Neuro Flashcards

1
Q

A patient has come in to discuss their epilepsy diagnosis. They want to know about SUDEP , their risk and what they can do about it.

A

-discuss lifestyle factors eg alcohol, new medications which may interact incl otcs, sleep hygiene, GI disturbances, importance of adherence to medications

  • explain risk is low but that it is a risk
  • many people have seizures and are complication free
  • aknowledge and legitimise the risk: ‘eg many people worry about seizures, theyre obviously unpleasant’

having seizures is bad

some seizures have complications: rarely this includes serious injury and death

some lifestyle choices impact on seizure frequency

arming patients with information to reduce impact of epilepsy is good.

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2
Q

discuss DVLA requirements of epilepsy. patient has had second seizure in a year

A
  • must inform DVLA
  • license is rebuked but they get it back if they are seizure free for 1 year
  • this includes aura, jerking, and aura, absence etc seizures
  • try to persuade patient, use personal factors eg own and family safety, feeling of guilt if they end up killing someone, void insurance
  • wider public safety
  • criminal offence
  • doctor will need to inform DVLA anyway if they don’t
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3
Q

A 23 year old lady is started on Lamotrigine following her first focal seizure. She is also on the OCP. Explain the drug to her and highlight any points for consideration in the discuss

A
  • takes a brief hx
    -explains why lamotrigine has been chosen and when to take it
  • explain ocp can have reduced effect with lamotrigine
    -explain risk of all aeds with pregnancy
    -explain side effects of Lamotrigine: common : sedation, dizziness, nausea, insomnia,
    rare but important side eggects are allergic skin rash and hypersensitivity reaction.
    -emphasise should seek medical attention if these rarer side effects occur
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4
Q

what is the acute management of status epilepticus?

A

Ensure airway patency if possible - 100% oxygen via rebreathe mask or nasal cannula

1st line: IV Lorazepam or Buccal or IM Midazolam (or other BDZ)
If still continuing then REPEAT BDZ
if still continuing then IV Valproate or IV Phenytoin

After 30 minutes use propofol to stop convulsion and ring ITU and Neuro

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5
Q

A patient presents following their first ever TLOC. They recover well and are able to go home that day. What investigation is most important?

A
  • An ECG
    All patients with TLOC must have an ECG to check for evidence of potentially life threatening cardiac rhythm disturbances (Eg prolonged QT). An EEG is rarely indicated after a first ever seizure and should never be performed in patients who give a history consistent with syncope. In patients who recover fully after TLOC and have no abnormal neurological signs on examination, immediate brain imaging is unnecessary. Such patients do need to be seen in a ‘first seizure’ clinic and MRI brain scanning may well be organised as an outpatient. MRI is far better for spotting small epileptogenic lesions than CT.
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6
Q

what is a febrile seizure?

A

common seizures in childhood. they occur after a high temperature (eg secondary to an URTI)
they can predispose people to seizures in later life
particularly seizures which originate in the temporal lobe as they can cause Mesial Temporal Sclerosis
(scarring and gliosis which is visible on MRI)

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7
Q

when is serum drug monitoring of anti epileptic medication indicated?

A
  • if there are concerns over drug toxicity
  • if there are concerns over compliance /adherence/ poor absorption
  • if there are concerns that another medication may have interacted with the anti epileptic medication and may be causing the drop
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8
Q

what issues are involved in switching anti epileptic mediations?

A
  • pt needs to simultaneously reduce current drug and increase new drug (in order to avoid breakthrough seizures)
  • the new drug may be less effective than the old!
  • potential interactions of the two medications
  • new side effects
  • potential interactions between the new drug and any other medication she may be on ESP contraception OCP
  • implications for driving: if she experienced a break through seizure she would not be allowed to drive … also the DVLA recommend (but don’t legally enforce) that patients do not drive during the changeover period
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9
Q

what implications does epilepsy have on a patient’s hobbies etc

A

best to avoid things such as extreme sports, showers safer than baths, heavy machinery is no no , cant drive,

ultimately , apart from the driving, it is up to the patient to make an informed decision about what level of risk they consider to be acceptable. A doctor or nurse can help them think this through.

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10
Q

what can cause seizures

A
  • poor sleep
  • systemic illness
  • GI upset (poor absorption)
  • alcohol
  • dehydration
  • electrolyte abnormalities
  • blood glucose
  • new medication
  • missing medication (on purpose and by accident)
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11
Q

derangements in which electrolytes can lead to limb weakness?

A
  • calcium
  • magnesium
  • potassium
  • phosphate
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12
Q

what are signs of worsening breathing due to GBS ?

A
  • weak neck
  • worse lying flat
  • worsening GBS signs (limb weakness)
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13
Q

what does an LP in GBS show?

A
  • normal WCC

- high protein

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14
Q

signs of neuromuscular weakness causing resp problems?

A
  • CO2 retention flap
  • neck weakness
  • reduced chest expansion
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15
Q

treatment for GBS

A

-plasma exchange or IVIG

supportive tmt: eg ventilator support & pulse and BP monitoring, DVT prophlaxis (heparin or enoxaparin)

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16
Q

what would the LP look like in a patient with neuropathy secondary to HIV look like?

A

high WCC (probably lymphocytes)

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17
Q

causes for GBS

A
  • EBV
  • CMV
  • Campylobacter Jejuni
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18
Q

what is the most common form of GBS?

A

AIDP

acute inflammatory demyelinating polyradiculopathy

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19
Q

investigations to order in GBS?

A
  • Nerve conduction studies
  • LP
  • LFTs (can get derangement)
  • spirometry
  • antiganglioside antibody
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20
Q

what is brown sequard syndrome?

A

-damage to a hemi section of the spinal cord

21
Q

standard investigation for carpal tunnel?

A

nerve conduction studies

22
Q

what investigations are required to diagnose Bells palsy?

A
  • none

- clinical diagnosis

23
Q

treatment of Bells palsy

A
  • steroids
  • some treat with acyclovir
  • tape eye shut
24
Q

how long does it take to recover from Bells palsy?

A

-may worsen after first few days
4-6 months
recurrence is also low

25
Q

what is Ramsay Hunt syndrome?

A

painful shingles of the facial geniculate ganglion

26
Q

how would you treat a venous sinus thrombosis?

A

anticoagulation

27
Q

what would a lesion in the dorsal columns lead to?

A

sensory ataxia

proprioception and vibration sense loss

28
Q

what leads to an isolated wrist drop?

A

radial nerve palsy

29
Q

where do the dorsal columns decussate?

A

the medulla

30
Q

acute neurology problems are likely to be

A
  • trauma

- vascular

31
Q

subacute neurology problems are likely to be

A
  • infective

- immune

32
Q

relapsing neurology problems are likely to be

A

immune

33
Q

chronic neurology problems are likely to be

A

hereditary
degenerative
neoplastic

34
Q

what is a spastic paraparesis?

A

bilateral UMN signs

35
Q

what are some causes of a spastic paraparesis

A
  • cord compression
  • cord trauma
  • tumour
  • bilateral stroke
  • MS
36
Q

what are some causes of cord compression

A
  • prolapsed intervertebral disc
  • extra dural tumor
  • spondolysis (where osteoarthritic vertebrae impinge on the spinal cord
37
Q

what is spondolithesis

A

where a vertebrae slips over the edge of another and presses on the spinal cord. can cause leg and or back pain

38
Q

what does Vitamin B12 / folate deficiency lead to?

A

subacute degeneration of the spinal cord

  • spastic paraparesis
  • upgoing plantars
  • reduced knee jerk
  • loss of ankle jerks
  • dorsal column loss: loss of vibration sense, sensory ataxia (positive rombergs), loss of joint position sense
39
Q

what could cause a sensory ataxia?

A
-dorsal column loss 
eg syphilis
MS
SCDC (vit b12 /folate def)
-sensory peripheral neuropathy
40
Q

what could cause a peripheral neuropathy

A
sensory
-diabetes
-uraemia (renal failure)
motor
-GBS
-CIDP
-lead poisoning
mixed
-thiamine deficiency
-vitamin b12 deficiency
-alcohol
-vasculitis /SLE
-charcot marie tooth
41
Q

the cauda equina is made up of which nerve roots

A

L2-S5

42
Q

causes of a foot drop

A
  • common peroneal nerve palsy
  • MS
  • vasculitis (mononeuritis)
  • MND
  • L4/L5 nerve root lesion
  • charcot marie tooth
43
Q

features of charcot marie tooth on examination

A
  • peripheral mixed neuropathy
  • foot drop
  • slapping gait
  • pes cavus (high arches) or pes planus (low arch)
  • stork legs (tibialis anterior and peroneal muscle wasting)
44
Q

how can you differentiate between a common peroneal nerve palsy and a L5 radiculopathy?

A

both may present with foot drop
BUT
L5 radiculopathy= back pain & loss of achilles reflex
CPN palsy=painless, ankle reflex preserved, hx compression

45
Q

how would you treat a foot drop palsy?

A

splint

46
Q

which antibody is implicated in neuromyelitis optica

A

NMO antibodies or aquaporin 4 antibodies

47
Q

what is L’Hermittes sign? and what causes it?

A

tingling sensation on flexion and extension of the neck
or
feeling of tightness around the ribcage

spinal cord lesion

48
Q

which conditions can cause cord lesions similar to MS?/ mimick MS

A
  • Sjorgens (Anti Ro/La)
  • Antiphospholipid antibdies (Anticardiolipin)
  • Neuromyelitis optica (longitudinally extensive transverse myelitis)
49
Q

risks with steroid use?

A

GI irritation
AVN femoral head
hyperglycaemia
steroid induced psychosis