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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

Mean onset of Parkinson’s

A

45-60

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2
Q

Pathology of Parkinson’s

A

Loss of dopaminergic neurons in the basal ganglia - substantia nigra. Surviving nuerons have aggregations of protein (a-synuclein) called Lewy bodies

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3
Q

Course of Parkinson’s

A

Slowly progressive disease with degeneration of neurons, without remission. 10-15 years

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4
Q

Triad of symptoms in Parkinson’s

A

Bradykinesia, tremor and rigidity (cogwheel). Power and sensory remain normal

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5
Q

Describe the gait seen in Parkinson’s

A

Slow shuffling steps, reduced arm swing, difficult to get started, stopped, narrow based

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6
Q

Other symptoms of Parkinson’s

A

Slow monotonous speech, mask like face, reduced blinking, agnosia, depression, dementia, hallucinations, violent dreams, handwriting smaller and spidery

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7
Q

Which drugs can cause Parkinson’s symptoms

A

Dopamine antagonists - Neuroleptics, metoclopramide, phenozanthines

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8
Q

Drug treatment of Parkinson’s

A

Levodopa - precursor of dopamine that can cross the BBB, short half life so usually given with carbidopa to prolong this

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9
Q

Side effects of l-dopa

A

Decreased efficacy over time, psychosis, compulsive behaviour, nausea, dyskinesia

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10
Q

Other drugs used in Parkinson’s

A

Amantadine - adjunct to ldopa

Anticholinergics - in pts on antipsychotics

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11
Q

How do you distinguish migraine from TIA

A

TIA - sudden onset, maximum deficits immediately, headache rare

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12
Q

Causes of migraine

A 
Chocolate
Hangover
Orgasm
Cheese/caffeine
Oral contraceptive
Lie ins
Alcohol
Travel
Exercise

Stress, puberty, menstruation, pregnancy

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13
Q

Clinical features of migraine

A

Visual aura - lines, scotoma, techopsia, 15-60 mins, reduced blood flow to occipital cortex
Throbbing, photophobia, unilateral, nausea and vomiting, heightened pain, no neuro signs

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14
Q

Pathology of migraines

A

Dilation and construction of cerebral vessels

Oligaemia causes aura then hyperaemia causes pain

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15
Q

Treatment of migraine

A

Analgesia, antiemetic if needed
Anticonvulsants eg lamotrigine
rebreathing into paper bag

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16
Q

Prophylaxis of migraine

A

Pizotifen, propranolol, amitriptyline

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17
Q

Tension headache

A

Bilateral, pressure throbbing, rubber band, no neuro signs, no vomiting. Caused by stress, fumes, visual stress

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18
Q

Cluster headache

A

M:F 5:1, episodic intense unilateral pain often behind eye for 30-90 mins. Wakes up from sleep, lacrimation and bloodshot

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19
Q

Treatment of cluster headache

A

100% oxygen, s/c sumatriptan

Prophylaxis verapamil, corticosteroids

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20
Q

Temporal arteritis

A

Inflammation of walls of arteries, vessels harden, pulse lost, scalp may be red.
Claudication of jaw, visual loss, scalp tenderness

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21
Q

Investigations in GCA

A

Raised ESR, low albumin, increased gamma GT, temporal artery biopsy - before or within 7 days of starting steroids
Intimal hypertrophy and inflammation

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22
Q

Treatment of GCA

A

Corticosteroids - prednisolone
Calcium and vitD while of steroids
Don’t use NSAIDS

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23
Q

Which disease if GCA associated with

A

Polymyalgia rheumatica

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24
Q

What is huntingtons disease

A

Autosomal dominant disorder that shows full penetrance

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25
Q

Genetics of Huntington’s

A

Defect in chromosome 4, Normal gene codes for glutamine, CAG repeats, 36-40 disease exists, 40+ full penetrance. Length of repeat determines disease severity and onset

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26
Q

Pathology of huntingtons

A

Cerebral and caudate nucleus/corpus striatum atrophy due to loss of GABA-nergic and cholinergic neurons

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27
Q

What would you see on imaging in HD

A

Squaring of ventricle edges - boxcar ventricles where caudate nucleus has atrophied

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28
Q

Presentation of HD

A

35-50, sporadic -> progressive

Chorea, agitation, dementia +_ seizures, death

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29
Q

What is chorea?

A

Involuntary short sharp muscle movements

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30
Q

Treatment of HD

A

Supportive, genetic testing for family, counselling

Antipsychotics can help reduce chorea and agitation

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31
Q

What is Guillain-Barré syndrome

A

Acute, inflammatory demyelination get polyneuropathy which typically comes on several weeks after a viral infection, also causes by HIV

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32
Q

Clinical features of Guillain Barre

A

Always motor and sometimes sensory, ascending symmetrical muscle weakness, buckle knees, progresses over 4 weeks, pain common, proximal muscles more affected, can affect cranial nerves and resp, autonomic signs

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33
Q

Pathology of GB

A

Viral infection causes production of autoimmune antibodies against peripheral nerves, myelin damaged leading to transmission reduced/blocked

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34
Q

Investigations and results in Guillain barre

A

LP - increased protein in CSF, WCC normal

Nerve conduction slowed

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35
Q

Treatment of Guillain barre

A

Intubate if necessary, maintain resp function, IV immunoglobulin, don’t use corticosteroids, plasmapheresis removes antibodies

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36
Q

Mechanism of subarachnoid haemorrhage

A

Rupture of blood vessel/aneurysm, berry aneurysm

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37
Q

Mechanism of subdural haemorrhage

A

Bridging veins, trauma could be minor and months ago, acute and or chronic, often in elderly due to cerebral atrophy

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38
Q

Mechanism of extradural

A

Direct moderate/severe trauma, typically around the eye causing fracture of parietal or temporal bone resulting in laceration of middle meningeal artery/vein

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39
Q

Describe the pain in subdural haemorrhage

A

Sudden onset, painful, usually back of head

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40
Q

Describe the pain in subdural haemorrhage

A

Possible minor dull headache

41
Q

Describe the pain in extradural headache

A

Likely severe pain but not sudden onset

42
Q

Describe the difference in consciousness in different brain haemorrhages

A

Subarachnoid - impaired quickly
Subdural - fluctuating over weeks/months
Extradural - initial lucid period followed by impaired consciousness

43
Q

Investigations and results in subarachnoid

A

CT shows star shaped bleed, LP xanthochromia in CSF (12 hours)

44
Q

Difference on imagine between subdural and extradural haemorrhage

A

Subdural - crescent shaped, midline shift

Extradural - lens shaped, biconvex, LP contraindicated

45
Q

Management of haemorrhages

A

Subarachnoid - clipping/cooking of aneurysm, nimodipine
Subdural - Burr hole/craniotomy
Extradural - surgery to evacuate blood and linage bleeding vessels

46
Q

What is motor neurone disease

A

Progressive degeneration of motor neurons in the motor cortex and spinal cord, affecting upper and lower motor neurons

47
Q

Features of amyotrophic lateral sclerosis

A

75% of cases, LMN and UMN in same muscle (fasciculations, wasting and hyperreflexia), progressive weakness and wasting of the limbs

48
Q

Features of progressive bulbar palsy

A

Speech and swallowing problems, bulbar and pseudobulbar signs

49
Q

Epidemiology of MND

A

5 per 100,000, male predominance, mean onset 60, 5 year survival from diagnosis <10%

50
Q

Potential causes of MND

A

Aging, genetics, chemicals, biochemical - associated with hyperparathyroidism

51
Q

Pathology of MND

A

Oxidative damage, aggregation of protein inside cell, glutamate problems, apoptosis, prolonged caspase activity

52
Q

Clinical features of MND

A 
Usually no pain
Muscle weakness and wasting usually at extremities
Fasciculations
Cramps
Dysphagia, dysarthria, choking
Eye movements spared
Reflexes lost/increased 
Dementia - frontotemporal  
NO SENSORY LOSS/SPHINCTER
DISTURBANCE
53
Q

Diagnosis and investigations in MND

A

Clinical diagnosis
EMG - denervation and fibrillation
Bloods - elevated CK due to muscle breakdown

54
Q

Drug therapies in MND

A

Riluzole - increases survival by 3-5 months
Baclofen - reduce spasticity
Amitriptyline - helps drooling

55
Q

What is myasthenia gravis

A

Acquired autoimmune condition

56
Q

Which receptors do the antibodies attack in myasthenia gravis

A

Nicotinic Acetylcholine receptors (AChR)

57
Q

Which muscles is mysathenia gravis likely to affect

A

Ocular, bulbar and proximal skeleton

58
Q

What is a key symptom of myasthenia gravis?

A

Fatiguability

59
Q

Which 2 groups of people are more susceptible to myasthenia gravis

A

Women 20-35 and men 60-75

60
Q

Pathology of myasthenia gravis

A

IgG autoantibodies attack the post synaptic AChR receptor at the neuromuscular junction

61
Q

What other pathologies is myasthenia gravis associated with

A

Diseases of the thymus - hyperplasia, thymoma

62
Q

Signs and symptoms of MG

A 
Crises and remittance 
Muscle fatigue and weakness
Ocular - Ptosis, diplopia
Bulbar - dysphagia, dysarthria
Proximal - shoulders, thighs
Axial - neck, trunk, resp
63
Q

How can you elicit fatiguability

A

Ask the pt to repeat a movement for 30-60s

Report that their symptoms get worse as day goes on

64
Q

Is their sensory disturbance in MG?

A

No, and no muscle wasting unless sever disease

65
Q

How do you test for myasthenia gravis

A

TENSILON test
Edrophipnium - prevents breakdown of ACh and atropine to prevent cardiac s/e
Within seconds dramatic improvement

Serum ACh antibodies positive, other autoantibodies likely present

Electromyography, CT/MRI thymus, spirometry

66
Q

Management of MG

A

Pyridostigmine - oral anticholinesyersae inhibitor

67
Q

What is Multiple Sclerosis?

A

An autoimmune inflammatory condition that affects the oligodendrocites of the CNS

68
Q

Mean age of onset of MS

A

20-45, twice as common in females

69
Q

What are oligodendrocites?

A

CNS equivalent of Schwann cells

70
Q

Pathology in MS

A

Destruction of myelin and axonal loss. Macrophages cannot normally cross BBB but in MS they exhibit a glycoprotein allowing them to cross. Plaques are sites of inflammation - common at optic nerves, brainstem and cerebellar connections. Conduction loss causes symptoms

71
Q

4 patterns of progression

A

Relapsing remitting
Primary progressive
Secondary progressive
Progressive - relapsing

72
Q

Clinical features of MS

A

Optic neuropathy, optic disc swelling
Sensory signs
Autonomic defects - urinary incontinence, constipation, sexual dysfunction
Fatigue

73
Q

What is Uthoff’s phenomenon?

A

MS symptoms are worse in heat - bath, exercise, weather due to heat slowing conduction

74
Q

What is Lhermitte’s sign?

A

On voluntary flexing of the head there is electric sensation travelling down spine and into limbs

75
Q

Investigations and results in MS

A

MRI - definitive - plaques
Visual evoked potential - delayed response
Oligoclonal bands on CSF

76
Q

Diagnosis of MS

A

Lesions disseminated in time and place

77
Q

Acute management of MS relapse

A

Steroids - methylprednisolone

To induce remission, shouldn’t use more than twice a year

78
Q

Managing MS - preventing relapse

A

B-interferon - doesn’t alter long term outcome - reduces relapse rate
Natalizumab - monoclonal antibody

79
Q

Conservative management of MS

A

Treat infections promptly, physio, cannabis? Avoid pressure sores

80
Q

2 non motor symptoms of Parkinson’s

A

Anosmia, depression, dementia (lewy body), REM sleep disorder

81
Q

What is trigeminal neuralgia?

A

Paroxysms of intense stabbing pain, lasting seconds, in the triennial nerve distribution. Brought on by.. washing face, cold wind, eating

82
Q

Treatment of trigeminal neuralgia?

A

Carbamazepine first line, surgery if unresponsive

83
Q

Define seizure

A

Spontaneous uncontrolled abnormal brain activity

84
Q

What is epilepsy?

A

Tendency to have seizures

85
Q

Causes of epilepsy

A

Genetic, development abnormalities, trauma, hypoxia, pyrexia, stroke, metabolic

86
Q

Pathology of epilepsy

A
  • abnormal synchronised discharge of neurones

- seizure threshold lowered, neurones hyperexciteable

87
Q

Triggers of seizures

A 
Sleep deprivation 
Flashing lights
Alcohol (intake and withdrawal)
Drug misuse
Physical/mental exhaustion
Infection
Metabolic disturbance
88
Q

Describe a tonic clinic seizure

A 
Often preceding aura
Tonic phase (10-60s) - rigidity, tongue biting, incontinence, hypoxia/cyanosis
Clonic phase (s-mins) - convulsions, jerking, eye rolling, tachy
89
Q

What is status epilepticus

A

Seizures that last >30 mins or seizures between which consciousness is not recovered
MEDICAL EMERGENCY
Cells swell due to electrolyte imbalance as body isn’t able to meet energy demands

90
Q

How do you treat status epilepticus

A

Acute - rectal/IM lorazepam midazolam
Phenobarbital 2nd line
Phenytoin IV

91
Q

Driving and epilepsy

A

Tell pt to inform DVLA
can’t drive if….
- changed meds in last 6 months
- seizure in last 12 months

92
Q

Drug treatment of epilepsy

A

After 2 fits
First line for partial - carbamazepine
First line for general - sodium valproate
Lamotrigine, phenytoin, phenobarbital

93
Q

What is meningitis?

A

Inflammation of the meninges

Caused by virus (most common) or bacterial (rarer and more severe)

94
Q

Features of meningitis

A

Headache, stiff neck, photophobia, tachy, fever, altered consciousness, vomiting, seizures shock
Bacterial - rash, Petechial and non blanching

95
Q

What is kernigs sign?

A

Flex the hip with knee flexed, positive if spasm of hamstrings

96
Q

What is brudzinkis sign?

A

Passively flex the neck, positive if flexion of hip or knee

97
Q

Causes of viral meningitis

A 
Echovirus
Mumps - rare in UK due to MMR
Herpes - simplex, EBV, chicken pox
Influenza 
Treat symptoms
98
Q

Describe the neuropathy seen in diabetes

A

Peripheral, motor or sensory but usually sensory, LMN only

99
Q

Describe what happens in Brown Sequard syndrome

A

Ipsilateral paralysis and loss of light touch and vibration

Contralateral loss of pain and temp

Phase 3A (2 decks)

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