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Neuro Flashcards

1
Q

Which gene is a risk factor for Parkinson’s?

A

LRRK2

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2
Q

Which area of the brain is affected in Parkinson’s?

A

Pars compacta of the substantia nigra

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3
Q

What non-specific and non-motor features of Parkinson’s may develop before onset of disease

A
  • Anosmia
  • Constipation
  • Depression/anxiety
  • Micrographia
  • Quiet speech
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4
Q

What are the triad of symptoms of Parkinson’s?

A
  • Bradykinesia (decreased rate and amplitude of repetitive movement)
  • Resting tremor
  • Rigidity
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5
Q

What are the features of tremor seen in PD?

A
  • Intention tremor (worse when reaching for objects)
  • Better when distracted with tasks in other hand
  • Can also improve on voluntary movement
  • Usually asymmetrical
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6
Q

What is the 1st line treatment of PD?

A

Levodopa if quality of life is impaired

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7
Q

What considerations must you make when prescribing levodopa?

A

Prescribe it with a dopa decarboxylase inhibitor such as benserazide or carbidopa to minimise nausea and hypotension

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8
Q

What other class of drugs (give examples) is used in combination with levodopa?

A

Dopamine agonists

-ropinirole, rotigotine

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9
Q

Side effects of ropinirole/rotigotine?

A

Impulse control disorders

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10
Q

Mode of action of MOAB inhibitor and give examples

A

Reduces dopamine catbolism in brain

-selegiline, rasagiline

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11
Q

When is use of amantadine indicated?

A

Helps dyskinesia in advanced PD

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12
Q

Which drugs can cause a worsening of parkinsonim?

A

Haloperidol/chlorpromazine

Metoclopramide

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13
Q

Name the 4 types of Parkinson plus syndromes and describe their features

A

All have features of Parkinsonism (bradykinesia, hypertonia, resting tremor)

  1. Progressive supranuclear palsy - Vertical gaze palsy
  2. Multiple system atrophy - Early autonomic clinical features (postural hypotension, incontinence, impotence)
  3. Cortico-basal degeneration - Spontaneous activity in affected limb/akinetic rigidity of limb
  4. Lewy-body dementia - Fluctuation in cognitive impairment, visual hallucinations
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14
Q

Mode of inheritance of Huntington’s?

A
  • Autosomal dominant
  • Trinucleotide repeat disorder (CAG)
  • Anticipation
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15
Q

What movement disorders are seen in Huntington’s?

A
  • Chorea
  • Eye movement disorder
  • Dysarthria
  • Dysphagia
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16
Q

What mutation is seen in muscle dystrophy?

A

Trinucleotide CTG repeat in the DMPK gene

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17
Q

What is myotonic dystrophy?

A

Disease of abnormal muscle contraction which results in weakness of muscles as well as inability for muscles to relax after contraction

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18
Q

Features of myotonic dystrophy?

A
  • Progresive distal muscle weakness
  • Ptosis
  • Weakness and thinning of face and sternocleidomastoid
  • Respiratory weakness
  • Myotonia
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19
Q

Pathophysiology of Duchenne MD?

A

X-linked recessive disorder. Lack of dystrophin

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20
Q

How does Becker’s MD differ from DMD?

A

Less severe lack of dystrophin and weakness only becomes apparent in adults

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21
Q

Clinical features of DMD?

A
  • Gower’s sign
  • Difficulty running and rising to feet leads to falls
  • Calf pseudohypertrophy and proximal muscle weakness
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22
Q

Pathophysiology of Charcot Marie Tooth?

A

Autosomal dominant disease causing dysfunction in myelin/axons of peripheral motor and sensory nerves

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23
Q

Features of CMT?

A
  • Pes cavus
  • Distal muscle wasting (champagne bottle legs)
  • Foot drop due to weakness of lower legs
  • Hand weakness
  • Peripheral sensory loss
  • Reduced tone and reflexes
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24
Q

Features of essential tremor?

A
  • Fine tremor
  • Symmetrical
  • Worsens with voluntary movement, tiredness, stress, after caffeine
  • Better with alcohol
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25
Q

Which drugs can help essential tremor?

A
  • Beta blockers (propranolol)
  • Alcohol
  • Primidone
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26
Q

What movement disorders can antipsychotics cause?

A
  • Dystonia (oculogyric crisis, torticollis)
  • Tardive dyskinesia
  • Akathisia
  • Parkinsonism
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27
Q

CN 3 palsy is associated with which circulatory abnormality?

A

Aneurysm of posterior communicating artery

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28
Q

Features of MCA stroke in the dominant hemisphere?

A
  • Global aphasia
  • Contralateral sensorimotor loss on face, upper limb and trunk
  • Homonymous hemianopia
  • Dysarthria, dysphagia
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29
Q

Features of MCA stroke in non-dominant hemisphere?

A
  • Neglect syndrome
  • Contralateral sensorimotor loss on face, upper limb, trunk
  • Homonymous hemianopia
  • Dysarthria, dysphagia
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30
Q

Features of ACA stroke?

A
  • Contralateral sensorimotor loss below the waist
  • Urinary incontinence
  • Personality defects
  • Split brain syndrome
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31
Q

Features of PCA stroke?

A
  • Contralateral homonymous hemianopia with macular sparing
  • Reading and writing deficit
  • Impaired memory
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32
Q

Features of PICA stroke?

A

Causes Wallenberg syndrome:

  • Ipsilateral Horner syndrome
  • Ipsilateral sensory deficits in pain and temp in face
  • Ipsilateral cerebellar ataxia
  • Contralateral sensory deficits in pain and temp in rest of body
  • Contralateral vertigo, nystagmus, N&V, diplopia
  • Contralateral loss of gag reflex, dysphagia, dysphonia
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33
Q

Which structures are affected in Wallenberg syndrome?

A
  • Ipsilateral descending sympathetic fibres
  • Ipsilateral CN V nucleus
  • Ipsilateral lateral medulla
  • Contralateral spinothalamic tract
  • Contralateral CN VIII nucleus
  • Contralateral CN IX and X nucleus
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34
Q

What would result from damage to the frontal cortex?

A
  • Personality changes
  • Deficit in executive function
  • Poor working memory
  • Disinhibition and impulsiveness
  • Apathy
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35
Q

How is the GCS scored?

A 
Eyes: 
4 - spontaneous eye opening
3 - opens eyes to sound
2 - opens eyes to pain
1 - none
Verbal:
5 - orientated to time, person, place
4 - speaks, but confused and not completely coherent 
3 - speaks some words
2 - minimal sounds
1 - none
Motor:
6 - follows commands
5 - localises to pain
4 - flexes past midline to pain
3 - abnormal flexion posturing
2 - abnormal extension posturing
1 - none
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36
Q

Extradural haemorrhage is usually caused by rupture of which artery?

A

Middle meningeal artery

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37
Q

What does CT show for extradural haemorrhage?

A

Hyperdense, biconcave lens shape that does not cross suture lines

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38
Q

How do acute bleeds and chronic bleeds differ on CT scan?

A

Acute bleeds appear brighter as they are more dense due to higher iron content

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39
Q

1st line investigation for subarachnoid haemorrhage? Positive scan shows what?

A

CT scan

+ive scan shows 5 point star shape

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40
Q

What investigation do you do if CT scan is negative for SAH? What do you test for?

A

Do a lumbar puncture. Look for elevated RBC and xanthochromia. Xanthochromia shows 12 hours later

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41
Q

Why do you test for xanthochromia in CSF?

A

It is caused by bilirubin from haemolysis in the CSF leading to a yellow appearance

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42
Q

What is the role of calcium channel blockers after SAH surgery?

A

Prevents vasospasm-induced cerebral ischaemia to optimise cerebral perfusion

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43
Q

Difference between CMT1 and CMT2?

A

Charcot Marie Tooth 1 is demyelinating. CMT2 is axonal

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44
Q

CSF findings consistent with MS?

A

oligoclonal bands

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45
Q

Pre-ganglionic causes of Horners

A

Pancoast tumour
Thyroidectomy
Trauma

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46
Q

Central causes of Horners

A

Stroke, syringomyelia, MS

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47
Q

Post-ganglionic causes of Horners

A

Carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis

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48
Q

How to differentiate between pre, post and central causes of Horners?

A

Central = anhydrosis of face and trunk

Pre-ganglionic = anhydrosis of face

Post-ganglionic = no anhydrosis

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49
Q

Features of cerebellar syndrome?

A 
DANISH:
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
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50
Q

Difference between Horners and CN 3 palsy?

A

Horner is a disruption of sympathetic innervation - there will be miosis and anhydrosis

CN 3 palsy results in unopposed sympathetic action leading to dilated pupil as well as a down and out appearance

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51
Q

Triggers of migraine?

A

Stress
Bright light
Strong smells
Foods (chocolate, alcohol, caffeine)

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52
Q

How to treat migraines?

A
  • Paracetamol and NSAIDs to treat pain
  • Triptans as soon as migraine starts
  • Antiemetics if needed
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53
Q

How do triptans work?

A
  • 5HT (serotonin) receptor agonists
  • Cause vasoconstriction of smooth muscle
  • Inhibit activation of pain receptors
  • Reduce CNS neuronal activity
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54
Q

Side effects of triptan use?

A

Tight chest and throat

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55
Q

What is given as migraine prophylaxis 1st line? 2nd line? Off-license?

A

1st: Propranolol
2nd: Topiramate

Off-license: Amitriptyline

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56
Q

Pain character and distribution for trigeminal neuralgia?

A

Shooting, electric type pain in jaw, teeth, gums, face that lasts for a few seconds to 2 minutes

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57
Q

Treatment for trigeminal neuralgia?

A

Carbamazepine

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58
Q

Pain character and distribution for cluster headache?

A

Severe and unbearable pain usually around eye.

3-4 attacks a day for a number of weeks then years of pain free before returning

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59
Q

Acute treatment for cluster headache?

A

Sumatriptan and 100% high flow oxygen

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60
Q

Prophylaxis for cluster headache?

A

Verapamil or lithium

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61
Q

How long does someone have to be taking analgesia for them to be classed as a medication overuse headache?

A

Taking analgesia 2/3x a week

or

> 10 days in a month

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62
Q

Features of raised ICP?

A
  • Headache
  • Vomiting
  • Altered consciousness
  • Papilloedema
  • Cushing’s triad (hypertension, bradycardia, irregular breathing)
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63
Q

Management of raised ICP?

A
  • IV mannitol as osmotic diuretic
  • Controlled hyperventilation
  • CSF drain
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64
Q

What role does controlled hyperventilation have on treatment of raised ICP?

A

Reduces CO2 so vasoconstriction of cerebral arteries and reduces ICP. Needs to be controlled as you are reducing blood flow to an ischaemic brain

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65
Q

What kind of demographic is idiopathic intracranial hypertension seen in ?

A

Young, overweight females

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66
Q

Management of IIH?

A

Weight loss
Acetazolamide
Topiramate

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67
Q

Romberg test findings in cerebellar disease?

A

Romberg test is negative

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68
Q

Features of absence seizure?

A

Loss of awareness and vacant expression for less than 10s

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69
Q

What can provoke an absence seizure?

A

Hyperventilation/stress

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70
Q

Feature of focal seizures localised to:

  • Temporal lobe
  • Frontal lobe
  • Occipital lobe
  • Parietal lobe
A
  • Feelings of déjà vu, olfactory/gustatory/auditory hallucination, gastric rising, automatisms
  • Jacksonian march, posturing, head/leg movements
  • Floaters and flashes
  • Paresthesia
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71
Q

Treatment of focal seizure?

A

Carbamazepine generally 1st line. Lamotrigine can be given

72
Q

What must be tried before IV phenytoin is used for termination of epilepsy?

A

2 doses of buccal midazolam/rectal diazepam/IV lozapem

73
Q

Which anti-epileptic should be given if pregnant and having generalised seizures?

A

Lamotrigine

74
Q

Side effects of sodium valproate?

A
  • Teratogenic
  • Weight gain
  • LFT derangement (hepatitis)
  • Hair thinning/alopecia
  • Tremor
  • Thrombocytopaenia
75
Q

Side effects of carbamazepine?

A
  • SIADH (hyponatremia)
  • SJS
  • Dizziness/ataxia
  • Nystagmus
  • Leucopaenia/agranulocytosis
  • Diplopia
76
Q

Side effects of lamotrigine?

A
  • SJS

- Lymphopaenia

77
Q

Side effects of phenytoin?

A
  • Gingival hyperplasia
  • Peripheral neuropathy
  • Lymphadenopathy
  • Acne, hirsutism
78
Q

Side effects of topiramate?

A
  • Weight loss
  • Renal stones
  • Glaucoma
  • Memory loss
79
Q

Rules on driving with epilepsy?

A
  • Patients cannot drive for 6 months after 1st seizure.

- For patients with established epilepsy, they must be fit free for 12 months

80
Q

What is the pathological hallmark of MND?

A

TDP-43 and FUS proteins seen in axons

81
Q

UMN lesion features?

A
  • Weakness
  • No/slight muscle wasting
  • Hyperreflexia
  • Hypertonia
  • No fasciculations
  • Babinski positive
82
Q

LMN lesion features?

A
  • Weakness/flaccid paralysis
  • Muscle wasting
  • Hyporeflexia
  • Fasciculations
  • Hypotonia
83
Q

Features of amyotrophic lateral sclerosis?

A

Involvement of UMN and LMN signs of one limb that spreads to other limbs and trunk

(Typically UMN signs in legs and LMN signs in arms)

84
Q

Features of progressive muscular atrophy

A
  • LMN signs only
  • Affects distal muscles then proximal
  • Starts in one limb then spreads to affect other spinal segments
85
Q

Features of primary lateral sclerosis?

A
  • UMN signs only

- Slowly progressive tetraparesis

86
Q

Features of progressive bulbar palsy?

A
  • Tongue fasciculation with slow, stiff tongue movements
  • Dysfunction of CN nuclei 9-12
  • Dysarthria, dysphagia, choking
  • Loss of gag reflex
87
Q

Features of progressive pseudobulbar palsy?

A
  • Dysarthria, dysphagia, emotional lability
  • Brisk jaw jerk reflex
  • Hot potato speech
88
Q

General features of MND?

A
  • Fasciculation
  • Absence of sensory symptoms
  • Mixture of UMN and LMN signs
  • Wasting of small hand muscles/tibialis anterior
  • Does not affect eye muscles
  • No cerebellar signs
89
Q

Management of MND?

A
  • Riluzole

- Respiratory support

90
Q

Mechanism of action of riluzole?

A

Glutamate receptor antagonist

91
Q

Classic demographic of MS patient?

A

White, 30yrs, woman

92
Q

What is MS?

A

Chronic, autoimmune, T-cell mediated inflammatory disorder of white matter of CNS

93
Q

What is the cardinal feature of MS?

A

Plaques of demyelination found in brain and spinal cord

94
Q

What feature of MS is crucial for diagnosis?

A

Dissemination in time and space

95
Q

Common features of MS?

A
  1. Optic neuritis
  2. Brainstem demyelination (diplopia, vertigo, dysarthria, dysphagia)
  3. Spinal cord lesions (paraparesis, difficulty walking)
96
Q

Other symptoms of MS?

A
  • Visual change
  • Sensory change
  • Clumsy hands
  • Ataxia
  • Urinary urgency/frequency
  • Fatigue
  • Spasticity
  • Depression
97
Q

What is the most common pattern of MS?

A

relapsing-remitting

98
Q

Describe disease course of secondary progressive MS

A

Initially relapsing-remitting but then sudden decline without remission

99
Q

Describe disease course of primary progressive MS

A

Worsening MS with no periods of relapse or remission

100
Q

Describe disease course of relapsing progressive MS

A

Disease getting worse overall but has periods of severe and worsening attacks

101
Q

Which investigation is definitive in MS?

A

MRI brain shows plaques and scars

102
Q

What does lumbar puncture show in MS?

A

Oligoclonal bands against myelin

103
Q

What medication can be given for MS? What does it do?

A

Steroids can help alleviate acute attacks

Beta-interferon or Natalizumab can modify course of inflammatory relapsing-remitting MS

104
Q

Treatment of transverse myelitis?

A

High dose steroids/immunosuppression

Antimicrobials if infective cause

105
Q

Triad of symptoms seen in meningitis?

A

Headache
Fever
Neck stiffness

106
Q

Other symptoms of meningitis?

A
  • Photophobia
  • Vomiting
  • Irritability
107
Q

CSF appearance in bacterial meningitis?

A
  • Cloudy
  • Low glucose (<50% of plasma glucose)
  • High protein
  • High WCC (polymorphs)
108
Q

CSF appearance in viral meningitis?

A
  • Clear/cloudy
  • 60-80% of plasma glucose
  • Proteins normal slightly raised
  • Lymphocytes
109
Q

How does tuberculous meningitis CSF differ from bacterial meningitis CSF?

A
  • Appearance has fibrin web

- Has lymphocytes

110
Q

Empirical antibiotics given in meningitis?

A

Cefotaxime

Benzylpenicillin if meningococcus sensitivity confirmed

111
Q

Complications of meningitis?

A
  • Sensorineural hearing loss
  • Seizure
  • Hydrocephalus
  • Focal neurological deficit
  • Sepsis
112
Q

What drug should be given with 1st dose of antibiotics to reduce neurological complications of meningitis?

A

Dexamethasone

113
Q

Most common causative organism of encephalitis?

A

HSV1

114
Q

Features of encephalitis?

A
  • Meningism
  • Focal neurological deficits
  • Seizures
  • Vomiting
  • Reduced consciousness
  • Personality and behavioural change
115
Q

Carpal tunnel syndrome is more common in those with which diseases?

A
  • Diabetes
  • Hypothyroid
  • 3rd trimester pregnancy
  • RA
116
Q

Sensory distribution of median nerve?

A

Lateral 3.5 fingers in the palmar hand

Top half of fingers 2, 3, half of 4 in the dorsal hand

117
Q

Describe Tinel and Phalen test

A

(Tapping)Tinnel: tap nerve in the carpal tunnel

(Phlexing)Phalen: hold the wrist in flexion

Both tests cause pain and tingling if positive

118
Q

Which nerve is affected in cubital tunnel syndrome?

A

Ulnar

119
Q

What hand signs are seen in cubital tunnel syndrome?

A
  • Claw hand
  • Wasting of interossei and hypothenar muscles
  • Wasting of medial 2 lumbricals
  • Sensory loss over medial 1.5 fingers
120
Q

What structure is damaged with spiral fracture of humerus?

A

Radial nerve - Wrist drop

121
Q

Signs of radial nerve palsy?

A
  • Wrist drop
  • Weakness of flexion (brachioradialis) and finger extension
  • Sensory loss to dorsum of 1st and 2nd metacarpals
122
Q

What is caused by meralgia paraesthetica?

A

Compression of lateral cutaneous nerve of thigh

123
Q

Signs of common peroneal nerve palsy?

A
  • Foot drop (deep peroneal nerve) and weak ankle eversion (superficial peroneal nerve)
  • Numbness over anterolateral border of dorsum of foot and lateral calf
124
Q

Common prodrome of Guillain-Barre Syndrome?

A

Gastroenteritis

125
Q

What are the causes of GBS?

A
  • Campylobacter jejuni

- CMV

126
Q

What kind of disease is GBS?

A

Autoimmune demyelinating disease of the PNS causing symmetrical ascending weakness

127
Q

Symptoms of GBS?

A
  • Leg/back pain
  • Ascending, symmetrical weakness in limbs
  • Reflexes reduced/absent
  • Mild sensory impairment
  • Respiratory failure
  • Diplopia, facial nerve palsy, oropharyngeal weakness
  • Urinary retention
128
Q

What is the classic finding in lumbar puncture of GBS?

A

Raised proteins with normal WCC

129
Q

What do nerve conduction studies show in GBS?

A

Decreased motor nerve conduction velocity due to demyelination

130
Q

What is important to be monitored in GBS and how is this done?

A

Respiratory function by FVC

131
Q

What is given to reduce the severity and duration of paralysis in GBS?

A

IV immunoglobulins

132
Q

What is Miller Fisher syndrome?

A

A variant of GBS associated with ophthalmoplegia, areflexia and ataxia. Eye muscles are typically affected first
(descending paralysis)

133
Q

Which antibodies are seen in Miller Fisher syndome?

A

Anti-GQ1b

134
Q

What deficits are seen in syringomyelia and how is this distributed?

A

Bilateral loss of pain, temperature sensation and motor weakness

Distributed in cape-like pattern (neck, shoulders, arms)

135
Q

What is the thrombolysis protocol of ischaemic stroke?

A

Thrombolysis with alteplase (tPA) only if:

  • Haemorrhagic stroke has been excluded
  • Administration is within 4.5hrs of symptoms
136
Q

What is the thrombectomy protocol of ischaemic stroke?

A

Can only be done if:

  • Haemorrhagic stroke has been excluded
  • Done within 6hrs of symptoms
137
Q

What is the medical management of ischaemic stroke?

A
  • 300mg aspirin for 14 days as soon as haemorrhagic stroke has been excluded
  • Statin if cholesterol is >3.5mmol/L
  • Clopidogrel 75mg after 14 days
138
Q

What 3 features are seen in an anterior circulation infarct?

A
  1. Contralateral hemiparesis
  2. Homonymous hemianopia
  3. High cognitive dysfunction such as dysphasia
139
Q

What is a TIA?

A

Transient, sudden loss of neurological function that has complete recovery

140
Q

What is the risk of full stroke with someone who has had a TIA?

A

10% risk of stroke within 90 days

141
Q

What is the management of TIA in the community?

A
  • 300mg aspirin

- Refer to TIA clinic ASAP with carotid imaging within 24 hours

142
Q

What is the management of TIA in the hospital?

A
  • Aspirin 300mg stat then 75mg daily
  • Full imaging screen: CT head, ECG, CTA/Doppler
  • Refer to TIA clinic
143
Q

Management of facial paralysis?

A
  • Otoscopy to check for Ramsay Hunt

- Prednisolone

144
Q

Treatment of Ramsay Hunt syndrome?

A

Oral aciclovir

Prednisolone

145
Q

Lesion in optic nerve causes which visual field defect?

A

Monocular vision loss

146
Q

Lesion in optic tract causes which visual field defect?

A

Contralateral homonymous hemianopia

147
Q

Lesion in superior fibres of optic radiation of parietal lobe?

A

Contralateral inferior quadrantianopia

148
Q

Lesion in the inferior fibres of optic radiation of temporal lobe?

A

Contralateral superior quadrantianopia

149
Q

Lesion in occipital lobe causes which visual field defect?

A

Contralateral homonymous hemianopia with macular sparing

150
Q

What is the pathophysiology of myasthenia gravis?

A

Antibodies against ACh receptors lead to insufficient functioning at the NMJ

151
Q

What happens in myasthenic crisis?

A

Respiratory muscles become weak leading to respiratory failure. Consider ventilation if FVC falls below 15ml/kg

152
Q

Which cancer is associated with myasthenia gravis? What imaging is required during investigation?

A

Thymoma - CT chest required

153
Q

What is seen on EMG in myasthenia gravis?

A

Repetitive stimulation of a nerve will show a characteristic decrement in muscle action potential

154
Q

Which antibodies are hallmark for myasthenia gravis?

A

Anti-AChR

155
Q

Which other antibodies are also seen in MG?

A

Anti-MuSK

156
Q

Pattern of weakness in those with anti-MuSK MG?

A

Weakness of face, neck and bulbar muscles

157
Q

1st line treatment of MG? Drug class?

A

Pyridostigmine - acetylcholinesterase inhibitor

158
Q

Which antibodies characterises Lambert Eaton syndrome?

A

Antibodies against voltage gated calcium channels (anti VGCC) in the PNS

159
Q

What cancer is associated with LEMS?

A

Small cell lung cancer

160
Q

What is seen on EMG with LEMS?

A

Repetitive stimulation shows incremental response

161
Q

Features of LEMS?

A

Proximal limb weakness affecting lower limbs and absent reflexes

These get better after repeated muscle contraction

162
Q

Treatment of LEMS?

A

Immunosuppression with prednisolone

163
Q

Features of normal pressure hydrocephalus?

A

Urinary incontinence
Dementia
Gait disorder/apraxia

“Wet, weird, wobbly”

164
Q

What causes normal pressure hydrocephlaus?

A

Enlarged lateral ventricles in elderly patients

165
Q

What kind of seizure does carbamazepine not have a role in treatment?

A

Absence seizures

Myoclonic seizures

166
Q

What is the difference between Wernicke’s aphasia and conduction aphasia?

A

Both have impaired repetition of words but comprehension is preserved in conduction.
“Wernicke = What? (no comprehension)”

167
Q

Which drugs can be given to help spasticity in MS?

A

Baclofen or gabapentin

168
Q

Stroke affecting which areas of the brain lead to expressive, receptive and conduction aphasias?

A 
Expressive = Broca = inferior frontal gyrus
Receptive = Wernicke = superior temporal gyrus
Conduction = arcuate fasciculus
169
Q

Features of Weber syndrome? Where is the location of stroke in this syndrome?

A
  • Ipsilateral CN 3 palsy
  • Contralateral weakness on whole side of body
  • Stroke in midbrain
170
Q

What is pituitary apoplexy, most common cause and how is it treated?

A
  • Bleeding of the pituitary
  • Most commonly caused by bleeding of pituitary tumour
  • Treat with steroids
171
Q

Which class of drugs worsen MG?

A

beta blockers

172
Q

What can cause a bitemporal hemianopia with superior quadrants more affected? Inferior quadrants more affected?

A

Superior more affected: pituitary macroadenoma

Inferior more affected: craniopharyngioma

173
Q

What is the MRC muscle power grading system?

A

Grade 5: normal strength
Grade 4: movement against resistance with reduced power
Grade 3: cannot move against resistance, can against gravity
Grade 2: can move with gravity eliminated
Grade 1: twitches and trace contractions
Grade 0: none

174
Q

When should carotid endarterectomy be done?

A

High grade symptomatic carotid stenosis with >70% narrowing

175
Q

CSF appearance in encephalitis?

A
  • Lymphocytes (raised WCC)
  • Normal glucose
  • Slightly raised protein
176
Q

How does CSF appear in T1 vs T2 weighted MRI?

A

T1: CSF is dark
T2: CSF is light

177
Q

Which mutation is seen in cases of familial MND?

A

SOD1

Revision all topics (11 decks)

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