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Phase 2a Lecture Notes > Neurology > Flashcards

Neurology Flashcards

1
Q

Types of stroke

A

Ischemic- clots
Haemorrhagic- bleeds
TIA (transient ischemic attack

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2
Q

Which is more common ischaemic or haemorrhagic stroke

A

Ischaemic stroke-85%
Haemorrhagic- 15%

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3
Q

Ischaemic Stroke

A

Interruption of cerebral blood supply:
Embolism
Thrombosis
Systemic hypoperfusion

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4
Q

Stroke- FAST

A

FACE
ARMS
SPEECH
TIME TO CALL 999

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5
Q

Anterior cerebral artery supplies

A

midline portions of the frontal lobe and parietal lobe

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6
Q

Middle cerebral artery supplies

A

majority of the lateral surface of the hemisphere

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7
Q

Posterior cerebral artery supplies

A

inferior portion of the temporal lobe and occipital lobe

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8
Q

Wernicke area

A

Controls the ability to understand the meaning of words

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9
Q

Broca’s area

A

premotor area for speech sounds

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10
Q

Wernicke’s area location

A

Usually found on left superior temporal gyrus

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11
Q

Broca’s area location

A

Left posterior inferior frontal gyrus

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12
Q

Wernicke’s area blood supply

A

Inferior division of the MCA

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13
Q

Broca’s area blood supply

A

Superior division of the MCA

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14
Q

Oxford Community Stroke Project (OCSP) Classification

A

Clinical classification of patterns of neurological deficit in acute ischaemic stroke

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15
Q

Oxford Community Stroke Project (OCSP) Classification- different classifications

A

Anterior Circulation Infarction- Partial (PACI) or Total (TACI)
Posterior Circulation Infarction (POCI)
Lacunar Infarction (LACI)

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16
Q

Anterior Circulation Infarction- arteries affected

A

Anterior and middle cerebral arteries

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17
Q

Anterior Circulation Infarction- signs and symptoms

A

Contralateral weakness
Contralateral sensory loss/sensory inattention
Dysarthria
Dysphasia (receptive, expressive)
Homonymous Hemianopia/visual inattention
Higher cortical dysfunction

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18
Q

Posterior Circulation Infarction- arteries affected

A

2 vertebral arteries, basilar artery, 2 posterior cerebral arteries

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19
Q

Posterior Circulation Infarction- signs and symptoms

A

Cranial nerve palsy and a contralateral motor/sensory deficit (‘crossed signs’)
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia, dysarthria)
Isolated homonymous hemianopia
Bilateral events can cause reduced GCS

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20
Q

Lacunar Infarction

A

Occlusion of deep penetrating arteries
Affects a small volume of subcortical white matter
Underlying process is often referred to as small vessel disease

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21
Q

Lacunar Infarction- symptoms

A

Do not present with cortical features as subcortical white matter affected e.g. dysphasia, apraxia, neglect, visual field loss

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22
Q

Lacunar syndromes

A

Pure motor hemiparesis
Ataxic hemiparesis
‘Clumsy hand’ and dysarthria
Pure hemisensory
Mixed sensorimotor

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23
Q

Total anterior circulation stroke (TACS)- criteria

A

All 3: Unilateral weakness, homonymous hemiopia, higher cerebral dysfunction

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24
Q
A
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25
Q
A
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26
Q

Partial anterior circulation stroke (PACS)- criteria

A

2 of: Unilateral weakness, homonymous hemiopia, higher cerebral dysfunction

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27
Q
A
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28
Q

Lacunar syndrome (LACS)

A

1 of: Pure sensory stroke, pure motor stroke, sensori-motor stroke, ataxic hemiparesis

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29
Q
A
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30
Q

Posterior circulation syndrome (POCS)

A

1 of: Cranial nerve palsy + contralateral motor/ sensory deficit, bilateral motor/sensory deficit, conjugate eye movement disorder, cerebellar dysfunction, Isolated homonymous hemiopia or cortical blindness

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31
Q
A
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32
Q

NIHSS- NIH Stroke Scale

A

Grade and track the severity
Monitor response to acute treatments

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33
Q
A
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34
Q

Stroke- 1st line investigation

A

Urgent CT Head (+/- CT angiography)

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35
Q
A
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36
Q

Stroke- Head CT purpose

A

Differentiae between ischemic and haemorrhagic stroke

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37
Q

Utility of CT in acute stroke- pros

A

Quick
Readily available 24/7
Sensitive for haemorrhage
May see a ‘hyperdense vessel’

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38
Q

Utility of CT in acute stroke- cons

A

Cannot usually diagnose an infarct in the acute phase
Less sensitive than MRI for picking up other abnormalities, LACS + PCS

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39
Q

ASPECTS- Alberta Stroke Program Early CT Score

A

Segmental estimation of early infarction on CT head in MCA stroke
RAPID software uses a machine learning algorithm to calculate this score.

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40
Q

Ischemic Stroke- treatment-Thrombolysis

A

Breaks down acute clot- potentially life saving
Within 4,5 hrs of symptoms on set
Risk- haemorrhage, allergic reaction

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41
Q

Ischemic Stroke- treatment-Thrombolysis- Contraindications

A

Symptoms only minor/ rapidly improving
Haemorrhage on CT/MRI
Active bleeding from any site
Recent GI/UT haemorrhage
Recent treatment with heparin/warfarin
Recent surgery/trauma
Plus many more

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42
Q

Post-thrombolysis care

A

More aggressive blood pressure monitoring
Vigilance for complications (bleeding)
24 hour CT head (haemorrhagic transformation)

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43
Q

Mechanical Thrombectomy

A

Mechanical recanalisation of the culprit vessel (catheter aspiration and/or stent retrievers)
6 hour time-window

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44
Q

Mechanical Thrombectomy- risk

A

femoral haematoma/ pseudoaneurysm, retroperitoneal bleeding, vessel rupture, arterial dissection

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45
Q

Ischaemic Penumbra

A

Reversibly injured brain tissue around ischemic core (irreversibly damaged brain tissue)

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46
Q

Pathological subtypes of ischaemic stroke (TOAST classification)

A

Large vessel disease (50%)
Small vessel disease (25%)
Cardioembolic (20%)
Unknown (cryptogenic) (3%)
Rare causes (2%) e.g. dissection, CVST, vasculitis

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47
Q

Stroke- treatment- lifestyle

A

Smoking cessation
Drug and alcohol cessation
Dietary modifications
Exercise
Driving advice

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48
Q

Stroke- treatment- medical

A

Thrombolysis
Antiplatelet
Anticoagulation
Statin therapy

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49
Q

Stroke- treatment

A

Thrombolysis +/- Mechanical Thrombectomy if indicated
or Aspirin 300mg

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50
Q

Neuroepithelial cells

A

stem cells that differentiate into neurons and glial cells

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51
Q

Glia (gilal cells or neuroglia)

A

non-neuronal cells in the CNS (brain and spinal cord) and the peripheral nervous system that do not produce electrical impulses.
They maintain homeostasis, form myelin, and provide support and protection for neurons.

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52
Q

Types of Glial cells

A

Astrocytes, ependymal cells, oligodendrocytes, microglial

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53
Q

Astrocytes

A

perform metabolic, structural, homeostatic, and neuroprotective tasks

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54
Q

Oligodendrocytes

A

produce the myelin sheath insulating neuronal axons

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55
Q

Gliomas

A

a common type of brain tumour, include astrocytoma, ependymoma, oligodendrocyte
WHO grade 1 and 2 – “low”
WHO grade 3 and 4 – “high”

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56
Q

Germ cell tumours

A

rare paediatric usually cancerous tumours in the pituitary/pineal region

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57
Q

Tumour of the sellar region

A

Craniopharyngiomas a usually benign, cystic tumours

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58
Q

Brain tumours- cranial nerves

A

Schwannoma e.g. eighth nerve - acoustic neuroma

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59
Q

Brain tumour- Haematopoietic

A

Lymph cells - primary CNS lymphoma

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60
Q

Brain tumour- Secondary /metastatic tumours

A

Lung
Breast
Colorectal
Testicular
Renal cell
Malignant melanoma

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61
Q

Brain tumour- WHO classification

A

Graded according to how fast they grow and how likely they are togrow back after treatment using both histology and genetics into four grades of malignancy
-1 most benign, 4 most malignant

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62
Q

Brain Tumour Grades 1

A

Slow growing, non-malignant, and associated with long-term survival

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63
Q

Brain Tumour Grades 2

A

Have cytological atypia. These tumours are slow growing but recur as higher-grade tumours.

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64
Q

Brain Tumour Grades 3

A

Have anaplasia and mitotic activity. These tumours are malignant

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65
Q

Brain Tumour Grades 4

A

Anaplasia, mitotic activity with microvascular proliferation, and/or necrosis. These tumours reproduce rapidly and are very aggressive malignant tumours

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66
Q

Low grade gliomas – grade 2

A

Slow growing but will undergo anaplastic transformation
Astrocytomas – 3-5 years
Oligodendroglioma – 7-10 years
Average Survival 10 years
Median age 35 years

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67
Q

High Grade Gliomas – 3 and 4

A

Most common type - 85% of all new cases of malignant primary brain tumour
Either as primary tumour or from pre-existing low grade

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68
Q

High Grade Gliomas – 3 and 4- natural history

A

Median age onset 45 for 3, 60 for 4
Survival times 3 – 3-5 years 4 – 12 months

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69
Q

Brain tumour- known causes

A

Majority no cause found
Ionising radiation
5% family history
Immunosuppression (CNS lymphoma)

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70
Q

Brain tumour- symptoms

A

Varied- dependent on tumour type, grade and site
-Headache
-Seizures
-Focal neurological symptoms
-Other non-focal symptoms

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71
Q

Brain tumour- headache

A

Woken by headache, worse in the morning, worse lying down, associated with N&V, exacerbated by coughing, sneezing, drowsiness
Typically 1st symptom and seen at presentation

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72
Q

Headache- brain tumour vs norm pop

A

70% patients with brain tumour will have headache (same as normal population)

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73
Q

Brain tumour- headache red flags

A

Headache PLUS
Headache and age (>50)
New/changed headache
Previous history of cancer

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74
Q

Frontal lobe function

A

Prefrontal area – Personality, Inhibition
Frontal - Motor function, Language production (Broca’s area)

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75
Q

Parietal lobe function

A

Sensory processing
Spatial orientation
Visual field pathway

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76
Q

Occipital lobe function

A

Visual processing

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77
Q

Cerebellum function

A

Balance, coordination

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78
Q

Temporal lobe function

A

Language comprehension
Auditory processing
Visual field pathway
Memory

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79
Q

Brainstem function

A

cranial nerve nuclei
control subconscious body functions

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80
Q

Focal symptoms

A

(progressive over days – weeks)
Weakness
Sensory loss
Visual/speech disturbance
Ataxia

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81
Q

Non-focal symptoms

A

Personality change/behaviour
Memory disturbance
Confusion

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82
Q

Brain tumour- seizures

A

21% presenting symptom
>80% patients with a brain tumour
First fit 2-6% = brain tumour

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83
Q

Frontal lobe- seizure

A

Limb jerking, head or eye deviation

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84
Q

Parietal lobe- seizure

A

Sensory disturbance – spreading tingling

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85
Q

Occipital lobe- seizure

A

Positive visual disturbance - coloured balls

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86
Q

Temporal lobe- seizure

A

Déjà vu
Jamais vu
Memories
Feeling of dread
Rising feeling

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87
Q

Seizure- signs

A

Papilloedema-
Focal neurological deficit- Hemiparesis, Hemisensory loss, Visual field defect, Dysphasia

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88
Q

Papilloedema

A

Swelling of the optic disc due to elevated intracranial pressure

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89
Q

Low grade brain tumour- presentation

A

typically present with seizures (can be incidental finding)

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90
Q

High grade brain tumour- presentation

A

rapidly progressive neurological deficit. Symptoms of raised intracranial pressure

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91
Q

Brain tumour- headache red flags

A
  • With features of raised intracranial pressure (including papilloedema and VIth nerve palsy)
    -With focal neurology. Check for field defect
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92
Q

Brain tumour- urgent referrals

A

New onset focal seizure
Rapidly progressive focal neurology (without headache)
Past history of other cancer

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93
Q

Brain tumour- 1st line investigations

A

Imaging- CT (with contrast), MRI
Functional MRI

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94
Q

Brain tumour- 2nd line investigation

A

Brain biopsy/surgery- Histology, molecular markers and genetics

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95
Q

Brain tumour- treatment

A

Depends on tumour type, grade and site
Treatment is non-curative (except for grade I)

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96
Q

Brain tumour prognosis

A

Brain cancer 5 year survival rate is 12%
Compare to breast cancer – 76% over 10 years

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97
Q

Brain tumour- treatment high grade glioma

A

Steroids, surgery, chemo
Radiotherapy is mainstay of treatment

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98
Q

Brain tumour- treatment low grade glioma

A

Surgery – early resection
Radiotherapy and early chemotherapy

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99
Q

Traumatic brain injury

A

Evidence of neurological dysfunction caused by external force

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100
Q

Traumatic brain injury- aetiology

A

RTC, falls (elderly), assaults, sports and recreation

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101
Q

Contrecoup injury

A

Counterblow, brain lies in CSF, collision on head causes “free floating” brain to head back of head

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102
Q

Primary vs secondary Traumatic brain injury

A

primary brain injury results from mechanical injury at the time of the trauma
secondary brain injury is caused by the physiologic responses to the initial injury

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103
Q

Contusions

A

Bruising of the brain, close to bony providences

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104
Q

Diffuse axonal injury

A

White matter lesions, high rotation or deceleration
Little haemorrhage- need MRI to see

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105
Q

Types of brain haemorrhage

A

epidural haemorrhage, subdural haemorrhage, subarachnoid haemorrhage, and intraparenchymal haemorrhage

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106
Q

Epidural haemorrhage

A

Most dangerous but if drained, good recovery
bleeding between the inside of the skull and dura mater

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107
Q

Subdural haemorrhage

A

Presents typically with milder trauma
Collection of blood under the dura mater

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108
Q

Subarachnoid haemorrhage

A

Can cause finger like extensions of blood that fill the sulci and bathe the brain as seen on CT
Accumulation of blood between the arachnoid and pia mater

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109
Q

Intraparenchymal haemorrhage

A

bleeding into the brain parenchyma proper

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110
Q

Secondary traumatic brain injury- treatment

A

Maintenance of homeostasis- (iv fluids, glucose ect)
Management of seizures- diazepam
Surgery- rarer

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111
Q

When to CT- presents with a head injury

A

Any form of clinical concern- not returned to pretty much near normal when under observations

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112
Q

Glasgow coma scale

A

Composed of three parameters: best eye response (E), best verbal response (V), and best motor response (M), 3-15, 3 being the worst and 15 the best

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113
Q

Chronic traumatic encephalopathy

A

Only found at autopsy
Thought to be linked to repeated head injuries and blows to the head

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114
Q

Basal ganglia disease

A

Hardware problem and software problems (no cell dead, problem with brain circuit)

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115
Q

Basal ganglia disease- hardware problems

A

Parkinson’s disease
Huntington’s disease

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116
Q

Basal ganglia disease- software problems

A

Essential tremor
Dystonia
Tourette

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117
Q

Parkinson’s disease- three cardinal features

A

Brady/Akinesia- (problems with buttons, writing smaller, walking deteriorated)
Tremor- (at rest, may be unilateral)
Rigidity

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118
Q

Spasticity vs rigidity

A

Spasticity- more resistance in one direction, more tone initial part of movement, velocity dependent
Rigidity- Same resistance in all directions, not velocity dependent

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119
Q

Spasticity vs rigidity- pathophysiology

A

spasticity arises as a result of damage to the corticoreticulospinal (pyramidal) tracts, rigidity is caused by dysfunction of extrapyramidal pathways

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120
Q

Bradykinesia

A

slowness of movement and speed (or progressive hesitations/halts) as movements are continued

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121
Q

Akinesia

A

inability to perform a clinically perceivable movement

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122
Q

Parkinson’s disease- aetiology

A

Cell loss in substantia nigra- Inherited factors, oxidative stress, mitochondrial dysfunction, environmental factors (risk factors, toxin induced)

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123
Q

Parkinson’s disease- pathophysiology

A

Loss of dopaminergic neurons in the substantia nigra

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124
Q

Parkinson’s disease- treatment overview

A

Non curative, to replace lost dopamine to reduce symptoms

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125
Q

Parkinson’s disease- treatment- L dopa

A

L-dopa > dopamine> dopamine receptor

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126
Q

Parkinson’s disease- treatment- dopamine agonist

A

Activate dopamine receptor like dopamine

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127
Q

Parkinson’s disease- treatment- COMT/MAO-B inhibitors

A

Inhibits Catechol-O-Methyl-Transferase + Monoamino-
oxidase- reponisble for removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain

128
Q

Parkinson’s and tremor on action

A

Unlikely to be Parkinson’s, more likely to be essential tremor

129
Q

Essential tremor- signs

A

Postural/action tremor
No/little rest tremor
No increased tone
No problems with fine finger movements

130
Q

Essential tremor- treatment

A

BBs, primidone
Deep brain stimulation useful

131
Q

Essential tremor-pathophysiology

A

Software issue- the result of an abnormally functioning central oscillator

132
Q

Meningitis

A

Inflammation of the meninges

133
Q

Meninges

A

Outermost- dura mater
Arachnoid
Pia Mater

134
Q

Causes of Meningitis- infective

A

Bacterial
Viral
Fungal
Parasitic

135
Q

Causes of Meningitis- non infective

A

Paraneoplastic
Drug side effects
Autoimmune(e.g. vasculitis/SLE

136
Q

Meningitis- infective routes

A

Via blood stream
Extracranial infection
Neurosurgical complications

137
Q

Meningitis- infective- pathophysiology

A

Bacteria enter CSF, either transcellularly (through endothelial cells) or paracellularly (next to endothelial cells)
Infected WBCs can act as trojan horse

138
Q

Meningitis- infective barriers

A

Blood-CSF and blood-brain barrier ordinarily protect against meningitis and encephalitis respectively

139
Q

Infective meningitis- classic triad

A

fever, headache, neck stiffness

140
Q

Infective meningitis- first line antibiotic in community

A

IM benzylpenicillin

141
Q

Infective meningitis- 1st line investigations

A

Assess GCS (Glasgow Coma Score)
Blood cultures

142
Q

Infective meningitis- 1st line treatment

A

Broad spectrum antibiotics
Steroids (IV dexamethasone)

143
Q

Infective meningitis- first line antibiotic in hospital

A

ceftriaxone or cefotaxime

144
Q

Infective meningitis- first line antibiotic- special considerations

A

Penicillin allergic
Immunocompromised 🡪 risk of listeria
Recent travel 🡪 risk of penicillin resistance

145
Q

Infective meningitis- diagnostic investigation

A

Lumbar puncture and lab tests

146
Q

Infective meningitis- gram Negative cocci

A

Neisseria

147
Q

Infective meningitis- gram positive cocci

A

Pneumococcus (strep.pneumoniae)

148
Q

Infective meningitis- bacterial clinical signs

A

May appear septic
Focal neurology
?purpuric rash

149
Q

Infective meningitis- viral clinical signs

A

Recent viral illness
Less severe

150
Q

Infective meningitis- TB clinical signs

A

Weight loss
Night sweats
Insidious onset

151
Q

Infective meningitis- cryptococcal clinical signs

A

HIGH OPENING PRESSURE!!!- when doing lumbar puncture

152
Q

Infective meningitis- bacterial RFs

A

Students
Travel
Immunosuppressed

153
Q

Infective meningitis- Viral RFs

A

Small children
Immunosuppressed

154
Q

Infective meningitis- TB RFs

A

TB contact
Immunosuppressed

155
Q

Infective meningitis- cryptococcal RFs

A

HIV
Immunosuppressed

156
Q

Infective meningitis- bacteria species- neonate

A

Strep B

157
Q

Infective meningitis- bacteria species- child

A

N. meningitidis, S. pneumoniae,
H. Influence

158
Q

Infective meningitis- bacteria species- adult

A

Neisseria meningitidis, S. pneumoniae

159
Q

Infective meningitis- bacteria species- elderly

A

N. meningitidis, S. pneumoniae

160
Q

Infective meningitis- bacteria species- immunocompromised

A

Listeria

161
Q

Encephalitis- causes

A

Usually viral
-Herpes Simplex
-Varicella Zoster
Tropical
Non-infective- autoimmune, paraneoplastic

162
Q

Encephalitis

A

Inflammation of the brain

163
Q

Encephalitis- signs

A

Preceding “flu-like” illness
Altered GCS: confusion, drowsiness, coma
Fever
Seizures
Memory loss
(+/- meningism)

164
Q

Encephalitis- investigations

A

MRI head
Lumbar puncture (Lymphocytic CSF, Viral PCR)

165
Q

Encephalitis- treatment

A

Mostly supportive
Aciclovir if HSV or VZV

166
Q

Tetanus

A

Inoculation through skin with Clostridium tetani spores (found globally in soil)
e.g. stepping on a nail, dirty wounds
Bacteria produce toxins!

167
Q

Tetanospasmin

A

travel retrogradely along axons
Interferes with neurotransmitter release 🡪 increased neuron firing 🡪 unopposed muscle contraction and spasm
Incubation around 8 days

168
Q

Tetanus- management

A

Vaccinate if risk injury
Supportive- Muscle relaxants
Paracetamol/cooling
Immunoglobulin to mop up toxin
Metronidazole to clear any residual bacteria

169
Q

Rabies

A

Virus- Inoculation through skin with saliva of rabid animal (dogs, cats, foxes etc)
e.g. lick, bite, splash
Travels retrogradely along nerves

170
Q

Stroke

A

a clinical syndrome, caused by cerebral infarction or
haemorrhage, typified by rapidly developing signs of focal and global disturbance of
cerebral functions lasting more than 24 hours or leading to death

171
Q

Transient ischemic attack (TIA)

A

acute loss of cerebral or ocular
function with symptoms lasting less than 24 hours caused by an inadequate
cerebral or ocular blood supply as a result of low blood flow, ischemia, or embolism
associated with disease of the blood vessels, heart or blood

172
Q

Ischemic stroke- aetiology

A

Blood vessel in the brain is blocked
Usually, an atherosclerotic plaque or a clot in a larger artery ruptures, travels
downstream, gets trapped in a narrower artery in the brain.
Embolic strokes are common complications of AF and atherosclerosis of
the carotid arteries

173
Q

Haemorrhagic stroke- aetiology

A

Bleeding from a blood vessel within the brain.
HTN is the main cause of intracerebral haemorrhagic stroke.

174
Q

Strokes- Differential Diagnosis

A

Hypoglycaemia Labyrinthine disorders
Migrainous aura
Mass lesions
Postictal weakness
Simple partial seizures
Functional hemiparesis

175
Q

ABCD2 Score

A

estimates risk of stroke (CVA) after a transient ischemic attack (TIA)

176
Q

ABCD2 Score- stands for

A

Age: >60yrs (1 point)
BP >140/90 (1 point)
Clinical features
-Unilateral weakness, 2 points
-Speech disturbance without weakness, 1 point.
Duration (60 mins< = 2 points, 10–59 mins =1 point)
Diabetes (1 point)

177
Q

High risk of TIA becoming stroke

A

ABCD2 >3
Or AF, 1< TIA in a week, TIA on anticoagulants

178
Q

TIA treatment

A

Low risk < 7 days, high risk <1 day
Statin, antiplatelet (clopidogrel or aspirin), treat BP, no driving until seen by a specialist

179
Q

Active Rehabilitation

A

Facilitating recovery through modification of the neural networks

180
Q

Active Rehabilitation techniques- Priming

A

Makes NS more receptive to rehabilitation interventions: Imagery, Touch, Transcranial direct current stimulation, Transcranial magnetic stimulation

181
Q

Active Rehabilitation techniques-Augmenting

A

Augment the effects of rehabilitation interventions- Robotics, Biofeedback

182
Q

Active Rehabilitation techniques- Specific interventions

A

Neurophysiological
Task Specific practice

183
Q

Adaptation

A

Incomplete Recovery- strategies facilitate recovery of function through training, use of aids and appliances or modification of environment

184
Q

Preventative rehabilitation

A

Reduce immobilisation: Passive range of motion exercises

185
Q

Gait in neurological disorders

A

Weakness
Balance
Stiffness
Slowness

186
Q

Walking

A

Heelstroke, footflat, midstance, pushoff, acceleration, midswing, deceleration

187
Q

Dropped foot

A

Inability to activate ankle dorsiflexors in swing phase of gait

188
Q

Dropped foot- pathophysiology

A

Lesion of CNS- corticospinal tract

189
Q

Balance treatment

A

Vestibular exercises
Physiotherapy
Increase the base
Improve vision

190
Q

Posture and slow treatment

A

Dopaminergic drugs
Metronomes

191
Q

Spasticity

A

Disordered sensori-motor control resulting from an UMN lesion, presenting as intermittent or sustained involuntary activation of muscles

192
Q

Headache classification- Primary

A

Migraine, Cluster, Tension Type

193
Q

Headache classification- Secondary

A

Meningitis, Subarachnoid Haemorrhage, GCA, Idiopathic Intracranial Hypertension, Medication overuse headache

194
Q

Brain tumour- headache red flags

A

New headache with Hx cancer, Cluster headache, Seizure, Significantly altered conciousness, memory, confusion, coordination, Papilloedema

195
Q

Kernig’s sign

A

Pts is kept in supine position, hip and knee are flexed to a right angle, and then knee is slowly extended- resistance or pain >135 degree= +ive kernig sign

196
Q

Positive Kernig’s sign

A

Meningitis

197
Q

Migraine signs

A

Attacks last 4-72 hours
Two of the following: Unilateral , Pulsing, Moderate/severe, Aggravation by routine physical activity
Nausea and /or vomiting
Photophobia and phonophobia

198
Q

Photophobia

A

abnormal sensitivity to light, especially of the eyes

199
Q

Phonophobia

A

persistent, abnormal, and unwarranted fear of sound

200
Q

Migraine pain

A

Unilateral, pulsing, Moderate/severe, Aggravation by routine physical activity

201
Q

Tension type headache signs

A

30 mins to 7 days
Bilateral
Pressing/tightening (non pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity
No nausea or vomiting (anorexia may occur)
No more than one of photophobia and phonophobia

202
Q

Tension type headache- characteristic

A

Bilateral
Pressing/tightening (non pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity

203
Q

Cluster headache

A

Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180
minutes if untreated
Accompanied by ipsilateral cranial autonomic features +/ a sense of
restlessness or agitation
Attacks have a frequency from 1 every other day to 8 per day

204
Q

Cluster headache- pain

A

Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 mins

205
Q

Trigeminal Neuralgia- definition

A

intense facial pain in the distribution of the trigeminal nerve

206
Q

Classical Trigeminal Neuralgia

A

distributions of the trigeminal nerve
Electric shock like, shooting, stabbing or sharp
Precipitated by innoculous stimuli to the affected side of the face

207
Q

Migraine- acute treatment

A

Oral triptan + NSAID/ paracetamol
DO NOT USE OPIOIDS

208
Q

Migraine- preventive treatment 1st line

A

topiramate or propranolol

209
Q

Migraine- preventive treatment 2nd line

A

Amitriptyline

210
Q

Meningitis signs

A

Drowsy, Pyrexial, Neck stiffness

211
Q

Subarachnoid Haemorrhage signs

A

Thunderclap headache – max severity within seconds

212
Q

Subarachnoid Haemorrhage- 1st line investigations

A

CT head

213
Q

Subarachnoid Haemorrhage- management

A

Surgery for aneurysms
Nimodipine- CCB to prevent vasospasm

214
Q

Raised Intracranial Pressure signs

A

Worse on waking, coughing, sneezing, straining, lying down (postural)
Nausea, vomiting
Papilloedema

215
Q

Papilloedema

A

swelling of the optic disc due to elevated intracranial pressure

216
Q

Idiopathic Intracranial Hypertension signs

A

Headache of raised ICP
Visual disturbance – acuity, fields
Papilloedema

217
Q

Idiopathic Intracranial Hypertension RFs

A

Obesity
Drugs (tetracycline)
Female

218
Q

Idiopathic Intracranial Hypertension investigations

A

CSF normal but pressure high
Imaging to exclude secondary cause and cerebral venous sinus thrombosis

219
Q

Idiopathic Intracranial Hypertension management

A

Management of RFs (ie wgt loss)
consider pharmacotherapy

220
Q

Idiopathic Intracranial Hypertension- pharmacotherapy

A

Acetazolamide / Topiramate/ Diuretics

221
Q

Giant Cell Arteritis (GCA)

A

> 50 yrs
Associated with PMR
Jaw claudication
Visual symptoms
Tender temporal arteries
Raised inflammatory markers

222
Q

Giant Cell Arteritis (GCA) diagnostic investigation

A

ultrasonography +/ temporal artery biopsy

223
Q

Giant Cell Arteritis (GCA) 1st line treatment

A

high dose steroid

224
Q

Chronic Daily Headache

A

Headache on ≥ 15 days per month

225
Q

Chronic headache- common primary causes

A

Chronic Migraine, Tension-type headache, cluster headache, paroxysmal hemicranias
Hemicrania continua
New daily persistent headache

226
Q

Chronic headache- common secondary causes

A

Medication overuse headache
Chronic post-traumatic headache
Raised intracranial pressure
Low CSF pressure headache
Chronic meningitis

227
Q

Medication overuse headache- common causes

A

Ergotamine, Triptans, Opioids or Combination analgesic medications

228
Q

Medication overuse headache

A

Regular use for >3 months of one or more symptomatic treatment
Headache has developed or markedly worsened during drug use

229
Q

Dystonia

A

Prolonged muscle contraction causing abnormal posture or related movements

230
Q

Idiopathic generalized dystonia

A

Childhood-onset dystonia often starting in 1 leg with ipsilateral progression
Genetic cause is common

231
Q

Focal dystonia

A

Dystonia confined to one part of the body

232
Q

Focal dystonia- examples

A

Spasmodic torticollis, blepharospasm, writer cramp

233
Q

Spasmodic torticollis

A

head pulled to one side

234
Q

Blepharospasm

A

involuntary contraction of orbicularis oculi (responsible for closing eyelids)

235
Q

Acute dystonia

A

Medication induced dystonia

236
Q

Acute dystonia- examples

A

Torticollis (head pulled back), trismus (oromandibular spasm) +/ oculogyric crisis (eyes drawn back)

237
Q

Acute dystonia- treatment

A

diphenhydramine or benzatropine- antidopaminergic agents

238
Q

Generalised dystonia- treatment

A

Levodopa + physio

239
Q

Focal dystonia- treatment

A

botulinum toxin + physio

240
Q

Tourette syndrome

A

complex neurodevelopmental disorder characterised by motor and vocal tics beginning in childhood

241
Q

Tourette syndrome- RFs

A

Male, 3-8 yrs, PMH/FH of OCD or ADHD, FM of tourette’s

242
Q

Tourette syndrome- pathophysiology

A

Unknown, multiple genetic loci implicated and neuroanatomical differences on MRI

243
Q

Tourette syndrome- tic paradox

A

Tics are voluntary, but often unwanted- the desire to tic comes from the relief of the odd sensation that builds up prior

244
Q

Tourette syndrome- non medical treatment

A

Cognitive behavioural approaches- 1st line

245
Q

Tourette syndrome- medical treatment

A

Alpha-2 agonist, antipsychotic, botox

246
Q

Epilepsy- differential diagnosis

A

Postural syncope, hypoglycaemia, migraine, Benign paroxysmal Positional vertigo, TIA, cardiogenic syndrome

247
Q

Epileptic Seizure

A

Paroxysmal event in which changes of behaviour, sensation and cognition are caused by excessive, hypersynchronous neuronal discharges in the brain

248
Q

Epileptic Seizures- characteristics

A

30-120 seconds
May occur from sleep
Stereotypical seizures / syndromal seizure types
May be associated with other brain dysfunction

249
Q

Epileptic Seizures- temporal lobe

A

Focal impaired awareness seizure

250
Q

Epileptic Seizures- Frontal lobe

A

Focal aware seizure

251
Q

Focal seizure

A

Originating within networks linked to one hemisphere + often seen with underlying structural disease

252
Q

Focal seizure without impairment of consciousness

A

Awareness is unimpaired with focal, motor, sensory, automimic or psychic symptoms
No post-ictal symptoms

253
Q

Focal seizure with impairment of consciousness

A

Awareness is impaired- either at seizure onset or following a simple partial aura
Commonly temporal lobe- post ictal symptoms is a feature

254
Q

Focal seizure evolving into a bilateral, convulsive seizure

A

2/3 pts with partial seizures, electrical disturbances start focally, spreads widely, causing generalized seizure, typically convulsive

255
Q

Generalized seizures

A

Originating at some point within an rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge with no localizing features (to one hemisphere)

256
Q

Absence seizures

A

Brief pauses eg suddenly stops talking mid sentence, then carries off where they left off, presents in childhood

257
Q

Tonic-clonic seizures

A

Loss of conscience, limbs stiffen (tonic) then jerk (clonic)- may have one without the other
Post-ictal confusion + drowsiness

258
Q

Myoclonic seizures

A

sudden jerk of a limb, face or trunk
Pts may be thrown to ground or have a violently disobedient limb- ‘flying saucer epilepsy’

259
Q

Atonic (akinetic) seizures

A

Sudden loss of muscle tone causing a fall, no LOC

260
Q

Syncope

A

Paroxysmal event in which changes in behaviour, sensation and cognition are caused by an insufficient blood or oxygen supply to the brain.

261
Q

Syncope- characteristics

A

Situational
Typically from sitting/ standing- rarely sleep
Duration 5-30 seconds- recovery in 30s
Presyncopal symptoms

262
Q

Cardiogenic syncope- characteristics

A

less warning, history of heart disease

263
Q

Functional / dissociative (nonepileptic) seizure

A

Paroxysmal event in which changes in behaviour, sensation and cognition are caused by mental processes triggered by internal or external aversive stimuli.

264
Q

Functional / dissociative (nonepileptic) seizure- characteristics

A

Situational
Duration 1-20 minutes
Dramatic motor phenomena or prolonged atonia, Eyes closed, Ictal crying and speaking
Rapid or slow postictal recovery
History of psychiatric illness, other somatoform disorders

265
Q

Epilepsy versus syncope: Factors suggestive of epilepsy

A

Tongue biting, head turning, muscle pain, cyanosis (blue/grey lips), postictal confusion

266
Q

Epilepsy versus syncope: Factors suggestive of syncope

A

Prolonged upright position, sweating prior to LOC, nausea, presyncopal symptoms (dizzy, nausea, sweating, palpitations), pallor

267
Q

Epilepsy vs. Functional / Dissociative Seizures- suggestive of FDS

A

Very frequent, prolonged attacks
Those in which the body movements come and go
Attacks where the person is emotionally upset afterwards
Pre-ictal anxiety

268
Q

Structural / metabolic (focal) epilepsy

A

Associated with focal brain abnormality, may start at any age

269
Q

Structural / metabolic (focal) epilepsy- types of seizures

A

Partial seizures +/- with impairment of consciousness, secondary generalised seizures

270
Q

Structural / metabolic (focal) epilepsy- first line treatment

A

Lamotrigine (anticonvulsant)/ carbamazepine (anticonvulsants)/ levetiracetam (anticonvulsants)

271
Q

Structural / metabolic (focal) epilepsy- first line investigation

A

MRI- anatomical temporal lobe abnormalities
EEG can be diagnostic but a normal EEG does not exclude epilepsy

272
Q

Genetic (idiopathic) generalised epilepsy

A

No associated brain abnormality, manifestation usually <30 years

273
Q

Genetic (idiopathic) generalised epilepsy- seizure types

A

Absence, myoclonic, primary generalised tonic clonic seizures

274
Q

Genetic (idiopathic) generalised epilepsy- first line treatment

A

Lamotrigine (anticonvulsant) / levetiracetam (anticonvulsant)/ valproate (anticonvulsant)

275
Q

Genetic (idiopathic) generalised epilepsy- diagnostic test

A

EEC- electroencephalogram

276
Q

Modes of action of Anti-seizure medications- presynaptic neurone

A

Inhibit voltage-gated Na+/ Ca2+
Increase activity of voltage-gated K+
Inhibit SV2A
Overall decrease in pre-synaptic excitability and neurotransmitter release

277
Q

Modes of action of Anti-seizure medications- inhibitory neurotransmitters

A

Increase activity of GABA receptor
Inhibit GABA transaminase/ transporter
Overall more GABA in synapse

278
Q

Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated Na+ channels

A

Na+ influx increases excitability and drives APs
Inhibited by carbamazepine, lamotrigine, oxcarbazepine

279
Q

Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated K+ channels

A

K+ efflux reduces neuronal excitability, channel activity increased

280
Q

Modes of action of Anti-seizure medications- presynaptic neurone- Voltage gated Ca2+ channels

A

Ca2+ influx drives neurotransmitter release, channel inhibited

281
Q

Modes of action of Anti-seizure medications- presynaptic neurone- SV2A

A

Requires for release of neurotransmitter from vesicles
Inhibited by levetiracetam

282
Q

Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA receptor

A

Reduces neuronal excitability
GABA receptor activity increased by benzodiazepines, barbiturates, felbamate, topiramate

283
Q

Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA transaminase

A

Degrades GABA, inhibited to elevate GABA levels

284
Q

Modes of action of Anti-seizure medications- inhibitory neurotransmitters- target the GABA transporter

A

Removes GABA from the synapse, inhibited to elevate GABA levels

285
Q

Other epilepsy therapies

A

Surgery
Vagus nerve simulation

286
Q

Cerebellum anatomy

A

largest part of the hindbrain, located in posterior cranial fossa
comprises of two hemispheres joined by the vermis- sub-divided into three lobes – anterior, posterior, and flocculonodular separated by two transverse fissures

287
Q

Role of the cerebellum- main

A

accuracy and coordination

288
Q

Role of the cerebellum

A

-accuracy and coordination
-motor control and learning
-contributes to timing and sensory acquisition
-involved in the prediction of the sensor consequences of action
-eye movements, speech, limb movements, fine motor skills, gait, posture,
balance, cognition

289
Q

Ataxia

A

Sign, not a disease + results from cerebellar dysfunction (problems with balance and co-ordination) can be caused by structural damage to the cerebellum or can be inherited or acquired

290
Q

Ataxia- aetiology

A

Inherited- autosomal dominant, autosomal recessive (Friedreich’s ataxia), X linked, mitochondrial
Acquired- toxic/metabolic (alcohol, vit def, drugs), immune mediated (gluten related) infective, degenerative, trauma, neoplastic

291
Q

Symptoms of cerebellar dysfunction

A

-dizzy – unsteady / wobbly / clumsy
-falls, stumbles
-difficulty focusing / double vision / ‘oscillopsia’
-slurred speech
-problems with swallowing
-tremor
-problems with dexterity / fine motor skill

292
Q

Nystagmus

A

rhythmical, repetitive and involuntary movement of the eyes

293
Q

Ataxia- clinical signs

A

Gait is unsteady with a tendency to falls
Hand coordination is impaired
Dysarthria or dysphagia may be present
Ocular symptoms- nystagmus
Intentional tremor

294
Q

Classification of ataxia

A

Scale for the Assessment and Rating of Ataxia (SARA)
Mild- mobilising independently or with one walking aid
Moderate- Mobilising with 2 walking aids or walking frame
Severe- predominantly wheelchair dependent

295
Q

Ataxia-first line investigation

A

MRI brain demonstrates cerebellar atrophy and / or dysfunction

296
Q

Ataxia- common blood test

A

For genetic testing, autoimmune screen (esp gluten related serology)

297
Q

Motor neurone disease (MND)

A

Cluster of neurodegenerative disease characterised by selective loss of neurone in motor cortex, cranial nerve nuclei, and anterior horn cells

298
Q

Motor neurone disease (MND) vs MS and polyneuropathies

A

Never sensory loss or sphincter disturbance in MND, unlike MS and polyneuropathies

299
Q

Motor neurone disease (MND) vs myasthenia

A

MND never affects eye movement, distinguishing from myasthenia

300
Q

Motor neurone disease (MND)- 4 types

A

ALS (amyotrophic lateral sclerosis or Lou Gehrig’s disease)- most common
Progressive bulbar palsy- 10-20%
Progressive muscular atrophy <10%
Primary lateral sclerosis- rare

301
Q

ALS (amyotrophic lateral sclerosis)

A

Loss of motor neurones in motor cortex + anterior horn of the cord, so combined UMN + LMN signs

302
Q

UMN symptoms

A

Weakness (pyramidal)
Spasticity
Hyperreflexia

303
Q

LMN symptoms

A

Wasting
Weakness
Fasiculation
Hypotonia/flaccidity
Reflexes are reduced

304
Q

Progressive bulbar palsy

A

disease of the nuclei of CN IX-XII

305
Q

Progressive bulbar palsy- signs

A

Progressive, relentless
Oropharyngeal muscles
Dysarthria
Dysphasia
Jaw spasms/bruxism

306
Q

Progressive muscular atrophy

A

Anterior horn cell lesion, so LMN signs only
Affects distal muscles groups before proximal
Better prognosis than ALS

307
Q

Primary lateral sclerosis

A

Loss of betz cells in motor cortex
Mainly UMN, marked leg spastic leg weakness and pseudobulbar palsy, no cognitive sign

308
Q

Motor neurone disease- investigations

A

Clinical diagnosis

309
Q

Motor neurone disease- treatment overview

A

Improve survival and QoL

310
Q

Motor neurone disease- treatment

A

Riluzole
Non-invasive ventilation- for Nocturnal respiratory insufficiency
Multi-disciplinary specialist care

311
Q

Motor neurone disease- treatment- riluzole

A

inhibitor of glutamate release and NMDA receptor antagonist
Only medication to improve survival

312
Q

Dementia

A

A neurodegenerative disease with progressive decline in several cognitive domains
20% of pop > 80 yrs

313
Q

Dementia subtypes

A

Alzheimer’s disease, vascular dementia, Lewy body dementia, frontotemporal dementia

314
Q

Alzheimer’s disease

A

Most common type of dementia, cognitive impairment is progressive, non-cognitive symptoms may come and go, but pts become sedentary

315
Q

Alzheimer’s disease risk factors

A

1st degree relative, Down’s syndrome, genetics, low physical/ cognitive activity, depression, loneliness, smoking

316
Q

Alzheimer’s disease pathophysiology

A

Atrophy in the temporal, frontal and parietal area
Senile plaques (beta-amyloid) and neurofibrillary tangles are the characteristic histopathological features postmortem

317
Q
A

Phase 2a Lecture Notes (14 decks)

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