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neuro Flashcards

1
Q

What are the 2 main types of stroke?

& definition

A

Ischaemic- Ischaemia or infarction of the brain tissue secondary to a disrupted blood supply
Haemorrhagic- Intracranial haemorrhage, with bleeding in or around the brain

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2
Q

What is the WHO definition of stroke?

A

a clinical syndrome consisting of rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

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3
Q

What is a transient ischaemic attack?

A

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

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4
Q

Risk factors for a TIA

A

atrial fibrillation
valvular disease
carotid stenosis
intracranial stenosis
congestive heart failure
hypertension
hyperlipidaemia
diabetes mellitus
cigarette smoking
alcohol-use disorder
advanced age

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5
Q

What are crescendo TIAs?

A

two or more TIAs within a week
indicate a high risk of stroke

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6
Q

What causes a TIA?

A

Thrombus or occlusion of vessel

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7
Q

When should TIA be suspected?

A

sudden-onset, focal neurological deficit that resolves spontaneously and cannot be explained by another condition

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8
Q

What are the key presentations of a TIA?

A

Sudden onset
Brief duration
Focal neurological deficit

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9
Q

What investigations should be done for a suspected TIA?

AFTER deemed not a stroke

A
  • Blood glucose (rule out other cause for symptoms)
  • FBC and platelets (rule out other cause, e.g. infection)
  • PT, INR, APTT
  • ECG
  • Serum electrolytes
  • fasting lipid profile
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10
Q

What are the differentials of TIA?

A

STROKE
Hypoglycaemia
Syncope
Seizure with post-seizure (Todd’s) paralysis
Complex migraine
Space-occupying lesion (intracranial haemorrhage, abscess, or mass)
Functional neurological disorder
Labyrinthine disorders
MS
Peripheral neuropathy

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11
Q

How should a TIA be managed?

A

Give a loading dose of aspirin immediately, unless contraindicated, to patients with suspected TIA
Once confirmed give secondary antiplatelet prevention, e.g. aspirin + clopidogrel

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12
Q

Complications of a TIA

A

Stroke
MI

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13
Q

What should be involved in secondary prevention after a TIA?

A

Risk factor modification (including blood pressure control and smoking cessation)
Managing comorbidities that predispose patients to stroke

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14
Q

What are the different pathological subtypes of ischaemic stroke according to the TOAST classification?

A

Large vessel disease
Small vessel disease
Cardioembolic
Unknown (cryptogenic)
Rare causes e.g. dissection, CVST, vasculitis

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15
Q

What are the potential mechanisms for ischaemic stroke?

A

Embolism: an embolus originating somewhere else in the body causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of the brain the vessel supplies.
Thrombosis: a blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
Systemic hypoperfusion: blood supply to the entire brain is reduced secondary to systemic hypotension (e.g. cardiac arrest).
Cerebral venous sinus thrombosis: blood clots form in the veins that drain the brain, resulting in venous congestion and tissue hypoxia.

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16
Q

How does the Bamford (oxford) classification system describe ischaemic strokes?

A

Partial Anterior Circulation Infarction
Total anterior circulation infarction
Posterior Circulation Infarction
Lacunar Infarction

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17
Q

Where does a total anterior cerebral infarction affect and how does it present?

A

affecting the areas of the brain supplied by both the middle and anterior cerebral arteries

All 3 present:
- Unilateral weakness (and/or sensory deficit) of the face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disorder)

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18
Q

Where does a partial anterior cerebral infarction affect and how does it present?

A

only part of the anterior circulation has been compromised.

Two of the following need to be present for a diagnosis of a PACI:

  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder) - this alone is enough for diagnosis
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19
Q

Where does a posterior cerebral infarction affect and how does it present?

A

involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).

One of the following need to be present for a diagnosis of a POCI:
- Cranial nerve palsy and a contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
- Isolated homonymous hemianopia

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20
Q

Where does a lacunar stroke affect and how does it present?

A

subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).

One of the following needs to be present for a diagnosis of a LACS:

  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
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21
Q

What % of strokes are ischaemic?

A

87%

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22
Q

What sudden focal neurological symptoms would be seen in stroke?

A

Unilateral weakness or paralysis in the face, arm, or leg
Unilateral sensory loss
Dysarthria or expressive or receptive dysphasia
Vision problems (e.g., hemianopia)
Headache (sudden severe and unusual headache)
Difficulty with coordination and gait
Vertigo or loss of balance

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23
Q

What are the risk factors for ischaemic stroke?

A

Age ≥55 years
Hx of TIA or ischaemic stroke
family hx of stroke at a young age
Hypertension
Smoking
Diabetes mellitus
Atrial fibrillation
Comorbid cardiac conditions
Carotid artery stenosis
Sickle cell disease
Dyslipidaemia

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24
Q

What should be the first investigation done for stroke?

A

Non-contrast CT head

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25
Q

What are the differentials for ischaemic stroke?

A

Intracerebral haemorrhage
TIA
Hypertensive encephalopathy
Hypoglycaemia
Complicated migraine
Seizure and postictal deficits
Functional neurological disorder
Wernicke’s encephalopathy
Brain tumour
Sepsis
Ingestion of toxic substances

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26
Q

What is important in the management of stroke?

A

Early initiation of reperfusion strategies (intravenous thrombolysis or mechanical thrombectomy) within 4.5 hours from onset of symptoms, if not contraindicated (haemorrhage ruled out)

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27
Q

What meds should be given for ischaemic stroke?

A

thrombolysis with either alteplase or tenecteplase in patients with acute ischaemic stroke within 4.5 hours of known onset

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28
Q

Complications of ischaemic stroke

A

DVT
Haemorrhagic transformation

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29
Q

What is a traumatic brain injury?

A

an acquired disruption of the normal function or structure of the brain caused by a head impact or external force

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30
Q

What is the GCS for a mild, moderate and severe TBI?

A

Mild TBI: GCS 13-15; mortality 0.1%
Moderate TBI: GCS 9-12; mortality 10%
Severe TBI: GCS <9; mortality 40%.

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31
Q

What is a blunt TBI and when could this occur?

A

occurs when external mechanical force leads to rapid acceleration or deceleration with brain impact.

motor vehicle-related injury, falls, crush injuries, or physical altercations.

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32
Q

What is a penetrating TBI and what can cause this?

A

occurs when an object pierces the skull and breaches the dura mater

seen commonly in gunshot and stab wounds

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33
Q

When and why would a blast TBI occur?

A

commonly occurs after bombings and warfare, due to a combination of contact and inertial forces, overpressure, and acoustic waves

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34
Q

What does a focal TBI include?

A

Specific lesions such as contusions, intracranial haematomas, infarctions, axonal tears, cranial nerve avulsions, and skull fractures

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35
Q

What does a diffuse TBI include?

A

diffuse axonal injury (DAI), hypoxic brain injury, diffuse cerebral oedema, or diffuse vascular injury

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36
Q

Difference between primary and secondary injury in TBI

A

Primary: due to the immediate mechanical force
Secondary: evolving pathophysiological consequences of the primary injury

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37
Q

What are the components of the GCS?

A

Eye opening
Verbal response
Best motor response

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38
Q

What is happening in Parkinsons?

basic

A

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

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39
Q

What are the 3 cardinal symptoms in parkinsons?

A

Resting tremor
Rigidity
Bradykinesia

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40
Q

What is the definition of parkinsons?

A

a chronic progressive neurological disorder characterised by the presence of bradykinesia with at least one of rest tremor or rigidity

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41
Q

What is tremor like in parkinsons?

A

worse on one side and has a 4-6 hertz frequency, meaning it cycles 4-6 times per second

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42
Q

How does rigidity show in parkinsons?

A

resistance to the passive movement of a joint

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43
Q

How can bradykinesia present in parkinsons?

A

Smaller and slower movements
micrographia (smaller handwriting)
small frequent steps (avoid falling)
difficulty initiating movements and turning around
hypomimia (reduced facial movements)

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44
Q

What are the differentials for parkinsons?

A

Essential tremor
Progressive supranuclear palsy
Dementia with Lewy bodies
Corticobasal degeneration
Alzheimer’s disease with parkinsonism
Drug-induced parkinsonism
Metabolic abnormalities

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45
Q

What are the pharmaceutical management options for parkinsons?

A

Levodopa
Dopamine agonist
MAO-B inhibitor

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46
Q

What non-pharmaceutical management options are available for Parkinson’s?

A

Physio
OT
Speech therapy

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47
Q

What are the complications of parkinsons?

A

levodopa-induced dyskinesias
motor fluctuations
dementia
constipation
bladder dysfunction
orthostatic hypotension
sleep disorders
dysphagia
psychosis
depression
anxiety

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48
Q

What is the prognosis for parkinsons?

A

Progressive
treatment is symptomatic not curative

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49
Q

What symptoms would be present if the anterior cerebral artery was affected in an ischaemic stroke?

medial and superior frontal + parietal lobes, corpus callosum, basal gan

A

Contralateral weakness (leg mostly, due to motor homonculus)
Contralateral sensory deficitis
Loss of willpower
Speech disturbance (aphasia)
Urinary incontinence
Ipsilateral ataxia + contralateral leg weakness

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50
Q

Signs and symptoms expected of an ischaemic stroke affecting the superior MCA

lateral frontal and superior parietal lobes

A

Contralateral weakness of upper limbs and face (only lower 1/3 of face affected)
Contralateral sensory loss
Aphasia if on left side

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51
Q

Signs and symptoms of an ischaemic stroke affecting the inferior MCA

lateral temporal lobe

A

Contralateral homonymous hemianopia
Contralateral upper quadrantanopia
Wernicke’s aphasia

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52
Q

What is Gerstmann syndrome and what 4 symptoms are associated with it?

A

Parietal lobe of dominant (left) side of brain around angular gyrus affected by disease (e.g. stroke)

acalculia, agraphia, finger agnosia, left-right disorientation

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53
Q

When does ataxic hemiparesis occur?

A

Damage to posterior limb of internal capsule or basis pontis of pons
MCA arteries involved, e.g. penetrating from basilar

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54
Q

What are the symptoms of ataxic hemiparesis?

A

Contralateral upper and lower limb weakness (more prominent in leg)
Ataxia in limbs
No facial involvment

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55
Q

Where would be affected if an ischaemic stroke was in the PCA?

A

Occipital, inferior temporal, thalamus and midbrain

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56
Q

What is going wrong in parkinsons?

A

Gradual degeneration of neurones within the substantia nigra pars compacta
Less dopamine released to the striatum so less stimulation of direct pathway

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57
Q

What is amaurosis fugax?

A

a sudden, short-term, painless loss of vision in one eye

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58
Q

What can a TIA with amaurosis fugax be a warning sign for?

A

Can be clinical evidence of internal carotid artery stenosis and a warning sign of possible ICA stroke

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59
Q

What are the 2 subtypes of haemorrhagic stroke?

A

Intracerebral haemorrhage
Subarachnoid haemorrhage

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60
Q

What are the 4 types of intracranial haemorrhage?

A

Intracerebral
Subarachnoid
Subdural
Extradural

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61
Q

What is a subarachnoid haemorrhage?

A

a type of stroke caused by bleeding outside of the brain tissue, between the pia mater and arachnoid mater
bleeds into subarachnoid space where the CSF is

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62
Q

What is an intracerebral haemorrhage?

A

Bleeding within the brain secondary to a ruptured blood vessel.
Intracerebral haemorrhages can be intraparenchymal (within the brain tissue) and/or intraventricular (within the ventricles)

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63
Q

How does a subarachnoid haemorrhage typically present?

A

a sudden, severe headache (thunderclap headache) that lasts more than an hour

typically alongside vomiting, photophobia, and non-focal neurological signs

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64
Q

Strong risk factors for all types of haemorrhagic stroke

A

HTN
family hx

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65
Q

Risk factors for subarachnoid haemorrhagic stroke

A

HTN
Family hx
Smoking
ADPKD

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66
Q

Risk factors for intracerebral haemorrhagic stroke

A

HTN
older age
male sex
Asian, black and/or Latino/Hispanic
heavy alcohol use / drug (cocaine, amphetamines) use
family hx of intracerebral haemorrhage
haemophilia, sickle cell
cerebral amyloid angiopathy
genetic mutations
anticoagulation
vascular malformations
pregnancy

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67
Q

How can hypertension cause intracerebral haemorrhage?

A

can lead to haemorrhage via arteriosclerosis or rupture of microaneurysms (Charcot-Bouchard aneurysms)

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68
Q

How does cerebral amyloid angiopathy cause intracerebral haemorrhage?

A

deposition of amyloid beta peptide in vessels leads to a weaker vessel structure so bleeding is easier

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69
Q

What can cause an intracerebral haemorrhagic stroke?

A

HTN
Cerebral amyloid angiopathy
Arteriovenous malformations
Cavernomas
Coagulopathies
Anticoagulants/thrombolysis

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70
Q

What can cause a subarachnoid haemorrhage?

A

Rupture of cerebral aneurysm, e.g. saccular (berry) aneurysm
Rupture of an arteriovenous malformation

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71
Q

Where are common sites for saccular (berry) aneurysms to form?

A

Junction of the anterior communicating artery with the anterior cerebral artery.
Junction of the posterior communicating artery with the internal carotid artery.
Bifurcation of the middle cerebral artery.

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72
Q

What proportion of strokes are haemorrhagic and how does the prognosis compare to ischaemic?

A

Haemorrhagic stroke accounts for about 10% of strokes, but is responsible for more deaths and disability-adjusted life-years lost than ischaemic stroke

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73
Q

Epidemiology of intracerebral haemorrhagic stroke

A

Increases with age
more common in men (difference less relevant as you get older)
black/Asian/Hispanic people

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74
Q

Epidemiology of subarachnoid haemorrhage

A

Increases with age (av 50-55yr)
more common in women
black and Hispanic people

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75
Q

Can an ischaemic stroke become haemorrhagic?

A

Yes
This is a haemorrhagic transformation as infarcted tissue is more prone to bleeding

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76
Q

What are the different locations for intracerebral haemorrhages?

A

Lobar intracerebral haemorrhage
Deep intracerebral haemorrhage
Intraventricular haemorrhage
Basal ganglia haemorrhage
Cerebellar haemorrhage

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77
Q

What are the symptoms of an intracerebral haemorrhage?

A

unilateral weakness or paralysis in the face, arm, or leg
sensory loss
dysphasia
dysarthria
visual disturbance
photophobia
headache
ataxia

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78
Q

What are the symptoms of a subarachnoid haemorrhage?

A

Thunderclap headache
Neck stiffness
Photophobia
Decreased consciousness
Focal neurological deficits
Diplopia

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79
Q

What would be seen on a CT head in an IC haemorrhagic stroke?

A

hyperattenuation (brightness), suggesting acute blood
often with surrounding hypoattenuation (darkness) due to oedema

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80
Q

What would a CT show in a SAH stroke?

A

hyperdense areas in the subarachnoid space/basal cisterns

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81
Q

What would a CT for an ischaemic stroke show?

A
  • hypoattenuation (darkness) of the brain parenchyma
  • loss of grey matter-white matter differentiation, and sulcal effacement
  • hyperattenuation (brightness) in an artery indicates clot
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82
Q

Differentials of SAH

A

Arterial dissection
Vasculitis
Saccular aneurysms of spinal arteries
Cocaine abuse
Anticoagulant-associated intracranial haemorrhage

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83
Q

Differentials of an ICH stroke

A

Ischaemic stroke
Hypertensive encephalopathy
Hypoglycaemia
Complicated migraine
Seizure disorder
Functional neurological disorders

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84
Q

In the management of ICH stroke, what BP are you aiming for?

A

130 to 140 mmHg within 1 hour of starting treatment

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85
Q

Management for ICH

A

Arrange immediate neurosurgical review
Consider rapidly lowering BP: 130 to 140 mmHg within 1 hour of starting treatment
Reverse any anti-coagulations

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86
Q

When would you offer rapid lowering of BP to ICH patients?

A

Within 6 hours of symptom onset
Not going to have surgery for haematoma
No underlying structural cause

BP of 150-220mmhg observed

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87
Q

What are patients with SAH at risk of?

A

haemodynamic instability
neurological deterioration

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88
Q

Management of an SAH

A

ABC approach
Stop and reverse anticoagulations
Neurosurgeon to consider giving nimodipine

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89
Q

Complications of ICH

A

Infection
DVT/PE
Delirium
Seizures

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90
Q

What are some complications of SAH?

A

Neuropsychiatric complications, e.g. mood and memory disorders
Chronic hydrocephalus

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91
Q

What underlying conditions can predispose a patient to stroke?

A
  • Hypertension
  • Hypercholesterolaemia
  • Type 1 and type 2 diabetes
  • Atrial fibrillation
  • TIA
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92
Q

What are some poor prognostic factors in ICH?

A

Advanced age
impaired consciousness at presentation
rupture of the haematoma into the ventricular system

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93
Q

Which artery is involved in 75% of extradural haematomas? + where is it particulary vulnerable?

A

Middle meningeal artery at the pterion

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94
Q

What is an extradural haematoma?

A

an acute haemorrhage between the dura mater and the inner surface of the skull

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95
Q

What happens in an extradural haematoma?

A

Artery bleeds into space between skull and external layer of dura mater (can’t cross suture lines)
This can cause compression of local brain structures, a midline shift and a rise in intracranial pressure, leading to tentorial herniation
Herniation can affect the brainstem

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96
Q

What is the standard presentation of an extradural haematoma?

A

Lucid interval: brief duration of unconsciousness followed by improvement then a rapid decline

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97
Q

What normally causes an extradural haematoma?

A

Head trauma

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98
Q

How does an extradural haematoma appear on a CT?

A

Biconvex dense lemon shape (doesn’t cross sutures)

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99
Q

What is cushing’s reflex?

A

a physiological response to raised ICP to attempt to improve perfusion

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100
Q

What is seen in cushing’s triad?

raised ICP

A

HTN (widened pulse pressure)
bradycardia
irregular breathing pattern

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101
Q

What are the signs and symptoms of an EDH?

A

Reduced GCS
Ipsilateral dilated pupil
Contralateral hemiparesis
Hyperreflexia
Cushing’s triad

Progressing to: bilateral fixed and dilated pupils, tetraplegia, respiratory arrest

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102
Q

How is an EDH managed?

A

Neurosurgery
Burr-holes to evacuate blood

Anti-coagulation, antibiotics to avoid infection, mannitol to decrease ICP

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103
Q

What are some possible complications of an EDH?

A

Infection: due to skull fracture or as a result of operative intervention
Cerebral ischaemia: typically occurs adjacent to the haematoma
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus due to obstruction of the ventricles
Brainstem injury: due to significantly raised ICP

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104
Q

What are some poor prognostic features of an EDH?

A

Low GCS at presentation
No history of a lucid interval
Pupil abnormalities
Decerebrate rigidity
Pre-existing brain injury

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105
Q

What is a subdural haematoma?

A

a collection of blood between the dura mater and arachnoid mater of the brain

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106
Q

What are the different timescales of a subdural haematoma?

A

acute (< 3 days)
subacute (3-21 days)
chronic (>21 days)

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107
Q

What % of intracranial haematomas are made up by SDH and when do they usually occur?

A

SDHs account for 50% to 60% of acute traumatic intracranial haematomas
more likely to occur after falls or assaults than after motor vehicle accidents

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108
Q

Who do chronic SDHs tend to affect?

A

Older (65+) people typically post fall

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109
Q

What causes subdural haematomas?

A

Trauma, e.g. fall, assault
Less common: rupture or aneurysm or AV malformation

caused by a rupture of the bridging veins in the outermost meningeal layer

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110
Q

What is the pathophysiology of a subdural haematoma?

A

Force causes disruption of bridging cortical veins emptying into the dural venous sinuses
Blood pools into subdural space and creates a haematoma.
Damaged veins are under low pressure so bleeding is slow and symptoms can develop slowly

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111
Q

How does acute SDH typically manifest?

A

acute neurological decline including alteration in consciousness, contralateral weakness, and signs of brainstem herniation

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112
Q

How does chronic SDH typically present?

A

range from acute neurological deficit to slow cognitive decline.

Because of brain atrophy over time, older patients with chronic SDH are often less symptomatic than younger patients, who are more susceptible to the mass effect from an intracranial haematoma

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113
Q

In SDH why are older patients typically less symptomatic?

A

Brain atrophy over time with aging makes the symptoms less obvious than that of a younger person

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114
Q

What are the risk factors for a subdural haematoma?

A

recent trauma
coagulopathy and anticoagulant use
advanced age (>65 years)

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115
Q

How does a subdural haematoma appear on a CT?

A

crescent shape
not limited by the cranial sutures

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116
Q

What are the signs and symptoms of a subdural haematoma?

A

Headache
Nausea/vomiting
Reduced GCS
Confusion
localised weakness
sensory changes
cognition changes
speech or vision changes
Seizure

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117
Q

What investigation should be done in the case of suspected haemorrhage?

A

non-contrast CT head

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118
Q

Basic management of a subdural haematoma

A

Surgical evacuation
Management of raised ICP
Correction of coagulopathy

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119
Q

How can some haemorrhagic bleeds be prevented in the brain?

A

Seat belts and helmets should be used when applicable
Coagulation profiles should be routinely monitored by physicians prescribing anticoagulants

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120
Q

What are the consequences of SDH?

A

neurological deficits
coma
stroke
surgical-site infection
epilepsy
recurrence of SDH post-operatively

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121
Q

What is bacterial meningitis?

A

a serious inflammation of the meninges caused by various bacteria

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122
Q

What are the risk factors for bacterial meningitis?

A

advanced age
crowding
exposure to pathogens
immunocompromising conditions
cranial anatomical defects/ventriculoperitoneal shunt
cochlear implants
sickle cell disease

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123
Q

Who is most at risk of acquiring bacterial meningitis?

A

infants
teenagers and young adults

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124
Q

In bacterial meningitis how do pathogens reach the meninges?

A

directly from ears, nasopharynx, cranial injury or congenital meningeal defect
by spread in the bloodstream

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125
Q

What are some non-infective causes of menigitis?

A

paraneoplastic
intrathecal drugs
autoimmune (e.g. SLE)

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126
Q

Which bacteria are the most common causes of meningitis?

A

Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae type b

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127
Q

What is the pathophysiology of bacterial meningitis?

A

Bacteria reach the meninges directly or through blood
Multiply quickly in the sub arachnoid space and trigger inflammatory mediators in the CSF
Inflammatory cascade leads to raised ICP and cerebral oedema, damaging brain

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128
Q

What bacteria causes pneumococcal meningitis?

A

Streptococcus pneumoniae

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129
Q

What bacteria causes meningococcal meningitis?

A

Neisseria meningitidis

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130
Q

What triad of symptoms makes up the meningitic sundrome?

A

Headache
Neck stiffness
Fever

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131
Q

Which meningitis would present with a petechial non-blanching rash?

A

Meningococcal

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132
Q

Clinical features of meningococcal meningitis

A

Petechial, non-blanching rash
Fever
Headache
Neck stiffness

vomiting and photophobia may also be present

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133
Q

General symptoms of meningitis

A

Headache
Neck stiffness
Fever
Petechial rash (meningococcal septicaemia)
Photophobia
Vomiting

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134
Q

How is meningococcal meningitis spread?

A

Meningococci colonise the human nasopharynx by adhering to non-ciliated columnar epithelial cells.
Transmission occurs by inhalation of respiratory droplets or by direct contact with infected secretions

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135
Q

What signs may be present in meningitis?

uncommon but can be seen

A

Kernig’s sign: Severe stiffness of the hamstrings causing inability to straighten the leg when the hip is flexed to 90 degrees
Brudzinksi’s sign: Severe neck stiffness causing the patient’s hips and knees to flex when the neck is flexed

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136
Q

What investigations would be carried out for meningitis?

A

Lumbar puncture within an hour of arriving
Blood culture
Blood glucose
Blood gases + lactate
FBC: leukocytosis

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136
Q

What is the gold standard investigation for meningitis?

A

CSF culture through lumbar puncture

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137
Q

Differentials for bacterial meningitis

A

Encephalitis
Viral meningitis
Drug-induced meningitis
Tuberculous meningitis
Fungal meningitis

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138
Q

What are examples of primary headaches?

A

Cluster
Tension
Migraine

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139
Q

What are some secondary causes of headaches?

A

Meningitis
Subarachnoid Haemorrhage
Idiopathic intracanial HTN
Medication overuse

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140
Q

What are primary headaches?

A

no identified pathology, such as migraine or tension-type headache

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141
Q

What are secondary headaches?

A

secondary to organic pathology

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142
Q

What does a headache with fever, photophobia or neck stiffness suggest?

red flags

A

meningitis, encephalitis or brain abscess

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143
Q

What does a headache with visual disturbances suggest?

A

giant cell arteritis, glaucoma or tumours

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144
Q

What does a headache that’s worse on coughing or straining and postural suggest?

A

raised ICP

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145
Q

What does a headache with a history of trauma suggest?

A

intracranial haemorrhage

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146
Q

What are some red flags of headache?

A
  • New severe or unexpected headache
  • Progressive or persistent headache
  • Headache that has changed dramatically
  • Associated features: meningitis type symptoms, papilloedema, New-onset focal neurological deficit, atypical aura, vomiting, dizziness
  • Contacts with similar symptoms
  • Precipitating factors
  • Comorbidities, e.g. immunocompromised
  • Pregnancy
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147
Q

What are some possible causes for secondary headache that should be urgent considerations?

A

Meningitis
Haematoma
SAH
HTN encephalopathy
Pre-eclampsia/eclampsia
Raised ICP

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148
Q

Features of a tension headache

A

non-disabling
bilateral
NO photophobia, phonophobia or nausea
typically described as tight band around head

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149
Q

What are the symptoms of a tension headache?

A

Bilateral, non-throbbing head pain
Head pressure
Generalised constricting head pain

nearby muscle pain

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150
Q

What are some possible features in a patient hx for a tension headache?

A

stress
missed meals
lack of sleep
fatigue
depression
previous tension headache

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151
Q

How common is a tension headache?

A

most prevalent form of primary headache in the general population
most prevalent neurological disorder worldwide
slightly more common in females
peaks ages 20-40

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152
Q

What are the differential diagnoses for tension type headaches?

A

Chronic migraine
Medicine overuse headache
Sphenoid sinusitis
Giant cell arteritis
Temporomandibular disorder (TMD)
Chronic subdural haematoma
Tumour

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153
Q

What are the risk factors for tension type headaches?

A

mental tension
stress
missing meals
fatigue
lack of sleep

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154
Q

How are tension type headaches usually managed?

A

self-treated with simple analgesics like paracetamol or nsaids

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155
Q

What are the trigeminal autonomic cephalalgias?

A

A group of primary headache disorders characterised by unilateral trigeminal distribution pain (usually in the opthalmic division)

most common form is a cluster headache

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156
Q

Epidemiology of cluster headache

A

most common trigeminal autonomic cephalalgia
more common in men
between ages 20-40

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157
Q

What are the key features of cluster headaches?

A

unilateral headache attacks lasting 15-180 mins
excruciating retro-orbital pain
patient restless and unable to lie still
repeated attacks

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158
Q

What are the risk factors for cluster headaches?

A

family history
male sex
head injury
heavy smoking
heavy drinking

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159
Q

What are the symptoms of a cluster headache?

A

Excruciating unilateral pain: sharp, piercing, burning, or pulsating, normally around eye/temples
Agitation/ restlessness
One autonomic feature: lacrimation, rhinorrhoea, partial horner’s

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160
Q

What are the differentials for cluster headaches?

A

Migraine
Paroxysmal hemicrania
Trigeminal neuralgia
Subarachnoid haemorrhage
Giant cell arteritis

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161
Q

What medication can be given to manage an acute cluster headache?

A

Triptans:
- subcut sumatriptan
- intranasal zolmitriptan

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162
Q

What are the main features of a migraine?

A

Unilateral but can become bilateral
Throbbing, moderate to severe pain
Motion sensitivity
Photophobia/phonophobia
Can have nausea/vomiting
Attacks last hours to days

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163
Q

What are the key features in a patient hx that may suggest migraine?

A

nausea
photophobia
reduced ability to function
headache
may have aura

164
Q

What is a migraine aura?

A

a complex of reversible visual, sensory, or speech symptoms, which precedes or occurs during headache

165
Q

What is the epidemiology of migraines?

A

migraine affects around 1 in 6 people
females more affected than males
most common between teenagers-adults (18-40ish)

166
Q

How long do migraines typically last?

A

4-72 hours

167
Q

What are the risk factors for migraines?

A

family history of migraine
female sex
obesity
stressful life events
medication overuse
sleep disorders

168
Q

What are the symptoms of a migraine?

A

Prolonged headache
Nausea
Sensitivity to light
Worse with movement
Unilateral, throbbing pain

169
Q

What are the differentials for a migraine?

A

Other forms of headache
SAH
CNS infection
Giant cell arteritis
Ischaemic stroke

170
Q

What are the management options for migraines?

A

Mild to moderate: analgesics, e.g. paracetamol or NSAIDs
Severe: triptans
Can also acutely give anti-emetics

171
Q

What can trigger migraines?

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

172
Q

What is the mechanism of action for triptans?

used for migraines and cluster headaches

A

Cranial vasoconstriction
Inhibiting the transmission of pain signals
Inhibiting the release of inflammatory neuropeptides

173
Q

What class of drug are triptans?

A

5-HT receptor agonists
(they bind to and stimulate serotonin receptors)

174
Q

What medications can be used in the prophylaxis of migraines?

A

Propranolol (a non-selective beta blocker)
Amitriptyline (a tricyclic antidepressant)
Topiramate (teratogenic and very effective contraception is needed)

175
Q

What is a classic hx of a patient with trigeminal neuralgia?

A

unilateral paroxysms of facial pain lasting seconds to minutes in a distribution along ≥1 divisions of the trigeminal nerve

176
Q

Epidemiology of trigeminal neuralgia

A

more common in females
increases with age, mean age of onset is 50s

177
Q

Features + symptoms of trigeminal neuralgia

A

Unilateral
Intense pain following distribution of trigeminal nerve
Attacks triggered by facial or oral mechanical stimulation
Last seconds to minutes

178
Q

What are the risk factors for trigeminal neuralgia?

A

increased age
multiple sclerosis
female
hypertension

179
Q

What are the differentials of trigeminal neuralgia?

A

Mandibular osteomyelitis
TMJ syndrome
Migraine
Glossopharyngeal neuralgia
Post-herpetic neuralgia
Giant cell arteritis
Atypical facial pain
Trigeminal autonomic cephalalgias

180
Q

What’s the management for trigeminal neuralgia?

A

anti-convulsants: carbamazepine
microvascular decompression

181
Q

What is meningoccocal meningitis?

A

bacteria infects the meninges and the cerebrospinal fluid

Neisseria meningitidis

182
Q

What is meningococcal septicaemia?

A

neisseria meningitidis bacterial infection is in the bloodstream
produces the non-blanching rash

183
Q

What is the management for bacterial meningitis?

A

IM benzylpenicillin (1200mg for age 10+) immediately if suspected
Intravenous cefotaxime or ceftriaxone (3rd gen cephalopsorins)

Assess GCS on arrival, monitor for sepsis

Ideally, blood cultures and a lumbar puncture should be performed before starting antibiotics. However, antibiotics should not be delayed if the patient is acutely unwell.

184
Q

What are some complications of meningitis?

A

Shock
Raised ICP
Sepsis
Seizures
Coagulopathy in meningococcal (DIC)
Subdural effusion

185
Q

Apart from IV ceftriaxone/ cefotaxime, what else can be given for pneumococcal meningitis?

A

intravenous dexamethasone for 4 days

186
Q

What is given to close contacts of meningitis for prophylaxis?

A

Ciprofloxacin or Rifampicin

187
Q

How can meningitis be prevented?

A

Vaccinations, e.g. Men B or N. meningitidis A, C, Y, and W-135

Prophylaxis in close contacts: antibiotics ciprofloxacin or Rifampicin

188
Q

What can cause viral meningitis?

A

coxsackievirus
echovirus
herpes simplex
mumps
influenza
HIV

(enteroviruses)

189
Q

How is viral meningitis managed?

A

Treat as bacterial until confirmed as viral
Viral is almost always benign
No specific treatment: analgesics, fluids, anti-emetics

190
Q

What is the pathological difference between meningitis and encephalitis?

A

encephalitis is the result of direct inflammation of the brain tissue, as opposed to the inflammation of the meninges

191
Q

What is encephalitis?

A

inflammation of the brain parenchyma associated with neurological dysfunction

192
Q

What ages tend to be most affected by encephalitis?

A

bimodal age distribution
highest incidence in those under one year and over 65 years

193
Q

What causes encephalitis?

A

Normally a virus: herpes simplex, varicella zoster or an enterovirus
Tropical: west nile, tick-borne, rabies
Autoimmune: paraneoplastic

194
Q

What is the pathology of viral encephalitis?

A

Virus enters and replicates in regional tissue, e.g. GI tract, UG or resp system
Virus travels to CNS through the blood or through retrograde axonal transport (e.g. herpes/rabies)
Infection and inflammation of brain tissue occurs

195
Q

What are some risk factors for encephalitis?

A

age <1 or >65 years
immunodeficiency
post-infection
blood/body fluid exposure (HIV or West-nile)
organ transplantation from infected donors
animal or insect bites

196
Q

What are the main differentials for transient loss of consciousness?

A

Epilepsy
Syncope
Functional neurological disorders

197
Q

What is a seizure?

A

transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

198
Q

What is epilepsy?

A

a neurological disorder in which a person experiences recurring seizures

199
Q

How does the ILAE define epilepsy?

A

any of:
- At least two unprovoked (or reflex) seizures occurring more than 24 hours apart
- One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
- Diagnosis of an epilepsy syndrome.

200
Q

What is ataxia?

A

a neurological syndrome characterised by clumsy and unco-ordinated movement of the limbs, trunk, and cranial muscles

201
Q

Where does ataxia come from?

A

results from pathology in the cerebellum and its connections, or in the proprioceptive sensory pathways

202
Q

What are some syptoms of cerebellar dysfunction?

A

dizzy - unsteady, wobbly, clumsy
falls, stumbles
difficulty focusing, double vision
slurred speech
problems with swallowing
tremor
problems with dextrity/ fine motor skills

203
Q

What are some clinical signs of cerebellar dysfunction?

A

nystagmus
dysarthria
intention tremor / myoclonus
dysmetria / past pointing / dysdiadochokinaesia
heel - shin ataxia
gait / limb / truncal ataxia

204
Q

What are some causes of ataxia?

A

Genetic: friedrich’s ataxia (AR), fragile X
Metabolic: alcohol, drugs, vitamin deficiencies
Immune mediated: paraneoplastic cerebellar degeneration, gluten related
Post infectious
Creutzfeldt-Jakob disease

205
Q

What are the different ratings of ataxia?

A

mild: mobilising independently or with one walking aid
moderate: mobilising with 2 walking aids or walking frame
severe: predominantly wheelchair dependent

206
Q

What happens to the motor neurones in MND?

A

degenerative condition that affects motor neurons, especially the anterior horn cells of the spinal cord and the motor cranial nuclei.
It causes LMN and UMN dysfunction, leading to a mixed UMN/LMN picture of muscular paralysis, (LMN signs usually predominant)

207
Q

What’s the epidemiology of MND?

A

peak incidence between 60 and 75 years
affects men more than women
approx. 5-10% of cases are familial

208
Q

What is motor neuron disease?

A

neurodegenerative condition that affects the motor neurones in brain and spinal cord, leading to progressive paralysis and eventual death

209
Q

What are some signs of lower motor neuron disease?

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

210
Q

What are some signs of upper motor neurone disease?

A

Increased tone or spasticity
Hyperreflexia
Abnormal reflexes: babinski

211
Q

What are the risk factors for MND?

A

Male sex, increasing age and hereditary disposition

212
Q

What are the different ways that MND can present?

A

Limb onset (75%)
Bulbar onset (20%)
Respiratory onset (5%)

213
Q

What are some limb symptoms of MND?

A

upper extremity weakness
stiffness, with poor co-ordination and balance
painful muscle spasms
difficulties in arising from chairs and climbing stairs
Head drop
Muscle atrophy
Hyperreflexia

214
Q

What are some bulbar symptoms of MND?

A
  • dyspnoea
  • coughing and choking on liquids (including secretions) and eventually on food
  • strained, slow speech
  • slurred, nasal, and, at times, dysphonic speech
  • hypophonic speech

inappropriate bursts of laughing and crying

215
Q

What are the cerebellar signs of dysfunction?

A

D- dysdiadochokinesia (can’t supinate/pronate) and dysmetria
A- ataxia
N- nystagmus
I - intention tremor
S - speech (slurred/inappropriate/slow)
H - hypotonia

216
Q

How does UMN dysfunction typically manifest?

A

weakness predominating in the arm extensors and leg flexors with evidence of hypertonia, hyperreflexia and upgoing plantar responses
the bulbar muscles may also show spasticity with an exaggerated jaw jerk

217
Q

How does LMN dysfunction typically manifest?

A

weakness, atrophy, fasciculations and hyporeflexia in the limbs

218
Q

What criteria is needed for a clinical diagnosis of MND?

A

Evidence of LMN and UMN degeneration
Progressive spread of symptoms and signs
Absence of other disease processes

219
Q

What is the management of MND?

A

There are no effective treatments for halting or reversing the progression of the disease.
Riluzole can slow the progression of the disease and extend survival by several months in ALS

care is supportive as MND incurable

220
Q

What should be monitored in MND?

A

Monitoring for resp decline and nutritional deficit
In patients taking riluzole: monitoring for hepatotoxicity (LFTs) and neutropenia (FBCs) should be done every month in the first 3 months and every 3 months afterwards

221
Q

What are some possible complications of MND?

A

Respiratory failure
Nutritional deficit
Aspiration pneumonia
Riluzole related hepatotoxicity or neutropenia

222
Q

What are the poor prognostic factors for MND at diagnosis?

A

Speech and swallowing problems (bulbar presentation).
Weight loss.
Poor respiratory function.
Older age.
Lower ALS Functional Rating Scale (ALSFRS or ALSFRS-R) score.
Shorter time from first developing symptoms to time of diagnosis.

223
Q

What is the most common form of MND?

A

amyotrophic lateral sclerosis

224
Q

What is amyotrophic lateral sclerosis?

A

a progressive disease characterised by degeneration of motor neurons with cortical, brainstem, and ventral cord locations

involves both LMN and UMN degeneration

Most common form of MND

225
Q

What typically causes amaurosis fugax?

A

result of stenosis or occlusion of the internal carotid artery or the central retinal artery, leading to hypoperfusion of the retina

226
Q

What are the risk factors for amaurosis fugax?

A

diabetes
smoking
cocaine use
htn
hyperlipidaemia

227
Q

What are the main symptoms of encephalitis?

A

Fever
Change in consciousness
Altered mental state
Seizures
Headache (meningism)
Movement disorders
Sensitivity to light (meningism)
Sensitivity to sound
Neck stiffness (meningism)

228
Q

What are the first line investigations for encephalitis?

A

Lumbar puncture: CSF analysis, culture, serology, CSF PCR
MRI: areas of inflammation and swelling
FBC: elevated WBC
Blood cultures
Throat swab

229
Q

What are the differentials for encephalitis?

A

Viral meningitis
Encephalopathy (toxic/metabolic)
Status epilepticus
Central nervous system vasculitis
Malignant htn
Ischaemic stroke
Intracranial bleed
Intracranial tumour

230
Q

What should be given as soon as encephalitis is suspected?

A

Antivirals: IV aciclovir

231
Q

What antiviral should be given for HSV or VZV encephalitis?

A

IV aciclovir (10mg/kg 3x a day for 14-21 days)

232
Q

What antiviral should be given for encephalitis caused by human herpes 6 or herpes B virus?

A

ganciclovir

HH6 can have aciclovir

233
Q

What are the complications of encephalitis?

A

death
hypothalamic and autonomic dysfunction
ischaemic stroke
encephalitis lethargica (Von Economo’s disease)
neurological sequelae
seizures
sleep disorders

234
Q

What are focal to bilateral seizures?

A

begin on one hemisphere but then involve both sides

234
Q

What is a tonic seizure like?

A

bilaterally increased tone of the limbs typically lasting 3 seconds to 2 minutes

235
Q

What is a clonic seizure?

A

bilateral sustained rhythmic jerking
loss of consciousness

236
Q

What is an atonic seizure?

A

sudden loss or diminution of muscle tone

very brief duration and remains awake
may involve the head, trunk or limbs

237
Q

What is a myoclonic seizure?

A

a single or series of jerks (brief muscle contractions)

238
Q

What is multiple sclerosis?

A

a demyelinating central nervous system condition clinically defined by two episodes of neurological dysfunction that are separated in space and time

239
Q

What are the 4 different phenotypes of MS?

A
  1. Clinically isolated syndrome: first episode of demyelination and neurological signs and symptoms
  2. Relapsing remitting: episodes of disease and neurological symptoms followed by recovery
  3. Primary progressive: progressive accumulation of disability from onset
  4. Secondary progressive: progressive accumulation of disability after an initial relapsing course
240
Q

What is the suspected aetiology of MS?

A

Genetic susceptibility + environmental trigger
- E-BV
- Low vitamin D
- Toxins, e.g. smoking

241
Q

What’s the epidemiology of MS?

A

most commonly diagnosed in people between 20 and 40 years old
female to male ratio of around 3:1
A geographic gradient, with higher incidence at latitudes closer to the poles

242
Q

What’s the basic pathophysiology of MS?

A

Demyelination and plaques in the CNS as a result of focal inflammation.
Myelin is lost and signalling is impaired.
Periods of remyelination, where some of the myelin sheath is restored.
More incomplete remyelination leads to scar tissue and plaques forming and further impairment

thought to be immune mediated oligodendrocyte destruction

243
Q

What is optic neuritis?

A

most common presentation of MS
demyelination of the optic nerve and presents with unilateral reduced vision
develops over hours - days

244
Q

How may MS present?

symptoms

A

Motor deficits:
- Weakness, spasticity, tremors, cerebellar ataxia
Sensory disturbances:
- Paraesthesia, loss of sensation, neuropathy
Bulbar dysfunction:
- Dysphagia, dysarthria, dysphasia
Vision changes + optic neuritis:
- Central monocular loss, diplopia, pain on ocular movement
- Cognitive impairment
- Depression/ anxiety
- Urinary urgency, incontinence, retention

optic neuritis big presentation

245
Q

What signs/ phenomena are present in MS?

A

Uhthoff phenomenon: deterioration in symptoms when exposed to high temperatures
Lhermitte’s sign: sensation of electrical shock running down back when neck is flexed

246
Q

What investigations should be run for MS and what would they show?

A

MRI of brain and spinal cord: demyelinating lesions
CSF lumbar puncture: oligoclonal bands and elevated CSF IgG
Vitamin B12 and TSH normal to rule out other diagnoses

247
Q

What are the possible differentials of MS?

A

Vitamin B12 deficiency + peripheral neuropathy
SLE
ALS
POTS
Fibromyalgia
Myelopathy from cervical spondylosis

248
Q

What’s the basic management of MS?

A

management of acute worsening/relapses
- IV or oral methylprednisolone
disease-modifying therapy
- Immunomodulators
symptomatic management

249
Q

What are the possible complications of MS?

A

UTI
Osteopenia/osteoporosis
Erectile dysfunction
Depression
Visual impairment
Impairment mobility
Cognitive impairment

250
Q

What’s Huntington’s disease?

A

an autosomal dominant genetic condition that causes progressive neurological dysfunction, characterised by chorea, incoordination and cognitive changes

251
Q

Who does huntington’s tend to affect?

A

affects men and women equally
typical onset is 35 to 45 years of age
less common in African and Asian populations

252
Q

What causes Huntington’s?

A

caused by an expanded CAG repeat in the HTT gene on chromosome 4, which codes for the huntingtin (HTT) protein

253
Q

What are the risk factors for Huntington’s?

A

expansion of the CAG repeat length at the N-terminal end of the huntingtin gene
family hx

254
Q

What is anticipation as seen in Huntington’s?

A

Anticipation is a feature of trinucleotide repeat disorders, where successive generations have more repeats in the gene, resulting in:
- Earlier age of onset
- Increased severity of disease

255
Q

What are the non-movement symptoms of Huntington’s?

A

depression, obsessions, and compulsions
personality change
irritability and impulsivity
concentration impairment
changes in personal habits/hygiene
disinhibition or unusually anxious behaviour

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

256
Q

What movement disorder symptoms are associated with Huntington’s?

A
  • Chorea (involuntary, random, irregular body movements)
  • Dystonia (abnormal muscle tone and postures)
  • Rigidity (increased resistance to the passive movement of a joint)
  • Eye movement disorders
  • Dysarthria (speech difficulties)
  • Dysphagia (swallowing difficulties)
257
Q

How is Huntington’s diagnosed?

A

Clinical diagnosis
CAG repeat testing

258
Q

What are the management options for Huntington’s?

A

Genetic counselling
Multidisciplinary team (MDT) input to support and maintain their quality of life
Physiotherapy
Speech and language therapy
Tetrabenazine may be used for chorea symptoms
Antidepressants (e.g., SSRIs) for depression

no treatment to slow or stop progression

259
Q

What’s the typical prognosis for Huntington’s?

A

duration of disease is approximately 10- 20 years from time of diagnosis to time of death
death often due to aspiration pneumonia or suicide

260
Q

What is Guillian barre?

A

an acute inflammatory polyneuropathy affecting PNS
divided into axonal and demyelinating forms

261
Q

What is going wrong in Guillain barre syndrome?

A

Molecular mimicry
B cells create antibodies against the antigens on the triggering pathogen.
These antibodies also match proteins on the peripheral neurones.
They may target proteins on the myelin sheath or the nerve axon itself

262
Q

What causes Guillain-barre syndrome?

A

immune-mediated attack on the myelin sheath or Schwann cells of sensory and motor nerves
frequently triggered by an antecedent infection

263
Q

What are the most common infectious triggers for Guillain-Barre?

A

C.jejuni
cytomegalovirus
EBV
Mycoplasma pneumoniae

Two-thirds of patients with GBS have had infections in the 6 weeks before symptom onset, most commonly upper respiratory tract infection or gastroenteritis

264
Q

What’s the classic presentation of Guillian-Barre syndrome?

A

progressive symmetrical muscle weakness affecting lower before upper extremities, and proximal muscles before distal muscles
paraesthesias in the feet and hands
typically flaccid with areflexia and progresses acutely over days

265
Q

What are some symptoms of Guillian barre?

A

Ascending muscle weakness
paraesthesia
back/leg pain
respiratory distress
speech problems
areflexia/hyporeflexia
facial weakness
bulbar dysfunction causing oropharyngeal weakness
dysautonomia

after trunk and limb involvement: diplopia, dysarthria, dysphagia

266
Q

What are the risk factors for guillain barre?

A

preceding viral illness or bacterial infection
hepatitis E infection

267
Q

What investigations should be done for Guillain Barre?

A

Nerve conduction studies (showing reduced signal through the nerves)
Lumbar puncture for cerebrospinal fluid (showing raised protein with a normal cell count and glucose)
Spirometry

268
Q

How is Guillain Barre syndrome managed?

A

Supportive care
VTE prophylaxis (PE is a leading cause of death)
IV immunoglobulins (IVIG) first-line
Plasmapheresis is an alternative to IVIG
Ventilation in cases of resp failure

269
Q

What is the course of Guillain Barre usually like?

A

continued disease progression for up to 2 weeks, followed by a plateau phase of 2 to 4 weeks, and then recovery of function

270
Q

What are some complications of Guillain Barre syndromes?

A

respiratory failure
bladder areflexia
adynamic ileus
paralysis
fatigue
immobilisation hypercalcaemia
deep vein thrombosis (DVT)
psychological problems

271
Q

What are the symptoms of raised intracranial pressure?

A

headache: starting when waking, worse on coughing or moving head
papilloedema
vomiting
altered mental state

Cushing’s Triad is composed of irregular respiration, bradycardia, and systolic hypertension

272
Q

What can cause raised intracranial pressure?

A

head injury
bleeding in the brain
tumour
infection
stroke
excess cerebrospinal fluid
swelling of the brain

273
Q

How is raised ICP treated?

A

IV mannitol
CSF drainage
Hyperventilation

274
Q

What goes wrong in raised ICP?

A

ICP is higher than MAP so the brain is no longer adequately perfused with oxygen
BP is increased and HR decreased

275
Q

What is dementia?

A

a syndrome characterised by deterioration in cognition, resulting in impairment in the activities of daily living.

Cognitive decline occurs in one or more cognitive domains

early onset: 65 or younger

276
Q

What are the subtypes of dementia?

A
  • Alzheimer’s (70%)
  • Vascular (15%)
  • Dementia with Lewy bodies
  • Frontotemporal
277
Q

What are the risk factors for dementia?

A

Increasing age
Family hx of first degree relative
Down’s
Cognitive reserve: reduced in social isolation
Ischaemic stroke (smoking, diabetes, AF, HTN, age)

278
Q

What is the pathophysiology of Alzheimer’s?

A

Accumulation of beta-amyloid ,forming extracellular plaques, and hyperphosphorylated TAU protein, forming neurofibrillary tangles

279
Q

What happens in vascular dementia?

A

Disturbance in the blood supply to the brain leading to ischaemia and loss of cells

280
Q

What is the pathophysiology of Lewy-body dementia?

A

Lewy body deposits in cytoplasm of neurones

281
Q

Which two proteins are involved in frontotemporal dementia?

A

TDP43 and TAU protein

282
Q

How does Alzheimer’s typically present?

A
  • Short term memory loss
  • Difficulty finding words
  • Problems with insight
  • Visuo-spatial difficulties
283
Q

How does vascular dementia present?

A
  • Impairments in planning, organisation, and judgement early on
  • Stepwise
284
Q

How does dementia with lewy-bodies present?

A
  • Fluctuating cognition
  • Parkinsonian
  • Hallucination
  • REM sleep disturbances
285
Q

How does frontotemporal dementia present?

A
  • Behaviour and personality changes
  • Language difficulties
  • Impairments in comprehension
286
Q

What is there typically impairment in in dementia?

A
  • Memory
  • Executive function
  • Language
  • Attention
  • Visuo-spatial functions
287
Q

What are the symptoms of early stages dementia?

A

Pre-dementia
- Loss of sense of smell
- Forgetfulness
Early-dementia
- Symptoms are apparent to other people
- E.g. forgetting meds, managing finances, difficulty completing household tasks

288
Q

How does mid-stage dementia typically present?

A
  • Require assistance with personal care and hygiene
  • Behavioural disturbances
  • Lack of insight
  • Can’t acquire new info
289
Q

How does late stage dementia present?

A
  • Time shift
  • Further regression in speech
  • Mood disturbances
  • Hallucinations
  • Restlessness
  • Recognition harder
  • Movement difficulties
  • Swallowing difficulties
290
Q

How is dementia diagnosed?

A

Clinical history
MMSE/MOCA
FBC: B12, TFTs

291
Q

How can dementia be managed?

A

Cholinesterase inhibitors: donepezil
NMDA antagonists: memantine
Behaviour and environment support:
- Maintaining familiar environment
- Monitor personal comfort
- Attention redirection
- Mental health support
- Aerobic exercise

292
Q

What is the pathophysiology of myasthenia gravis?

A

At NMJ, NTs release Ach which attaches to receptors on the postsynaptic membrane, simulating muscle contraction

In myasthenia gravis: Acetylcholine receptor (AChR) antibodies are found and bind to postsynaptic ACh receptors, blocking them and preventing stimulation by ACh.

The more the receptors are used during muscle activity, the more they become blocked.
Less effective stimulation of the muscle with increased activity.
With rest, the receptors are cleared, and the symptoms improve.

antibodies also activate the complement system within the neuromuscular junction, leading to cell damage at the postsynaptic membrane, further worsening symptoms

293
Q

What is myasthenia gravis?

A

a chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction in skeletal muscle
causes muscle weakness that progressively worsens with activity and improves with rest

294
Q

What ages does myasthenia gravis tend to affect?

A

affects men and women at different ages
typically affecting women under 40 and men over 60

295
Q

What antibodies are associated with myasthenia gravis?

A

ACh receptor antibodies
MuSK and LRP4 (important proteins for the creation and organisation of the ACh receptor, destruction of these proteins leads to inadequate acetylcholine receptors)

296
Q

What is the basic presentation of myasthenia gravis?

A

muscle weakness that increases with exercise (fatigue) and improves on rest
Symptoms are typically best in the morning and worst at the end of the day

297
Q

What are the symptoms of myasthenia gravis?

A

Muscle weakness with exercise
drooping eyelids
double vision
dysphagia
facial paresis
SOB
Proximal limb weakness
Speech difficulties

298
Q

What investigations should be done for myasthenia gravis?

A

Antibody tests look for:
- AChR antibodies (around 85%)
- MuSK antibodies
- LRP4 antibodies

CT chest: thymoma
Pulmonary function tests in myasthenic crisis: low fvc

299
Q

What is the management for myasthenia gravis?

A

Cholinesterase inhibitor: Pyridostigmine (prolongs the action of Ach)
Consider:
* Immunosuppression (e.g., prednisolone) suppresses the production of antibodies
* Thymectomy can improve symptoms, even in patients without a thymoma
* Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail

300
Q

What is myasthenic crisis?

A

often triggered by another illness, such as a respiratory tract infection.
Respiratory muscle weakness can lead to respiratory failure. Patients may require non-invasive ventilation or mechanical ventilation.

Treatment is with IV immunoglobulins and plasmapheresis

301
Q

What is an absence seizure?

A

patient becomes blank, stares into space, and then abruptly returns to normal.
unaware of their surroundings and do not respond.
typically last 10 to 20 seconds.
usually in childhood

302
Q

What happens during a tonic clonic seizure?

A

Tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness.
tongue biting, incontinence, groaning and irregular breathing

aura before sometimes, post-ictal after

303
Q

How may a person act post-ictally?

A

confused, tired, and irritable or low.

304
Q

What symptoms may be present in a partial seizure?

A

Déjà vu
Strange smells, tastes, sight or sound sensations
Unusual emotions
Abnormal behaviours

305
Q

What is a partial seizure?

A
  • occur in an isolated brain area, often in the temporal lobes.
  • affect hearing, speech, memory and emotions.
  • Patients remain awake
  • They remain aware during simple partial seizures but lose awareness during complex partial seizures
306
Q

What are some differentials for epileptic seizures?

A

Vasovagal syncope (fainting)
Pseudoseizures (non-epileptic attacks)
Cardiac syncope
Hypoglycaemia
Hemiplegic migraine
TIA

307
Q

What is going wrong in seizures?

A

inappropriate hyperexcitability and hypersynchrony

308
Q

What are the risk factors for epilepsy?

A

family hx of onset epilepsy
previous CNS infection
head trauma
CNS lesion
stroke
antenatal or perinatal brain insult
intellectual disability
HIV
prior seizure events

309
Q

What investigations are done for epilepsy?

A

electroencephalogram (EEG)
MRI to detect pathology

310
Q

What safety precautions should be taken in epilepsy?

A

The DVLA will remove their driving licence until specific criteria are met (e.g., being seizure-free for one year)
Taking showers rather than baths
Particular caution with swimming, heights, traffic and dangerous equipment

311
Q

Which seizures are managed with sodium valproate?

A

Tonic-clonic
Myoclonic
Tonic
Atonic

312
Q

What medication can be given for an epileptic seizure?

A

BZs: diazepam, midazolam
Phenytoin

313
Q

When is lamotrigine or levetiracetam used to manage seizures?

A

partial seizures
when sodium valproate can’t be used, e.g in pregnancy

314
Q

How does sodium valproate work?

A

increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brain

315
Q

What are the side effects of sodium valproate?

A

Teratogenic (harmful in pregnancy): neural tube defects
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

316
Q

What is status epilepticus?

A

A seizure lasting more than 5 minutes
Multiple seizures without regaining consciousness in the interim

317
Q

What are some anti-epileptics?

A

Sodium valproate
Carbamazepine (tegretol)
Lamotrigine
Ethosuximide (absence seizures)

318
Q

What are the cardinal signs of an UMN lesion?

A

Hypertonia
Hyperreflexia
Clonus
Babinski sign
Muscle weakness

319
Q

Where does a lower motor neuron lesion affect?

A

A lower motor neurone (LMN) lesion affects anywhere from the anterior horn cell to the muscle

320
Q

Where is an UMN lesion?

A

CNS

corticospinal

321
Q

What is seen in a lower motor neuron lesion?

A

Marked atrophy
Fasciculations
Hypotonia
Variable patterns of weakness
Hyporeflexia or areflexia
Downgoing plantars or absent response

322
Q

What are the differences between an UMN and LMN lesion?

A

UMN: hypertonia and spastic paralysis, hyperreflexia
LMN: hypotonia and flaccid paralysis, hyporeflexia

323
Q

What happens when an UMN is damaged?

A

a loss of inhibitory tone of muscles leading to constant contraction of muscles.

This leads to the typical hypertonia, spastic paralysis and hyperreflexia

324
Q

What happens when a LMN is damaged?

A

If LMNs are damaged or lost, there is nothing to tell the muscles to contract, resulting in hypotonia and flaccid paralysis

325
Q

What conditions may have a LMN lesion?

A

Peripheral nerve trauma/compression
Spinal muscular atrophy
ALS
Guillain-Barré syndrome
Poliomyelitis

326
Q

What conditions may have UMN lesions?

A

Ischaemic or haemorrhagic stroke (including brainstem strokes)
ALS
MS

327
Q

What is cauda equina syndrome?

A

Cauda equina is a neurosurgical emergency caused by compression of the lumbosacral nerve roots of the cauda equina

328
Q

What is the cauda equina and what does it supply?

A

a collection of nerve roots that travel through the spinal canal after the spinal cord terminates around L2/L3

  • 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
329
Q

What can cause compression of the spinal cord in cauda equina?

A

**Herniated disc at L4/5 or L5/S1 **(the most common cause)
Stenosis of the spinal cord
Tumours, particularly metastasis
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Abscess (infection)
Trauma

330
Q

What are the red flags to look out for in cauda equina?

A

Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus)
Loss of sensation in the bladder and rectum (not knowing when they are full)
Urinary retention or incontinence
Faecal incontinence
Bilateral sciatica
Bilateral or severe motor weakness in the legs
Reduced anal tone on PR examination

331
Q

What is metastatic spinal cord compression?

A

a metastatic lesion compresses the spinal cord
different to cauda equina

332
Q

What are the risk factors for cauda equina?

A

lumbar disc herniation
spinal trauma
spinal surgery
spinal epidural abscess
anticoagulation therapy (risk of haematoma)

333
Q

What are the symptoms of cauda equina syndrome?

A

low back pain
sciatica
progressive neurological deficits
bladder dysfunction:
- difficulty starting or stopping urination
- impaired sensation of urinary flow
- urgency
- urinary retention with overflow urinary incontinence
loss of sensation of rectal fullness
faecal incontinence
laxity of the anal sphincter
saddle anaesthesia or paraesthesia
sexual dysfunction

334
Q

What imaging is done for cauda equina syndrome and how is it treated?

A

MRI lumbar spine
urgent surgical decompression of the spinal canal

335
Q

What is spinal stenosis?

A

narrowing of part of the spinal canal, resulting in compression of the spinal cord or nerve roots.
usually affects the cervical or lumbar spine

336
Q

What can cause spinal stenosis?

A

Congenital spinal stenosis
Degenerative changes
Herniated discs
Thickening of the ligamenta flava or posterior longitudinal ligament
Spinal fractures
Spondylolisthesis
Tumours

337
Q

What are the risk factors for spinal stenosis?

A

age >40 years
previous back surgery
previous injury
achondroplasia
acromegaly

338
Q

How does spinal stenosis present?

A

Gradual onset
Neurogenic claudication
Back pain
Leg pain when walking
Stooped when walking
Leg numbness

339
Q

What imaging can be done for spinal stenosis?

A

plain x-ray
MRI (T2-weighted)

340
Q

What are the management options for spinal stenosis?

A

Physiotherapy + exercise
NSAIDs
Consider corticosteroids if NSAIDs uneffective

341
Q

What can spinal stenosis develop into?

A

Cauda equina compression

342
Q

What forms the sciatic nerve and what does it supply?

A

L4-S3
sensation to the lateral lower leg and the foot
motor function to the posterior thigh, lower leg and foot.

343
Q

How does sciatica present?

A

unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet
paraesthesia
numbness
motor weakness

344
Q

What is Lambert-Eaton Syndrome?

A

An autoimmune disorder of the neuromuscular junction
In most cases, it is a paraneoplastic syndrome occurring alongside small-cell lung cancer (SCLC).
Can occur as a primary autoimmune disorder without the presence of SCLC

345
Q

What are the main presentations of Lambert-Eaton?

A

Proximal muscle weakness: difficulty climbing stairs, standing from a seat or raising the arms overhead
Autonomic dysfunction: dry mouth, blurred vision, impotence and dizziness
Reduced or absent tendon reflexes

improve after periods of muscle contraction, which is the reverse of what is seen in myasthenia gravis

346
Q

What are the risk factors for lambert-eaton?

A

underlying small cell lung cancer or other malignancy
co-existing autoimmune disorder
cigarette smoking
family hx of autoimmune disease

347
Q

What is the pathophysiology of lambert-eaton?

A

antibodies against voltage-gated calcium channels
antibodies may be produced in response to small-cell lung cancer (SCLC) cells that express voltage-gated calcium channels
When the voltage-gated calcium channels are destroyed, less acetylcholine is released into the synapse, resulting in a weaker signal and reduced muscle contraction

348
Q

What is the typical aetiology of lambert eaton?

A

Autoimmune state or in association with a cancer

349
Q

What investigations should be done for lambert eaton?

A

nerve conduction studies: doubling after exercise
low-frequency repetitive nerve stimulation
anti-P/Q voltage-gated calcium-channel serology: positive
chest CT scan: may show malignancy
anti-acetylcholine receptor (AChR) serology: negative

350
Q

What is the treatment for lambert eaton?

A

Treatment of underlying cause
Amifampridine (works by blocking voltage-gated potassium channels in the presynaptic membrane, which prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action)

351
Q

What is bitemporal hemianopia?

A

two halves lost are on the outside of each eye’s peripheral vision
effectively creating a central visual tunnel
optic chiasm compression

352
Q

What is homonymous hemianopia?

A

two halves lost are on the corresponding area of the visual field in both eyes
lesion behind the optic chiasm

353
Q

How do LMN and UMN lesions differ in the face?

A

LMN: upper and lower facial paralysis
UMN: lower facial paralysis only

UMN requires urgent treatment, LMN less urgent

354
Q

What is Bell’s palsy?

A

a unilateral lower motor neurone facial nerve palsy

355
Q

How can Bell’s palsy be treated?

A

lubricating eye drops
prednisolone

356
Q

What causes Ramsay hunt syndrome and how is it treated?

A

varicella zoster virus (VZV)
Mx: aciclovir and pred

357
Q

What is Ramsay Hunt syndrome?

A

unilateral lower motor neurone facial nerve palsy
stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side

358
Q

What is mononeuritis multiplex?

A

a type of peripheral neuropathy, happens when there is damage to at least two different areas of the peripheral nervous system

simultaneous or sequential involvement of ≥ 2 separate nerves

classic presentation of vasculitis

359
Q

How does peripheral neuropathy present?

A

glove and stocking distribution

360
Q

What can cause peripheral neuropathy?

A

Diabetes mellitus
Chronic alcohol
Vitamin B12 or folate deficiency
Infective
Vasculitis
Charcot-Marie tooth
Drugs: isoniazid, amiodarone, leflunomide and cisplatin

361
Q

What investigations are done for peripheral neuropathy?

A

Electromyography and nerve conduction studies

362
Q

What is the basic pathophysiology of peripheral neuropathy?

A

axonal degeneration
demyelination

363
Q

How does carpal tunnel present?

A

numbness and tingling mainly in the thumb and radial fingers
aching and pain in the anterior wrist and forearm
clumsiness in the hand.

363
Q

What is carpal tunnel?

A

collection of symptoms and signs caused by compression of the median nerve in the carpal tunnel

364
Q

Who is most at risk of carpal tunnel?

A

Females age 40-60

365
Q

What are the risk factors for carpal tunnel?

A

Repetitive strain
Obesity
Perimenopause
Rheumatoid arthritis
Diabetes
Acromegaly
Hypothyroidism

366
Q

How can carpal tunnel be diagnosed?

A

Electromyogram
Phalen’s test
Tinel’s test

367
Q

How is carpal tunnel managed?

A

Wrist splint
Consider corticosteroid injection and surgery

368
Q

Damage to what nerve causes wrist drop?

A

Radial

369
Q

Damage to what nerve causes claw hand?

A

Ulnar

370
Q

What nerve injury causes foot drop?

A

common peroneal nerve

371
Q

What is syncope?

A

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

372
Q

What happens in a vasovagal episode?

A

Vagus nerve receives a strong stimulus (emotional event, painful sensation or change in temperature)
Parasympathetic nervous system stimulated and counteracts SNS constriction of blood vessels.
BP in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”

373
Q

What symptoms are typically present before fainting (prodrome)?

A

Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache

374
Q

What can cause primary syncope?

A
  • Dehydration
  • Missed meals
  • Extended standing in a warm environment, such as a school assembly
  • A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood
375
Q

What can cause secondary syncope?

A

Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy

376
Q

What advice can be given for simple syncope management?

A

Avoid dehydration
Avoid missing meals
Avoid standing still for long periods
When experiencing prodromal symptoms such as sweating and dizziness, sit or lie down, have some water or something to eat and wait until feeling better

377
Q

What are some symptoms of Charcot-Marie-Tooth disease?

A

High foot arches
Distal muscle
Lower leg weakness, particularly loss of ankle dorsiflexion (with a high stepping gait due to foot drop)
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

378
Q

What is Charcot-marie-tooth?

A

autosomal dominant inherited disease that affects the peripheral motor and sensory neurones (peripheral neuropathy)

symptoms typically develop before age of 10, can be up to 40

no treatment, MDT approach

379
Q

What is the aetiology of Duchenne?

A

X-linked recessive
defective gene for dystrophin on the X-chromosome

380
Q

What investigations should be done for duchenne?

A

serum creatine kinase (CK): elevated
genetic testing

381
Q

What are some complications of duchenne muscular dystrophy?

A

respiratory failure
loss of mobility
weight loss/malnutrition
sexual dysfunction
impaired growth
delayed puberty
constipation
cardiac failure
excessive daytime sleepiness and morning headaches

382
Q

How might duchenne first present?

A

Boys with Duchennes present around 3 – 5 years with weakness in the muscles around their pelvis

383
Q

How is Duchenne managed?

A

Corticosteroid: prednisolone
Physiotherapy
Psychosocial care
Management of complications

384
Q

What does brown-sequard result from?

A

a hemisection (one sided lesion) of the spinal cord, often c spine

most common cause is trauma

385
Q

What goes wrong in brown-sequard?

A

Interruption
- lateral corticospinal tracts
- lateral spinothalamic tract
- occasionally the posterior columns.

386
Q

How does brown-sequard present?

A

DCML: ipsilateral loss of touch, vibration and proprioception
Anterolateral: contralateral loss of pain and temperature sensation
ipsilateral hemiparesis

387
Q

What are the symptoms of horner’s syndrome?

A

Partial ptosis (drooping or falling of upper eyelid)
Miosis (constricted pupil)
Facial anhidrosis (loss of sweating)

due to a disruption in the sympathetic nerve supply

388
Q

What cancers most often spread to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

389
Q

What can pituitary tumours cause?

A

Acromegaly (excessive growth hormone)
Hyperprolactinaemia (excessive prolactin)
Cushing’s disease (excessive ACTH and cortisol)
Thyrotoxicosis (excessive TSH and thyroid hormone)
Bitemporal hemianopia

390
Q

What are the different brain tumour?

A

range from benign (e.g., meningiomas) to highly malignant (e.g., glioblastomas)
pituitary tumours

391
Q

What are gliomas?

A

tumours of the glial cells in the brain or spinal cord

392
Q

What are meningiomas?

A

tumours growing from the cells of the meninges

393
Q

What are the different gliomas?

A
  • Astrocytoma (the most common and aggressive form is glioblastoma)
  • Oligodendroglioma
  • Ependymoma
394
Q

What are acoustic neuromas?

A

benign tumours of the Schwann cells that surround the auditory nerve

395
Q

What are the investigations for a brain tumour?

A

MRI brain
Biopsy after surgical removal

396
Q

What are the different management options for a brain tumour?

A

Surgery
Chemotherapy
Radiotherapy
Palliative care

397
Q

What is giant cell arteritis?

A

a granulomatous vasculitis of large and medium-sized arteries
It primarily affects branches of the external carotid artery

398
Q

Who does GCA tend to affect?

A

most common form of systemic vasculitis in adults.
GCA typically occurs in people aged 50 years or older
more common in women

399
Q

What investigations should be done for GCA?

A

Clinical presentation
Raised inflammatory markers, particularly ESR
Temporal artery biopsy (showing multinucleated giant cells)
Duplex ultrasound (showing the hypoechoic “halo” sign and stenosis of the temporal artery)

400
Q

What are the symptoms of GCA?

A

Unilateral headache around temples and forehead
Scalp tenderness (e.g., noticed when brushing the hair)
Jaw claudication
Blurred or double vision
Loss of vision if untreated

401
Q

What are the risk factors for GCA?
and suspected aetiology

A

age over 50 years
female sex
northern European ancestry

genetic (HLA II) and environmental

402
Q

What is the management for GCA?

A

Steroids: prednisolone, immediately started
Aspirin 75mg daily
For steroid adverse effects:
- PPI (e.g., omeprazole) for gastroprotection while on steroids
- Bisphosphonates and calcium + vit D for bone protection while on steroids

403
Q

What’s the main complication of GCA?

A

Irreversible vision loss
hence start steroids straight away

404
Q

What are some tools for scoring stroke?

A

FAST and ROSIER

405
Q

Components of the ROSIER score

A

Loss of consciousness or syncope - 1 point
Seizure activity - 1 point
New, acute onset of:
* asymmetric facial weakness + 1 point
* asymmetric arm weakness + 1 point
* asymmetric leg weakness + 1 point
* speech disturbance + 1 point
* visual field defect + 1 point

stroke likely if score more than 1

Phase 2a (14 decks)

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