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Baz Y2 Semester 1 > Week 3 Neurology > Flashcards

Week 3 Neurology Flashcards

1
Q

What is a seizure?

A

Abnormal excessive or synchronous discharge of cortical neurones

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2
Q

What is the difference between focal and generalised seizures

A

Whole brain (generalised seizures)
Part of the brain (focal seizures)

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3
Q

What makes a seizure epileptic?

A

If it is unprovoked

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4
Q

Genetic generalised epilepsy.
Focal onset epilepsy.

Which is a “software” and “hardware” problem?

A

Genetic generalised epilepsy
Software problem

Focal onset
Hardware problem

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5
Q

Three frist line drug treatments for epilepsy

A

Lamotrigine
Levetiracetam
Sodium valproate

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6
Q

What is the reticular activating system?

A

It is located int he brainstem and is responsible for activating consiousness in the cerebral cortex and the diencephalon.

During sleep it inhibits sensory information.

It can be turned off with aneasthetics and damage can result in comas and narcolepsy.

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7
Q

What are the two things you need for conciousness?

A

Arousal - activation of content, originates from reticular formation

Content - requires functioning hemispheres & diencephalon (don’t need both)

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8
Q

What does tonic clonic refer to?

A

Tonic-clonic refers to a specific type of seizure characterized by two distinct phases:

Tonic phase:

The body becomes stiff as muscles contract continuously.
This phase usually lasts for about 10 to 20 seconds.
The person may fall if standing and might cry out as air is forced out of the lungs due to sudden muscle contraction.

Clonic phase:

The muscles go through rhythmic jerking movements, typically involving the arms, legs, and face.
This phase can last from a few seconds to a couple of minutes.

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9
Q

Which part of the nervous system is impaired during coma?

A] Cerebellum

B] Both cerebral hemispheres

C] Reticular activating system in the brainstem

D] Spinal cord

E] Neuromuscular junction

A

B] Both cerebral hemispheres

OR

C] Reticular activating system in the brainstem

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10
Q

Most common causes of coma?

A

Structural lesions 20%
Metabolic 35 %
Drugs & Toxins 25%
CNS infections
Stroke

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11
Q

Which of the following can cause coma?

A] Trauma

B] Sepsis

C] Hypoglycaemia

D] Hypothermia

E] Carbon monoxide poisoning

A

All baby

A] Trauma

B] Sepsis

C] Hypoglycaemia

D] Hypothermia

E] Carbon monoxide poisoning

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12
Q

If there is a focal mass applying pressure and it causes coma where is it likely to be?

A

Could be tumour, haematomas, abscess.

Pressure on and displacement of diencephalon/ brainstem (RAS)

Especially common with posterior fossa masses eg cerebellar haematoma

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13
Q

If there is a mass applying pressure on the brainstem and/or diencephalon causing coma what other features might be present?

A

Focal neurological signs eg hemiparesis in the case of herniation from cerebral hemisphere.

Papilloedema due to general increased cranial pressure.

IIIrd nerve palsy may be present as oculomotor enters here (down and out position, ptosis, dilated pupils)

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14
Q

How does occulomotor nerve palsy present?

A
  1. Eye Position:
    The affected eye often appears “down and out” due to unopposed action of the lateral rectus (CN VI) and superior oblique (CN IV), which are not controlled by CN III.
  2. Ptosis (Drooping of the Eyelid):
    The levator palpebrae superioris muscle, which lifts the upper eyelid, is weakened or paralyzed, leading to drooping of the eyelid on the affected side.
  3. Pupil Involvement:
    Dilated pupil (mydriasis):
    The parasympathetic fibers of CN III control pupil constriction. Damage results in an enlarged pupil that does not constrict properly in response to light.
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15
Q

If the one cerebral hemisphere isn’t responsible for conciousness by itself how could a mass in one cerebral hemisphere result in coma?

A

Through herniation of the medial temporal lobe

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16
Q

Describe the whole of the glasgow coma scale

A
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17
Q

If when you approach a patient and they are awake and looking at you, how would you record this on the Glasgow Coma Scale?

GCS 15
Spontaneous eye opening
Orientated
Obeying commands
Eye opening response sub domain score on GCS of 6

A

Spontaneous eye opening

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18
Q

Your patient’s vocal response is confused, but they are still able to speak in full sentences. What score would you give them for the verbal portion of the GCS?

1
2
3
4
5

A

4

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19
Q

Thinking about focal signs and meningism what is the rule of thumb for cause of coma?

A
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20
Q

What happens to the pupils during opiate overdose and pontine lesions?

A

You get pinpoint pupils

This is due to sympathetic surpression resulting in overactive parasympathetic

Opiates aurpress the sympathetic nervous system. Sympathetic fibres run hrough the pons

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21
Q

What can pupils tell you about the cause of coma?

A

Asymmetric dillation - IIIrd nerve palsy?

Equal & reactive - metabolic/ toxic

Pinpoint - Opiates/ Pontine lesion

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22
Q

What is the overview of coma treatment?

A

Depends on cause.

All - Airway Breathing Circulation

Hypoglycemia: Give dextrose (25ml 50%)

Thiamine if due to thiamine deficiency in chronic alcohol abuse

Naloxone iv should be considered if opiates

Treat seizures with anti seizures meds

Antibiotics iv if patient pyrexial with meningism

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23
Q

What is tension type headache?

A

Standard headache, no other associated symptoms.

Classified as disease it occurs frequently and suddenly.

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24
Q

What does a tension type headache feel like?

A
  • Whole head
  • Dull, pressing character
  • Mild - moderate severity
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25
Treatment for tension type headaches?
Acute: NSAIDs Preventative: Not really any but maybe amitriptyline
26
What class of drugs is amitriptyline
tricyclic antidepressant
27
What is a Trigeminal Autonomic Cephalgias? Presentation? Frequency? Also known as?
Activation of the trigeminal nerve and autonomic pathways of the face Presents as unilateral headache attacks with ipsilateral autonomic features (red eye, ptosis, lacrimation, rhinorrhea). It is often circadian and comes in clusters i.e. periodically for a few days then stops then comes back. Also known as cluster headaches
28
Types of migraine?
Headache without aura Headache with aura Aura without headache - mistaken for TIA
29
Timeline of migraine
T-Hours/Days: Prodromal - fatigue, phonophobia, irritability T0: Aura T+20mins: Headache plus photosensitivity T+Hours/Days: Postdromal - Blurry vision, tiredness, lack of concentration
30
What defines chronic migraine?
Chronic migraine * Headache ≥15 days/month for ≥ 3 months * Characteristic migraine features ≥ 8 days/month * Often associated with analgesia overuse
31
Acute drug treatment for migraine
Aspirin: ideally soluble and high dose 600-900mg NSAIDs Triptans: try several types and several routes before giving up Analgesics shouldn't be used preventitavely as can cause headaches
32
Classical preventative migraine treatment
Need to take regularly and let it build up Some examples (kind if discovered randomly) Maybe just remember some key ones * **Propranolol (beta blocker)** common with GPs but side effects of weight gain * **Pizotifen** (antihistamine with serotonin antagonist) * **Amitryptiline / Nortyryptiline** (tricyclic antidepressants) not used much anymore as very non-specific drug with lots of side effects * Candesartan (angiotensin II receptor antagonist) * Topiramate (antiseizure drug increasing GABA activity, inhibiting glutamate) * Flunarizine (calcium channel blocker with antihistamine effects) * Riboflavin (vitamin B2, role in cellular energy production /mitochondria) * Botulinum injections (neurotoxin blocking presynaptic release of Ach)
33
Novel migraine treatment. Why might you not use it first?
Calcitonin Gene Related Peptide drugs (CGRP) Monoclonal antibodies against CGRP or CGRP receptor for migraine prevention * CGRP = neuropeptide in trigeminal ganglion neurones * CGRP release triggers a cascade resulting in sensitization of trigeminal nerves * CGRP has key role in migraine pain pathways through trigeminovascular system Very effective but very expensive so try other things first
34
What parts of the nervous system does MS affect?
CNS Brain, Spinal chord, Optic nerve
35
How is MS thought to start?
It is an immune response and certain alles of MHC class I & II are thought to make you more susceptible.
36
Which virus is most associated with MS as a trigger?
Epstein-Barr Virus
37
What would you expect to find in a biopsy of a nerve affected by MS?
De-myelinating plaques
38
Is MS genetic?
There is definately some genetic susceptibility. You don't need ot remember this but just to demonstate: * 1/330 lifetime risk MS in UK * 1/5 identical twin, 1/22 non-identical twin * 1/37 sibling * 1/48 offspring
39
What are the four subtypes of MS based on the pattern of progression?
* Relapsing Remitting MS * Primary Progressive MS * Secondary Progressive MS * Progressive Relapsing MS
40
Which subtype of MS is the most common?
Relapsing Remitting MS - this affects 85% of patients
41
MS presentation
Presentation depends on the sites that are affected first. But common presentations include: * Optic neuritis (unilateral) * Transverse myelitis * Brainstem or cerebellar syndrome * Focal supratentorial presentation
42
What is optic neuritis?
Optic neuritis is an inflammatory condition affecting the optic nerve. It is often associated with autoimmune conditions, including multiple sclerosis (MS). It is often unilateral Presents with vision loss, eye pain due to inflammation and other visual symptoms
43
Which side is optic neuritis likely to affect?
Either, but nearly always unilateral
44
What is transverse myelitis?
Transverse myelitis is an inflammatory condition of the spinal cord. The term "transverse" refers to the fact that the inflammation often affects a cross-section of the spinal cord, impairing sensory, motor, and autonomic functions below the level of the lesion. Presents as complete neurological below the lesion. Sensory loss or burning/tingleing pain. Weakness. Autonomic function such as bowel and bladder control.
45
What does supratentorial mean?
Top half of brain. Cerebral hemispheres, basal ganglia, thalamus and hypothalamus
46
What is the diencephalon?
Thalamus and hypothalamus
47
Which MS subtype typically has the youngest age of onset? A: RRMS B: SPMS C: PPMS
RRMS is correct. Typical age of onset is 20-40. Almost all cases of pediatric onset MS are RRMS. PPMS onsets later, typically in the 40s to 50s. SPMS is a progression of RRMS so naturally comes later.
48
What does form if imaging do you use to diagnose MS?
A type of MRI T2 imaging called flare imaging. As with all T2 imaging fluid comes up white so can be used to detect damage and iflamation. However in flare CSF signals are surpressed meaning you only detect other fluid in the brain.
49
What is characteristic feature of MS in a sagital brain MRI?
Dorson's fingers or periventricular lesions on a sagital view
50
What would you look for in a CSF sample for someone with MS
Oligoclonal bands. This is where the antibodies in a sample are all removed are separated by size. If there is a problem like infection or autoimmune disease certain antibodies will be much more present (cloned) and appear as dark patches. Specifically oyu are looking ones that are present only in the CSF implying there isn't a generalised antibody pattern. You also need more than one.
51
What characteristic featurs of MS might you look for in a spinal chord MRI?
Bright white down the centre of the chord
52
What MS characteristics might you look for in a planel view MRI of the lower brain?
Infratentorial lesions of the brainstem and cerebellum
53
What MS characteristic might you look for in a coronal view brain MRI
Juxtacortical lesions
54
What investigations would you prioritise for an MS diagnosis?
Symptoms and MRI first. CSF sample if still not sure.
55
* What clinical presentation is NOT typical of MS? A: Optic neuritis B: Slowly progressive cognitive difficulties C: Unilateral weakness developing over 24 hours D: Ataxia E: Diplopia with weakness of adduction of one eye and nystagmus of contralateral eye on lateral gaze
A: Optic neuritis - common **B: Slowly progressive cognitive difficulties** - could happen but is rare C: Unilateral weakness developing over 24 hours - common sign of motor cortex lesion which could be in MS D: Ataxia - common cerrabella MS E: Diplopia with weakness of adduction of one eye and nystagmus of contralateral eye on lateral gaze - occurs due to a lesion in the medial longitudinal fasciculus (MLF) of the brainstem. If oyu seen this in young people it is 9/10 times MS
56
What is Internuclear Ophthalmoplegia (INO)
INO results from a lesion in the medial longitudinal fasciculus (MLF), a key brainstem tract that coordinates eye movements between the nuclei of cranial nerves III (oculomotor) and VI (abducens) for conjugate gaze. Presents as "diplopia with weakness of adduction of one eye and nystagmus of the contralateral eye on lateral gaze"
57
Why is the "multiple" part of multiple sclerosis so important in the diagnoses of MS?
* Multiple lesions in different parts of the CNS = dissemination in space * Multiple lesions forming over different time points = dissemination in time
58
How do the disease modifying treatments for MS work?
Surpress immune system leading to fewer episodes of immune cells traveling into the CNS causing relapses As such fewer relapses, and fewer new lesions on MRI
59
What is the overview of MS prognosis?
* MS is a chronic condition * Majority do not end up in a wheelchair * Lifespan is reduced on average by approx. 10 years although wide variation, and beyond aged 70 no difference in excess death rates * In most patients the most disabling relapses are early on, and this is becoming less common with DMTs
60
What is transverse myelitis?
Inflamation of the spinal chord. Can occur as a consequence other diseases such as MS. Or it can be a standalone condition after infection etc. Sort it out with steroids.
61
What is Acute Disseminating Encephomylitis?
ADEM where there are very large oval shaped areas of inlfamation seen on an MRI. Can occure anywhere in CNS. Again it could be part of MS but could also be standalone. If it's massive think acute disseminating encephomylitis.
62
What is Autoimmune Encephalitis?
It is a form of CNS inflammation where the immune system makes antibodies against the nurological synapses. It presents as dementia or phychosis but is treatable and reversible so it is very important to pick up on especially if you see dementia with inflammatory signals.
63
What does a Paraneoplastic Neurological Disorder mean?
It is ascosiated with malignancy
64
What should you also check for in someone with autoimmune encephalitis?
Scan for tumours. Malignancy is a hot bed for autoimmune diseases.
65
What are the two types of autoimmune encephalitis?
66
Which type of autoimmune encephalitis presents similarly to alzheimer's?
LGI1/CASPR It affects the hippocampus
67
Which type of autoimmune encephalitis presents similarly to phychosis, movement disorders and autonomic functions?
NMDA (atacks the glutamate receptors)
68
What is neuromyelitis optica spectrum disorder broadly and how is it?
NMO is again an autoimmune disorder again the CNS charcterised optic neuritis and spinal chord lesions travelling longitudinally down the entire chord (as opposed the transverse just affecting one area) so extremely damaging.
69
What parts of CNS microanatomy are particularly targeted in neuromyelitis optica spectrum disorder?
Astrocyte's aquaporin channels are targetted causing swelling and death. This loss of astrocytes then causes the oligodendrocytes and odema causeing gross damge to surrounding tissue
70
Which of the following is a risk factor for development of multiple sclerosis? Vitamin D insufficiency BMI < 25 Non-smoker Male sex Age > 50
Vitamine D insufficiency Remember the northerly spread? Lots in Orkney
71
What is the criteria for diagnosing MS called?
McDonald Criteria Diagnoses of exclusion Disemination in space Disemination in time
72
What does it mean to be male with regard to MS?
You are less likely to get it It is a worse prognosis of you do
73
When might you not treat an epileptic presenting seizure?
If they have only had one seizure and there no other risk factors
74
If someone presents with symptoms of a temporal/limbic seizure then what investigation should you perform?
MRI as the cause could be structural. EEG is good for confirming generalised siezures in younge people with genetic epilepsy.
75
After giving benzos to stop an ongoing siezure what should you consider?
levetiracetam or sodium valporate (not lamotrigine) Hint: levetiracetam and sodium valporate are 2nd line treatments for both preventative and ongoing seizures. For preventative try lamotrigine first. For ongoing benzos.

Baz Y2 Semester 1 (17 decks)

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