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Phase 2a > The Brain > Flashcards

The Brain Flashcards

1
Q

Define multiple sclerosis

A

Chronic and progressive autoimmune condition involving demyelination in the CNS

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2
Q

Describe the pathophysiology of multiple sclerosis

A

Immune system attacks the myelin sheath of the myelinated neurones

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3
Q

What cell produces myelin in the CNS

A

Oligodendrocytes

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4
Q

What cell produces myelin in PNS

A

Schwann cell

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5
Q

What happens in early disease in multiple sclerosis to myelin

A

Re-myelination can occur symptoms resolve

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6
Q

What happens in later disease in multiple sclerosis to myelin

A

Re-myelination is incomplete

Symptoms gradually become more permanent

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7
Q

Why in multiple sclerosis do symptoms change overtime

A

Lesions vary in location = affected sites change overtime

Lesions - ‘disseminated in time and space’

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8
Q

What is the epidemiology of multiple sclerosis

A

Presents in young adults - under 50

More common in women

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9
Q

What are the causes of multiple sclerosis

A

Unclear - by may be influenced by:

Multiple genes
Epstein-Barr virus
Low vitamin D
Smoking
Obesity

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10
Q

Name the risk factors for multiple sclerosis

A

Female sex
History MS
Northern latitude

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11
Q

Describe the onset of multiple sclerosis

A

Usually progresses over more than 24 hours

Symptoms tend to last days to weeks after 1st presentation and then improve

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12
Q

Describe the clinical features of multiple sclerosis

A

Depend on site of the lesion

Optic neuritis (most common)
Eye movement abnormalities
Focal neurological symptoms
Ataxia

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13
Q

Name the investigations for multiple sclerosis

A

MRI

Lumbar puncture

Other
- FBC
- Thyroid stimulating hormone
- Vitamin B12

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14
Q

Describe the disease patterns of multiple sclerosis

A

Clinically isolated syndrome
Relapsing remitting
Secondary progressive
Primary progressive

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15
Q

Describe the clinically isolated syndrome pattern of multiple sclerosis

A

1st episode of demyelination and neurological signs and symptoms

May never go on to have another lesion or develop MS

Lesions on MRI can suggest likelihood to progress onto MS

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16
Q

Describe the relapsing-remitting stage of multiple sclerosis

A

Most common pattern when 1st diagnosed

Characterised by episodes of disease and neurological symptoms followed by recovery

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17
Q

What are the classifications of relapsing remitting stage of multiple sclerosis

A

Active - new symptoms/lesions

Not active - no new symptoms/lesions

Worsening

Not worsening

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18
Q

Describe secondary progressive stage of multiple sclerosis

A

Was relapsing emitting, no progressive worsening of symptoms with incomplete remission

Symptoms becoming increasingly more permanent

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19
Q

Describe the primary progressive stage of multiple sclerosis

A

Worsening disease and neurological symptoms from the point of diagnosis without relapses and remissions

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20
Q

How is multiple sclerosis diagnosed

A

Clinical picture + symptoms suggesting lesions that change location overtime

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21
Q

Describe the management of multiple sclerosis

A

Optic neuritis = high dose steroids

Disease modifying therapies

Relapses - may be treated with steroids

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22
Q

Name 5 differential diagnosis of multiple sclerosis

A

Fibromyalgia
Sjogren syndrome
Vitamin B12 deficiency
Ischaemic stroke
Peripheral neuropathy

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23
Q

Name 5 complications of multiple sclerosis

A

UTI
Osteopenia and osteoporosis
Depression
Visual impairment
Erectile dysfunction

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24
Q

What is the prognosis of multiple sclerosis

A

Difficult to know

Depends on response to treatment

MRI useful to assist prognosis

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25
Q

Define Guillain-Barre Syndrome

A

Acute paralytic polyneuropathy that affects the peripheral nervous system

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26
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Molecular mimicry

B cells create antibodies against the antigens on the triggering pathogen

Antibodies match proteins on the peripheral neurones

May target proteins on the myelin sheath or the nerve axon itself

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27
Q

Describe the epidemology Guillain-Barre syndrome

A

More common in males

> 50 years

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28
Q

Describe the causes of Guillain-Barre syndrome

A

Usually triggered by an infection

Gastroenteritis or influenza like illness before onset of neurological symptoms

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29
Q

Name 4 risk factors of Guillain-Barre syndrome

A

Preceding:
viral illness
bacterial infection
mosquito-borne viral infection

Hepatitis E infection

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30
Q

Describe the clinical feature of Guillain-Barre syndrome

A

Usually start within 4 weeks of triggering infection

Symptoms peak 2-4 weeks

  • Begin in the feet and progress upwards
  • Acute, symmetrical, ascending weakness
  • sensory symptoms
  • reduced reflexes
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31
Q

What are the investigations Guillain-Barre syndrome

A

Nerve conduction studies

Lumbar puncture for CSF

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32
Q

What criteria can be used for Guillain-Barre syndrome

A

Brighton criteria

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33
Q

Describe the Brighton criteria

A

Diagnostic tool - helps identification and monitoring

Help distinguish low and high-risk patients

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34
Q

How is a clinical diagnosis of Guillain’s-Barre syndrome made

A

Clinical (Brighton criteria) = supporting investigations

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35
Q

What is the clinical definition of Guillain’s-Barre syndrome

A

Syndrome characterised by motor difficulty, absence of deep tendon reflexes, Paraesthesias without objective sensory loss and increased CSF albumin with a normal cell count

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36
Q

What is the 1st line treatment in Guillain’s-Barre syndrome

A

IV immunoglobulins

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37
Q

Describe the management of Guillain’s-Barre syndrome

A

1st line - immunoglobulins

Supportive care

VTW prophylaxis

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38
Q

Describe Guillain’s Barre syndrome

A

Transverse myelitis
Myasthenia gravis
Botulism
Polymyositis
Vasculitis neuropathy

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39
Q

What is the leading cause of death of Guillain’s-Barre syndrome

A

Pulmonary embolism

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40
Q

Describe the prognosis of Guillain’s-Barre syndrome

A

Recovery can take months to years.

Can continue regaining function 5 years after acute illness.

Either full recovery or minor symptoms.

Some left with significant mortality

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41
Q

What is the mortality of Guillain’s-Barre syndrome

A

5%

Mainly due to respiratory or cardiovascular complications

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42
Q

What is the % of people with Guillain’s-Barre syndrome who will go on to develop respiratory muscle weakness required ventilation

A

20-30%

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43
Q

Define Parkinson’s Disease

A

Progressive reduction in dopamine in the basal ganglia, leading to disorders of movement

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44
Q

Define the pathophysiology of Parkinson’s disease

A

Unknown

Selective loss of nigrostriatal dopaminergic neurones in the substantia nigra pars compacta

Intracytoplasmic eosinophilic inclusions (Lewy bodies) and neuritis

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45
Q

Parkinson’s - What is the most characteristic feature of basal ganglia dysfunction

A

Bradykinesia

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46
Q

Describe the epidemiology of Parkinson’s disease

A

Older age - 70 years

Male

Gradual onset of symptoms

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47
Q

Name the causes of Parkinson’s disease

A

Sporadic

Unknown
- Genetic predisposition
- Environmental factors/exposures

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48
Q

Name the 3 risk factors of Parkison’s disease

A

Increasing age

History of familial PD in younger-onset disease

Mutation in gene encoding glucerebrosidase

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49
Q

Describe the clinical signs of Parkinson’s disease

A

Asymmetrical

Resting tremor - a tremor worse with rest

Rigidity - resisting passive movement

Bradykinesia - slowness of movement

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50
Q

Describe the presentation of Parkinson’s disease

A

Stooped posture
Facial masking
Forward tilt
Reduced arm swing
Shuffling gait

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51
Q

Describe Parkinson’s-Plus syndrome

A

Multiple system atrophy
Dementia with Lewy bodies

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52
Q

Name the investigations Parkinson’s disease

A

Dopaminergic agent trial - improvement of symptoms

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53
Q

Describe the diagnosis of Parkinson’s disease

A

History + examination findings

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54
Q

Describe the management of Parkinson’s disease

A

No cure

Treatment options
- Levodopa
- COMT inhibitors
- Dopamine agonists
- Monoamine oxidase B-inhibitors

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55
Q

Name the differential diagnosis Parkinson’s disease

A

Essential tremor
Multiple system atrophy
Dementia with Lewy bodies
Corticobasal degeneration
Alzheimer’s disease with parkinsonism

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56
Q

Name the complications of Parkinson’s disease

A

Levodopa-induced dyskinesias
Motor fluctuations
Dementia
Constipation
Bladder dysfunction
Orthostatic hypotension
Sleep disorders
Dysphagia

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57
Q

Describe the prognosis of Parkinson’s disease

A

Course is progressive

Unilateral symptoms become bilateral

After 5 years - motor complications develop

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58
Q

Define Huntington’s Disease

A

Autosomal dominant genetic condition that causes progressive neurological dysfunction

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59
Q

Describe the pathophysiology of Huntington’s disease

A

CAG repeat generates elongated polyglutamine tail of the huntingtin protein.

Leads to cleavage and generation of toxic fragments of this abnormal protein

Toxic fragments can cross-link

Forms aggregates that resist degradation, interfere with normal cell function

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60
Q

Describe the epidemiology of Huntington’s disease

A

Symptoms begin aged 30-50

Men and women equally

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61
Q

Describe the causes of Huntington’s disease

A

Autosomal dominant

Trinucleotide repeat disorder CAG

HTT gene mutation of chromosome 5 - encodes for huntingtin (HTT) protein

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62
Q

Name of feature of trinucleotide repeat disorders

A

Successive generations have more repeats in the gene

Results in:

Earlier age of onset

Increased severity of disease

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63
Q

Name the risk factors (2) of Huntington’s disease

A

Expansion of CAG repeat in huntingtin gene

Family history

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64
Q

Name the progression of the clinical features of Huntington’s disease

A

Insidious, progressive worsening of symptoms

Typically, begins with cognitive, psychiatric or mood problems, followed by development of movement disorders

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65
Q

Name the movement disorder clinical features of Huntington’s disease

A

Chorea
Dystonia
Rigidity
Eye movement disorders
Dysarthria
Dysphagia

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66
Q

Name the investigations of Huntington’s disease

A

No initial tests

Genetic testing - CAG repeat testing

MRI or CT scan

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67
Q

How is the clinical diagnosis of Huntington’s disease

A

Genetic testing (with pre and post-test counselling)

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68
Q

Describe the treatment of Huntington’s disease

A

No treatment options for slowing or stopping progression

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69
Q

Describe management of Huntington’s disease

A

Genetic counselling
MDT
Physiotherapy
Speech and language therapy
Tetrabenazine
Antidepressants
Advanced directives
End-of-life care

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70
Q

Name 4 differential diagnosis of Huntington’s disease

A

Tardive dyskinesia
DRPLA
Neuroacanthocytosis
Spinocerebellar ataxia 17

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71
Q

Describe the prognosis of Huntington’s disease

A

Progressive condition

Life expectancy 10-20 years after onset of symptoms

Progresses - more frail and susceptible to illness

Death often due to aspiration pneumonia

Suicide common

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72
Q

Name 4 complications of Huntington’s disease

A

Weight loss
Dysphagia
Falls
Suicide risk

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73
Q

Name some key red flags of headaches

A

Fever, photophobia or neck stiffness

Sudden-onset occipital headache

Postural, worse on standing, lying or bending over

Vomiting

History of trauma or cancer

Pregnancy

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74
Q

Define a migraine

A

Complex neurological disorder causing episodes or attacks of headache and associated symptoms

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75
Q

Describe the pathophysiology of migraines

A

Results from neurological inflammation of first division trigeminal sensory neurones that innervate the large vessels and meninges in the brain

When trigeminal neurones are activated - release substances that cause dilation of meningeal blood vessels, leakage of plasma proteins into surrounding tissue and platelet activation

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76
Q

Describe the pathophysiology of Aura in migraines

A

Waves of excitation spread anteriorly in the cortex followed by a prolonged period of decreased neuronal activity then neuronal recovery

Results in activation of nociceptors in adjacent dura and blood vessels

Leads to activation of trigeminal sensory nucleus

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77
Q

What are the 4 types of migraine headaches

A
  1. Migraine with aura

2.Migraine without aura

  1. Silent migraine - migraine with aura without headache
  2. Hemiplegic migraine
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78
Q

Describe the epidemiology of migraines

A

Very common

Affect women more than men

Common among teenagers and young adults

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79
Q

What are the causes of migraines

A

Genetic factors

Brain of people who experience migraines = hyperexcitable to a variety of stimuli

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80
Q

What are the 5 stages of migraines

A
  1. Premonitory or prodromal stage
  2. Aura
  3. Headache stage
  4. Resolution stage
  5. Postdromal or recovery phase
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81
Q

Describe the premonitory or prodromal stage of migraines

A

Can begin several days before the headache

Could be yawning, fatigue or mood change

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82
Q

Describe the aura stage of a migraine

A

Lasts up to 60 minutes

Can affect vision, sensation or language

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83
Q

Describe the headache stage of migraines

A

Lasts 4-72 hours

Main features
- unilateral
- moderate-severe intensity
- pounding or throbbing nature
- photophobia
- phonophobia
- osmophobia
- aura
- nausea and vomiting

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84
Q

Describe the resolution stage of migraines

A

Headache may fade away or be relieved abruptly by vomiting or sleeping

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85
Q

Describe the investigations of a migraine

A

= clinical diagnosis

Headache diary may be useful

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86
Q

Name some triggers of migraines

A

Stress
Bright lights
Strong smells
Certain foods
Dehydration
Mensuration
Disturbed sleep
Trauma

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87
Q

How is the clinical diagnosis of migraines made

A

By international classification of headache disorders (ICHD)- 3 criteria for migraines

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88
Q

What does the ICHD-3 criteria define a migraine as

A

At least 5 or more attacks in a lifetime

Headache attack lasting 4-72 hours

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89
Q

Define a migraine with aura

A

Having full reversible visual symptoms, sensory symptoms or dysphasic speech disturbance

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90
Q

Describe the acute management of migraines

A

Retreat to dark, quiet room, sleeping

Medical
- NSAIDs
- Paracetamol
- Triptans
- Antiemetics

NO opioids

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91
Q

Describe the prophylaxis of migraines

A

Depends on the frequency and severity of the attacks

Usual:
- propranolol
- amitriptyline
- topiramate

Other
- cognitive behavioural therapies
- mindfulness and medication
- acupuncture
- vitamin B12

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92
Q

Name 5 differential diagnosis of migraines

A

Headache tension

Headache cluster

Medication-overuse headache

Headache after head or neck trauma

Subarachnoid haemorrhage

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93
Q

Describe a hemiplegic migraine

A

Key features
- hemiplegia
- ataxia
- impaired consciousness

Autosomal dominant or no genetic link

Can mimic a stroke/TIA

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94
Q

What medication is contraindicated in migraines due to increasing the risk of stroke

A

Combined pill

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95
Q

Describe the prognosis of migraines

A

Tend to become less frequent and severe or stop altogether with time - particularly after menopause

Slight increase in risk - especially with aura

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96
Q

Describe the pathophysiology of tension headaches

A

Not fully understood

Similar to migraine - central hypersensitivity

Chronic = state of generalised hyperalgesia.

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97
Q

Name 5 associations of tension

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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98
Q

Describe the epidemiology of tension headaches

A

Very common

Episodic = most common type of headache

Most common between 20-39

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99
Q

Describe the causes of tension headaches

A

Involvement of peripheral factors - pericranial muscles

Genetic factors, specific genes = unknown

Common trigger = psychological stress

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100
Q

Name 5 risk factors of tension headaches

A

Mental tension
Stress
Missing meals
Fatigue
Lack of sleep

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101
Q

Name the clinical features of tension headaches

A

Either episodic or chronic

Mild ache or pressure in band-like pattern around head
- dull
- non-pulsatile
- bilateral
- pressing/pressure-like pain
- pericranial tenderness = common

No visual changes

Develop gradually

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102
Q

Describe the investigations of tension headaches

A

History + physical examination

Headache diaries can help

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103
Q

What is the 1st line treatment in tension headaches

A

Amitriptyline

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104
Q

Describe the management of tension headaches

A

1st line = amitriptyline

  • reassurance
  • simple analgesia
  • non-drug therapies
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105
Q

Name the differential diagnosis of tension headaches

A

Chronic migraine
Medicine overuse headache
Sphenoid sinusitis
Giant cell arteritis
Temporomandibular disorder
Pituitary tumour

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106
Q

Describe the prognosis of tension headaches

A

Depression, anxiety, poor sleep and stress - potential of poor prognosis

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107
Q

What is the difference between tension headaches and migraines

A

Tension headaches do not have:

Significant nausea

No vomiting

Little or no photophobia or phonophobia

Lack of aggravation by routine physical activity

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108
Q

What are the 3 cardinal features of the disorder are:

A
  1. Trigeminal disruption of the pain
  2. Ipsilateral cranial autonomic symptoms
  3. Circadian/circannual pattern of attacks
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109
Q

Describe the pathophysiology of cluster headaches

A

Physiological reflex arc, the trigeminal autonomic reflex.

Increased firing of parasympathetic nerve fibres (trigeminal nerve) innervating facial structures - causes autonomic features seen in an attack

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110
Q

What is the typical presentation (epidemiology) of cluster headaches

A

30-50 year old male

Male

Smoker

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111
Q

Describe the aetiology of cluster headaches

A

Unknown - potentials:

Head trauma
Heavy cigarette smoking
Heavy alcohol intake

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112
Q

Name 5 risk factors of cluster headaches

A

Male sex
Family history
Head injury
Cigarette smoking
Heavy drinking

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113
Q

Describe the clinical features of cluster headaches

A

Severe and unbearable unilateral headaches - usually around the eye

Clusters of attacks then disappear for extended periods

‘Suicide headache’ due to severity

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114
Q

What are the associated symptoms of the unilateral cluster headache

A

Red, swollen and watering eye

Pupil constriction (miosis)

Eyelid dropping (ptosis)

Nasal discharge

Facial sweating

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115
Q

Describe the investigations of cluster headaches

A

Brain and pituitary MRI without and with intravenous contrast

Erythrocyte sedimentation rate

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116
Q

Name 3 triggers of cluster headaches

A

Alcohol
Strong smells
Exercise

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117
Q

What’s the 1st line treatment for cluster headaches

A

Prophylaxis - verapamil

Prevent attacks

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118
Q

What is given to cluster headaches during an acute attack

A

Triptans

High flow 100% oxygen

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119
Q

What are the differential diagnosis of cluster headaches

A

Migraine
Paroxysmal hemicrania
Trigeminal neuralgia
Cluster-tic syndrome
Angel-closure glaucoma
Subarachnoid haemorrhage
Giant cell arteritis

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120
Q

Define meningitis

A

Inflammation of the meninges, usually due to an infection

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121
Q

Define meningococcal meningitis

A

When the bacteria infect the meninges and the CSF

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122
Q

Define meningococcal septicaemia

A

When meningococcus bacterial infection is the blood stream.

Can cause a non blanching rash

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123
Q

What are the causes of meningitis

A

Bacterial

Viral

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124
Q

What are the causes of bacterial meningitis

A

Neisseria meningitidis

Streptococcus pneumonia

Group B streptococcus (neonates)

Listeria monocytogenes (neonates)

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125
Q

What are the causes of viral meningitis

A

Enterovirus

Herpes simplex virus (HSV)

Varicella zoster virus (VZV)

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126
Q

Name the risk factors of bacterial meningitis

A

Most = young age

Winter season
Absent/non-functioning spleen
Older age > 65
Immunocompromised
Incomplete immunisation
Cancer
Smoking

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127
Q

Name the risk factors of viral meningitis

A

Infants and young children
Young adults
Older people
Summer and autumn
Exposure to mosquito or tic vector
Unvaccinated for mumps

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128
Q

Name the clinical features of meningitis

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash

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129
Q

In what type of meningitis is a non-blanching rash seen

A

Meningococcal septicaemia

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130
Q

Name the investigations of meningitis

A

Lumbar puncture

Viral PCR testing on CSF sample

Blood culture

Meningococcal PCR

Kernig’s test

Brudzinski’s test

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131
Q

Describe a lumbar puncture

A

Insert needle into lower back CSF at L3-4 or L4-5 intervertebral space

Samples sent for bacterial culture, viral PCR, cell count, protein and glucose

Blood glucose sent at same time

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132
Q

What two tests look for meningeal infection

A

Kernig’s test
Brudzinski’s test

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133
Q

Describe Kernig’s test

A

Lay patient on back, flex one hip and knee to 90 degrees

Slowly straighten the knee while keeping hip flexed at 90

Created slight stretch in the meninges

If meningitis = produce spinal pain or resistance to movement

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134
Q

Describe the Brudzinski’s test

A

Lie patient flat on back, gently using hands to life head and neck of bed, flexing chin to chest

Positive test = causes patient to flex their hips and knees involuntary

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135
Q

Describe the management of meningitis

A

Blood cultures and lumbar puncture before antibiotics

Aciclovir
- viral meningitis (HSV, VZV)

Bacterial
- steroids
- benzylpenicillin

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136
Q

What medication is used in viral meningitis

A

Aciclovir

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137
Q

What medication is used in bacterial meningitis

A

Steroids

Benzylpenicillin

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138
Q

Describe post exposure prophylaxis of meningitis

A

Significant exposure to meningococcal infection puts contacts at risk

Highest risk within 7 days of onset of illness

Single dose = ciprofloxacin

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139
Q

Name the differential diagnosis of meningitis

A

Bacterial/viral
Encephalitis
Encephalopathy
Drug induced meningitis
TB meningitis

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140
Q
A
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141
Q

Name complications of meningitis

A

Hearing loss - key
Seizure and epilepsy
Cognitive impairment
Memory loss
Focal neurological defects

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142
Q

Define trigeminal neuralgia

A

Facial pain syndrome in the distribution of 1 or more divisions of the trigeminal nerve

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143
Q

What is the main presentation of trigeminal neuralgia

A

Cause intense facial pain in the distribution of the trigeminal nerve

90% cases are unilateral

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144
Q

What are the 3 branches of the trigeminal nerve

A

Ophthalmic nerve (V1)

Maxillary (V2)

Mandibular (V3)

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145
Q

In what condition is trigeminal neuralgia common in

A

Multiple sclerosis

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146
Q

Describe the pathophysiology of trigeminal nerve neuralgia

A

Focal demyelination and the resultant conduction aberrations

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147
Q

Name the causes of trigeminal neuralgia

A

Majority of patients - focal compression of the trigeminal nerve root at the entry zone by an aberrant vascular loop

Multiple sclerosis - demyelinating plaques in the pons that encompass the root entry zone of the trigeminal nerve

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148
Q

Name 2 risk factors of trigeminal neuralgia

A

Increased age

Multiple sclerosis

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149
Q

Name the clinical features of trigeminal neuralgia

A

Pain comes on suddenly can last seconds to hours

Electricity like
Shooting
Stabbing
Burning pain

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150
Q

Name 4 things in which trigeminal neuralgia can be triggered by

A

Touch
Eating
Shaving
Cold

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151
Q

How is the diagnosis of trigeminal neuralgia made

A

Clinical + history of paroxysms of sharp, stabbing, intense pain lasting up to 2 minutes

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152
Q

What is the 1st line management in trigeminal neuralgia

A

Carbamazepine

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153
Q

Describe the treatment of trigeminal neuralgia

A

1st line = carbamazepine

Medical therapies

Vascular decompression

Ablative decompression

Surgical interventions

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154
Q

What are the differential diagnosis of trigeminal neuralgia

A

Dental caries/fractures
Mandibular osteomyelitis
Migraine
Temporomandibular joint syndrome
Glossopharyngeal neuralgia

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155
Q

Define Alzheimer’s disease

A

Chronic neurodegenerative disease with an insidious onset and progressive but slow decline

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156
Q

What does Alzheimer’s often co exist with

A

Vascular dementia

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157
Q

Describe the pathophysiology of Alzheimer’s disease

A

Reduced brain weight

Cortical atrophy in temporal, frontal and partial area

Changes in senile plaques and neurofibrillary tangles seen

Beta-amyloid induced injury to brain cells.

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158
Q

What is a useful indicator for the severity of Alzheimer’s disease and its cognitive incline

A

Abundance of tangles is roughly proportional to the severity of clinical disease and cognitive decline

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159
Q

Name the causes of Alzheimer’s dementia

A

Amyloid plaques - clumps of beta-amyloid

Neurofibrillary tangles

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160
Q

What are the risk factors of Alzheimer’s disease

A

Advanced age
Family history
Genetics
Down’s syndrome
Cerebrovascular disease
Lifestyle factors and medications
Less than secondary school education

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161
Q

What are the hallmark symptoms of Alzheimer’s disease

A

Memory loss

Impairment of daily activities

Neurobehavioral abnormalities

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162
Q

Name the investigations for Alzheimer’s disease

A

Bedside cognitive testing

MRI or CT

Tests to rule out other conditions

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163
Q

What is the management of Alzheimer’s disease

A

Assess and manage other long-term conditions

Possible referral

AChE inhibitors

Reduce polypharmacy

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164
Q

Name some possible complications of Alzheimer’s disease

A

Pneumonia
Institutionalisation
UTI
Falls and their complications
Weight loss
Elder abuse

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165
Q

Define frontotemporal dementia

A

Primary neurodegenerative brain disease in adults > 65 years of age.

Spectrum compromises a heterogenous group of conditions that are heritable in some cases

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166
Q

Describe the pathophysiology of frontotemporal dementia

A

Frontal lobar degeneration - neural loss, gliosis and microvascular changes of frontal lobes, anterior temporal lobes, anterior cingulate cortex and insular cortex

Several subtypes

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167
Q

How are the subtypes of frontotemporal dementia labelled

A

According to main protein component of neuronal and glial abnormal inclusions and their distributions

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168
Q

Describe the epidemiology of frontotemporal dementia

A

Average age of onset 45-65 years

Peak prevalence 7th decade

Affects both sexes equally

Average life expectancy post diagnosis = 8 years

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169
Q

Describe the causes of frontotemporal dementia

A

Neuron damage and death occurring in frontal and temporal lobes

Atrophy - due to deposition of abnormal proteins (tau protein)

Genetic component 1/4 cases

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170
Q

Name 3 risk factors of frontotemporal dementia

A

Mutations in:

MAPT gene
CRN gene
C9orf72 gene

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171
Q

What are the 3 clinical pictures of frontotemporal dementia

A

Behavioural presentation
Semantic presentation
Non fluent presentation

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172
Q

Name the investigations of frontotemporal dementia

A

Formal cognitive testing

Imaging - brain MRI or CT

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173
Q

Describe the management of frontotemporal dementia

A

No cure

Care plan

Medicine
- antidepressants
- antipsychotics

Other support

End of life plans

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174
Q

Name 5 differential diagnosis of frontotemporal dementia

A

Other forms of dementia

Bipolar disorder
Major depression
OCD
Primary brain tumour
Hyperthyroidism

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175
Q

Describe the prognosis of frontotemporal dementia

A

Shorter survival and faster rates of cognitive and functional decline that patients with Alzheimer’s disease

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176
Q

Define lewy body dementia

A

Neurodegenerative disorder with parkinsonism, progressive cognitive decline, prominent executive dysfunction, behavioural and sleep disturbances and visuospatial impairment

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177
Q

Describe the pathophysiology of lewy body dementia

A

Accumulation of lewy bodies at vulnerable sites

Lewy bodies - composed of protein alpha-synuclein - cytoplasmic protein associated with synaptic vesicles

Normal function of this protein - role in transportation of synaptic vesicles and synaptic plasticity

Distribution linked to clinical symptoms

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178
Q

Describe the epidemiology of lew body dementia

A

> 50

Affects men slightly more than women

Rapid progression

Death 7 years post diagnosis

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179
Q

Name the aetiology of Lewy body dementia

A

Spherical lewy proteins (alpha-synuclein) deposited in the brain

Toxic protein aggregation

Abnormal phosphorylation

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180
Q

Describe the difference between the presence or lewy bodies in Parkinson’s vs. lewy body dementia

A

Parkinson’s = deposited in substantia nigra

Lewy body dementia = more widespread

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181
Q

What is the risk factor of Lew body dementia

A

Older age

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182
Q

Name 4 clinical features of Lewy body dementia

A

Cognitive fluctuations

Recurrent visual hallucinations

Rapid eye movement (REM) sleep behaviour disorder

+ one or more spontaneous cardinal motor features of Parkinsonism.

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183
Q

Name the investigations in Lewy body dementia

A

Serum thyroid stimulating hormone

Serum vitamin B12

Ct head

MRI head

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184
Q

What is the clinical diagnosis of lewy body dementia

A

Clinical + confirmed pathologically presence of Lewy bodies

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185
Q

Describe the management of Lewy bodies

A

1st line pharmacological = cholinesterase inhibitors

Other medications

Main goal = improve or stabilise cognition, behaviour, and activities of family living and to maintain safety

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186
Q

What is the 1st line pharmacological treatment in Lewy body dementia

A

Cholinesterase inhibitors

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187
Q

Name 5 differential diagnosis for Lewy body dementia

A

Alzheimer’s disease
Parkinson’s disease
Frontotemporal dementia
Vascular dementia
Prion disorders

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188
Q

Describe the prognosis of Lewy body dementia

A

Progressive

Treatment = symptomatic

Mean survival 5 years

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189
Q

Define vascular dementia

A

Chronic progressive disease of the brain characterised by a chronic progressive multifaceted impairment of cognitive function

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190
Q

Describe the pathophysiology of infarction causing vascular dementia

A

Large - affect individual regions, will exhaust the brain’s compensatory mechanisms and lead to dementia

Small - in strategic areas

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191
Q

Describe the pathophysiology of leukoaraiosis as a cause of vascular dementia

A

Causes white matter pallor to naked eye

Loss of axons, myelin and oligodendrocytes

Perivascular tissue loss and dilation of perivascular spaces

Damage to capillaries with breakdown of the BBB and protein leakage

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192
Q

Describe the pathophysiology of haemorrhage as a cause of vascular dementia

A

Large parenchymal haemorrhages centred in basal ganglia (often due to hypertension)

Multiple haemorrhages occur in cortex and white matter

Angioplasty due to amyloid beta protein

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193
Q

Describe mixed dementia

A

Alzheimer’s dementia + vascular dementia

Act synergistically with each other

Co-exist - affected to greater degree compared to only one pathology

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194
Q

Describe the epidemiology of vascular dementia

A

More common in males

Prevalence increases in those who have had a stroke

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195
Q

Describe the aetiology of vascular dementia

A

Most common = cerebrovascular infarcts

Infarction

Leukoriosis

Haemorrhage

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196
Q

Name the risk factors of vascular dementia

A

Age > 60
Obesity
Hypertension - major
Cigarette smoking
Vascular risk factors

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197
Q

Describe the clinical features of vascular dementia

A

Progressive in step wise fashion

Single infarct vascular disease - cognitive impairment following an event

Motor and mood changes

Mood disturbances

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198
Q

Name the investigations of vascular dementia

A

FBC
Erythrocyte sedimentation rate
Blood glucose level
Renal and liver function tests
Vitamin B12
Folate
Thyroid function
CT or MRI brain
ECG

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199
Q

Describe the management of vascular dementia

A

Early aggressive treatment of vascular risk factors

Prevention of further cerebrovascular disease

Supportive care

Cholinesterase inhibitors
Antihypertensives
SSRIs
Cognitive stimulation therapy

Supportive care

End of life care

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200
Q

Name 5 differential diagnosis of Vascular dementia

A

Depression
Alzheimer’s disease
Mild cognitive impairment
Other forms of dementia
Primary brain tumour

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201
Q

Name 4 complications of vascular dementia

A

Depression
Aggression
Falls
Stroke

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202
Q

Name the prognosis of vascular dementia

A

Life expectancy significantly shortened - similar to AD

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203
Q

Define Amaurosis Fugax

A

Describes transient monocular vision loss because of ischemia to retina, choroid or optic nerve (retinal transient ischaemic attack)

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204
Q

Name the causes of amaurosis fugax

A

Due to narrowing (stenosis) or occlusion of the internal carotid artery or the central retinal artery

Arterial embolus (atherosclerotic emboli)

Thrombotic vascular events

Inflammation of optic nerve

Giant cell arteritis

Diabetes, smoking, cocaine

Hypertension - old age

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205
Q

Describe the pathophysiology of an artherosclerotic emboli causing amaurosis fugax

A

Usually in retinal artery from ipsilateral carotid artery disease

Accumulation of fat detaches from the inner lining of an artery and blocks blood flow elsewhere

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206
Q

Name the risk factors of amaurosis fugax

A

> 50

Vascular risk factors
- hypertension
- hypercholesterolemia
- smoking
- previous history TIA/stroke

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207
Q

Name the clinical features of amaurosis fugax

A

Typical presentation - transient vision loss in one or both eyes occurring abruptly

Maximum severity within seconds and lasts seconds - followed by full visual recovery

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208
Q

Describe the investigations of amaurosis fugax

A

Opthalamogical examination - typically normal

Inflammatory markers (exclude)
Carotid artery imaging
Cardiac investigations

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209
Q

Describe the management of amaurosis fugax

A

Aspirin
Urgent referral

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210
Q

Describe secondary prevention in amaurosis fugax

A

After diagnosis

Statin therapy

Antiplatelet therapy

Optimising blood pressure control

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211
Q

Name 6 differential diagnosis of amaurosis fugax

A

Central retinal artery/vein occlusion
Giant cell arteritis
Multiple sclerosis
Papilledema
Epilepsy
Sickle cell anaemia

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212
Q

Name the complications of amaurosis fugax

A

Ischaemic stroke - 2%

Death

Adverse cardiac events

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213
Q

Name the prognosis of amaurosis fugax

A

Untreated = major risk of stroke

Carotid endarterectomy - good prognosis

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214
Q

Define cauda equina

A

Caused by compression of the lumbosacral nerve roots that extend below the spinal cord

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215
Q

Describe the emergency of cauda equina

A

Requires emergency decompression surgery to prevent permanent neurological dysfunction

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216
Q

Describe the pathophysiology of cauda equina

A

Collection of nerve roots that travel through the spinal canal after the spinal cord terminates around L2/3.

Nerve roots exit either side of their column at their vertebral level L3-5, S1-5 and Co.

These nerves are compressed

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217
Q

What nerves are supplied by the cauda equina

A

Sensation to the lower limbs, perineum, bladder and rectum

Motor innervation to the lower limbs, and the anal and urethral sphincters

Parasympathetic innervation of the bladder and rectum

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218
Q

Name the causes of cauda equina

A

Herniated disc = most common

Tumours - metastasis

Spondylolisthesis

Abscess - infection

Trauma

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219
Q

Name 5 risk factors of cauda equina

A

Lumbar disc herniation
Spinal trauma
Spinal surgery
Spinal epidural abscess
Anticoagulation therapy

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220
Q

Describe the clinical features of cauda equina

A

Presents LMN signs - reduced tone and reflexes

Bladder dysfunction - always

Other symptoms

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221
Q

Why does cauda equina present with LMN signs

A

Nerves being compressed are LMN that have already exited the spinal cord

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222
Q

Name 2 investigations of cauda equina

A

MRI - ASAP

CT lumbar spine

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223
Q

Describe the management of cauda equina

A

Lumbar decompression surgery

Increases chance of regaining function

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224
Q

How successful is lumbar decompression surgery in cauda equina

A

May still be left with bladder, bowel, sexual dysfunction, leg weakness and sensory impairment

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225
Q

Describe the metastatic spinal cord compression as a differential diagnosis of cauda equina

A

Metastatic lesion compresses the spinal cord

Presents similar to cauda equina

Will be UMN signs - metastatic spinal cord compression is higher

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226
Q

Name the red flags of cauda equina

A

Saddle anaesthesia

Loss of sensation in the bladder and rectum

Faecal incontinence

Bilateral sciatica

Bilateral or severe motor weakness in the legs

Reduced anal tone on PR examination

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227
Q

What is the prognosis of cauda equina

A

Even with immediate decompression - patients still may not regain full function

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228
Q

Define depression

A

Disorder that causes persistent feelings of low mood, low energy, and reduced interest

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229
Q

Describe the causes of depression

A

Multifactorial - biological, psychological, social

Factors can be: predisposing, precipitating, perpetuating

Often triggered by life events

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230
Q

Name 3 protective features of depression

A

Current employment
Good social support
Marital status being married

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231
Q

What are the risk factors for depression

A

Not a single identifiable cause or trigger for cases of depression

Biological factors
Psychological factors
Social factors

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232
Q

What are the 3 core symptoms of depression

A
  1. Low mood
  2. Anhedonia - low interest or pleasure in most activities of the day
  3. Lack of energy - anergia
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233
Q

Describe the investigation of depression

A

Screening questions

Investigations for exclude physical/organic causes

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234
Q

How is depression diagnosed clinically

A

ICD-10/11 criteria

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235
Q

Describe the management of depression

Mild vs. Moderate/severe

A

Mild depression = watchful waiting + advice about healthy habits. Follow up 2 weeks

Severe depression = 1st line = antidepressant therapy + high-level psychosocial interventions

Electroconclusive therapy

236
Q

What are 5 psychiatric differentials of depression

A

Bipolar affective disorder
Premenstrual dysphoric disorder
Bereavement
Anxiety disorders
Alcohol-use disorders

237
Q

Name 3 organic illness differentials of depression

A

Hypothyroidism
Cushing’s disease or syndrome
Vitamin B12 deficiency

238
Q

Name the complications of depression

A

Suicide risk - 4x higher
Substance/alcohol misuse
Recurrence of depressive episodes
Reduced quality of life reduction
Antidepressant side effects

239
Q

What’s the prognosis of depression

A

Typically - lasts 3-6 months

Most people recover within 12 months

Illness episodic

Feel well in-between acute depressive episodes

240
Q

Define motor neurone disease

A

Encompasses a variety of specific diseases affecting motor nerves

241
Q

What is the most common form of motor neurone disease

A

Amyotrophic lateral sclerosis

242
Q

Describe the pathophysiology of motor neurone disease

A

Involves degeneration of both the upper and lower motor neurones

Sensory neurones = spared

243
Q

Describe the presentation of motor neurone disease

A

Late middle-aged e.g. 60

Man

Possibly affected relative

244
Q

Name the causes of motor neurones disease

A

Exact cause = unclear

Genetic links

Family history 10-15%

Increased risk with smoking, exposure to heavy metals and certain pesticides

245
Q

Name the risk factors of motor neurone disease

A

Genetic factors

Lifestyle and environment
- mechanical and/or electrical trauma
- military service
- high levels of exercise
- exposure to agricultural chemicals
- exposure to variety of heavy metals

246
Q

Name the clinical features of motor neurone disease

A

Insidious, progressive weakness of muscles - first noticed in upper limbs

Affects limbs, trunk, face and speech

May be increased when exercising

Clumsiness

Slurred speech

247
Q

What are the signs of lower motor neurone disease

A

Muscle wasting
Reduced tone
Fasciculations
Reduced reflexes

248
Q

What are the signs of upper motor neurone disease

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflexes

249
Q

Name the investigations of motor neurone disease

A

Clinical diagnosis + examination

Electrophysiological studies

250
Q

Describe the management of motor neurone disease

A

No effective management for halting or reversing the progression of the disease

Riuzole

Non-invasive ventilation

Supporting person and their family

251
Q

What medication can slow progression of ALS and extend survival by several months

A

Riluzole

252
Q

What symptom would suggest an alternative diagnosis of motor neurone disease

A

Affect on sensory neurones

253
Q

Name 5 differential diagnosis of ALS

A

Cervical spondylosis with myelopathy and radiculopathy

Multifocal motor neuropathy

Inclusion body myositis

Myasthenia gravis

Progressive muscular atrophy

254
Q

What is the prognosis of motor neurone disease

A

Progressive - eventually fatal

Tend to due of respiratory failure or pneumonia

255
Q

Define myasthenia gravis

A

Chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction in skeletal muscle

256
Q

Describe the pathophysiology of myasthenia gravis

A

Circulating antibodies against the nicotinic receptor or associated protein impair neuromuscular transmission

257
Q

Describe the epidemiology of myasthenia gravis

A

Affects men and women at different ages

Women under 40
Men over 60

258
Q

What are the antibodies which are associated with myasthenia gravis

A

Acetylcholine receptor antibodies

Muscle-specific kinase (MuSK) antibodies

Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies

259
Q

What is the cause of myasthenia gravis

A

Antibodies present at the neuromuscular junction

260
Q

Describe the role of MuSK and LRP4 in the pathophysiology of myasthenia gravis

A

Important in creation and organisation of Ach receptor

Destruction of these proteins leads to inadequate Ach receptors

261
Q

Name the risk factors of myasthenia gravis

A

Thymomas

Family history of autoimmune disorders

Genetic markers

Cancer-targeted therapy

262
Q

Describe thymomas in myasthenia gravis

A

Thymus gland tumours

10-20% of patients have thymoma

30% patients with thymoma will develop mg

263
Q

Describe the clinical features of myasthenia gravis

A

From mild to life-threatening severe

Weakness that worsens with muscle use and improves with rest

Symptoms better in morning, worse at end of day

Affect proximal muscles of the limbs and small muscles of the head and neck

264
Q

Describe the examination investigations of myasthenia gravis

A

Examination - fatigue in muscles

Look for thymectomy scar

Forced vital capacity

265
Q

Describe the antibody investigations of myasthenia gravis

A

AChR antibodies - around 85%

MuSK antibodies - < 10%

LRP4 antibodies - < 5%

266
Q

Describe the imaging investigation of myasthenia gravis

A

CT or MRI of thymus gland

Edrophonium test - helpful for diagnosis

267
Q

Describe the examination of looking for fatigue in muscles in myasthenia gravis

A

Repeated blinking will exacerbate ptosis

Prolonged upward gazing will exacerbate diplopia

Repeated abduction of one arm 20x will result in unilateral weakness

268
Q

Describe the edrophonium test of myasthenia gravis

A

Given IV edrophonium chloride

Edrophonium blocks the enzymes which break down Ach at the neuromuscular junction

Result = level of Ach at the neuromuscular junction rises - temporarily relieves the weakness

Suggests diagnosis

269
Q

Describe the management of myasthenia gravis

A

Pyridostigmine

Immunosuppression

Thymectomy (even if do not have thymoma)

Rituximab (last resort)

270
Q

Name 4 differential diagnosis of myasthenia gravis

A

Lambert-eaton myasthenic syndrome

Botulism

Penicillamine-induced myasthenia gravis

Primary myopathies

271
Q

Describe myasthenic crisis as a complication of myasthenia gravis

A

Potentially life-threatening

Can cause acute worsening symptoms

Respiratory muscle weakness - require non invasive ventilation or mechanical

Treatment = IV immunoglobulin and plasmapheresis

272
Q

Name 5 complications of Myasthenia gravis

A

Respiratory failure
Impaired swallowing
Acute aspiration
Secondary pneumonia
Cardiac complications

273
Q

Where are upper motor neurone lesions found

A

CNS - brain and spinal cord

274
Q

Where are lower motor neurone lesions found

A

Anywhere from the anterior horn cell to the muscle

275
Q

Name 5 signs of an upper motor neurone lesion

A

Disuse atrophy or contractures

Increased tone (spasticity/rigidity) +/- ankle clonus

Pyramidal pattern of weakness

Hyperreflexia

Babinski sign

276
Q

Describe the Babinski sign

A

Occurs when stimulation of the lateral plantar aspect of the foot leads to extension

277
Q

Name 6 signs in lower motor neurone lesions

A

Marked atrophy

Fasciculations

Reduced tone

Variable patterns of weakness

Reduced or absent reflexes

Down going plantars or absent response

278
Q

Why does UMN lesions cause their associated symptoms

A

Loss of inhibitory tone in muscles leads to constant contraction of muscles

279
Q

Why does LMN lesions cause their related symptoms

A

Suppression by CNS, but the LMNs are damaged or lost, so there is nothing to tell the muscles to contract

280
Q

Define syncope

A

Describe the event of temporarily losing consciousness due to a disruption of blood flow to the brain - often leading to a fall

281
Q

Describe two other names for syncope

A

Vasovagal episodes

Fainting

282
Q

Describe the pathophysiology of syncope

A

Caused be a problem with the autonomic nervous system regulating blood flow to the brain

When vagus nerve received a strong stimulus it can stimulate PNS

PNS activation contracts SNS - blood vessels constricted

As blood vessels delivering blood to the brain relax = hypoperfusion of brain tissue

Leading to ‘faint’

283
Q

Name 4 causes of primary syncope

A

Dehydration

Missed meals

Extended standing in a warm environment

A vasovagal response to a stimulus

284
Q

Name 6 causes of secondary syncope

A

Hypoglycaemia

Dehydration

Anaemia

Infection

Anaphylaxis

Arrythmias

285
Q

What is primary syncope

A

Simply fainting

286
Q

What is secondary syncope

A

Loss of consciousness due to an underlying cause

287
Q

What are the possible categories of causes of syncope

A

Cardiac

Non cardiac

Unknown Causes

1/3 idiopathic aetiology

288
Q

Describe the clinical features of syncope

A

Prodrome
- hot and clammy
- sweaty
- heavy
- dizzy or lightheaded
- vision going blurry or dark
- headache

289
Q

What is recommended when someone is experiencing prodromal symptoms (syncope)

A

Sit or lie down

Have some water

Have something to eat

Wait till feel better

290
Q

Describe the investigations in syncope

A

Examination

ECG
24-hour ECG

Echocardiograms

Bloods

291
Q

Describe the management of syncope

A

Reassurance + simple advice

Avoid dehydration, missing meals, standing still for long periods of time.

292
Q

What are the 6 differential diagnosis of syncope

A

Seizure
Acute coronary syndrome
Ventricular arrythmias
Atrioventricular block
Acute atrial fibrillation
Congestive heart failure

293
Q

Define encephalitis

A

Inflammation of the brain parenchyma associated with neurological dysfunction (altered state of consciousness or focal neurological signs).

294
Q

Describe the pathophysiology of viral encephalitis

A

Virus initially gains entry and replicates in local or regional tissue.

Dissemination to the CNS occurs by haematogenous routes or via retrograde axonal transport

295
Q

Describe the pathophysiology of autoimmune encephalitis

A

Result form antibodies directed against normal brain components

Play a role in anti-N-methyl-D-aspartate receptor encephalitis and other paraneoplastic syndromes

296
Q

Describe the epidemiology of encephalitis

A

Bimodal age pattern <1 and > 65

Seasonal and geographical variations - viral

297
Q

What is the main cause of encephalitis

A

Virus

  • Herpes virus
  • Ticks and mosquitos as vectors
  • HIV
298
Q

What are the causes of encephalitis

A

Virus
Bacterial
Fungal
Parasitic
Para-infectious
Prion diseases
Paraneoplastic syndromes

299
Q

What are the risk factors of encephalitis

A

Age <1 or > 65
Immunodefiency
Post-infection
Blood/body fluid exposures
Organ transplantation
Animal or insect bites
Location
Season
Swimming or diving in warm freshwater

300
Q

Describe the clinical features of encephalitis

A

Often - mild flu like symptoms

Can be more severe

301
Q

What are the clinical features of severe encephalitis

A

Problems with speech and hearing

Double vision

Hallucinations

Personality changes

Loss of consciousness/sensation

Muscle weakness

Partial paralysis

Impaired judgement

Seizures

Memory loss

302
Q

Describe the investigations of encephalitis

A

Medical (+ neurological) exam + history

Lab screening - blood, urine an bodily secretions

Lumbar puncture

Brain imaging

303
Q

Describe the management of viral encephalitis

A

Antivirals - acyclovir and ganciclovir

304
Q

Describe the management of autoimmune encephalitis

A

Immunosuppressants

Steroids

305
Q

Describe the general management of encephalitis

A

Specific for the cause

Anticonvulsants

Corticosteroids

Artificial respiration

Cognitive rehabilitation

Physical speech

Occupational therapy

306
Q

Name 6 differential diagnosis of encephalitis

A

Viral meningitis

Encephalopathy - toxic/metabolic

Status epilepticus

CNS vasculitis

Confusional migraine with pleocytosis

Malignant hypertension

307
Q

Name 8 complications of encephalitis

A

Hearing and/or speech loss

Blindness

Permeant brain and nerve damage

Behavioural changes

Cognitive disabilities

Lack of muscle control

Seizures

Memory loss

308
Q

Describe the prognosis of encephalitis

A

May need long term therapy, medication and supportive care

Mortality and morbidity vary depending on aetiology

309
Q

What is the most common cause of fungal meningitis

A

Cryptococcus neoformans

310
Q

What fungal pathogens are able to cause meningitis

A

All major fungal pathogens have capacity to cause meningitis

Rapid aetiological diagnosis needed for antifungal therapy

311
Q

Name 5 risk factors of fungal meningitis

A

HIV infection

Corticosteroid use

Underlying chronic disease

Exposure to distributed soil, chicken guano or bat caves

Neurosurgery

312
Q

What would be seen on a lumbar puncture of fungal meningitis

A

Lymphocytic pleocytosis

Elevated protein

Low glucose

313
Q

Describe what would be seen on a lumbar puncture of bacterial meningitis

A

Cloudy

Protein - high

Glucose - low

High neutrophils

Culture = bacterial

314
Q

What would a lumbar puncture of viral meningitis show

A

Clear

Protein would be mildly raised or normal

Glucose - normal

High lymphocytes

Culture - negative

315
Q

What would be the investigations of fungal meningitis

A

Fungal blood cultures - 3 sets

Serum cryptococcal antigen test

Serum + urine histoplasma antigen

316
Q

Describe the treatment of fungal meningitis

A

Aggressive therapy with antifungal agents

Coccidoidal meningitis requires lifelong therapies

317
Q

Describe the prognosis of fungal meningitis

A

Poor prognosis with HIV-associated

Mortality of non-HIV is associated with chronic renal failure, liver failure or haematological malignancy

Mortality rates remain high

318
Q

Define Lambert Eaton Syndrome

A

Autoimmune condition affecting the neuromuscular junction (similar to myasthenia gravis)

319
Q

Describe the pathophysiology of Lambert Eaton Syndrome

A

Antibodies against voltage-gated calcium channels

Antibodies may be produced in response to small-cell lung cancer cells that express voltage-gated calcium channels

Target and damage these channels in the presynaptic membrane of the neuromuscular junction

= less Ach released into the synapse = weaker signal = reduced muscle contraction

320
Q

Describe the causes of Lambert Eaton syndrome

A

50% paraneoplastic syndrome - small cell lung cancer

Primary autoimmune disorder (usually autoimmune thyroid disease)

321
Q

Describe the epidemiology of Lambert Eaton Syndrome

A

40% underlying cancer

Median age onset 60s

More frequent in males

Underlying cancer = bimodal pattern
Female < 45 yrs
Male > 60 yrs

322
Q

Name 3 clinical features of Lambert Eaton syndrome

A

Proximal muscle weakness

Autonomic dysfunction

Reduced or absent tendon reflexes

323
Q

Name 4 risk factors of Lambert Eaton Syndrome

A

Underlying small cell lung cancer or other malignancy

Co-existing autoimmune disorder

Cigarette smoking

Family history of autoimmune disease

324
Q

Describe the difference between Myasthenia gravis and Lambert Eaton Syndrome

A

Lambert Eaton syndrome = reverse

Reflexes may be absent in a rested patient but present when testing immediately after maximal muscle contraction

325
Q

Name the investigations of Lambert Eaton syndrome

A

Nerve conduction studies

Low frequency repetitive nerve stimulation

Chest CT (cancer)

Serology

Thyroid-stimulating hormone

326
Q

Describe the first line management of Lambert Eaton syndrome

A

1st line - amifampridine

327
Q

Describe the management of Lambert Eaton syndrome

A

Exclude underlying malignancies

Amifampridine

Other options
- pyridostigmine
- immunosuppressants
- IV immunoglobulins
- Plasmapheresis

328
Q

Name 5 differential diagnosis of Lambert Eaton syndrome

A

Botulism
Myasthenia gravis
Myopathy
Chronic inflammatory demyelinating neuropathy
Guillain-Barre syndrome

329
Q

Name 2 complications of Lambert Eaton syndrome

A

Osteoporosis

Other corticosteroid-related adverse effects

330
Q

Describe the prognosis of Lambert Eaton syndrome

A

Determined by presence and type of underlying cancer/autoimmune disease, the severity and distribution of weakness

Weakness improves with cancer treatment

331
Q

What are the types of primary brain tumours

A

Meninges = meningioma

Sellar region = craniopharyngioma

Germ cell tumours

Cranial nerves - schwannoma

Hematopoietic - primary CNS lymphoma

332
Q

Name 6 secondary brain tumours

A

Lung
Breast
Colorectal
Testicular
Renal cell
Malignant melanoma

333
Q

What is the most common type of primary brain tumour

A

Glioma

334
Q

Describe a glioma

A

Tumour of glial cell - astrocytes/oligodendrocytes/ependymal cells

335
Q

How are primary brain tumours classified

A

WHO grading system

1- 2 = low
3- 4 = high

336
Q

Describe grade 2 gliomas

A

Slow growing but will undergo anaplastic transformation

337
Q

Describe the epidemiology of primary brain tumours

A

55% malignant

9th commonest cancer

Commonest cause in men < 45, women < 35

Common differential diagnosis

338
Q

Describe the causes of primary brain tumours

A

Majority no cause

Ionising radiation to the brain

5% family history

Immunosuppression (CNS lymphoma)

339
Q

Name 4 risk factors of primary brain tumours

A

Age

Overweight and obesity

Medical radiation - ionising radiation

Family history

340
Q

Name the possible clinical features of a primary brain tumour

A

Headache

Seizures

Focal neurological symptoms

Other non-focal symptoms
- personality change/behaviour
- memory disturbance
- confusion

341
Q

Name the signs of primary brain tumours

A

Papilledema

Focal neurological deficit
- hemiparesis
- hemisensory loss
- visual field defect
- dysphasia

342
Q

Describe a headache as a symptom as a primary brain tumour

A

Woken by headache, worse in the morning and lying down

Exacerbated by coughing, sneezing and drowsiness

343
Q

When would a headache be a possible red flag of a primary brain tumour

A

Headache PLUS

Aged > 50
New/changed headache
Previous history of cancer

344
Q

What are the clinical features of a low grade primary brain tumour

A

Typically present with seizures

Can be incidental finding

345
Q

What are the clinical features of a high grade primary brain tumour

A

Rapidly progressive neurological deficit

Symptoms of raised intracranial pressure

346
Q

Describe the investigations of primary brain tumours

A

CT - with contrast

MRI - better for pituitary lesions

Biopsy/surgery

347
Q

Describe the management of high grade glioma

A

No cure

Steroids

Surgery

Radiotherapy

Chemotherapy

348
Q

Describe the prognosis of high grade glioma

A

6 months no treatment

18 months with

349
Q

Describe the management of low grade glioma

A

Surgery - early resection

Radiotherapy

Chemotherapy

350
Q

Describe the prognosis of low grade glioma

A

Median survival 10 years

351
Q

Is the treatment of glioma curative

A

No - except grade 1

352
Q

Name 6 differential diagnosis of gliomas

A

Brain metastasis

Brain abscess

Multiple sclerosis

Necrosis

Acute stroke

Encephalitis

353
Q

What features of a headache would result in an urgent referral for primary brain tumours

A

Features of raised intracranial pressure

Other
- new onset seizures
- rapidly progressive focal neurology
- past history of other cancer

354
Q

Define Charcot-Marie Tooth Disease

A

Inherited disease that affects the peripheral and sensory neurones

355
Q

Describe the pathophysiology of Charcot-Marie Tooth Disease

A

Genetic mutations primarily affect the Schwann cell and myelin leads to demyelinating CMT

Those affecting axons lead to axonal CMT

356
Q

Name the causes of Charcot-Marie Tooth Disease

A

Autosomal dominant

Autosomal recessive

X-linked

Heterogenous condition = most common

357
Q

Name the risk factor of Charcot-Marie Tooth Disease

A

Family history

358
Q

Describe the epidemiology of Charcot-Marie Tooth Disease

A

Symptoms start before the age of 10

Can be delayed until after 40

359
Q

Name the clinical features of Charcot Marie Tooth Disease that will always be present in patients

A

High foot arches - pev cavus

Distal muscle wasting

Lower leg weakness

Weakness in the hands

Reduced tendon reflexes

Reduced muscle tone

Peripheral sensory loss

360
Q

What is a characteristic feature of Charcot Marie Tooth

A

Peripheral neuropathy

Reduced sensory and motor function in peripheral nerves, typically affecting the feet and hands

361
Q

Name the possible causes of Peripheral neuropathy

A

Charcot Marie Tooth syndrome

ABCDE
Alcohol
B12 deficiency
Cancer and chronic kidney disease
Diabetes and drugs
Every vasculitis

362
Q

Name the investigations of Charcot Marie Tooth disease

A

Nerve conduction studies

Genetic testing

363
Q

Describe the management of Charcot Marie Tooth Disease

A

No cure or treatment to stop from progressing

Supportive management

364
Q

Name 5 differential diagnosis of Charcot Marie Tooth Disease

A

Diabetes neuropathy

Chronic inflammatory demyelinating polyneuropathy

Acquired peripheral neuropathy

Hereditary spastic paraplegia

Spinocerebellar degeneration

365
Q

Name 2 complications of Charcot Marie Tooth Disease

A

Osteoarthritis

Pain

366
Q

Describe the prognosis of Charcot Marie Tooth Disease

A

Progressive condition

Symptoms do not remit - worsen overtime

No affective treatment or cure

367
Q

Define muscular dystrophy

A

Umbrella term for genetic conditions that cause gradual weakening and wasting of muscles

368
Q

What is the most common and most rapidly progressive muscular dystrophy

A

Duchenne Muscular Dystrophy

369
Q

What gender does Duchenne’s Muscular dystrophy usually only affects

A

Boys

370
Q

What type of inheritance pattern is Duchenne’s muscular dystrophy

A

X-linked recessive condition

371
Q

Describe the pathophysiology of Duchenne’s Muscular Dystrophy

A

Defective gene for dystrophin on the X-chromosome

Dystrophin = protein that helps hold muscles together on the cellular level

Absence results in ongoing cell membrane depolarisation

Degeneration is faster than regeneration - muscle fibres undergo necrosis

Muscle fibres are replaced by adipose and connective tissue = muscle progressively weaken

372
Q

Name 2 risk factors of Duchenne’s Muscular Dystrophy

A

Family history

Male sex

373
Q

Describe the clinical presentation of Duchenne’s Muscular Dystrophy

A

Boys

Present at 3-5 years

Weakness in the muscles around their pelvis

Weakness = progressive, eventually all muscles will be affected

374
Q

Name 7 signs of Duchenne’s Muscular Dystrophy

A

Delayed motor milestones

Frequent falls

Abnormal gait

Muscle Pain

Calf hypertrophy

Speech and language delay

Difficulty jumping, running, climbing steps and rising from the floor

375
Q

Name the investigations for Duchenne’s Muscular Dystrophy

A

Serum creatinine kinase

Genetic testing (Xp21 mutation)

Gower’s sign

376
Q

Describe the Gower’s sign

A

Shows proximal muscle weakness

To stand up from lying position will have to get onto hands and knees, push their hips and backwards like a downward dog pose

377
Q

How is Duchenne’s Muscular Dystrophy diagnosed

A

Genetic testing

378
Q

Describe the management of Duchenne’s Muscular Dystrophy

A

Oral steroids

Creatinine supplementation

Genetic trials

Supportive treatment

379
Q

What is the aim of management in Duchenne’s Muscular Dystrophy

A

Allowing the person to have highest quality of life for the longest time possible

380
Q

Name 2 differential diagnosis of Duchenne’s Muscular Dystrophy

A

Other muscular dystrophies

Polymyositis

Static encephalopathies - cerebral palsy

381
Q

Describe the prognosis of Duchenne’s Muscular Dystrophy

A

Most patients lose ability to walk at 12 years

Require ventilation support by 20

Life expectancy 25-35 years - due to cardiac and respiratory complications

382
Q

Name the complications of Duchenne’s Muscular Dystrophy

A

Respiratory failure
Loss of mobility
Osteoporosis
Weight loss/malnutrition
Sexual dysfunction
Impaired growth
Delayed puberty
Constipation

383
Q

Define Brown-Sequard Syndrome

A

Occurs due to damage to one lateral side of the spinal cord and most commonly occurs in the cervical region

Incomplete spinal injury

384
Q

Describe the pathophysiology of Brown-Sequard syndrome

A

Partial hemi section

Often includes the nerve tracts lying along the path of the injured area involved

385
Q

Name the causes of Brown’s Sequard syndrome

A

Trauma

Tumour

Inadequate or blocked blood flow through a blood vessel to part of the body

Infectious disease e.g. TB

Inflammatory disease e.g. multiple sclerosis

386
Q

Describe the clinical presentation of Brown’s Sequard syndrome (thoracic spinal cord hemi section)

A

Ipsilateral spastic paralysis below the level of the lesion

Ipsilateral loss of fine touch, proprioception and vibration sense

Contralateral loss of pain and temperature sensation

387
Q

Damage to which pathway would cause ipsilateral loss of touch, vibration and proprioception

A

DCML pathway

388
Q

Damage to which pathway would cause contralateral loss of pain and temperature sensation

A

Anterolateral system

389
Q

Describe the investigations of Brown’s Sequard syndrome

A

Detailed history

Examination

Lab tests

Diagnostic testing - MRI

390
Q

Describe the first line management of Brown’s Sequard syndrome

A

High-dose steroids

391
Q

Describe the management of Brown’s Sequard syndrome

A

High dose steroids

Perioperative prophylactic antibiotics

Address underlying cause

392
Q

Name the 5 differential diagnosis

A

Stroke
Tumour or cysts
Spinal infection
Spinal cord tumour, primary or metastatic
Spinal cord herniation

393
Q

What the prognosis of Brown’s Sequard syndrome

A

Varies on cause

Potential for significant recovery is strong (50%)

Take up to 2 years for neurological recovery

394
Q

Name 4 differential diagnosis of Brown’s Sequard syndrome

A

Hypotension or spinal shock

Depression

Pulmonary embolism

Infections - UTI, lungs

395
Q

Name the function of the olfactory nerve (I)

A

Special visceral afferent fibres for the sense of smell

Passes through the cribriform plate of the skull

396
Q

Name the possible problem and signs of an the olfactory nerve lesion

A

Trauma, tumour

Decreased ability to smell

397
Q

Name the functions of the optic nerve (II)

A

Special somatic afferent fibres for vision

Afferent limb for pupillary light reflex

Passes through the optic canal of the skull

398
Q

Name the possible problem and sign of the optic nerve (II)

A

Trauma, tumour (pituitary adenomas and craniopharyngioma), MS, stroke

Blindness, visual field defect

399
Q

Name the function of the oculomotor nerve (III)

A

General somatic efferent and general visceral efferent fibres to the extraocular muscles and pupillary constrictor muscles

Efferent limb for the pupillary light reflex

400
Q

What muscles do the oculomotor nerve innervate

A

Levator palpebrae superiors

Inferior oblique

Superior, medial and inferior recti

401
Q

Where does the oculomotor nerve travel

A

Passes through the superior orbital fissure of the skull

402
Q

Name the function and sign of an oculomotor nerve lesion

A

Diabetes, increased intra-cranial pressure

CN III causes a ‘down and out’ eye

Dilated pupils

Ptosis

403
Q

Name the function of the trochlear nerve (IV)

A

Provides general somatic efferent to the extraocular superior oblique muscles

Depresses and abducts the eye

Passes through the superior orbital fissure.

404
Q

What is the possible problem and sign of the trochlear nerve

A

Trauma

Diplopia

405
Q

Name the 3 functions of the trigeminal nerve (V)

A

3 sensory nuclei
1. Mesencephalic - proprioception

  1. Principal - light touch and discrimination
  2. Spinal - pain and temperature, crude touch
406
Q

Describe the possible problem and sign of a trigeminal nerve lesion

A

Sensory - idiopathic, trauma, inguinal nerve damage

Motor - bulbar palsy

No signs - sensory deficit on testing

May have decreased facial sensation

407
Q

What is the function of the trigeminal nerve - ophthalmic (V1)

A

General somatic afferent to above the lower eyelid

408
Q

What is the function of the trigeminal nerve (V) maxillary V2

A

General somatic afferent of the lower eyelid to the upper lip

409
Q

What is the function of the trigeminal (V) nerve mandibular branch (V3)

A

General somatic afferent and special visceral efferent to below the upper lip

410
Q

Name the functions of the abducens (VI) nerve

A

General somatic efferent fibres for eye abduction

Innervates the lateral rectus muscle

Passes through the superior orbital fissure of the skull

411
Q

Name the possible problems and signs of an abducens nerve lesion

A

MS, some strokes

Inability of the eye to look laterally

Eye deviated towards the nose

412
Q

Name the functions of the facial (VII) nerve

A

General somatic afferent - skin behind the ear

Special visceral afferent - taste to anterior 2/3 of the tongue

General visceral efferent - parasympathetic to the lacrimal, subinguinal and submandibular gland

Special visceral efferent - muscles of facial expression

413
Q

Name the possible problems and signs of a facial nerve lesion

A

LMN - Bell’s palsy, skull fracture, parotid tumour = total facial weakness

UMN - stroke, tumour = forehead sparing weakness

414
Q

Name the functions of vestibulocochlear (VIII) nerve

A

Provide special somatic afferent = hearing and balance

Does not leave the skull

Cochlea = sound waves to mechanical ossicle movements

Vestibular apparats = detect changes in head motion

415
Q

Name the possible problems and signs of Vestibulocochlear nerve lesion

A

Excess noise, Paget’s, acoustic neuroma

Deafness

416
Q

Name the functions of Glossopharyngeal (IX) nerve lesion

A

General somatic afferent = sensation from the posterior

Special visceral afferent = taste to posterior 1/3 of the tongue

General visceral efferent = parasympathetic to parotid glands

Special visceral efferent = motor to stylopharyngeus

417
Q

Name the glossopharyngeal nerve possible problems and function

A

Trauma, tumour

Impaired gag reflex

418
Q

Describe the function of the vagus nerve (X)

A

General somatic afferent = skin around the ear

Special visceral afferent = taste and sensation to the epiglottis

General visceral afferent = sensory information to body viscera

General visceral efferent = parasympathetic to glands of GI tract

Special visceral efferent = motor innervation to soft palate, pharynx and larynx

419
Q

Name the possible problems and function of the Vagus Nerve

A

Trauma, brainstem lesions

Impaired gag reflex, soft palate moves ‘good’ side on saying ‘ahh’

420
Q

Name the function of the accessory (XI) nerve

A

General somatic efferent fibres to the trapezius and sternocleidomastoid

421
Q

Name the possible problems and sign of an accessory nerve lesions

A

Polio, stroke

Weakness turning the head away from the affected side (sternocleidomastoid)

Weakness shrugging shoulders (trapezius)

422
Q

Name the functions of the hypoglossal nerve

A

General somatic efferent fibres for controlling tongue muscles

423
Q

Name the possible problems and signs of a hypoglossal nerve lesion

A

Trauma, brainstem lesions

Tongue deviated to affected side on protrusion

424
Q

Define Carpel tunnel syndrome

A

Compression of the medial nerve as it travels through the carpal tunnel in the wrist.

Causes pain and numbness in the median nerve distribution on the hand.

425
Q

What does compression of the median nerve in the carpel tunnel cause

A

Either:

Swelling of the contents - swelling of the tendon sheaths due to repetitive strain

Narrowing of the tunnel

426
Q

What does the median nerve supply motor function to

A

Abductor pollicis brevis - thumb abduction

Opponens pollicis - thumb opposition

Flexor pollicis brevis - thumb flexion

427
Q

What is the palmar digital cutaneous branch of the median nerve responsible for

A

Sensory innervation of the palmar aspects and full fingertips of the:

Thumb
Index and middle finger
The lateral half of the ring finger

428
Q

Who is at the highest risk of carpal tunnel syndrome

A

Females between 40-60 years

429
Q

Name the cause of carpal tunnel syndrome

A

No clear cause found

Idiopathic

430
Q

Name 7 risk factors for carpal tunnel syndrome

A

Repetitive strain
Obesity
Perimenopause
Rheumatoid arthiritis
Diabetes
Acromegaly
Hypothyroidism

431
Q

Describe the clinical presentation of carpal tunnel syndrome

A

Gradual onset - start intermittent

Worse at night time

432
Q

Describe the sensory symptoms of carpel tunnel syndrome

A

Palmar digital cutaneous branch of the median nerve

  • Numbness
  • paraesthesia
  • Burning sensation
  • Pain
433
Q

Name 4 motor symptoms of carpal tunnel syndrome

A

To thenar muscles

  • weakness of thumb movements
  • weakness of grip strength
  • difficulty with fine movements involving the thumb
  • Wasting of the thenar muscle - atrophy
434
Q

Name 2 tests of carpal tunnel syndrome

A

Phalen’s test

Tinel’s test

435
Q

Describe Phalen’s test

A

Full flexing and holding it in its position

Test positive = position submandibular sensory symptoms of the carpal tunnel

436
Q

Describe Tinel’s test

A

Tapping the wrist at the location where the median nerve travels through the carpal tunnel

Positive = triggers sensory symptoms of carpal tunnel

437
Q

What is the 1st line diagnostic test for Carpal Tunnel syndrome

A

Electromyogram (EMG)

438
Q

Name 2 options of the management of Carpal tunnel syndrome

A

Wrist splint

Corticosteroid injection

Surgical release

439
Q

Name 5 differential diagnosis of Carpal tunnel syndrome

A

Osteoarthritis
Stroke
Ulnar neuropathy
MND
De Quervain’s tenosynovitis

440
Q

Define Radial neuropathy (Wrist drop)

A

Radial nerve damage leading to weakness in the wrist and fingers

441
Q

Describe the pathophysiology of wrist drop

A

Radial nerve exists the upper spinal cord, travels down the upper arm very close to humerus.

Gives off several branches.

May be damaged at the level of the humerus or in the elbow/forearm

442
Q

Describe the epidemiology of wrist drop

A

Named ‘Saturday night palsy’

Aged between 75-84

443
Q

Where can the radial nerve (wrist drop) be damaged

A

Humerus (upper arm)

Forearm

444
Q

What are the possible causes of wrist drop

A

Fracture

Sitting or sleeping with arm over back of chair

Repetitive use

Injuries - stab wombs

Lead poisoning and thiamine deficiency

Limb onset ALS

Acute upper limb ischemia

445
Q

Describe the clinical features of wrist drop

A

Weak wrist/fingers/thumb

Close to origin = weak elbow

Numbness or tingling present over the back of the thumb

446
Q

Name 4 investigations of wrist drop

A

Nerve conduction and needle electromyography

Plain x-ray

MRI

High resolution ultrasound

447
Q

Describe the management of wrist drop

A

Usually recover without treatment - weeks or months

Possible
- wrist splint
- physical therapy
- possible surgery

448
Q

Name differential diagnosis of wrist drop

A

Posterior interosseous neuropathy

Posterior cord

Radial neuropathy in the spinal groove/axilla

449
Q

Define claw hand

A

Deformity with hyperextension of the MCP joints and flexion of the IPJ due to weakness of the intrinsic muscles of the hand

450
Q

Describe the type of claw hand

A

Complete
- involves all digits
- results from both ulnar and median palsy

Incomplete/partial
- involves only ulnar 2 digits
- referred to as isolated ulnar nerve palsy

451
Q

Name the causes of claw hand

A

Nerve damage in the arm

Congenital birth defect

Some genetic diseases e.g. Charcot-Marie Tooth Disease

Bacterial infections e.g. leprosy

Scarring after a severe hand or forearm burn

Compartment syndrome of the hand

452
Q

Name 3 risk factors of claw hand

A

External compression at the elbow

Body weight pressure onto tools

Prolong movements causing the elbow to lean e.g. cyclists, desk jobs

453
Q

Name 4 clinical features of claw hand

A

Muscle wasting on the interosseous and hypothenar

Numbness along the nerve involved

Inability to extend the IP joints during extension of the fingers - abduct and adduct fingers

Unopposed action of the extensor and the flexor digitorum profundus.

454
Q

Name 2 investigations of claw hand

A

Electromyography

Nerve conduction studies

455
Q

Describe the management of claw hand

A

Splinting
Surgery
Tendon transfer (graft)
Therapy to straighten fingers

Physiotherapy management

456
Q

Name 4 differential features of claw hand

A

Cervical radiculopathy

Dypuytren contracture

Klumpke’s paralysis

Lower brachial plexopathy

457
Q

Define foot drop

A

Not a disease

Symptom of neurological, anatomical or muscular problem.

Inability to lift the forefoot due to the weakness of dorsiflexors of the foot

458
Q

Describe the pathophysiology of foot drop

A

Damage to the common peroneal nerve - weakness of tibialis anterior and other key dorsiflexors of the foot

459
Q

Name the causes of foot drop

A

Compression disorders

Traumatic injuries

Neurological disorders

460
Q

Name the compression disorders which could result in foot drop

A

Fibular nerve compression

Sciatic nerve compression

Lumbar disc herniation or spondylitis of the spine

461
Q

Name 2 neurological disorders which could result in foot drop

A

Charcot-Marie Tooth

Stroke

462
Q

Name the clinical features of foot drop

A

No active dorsiflexion in a non-weight bearing position

Gait assessment

Pain
- Neurogenic pain
- Sensory changes

463
Q

Name 5 investigations of foot drop

A

Gait assessment

History

Assessment of ankle dorsiflexion

Neurological exam

Electromyography/nerve conduction studies

464
Q

Describe the management of foot drop

A

2/3 resolve within 1 year

Analgesia

Splinting

Physiotherapy - exercise

Surgery

465
Q

Name 5 differential diagnosis of foot drop

A

L5 radicopathy

UMN lesion

Chronic/persistent pain

Sciatic nerve injury

466
Q

Name 2 examples of spinal cord compression

A

Sciatica

Spinal stenosis

467
Q

Define spinal stenosis

A

Narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots typically resulting from degenerative changes in the lumbar spine

468
Q

Describe the pathophysiology of spinal stenosis

A

Degenerative disease of lumbar spine may reduce the diameter of the spinal canal

May produce narrowing of the lateral recess and neural foramina

Stenosis results from a cascade of micro-degenerative changes

469
Q

Name 3 types of spinal stenosis

A

Central stenosis - narrowing of the central spinal canal

Lateral stenosis - narrowing of the nerve root canals

Foramina stenosis - narrowing of the intervertebral foramina

470
Q

What age does spinal stenosis affect

A

> 60 - degenerative changes

471
Q

Name the causes of spinal stenosis

A

Congenital spinal stenosis

Degenerative changes

Herniated discs

Thickening of the ligamenta flava or posterior longitudinal ligament

Spinal fractures

Spondylolisthesis

Tumours

472
Q

Name 5 risk factors of spinal stenosis

A

Age > 40

Previous back surgery

Previous injury

Achondroplasia

Acromegaly

473
Q

Describe the clinical features of spinal compression

A

Gradual onset

Severity of symptoms will depend on the degree of narrowing and spinal cord compression

474
Q

Describe the symptoms of severe spinal compression

A

Symptoms of cauda equina syndrome

  • Saddle anaesthesia
  • sexual dysfunction
  • incontinence of bladder and bowel

Requires emergency management

475
Q

Key presenting features of spinal cord compression

A

Intermittent neurogenic claudication of lumbar spine stenosis with central stenosis

  • Lower back pain
  • Buttock and leg pain
  • Leg weakness
476
Q

Define radiculopathy

A

Compression of the nerve roots as they exit the spinal cord and spinal column - leads to motor and sensory symptoms

477
Q

What is the 1st line investigation in spinal cord compression (spinal stenosis)

A

MRI

Other - angiogram

478
Q

What is the 1st line management in spinal cord compression (spinal stenosis)

A

NSAIDs + physiotherapy

479
Q

Describe the management in spinal cord compression (spinal stenosis)

A

1st line - NSAIDs + physiotherapy

Epidural corticosteroid injections

Decompressive spinal surgery

Laminectomy

480
Q

Name 5 differential diagnosis of spinal cord compression

A

Peripheral vascular disease

Lumbosacral intervertebral disc herniation

Spinal compression fracture

Metastatic disease of spine

Ankylosing spondylitis

481
Q

Describe the pathophysiology of sciatica

A

Supplies sensation to the lateral lower leg and the foot

Motor function to the posterior thigh, lower leg and foot

482
Q

Define sciatica

A

Symptoms associated with irritation of the sciatic nerve

483
Q

Name the main causes of sciatica

A

Due to lumbosacral nerve root compression

Herniated disc

Spondylolisthesis

Spinal stenosis

484
Q

Describe the clinical features of sciatica

A

Unilateral pain from buttock radiating down the back of the thigh to below the knee or feet

Paraesthesia

Numbness

Motor weakness

Reflexes may be affected

485
Q

Describe the management of sciatica

A

Amitriptyline

Duloxetine

NO opioids

486
Q

Define a cerebrovascular accident (CVA)

A

Either:

Ischaemic stroke

Intracranial haemorrhage

487
Q

Define ischemic stroke

A

Ischemia (inadequate blood supply) or infarction (tissue death due to ischemia) of the brain secondary to a disrupted blood supply

Blood supply in a cerebral vascular territory is critically reduced due to occlusion or critical stenosis of a cerebral artery

488
Q

Define intracranial haemorrhage

A

Bleeding in or around the brain

489
Q

Define transient ischaemic attack (TIA)

A

Involves temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction

490
Q

Define crescendo TIA

A

2 or more TIAs within a week and indicate a high risk of stroke

491
Q

Describe the pathophysiology of TIA

A

Cerebral blood flow falls - brain compensates by increasing oxygen extraction

Partial blood flow = neuronal function is impaired.

Cell death is delayed by minutes to hours

Restoration of flow via autolysis of occluding thrombus, can arrest the progression to infarction

492
Q

Name causes of ischaemic stroke

A

Caused by transient or permeant critical reduction in cerebral blood flow due to arterial occlusion or stenosis

Thrombus or embolus
Atherosclerosis
Shock
Vasculitis

493
Q

Name the causes of a TIA

A

In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque

Occlusion due to
- hypercoagulability
- dissection
- vasculitis
- vasospasm
- sickle cell occlusive disease

494
Q

Name the risk factor of stroke or TIA

A

Previous history

AF

Carotid artery stenosis

Hypertension

Diabetes

Raised cholesterol

Family history

Smoking

Obesity

Vasculitis

Combined contraceptive pill

495
Q

Describe the general clinical features of a stroke

A

Sudden onset of neurological features

Asymmetrical

Limb/facial weakness
Dysphasia
Visual field defect
Sensory loss
Ataxia and vertigo

496
Q

Describe FAST

A

For a stroke

Face
Arm
Speech
Time - act fast and call 999

497
Q

What tool can be used for the recognition of stroke in the emergency room

A

ROSIER tool

498
Q

Describe the ROSIER tool

A

Recognition of a stroke

Gives a score based on clinical features and duration

Stroke possible in patients scoring 1 or more

499
Q

What is the 1st line investigation in a TIA

A

Diffusion weighted MRI

500
Q

What is the 1st line investigation of a stroke

A

Non-contrast CT

501
Q

Describe the management of a TIA

A

Symptoms usually resolve within 24 hours of onset

Initial
- Aspirin
- Referral for specialised assessment
- MRI

Assessment of underlying cause

502
Q

Describe the initial management of a stroke

A

Exclude hypoglycaemia

Immediate CT brain (exclude haemorrhage)

Aspirin

Admission

503
Q

Define the possible management options for an ischemic stroke once haemorrhage has been excluded

A

Thrombolysis with alteplase

Thrombectomy

504
Q

Describe thrombolysis as a treatment for ischemic stroke

A

With alteplase - tissue plasminogen activation that rapidly breaks down clots

Given 4.5 hours within symptom onset

Close monitoring for complications

505
Q

Describe the thrombectomy as a treatment for ischaemic stroke

A

Blockage of the proximal anterior circulation or proximal posterior circulation

Within 24 hours of the symptom onset

Alongside IV thrombolysis

506
Q

How is blood pressure treated in ischemic stroke

A

Lowering blood pressure can worsen the ischemia

High blood pressure treatment only indicated in hypertensive emergency or reduce risks when giving IV thrombolysis

507
Q

How is blood pressure treated in a haemorrhagic stroke

A

Aggressively treated

508
Q

Name the differential diagnosis of a stroke

A

Ischemic/haemorrhagic

TIA

Hypoglycaemia

Complicated migraine

Wernicke’s encephalopathy

509
Q

What can be given as a secondary prevention in strokes

A

Clopidogrel

Atorvastatin

Blood pressure and diabetes control

Addressing risk factors

510
Q

Name 4 complications of an ischemic stroke

A

Aspiration

Pneumonia

Depression

DVT

511
Q

What is the prognosis in a TIA

A

Risk of recurrent stroke is high in the first 7 days following a TIA

512
Q

Describe the pathophysiology of a haemorrhagic stroke

A

Caused by vascular rupture into the brain parenchyma

Results in primary mechanical injury to the brain tissue.

Expanding haematoma may shear additional neighbouring arteries

Results in secondary ischemic injury

513
Q

Name the risk factors of ischaemic stroke

A

Head injuries
Ischemic stroke
Aneurysms
Ischemic stroke - progressing to bleeding
Brain tumours
Thrombocytopenia
Bleeding disorders
Anticoagulants

514
Q

Name the clinical features of haemorrhagic stroke

A

Key feature = sudden-onset headache

Seizures
Vomiting
Reduced consciousness
Focal neurological symptoms

515
Q

Describe the investigations in haemorrhagic stroke

A

Immediate CT head

Bloods
- FBC
- Coagulation screen

516
Q

What is the universal assessment tool for level of consciousness

A

Glasgow Coma Score

517
Q

Describe the Glasgow Coma Score

A

Score based on eyes, verbal response and motor response

Maximum score 15/15

8/15 needs airway support

518
Q

Describe the management of haemorrhagic stroke

A

Correct clotting abnormality

Small bleeds - manage conservatively

Extradural or subdural
- craniotomy
- Burr holes

519
Q

Name the clinical features of haemorrhagic stroke

A

Ischaemic stroke
Hypertensive encephalopathy
Hypoglycaemia
Complicated migraine
Seizure disorder

520
Q

Define a extradural haemorrhage

A

Between the skull and dura mater

521
Q

Name the cause of an extradural haemorrhage

A

Rupture of the middle meningeal artery in the temporoparietal region

Associated with a fracture of the temporal bone

522
Q

Describe the typical history of extradural haemorrhage

A

Young patient

Traumatic head injury

Ongoing headache

Period of improved neurological symptoms and consciousness

Followed by rapid decline over hours as the haematoma gets large enough to compress the intracranial contents

523
Q

Describe the investigations of an extradural haemorrhage

A

CT scan

  • Bi-convex shape
  • limited by cranial sutures
524
Q

Define the subdural haemorrhage

A

Occurs between the dura and arachnoid mater

525
Q

Describe the epidemiology of subdural haemorrhage

A

Elderly and alcoholic patients - more atrophy in the brains = vessels more prone to rupture

526
Q

Name the cause of subdural haemorrhage

A

Rupture of the bridging veins in the outermost meningeal layer

527
Q

Describe the investigations of subdural haemorrhage

A

CT

  • Crescent shape
  • not limited to cranial sutures
528
Q

Define the intracerebral haemorrhage

A

Involves bleeding in the brain tissue

529
Q

Where can intracerebral haemorrhage occur

A

Lobar
Deep
Intraventricular
Basal ganglia
Cerebellar

530
Q

Define the cause of intracerebral haemorrhage

A

Occur spontaneously

OR

Secondary to ischemic stroke, tumours, or aneurysm stroke

531
Q

Describe the clinical features of intracerebral haemorrhage

A

Presents like an ischemic stroke

Sudden onset focal neurological symptoms
- limb weakness
- dysphasia
- vision loss

532
Q

Define subarachnoid haemorrhage

A

Bleeding in the subarachnoid space when the CSF is located - between the pia mater and the arachnoid membrane

533
Q

Define the cause of subarachnoid haemorrhage

A

Ruptured cerebral aneurysm

534
Q

Describe the clinical features of a subarachnoid haemorrhage

A

Sudden onset occipital headache during strenuous activity

Sudden or severe onset - leads to thunderclap headache description

535
Q

Name the major differential diagnosis for seizures

A

Epileptic seizures

Syncope (vasovagal)

Postural (orthostatic) hypotension

Hypoglycaemia

Non-epileptic attack disorder

536
Q

What be suggestive features that a seizure is an epileptic seizure

A

Prodromal aura
Conclusive jerk
Eyes open
Automatism, lateral tongue biting
Cyanotic/pale
Post-ictal confusion
Long recovery period

537
Q

What would the following symptoms in a seizure be suggestive off

Prodromal aura
Conclusive jerk
Eyes open
Automatism, lateral tongue biting
Cyanotic/pale
Post-ictal confusion
Long recovery period

A

Epileptic seizure

538
Q

What would be the symptoms of syncope (vasovagal)

A

Trigger e.g. blood, standing, needles
Prodrome - nausea, light-headiness, pallor
Incontinence may feature
Brief convulsive jerks

539
Q

What would the following symptoms of a seizure be suggestive off

Trigger e.g. blood, standing, needles
Prodrome - nausea, light-headiness, pallor
Incontinence may feature
Brief convulsive jerks

A

Syncope (vasovagal)

540
Q

Name the symptoms of cardiac syncope

A

Features/history of arrythmias/structural abnormalities

541
Q

What type of seizure would the following symptoms suggest

Features/history of arrythmias/structural abnormalities

A

Cardiac syncope

542
Q

Name the features of a seizure in postural (orthostatic) hypotension

A

Use of vasodilators, antidepressants

543
Q

What would the following symptoms of a seizure be suggestive of

Use of vasodilators, antidepressants

A

Postural (orthostatic) hypotension

544
Q

Name the symptoms of a hypoglycaemic seizure

A

Features of adrenaline release - palpitations, sweating, agitation

545
Q

What would the following symptoms in a seizure be suggestive of

Features of adrenaline release - palpitations, sweating, agitation

A

Hypoglycaemia

546
Q

Describe the symptoms of a non-epileptic attack disorder

A

Normal colour
Eye closed with active resistance to opening
Retained consciousness, combative
Pelvic thrust, arching back, erratic mvt

547
Q

In a seizure what would the following symptoms be suggestive of

Normal colour
Eye closed with active resistance to opening
Retained consciousness, combative
Pelvic thrust, arching back, erratic mvt

A

Non-epileptic attack disorder

548
Q

What is the screening for dementia in GP

A

6 questions

549
Q

What are the screening for secondary care

A

MOCA - Montreal cognitive assessment

MMSE - mini-mental state examination

550
Q

What do you have to score on the MMSE for it to be abnormal

A

23 or lower indicates dementia

551
Q

In dementia if the temporal lobe is affected what would be the presenting symptoms

A

Hearing
Language compression
Sematic knowledge
Memory
Emotional/affective disorder behaviour

Amnesic

552
Q

Describe amnesic as a symptom of dementia

A

Failure to create new memories.

553
Q

What can you do to reduce your risk of dementia

A

Stop smoking

Body mass index - 18-25 kg/m2

Diet - consumption of 3+ fruit/vegetables + < 30% of calories from fat

Physical activity - 2+ miles walk or 10+ cycling, vigorous exercise

Alcohol < 3 units per day

554
Q

What is the 1st line management in dementia

A

Acetyl choline esterase inhibitors (cholinesterase inhibitors)

Slows down progression

555
Q

What is the reason for contrast in a CT scan

A

To dye blood vessels

556
Q

A patient presents with a sudden onset headache. What is the diagnosis?

A

Subarachnoid headache

557
Q

If someone has power loss and the source is in the brain how would this present

A

Unilateral

558
Q

Name 3 differentials for bilateral leg weakness and numbness. Difficulty passing urine and compression

What investigation would be done?

A

Spinal cord compression
Cauda equina
Pathological fractures
Prolapse disk
Metastasis
Multiple sclerosis

MRI

559
Q

What would oligoclonal bands on a lumbar puncture indicate

A

Multiple sclerosis

560
Q

What is the initial treatment for multiple sclerosis

A

High dose steroids - prednisolone

561
Q

What treatments are available for MND

A

Riluzole

Sodium channel blocker which inhibits glutamate release

562
Q

What is the most important treatment in a patient who presents to A&E with collapse/seizure

A

Blood glucose - hypoglycaemia

ECG - heart conditions

563
Q

What anti epileptic drug can you NOT give if you have a women of childbearing age

A

Sodium valproate

564
Q

If you are looking at peripheral nerves what is the broad rule for imaging

A

Nerve conduction studies

565
Q

On examination what would be seen on a third nerve palsy

A

Globe depressed and abducted

Fixed dilated pupil

566
Q

Describe lateral medullary syndrome

A

Ipsilateral side
- Horner’s syndrome
- limb ataxia
- loss of facial sensation of pain, temp on face, reduced corneal reflex.
- dysarthria
- dysphagia

Contralateral side
- loss of pain and temp sensation

567
Q

Define Horner’s syndrome

A

Lesion of sympathetic chain supplying the eye

568
Q

What 3 important structures does the SNS innervate

A

Dilator pupillae - involved in mydriasis or dilation of the pupil

Superior tarsal muscle - aids in elevating the upper eyelid with levator palpebrae superioris

Sweat glands

569
Q

What are the two common presentations of a brain tumour

A

Localising or pressure related

570
Q

Describe the Monro-Kellie Doctrine

A

Describes the relationship between the contents of the cranium and intracranial pressure.

3 components
- CSF volume (150ml 10%)
- Blood volume (150ml 10%)
- Brain parenchyma volume (1400ml 80%)

571
Q

Describe the Monro-Kellie Doctrine effect on intracranial pressure

A

= Pressure within the cranium of the skull.

Cranium is fixed, increase in volume of one of the other intracranial components will result in increased pressure.

Equilibrium between these components

572
Q

What is the 1st line investigation for a suspected brain tumour

A

MRI head with contrast (gadolinium) +/- spine

573
Q

How brain tumours (glioblastoma) appear on radiological scans

A

Ring enhancement around the outer edge of the tumour

Differentials - abscesses

574
Q

Describe the radiological appearance of lymphoma

A

Periventricular - around the tumour

Steroids can cause temporary shrinking - can make biopsy difficult

575
Q

Name 4 causes which could affect LMN

A

Brainstem motor nuclei
Cranial nerve
Neuromuscular junction
Muscle

576
Q

Name 2 causes which could affect UMN

A

Motor cortex
Corticobulbar tract

577
Q

Define a bulbar palsy

A

LMN problem affecting bilateral IX, X, XI and XIII (at the level of the brainstem nuclei, nerve fascicles or lower cranial nerves outside the brainstem

578
Q

Define pseudobulbar palsy

A

UMN problem occurring above the level of the brainstem nuclei e.g. affecting bilateral corticobulbar tracts (also associated with emotional lability)

579
Q

Name the problems bulbar palsy

Voluntary palatal movements
Gag reflex
Tongue
Speech
Limb involvement

A

Absent
Absent
Wasting and fasciculations
Nasal
LMN signs

580
Q

Name the problems of pseudobulbar palsy

Voluntary palatal movements
Gag reflex
Tongue
Speech
Limb involvement
Other features

A

Absent
Increased
Spastic, hard to protrude
Spastic dysarthria - ‘hot potato speech’
UMN signs
Emotional labiality, brisk jaw jerk

581
Q

Define dysarthria

A

Difficulty speaking because the muscles used to speak are weak

582
Q

Define dysphonia

A

Having difficulty making sounds when attempting to speak

583
Q

Define dysphasia

A

Language disorder that affects the ability to produce and understand spoken language

584
Q

Define expressive aphasia (Broca)

A

Difficulty expressing what you want to say

585
Q

Define receptive aphasia (Wernicke)

A

Difficulty understanding the speech of others

586
Q

What causes encephalitis

A

HSV-1

587
Q

What is the 1st line management in myasthenia gravis

A

Pyridostigmine

Long acting acetylcholinesterase

Phase 2a (15 decks)

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