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Belle Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

Pathological basis of meningitis

A

Inflammation of the pia and arachnoid mater
Microorganisms infect the CSF
Not always an infective cause e.g. can be post surgical

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2
Q

Symptoms of meningitis

A

TRIAD: Stiffness of the neck, Severe headache, and Fever (infective)
Photophobia
Meningococcal meningitis: petechial non blanching rash

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3
Q

Two most common bacterial causes of meningitis in adults

A 
Diplococcus bacteria: 
Neisseria Meningitidis (meningococcal meningitis) -ve (non-blanching rash) 
Streptococcus Pneumoniae (pneumococcal meningitis) +ve
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4
Q

Viral causes of meningitis

A

Mumps virus
Coxsackie virus
HSV

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5
Q

Drug induced meningitis

A

NSAIDs

Trimethoprim

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6
Q

Diagnosis of meningitis

A

Blood culture

Brain imaging

CSF sample (lumbar puncture at L4) for microscopy and sensitivity testing

  • bacteria: turpid yellow colour, neutrophil polymorphs, raised protein, low glucose
  • viral: lymphocytes, normal protein, normal glucose
  • TB: lymphocytes, raised protein, low/normal glucose

PCR swab for viral

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7
Q

Treatment for bacterial meningitis

A

If suspected, give broad spectrum antibiotics before tests come back

Cephalosporins: IV ceftriaxone/IV cefotaxime

Over 50/immunocompromised: add IV amoxicillin

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8
Q

Treatment for viral meningitis

A

Supportive treatment
Self-limiting in 4-10 days
Acyclovir for HSV meningitis

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9
Q

Types of STROKE

A

Cerebral infarction (ischaemic stroke)
Intracerebral haemorrhage
Subarachnoid haemorrhage

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10
Q

Transient ischaemic attack Px

A

SUDDEN ONSET
Brief episode of neurological deficit
Symptoms are maximal at onset (usually last 5-15 mins)
LASTS <24 HOURS
WITHOUT INFARCTION (temporary, focal cerebral ischaemia)

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11
Q

TIA epidemiology

A

MALES

African-Caribbean heritage (HTN and atherosclerosis)

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12
Q

TIA and ischaemic stroke RFs

A 
Age
HTN
Smoking
Diabetes
Combined pill
Atrial fibrillation 
Male
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13
Q

Causes of a TIA

A

Atherothromboembolism
- carotid artery = main cause (carotid bruit)

Cardioembolism

  • atrial fibrillation
  • post-MI
  • valve disease/prosthetic

Hyperviscosity

Hypoperfusion

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14
Q

DDx TIA

A 
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis 
Syncope
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15
Q

Clinical presentation of a TIA (carotid territory Sx - 90%)

A 
Amaurosis fugax
Aphasia
Hemiparesis
Hemisensory loss
Hemianopic visual loss
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16
Q

Amaurosis fugax

A

Temporary occlusion of retinal artery (temporary retinal hypoxia)

Unilateral sudden vision loss

Transient (minutes)

“like a curtain descending”

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17
Q

ABCD2 score

A

Risk of stroke after TIA

Age
Blood pressure
Clinical features (unilateral weakness, speech disturbance w/o weakness)
Duration (<60 mins = 1, >60 mins = 2) 
Diabetes mellitus
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18
Q

Ix for TIA

A

CLINICAL DIAGNOSIS based off symptoms description

Bloods: glucose, FBC (polycythaemia), ESR (vasculitis), U&Es, cholesterol, INR (if on warfarin)

Imaging: diffusion weighted MRI or CT

Carotid imaging: doppler ultrasound, MR/CT angiography if stenosis

ECG

Echocardiogram

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19
Q

IMMEDIATE Mx for TIA

A

Aspirin 300mg

Refer to specialist (within 24h of symptom onset)

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20
Q

Long term Mx of TIA

A

Control CV risk factors

  • BP control
  • Smoking cessation
  • Statin e.g. simvastatin
  • No driving (1 month)

Antiplatelet therapy: CLOPIDOGREL

AF: anticoagulation (e.g. warfarin)

> 70% carotid stenosis: carotid endartectomy (reduces stroke risk by 75%)

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21
Q

Stroke

A

rapid onset neurological deficit lasting for over 24 hours

poor blood flow to the brain causes cell death

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22
Q

Two types of stroke

A

Ischaemic (85%)
Haemorrhagic (15%)
1st line Ix: CT HEAD

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23
Q

Penumbra

A

Infarcted area in ischaemic stroke is surrounded by a swollen area (oedema) which can regain function with neurological recovery

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24
Q

Causes of ischaemic stroke

A

Small vessel occlusion by thrombus

Atherothromboembolism (e.g. from carotid artery)

Cardioembolism (AF, post-MI, valve disease, IE)

Hyperviscosity
Vasculitis
Hypoperfusion

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25
Q

Clinical Px of ischaemic stroke (cerebral infarct)

A

Depends on the site (ACA, MCA, PCA)

Contralateral sensory loss
Contralateral hemiplegia: initially flaccid, becomes spastic (UMN lesion)
UMN facial weakness (forehead sparing)
Dysphasia 
Homonymous hemianopia 
Visuo-spatial deficit

Weakness may recover gradually

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26
Q

Human homunculus blood supply

A

ACA (medial supply): lower limbs

MCA (lateral supply): face, upper limbs

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27
Q

Clinical Px of ischaemic stroke (brainstem infarct)

A 
Quadriplegia
Locked-in syndrome
Facial numbness and paralysis
Vision disturbances
Vertigo, nausea
Cerebellar signs
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28
Q

Lacunar infarct

A 
Small infarcts
Occur in single small perforating artery supplying a subcortical area
- Internal capsule
- Basal ganglia
- Thalamus
- Pons

Px one of: sensory loss, weakness (unilateral), ataxic hemiparesis, dysarthria (motor speech)

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29
Q

Ischaemic stroke and intracerebral haemorrhage Ix

A

CT scan

  • distinguish ischaemic from haemorrhagic
  • site of infarct
  • identify mimics

Diffusion-weighted MRI:

  • more sensitive
  • CT may be -ve in first few hours
  • unclear diagnosis

Bloods: glucose (rule out hypoglycaemia), FBC (polycythaemia), ESR (vasculitis), U&Es, Cholesterol, INR (warfarin)

ECG: AF, MI

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30
Q

Immediate ischaemic stroke Mx

A

EXCLUDE HAEMORRHAGE

loading dose: Aspirin 300mg

Admit to acute stroke unit

Thrombolysis (must happen within 4.5 hours of symptom onset for risk/benefit ratio)

  • IV alteplase
  • MANY contraindications
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31
Q

Long term ischaemic stroke Mx

A

Aspirin 300mg for 2 weeks
Clopidogrel daily long term

Anticoagulation (e.g. warfarin) for patients with AF

Rehabilitation

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32
Q

Intracerebral haemorrhage epidemiology

A

around 10% of strokes

higher mortality: up to 50%

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33
Q

Pathophysiology of increased ICP in an intracerebral haemorrhage

A

Pooling blood puts pressure on skull, brain & blood vessels - healthy tissue can die

CSF obstruction - hydrocephalus

Midline shift

Tentorial herniation

Coning (compression of the brainstem)

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34
Q

Intracerebral haemorrhage RFs

A

HYPERTENSION
Anticoagulation
Thrombolysis
Age, Alcohol, Smoking, Diabetes

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35
Q

Two causes of intracerebral haemorrhage

A

HYPERTENSION: stiff and brittle vessels are prone to rupture + microaneurysms

SECONDARY to ischaemic stroke (bleeding after reperfusion)

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36
Q

Clinical presentation of intracerebral haemorrhage

A
  • similar to ischaemic stroke -
Pointers to haemorrhage:
SUDDEN LOSS of consciousness
SEVERE HEADACHE
MENINGISM
COMA
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37
Q

Intracerebral haemorrhage Tx

A

Stop anticoagulants immediately

Control BP

Reduce ICP

  • mechanical ventilation
  • IV MANNITOL

Neurosurgical evaluation if:

  • hydrocephalus
  • coma
  • brainstem compression
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38
Q

Vessels in subarachnoid space

A

circle of willis arteries

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39
Q

Vessels in subdural space

A

bridging veins (drain from cortex into dural venous sinus > IJV)

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40
Q

Vessels in extradural space

A

middle meningeal artery

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41
Q

most common type of brain aneurysm

A 
berry aneurysm (90%) - bursting most commonly results in SUBARACHNOID
(70-80% of SAH cases) at circle of willis (ACA, MCA, PCA)
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42
Q

SAH typical age

A

35-65

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43
Q

RFs associated with berry aneurysms

A

Polycystic kidney disease
Coarctation of aorta
Connective tissue disorders

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44
Q

SAH RFs

A 
Hypertension
Known aneurysm
Previous aneurysmal SAH
Berry aneurysm RF e.g. PKD
Smoking, alcohol
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45
Q

Berry aneurysms make up 70-80% of SAH cases, what are the other causes?

A

Traumatic injury
ARTERIOVENOUS MALFORMATIONS (15%): abnormal tangle of blood vessels connecting arteries and veins
IDIOPATHIC (15-20%)

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46
Q

Complications of SAH

A

Rebleeding

Hyponatraemia

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47
Q

SAH pathophysiology

A

Tissue ischaemia
- less blood to reach tissue > less O2 + nutrients > cell death

Raised ICP

Space-occupying lesion (puts pressure on brain)

Meningism

  • blood irritates meninges
  • can obstruct CSF outflow (hydrocephalus)

Vasospasm

  • bleeding irritates other vessels
  • ischaemic injury
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48
Q

SAH symptoms

A

SUDDEN ONSET EXCRUCIATING HEADACHE

  • “Thunderclap” “worst ever headache”
  • Typically OCCIPITAL

Nausea, vomiting, collapse, loss of consciousness

Seizures, vision changes, coma

Mild photophobia/neck stiffness

Sentinel headache before main rupture in some cases

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49
Q

SAH signs

A

Meningeal irritation:

  • Neck stiffness
  • Kernig’s sign
  • Brudzinski’s sign

Retinal bleed -/+ papilloedema (worse prognosis)

Focal neurological signs e.g. 3rd nerve palsy

Increased BP

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50
Q

DDx in SAH

A

Headache

  • MIGRAINE
  • Cluster headache

MENINGITIS

Intracerebral haemorrhage

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51
Q

CT scan in SAH

A

ASAP
Detects >95% of SAH in first 24 hours
Findings of subarachnoid or intraventricular blood
“Star” shaped sign

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52
Q

Lumbar puncture in SAH

A

Only do a lumbar puncture if NORMAL ICP (to prevent CONING)
Indication: if -ve CT but strong suspicion of SAH remains
- after 12 hours

Finding: XANTHOCHROMIA (yellowish CSF with RBC breakdown products e.g. bilirubin)

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53
Q

Mx in SAH

A

Immediately refer to neurosurgeon

IV fluids (maintain cerebral perfusion)

Hydrocephalus: ventricular drainage

NIMODIPINE: calcium antagonist, reduces vasospasm (reducing ischaemic risk)

Surgery: if angiography has shown aneurysm, endovascular coiling

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54
Q

Main cause of subdural haematoma

A

Head trauma

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55
Q

Px SDH

A

MASSIVE LATENT INTERVAL (weeks to months)
[often cannot remember the traumatic injury as it was so long ago]

Symptoms: fluctuating level of consciousness, drowsiness, headache, confusion

Signs: raised ICP, seizures, neurological signs (hemiparesis, unequal pupils)

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56
Q

SDH epidemiology + risk factors

A

BABIES: “shaking baby syndrome” traumatic injury

DEMENTIA, ELDERLY, ALCOHOLICS

  • BRAIN ATROPHY (veins are more susceptible to rupture)
  • more accident-prone (risk of falls) + epileptics

Anticoagulation

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57
Q

Ix SDH

A

CT:

  • CRESCENT SHAPED (BANANA)
  • Unilateral
  • MIDLINE SHIFT
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58
Q

Subdural haemotoma pathophysiology

A

Bridging vein bleeding > haemotoma > bleeding stops > weeks/months later = haemotoma AUTOLYSES = massive increase in ONCOTIC and OSMOSTIC pressure = WATER SUCKED IN = haemotoma enlarges

Gradual rise in ICP over WEEKS

Midline structures shifted away from side of clot = tentorial herniation + coning

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59
Q

Ix SDH

A 
CT:
Haematoma:
- CRESCENT SHAPED (BANANA)
- Unilateral
- MIDLINE SHIFT

MRI scan

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60
Q

Mx SDH

A

SURGERY
depends on clot SIZE, CHRONICITY, CLINICAL PICTURE
- clot evacuation
- craniotomy

IV MANNITOL (reduce ICP)

Reverse clotting abnormalities

Address cause of trauma (falls, abuse)

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61
Q

EDH epidemiology

A

mostly in YOUNG PEOPLE

more common in MALES

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62
Q

EDH pathophysiology

A

After LUCID INTERVAL:

  • rapid rise in ICP
  • midline shift
  • tentorial herniation
  • coning
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63
Q

EDH clinical Px

A 
Lucid interval
Rapidly declining GCS (consciousness level)
Increasingly severe headache
Vomiting
Seizures
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64
Q

EDH Ix

A

CT:

  • LENS SHAPED (LEMON)
  • Doesn’t cross suture lines (trapped in skull)
  • Unilateral
  • Midline shift

Skull X-Ray: fractures

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65
Q

EDH clinical Px

A 
Lucid interval
RAPIDLY DECLINING GCS (consciousness level)
Increasingly severe HEADACHE
VOMITING
SEIZURES
Hemiparesis
UMN signs
COMA
Deep and irregular breathing (due to coning)
DEATH (respiratory arrest)
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66
Q

EDH Ix

A 
CT:
Haematoma:
- LENS SHAPED (LEMON)
- DOESN'T cross suture lines (trapped in skull)
- Unilateral
- Midline shift

Skull X-Ray: fractures

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67
Q

What is a migraine?

A

RECURRENT throbbing UNILATERAL headache often preceded by an AURA and associated NAUSEA, VOMITING, and VISUAL CHANGES

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68
Q

Most common cause of episodic headaches

A

Migraines

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69
Q

Migraines epidemiology

A

90% onset before 40 years

More common in females (roughly 3x)

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70
Q

Migraines RFs

A

Genetics (FHx)
Female
Age (majority of first ones occur in adolescence)

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71
Q

Migraine triggers

A 
CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult i.e. loud noises
Exercise
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72
Q

Migraine prodrome

A

yawning, cravings, mood/sleep changes

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73
Q

Aura

A

precedes migraine attack
variety of symptoms:
visual disturbance e.g. lines, dots, zig-zags
somatosensory e.g. parasthesia, pins & needles

migraines can be classified WITH or WITHOUT AURA

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74
Q

Aura preceding migraine attack

A

variety of symptoms:
visual disturbance e.g. lines, dots, zig-zags
somatosensory e.g. parasthesia, pins & needles

migraines can be classified WITH or WITHOUT AURA

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75
Q

Migraine diagnostic criteria

A 
ATLEAST 2 OF:
Unilateral pain (usually 4-72 hours)
Throbbing-type pain
Moderate-severe intensity
Motion sensitivity

PLUS, AT LEAST 1 OF:
Nausea/vomiting
Photophobia/phonophobia

ALSO: NORMAL EXAMINATION & NO ATTRIBUTABLE CAUSE

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76
Q

Migraine Ix

A

Clinical diagnosis with few or no Ix required

Certain cases may require rule outs e.g. blood tests, CT/MRI, lumbar puncture

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77
Q

Migraine red flag indications for CT/MRI

A 
Thunderclap headache
Change in pattern
Abnormal neuro exam
Onset > 50 years
Epilepsy
Posteriorly located headache
78
Q

Migraine treatment

A

1st line acute = ORAL TRIPTANS E.G. SUMATRIPTAN

  • c/i in IHD + uncontrolled HTN
  • s/e: arrhythmias, angina

NSAIDs e.g. naproxen

Anti-emetics e.g. prochlorperazine

AVOID OPIOIDS & ERGOTAMINE

79
Q

Migraine PROPHYLAXIS

A

Required if >2 attacks per month OR if acute meds are required >2 per week

Triad:

  1. BETA BLOCKERS e.g. propranolol
  2. TCAs e.g. amitriptyline
  3. Anti-convulsant e.g. topiramate
80
Q

Triptan MOA

A

5-HT receptor

at trigeminal nerve, prevents neuropeptide release that would lead to

  • vasodilation
  • neurogenic inflammation
  • PAIN

on cranial vasculature, leading to vasoconstriction

81
Q

Cluster headache definition

A

Episodic headaches lasting from 7 days up to 1 year (usually 2-3 weeks) with pain-free periods that last around 4 weeks

Considered the MOST DISABLING of primary headaches

82
Q

Cluster headache epidemiology

A

Much rarer than migraines
More common in MALES (x4)
Typically affects adults with onset 20-40 years

83
Q

Cluster headache risk factors

A

SMOKER
ALCOHOL
Male
Genetics (FHx)

84
Q

Px of cluster headache

A

RAPID ONSET EXCRUCIATING PAIN, CLASSICALLY AROUND THE EYE
- other common areas = temples or forehead

UNILATERAL and LOCALISED PAIN
- rises to a crescendo

IPSILATERAL AUTONOMIC FEATURES

  • watery & bloodshot eye
  • miosis +/- ptosis
85
Q

Management of acute cluster headache attack

A

15L 100% O2 for 15 minutes via non-rebreather mask

TRIPTANS e.g. SUMATRIPTAN

(Analgesics are UNHELPFUL)

86
Q

Cluster headache prevention

A

1st LINE: VERAPAMIL (CCB)

Prednisolone

Reduce alcohol consumption & stop smoking

87
Q

Is a tension headache episodic or chronic?

A

Usually chronic but can be episodic

  • episodic <15 days/month
  • chronic >15 days/month (for atleast 3 months)
88
Q

Tension headache triggers

A 
Stress
Sleep deprivation
Bad posture
Hunger
Eyestrain
Anxiety
Noise
89
Q

Tension headache Px

A

Usually at least 1 of the following:

  • BILATERAL
  • Pressing/tight & NON-PULSATILE (like an elastic band)
  • mild/moderate intensity

NO AURA, vomiting, or sensitivity to head movement

can be “pressure” behind eyes but the pain isn’t localised here

90
Q

Tension headache Mx

A

Avoidance of triggers & stress relief

Symptomatic relief: NSAIDs (aspirin, ibuprofen), paracetamol
AVOID OPIOIDS

limit analgesics to no more than 6 days per month to reduce the risk of medication-overuse headaches

91
Q

Examples of secondary headaches

A 
Giant cell/temporal arteritis
Sentinel headache
Thunderclap headache
Trauma
Medication overuse
Trigeminal neuralgia
Systemic infection
Meningitis
92
Q

Epilepsy diagnostic criteria

A

At least 2 UNPROVOKED seizures occurring MORE THAN 24 HOURS apart

93
Q

Epilepsy aetiology

A

2/3rds are IDIOPATHIC

Other:
Cortical scarring e.g. trauma, stroke, infection
Tumours/space-occupying lesions
Alzheimer's 
Alcohol withdrawal (delirium tremens)
94
Q

Epilepsy risk factors

A

FHx
Premature birth
Abnormal cerebral blood vessels
Drugs e.g. cocaine

95
Q

Aura in seizures

A

Part of the seizure where the patient is AWARE and often PRECEDES other manifestations

  • e.g. strange feelings in gut, deja vu, strange smells, flashing lights
  • often implies a PARTIAL SEIZURE
96
Q

Post-ictal period of seizures

A

PERIOD AFTER SEIZURES

Headache, confusion, myalgia, sore tongue (often bitten)

Post-ictal Todd’s palsy = temporary weakness after focal seizure in MOTOR CORTEX

Dysphagia following temporal lobe seizure

97
Q

Types of seizure

A

Primary generalised (40%)

  • generalised = whole cortex
  • ALWAYS ASSOCIATED WITH LOSS OF CONSCIOUSNESS & LACK OF AWARENESS
  • BILATERAL and SYMMETRICAL motor manifestations

Partial (focal) (60%)

  • SINGLE LOBE IN ONE HEMISPHERE e.g. temporal lobe
  • often seen with underlying structural disease
  • may later progress to generalised
98
Q

Types of primary generalised seizure

A

Tonic = rigid, stiff limbs

Clonic = rhythmic muscle jerking

TONIC-CLONIC (Grand Mal) = stereotypical shaking seizures

Myoclonic = isolated jerking of a limb

Atonic = opposite to tonic: loss of muscle tone (floppy)

Absence (Petit Mal) = blank stare, common in childhood + increases risk of developing tonic-clonic as adult

99
Q

Types of partial (focal) seziure

A

Simple partial seizure = no effect on consciousness or memory, no post-ictal symptoms

Complex partial seizure = memory/awareness is affected at some point, most commonly TEMPORAL (speech, memory, emotion), post-ictal confusion in temporal (frontal has swift recovery)

Partial seizure with secondary generalisation = 2/3 patients with partial seizures will develop generalised (usually T-C)

100
Q

Temporal lobe seizure characteristics

A

AURA (80%)
Automatisms e.g. lip smacking
Anxiety, out-of-body experiences

101
Q

Frontal lobe seizure characteristics

A

Motor features e.g. posturing, peddling legs
JACKSONIAN MARCH (seizures march up/down the motor homunculus)
Post-ictal Todd’s palsy (starts distally in a limb and works its way up to the face)

102
Q

Parietal lobe seizure characteristics

A

Sensory disturbances e.g. tingling/numbness

103
Q

Occipital lobe seizure characteristics

A

Visual phenomena e.g. spots, lines, flashes

104
Q

Non-epileptic seizure characteristics

A

Entirely situational e.g. metabolic disturbances, low Na+, hypoxia

Typically longer with closed eyes + mouth

DO NOT OCCUR DURING SLEEP
do not involve incontinence or tongue biting

Pre-ictal anxiety symptoms

105
Q

Epilepsy Ix

A

ELECTROENCEPHALOGRAM (EEG)
Not diagnostic but can help support a diagnosis/type of epilepsy

MRI/CT HEAD
- rules out other potential causes e.g. space-occ lesion

BLOODS
- rules out other potential causes e.g. metabolic

Genetic testing
e.g. juvenile myoclonic epilepsy

106
Q

Wernicke’s encephalopathy

A

Depletion of thiamine (Vitamin B1)

Classic triad:
Confusion
Ataxia
Opthalmoplegia

Sign: Asterixis (liver flap) - sign of metabolic encephalopathy

107
Q

Epilepsy Tx: generalised tonic-clonic, tonic, atonic

A

Sodium valproate for males & women unable to bear children

Lamotrigine for females of childbearing potential

108
Q

Epilepsy Tx: myoclonic

A

Sodium valproate for males & women unable to bear children

Levetiracetam/Topiramate for females of childbearing potential

109
Q

Epilepsy Tx: absence

A

Sodium valproate for males & women unable to bear children

Ethosuximide for females of childbearing potential

110
Q

Epilepsy Tx: partial (focal)

A

Lamotrigine

111
Q

Example of primary brain tumour

A

Much less common than secondary

Gliomas e.g. astrocytoma (most common)
Others e.g schwannoma

112
Q

Most common origins of secondary brain tumours

A 
Non-small cell lung cancers (most common)
SCLC
Breast
Renal cell carcinoma
GI
113
Q

Alzheimer’s disease epidemiology

A

Most common type of dementia

Mainly affects >65

114
Q

Parkinson’s disease patho

A

Progressive destruction of dopaminergic neurones in the substantia nigra of the basal ganglia

Basal ganglia = habitual movements, voluntary movements + learning of specific movement patterns

115
Q

Clinical Px Parkinson’s disease

A

TRIAD:
Unilateral RESTING tremor (pill-rolling) - diminishes with intentional movement
Cogwheel rigidity (resistance to passive movement of the joint)
Bradykinesia: shuffling gait + ‘freezing’ when starting to walk (difficulty initiating movement)

Cognitive impairment
Depression
Visual hallucinations
Sleep disorders

NO WEAKNESS

116
Q

PD Ix

A

DaT scan (injected drug assesses dopaminergic neurones)

A normal CT scan will show no pathology

117
Q

PD Mx

A
  1. Dopamine agonists e.g. carbergoline
  2. MAO-B inhibitors e.g. sergeline
  3. Co-careldopa (Levodopa + carbidopa)
118
Q

PD vs Benign resting tremor

A

PD: worse at rest, improves with intentional movement

BRT: improves at rest, improves with ALCOHOL, worse with intentional movement

119
Q

Parkinson’s histopathological findings

A 
Loss of dopaminergic neurones 
Lewy bodies (eosinophilic cytoplasmic inclusions made of alpha synuclein)
120
Q

Huntingtons disease

A

HTT mutation on c4 = CAG trinucleotide repeat
>35 CAG = HD

Loss of GABAergic neurones = hyperexcitation of dopaminergic pathways in the striatum = excessive thalamic stimulation = chorea

121
Q

Clinical Px of HD

A 
Chorea
Dystonia
Incoordination
Cognitive + behaviour difficulties
Irritability, agitation, anxiety
122
Q

HD Ix

A

GENETIC TESTING

MRI/CT = loss of striatal volume

123
Q

HD Tx

A

Benzodiazepines/valproic acid (for chorea)
SSRIs (for depression)
Haloperidol (for psychosis)

124
Q

HD prognosis

A

Poor
Most common cause of death = pneumonia
Second most common cause of death = suicide

125
Q

Differential diagnosis in HD

A

Sydenham’s chorea (Rheumatic fever)

126
Q

Alzheimer’s disease RFs

A

Down’s syndrome
Depression
ApoE E4 allele homozygosity

127
Q

Pathological hallmarks of AD

A

EXTRACELLULAR deposition of B-amyloid plaques

INTRACELLULAR neurofibrillary tangles (tauopathy)

128
Q

Alzheimer’s treatment

A

Acetycholinesterase inhibitors e.g. rivastigmine, donepezil

129
Q

AD Ix

A

Entirely clinical diagnosis
MRI = cerebral atrophy
Rule out: bloods (TFTs, B12)

130
Q

Vascular dementia

A

Caused by MULTIPLE INFARCTS

Sudden onset
Stepwise deterioration

131
Q

Lewy body dementia

A

Presence of Lewy Bodies in brainstem + occipto-parietal region (misfolded a-synuclein/eosinophilic inclusions)

Fluctuating cognitive dysfunction, visual hallucinations + parkinsonism

Tx: cholinesterase inhibitors

132
Q

Frontotemporal dementia

A 
Progressive
More common dementia in those under 65
Atrophy in frontal and temporal lobes with no plaque formation 
Tauopathy (which leads to apoptosis)
Pick bodies

Px: behavioural issues e.g. disinhibition, progressive aphasia e.g. slow, difficult speech, dementia symptoms

Tx: cholinesterase inhibitors

133
Q

Age of onset multiple sclerosis

A

Early adult life (20-40 years)

134
Q

Pathophysiology of multiple sclerosis

A 
Autoimmune destruction (CD4 mediated - Type 4 HS)
CNS oligodendrocyte myelin sheath attack = plaques (sclera) 
Remission = regulatory T cells > remyelination in early disease
135
Q

MS patterns

A

Relapsing remitting (most common)
Primary progressive
Secondary progressive
Progressive relapsing

136
Q

Charcot’s neurological triad (MS)

A

Nystagmus (painful, shaking eyes) - optic nerve plaques: optic neuritis

Intention tremor - motor pathway plaques

Staccato speech (dysarthria) - brain stem attacks: conscious movement (eating, talking) + unconscious (swallowing)

137
Q

What is Uhthoff’s phenomenon in MS?

A

Worsening symptoms with increase in body temperature

138
Q

What is Lhermitte’s sign in MS?

A

Sudden electrical sensation passing down the neck, spine, radiating out to the limbs when bending the neck forward

139
Q

McDonald’s diagnostic criteria for MS

A

2 or more CNS attacks, at least 30 days apart and affecting different parts of the CNS
“Disseminated in space and time”

140
Q

MS Ix

A

Clinical diagnosis

LUMBAR PUNCTURE: Oligoclonal IgG bands

MRI: plaque detection, white matter abnormalities, periventricular lesions

141
Q

MS Tx

A

Acute: IV METHYLPREDNISOLONE

Other:
Vitamin D supplements 
B-IFN (decreases inflammatory cytokines in brain) 
Biologicals e.g. Monoclonal antibodies 
Symptomatic: baclofen, amitriptyline
DMARDs
142
Q

Px MS

A 
TEAM:
Tingling (parathaesia)
Eye: optic neuritis 
Ataxia
Motor: paraparesis

Autonomic: bladder and bowel, sexual dysfunction
Decreased vibration sense
Dysphagia, constipation
Falls

143
Q

Risk factors MS

A

Genetic: female, HLA DR2
Environmental: infections, vitamin D deficiency

144
Q

UMN symptoms in MND

A

EVERYTHING GOES UP

Increased muscle tone
Brisk reflexes
Positive BABINSKI sign
Impaired fine movement

145
Q

LMN symptoms in MND

A

EVERYTHING GOES DOWN

Decreased muscle tone and reflexes
Muscle WASTING
Fasciculations

146
Q

MND epidemiology

A

> 50 y/o males

147
Q

Typical MND patient Px

A 
>40 
Stumbling, spastic gait
FOOT DROP, weak grip 
NO SENSORY LOSS
NO EYE MOVEMENT DISTURBANCES
148
Q

Types of MS

A 
ALS: UMN+LMN
PBP (progressive bulbar palsy): UMN+LMN
PMA (progressive muscular atrophy): LMN only 
PLS (primary LS): UMN only 
Corticobulbar (pseudobulbar) palsy
149
Q

ALS Px

A

MOST COMMON

Weakness, UMN + LMN signs, fasciculations
Drifting thumb
Wrist, foot drop

150
Q

Progressive bulbar palsy Px

A

WORST PROGNOSIS

Affects cranial nerves IX-XII
Dysarthria, dysphagia

151
Q

Progressive muscular atrophy Px

A

Only LMN signs

Affects muscles distally to proximally

152
Q

MND Ix

A

Clinical diagnosis: LMN + UMN signs in 3 regions

Blood tests
MRI
Lumbar puncture

153
Q

MND Tx

A

Antiglutamatergic drugs e.g. RILUZOLE (sodium channel blocker that inhibits glutamate release)
Spasticity: baclofen
Respiratory: non-invasive ventilation

154
Q

What is myasthenia gravis?

A

Autoimmune destruction of acetylcholine receptors

155
Q

What is myasthenia gravis exacerbated by?

A

Pregnancy
Infection
Emotion
Drugs

156
Q

Myasthenia gravis Px

A

Symptoms worse after muscle use (increasing muscle fatigue)

157
Q

Myasthenia gravis Ix

A

Acetylcholine receptor (ACh-R) antibodies (85% of patients)

Positive tensilon test
- edrophonium (neostigmine) injection = temporary relief (due to increase in ACh)

A CT or MRI of the thymus gland to look for a thymoma

158
Q

Myasthenia gravis Tx

A

Immunosuppression
Neostigmine
Thymectomy

159
Q

Guillane-Barré pathophysiology

A

Peripheral neuropathy often occurring after infection (molecular mimicry against pathogenic antigen AND peripheral nerves)

160
Q

Kernigs sign

A

Resistance to extension of the leg while the hip is flexed

+ve in meningitis

161
Q

Brudinskis sign

A

Flexion of the hips and knees in response to neck flexion

+ve in meningitis

162
Q

Syncope

A

Temporary loss of consciousness due to disruption of blood flow to the brain (Vasovagal)

163
Q

Primary syncope

A

Dehydration
Missed meals
Extended standing in a warm environment
Stimuli E.g. sight of blood

164
Q

Syncope Ix

A

ECG
24 hour ECG
Echocardiogram
Bloods

165
Q

Spina bifida aetiology

A

Combination of genetic, nutritional and environmental risk factors e.g. folate deficiency

166
Q

Autonomic vs somatic NS receptors

A
167
Q

Cerebral stroke patterns: MCA vs ACA

A
168
Q

Tonic seizure

A
169
Q

Tonic clonic seizure

A
170
Q

Selective colour vision deficit on red-green colour test

A

MS

171
Q

Most common causative organism of meningitis in children 3 months-12 years

A

Strep pneumoniae (think snotty kids)

172
Q

Saddle anaesthesia

A

Associated with CAUDA EQUINA SYNDROME
Erectile dysfunction
Loss of bowel control

173
Q

Change in CSF parameters BACTERIAL meningitis

A

Turbid (yellow) fluid, with neutrophils, raised protein (bacteria produce enzymes etc), low glucose

174
Q

Change in CSF parameters VIRAL meningitis

A

Clear fluid, with lymphocytes, normal glucose, normal protein

175
Q

Change in CSF parameters in FUNGAL meningitis

A
176
Q

Change in CSF parameters TB meningitis

A
177
Q

Uhthoff’s phenomenon

A

MS symptoms get worse with heat (E.g. shower)

178
Q

Resperidone

A

Dopamine receptor antagonist: manages aggression and chorea in HD

179
Q

Guillain Barre syndrome Tx

A

IV immunoglobulins

180
Q

Encephalitis

A

Inflammation of the brain
Can be caused by herpes simplex virus
Triad: fever, altered mental state, headache
Community Tx: IM Benpen (suspect meningitis)
Hospital: acyclovir

181
Q

Shingles (Herpes Zoster) neurological manifestation

A

Post-herpetic neuralgia

182
Q

Sciatica

A
183
Q

Trigeminal neuralgia

A

Sudden severe facial pain in the trigeminal regions

184
Q

Difference between Lambert Eaton syndrome and myasthenia gravis

A 
LES = autoimmune attack of calcium gated channels 
MG = autoimmune attack of ACh receptor
185
Q

Brown Sequard syndrome

A

Ipsilateral loss:
Corticospinal
Dorsal column

Contralateral (1-2 levels down):
Spinothalamic

186
Q

Charcot-Marie-Tooth syndrome

A

Autosomal dominant
Demyelination of peripheral motor and sensory nerves
Classical features: inverted champagne bottle legs, high foot arches

187
Q

Duchenne Muscular dystrophy

A

X-linked recessive disease (only men can be affected)

Characterised by progressive muscle degeneration and weakness due to the alterations of a protein called dystrophin that helps keep muscle cells intact

188
Q

Beckers muscular dystrophy

A
189
Q

Cauda equina vs conus medullaris

A

Cauda Equina = L1/L2 (level at which spinal cord terminates) = LMN features only

Conus medullaris = UMN features (hyperreflexic)

190
Q

Stroke definition

A

Sudden onset neurological deficit due to ischaemic or haemorrhagic compromise with symptoms lasting over 24 hours

Belle Phase 2a (14 decks)

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