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Phase 2a Basic Knowledge > Neurology > Flashcards

Neurology Flashcards

1
Q

Define transient Ischaemic attack (TIA)

A

Transient / temporary neurological dysfunction secondary to ischaemia without infarction; within 24hrs

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2
Q

Blood supply entering the brain with which arteries……

A

Internal carotid artery (ICA) - 90%

Vertebral (posterior) - 10%

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3
Q

Main cause of TIA

A

Carotid thrombo-emboli

Increased emboli risk when Px has Afib - Remember CHA2DS2 VASc score is used as stroke risk in Afib Px.

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4
Q

Risk factors for transient Ischaemic attack

A

HTN
Hypercholestraemia
T2DM
Afib
Obesity
IHD
Smoking
Ventricular septal defect

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5
Q

Sx of TIA

A

Slurred speech
Facial weakness
Limb weakness

Amaurosis fugax - temporary painless vision loss; usually one eye.

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6
Q

What signs are seen in TIA

A

Focal neurology: depending on which vessel is affected, have different signs

Anterior cerebral.A - Contralateral leg weakness
Middle cerebral.A - Contralateral body weakness + facial drooping forehead sparing + dysphasia
Posterior cerebral.A - Vision loss; contralateral hamonymous hemianopia
Vertebral.A - Cerebellar syndrome - D.A.N.I.S.H; +ve Ramberg test (sensory and motor ataxia)
Opthalmic/Retinal/Ciliary.A

Irregular pulse - if AFib is cause
Carotid bruit - suggests carotid artery stenosis

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7
Q

How do you initially differentiate between TIA and Stroke

A

Can’t tell until after recovery:
TIA —> Sx resolve <24hrs with no infarct
Stroke —> Sx last ≥24hrs with infarction

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8
Q

What investigation and Dx are needed for TIA

A

Clinical Dx; usually obvious if TIA/stroke is suspected
2 scoring systems that can be used:
FAST —> Face Arms Speech Time (public health campaign)

ABCD2 —> Age >60; BP >140/90; Clinical Sx unilateral weakness (2pt) / slurred speech (1pt); Duration Sx >1hr (2pt) / <1hr (1pt); DMT2 (1pt)
- refer to neurology ASAP (sig. increased risk of stroke)

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9
Q

Treatment for TIA

A

Acutely —> Aspirin

Prophylaxis long term/2º prevention —> Clopidogrel (75mg) and Atorvastatin (80mg)

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10
Q

Define stroke

A

AKA a Cerebrovascular accident.
Focal neurological defect lasting >24hrs with infarct

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11
Q

What types of stroke are there

A

Ischaemic (85%)
Essentially prolonged TIA
Lacunar Ischaemic stroke

Haemorrhagic (15%)
Ruptured blood vessel
Intracerebral
Subarachnoid
Extradural/epidural not considered haemorrhagic strokes

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12
Q

Causes of each type of stroke

A

Ischaemic stroke
Cardiac
Atherosclerosis; Carotid thrombo-emboli: thrombosis ± AFib embolisation, AFib, smoking, HTN, hyperlipidaemia
Vascular
Aortic dissection
haematological
Hypercoagubility; Antiphospholipid syndrome
Polycythaemia, sickle cell disease

Haemorrhagic stroke
Intracerebral
HTN, trauma
Subarachnoid
Berry aneurysm rupture, trauma
Intraventricular
* - bleeding within the ventricles; prematurity is a very strong risk factor in infants*

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13
Q

Risk factors for stroke

A

TIA
HTN
Smoking
Obesity
T2DM
AFib
Hypercoagulability; polycythaemia, sickle cell

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14
Q

Sx of a stroke

A

Focal neurology like TIA

+ For haemorrhagic stroke
Increased ICP —> Midline shifts; risk of tentorial herniation (the movement of brain tissue from one intracranial compartment to another.)

+ For lacunar strokes
V. Common type of Ischaemic stroke of lenticulostriate arteries (branches of MCA;supplying deep structures) —> ischaemia to basal ganglia, internal capsule, thalamus & pons

If a Px is on oral anticoagulants - suspect haemorrhagic stroke.

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15
Q

What are the focal neurology signs *esp witnessed in a stroke/TIA *

A

Focal neurology = neurological defect; depending on which vessel is affected, presents with different signs

Anterior cerebral.A - Contralateral leg weakness
Middle cerebral.A - Contralateral body weakness + facial drooping forehead sparing + dysphasia
Posterior cerebral.A - Vision loss; contralateral hamonymous hemianopia
Vertebral.A - Cerebellar syndrome - D.A.N.I.S.H; +ve Ramberg test (sensory and motor ataxia)
Opthalmic/Retinal/Ciliary.A - Amaurosis fugax

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16
Q

Name a specific sign in stroke

A

Pronator drift

Ask a Px to lift arms to ceiling; pronators takeover so the arm of the affected side will pronate and the palm of hand faces down.

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17
Q

Investigation and Dx of stroke

A

G.Standard: Non-contrast CT head
Ischaemic stroke - usually normal
Haemorrhagic stroke - hyperdense blood

Could do MRI as alternative.
1st line: FBC, serum glucose, electrolytes, cardiac enzymes, PTT
± CT angiogram

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18
Q

Tx for stroke

A

Ischaemic
When presented within 4.5hrs —> use CLOT BUSTER / fibrinolytic agent (Alteplase)
+ Aspirin

Haemorrhagic
Neurosurgery referral
IV Mannitol (for increased ICP)

2º prevention / prophylaxis for both: atorvastatin + Clopidogrel; could give Ramipril for haemorrhagic stroke.

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19
Q

What does the DVLA say about strokes / TIAs

A

For cars/motorcycle:
Must not drive for 1month after TIA/strokes

For heavy vehicles:
Must not drive for 1 year

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20
Q

What classification is used to categorise a stroke according to area affected

A

Bamford classification

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21
Q

What does D.A.N.I.S.H acronym stand for and when is it used

A

Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Scanning dysarthria
Heel-shin test positivity

Used for cerebellar syndrome

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22
Q

A 38-year-old female presents by ambulance with a severe occipital headache, which started suddenly 1 hour ago. She collapsed due to the pain. She has a history of hypertension.
What is the most likely Dx

A

Subarachnoid haemorrhage

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23
Q

Describe the Pathophysiology of subarachnoid haemorrhages

A

Type of intracranial haemorrhage characterised by blood within the subarachnoid space where the cerebrospinal fluid is located (inbetween pia mater and arachnoid mater)

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24
Q

What are the causes of a subarachnoid haemorrhage

A

Trauma

Atraumatic (i.e. spontaneous)
Ruptured berry (/ saccular) aneurysm

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25
Q

Describe what a berry aneurysm is and what it can cause

A

Known as berry aneurysm as it looks like a berry off a vine.

Arise at points of arterial bifurcation within the Circle of Willis; most commonly junction between the anterior communicating and anterior cerebral arteries

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26
Q

Risk factor for subarachnoid haemorrhages

A

Traumas
Htn
Polycystic kidney disease
FHx
Increased age
Marfan’s/EDS

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27
Q

Signs and Sx of subarachnoid haemorrhages

A

Occipital thunderclap headache
Sudden onset
“The worst headache of my life”: 0–>10 severity instantly

Meningism (photophobia + neck stiffness)
Kernig sign - when hip and knee are flexed, hard to extend knee again
Brudzinski sign - automatic knee flexion when neck is flexed - Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed

Reduced GCS
Nerve palsies (CN3-6)
Cn3 - fixated eye pupils
Cn6 - non-specific sign of increased ICP

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28
Q

What type of headache might be experienced preceding a berry aneurysm rupture

A

Sentinel headache

precedes the rupture by weeks ≈50% of cases - throbbing occipital pain

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29
Q

What is the differential Dx of subarachnoid haemorrhage

A

Meningitis (no thunderclap headache but w/ signs of infection)

Migraine (no meningism / thunderclap)

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30
Q

What is GCS referring to…

A

Out of /15
Eyes /4
Verbal /5
Motor /6

15: normal
≤ 8: comatose
≤ 3: unresponsive

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31
Q

Investigations and Dx of subarachnoid haemorrhages

A

Diagnostic - non-contrast CT Head
- ‘STAR shape’ on superior view

If positive: CT Angiogram - to see extent of rupture

If negative: Lumbar puncture - wait ~12hrs; results are most sensitive >12hrs
- Will see Xanthocheomia (yellowish CSF due to RBC haemolysis)

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32
Q

Treatment for subarachnoid haemorrhages

A

1st line:
Neurosurgery referral; endovascular coiling
+ Nimodipine (* CCB; decreased vasospasms + decreased BP*)

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33
Q

Define subdural haemorrhage

A

When blood accumulates between the dura mater and arachnoid mater (subdural space)
There’s bridging veins in that area; blood from the brain —> dural venous sinuses
Rupturing these veins (“in surgery is known as a very bad thing ;) loveland jk !”) and usually due to shearing injury (met with pressure and separation of the 2 layers)

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34
Q

Risk factors for subdural haemorrhages

A

Trauma
Child abuse - shaken baby syndrome
Increased age (Cortical atrophy e.g. dementia)

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35
Q

Signs and Sx of subdural haemorrhages

A

Acute sx incited within 3 days of an incident
Reduced conciousness
Headaches & vomiting
Signs of increased ICP - CUSHING TRIAD + papilloedema
* - Widened pulse pressure, bradycardia, reduced respiration*

chronic
Start seeing focal neurological deficit (CN3 palsy)

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36
Q

Investigation and Dx of subdural haemorrhage

A

Non contrast CT head:
Banana / crescent shaped haematoma; not confined to suture lines, midline shift
- If acute = hyperdense (bright)
- if subacute = Isodense
- if chronic (late) = hypodense (darker than the brain image)

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37
Q

Tx for subdural haemorrhage

A

Surgery; Burr hole + craniotomy

To reduce ICP: IV mannitol

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38
Q

Complication of subdural haemorrhage

A

Brain stem herniation
+
Respiratory arrest

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39
Q

Define extradural haemorrhage

A

Haematoma found within the potential space and dura mater.

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40
Q

What is the most common cause of an extradural haemorrhage

A

Trauma

Mainly leads to arterial bleeding - middle meningeal artery
Due to damage of the pterion (thinnest part of the skull) / temporal region

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41
Q

Risk factors for extradural haemorrhages

A

Seen in 20-30y/o
As age increases, risk decreases… as the dura is more firmly adhered to the skull

Head trauma

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42
Q

Signs and Sx of extradural haemorrhages

A

Acutely
Initial loss of consciousness —> lucid intervals of feeling okay —> rapid deterioration because of ICP

Reduced GCS
Increased ICP signs; Cushing triad (bradycardia, widened pulse pressure, irregular breathing) + papilloedema

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43
Q

What causes the rapid deterioration in extradural haemorrhages…

A

Increased ICP

Blood clots become haemolysed and take up water (i.e. they’re osmotically active) so they increase in volume, increasing the pressure.

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44
Q

Complication of extradural haemorrhages

A

Death for respiratory arrest
- herniation + coning of the brain = compressed respiratory centres
- due to untreated ICP

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45
Q

Investigation and Dx of extradural haemorrhage

A

Non-Contrast CT head
Lens shaped hyperdense bleed.
Confined to suture lines
Midline shift

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46
Q

Tx for extradural haemorrhages

A

Urgent surgery
IV mannitol to decrease ICP

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47
Q

What types of headaches are there….

A

1º headaches
Migraines
Cluster
Tension
Trigeminal neuralgia
Drug overdose

2º headaches cause is more specific; coz of an underlying condition
Giant cell artiritis
Infection
Head injury — subarachnoid haemorrhage
Carbon monoxide poisoning

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48
Q

Give an example of primary headaches

A

Tension
Cluster
Migraines
Trigeminal neuralgia
Drug-induced

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49
Q

Give an example of secondary headaches

A

Giant cell arteritis
Meningitis
Subarachnoid haemorrhages
Carbon monoxide poisoning

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50
Q

Give 6 questions you’d ask that are important when taking a history for a headache

A

Time; Onset / Duration / Frequency / Pattern
Triggers; any factors aggravating / alleviating the headaches
Type of pain; Severity / Site / Does pain spread? / Is it impacting QoL?
Associated Sx; Photophobia, Phonophobia, V&N
Response; to medication
Sx in between attacks

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51
Q

Give red flags for more serious conditions (raised ICP/intracranial haemorrhage) when presenting with a headache

A

Rapid/new onset headache
Fever + neck stiffness
Seizures
Papilloedema
Significantly altered consciousness / confusion

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52
Q

Describe the pain of a migraine

A

Unilateral
Throbbing
Moderate—>Severe
Worsened on exercise

±

Photophobia / phonophobia
N &/ V

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53
Q

Types of migraine

A

Episodic with Aura (20%) / without Aura (80%)
Chronic

May also have:
Silent migraines
migraines with aura but without headache

Hemiplegic migraines
Migraine mimicking a stroke; typical Sx of migraine + hemiplagia (unilateral weakness of limbs)

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54
Q

What do Px with migraine + aura complain of …

A

Visual disturbance / phenomena; ZIGZAG lines

Sparks in vision
Blurring vision
Lines across vision
Loss of different visual fields

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55
Q

What triggers are there for migraine

A

CHOCOLATE

C . Hocolate
Oral contraceptives
Cheese
AlcohO . L
Anxiety
Travel
Exercise

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56
Q

How long does migraine last

A

Prodrome (stage before the headache); mood ∆

± Aura (part of the attack, minutes before the headache)

Throbbing headache
4 - 72hrs

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57
Q

With a women complaining of migraines and is on oral contraceptive… what would you do as her dr

A

Stop O.C.

Offer alternatives; as it acts as a trigger, increases stroke risk, decreases Triptan efficacy

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58
Q

Investigation and Dx of migraine

A

Dx: clinical; unless a different pathway is suggested

The clinical Sx (Should meet this requirement):
≥2 of…
Unilateral pain
Throbbing
Moderate —> severe
Motion-sickness
+
≥1 of…
N &/ V
Photophobia / Phonophobia

with normal neuro exam

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59
Q

Tx for migraines

A

Acute
Oral Triptan (Sumotriptan)
Or
Aspirin 900mg

Prophylaxis
Beta-blocker (propanolol); if asthmatic give Topiromate (anti-convulsant)
Amitryptiline (TriCyclic Antidepressant)

Avoid Opiates
Consider Anti-emetics; Metoclopramide (if N &/V)

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60
Q

What drug class is Triptan

A

5-HT receptor agonist (serotonin receptor agonists)

61
Q

MoA of Triptans and what condition can they be used in

A

Smooth muscle in arteries to cause vasoconstriction
Peripheral pain receptors to inhibit activation of pain receptors
Reduce neuronal activity in the central nervous system

  • Headaches; migraines / cluster headaches
62
Q

What are the pharmacological and non-pharmacological prophylaxis for migraines

A

Pharmacological
Propanolol (B. Blocker) / topiromate (anti-convulsant)
Amitryptiline

Non-Pharmacological
Acupuncture
Vit B supplement (riboflavin)

63
Q

Wheat is the most common type of 1º headache

A

Tension headaches

64
Q

Describe the pain of a tension headache

A

Bilateral
Generalised pain; pressing/tight
Mild —> moderate
Not exercise induced

Pain in Frontalis, temporalis and occipitalis muscles
Rubber band, tight around head

65
Q

What is the duration of a tension headache

A

30 mins —> 7days

66
Q

Excluding the generalised pain in tension headaches, are there any other sx

A

No
No motion sickness
No aura
No photophobia / phonophobia

67
Q

Tx for tension headache

A

Analgesia:
Aspirin or paracetamol

Avoid opiates - dependence

68
Q

Describe the pain of a cluster headache

A

Unilateral
Pain around an eye / temporal area
Severe —> very severe
Headache is accompanied by cranial autonomic features

Classified as Trigeminal Autonomic Cephalgia (TAC) - thought to happen because of hypersensitivity of trigeminal autonomic reflex arc (vascular dilation + nerve stimulation) & increased histamine release from mast cells — adding to the Sx

69
Q

How long do cluster headaches last

A

15 min —> 3hrs

70
Q

What is the most disabling 1º headache

A

Cluster headaches

71
Q

Risk factors of cluster headaches

A

Male
Smoking
Genetics

72
Q

Signs and Sx of cluster headaches

A

Crescendo unilateral peri-orbital excruciating pain - AKA suicide headaches

With ipsilateral autonomic features
Ptosis (droopy eye);
miosis (constricted unilateral pupil);
lacrimation (watery blood shot eyes);
rhinorrhoea (runny nose)

73
Q

Investigation and Dx of cluster headaches

A

Clinical Dx; ≥ 5 similar attacks confirms Dx

But remember these headaches come in clusters and so they may experience Sx for like a week — month but then not experience them for years before the next cluster.

74
Q

Tx of cluster headache

A

Acute
Triptans; Sumatriptan
High flow O2 (can be given at home)

Prophylaxis
Verapamil (CCB)

75
Q

Describe the pain of Trigeminal neuralgia

A

Unilateral electric shock pain
Across the face (V1, 2, 3) - mainly V3 is affected
Very severe

76
Q

What are the branches of trigeminal nerve

A

Cranial nerve 5

V1 —> Opthalmic

V2 —> Maxillary

V3 —> Mandibular

77
Q

What is the duration of pain for trigeminal neuralgia

A

A few seconds
(Secs —> 2mins)

78
Q

Name some triggers of trigeminal neuralgia

A

Eating (spicy foods / citrus fruit)
Cold weather
Brushing teeth
Talking

79
Q

Name 3 risk factors for trigeminal neuralgia

A

Multiple sclerosis
Increased age
Female

80
Q

Investigations and Dx of trigeminal neuralgia

A

Clinical; ≥ 3 attacks of the Sx

81
Q

Tx for trigeminal neuralgia

A

Carbamazepine (anti-convulsant)

Surgery if all else fails

82
Q

Define giant cell arteritis

A

Systemic vasculitis affecting large arteries; esp. temporal arteries

83
Q

Key complication of giant cell arteritis

A

Vision loss (amaurosis fugax )

HIgh dose steroid used to prevent development/progression of the vision loss

84
Q

Which condition does giant cell arteritis have a strong link with

A

Polymyalgia rheumatica

85
Q

What are the sx of giant cell arteritis

A

Severe Unilateral scalp tenderness and headache around temple and forehead

Jaw claudication

Blurred / double vision (curtains over field of view)

86
Q

Investigation and Dx of giant cell arteritis

A

Temporal artery biopsy (do a big sample to capture as many skip lesions):
Granulomatous non-caseating inflammation of intima+media; with skip lesions — multinucleated giant cells

Raised ESR / CRP

Normacytic normochromic anaemia

87
Q

Tx of giant cell arteritis

A

Corticosteroids (prednisolone)
Any signs of amaurosis fugax —> high dose methylprednisolone STAT

88
Q

Define epilepsy

A

Neurological disorder characterised by recurrent seizures.

Seizure = paroxysmal alteration of neurological function leading to hypersynchronous discharge of neurons within the brain
(I.E. sudden uncontrollable burst of electrical activity)

89
Q

What types of seizures are there?

A

Generalised seizures:
Motor seizures;
Tonic-clonic seizures; Typical epileptic seizure
Tonic - stiffening of arms, leg / trunk
Clonic - Jerking of arms/legs on 1 or both sides of body

Non-Motor seizures;
Absence seizures

Focal seizures
Simple

Complex

Myoclonic - Some or all of body twitches lasting < 1sec.
Atonic - Sudden loss of muscle strength (floppy). Can cause person to drop to the ground. - THESE CAN BE GENERALISED / FOCAL

90
Q

Define tonic-clonic seizures

A

AKA ‘Grand male’
Typically, tonic comes before clonic!
Generalised seizures involve both hemispheres of the brain at onset

  • No aura
  • Tonic phase; muscle tensing/Rigidity, so fall to the floor
  • Clonic phase; muscle jerking
    You see… Upgazing open eyes, incontinence, tongue-biting
91
Q

Define an absence seizure

A

Generalised seizures involve both hemispheres of the brain at onset

Manifests in childhood; moments of blankly staring into space (secs—>mins) then carrying on from where they left / repeated movements like lip-smacking

92
Q

What’s seen on an EEG of an absent seizure

A

3Hz spike

93
Q

What can cause seizures

A

Remember V.I.T.A.M.I.N…D.E

Vascular
Infection
Trauma
Autoimmune conditions (SLE)
Metabolic (hypocalcaemia)
Idiopathic —> EPILEPSY
Neoplasm
Dementia / Drugs
Eclampsia

94
Q

Define epilepsy relative to its seizures

A

Epilepsy = idiopathic cause of seizures
≥2 episodes more than 24hrs apart

95
Q

Risk factor for epilepsy

A

Inherited
Family Hx
Metabolic disorders

Acquired
Dementia
Ischaemic stroke

96
Q

What’s the difference between epileptic and non-epileptic seizures

A

Eyes open
Synchronous movement
Can occur in sleep

For epileptic seizures

97
Q

Pathophysiology of an epileptic seizure

A

Imbalance between excitation (glutamate) and inhibition (GABA) within the neurons of the brain…

Balance shifts towards the excitatory neurotransmitter (glutamate) by stimulation + inhibition of GABA

98
Q

Describe what a seizure period is

A

Pre-ictal
Aura / deja vu / triggers
Ictal
Seizure
Post-ictal
headache / confusion / reduced GCS / amnesia
TODD’s paralysis; if motor cortex affected (frontal lobe), may have temporary paralysis / muscle weakness

99
Q

Define a focal seizure

A

Features are confined to a specific region; depending on which lobe of the brain is affected will depend on the Sx experienced
- Could progress to 2º generalised seizures

Simple focal; Px is Awake and Aware, just got uncontrolled muscle jerking

Complex focal; Px is Unaware / has impaired consciousness during the seizure.

100
Q

What is jacksonian march

A

If jerking activity starts in specific muscle group and spreads to surrounding muscle groups as more neurones are affected its referred to as a JACKSONIAN MARCH.
Usually from more distal areas towards the face

101
Q

What sx are seen if temporal region of brain is affected in epilepsy

A

Temporal lobe i.e., Memory, understanding speech, emotion
• Aura (80%); Deja-vu, auditory hallucinations, funny smells, fear
• Automatisms e.g., lip smacking

102
Q

What sx are seen if frontal region of brain is affected in epilepsy

A

Frontal lobe i.e., Motor, thought processing
• Motor features e.g., posturing, peddling movements of leg
• JACKSONIAN MARCH – seizures march up/down the motor homunculus
• Post-Ictal Todd’s palsy
• Starts distally in a limb & works its way upwards to the face

103
Q

What sx are seen if parietal region of brain is affected in epilepsy

A

Parietal lobe i.e., Sensation
• Sensory disturbances e.g. tingling/numbness

104
Q

What sx are seen if occipital region of brain is affected in epilepsy

A

Occipital lobe i.e., Vision
• Visual phenomena e.g. spots, lines, flashes

105
Q

Most common lobe saffected in epilepsy

A

Temporal

106
Q

What investigation and Dx are the for epilepsy

A

Blood glucose, FBC Electrolyte panel, Tox screen, CSF lumbar puncture analysis- rule out other potential causes

MRI/CT head

Electroencephalogram (EEG)- not diagnostic but can help support diagnosis and may help determine type of epileptic syndrome

107
Q

Tx of epilepsy

A

Generalised:
Tonic-clonic
1st line:Sodium valproate
2nd line: Lamotrigine

Absence
1st line:Sodium valproate
2nd line:Ethosuximide

Focal:
1st line: Lamotrigine
2nd line: Carbamazapine

108
Q

Complication of generalised seizures

A

Status epilepticus
-It is a medical emergency. It is defined as seizures lasting more than 5 minutes or more than 3 seizures in one hour.

Tx:
A-E approach
Give Benzodiazepine IV lorazepam; repeated after 10 minutes if seizure continues

109
Q

Define syncope

A

Insufficient blood / oxygen supply to the brain causing paroxysmal changes (periodic marked changes) in behaviour, sensation and cognitive processes

110
Q

Give 5 signs that transient loss of conciousness is due to syncope

A

Situational
5 - 30 secs
Pallor
Nausea
Sweating
Dehydration

111
Q

Which seizure is likely to last longer: epileptic / non-epileptic seizure

A

Non-epileptic *lasts around 1-20 mins

Whereas epileptic lasts around 30-120 secs*

112
Q

A Px complains of having black-outs. They tell you before the black out they felt nauseous and were sweating. They tell you that their friends all said they looked pale. Is this a blood circulation problem or a disturbance of brain function

A

Likely to be a blood circulation issue e.g. syncope

113
Q

How does carbamezapine work as an anti-epileptic drug

A

Inhibits pre-synaptic Na+ channels and so prevents axonal firing

114
Q

What’s the major side effect of sodium valproate

A

Teratogenic

115
Q

What is dopamine produced from

A

Tyrosine —> L-DOPA —> Dopamine

116
Q

Define Parkinson’s disease

A

Loss/degeneration of dopaminergic neurones in the substantia niagra, pars compacta

Pars compacta is a sub-portion of substantia niagra

  • 2nd most common neurodegenerative disorder
  • Idiopathic
117
Q

Where is substantia niagra found and where does the substantia niagra project to

A

Found on either side of the midbrain and part of the basal ganglia

Project to the Striatum (which consists of Caudate + Putamen)

The Pars compacta sends messages to the striatum via neuron rich neurotransmitter dopamine.
- Forming nigrostriatal pathway; helps stimulate cerebral cortex to initiate movement by signalling striatum to stop firing to pars reticulata to then stop movement inhibition

The other region of substantia niagra (pars reticulata) receives signals from the striatum which are then relayed to the thalamus using neurons rich in neurotransmitter GABA; which send signals to cortex to inhibit movement

118
Q

Pathophysiology of Parkinson’s

A

The Pars compacta sends messages to the striatum via neuron rich neurotransmitter dopamine.
- Forming nigrostriatal pathway; helps stimulate cerebral cortex to initiate movement by signalling striatum to stop firing to pars reticulata to then stop movement inhibition

The other region of substantia niagra (pars reticulata) receives signals from the striatum which are then relayed to the thalamus using neurons rich in neurotransmitter GABA; which send signals to cortex to inhibit movement

Degeneration of substantia niagra pars compacta means reduced signalling so harder to initiate movement.

119
Q

Risk factor for Parkinson’s

A

FHx
Increased age (since its progressive)
Males

120
Q

Aetiology of Parkinson’s

A

Idiopathic
May be genetic; Mutation in PINK1 / Parkin / ∂-synuclein

Rare: Parkinsonians Sx may be caused by recreational drugs (MPPP)

121
Q

Signs and symptoms of Parkinson’s

A

Cardinal Sx:
TRIAD; Tremor, Rigidity, Bradykinesia
+ Postural instability

Tremor; Pill-rolling resting tremor
Rigidity; Cogwheel rigidity = tension in arms/legs when passively moved gives movement in small increments (jerk movement)
Bradykinesia; Shuffling gait as a result of Bradykinesia and Hypomimia - reduced facial expressions

+ Amnosia

122
Q

Would you describe the Parkinson’s Sx as symmetrical or asymmetrical

A

One side is always worse than the other
- Sx are asymptomatic / unilateral

123
Q

Investigation and Dx of Parkinson’s

A

Clinical

(Bradykinesia + ≥1 cardinal sign)

124
Q

Give a differential Dx for Parkinson’s

A

Lewy body dementia (associated with Parkinson’s)
Parkinson’s Sx then dementia = Parkinson dementia
Parkinson’s Sx after dementia = Lewy body dementia with Parkinsonism

125
Q

Tx of Parkinson’s

A

Doesn’t stop neurodegeneration; helps with Sx
Main aim is to increase dopamine signalling in the brain
Dopamine doesn’t cross the Blood-Brain Barrier… its precursor Levadopa does; converted in the brain to dopamine by decarboxylase inhibitor; carbidopa - given as combination with L-Dopa; Co-careldopa - but theres also peripheral dopa decarboxylase which converts dopamine —> epinephrine… we dont want this so use decarboxylase inhibitors as that’ll stop dopamine breakdown and wont pass the BBB either.

L-Dopa + decarboxylase inhibitor (carbidopa) = Co-careldopa

Could also give:
Dopamine agonist - Bromocriptine / Cabergoline
Can also give enzyme inhibitors to stop dopamine breakdown in different pathways
COMT inhibitors - Entacapone
MAO inhibitors - Selegiline

126
Q

You ask a Px who you suspect might have PD to walk up and down the corridor so that you can assess their gait. What features would be suggestive of PD

A

Stooped posture
Assymetrical arm swing
Small steps
Shuffling

127
Q

Histological findings in Parkinson’s disease

A

Lewy bodies

Loss of dopaminergic neurones in substantia niagra

128
Q

Give an example of a dopamine agonist

A

Bromocriptine

Cabergoline

129
Q

Give an example of a COMT inhibitor

A

Entacapone

130
Q

Give an example of a MAO inhibitor

A

Selegiline

131
Q

Give side effects of levodopa

A

Dyskinesia (involuntary movement)
Has an “on/off” effect i.e. there’ll be well controlled periods w/ sudden declines

132
Q

Define huntington’s chorea

A

Autosomal dominant genetic disorder trinucleotide repeat that causes progressive deterioration of the nervous system

133
Q

What mutation is found in Huntington’s chorea

A

Trinucleotide repeat disorder; genetic mutation in HTT gene on chromosome 4

134
Q

What triplet code is repeated in Huntington’s disease

A

CAG triplet repeats
≥36 times

135
Q

Define anticipation

A

Genetic anticipation is a feature seen in trinucleotide repeats.
As generation earlier age onset
The more repeats, the increased severity of disease

136
Q

Pathophysiology of Huntington’s

A

The trinucleotide repeat (of CAG) leads to mutated HTT proteins formation but they also affect the DNA replication itself.
These can aggregate in neuronal cells of the basal ganglia (caudate nucleus; striatum) causing neuronal cell death.

Neurotransmitter affected = GABA (lack of) + excessive nigrostriatal pathway

137
Q

What features and signs are seen in Huntington’s

A

Early onset
Irritability
Depression
Personality change

Later onset
Chorea (fidgety)
Athetosis (slow involuntary movement)
Psychiatric problems
Dementia

138
Q

Investigation and Dx of huntingtons

A

Clinical; FHx of earlier + severe huntingtons
Genetic test to count CAG repeats

139
Q

Tx for Huntingtons

A

Extensive counselling

Medication
Dopamine antagonist for chorea; Tetrabenazine
Could also give:
Antipsychotics; Olanzapine
Benzodiazepines; Diazepam

140
Q

Define multiple sclerosis

A

Chronic autoimmune, cell-mediated demyelinating disease of the CNS.

141
Q

Epidaemiology of multiple sclerosis

A

Females
20-40y/o
Rare in the tropics

142
Q

Risk factors for multiple sclerosis

A

Other autoimmune conditions
Female
20-40y/o
EBV

143
Q

Describe the aetiology of multiple sclerosis

A

Environmental
Genetic predisposition
Idiopathic

144
Q

Pathophysiology of multiple sclerosis

A

Genetic susceptibility + environmental trigger —> T-Cell activation —> B-cells and macrophage activation —> Inflammation, demyelination and axon destruction

145
Q

Where would the plaques be seen histologically

A

Around blood vessels; perivenular

146
Q

Does myelin regenerate in someone with multiple sclerosis

A

Yes but its much thinner which causes inefficient nerve conduction

147
Q

Give 3 main features of MS plaque

A

Inflammation

Demyelination

Axon loss

148
Q

What types of multiple sclerosis is thee

A

Relapsing - remitting
Sx; the Px has random attacks over a number of years and inbetween the attacks theres no progression

1º progressive
Gradual deterioration without recovery

2º progressive
Relapsing-remitting —> 1º progressive

149
Q

Signs and Sx of multiple sclerosis

A

Symptoms:
Paraesthesia
Blurred vision
Uhtoff’s phenomenon - worsening Sx following a rise in temperature (hot shower)

Signs:
Optic neuritis (inflamed optic nerve + can’t see red properly) —> 1st presenting Sx

Phase 2a Basic Knowledge (13 decks)

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