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MRCP > MRCP Neuro > Flashcards

MRCP Neuro Flashcards

1
Q

What MRI brain changes are usually seen in herpes simplex encephalitis T1?

A

MRI brain normally shows changes in the temporal lobes. Swelling, mass effect and high signal in mesial temporal structures.

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2
Q

What test can you do for herpes simplex virus encephalitis? What are the CSF findings?

A

PCR for herpes simplex virus on cerebral spinal fluid (CSF) is a highly specific test. Other CSF findings are lymphocytosis and mildly raised red cells.

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3
Q

What virus commonly causes encephalitis?

A

Herpes simplex (HS) type 1 (70% in immunocompetent patients).

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4
Q

What does damage to the ulnar nerve result in?

A

Damage at the wrist results in wasting of the intrinsic hand muscles (other than the lateral two lumbricals) and the hypothenar eminence. This produces the classic claw hand

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5
Q

What is the sensory supply of the ulnar nerve?

A

Supplies sensation to the medial one and a half fingers

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6
Q

What muscles does the median nerve innervate?

A

The lateral two lumbricals and the thenar eminence (oppenens pollicis, abductor pollicis and flexor policis brevis). It supplies sensation to the lateral three and a half fingers

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7
Q

What does motor damage to the median nerve result in?

A

Damage to the motor branch, the anterior interosseous nerve results in inability to form and pinch grip, tip to tip, instead holding the paper between the pulp of the thumb and index finger

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8
Q

What is Lambert-Eaton myasthenic syndrome?

A

It is a pre-synaptic disorder of auto-antibody IgG directed against the pre-synaptic calcium channel leading to impaired acetylcholine release. Clinically, patients present with muscle weakness that improves with exercise.

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9
Q

Which kind of lung cancer is more commonly associated with paraneoplastic syndromes? Why?

A

Small cell lung cancers.
Due to its neuroendocrine cell origin.

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10
Q

Why do Paraneoplastic syndromes occur?

A

Result from antibody generation from or against malignant cells attacking normal tissue. Examples include antineuronal antibodies directed against the Purkinje cells of the cerebellum leading to cerebellar syndrom
Check Anti-Purkinje cell antibody levels

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11
Q

What is the mechanism of action of tetrabenazine?

A

VMAT-inhibitor (vesicular monoamine transporter 2), involved in transportation of monoamines

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12
Q

Indication for Tetrabenazine

A

Huntington’s chorea to reduce hyperkinetic movements

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13
Q

Which structure is implicated in chorea?

A

Caudate nucleus pathology is associated with chorea (for example, in Huntington’s disease).

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14
Q

Which structure is implicated in AD?

A

Hippocampus pathology is associated with short term memory impairment (for example, Alzheimer’s disease).

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15
Q

How does Guillain-Barre present?

A

Gradual development of ascending weakness with autonomic involvement

e.g.

Two week history of difficulty walking and weakness in her arms.

On examination, there was proximal and distal limb weakness which was more marked in the legs than the arms. All tendon reflexes were absent and the plantar responses were flexor. There was no sensory loss.

Blood pressure in the supine position was 140/78 mmHg (lying) and was 110/70 mmHg on standing.

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16
Q

How does Brown-Séquard’s syndrome present?

A

clinical presentation is that of ipsilateral weakness and a loss of position and vibration below the lesion with contralateral loss of pain and temperature

27M with three months of difficulty walking.

Examination reveals motor weakness of left leg in a pyramidal distribution with increase in tone. There is impaired pinprick sensation of right leg extending into the groin.

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17
Q

Clinical features of lateral medullary syndrome

A

Ipsilateral signs of Horner’s syndrome
Pharyngeal weakness and ataxia and
Contralateral signs of spinothalamic sensory loss of the limbs.

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18
Q

CSF features of bacterial meningitis?

A

high protein
low glucose, and
neutrophil pleocytosis.

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19
Q

How would you differentiate between mechanical and neurogenic dysphagia?

A

Mechanical dysphagia (for example, oesophageal and gastric carcinoma, oesophageal stricture, etc) causes dysphagia that is worse with solids than liquids

Nasal regurgitation, coughing and choking episodes during meals, dysphagia that is worse with liquids than solids and dysarthria indicate neurogenic dysphagia.

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20
Q

What could cause neurogenic dysphagia?

A

In 60+ think of myasthenia gravis and motor neuron disease.

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21
Q

Levetiracetam MoA?

A

Binds to the synaptic vesicle protein SV2A in the brain
Modulates neurotransmitter release

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22
Q

What is the inheritance pattern of Maple syrup urine disease?

A

autosomal recessive inheritance pattern

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23
Q

Name X-linked dominant conditions

A

Alport’s syndrome (in around 85% of cases - 10-15% of cases are inherited in an autosomal recessive fashion with rare autosomal dominant variants existing)

Rett syndrome

Vitamin D resistant rickets

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24
Q

What are the features of polyarteritis nodosa?

A

Mononeuritis multiplex
Fever
HTN
Nephritic renal involvement

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25
Q

Which viral infection is PAN associated with?

A

hepatitis B
Hepatitis B surface antigen is postivie in 30%, and p-ANCA is usually positive. Angiography demonstrates microaneurysms in affected organs, and biopsy shows necrotising inflammation.

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26
Q

Neurological manifestations of Whipple’s disease?

A

Chronic progressive impairment of higher mental function in association with:
Seizures
Myoclonus ataxia and
Oculomasticatory myorhythmia- found uniquely in Whipple’s.

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27
Q

What is is the underlying pathology in dementia with Lewy bodies?

A

Insoluble alpha-synuclein accumulation

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28
Q

What are the underlying pathological changes in Alzheimer’s disease?

A

Tau tangle and beta amyloid plaque formation

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29
Q

Why is Haloperidol contraindicated in Lewy Body dementia

A

risk of severe neuroleptic reactions -fatal

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30
Q

How does Diffuse Lewy body disease present?

A

cognitive Impairment, visual hallucinations, and parkinsonism.

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31
Q

Clinical features of progressive supranuclear palsy (PSP)

A

triad of parkinsonism, vertical gaze palsy and cognitive impairment

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32
Q

What comprises a TACI infarct?

A

higher cortical dysfunction which includes visuospatial disturbance (in this case visuospatial neglect), dysphasia, and/or a decreased level of consciousness
contralateral homonymous hemianopia, and
motor and sensory deficits in two or more of the contralateral face/arm/leg.

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33
Q

What conditions are associated with Absent ankle jerks? / extensor plantars

A

Subacute combined degeneration of the cord
Motor neuron disease
Friedreich’s ataxia
Syringomyelia
Taboparesis (syphilis)
Conus medullaris lesion

Neuropathy (B12 deficiency, systemic lupus erythematosus [SLE], cerebrotendinous xanthomatosis)

Dorsal root disease (tabes dorsalis).

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34
Q

What is Cerebrotendinous xanthomatosis?

A

inherited condition, associated with accumulation of cholesterol in tissues including brain, peripheral nerve and tendons which produces a clinical picture of:

Early onset dementia
Gait ataxia
Loss of vibration sense
Cataracts
Large tendon xanthomata.

cholestanol is a derivative of cholesterol. In cerebrotendinous xanthomatosis there is a deficiency in sterol storage, and diagnosis is based on high serum (and tendon) cholesTANOL. Serum cholesterol may be normal or low.

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35
Q

Three syndromes of MSA? -multi system atrophy

A

Strionigral degeneration leading to parkinsonism
Autonomic failure
Olivopontocerebellar degeneration.

36
Q

Differentiate between subarachnoid haemorrhage rather than bacterial meningitis?

A

A family history of polycystic kidney disease- berry aneurysm -SAH

37
Q

What would be the result of a spinal lesion at the level of C8?

A

Weakness of finger flexion

38
Q

Anterior spinal artery occlusion symptoms?

A

sudden onset weakness of his legs associated with urinary retention

lesion is involving the anterior two thirds of the spinal cord which spares light touch, vibration and position sense, but causes loss of pain and temperature sensation distally

39
Q

Raised protein in CSF?

A

Guillain-Barre syndrome
tuberculous, fungal and bacterial meningitis
Froin’s syndrome*
viral encephalitis

40
Q

What is Wallerian degeneration

A

Degeneration of the portion of the nerve distal to the injury. It occurs following axonal injury in both the peripheral and central nervous systems and usually begins within 24-36 hours of injury.

41
Q

Rett syndrome

A

girl rubbing hands
MECP2 gene on the X chromosome.

42
Q

Organophosphate level poisoning symptoms?

A

Salivation
Bradycardia
Bronchospasm and urination, diarrhoea and miosis.

43
Q

What is the classic triad of symptoms of carotid dissection ?

A
  1. Unilateral (ipsilateral) headache
  2. Ipsilateral Horner’s syndrome
  3. Contralateral hemisphere signs (aphasia, neglect, visual disturbance, hemiparesis).
44
Q

What causes Horner’s syndrome in carotid dissection?

A

Compression of the ascending sympathetic supply within the carotid sheath, and results in ptosis and miosis.

Anhydrosis is classically not present as the sympathetic supply to the sweat glands is along the external carotid plexus and is therefore spared.

45
Q

How does cortical venous thrombosis present?

A

Headache
Seizures
Focal neurological deficit

more common in the postpartum period.

46
Q

List associations of acromegaly?

A
  • Impaired glucose tolerance (~40%), DM (~15%)

*Vascular: Raised BP, left ventricular hypertrophy (±dilatation/CCF), cardiomyopathy, arrhythmias. There is risk of ischaemic heart disease and stroke (?due to raised BP ± insulin resistance and GH-induced increase in fibrinogen and decrease in protein S)

  • Neoplasia: colon cancer risk increases colonoscopy may be needed.

Thirty percent have:
- elevated prolactin levels
- a combination of a damaged pituitary stalk reducing the dopamine suppression signal
-reduced thyroid-stimulating hormone levels leading to increased thyrotropin-releasing hormone which stimulates prolactin secretion.
1. Pseudogout
2. Hypertension, heart failure and cardiomyopathy may occur.
3. Goitre is seen in 20%, along with other soft tissue swelling.
4. Phosphate levels are elevated but calcium levels are not significantly increased

47
Q

What are some features associated with Wilsons disease?

A
  • Extrapyramidal features (tremor, parkinsonism, dystonia)
  • Dysarthria
  • Psychiatric features
  • Cirrhosis
  • Kayser-Fleischer ring (a deposit of brownish-green pigment around the margin of the cornea)
48
Q

Complete the sentence:

Variant Creutzfeldt-Jakob disease is characterised by

A

myoclonus and rapid onset dementia

49
Q

What is myoclonus

A

Sudden shock-like involuntary movement:
* Positive myoclonus: brief muscle contraction.
* Negative myoclonus: pause in muscle activity (asterixis).

50
Q

Hemiballismus is characeteristic of damage to which structure ?

A

contralateral subthalamic nucleus infarction

51
Q

What is Opercular syndrome?

A

facio-labio-pharyngo-masticatory syndrome with automato-voluntary dissociation.

signs limited to bulbar and masticatory muscles, especially for voluntary actions

52
Q

What is Grestman syndromes?

A

Finger anomia
Right-left confusion
Acalculia

mainly higher cortical dysfunction like finger anomia, right-left confusion and acalculia. It does not have such prominent bulbar motor signs.

53
Q

What is Foster Kennedy’s syndrome

A

Combination of optic atrophy and central scotoma, contralateral papilloedema and anosmia.

It is caused by optic and olfactory nerve compression and raised intracranial pressure.

This is often secondary to a mass such as an olfactory groove meningioma.

54
Q

What is Leber’s herditary optic neuropathy?

A

mitochondrial disorder causing visual loss in young men but would not account for his other symptoms.

55
Q

What is the blood supply of the spinothalamic tracts?

A

anterior spinal artery

56
Q

Central spinal cord lesions destroy

A

Contiguous structures like the anterior horn cells (lower motor neurone signs)
Decussating sensory fibres (pain and temperature) and
The lateral corticospinal tracts (upper motor neurone signs).

57
Q

Conus medullaris lesion causes

A

Wasting and weakness of leg muscles with fasiculations (lower motor neurone signs) and
Hyper-reflexia especially distally (upper motor neurone signs) supplied by the lower sacral segments (glutei)
with sensory loss of buttocks and perineum.

58
Q

Where does the spinal cord end?

A

lower border of L1 vertebra.

59
Q

What do the anterior spinal arteries supply?

A

Corticospinal and spinothalamic tracts, and anterior horns of the grey matter.

60
Q

Ulnar neuropathy causes?

A

Ring and little finger paraesthesia
Hypothenar wasting
Weak thumb adduction.

61
Q

median nerve movements?

A

Abduction and opposition of the thumb and flexion of the index finger

62
Q

radial nerve movements in the hand?

A

Extension of the little finger

63
Q

What is the difference between idiopathic Parkinson’s disease and Neuroleptic-induced parkinsonism?

A

Neuroleptic-induced parkinsonism is usually bilateral and symmetrical.

64
Q

Match the muscle to the nerve supply: Deltoid

A

C5

65
Q

Match the muscle to the nerve supply: Triceps

A

C7

66
Q

Match the muscle to the nerve supply: Gastrocnemius

A

S1

67
Q

Quadriceps

A

L3

68
Q

Finger flexors and extensors

A

C8

69
Q

Hair loss is most common with which antiepileptic?

A

Valproate -happens with carbazepine but only 6%

70
Q

What are the symptoms of L5/S1 disc prolapse affects the S1 nerve root?

A

Sensory loss to the posterior calf and the plantar surface of the foot
Motor loss to gastrocnemius and soleus, and
Loss of ankle jerk

71
Q

L3/4 disc prolapse affects the L4 nerve root, causing:

A

Pain in the anterior thigh
Quadriceps weakness
Reduced knee jerk
Loss of sensation over the thigh

72
Q

L4/5 disc prolapse affects the L5 nerve root, causing:

A

Pain over lateral aspect of thigh and leg
Loss of sensation to lateral aspect of leg and dorsum of foot
Weakness of dorsiflexion (‘foot drop’)
Reflexes often unaffected

73
Q

Amyotrophic lateral sclerosis signs

A

Degeneration of upper (UMN) and lower motor neurones (LMN), therefore giving a mixed picture fasciculations and spasticity,
weakness and
hypo- or hyperreflexia.

74
Q

Imaging changes in frontotemporal dementia (FTD) start initially in which parts of the brain?

A

Orbitofrontal cortex and anterior cingulate regions of the frontal lobes, along with the anterior insula

75
Q

A 35-year-old woman presents with a one-week history of blurred vision in her right eye and pain with eye movement. One year prior, she experienced sudden weakness and stiffness in her left leg, which resolved over three days. She also reports a transient decrease in colour perception six months ago. Examination reveals a relative afferent pupillary defect and optic disc swelling on the right side.

Which MRI sequence is most appropriate for identifying the characteristic lesions associated with this condition?

A

Use MRI FLAIR sequence in diagnosis of multiple sclerosis vs. MRI STIR in flares of thyroid eye disease

76
Q

Why are flair sequences used for MS?

A

MRI FLAIR sequences are particularly adept at identifying hyperintense lesions on T2-weighted images, which are characteristic of MS; they effectively reveal lesions within periventricular areas and can detect the pathognomonic Dawson fingers that extend perpendicular to the corpus callosum. This imaging modality is proficient at detecting disseminated lesions across both time and space, which are crucial criteria for diagnosing MS.

77
Q

What are MRI diffusion-weighted sequence used for

A

detecting acute ischaemic strokes by highlighting areas of restricted diffusion

-focuses on changes in water molecule diffusion within brain tissue

78
Q

What is MRI STIR sequence used for?

A

soft tissue imaging and is particularly useful for detecting oedema and inflammation in various conditions
-thyroid eye disease

79
Q

What is MRI susceptibility-weighted sequence used for?

A

microhaemorrhages or iron deposits within cerebral tissues in conditions such as haemochromatosis

80
Q

When are T1 weighted MRI images useful?

A

high-resolution images that delineate anatomical structures clearly and can be essential when assessing brain anatomy and atrophy

81
Q

MS features on MRI

A

high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

82
Q

MS features on Visual evoked potentials

A

delayed, but well preserved waveform

83
Q

What is conduction aphasia

A

poor repetition and naming but intact comprehension and fluent verbal output.

84
Q

Features of Charcot-Marie-Tooth

A

distal muscle weakness and atrophy
weak ankle dorsiflexio
depressed tendon reflexes
pes cavus foot deformity

85
Q

Features of subacute combined degeneration of the spinal cord

A

Distal sensory loss, tingling + absent ankle jerks/extensor plantars + gait abnormalities/Romberg’s positive

86
Q

Causes of gingival hyperplasia

A

phenytoin, ciclosporin, calcium channel blockers and AML

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