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MRCPsych Part A big > Clinical Examination > Flashcards

Clinical Examination Flashcards

1
Q

Concepts to approach threatening topics

A

Normalizing questions
Symptom expectation and reduction of guilt
Symptom exaggeration
Familiar language when asking about behaviours

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2
Q

Purpose of normalizing questions?

A

Decrease patients embarrassment about feeling or behaviour

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3
Q

Purpose of symptom expectation?

A

Defuse admission of embarrassing behaviour

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4
Q

Purpose of symptom exaggeration?

A

Determine actual frequency of sensitive or shameful behaviour

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5
Q

Techniques to change topics?

A

Smooth transitions
Referred transitions
Introduced transitions

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6
Q

When to use smooth transitions?

A

To hint at something the patient just said

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7
Q

When to use referred transitions?

A

Hint at something mentioned earlier

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8
Q

When to use introduced transitions?

A

To pull a new topic from thin air

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9
Q

What are directive techniques?

A

Focused on seeking a particular answer or driven by motives of doctor.

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10
Q

Give e.g. of limit setting

A

I am going to interrupt you as there are a few things to cover.

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11
Q

Name some directive techniques

A 
Limit setting
Closed questions
Question rephrasing
Redirection
Transition
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12
Q

Describe confrontation

A

Point out to a patient something which the doctor thinks the patient is missing or denying

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13
Q

Give e.g. of suggestive question

A

These voices are not from your head. Am I right?

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14
Q

What is functional analysis?

A

Attempts to explain and predict functions of a phenomenon by examining any relationships to the outcome.

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15
Q

What medical intervention can confirm a panic disorder?

A

Lactate provocation
Hyperventilation
CO2 inhalation

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16
Q

What inhibits panic attacks triggered by sodium lactate?

A

Benzos

TCAs

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17
Q

In which psychiatric diagnosis is infusion of amobarital (narcoanalysis) helpful?

A 
Catatonia
Stupor
Muteness
Repression
Dissociation
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18
Q

What happens to organic conditions when infused of amobarbital?

A

They worsen

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19
Q

Why do non-organic conditions get better with infusion of amo-barbital?

A

Due to disinhibition, decreased anxiety or increased relaxation

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20
Q

What can be substituted for amo-barbital?

A

Benzos

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21
Q

Investigations for suspected encephalitis syndrome

A

NMDA receptor and voltage-gated K+ channel receptor auto-antibodies (IgG0

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22
Q

Investigations for porphyria

A

Spot urine sample for porphobilinogen during acute attack and 24 hour urine for porphyrins, porphobilinogen and delta-aminolevulinic acid

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23
Q

Investigations for Wilsons Disease

A

Serum ceruloplasmin

24 hour copper excretion test

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24
Q

Investigations for lysosomal storage disease

A

Skin biopsy
Genetic tests
Detection of serum alpha-galactosidase enzyme

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25
Q

Investigations for Homocystinuria?

A

Homocysteine in urine and blood

Molecular genetic testing

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26
Q

Investigations for metachromatic leukodystrophy

A

Arylsulfate A enzyme activity in WCCs or in cultured skin fibroblasts

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27
Q

Investigations in malnourishment

A 
Serum homocystine and folate
Vitamin B12
Niacin
Trytophan
Nicotinamide adenine
Dinucleotide (NAD) and NADP
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28
Q

Difference between AIP and porphyria?

A

AIP does not present with rash

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29
Q

Onset of porphyria

A

18-40 years of age

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30
Q

What triggers AIP?

A

Oestrogens
Barbituates
Benzos
Diclofenac

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31
Q

Treatment for AIP

A

Haemin - reduces haem synthesis

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32
Q

important receptors involved in autoimmune encephalitis

A 
Voltage gated K+ channel complex - LGI1, CASPR2, contactin-2
NMDA
AMPA receptor
GABA-B
Glycine receptor
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33
Q

How do anti-NMDA receptor antibodies work?

A

Titre-dependent destruction of synaptic NMDAR through crosslinking and internalisation

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34
Q

Gender variability in anti NMDAR encephalitis?

A

80% are female

50% of women with it have underlying ovarian teratoma

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35
Q

How does psychosis with anti NMDAR first present usually?

A

Fever, headache, malaise

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36
Q

EEG in anti-NMDAR encephalitis?

A

Disorganized delta/theta activity

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37
Q

What to look for in MRI in anti-NMDAR encephalitis?

A

Medial temporal hyperintensity in hippocampi, frontobasal and insular regions in basal ganglia

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38
Q

How to confirm anti-NMDAR encephalitis?

A

CSF: lymphocytic pleocytosis, elevated protein and oligloclonal bands in 60%, anti-NMDAR antibodies.

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39
Q

Treatment of anti-NMDAR encephalitis

A

3 days of methylprednisolone PO/IV followed by PO prednisolone in association with 5 days of plasma exchange

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40
Q

Why must you not give antipsychotics in anti-NMDAR encephalitis?

A

Dystonic reactions and NMS-like syndrome can occur

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41
Q

What type of thyroid problem can cause cognitive impairment?

A

Low T4

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42
Q

When would EEG be required to diagnose dementia?

A

Rapid onset; may suggest CJD.

Need EEG and MRI

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43
Q

TFTs in patients with anorexia

A

Low T3
Low normal range T4
Normal TSH
(low T3 syndrome)

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44
Q

GI effects of anorexia

A

Delayed gastric emptying
Decreased colonic motility - secondary to chronic laxative misuse
Acute gastric dilatation - rare, secondary to binge eating

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45
Q

Haematological signs of anorexia

A

Moderate normocytic anaemia
Mild leucopenia with relative lymphocytosis
Thrombocytopenia

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46
Q

Electrolyte result of laxative misuse

A

Metabolic acidosis
Hyponatraemia
Hypokalaemia

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47
Q

Brain abnormalities resulting in anorexia

A

Enlarged cerebral ventricles and external CSF spaces (pseudo atrophy)

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48
Q

BMI for obesity

A

30 or greater

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49
Q

Most specific and sensitive test for detecting heavy alcohol use over 10 days

A

Carbohydrate deficiency test

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50
Q

What is Marchiafava syndrome?

A

Corpus callosum damage often due to alcohol misuse

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51
Q

Normal QTc for men

A

440ms

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52
Q

Normal QTc for women

A

470ms

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53
Q

Which recreational drugs increase risk of QTc prolongation?

A

Stimulants

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54
Q

Method of testing drug use aside from urine

A

Specific gravity in urine

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55
Q

How long is alcohol present in urine?

A

Up to 12 hours

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56
Q

How long is amphetamine present in urine?

A

Up to 48 hours

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57
Q

How long is benzo present in urine?

A

3 days depending on half life

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58
Q

How long does cannabis last in urine if occasional use?

A

Up to 3 days

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59
Q

How long does cannabis last in urine if high daily use?

A

Up to 4 weeks

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60
Q

How long does cocaine last in urine?

A

6-8 hours

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61
Q

How long does cocaine metabolite last in urine?

A

2-4 days

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62
Q

How long does codeine stay in urine?

A

48 hours

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63
Q

How long does heroin last in urine?

A

1-3 days

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64
Q

How long does methadone stay in urine?

A

3 days or more

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65
Q

How long does morphine last in urine?

A

2-3 days

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66
Q

How long does PCP stay in urine?

A

8 days

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67
Q

Which recreational drugs are associated with renal disease?

A

Cocaine

Heroin

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68
Q

Common renal dysfunction in black patients with drug misuse

A

Segmental glomerulosclerosis

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69
Q

Common renal dysfunction in white patients

A

Membranoproliferative glomerulonephritis

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70
Q

Plasma and urine osmolality in diabetes insipidues

A

Plasma: High (>295)
Urine: low

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71
Q

Plasma and urine osmolalities in psychogenic polydipsia?

A

Plasma: Low (<280)
Urine: Low

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72
Q

Plasma and urine osmolalities in SIADH

A

Plasma: low
Urine: high

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73
Q

At what Na level do symptoms of hyponatraemia occur?

A

Na <125

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74
Q

At what Na level can seizures and irreversible brain damage occur?

A

Below 110-115

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75
Q

Most common cause of Argyll-Robertson pupil

A

Diabetes

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76
Q

What is checker-board abdomen?

A

Multiple surgical scars in factitious disease

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77
Q

In which drug misuse is piloerection seen?

A

Opiate withdrawl

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78
Q

How can one rate Minor Physical anomalies?

A

Lane Scale

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79
Q

In what type of patients are Minor Physical Anomalies noted?

A

Developmental disorders

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80
Q

Which tuning fork is used to test auditory function?

A

512Hz

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81
Q

Which tuning fork is used to test peripheral neuropathy?

A

128 Hc

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82
Q

What type of diseases result in a positive Romberg test?

A

Polyneuropathies

Disease of dorsal column

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83
Q

Normal caloric testing result

A

On cold water testing, nystagmus noted to opposite side.

On warm water, nystagmus to same side

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84
Q

What are hard neurological signs?

A

Imapirments of basic motor and sensory functions that are localisable to pyramidal, extrapyramidal or cranial nerve systems.

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85
Q

what are neurological soft signs?

A

Non-localisable neurological findings thought to reflect neurodevelopmental aberrations when seen in psychiatric disorders.

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86
Q

Three groups of soft signs

A

Abnormalities of motor coordination, sensory integration and signs of cortical disinhibition

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87
Q

Signs of midline cerebellar dysfunction

A

Ataxic gait
Difficulty in maintaining upright posture
Truncal ataxia

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88
Q

What is the neocerebeullum?

A

Lateral cerebellar hemispheres

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89
Q

What does neocerebeullum control?

A

Movement of ipsilateral limb

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90
Q

What is the midline vermis involved in?

A

Control of truncal tone, speech and eye movements

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91
Q

What is the archicerebeullum?

A

Flocculonodular lobe

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92
Q

What does flocculonodular lobe do?

A

Vestibular functions

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93
Q

What part of the cerebellum controls vestibular functions?

A

Archicerebellum/flocculonodular lobe

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94
Q

How to test for ataxia

A

Tandem gait

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95
Q

Which type of tremor accelerates in pace on approaching the target

A

Intention tremor

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96
Q

What is dyssynergia?

A

Incoordination

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97
Q

What is dysmetria?

A

Past pointing

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98
Q

What is dysrhythmia?

A

Inability to tap and keep to a rhythm

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99
Q

What is dysarthria a sign of?

A

Diffuse involvement of cerebellum

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100
Q

What is the Brudzinski sign?

A

Flexion of hips and knees when you try to flex the neck

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101
Q

What is Kernigs sign?

A

Flexing one hip and knee and then extending knee with hip still flexed. If opposite knee flexes, this test is positive

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102
Q

What is another name of the straight-leg raising test?

A

Lasegue

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103
Q

Describe the straight leg raising sign

A

Passively flexing hip with knees straight while patient is in supine position.
Limitation of flexion due to hamstring spasm or pain indicates local irritation of lower lumbar nerve roots

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104
Q

Describe reverse straight leg raise sign

A

Passively hyperextending hip with knees straight while prone; limitation of extension due to spasm or pain in anterior thigh muscle indicates local irritation of upper lumbar nerve roots

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105
Q

Functions of cortical sensory system

A 
Kinaesthetic sensation
Stereognosis
Graphesthesia
Tactile localization
Tactile 2 point discrimination on both sides of body
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106
Q

Which type of fibrillations are visible?

A

TOngue

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107
Q

Describe myoclonus

A

Brief <0.25 second muscle jerk, generalized.

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108
Q

What is myoclonus associated with

A

Generalized epilepsy
CJD
Severe Alzheimers

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109
Q

What is athetosis

A

Slow writhing spasms along long axis of limbs or body itself.

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110
Q

What is chorea

A

Quasi-purposeful movements affecting multiple joints with distal preponderance.

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111
Q

What lesion is chorea associated with?

A

Caudate

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112
Q

What is hemiballismus?

A

Violent flinging of half of body

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113
Q

What area of the brain is hemiballismus associated with?

A

Lesion of subthalamic nucleus

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114
Q

Give examples of primary reflexes

A 
Glabellar tap
Rooting
Snout
Sucking
Palmomental
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115
Q

What are primary reflexes?

A

Absent in adults

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116
Q

What does primary reflex in adult suggest?

A

Possible frontal lobe damage

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117
Q

What are superficial reflexes?

A

Responses that indicate integrity of cutaneous innervation and corresponding motor outflow

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118
Q

What are the superficial reflexes?

A

Corneal and conjunctival
Abdominal
Cremasteric
Plantar

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119
Q

What controls corneal and conjunctival reflexes?

A

Afferent: 5th nerve
Efferent: 7th nerve

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120
Q

What is the abdominal reflex/

A

Drawing line away from umbilicus in diagonals of 4 abdominal quadrants. Normal reflex draws umbilicus towards direction of line.

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121
Q

Describe cremasteric reflex

A

Scratching medial surface of thigh to elicit scrotal contraction or lift.
Normal: elevation of ipsilateral testis.

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122
Q

What does lack of both positive and negative Babinski sign suggest?

A

Absence of cutaneous innervation in S1 or loss of motor innervation in L5

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123
Q

What is required for a deep tendon reflex?

A

Intact cutaneous innervation
Motor supply
Cortical input to corresponding spinal segment

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124
Q

Spinal roots of biceps reflex

A

C5, C6

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125
Q

Spinal roots of brachoradialis reflex

A

C6

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126
Q

Spinal roots of triceps reflex

A

C7

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127
Q

Spinal roots of patellar reflex

A

L2-L4

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128
Q

Spinal roots of Achilles reflex

A

S4

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129
Q

What type of lesion is a pseudobulbar palsy?

A

UMN lesion

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130
Q

What type of lesion is exaggerated jaw jerk?

A

UMN lesion

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131
Q

What type of lesion is bulbar palsy?

A

LMN

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132
Q

Which disease is frontal baldness associated with?

A

Myotonic dystrophy

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133
Q

Neurocutaneous signs of Tuberous Sclerosis

A

Dermatomal eruptions
Ash leaf macules
Ungual fibromas
Café au lait spots

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134
Q

Neurocutaneous signs of Neurofibroma

A

café au lait spots

Axillary freckling

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135
Q

Describe spastic dysarthria

A

Strained, hoarse voice
Hypernasality
Slow, imprecise articulation

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136
Q

Cause of spastic dysarthria

A

Bilateral UMN lesions

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137
Q

Cause of flaccid dysarthria

A

LMN

XII nerve involved if tongue is small due to loss of tone

138
Q

Cause of ataxic dysarthria

A

Cerebellar

139
Q

What is ataxic dysarthria?

A

Excess loudness, tremor and irregular articulatory breakdowns (scanning speech)

140
Q

What is hypokinetic dysarthria

A

Breathy monotone voice with reduced loudness and articulation leads it to be accelerated and imprecise

141
Q

Damage leading to hypokinetic dysarthria?

A

Motor control circuit

142
Q

Which type of speech is associated with basal ganglia damage?

A

Hyperkinetic dysarthria

143
Q

Describe hyperkinetic dysarthria

A

Strained hoarseness and voice arrests

144
Q

Describe mixed dysarthria

A

Similar to spastic, accompanied by wet sounding voice with rapid tremor, poor laryngeal and tongue movements and poor control of lips

145
Q

What results in mixed dysarthria?

A

Damage to more than one motor control system

146
Q

What happens in hysterical aphonia?

A

Sudden loss of voice but preserved vocal cord activity

Normal examination

147
Q

What type of dysarthria results from bilateral UMN lesions

148
Q

What type of dysarthria results from LMN lesion?

149
Q

What type of dysarthria results from motor control circuit?

A

Hypokinetic

150
Q

What type of dysarthria results from multiple motor system damage?

151
Q

What disorder leads to hemiparetic gait?

A

Stroke affecting pyramidal system

152
Q

How does hemiparetic gait present?

A

Clenched hand with extended knee and plantarflexed ankle.

Makes paralyzed leg appear longed than other. Results in circumduction of affected leg when walking.

153
Q

What results in patient veering to one side with ataxic gait?

A

Unilateral cerebellar lesion - patient veers to side of lesion

154
Q

What causes steppage gait

A

Chronic peripheral neuropathies e.g. drop foot and dorsal column disorders

155
Q

What compensation occurs in proximal myopathy resulting in waddling gait

A

Forward curvature of lumbar spine adds to body swing.

156
Q

What diseases result in waddling gait?

A

Proximal myopathy
Congenital hip dislocation
Near term pregnant women

157
Q

What disease causes scissoring gait?

A

Spastic paraplegia

158
Q

How does scissoring gait present?

A

Marked rigidity and excessive adduction of swinging leg together with plantar flexion of ankle and flexion at knee due to contractures of all spastic muscles leads to forced tip-toe walking with knees rubbing together and crossing like scissors.

159
Q

What condition caused gait apraxia/magnetic gait?

A

Hydrocephalus

160
Q

Conditions causing high stepping gait due to foot drop?

A

Neuropathic
Polio
Peripheral lesions in MS

161
Q

What type of gait occurs in Huntingtons?

A

Lurching, chaotic gait

162
Q

What conditions lead to pigeon gait?

A

Torsional abnormalities seen in hip dysplasia

163
Q

What gait occurs with Carbon monoxide poisoning?

A

Propulsive

164
Q

What conditions cause stiff, scissoring gait?

A

UMN lesions
Cerebral lesions
Cortical lesions in MS
Stroke

165
Q

What conditions cause stomping gait?

A

Friedreich’s ataxia
Pernicious anaemia
Tabes Dorsalis (Syphilis)

166
Q

What causes Trendelenburg gait?

A

Weakness of abductor muscles of lower limb, mainly gluteus medius

167
Q

Conditions causing absent ankle jerks and upgoing plantars?

A

Subacute combined degernation cord
Syphilitic taboparesis
Friedrich’s ataxia
MND

168
Q

Underlying pathology causing absent ankle jerks and upgoing plantars

A

Absence of absence jerk as spinal reflex pathway is affected (afferent) while UMN type damage still produces Babinski

169
Q

What is anisocoria?

A

Pupil asymmetry

170
Q

Which type of nervous system deficit leads to tonic pupil?

A

Parasympathetic dysfunction

171
Q

What is Argyll-Robertson pupil?

A

Irregular and small

Doesn’t react to light but does accommate

172
Q

Damage leading to anosognosia

A

Right frontoparietal lesions resulting in left hemiplegia that patient denies

173
Q

What is Beevor sign?

A

Upward deviation of umbilicus when patient tries to raise head and sit up from supine position

174
Q

When is Beevor sign seen?

A

Bilateral lower abominal paralysis

175
Q

Signs of lateral corticospinal damage

A

Ipsilateral spastic paralysis below level of lesionn
Babinski sign ipsilateral to lesion
UMN type hyper-reflexia

176
Q

Signs of posterior column damage

A

Ipsilateral loss of tactile discrimination, vibratory and position sensation below level of lesion

177
Q

Signs of lateral spinothalamic damage

A

Contralateral loss of pain and temperature sensation, usually 2-3 segments below level of lesion

178
Q

Describe Chvoestek sign

A

Tapping cheek at angle of jaw precipitates tetanic facial contractions

179
Q

What does Chvoestek sign occur?

A

Hypocalcaemia

180
Q

Describe Doll’s eye maneuver?

A

Turning head passively with patient awake and fixated or patient in coma.

181
Q

Result of Doll’s eye maneuver in awake patient?

A

Eyes remain fixated at original focus when all gaze pathways normal

182
Q

Result of Doll’s eye maneuver in coma?

A

Eyes deviate in opposite direction with brainstem intact

183
Q

What type of disease is Friedreich’s ataxia?

A

Trinucleotide repeat

184
Q

Signs in Friedreich’s ataxia?

A 
Pes cavus
Kyphoscoliosis
Cerebellar signs
Impaired joint position/vibration
Cardiomyopathy
Optic atrophy
185
Q

What is seen in Holmes Adie syndrome?

A

Benign tonic pupil

Absent patellar and achilles reflexes

186
Q

Signs in Horner’s syndrome

A 
Ptosis
Anhidrosis
Miosis
Enophtholmos
Loss of cilospinal reflex
187
Q

Describe Marcus Gunn pupil

A

Abnormal pupil dilates as light swings back from normal side.

188
Q

Pathology underlying Marcus Gunn pupil

A

Afferent (optic nerve) pupillary defect

189
Q

Describe mononeuritis multiplex

A

Painful asymmetric asynchronous sensory and motor peripheral neuropathy with isolated damage to at least 2 separate nerve areas

190
Q

Causes of mononeuritis multiplex

A 
Diabetes
Vasculitis
Amyloidosis
Direct tumour involvement
Autoimmune disorders
Paraneoplastic
191
Q

What is milkmaid’s grip

A

Inability to maintain sustained grip

192
Q

What pathology does Milkmaids grip occur in

193
Q

What is Myerson sign?

A

Continuing to blink with repeated glabellar taps

194
Q

In which diseases does Myerson sign occur

A

Parkinsons, particularly those with bilateral frontal lobe dysfunction

195
Q

Triad of optic neuritis

A 
Loss of vision
Eye pain
Dyschromatopsia
(70% unilateral)
Spontaneous recovery
196
Q

Describe Uhthoff symptom

A

Exercise/heat-induced vision loss - MS

197
Q

Cause of subacute combined degeneratio

A

Vitamin B12 deficiency

198
Q

Signs of subacute combined degeneration

A

Peripheral neuropathy

Posterior column signs with pyramidal signs below wait

199
Q

Which types of patients show trombone tongue?

A

Patients with chorea

200
Q

What is trombone tongue?

A

Unsteadiness of tongue when patient tries to protrude it outside mouth

201
Q

Signs of UMN lesion

A

Rigidity
Hypertonia
Exaggerated reflexes
Mild atrophy

202
Q

Signs of LMN lesion

A

Atonia/hypotonia
Loss of deep tendon reflexes
Atrophic, wasted
Fasciculations

203
Q

Cause of bulbar palsy

A

LMN weakness of CN 9-12

204
Q

Cause of pseudobulbar palsy

A

Bilateral supranuclear (UM) lesions of lower CN

205
Q

Signs of Bulbar palsy

A

Wasted, fasciculating tongue
Nasal speech
Loss of jaw jerk and gag reflex

206
Q

Diseases in Bulbar palsy

A 
MND
Polio
Botutilism
Myasthenia Gravis
Muscular dystrophies
207
Q

Signs of pseudobulbar palsy

A

Stiff tongue - wasting only in later stages
Donald-duck speech
Exaggerated jaw jerk, preserved gag reflex
Emotional lability

208
Q

Diseases in pseudobulbar palsy

A

MND
MS
Multiinfarch dementa
Severe HI

209
Q

In which type of lesion is there Donald Duck speech?

210
Q

In which type of lesion is there loss of jaw jerk and gag reflex?

211
Q

Who created the MMSE?

A

Folstein, 1976

212
Q

How many points in MMSE

213
Q

Cut off for dementia in MMSE

A

23/24

21/22 if less than 9 years formal education

214
Q

What is MMSE insensitive to

A

Early decline

215
Q

What does MMSE not pick up

A

Frontal executive defects

216
Q

Items in MMSE

A 
Orientation (10)
Registration (3) and recall (3)
Attention (5)
Multistep command (3)
Naming (2)
Repetition language (1)
Reading comprehension (1)
Writing (1)
Visual construction (1)
217
Q

What does clock drawing test require

A

Verbal understanding
Short-term memory
Spatially coded knowledge
Constructive skills and planning - executive function

218
Q

Which subjects perform poorly in clock drawing test?

A

Low education
Advanced age
Depression

219
Q

What can normal clock drawing ability reasonably exclude?

A

Cognitive impairment

220
Q

Who created the Clock drawing test?

221
Q

What is the clock drawing test scored out of?

222
Q

Normal score for clock drawing test

223
Q

How many digits is deemed to be correct in clock drawing test

A

Placing of any three digits in a quadrant

224
Q

What does Addenbrookes test

A 
Orientation
Attention
Memory
Verbal fluency
Language
Visuospatial ability
225
Q

What test helps to differentiate subtypes of dementia?

A

Addenbrookes

226
Q

Cut off for dementia in Addenbrookes

227
Q

Major area of scoring in Addenbrookes

228
Q

What determines CT image contrast?

A

Degree to which tissues absorb x-rays

229
Q

Which structures are likely to be obscured in CT?

A

Those close to bone e.g. brainstem

230
Q

Plane of rotation of CT?

A

One - axial

231
Q

How can one visualise tumours and inflammation in CT?

A

Infusion of iodine-containing contrast agents; once in vascular compartments, iodinated compounds absorb more irradiation than brain tissue

232
Q

What area of the brain does CT have poor visualization capacity for

A

Posterior fossa

233
Q

What are MRI magnets rated in

A

Tesla units of magnetic field strength

234
Q

What happens when atoms are placed in a magnetic field

A

Axes of all odd-numbered nuclei (i.e. H1) align with magnetic field
This axis deviates away from magnetic field when exposed to pulse of radiofrequency electromagnetic radiation oriented at 90 or 180 degrees to magnetic field.
When pulse terminates, axis of spinning nucleus realigns itself with magnetic field and emits its own radiofrequency signal.
This is collected by MRI scanners

235
Q

Planes of MRI

A

Axial
Coronal
Sagittal

236
Q

What affects the realignment of H1 axis?

A

Immediate environment and degree of water content

237
Q

Difference between hydrogen in fat and wat

A

Fat: realign rapidly
Water: realign slowly

238
Q

Describe pulses in T1 images

239
Q

What is emphasised in T1 images?

A

Hydrophobic environments - i.e. fat is bright, CSF is dark

240
Q

In which type of MRI is CSF dark?

241
Q

Which type of MRi scan closely resembles CT?

242
Q

Which MRI scan allows contrast enhancement with contrast agent gadolinium-DTPA?

A

T1 - these appear white

243
Q

Pulses in T2

A

Four times as long as T1

244
Q

What images are emphasised in T2?

A

Signal from hydrophilic areas - brain tissue is dark, CSF is whtie

245
Q

What is revealed in T2 images?

A

Brain tissue with abnormally high water content - tumours, inflammation, strokes

246
Q

What is protein density sequence in MRI helpful for?

A

Periventricular structures

247
Q

What is fluid attenuated inversion recovery (FLAIR) in MRI?

A

When T1 image is inverted and added to T2 image to double contrast between gray and white matter

248
Q

What is FLAIR in MRI images helpful for?

A

Detecting sclerosis of huppocampus caused by temporal lobe epilepsy
Localizing areas of abnormal metabolism in degenerative neurological disorders

249
Q

When are MRI scans contra-indicated?

A

PPM

Implants of ferromagnetic metals

250
Q

Radiation in MRI?

251
Q

Which scan has good sensitivity to early ischaemia?

252
Q

How does infarct appear in T2 image?

253
Q

How does infarct appear in T1 image?

254
Q

How does infarct appear in CT?

255
Q

How does haemorrhage apear in T2?

256
Q

How does haemorrhage appear in T1?

257
Q

How do tumours appear in T2?

258
Q

How do tumours appear in T1?

259
Q

How do tumours appear in CT?

260
Q

How does bone appear in T2?

261
Q

How does bone appear in T1?

262
Q

How does air appear in T2?

263
Q

How does air appear in T1?

264
Q

How does fat appear in T2?

265
Q

How does fat appear in T1?

266
Q

How does fat appear in CT?

267
Q

How does white matter appear in T1?

268
Q

What can MR spectroscopy detect?

A

Several biologically important nuclei with odd number of protons and neutrons

269
Q

What is H1 proton spectroscopy useful for?

A

To quantify N-acetyl aspartate, creatinine and choline-containing molecules

270
Q

What cannot be detected with MRS

271
Q

What can phosphorus-31 MRS determine

A

pH of brain regions and concentrations of phosphorus-containing compounds i.e. metabolic activity of brain

272
Q

Other indications of MRS

A

Measure concentration of psychotherapeutic drugs such as lithium, fluoxetine and trifluoperazine which contain fluorine-19

273
Q

What is blood oxygen level dependent technique?

A

Neuronal activity = local increase in o2 consumption, so local conc of deoxyhaemoglobin increases relative to oxyhaemoglobin.
Oxyhaemoglobin is diamagnetic (weak magnetic contrast)
Deoxyhaemoglobin is paramegnetic, producing MR signal detected in T2.

274
Q

What is fMRI based on?

A

Blood oxygen level dependent technique

275
Q

What is fMRI a measure of?

A

Proxy measure of tissue activity that depends on relative changes in perfusion

276
Q

Advantage of fMRI over PET and SPECT

A

No radioactive isotopes used

277
Q

Structures studied in resting fMRI

A

Brain regions with high levels of activity during rest: precuneus, lateral parietal regions and medial prefrontal cortex

278
Q

What are brain networks that show higher baseline activity at rest in fMRI called?

A

Default mode network

279
Q

What does SPECT stand for?

A

Single Photon Emission Computed Tomography

280
Q

How does SPECT work?

A

Uses radioactive compounds to study regional differences in cerebral blood flow in brain.
This records patterns of photon emission from bloodstream which varies according to level of perfusion

281
Q

What does SPECT use?

A

Compounds labeled with single photon-emitting isotopes

282
Q

Name the three isotopes used in SPECT

A

Iodine-123
Technetium-99m
Xenon-133

283
Q

What type of SPECT is referred to as the cerebral blood flow technique?

A

Xenon-SPECT

284
Q

How does Xenon-133 work in SPECT?

A

Enters blood quickly and is distributed to areas of the brain as a function of regional blood flow

285
Q

Limitation of Xenon-SPECT

A

Can only measure blood flow on surface of brain

286
Q

What do you need to use to assess blood flow in the whole brain?

A

Injectable tracers such as HMPAO

287
Q

How does HMPAO work in SPECT?

A

Attaches to highly lipophilic molecules that cross Blood brain barrier to enter brain cells. Once inside, ligands are enzymatically converted to charged ions, which remain trapped in cell.
Over time, tracers concentrate in areas of high blood flow.

288
Q

Which compound is used to study receptors in SPECT?

A

Iodine-123-labeled ligands

289
Q

What can Iodine-123 ligands be used to study in SPECT?

A

Muscarinic
Dopaminergic
Serotonergic
(occupancy and distribution)

290
Q

What compound is used to study D1/D2 receptors in SPECT?

A

Iodobenzamide

291
Q

What compound is used to study GABA-A receptors in SPECT?

292
Q

What compound is used to study dopamine and serotonin transporters in SPECT?

A

Nor-beta-CIT

293
Q

What compound is used to study D2/D3 receptors?

A

Epidepride

294
Q

What can PET study?

A

Blood flow
Receptor distribution
Metabolic activity

295
Q

Difference between SPECT and PET

A

SPECT; single particle is emitted

PET: two particles are emitted, thus more precise location for event and better resolution of image

296
Q

What happens to isotopes used in PET?

A

Decay by emitting positrons with resolution closer to its theoretical minimum of 3mm

297
Q

Limitation of PET

A

Require on-site cyclotron

298
Q

Most commonly used isotopes in PET

A

Fluorine-18
Nitrogen-13
Oxygen-15

299
Q

Which isotope used in PET is not linked to another molecule?

300
Q

Advantage of fluorine-18 used in PET?

A

Gives direct information about neuronal metabolism

301
Q

PET ligand used in blood flow

302
Q

PET ligand used for glucose metabolism

A

F18 deoxyglucose

303
Q

PET ligand used for D2 receptors

A

11C raclopride

304
Q

PET ligand used for ropamine neuron density

A

18F dopa

18F metatyrosine

305
Q

PET ligand used for GABA-A receptors

A

11C Flumazenil

306
Q

PET ligand used for 5HT2 receptors

A

18F altanserin

Setoperone

307
Q

PET ligand used in striatal D2 and cortical 5HT2

A

11C methylspiperone

308
Q

What PET ligand is used for seretonin synthesis rate

A

11C methyltryptophan

309
Q

PET ligand used for muscarinic receptors

A

11C scopolamine

310
Q

What does DTI stand for

A

Diffusion tensor imaging

311
Q

How does DT1 work

A

Combines principle of nuclear magnetic resonance and molecular diffusion

312
Q

What is diffusion in DT1?

A

Random translational motion of molecules - Brownian notion - that results from energy carried by these molecules

313
Q

How does DT1 work

A

During random Brownian motion, molecules probe tissue structure at a microscopic scale beyond usual image resolution; direction of movement determines integrity and trace of white matter tracts

314
Q

Gradients allowed via DT1

315
Q

In which scan can Fractional Anisotrophy be calculated?

316
Q

What is Fractional Anisotrophy?

A

Index of integrity of white matter

317
Q

What is tractography?

A

Using principal direction of diffusion tensor to infer white-matter connectivity of brain

318
Q

Neuro-imaging findings in depression re metabolism

A

Decreased metabolism in prefrontal cortex, anterior cingulate and amygdala

319
Q

Brain volumes seen in depression

A

Decreased frontal and basal ganglia volumes

320
Q

Hyperintensities seen in neuroimagingin depression

A

Periventricular and deep white matter

Subcortical - thalamic and striatal

321
Q

Neuroimaging findings in treatment response for depression

A

Higher prefrontal metabolism (anterior cingulate) predict better treatment response

322
Q

Neuroimaging findings in patients with depression with higher dysfunctional negative thoughts

A

Higher 5HT2A receptor density

323
Q

Neuroimaging findings in women with depression

A

Increased MAO-A activity

324
Q

Neuroimaging findings in psychomotor retardation in depression

A

Elevated D2 binding in untreated depression

325
Q

Neuro-imaging findings in patients on therapeutic dose of SSRIs

A

80% of 5HT transporters occupied

326
Q

Neuro-imaging findings in schizophrenia

A

Ventricular enlargement

Loss of grey matter - insular cortex, anterior cingulate (medical prefrontal cortex) and medial temporal lobe

327
Q

Neuro-imaging findings in first few years of diagnosis?

A

Progressive loss of brain volume

328
Q

Neuro-imaging findingin schizophrenia linked with executive tasks

A

fMRI revealrs poor DLPFC activation

329
Q

MRS findings in schizophrenia

A

Decreased n-acetyl aspartate in PFC (neuronal loss)

330
Q

Findings in DT1 in schizophrenia

A

Widespread reduction

Fractional anisotrophy: frontal and corpus callosum - more in chronic treated patients

331
Q

Neuro-imaging findings in Alzheimers

A

Ventricular enlargement
Loss of temporal lobe volume - hippocampus
Decreased parieto-temporal fMRI activation and SPECT blood flow

332
Q

Neuro-imaging findings in OCD

A

Reduced and increases volumes of caudate nuclei noted (both)

Higher caudate blood flow - increased metabolism

333
Q

What neuro-imaging findings decrease with effective treatment of OCD?

A

Higher caudate blood flow reduces with treatment

334
Q

Neuro-imaging findings in childhood-onset schizophrenia

A

Ventricular enlargement at baseline and slower growth rates (right hemispheric) white matter also noted

335
Q

A non-invasive perfusion MRI methodology used to quantify cerebral blood flow is?

A

Arterial spin labelling

336
Q

What is used in MRS to measure cellular metabolism?

337
Q

What is used in MRS to quantify N-acetylaspartate, choline, glutamatate, lactate and creatinine?

338
Q

What is used in MRS to study labelled drugs and deoxyglucose?

339
Q

What is Gedankenlautwerden?

A

Thought echo

340
Q

What is moria?

A

Tendency to be inappropriately euphoric

341
Q

Who came up with the idea of autochthonous delusions?

MRCPsych Part A big (22 decks)

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