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Phase 3a > Neuro > Flashcards

Neuro Flashcards

1
Q

What are differential diagnoses for recurrent black outs?

A

Syncope

  • Cardiopulmonary- structural (aortic stenosis, PE), arrhythmias
  • Vasovagal (reflexive)- postural hypotension, carotid sinus sensitivity, situational (coughs, micturation, postexertional)

Epilepsy

Hypoglycaemia

Pychogenic

  • NEAD
  • Panic attacks/ hyperventilation
  • Narcolepsy
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2
Q

What is a Jacksonian March?

A

Simple focal seizure spreads to include more muscles etc.

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3
Q

What is a partial/focal seizure?

+ what is simple vs complex partial seizures?

A

Only effects one part of the brain- a set few symptoms

Simple- remains conscious and is usually aware
Complex- unconscious and unaware, doesn’t remember

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4
Q

What is a generalised seizure?

Tonic?
Atonic?
Clonic?
Tonic-Clonic?
Myoclonic?
Absent?
A
  • includes the whole brain

Tonic- muscles stiffen
Atonic- muscles all relax
Clonic- muscles spasm
Tonic-Clonic- muscles have periods of spasm and relaxation (grand mal)
Myoclonic- short muscle twitches
Absent- lose consciousness and then regain- “spaced out” (petit mal)

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5
Q

What classifies a diagnosis of “epilepsy”?

A

recurring 8 unpredictable seizures

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6
Q

What is status epilepticus?

  • causes?

How do you manage this?

A

Seizure(s) for >5 minutes without a break.
- usually tonic-clonic

Causes

  • stopping epileptic medication (suddenly)
  • alcohol/ drug abuse
  • infection

MANAGEMENT: ABCDE, Benzodiazepines (Lorazepam, diazepam, phenytoin)

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7
Q

What is Todd’s Paralysis?

A

Post-epileptic paralysis, usually in the area where the seizure was

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8
Q

How do you investigate recurrent LOC?

A

Bloods

  • FBC (anaemia)
  • U+E (arrhythmias)
  • Glucose (Hypoglycaemia)
  • LFTs (alcoholism)
  • Calcium

ECG

Imaging: CT, MRI (to exclude other lesions)
- EEG

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9
Q

What can causes/risk factors epilepsy?

A
  • cerebrovascular accidents
  • tumours
  • alcohol
  • Post traumatic epilepsy
  • metabolic disturbances
  • previous seizures (e.g. febrile convulsions)
  • increasing age
  • Family history
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10
Q

What is the first line treatment for generalised tonic clonic seizures?

A

Sodium valproate

Lamotrigine

Carbamazepine

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11
Q

What is the first line treatment for absence seizures?

A

sodium valproate

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12
Q

What is the first line treatment for focal seizures?

A

Lamotrigine
Carbamazepine

Sodium valproate

Neurosurgery !

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13
Q

What are the side effects for sodium valproate?

A

weight gain
hair loss
liver damage

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14
Q

What are the side effects for Carbamazepine?

A

Rashes, leucopenia, toxic epidermal necrolysis

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15
Q

What are the side effects for Lamotrigine?

A

toxic epidermal necrolysis

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16
Q

What is non-epileptic attack disorder?

  • characteristics
  • management
A

Pseudoseizures, usually psychogenic

Characteristics of NEAD:

  • flapping
  • eyes and mouth open (can tongue bite)
  • sometimes responsive
  • normal vital signs
  • unresponsive to medication
  • many external physical and emotional triggers

commonly from shoulders and pelvis

Management
- Psychiatric referral

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17
Q

What are causes of acute single episodes of headache?

A 
Meningism 
Subarachnoid haemorrhage 
Head trauma 
Sinusitis 
Low/high pressure headache- CSF leak/ haemorrhage
Acute glaucoma 
Giant cell arteritis
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18
Q

What are causes of recurrent headaches?

A

Tension headaches
Migraines
Trigeminal neuralgia

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19
Q

What are causes of chronic headaches?

A

Tension
Raised ICP (lesion, haemorrhage)
Medication overuse headache (after stopping)

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20
Q

What is the presentation of a tension headache?

A
  • bilateral
  • non-pulsatile
  • scalp tenderness
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21
Q

What is the management of a tension headache?

A
  • analgaesia

- antidepressants

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22
Q

What is the presentation of a migraine?

A
  • Aura
  • unilateral
  • pulsatile
  • photophobia
  • phonophobia
  • worsens on head movement
  • vomiting/ nausea

4-72h

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23
Q

What is the management of a migraine?

A

Analgaesia: paracetamol, ibuprofen, aspirin

Acute treatment: Sumatriptan, Zolmitriptan

Preventative: Propanolol

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24
Q

What is the presentation of trigeminal neuralgia?

  • pathophysiology
A

paroxysmal stabbing pain in trigeminal distribution, screws up face
exacerbated by washing/shaving/ eating/ talking
Asian men >50

Pathophys; compression of trigeminal nerve root, causing chronic demyelination

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25
Q

What is the management of trigeminal neuralgia?

A

Carbamazepine

Lamotrigine

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26
Q

What is the presentation of a cluster headache?

+ management

A

rapid onset, excruciating pain
- around one eye - red, watery
unilateral
15-160min

Management: Subcut sumatriptan+ Oxygen!!

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27
Q

What is a stroke?

A

Brain infarction causing focal CNS signs

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28
Q

What are the 2 types of stroke?

A

Ischaemic (80%)

Haemorrhagic (20%)

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29
Q

What are risk factors for ischaemic stroke?

A
  • hypertension +++
  • smoking ++
  • heart disease, coronary artery stenosis
  • poor lifestyle
  • AF
  • Diabetes
  • High cholesterol
  • Alcohol intake
  • Age, Race (Black),
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30
Q

What are risk factors for a haemorrhagic stroke?

A
  • hypertension
  • smoking
  • lifestyle
  • AF
  • Obesity
  • Age
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31
Q

What is a common presentation of a stroke?

A

ROSIER TOOL- LOC, seizures, asymmetrical arm/leg/face movements, speech and vision defects

Contralateral

  • hemiparesis
  • hemiplegia
  • absent or hyporeflexive
  • facial weakness
  • hemianopia
  • Dysarthria, dysphasia (when dominant lobe)
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32
Q

What is a lacunar infarct?

A

Very localised infarct, usually from deep cerebral arteries

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33
Q

What investigations do you do in ?stroke

A
  • MRI
  • CT
  • ECG
  • Bloods- GLUCOSE
  • examination- BP, carotid bruit, arrythmias
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34
Q

What are the differential diagnoses for stroke?

A 
TIA 
Head injury 
Subdural haemorrhage 
tumours 
migraine 
epilepsy- Todd's palsy 
Wernicke's
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35
Q

What is the management for an acute stroke?

A

ABCDE
Imaging- urgent head CT to rule out haemorrhagic
ONCE RULED OUT
- Aspirin or clopidegrel
- thrombolysis (alteplase) if onset <4.5h

Haemorrhagic
- supportive

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36
Q

What are the contraindications for a thrombolysis?

A
  • Haemorrhagic stroke
  • Previous haemorrhagic stroke
  • Major surgery or trauma in the last 2 weeks
  • active internal bleeding
  • prolonged CPR
  • Pregnancy or postnatal
  • hypertension 200/120
  • allergy
  • previous ischaemic stroke in <3 months
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37
Q

What is the presentation of a TIA?

A
  • Stroke symptoms that resolve within 24h

- amaurosis fugax

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38
Q

What are notable points in the history/ examination of a TIA?

A
  • Cardiac arrhythmias - AF++
  • Carotid bruits
  • Recent MI/ CVA
  • radioradial delay - brachial artery stenosis
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39
Q

What is the management of a TIA?

A
  • Stroke protocol if suspected

Investigations:

  • ABCD2 score + CT immediate or within a week (<4>)
  • Blood pressure
  • ECG
  • Bloods: FBC, U+E, Glucose, cholesterol

Management:

  • Aspirin + continued aspirin/ clopidogrel
  • second line: dipyramidole
  • htn/ cholesterol management
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40
Q

What is the primary prevention of stroke/ TIA?

A

Reducing risk of stroke in people who have never had a stroke before

  • Lifestyle: diet, exercise, smoking, alcohol
  • Managing bp and cholesterol
  • anticoagulation therapies for those at risk (e.g. AF, rheumatic heart disease)
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41
Q

What is the secondary prevention of stroke/ TIA?

A

Reducing risk of another stroke in people who have had a stroke before

  • Lifestyle: diet, exercise, smoking, alcohol
  • Managing bp and cholesterol
  • Asprin/ warfaring + clopidogrel
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42
Q

What is the presentation of cerebellar dysfunction?

A

Acute:

  • nausea/ vomiting
  • vertigo
  • altered level of consciousness
Ataxias:
- gait 
- truncal 
- limb (heel-shin, fingers) IPSILATERAL 
Dysarthria (broken speech)

Signs:

  • past pointing
  • dysdiadochokinesia
  • tremor
  • nystagmus
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43
Q

What is the aetiology of cerebellar dysfunction?

A

Vascular:
- infarction- posterior cerebellar artery

Other disease:

  • MS
  • cerebral oedema
  • Wilson’s disease (excess copper)
  • developmental: cerebral palsy, cerebella hypoplasia, Dandy-Walker

Space occupying lesion

Nutritional

  • thiamine deficiency (wernicke’s)
  • vitamin E deficiency

Infection

  • meningitis
  • encephalitis
  • abscess

Toxins

  • alcohol
  • drugs
  • mercury
  • CO
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44
Q

What is narcolepsy?

management

A

Brain’s inability to regulate sleep
- hypocretin deficiency

managed with psychotherapies and occupational therapies

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45
Q

What is cataplexy?

A

Temporary loss of muscle control as a result of emotions

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46
Q

What is shingles?

A

Reactivation of varicella zoster infection, often during times of immunosuppression
(virus lies dormant in dorsal root ganglia)

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47
Q

What is the presentation of shingles?

A

pain in dermatomal presentation
malaise fever

erythematous swollen plaques, in clusters
neuritic pain

crust over after 7-10 days (no longer infectious)

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48
Q

What is the management of shingles?

A

Acyclovir

analgaesia

Post herpetic pain: amitryptilline

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49
Q

What is the role of thiamine (B1) in the body and specifically brain?

A

Generally:
- glucose metabolism
Brain:
- metabolises carbohydrates and lipids
- maintains levels of neurotransmitters and amino acids
- can help with propagating neural signals

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50
Q

What condition is related to thiamine (B1) deficiency?

A

Wernicke-Korsakoff Syndrome

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51
Q

What is the pathophysiology and aetiology of thiamine (B1 deficiency)

A

thiamine deficiency–> impaired glucose metabolism and brain function (as brain uses so much energy)–>

Alcohol

  • prevents thiamine becoming activated
  • ethanol also prevents thiamine absorption
  • fatty liver/ cirrhosis- stops storage of thiamine

Nutritional

  • deficiency- malnutrition/ anorexia
  • absorption (stomach cancer, IBD etc.)

Chronic Illness

  • HIV/ Aids
  • thyrotoxicosis
  • vomiting (hyperemesis)
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52
Q

What is the presentation of Wernicke’s Encephalopathy?

A 
Cerebellum 
KEY
- opthalmoplegia
- ataxia 
- confusion

other:

  • unsteady gait
  • personality change
  • coma/ death
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53
Q

What is the presentation of Korsakoff’s Syndrome

A

Limbic system

  • memory impairment- antero/retrograde amnesia
  • confabulation- make up stories
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54
Q

How do you diagnose Wernicke- Korsakoff syndrome?

A
  • clinical history
  • blood thiamine (B1) levels
  • MRI- mammilary body degeneration
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55
Q

What investigations would you want to do in ?Wernicke-Korsakoff?

A

Bloods

  • FBC
  • U+E- rule out other metabolic disturbances
  • LFTs- alcoholism
  • Urine (UTI- delirium)
  • THIAMINE LEVELS

Imaging
- CT scan if acute- periaqueductal punctate haemorrhages, brain damage

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56
Q

What is the management of Wernicke-Korsakoff syndrome?

A
  • thiamine infusion
  • Alcohol cessation referral
  • dietician input
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57
Q

What is Huntington’s Disease?

A

Autosomal Dominant Disease
Neuronal damage due to abnormal HTT gene
Loss of GABAnergic and Cholinergic neurons

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58
Q

What is the presentation of Huntington’s disease?

inc. signs

A

Onset: 35-50yo

Chorea- jerky movements 
Agitation 
Dementia 
Seizures 
Death

Signs:

  • squaring off of ventricles on MRI
  • cerebral and caudate nucleus atrophy
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59
Q

What is the management of Huntington’s Disease?

A

Antipsychotics- haloperidol, chlorpromazine

+ genetic counselling

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60
Q

What is the pathology of Parkinson’s Disease?

A

Loss of dopaminergic neurones in substantia nigra (basal ganglia)
Cell loss–> akinesia
Left over aggregates of protein known as Lewy body’s- if found all around the brain–> Lewy Body Dementia

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61
Q

What is the presentation of Parkinson’s Disease?

A
  • Tremor (at rest)
  • Rigidity
  • Bradykinesia

Gait:

  • shuffling gait
  • reduced arm swing
  • stooped
  • frequent falls

Face:

  • Masked expression
  • Slow speech

Psych:

  • Depression
  • Hallucination
  • Dementia (if cell degeneration occurs in the whole brain)
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62
Q

What diseases cause Parkinsonism?

A

Idiopathic Parkinson’s Disease- L-Dopa

Drug induced (e.g. dopamine antagonists- antiemetics)

Progressive supranuclear palsy (Steel-Richardson-Olszewski Syndrome)

Multisystem atrophy (neurodegenerative disease)

Wilson’s Disease- Parkinsonism+ liver/renal failure, personality problems. Copper metabolism pathology- deposits in the brain (SN), liver, eyes etc.) Penicillamine

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63
Q

What investigations are done for ?Parkinson’s disease?

A

Clinical diagnosis

?MRI for differentials

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64
Q

What is the management of Parkinson’s disease?

A
  • Levodopa (dopamine precursor) + Carbidopa

- Ropinirole (dopamine agonist)

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65
Q

What are the side effects of L-Dopa and Carbidopa?

A
  • Psychosis/ Hallucinations (due to increased dopamine)
  • Risky behaviours
  • Vomitting/ nausea
66
Q

What are the risk factors for Alzheimer’s Disease?

A
  • Insulin resistance
  • cholesterol/ atherosclerosis
  • Family history
  • Depression
  • Hypothyroidism
  • Head injury
  • HIV
  • Parkinson’s disease
67
Q

What are the symptoms of dementia?

A 
Memory loss (short term ++) 
Visuospacial disturbances 
Emotional disturbances 
Loss of normal social behaviour 
Behaviour- aggression, depression, irritable, 
Personality changes
68
Q

How do you diagnose dementia?

A

Mini-Mental-State-Exam
+ DSM IV criteria;

One of:

  • Aphasia
  • Apraxia
  • Agnosia
  • Reduced executive function (e.g. planning)

And not linked with:

  • organic causes
  • delirium
  • mental health disorder
69
Q

What are the differential diagnoses for dementia?

A
  • Delirium (Infection, Diabetes, Parkinson’s, Substance misuse)
  • Head injury
  • Depression
  • Normal reduced cognition with age
70
Q

What investigations would you want to do in ?dementia?

A

Bloods:

  • FBC (anaemia)
  • Calcium, U+E (metabolic disturbances)
  • CRP (infection)
  • Glucose

Urine:
- MC+S (UTI)

CT/MRI in ?SOL (general atrophy)

71
Q

What is the pathogenesis of Alzheimer’s disease?

A

B-amyloid plaque deposits
Atrophy of brain tissue + compensatory ventricle dilation (hydrocephalus)
Cholinergic fibre atrophy + reduction of acetylcholine production

= reduced brain function

72
Q

What is the pathogenesis of vascular dementia?

A

Multiple small infarcts

73
Q

What is the management of dementia?

A

Lifestyle: physio and occupational therapy
Advance Care Planning
Report to DVLA

Drugs:
Acetylcholinesterase inhibitors- Donepazil, Galantamine, Rivastigmine (hallucinations)
NDMA receptor antagonists- Memantine

Slows progression. No cure.

74
Q

What is the role of CSF?

A
  • Protects brain from damage
  • Provides nutrients
  • Removes waste
75
Q

What is hydrocephalus?

A

Abnormal build up of CSF in the cerebral ventricles

76
Q

What are the mechanisms of damage in hydrocephalus?

A

Increased secretion OR decreased/ impaired absorption

77
Q

What is normal pressure hydrocephalus?

  • presentation
  • causes
A

build up of CSF due to blockage of the spinal cord- build up of pressure

  • causes dementia like symptoms +urinary incontinence + instability (wet, whacky and wobbly)

caused by:
Haemorrhages, stroke, tumour, meningitis

78
Q

What are some causes of congenital hydrocephalus?

A
  • Spina bifida
  • Congenital malformations: e.g. Dandy-walker
  • maternal infections- rubella, mumps, toxoplasmosis
79
Q

How do you manage a hydrocephalus

- inc investigations

A

History- acute-ish onset
CT/MRI

  • ventriculoperitoneal shunt
  • Third Ventriculostomy (put a hole in the third ventricle)
80
Q

What cells are affected in MS?

A

Oligodendrocytes in the CNS

81
Q

What is the pathophysiology of MS?

A

Autoimmune attack against the myelin and oligodendrocytes (CNS version of Schwann cells) + subsequent axonal loss

Causes inflammation (plaques of active lesions)- show up on MRI as white blobs

Symptoms as a result of conduction loss

82
Q

What are the types of MS?

A
  1. Primary progressive (linear line)
  2. Secondary Progressive (Relapses and then a linear line)
  3. Progressive- relapsing ( relapses with linear lines in between)
  4. Relapsing-remitting (relapses only, no progression between)
83
Q

What is the presentation of MS?

  • Symptoms
  • Signs
A

20-50y/o

Symptoms:

  • Vision loss (optic neuritis)
  • incontinence
  • sexual dysfunction
  • weakness
  • sensory loss
  • fatigue
  • Worse in heat

Signs:

  • UMN LESIONS!!!!!!
  • Spasticity, weakness, hyperreflexive
  • Numbness, paraesthesia
  • Autonomic: urinary incontinence, constipation, sexual dysfunction
  • Cerebellar: ataxia, nystagmus
  • Lhermitte’s- electric shock down spine when flexes neck
84
Q

What investigations do you do in ?MS ?

A

MRI

LP: oligoclonal bands

85
Q

What is the management of MS?

A

For acute attacks: Methylprednisolone

For prevention: INF1a/ INF1b, monoclonal antibodies

Symptomatic relief:

  • urinary: catheter
  • Sexual: mechanical aids
  • Psych: antidepressants
86
Q

What is Guillain Barre Syndrome (GBS)?

A

Acute inflammatory demyelinating polyneuropathy

87
Q

What is the pathophysiology (inc. aetiology) of GBS?

A

Aetiology:
- Often post infectious (campylobacter, EBV, CMV) (several weeks after)

Pathophys:

  • autoimmune reaction against myelin and peripheral nerves
  • resulting in reduced transmission
88
Q

What is the presentation of GBS?

A

LMN lesions in ascending pattern

  • Paralysis (usually symmetrical)
  • Numbness
  • Areflexia
  • Pain
89
Q

What is the management of GBS?

A

ABCDE (respiratory distress)

IV immunoglobulins

Supportive- can recover by themselves

90
Q

What is Motor Neurone Disease (MND)?

+ most common type?

A

Relentless degeneration of UMN and anterior cells horns

Given UMN AND LMN signs!!!!!!!!!

ALS- Amylotropic Lateral Sclerosis

91
Q

What is bulbar palsy?

A

CN 9,10,11,12 impairment

  • flaccid paralysis of the pharynx and larynx

Presentation:

  • dysphagia
  • difficulty chewing
  • difficulty speaking- slurring words
  • aspiration
  • dribbling
  • ABSENT GAG REFLEX
  • FLACCID TONGUE

Causes:

  • Medullary infarct
  • GBS
  • MND
  • Toxins (scorpion/snake venom)
  • Botulism
  • Malignancy

Management:

  • supportive: feeding tubes, ventilation
  • management of causes
92
Q

What is pseudobulbar palsy?

A

UMN lesion
Spastic paralysis of CN 9,10,11,12

Causes: (UMN)

  • infarction (stroke)
  • malignancy
  • MND
  • MS
  • Parkinsons

Presentation:

  • dysphagia
  • difficult speech
  • drooling
  • SMALL STIFF TONGUE
  • BRISK JAW REFLEX
  • NORMAL, ABSENT OR HYPER GAG REFLEX

Management:

  • SSRIs
  • Supportive
93
Q

What is the presentation of MND?

A
  • middle aged onset

NO PAIN, NO SENSORY INVOLVEMENT
NO BLADDER INVOLVEMENT
NO EYE INVOLVEMENT
can see, can pee, can feel a tree

Combination of UMN and LMN signs

  • Symmetrical weakness and wasting (LMN)
  • Fasciculations (LMN)
  • Hyperreflexia OR areflexia (in anterior horns)
  • ALS (spastic paraperesis + muscle wasting (UMN+LMN))
  • Progressive bulbar and pseudobulbar palsy
94
Q

What is the pathology of MND?

A

Unknown causes (?genetic)

oxidative damage of neurones
protein aggregation inside cells

95
Q

What investigations do you do in ?MND?

A

EMG (electromyography)- denervation
NCS

Bloods:
Calcium/thyroid bloods (to rule out)
Creatinine kinase (raised)

96
Q

What is the management for MND?

A

Riluzole (Sodium channel blocker)

ABCDE + feeding

Palliation

97
Q

What is myasthenia gravis?

A

Autoimmune condition which attack the nicotinic ACh receptors in the NMJ

98
Q

What is the presentation of myasthenia gravis?

A
  • young women (20-35) and older men (60-75)

FATIGABILITY- worse at end of the day, has relapses and remissions
- muscle fatigue and weakness

EYES, SHOULDERS, NECK and TRUNK

Eyes: diplopia, ptosis
Shoulders: and thighs
Neck: bulbar palsy, enlarged thymus!!!!!
Trunk: problems with respiration

no sensory, normal reflexes

99
Q

What is the management of Myasthenia Gravis?

A

Acetylecholinesterase inhibitors- Pyridostigmine

Corticosteroids

Thymectomy

100
Q

What is cerebral palsy?

A

Non-progressive lesion on motor pathways in the developing brain, leading to abnormalities in movement and posture

101
Q

What is Neurofibromatosis?

A
  • Benign tumours of neurones.
102
Q

What are the types and causes of neurofibromatosis?

A

2 Types; Both autosomal dominant (50% chance)

1: common, skin or other PNS lesions- linked with cafe au lait spots
2: In the head, most commonly presents with hearing loss (due to bilateral vestibular schwannomas)

103
Q

What is the management of neurofibromatosis?

A

Surgical removal if necessary/ SOL

Monitor hearing

Genetic counselling

104
Q

What are the causes of meningitis?

A

Commonly; Meningococcus (neisseria meningitidis) or Pneumococcus (Strep. Pneumoniae)

Less commonly; Haemophilus influenzae, listeria monocytogenes

105
Q

What is the presentation of meningitis?

A

Symptoms:

  • headache
  • neck stiffness
  • fever

Signs:

  • photophobia
  • Kernig’s (pain on passive extension of knee in flexed hip)
  • petechial rash
106
Q

What investigations do you do in meningitis?

A

Bloods:

  • FBC (WCC)
  • CRP
  • Blood culture
  • coagulation screens
  • LFT U+E Glucose

LP- raised protein, cloudy if bacterial, reduced glucose , raised white cells (neutrophils in bacterial)

107
Q

What white cells are raised in CSF in bacterial meningitis?

A

Neutrophils

108
Q

What white cells are raised in CSF in viral meningitis?

A

Lymphocytes

109
Q

What is the management of meningitis?

A

IV cefotaxime

110
Q

What is the presentation of encephalitis?

A
  • Fever
  • Bizarre behaviour/ confusion
  • Headache
  • Lowered GCS
  • Focal seizures
  • History of travel or animal bite
111
Q

What are the common causes of encephalitis?

A

Viral- HSV 1+2,3,4,5, measles, mumps, rabies

Non-viral: bacterial meningitis (meningococcus, pneumococcus)

112
Q

What investigations would you do in ?encephalitis?

A 
Bloods: 
FBC (WCC)
Glucose 
Cultures 
Viral PCR

Swabs/ culture:
Throat + PCR
Urine
CSF culture+ pcr

Imaging: CT head
EEG

LP: raised protein, low glucose

113
Q

What is the management of encephalitis?

A

IV aciclovir

114
Q

What is Horner’s Syndrome?

A

Ipsilateral damage of sympathetic fibres that supply the eyes

115
Q

What is the presentation of Horner’s Syndrome?

A

Ptosis
Anhydrosis
Miosis (pupil consitriction)

116
Q

What causes Horner’s Syndrome?

A

MS
CVA
Trauma
Brain tumours

Thyroidectomy
Goiter
Thyrocarcinoma

Migraine
Cluster headache
Middle ear infection

117
Q

What investigations do you do for ?Horner’s Syndrome?

A

CT/ CXR/ Carotid angio

COCAINE EYEDROPS- fail to elicit pupil dilation in Horners

Paredrine test to localise lesion to which order neuron

118
Q

What is Bell’s Palsy?

A

Facial nerve palsy (CNVII)

most common mononeuropathy

119
Q

What is the presentation of Bell’s Palsy?

A

Rapid onset unilateral facial paralysis

120
Q

What is the management of Bell’s Palsy?

A

70% self resolve

Prednisolone

Aciclovir

Lubricating eye drops

121
Q

What are the causes of peripheral neuropathy?

A 
Diabetes 
Alcoholism 
Vitamin B12 deficiency 
Infection- GBS/ charcot-marie tooth 
Drugs- Isoniazid
122
Q

How could peripheral neuropathy resolve?

A

remyelination

axonal regrowth

123
Q

What are the domains assessed in the Glasgow Coma Scale?

A
  1. Eye response (/4)
  2. Verbal response (/5)
  3. Motor response (/6)

/15

124
Q

What is a myasthenic crisis?
- precipitating factors

+ management

A

Respiratory failure due to myasthenia gravis

Precipitating factors:

  • infection
  • pain
  • sleep deprivation
  • antibiotics
  • emotional causes
  • perimenstruation
  • antiepileptics

Management:

  • ABCDE
  • IVIg
  • Plasma exchange
  • antibiotics (Myathenic crisis pt. have increased risk of sepsis)
125
Q

What is a cholinergic crisis?
- Presentation

  • Management
A

Too much cholinergics (often seen in myasthenia gravis pts)

Presentation: wet and weak
Nicotinic toxicity:
- muscle weakness 
- fasiculations 
Muscarinic toxicity:
- Nausea 
- Vomitting
- sweating 
- tearing 
- diarrhoea

Management:
ABCDE
atropine
withdraw from anticholinesterases (pyridostigmine)

126
Q

What is cord compression?

A

Pressure of spinal cord causing neurological symptoms from that level down (e.g. weakness, incontinence)

127
Q

What is the presentation of cord compression?

A

Commonly:
Leg weakness/ paralysis, loss of sensation
Urinary/ bowel symptoms- incontinence, retention, frequency, constipation, hesitancy etc.
arm paralysis: cervical lesion

LMN SIGNS AT THE LEVEL
UMN SIGNS BELOW THE LEVEL

128
Q

What are the causes of cord compression?

A
  • Malignancy (secondary tumour)
  • Infection (epidural abscess)
  • Disc prolapse
  • Haematoma (?warfarin)
  • Myeloma
129
Q

What is the presentation of cauda equina syndrome?

A

Cord compression from L2 onwards

  • Mixed UMN and LMN
  • Urinary retention and constipation
  • back pain/ leg pain
  • Saddle paraesthesia
  • decreased sphincter tone
130
Q

What are the differential diagnoses for cord compression?

A
  • MS
  • MND
  • GBS
  • Trauma
  • Transverse Myelitis
131
Q

What are the investigations for spinal cord compression?

A
  • URGENT IMAGING: CT or MRI (+ biopsy)
    PET scan

Bloods:
FBC (WCC)
ESR, CRP (?infection)
cultures

LP:
- culture

Urodynamics

132
Q

What is the management of spinal cord compression?

A 
ABCDE
Immobilisation 
IV methylprednisolone or dexamethasone (in malignancy)
Surgical correction
ABx if abscess
133
Q

What are common mononeuropathies?

A
  • carpal tunnel syndrome
  • common peroneal nerve palsy
  • axilliary
134
Q

What is the causes of mononeuropathies?

A

Injury

Long term pressure (RSI, swelling, kneeling)

135
Q

What is the presentation of carpal tunnel syndrome?

A

Median nerve entrapment

Pain or tingling in the arm and hand
Paraesthesia in the thumb, index and middle finger
Relieved by hanging arm over bed

Tinel’s + Phalen’s positive

136
Q

What nerve is effected in carpal tunnel syndrome?

A

Median nerve

137
Q

What’s the management of carpal tunnel syndrome?

A
  • splints
  • local steroid injection
  • decompression surgery
138
Q

What is the pathology of sciatica?

A

L4/L5/S1 nerve compression due to bulging disc or herniated disc

This causes back and leg pain and weakness

139
Q

What is a radiculopathy?

+ what can cause it

A

Nerve root compression causing pain (dorsal root) and weakness (anterior root)

Disc prolapse (weakened anulus fibrous), trauma, heavy lifting, osteoarthritis, spinal stenosis

140
Q

Where are common radiculopathies?

A

C6/7= median/ radial nerve

L4/5,S1= sciatica

141
Q

What is the presentation of sciatica?

A

shooting pain down leg/ back + weakness

142
Q

What is the management of radiculopathies?

A

Conservative: physiotherapy, lifestyle- diet and exercise, stay active, heat pads, cushion between knees

Medical: NSAIDs (ibuprofen or naproxen), analgaesics (cocodamol, codeine)

Surgical: discectomy

143
Q

What is a subarachnoid haemorrhage?

+ presentation

A

rupture of blood vessel in the circle of willis or connecting

(Berry aneurysm)

thunderclap headache
neck stiffness (chemical meningitis) + Kernig’s sign +
altered consciousness
hemiplegia

144
Q

What are the risk factors of subarachnoid haemorrhages?

A
  • raised BP
  • smoking
  • known aneurysm
  • aneurysm causing disease- PKD, ehler-danlos, coarctation of the aorta
  • family history
145
Q

What are investigations and management of a subarachnoid haemorrhage?

A

CT: star shaped lesions (circle of wilis)

LP: (contraindicated in raised ICP)

  • billirubin
  • xanthochromia

Management:

ABCDE
Neurosurgical referral- drain

146
Q

What is a subdural haemorrhage?

+ presentation

A

Haemorrhage between the dura and the arachnoid.
Due to damage of the bridging veins, commonly a venous bleed

Drowsiness
LOC
Personality change
focal symptoms: seizures, unequal pupils, hemiparesis (after 2 months)

147
Q

What are the risk factors of a subdural haemorrhage?

A
  • Old age (smaller brain)
  • Alcoholism (smaller brain)
  • Epilepsy
  • Anticoagulant therapy
  • Trauma- mild or severe
148
Q

What is the investigations and management of a subdural haemorrhage?

A

CT: Cresent shape inside skull, midline shift

Management:

  • ABCDE
  • Burr hole- craniostomy- irrigation or evacuation
  • Craniotomy
  • Manage cause of falls/ trauma
149
Q

What is a Extradural haemorrhage?

+ presentation

A

Haemorrage between the cranium and the dura
Often as a result of damage to the middle meningeal artery, commonly arterial bleed

Commonly presents with fracture to parietal or temporal bone (near the eye)
Trauma followed by dull headache and drowsiness, which resolves
THEN neurological signs (drowsiness and headache++, unequal pupils, vomitting, seizures, hemiparesis

150
Q

What are the risk factors of a extradural haemorrhage?

A

skull trauma

151
Q

What is the investigations and management of a extradural haemorrhage?

A

CT: convex shaped lesion
Head Xray for fractures
LP IS CONTRAINDICATED

Management:

  • ABCDE
  • Surgery to remove blood and ligate bleeding vessels
152
Q

What is the management of spinal stenosis?

A

Conservative: physiotherapy and exercise

Medical: NSAIDs, Steroid injection

Surgical: laminectomy, discectomy, spinal fusion

153
Q

What is anterior cord syndrome?

A

Interruption of the anterior 2/3 of the spinal cord

154
Q

What is the presentation of anterior cord syndrome?

A

Complete loss of motor, temp and pain

Retention of vibration and fine touch

155
Q

What is the presentation of Brown Sequard’s syndrome?

A

ipsilateral loss of motor and vibration and fine touch

contralateral loss of temperature and pain after 1-2 levels

156
Q

What is muscular dystrophy?

A

Genetically caused weakened muscles without any nerve damage

157
Q

What is the aetiology of muscular dystrophy?

A

X-linked recessive. (More common in boys)

Missing or damaged Dystrophin gene

158
Q

What is the presentation of muscular dystrophy?

A

Ataxic gait- waddling, walking later, calf pseudohypertrophy

Later: respiratory distress, cardiac arrhythmias

159
Q

How do you diagnose muscular dystrophy?

A

High serum creatinine kinase (++++ as creatinine kinase leaves cells)

muscle biopsy staining for dystrophin

Karyotyping

160
Q

What is the management of muscular dystrophy?

A

Corticosteroids

Physio, occupational therapy

161
Q

What are non-medical managements of epilepsy?

A
  • ketogenic diets
  • surgery
  • canniboids

Phase 3a (9 decks)

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