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Year 2 > NEURO: Part 6 > Flashcards

NEURO: Part 6 Flashcards

1
Q

Define Huntington’s Chorea

A
  1. Cause of chorea and is a neurodegenerative disorder characterised by lack of inhibitory GABA
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2
Q

What is CHorea

A

Continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another

Interfere with voluntary movements but cease during sleep

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3
Q

Genetic cause of Huntington’s

A

AUTOSOMAL DOMINANT condition

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4
Q

At what age does HUNTINGTON’s present

A

Middle age

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5
Q

What type of symptoms are presented when huntington’s manifests

A

Prodromal phase (irritability, depression and incoordination)

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6
Q

Where does huntington’s mutation take place

A

CHROMOSOME 4 resulting in REPEATED EXPRESSION OF CAG sequence

  • leads to translation of expanded polyglutamine repeat structure in huntington gene, protein gene product the function of which is unclear
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7
Q

How does symptom onset correlate with CAG repeats

A

More repeats = earlier symptoms

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8
Q

How many repeats are seen in middle aged men

A

36-55

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9
Q

How many repeats are seen in huntington’s childhood

A

60!

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10
Q

Pathophysiology caused by gene mutation in huntington’s

A
  1. Progressive cerebral atrophy with loss of neurones in DORSAL STRIATUM of basal ganglia - loss of GABANERGIC and CHOLINERGIC neurones
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11
Q

How does GABA effect Dopamine release

A

Loss of Gaba removes inhibition against dopamine = excessive thalamic stimulation and movements = chorea

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12
Q

Clinical presentation of Huntington’s

A
  1. PRODROMAL STAGE
  2. THEN CHOREA: Relentlessly progressive, jerky, explosive, rigidity INVOLUNTARY movements that cease when sleeping

CAN’T SIT STILL

  1. Dysarthria, dysphagia and abnormal eye movements
  2. BEHAVIOURAL CHANGES: Depression, anxiety and aggression + apathy
  3. Dementia (+ associated seizures)
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13
Q

What causes death in huntington’s

A

DEMENTIA within 15 years of diagnosis = infections

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14
Q

Differential diagnosis

A

CAUSES OF CHOREA:

  1. Sydenham’s chorea
  2. Creutzfeldt-Jakob Disease (prion)
  3. Wilson’s disease
  4. SLE
  5. Stroke of basal ganglia
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15
Q

How is huntington’s diagnosed

A
  1. Genetic testing

2. CT/MRI

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16
Q

What will genetic testing show in huntington’s

A
  1. CAG REPEATS
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17
Q

What would CT/MRI

A

CAUDATE NUCLEUS atrophy and increased size of frontal horns of LATERAL VENTRICLES (sign of brain matter destruction)

Can’t be used early on

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18
Q

How is huntington’s treated

A
  1. GENETIC COUNSELLING
  2. BENZODIAZEPINES
  3. SULPIRIDE (depresses nerve function)
  4. TETRABENAZINE (dopamine depleting agent)
  5. SEROXATE (SSRI antidepressant)
  6. HALOPERIDOL (antipsychotic medication)
  7. RISPERIDONE (to treat aggression)
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19
Q

What are primary causes of headache examples

A
  1. MIGRAINES
  2. CLUSTER HEADACHES
  3. TENSION HEADACHE
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20
Q

What are cluster headaches

A

Severe headaches around the eye

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21
Q

What are tension headaches

A

Headache effecting both sides of the head due to environmental stresses

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22
Q

What causes secondary headaches

A
  1. UNDERLYING CAUSES:
HIV
FEVER
THUNDERCLAP HEADACHE
SEIZURE
SUSPECTED MENINGITIS
SUSPECTED ENCEPHALITIS
RED EYE
HEADACHE + NEW FOCAL NEUROLOGY (papilloedema(
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23
Q

Define Migraine

A
  1. Recurrent throbbing headache often proceeded by aura and associated with nausea, vomiting and visual changes
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24
Q

What kind of headache are migraines

A

EPISODIC

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25
Q

In what gender are migraines common

A

FEMALES

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26
Q

How does severity of headaches change with age

A

DECREASES

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27
Q

Causes of migrianes

A 
CHOCOLATE
C - Chocolate
H - Hangovers
O - Orgasms
C - Cheese
O - Oral Contraceptives
L - Lie Ins
A - Alcohol 
T - TUMULT (loud noise)
E - Excersise
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28
Q

What nerve may cause migraines

A

Trigeminal nerve

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29
Q

Risk factors for migraines

A
  1. FEMALE
  2. AGE
  3. FAM HISTORY
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30
Q

Why do genetic factors have an effect on migraines

A

EFFECT NEURONAL-HYPER_EXCITABILITY

change sin brainstem blood flow lead stop unstable trigeminal nerve nucleus and nuclei in basal thalamus

Cortical spreading depression occurs

Results in release of vasoactive neuropeptides including calcitonin-gene-related peptide and substance P: causes neurogenic inflammation (vasodilatation and plasma protein extravasation leading to pain all over cerebral cortex

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31
Q

What is cortical spreading depression

A

Self-propagating waves of neuronal and glial depolarisation that spreads across cerebral cortex that causes aura of migraines and release of inflammatory mediators which impact trigeminal nerve nucleus

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32
Q

Clinical presentation of Migraine without aura

A
  1. TWO OF FOLLOWING:
    - Unilateral
    - Pulsing
    - Moderate/severe pain in head
    - Aggravated by routine physical activity

Nausea or vomiting during headache

Photophobia and Misophobia

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33
Q

Clinical presentation of migraine with prodrome

A
  1. Yawning
  2. Cravings
  3. Mood/sleep changes
34
Q

Clinical presentation of migraine with aura

A
  1. @ attacks
  2. Aura precedes attack by minutes
  3. Visual: Chaotic cascading, jumbling, distorting lines, dots or zigzags
  4. Scotoma (black hole in visual field)
  5. Hemianopia
  6. Paraesthesiae spreading from fingers to face

UNILATERAL PULSLABILE HEADACHE

35
Q

General migraine features

A

AT LEAST 2 of:

  1. Unilateral pain
  2. Throbbing-type pain
  3. Moderate to severe intensity
  4. Motion sensitivity

AT LEAST ONE OF:
Nausea/vomiting
PHOTOPHOBIA/PHONOPHOBIA
Normal examination with no other caues

36
Q

Differential diagnosis of migraines

A
  1. Tension headache (bilateral around head)
  2. Cluster headache (PAINFUL, around eye)
  3. Mediction headaches
    4, SUDDEN” Meningitis or subarachnoid haemorrhage
  4. TIAs can cause visual and hemisensory symptoms
  5. Tumour mass or temporal arteritis
37
Q

How are migraines diagnosed

A
  1. EYES (papilloedema using fundocscopy)
  2. BP
  3. HEAD + NECK arteries

——-Exclude other causes—–

FBC (CRP and ESR)
CT/MRI
Lumbar puncture

38
Q

When is CT/MRI done for migraines (red flags)

A
  1. SEVERE thunderclap headache
  2. Changes in pattern of migraine
  3. Abnormal neuro exam
  4. Onset over 50
  5. Epilepsy
  6. Posteriorly located
39
Q

Indications for lumbar puncture in migraines

A
  1. thunderclap headache
  2. Severe onset, progressive headaches
  3. NEUROIMAGING should precede lumbar puncture to rule out raised ICP
40
Q

Treatment of migraines

A 
1. Reduce triggers
ACUTE:
1. No ERGOTS
2. SUMATRIPTAN 
3. NSAIDs
4. Anti-emetic (PROCHLORPERAZINE)
41
Q

Why are triptans given

A

The selectively stimulate 5-hydroxytryptamine receptors in the brain

42
Q

When are sumatriptan contraindicated and why

A

IHD, coronary spasms

Causes arythmies and angina

43
Q

Preventative treatment of migraines

A

DONE when more than 2 attacks a month

  1. PROPRANOLOL (not for asthmatics)
  2. AMITRIPTYLINE
  3. TOPIRAMATE (anti-convulsant)
44
Q

When is acute migraine treatment given

A

when they are 2x a week

45
Q

Define tension headache

A

MOST CHRONIC DIALY + RECURRENT HEADACHES are tension headaches

46
Q

What type of headache are tension headahces

A
  1. EPISODIC (<15 days/month)

2. CHRONIC ( more than 15 days for at least 3 months)

47
Q

What causes tension headaches

A

No organic cause

48
Q

Risk factors for tension headaches

A
  1. Stress
  2. Sleep deprivation
  3. Bad posture
  4. Hunger
  5. Eyestrain
  6. Anxiety
  7. Noise
49
Q

Clinical Presentation of tension headaches

A
  1. BILATERAL
  2. Non=pulsatile (tight)
  3. Mild intensity
  4. Scalp muscle tenderness
  5. No vomitiing or aura
  6. Not aggravated by physical activity
  7. Pressure behind eyes
  8. Lasts from 30 mins to 7 days
50
Q

Differential diagnosis of tensions headahces

A
  1. Migraine
  2. Cluster headaches
  3. Giant cell arteritis
  4. Drug-induced headaches
51
Q

How is tension headache diagnosed

52
Q

Treatment of tension headaches

A
  1. Lifestyle advice (regular excersise, avoidance of triggers)
  2. Stress relief
  3. Symptom relief
53
Q

Symptom relief of tensions headaches

A
  1. ASPIRIN
  2. PARACETAMOL
  3. NSAIDS
    no opcodes
  4. AMITRYPTYLINE
54
Q

Why do we not give opioids

A

Strong analgesics can cause medication-overdose headaches

55
Q

How do we stop medication-overdose headaches in aspirin, paracetamol dosages

A

No more than 6 days a month

56
Q

In what gender are cluster headaches common in

57
Q

What age do cluster headaches effect

58
Q

What risk factors for cluster headaches

A
  1. SMOKER
  2. MALE
  3. AUTOSOMAL DOMINANT GENE has a role
59
Q

What causes cluster headaches

A

Superficial temporary artery smooth muscle hyper-reactivity to serotonin (5HT)

Hypothalamic grey matter abnormalities too

60
Q

Clinical presentation of cluster headaches

A
  1. ACUTE
  2. Pain around one eye, temple or forehand
  3. IPSILATERAL CRANIAL AUTONOMIC FEATURES
  4. Pain is UNILATERAL
  5. Rises to crescendo over minutes (15-160 mins once or twice a day)
  6. Often nocturnal/early morning
  7. VOmiting
  8. Episodic: 4-12 weeks and pain-free periods for months or years
  9. Chornic
61
Q

Differential diagnosis of cluster headaches

62
Q

Ipsilateral cranial autonomic features of cluster headaches

A
  1. Blud shot water eyes with lid swelling
  2. Facial flushing
  3. Rhinorrhea
  4. Miosis (excessive pupil constriction) + ptosis (drooping of upper eyelid)
63
Q

How is cluster headaches diagnosed

A
  1. At least five headache attacks that fulfil above criteria

HISTORY

64
Q

Treatment for cluster headaches

A

ACUTE: Analgesics
100% 15L O2 for 15 mins with non-rebreathable mask
3. SC SUMATRIPTAN reduces vascular inflammation

65
Q

Preventative treatment for cluster headaches

A
  1. VERAPAMIL
  2. Avoid alcohol during cluster period
  3. PREDNISOLONE
66
Q

Branches of trigeminal nerve

A
  1. OPTHALMIC
  2. MAXILLLARY
  3. MANDIBULAR
67
Q

What trigeminal nerve supplies muscles of mastication

A

MANDIBULAR branch

68
Q

What age is effected in trigeminal neuralgia

69
Q

Is trigeminal neuralgia bi or unilateral

A

UNILATERAL

70
Q

What causes trigeminal neuralgia

A

Compression of trigeminal nerve by vein or artery

LOCAL PATHOLOGICAL (meningeal inflammation, aneurysms) - young people

FIFTH NERVE LESIONS due to pathology

71
Q

What would cause fifth nerve lesion at brainstem

A

TUMOUR
MS
INFARCTION

72
Q

What would cause fifth nerve lesion at cerebellopontine angle

A

ACOUSTIC NEUROA

TUMOUR

73
Q

What would cause fifth nerve lesion at petrous bone

A

spreading middle ear infection

74
Q

What would cause fifth nerve lesion at cavernous sinus

A

Aneurysms of internal carotid, tumour or thrombosis of cavernous sinus

75
Q

Risk factors for trigeminal neuralgia

A
  1. HYPERTENSION

2. TRIGGERS: washing affected area, shaving, eating and talking

76
Q

What happens to the nerve in compression during trigeminal neuralgia

A
  1. DEMYELINATION and excitation of nerve = erratic pain signalling
77
Q

Clinical presentation of trigeminal neuralgia

A
  1. UNILATERAL
  2. Facial pain in one or more distributions of nerve (no further than what is supplied by trigeminal nerve)
  3. PAIN HAS THREE OF THE FOLLOWING:
    - Reoccurring in paroxysmal attacks from a fraction of a second to 2 minutes
    - severe intensity
    - electric shock like, shooting, stabbing or knife-like
    - precipitated by innocuous stimuli (washing or shaving)
78
Q

Differential diagnosis of trigeminal neuralgia

A
  1. GIANT CELL ARTERITIS/TEMPORAL ARTERITIS
  2. Dental pathology
  3. TEMPOROMANDIBULAR JOINT DYSFUNCTION
  4. MIGRAINE
  5. CLUSTER
  6. HEADACHES
79
Q

Treatment of trigeminal neuralgia

A
  1. ORAL CARBAMAZEPINE (surpasses attack)
  2. ORAL PHEYTOIN< GABAPENTIN or LAMOTRIGINE
  3. spontaneously remit after 6-12 months
    IF drugs fail then surgery
80
Q

What surgery can be done for trigeminal neuralgia

A
  1. MICROVASCULAR DECOMPRESSION (anomalous vessels separated form trigeminal root)
  2. GAMMA KNIFE SURGERY (directly at trigeminal nerve ganglion or nerve root)
  3. Stereotactic radio surgery

Year 2 (155 decks)

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