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GI P2a > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the condition that presents with headache, scalp tenderness and jaw claudication, and potential systemic symptoms? What would be seen on a biopsy (and where would this be done?)

A

Giant cell arteritis.

Granulomatous arteritis on a temporal artery biopsy

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2
Q

What condition and sign is associated with giant cell arteritis?

A

Polymyalgia rheumatica and amourosis fugax

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3
Q

What is the extra pyramidal triad that Parkinson’s presents with? what are other symptoms?

A

Pill rolling tremor (at rest), bradykinesia, hypertonia = triad. other symptoms: decreased arm swing in gait, stoop, depression, constipation, urinary incontinence

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4
Q

What is the pathophysiology of Parkinson’s?

A

progressive loss of dopamine secreting cells in the substantial nigra. Alteration in the basal ganglia which regulate movement (and of which dopamine is a key neurotransmitter). Loss of striatal pathways. Also accumulation of Lewy-bodies

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5
Q

Dx of Parkinson’s and conditions that should be excluded:

A

Exclude cerebellar disease and frontal temporal dementia. Clinical dx based on extra pyramidal triad. Clinical response to dopaminergic tx. MRI rules out structural pathology and CT shows atrpohy of the substantial nigra

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6
Q

What is the treatment for Parkinsons?

A
  • Levodopa (dopamine precursor) with DOPA- decarboxylase inhibitor
  • dopamine agonst (ropinirole)
  • MAO-B inhibitors: efficacy decreases with time
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7
Q

What neurotransmitters are lost in Huntington’s disease, and what is maintained, and where in the brain does this occur?

A

ACh and GABA lost, dopamine spared. Occurs in the caudate nucles and basal ganglia

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8
Q

what is the aetiology of Huntingtons?

A

Autosomal dominant. CAG repeats due to genetic stutter; Huntingtin protein.

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9
Q

What is the tx of Huntingtons?

A
  • no disease modifying treatment available.

- treat chorea: sodium valproate, benzodiazepines

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10
Q

What is Guillain Barre syndrome?

A

Demyelination and axonal degeneration. Rapid progressive ascending neuropathy

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11
Q

What is the presentation of Guillain Barre syndrome and associated syndrome?

A
  • progressive ascending limb weakness (usually symmetrical)
  • Peaks at 4 weeks
  • decreased reflexes
  • parasthesia
  • no muscle wasting

Miller Fischer syndrome: related variant that affects cranial nerves of the eye muscles

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12
Q

What is the cause of gullian barre syndrome and why does it happen?

A

Preceding infection, usually resp or GI. Antibodies attack peripheral nerves

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13
Q

What are common bacteria that cause GBS?

A
  • campylobacter jejuni

- CMV: cytomegalovirus

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14
Q

What is the presentation of upper motor nerve lesion?

A
  • affects groups of muscles
  • pyramidal pattern: extensors of warm and flexors of legs weakened
  • spasticity, increased tone ( the faster muscles are moved, the more resistances)
  • increased reflexes
  • no muscle wasting
  • positive Babinski sign (plantar up)
  • loss of fine finger movement
  • less control of active movement
  • protonator drift
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15
Q

What is the presentation of a lower motor nerve lesion?

A

Patterns of weakness corresponds to the muscles supplied by the involved neurons

  • flaccid weakness
  • hypotonia: little resistance to passive stretch
  • decreased reflexes
  • muscle paralysis
  • fasciculation (involuntary twitching)
  • absent Babinski reflex
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16
Q

What are acute causes of peripheral neuropathy?

A

Guillan barre, nerve entrapment/trauma/lesion

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17
Q

What are chronic causes of peripheral neuropathy?

A

Diabetes, alcohol

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18
Q

What is amitriptyline commonly used for?

A

Nerve pain

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19
Q

What is trigeminal neuralgia and how does it present?

A

Knife like pain in the trigeminal/sensory division. Severe, short lasting electric shock like pain, normally unilateral. Usually a trigger

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20
Q

What is the given duration of a migraine?

A

4-72 hours

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21
Q

What are the classifications of headaches (and 2 examples of each(

A

primary (migraine, cluster) secondary (meningitis, SA haemorrhage), tension type

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22
Q

What are the red flags for headaches?

A

SNOOP10:

  • S: systemic disturbance
  • N: neurological symptoms/signs
  • O: onset (sudden)
  • O: onset age (>50 years)
  • P: phenotype
  • P: pattern change
  • P: pregnancy
  • P: papilloedema
  • P: pathology existing
  • P: painful eye
  • P: precipitation (coughing, straining)
  • P: posture
  • P: past trauma
  • P: painkiller useage
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23
Q

What is a cluster headache

A

Unilateral, very severe. Usually last 15mins to 3 hours. Cranial autonomic features (watery eyes/runny nose)

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24
Q

What is the pathophysiology of Alzheimer’s?

A

Accumulation of beta amyloid plaque, a degradation product of amyloid precursor protein. Results in progressive neuronal damage, neurofibrillary tangles, increased number of amyloid plauqes, loss of ACh. Neuronal loss: amygdala, hippocampus, subcortical nuclei.

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25
Q

What is the tx for Alzheimers?

A

ACh-esterase inhibitors. BP control

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26
Q

What are the subtypes of dementia?

A
  • Alzheimers
  • Vascular dementia (if hx of strokes/TIAs, or evidence of atheropathy)
  • Lewy body dementia: fluctuating cognitive impairment, detailed hallucinations, later Parkinsons
  • Fronto-temporal dementia: mixed dementia. Frontal and temporal atrophy with loss of neurons
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27
Q

What scan is done for dementia dx?

A

MRI

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28
Q

What is the presentation of a lesion in CN I:

A

decreased ability to smell

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29
Q

What is the presentation of a lesion in CN II

A

blindness, visual field defect

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30
Q

What is the presentation of a lesion in CN III

A

dilated pupil, ptosis (eye drooping)

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31
Q

What is the presentation of a lesion in CN IV

A

diplopia (double vision)

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32
Q

What is the presentation of a lesion in CN V:

A

Sensory deficit. Decreased facial sensation

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33
Q

What is the presentation of a lesion in CN VI

A

Inability of eye to look laterally (Eye to nose)

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34
Q

What is the presentation of a lesion in CN VII

A

LMN: total facial weakness
UMN: forehead sparing weakness

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35
Q

What is the presentation of a lesion in CN VIII

A

deafness

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36
Q

What is the presentation of a lesion in CN IX

A

impaired gag reflex

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37
Q

What is the presentation of a lesion in CN X

A

impaired gag reflex. Soft palate to good side when ‘aah’

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38
Q

What is the presentation of a lesion in CN XI

A

weakness turning head to affected side. Can’t shrug

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39
Q

What is the presentation of a lesion in CN XII

A

Tongue deviates to affected side

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40
Q

What is affected first in a nerve root lesion?

A

sensory then motor

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41
Q

What is Cauda Equina synrome, and where does the pathology occur?

A

Compression of the spinal cord at the level of cauda equina. Cord ends at L2 level

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42
Q

What is the classic presn of Cauda equina

A
  • saddle anaesthesia
  • lower back pain, bilateral sciatic
  • bowel and/or bladder dysfunction
  • sexual dysfunction
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43
Q

What ion is affected in Eaton Lambert syndrome and what is the effect?

A
  • calcium ion channel blocked
  • affects ACh release
  • leads to muscle weakness
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44
Q

What condition has the following symptoms?proximal muscle weakness, strength that increases with more effort. Diminshed/absent reflexes. Rapid progression, dysarthria

A

Eaton Lambert syndrome

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45
Q

What is the treatment for Eaton Lambert syndrome?

A

Block K+ channels in post synaptic channel. Increases AP duration, as it doesn’t repolarise. Thus, calcium channels open longer, more ACh release

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46
Q

What is myasthenia gravis?

A

AID, attack ACh receptors (post synaptic). Autoantibodies to nicotinic ACh receptors or MuSK (muscle specific tyrosine kinase), on the post synaptic membrane.

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47
Q

What are the symptoms of myasthenia gravis?

A

Weakness, fatiguability of occular (ptosis: eyelids droop), bulbar weakness (dysphagia, dysarthria), proximal limb weakness that improves after rest

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48
Q

What condition is myasthenia gravis associated with?

A

Thymic hyperplasia. In 10% cases, a thymic tumour can be found (thymoma).

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49
Q

What is the dx of myasthenia gravis?

A
  • anti ACHr antibodies in serum
  • nerve stimulation test (characteristic decrement of evoked action potential following motor nerve stimulation)
  • Ice test: improvement of ptosis with ice pack
  • Cogan’s eye twitch: sign elicited by instructing patient to look down for 15 seconds, gaze upwards and return to normal
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50
Q

What is the treatment of myasthenia gravis?

A

Pyridostigmine: acetylchinesterase inhibitor

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51
Q

What is the colloquial name of shingles and what virus causes it?

A
  • Herpes Zoster

- Varicellar Zoster virus reaction: herpes virus 3

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52
Q

Describe chicken pox rash and systemic symptoms

A

fever, malaise, headache, abdominal pain. Rash, then scabbed over vesciles

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53
Q

Describe the events in shingles:

A
  • pre eruptive: no skin lesions, but burning and itching on one dermatome
  • eruptive: skin lesions appear. erythmatous, swollen plaques, doesn’t cross deratomes
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54
Q

How does shingles develop

A

Chicken pox primary infection via respiratory droplets, invades the lymph nodes, infects skin epithelial cells. LEads to virus containing vesicles (chicken pox). Remainns dormant in sensory nerve roots. Reactivated= shingles

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55
Q

What is shingles treatment?

A

oral aciclovir

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56
Q

What are the majority of brain tumours?

A

Gliomas or meningioma

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57
Q

Where are common primary sites for brain mets?

A

Bronchus, breast, kidney, thyroid, stomach, pancreas

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58
Q

Presentation of meningitis vs encephalitis

A

The hallmark signs of meningitis include some or all of the following: sudden fever, severe headache, nausea or vomiting, double vision, drowsiness, sensitivity to bright light, and a stiff neck. Encephalitis can be characterized by fever, seizures, change in behavior, and confusion and disorientation.

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59
Q

What is encephalitis?

A

inflammation of brain parenchyma

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60
Q

What are common causes of encephalitis?

A

often presumed viral, but never identified. Herpes simplex virus, coxsackie. mumps. Tick norne. HIV, MMR

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61
Q

What is typically seen in a lumbar puncture for encephalitis?

A

increased protein and lymphocytes, decreased glucose

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62
Q

What is the clinical presentation of acute bacterial meningitis?

A

Headache, neck stiffness, fever, photophobia, vomiting. Kernig’s sign. Papilloedema. Progressive drowsiness

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63
Q

What is Kernig’s sign?

A

Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

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64
Q

What is a specific symptom of meningococcal septicaemia?

A

purpuric, non blanching rash

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65
Q

What is the differences between viral and bacterial meningitis?

A

Viral has all the same presentation but is usually more self limiting and benign. Also, no rash

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66
Q

What is the LP is bacterial meningitis?

A

Polymorphs seens, cloudy apperance, increased protein and glucose

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67
Q

What is the LP if viral meningits?

A

lymphocytes seen, clear. Increased protein. Decrease glucose

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68
Q

What is the empirical tx for meningitis?

A
  • empirical cefotaxime (can penetrate BBB, works on gram neg and positive)
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69
Q

What reduces the long term effects of menginitis?

A

dexamethasone

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70
Q

What antibiotic is added if risk of listeria mengintis?

A

Ampicillin

71
Q

What is the cause of extra dural haemorrhage?

A

fractured temporal bone. ruptured middle meningeal artery

72
Q

What is the identifying presentation of a ED haemorrhage

A

head injury –> unconscious –> lucid recovery –> rapid deterioration

73
Q

What is the CT apperance in ED haemorrhage?

A

Convex lens

74
Q

What is the cause of SD haemorrhage?

A

Minor trauma, around 9 months before. Rupture of bridging vein

75
Q

What is the presentation of a SD haemorrhage?

A
  • people at increased falls risk: epileptics, alcoholics, elderly
76
Q

What is the CT apperance in SD haemorrhage?

A

crescent shaped with midline shift

77
Q

what is the key presentation of a SA haemorrhage?

A

thunderclap headache

78
Q

What is the cause of a SA haemorrhage?

A

berry aneurysm rupture, in the circle of willis. Junction of posterior artery communicating with the internal carotid artery.

79
Q

What is the pattern of a SA haemorrhage on a CT?

A

Star pattern.

80
Q

What is the tx for a SA haemorrhage?

A

maintain cerebral perfusion. Nimidopine will reduce vasospasm and cerebral ischaemia. calcium channel blocker.

81
Q

What most be done before any stroke treatment?

A

exclude that it is not a hamoerrhagic stroke (rather than embolism)- CT.

82
Q

What is the ABCD^2 scored?

A

TIA patients risk of a stroke. Age (>60 years), Blood pressure, HTN, clinical features. Duration of symptoms. diabetes.

83
Q

What is the cause of death in most people with motor neurone disease?

A

respiratory failure due to bulbar palsy and pneumonia

84
Q

What is the key features of motor neurone diseases?

A

relentless destruction of neurones in the motor cortex, cranial nerve nuclei, anterior horn cells.

85
Q

What are the four types of MND?

A
  1. amyotrophic lateral sclerosis
  2. progressive bulbar palsy
  3. progressive muscular atrophy
  4. primary lateral sclerosis
86
Q

What are the clinical features of MND?

A

upper limbs: decreased dexterity, stiffness, wasting of intrinsic muscles of hand.
Lower limbs: tripping, stumbling gait, foot drop.
Bulbar: slurred speech, dysphagia
LMN and UMN signs.

87
Q

What is the tx for MND?

A

Riluzole. Sodium channel blockers. Stops glutamate release. Slows progression

88
Q

What do vertebral tumours often cause?

A

Spinal cord compression. Leads to UMN lesion pattern.

89
Q

What nerve is affected in carpal tunnel syndrome?

A

entrapment of median nerve against carpal tunnel

90
Q

What is tinnel’s sign? what condition does it relate to?

A

Tapping nerve elicits pins and needles in carpal tunnel syndrome

91
Q

What is Phalen’s test? what condition does it relate to?

A

Keep wrists flexed for one minute, see if any symptoms. Carpal tunnel syndrome

92
Q

What is Lhermittes sign?

A

tingling down back into limbs when neck is flexed. Related to MS

93
Q

What is the diagnostic criteria for MS dx?

A

two discrete instances of CNS dynsfunction.

94
Q

What is the characteristic areas of presentation of multiple sclerosis?

A
  1. optic: blurred vision, unilateral eye pain
  2. brainstem: diplopia, vertigo, dysphagia, nystagmus
  3. spinal cord: numbness, pins and needles
95
Q

What is the pathophysiology of MS

A

T lymphocytes activated. Complete inflammatory attack. Demyelination and axonal degeneration of oligodendrocytes.

96
Q

What is Uhthoff’s phenomen?

A

remyelinated sections= temperature dependent. Cold relieves symptoms

97
Q

What is the nature of the plaques in MS?

A

perivenular (around a vein)

98
Q

What viral exposure in early life predilects to MS?

99
Q

What is seen on a LP in MS?

A

oligoclonal bands of IgG in CSF, not blood serum. Duggests inflammation

100
Q

What is a generalised tonic clonic seizure?

A
  • generalised: orginating at some point then rapidly engaging both networks. No single starting point
  • sudden onset tonic phase followed by clonic phase. Tongue biting, incontinence, followed by drowsiness/coma
101
Q

what is the tx for a generalised tonic clonic seizure?

A
  1. Sodium valproate (increases GABA0

2. lamotrigine

102
Q

What is a absence seizure

A
  • generalised seizure.
  • cease activity, staring and pales
  • presents in childhood
103
Q

What is the tx of a absence seizure?

A
  1. sodium valproate

2. Ethosuximide

104
Q

What is a partial seizure?

A

Focal seizure. Symptoms depend on lobe of origination

105
Q

What is the difference between a simple and complex seizure?

A
  • simple: no impairment of consciousness. no post ictal symptoms
  • complex: lose consciousness. Most commonly from temporal lobe. post ictal confusion
106
Q

What is the tx for a partial seizure?

A
  1. carbamazepine

2. lamotrigine

107
Q

What does the dorsal root ganglion contain? where is it in the spinal cord?

A

nerve bodies of peripheral sensory neurones. posterior spinal cord

108
Q

What is the DCML? what nerves does it contain? where does it decussate?

A
  • ascending (Sensory)
  • cuneate and gracile
  • decussate at medulla
  • proprioception, vibration, fine touch
109
Q

Where does gracile begin (DCML)

110
Q

What is the spinothalamic tract. Where does it decussate?

A
  • ascending
  • decussate two levels above
  • crude touch, pain, temp
111
Q

What is the corticobulbar tract?

A
  • descending

- facial and neck, and cranial nerve control

112
Q

What is the corticospinal tract? lateral vs anterior?

A
  • lateral: extremity muscles. 85%. decussate at medulla

- anterior: axial and trunk. 15%. decussate at spinal cord

113
Q

axonal vs demyelination damage affects?

A
  • axonal: reduced amplitudes of AP

- demyelination: reduced conduction velocities

114
Q

What is Horner’s syndrome?

A

miosis (pupil constriction), ptosis (drooping eyelide) and anhidrosis (lack of sweating of the face)

115
Q

What does presence/lack of pupillary sparing in third nerve palsy suggest?

A
  • presence: compression. tumour

- lack: ischaemia, no compression, eg via tumour

116
Q

What assymetric eye movement diagnostic of?

117
Q

What is Cushing’s triad?

A

wide pulse pressure, tachycardia, irregular respiration

118
Q

Why does Cushing syndrome occur?

A

Increase ICP. LEads to hypoxia in brain. ICP >MAP. Lack of perfusion: ischaemia. Leads to irregular respiration, as increasing ICP affects the respiratory centre in the medulla

119
Q

Focal vs non focal sign:

A
  • focal: speech, vision, hearing problems. Indicate what area of the brain is affected
  • non focal: not specific to one area
120
Q

What are seizure symptoms classed as:

A

Gain of function.

121
Q

Frontal seizure symptoms:

A

limb jerking, head or eye deviation

122
Q

Parietal lobe seizure symptoms:

A

sensory disturbance. Spreading of tingling

123
Q

Temporal lobe seizure symptoms:

A

feeling of dread: deja vu

124
Q

Occipital lobe seizure symptoms:

A

positive visual disturbance: eg, coloured balls

125
Q

What type/location of seizure is a prodromal aura indicative of?

A

Focal seizure from the temporal lobe

126
Q

What is substance p associated with?

A

Pain and inflammatory processes

127
Q

what is bells palsy?

A

LMN of facial nerve (7)

128
Q

What are lewy bodies?

A

Eosinophilic intra cytoplasmic inclusion bodies. aggregation of proteins

129
Q

What is claw hand indicative of?

A

Ulnar nerve damage

130
Q

What is first line tx for trigeminal nerve palsy?

A

carbamazepine

131
Q

What is topiramate tx for?

A

prophylaxis for migraine

132
Q

What does ACA supply?

A

Medial frontal lobe and superior medial parietal love: lower limb supply

133
Q

What does MCA supply?

A

areas of frontal, temporal and parietal lobe. Including areas of facial, throat, hand/arm innervation. Snesory and motor

134
Q

PCA supply?

A

occipital and hippocampus

135
Q

What cranial nerves does bulbar palsy affect?

A

9,10,11,12

136
Q

What are the common bacterial causes of meningitis?

A
  1. neisseria meningitidis: common in young adults
  2. haemophilus influenzae
  3. streptococcus pneumoniae: most common in young
137
Q

By definition, what is the time length of a TIA?

138
Q

Where are most atherothromboembolisms from in TIAs/strokes?

A

Carotid artery.

139
Q

What are the different signs of carotid territory and vertebrobasilar territory strokes?

A
  • carotid: amorousis fugax, aphasia

- VB: diplopia, vomiting, vertigo, choking

140
Q

What region of the brain are strokes most and least likely to occur in?

A
  • most: MCA

- least: ACA

141
Q

Why would a diffusion weighted MRI be done for a SAH?

A

more sensitive, and a CT may be negative within a few hours

142
Q

What is the maximum time after a stroke IV alteplase can be given?

143
Q

Why does haemorrhagic strokes have higher mortality?

A

pooling of blood increases ICP.

144
Q

what are conditions associated with Berry aneurysms? And SAH?

A
  • polycystic kidney disease
  • coartication of the aorta
  • connective tissue disorders such as Marfans and ED
145
Q

What signs are associated with meningism in SAH?

A
  • those seen in meningitis
  • Brudzinksi’s sign (passive neck flexion = hip and knee flexion)
  • Kernigs sign
146
Q

What colour is a LP in a SAH and why?

A

yellow (xanthochromia). Due to bilirubin breakdown

147
Q

What acronym is used to remember the causes of migraines?

148
Q

What is the first line tx for migraines and what is their MoA?

A
  • triptans: eg, sumatriptans. Prevents peptide release from trigeminal nerve that would lead to vasodilation, neurogenic inflammation and pain
149
Q

What is the definition of cluster headaches?

A

episodic headaches from 7 days up to 1 year with pain free periods that last ~4 weeks inbetween

150
Q

What is the presentation of cluster headaches?

A

Rapid onset of excruciating pain, classically around one eye. strictly unilateral and localised to one area. Rises to a crescendro and lasts for a few hours. Also ipsilateral autonomic features (watery eyes, nose, mitosis, rhinorrhea)

151
Q

What are the symptoms are tx of cluster headache?

A
  • verapamil CCB (1st line prophylaxis)
152
Q

What is the cause of most seizures?

A

idiopathic

153
Q

What is Jacksonian march?

A

seizures march up and down the motor homonculus

154
Q

What are primary generalised seizures always associated with?

A

loss of consciousness and awareness

155
Q

What is the identifying features of vascular dementia?

A

progresses in step wise progression

156
Q

What treats chorea?

A

valproic acid and benzodiazepines

157
Q

what nerve is affected in foot drop?

A

common peroneal nerve

158
Q

What cancer is associated with lambert eaton syndrome?

A

small cell lung cancer

159
Q

What is the crushed ice test used in and what are positive results?

A

myasthenia gravis. Ptosis would improve

160
Q

What is the first line treatment for trigeminal neuralgia?

A

carbamazepine

161
Q

What is the maximum dose of sumatriptan?

162
Q

What is a presentation that points diagnosis towards Lewy body dementia?

A

hallucinations

163
Q

If a patient has a down and out eye, what cranial nerve is affected and which artery is the stroke in?

A
  • oculomotor (III)

- posterior communicating artery

164
Q

What is gold standard Dx for guillan barre syndrome?

A

LP and CSF for antibodies

165
Q

What cancer can cause cauda equina?

166
Q

What is riluzole used in?

A

ASL. Prevents too much glutamate production

167
Q

What is ropinirole?

A

MAO-B inhibitor. Parkinsons tx

168
Q

What cranial nerve is responsible for down and out eyes?

169
Q

What CN is responsible for double vision?

170
Q

What are cafe-au-lait presentation of?

A

neurofibromatosis

171
Q

What is the most common cause of meningitis in neonates?

A

streptococcus aeruginosa

172
Q

What is the tx for GBS?

A

IV immunoglobulins

173
Q

What is chorea treatment?

A

Risperidone

GI P2a (12 decks)

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