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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
In what gender are migraines common
FEMALES
26
How does severity of headaches change with age
DECREASES
27
Causes of migrianes
``` CHOCOLATE C - Chocolate H - Hangovers O - Orgasms C - Cheese O - Oral Contraceptives L - Lie Ins A - Alcohol T - TUMULT (loud noise) E - Excersise ```
28
What nerve may cause migraines
Trigeminal nerve
29
Risk factors for migraines
1. FEMALE 2. AGE 3. FAM HISTORY
30
Why do genetic factors have an effect on migraines
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
31
What is cortical spreading depression
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
32
Clinical presentation of Migraine without aura
1. TWO OF FOLLOWING: - Unilateral - Pulsing - Moderate/severe pain in head - Aggravated by routine physical activity Nausea or vomiting during headache Photophobia and Misophobia
33
Clinical presentation of migraine with prodrome
1. Yawning 2. Cravings 3. Mood/sleep changes
34
Clinical presentation of migraine with aura
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
General migraine features
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
Differential diagnosis of migraines
1. Tension headache (bilateral around head) 2. Cluster headache (PAINFUL, around eye) 3. Mediction headaches 4, SUDDEN" Meningitis or subarachnoid haemorrhage 5. TIAs can cause visual and hemisensory symptoms 6. Tumour mass or temporal arteritis
37
How are migraines diagnosed
1. EYES (papilloedema using fundocscopy) 2. BP 3. HEAD + NECK arteries -------Exclude other causes----- FBC (CRP and ESR) CT/MRI Lumbar puncture
38
When is CT/MRI done for migraines (red flags)
1. SEVERE thunderclap headache 2. Changes in pattern of migraine 3. Abnormal neuro exam 4. Onset over 50 5. Epilepsy 6. Posteriorly located
39
Indications for lumbar puncture in migraines
1. thunderclap headache 2. Severe onset, progressive headaches 3. NEUROIMAGING should precede lumbar puncture to rule out raised ICP
40
Treatment of migraines
``` 1. Reduce triggers ACUTE: 1. No ERGOTS 2. SUMATRIPTAN 3. NSAIDs 4. Anti-emetic (PROCHLORPERAZINE) ```
41
Why are triptans given
The selectively stimulate 5-hydroxytryptamine receptors in the brain
42
When are sumatriptan contraindicated and why
IHD, coronary spasms Causes arythmies and angina
43
Preventative treatment of migraines
DONE when more than 2 attacks a month 1. PROPRANOLOL (not for asthmatics) 2. AMITRIPTYLINE 3. TOPIRAMATE (anti-convulsant)
44
When is acute migraine treatment given
when they are 2x a week
45
Define tension headache
MOST CHRONIC DIALY + RECURRENT HEADACHES are tension headaches
46
What type of headache are tension headahces
1. EPISODIC (<15 days/month) | 2. CHRONIC ( more than 15 days for at least 3 months)
47
What causes tension headaches
No organic cause
48
Risk factors for tension headaches
1. Stress 2. Sleep deprivation 3. Bad posture 4. Hunger 5. Eyestrain 6. Anxiety 7. Noise
49
Clinical Presentation of tension headaches
1. BILATERAL 2. Non=pulsatile (tight) 3. Mild intensity 4. Scalp muscle tenderness 5. No vomitiing or aura 6. Not aggravated by physical activity 6. Pressure behind eyes 7. Lasts from 30 mins to 7 days
50
Differential diagnosis of tensions headahces
1. Migraine 2. Cluster headaches 3. Giant cell arteritis 4. Drug-induced headaches
51
How is tension headache diagnosed
History
52
Treatment of tension headaches
1. Lifestyle advice (regular excersise, avoidance of triggers) 2. Stress relief 4. Symptom relief
53
Symptom relief of tensions headaches
1. ASPIRIN 2. PARACETAMOL 3. NSAIDS no opcodes 4. AMITRYPTYLINE
54
Why do we not give opioids
Strong analgesics can cause medication-overdose headaches
55
How do we stop medication-overdose headaches in aspirin, paracetamol dosages
No more than 6 days a month
56
In what gender are cluster headaches common in
MALES
57
What age do cluster headaches effect
20-40
58
What risk factors for cluster headaches
1. SMOKER 2. MALE 3. AUTOSOMAL DOMINANT GENE has a role
59
What causes cluster headaches
Superficial temporary artery smooth muscle hyper-reactivity to serotonin (5HT) Hypothalamic grey matter abnormalities too
60
Clinical presentation of cluster headaches
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
Differential diagnosis of cluster headaches
Migraines
62
Ipsilateral cranial autonomic features of cluster headaches
1. Blud shot water eyes with lid swelling 2. Facial flushing 3. Rhinorrhea 4. Miosis (excessive pupil constriction) + ptosis (drooping of upper eyelid)
63
How is cluster headaches diagnosed
1. At least five headache attacks that fulfil above criteria HISTORY
64
Treatment for cluster headaches
ACUTE: Analgesics 100% 15L O2 for 15 mins with non-rebreathable mask 3. SC SUMATRIPTAN reduces vascular inflammation
65
Preventative treatment for cluster headaches
1. VERAPAMIL 2. Avoid alcohol during cluster period 3. PREDNISOLONE
66
Branches of trigeminal nerve
1. OPTHALMIC 2. MAXILLLARY 3. MANDIBULAR
67
What trigeminal nerve supplies muscles of mastication
MANDIBULAR branch
68
What age is effected in trigeminal neuralgia
FEMALES
69
Is trigeminal neuralgia bi or unilateral
UNILATERAL
70
What causes trigeminal neuralgia
Compression of trigeminal nerve by vein or artery LOCAL PATHOLOGICAL (meningeal inflammation, aneurysms) - young people FIFTH NERVE LESIONS due to pathology
71
What would cause fifth nerve lesion at brainstem
TUMOUR MS INFARCTION
72
What would cause fifth nerve lesion at cerebellopontine angle
ACOUSTIC NEUROA | TUMOUR
73
What would cause fifth nerve lesion at petrous bone
spreading middle ear infection
74
What would cause fifth nerve lesion at cavernous sinus
Aneurysms of internal carotid, tumour or thrombosis of cavernous sinus
75
Risk factors for trigeminal neuralgia
1. HYPERTENSION | 2. TRIGGERS: washing affected area, shaving, eating and talking
76
What happens to the nerve in compression during trigeminal neuralgia
1. DEMYELINATION and excitation of nerve = erratic pain signalling
77
Clinical presentation of trigeminal neuralgia
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
Differential diagnosis of trigeminal neuralgia
1. GIANT CELL ARTERITIS/TEMPORAL ARTERITIS 2. Dental pathology 3. TEMPOROMANDIBULAR JOINT DYSFUNCTION 4. MIGRAINE 5. CLUSTER 6. HEADACHES
79
Treatment of trigeminal neuralgia
1. ORAL CARBAMAZEPINE (surpasses attack) 2. ORAL PHEYTOIN< GABAPENTIN or LAMOTRIGINE 3. spontaneously remit after 6-12 months IF drugs fail then surgery
80
What surgery can be done for trigeminal neuralgia
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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