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Phase 1c: Conditions > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the definition of a transient ischaemic attack?

A

A transient episode of neurological dysfunction caused by ischaemia, but not acute infarction; sudden onset and symptoms last less than 24 hours (longer than this is a stroke)

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2
Q

What are the key diagnostic factors for a transient ischaemic attack?

A

Sudden onset and brief duration of symptoms
Unilateral weakness or paralysis
Dysphasia (disruption in language production and comprehension)
Ataxia, vertigo, or loss of balance
Vision loss, diplopia

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3
Q

What are the risk factors for TIA?

A

Cardiovascular disease (atrial fibrillation, valvular heart disease, carotid stenosis, congestive heart failure, hypertension)
Diabetes mellitus
Hyperlipidaemia
Excessive alcohol and smoking

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4
Q

What are the 1st line investigations for a TIA?

A

Blood glucose (to exclude hypoglycaemia as cause)
FBC and platelet count (to exclude infection)
Fasting lipid profile (to evaluate for treatable atherosclerotic risk factors)
Serum electrolytes (to exclude electrolyte imbalance)
ECG (AF/arrhythmias/myocardial infarction?)
CT scan only if patient has bleeding disorder or taking anticoagulants
MRI
Carotid doppler

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5
Q

How is TIA treated?

A

300mg aspirin - unless patient has bleeding disorder or taking anticoagulant
secondary prevention: clopidogrel, 20-80mg atorvastatin

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6
Q

How does a migraine present?

A

Prolonged headache (4 to 72 hours) that is worse with activity - throbbing sensation, often unilateral
Nausea
Photophobia and phonophobia
Aura

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7
Q

What are the characteristics of aura?

A

Positive phenomena (visual sparkles, flashing lights)
Negative phenomena (visual loss or scintillating scotoma)
Sensory symptoms (numbness, tingling)

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8
Q

What are some risk factors for migraine?

A

Family history
Female sex
Obesity
Stressful life events
Medication overuse
Sleep disorders

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9
Q

How is migraine treated?

A

1st line: oral triptan (sumatriptain) and NSAID (aspirin, diclofenac, ibuprofen, naproxen)/paracetamol
Anti-emetic (metoclopramide or promethazine) - non-oral preparation
Oral or IV fluids
Can use corticosteroids (e.g. dexamethasone or prednisolone)

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10
Q

What preventative therapies are given for migraines?

A

Propranolol or topiramate (although, topiramate is teratogenic) - propranolol should be avoided in asthmatics
2nd line: acupuncture, riboflavin, frovatriptan for people with predictable menstrual migraines

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11
Q

How does a tension-type headache present?

A

Generalised head pain (often bilateral pressure-like and non-throbbing, constricting pain) - frontal or occipital
Not aggravated by routine physical activity
Mild-to-moderate intensity
May have peri-cranial tenderness

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12
Q

How is tension-type headache treated?

A

Simple analgesics (aspirin, paracetamol, ibuprofen, naproxen)
Low-dose tricyclic antidepressants (amitriptyline) may reduce the frequency and intensity of attacks

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13
Q

How does idiopathic raised intracranial hypertension present?

A

headache (pressure-like or throbbing) - worst first thing in morning and last thing at night
visual field loss (enlarged blind spot)
photophobia
optic disc swelling
blurred vision
sixth nerve palsy - cannot abduct the eye

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14
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Female sex
Obesity and weight gain
Certain medication use (OCP, steroids, tetracyclines, lithium)

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15
Q

How is idiopathic intracranial hypertension investigated?

A

Visual field testing (enlarged blind spot, inferonasal loss, other nerve fibre bundle defects, or constriction of the field)
Dilated fundoscopy (papilloedema)
MRI brain
Lumbar puncture at L3/L4 (raised pressure)

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16
Q

How is idiopathic intracranial hypertension treated?

A

Weight loss
Acetazolamide or furosemide (diuretics) or topiramate
Analgesia (amitriptyline or naproxen)
Surgery (optic nerve sheath decompression, CSF shunting)

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17
Q

What are the key diagnostic factors of trigeminal neuralgia?

A

Facial pain (restriction to trigeminal distributions)
Usually unilateral
Electric shock-like, sharp, shooting
Multiple attacks a day, lasting few seconds - minutes; periods of remission for months

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18
Q

What are the possible triggers of trigeminal neuralgia?

A

Vibration
Skin contact (e.g. shaving, washing)
Brushing teeth
Oral intake
Exposure to the wind

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19
Q

What are the risk factors for trigeminal neuralgia?

A

Increased age
Multiple sclerosis
More common in females

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20
Q

How is trigeminal neuralgia diagnosed?

A

Diagnosis is usually clinical
Brain MRI to exclude other causes

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21
Q

How is trigeminal neuralgia treated?

A

anticonvulsant (carbamazepine)
referral to neurology if unresponsive to carbammazepine
Baclofen if unresponsive to anticonvulsants
Microvascular decompression or ablative surgery if unresponsive to medication

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22
Q

What are the key diagnostic factors for chronic fatigue syndrome?

A

Persistent disabling fatigue (>50% of time) not alleviated by rest
Exertional exhaustion
Short-term memory/concentration impairment
Sore throat
Generalised arthralgia without inflammation
Headaches
Orthostatic intolerence
Widespread muscle pain
Tender lymph nodes and flu-like symptoms
Dizziness/lightheadedness
Temperature hypersensitivity
Co-morbid depression/anxiety

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23
Q

What are the risk factors for chronic fatigue syndrome?

A

Female sex
30-50 years
Epstein-Barr infection in adolescents

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24
Q

How is chronic fatigue syndrome investigated?

A

DePaul symptom questionnaire
FBC, ESR, CRP, TSH, HIV antibody test (normal)

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25
Q

What are the symptoms of an anterior cerebral artery stroke?

A

MEDIAL FRONTAL AND TEMPORAL LOBES
Paralysis of contralateral structures (leg >arm, face)
Disturbance of intellect and executive function
Loss of appropriate social behaviour

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26
Q

What are the symptoms of a middle cerebral artery stroke?

A

LATERAL FRONTAL AND TEMPORAL LOBES
Contralateral hemiplegia (arm>face)
Contralateral hemisensory deficits
Hemianopia
Aphasia (left sided weakness)

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27
Q

What are the symptoms of a posterior cerebral artery stroke?

A

Visual agnosia
Homonymous hemianopia

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28
Q

What are the risk factors for stroke?

A

CVD, e.g. angina, MI, peripheral vascular disease
Previous stroke or MIA
Atrial fibrillation
Hypertension
Diabetes
Smoking
Combined contraceptive pill
Vasculitis
Thrombophilia

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29
Q

How is stroke investigated?

A

Non-contrast CT head (first line)
Diffuse-weighted MRI
Angiography
Carotid ultrasound to assess for carotid stenosis
Serum glucose (exclude hypoglycaemia)
Serum electrolytes (exclude hyponatraemia)

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30
Q

How is ischaemic stroke treated?

A

Thrombolysis with alteplase (tissue plasminogen activator that breaks down clots) - only if hemorrhage excluded and within 4.5 hours of symptom onset
Aspirin 300mg to prevent further clots
Thrombectomy if occlusion confirmed on imaging - within 6 hours
Secondary prevention: clopidogrel, atorvastatin, carotid endarterectomy/stenting

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31
Q

What are the features of a total anterior circulation infarct (TACI)?

A

Involves middle and anterior cerebral arteries
Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
Homonymous hemianopia
Higher cognitive dysfunction e.g. dysphasia

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32
Q

What are the features of a partial anterior circulation infarct (PACI)?

A

Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of:
Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
Homonymous hemianopia
Higher cognitive dysfunction e.g. dysphasia

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33
Q

What are the features of a lacunar infarct?

A

Involves perforating arteries around the internal capsule, thalamus, and basal ganglia
Presents with 1 of the following:
Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
Pure sensory stroke.
Ataxic hemiparesis

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34
Q

What are the features of a posterior circulation infarct?

A

Involves vertebrobasilar arteries
Presents with 1 of the following:
Cerebellar or brainstem syndromes
Loss of consciousness
Isolated homonymous hemianopia

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35
Q

What are the risk factors for subdural haemorrhage?

A

Head trauma
Coagulopathy and anticoagulant use
Advanced age (>65 years)
Chronic alcohol use

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36
Q

What are the symptoms of subdural haemorrhage?

A

Evidence of trauma
Headache
Nausea and vomiting
Diminished eye, motor and verbal response
Confusion
Loss of consciousness/decreased alertness
Seizure
Speech, vision, sensory changes

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37
Q

How is subdural haemorrhage investigated?

A

Non-contrast CT scan (crescent shape, can cross over sutures)

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38
Q

How is an acute subdural haemorrhage treated?

A

If small or incidental finding, conservative management
Surgical options include monitoring of ICP and decompressive craniectomy

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39
Q

What are some causes of subarachnoid haemorrhage?

A

Head trauma
Ruptured intracranial aneurysm (most common)
Arteriovenous malformations
Anticoagulant use

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40
Q

How is a chronic subdural haematoma treated?

A

If small in size or incidental finding with no associated deficit, can be managed conservatively
If patient is confused, has neurological deficits or severe image findings, surgical decompression with burr holes

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41
Q

What are the risk factors for subarachnoid haemorrhage?

A

Hypertension
Smoking
FHx
Autosomal dominant polycystic kidney disease
Alcohol use
Age >50 years
Marfan’s/Ehlers-Danlos

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42
Q

What are the symptoms of subarachnoid haemorrhage?

A

Severe sudden-onset thunderclap headache (lasts an hour)
Loss of/depressed consciousness
Neck stiffness and muscle aches
Photophobia
Nausea and vomiting
Seizures
Can compress CNIII, causing eyelid drooping, diplopia, orbital pain

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43
Q

How is subarachnoid haemorrhage investigated?

A

Non-contrast CT head (hyperdense areas in subarachnoid space)
U&Es (hyponatraemia due to SIADH)
ECG (arrhythmias, long QT, ST segment or T-wave abnormalities)
CT angiography to identify causal pathogen
Lumbar puncture: xanthochromia, blood in CSF

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44
Q

How is subarachnoid haemorrhage treated?

A

Nimodipine (CCB) to prevent vasospasm/delayed cerebral ischaemia
Consider prophylactic sodium valproate if seizures occurring
Stop and reverse anticoagulation
Endovascular coiling for intracranial aneurysms

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45
Q

What are the symptoms of extradural haemorrhage?

A

Patient initially loses, briefly regains and then loses consciousness again after low-impact head injury - lucid period
Fixed and dilated pupil (compression of parasympathetic fibres of CNIII)

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46
Q

What is the most common cause of extradural haemorrhage?

A

Damage to the pterion, leading to rupture of the middle meningeal artery

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47
Q

How is extradural haemorrhage investigated?

A

CT head shows biconvex haematoma

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48
Q

How is extradural haemorrhage managed?

A

No neurological deficit: cautious clinical and radiological observation
Otherwise, craniotomy and evacuation of haematoma

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49
Q

What are the symptoms of Bell’s palsy?

A

Facial nerve palsy (CNVII) - involvement of all nerve branches
Unilateral facial weakness and drooping (non-forehead sparing)
Keratoconjunctivitis sicca (dry eye) - inability to close eye
Post-auricular pain
Hyperacusis (sensitivity to sound)
Loss of taste on anterior 2/3 of tongue

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50
Q

How is Bell’s palsy diagnosed?

A

Clinical diagnosis of exclusion
Exclude stroke, infections (Lyme, TB, HIV), systemic disease (DM, sarcoidosis)

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51
Q

How is Bell’s palsy treated?

A

Oral prednisolone
Eye protection (e.g. eye drops) as dry eye is common - may lead to exposure keratopathy
Surgical Decompression & Anti-Virals (Acicolvir) if severe palsy

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52
Q

What are the risk factors for Bell’s palsy?

A

Intranasal influenza vaccination
Pregnancy (particularly in third term)
Upper RTI
Arid/cold climate
FHx

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53
Q

What are the symptoms of Parkinson’s disease?

A

CLINICAL DIAGNOSIS
Resting unilateral ‘pill rolling’ tremor
Cogwheel rigidity
Bradykinesia (shuffling gait, hypomimia, smaller handwriting)
Depression
Postural instability
Cognitive impairment and memory problems
Insomnia

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54
Q

How is Parkinson’s treated?

A

Levodopa (synthetic dopamine) - co-careldopa or co-benyldopa, becomes less effective over time
COMT inhibitor (stops degradation of levodopa) - entacapone
Dopamine agonists - cabergoline, pergolide (prolonged use can cause pulmonary fibrosis)
Monoamine oxidase-B inhibitors - rasagiline

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55
Q

What are the side effects of levodopa?

A

Dyskinesias (excessive motor activity)
Dystonia (abnormal postures or exaggerated movements)
Chorea (jerking movements)
Athetosis (writhing movements)

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56
Q

What is the difference between Parkinson’s and an essential tremor?

A

Parkinson’s: worse with rest, unilateral, improves with intentional movement, no change with alcohol
Essential tremor: improves with rest, symmetrical, worse with intentional movement, improves with alcohol

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57
Q

What are the risk factors for essential tremor?

A

Advancing age
Family history
White ancestry
Environmental toxins (pesticides, lead, mercury)

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58
Q

What are the symptoms of essential tremor?

A

Bilateral upper limb tremor
More prominent with intentional movement
Improved by alcohol
CLINICAL DIAGNOSIS

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59
Q

How is essential tremor managed?

A

Not treated if no functional or psychological problems
Propranolol
Primidone (anti-epileptic)

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60
Q

What are the risk factors for myasthenia gravis?

A

Family history of autoimmune disorders (pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE)
Cancer of the thymus gland - thymoma

61
Q

What are the symptoms of myasthenia gravis?

A

Weakness that worsens with muscle activity and improves with rest - symptoms minimal in the morning and worse at the end of the day
Diplopia (double vision) - extraocular eye weakness
Ptosis (drooping of eyelids)
Dysphagia (difficulty swallowing)
Slurred speech
Facial weakness
Shortness of breath

62
Q

How is myasthenia gravis investigated?

A

FVC - may drop due to respiratory muscle weakness
Serum acetylcholine receptor antibodies
CT thorax to exclude thymoma
EMG - diminished response to repetitive stimulation
Muscle-specific tyrosine kinase antibodies
Tensilon test

63
Q

What is the tensilon test?

A

IV edrophonium is given - blocks cholinesterase enzymes so more Ach stays in the synapse
Briefly and temporarily reduces muscle weakness

64
Q

How is myasthenia gravis treated?

A

Long-acting acetylcholinesterase inhibitors (pyridostigmine)
Immunosuppression - suppresses production of autoantibodies (azathioprine, prednisolone)
Rituximab

65
Q

What is myasthenic crisis?

A

Often triggered by illness, e.g. respiratory tract infection
Weakness in respiratory muscles, leading to respiratory failure

66
Q

How is myasthenic crisis treated?

A

Intubation and mechanical ventilation
Plasma exchange or IV immunoglobulin

67
Q

What are the risk factors for MS?

A

Young adult (<50)
Female
Family history
Epstein-Barr virus
Low vitamin D
Smoking
Obesity

68
Q

What are the symptoms of MS?

A

Lethargy and headache
Optic neuritis (pain with eye movement and temporary vision loss in one eye)
Uhthoff’s phenomenon: worsening of vision with rise in body temp
Internuclear opthalmoplegia
Lhermitte’s sign: electric shock sensation in limbs on neck flexion
Paraesthesia and numbness
Trigeminal neuralgia
Urinary incontinence
Sexual dysfunction
Sensory or cerebellar ataxia
Spastic weakness
Leg cramping

69
Q

What are the subtypes of MS?

A

Relapsing-remitting (most common) - active or worsening? episodes of disease (lasting 1-2 months) followed by recovery
Secondary progressive - relapsing-remitting at first (after 10-15 years), but now progressive worsening of symptoms
Primary progressive - worsening of disease from point of diagnosis

70
Q

How is MS diagnosed?

A

Requires demonstration of lesions disseminated in space and time (lesions must have occurred in at least 2 different places at least 2 different times)
MR with contrast: shows lesions
Lumbar puncture: shows oligoclonal bands in CSF - NOT SEEN IN THE SERUM
Visually evoked potentials - slower electrical conduction

71
Q

How is MS managed?

A

Acute relapse: oral or IV methylprednisolone
Relapsing: DMARDs and biologics (natalizumab), immunomodulators (beta-interferon)
Spasticity: gabapentin, baclofen
Neuropathic pain: gabapentin, amitriptyline

72
Q

What are the subtypes of motor neurone disease?

A

Amyotrophic lateral sclerosis: LMN signs in arms and UMN signs in legs
Primary lateral sclerosis: UMN signs only
Progressive muscular atrophy: LMN signs only, affects distal muscles before proximal
Progressive bulbar atrophy: loss of function of brainstem motor nuclei - palsy of tongue, muscles of chewing/swallowing, facial muscles

73
Q

What are the symptoms of motor neurone disease?

A

LMN signs: muscle wasting, reduced tone, fasciculations (twitches in the muscles), reduced reflexes
UMN signs: increased tone/spasticity, brisk reflexes, upgoing plantar responses
Absence of sensory symptoms
Wasting of thenar muscles and wasting of tongue base
Asymmetrical symptoms
Dysphagia
Shortness of breath

74
Q

How is motor neurone disease investigated?

A

Clinical diagnosis
Nerve conduction studies: normal motor conduction
EMG shows signs of denervation (decreased APs with increased amplitude)
MRI to exclude cord compression

75
Q

How is motor neurone disease managed?

A

Patients usually die of respiratory failure or pneumonia - Non-invasive ventilation (NIV) at home
Riluzole
Edaravone

76
Q

What organism causes meningitis most commonly in neonates?

A

Group B Streptococcus (contracted during birth from mother’s vagina)

77
Q

What organisms commonly cause bacterial meningitis?

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae

78
Q

What organisms commonly cause viral meningitis?

A

Herpes simplex virus (HSV)
Enterovirus
Varicella Zoster virus

79
Q

What are the signs and symptoms of meningitis?

A

Headache
Fever
Neck stiffness
Altered mental status
Nausea and vomiting
Photophobia
Seizures
Purpuric rash
Non-blanching rash (meningococcal septicaemia)
Kernig’s and Brudzinski’s sign

80
Q

How is meningitis investigated?

A

Lumbar puncture (CSF protein, WCC, glucose, culture, PCR)
Blood culture

81
Q

How is meningitis managed?

A

IV/IM benzylpenicillin (community)
IV cefotaxime and amoxicillin (<3 months, hospital)
IV ceftriaxone (>3 months, hospital)
Vancomycin if risk of penicillin-resistant pneumococcal infection (recent foreign travel, prolonged antibiotic exposure)
Dexamethasone - reduce frequency and severity of neurological damage

82
Q

When is lumbar puncture contraindicated?

A

Raised ICP
focal neurological signs
papilloedema
significant bulging of the fontanelle
disseminated intravascular coagulation
signs of cerebral herniation
Meningococcal septicaemia

83
Q

What are the complications of meningitis?

A

Sensorineural hearing loss
Seizures
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits, e.g. limb weakness or spasticity

84
Q

What does CSF analysis look like for bacterial meningitis?

A

Cloudy appearance
High protein
Low glucose
High WCC (neutrophils)

85
Q

What does CSF analysis look like for viral meningitis?

A

Clear appearance
Mildy raised/normal protein
Normal glucose
High WCC (lymphocytes)

86
Q

What are the causes of optic neuritis?

A

MS
Sarcoidosis
Systemic lupus erythematosus
Diabetes
Syphilis
Measles
Mumps
Lyme disease

87
Q

What are the features of optic neuritis?

A

Unilateral decrease in visual acuity over hours or days
Central scotoma (enlarged blind spot)
Pain on eye movement
Relative afferent pupillary defect (pupils respond differently to light stimuli)
Impaired colour vision

88
Q

How is optic neuritis investigated?

A

MRI brain and orbits with gadolinium contrast

89
Q

How is optic neuritis treated?

A

Methylprednisolone and prednisolone
Recovery usually takes 4-6 weeks

90
Q

How does a focal seizure present?

A

With (simple) or without impaired consciousness or awareness
Hallucinations
Memory flashbacks
Deja vu or jamais vu
Jacksonian march

91
Q

What are the features of generalised tonic-clonic seizures?

A

Tongue biting
Urinary incontinence
Post-ictal period (patient is drowsy/tired for 15 minutes)
Irregular breathing
Loss of consciousness
Muscle tensing and muscle jerking

92
Q

How are seizures treated?

A

Generalised tonic-clonic: sodium valproate for males, lamotrigine or levetiracetam for females
Focal seizures: lamotrigine, levetiracetam
Absence seizures: ethosuximide
Myoclonic: sodium valproate for males, levetiracetam for females
Tonic: sodium valproate for males, lamotrigine for females

93
Q

What is status epilepticus?

A

A seizure lasting >5 minutes
>2 seizures within a 5 minute period

94
Q

How is status epilepticus treated?

A

ABC
IV lorazepam in hospital
PR diazepam or buccal midazolam in prehospital setting
IV phenytoin if seizure persists

95
Q

How is epilepsy investigated?

A

Clinical diagnosis - two or more unprovoked seizures 24 hours apart
EEG - classifies epilepsy and confirms diagnosis
MRI brain
Capillary blood glucose

96
Q

What are the side effects of sodium valproate?

A

Teratogenic
Liver damage and hepatitis
Hair loss
Tremor
Ataxia
Increased appetite and weight gain

97
Q

What are the side effects of carbamazepine?

A

Agranulocytosis
Aplastic anaemia
Induces the P450 system so there are many drug interactions
Steven-Johnson syndrome
Dizziness
Hyponatraemia due to SIADH

98
Q

What are the side effects of lamotrigine?

A

Steven-Johnson syndrome or DRESS syndrome
Leukopenia

99
Q

What are the side effects of phenytoin?

A

Folate and vitamin D deficiency
Megaloblastic anaemia (folate deficiency)
Osteomalacia (vitamin D deficiency)

100
Q

How does drug-induced parkinsonianism differ from Parkinson’s disease?

A

Drug-induced motor symptoms are rapid onset and bilateral
Rigidity and rest tremor are less common

101
Q

What are the risk factors for Meniere’s disease?

A

FHx
Recent viral illness
Autoimmune disorders
Middle-aged adult

102
Q

What are the symptoms of Meniere’s disease?

A

Vertigo
Tinnitus
Hearing loss (sensorineural)
Feeling of fullness in the ear
Unexplained falls (‘drop attacks’) without loss of consciousness
Spontaneous nystagmus during an attack (usually unidirectional)
Positive Romberg test (swaying or falling when asked to stand with feet together and eyes closed)
TYPICALLY UNILATERAL SYMPTOMS

103
Q

How is Meniere’s disease diagnosed?

A

Clinical diagnosis by ENT specialist
Audiology assessment to evaluate hearing loss

104
Q

How is Meniere’s disease treated?

A

ACUTE ATTACKS: prochlorperazine, antihistamines
PROPHYLAXIS: betahistine

105
Q

What are the risk factors for brain abscess?

A

Sinusitis, otitis media (adults, Streptococcus species)
Meningitis
Recent neurosurgery
Endocarditis

106
Q

What are the symptoms of brain abscess?

A

Dull, persistent headache - ruptured abscess is associated with sudden worsening of headache and meningism
Raised ICP - nausea, vomiting, papilloedema, seizures
Fever
Focal neurology (3rd or 6th nerve palsy secondary to raised ICP)
Positive Kernig or Brudzinki signzol

107
Q

How is brain abscess diagnosed?

A

MRI with contrast (ring enhancing lesions) - best initial test
FBC (leukocytosis)
ESR and CRP (raised)
Biopsy - best confirmatory test

108
Q

How is brain abscess treated?

A

Surgery (craniotomy)
IV antibiotics (ceftriaxone and metronidazole)
Dexamethasone for ICP

109
Q

What are the risk factors for encephalitis?

A

Age <1y or >65y
Immunodeficiency
Viral infections (most common is HSV)
Organ transplant
Animal or insect bites

110
Q

what organism typically causes encephalitis?

A

HSV-1
typically affects temporal and inferior frontal lobes

111
Q

What are the symptoms of encephalitis?

A

fever
headache
seizures
psychiatric symptoms
vomiting
focal features, e.g. aphasia

112
Q

How is encephalitis investigated?

A

CSF analysis (lymphocytosis, elevated protein, normal glucose)
CSF viral PCR will confirm HSV
CT/MRI - CT showing temporal lobe changes is herpes simplex encephalitis

113
Q

How is encephalitis treated?

A

IV aciclovir

114
Q

What are the symptoms of benign paroxysmal positional vertigo?

A

Recurrent episodes of vertigo
Triggered by changes in head movements
20-60 second episodes, patients asymptomatic between attacks

115
Q

What are the risk factors for BPPV?

A

Female sex
Age >50 years

116
Q

How is BPPV diagnosed?

A

Dix-Hallpike manoeuvre - rotational beats of nystagmus towards the affected ear

117
Q

How is BPPV treated?

A

Epley manoeuvre
Brandt-Daroff exercises
Betahistine (prescribed but of limited use)

118
Q

What are the causes of Wernicke’s encephalopathy?

A

Thiamine (B1) deficiency
Most commonly seen in alcoholics
Persistent vomiting
Stomach cancer
Dietary deficiency

119
Q

What are the symptoms of Wernicke’s encephalopathy?

A

Oculomotor dysfunction: nystagmus, opthalmoplegia
Gait ataxia (Wide-based, small steps)
Encephalopathy: confusion, disorientation, apathy

120
Q

How is Wernicke’s encephalopathy treated?

A

IV thiamine

121
Q

What are the causes of spinal cord compression?

A

Trauma
Disc herniation
Vertebral metastases
Infection (esp TB)
Epidural haematoma

122
Q

What are the features of spinal cord compression?

A

UMN signs below level of lesion, LMN signs at level of lesion
Back pain (worse when coughing or lying down is red flag)
Numbness or paraesthesia
Faecal incontinence
Urinary retention
Hyper-reflexia

123
Q

How is spinal cord compression investigated?

A

MRI spine - recommended within 24 hours of presentation

124
Q

How is spinal cord compression managed?

A

Surgical decompression
High-dose oral dexamethasone for malignancy

125
Q

What are the features of a lacunar infarct?

A

Involves perforating arteries around the internal capsule, thalamus, and basal ganglia
Presents with 1 of the following:
Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
Pure sensory stroke.
Ataxic hemiparesis

126
Q

What are the features of Guillain-Barré syndrome?

A

Back/leg pain as initial symptom
Symmetrical ascending weakness (starting at the feet and moving up the body)
Reduced reflexes
Peripheral loss of sensation or neuropathic pain
May have facial nerve weakness
Preceding campylobacter jejuni infection

127
Q

How is Guillain-Barré diagnosed?

A

Clinically - uses the Brighton criteria
Nerve conduction studies (reduced signal through the nerves)
Lumbar puncture for CSF (raised protein with a normal cell count and glucose)

128
Q

How is Guillain-Barré managed?

A

IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis

129
Q

What is carpal tunnel syndrome?

A

Compression of the median nerve (C6-T1) in the carpal tunnel

130
Q

What are the causes of carpal tunnel syndrome?

A

idiopathic
pregnancy
oedema e.g. heart failure
lunate fracture
rheumatoid arthritis

131
Q

What are the features of carpal tunnel syndrome?

A

Paraesthesia/pain in thumb, index and middle fingers
Weakness of thumb movements
Weakness of grip strength
Difficulty with fine movements involving the thumb
Wasting of the thenar muscles (muscle atrophy)

132
Q

How is carpal tunnel syndrome investigated?

A

Nerve conduction studies
Tinel’s sign: tapping causes paraesthesia
Phalen’s sign: flexion of wrist causes symptoms

133
Q

How is carpal tunnel syndrome managed?

A

corticosteroid injection
wrist splints at night
surgery: flexor retinaculum is cut to release the pressure on the median nerve

134
Q

How is GCS (eyes) scored?

A

Spontaneous = 4
Speech = 3
Pain = 2
None = 1

135
Q

How is GCS (verbal) scored?

A

Orientated = 5
Confused conversation = 4
Inappropriate words = 3
Incomprehensible sounds = 2
None = 1

136
Q

How is GCS (motor) scored?

A

Obeys commands = 6
Localises pain = 5
Normal flexion = 4
Abnormal flexion = 3
Extends = 2
None = 1

137
Q

What are the causes of raised intracranial pressure?

A

idiopathic intracranial hypertension
traumatic head injuries
infection (meningitis)
tumours
hydrocephalus

138
Q

What are the features of raised ICP?

A

headache
vomiting
reduced levels of consciousness
papilloedema
Cushing’s triad (widening pulse pressure, bradycardia, irregular breathing)

139
Q

how is raised ICP investigated?

A

CT/MRI
invasive ICP monitoring

140
Q

how are cluster headaches treated?

A

acute attacks: 100% oxygen via non-rebreathe mask, subcutaneous/nasal triptan
verapamil prophylaxis

141
Q

what are the features of giant cell arteritis?

A

typically patient >60 years old
usually rapid onset (e.g. <1 month)
headache
jaw claudication (pain on chewing food)
scalp tenderness
tender, palpable temporal artery - may be pulselss
diplopia, temporary visual loss
may have features of polymyalgia rheumatica

142
Q

how is giant cell arteritis investigated?

A

raised ESR
temporal artery biopsy - skip lesions may be present
start steroids as soon as temporal arteritis is suspected, do not wait for biopsy

143
Q

how is giant cell arteritis treated?

A

high dose prednisolone if no visual loss
IV methylprednisolone if evolving visual loss
alternative diagnosis considered if no dramatic response

144
Q

what are the features of subacute combined degeneration of the cord?

A

symmetrical distal burning/tingling - more legs, than arms
muscle weakness, hyperreflexia, spasticity
brisk knee reflexes, absent ankle reflexes
positive Romberg’s sign
sensory ataxia: gait abnormalities

145
Q

what are the features of intracranial venous thrombosis?

A

headache
confusion/drowsiness
impaired vision
nausea and vomiting
seizures
cranial nerve palsies
papilloedema

146
Q

how is intracranial venous thrombosis investigated?

A

MR venography (gold standard)
non-contrast CT (hyperdensity in affected sinus)

147
Q

what are the risk factors for intracranial venous thrombosis?

A

COP
pregnancy
prothrombotic haematological conditions
dehydration, sepsis

148
Q

how is intracranial venous thrombosis treated?

A

LMWH

Phase 1c: Conditions (18 decks)

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