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Y4 - Finals Edition > Neuro CBLS > Flashcards

Neuro CBLS Flashcards

1
Q

A 29-year-old woman is brought to A and E by her husband.

She has been convulsing on and off for ~ 45 minutes with partial recovery between episodes.

Her epilepsy, which started four years ago, has never been controlled with medication and this is her third such presentation to A and E in the last six months despite her being on high doses of two anti-epileptic drugs - carbamazepine and levetiracetam.

2 diagnostic possibilities

A
  1. Non-Epileptic status
    • change in mental status or behaviour from baseline, associated with continuous seizure activity on EEG
  2. Convulsive Status Epilepticus
    • seizure > 5mins
    • no recovery in between seizures
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2
Q

How might you distinguish GCSE and NES

Generalised convulsive status epilepticus with non-epileptic status

A
  1. Movement
  2. Cardiorespiratory status
  3. Conscious level

GCSE
- rhythmic clonic jerking
- cyanosis
- deeply unconscious

NES
- arrhythmic flailing, stop start
- pink
- resistance to eye opening
- gaze aversion
- responsiveness during stop phases
- emotional post ictal phase

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3
Q

Who gets PNEAD and why?

PNEAD = psychologically derived non-epileptic attack disorders

A
  • majority are young women wo have experienced abuse in childhood
  • trauma conditions the brain to dissociate and this manifests by somatic symptoms
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4
Q

PNEAD management and role of neurologist

A
  1. Explain to patient symptoms are real but are not due to structural disease in the brain
    • attacks occurring at a sub conscious level
    • over stress may trigger
  2. PNEAD is treatable
    a. neuropsychologist : to identify whether she can connect remote trauma to her current symptomsb. psychiatrist : recommend drug treatment for mood disturbance or anxiety or both
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5
Q

56 M , BIBA, AED

pc: convulsion, fluttering sensation in chest before losing consciousness.

witness: his wife says his puts his hand on his chest, his eyes flicker rapidly and he shakes uncontrollably “like a very bad tremor.”

breathing can be erratic but not cyanosed

hpc: 3rd episode in 1 month

pmh: pacemaker in situ since having an inferior MI nine months previously

likely diagnosis

A

Late onset psychogenic non-epileptic attacks

  • may be triggered by life changing physical health problems
  • patients often have insight into origin of the problem and are responsive to psychological interventions
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6
Q

What are refractory seizures:

A
  • ongoing seizures despite two I.V treatments
  • one of which is a benzodiazepine AND 2nd line treatment within 30 mins
    • HDU / ITU input
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7
Q

STATUS EPILEPTICUS

What if the first dose of Lorazepam doesn’t stop the seizures:

A

Second can be given.

If seizures continue for 15 mins —> 2nd line treatment will be needed

PHENYTOIN (slow infusion with cardiac monitoring)

If seizures continue for 30 mins

  • refractory status —> ITU
    • anaesthesia and sedation
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8
Q

Typical presentation of GBS

A
  1. Symmetrical ascending weakness (feet moves up body)
  2. Reduced reflexes
  3. Peripheral loss of sensation or neuropathic pain
  4. May progress to cranial nerves and cause facial nerve weakness
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9
Q

Criteria for diagnosis of GBS

A

BRIGHTON CRITERIA

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10
Q

Investigations which may support diagnosis of GBS

A
  1. Nerve conduction studies
    • reduced signal through the nerves
    • demyelination leading to acute inflammatory demyelinating poly radiculo neuropathy
  2. Lumbar puncture for CSF
    • raised protein?
    • normal cell count and glucose?
    • rule out infection
      CYTOALBUMINIC DISSOCIATION
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11
Q

Management of GBS

A
  1. IV immunoglobulins
  2. Plasma exchange
  3. supportive care
  4. VTE prophylaxis (PE)
  5. Intubation and Ventilation in respiratory failure
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12
Q

What would be the difference between a patient with classical locked in syndrome and a patient with severe GBS?

A

Locked in syndrome

  • pontine infarction
    • CN3,4 come out of midbrain so vertical movements of eyes preserved
    • pontine controls horizontal eye movements (abducens, CN 6)

Patient would be able to undertake vertical eye movement and eyelid opening (cn3,4)

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13
Q

Who is involved in the neurorehabilitation unit:

A
  1. Occupational therapists
    - upper limb posture, movement, dexterity
  2. Physio
    - supporting weak joint
    - strengthening resp muscles
  3. SALT
    - optimise speech and swallowing
  4. NURSES AND HCA
    - therapy sessions
  5. Psychologist
    - emotional support
  6. Dieticians
    - dietary needs, route of feeding
  7. Rehab doctors
    - oversee the rehab team
    - manage symptoms and medication
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14
Q

Cotton wool spots in eye indicate

A

lack of blood flow to small retinal blood vessels

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15
Q

Key features of Temporal lobe seizures

A
  • with or without impairment of consiousness
  • aura!
  • 1 min (lip, smacking, grabbing, plucking)
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16
Q

Key features of frontal lobe seizures

A

Head / leg movements

Posturing

Post ictal weakness

JACKSONIAN MARCH: patient does not lose awareness

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17
Q

Key feature of seizure in parietal lobe

A

Sensory, paraesthesia

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18
Q

Key features of seizure in occipital lobe

A
  • floaters / flashes
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19
Q

Area of brain which involves comprehension

A

WERNICKES AREA

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20
Q

Management for high blood pressure

A

LABETALOL
- beta blocker
- and acts on alpha adrenoreceptors reducing vascular resistance

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21
Q

Does upper motor neuron lesion have forehead sparing or not?

A

UPPER = forehead sparing

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22
Q

Type of brain aneurysm commonly caused by chronic hypertension

A

Charcot-Bouchard aneurysm

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23
Q

56 Male, HTN, T2DM suddenly declines with severe headache, nausea and intermittent vomiting

key investigations

A

CT brain without 12 hours

  • need to exclude SAH

Thunderclap headache and no blood on CT scan would indicate need for Lumbar puncture after 12 hours:

  • allow haemoglobin ring to metabolised to the yellow coloured bilirubin (xanthochromia)
    • needs to be transported in a light protected container because bilirubin is broken down by UV light
24
Q

What are the principles of management of a patient with confirmed spontaneous subarachnoid haemorrhage?

A

Identify presence of aneurysm with CT Brain

  1. endovascular coil embolization
  2. clipping
25
Q

What are complications of subarachnoid haemorrhage and how might these be managed?

A

Manage complications:
1. SAH —> sympathetic storm —> excess catecholamines being released —> HTN, t.cardias, GI ischaemia (peptic ulcers and bowel infarction)
- NOTE ABOUT HTN: normal autoregulation of cerebrals can be lost hence HTN may be tolerated by clinicians. Hypotension could lead to profound ischaemia and stroke.
- MAP targets in first week of SAH = 80-90mmHg

  1. Hydrocephalus (tx w/ lumbar drain or repetitive LPs)
  2. Hyponatraemia
    - due to SAIDH?
  3. delayed cerebral ischaemia (DCI)
    - VASOPASM
    - blood products —> release of inflammatory cytokines
    - inflammatory response facilitates blood vessel spasm —> spasm reduces further blood loss. However the spasm reduces delivery of blood to the rest of the healthy brain
    - CEREBRAL ISCHAEMIA
26
Q

What is given to prevent vasospasm in brain?

A

calcium channel blocker (nimodipine)

27
Q

Treatment of subdural haematoma

A

In the acute setting

  • acute A-E assessment
  • anti-epileptics (1 week after presentation of SHD)
  1. Trauma craniotomy
    • large opening in the skull to create evacuate the haematoma and relieve the associated mass effect
  2. Decompressive craniotomy
    • bone flap may be left out at surgery.
28
Q

Management of chronic SDH

A

Burr Hole craniotomy with irrigation or twist drill craniotomy with drain placement

29
Q

Differential diagnoses for decline in conscious level

A

AEIOU TIPS

A-alcohol
E-epilepsy
I-insulin
O-overdose
U- uraemia (renal failure)

T- trauma
I - infection (sepsis)
P - psychiatric condition
S - stroke / shock

30
Q

What does the brain require to maintain consciousness?

A
  1. Reticular activating system
  2. Brainstem
  3. Cerebral cortex

Brain requires glucose and oxygenated blood at perfusion pressure of 50-60mmHg

31
Q

Formula for cerebral perfusion pressure:

A

CPP = Mean arterial pressure - Intracranial pressure

32
Q

GCS

A

Motor Response
6 = obeys commands
5 = localises to pain
4 = withdraws from pain
3 = abnormal flexion to pain (decorticate)
2 = extending to pain
1 = none

Verbal response
5 = orientated
4 = confused
3 = words
2 = sounds
1 = none

Eye opening
4 = spontaneous
3 = to speech
2 = to pain
1 = none

33
Q

Uncal herniation management

A

1. URGENT INTUBATION FOR AIRWAY protection
—-> ANAESTHESIA
a) reduces depolarisation of neurons so reduces the energy demand in a situation where oxygen limited.
b) reduces blood supply, reduces intracranial blood volume —> lowers ICP

2. OSMOTHERAPY
—–> Mannitol or hypertonic saline
a) reduce ICP
b) may stimulate v. constriction –> reducing ICP

3. CT scan

34
Q

Commonest cause of extradural haematoma

A

middle meningeal artery

35
Q

Treatment for tonic or atonic seizures

A

M - SODIUM VALPROATE

F - lamotrigine

36
Q

Generalised tonic clonic treatment

A

M = sodium valproate

F = lamotrigine / Leve

37
Q

Focal seizures treatment

A

1st line = Lamotrigine / Leve

2nd line = carbamazepine, oxcarbazepine, zonisamide

38
Q

What AED may exacerbate absent seizures

A

carbamazepine

39
Q

Treatment for absent seizures

A

1st line = ethosuximide

2nd line =
MALE - sodium valproate
FEMALE - lamotrigine

40
Q

Treatment for myoclonic seizures

A

Males - sodium valproate
Females - leve

41
Q

Mnemonic for potentially life threatening headaches

A

SNOOP
S- systemic signs and disorder

N-neurologic symptoms

O- onset new or changed and patient > 50

O- onset in thunderclap presentation

P- papilloedema, pulsatile tinnitus, positional provocation, precipitated by exercise

42
Q

Migraine acute treatment

A

Acute treatment:

Simple analgesia
- Aspirin 900 mg or
- Ibuprofen 400mg or
- Paracetamol 1000 mg

+/- Triptan (Oral sumatriptan first choice)
+/- antiemetic (metoclopramide 10 mg or prochlorperazine 10 mg)

43
Q

Migraine prophylaxis treatment

A
  • PROPRANOLOL
  • TOPIRAMATE (teratogenic)
  • Acupuncture (10 sessions over 5 weeks)
    Not in guidelines
    Candesartan
    Monoclonal antibodies against CGRP
44
Q

Cluster headache management

A

Acute
100% oxygen
Subcutaneous triptan

Prophylaxis
VERAPAMIL

45
Q

Tension type headache treatment

A

Acute treatment: aspirin, paracetamol or NSAID first line

Prophylaxis
- up to 10 sessions of acupuncture over 58 weeks
- low dose amitriptyline

46
Q

Temporal arteritis investigations

A
  • raised inflammatory markers ESR > 50
  • temporal artery biopsy
47
Q

Treatment of temporal arteritis

A

Treatment : ASAP don’t wait for biopsy

If no vision loss → HIGH DOSE PRED
Vision loss→ IV METHYL PRED
URGENT OPTHAL REVIEW

48
Q

Management for trigeminal neuralgia

A
  1. Carbamazepine is 1st line
  2. Failure to respond to treatment or atypical features should prompt referral to neurology
49
Q

Key features of subdural haematoma

A

Key features
- Age
- Trauma
- Fluctuating confusion
- Decreased consciousness
- Anticoag use
- Alcohol use

50
Q

acute subdural haematoma treatment

A
  • trauma craniotomy flap to evacuate haematoma
51
Q

larger acute subdural haematoma w/ mass effect

A
  • decompressive craniotomy
52
Q

chronic subdural haematoma treatment

A

burr hole craniotomy

53
Q

key investigations for subarachnoid haemorrhage

A

non-contrast CT head 1st line

LP if CT normal after 12 hours

54
Q

Management of subarachnoid haemorrhage

A

MX
NEUROSURGERY URGENT REFERRAL
Supportive: rest, analgesia, VTE prophylaxis
NIMODIPINE - stop vasospasm
Surgery - Coil or clipping !

55
Q

Extradural haemorrhage management

A

MX
URGENT NEUROSURGERY REFERRAL

Conservative (<30cm3, minimal midline shift, GCS > 8 w/o focal neurological deficits)
SURGICAL
—> Craniotomy , Burr Holes
—> Ligate / cauterise bleeding source

LUCID INTERVAL

Y4 - Finals Edition (40 decks)

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