neuro Flashcards

1
Q

what nerve palsy causes diplopia worse going down stairs of reading?

A

fourth CN

  • usually after bang to head
  • classically noticed when reading a book or going downstairs
  • vertical diploplia
  • tilt head to make vision seem more natural
  • otherwise well
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2
Q

what is the clinical purpose of the corneal reflex?

A

check integrity of CN5 (sensory) and CN7 (motor)

when corneal is touched sensory fibres -> spinal trigeminal nucleus -> facial motor nucleau bilaterally -> orbicularis oculli muscles bilaterally -> blink

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3
Q

what nerve palsy causes horizontal diplopia with the distance between the objects being greater when looking at things far away. and the inability to abduct the eye?

A

CN6

  • no ptosis
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4
Q

what symptoms does 3rd nerve palsy cause?

A

ptosis, diplopia (horizontal), and dilated pupil

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5
Q

what clinical signs suggest damage to the common peroneal nerve (L4-S2)?

A

pt cannot evert, dorsiflex at the ankle joint or extend the digits of the foot

  • common injury if fracture head of fibula or use of a tight plaster cast
  • pt present with footdrop and associated characteristic gait
  • loss of sensation over the dorsum of the foot, and lateral side of the leg.
  • Innervation is preserved on the medial side of the leg (supplied by the saphenous nerve, a branch of the femoral), and the heel and sole (supplied by the tibial nerve, a branch of the sciatic).
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6
Q

what is the underlying molecular pathology behind the different types of dementia?

A
  1. alzheimer’s:
    - most common!
    - cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
    - reduction of Ach reduces neuronal signalling
    - insidious onset, with steady progression
    - loss of short term memory usually early symptom
    - slow disintegration of personality and intelect, eventually affecting all aspects of corticol function
    - decline in language (understanding what is being said), visuospacial skills, apraxia (cant carry out skilled motor tasks) and agnosia (cant recognise objects)
  2. vascular:
    - second most common
    - atherosclerosis in the cerebral arteries
    - stepwise deterioration and decline followed by short periods of stability
    - hx of TIAs and/or other CVD
    - less insidious onset, emotional lability (amygdala), preserved personality
  3. dementia with lewy body:
    - presence of LB
    - fluctuating cognition with pronounced variation in attention and alertness
    - prominent or persistent memory loss may not occur in early stages
    - impairment in attention, frontal, subcorticol and visuospacial ability
    - depression and sleep disorders
    - visual hallucinations, parkinisonism, delusion and transient LOC
    * DON’T GIVE ANTI-PSYCHOTICS*
  4. fronto-temporal dementia:
    - personality changes
    - behavioural changes
    - language problems
    - memories relatively preserved (no hipocampus involvement)
    - younger onset
    * ACHEi are not effective
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7
Q

night terrors, nocturnal enuresis, sleepwalking occur during what stage of sleep?

A

Non-REM stage 3

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8
Q

posterior communicating artery stroke can cause what nerve palsy?

A

third (diabetes mellitus, vasculitis, posterior communicating artery aneurysm, cavernous sinus thrombosis)

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9
Q

bilateral acoustic neuromas are associated with what genetic condition?

A

neurofibromatosis type 2

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10
Q

chiari malformations (where lower part of the brain pushes into the spinal cord) are associated with what kind of spinal pathology?

A

syringomyelia -> a fluid filled cavity, called a syrinx develops in the spinal cord. if not treated can lead to SCI/damage

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11
Q

transient loss of function of a nerve is know as what?

A

neuropraxia

Nerve intact but electrical conduction is affected
Myelin sheath integrity is preserved
Full recovery
Autonomic function preserved
Wallerian degeneration does not occur
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12
Q

what are the muscles that attach to the greater trochanter?

A

Mnemonic for muscle attachment on greater trochanter is POGO:

  • Piriformis
  • Obturator internus
  • Gemelli
  • Obturator externus
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13
Q

what do the following fibres transmit?
C fibres.
A α fibres
A β fibres

A

Slow transmission of mechanothermal stimuli is transmitted via C fibres.
A α fibres transmit information relating to motor proprioception, A β fibres transmit touch and pressure and B fibres are autonomic fibres

Peripheral nociceptors are innervated by either small myelinated (hence fast) fibres (A-gamma) fibres or by unmyelinated (hence slow) C fibres.
The A gamma fibres register high-intensity mechanical stimuli. The C fibres usually register high-intensity mechanothermal stimuli.

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14
Q

after confirmed epilepsy Dx (>2 seizures), what are the treatment options?

A

focal:

  • 1st line = carbamazepine (strong sedating effect and will affect CONTRACEPTION) or lamotrigine
  • 2nd line = sodium valproate or levetiracetam

tonic clonic:

  • 1st = sodium valproate
  • 2nd = lamotrigine or carbamazepine

absent:
- 1st = sodium valproate or ethosuxamide

atonic:

  • 1st sodium valproate
  • 2nd lamotrigine

myotonic:

  • 1st sodium valporate
  • 2nd lamotrigine, levetiracetam, topiramate

infantile spasms:
- 1st line prednisolone and vigabatrin

  • adjuncts: relaxation/CBT/surgical intervention (if epileptogenic focus like hippocampal sclerosis or small low-grade tumour)/ vagal nerve stimulation
  • start with monotherapy and increase to max dose before switching drug. dual therapy if all appropriate drugs have been tried
  • stopping can be considered if seizure free for >2years. decreased slowly over 2-3months
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15
Q

what seizure type may be a sign of lennox-gastaut syndrome

A

atonic seizure

LGS = usually begins between 3 and 5, but can start as late as adolescence. Children may have several different types of seizure with this syndrome. These include tonic (where the muscles suddenly become stiff), atonic (where the muscles suddenly relax), myoclonic, tonic clonic and atypical absences. Atypical absences often last longer than normal absences and are different as a child may be responsive and aware of their surroundings.

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16
Q

what AED is a cause of SJS or DRESS syndrome?

A

lamotrigine

17
Q

what does allodynia and hyperalgesia mean and what syndrome is it associated with?

A

allodynia - lowered pain threshold. non-painful stimuli elicits intense pain
hyperalgesia - normal pain threshold but painful stimuli ellicits intense pain more then usual

both associated with/ almost always present in complex regional pain syndrome

18
Q

what is the first line treatment of trigeminal neuralgia?

A

Carbamazepine in the acute stages (reduces frequency and severity of attacks). SEs = dizziness. will interact with some contraception.

2nd line - phenytoin (can be given IV)

surgery may be treatment of choice in many pt’s

(Once pain is in remission, the dosage should be gradually reduced to the lowest possible maintenance level, or the drug can be discontinued until a further attack occurs)

19
Q

list causes of anterior mediastinal mass on CXR

A

Thymic mass / thymoma
Thyroid mass
Teratoma
Lymph nodes (‘Terrible’ lymphoma or carcinoma)

20
Q

what is the difference between receptive and expressive dysphagia?

A
receptive = cant comprehend instructions
expressive = cant get words out
21
Q

what may an isolated loss of reflex suggest?

A

radiculopathy (‘pinched nerve’)

  • affects only the segment of the nerve
  • e.g. loss of ankle jerk if slipped disc at S1
22
Q

name some stroke mimic

A

MS

seizure

SOL

sepsis

syncope

hypoglycaemia - simple bedside test

migraine - ass with +ve symptoms i.e. aura, stroke is ass with -ve i.e. loss of neurological function

23
Q

what scoring system is used to assess the risk of stroke after a TIA (<24hrs)

A

ABCD2 score

24
Q

what is the management of TIA?

A
  • antiplatlet drugs: if person had a suspected TIA in the last week give 300mg OD of Aspirin for 2 weeks (+PPI) then switch to clopidogrel 75mg OD
  • control CV risk factors e.g. BP, hyperlipidaemia, DM, stop smoking
  • anticoagulation indications: cardiac source of emboli
  • carotid endarterectomy - perform within 2wks of 1st presentation if 70-99% stenosed and op risk is acceptable
  • remember driving prohibition for 1month
  • calculate stroke risk. if >4 must see specialist within 24hrs if <3 in 1 week
25
Q

nice recommend that brain imaging for acute stroke should be performed immediately if any of what are present…

A
  1. indications for thrombolysis or early anti-coag Rx
  2. on anticoagulant Rx
  3. a known bleeding tendency
  4. depressed level of conciousness (GCS <13)
  5. unexplained progressive or fluctuating symptoms
  6. papilloedema, neck stiffness or fever
  7. severe headache at onset of stroke symptoms
26
Q

what severe type of ischaemic stroke has a high mortality rate and why?

A

malignant middle cerebral artery infarct (kills 80%)

  • large extent of ischamic lesion occupying >50% of the MCA
  • at risk of developing odema and elevating ICP
  • if left untreated, oedema compromises blood flow and causes brain herniation
27
Q

what is an important cause of stoke to consider in pts <50y/o?

A

carotid artery dissection

  • commonest in males
  • head and neck trauma is a known precipitating factor.. also aneurysm, HTN, atherosclerosis
  • can be asymptomatic or sudden, severe, persistent neck pain alone. other CFs = ipsilateral headache, face or neck pain, Horners syndrome
  • Dx = CT angiography or MRA
  • Rx = full resolution
28
Q

list key differential diagnoses of tremor

A
  • parkinsons disease
  • MS
  • Huntingtons chorea
  • hyperthyroidism
  • fever
  • medication (e.g. antipsychotics)
29
Q

what is the management of benign essential tremor?

A

No definitive Rx

can try improve symptoms with propanolol (non-selective BB) or primidone (barbiturate anti-epileptic med)

30
Q

define myasthenia gravis

A

AI disorder characterised by presence of nicotinic ACh receptor antibodies and depletion of Ach receptors on the post synaptic side of NMJ

causes gradual worsening of generalised muscle weakness (e.g. slurring of speech, bulbar/ swallowing and chewing/ face and neck), fatigue, SOB, double vision

signs = ptosis, diplopia, orbicularis fatigue, counting to 50 voice fades. tendon reflexes are normal.

exacerbated by pregnancy, hypokalaemia, infection, over Rx, exercise. ASSOCIATED with thymoma (20%. tumour originating from epithelial cells of thymus. benign or malignant)

31
Q

what are the tests for MG?

A

anti-AchR antibodies

EMG studies (muscle response to repetative nerve stimulatio)

ice pack cooling test to affected eye (ptosis improves by >2mm after ice application)

thyroid function test/ CT to exclude thymoma

32
Q

what is the treatment of MG?

A

symptom control with anticholonesterases such as pyrostigmine

immunosuppression with prednisolone is the mainstay of drug Rx. steroid sparing drugs like azathioprine (DMARD) may be used long term

thymectomy - beneficial effect, even in pts without thymoma

33
Q

what is MG crisis and how is it managed?

A

life-threatening weakness of resp.muscles during a relapse (can be difficult to distinguish from cholinergic crisis)

monitor FVC

ventilator support

Rx with plasmapheresis (removes AChr antibodies from circulation) or IV immunoglobulins and identify trigger for relapse (infection/medication etc)

34
Q

what cranial nerves are at risk from damage/lesion of the cerebellarpontine angle?

A

CN V, VI, VII, VIII, IX, X

(e.g. vestibular schwannomas

Progressive sensorineural hearing loss
Gait disequilibrium
Vertigo)

35
Q

what are the common cancers that metastasise to brain?

A

lung
breast
colorectal
prostate

36
Q

what is the pharmacological treatment of the following pituitary tumours:

  1. prolactin secreting
  2. GH secreting
A
  1. bromocriptine

2. somatostatin analogues e.g. ocreotides

37
Q

what can the edrophonium test aid in the diagnosis of?

A

myasthenia gravis

38
Q

list SEs of sodium valproate

A

hepatotoxicity, gastrointestinal symptoms (nausea, vomiting), hair loss and tremor. Hepatotoxicity is particularly important as it typically occurs in the first 6 months of treatment, and is rarely associated with fulminant liver failure and death