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Y4 Neuro and Special Senses > Neurological Conditions > Flashcards

Neurological Conditions Flashcards

1
Q

Define Epilepsy

A

Chronic neurological condition characterised by recurrent seizures

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2
Q

Define Seizure

A

Transient neurological change due to synchronous hyperexcited neuronal activity

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3
Q

Give 5 causes of unprovoked seizures

A 
Genetic
Structural (eg congenital malformation)
Metabolic 
Immune
Infection (HIV)
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4
Q

Describe the pathophysiology of Epilepsy

A

Due to imbalance of excitatory and inhibitory signals in the brain

High frequency excitable Action Potentials lead to synchronous hyperexcitable activity and propagation to other neurones

Transformed long lasting structural/biochemical changes

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5
Q

Name three risk factors for Epilepsy

A

Cerebral infections
Family history
Prematurity

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6
Q

How can you classify seizure type?

A

Area of onset
Awareness
Clinical Features

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7
Q

Describe the subtypes of ‘area of onset’ in epilepsy

A

Focal (networks of neurones in one hemisphere)
Generalised (affecting both hemispheres)
Focal to Bilateral (Secondary Generalised Seizure)

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8
Q

Describe the subtypes of ‘awareness’ in epilepsy

A

Fully aware
Impaired Awareness

Only relevant for Partial

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9
Q

Describe the subtypes of ‘Clinical Features’ in epilepsy

A 
Motor (Tonic, Clonic, Myoclonic, Atonic, Spasms)
Non Motor (any sensory/cognitive/emotional dysfunction or generalised absence)
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10
Q

Name four epilepsy classifications

A

Focal
Generalised
Generalised and Focal
Unknown

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11
Q

Name two Epilepsy Syndromes

A

West Syndrome

Lennox Gastout Syndrome

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12
Q

What are the four periods of different clinical features in Epilepsy?

A

Prodromal
Early Ictal (ie Aura - normally seen in general)
Ictal
Post Ictal

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13
Q

How is Epilepsy diagnosed?

A

One of:

  • More than two unprovoked seizures occurring more than 24h apart
  • 1 unprovoked seizure with probability of further
  • Diagnosed epilepsy syndrome
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14
Q

Give three differentials for Epilepsy

A

Anoxic Seizures
Sleep Associated
Migraine Associated

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15
Q

How is an EEG used in suspected Epilepsy?

A

To support diagnosis, assess recurrence risk and determine seizure type

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16
Q

When is an MRI required in Epilepsy?

A

<2 years old
Refractory to AEDs
Focal

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17
Q

Name four education/safety points in terms of Epilepsy

A

Avoid taking baths
Avoid operating heavy machinery
Always use contraception while on AEDs
Inform DVLA

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18
Q

What are the DVLAs rules on driving after seizures?

A 
First seizure - 6m
Epileptic Seizure - 12m
No LOC - ask DVLA
First Seizure + Lorry - 5y
Epileptic Seizure + Lorry - 10y
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19
Q

What is done at the ‘First Fit Clinic’

A

Formal Assessment and relevant EEG/MRI

If diagnosis is made and risk of another is felt to be high - AED started

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20
Q

Name three SE of Sodium Valproate

A

Teratogenic
DILI
Pancreatitis

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21
Q

Name two SE of Lamotrigine

A 
Slightly teratogenic
Skin reactions (life threatening)
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22
Q

Name two SE of Levetiracetam

A

CNS and Neuropsych disturbance

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23
Q

Name three SE of Phenytoin

A

Arrhythmia
Teratogenic
Gum Hypertrophy

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24
Q

What are the AEDs of choice for Focal Seizures?

A

1) Lamotrigine

2) Sodium Valproate

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25
Q

What are the AEDs of choice for General Seizures?

A

Sodium Valproate or Lamotrigine

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26
Q

What are the AEDs of choice for Absence Seizures?

A

Ethosuxamide or Sodium Valproate

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27
Q

What are the AEDs of choice for Myoclonic Seizures?

A

Sodium Valproate

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28
Q

Define Migraine

A

A primary headache characterised by recurrent moderate to severe headaches and associated with nausea/vomiting/photophobia/phonophobia

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29
Q

Migraines can be episodic or chronic. How does a patient qualify for ‘Chronic Migraines’?

A

Headaches >15d a month, at least 8 of which have migraine features

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30
Q

Describe the diagnostic criteria for Migraines without Aura

A

Atleast 5 fulfilling:

  • Headaches lasting 4-72 hours
  • Atleast 2 of - unilateral/pulsating/mod to severe/aggravated by physical activity
  • Not accounted for
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31
Q

Describe the diagnostic criteria for Migraines with Aura

A

Atleast two attacks fulfilling:

  • One or more reversible aura (scintillating scotoma most commonly)
  • Atleast 3 of - one>5 mins/two or more in succession/one unilateral/one positive/one followed by a headache within 60 mins
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32
Q

Migraines without Aura are commonly associated with the Menstrual Cycle. If first line Migraine management fails in these women, what can be used?

A

Frovatriptan

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33
Q

Name 5 Migraine Red Flags

A 
Motor Weakness
Double Vision
Aura without headache
Severe Sudden Onset 
Worse on Standing (CSF leak)
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34
Q

How is an Acute Migraine managed?

A

Simple Analgesia (eg rectal diclofenac) and Antiemetic (buccal prochlorperazine)
Severe - Sumatriptans (5HT1 agonist)
Come off COCP

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35
Q

How can Migraines be prevented?

A

Propanolol
Topirimate
Amitryptyline

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36
Q

How can inretractable Migraines be prevented?

I.E more than 3 medications tried

A

Galcenezumab

Botox

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37
Q

Name three complications of Migraines

A

Status Migrainosus (>72h)
Migrainal Infarction
Ischaemic Stroke

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38
Q

How can Tension Headaches be classified?

A

Infrequent Episodic - 10 episodes occuring on <12d per year
Frequent - 1 to 14d a month for >3m
Chronic - >15d a month for >3m

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39
Q

How are chronic Tension Headaches managed?

A

Accupuncture
Low dose Amitryptyline
Lifestyle

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40
Q

Define Trigeminal Neuralgia

A

Episodes of acute severe facial pain in the distribution of the trigeminal nerve (commonly affecting maxillary and mandibular)

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41
Q

Trigeminal Neuralgia can be primary or secondary. Describe the Primary pathophysiology

A

Vascular compression at the nerve root entry zone leading to demyelination and abnormal electrical activity

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42
Q

Trigeminal Neuralgia can be primary or secondary. Describe the Secondary pathophysiology

A

Disease occuring due to another condition

eg Vestibular Shwannoma, Meningioma, Cysts, MS

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43
Q

Describe the diagnostic criteria for Trigeminal Neuralgia

A

Pain lasting up to two minutes of severe electric shock like intensity
Precipitated by innocuous stimuli within the region (eg cold)
Not accounted for by alternate diagnosis

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44
Q

Describe the medical management options for Trigeminal Neuralgia

A

Carbemazepine (titrate up to remission and then back down to lowest possible maintenance)

Second Line - Gabapentin, Lamotrigine

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45
Q

Describe the surgical management for Trigeminal Neuralgia

A

Microvascular Decompression

Gamma Knife Radiosurgery

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46
Q

Cluster Headaches can be chronic or episodic, what is the difference?

A

Episodic - in periods lasting between 7d and 1y with pain free episodes in between

Chronic - Occurring for one year without/short lived remissions

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47
Q

What hormone do Cluster Headaches have a link to?

A

Melatonin

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48
Q

Describe the nature of Cluster Headaches

A

Rapid Onset over 10 minutes, often at night, excruciating around one eye lasting up to 90 mins

Associated lacrimation and rhinorrhoea

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49
Q

Name three triggers for Cluster Headaches

A

Alcohol
Histamine
Disrupted Sleep

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50
Q

Describe the diagnostic criteria for Cluster Headaches

A

5 attacks qualifying:

  • Severe unilateral pain lasting 15-180 minutes untreated
  • Accompanied by lacrimation/congestion/rhinorrhoea
  • Attacks occurring from one every other day to 8 times a day
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51
Q

How can an Acute Cluster Headache be treated?

A

Sumatriptans and 100% O2

Could use Indometacin/Lidocaine

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52
Q

How can a Cluster Headache be prevented?

A

Stop Smoking, Stop Alcohol, Maintain good sleep hygiene

Verapamil, Prednisolone, Lithium

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53
Q

Define Parkinson’s

A

Chronic progressive neurodegenerative condition occurring secondary to loss of dopaminergic neurones in substantia nigra

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54
Q

Define Parkinsonism

A

Bradykinesia plus one of resting tremor/rigidity/postural instability

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55
Q

Name three roles of the Basal Ganglia

A

Inhibit muscle tone
Initiation of movement
Suppression of useless movement

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56
Q

Describe the direct Basal Ganglia pathway

A

Stimulatory pathway associated with D1 receptors

Activation leads to neural connections and movement initiation (via dopamine from substantia nigra)

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57
Q

Describe the indirect Basal Ganglia pathway

A

Inhibitory pathway associated with D2 receptors. Activation leads to inhibition of muscular tone, inhibition of movement initiation and inhibition of direct pathway

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58
Q

How does Bradykinesia of Parkinsons present?

A 
Slowing of voluntary movements
Reduced arm swing
Reduced amplitude with repetitive movements
Expressionless face
Micrographia
Shuffling Gait (festinant)
Freezing at obstacles such as doors
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59
Q

How does Tremor of Parkinsons present?

A

Worse at rest
Described as pill rolling
4-6Hz
Can be induced by distraction

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60
Q

How does Rigidity of Parkinsons present?

A

Increased resistance to passive movement

Cogwheel rigidity due to superimposed tremor

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61
Q

Other than the classic triad, give three other clinical features of Parkinsons

A

autonomic dysfunction - postural hypotension, constipation, urinary frequency/urgency, dribbling of saliva
sleep disturbance - REM sleep behaviour disorder
reduced sense of smell
neuropsychiatric complications - depression, dementia, psychosis

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62
Q

Name three exclusion criteria for Parkinsons

A

Cerebellar Abnormalities
Restricted to lower limbs for >3y
Suspected Frontotemporal Dementia

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63
Q

Parkinsonism is an umbrella term. Other than Idiopathic Parkinsons Disease, name three other causes

A

Parkinson Plus Syndromes
Drug Induced (Antipsychotics, Antiemetics, Lithium)
Other (Post Encephalitis, Trauma)

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64
Q

Parkinson Plus Syndromes affect a wider area of nervous system causing more complex disease and increased survival. Name four causes

A

Multiple System Atrophy
Progressive Supranuclear Palsy
DLB
Corticobasal Degeneration

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65
Q

How does Multiple System Atrophy present?

A

Rapidly progressive disease characterised by profound autonomic dysfunction leading to severe postural hypotension and urogenital dysfunction

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66
Q

How does Progressive Supranuclear Palsy present?

A 
Early postural instability
vertical gaze palsy +/- falls
rigidity of trunk>limbs
symmetrical onset 
speech and swallowing problems
little tremor
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67
Q

How does Corticobasal Degeneration present?

A

akinetic rigidity involving one limb
cortical sensory loss
apraxia

Severe - Alien Limb Syndrome

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68
Q

Idiopathic Parkinsons Disease is largely a clinical diagnosis. Name three possible investigations

A

CT/MRI - if strong suspicion of underlying cause/failed response to treatment
PET with Fluorodopa - can localise dopamine deficiency in Basal Ganglia
DaTscan - differentiates Parkinsons from Essential Tremor

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69
Q

Parkinsons Disease requires early initiation of treatment. What are the three mainstay treatment options?

A

Levodopa
Ropinorole (Dopamine Agonists)
Rasigiline (MAO-B Inhibitors)

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70
Q

Describe the use of Levodopa in Parkinsons

A
  • Effective, for mostly 5-6y
  • Can cross BBB and be converted to Dopamine by Dopa-Decarboxylase
  • Some peripheral conversion
  • Treats motor symptoms well but also causes dyskinesia/on off fluctuations
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71
Q

Describe the use of Ropinorole in Parkinsons

A
  • Dopamine Agonist

- Less motor effects but can cause problems with impulse control and sedation

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72
Q

Eventually, all Parkinsons patients will require more than monotherapy. Name four adjuvant options

A
  • COMT Inhibitors (Entacapone- given with Levodopa)
  • Antimuscarinics (Procyclidine)
  • Amantadine
  • Apomorphine (Dopamine Agonist for advanced disease)
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73
Q

Another treatment option for Parkinsons is Deep Brain Stimulation. Name two advantages and two disdvantages to this method

A

Advantages - Reduces rigidity and tremor

Disadvantages - Haemorrhage and Confusion

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74
Q

Name two motor and two non motor complications of Parkinsons Disease

A

Motor - Freezing of Gait, Falls

Non Motor - Aspiration Pneumonia, Pressure Sores

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75
Q

Name four causes of Neuromuscular Weakness

A

Guillaine Barre Syndrome
Myasthenia Gravis
Motor Neurone Disease
Muscular Dystrophy

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76
Q

Define Guillaine Barre Syndrome (GBS)

A

Acute inflammatory polyneuropathy characterised by progressive ascending neuropathy with weakness and reduced reflexes

Often triggered by infections such as Campylobacter

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77
Q

Describe the pathophysiology of GBS

A

Immune mediated damage to peripheral nerves (proposed antigenic mimicry)

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78
Q

What are the four subtypes of GBS?

A

Acute Inflammatory Demyelinating Polyneuropathy (90%)
Acute Motor Axonal Neuropathy
Acute Motor Sensory Neuropathy
Miller Fisher Syndrome

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79
Q

How does the AIDP subtype of GBS present?

A

Progressive symmetrical weakness (often ascending from distal muscles)
Reduced/absent reflexes
Reduced sensation

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80
Q

What is the destructive target in Acute Motor Axonal Neuropathy (GBS)?

A

The Axons

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81
Q

How does the Miller Fisher subtype of GBS present?

A

Ataxia
Areflexia
Opthalmoplegia

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82
Q

Name five investigations for suspected GBS

A
  • Viral Screen
  • CXR (Rule out Sarcoidosis)
  • Electrophysiology (confirms diagnosis and differentiates axonal and demyelinating)
  • LP (increased protein and normal WCC)
  • AB for Miller Fisher
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83
Q

The management for GBS is normally supportive, if required, what management can be given?

A

FVC<20ml/kg - ITU and intubation

IVIG/Plasma Exchange

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84
Q

What is Hughes Disability Score?

A 
Severity scoring for GBS 
0 - Healthy
4 - Bedridden
5 - Assisted Ventilation
6 - Death
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85
Q

Define Myasthenia Gravis

A

Antibody mediaed blockage of Neuromuscular Transmission due to ACh receptor AB

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86
Q

Describe the pathophysiology of Myasthenia Gravis

A
  • Type II Hypersensitivity reaction
  • Cross links receptors causing destruction and activates –Membrane Attack Complexes to destroy membrane
  • Disease fluctuates as NMJ can repair itself and create more receptors easily
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87
Q

What are the three stages of Myasthenia Gravis?

A

1 - Fluctuating muscle weakness with most severe symptoms happening here
2 - Persistent but stable symptoms
3 - Remission

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88
Q

What is the relation of Myasthenia Gravis to the Thymus?

A

10-15% have a Thymoma
Up to 85% have Thymic Hyperplasia

There are myoid cells in the thymus which may start the target for autoimmunity

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89
Q

What are the two clinical subtypes of Myasthenia Gravis?

A

Ocular

Generalised

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90
Q

Name three antibodies associated with Myasthenia Gravis

A

AChR - Ab
Anti MuSK
Anti - LRP4

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91
Q

Name four ocular features of Myasthenia Gravis

A

Diplopia (improved on occluding one eye)
Ptosis
Weak eye movements
Pupillary sparing

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92
Q

Name four features of Generalised Myasthenia Gravis

A
  • Bulbar - Fatiguable chewing
  • Facial - Expressionless
  • Neck - Dropped head towards EOD
  • Proximal limb weakness more than distal
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93
Q

What is the Ice Pack Test for Myasthenia Gravis?

A

Improvement of ptosis after ice applied to closed eye for one minute
Neuromuscular transmission is better at lower temperatures

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94
Q

Other than the Ice Pack Test, name four investigations for Myasthenia Gravis

A
  • Tensilon Test (improvement after AChesterase inhibitors)
  • Serological Antibodies
  • Repetitive Nerve Stimulation (showing decline)
  • CT/MRI thymus
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95
Q

Name three options for treating Myasthenia Gravis

A

Pyridostigmine
Prednisolone
Azathioprine

Could also do a Thymectomy

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96
Q

What is a Myasthenic Crisis?

A

Worsening of weakness requiring respiratory support

Precipitants include warmth/surgery/stress/infection

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97
Q

How are Myasthenic Crises managed?

A

IVIG
Plasma Exchange
Steroids

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98
Q

Define Motor Neurone Disease

A

Umbrella term for progressive and ultimately fatal condition where motor neurones stop functioning

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99
Q

What are the four subtypes of Motor Neurone Disease?

A

Amyotrophic Lateral Sclerosis
Progressive Bulbar Palsy
Progressive Muscular Atrophy
Primary Lateral Sclerosis

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100
Q

How does the Amyotrophic Lateral Sclerosis subtype of MND present?

A 
Mid to Late 50s
Asymmetrical weakness (spreading sequentially)
Wrist or Foot Drop
Can have UMN or LMN signs 
Can have Bulbar involvement
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101
Q

Amyotrophic Lateral Sclerosis is more of a clinical diagnosis. What investigations can be done?

A

EMG (sensory intact)
Genetics
MRI?CT
Antibodies to exclude MG/Lambert Eaton

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102
Q

Amyotrophic Lateral Sclerosis is incurable. Name four managements to ease symptoms and slow progression

A

Riluzole/Edavarone - slows progression and increases survival by a few months
Baclofen - muscle cramps
Opioids - Breathlessness
Physiotherapy

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103
Q

Define Muscular Dystrophy

A

Umbrella term that causes gradual wasting and weakness of muscles

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104
Q

Describe Duchennes Muscular Dystrophy

A
  • X linked inherited abnormal gene
  • If mother is a carrier, son has 50% chance of being affected
  • Boys present at 3-5y with pelvic muscular weakness
  • Life expectancy of 25-35y
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105
Q

How is Duchennes MD managed?

A

Steroids to slow progression and creatine supplements

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106
Q

Describe Beckers MD

A

Dystrophin gene is less severely affected than in Duchennes

Symptoms start around 8-12y and may require a wheelchair by 20-30y

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107
Q

Describe Myotonic Muscular Dystrophy

A
  • Genetic disorder presenting in adulthood

- Progressive muscle weakness, prolonged contractions, cataracts, cardiac arrhythmia

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108
Q

Describe Facioscapulohumeral MD

A

In childhood, weakness around face progressing to shoulders and arms

Sleep with eyes open, can’t purse lips, can’t blow out cheeks

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109
Q

Describe Oculopharyngeal MD

A

Bilateral Ptosis
Restricted eye movements
Swallowing problems

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110
Q

Describe Emery Dreifuss MD

A
  • Contractures (usually at elbow and ankles)

- Progressive weakness and muscle wasting

111
Q

Define Multiple Sclerosis

A

Chronic immune mediated inflammatory disease of the CNS - multiple plaques of demyelination in the brain and spinal cord disseminated in time and place (occurring at multiple sites with >30 days between attacks)

Type 2 hypersensitivity

112
Q

What causes Multiple Sclerosis?

A

Abnormal immune reaction to an unknown trigger in genetically predisposed individual

More than 200 polymorphisms of genetic succeptibility

Risks - EBV, Low sunlight, adolescent obesity, smoking

113
Q

Describe the pathophysiology of Multiple Sclerosis

A

Oligodendrocytes are destroyed which leads to demyelination and axonal loss (due to poor healing) = poor transmission of signals passed down nerve

B lymphocytes, macrophages and microglia create MS plaques (optic nerves, spinal cord, brainstem)

114
Q

What are the classifications of Multiple Sclerosis?

A
  • Relapsing/Remitting (getting residual damage each time)
  • Primary Progressive
  • Secondary Progressive (after 15y of Relapse/Remit)
  • Clinically Isolated (clinical episode but no evidence on neuroimaging)
115
Q

What are the possible visual features of Multiple Sclerosis?

A

Optic Neuritis (visual loss, poor colour, pain, scotoma)

Internuclear Opthalmoplegia (disconjugate lateral gaze - abducens moves fine, oculomotor doesn’t)

Abducens Palsy

116
Q

What Motor Symptoms are classical of Multiple Sclerosis?

A

Weakness
Ataxia
UMN signs

117
Q

What specific Motor Syndromes can you get within Multiple Sclerosis?

A

Transverse Myelitis - focal inflammation within the spine and sensorimotor symptoms below with bladder/bowel involvement

Cerebellar Syndrome - DANISH

118
Q

What sensory features can you get in Multiple Sclerosis?

A

Paraesthesia and Pain

L’hermitte Phenomenon - Electric shock feeling triggered by neck flexion

Uhthoff Phenomenon - Transient worsening of neuro symptoms with heat

119
Q

What is the criteria for diagnosing MS based on MRI called?

A

McDonald Criteria

120
Q

Define an MS attack

A

Episode of neurological symptoms lasting >24h with or without recovery (but with at least 30 days between attacks)

121
Q

Name four differentials for Multiple Sclerosis

A

Transverse Myelitis
Lyme Disease
B12 Deficiency
Diabetic Neuropathy

122
Q

Name three supportive investigations for Multiple Sclerosis

A

CSF Oligoclonal Bands (not identified in serum)

Visual Evoked Response (measures electrical activity over occipital cortex in response to light)

AB Testing

123
Q

How is an acute MS attack managed?

A

After ruling out any infection

Oral/IV Methylprednisolone + PPI

124
Q

Name two disease modifying therapies for MS

A

Interferon Beta

Glatiramir Acetate

125
Q

What other general care managements do you need to consider in MS?

A 
Bladder dysfunction (Oxybutinin)
Depression
Fatigue
Neuropathic Pain
Spasticity (Baclofen)
126
Q

Define Benign Essential Tremor

A

Relatively common condition characterised by fine trmor affecting voluntary muscles, most noticable in hands but can affect other areas

127
Q

Name four features of Benign Essential Tremor

A

Fine Tremor
Symmetrical
Improved by alcohol
More prominent on voluntary (eg outstretched)

128
Q

How is Benign Essential Tremor managed?

A

No definitive management

Propranolol or Primidone can be tried

129
Q

What is Bell’s Palsy?

A

Idiopathic facial nerve palsy

130
Q

Name four symptoms of Bell’s Palsy

A

Difficulty chewing
Tingling
Ear Pain
Hyperacusis

131
Q

Name four signs of Bell’s Palsy

A

Loss of nasolabial folds
Drooping corner of mouth
Drooping eyebrow
Asymmetric smile

132
Q

How can Bell’s Palsy be differentiated from a stroke?

A

A stroke affected UMN so is forehead sparing

133
Q

What is the grading system for Bell’s Palsy?

A

House Brackmann Grading System

134
Q

When would you consider an alternative diagnosis to Bell’s Palsy?

A

Overt pain
Systemic Illness
Hearing abnormalities

135
Q

How is Bell’s Palsy managed?

A

Prednisolone if within 72 hours
Eye drops and tape for protection

May take several months to recover

136
Q

Name two complications of Bell’s Palsy

A

Corneal Abrasion

Aberrant Reinnervation (voluntary contraction of one muscle leads to involuntary contraction of another muscle)

137
Q

Name five presenting features of Cervical Spondylosis

A
  • Cervical pain worsened by movement
  • Cervical stiffness
  • Vague numbness/tingling/weakness of upper limbs
  • Radiculopathy
  • Retro orbital/Temporal pain
138
Q

How can you demonstrate dural irritation in Cervical Spondylosis?

A

Lateral flexion and pressure on top of head

139
Q

Name three read flags for Cervical Spondylosis

A
  • Age of onset <20 ir >55
  • Weakness/ Sensory loss in more than one Dermatome/Myotome
  • Constitutional symptoms
140
Q

How would you manage Cervical Spondylosis initially?

A

First 3-4 weeks reassure patient that it is common and will resolve
Stay active
One firm pillow at night

141
Q

After four weeks how should Cervical Spondylosis be managed?

A

Physiotherapy, Occupational health referral, Pain Clinic, Surgery

142
Q

What is a Radiculopathy?

A

Sensory/Motor symptoms in response to nerve root damage by any cause

143
Q

How does Posterior Sciatica present?

A

Pain along posterior thigh and posterolateral leg due to L5/S1 radiculopathy

144
Q

How does Anterior Sciatica present?

A

Pain along anterior leg/thigh due to L3/L4 radiculopathy

145
Q

Name the nerve roots for upper limb reflexes

A

Biceps - C5
Triceps - C7
Wrist - C8

146
Q

Name the nerve roots for lower limb reflexes

A

Knee - L3/L4

Achilles - S1/S2

147
Q

What is Carpal Tunnel Syndrome?

A

Compression/Entrapment/Irritation of Median Nerve

148
Q

Carpal tunnel syndrome is normally idiopathic, give three associations

A

Pregnancy
Obesity
Hypothyroid

149
Q

How does Carpal Tunnel Syndrome present?

A

Tingling/numbness/pain in median nerve distribution
Often worse at night (patient may hang arm out of bed to revive)
Weakness if hand grip
Severe- Thenar wasting

150
Q

What are the two clinical tests for Carpal Tunnel Syndrome

A

Tinnel’s

Phalen’s

151
Q

Carpal Tunnel Syndrome is normally a clinical diagnosis . What investigations could be done?

A

Electroneurography

Ultrasound

152
Q

How is Carpal Tunnel Syndrome managed?

A

Splint at night and NSAIDs

Corticoteroid injections, Accupuncture

Surgical cutting the transverse carpal ligament

153
Q

Name three causes of Ulnar Nerve Palsy

A

Dislocation/Fracture of elbow
Ulnar artery aneurysm
Synovial inflammation

154
Q

How does Ulnar Nerve palsy at the elbow present?

A

Wasting along medial forearm
Weakness in hand muscles and finger flexion
Sensory Loss
Ulnar Claw

155
Q

How does Ulnar Nerve palsy at the wrist present?

A

Cutaneous often spared

156
Q

How can Ulnar Nerve Palsy be investigated?

A

USS Cubital tunnel
EMG
CXR (pancoast)

157
Q

Describe the conservative management for Ulnar Nerve Palsy

A

Anterior elbow splinting
Ergonomic correction
NSAIDs

If not then surgery

158
Q

Diabetic Neuropathy is the most common cause of Peripheral Neuropathy. Give three risk factors

A

Smoker
>40
Periods of poor glycaemic control

159
Q

Patients with Diabetic Neuropathy may not notice themselves. What are the five different types?

A 
Peripheral Sensorimotor
Acute Diffuse Painful
Autonomic
Mononeuropathy
Diabetic Amyotrophy
160
Q

How does Peripheral Sensorimotor Diabetic Neuropathy present?

A

Sensory nerves affected more (glove and stocking)
Loss of ankle jerks and later knee
Hands only in long standing

161
Q

How does Acute Diffuse Painful Diabetic Neuropathy present?

A

Abrupt onset but can resolve completely
Burning foot pain (worse at night)
Associated with poor glycaemic control

162
Q

How does Autonomic Diabetic Neuropathy present?

A

Cardiac abnormalities
Exercise intolerance
Reduced respiratory drive
Reduced baroreceptor sensitivity

163
Q

How does Mononeuropathic Diabetic Neuropathy present?

A

E.G Carpal Tunnel

164
Q

How does Diabetic Amyotrophy present?

A

Pain and paraesthesia in upper legs with weakness and wasting of muscle

165
Q

How is Diabetic Neuropathy investigated?

A

Diabetic Control
Measuring BP
Nerve conduction studies
Electromyography

166
Q

How is Diabetic Neuropathy managed?

A

Regular surveillance and foot care
Good diabetic control
bed foot cradles
Neuropathic pain relief if required

167
Q

What are the two types of ADLs?

A

Personal - Washing/Dressing/Toileting/Continence

Domestic - Cooking/Cleaning/Shopping

168
Q

Define Alzheimer’s

A

Progressive neurodegenerative disorder that causes reduced mental performance and impairment in social and occupational function

169
Q

What causes Alzheimer’s?

A

A combination of factors

Older Age, Genetics (Sporadic/APP/Presenilin), CVS Disease

170
Q

What are the two main pathological features associated with Alzheimer’s Disease?

A

Senile Plaques (Beta Amyloid deposits extracellularly, they are seen in normal ageing)

Neurofibrillary Tangles (Hyperphosphorylated Tau Proteins in regions involved in memory, promoting cell death)

171
Q

Name two cognitive and two non cognitive symptoms of Alzheimer’s disease

A

Cognitive - Poor Memory, Language

Non Cognitive - Agitation, Emotional Lability

172
Q

Name four cognitive assessments

A
  • Mini - Cog (three item word memory and clock drawing)
  • AMT (ten item tool)
  • MMSE (eleven item tool)
  • MoCA (several domains including executive function, attention, language, memory and visuospatial)
173
Q

How is Alzheimer’s Disease diagnosed?

A 
Functional Inability (and decline from previous)
Cognitive (impairment in >2 domains)
Differentials excluded (via neuroimaging etc)
174
Q

Name three non pharmacological managements of Alzheimer’s Disease

A

Advanced Care Planning
Inform DVLA
Encourage groups and activities

175
Q

What are the pharmacological options for Alzheimer’s management?

A

Mild to Mod - AChesterase inhibitors (Donepazil)

Mod to Severe - NMDA Antagonists (Memantine)

176
Q

Frontotemporal dementia has prominent disturbances in social behaviour, language and personality. What are the subtypes?

A

Behavioural Variant - Progressive personality and behavioural change

Primary Progressive Aphasia (Non Fluent or Semantic)

177
Q

Describe the pathophysiology of Frontotemporal Dementia

A

Phosphorylated Tau Proteins/Pick Bodies

Some familial cases with AD Inheritance

Atrophy of frontal and temporal lobes

178
Q

Frontotemporal Dementia can present in many different ways. How does the Behavioural Variant present?

A

Disinhibition, Loss of empathy, Apathy

179
Q

Frontotemporal Dementia can present in many different ways. How does the Primary Progressive Aphasia present?

A

Effortful/Halting Speech
Speech Apraxia
Difficulty finding words

180
Q

Frontotemporal Dementia can present in many different ways. How do the Motor Syndromes present?

A
  • MND
  • Corticobasal Syndrome (Dystonia, Asymmetrical Akinesia, Alien Limb)
  • Progressive Supranuclear Palsy (difficulty looking up)
181
Q

What would the MRI of Frontotemporal Dementia show?

A

Frontal and temporal lobe atrophy

182
Q

How would you manage Frontotemporal Dementia?

A

Financial advice, SALT input, Supervision

SSRIs (decrease impulsivity)/Atypical Antipsychotics

183
Q

State the five subtypes of Vascular Dementia

A
  • Subcortical
  • Stroke Related (Large Cortical)
  • Single/Multiple Infarct
  • Mixed (with Alzheimers)
  • Autosomal Dominant
184
Q

How does Vascular Dementia present?

A

Stepwise cognitive decline

Can have focal neurological symptoms

185
Q

How is Vascular Dementia managed?

A

Donepazil/Memantine

Control CVS factors

186
Q

What is Horner’s Syndrome?

A

Classic triad of Miosis/Ptosis and anhidrosis/enopthalmos due to a lesion along oculosympathetic pathway

187
Q

What is the Oculosympathetic Pathway?

A

First Order - Hypothalamus to Spinal Cord
Second Order - Preganglionic (spinal cord to sympathetic chain)
Third Order - Post Ganglionic (within adventitia of IC, travelling to dilator pupillae and muller’s muscle)

188
Q

What are the causes of Horner’s Syndrome if first order neurones are affected? (4S’s)

A

Stroke
multiple Sclerosis
SOL
Syringomyelia

Anhidrosis on one half of body

189
Q

What are the causes of Horner’s Syndrome if second order neurones are affected? (4T’s)

A

Tumour
Trauma
Thyroidectomy
Top Rib

190
Q

What are the causes of Horner’s Syndrome if third order neurones are affected? (3C’s)

A

Carotid Aneurysms
Carotid Artery Dissection (no other sx)
Cavernous Sinus Thrombosis

No Anhidrosis

191
Q

How can Horner’s Syndrome be investigated?

A

CT Angiography (exclude dissection)
MRI (if brainstem features)
CXR (Pancoast)

192
Q

How can Horner’s Syndrome be confirmed?

A

Cocaine Eye Drops - blocks NA reuptake, only unaffected eye constricts

Apraclonidine - Alpha agonist causing affected pupil to dilate and normal pupil to constrict

Hydroxyamphetamine - all dilate except post ganglionics

193
Q

Name two cerebellopontine angle lesions

A

Acoustic Neuroma

Meningioma

194
Q

What are Acoustic Neuromas?

A

Tumours of the vestibulocochlear nerve arising from schwann cells
Typically benign and slow growing but causes pressure on surrounding tissues

195
Q

Name two risk factors for Acoustic Neuromas

A

Neurofibromatoses

High dose ionising radiation

196
Q

What initial symptoms can Acoustic Neuromas present with?

A

Unilateral/Asymmetric hearing loss/tinnitus
Impaired facial sensation
Balance problems without explanation

197
Q

As an Acoustic Neuroma grows, what further symptoms can it cause?

A

Facial Pain/Numbness
Earache
Ataxia
Hydrocephalus

198
Q

What investigations are required for Acoustic Neuromas?

A

Audiology

MRI

199
Q

If the Acoustic Neuroma is small, you can just manage with serial scans. What other management options are there?

A

Microsurgery (can cause CSF leak or stroke)

Radiotherapy (sterotactic, fractionated, proton beam)

200
Q

What are Meningiomas?

A

Slow growing benign tumours arising from Dura Mate

Normally well circumscribed

201
Q

How are Meningiomas graded?

A

I - Generally Benign
II - Higher rate of recurrence post surgery
III - Anaplastic

202
Q

How do Meningiomas present?

A 
Seizures
Raised ICP
Changes in personality
Nerve palsies
Can be spinal - Brown Sequard
203
Q

How do Meningiomas appear on MRI?

A

Well defines
Central Cystic Degeneration
Oedema of nearby white matter

204
Q

What are the management options for Meningiomas?

A

Endovascular Embolisation (Coil or Glue)
Surgical Removal
Stereotactic Radiotherapy

205
Q

What is Subacute Combined Degeneration of the Cord?

A

Degeneration of the posterior and lateral columns as a result of B12/Vitamin E/Copper deficiency

206
Q

Name three underlying causes of Subacute Combined Degeneration of the Cord

A

Dietary Deficiency
Lack of IF
Low Gastric pH

207
Q

What would be the underlying investigative abnormality in Subacute Degeneration of the Spinal Cord?

A

B12 and folate deficiency leading to megaloblastic anaemia

208
Q

How does Subacute Degeneration of the Spinal Cord present?

A

Weakness of leg/arms/trunk
Progressive tingling and numbness
Posterior Column - reduced vibration and proprioception
Lateral Column - UMN signs, Ataxia

209
Q

How is Subacute Degeneration of the Spinal Cord managed?

A

Replace B12

If folate also deficient, treat B12 first

210
Q

What is Cavernous Sinus Syndrome?

A

Any pathology involving Cavernous Sinus which may present as a combination of unilateral opthalmoplegia, autonomic dysfunction, or sensory loss

211
Q

Give four causes of Cavernous Sinus Syndrome

A

Meningioma
Sarcoidosis
Basal Skull Fracture
Cavernous Sinus Thrombosis

212
Q

How does Cavernous Sinus Syndrome present?

A

Can compress any nerves leading to isolated palsies or post ganglionic Horners
May get Proptosis and Chemosis secondary to pressure

213
Q

How is Cavernous Sinus Syndrome investigated?

A

Bloods
MRI
CT

214
Q

How is Cavernous Sinus Syndrome managed?

A

Tumour - Surgery or Radio
Traumatic - Orbital Decompression
Inflammatory - Steroids
Vascular - Embolisation/Clipping

215
Q

What is Wernicke’s Encephalopathy?

A

Spectrum of diseases resulting from Thiamine deficiency (usually related to alcohol abuse although can be secondary to Bariatric Surgery/Hyperemesis Gravidarum etc)

216
Q

Describe the pathophysiology of Wernicke’s Encephalopathy

A

Inadequate nutritional thiamine/decreased absorption from GI tract/impaired thiamine utilisation

Thiamine is a cofactor required by three enzymes for carbohydrate synthesis so causes metabolic disruption

217
Q

What is the classic triad of Wernicke’s Encephalopathy? Name two other symptoms

A

Ataxia, Opthalmoplegia, Confusion

Unexplained hypotension/hypothermia
Hallucinations

218
Q

What is required to diagnose Wernicke’s Encephalopathy?

A

At least 2 of:

Dietary Deficiency
Oculomotor Abnormalities
Cerebellar Dysfunction
Altered Mental State/Impairment

219
Q

How is Wernicke’s Encephalopathy managed?

A

Thiamine + Pabrinex

Alcoholics should have prophylactic thiamine as long as they are malnourished/have decompensated liver disease

May have to use Mental Health Act

220
Q

One of the complications of Wernicke’s Encephalopathy is Korsakoff Syndrome. Name three features of this

A

Confabulation
Anterograde and Retrograde Amnesia
Psychosis

221
Q

What is an Argyll Robertson Pupil?

A

Small irregular pupils that have little/no constriction to light but do accommodate

Classically caused by neurosyphilis

222
Q

Describe the pathophysiology behind an Argyll Robertson Pupil

A

Damage to dorsal aspect of EWN disrupts inhibitory neurones causing constant constriction

223
Q

What is Creutzfeld-Jakob Disease?

A

Best known Human Prion Disease

Accumulation of small infectious pathogens, containing protein but lacking nucleic acids

224
Q

Name the four main variants of CJD

A
  • Sporadic (85% of cases)
  • Hereditary (Familial clusters with dominant inheritance)
  • Iatrogenic (Neurosurgery, tissue grafts)
  • New Variant (linked to eating BSE infected cattle products)
225
Q

CJD presents very non specifically and can’t be reliably diagnosed until death. Give some presentations

A
  • Myoclonus
  • Progressive Ataxia/Choreiform
  • Visual Disturbance
  • Rapidly progressing cognitive and functional impairment
226
Q

How is CJD investigated?

A
  • Brain Biopsy (can use tonsil biopsy if new variant)
  • CSF markers
  • EEG (Periodic wave complexes in sporadic)
  • MRI (increased intensity in certain brain regions depending on subtype)
227
Q

Define Syringomyelia

A

Fluid filled tubular cyst in central spinal cord that can elongate/enlarge and expand into grey/white matter, compressing tracts

228
Q

Define Syringobulbia

A

Where Syringomyelia has extended into brainstem

Can cause nerve palsies

229
Q

Describe the aetiology of Syringomyelia

A

Blockage of CSF (normally secondary to Chiari malformation)

SOL, Arachnoiditis, Post Traumatic

230
Q

How does Syringomyelia present in terms of sensory features?

A

Spinothalamic lost in a shawl like distribution
Extends into Dorsal Column

Dysaesthesia - Pain when skin is touched

231
Q

How does Syringomyelia present in terms of motor features?

A

As t extends and damages LMN of anterior horn

Muscle wasting and weakness beginning in hand
Reduced tendon reflexes
Claw hand

232
Q

How does Syringomyelia present in terms of autonomic features?

A

Can affect bowel/bladder/sexual organs

Horners

233
Q

How can Syringomyelia be investigated?

A

MRI - shows soft tissue causes

CT - shows bony causes

234
Q

How can Syringomyelia be managed?

A

Physio and rehab
Taught to avoid damage which may occur in the absence of pain

Surgery - Shunt/Laminectomy/Syringotomy

235
Q

What is Hypoxic Ischaemic Encephalopathy?

A

Entire brain is derived of adequate oxygen supply but loss is not total. Normally associated with neonates but can occur in adults (eg post cardiac arrest)

236
Q

How does HIE present?

A

Cyanosis as blood is redirected

Fainting/Coma/Seizures/Brain Death

237
Q

What would be seen on CT of HIE?

A

Diffuse oedema

Reduced cortical grey matter

238
Q

What Syndrome can Pituitary Tumours be associated with?

A

MEN1

239
Q

Name four types of Pituitary Tumour

A

Non functioning adenoma
Prolactinoma
GH secreting
ACTH secreting

240
Q

Describe the local effects of a Pituitary Tumour

A

Headache (retro-orbital or bitemporal, worse on waking)
Visual Field Defects
Facial Pain

If extending into hypothalamus - Diabetes Insipidus etc

241
Q

How can the cause of Bitemporal Hemianopia be distinguished?

A

If initially lower quadrants affected - Craniopharyngoma

If upper - Pituitary Adenoma

242
Q

What is the order of hormones affected in Hypopituitarism

A

LH, GH, TSH, ACTH, FSH

243
Q

The management for Pituitary Adenomas is often Trans-sphenoidal surgery. Name four complications

A

SIADH
DI
Addisons
CSF leak

244
Q

How can you manage Pituitary Adenomas medically?

A

Acromegaly - Octreotide

Prolactinoma - Bromacriptine

245
Q

When would you use Radiotherapy for Pituitary Adenoma?

A

Incomplete resection

246
Q

Name three causes of Olfactory Nerve Damage

A

Trauma
Frontal Lobe Tumour
Meningitis

247
Q

Name three causes of Oculomotor Nerve Damage

A

DM
GCA
PCA

248
Q

Name two causes of Trochlear Nerve Damage

A

Rare -Orbital trauma, Diabetes

249
Q

Name three causes of Abducens Nerve Damage

A

MS
Pontine CVA
Raised ICP

250
Q

Name two causes of Facial Nerve Damage

A

Upper - Stroke

Lower - Bells

251
Q

Name three causes of Vestibulocochlear Nerve Damage

A

Loud Noises
Pagets
Acoustic Neuroma

252
Q

Name three causes of Glossopharyngeal Nerve Damage

A

Trauma
GBS
Polio

253
Q

Name two causes of Vagus and Accessory Nerve Damage

A

Trauma

Brainstem pathology

254
Q

Name three causes of Hypoglossal Nerve Damage

A

Polio
Syringomyelia
TB

255
Q

What AED is tolerated really well?

A

Levetiracetam (Keppra)

256
Q

Name three stroke mimics

A

Migraines
Todd’s Paresis (post seizure)
Bells Palsy

257
Q

Name three Chameleons (atypical strokes)

A

Bilateral thalami stroke
Bilateral occipital stroke
Limb shaking TIA

258
Q

What can affect the seizure threshold?

A

Medications
Drugs
Sleep
Flashing Lights

259
Q

What is the pregnancy prevention programme for epilepsy?

A

At least 1 form of contraception (ideally 2)

Should be started Atleast one month before starting the medication

260
Q

MCA infarcts make up 2/3 of Ischaemic strokes. How would ACA strokes present differently?

A

Contralateral Lower limb > upper limb

Disorder of executive function

261
Q

What is characteristic on an epileptic EEG?

A

Spike and wave discharge

Hz is how many spikes and waves in a second

262
Q

What are the four recognised stages of Parkinson’s

A

Early
Maintenance
Advanced
Palliative

263
Q

What is Restless Leg Syndrome?

A

Urge to move legs (aka this is) associated with par aesthetics (crawling,throbbing), and night time movements (often noticed by partner)

264
Q

Give 5 associations of Restless Leg Syndrome

A 
Family History
Uraemia
Iron Deficiency Anaemia (check ferritin)
Pregnancy 
Diabetes Mellitus
265
Q

How is Restless Leg Syndrome managed?

A

Simple exercises such as walking and stretching

Dopamine agonists such as Ropinorole first line

266
Q

Name two scoring systems for Parkinson’s

A

Heohn Yahr

UPDRS

267
Q

Describe the Heohn Yahr Scale for Parkinson’s Disease

A

I - Unilateral Disease
II - Bilateral Disease with intact posture
III - Mod Bilateral disease with postural instability
IV - Severe Bilateral Disease but can still walk independently
V - Wheelchair only or bed bound

268
Q

Describe the UPDRS

A

Measured on 4 categories (Non Motor Symptoms of ADL, Motor Symptoms of ADL, Motor Assessment, Motor Complications), rated out of 5

269
Q

Head injuries caused by high energy impacts can be divided into 2 groups, how?

A

blunt - falls, RTIs, sports injury, assault

penetrating - bullet and knife wounds

270
Q

what are the 3 i’s of head injury?

A

impulsivity
irritability
instability

271
Q

what are some changes often reported by patients relatives following head injuries?

A

lose of executive function, loss of problem solving, memory and learning difficulties, difficulties with speech and language, more impulsive, irritable and unstable

272
Q

describe the pathophysiology of a head injury

A

coup injury occurs at the site of impact ipsilateral to the direction of the initial blow and happens as a result of the cranial vault being pushed backwards onto the brain. Then get a contrecoup injury where due to density differences between CSF and brain, the brain is left behind as skull acceletrates pushing it backwards in the skull hitting the occipital bone - secondary impact

273
Q

how does indirect damage occur in a head injury

A

diffuse axonal injury - high shear forces generated in rapid acceleration and deceleration cause damage to the myelinated white matter disrupting axonal transport = microglial activation and scarring. can also cause disconnected white matter tracts = neurobehavioral changes = traumatic brain injury

Y4 Neuro and Special Senses (9 decks)

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