Phase 2 Flashcards

1
Q

what does CVA stand for?

A

cerebrovascular accident

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2
Q

a man having recently undergone surgery on his carotids experiences difficulty swallowing and speaking. his tongue deviates to the right slighlty. Which nerve has been damaged?

A

right hypoglossal

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3
Q

a man with a 40 year pack history presents with a 4 week history of a hoarse voice. Which nerve is most likely to have been damaged?

A

recurrent laryngeal

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4
Q

where does the anterior and lateral coricospinal tracts decussate?

A

anterior corticospinal tract decussates at the level it exits the spine
lateral corticospinal tract decussates at the medulla pyramids

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5
Q

what is paraplegia?

A

loss of motor and sensory function of the lower limbs due to a spinal cord injury

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6
Q

what are the key features of a TIA?

A

subacute onset of CNS focal phenomena due to a temporary occlusion of part of the cerebral circulation lasting for less than 24 hours

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7
Q

what is amaurosis fugax?

A

the sudden loss of vision in one eye- caused by an infarct int the retinal artery

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8
Q

where is the thromobus likely to have arised from if the patient presents with contralateral weakness, dysphagia and homonomos hemaiopia?

A

anterior ciruclation of the cerebra has been effected- usually from the carotids

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9
Q

if a patient presents with vomiting, chocking, hemiplegic sensory loss, tinnitus which area of the cerebral ciruclation is likely to have been occluded?

A

posterior circulation

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10
Q

if there is temporary occlusion to the posterior circulation, where is the thrombi likeli to have arisen from?

A

verterbrobasilar system

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11
Q

in huntingtons chorea which areas of the brain are affected by axonal loss?

A

caudate nucleus

basal ganglia

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12
Q

what is the name of the type of stroke which results in small infarcts around the basal ganglia and internal capsule?

A

lacuna infarct

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13
Q

what is papilloedema

A

swelling of the optic disc

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14
Q

which type of receptors do the antibodies in Myasthenia Gravis attack?

A

nicotinic Ach receptors on the post synaptic neurone

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15
Q

which muscles does Myasthenia gravis commonly affect>

A

extra-ocular, bulbar, face and neck, limbs (proximal)

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16
Q

what investigations would you do if suspecting MG

A

Tensilon test: Administer edrophonium (achesterase inhibitor) and observe if the symptoms improve- need to have atropine to hand due to risk of bradycardia.
CT thymus, nerve conduction studies

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17
Q

how does a subdural haemorrhage present on CT?

A

concave / crescent shaped (tends to progress more slowly, but can be acute)

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18
Q

what are 4 bedside tests you can do to asses a subarachnoid haemorrhage?

A
  1. look for papilloedema (swelling of the optic discs)
  2. blood pressure- generally increased
  3. glasgow coma scale- consicousness
  4. pulse and resp rates
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19
Q

describe the typical appearance of a subarachnoid haemorrhage

A

sudden onset thundercalp headache, photophobia, neck stiffness.

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20
Q

what is the first line investigation if you suspect a SAH?

A

CT scan

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21
Q

how might a SAH appear on a ECG?

A

prolongued QT, dysarthrithmias and ST elevation

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22
Q

what score would you use to classify the severity of a subarachnoid haemorrhage?

A

Hunt and Hess score

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23
Q

define a seizure

A

a paroxymal event in which changes in behaviour sensation or cognition are affected by excessive hypersynchronous neuronal discharges in the brain

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24
Q

define epilepsy

A

the recurrent tendendy to seizures

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25
Q

what is staus epilepticus?

A

a seizure which lasts longer than 30 minutes

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26
Q

name 8 causes of epilepsy

A
  1. idiopathic
  2. cortical scarring
  3. tumours
  4. Stroke
  5. SLE
  6. fever/sepsis
  7. alcohol withdrawl
  8. raised ICP
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27
Q

what is the difference between a simple partial seizure and a complex partial seizure?

A

Simple partial seizure= the patient is aware throughout the seizure; there is no post-ictal symptoms
A complex partial seizure= awareness is impaired; most commonly arise in the temporal lobe

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28
Q

name 4 different types of primary generalised seizures

A
  1. absent seizure- brief pause mid-sentence then continues
  2. tonic-clonic; limbs stiffen then jerk, and there is often post-ictal symptoms
  3. myoclonic: sudden jerk of the limb or face or hand
  4. atonic: patient loses all muscle tone and falls to the ground.
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29
Q

a patient experiencing a seizure presents with kicking of the legs, and versive movements of the head and eyes- what part of the brain is the seizure likely to originate from?

A

frontal lobe

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30
Q

a patient experiences tingling and pins and needles (and any other sensory feature) in their fingertips prior to their seizures- which part of the brain is it likely to originate from?

A

parietal lobe

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31
Q

the patient see’s stars and flashes of light prior to a seizure- which lobe is the seizure likely to arise from?

A

occipital

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32
Q

name 4 features which you would expect a patient to experience if their seizure began in the temporal lobe

A

De ja vu aura
dysphagia
automatisms- lip smacking, grabbing, chewing
emotional disturbance- sudden fear, crying, terror
auditory hallucinations- eg hearing music

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33
Q

how do you diagnose epilepsy?

A

MRI/CT to exclude alternative causes

need to have had 2 unprovoked seizures to have a diagnosis

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34
Q

when are epilepsy patients allowed to drive again?

A

when they have been 1 year seizure free

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35
Q

what are the side effects of Valproate? VALPROATE

A
VALPROATE
Appetite increases
Liver failure
Pancreatitis
Reversible hair loss
Oedema
Ataxia
Teratogenicity, tremor
Encephalopathy
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36
Q

why do drugs which block the neuromuscular receptors not have central side effects>

A

they are not lipid soluble and therefore cannot pass the blood:brain barrier

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37
Q

what is the treatment for schizophrenia?

A

dopamine

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38
Q

name 2 side effects of anti achetylcholinesterase inhibitors

A

dry mouth

urinary retention

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39
Q

what drug do you need to give with L-dopa and why?

A

Carpidopa; it inhibits dopa decarboxylase, preventing L-dopa from being converted into dopamine in the peripherise

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40
Q

name a side effect of carbamazepine

A

hyponatraemia

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41
Q

how do benzodiazepines work?

A

they are allosteric modulators, enhancing the binding of GABA to the GABA-A receptor

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42
Q

how do barbituates work?

A

they modulate the Cl- channel permeability enabling hyperpolarisation

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43
Q

what is multiple sclerosis

A

a relapsing and remitting chronic inflammatory disorder due to multiple plaques of demyelination within the CNS. require 2 or more CNS lesions disseminated in time and space. More common away from equator and in female caucasians

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44
Q

name 3 cardinal features of MS and their symptoms and signs

A

optic neuropathy; blurring in one eye, mild occular pain- affecting the trigeminal nerve
Brainstem demylination- facial numbness, dysphagia,
Spinal cord lesions- urinary incontinence, sexual dysfunction, spastic paraparesis

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45
Q

what is urcoffs phenomenon and what condition is it typically seen in?

A

symptoms and signs of MS are worse on a hot day or after exercise- heat slows the conduction in nerve fibres.

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46
Q

name 2 other types of MS other than relapsing and remitting

A

primary progressive- the illness gets worse progressively without any epidoses of marked improvement.
Secondary progressive- intitially starts relapsing and remitting but then becomes continuous without marked improvement

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47
Q

state 2 histological changes may be observed in an active MS lesion

A

demyelination, variable oligodendrocytes loss, hypercellular plaque edge due to infiltration of tissues with inflammatory cells- mainly macrophages

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48
Q

what investigations would you do for MS?

A

MRI of brain and spinal cord- typical lesions are multifocal
Lumbar puncture: may see oligoclonal bands of IgG in the CSF

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49
Q

what is the treatment for MS?

A

acute relapse: methyprednisolone

Maintenance: beta interferon or Nataliluzab if severe

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50
Q

what is rehabilitation?

A

this is the changes that can be made to help the person live with their disease- about setting attainable goals, and providing support for them to reach these goals.

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51
Q

name an anti-spasticity drug which may help with symptoms of MS

A

baclofen

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52
Q

name the organism commonly causing infection which 1-3 weeks later presents with acute paralysis (guillian barre syndrome)

A

CMV or campylobacter pylori

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53
Q

how does guillian barre syndrome commonly present?

A

pain, tingling and numbness, progressive muscle weakness. Temporary progressive paralysis of the legs-arms-face-respiratory muscles!!!

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54
Q

give 4 signs of Guillian barre syndrome

A
  1. abscent reflexes
  2. hypotonia
  3. autonomic dysfunction- arrhythmias, reduced sweating and heat tolerance
  4. altered sensation- paraesthesia
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55
Q

which parts of the brain are affected the most in parkinsons?

A

substantia niagra and basal ganglia

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56
Q

which neurones are lose in parkinsons disease?

A

loss of the nigrostriatal cells

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57
Q

name the 2 protiens often seen within the eosinophilic aggregations in the pars compacta of the substantia niagra

A

ubiquitin and alpha synuclein

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58
Q

name 3 key symptoms of parkinsons disease

A

tremor, rigidity and Akinesia
handwriting becomes very small, pill rolling tremour at rest decreasing with action. Cogwheel rigidity, difficulty initiating movements, slurring dyarthria, depression, postural instability

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59
Q

name 4 signs of parkinsons disease

A

slow shuffling gait, stooping appearance, poor arm swing. Urinary difficulties, dysphagia, dribbling, lead pipe rigidity, difficulty initiating movements

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60
Q

name 2 treatments of parkinsons disease apart from L-dopa

A

Carpidopa (dopadecarboxylase inhibitor- needs to be given with L-dopa to inhibit conversion to dopamine in the peripheries)
MOAB inhibitor- Selegiline
Dopamine agonist- Ropinirole

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61
Q

which part of the brain shows marked axonal loss in huntingtons chorea?

A

caudate nucleus, putamen and basal ganglia

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62
Q

what is the meaning of chorea?

A

dance like jerky quasi-purposive movements flitting around the body

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63
Q

name 4 clinical features of huntingtons chorea

A

jerky involuntary movements- these are relentless and progressive. early onset behavioural changes and irritability progressing to dementia. Dyarthria and dysphagia are also common.

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64
Q

what is the pathology behind huntingtons Chorea?

A

There is a mutation in the huntingtin gene on chromosome 4- shows variable CAG (cysteine, adenosine, guanine) base sequence repeats- the more repeats in the gene the earlier the onset on huntingtons. It causes axonal degeneration and atrophy in the caudate nucleus, putamen and basal ganglia. They end up with aggregations of dompaine within the synapses-stimulation-causing these jerky uncontrollable movements.

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65
Q

what is the treatment of Huntingtons chorea

A

treatment does not prevent progression it is only symptomatic , domamine antagoinst- Terabenazine

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66
Q

what is the prognosis of huntingtons Chorea after diagnosis?

A

death within 10-20 years

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67
Q

name 4 complications of a SAH

A
  1. rebleeding- death
  2. cerebral ischcaemia- due to vasospasm- permanent CNS deficit
  3. hydrocephalus- due to blockage of the arachnoid granulations (resorb CSF)
  4. hyponatraemia
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68
Q

name 2 findings you may see in a lumbar puncture after a SAH

A
  1. xanthochromic fluid- yellow looking due to the break down in haemoglobin after 12 hours of SAH
  2. mononuclear polycytosis secondary do chemical meningitis caused by the degradation products in subarachnoid blood.
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69
Q

why do you need to take 3 samples of LP after a SAH

A

one for virology, one for microscopy and one for biochemistry

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70
Q

why do you need to wait 12 hours after SAH before undertaking LP?

A
  1. to prevent the risk of cerebral herniation through the foramen magnum when LP decreased the ICP
  2. xanthochromic fluid is most commonly found 12 hours after SAH, making the sample collected more sensitive to confirm whether there was a SAH or not.
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71
Q

why might patients experience a sentinel headache prior to the SAH?

A

perhaps due to a small warning leak from the offending aneurysm

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72
Q

what is the pathophysiology of giant cell arteritis?

A

inflammatory granulomatous arteritis of the large cerebral arteries

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73
Q

how might giant cell arteritis present?

A

jaw claudication

tenderness of the scalp, severe headaches, sudden painless loss of vision, malaise, tireness and fever

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74
Q

what investigations might you do for giant cell arteritis?

A

FBC: normocytic anaemia, ESR raised, temporal artery biopsy

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75
Q

what will you see on a temporal artery biopsy in giant cell arteritis?

A

intimal hypertrophy, inflammation of the intima and sub intima, breaking up the elastic lamina, giant cells, lymphocytes and plasma cells in the elastic lamina.

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76
Q

what is the treatment for giant cell arteritis?

A

prednisolone

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77
Q

name a secondary cause of trigeminal neuralgia?

A

compression by anomalous or aneurysmal intracranial vessels/a tumour, MS, causing demyelination.

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78
Q

how might trigeminal neuralgia present?

A

knife like or electric shock like pain lasting seconds in the distribution of the 5th CN. Pain when washing, shaving or a cold wind brushing the face.

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79
Q

what is the treatment for trigeminal neuralgia

A

carbamazipine

80
Q

name 3 causes of cauda equina syndrome

A
  1. slipped vertebral disc (herniation)
  2. Tumours and leisons
  3. trauma to the spine causing pressure on the cauda equina
  4. lumbar spinal stenosis
81
Q

what is cauda equina syndrome

A

acute loss of function below the conus medullaris L1-2

82
Q

how does cauda equina syndrome present?

A

alternating unilateral or bilateral pain radiating down the leg causing asymmetrical and incomplete paralysis of the legs, saddle aesthesia, loss of anal tone on PR, urinary ± bowel incontinence. (lower back pain)

83
Q

how do you diagnose cauda equina syndrome?

A

MRI of the spine

84
Q

how does spinal cord compression present?

A

back pain, spastic paralysis and decreased sensation below the level of compression. Hyper-reflexia may be present

85
Q

what is the pathophysiology of brown sequard syndrome?

A

lateral hemisection of the spinal cord

86
Q

signs of brown sequard syndrome

A

Babinski’s sign

87
Q

symptoms of brown sequard syndrome

A

ipsilateral paralysis at the level of the lesion (corticospinal)- loss of LWN at the level, loss of UMN below the level
ipsilateral loss of fine touch, vibration and conscious proprioception at the level of the lesion (dorsal columns)
contralateral loss of pain and temperature 2 segments down from the lesion (spinothalamic)

88
Q

name 5 differences between UMN lesions and LMN lesions

A

UMN: spastic paralysis, no muscle wasting, no fasciculations, hyper-reflexia, upgoing plantar. LMN: flaccid paralysis, atrophy of muscles, fasciculations, hypo-reflexia (or abscent), normal or absent plantar.

89
Q

how do you distinguish MND and MG?

A

MND never affects eye movements whereas MG does

90
Q

how do you distinguish MND and MS?

A

there is no sphincter disturbance or sensory loss distinguishing it from MS and polyneuropathies

91
Q

What is motor neuron disease?

A

progressive degeneration of lower and UMN in the spinal cord, cranial nerve motor nuclei and within the cortex. It does NOT affect SENSORY!!! NOR THE EYES!!

92
Q

what are the triggers of a migrane? CHOCOLATE

A
CHeese
Oral Contraceptives
Caffeine
alcohOL
Anxiety
Travel 
Exercise
93
Q

what are the symptoms of a migrane

A

unilateral throbbing pain lasting 4hours or more. Can follow a visual of other aura lasting 15-30 minutes. Photophobia, nausea, vomiting are common

94
Q

what is the treatment for a migraine?

A

NSAIDS then amilotriptan

95
Q

prophylaxis of migraines?

A

amitriptyline and propranolol.

96
Q

what is an aura? (epilepsy)

A

part of a seizure in which the patient is aware and may precede its other manifestations. (visual, strange feeling in the gut, smells or flashing lights.)

97
Q

name 5 causes of epilepsy

A
  1. idiopathic
  2. head injury
  3. space occupying lesion
  4. stroke
  5. metabolic disturbances
98
Q

what is status epilepticus?

A

continous seizures without recovery of consicousness lasting 30 minutes or more.

99
Q

what investigations would you do in a patient with epilepsy?

A

EEG, patient and family history
CT MRI to exclude tumours
Drug levels?

100
Q

Name a side effect for each of these drugs: carbamazepine, lamotrigine and sodium valproate

A

Carbamazepine: leucopenia
Lamotrigine: Steven Jonnsons syndrome
sodium valproate: nausea, increased appetite, tetragenicity

101
Q

what is a mononeuritis complex?

A

when 2 or more peripheral nerves are affected by the lesion

102
Q

what are the causes of mononeuritis complex? WARDS PLC

A

Wegeners granulomatosis, Amyloidosis, Rheumatoid, diabetes mellitus, Sarcoidosis, Polyarteritis nodosa, Leprosy and Carcinomatosis

103
Q

what investigations would you do for mononeuropathies?

A

Electromyography

104
Q

give 6 broad causes of polyneuropathies

A
  1. diabetes mellitus
  2. inflammation- sarcoidosis
  3. toxins- lead, arsenic
  4. drugs- alcohol, phenytoin
  5. infection- lyme disease
  6. vasculitides- RA
    nutritional- vit B12 folate deficiencies
105
Q

what would you expect to see in a cranial nerve polyneuropathy?

A

swallowing and speaking difficulties, diplopia- double vision

106
Q

what is the pathophysiology of meningitis?

A

serious infection in the meninges; acute bacterial shows pi-arachnoid congestion with polymorphs, a layer of pus forms.

107
Q

name 3 common bacteria causing meningitis

A

strept pyogenes,

Neisseria meningitidis. Haemophilus inflenxae

108
Q

name 2 signs of meningitis

A
  1. Kernigs sign

2. Petechial rash; due to a viral meningitis (very small red dots on the skin)

109
Q

name the type of gait seen in each of the following conditions: Parkinsons, Cerebellar disease, and stroke

A

Parkinsons: bradykinesic gait: slow shuffling gait, reduced arm swing and freezing at obstacles or doors.
Cerebellar disease: ataxic gait (staggering, unstable)
Stroke: hemiparetic gait (affected side does not move) or marche a petit pas- slow shuffling wide based gait.

110
Q

name 3 complications of menigitis

A
  1. seizures
  2. deafness
  3. reduced IQ
111
Q

name 4 complications of septicaemia arising from meningitis

A
  1. death
  2. coma
  3. shock
  4. septic arthritis
112
Q

what investigations would you do if a patient presents with peripheral neuropathy?

A

FBC, ESR, glucose, U&E, LFT B12, electrophoresis for ANA, ANCA, CXR, urinanalysis, genetic tests, nerve conduction studies to distinguish between demyelination and axonal neuropathies.

113
Q

how might CSF appear with bacterial meningitis?

A

cloudy, elevated neutrophils, high protein and low glucose

114
Q

name 3 differential diagnosis of meningitis

A

encephalitis
septicaemia
subarachnoid haemorrhage

115
Q

name 3 causes of chronic meningitis

A

TB, symphilis, lyme disease

116
Q

name 3 causes of encephalitis

A
  1. Epstein-Barr virus
  2. EBV infection
  3. Coxsackie virus
117
Q

how might encephalitis present?

A

mood change, headache, high fever, drowsiness over hours/days.

118
Q

what is myelitis?

A

this is inflammation of the spinal cord causing paraparesis or tetraparesis (usually due to varicella zoster infection)

119
Q

how might you diagnose and treat HSV encephalitis?

A

MRI of the brain- showing areas of oedema. LP taking CSF sample for cultures (PCR). Treatment IV acyclovir

120
Q

describe 3 neurological complications of tetanus infection

A
  1. jaw lock
  2. sustained muscle contraction
  3. paroxysmal generalised spasms
121
Q

how do you treat a botilun toxin overdose?

A

human or equine antitoxin

122
Q

how might an extradural haemorrhage present?

A

lucid interval; no loss of consciouness after initial trauma, followed several hours later by deteriorating consciousness, severe headaches, vomiting, confusion fits ± hemiparaesis. Breathing becomes deep and irregular

123
Q

name 3 dd for subarachnoid haemorrhage

A
  1. migraine
  2. meningitis
  3. intracerebral bleeds
124
Q

state 3 causes of stroke

A
  1. haemorrhagic
  2. ischaemia
  3. vasculitis, venous sinus thrombosis, aortic dissection
125
Q

how do you distinguish between an anterior and posterior stroke?

A

anterior stroke: hemiplagia, high function disturbance, homonymous hemianopia. posterior stroke: cerebellar dysfunction- dysphagia, dizziness, dystaxia, cranial nerve lesions, cortical blindness

126
Q

what are the differences between Duchenne muscular dystrophy and becker’s muscular dystrophy?

A

Duchenne muscular dystrophy dytrophin gene is abscent- progressive (faster) muscle atrophy than beckers- some of the dytrophin levels are present, but still low; less severe and weakness is only apparent in young adults.

127
Q

what might the blood results show in an individual with duchenne muscular dystrophy?

A

high levels of creatine kinase- released from atrophic muscles

128
Q

what is cerebral palsy?

A

a group of conditions apparent at birth or in childhood with abnormal development of movement and posture causing activity limitation. (defects are non progressive)

129
Q

name 4 causes of cerebral palsy

A

hypoxia, neonatal cerebral haemorrhage, trauma, prolongued seizures. Hypoglycaemia

130
Q

describe features of a tension headache

A

bilateral head pain, like a tight band. Long lasting, from minutes-days. Induced by stress

131
Q

describe the features of a cluster headache

A

excruciatingly painful, attacks in clusters that occur once of 2x daily. typically for 4-12 weeks followed by attack free periods. May have unilateral pain around one eye, associated with lacrimation, lid swelling and facial flushing.

132
Q

what are the features of sinusitis linked to headache?

A

pain above or around the eyes, facial tenderness made worse by bending over. post nasal drip± fever and malaise

133
Q

what questions would you ask about increased ICP?

A

does it get worse when you bend over?
what medications are you taking?
have you experienced any vomitting, blurred vision, seizures.

134
Q

name 4 cancers that commonly metastasise to the brain

A
  1. lung (bronchus)
  2. breast
  3. prostate
  4. kidney
135
Q

where are gliomas normally found?

A

a glioma is a malignant tumour of neuroepithelial origin. Usually in the hemisphere.

136
Q

which cells do neurofibromas arise from and where do they usually occur?

A

schwann cells, normally in the cerebellopontine angle- arising from CN8 nerve sheath

137
Q

what are the 3 general effects of brain tumours?

A

destruction of the brain, increased ICP, shift of the intracranial contents provoking seizures

138
Q

how might you treat cerebral oedema?

A

IV dexamethasone or mannitol

139
Q

what is bells palsy?

A

this is a common acute isolated lesion on CN 7

140
Q

how does bells palsy present?

A

sudden unilateral facial weakness, sometimes with loss of taste in the tongue. Weakness progresses over hours

141
Q

what is the treatment of bells palsy?

A

prednisolone. antivirals in sever palsy

142
Q

name 8 causes of sensorineuronal deafness

A
  1. acoustic neuroma at the cerebellopontine angle
  2. CMV infection in the middle ear
  3. congenital malformation of the cochlea
  4. idiopathic
  5. induced by autoimmune destruction; wegeners granulomatosis
  6. ischaemia to the inner ear
  7. meningitis or a meningioma
  8. physical trauma- damage to the temporal bone or CN8 nuclei
    noise induced; prolongued exposure to loud noise decreases the sensitivity and damages the hair cells
143
Q

name the 2 muscles which influence the vibration of the bones in the ear

A

stapedius muscle and tensor tympani; they contract to protect the ear from very loud noise

144
Q

name 6 causes or polyneuropathies

A
guillian barre syndrome
lead poisoning
renal failure
polyarteritis nodosa
rheumatoid arthritis
HIV infection
B12 deficiency
Alcohol
Phenytoin
Amyloidosis
145
Q

what would you expect to see in a CN3 palsy?

A

“down and out stare”- only the lateral rectus and superior oblique muscles are contracting as the rest of the eye muscles are supplied by CN3

146
Q

what area of the brain connects wernicke’s and Broca’s areas?

A

arcuate fasciculus

147
Q

which enzyme converts L-Dopa/dopamine to inactive precursors?

A

monoamine oxidase

148
Q

what is the complication that may arise if you stop parkinsons drugs abruptly?

A

neuroleptic malignant syndrome- fever, muscle rigidity, altered mental status, impairment in thermal homeostasis and autonomic dysfunction

149
Q

give an example of a high grade glioma

A

anaplastic astrocytoma

150
Q

what is the 2nd most common cancer in children?

A

astrocytoma; 60% occurs in the posterior fossa

151
Q

where are LMN cell bodies located?

A

in the anterior horn of the spinal column and in the cranial nerve nuclei in the brainstem

152
Q

what is a motor unit

A

a single alpha motor neuron which supplies a group of muscle fibres

153
Q

define a seizure

A

a paroxysmal event in which changes in behaviour, sensation or cognitive processes are caused by excessive hypersynchronous neuronal discharege in the brain

154
Q

how might you treat an essential benign tremor?

A

beta blockers, low dose primidone

155
Q

2 risk factors for developing idiopathic intercranial hypertension

A

obesity, tetracycline

156
Q

what treatments could you give for idiopathic intercranial hypertension?

A

CSF shunt, acetazolamide

157
Q

name 2 autonomic features of a cluster headache

A

pstosis, tearing

158
Q

name 2 conservative treatments you would give to a patient with bells palsy

A

tape down eyes at night, lubricating eye drops

159
Q

how might a hemiplegic gait look?

A

arching leg when they walk, wrist held in flexion, thumb tucked under hand. other side (unaffected) is normal

160
Q

name 3 features of neurofibromatosis 1

A

cafe au lait spots
axillary freckling
neurofibromas

161
Q

name 3 contraindications of thrombolysis after a stroke

A

symptoms onset >4.5 hours ago
seizures at presentation
uncontrolled BP
major trauma within the last 2 weeks

162
Q

what does hypominia mean and what condition is it associated?

A

reduced facial expression- parkinsons

163
Q

where are CN nuclie 3-12 found?

A

3,4= midbrain, 5,6,7,8= pons 9,10,11,12= medulla

164
Q

what type of nerves are involved in MND?

A

motor- UMN, LMN there is no sensory involvement. Tongue fasciculations.

165
Q

give 3 presentations which may give MS a better prognosis

A

fewer lesions on MRI
optic neuritis instead of cerebellar involvment
long intervals between relapses
age

166
Q

black curtain descending?

A

amaurosis fugax (temporary unilateral visual loss)

167
Q

what is hypertensive encephalitis?

A

increased BP compromises the blood-brain-barrier causing cerebral perfusion and oedema

168
Q

what factor should be used to determine the survival rate of someone with malignant melanoma?

A

Breslow thickness (thickness of the lesion)

169
Q

how might you treat hypercalcaemia of malignancy?

A

stabilise with IV saline then IV bisphosphonates

170
Q

what is the difference between hemiplagia and hemiparesis?

A

hemiplagia= paralysis of one 1/2 of the body, hemiparesis= weakness on one 1/2 of the body

171
Q

what is Todds paraesis?

A

focal weakness in a part of the body after a seizure

172
Q

give an example of a MOA-B inhibitor

A

selegiline

173
Q

give an example of a dopamine agonist

A

ropinirole

174
Q

give an example of an antiglutaminergic drug used to treat MND

A

RILUZOLE

175
Q

what might you see histologically in a patient with alzheimers disease

A

amyloid plaques and neurofibrillary tangles, lewy bodies

176
Q

what might you want to rule out if someone presents with a headache and a CN3 palsy?

A

posterior comminicating artery aneurysm

177
Q

where is brocas area found and what is its function?

A

found in the dominant frontal lobe, speech production

178
Q

Define pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

179
Q

what is dementia

A

a progressive decline in motor function without the impairment of consciousness

180
Q

how do you diagnose dementia?

A

must have: an acquired loss of higher cognitive function affecting 2 or more cognitive domains, sufficient severity to cause social impairment and occur in a clear consicousness

181
Q

what investigations would you do in a patient with dementia

A

FBC: rule out any electrolyte/ vitamin abnormalities
CT scan; rule out tumour, hydrocephalus
MRI: show level of atrophy in the brain for type of dementia
CSF sample: TAU protein (high in alzheimers) and Abeta42- low in creutzfelt-Jakob disease

182
Q

what protein might you find to be elevated in a CSF sample of a patient with Alzheimers?

A

TAU protien

183
Q

what protein might you find to be low in the CSF sample of a patient with creutzfelt Jakob disease?

A

Abeta42

184
Q

what is the cause of creutzfelt jakob disease?

A

misfolding of the prion protien- infectious to other proteins; causes rapid damage to neuronal cells and spongiform changes (tiny holes) in the cortex. Death within 6 months

185
Q

which artery supplies the occipital lobe?

A

posterior cerebral artery

186
Q

what is the difference between anaesthesia and analgesia?

A

analgesis= pain relief without the loss of consciousness, anaesthesia is pain relief, loss of consciousness and amnesia

187
Q

what is the immediate treatment for an acute onset of MS

A

oral steroids have been show to be effective in immediate treatment

188
Q

what disease modifying drug is used in the treatment of a relapsing and remitting MS?

A

Interferon beta

189
Q

name 4 poor prognostic features in MS

A
  1. onset after the age of 25
  2. cerebellar symptoms at onset rather than optic neuritis or sensory
  3. short interval between relapses
  4. multiple lesions seen on MRI in the cortex and spine
190
Q

name 3 absolute contraindications for thrombolysis in an ischaemic stroke

A
  1. uncontrolled BP
  2. onset of symptoms more than 3 hours (thrombolysis is ineffective after 3 hours)
  3. previous intracranial bleed
  4. head injury in the last 3 months
191
Q

how does spinal claudication present?

A

lower back pain and sciatica on walking. The pain worsens when spine is extended- waslking downhill and improves when flexed- uphill.

192
Q

what is the cause of spinal claudication

A

narrowing of the spinal canal as a result of spondylisis (degenerative disease)

193
Q

does parkinsons disease present with a narrow or wide based gait?

A

narrow

194
Q

what is the 1st line treatment for status epilepticus?

A

Phenytoin loading

195
Q

a patient has experienced a stroke as a result of atrial fibrillation- what secondary prevention measures would you undertake to prevent further strokes from occuring?

A

Anticoagulate with wafarin

196
Q

a patient has experienced a stroke what secondary prevention measures would you take to prevent further strokes from occuring?

A

Antiplatelets- Clopidogrel

197
Q

which areas of the brain are most sensitive to ischaemia?

A

watershed areas between the anterior and middle cerebral arteries- large pyradimal neurones are most sensitive to hypoxic and hypoglycaemic stress