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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the pathophysiology of an ischaemic stroke?

A

Stenosis or occlusion of a cerebral artery, often associated with prothrombotic states.

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2
Q

What are the three pathophysiologies of ischaemic stroke?

A
  • Primary vascular pathology (directly reduce cerebral perfusion)
  • Cardiac pathologies (cerebral artery occlusion)
  • Haematological pathologies (cerebrovascular thrombus)
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3
Q

What are the risk factors for an ischaemic stroke?

A
  • Age
  • Family history
  • Hypertension
  • Smoking
  • Diabetes mellitus
  • Atrial fibrillation
  • Comorbid cardiac condition
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4
Q

What are the signs and symptoms of an ischaemic stroke?

A
  • Vision loss/field defect
  • Muscle weakness
  • Aphasia
  • Ataxia
  • Sensory loss
  • Headache
  • Diplopia
  • Dysarthria (slurred words)
  • Gaze paresis
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5
Q

How is an ischaemic stroke diagnosed?

A

Non-contrast CT head

  • Hypoattenuation of brain parenchyma
  • Loss of grey matter-white matter differentiation
  • Hyperattentuation in an artery
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6
Q

What are the differentials for an ischaemic stroke?

A
  • Intracerebral haemorrhage
  • Epileptic seizure
  • Space occupying lesion
  • Infection
  • MS
  • FND
  • Migraine
  • Metabolic changes (eg. alcohol/drugs)
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7
Q

How is an ischaemic stroke managed?

A
  • Mechanical thrombectomy
  • Thrombolysis
  • Aspirin
  • Statins 48 hours after
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8
Q

What are the possible complications of an ischaemic stroke?

A
  • DVT
  • Haemorrhagic transformation
  • Depression
  • Aspiration pneumonia
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9
Q

What is the pathophysiology of a haemorrhagic stroke?

A

Vascular rupture → bleeding into brain parenchyma → primary mechanical injury to brain

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10
Q

What are the risk factors for haemorrhagic stroke?

A
  • Hypertension
  • Old age
  • Male sex
  • Asain/black/hispanic
  • Alcohol use
  • Sympathomimetic drugs
  • FHx
  • Anticoagulation
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11
Q

What are the signs and symptoms of haemorrhagic stroke?

A
  • Unilateral weakness
  • Sensory loss
  • Dysphasia/dysarthria
  • Photophobia
  • Headache
  • Confusion
  • N+V
  • Decreased consciousness
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12
Q

How is haemorrhagic stroke diagnosed?

A

Non-contrast CT head
- Hyperattenuation suggesting acute blood
- Surrounding hypoattenuation due to oedema

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13
Q

What are the differentials for haemorrhagic stroke?

A
  • Ischaemic stroke
  • Hypersensitivity encephalopathy
  • Hypoglycaemia
  • Complicated migraine
  • Seizure disorder
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14
Q

How are haemorrhagic strokes managed?

A
  • Manage comorbidities
  • Craniotomy
  • Drugs to relieve pressure (eg. manitol)
  • Stereotactic aspiration

Management depends on type of stroke

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15
Q

What are the complications of haemorrhagic strokes?

A
  • Infection
  • DVT/PE
  • Seizures
  • Delirium
  • Aspiration pneumonia
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16
Q

What is a transient ischaemic attack?

A

A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia.

No acute infarction, sudden onset and usually lasts between 1 and 24 hours.

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17
Q

What is the pathophysiology of a TIA?

A

Severity depends on a combination of:
- Degree of obstruction
- Area and function of tissue supplied by the vessel
- Length of time thrombus obstructs the vessel
- Ability of collateral circulation to provide supplemental perfusion

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18
Q

What are the causes of TIA?

A
  • Stenosis or unstable atherosclerotic plaques
  • Cardioembolic events (impaired ejection fraction)
  • Microatheromas, fibrinoid necrosis etc
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19
Q

What are the risk factors for a TIA?

A
  • CVD
  • Diabetes mellitus
  • Hyperlipidaemia
  • Smoking
  • Alcohol
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20
Q

What are the signs and symptoms of a TIA?

A
  • Sudden onset and brief duration
  • Focal neurological deficit
  • Unilateral weakness
  • Dysphasia
  • Ataxia, vertigo/loss of balance
  • Homonymous hemianopia/diplopia
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21
Q

How is a TIA diagnosed?

A

Clinical diagnosis

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22
Q

What are the differentials for TIA?

A
  • Stroke
  • Hypoglycaemia
  • Post-seizure paralysis
  • Complex migraine
  • Conversion disorder
  • MS
  • Peripheral neuropathy
  • Labyrinthine disorders
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23
Q

What is the management of a TIA?

A

Aspirin and clopidogrel

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24
Q

What are the possible complications of a TIA?

A
  • Stroke
  • MI
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25
Q

What is the pathophysiology of a subarachnoid haemorrhage?

A
  • Usually caused by cerebral aneurysms
  • Bifurcation of major arteries that form the circle of Willis
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26
Q

What factors increase the risk of aneurysm rupture?

A
  • Size
  • Location
  • Presence of symptoms
  • Multiple aneurysms
  • History of ruptured aneurysms
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27
Q

What are the risk factors for subarachnoid haemorrhage?

A
  • Age
  • Female sex
  • Smoking
  • Hypertension
  • Alcohol misuse
  • FHx
  • Acute cocaine use
  • Adrenergic/seretonergic drugs
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28
Q

What are the signs and symptoms of subarachnoid haemorrhage?

A
  • Severe sudden-onset headache
  • Depressed/loss of consciousness
  • Neck stiffness and muscle aches
  • Photophobia
  • N+V
  • Confusion
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29
Q

How are subarachnoid haemorrhages diagnosed?

A
  • Non-contrast CT scan (hyperdense areas in subarachnoid space)
  • LP after 24 hours
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30
Q

What are the differentials for subarachnoid haemorrhage?

A
  • Aortic dissection
  • Cerebral arteriovenous malformation
  • Dural arteriovenous fistulae
  • Vasculitis
  • Cardiac myxoma
  • Cocaine abuse
  • Sickle cell disease
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31
Q

What is the management of a subarachnoid haemorrhage?

A
  • Nimodipine (prevents ischemia)
  • Neurosurgery to secure aneurysm
  • Observe for signs of deterioration
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32
Q

What are the possible complications of subarachnoid haemorrhage?

A
  • Neuropsychiatric problems
  • Chronic hydrocephalus
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33
Q

What is the pathophysiology of a subdural haemorrhage?

A

The result of torsional or sheer forces → disruption of bridging cortical veins → empty into dural venous sinuses

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34
Q

What are the causes of subdural haemorrhage?

A
  • Trauma (most common)
  • Increased intracranial pressure
  • Mets
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35
Q

What are the risk factors for subdural haemorrhage?

A
  • Alcoholism
  • Aspirin/blood thinners
  • Age
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36
Q

What are the signs and symptoms of a subdural haemorrhage?

A
  • Drowsiness
  • Consciousness fluctuation
  • Personality change
  • Increased ICP
  • Seizures
  • Focal neurological signs (unequal pupils)
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37
Q

How are subdural haemorrhages diagnosed?

A

CT/MRI
- Concave crescent of blood around the edge of the brain
- Midline shift of brain structures

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38
Q

What are the differentials for subdural haemorrhage?

A
  • Stroke
  • Dementia
  • Mass lesion
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39
Q

What is the management of subdural haemorrhage?

A
  • Irrigation/evacuation/burr hole craniostomy
  • Craniotomy
  • Identify cause
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40
Q

What are the possible complications of a subdural haemorrhage?

A
  • Neurological deficits
  • Coma
  • Stroke
  • Epilepsy
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41
Q

What is intracerebral haemorrhage?

A

Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system

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42
Q

What are the symptoms of posterior circulation strokes?

A
  • Unsteadiness
  • Visual disturbance
  • Slurred speech
  • Headache
  • Vomiting
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43
Q

What is the pathophysiology of an extradural haemorrhage?

A

Usually a bleed from the middle meningeal artery and/or vein, normally due to trauma around the eye (fracture of temporal/parietal bone).

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44
Q

What is the presentation of extradural haemorrhage?

A
  • Drowsiness
  • Pupil asymmetry
  • Impaired consciousness/coma
  • Severe headache
  • Vomiting
  • Seizures
  • Hemiparesis
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45
Q

How is an extradural haemorrhage diagnosed?

A

CT or MRI

Convex lesion

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46
Q

What are the differentials for extradural haemorrhages?

A
  • Subdural haemorrhage
  • Meningioma
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47
Q

How is an extradural haemorrhage managed?

A
  1. Surgery - 1st line
    - Evacuation of blood
    - Bleeding lesion ligation
  2. Decompression if required
  3. Sit up in bed
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48
Q

What is epilepsy?

A

The tendency to have seizures (not a true condition, more a symptom).

Diagnosed after a minimum of 2 seizures.

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49
Q

What is the pathophysiology of epilepsy?

A
  • Abnormal synchronised discharge of neurones (usually glutamate and GABA neurones)
  • Failure of inhibitory mechanisms
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50
Q

What does ‘seizure threshold’ mean?

A

The level of excitability at which cells will discharge uncontrollably, in epilepsy this is lowered (neurones are hyperexcitable).

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51
Q

What triggers can push neurones past the seizure threshold?

A
  • Sleep deprivation
  • Alcohol
  • Drug misuse
  • Physical/mental exhaustion
  • Flickering lights
  • Infection/metabolic disturbance
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52
Q

What are the causes of epilepsy?

A
  • Genetic
  • Developmental abnormalities
  • Trauma/surgery
  • Hypoxia
  • Pyrexia
  • Mass lesion in the skull
  • Drugs
  • CNS infection
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53
Q

What are the risk factors for epilepsy?

A
  • Age
  • FHx
  • Head injury
  • Stroke (vascular diseases)
  • Dementia
  • Brain infection
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54
Q

What are the signs and symptoms of a simple partial seizure?

A
  • Remains consciousness
  • Isolated limb jerking
  • Isolated head turning
  • Isolates paraesthesia
  • Weakness of limbs follows
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55
Q

What are the signs and symptoms of a complex partial seizure?

A
  • May impair consciousness
  • Deja vu
  • Vertigo
  • Hallucinations
  • Lip-smacking (other motor disturbances)
  • Tachycardia
  • Post-ictal confusion and drowsiness
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56
Q

What are the signs and symptoms of absence seizures?

A
  • Unresponsive to stimuli but still conscious
  • Stares/pallor
  • Muscle jerking
  • Multiple episodes in one day
  • Normal function quickly resumes post episode
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57
Q

What are the signs and symptoms of Tonic-Clonic seizures? §

A
  1. Aura prior to the episode
  2. Tonic phase
    - Rigidity
    - Epileptic cry
    - Tongue biting
    - Incontinence
    - Hypoxia
  3. Clonic phase
    - Convulsions
    - Eye rolling
    - Tachycardia
    - Random or uncontrolled breaths
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58
Q

What are the features of generalised epilepsy?

A
  • Absence seizures
  • Tonic-Clonic seizures
  • Tonic only seizures
  • Atonic seizures (presents similar to syncope)
  • Myoclonic seizures
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59
Q

What are the features of focal epilepsy?

A
  • Simple partial seizure
  • Complex partial seizure
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60
Q

What are the signs and symptoms of status epilepticus?

A

Seizure >30 minutes
OR
Multiple seizures without regaining consciousness lasting >30 minutes

The brain swells and can cause herniation due to electrolyte imbalance

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61
Q

How is epilepsy diagnosed?

A
  • EEG
  • CT/MRI (focal lesions)
  • PET scan
  • Bloods (CK)
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62
Q

What are the differentials for epilepsy?

A
  • Other causes of falls
  • Pseudoseizures
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63
Q

How is epilepsy managed?

A
  • Avoid triggering factors
  • Focal seizures - carbamazepine
  • Generalised TC - Sodium valproate
  • Surgery
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64
Q

How is status epilepticus managed?

A

Benzodiazepines.

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65
Q

What is meningitis?

A

Inflammation of the meninges.

Notifiable disease.

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66
Q

What is the pathophysiology of infective meningitis?

A
  1. Haematogenous spread
    - Binding to surface receptors
    - Vulnerable spots/areas of damage
  2. Direct spread
    - Anatomical
    - Through the nose
    - Through overlaying skin
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67
Q

What are the causes of bacterial meningitis? §

A
  • Neisseria meningitides (gram-negative diplococci)
  • Strep pneumoniae or pneumococcus
  • Haemophilus influenzae
  • Listeria monocytogenes (pregnant women)
  • E. coli (neonates)
  • TB
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68
Q

What are the causes of viral meningitis?

A
  • HSV
  • VZV
  • Enteroviruses
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69
Q

What are the causes of fungal meningitis?

A

Cryptococcus neoformans

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70
Q

What are the causes of parasitic meningitis?

A

P. Falciparum

71
Q

What are the risk factors for infective meningitis?

A
  • Elderly
  • Pregnant
  • Bacterial endocarditis
  • Crowding
  • Diabetes
  • Malignancy
  • IV drugs
72
Q

What is the clinical presentation of infective meningitis?

A

Classic triad:
- Headache
- Fever
- Neck stiffness

73
Q

What are the early signs of meningitis?

A
  • Headache
  • Fever
  • Leg pain
  • Cold hands and legs
  • Abnormal skin colour
74
Q

What are the chronic signs of meningitis?

A
  • Meningism
  • Papilloedema
  • Impaired consciousness
  • Petechial rash (non-blanching)
  • Seizures
75
Q

What is meningism?

A

Positive Kernig’s and Brudzinski’s sign
- Neck stiffness
- Photophobia

76
Q

How is infective meningitis diagnosed?

A

Lumbar puncture

Bacteria:
- Appears cloudy
- High protein
- High WCC
- Neutrophil polymorphs

Virus:
- Appears normal
- Normal protein and glucose
- High WCC
- Lymphocytes

77
Q

What are the differentials for meningitis?

A
  • Malaria
  • Encephalitis
  • Sepsis
  • Subarachnoid haemorrhage
  • Dengue fever
  • Tetanus
78
Q

What is the management of meningitis?

A
  • Benzylpenicillin
  • Cefotaxime (in hospital)
79
Q

What are the possible complications of meningitis?

A
  • Hearing or vision loss
  • Epilepsy
  • Memory and concentration problems
  • Coordination, movement and balance problems
  • Learning difficulties
  • Loss of limbs
80
Q

What is Guillain-Barre syndrome?

A

Acute inflammatory demyelinating polyneuropathy.

Usually follows a GI/URT infection or HIV.

81
Q

What is the pathophysiology of Guillain-Barre syndrome?

A

The viral infection causes the production of auto-immune antibodies against peripheral nerves, damaging myelin, reducing/blocking transmission.

82
Q

What are the risk factors for Guillan-Barre syndrome?

A

Preceding viral/bacterial infection.

83
Q

What is the clinical manifestation of Guillan-Barre syndrome? (most common)

A
  • Muscle weakness
  • Respiratory distress
  • Speech problems
  • Paraesthesia
  • Facial weakness
  • Areflexia/hyporeflexia
  • Facial droop
84
Q

How is Guillain-Barre syndrome diagnosed?

A
  • Lumbar puncture (raised protein)
  • Slowed nerve conduction
85
Q

What are the differentials for Guillain-Barre syndrome?

A
  • Transverse myelitis
  • Myasthenia gravis
  • Botulism
  • Lambert-Eaton myasthenic syndrome
  • Vasculitic neuropathy
86
Q

How is Guillain-Barre syndrome managed?

A
  • Intravenous immunoglobulin
  • Plasma exchange
  • Supportive treatment
87
Q

What are the possible complications of Guillain-Barre syndrome?

A
  • Respiratory failure
  • Bladder areflexia
  • Adynamic ileus
  • Paralysis
  • Fatigue
  • Immobilisation hypercalcaemia
  • DVT
88
Q

What is the pathophysiology of Parkinson’s disease?

A
  • Progressive loss of dopaminergic neurones in the basal ganglia
  • Lewy bodies accumulate in surviving neurones
  • Slowly progressive with no remission
  • Symptoms at 20-40% loss
89
Q

What are the risk factors for Parkinson’s disease?

A
  • Age
  • Hereditary
  • Male sex
  • Exposure to toxins (herbicides/pesticides)
90
Q

What are the clinical features of Parkinson’s disease?

A
  • Tremor (usually in hands)
  • Bradykinesia
  • Rigidity (no sensory deficit)
  • Slow shuffling gait
  • Stooped posture
  • Slow and monotonous speech
  • Depression
  • Dementia
91
Q

How is Parkinson’s disease diagnosed?

A

Usually completely clinical.

92
Q

What are the differentials for Parkinson’s disease?

A

VODKA:
- Vascular events (stroke/MI)
- Orthostatic hypotension with atonic bladder
- Dementia with vertical gaze paralysis
- Kayser-Fleisher rings
- Apraxic gait

93
Q

How is Parkinson’s disease managed?

A

Exercise and physiotherapy can improve mobility.

L-DOPA

94
Q

What is Huntington’s disease?

A
  • Autosomal dominant disease
  • Causes degeneration of neurones in the brain
95
Q

What is the clinical presentation of Huntington’s disease?

A
  • Personality change
  • Irritability and impulsivity
  • Chorea
  • Twitching and restlessness
  • Loss of coordination
  • Dementia and seizures
96
Q

How is Huntington’s disease diagnosed?

A

Clinical diagnosis.

97
Q

How is Huntington’s disease managed?

A

Management is supportive - no cure.

98
Q

What are the complications of Huntington’s disease?

A
  • Weight loss
  • Dysphasia
  • Falls
  • Suicide risk
  • Incontinence
99
Q

What can trigger a migraine?

A

CHOCOLATE:
- CHocolate
- Oral contraceptive
- Caffeine
- AlcohOL
- Travel
- Exercise

100
Q

What are the risk factors for migraines?

A
  • Family history
  • Age
  • Female sex
  • Hormonal changes (menstruation, pregnancy, menopause)
101
Q

What is the clinical presentation of a migraine?

A
  • Visual aura
  • Throbbing/pulsing sensation
  • Photophobia
  • Unilateral pain
  • Nausea and vomiting
  • Hyperalgesia
  • Onset in morning
102
Q

How are migraines diagnosed?

A

Clinical diagnosis

103
Q

How are migraines managed?

A
  • Aspirin/NSAIDs
  • Antiemetic
  • Triptans (serotonin receptor agonists)
104
Q

What are the causes of tension headaches?

A
  • Stress
  • Noise
  • Concentrated visual effort
  • Fumes/smells
105
Q

What are the signs and symptoms of a tension headache?

A
  • Bilateral headache
  • Tight band sensation
  • Pressure behind the eyes
  • Frequent occurence
  • Not sensitive to head movement
  • No N+V or neurological signs
106
Q

How is a tension headache diagnosed?

A

Clinical diagnosis

107
Q

How are tension headaches managed?

A

Analgesia
- Avoid strong analgesics (risk of medication overuse headache)

108
Q

What are the risk factors for cluster headaches?

A
  • Male sex
  • Age
  • Smoking
  • Alcohol use
  • FHx
109
Q

What are the clinical features of cluster headaches?

A
  • Episodic, intense unilateral pain
  • Onset early in the morning
  • Can have multiple episodes in one day
  • Unilateral lacrimation and rhinorrhoea
  • Miosis and ptosis
  • No N+V
110
Q

How are cluster headaches diagnosed?

A

Clinical diagnosis

111
Q

How are cluster headaches managed?

A
  • 100% O2
  • Subcut sumatriptan
  • Analgesia not effective
112
Q

What is Mulitple Sclerosis?

A

Chronic inflammation of the CNS
- Demyelination and axonal loss of nerves
- Peripheral nerves are spared

113
Q

What is the pathophysiology of Multiple Sclerosis?

A
  • Demyelination condition with axonal loss
  • Autoimmune reaction (CD4 cells attack oligodendrocytes)
  • Macrophages can cross BBB
114
Q

Describe the progression of Multiple Sclerosis.

A

Relapse-remission disease
- Relapse - local inflammation and damage to myelin/oligodendrocytes/conduction block
- Remission - inflammation subsides, remyelination of damaged areas

115
Q

What are the risk factors for Multiple Sclerosis?

A
  • Age (20-40)
  • Female sex
  • FHx
  • Certain infections (eg. EBV)
  • White people
  • Colder climates
  • Smoking
116
Q

What are the clinical features of Multiple Sclerosis?

A

Any neurological sign can be present in MS, episodes don’t always present with the same S+S

117
Q

How is Multiple Sclerosis diagnosed?

A

MRI - presence of plaques

118
Q

What are the differentials for Multiple Sclerosis?

A
  • Migraine
  • Cerebral neoplasms
  • Nutritional deficiencies (B12 and copper)
  • Infections (HIV)
  • MND
  • Psychiatric disease
  • Vascular causes
119
Q

What is the management of Multiple Sclerosis?

A
  • No cure
  • Smoking cessation
  • Steroids for relapse (methylprednisolone)
  • Glatiramer (may prevent relapse)
120
Q

What are the complications of Multiple Sclerosis?

A
  • UTI
  • Osteoporosis
  • Depression
  • Visual/cognitive impairment
  • Erectile dysfunction
121
Q

What is motor neurone disease?

A

General term for several types of motor neurone degeneration:
- Amyotrophic lateral sclerosis (ALS)
- Progressive bulbar palsy (PBP)
- Progressive muscular atrophy (PMA)
- Spinal muscular atrophy (SMA)

122
Q

What is the pathophysiology of MND?

A

Degeneration of motor neurones in the motor cortex and spinal cord (never causes sensory issues)
- Oxidative neuronal damage
- Abnormally large amounts of protein inside cells
- Glutamate problems
- Apoptosis

123
Q

What are the risk factors for MND?

A
  • Inherited
  • Age (40-60)
  • Male sex (up to 65, then equal)
  • Genetics
124
Q

What are the clinical features of MND?

A
  • Symmetrical weakness and wasting
  • Bulbar and pseudobulbar features
  • Reflex problems
  • Does NOT affect eye movement
  • Dementia
125
Q

How is MND diagnosed?

A
  • Normally clinical
  • EMG may be used (shows denervation)
  • Needs both UMN and LMN and no sensory signs with a progressive pattern
126
Q

What are the differentials for MND?

A
  • Motor neuropathy
  • Spinal muscular atrophy
  • Kennedy’s syndrome
  • Hyperthyroidism and hyperparathyroidism
  • Pseudobulbar palsy
  • Spinal tumours
127
Q

What is the management for MND?

A
  • Na channel blocker (riluzole)
  • GABA agonist (Baclofen)

No remission, death is usually due to bronchopneumonia.

128
Q

What is myasthenia gravis?

A
  • Acquired autoimmune condition
  • Affects NMJ
  • Antibodies against ACh receptors
  • Results in weakness of the muscles
129
Q

What is the pathophysiology of myasthenia gravis?

A
  • B and T cell-mediated IgG (attack post-synaptic AChR)
  • Antibodies block the receptor, stopping ACh from binding - nerve signal is not fully transmitted
130
Q

What are the risk factors for Myasthenia Gravis?

A
  • FHx of autoimmune disorders
  • Genetic markers
  • Cancer-targeted therapy
131
Q

What is the clinical manifestation of myasthenia gravis?

A
  • Pattern of remission and crises
  • All muscles are affected, most notably ocular, bulbar, proximal, and axial muscles
  • Fatigability of muscles
  • Symptoms better in morning, worse throughout the day
  • Rarely muscle wasting
132
Q

How is Myasthenia Gravis diagnosed?

A

Serum AChR antibody analysis = positive

133
Q

What are the differentials for Myasthenia Gravis?

A
  • Lambert-Eaton myasthenic syndrome
  • Botulism
  • Penicillamine-induced myasthenia gravis
  • Primary myopathies
134
Q

How is myasthenia gravis managed?

A
  • Pyridostigmine
  • Corticosteroid (prednisolone) as adjunct
135
Q

What are the complications of Myasthenia Gravis?

A
  • Respiratory failure
  • Impaired swallowing
  • Acute aspiration
  • Secondary pneumonia
136
Q

What is encephalitis?

A

Inflammation of brain parenchyma, usually caused by infection (normally viral).

137
Q

What is the pathophysiology of encephalitis?

A

Intracranial infection causes inflammatory response.

Inflammation of cortex, white matter, basal ganglia and brain stem.

138
Q

What are the risk factors for encephalitis?

A
  • Extremes of age
  • Immunodeficiency
  • Viral infections
  • Body fluid exposure
  • Organ transplantation
  • Location/season
139
Q

What are the clinical features of encephalitis?

A
  • Normally mild self-limiting illness
  • Headache
  • Drowsiness
  • Pyrexia
  • Malaise
  • Meningism symptoms
  • Parenchymal signs
140
Q

How is encephalitis diagnosed?

A

Lumbar puncture:
- Viral PCR
- MCS
- Glucose (raised in bacterial)
- Protein (raised in bacterial)
- Cloudy if bacterial

141
Q

What are the differentials for encephalitis?

A
  • Diabetic ketoacidosis
  • Hepatic encephalopathy
  • Hypoglycaemia
  • Drug overdose
  • SLE
  • Hypoxia
142
Q

How is encephalitis managed?

A
  • IV anciclovir if HSV
  • Dexamethasone treats high ICP
143
Q

What are the possible complications of encephalitis?

A
  • Death
  • Hypothalamic and autonomic dysfunction
  • Ischaemic stroke
  • Seizures
  • Cerebral haemorrhage
  • Cerebral vasculitis
144
Q

What are gliomas?

A

Tumour of glial cells in the brain or spinal cord

145
Q

What are the three types of gliomas?

A
  • Astrocytoma
  • Oligodendroglioma
  • Ependymoma
146
Q

What are meningiomas?

A

Grow from arachnoid, normally benign but can cause raised ICP and neurological signs.

147
Q

What are pituitary tumours?

A

May cause hormone deficiencies or excess hormone production leading to:
- Acromegaly
- Hyperprolactinaemia
- Cushing’s disease
- Thyrotoxicosis

Tend to be benign.

148
Q

What are hemangioblastomas?

A

Tumours with blood vessel origin

149
Q

What are acoustic neuromas?

A

AKA vestibular schwannoma

Schwann cell tumour of the auditory nerve that innervates the ear

150
Q

What are the classic symptoms of acoustic neuromas?

A
  • Hearing loss
  • Tinnitus
  • Balance problems
151
Q

What are the risk factors for primary brain tumours?

A
  • Affluent groups
  • Ionising radiation
  • Vinyl chloride
  • Immunosuppression
  • FHx
152
Q

What are the clinical manifestations of primary brain tumours?

A
  • Tend to be asymptomatic while small
  • Focal neurological symptoms
  • Signs and symptoms usually associated with raised ICP
153
Q

What are the signs and symptoms associated with raised ICP?

A
  • Headache
  • Vomiting
  • Altered medical state
  • Visual field defects
  • Seizures
  • Unilateral ptosis
  • 3rd and 6th nerve palsies
154
Q

How are primary brain tumours diagnosed?

A
  • CT/MRI (lesions)
  • Tissue biopsy to identify gradec§
155
Q

What are the differentials for brain tumours?

A
  • Aneurysm
  • Abscess
  • Cyst
  • Haemorrhage
  • Idiopathic intracranial hypertension
156
Q

How are primary brain tumours managed?

A
  • Steroids
  • Surgery
  • Chemotherapy
  • Radiotherapy
  • Palliative care
157
Q

What are the possible complications of primary brain tumours?

A
  • Hydrocephalus
  • Midline shift and herniations through foramen magnum
158
Q

What are the common causes of secondary brain tumours?

A
  • Lung
  • Breast
  • Melanoma
  • Renal
  • GI
159
Q

What are the clinical manifestations of secondary brain tumours?

A
  • Headache
  • Focal neurological symptoms
  • Ataxia
  • Seizures
  • Nausea + vomiting
  • Papilloedema
160
Q

How are secondary brain tumours diagnosed?

A

CT/MRI

161
Q

How are secondary brain tumours diagnosed?

A
  • Steroids (eg. dexamethasone)
  • Radiotherapy
  • Chemotherapy
  • Surgery
  • Palliative care
162
Q

What are the causes of spinal cord compression?

A
  • Degenerative disc lesions
  • Degenerative vertebral lesions
  • TB
  • Epidural abscess
  • Vertebral neoplasm
  • Epidural haemorrhage
163
Q

What are the risk factors for spinal cord compression?

A
  • History of trauma
  • High risk occupation
  • High risk sports activity
164
Q

What are the clinical manifestations of spinal cord compression?

A
  • Back pain
  • Numbness/paraesthasia
  • Weakness/paralysis
  • Bladder/bowel dysfunction
  • Hyperreflexia
  • Sensory loss
  • Loss of tone below suspected injury
  • Neurogenic shock
165
Q

How is spinal cord compression diagnosed?

A
  • MRI spine
  • Plain spine X-ray
  • CT spine
  • CT myelography
166
Q

What are the differentials for spinal cord injury?

A
  • Transverse myelitis
  • Guillain-Barre syndrome
  • HIV-related myelopathy
  • ALS
  • MS
  • Diabetic/peripheral neuropathy
167
Q

How is spinal cord compression treated?

A
  • Treat underlying cause
  • Surgery
  • Antibiotics
  • Steroids
  • Radiotherapy
168
Q

What are the possible complications of spinal cord compression?

A
  • Pressure ulcers
  • Cardiovascular dysfunction
  • DVT
  • PE
  • MRSA infection
169
Q

What are the causes of cauda equina syndrome?

A
  • Lumbar disc herniation
  • Trauma
  • Spinal tumour
  • Epidural abscess/haematoma
170
Q

What is the clinical manifestation of cauda equina syndrome?

A
  • Bilateral lower limb weakness
  • Decreased/absent lower limb reflexes
  • Reduced perianal sensation and anal tone
  • Lower back pain and sciatica
  • Bladder and bowel dysfunction
  • Leg weakness/paralysis
171
Q

How is cauda equina syndrome diagnosed?

A

MRI

172
Q

What are the differential diagnoses for cauda equina syndrome?

A
  • Conus medullaris syndrome
  • Vertebral fracture
  • Peripheral neuropathy
  • Mechanical lower back pain
173
Q

How is cauda equina syndrome managed?

A
  • Surgery
  • Antibiotics
  • Corticosteroids
174
Q

What are the possible complications for cauda equina syndrome?

A
  • Permanent leg weakness
  • Sexual/urinary dysfunction
  • Chronic pain
  • DVT

Phase 2a (11 decks)

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