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nicks phase 2a flaschards > neurology > Flashcards

neurology Flashcards

1
Q

what are the clinical features of a TIA?

A
  • carotid territory symptoms- amaurosis fugax, aphasia, hemiparesis, hemianopic visual loss
  • vertobrobasilar territory symptoms- diplopia, vertigo, vomiting, ataxia, hemisensory loss
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2
Q

what are some differential diagnoses of TIA?

A
  • hyoglycaemia
  • migraine aura
  • focal epilepsy
  • hyperventilation
  • retinal bleeds
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3
Q

what is the ABCD2 score?

A 
•	6+ strongly predicts a stroke (35.5% in next week)
o	Age >60yrs old – 1pt
o	BP >140/90 – 1pt
o	Clinical features
	Unilateral weakness – 2pt
	Speech disturbance without weakness – 1pt
o	Duration of symptoms
	>1h – 2pt
	10-59min – 1pt
o	Diabetes – 1pt
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4
Q

how would you treat a patient with a TIA?

A
  • control CV risk- hypertension, diabetes, smoking cessation
  • anti platelet- clopidogrel, high dose aspirin
  • warfarin
  • carotid endarterectomy
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5
Q

what can cause a stroke?

A
  • cardiac emboli
  • atherothromboembolism
  • CNS bleeds
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6
Q

how can you diagnose a stroke?

A
  • CT/MRI
  • CXR- cardiomyopathy
  • cardiac source of emboli- ECG for AF
  • carotid artery stenosis- carotid doppler ultrasound
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7
Q

what is the acute management of a stroke?

A
  • protect airway
  • check pulse, BP and ECG
  • blood glucose
  • CT/MRI
  • thrombolysis- IV altepase
  • anti platelet agents- aspirin
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8
Q

what is a subarachnoid haemorrhage?

A

spontaneous bleeding into subarachnoid space

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9
Q

what can cause a subarachnoid haemorrhage?

A
  • rupture of saccular aneurysms
  • AV malformations
  • idiopathic
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10
Q

where are the common sites for berry aneurysms to occur?

A
  • junction of posterior communicating with the internal carotid
  • junction of anterior communicating with the anterior cerebral artery
  • bifurcation of middle cerebral artery
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11
Q

what signs and symptoms would a patient with a subarachnoid haemorrhage present with?

A

symptoms- sudden occipital headache, vomiting, collapse, seizures
signs- neck stiffness, Kernig’s sign, retinal bleeds, focal neurology

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12
Q

how would you treat a patient who has suffered a subarachnoid haemorrhage?

A
  • nimodipine
  • endovascular coiling
    maintain cerebral perfusion
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13
Q

what is a subdural haemorrhage?

A

Bleeding from bridging veins between cortex and venous sinuses

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14
Q

what’s the most common cause of a subdural haemorrhage?

A

trauma

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15
Q

how does a subdural haemorrhage present clinically?

A
  • symptoms- fluctuating consciousness, sleepiness, headache, personality change
  • signs- raised ICP ,seizures
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16
Q

how would a subdural haemorrhage appear of a CT scan?

A

crescent-shaped collection of blood over one hemisphere

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17
Q

how would you treat a subdural haemorrhage?

A

irrigation/ evacuation- burr hole craniotomy

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18
Q

what is an extradural haemorrhage?

A

accumulation of blood between the bone and the dura, caused by laceration of the middle meningeal artery and vein due to a fractured temporal or parietal bone

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19
Q

how does the shape of an extradural haemorrhage differ from that of a subdural haemorrhage?

A

extradural appears round, subdural appears sickle shaped

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20
Q

how would you treat a subdural haemorrhage?

A

clot evacuation and ligation of the bleeding vessel

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21
Q

what is epilepsy?

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in a part of the brain- seizures

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22
Q

what are the elements of a seizure?

A
  • prodrome- precedes seizure
  • aura- part of the seizure, feeling of deja vu/ flashing lights/ strange smells
  • post-ictal state- after the seizure the patient experiences a headache,e confusion, myalgia and a sore tongue
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23
Q

what are some non-epileptic causes of seizures?

A

trauma, stroke, haemorrhage, raised ICP, alcohol withdrawal, metabolic disturbance, liver disease, HIV, meningitis, encephalitis, fever

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24
Q

what is a simple partial seizure?

A
  • awareness impaired
  • focal motor, sensory, autonomic symptoms
  • no post-ictal symptoms
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25
Q

what is a complex partial seizure`?

A
  • awareness impaired
  • possible aura
  • arise from temporal lobe
  • post ictal confusion
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26
Q

what are primary generalised seizures?

A

simultaneous onset of electrical discharge throughout cortex with no localising features referable to only one hemisphere

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27
Q

what are examples of primary generalised seizures?

A
  • absence seizures
  • tonic-clonic seizures
  • myoclonic seizures
  • atonic seizures
  • infantile spasms
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28
Q

what is an absence seizures?

A

brief pauses less that 10 seconds- e.g. suddenly stopping mid sentence- occur in childhood

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29
Q

what is a tonic-clonic seizure?

A
  • loss of conciousness
  • limb stiffen then jerk
  • post ictal confusion and drowsiness
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30
Q

what is a myoclonic seizure?

A

a sudden jerk of a limb/ trunk/ face

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31
Q

what is an atonic seizure?

A

sudden loss of muscle tone causing a fall with no loss of consciousness

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32
Q

what are some locating features of a temporal lobe seizure?

A
  • automatisms
  • abdominal rising sensation or pain
  • dysphasia
  • deja vu
  • auditory hallucinations
  • delusional behaviour
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33
Q

what are some locating features of a frontal lobe seizure?

A
  • motor- posturing and peddling movements of legs
  • Jacksonian march
  • motor arrest
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34
Q

what are some locating features of a parietal lobe seizure?

A
  • sensory- tingling, numbness, pain

- motor- spread to pre-central gyrus

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35
Q

what are some locating features of an occipital lobe seizure?

A

visual phenomena- spots/ lines/ flashes

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36
Q

how would you treat generalised tonic clonic seizures?

A

sodium valproate or lamotrigine

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37
Q

how would you treat absence seizures?

A

sodium valproate

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38
Q

what is the cardinal triad of symptoms for a patient with Parkinson’s disease?

A
  • tremor- worse at rest, pill rolling of thumb over fingers
  • rigidity/ increased tone- cogwheel rigidity
  • bradykinesia
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39
Q

what can cause Parkinson’s disease?

A
  • idiopathic
  • drugs- e.g. neuroleptics
  • also trauma, encephalopathy, post-flu, copper toxicity, HIV
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40
Q

what is the pathophysiology behind Parkinson’s disease?

A

Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurons in the substantia nigra pars compacta

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41
Q

how can Parkinson’s disease be treated?

A
  • weight lifting
  • levodopa- start late
  • dopamine agonists
  • MAO-B inhibitors
  • deep brain stimulation
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42
Q

what is Huntington’s chorea?

A

an autosomal dominant neurodegenerative disorder that can lead to the progression of chorea and dementia

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43
Q

how does a tension headache present clinically?

A

bilateral, non-pulsatile headache and scalp muscle tenderness with no vomiting or sensitivity to head movement

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44
Q

how does a cluster headache present clinically?

A
  • rapid onset excruciating pain around one eye
  • unilateral pain
  • lasts 15-60 mins
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45
Q

how would you treat a cluster headache?

A

100% O2 for 15 mins via a non-rebreathable mask

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46
Q

how does a migraine present clinically?

A

aura lasting 15-30 mins followed within 1 hour by unilateral, throbbing headache

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47
Q

what can trigger a migraine?

A

chocolate, hangovers, orgasms, cheese, oral contraceptives, alcohol, loud noise

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48
Q

what is the treatment for a migraine?

A

topiramate or propanolol

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49
Q

how does giant cell arteritis present clinically?

A
  • headache
  • temporal artery and scalp tenderness
  • jaw claudication
  • amaurosis fugax
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50
Q

how is giant cell arteritis diagnosed clinically?

A
  • raised ESR and CRP
  • low Hb
  • temporal artery biopsy
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51
Q

how is GCA treated?

A

oral prednisolone

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52
Q

what are some secondary causes of trigeminal neuralgia?

A
  • compression of trigeminal root by a tumour
  • chronic meningeal infection
  • MS
  • herpes zoster
  • skull base malformation
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53
Q

how would a patent with trigeminal neuralgia present?

A
  • paroxysms of intense, stabbing pain, lasting seconds
  • unilateral
  • face screwed up in pain
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54
Q

what can trigger trigeminal neuralgia?

A

washing the affected area, shaving, eating, talking

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55
Q

how you treat a patient with trigeminal neuralgia?

A

carbamazepine or lamotrigine

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56
Q

what is the aetiology of spinal cord compression?

A
  • secondary malignancy in spine- breast, lung, prostate, thyroid, kidney
  • rarer- epidural abscess, cervical disc prolapse, haematoma, myeloma
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57
Q

what are some of the differential diagnoses of spinal cord compression?

A

transverse myelitis, MS, carcinomatous meningitis, spinal artery thrombosis, trauma, dissecting aneurysm

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58
Q

how would you diagnose spinal cord compression?

A
  • MRI

- CXR to look for secondary malignancy or TB

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59
Q

what is cauda equina syndrome?

A

damage to the spine at or distal to L1 injures the cauda equina

60
Q

what can cause cauda equina syndrome?

A

congenital lumbar disc disease, lumbrosacral nerve lesions, lumbar disc prolapse

61
Q

what are the key clinical signs a patient with cauda equina syndrome will present with?

A

back pain, radicular pain down the legs, sensory loss in a root distribution

62
Q

what is the aetiology of MS?

A

discrete plaques of demyelination occur at multiple CNS sites from a T cell-mediated immune response. this demyelination causes axonal loss and clinically progressive symptoms.

63
Q

how does MS present clinically?

A
  • mono symptomatic

- can be unilateral optic neuritis, numbness/ tingling in limbs, leg weakness, ataxia

64
Q

what are some systemic signs of MS?

A
  • sensory- paraesthesia
  • motor- spastic weakness
  • sexual- ED, incontinence
  • GI- swallowing disorders
  • eye- hemianopia, optic neuritis
  • cerebrellum- trunk and limb ataxia
  • cognitive and visuospatial decline
65
Q

how is MS diagnosed?

A

more than 1 CNS lesion disseminated in space and time, with no other attributable cause
- plaques seen on MRI

66
Q

how can you treat a patient with MS?

A
  • vitamin D supplements
  • monoclonal antibodies- alemtuzumab
  • non-immunosuppressives
  • azathioprine
67
Q

what is myasthenia gravis?

A

an autoimmune disease mediate day antibodies to nicotinic acetylcholine receptors. these interfere with the neuromuscular transmission via depletion of working post-synaptic receptor sites.

68
Q

what is the order that muscle groups are affected in in myasthenia gravis?

A

extra-ocular, bulbar, face, neck, limb girdle, trunk

69
Q

how can myasthenia gravis be diagnosed?

A
  • voice fades counting to 50
  • other causes ruled out
  • raised anti- AChR antibodies
  • look for ptosis, diplopia and myasthenic snarl on smiling
70
Q

what are some fo the differential diagnoses of myasthenia gravis?

A

polymyositis, systemic lupus erythematosus, Takayasu’s arteritis, botulism

71
Q

how can you treat myasthenia gravis?

A
  • symptomatic control- anticholinesterase
  • immunosuppression- prednisolone
  • thymectomy
72
Q

what is motor neurone disease?

A

a cluster of major degenerative diseases characterised by the selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells

73
Q

what is the aetiology of MND?

A
  • sporadic

- rare mutations in SOD-1

74
Q

what are the 4 clinical patterns of MND?

A
  • ALS- loss of motor neurones in motor cortex and the anterior horn of the spinal cord
  • progressive bulbar palsy- only affects CN- IX-XII, resulting in jaw jerk, hoarse speech and flaccid tongue
  • progressive muscular atrophy- anterior horn cell lesion only
  • primary lateral sclerosis- loss of betz cells in motor cortex
75
Q

how would you treat a patient with MND?

A

treat symptoms

76
Q

what can cause Gullian- Barre syndrome?

A
  • Campylobacter jejuni
  • CMV
  • Mycoplasma zoster
  • HIV
  • EBV
77
Q

how does Gullian-Barre present clinically?

A
  • advancing muscle weakness

- progressive phase of 4 weeks followed by recovery

78
Q

how would you treat Gullian-Barre syndrome?

A

IV immunoglobulin for 5 days

79
Q

how does dementia present clinically?

A

initial= memory loss over months and years

later- agitation, agression, apathy, hallucinations

80
Q

what is the aetiology of dementia?

A
  • alzheimers dementia
  • vascular dementia
  • Lewy body dementia
  • fronto-temporal dementia
81
Q

how is dementia treated?

A
  • developing routines
  • trazodone
  • lorazepam
82
Q

what is the aetiology of Alzheimers disease?

A

accumulation of beta-amyloid peptide results in progressive neuronal damage and raised numbers of amyloid plaques and a loss of acetylcholine.

83
Q

what are some risk factors of Alzheimers disease?

A
  • first degree relative with the condition
  • downs syndrome
  • vascular- hypertension, diabetes
  • depression
  • loneliness
84
Q

how is Alzheimers disease treated?

A
  • acetylcholinesterase inhibitors

- antiglutamatergic treatment

85
Q

what are some examples of mono neuropathies?

A

Wegener’s, AIDS, rheumatoid, sarcoidosis, leprosy

86
Q

what does a median nerve mononeuropathy present like?

A
  • weakness of abductor policis previs
  • sensory loss of radial 3.5 fingers and palm
  • weakness of flexion of distal phalanx
87
Q

what are the signs of an ulnar nerve mononeuropathy?

A

weakness and wasting of the medial wrist flexors, interossi and medial 2 lumbricals- claw hand

88
Q

what is the key sign of radial nerve mononeuropathy?

A

wrist and finger drop

89
Q

what muscles are involved in a radial nerve mononeuroapthy?

A

brachioradialis, extensors, supinator, triceps (BEST)

90
Q

what can cause brachial plexus mononeuropathy?

A

trauma, radiotherapy, cervical rib, prolonged wearing of a heavy rucksack

91
Q

what can cause phrenic nerve mononeuropathy?

A

lung cancer, myeloma, thymoma, thoracic surgery, HIV, Lyme disease, TB, muscular dystrophy

92
Q

what are the signs of a common peroneal nerve mononeuropathy?

A
  • foot drop
  • weak ankle dorsiflexion
  • sensory loss over dorsum of foot
93
Q

what are the clinical features of carpel tunnel syndrome?

A

oAching pain in hand and arm, especially at night
oParaesthesiae in thumb, index and middle fingers
oAll relieved by dangling hand over edge of bed and shaking it – wake and shake
oSensory loss and weakness of abductor pollicis brevis ± wasting of thenar eminence

94
Q

what can cause carpal tunnel syndrome?

A
  • Myxoedema
  • Enforced flexion – e.g. Colles’ splint
    Diabetic neuropathy
  • Idiopathic
  • Acromegaly
  • Neoplasms e.g. myeloma
  • benign Tumours – lipomas, ganglias
  • Rheumatoid arthritis
  • Amyloidosis
  • Pregnancy/premenstrual oedema
  • Sarcoidosis
95
Q

how can you diagnose carpel tunnel syndrome?

A
  • Phalen’s test- maximal wrist flexion for 1 min

- Tinel’s test- tapping over nerve at wrist induces tingling

96
Q

how can you treat carpel tunnel syndrome?

A

splinting, local steroid injection or decompression surgery

97
Q

what can cause poly-neuropathies?

A
  • metabolic- diabetes mellitus, renal failure
  • malignancy
  • Gullian-Barre, sarcoidosis
  • infections- HIV, Lyme
  • deficiency of B1, B6, B12, E, folate
98
Q

what can cause an olfactory nerve lesion?

A

trauma, respiratory tract infection, meningitis

99
Q

how would a trigeminal nerve palsy present clinically?

A

motor palsy on opening mouth

jaw deviates to side of lesion

100
Q

what would an accessory nerve lesion present as clinically?

A

patient is unable to:

  • shrug shoulders against resistance
  • unable to urn head left or right against resistance
101
Q

what are the types of common brain tumour?

A
  • primary malignant- glioma, lymphoma, medulloblastoma
  • benign- meningioma, neurofibroma
  • metastases- bronchus, breast, stomach, prostate, thyroid, kidney
102
Q

what do the clinical features of a brain tumour result from?

A
  • progressive focal neurological deficit due to mass effect and surrounding oedema
  • raised ICP
  • focal/ generalised epilepsy
103
Q

what is the differential diagnosis of a brain tumour?

A

other intracranial mass lesions- cerebral abscess, tuberculoma, subdural haematoma, intracranial haematoma

104
Q

how is a brain tumour treated?

A
  • surgery- removal of mass
  • radiotherapy
  • oral dexamethasone
  • anti-convulsants
105
Q

what can cause meningitis?

A
  • meningococcus
  • haemophilus influenza
  • listeria monocytogenes
106
Q

how does meningitis present clinically?

A
  • early- headache, leg pains, cold hands

- later- meningism, decreased consciousness, seizures, non-blanching petechial rash

107
Q

what are some differential diagnoses of meningitis?

A

malaria, encephalitis, septicaemia, subarachnoid, tetanus

108
Q

how would you treat a patient with meningitis?

A
  • cefotaxime and ampicillin

- dexamethasone

109
Q

what is encephalitis?

A

inflammation of the brain parenchyma

110
Q

what are the viral causes of encephalitis?

A

herpes simplex, CMV, EBV, VZV, HIV, measles, rabies

111
Q

what are non-viral causes of encephalitis?

A

bacterial meningitis, TB, malaria, listeria, Lyme disease, legionella, typhus, aspergillosis

112
Q

how does encephalitis present clinically?

A
  • confusion
  • decreased GCS
  • fever
  • headache
  • seizures
113
Q

how is encephalitis treated?

A

IV acyclovir

114
Q

what is herpes zoster?

A

occurs after a previous primary infection with chickenpox- the virus remains dormant in dorsal root ganglia- reactivation of this causes shingles

115
Q

what dermatome distribution does shingles present with?

A

rash- papules and vesicles
pain and tingling
occurs in lower thoracic dermatomes

116
Q

how is shingles treated?

A

oral acyclovir/ valaciclovir/ famiciclovir

117
Q

what are some modifiable risk factors of a stroke?

A
  • hypertension
  • smoking
  • DM
  • heart disease
  • PVD
  • OCP
118
Q

how does a cerebral infarct present clinically?

A
  • contralateral sensory loss
  • initially flaccid, becomes spastic
  • dysphasia
  • homonymous hemianopia
119
Q

how does a brainstem infarct present clinically?

A
  • quadraplegia
  • disturbances of gaze and vision
  • locked-in syndrome
120
Q

what does a lacunar infarct affect?

A

basal ganglia, internal capsule, thalamus and pons

121
Q

what are some differential diagnoses of a stroke?

A
  • trauma
  • hypo/hypergylcaemia
  • subdural haemorrhage
  • epilepsy
  • intracranial tumour
  • CNS lymphoma
122
Q

How can a suspected diagnosis of a subarachnoid haemorrhage be confirmed via a lumbar puncture?

A

CSF is bloody early on then becomes yellow due to bilirubin- xanthochromia confirms

123
Q

what is amaurosis fugax?

A

common symptom of a TIA- patient describes visual loss as being ‘like a curtain descending’

124
Q

How is a partial seizure treated?

A

carbamazepine

125
Q

what are some symptoms of Huntington’s chorea?

A
  • irritability
  • depression
  • incoordination
  • chorea
  • dementia
126
Q

How is a tension headache treated?

A
  • stress relief- massage, tricyclic antidepressants

- analgesia withdrawl

127
Q

what can cause a secondary headache?

A
  • meningitis
  • subarachnoid haemorrhage
  • raised ICP
  • idiopathic intracranial hypertension
  • GCA
  • medication over-use
128
Q

how can a medication over-use headache be diagnosed?

A
  • Headache for over 15 days/ month
  • Regular use for over 3 months of a symptomatic treatment drug (e.g. ergotamine, triptans, opioids)
  • Headache has worsened during drug use
129
Q

how can motor neurone disease be differentiated from myasthenia gravis?

A

MND never affects eye movements

130
Q

How can sensory polyneuropathy be diagnosed?

A
  • numbness
  • pins and needles
  • affects extremities first
  • difficulty handling small objects
131
Q

how can motor polyneuropathy be diagnosed?

A
  • weak hands

- difficulty walking and breathing

132
Q

how can cranial nerve polyneuropathy be diagnosed?

A
  • swallowing/ speaking difficulty

- diplopia

133
Q

how do upper motor nerve lesions present clinically?

A
  • no muscle wasting
  • loss of skilled fine finger movements
  • spasticity
  • hyperreflexia
134
Q

how do lower motor nerve lesions present clinically?

A
  • muscle wasting and fasciculation
  • hypotonia
    absent reflexes
135
Q

what can an olfactory nerve lesion cause?

A

anosmia- loss of sense of smell

136
Q

what can an optic nerve lesion cause?

A
  • monocular blindness
  • bilateral blindness
  • bitemporal hemianopia
  • homonymous hemianopia
  • optic neuritis
  • pailloedema
137
Q

how does a palsy of cranial nerve 3 present clinically?

A

ptosis, eye pointing down and out

138
Q

how does a palsy of the facial nerve present clinically?

A

facial droop and weakness

139
Q

how does a palsy of the vestibulocochlear nerve present?

A

problems with hearing, balance and vertigo

140
Q

how does a palsy of the glossopharyngeal and vagus nerve present clinically?

A

gag reflex problems

141
Q

how does a hypoglossal nerve palsy present clinically?

A

Tongue deviates to the side of the lesion

142
Q

what symptoms indicate a medical emergency in a patient with meningitis and what is the treatment offered?

A

2 of headache, pyrexia, neck stiffness, altered mental state

- IV benzypenicillin

143
Q

how does a peripheral polyneuropathy present clinically?

A

ataxia, muscle cramps, weakness, fasciculations, atrophy

144
Q

what is the aetiology of peripheral polyneuropathy?

A
  • infectious- hepatitis, HIV, Lyme
  • vasculitis
  • porphyria
  • toxins
145
Q

how can peripheral polyneuropathy be treated?

A

symptomatic aim

  • pain- amitryptilline
  • cramps- quinine
  • balance problems- walking aids

nicks phase 2a flaschards (15 decks)

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