Neuro Flashcards

1
Q

what differentiates between stroke and TIA?

A

Stroke, symptoms lasting for > 24 hours

TIA, symptoms lasting < 24 hours

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2
Q

what is crescendo TIA

A

> 2 TIA in 1 week

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3
Q

aetiology of ischaemic infarction

A

small vessel occlusion or thrombosis in situ
cardiac emboli –> AF, endocarditis
atherothoromboembolism eg carotids
vasculitis

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4
Q

aetiology of haemorrhagic infarction

A

CNS bleeding –> HTN, ruptured aneurysm, anticoagulation, thrombolysis

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5
Q

what are some rapid recognition screening tools which can be used to identify stroke

A

in primary care - FAST - face, arm, speech, test (any focal neuro loss)

in ER - ROSIER

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6
Q

what are the different types of stroke according to oxford/Bamford classification for ischaemic stroke

A

total anterior circulation syndrome
Partial anterior circualtion syndrome
Posterior circulation syndrome
Lacunar syndrome

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7
Q

what are the criteria for total anterior circulation syndrome

A

must have all 3

1) unilateral weakness +/- a sensory deficit of face, arm or leg
2) homonymous hemianopia
3) high cognitive unction - dysphagia, visuospatial disorder

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8
Q

what are the criteria for partial anterior circulation syndrome

A

must have 2

1) unilateral weakness +/- a sensory deficit of face, arm or leg
2) homonymous hemianopia
3) high cognitive unction - dysphagia, visuospatial disorder

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9
Q

what are the criteria for posterior circulation syndrome

A

1 of the following:
cerebellar or brainsteam syndrome - Webner’s syndrome etc
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
loss of consciousness
isolated homonymous hemianopia
Conjugate eye movement disorder – gaze palsy
Cerebellar dysfunction – ataxia, nystagmus, vertigo

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10
Q

clinical features of TIA

A
•	Suspect TIA if sudden onset focal neurological deficit which has completely resolved within 24 hrs
	Unilateral weakness or sensory loss.
	Dysphasia.
	Ataxia, vertigo, or incoordination.
	Syncope.
	Sudden transient loss of vision in one eye (amaurosis fugax). 
	Homonymous hemianopia.
	Cranial nerve defects.
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11
Q

clinical features of stroke

A

o Weakness − sudden loss of strength in the face or limbs.
o Sensory loss – paraesthesia or numbness.
o Speech problems such as dysarthria.
o Visual problems – normally homonymous hemianopsia
o Dizziness, vertigo or loss of balance — isolated dizziness is not usually a symptom of TIA.
o Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosis).
o Inattention/neglect
o Confusion, altered level of consciousness and coma.
o Difficulty with fine motor co-ordination and gait.
o Neck or facial pain (associated with arterial dissection).
o Initially flacid and no reflexes then Spasticity +/- clonus, ↑ tendon reflexes
o Weakness in extensors of arms and flexors of legs = hemiplegic gait – UMN lesion
o Posterior circulation strokes:
 Acute, persistent continuous vertigo
 Dizziness with nystagmus
 N+V
 Head motion intolerance
 New gait unsteadiness

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12
Q

what are the criteria for Lacunar syndrome

A

1 of the following

  • unilateral weakness +/- sensory deficit of face and arm and leg or all 3
  • pure sensory stroke
  • ataxic hemiparesis
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13
Q

what are some differentials for stroke

A

Bell’s palsy - don’t have forehead sparing

migraines - with aura, aura without headache etc

Metabolic causes - hypo/hypergycaemia, hypocalcemia

MS
epilepsy
blackouts/syncope
subdural haemorrhage (trauma-related)

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14
Q

what are the criteria for immediate CT head (next available slot or within 1 hour)?

A
  • indications for thrombolysis or early anticoagulation treatment
  • on anticoagulant treatment/known bleeding tendency
  • GCS < 13
  • unexplained progressive or fluctuating symptoms
  • papilloedema, neck stiffness or fever
  • severe headache at onset of stroke symptoms
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15
Q

what is the management of an ischaemic stroke

A

thrombolysis with altepase (IV) - within 4.5 hours of symptoms onset

CT head again at 24 hours after alteplase

aspirin 300mg from Day 2 for 2 weeks

SALT team involvement for swallowing assessment

early mobilisation

screen for malnutrition

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16
Q

what happens if alteplase cannot be given

A

300mg aspirin for 2 weeks

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17
Q

what specialist managements are there for stroke

A

maintenance or restoration of homeostasis

  • O2 if stats < 95%
  • BM between 4 -11
  • IV insulin and glucose for DM pts
  • antihypertensive therapy only in hypertensive emergency
  • consider BP reduction to 185/110 to lower
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18
Q

Pharmacological management of ischaemic stroke

A

aspirin 300mg for 2 weeks from alteplase then switch to clopidogrel 75mg long-term

statin - start 48 hours after alteplase if not already on it

warfarin/dabigatran if potential causes of cardiac thromboembolism (AF, prosthetic valves)

defer antihypertensive for 1-2 weeks as inc BP can be physiological

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19
Q

what are some management for hemorrhagic stroke which can be carried by the neurosurgeons?

A

decompressive hemicraniectomy for MCA infarct

intracerebral haemorrhage - surgery for hydrocephalus, combination of prothrombin and Vit K in patients on anticoagulants

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20
Q

definition of meningitis

A

viral or bacterial infection to the meninges of the brain

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21
Q

what is the bacterial cause of meningitis in neonates

A

Listeria

Group B streptococcus

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22
Q

what is the bacterial cause of meningitis in infants/young children

A

H.influenza

strep. pneumoniae

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23
Q

what is the bacterial cause of meningitis in adult

A

strep. pneumoniae

Neisseria meningitis

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24
Q

what are some viral causes of meningitis

A

herpes
enterovirus
varicella zoster

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25
Q

clinical features of meningitis in children and adult

A

headache
fever
N+V
photophobia
neck stiffness
altered consciousness - confusion
seizure
• focal neurological signs  non-reactive pupil, abnor of ocular motility, abnor visual fields, gaze palsy, arm or leg drift
• non-blanching rash  meningococcal meningitis
• Kernig’s sign – pain in lower back or back of thigh on extension of knee when hip is flexed at 90 degree
• Brudzinski’s sign – forced flexi of the neck elicit a reflex flexion of the hips

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26
Q

clinical features of meningitis in neonates and babies

A

non-specific signs and symptoms - hypotonia, poor feeding, lethargy, hypothermia, bulging fontanelle

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27
Q

investigation for meningitis

A
LP + blood culture (prior to abx)
blood glucose
pneumococcal and meningococcal PCR 
FBC, U&E, CRP, LFT, Clotting, VBG
viral PCR 
serum HIV
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28
Q

what does the lumbar puncture show if bacterial meningitis

A
cloudy appearance 
inc protein 
reduce glucose 
inc WCC and neutrophils dominant 
culture - usually +ve
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29
Q

what does the lumbar puncture show if viral meningitis

A
clear appearance 
normal protein level 
normal glucose level 
inc WCC lymphocytes 
usually can not be cultured
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30
Q

management of meningitis

A

if discovered in the community –> IV/IM benylpenicillin
< 1 year - 300mg
1-9 years - 600 mg
> 10 - 1200mg

if discover in the hospital
< 3 months - cefotaxime + amoxicillin (cover listeria contracted during pregnancy from mother)

> 3 months - ceftriaxone or cefotaxime

Dexamethasone for 4 days can help reduce inflammation and preserve hearing in children

• Single dose ciprofloxacin for close contact within 7 days prior to the onset of symptoms.

public health notifiable

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31
Q

what prophylaxis do you provide with those who had close contact with a patient who is confirmed to have bacterial meningitis

A

single-dose ciprofloxacin

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32
Q

what is another name for acute confusional state

A

delirium - alternating cognition with a fluctuating course

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33
Q

what is the ICD-10 definition for acute confusional state

A

Aetiology non-specific syndrome characterised by concurrent disturbances of consciousness and attention, perception, thinking, memory, psychomotor behaviour, emotion and the sleep-wake cycle (that is) transient and of fluctuating intensity.

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34
Q

causes of acute confusional state?

A

PINCH ME

pain 
infection 
nutririon/electrolyte imbalance/meatbolic disturbances 
constipation 
hydration 

medications
environmental

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35
Q

RF for acute confusional state

A
  • Age > 65
  • Hospitalisation
  • Dementia
  • Frailty/multiple co-morbidities
  • Significant injuries such as hip fracture
  • Functional impairment (for example immobility and the use of physical restraint’s)
  • Hx of /current excess alcohol use
  • Sensory impairment
  • Poor nutrition
  • Lack of stimulation
  • Terminal phase of illness
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36
Q

clinical features of acute confusional state

A
acute onset 
fluctuating course (lucid interval during day and worse at night) 
2 types - hypoactive/hyperactive 

cognitive/consciousness - clouded, poor concentration, confusion, slow response, memory and language impairment

inattention - person is easily distractible and have difficulty focusing

disorganised thinking

perception - visual and auditory hallucination possible

physical
if hypoactive - more lethargic, reduced mobility, lack interest in daily activities, reduced appetite, become quiet and withdrawn

if hyperactive - increased sensitivity to their immediate surroundings with agitation, restlessness, sleep disturbance, and hyper-vigilance. Restlessness and wandering are common.

social - lack of co-operation with a reasonable request, withdrawal or alterations in communication, mood, and attitude

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37
Q

investigation for acute confusional state

A

initial screening - history (both patient and collateral hix to assess acute onset and fluctuating course)

assess cognition - AMTS

A-E assessment - full assessment looking for signs of infection and any other causes for deirium

confusion bloods- FBC, U&E, LFT, TFT, Ca2+, glucose, B12, folate, CRP/ESR, syphilis

urine dip +/- urine drug screen
review medication charts

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38
Q

management of acute confusional state

A

biological

  • identify any underlying causes
  • supportive management eg hydration, nutrition, address pain, restrict use of catheters
  • antipsychotics or sedation in pt who are aggressive (haloperidol/olanzapine)
  • Benzo for alcohol withdrawal (delirium tremens)

psychological

  • Identify and treat reversible cause e.g. dementia.
  • Supportive: safety, encourage engagement reminders of time, orientation, familiar objects/people, maintain a sleep-wake cycle, calm manner, avoid physical restraints, encourage them to walk.

social -

  • Minimise change and moving of environment.
  • Control environment e.g. single room, quiet.
  • Control disruptive behaviours which may harm other patients
  • No driving until delirium has resolved
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39
Q

definition of subarachnoid hemorrhage

A

bleeding into the subarachnoid space (between the pica and archnoid matter) –> usually result of ruptured cerebral aneurysm

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40
Q

aetiology of subarachnoid hemorrhage

A

rupture of berry aneurysm (circle of willis)

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41
Q

RF for subarchnoid haemorrhage

A
hypertesnion 
smoking 
excessive alcohol consumption 
cocaine use 
female 
45-70 yrs old 
black 
FHx 
sickle cell anaemia 
Av malformation, coarctation of aorta 
PCKD, ehlers danlos, marfans 
neurofibromatosis
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42
Q

clinical features of subarchnoid haemorrhage

A

sudden onset thunderclap headache - occurs during strenuous activity eg exercise/sex

depressed/loss of consciousness

CN3 compression - eyelid dropping, diplopia with mydriasis, orbital pain

papilloedema, retinal bleed

meningism - stiff neck photophobia, N+V

+ve Kernig (extend leg pain) and Brudzinski (bow)

neuro signs - speech changes, weakness, seizures

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43
Q

investigation for subarachnoid hemorrhage

A

non-contrast CT head - if SAH - blood around the circle of willis ie starfish of death

FBC, U&E, LFT, Clotting, BM (hypoglycemia)

ECG - arrythmia, prolong QT, ST segement, tall T-wave

LP - if CT inconclusive & after 12 hours - red cell count high + xanthochromic, 3 samples needed

CT angiography - once confirmed SAH to look for bleeds location for fixation prep

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44
Q

management of SAH

A

A-E assessment, urgent referral to a specialist neurosurgical unit. monitor CNS, BP, pupils, GCS

anaesthetist if GCS < 8

fluid to inc cerebral perfusion (aim system > 160)

nimodipine (Ca antagonist) to dec vasospasm and cerebral ischaemia risk

dexamethason - dec cerebral oedema

analgesia and anetiemtics

antiepileptic - treat seizures

surgery to treat aneurysm - endovascular coiling, Stents, Ballon, clipping

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45
Q

what is the most common complications of SAH

A

hyponatremia - can lead to arrhythmia - cardiac arrest

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46
Q

definition of sub-dural haematoma

A

collection of blood between the dural and arachnoid covering of the brain

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47
Q

aetiology of sub-dural haematoma

A
  • Most common cause = trauma (in both Acute and chronic)
  • Rupture of a cerebral aneurysm (less common)
  • Vascular malformation – AV malformation or dural fistula
  • All of the above  damage to the bridging vein leading to subdural bleeds
  • Common in elderly and alcoholics
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48
Q

what are the different classification of subdural haematoma

A
  • Acute  < 3 days old, diffusely hyperdense
  • Subacute  3-21 days old, heterogeneously hyperdense/isodense
  • Chronic  > 21 days, diffusely hypodense
  • Acute-on-chronic  areas of hyperdensity within hypodense haematoma
49
Q

clinical feaures of subdural haematoma

A
  • Physical signs of trauma
  • Headache – inc intracranial pressure
  • N+V – inc intracranial pressure
  • Diminished eye response  anisocoria (unequal pupil response, can be a sign of brainstem herniation)
  • Reduced GCS
  • Confusion
  • LOC
  • Seizures
  • Loss of bowel and bladder continence
  • Localised weakness
  • Sensory changes
  • Speech or vision changes
  • Otorrhoea – basal skull fracture
  • Rhinorrhoea – basal skull fracture
50
Q

investigation for a subdural haematoma

A

non-contrast CT  banana shaped (crescentic in shape and can cross suture line), density of the lesion = age of haematoma

  • MRI scan  can help to determine the degree of damage
  • Plain skull X-ray  possible skull fracture
51
Q

Mx of acute sub-dural haematoma

A

If < 10 mm size, midline shift < 5mm non-expansile without significant neuro dysfunction
o Observation + monitoring (cerebral pressure monitoring)
o Prophylactic antiepileptics (7 days) phenyton or levetiracetam
o Correct any anticoagulant used eg warfrain
o Lower intracranial pressure  bed head @ 30 degree, adequate analgesia and sedation, hyperosmolar therapy (to draw fluid back into serum), mannitol (osmotic diuretis)

If > 10 mm, midline shift > 5mm or expansile or significant neuro dysfunction
o Surgery  what type of surgery depends on the location of the haematoma  burr hole craniotomy, hemicraniectomy and duraplasty
o All of the other observation, monitoring, prophylactic antiepileptics, lower intracranial pressure

52
Q

managment of chronic haematoma

A
  • Antiepilictics – phenytoin, levetiracetam
  • Elective surgery eg twist-drill craniotomy with coninuous catheter drainage
  • Correction of coagulopathy
  • Lowering intra-cranial pressure
53
Q

definition of extra-dural haematoma

A

• Collecition of blood in the potential space between the dura and the bone. Can occur in the spinal column

54
Q

aetiology of extra-dural haematoma

A
  • Fracutred temporal or parietal bone damaging the middle meningeal artery or vein  blood collecting between the dura and the skull
  • Trauma to the temple
  • Dural venous sinuses
  • Can occur in the spinal olumn – after trauma of epidural anaesthesia or LP
55
Q

clinical features of extra-dural hematoma

A
  • Hx of trauma to the head
  • A lucid period then rapid deterirations  extra-time
  • Headaches
  • N+V
  • Seizures
  • Bradycardia +/- hypertension  inc intracranial pressure
  • CSF otorrhea or rhinorrhoea resulting from skull fracture with a tear of the dura
  • Dec GCS
  • Unequal pupils  anisocoria
  • Facial nerve injury
  • Weakness of limbs
  • Focial neuro deficit
56
Q

investigation for extra-dural hematoma

A

Plain x-ray  can show skull fracture

Cervical spine x-ray  can see the spinal injury and must be excluded

Non-enhanced CT head  lenticular shape (lemon) & & can not cross suture line repeat CT head if any deterioration

Bloods  FBC, U&Es, coag, group & save

57
Q

mx of extradural haematoma

A

If acute  trauma A-E assessment
If subacute  can be treated conservatively + supportive management
If intra-cranial pressure inc  IV osmotic diuretics (mannitol), hypertonic saline, positioning of the patient
Large haematoma + unstable patient  surgery eg burr holes

v.similar to sub-dural haematoma

58
Q

definition of seziure

A

• A transient occurrence of signs and/or symptoms due to abnor excessive or synchronous neuronal activity in the brain’
• Defined by the following
 At least 2 unprovoked (or reflex) seizures occurring >24 hours apart
 1 unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years
 Diagnosis of an epilepsy syndrome

59
Q

what are the different types of epilepsy?

A

general - motor

general - non-motor eg abscence

focal - being aware or impaired awareness

unknow onset

60
Q

causes of epilepsy

A
anoxia 
head injuries  
brain tumors 
infections - meningitis, encephalitis
stroke 
metabolic abnor - eg hypoglycaemia 
genetic and congenital malformations
61
Q

definition of focal epilepsy

A

 Electrical and clinical manifestations arise from one portion of the brain

62
Q

what are the subtypes of focal epilepsy?

A

focal aware

focal impaired awareness

63
Q

clinical features of focal seizures

A

 Either focal aware or focal impaired awareness of seizure
 Movement in one side of the body or one part of the body
 Premonitory sensation or sequence of sensation  more likely to indicate a focal seizures in temporal lobed  fear, epigastric sensation, déjà vu, jamais vu)
 Automatisms  picking at clothes, smacking of the lips

 Can develop into bilateral tonic-clonic epilepsy
 Can have post-ictal focal neuro deficit  Todd’s paralysis, aphasia

64
Q

clinical features of generalized tonic clonic seizures

A

 LOC with tonic (muscle tensing) and clonic (muscle jerking)
 Associated tongue biting, incontinence, groaning, irregular breathing.
 Post-ictal- confused, drowsy, irritable, depressed

65
Q

clinical features of generalized atonic seizures

A

 Indicative of lennox gastaut syndrome
 Aka drop attacks
 Brief lapses of muscle tone
 Last around 3 minutes.

66
Q

clinical features of generalized myoclonic seizures

A

 Sudden brief muscle contraction like a “jump”

 Common in children as juvenile myoclonic epilepsy

67
Q

clinical features of generalized infantile seizures

A

West syndrome

  • 6 months - clusters of full body spasms
  • might draw leg towards chest
68
Q

clinical features of generalized absence seizures

A

common in children
patient becomes blank stares into space and abruptly return to normal
- lasting 10-20 seconds
- most stop having seizures at older ages

69
Q

what are the investigations for epilepsy

A

• 1st seizure not Ix with EEG.
• EEG indicative after unprovoked seizures
o EEG- typical patterns in different forms of epilepsy
• Bloods  BM, FBC, U&Es, urinary drug screen, LP and CSF analysis (evidence of infection)
• CT head – any structural/stroke
• MRI brain: structural abnormalities.
• Can do video/EEG long-term monitoring

70
Q

management of generalised tonic clonic, atonic, myoclonic and absence epilepsy

A

1st line - sodium valporate
2nd line - lamotrigine
3rd line - dual therapy

avoid carbamazepine in myoclonic and absence - can exacerbate the symptoms

avoid sodium valproate in pregnancy, but can continue using it if other meds trailed and failed

71
Q

management of focal epilepsy

A

1st line - carbamazepine
2nd line - sodium valproate
3rd line - dual therapy
4th line - surgery

72
Q

how long do you have to stop driving if you have epilepsy

A

6 months if one-off seizure

1 year if multiple seizures

73
Q

definition of status epilepticus

A

seizure klasting > 5 minutes or > 3 seizures in 1 hour

74
Q

aetiology of status epilepticus

A
low AED dose
stroke 
alcohol 
withdrawal 
anoxic brain injury 
infection 
metabolic disturbances - hypoglycaemia
75
Q

what is the most important thing to do when you see somebody having a seizure?

A

start a timer + call for help + establish IV access if possible

76
Q

management of status epilepticus in the first 0-5 minutes

A

secure airway - semi-prone position, nasoparyngeal airway

start regular monitoring - GCS, pulse, BP, temp, ECG

give high concentration oxygen

give high potentcy thiamine if there is any suggestion of alcohol abuse or impaired nutrition

give glucose if pt is hypoglycaemic

77
Q

management of status epilepticus in the 5-20 minutes

A

if seizures continue, the ngive benzos

  • if in community, buccal midazolam or rectal diazepam
  • if IV access established - 4mg lorazepam stats
  • if no response to 1st benzo after 10-20 minutes, give another dose
78
Q

what are the investigations regimen for status epileptics

in 5-20 minutes

A

bloods - FBC, U&E, LFT, blood gas, calcium, magnesium, CRP, clotting, glucose, anticonvulsant drug levels

establish medical history

request CXR to assess for possible aspiration

request urgent CT head if no previous history of epilepsy or new focal nuerology

79
Q

management of status epilepticus at 20-40 minutes

A

> 30 minutes = satus epilepticus

alert anaesthetist and ICU & consider phenytoin. Senior decision

80
Q

when should you call an ambulance if someone has a seizure in a GP practice

A

5 minutes after 1st dose of Benzo + still seizure

81
Q

what is the most common aetiology of olfactory nerve damage/lesion

A

trauma - impact to the lateral and occipital regions

intracranial space - occupying lesion

82
Q

clinical features of olfactory nerve lesion

A

anosmia

83
Q

what is the most common aetiology of optic nerve damage/lesion

A

ischaemic optic neuropahty

trauma

optic nerve glioma

amiodarone/ethambutol

84
Q

clinical features of olfactory nerve lesion

A

impaired vision

complete transection - ipsilateral blindness and loss of direct pupillary response

85
Q

what is the most common aetiology of oculomotor damage/lesion

A

diabetic cranial mononeuropathy

posterior communication artery aneurysm

86
Q

clinical of oculomotor nerve lesions

A

paralyic squint - adduction weakness

ptosis

the affected eye will have a down and outward appearances

horizontal diplopia - worse when head is turned away from the side of nerve palsy

87
Q

diagnostic test for oculomotor nerve lesion

A

if dilated pupil

  • compressive lesion eg posterior communicating aneurysm
  • MRI imaging

pupillary sparing

  • ischaemic microangiopathy
  • assess for RF of atherosclerosis if no improvement in 3 months –> MRI
88
Q

management of oculomotor nerve lesion

A

if compressive lesion - surgery

posterior communicating aneurysm - endovascular coiling and clipping

89
Q

what is the most common aetiology of damage to trochlear nerve?

A

microvascular damage

Cavernous sinus thrombosis

90
Q

clinical features of trochlear nerve damage

A

affected side –> eyeball drift upward and inward

diplopia

91
Q

function of cranial nerve 5

A

trigeminal nerve

sensory - 3 branches for the 3 areas of the face . afferent arm of corneal reflex

motor - muscle of mastication

92
Q

what is the most common aetiology of damage to trigeminal nerve?

A

inflammation of the nerve

cavernous sinus thrombosis

93
Q

clinical features of trigeminal nerve damage

A

inability to feel in all 3 branches of the face eg opthalmic, maxillary and mandibular region

jaw deviates towards side of the lesion

can get trigeminal neurolgia

94
Q

what is the most common aetiology of damage to abducens nerve?

A

cavernous sinus thrombosis

95
Q

clinical featuers of abducen nerve damage

A

horizontal diplopia

esotropia - affected eye in-turning

96
Q

what is the commonest facial nerve damage/lesions

A

trauma

Bell’s palsy - viral infection leading to temporary dysfunctioning of the nerve

97
Q

what is the commonest Vestibulocochlear nerve damage/lesions

A

Lyme’s disease - ticks

98
Q

clinical features of vestibulocochlear nerve damage/lesions

A

sensorineural hearing loss
vertigo
horizontal nystagmus

99
Q

what is the commonest glossopharyngeal nerve damage/lesions

A

often unknown and rarely a mononeuronal damage

100
Q

clinical features of glossopharyngeal nerve damage/lesions

A

loss of gag reflex
loss of carotid sinus reflux

sensory loss soft palate, upper phalanx, posterior 1/3 of tongue

mild dysphagia

101
Q

what is the commonest vagus nerve damage/lesions

A

trauma
DM
inflammation
aortic anuerysm

102
Q

clinical features of vagus nerve damage/lesions

A

gag reflex absent

deviation of uvula away from the the side of lesion

epiglottic paralysis

dysphage

vocal cord paralysis - hoarseness

103
Q

what is the commonest accessory nerve damage/lesions

A

surgeries in the lateral cervical regions

104
Q

clinical features of accessory nerve damage/lesions

A

paralysis of SCM and trapezius

105
Q

what is the commonest hypoglossal nerve damage/lesions

A

tumours

trauma

106
Q

clinical features of hypoglossal nerve damage

A

atrophy and fasciculation of the tongue

tongue deviates towards the side of lesions

107
Q

what are some of the investigations for peripheral nerve injury

A

clinical examination

neurological exmaination of the area/limbs affected eg upper limb neuro exam

CT/MRI - evaluation of causes like nerve tumours, avulsions and focal soft tissue pathologies

nerve conduction studies

108
Q

what are the 2 conditions results from brachial plexus injuries

A

Erbs’ palsy - injury to the upper trunk of the brachial plexus (c5-c6)
 Excessive lateral flexion of the neck, physio,
 Waiters tip position
 Rx: immobilisation in flexion/extension with and abduction brace, physio, surgery

klumpke palsy - injury to lower trunk of the brachial plexus (c8-t1)
 Hyperabduction of the arm/ compression (Pancoast tumour)
 Claw hand
 Rx: splint, physio, surgery.

109
Q

which nerve is damage if infraspinatus and supraspinatues muscle injury

A

suprascapular nerve - limited abduction and abbuction and external rotation of the arm

shoulder instability

110
Q

which nerve is damage if latissimus dorsi and teres major muscle injury

A

thoracodorsal nerve - limited shoulder retarction, impaired adduction and internal rotation of the arm

111
Q

which nerve is damage if serratus anterior muscle injury

A

long thoracic nerve injury - medial winging of the scapula, impaired abduction of the arm

112
Q

which nerve is damage if rhomboid major and minor, levator scapulae muscle injury

A

dorsal scapular nerve injury - lateral winging of the scapula

113
Q

which nerve is damage if gluteus medius and minimus muscle injury

A

superior gluteal nerve injury - paralysis of gluteus medius and minimus, Tension fascia lata –> Inter hip abduction

Positive Trendelenburg sign - lateral pelvic titlt towards the opposite side

114
Q

which nerve is damage if Gluteus maximus muscle injury

A

inferior gluteal nerve - paralysis of gluteus maximus - impaired thigh extension

Standing from sitting position and climbing stairs

Backward lunching gate - Trying to use backwards during the heelstrike face in the lane with a weak hip extension

forward pelvic tilt

115
Q

which nerve is damage if hip flexion is impaired

A

femoral nerve injury - paralysis of quadricep muscle and anterior medial thigh sensation

116
Q

which nerve is damaged if pain and paresthesia on the lateral surface of the anterior thigh

A

lateral femoral cutaneous nerve

117
Q

which nerve is damaged if paralysis of hip adductors

A

obturator nerve - usually due ot pelvic ring fracture

118
Q

which nerve is damaged if paralysis of foot and toe extensor (dorsiflexor)

A

common peroneal nerve injury - paralysis of foot and toe extensor (dorsiflexors) - foot drop - high-steeping gait

impaired pronation of the foot

119
Q

which nerve is damage if posteriolateral side of the lower leg, the lateral border of the foot and small area under the heel

A

sural nerve injury