memory loss - retrograde only

181
Q

What is the problem in dissociative amnesia?

A

Complete unavailability of memories which were formed normally and previously accessible.
Forgotten events are generally traumatic or stressful.

182
Q

Define aphasia

A

Higher-level language defect despite intact hearing, sound production and articulation mechanisms.

183
Q

What is anomia?

A

Naming defects

184
Q

Where is sound from the ears transmitted to?

A

Wernicke’s area

Auditory association cortex that processes language component

185
Q

What is Broca’s area?

A

Higher motor area of language production

186
Q

Where do signals from Broca’s area go on to?

A

To motor area to coordinate delivery of language via tongue, lips and vocal cords

187
Q

What are the three components of language?

A

Fluency
Comprehension
Repitition

188
Q

What does fluency of language depend upon?

A

Intact Broca’s area and its forward connections

189
Q

What does language comprehension depend upon?

A

Intact Wernicke’s area and its connection with association cortex and sensory input

190
Q

Which component of language requires no higher-level processing?

A

Repitition

191
Q

When can repetition occur?

A

When Broca’s, Wernicke’s and arcuate fasciculus are intact.

192
Q

What is lost in Wernicke’s sensory aphasia?

A

Repetition
Comprehension - reading and writing
Naming

193
Q

What is left intact in Wernicke’s sensory aphasia?

A

Fluency

194
Q

What is lost in Broca’s motor aphasia?

A

Fluency
Repetition
Naming

195
Q

What is left intact in Broca’s motor aphasia?

A

Comprehension

196
Q

What is lost in Conduction aphasia?

A

Repetition

Naming

197
Q

What is left intact in Conduction aphasia?

A

Fluency

Comprehension

198
Q

What is left intact in Transcortical sensory aphasia?

A

Fluency

Repetition

199
Q

What is lost in Transcortical sensory aphasia?

A

Comprehension

200
Q

What is kept intact in Transcortical motor aphasia?

A

Repetition

Comprehension

201
Q

What is lost in transcortical motor aphasia?

A

Fluency

Naming

202
Q

How does Broca’s aphasia present?

A

Speech is nonfluent; appears laboured with many interruptions and pauses.
Function words are most affected.
Abnormal word order and agrammatism.
Speech is telegraphic.

203
Q

E.g. of Broca’s ahasia

A

I see…. the dotor, dotor sent me…. Bosson.

204
Q

How does Wernicke’s aphasia present?

A

language output is fluent but highly paraphasic, sometimes with string of neologisms and circumlocutions - jargon aphasia.
Speech contains large number of function words but few nouns/verbs.
Output is voluminous but uninformative, like schizophrenic speech disturbance.

205
Q

What is pure word deafness?

A

Patient can speak, read and write fluently but comprehension is impaired only for spoken language.

206
Q

What damage leads to pure word deafness?

A

Bilateral (or left sided with disrupted connections to non-dominant circuit) damage to superior temporal pole

207
Q

What is pure word blindness?

A

Alexia, no agraphia

patient can speak and comprehend normally, and write spontaneously, but reading comprehension is impaired.

208
Q

Damage leading to pure word blindness.

A

Left posterior cerebral artery affecting splenium of corpus callosum and left visual cortex

209
Q

What is pure word dumbness?

A

Spoken language cannot be produced clearly but patient can comprehend language, read and write.

210
Q

What is pure agraphia?

A

Isolated inability to write while everything else is preserved.

211
Q

Define apraxia

A

Varying combination of the following disturbances in order of progressive dysfunction:
Failure to produce correct movement in response to verbal command
Failure to correctly imitate movement performed by examiner
Failure to perform movement correctly in response to seen object
Failure to handle object correctly

212
Q

Damage related to apraxia?

A

Left parietal and frontal lobes

213
Q

What is isolated limb apraxia diagnostic of?

A

Corticobasal degeneration

214
Q

Functional classification of apraxia

A

Constructional apraxia
Ideational/conceptual
Ideomotor (most common)

215
Q

Define constructional apraxia

A

Inability to construct elements into meaningful whole

216
Q

E.g. of constructional apraxia

A

Unable to draw or copy simple diagrams or figures

217
Q

Localization of constructional apraxia?

A

Right cerebral hemisphere, often parietal lobe

218
Q

Define ideational/conceptual apraxia

A

Impairment in carrying out a sequence of actions requiring use of various objects in correct order.

219
Q

Localization of ideational/conceptual apraxia

A

Left parieto-occipital and parietotemporal regions

220
Q

Definition of ideomotor apraxia

A

Disorder of goal-directed movement.

Patient knows what to do but not how to do it.

221
Q

E.g. of ideomotor apraxia

A

Patient uses own fingers to represent toothbrush when asked to brush teeth.
Improves on imitation and use of actual tool.
Tool more effective than gestures.

222
Q

Localization of ideomotor apraxia

A

Mainly left hemisphere; frontal and parietal association areas.

223
Q

What results in bilateral ideomotor apraxia?

A

Unilateral lesions of left hemisphere in right-handed patients, usually less severe in left limb.

224
Q

Regional classifications of apraxia

A

Buccofacial

Limb-kinetic

225
Q

Define buccofacial apraxia

A

Inability to coordinate and carry out facial and lip movements such as whistling, winking, coughing on command.

226
Q

Localization of buccofacial apraxia.

A

left inferior frontal lobe and insula

Commonly accompanies aphasia caused by lesion of Broca’s area.

227
Q

Define limb-kinetic apraxia?

A

Loss of hand and finger dexterity resulting in inability to connect or isolate individual movements.

228
Q

What does limb-kinetic apraxia result in?

A

Affects use of tools, gestures, particularly finger movements.

229
Q

Localization of limb-kinetic apraxia?

A

Dominant frontoparietal or primary motor cortex.

230
Q

What is visual agnosia?

A

Failure of object recognition despite adequate perception

231
Q

What happens in appreceptive visual agnosia?

A

Patients have normal vision but cannot identify and name objects
they can name objects by description or touch.

232
Q

Pathology leading to appreceptive visual agnosia?

A

Bilateral occipitotemporal infarction

233
Q

What happens in associative visual agnosia?

A

Stored semantic knowledge is affected.

234
Q

Pathology leading to associate visual agnosia?

A

Lesions of anterior left temporal lobe

235
Q

How to test for visual agnosia?

A

Assess visual object naming/description and tactile naming, naming described objects and providing semantic information about unnamed items.

236
Q

What is prosopagnosia?

A

Ability to recognise familiar faces.

237
Q

Pathology leading to prosopagnosia?

A

Face processing is a bilateral function, more key areas on right.
Associated with bilateral or right-sided lesions of occipital-temporal junction (fusiform gyrus).

238
Q

What is the fusiform gyrus?

A

Occipital-temporal junction

239
Q

What is achromatopsia?

A

Loss of ability to discriminate colours

240
Q

Pathology resulting in achromatopsia?

A

Medial occipitotemporal damage due to left posterior cerebral artery infarct

241
Q

What is colour agnosia?

A

Loss of ability to retrieve colour information stored in semantic knowledge base e.g. what colour is a banana?

242
Q

Damage leading to colour agnosia?

A

Left occipito-temporal damage

243
Q

What is colour anomia?

A

Disorder of colour naming despite intact perception and colour knowledge.

244
Q

Damage leading to colour anomia?

A

Disconnection of language structures in temporal lobe from visual cortex.

245
Q

What is acalculia?

A

Inability to read, write and comprehend numbers.

246
Q

What are the symptoms of Balint syndrome?

A

Simltanagnosia
Optic Ataxia
Oculomotor apraxia

247
Q

What results in Balints syndrome?

A

Bilateral superior-parietoocipital damage (disruption to dorsal ‘where’ strand linking visual and parietal association areas).

248
Q

Possible causes of Balints syndrome?

A

CO poisoning
Infarct
Alzheimers

249
Q

What is simultanagnosia?

A

Inability to attend to more than one item at a time

250
Q

What is optic ataxia?

A

Inability to guide reaching or pointing despite adequate vision

251
Q

What is oculomotor apraxia?

A

Inability to voluntarily direct saccades to a visual target

252
Q

Lesion resulting in Gerstmann syndrome

A

Lesinos in dominant angular and supramarginal gyri (parietal lobe)

253
Q

Symptoms of Antons syndrome

A

Denies any deficit

254
Q

Damage in Antons syndrome

A

Bilateral occipital damage

255
Q

Damage in Marchiafava-Bignami disease?

A

Symmetrical demyelination and necrosis of corpus callosum and adjacent anterior commissure.

256
Q

Signs in Marchiafava-Bignami disease?

A

Sudden onset stupor/coma/seizures.

Chronic onset of dementia and/or gait problems

257
Q

Stereotypical patient who gets Marchiafava-Bignami disease?

A

Alcoholics drinking red wine

258
Q

What is the only sensory nerve to have no thalamic relay?

A

Olfactory

259
Q

What does unilateral anosmia suggest?

A

Lesion affecting olfactory nerve filaments, bulb, tract or stria

260
Q

Describe cortical representation for smell

A

Bilateral in piriform cortex

261
Q

Given the fact that cortical representation of smell is bilateral, what type of lesion would not cause any olfactory impairment?

A

Unilateral lesion distal to decussation of olfactory fibres (temporal/uncinate)

262
Q

What can cause unilateral anosmia?

A

Frontal meningiomas

263
Q

E.g. of diseases causing hyposmia

A

Early feature in Parkinsons and Alzheimers

264
Q

Where is the lesion in unilateral blindness?

A

Anterior to optic chiasm (optic nerve or retina)

265
Q

Where is the lesion in bitemporal hemianopia?

A

Optic chiasm

266
Q

E.g. of diseases causing bitemporal hemianopia?

A

Pineal tumours

Cranipharyngioma

267
Q

Lesion causing left-sided homonymous hemianopia?

A

Lesion of right optic tract, lateral geniculate body, optic radiations and striate cortex

268
Q

Lesion causing right-sided homonymous hemianopia

A

Lesions of left retro-chiasmatic structures

269
Q

Pathology causing enlargement of blind spot?

A

Any process causing disc swelling

270
Q

Lesion causing superior quadrantanopia?

A

Optic irradiation lesion at temporal lobe of contralateral side

271
Q

Lesion causing inferior quadrantanopia?

A

Optic irradiation lesion at parietal lobe of contralateral side

272
Q

What causes cortical blindness?

A

Occipital cortex lesion

Bilateral posterior cerebral artery occlusion

273
Q

What diseases does funnel vision occur in?

A

Glaucoma
Retinitis pigmentosa
Post-papilloedema optic atrophy
Bilateral occipital infarcts with macular sparing

274
Q

What is tunnel vision?

A

Absence of disparity between 2mm and 1mm fields on confrontation test.

275
Q

Symptoms of cortical blindness

A

Bilateral homonymous hemianopia with small central field around point of fixation (macular sparing) or
complete blindness

276
Q

How can one test the optic nerve?

A

Fundoscopy
Colour vision - Ishihara chart
Visual fields - confrontation test or perimetry
Acuity - Snellen chest

277
Q

Where do afferent fibres in optic nerve go to?

A

Lateral geniculate bodies and relay to Edinger-Westphal nuclei via pretectal nucleus

278
Q

Where is the Edinger-Westphal nucleis?

A

Midbrain

279
Q

Where do efferent (parasympathetic) fibres go from Edinger-Westphal nucleus?

A

Via third nerve to ciliary ganglion and then to pupil.

280
Q

Which nerve carries efferent fibres from the Edinger-Westphal nucleus?

A

3rd cranial nerve

281
Q

What happens when one fixates on an object?

A

Convergence

Pupillary constriction

282
Q

Which fibres carry convergence information?

A

Afferent fibres from optic nerve relay to convergence centre.

283
Q

What does the convergence centre do?

A

Receives muscle spindle afferent fibres from extraocular muscles (mainly medial recti) which are innervated by the 3rd CN.

284
Q

What is the efferent route from the convergence centre?

A

To Edinger-Westphal nucleus, ciliary ganglion and then to the pupils.

285
Q

What is light-near dissociation?

A

Pupils that accommodate but do not reacte.

286
Q

Causes of light-near dissociation?

A

Argyll Robertson pupil
Diabetes
Aldie pupil

287
Q

When is Argyll Robertson pupil seen?

A

Neurosyphillis

288
Q

What happens in Aldie pupil?

A

Peripheral pupillary defect producing tonic pupil.

289
Q

What happens in absent light reflex?

A

Due to afferent defect in pupillary reflex pathway - possibly pretectal.

290
Q

Where is the oculomotor nerve nucleus located?

A

Midbrain

291
Q

What does CN III supply?

A

Levator palpebrae superioris
Superior, inferior and medial recti
Inferior oblique muscles

292
Q

Signs of lesion of CN III?

A

Paralysis of ipsilateral upper eyelid and pupil
Patent cannot adduct, look up or down.
Pupil looks out (exotropia)

293
Q

What does lesion of nucleus of third nerve result in?

A

Bilateral ptosis

Ipsilateral paralysis of upper eyelid and pupil.

294
Q

What pathology results in diplopia in more than one direction?

A

Paralysis CN III

295
Q

What diseases result in pupil-sparing CN III paralysis?

A

Diabetes
Vasculitis
Brainstem lesions such as MS

296
Q

Where is the trochlear nerve nucleus located?

A

Midbrain

297
Q

What does the trochlear nerve innervate?

A

Superior oblique muscle

298
Q

Which nerve allows a person to visualise the tip of their nose?

A

Trochler

299
Q

Path of trigeminal nerve?

A

From midbrain through pons (main sensory nucleus and motor nucleus) to cervical region (spinal tract of trigeminal nerve)

300
Q

Function of trigeminal nerve

A

Sensory innervation of face

Muscles of mastrication

301
Q

What supplies the corneal reflex?

A

Afferent - V nerve

Efferent - facial nerve

302
Q

What does complete paralysis of CN V result in?

A

Sensory loss of ipsilateral face and weakness of mastication muscles.
Attempted opening of mouth results in deviation of jaw to paralyzed side.

303
Q

What can lead to loss of corneal reflex?

A

Acoustic neuroma pressing on 5th nerve

304
Q

Where is the CN VI nerve located?

A

Paramedian pontine region on floor of 4th ventricle

305
Q

What does abducens nerve innervate?

A

Lateral rectus

306
Q

Signs in CN VI palsy?

A

Double vision on horizontal gaze only - horizontal homonymous diplopia

307
Q

Why is paralysis of CN VI a false localizing sign?

A

It may result from increased intra cranial pressure

308
Q

Motor function of CN VII?

A

Motor supply to facial muscles from motor nucleus

309
Q

Sensory function of CN VII?

A

Innervates skin of posteromedial aspect of pinna and around external auditory canal.
Taste senation of anterior 2/3 of tongue and relays to sensory nucleus tractus solitarius

310
Q

Secrotomotor function of CN VII?

A

Parasympathetic relay to lacrimal, lingual and submandibular glands

311
Q

Signs of lower motor neuron lesion of CN VII?

A

Complete ipsilateral facial paralysis
Facial draws to opposite side as patient smiles
Eye closure impaired
Ipsilateral palpebral fissue is wider

312
Q

What causes LMN lesion of CN VII?

A

Bells palsy

313
Q

Sign of UMN CN VII lesion?

A

Lower half of face is paralyzed

Eye closure is preserved

314
Q

What is used to test CN VIII?

A

512 Hz tuning fork

315
Q

How does CN VIII communicate balance?

A

Vestibular portion transmits information about linear and angular accelerations of the head from urticle, saccule and semicircular canals of membranous labyrinth to vestibular nucleus.

316
Q

Result of Rombergs test if loss of CN VII

A

Patient will fall towards side of vestibular hypofunction

317
Q

Diseases where Rombergs is positive

A

CN VIII dysfunction
Disease of dorsal column
Polyneuropathies

318
Q

What is caloric testing?

A

Water testing

319
Q

Normal caloric testing results

A

Cold water; nystagmus to opposite side.

Warm water; nystagmus towards same side.

320
Q

Why is nucleus of CN IX and CN X called nucleus ambiguous?

A

Both are anatomically indistinuighable

321
Q

Sensory function of CN IX?

A

Sensory innervation of posterior third of tongue and pharynx.

322
Q

Motor funciton of CN IX?

A

Pharyngeal muscules - stylopharyngeus (with CN X)

323
Q

Which CN is important for BP control?

A

IX

324
Q

How is CN IX involved in BP control?

A

Vascular stretch afferents from aortic arch and carotid sinus travel via CN IX to nucleus solitarius

325
Q

Signs of CN IX palsy

A

Loss of taste in posterior 1/3 of tongue

Loss of pain and touch sensation in 1/3 of posterior tongue, soft palate and pharyngeal walls

326
Q

Where does CN X start?

A

Nucleus ambiguous

327
Q

Which CN has the longest peripheral course?

A

CN X

328
Q

Where does CN x stretch up to?

A

Splenic flexure of colon

329
Q

Function of CN X

A

Motor supply to pharyngeal muscles, palatoglossus and larynex
Smooth muscle of tracheobronchial tree, oesophagus, Gi tract up to middle-distral 1/3 of transverse colon

330
Q

Which pharyngeal muscle does CN X not supply?

A

Stylopharyngeus

331
Q

Where is the somatic sensation carried by CN X?

A

Back of ear
External auditory canal
Parts of tympanic membrane, pharynx, larynx and dura of posterior foss

332
Q

What innervates pharyngeal gag reflex and palatal reflex?

A

CN IX and X

333
Q

What is the palatal reflex?

A

Elevation of soft palate and ipsilateral deviation of uvula on stimulation of soft palate

334
Q

Sign of CN IX and X paralysis?

A

Pharyngeal gag reflex and palatal reflex will result in deviation of uvula to normal side (away from lesion)

335
Q

Functino of CN XII

A

Motor innervation of all extrinsic and intrinsic muscles of tongue

336
Q

Sign of CN XII palsy?

A

Tongue deviates to side of paralysis on protrusion

337
Q

What is concussion?

A

Transient coma for hours followed by apparent complete clinical covery.

338
Q

What is contusion?

A

Prolonged coma, focal signs and lasting brain damage.

339
Q

Where does contusino occur?

A

Beneath (coup injury) or contralateral (contracoup injury) to site of impact.

340
Q

Where is contre-coup contusion most common?

A

Orbito-frontal area and temporal tips where acceleration/deceleration forces cause brain to impact on bony protuberances of skull.

341
Q

What type of HI occurs in bilateral orbitofrontal injury?

A

Behavioural dyscontrol syndrome

342
Q

Mechanisms of traumatic brain injury

A

Axonal and neuronal damage from direct trauma
Shearing and rotational stresses on declerating brain
Brain oedema and raised ICP
Brain hypoxia and ischaemia

343
Q

What causes diffuse axonal injury?

A

Differential motion of brain within skull resulting in shearing and stretching of axons

344
Q

Difference between diffuse axonal injury and focal brain injury?

A

Diffuse axonal injury is more widespread with extensive lesions in white matter tracts.

345
Q

What is diffuse axonal injury more often associated with (signs)?

A

Persistent vegetative state

Coma

346
Q

Types of amnesia post head injury?

A

Post-traumatic amnesia

Retrograde amnesia

347
Q

What is post-traumatic amnesia?

A

Anterograde amnesia for period of injury and period following injury until normal memory resumes

348
Q

What is retrograde amnesia after HI?

A

Dense amnesia for period between last clearly recalled memory prior to injury and injury itself.

349
Q

Normal post-traumatic amnesia time?

A

Minutes

350
Q

What is used to assess HI severity?

A

GCS 24 hours after injury.
Length of coma
Post-traumatic amnesia

351
Q

What is used to predict functional outcome after HI?

A

LOC

PTA

352
Q

Poor prognostic factors with respect to psychiatric morbidity following HI?

A 
Long duration of LOC
Long PTA
Elderly
Chronic alcohol use
Diffuse brain damage
New onset seizures
Focal damage to dominant lobe
353
Q

Classification of mild HI

A

PTA <60 minutes

354
Q

Functional outcome of mild HI?

A

May return to work in <1 month

355
Q

Classification of moderate HI?

A

PTA between 1-24 hours

356
Q

Functional outcome of moderate HI?

A

Return to work in 2 months

357
Q

Classification of severe HI?

A

PTA between 1-7 days

358
Q

Functional outcome of severe HI?

A

Return to work in 4 months

359
Q

Classification of very severe HI?

A

Pta >7 days

360
Q

Functional outcome of very severe hI?

A

May require >1 year to return to work

361
Q

When is cognitive imppairment most likely after HI?

A

After closed HI with PTA lasting >24 hours

362
Q

When is personality change most likely after HI?

A

HI to orbitofrontal lobe or anterior temporal lobe

363
Q

What is post-concussional syndrome characterised by?

A

Headache
Dizziness
Insomnia
Irritability/emotional lability/anxiety/depression
Increased sensitivity to noise, light etc
Fatigue/poor concentration

364
Q

When is schizophrenia-like psychoses (paranoia) likely after HI?

A

Right temporal and orbitofrontal injury

365
Q

Prevalence of schizophrenia post HI?

A

2-5%

366
Q

% in which post-traumatic epilepsy is seen?

A

5% closed HI
30% open HI (usually during first year)
Worsens progress

367
Q

Where does working memory occur?

A

Frontal & parietal lobes

MRCPsych Part A - Al-Rashid Hospital (22 decks)

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