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2a high tier > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the aetiology of an ischaemic stroke?

A
  • Small vessel occlusion/ thrombosis in situ
  • Cardiac emboli from AF, MI or infective endocarditis
  • Large artery stenosis
  • Atherothromboembolism
  • Hypoperfusion, vasculitis, hypervisocity
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2
Q

What is the aetiology of a haemorrhagic stroke?

A

CNS bleeds due to:

  • Trauma
  • Aneurysm rupture
  • Anticoagulation
  • Thrombolysis
  • Carotid artery dissection
  • Subarachnoid haemorrhage
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3
Q

What is the pathophysiology of an ischaemic stroke?

A
  • Arterial disease and atherosclerosis
  • Thrombosis occurs at the site of an atheromatous plaque in the carotid/ vertebral/ cerebral arteries
  • Large artery stenosis acts as an embolism source rather than occluding the vessel
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4
Q

What is the pathophysiology of a haemorrhagic stroke?

A

Hypertension resulting in micro aneurysm rupture

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5
Q

What are the risk factors for a stroke?

A
  • Male
  • Black or Asian
  • Hypertension
  • Past TIA
  • Smoking
  • Diabetes mellitus
  • Increasing age
  • Heart disease
  • Alcohol
  • Polycythaemia
  • AF
  • High cholesterol
  • Combined oral contraceptive pill
  • Vasculitis
  • Infective endocarditis
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6
Q

What is the clinical presentation of an anterior cerebral artery stroke?

A
  • Leg weakness more likely than arm weakness
  • Sensory disturbances in legs
  • Gait apraxia
  • Truncal apraxia
  • Incontinence
  • Drowsiness
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7
Q

What is the clinical presentation of a middle cerebral artery stroke?

A
  • Contralateral arm and leg weakness
  • Contralateral sensory loss
  • Hemianopia
  • Aphasia
  • Dysphasia
  • Facial droop
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8
Q

What is the clinical presentation of a posterior cerebral artery stroke?

A
  • Contralateral homonymous hemianopia
  • Cortical blindness (eyes healthy but brain issues)
  • Visual agnosia (can see but can’t interpret)
  • Prosopagnosia (can’t see faces)
  • Problems naming and distinguishing colours
  • Unilateral headache
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9
Q

What is the clinical presentation of a posterior circulation stroke?

A
  • More catastrophic (wide region supplied)
  • Motor deficits
  • Dysarthria and speech impairment
  • Vertigo, nausea, vomiting
  • Visual disturbance
  • Altered consciousness
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10
Q

What are the differential diagnoses of a stroke?

A
  • Always exclude hypoglycaemia
  • Migraine aura
  • Focal epilepsy
  • Intracranial lesion
  • Syncope due to arrhythmia
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11
Q

How is a stroke diagnosed?

A
  • Urgent CT/ MRI head before treatment to rule out haemorrhagic before starting thrombolysis
  • Pulse, BP and ECG to look for AF
  • Bloods – thrombocytopenia and polycythaemia on FBC; hypoglycaemia on blood glucose
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12
Q

How is a stroke managed?

A
  • Maximise reversible ischaemic tissue
  • Thrombolysis up to 4.5h after onset of symptoms (give tissue plasminogen activator e.g. IV alteplase then antiplatelet therapy 24h later e.g. clopidogrel)
  • If time of onset is unknown, then daily aspirin and lifelong clopidogrel

In haemorrhagic:

  • No antiplatelets
  • Control hypertension
  • Reduced ICP (manually or with diuretics)
  • May need surgery

Risk management for stroke prevention:

  • Platelet treatment (e.g. aspirin with clopidogrel)
  • Cholesterol treatment
  • AF treatment (e.g. warfarin)
  • BP treatment (e.g. Ramipril)
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13
Q

What is the aetiology of a TIA?

A
  • Small vessel occlusion
  • Atherothromboembolism
  • Cardioembolism
  • Hyperviscosity
  • Can result from hypoperfusion in younger people
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14
Q

What is the pathophysiology of a TIA?

A
  • Cerebral ischaemia resulting in a lack of O2 and nutrients to the brain causing cerebral dysfunction
  • Period of ischaemic is short lived and symptoms rarely last more than 15m and resolve before irreversible cell death
  • Gradually progressing symptoms suggests a different pathology e.g. demyelination, tumour or migraine
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15
Q

What are the risk factors of a TIA?

A
  • Increasing age
  • Hypertension
  • Smoking
  • Diabetes
  • Heart disease (valvular, ischaemic, AF)
  • Past TIA
  • Raised packed cell volume
  • Peripheral arterial disease
  • Combined oral contraceptive pill
  • Hyperlipidaemia
  • Excess alcohol
  • Clotting disorder
  • Vasculitis e.g. SLE, GCA
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16
Q

What is the clinical presentation of an anterior circulation TIA?

A
  • Weak, numb contralateral leg ± similar arm symptoms
  • Hemiparesis (weakness on an entire side of the body)
  • Hemi sensory disturbance
  • Dysphagia
  • Sudden transient loss of vision in one eye
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17
Q

What is the clinical presentation of a posterior circulation TIA?

A
  • Double vision
  • Vertigo
  • Vomiting
  • Choking and dysarthria
  • Ataxia
  • Hemisensory loss
  • Hemianopia vision loss
  • Loss of consciousness (rare)
  • Transient global amnesia (episode of confusion/ amnesia lasting several hours followed by complete recovery)
  • Tetraparesis (muscle weakness in all 4 limbs)
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18
Q

What are the differential diagnoses of a TIA?

A
  • Impossible to differentiate from a stroke until a full recovery has been made
  • Hypoglycaemia\migraine aura
  • Focal epilepsy
  • Intracranial lesion
  • Syncope
  • Todd’s paralysis
  • Retinal or vitreous haemorrhage
  • GCA
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19
Q

How is a TIA diagnosed?

A
  • Often based solely on description
  • Bloods: FBC (for polycythaemia), ESR (for vasculitis), glucose (for hypoglycaemia), creatinine, electrolytes, cholesterol
  • Carotid artery doppler ultrasound for stenosis/ atheroma
  • CT/ MRI head
  • ECG (look for AF or evidence of MI ischaemia)
  • CT or diffusion weighted MRI
  • Echocardiogram/ cardiac monitoring to assess for a cardiac cause
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20
Q

How is a TIA managed?

A
  • Immediate aspirin and dipyridamole for 2 weeks then a lower dose
  • P2Y12 inhibitor long term
  • Anticoagulant if they have AF, mitral stenosis or recent septal MI
  • Statin long term
  • Control cardiovascular risk factors
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21
Q

What is the aetiology of a subarachnoid haemorrhage?

A
  • Rupture of saccular aneurysms (e.g. Berry aneurysm) = rupture of the junction of the posterior communicating artery with the internal carotid or the anterior comm with the arterial cerebral
  • Arteriovenous malformation = vascular development malformation
  • Rare = bleeding disorder, mycotic aneurysms, acute bacterial meningitis, tumours
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22
Q

What is the pathophysiology of a subarachnoid haemorrhage?

A

Most common cause is a ruptured aneurysm which leads to tissue ischaemia and rapidly raised ICP

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23
Q

What are the risk factors of a subarachnoid haemorrhage?

A
  • Hypertension
  • Known aneurysm
  • Family history
  • Disease that predispose to aneurysm (polycyctic kidney disease, Ehler’s Danlos, coarctation of aorta)
  • Smoking
  • Bleeding disorders
  • Post-menopausal decreased oestrogen
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24
Q

What is the clinical presentation of a subarachnoid haemorrhage?

A
  • Sudden onset severe occipital headache (incredibly painful)
  • Vomiting, collapse, seizures, coma often follow
  • Depressed level of consciousness
  • Coma/drowsiness may last for days
  • Neck stiffness
  • Kernig’s signs (unable to extend leg at the knee when the thigh is flexed)
  • Brudzinski’s sign (when neck is manually flexed, patient will flex hips and knees)
  • Retinal and vitreous bleeds
  • Papilloedema
  • Vision loss or diplopia
  • Focal neurology
  • Marked increase in BP (reflex following haemorrhage)
  • Sentinel headache (may present earlier, so ask about it in history)
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25
Q

What are the differential diagnoses of a subarachnoid haemorrhage?

A
  • Must be differentiated from a migraine
  • Meningitis
  • Intracranial bleeds
  • Cortical vein thrombosis
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26
Q

How is a subarachnoid haemorrhage diagnosed?

A
  • ABG to exclude hypoxia
  • Head CT = gold standard (seen as a ‘star shaped’ lesion)
  • CT angiogram if aneurysm is confirmed to see extent
  • Lumbar puncture
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27
Q

How is a subarachnoid haemorrhage managed?

specific interventions

A
  • Refer to neurosurgery immediately
  • IV fluids to maintain cerebral perfusion
  • Ca2+ blocker to reduce vasospasm and morbidity
  • Endovascular coiling – FIRST LINE when angiography shows aneurysm
  • Surgery – intracranial stents and balloon remodelling for wide-necked aneurysms
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28
Q

What is the aetiology of a subdural haemorrhage?

A

Trauma due to deceleration from violent injury or dural metastases results in bleeding from the bridging veins between cortex and venous sinuses

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29
Q

What is the pathophysiology of a subdural haemorrhage?

A
  • Bridging veins bleed and form a haematoma between dura and arachnoid, reducing pressure and stopping the bleeding
  • The haematoma starts to autolyse due to the massive increase in oncotic and osmotic pressure, so water is sucked into the haematoma, causing it to enlarge
  • ICP rises gradually over many weeks
  • Midline structures shift away from the side of the clot and if untreated can result in herniation and coning
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30
Q

What are the risk factors of a subdural haemorrhage?

A
  • Traumatic head injury, cerebral atrophy and increasing age (all make bridging veins more vulnerable)
  • Alcoholism, anticoagulation and physical abuse in infancy
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31
Q

What is the clinical presentation of a subdural haemorrhage?

A
  • Interval between injury and symptoms can be days to weeks to months
  • Fluctuating levels of consciousness ± insidious physical or intellectual slowing
  • Sleepiness
  • Headache
  • Personality change
  • Unsteadiness
  • Signs of raised ICP e.g. headache, vomiting, nausea, seizures and raised BP
  • Focal neurology e.g. hemiparesis or sensory loss
  • Occasionally seizures
  • Stupor, coma and coning may follow
  • Symptoms will develop much slower in the elderly due to decrease in brain weight
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32
Q

What are the differential diagnoses of a subdural haemorrhage?

A
  • Stroke
  • Dementia
  • CNS masses e.g. tumours or abscess
  • Subarachnoid haemorrhage
  • Extradural haemorrhage
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33
Q

How is a subdural haemorrhage diagnosed?

A
  • CT head: diffuse spreading, hyperdense crescent shaped collection of blood over 1 hemisphere (sickle/crescent shaped differentiates subdural from extradural)
  • MRI head for subacute haematomas and smaller haematomas
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34
Q

How is a subdural haemorrhage managed?

A
  • Assess and manage ABCs
  • Prioritise head CT
  • Stabilise patient
  • Refer to neurosurgeons
  • Address cause of trauma
  • IV mannitol to reduce ICP
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35
Q

What is the aetiology of an extradural haemorrhage?

A

Most commonly due to a traumatic head injury resulting in fracture of the temporal or parietal bone causing laceration of the middle meningeal artery, typically after trauma to the temple

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36
Q

What is the pathophysiology of an extradural haemorrhage?

A

Blood accumulates rapidly over minutes to hours between the bone and the dura

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37
Q

What is the clinical presentation of an extradural haemorrhage?

A
  • Characteristic history: head injury, brief post-traumatic loss of consciousness or initial drowsiness, lucid interval while haematoma is still small
  • Severe headache, nausea and vomiting, confusion and seizures (due to rising ICP) ± hemiparesis with brisk reflexes
  • Ipsilateral pupil dilates, coma deepens, bilateral limb weakness and breathing becomes deep and irregular
  • Decreased GCS and coning (brain herniates through foramen magnum)
  • Death from respiratory arrest if surgical intervention not fast enough
  • Bradycardia and raised BP are late signs
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38
Q

What are the differential diagnoses of an extradural haemorrhage?

A
  • Epilepsy, carotid dissection and carbon monoxide poisoning

- Subdural haematoma, subarachnoid haemorrhage, meningitis

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39
Q

How is an extradural haemorrhage diagnosed?

A
  • CT head = gold standard (shows hyperdense haematoma)

- Skull XR to see fracture lines (fracture would increase extradural haemorrhage risk)

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40
Q

How is an extradural haemorrhage managed?

A
  • ABCDE emergency management (assess and stabilise patient)
  • IV mannitol for increased ICP
  • Refer to neurosurgery (clot evacuation ± litigation of bleeding vessel)
  • Maintain airway via intubation and ventilation in unconscious patient
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41
Q

What is the aetiology of epilepsy?

A
  • 2/3 idiopathic (often familial)
  • Cortical scarring (head injury years before onset, cerebrovascular disease e.g. cerebral infraction, haemorrhage, CNS infection e.g. meningitis, encephalitis)
  • Space-occupying lesion e.g. tumour
  • Stroke
  • Tuberous sclerosis
  • AD or other dementia
  • Alcohol withdrawal
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42
Q

What is the pathophysiology of primary generalised seizures?

A
  • Simultaneous onset of electrical discharge throughout the whole cortex with no localising features referable to only one hemisphere
  • Bilateral symmetrical and synchronous motor manifestations
  • Always associated with a loss of consciousness
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43
Q

What is the pathophysiology of partial/ focal seizures?

A
  • Focal onset with features referable to a part of one hemisphere e.g. temporal lobe
  • Often seen with underlying structural disease
  • Electrical discharge is restricted to a limited part of the cortex of one cerebral hemisphere
  • These may later become generalised (e.g. secondary generalised tonic-clonic seizures)
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44
Q

What are the risk factors of epilepsy?

A
  • Family history
  • Premature baby small for age
  • Abnormal blood vessels in the brain
  • AD or other dementia
  • Use of drugs e.g. cocaine
  • Stroke/ brain tumour/ infection
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45
Q

What are the 5 types of primary generalised seizure?

A
  • Generalised tonic-clonic
  • Typical absence seizure
  • Myoclonic seizure
  • Tonic seizure
  • Atonic seizure
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46
Q

What is the clinical presentation of the 5 types of primary generalised seizure?
(Generalised tonic-clonic, typical absence, myoclonic, tonic, atonic)

A

GENERALISED TONIC-CLONIC

  • Often no aura
  • Loss of consciousness
  • Tonic phase = rigid stiff limbs (patient will fall to the floor if standing)
  • Clonic phase = generalised bilateral, rhythmic muscle jerking lasting for seconds to minutes
  • Eyes remain open and tongue often bitten
  • May be incontinence of urine/faeces
  • Followed by a period of drowsiness, confusion or coma for several hours

TYPICAL ABSENCE SEIZURE

  • Usually in childhood
  • Ceases activity, stares and pales for a few seconds (suddenly stops talking mid-sentence then carries on where they left off)
  • Often don’t realise they’ve has an attack

MYOCLONIC SEIZURE

  • Sudden isolated jerk of a limb, face or trunk
  • Patient may be thrown suddenly to the ground or have a violently disobedient limb

TONIC SEIZURE

  • Sudden sustained increased tone with a characteristic cry/grunt
  • Intense stiffening of body
  • Stiffening not followed by jerking

ATONIC SEIZURE
- Sudden loss of muscle tone and cessation of movement resulting in a fall

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47
Q

What are the 2 types of partial/ focal seizures?

A
  • Simple partial seizure

- Complex partial seizure

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48
Q

What is the clinical presentation of the 2 types of partial/ focal seizures?
(General symptoms for simple partial seizures and symptoms for each lobe for complex partial seizures)

A

SIMPLE PARTIAL SEIZURE

  • Not affecting consciousness or memory
  • Awareness is unimpaired with focal motor, sensory, autonomic or psychic symptoms
  • No post-ictal symptoms

COMPLEX PARTIAL SEIZURE

  • Affecting awareness or memory before, during, or immediately after the seizure
  • Most commonly arise from the temporal lobe
  • Temporal lobe → aura (deja-vu, auditory hallucinations, funny smells, fear), anxiety or out of body experience, automatisms (lip smacking, chewing, fiddling), post-ictal confusion
  • Frontal lobe → motor features (posturing or peddling movements of the leg), Jacksonian march (seizure ‘marches’ up/down the motor homunculus starting in the face/thumb), post-ictal Todd’s palsy (paralysis of limbs involved in seizure for several hours)
  • Parietal lobe → sensory disturbances (tingling/ numbness)
  • Occipital lobe → visual phenomena (spots, lines or flashes)
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49
Q

What are the differential diagnoses of epilepsy?

A
  • Postural syncope
  • Cardiac arrhythmia
  • TIA
  • Migraine
  • Hyperventilation
  • Hypoglycaemia
  • Panic attacks
  • Non-epileptic seizures
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50
Q

How is epilepsy diagnosed?

A
  • Need at least 2 unprovoked seizures occurring >24h apart to make a clinical diagnosis
  • EEG – not diagnostic, but used to support a diagnosis, may determine seizure type
  • MRI to view hippocampus
  • CT head in emergencies to look for tumours and exclude structural abnormalities
  • Bloods – FBC, electrolytes, Ca2+, renal function, liver function, urine biochemistry, blood glucose
  • Genetic testing e.g. in juvenile myoclonic epilepsy
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51
Q

What are the emergency measures for managing epilepsy?

A
  • ABCDE, glucose, prolonged/ repeated seizure treated with IV/rectal diazepam or lorazepam
  • IV phenytoin loading
  • Anaesthetic and ventilation if still fitting
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52
Q

How are primary generalised seizures managed?

3 medications for each of generalised tonic-clonic and absence seizures

A

GENERALISED TONIC-CLONIC

  • Oral sodium valproate
  • Oral lamotrigine
  • Oral carbamazepine

ABSENCE SEIZURE

  • Oral sodium valproate
  • Oral lamotrigine
  • Oral ethosuximide
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53
Q

What are the neurosurgical treatment options for epilepsy?

A
  • Only if drugs not working
  • If a single defined cause is found (e.g. hippocampal sclerosis or low-grade tumour) then surgical resection can stop seizures
  • Vagal nerve stimulation can reduce seizure frequency and severity
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54
Q

What is the aetiology of Parkinson’s disease?

A
  • Idiopathic
  • Drug induced
  • Combination of environmental factors (pesticides, methyl-phenyl tetrahydropyridine), Parkinson genes, oxidative stress and mitochondrial dysfunction
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55
Q

What is the pathophysiology of Parkinson’s disease?

A
  • Parkinson’s results from mitochondrial dysfunction and oxidative stress causing progressive degeneration of dopaminergic neurons
  • Therefore, reduced striatal dopamine levels due to loss of dopaminergic neurones
  • Less dopamine → thalamus is inhibited resulting in a decrease in movement therefore symptoms of Parkinson’s
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56
Q

What is the clinical presentation of Parkinson’s disease?

General, before motor symptoms, classic triad symptoms

A
  • Onset of symptoms is gradual and commonly presents with impaired dexterity or unilateral foot drop
  • Onset is asymmetrical (one side is always worse than the other)
  • Difficulty with fine movements e.g. doing up buttons
  • Parkinsonian gait = stooped posture, small shuffling steps, reduced arm swing, narrow base, difficulty initiating movement and turning and poor balance
  • Drooling of saliva and difficulty swallowing is a late feature (can lead to aspiration pneumonia as a terminal event)
  • Depression, constipation and increased urinary frequency are all common

Before motor symptoms develop:

  • Anosmia
  • Depression/ anxiety
  • Aches and pains
  • REM sleep disorders
  • Urinary urgency
  • Hypotension and constipation

Classic triad:

  1. TREMOR
    • Worse at rest and often asymmetrical
    • Usually most obvious in the hands
    • Improved by voluntary movements and made worse by anxiety
    • Rhythms gets worse the longer attempted (unique to PD)
  2. RIGIDITY
    • Increased tone in limbs and trunk
    • Limbs resist passive extension through movement
    • Can cause pain and problems turning in bed
  3. BRADYKINESIA/HYPOKINESIA
    • Slow to initiate movement and low, low-amplitude excursions in repetitive actions
    • Reduced blink rate
    • Monotonous hypophonic speech
    • Micrographia (smaller writing)
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57
Q

What are the differential diagnoses of Parkinson’s disease?

A
  • Benign essential tremor (worse on movement and rare while at rest)
  • Multiple cerebral infarcts, Lewy body dementia, drug-induced, Wilson’s disease, trauma, dopamine antagonists
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58
Q

How is Parkinson’s disease diagnosed?

A
  • Clinical based on history and examination
  • Can confirm by response to levodopa
  • MRI head (will show atrophy)
  • Signs that it’s not PD if present early = dementia, incontinence, symmetry in symptoms and early falls
59
Q

How is Parkinson’s disease managed?

A
  • Need to compensate for the loss of dopamine
  • Physiotherapy for balance problems, speech and gait disturbances
  • Oral levodopa with a decarboxylase inhibitor (e.g. co-careldopa) is gold standard of treatment
  • Levodopa has a lot of complications though, so should only be used when other treatments are ineffective
  • Dopamine agonists e.g. oral ropinirole
  • Monoamine Oxidase B (MAO-B) inhibitors e.g. oral selegiline
  • Catechol-O-methyl transferase inhibitors e.g. oral entacapone
  • Deep brain stimulation may help those who are partly-dopamine responsive
60
Q

What is the aetiology of Alzheimer’s dementia?

more than just atrophy

A
  • Degeneration of cerebral cortex with cortical atrophy
  • Accumulation of beta-amyloid peptide results in progressive neuronal damage, neurofibrillary tangles and increases in the number of amyloid plaques and the loss of ACh
61
Q

What is the aetiology of vascular dementia?

A

Brain damage due to cerebrovascular disease (either major stroke, multiple smaller unrecognised strokes or chronic changes in smaller vessels)

62
Q

What is the aetiology of dementia with Lewy bodies?

A
  • Deposition of abnormal protein within neurons in the brain stem and neocortex
  • Associated with Parkinson’s
63
Q

What is the aetiology of fronto-temporal dementia?

A
  • Specific degeneration/ atrophy of the frontal and temporal lobes
  • Behavioural and personality change, early preservation of episodic memory and spatial orientation, emotional unconcern, lowers inhibitions
64
Q

What are other aetiologies of dementia?

A
  • Parkinson’s disease
  • Mixed dementia
  • Huntington’s
  • Liver failure
  • HIV
  • Prion diseases
  • Vitamin B12/ folate deficiency
65
Q

What are the risk factors of dementia?

A
  • Family history
  • Age
  • Down’s syndrome
  • Alcohol use, obesity, high BP, high cholesterol, diabetes
  • Atherosclerosis
  • Depression
  • High oestrogen
66
Q

What is the clinical presentation of Alzheimer’s?

A
  • Insidious onset with steady progression over years
  • Short-term memory loss is usually the most prominent early symptoms
  • Slow disintegration of personality and intellect, eventually affecting all aspects of cortical function
  • Decline in language (difficulty naming and in understanding what is being said), visuospatial skills, apraxia (difficulty carrying out skilled motor tasks) and agnosia (failure to recognise objects)
67
Q

What is the clinical presentation of vascular dementia?

A
  • Stepwise deterioration with declines followed by short periods of stability
  • History of TIAs and strokes
  • Evidence of artheropathy
  • Signs of vascular pathology e.g. raised BP, past strokes and focal CNS signs
68
Q

What is the clinical presentation of dementia with Lewy bodies?

A
  • Fluctuating cognitive impairment with pronounced variation in attention and alertness
  • Prominent or persistent memory loss may not occur in early stages
  • Depression and sleep disorders occur
  • Visual hallucinations
  • Parkinson’s
  • Loss of inhibitions
69
Q

What are the differential diagnoses of dementia?

A
  • Substance abuse
  • Hypothyroidism
  • Space-occupying intracranial lesions
  • Huntington’s
70
Q

How is dementia diagnosed?

A
  • History – assess cognitive functions by asking various questions
  • MMSE score/30 (>25 = normal; 18-25 = mild/moderate impairment; >17 = serious impairment)
  • Blood tests (FBC, liver biochemistry, TFT, B12 and folate)
  • Neuropsychology
  • Brain CT in younger patients or those with atypical presentation
  • MRI to see extent of atrophy
  • Brain function assessment through PET/SPECT scanning and functional MRI
71
Q

How is dementia managed?

prevention, support, meditation

A
  • No specific therapy

PREVENTION:

  • Healthy behaviours
  • Smoking cessation
  • > 6 leisure activities
  • Education
  • Occupation

SUPPORT:

  • Socially active
  • Cognitively active (cognitive stimulation programmes, board games etc.)
  • Specialist memory service
  • Carers may be required

MEDICATION:

  • Blood pressure control to reduce further vascular damage e.g. ramipril
  • Acetylcholinesterase inhibitors to increase ACh (especially in vascular dementia) e.g. oral donepezil or oral rivastigmine
72
Q

What is the aetiology of migraines?

A
  • No specific cause, but there are partial triggers: chocolate, hangovers, orgasms, cheese, oral contraception, lie-ins, alcohol, tumult (load noise), exercise
  • Brain chemical imbalance may be a cause
  • May be caused by changes in the brainstem and its interactions with the trigeminal nerve
73
Q

What is the pathophysiology of migraines?

A
  • Genetic and environmental factors play a role
  • Genetic factors play a role in causing neuronal-hyperexcitability
  • Changes in brainstem blood flow leads to an unstable trigeminal nerve nucleus and nuclei in the basal thalamus
  • Cortical spreading depression – self-propagating wave of neuronal and glial depolarisation that spreads across the cerebral cortex is thought to cause the aura

→ Release of vasoactive neuropeptides results in the process of neurogenic inflammation leading to pain

74
Q

What are the risk factors of migraines?

A
  • Family history (has a strong genetic component)
  • Female
  • Age (majority start in adolescence)
75
Q

What is the clinical presentation of a migraine prodrome?

A
  • May precede the headache by hours/days

- Yawning, cravings and mood/sleep changes

76
Q

What is the clinical presentation of a migraine without aura?

A
  • Attacks last 4-72h
  • Two of the following: unilateral, pulsing, moderate/severe pain in head, aggravated by routine physical activity
  • During headache at least one of: nausea and/or vomiting, photophobia and phonophobia (sound sensitive) during the headache
  • Not attributable to another disorder
77
Q

What is the clinical presentation of a migraine with aura?

A
  • At least 2 attacks
  • Aura precedes the attack by minutes and may persist during it
  • VISUAL: chaotic cascading, jumbling, distorting lines, dots, zigzags, black hole in visual field (scotoma), hemianopia
  • SOMATOSENSORY: paraesthesia spreading from fingers to face
  • Unilateral, pulsatile headache
78
Q

What is the general clinical presentation of a migraine?

A

At least 2 of:

  • Unilateral pain
  • Throbbing-type pain
  • Moderate to severe intensity
  • Motion sensitivity (made worse by head movement of physical activity)

At least 1 of:

  • Nausea/vomiting
  • Photophobia/phonophobia
  • Normal examination with no other attributable cause
79
Q

What are differential diagnoses of a migraine?

A
  • Tension headache (bilateral, tight-band around head)
  • Cluster headache (excruciating, autonomic symptoms)
  • Medication over-use headache
  • Sudden migraine may resemble meningitis or subarachnoid haemorrhage
  • Thromboembolic TIA
  • Brain tumour
  • Temporal arteritis
80
Q

How are migraines diagnosed?

including red flag indications for neuroimaging and indications for lumbar puncture

A
  • Mainly a clinical diagnosis
  • Always examine eyes (papilloedema and other eye issues) and head & neck (scalp, neck muscles and temporal arteries)
  • Lab tests – CRP, ESR
  • Red flag indications for neuroimaging: worse/severe headache, change in migraine pattern, abnormal neuro exam, onset >50y, epilepsy, posteriorly located headache
  • Indications for lumbar puncture: worst headache of life, severe rapid onset, progressive headaches, unresponsive headaches
  • Neuroimaging should precede lumbar puncture to rule out mass/ lesion/ raised ICP
81
Q

How are migraines managed?

lifestyle, acute attack and prevention

A
  • Reduce triggers e.g. avoid dietary factors

ACUTE:

  • No ergots (e.g. opioids)
  • Triptans e.g. sumatriptan
  • NSAIDs (avoid paracetamol or ibuprofen)
  • ± anti-emetic e.g. prochlorperazine

PREVENTION:

  • If >2 attacks per month or if acute treatment is needed >2 times per week
  • Beta-blocker
  • Tricyclic anti-depressant
  • Anti-convulsant
82
Q

What is the aetiology of a tension headache?

A
  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger
  • Eyestrain
  • Anxiety
  • Noise
83
Q

What are the risk factors of a tension headache?

A
  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger
  • Eyestrain
  • Anxiety
  • Noise
84
Q

What is the clinical presentation of a tension headache?

A
  • Episodic (<15d/month) or chronic (>15d/month for at least 3m)
  • Usually has one of the following: bilateral, pressing/tight non-pulsatile, mild/moderate intensity ± scalp muscle tenderness
  • Without vomiting or sensitivity to head movement, no aura
  • Not aggravated by physical activity
  • Tight band-like sensation
  • Pressure behind eyes, mild-moderate pain
  • Headaches can last from 30m to 7d
  • Not attributed to any other disorder
85
Q

What are the differential diagnoses of a tension headache?

A
  • Migraine
  • Cluster headache
  • Giant cell arthritis
  • Frug-induced headache
86
Q

How is a tension headache diagnosed?

A

Clinical diagnosis from history

87
Q

How is a tension headache managed?

A
  • Reassurance and lifestyle advice e.g. regular exercise, avoidance of triggers
  • Stress relief e.g. massage or acupuncture
  • Symptomatic treatment for episodes occurring >2d/week (aspirin, paracetamol, NSAIDs, no opioids, limited analgesia, tricyclic antidepressants)
  • Beware of medication over-use headaches
88
Q

What is the aetiology of a cluster headache?

A
  • Unknown
  • May be due to superficial temporary artery smooth muscle hyper-reactivity to serotonin
  • Hypothalamic grey matter abnormalities
  • Autosomal dominant gene
89
Q

What are the risk factors of cluster headaches?

A
  • Smoker
  • Male
  • Autosomal dominant gene has a role
90
Q

What is the clinical presentation of a cluster headache?

A
  • Abrupt onset
  • Rapid onset of excruciating pain around on eye, temple or forehead
  • Ipsilateral cranial autonomic features: eye may become watery and bloodshot with lid swelling and lacrimation, facial flushing, rhinorrhoea (blocked nose), miosis (excessive pupil constriction) ± ptosis (drooping or falling of upper eyelid)
  • Pain is strictly unilateral and almost always affects the same side
  • Rises to crescendo over minutes and lasts 15-160m once or twice a day
  • Often nocturnal/early morning (often wakes patient from sleep)
  • ± vomiting
  • Episodic = clusters last 4-12w followed by pain-free periods of months or even 1-2y
  • Can be chronic (attacks from >1y without remission)
91
Q

What is the differential diagnosis of a cluster headache?

A

Migraine

92
Q

How is a cluster headache diagnosed?

A
  • Clinical diagnosis

- >5 headaches fulfilling the clinical presentation pattern

93
Q

How is a cluster headache managed?

acute attack and prevention

A

ACUTE ATTACK:

  • Analgesics are unhelpful
  • 100% 15L O2 for 15m via a non-rebreathable mask (not if COPD)
  • Tripan e.g. sub-cut sumatriptan (selective serotonin agonist)

PREVENTION:

  • Calcium channel blocker (FIRST LINE)
  • Avoid alcohol during cluster period
  • Corticosteroids may help during cluster
94
Q

What is the aetiology of a drug overuse headache?

A

Mixed analgesics e.g. paracetamol + codeine/ opiates, ergotamine and triptans

95
Q

What is the clinical presentation of a drug overuse headache?

A

Worsens while on regular analgesia (especially opioids)

96
Q

What is the aetiology of motor neurone disease?

A
  • Usually sporadic and of unknown cause

- Small proportion of cases are familial

97
Q

What is the pathophysiology of motor neurone disease?

A
  • Characterised by selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells
  • Degenerative condition affecting motor neurons, mainly anterior horn cells
  • Relentless and unexplained destruction of upper motor neurones and anterior horn cells in the brain and spinal cord, causing UMN and LMN disorders
  • Caused by reactive oxygen species which damage DNA, lipids and proteins
  • No sensory loss or sphincter disturbance (this distinguishes MND from MS and polyneuropathies)
  • Never affects eye movements (distinguishes from MG)
98
Q

What are the risk factors of motor neurone disease?

A

No established risk factors

99
Q

What are the 4 clinical patterns of motor neurone disease?

A
  • Amyotrophic lateral sclerosis
  • Progressive muscular atrophy
  • Progressive bulbar palsy
  • Primary lateral sclerosis
100
Q

What is the general clinical presentation of motor neurone disease?

A
  • No sensory symptoms or rectal/bladder sphincter issues
  • Think of MND in those >40y with stumbling spastic gait, foot drop ± proximal myopathy weak grip and shoulder abduction or aspiration pneumonia
  • Frontotemporal dementia in 25%
  • Weakness and atrophy spread to other parts of the body regardless of starting body part, with a varying amount of UMN symptoms until the muscles of all 4 extremities and the trunk + bulbar muscles are involved
101
Q

What is the clinical presentation of amyotrophic lateral sclerosis in motor neurone disease?

A
  • UMN + LMN involvement
  • Most common type
  • Loss of motor neurones in motor cortex and anterior horn of the cord
  • Weakness with UMN signs and LMN wasting/ fasciculations (usually in one limb)
  • Split hand sign – thumb side of the hand seems adrift due to excessive wasting around it (much less hypothenar wasting)
  • Cramps are a common but non-specific symptom
  • Examination shows UMN signs e.g. brisk reflexes, extensor plantar response and spasticity
  • Wrist and foot drop
102
Q

What is the clinical presentation of progressive muscular atrophy in motor neurone disease?

A
  • LMN involvement only
  • Presents with weakness, muscle wasting and fasciculations usually starting in one limb and gradually spreading to involve other adjacent spinal segments
  • Affects distal muscle group before proximal
103
Q

What is the clinical presentation of progressive bulbar palsy in motor neurone disease?

A
  • Lower cranial nerves and nuclei initially only affected (CN 9,10,11,12)
  • Dysarthria, dysphagia, nasal regurgitation of fluids and choking
  • LMN lesion of the tongue and muscles of talking and swallowing
  • Flaccid, fasciculating tongue
  • Normal/absent jaw jerk
  • Speech is quiet, horse or nasal
104
Q

What is the clinical presentation of primary lateral sclerosis in motor neurone disease?

A
  • Least common
  • Loss of Betz cells in motor cortex
  • Mainly UMN signs and marked spastic leg weakness with progressive tetraparesis and pseudobulbar palsy
  • No cognitive decline
105
Q

What are the differential diagnoses of motor neurone disease?

A
  • MS or polyneuropathies
  • Myasthenia gravis
  • Diabetic amyotrophy
  • Guillain-Barre syndrome
  • Spinal cord tumours
106
Q

How is motor neurone disease diagnosed?

A

Diagnosis based on clinical findings:

  • Definite = LMN + UMN signs in 3 regions
  • Probable = LMN + UMN signs in 2 regions
  • Probable with lab support = LMN + UMN (or UMN in >1) + EMG showing acute denervation in >2 limbs
  • Possible = LMN + UMN signs in 1 region
  • Suspected = LMN or UMN only in 1+ regions
  • Brain/ cord MRI excludes structural causes
  • Lumbar puncture to exclude inflammatory causes
  • Nerve conduction studies + electromyography to confirm denervation of muscles
107
Q

How is motor neurone disease managed?

A
  • Antiglutamatergic drugs e.g. oral riluzole (prolongs life by 3m)
  • FOR DROOLING: oral propantheline or oral amitriptyline
  • FOR DYSPHAGIA: blend food, nasogastric tube, percutaneous catheter gastrostomy
  • FOR SPASMS: oral baclofen
  • Non-invasive ventilation if respiratory failure
  • Analgesia e.g. NSAIDs
  • Specialist MDT support (neurologist, speech & language therapist, occupational therapist, specialist nurse, physiotherapist etc)
108
Q

What is the aetiology of MS?

A
  • Aetiology is not understood

- Mix of genetic and environmental factors (EBV exposure in childhood may predispose to later MS development)

109
Q

What is the pathophysiology of MS?

A
  • Autoimmune demyelination at multiple CNS sites
  • T-cell mediated (T cells activate B cells to produce autoantibodies against myelin)
  • T lymphocytes cross the BBB and cause a cascade of destruction in the brain’s neuronal cells, resulting in demyelination and therefore conduction disruption
  • Myelin sheath regenerates but is less efficient
  • Repeated demyelination leads to axonal loss and incomplete recovery between attacks
  • Plaques of demyelination are perivenular (occurs around veins) and can occur everywhere in the CNS, but particularly optic nerves, around ventricles, corpus callosum, brainstem, cerebellar connections and cervical cord
110
Q

What are the risk factors of MS?

A
  • EBV exposure
  • Low levels of sunlight and vitamin D
  • Female
  • White
  • Living far from the equator
111
Q

What are the types of MS?

A

RELAPSING AND REMITTING:

  • Most common pattern
  • Symptoms occur in attacks (relapses) with onset over days
  • Recovery (partial or complete) happens over weeks
  • Periods of good health or remission are followed by sudden symptoms or relapses
  • Patients may accumulate disability over time if they don’t fully recover after relapses

SECONDARY PROGRESSIVE:

  • Follows on from relapsing and remitting MS (majority will evolve within 35y of onset)
  • Late stage that consists of gradually worsening symptoms with fewer remissions

PRIMARY PROGRESSIVE:

  • Gradually worsening disability without relapses or remission
  • Typically presents later and is associated with fewer inflammatory changes on MRI
112
Q

What is the clinical presentation of MS?

A
  • Usually presents in young adults (20-40y)
  • Initially monosymptomatic
  • Symptoms may worsen with heat/ exercise (new myelin is inefficient and doesn’t work well in heat)
  • Unilateral optic neuritis (pain in one eye on movement and reduced central vision)
  • Numbness or tingling in the limbs
  • Leg weakness
  • Brainstem demyelination causes diplopia, vertigo, facial numbness/ weakness, dysarthria/ dysphagia and a clumsy/useless hand or limb due to loss of proprioception
  • Cerebellar symptoms e.g. ataxia
  • Trigeminal neuralgia
  • Constipation
  • Spasticity and weakness (can result in stiffness/ tightness of muscles that can interfere with normal movement, speech and gait)
  • Intention tremor
  • Bladder dysfunction e.g. urgency, frequency and incontinence
  • Sexual dysfunction e.g. erectile dysfunction
  • Cognitive decline
  • Amnesia
113
Q

What are the differential diagnoses of MS?

A
  • Hereditary spastic paraplegia
  • Cerebral variant of SLE
  • Sarcoidosis
  • HIV
114
Q

How is MS diagnosed?

A
  • Diagnosis requires 2 or more attacks affecting different parts of the CNS (i.e. 2 CNS lesions disseminated in time and space)
  • Exclude differentials with FBC, inflammatory markers, U&E, LFTs, glucose, HIV serology, auto-antibodies, Ca2+ and vitamin B12
  • MRI scan brain and cord: diagnostic if history matches
  • Lumbar puncture shows oligoclonal IgG bands
  • Electrophysiology (delayed nerve condition suggests demyelination)
115
Q

How is MS managed?

lifestyle, acute relapse, frequent relapse, symptomatic treatment

A
  • Encourage reducing stress as much as possible to reduce number of new lesions
  • Vitamin D supplement if poor diet and sun exposure

ACUTE RELAPSE:
- IV methylprednisolone for less than 3d to shorten relapse

FREQUENT RELAPSE:

  • SC interferon 1B or 1A
  • Disease modifying agents (monoclonal antibodies): IV alemtuzumab or IV natalizumab
  • Dimethyl fumarate

SYMPTOMATIC TREATMENT :

  • For spasticity: physiotherapy, Baclofen, Tizanidine, botox injection
  • For urinary urgency/ frequency: intermittent self-catheterisation
  • Incontinence: anticholinergic alpha-blocker drugs e.g. doxazosin
  • Aggressive treatment is stem cell transplant
116
Q

What is the aetiology of meningitis in adults and children?

A
  • Neisseria meningitides (G-ve diplococci)
  • Streptococcus pneumoniae/ pneumococcus
  • Less common cause is haemophilus influenza
117
Q

What is the aetiology of meningitis in pregnant women and older adults?

A

Listeria monocytogenes (found in cheese which is why it’s avoided in pregnancy)

118
Q

What is the aetiology of meningitis in neonates?

A
  • Escheria coli

- Group B haemolytic streptococcus

119
Q

What is the aetiology of meningitis in the immunocompromised?

A
  • Cytomegalovirus
  • Cryptococcus neoformans
  • TB – mycobacterium tuberculosis
  • HIV
  • Herpes simplex virus
120
Q

What is the pathophysiology of meningitis?

how do the microorganisms reach the meninges?

A

Microorganisms reach the meninges either by direct extension from the ears, nasopharynx, cranial injury or congenital meningeal defect / by bloodstream spread

121
Q

What is the pathophysiology of acute bacterial meningitis?

A
  • Typically sudden
  • Neisseria meningitides transmitted by droplet spread
  • Can lead to meningococcal septicaemia when bacteria invade blood and the presence of endotoxin leads to an inflammatory response causing petechial rash and signs of sepsis
  • Pia arachnoid is congested with polymorphs so a layer of pus forms which may organise to form adhesions causing cranial nerve palsies and hydrocephalus
122
Q

What is the pathophysiology of viral meningitis?

A
  • Predominantly lymphocytic inflammatory CSF reaction without pus formation
  • Little or no cerebral oedema unless encephalitis develops
123
Q

What are the risk factors of meningitis?

A
  • Intrathecal drug administration (into spinal canal)
  • Immunocompromised
  • Elderly
  • Pregnant
  • Bacterial endocarditis
  • Crowding (e.g. military base, university students)
  • Diabetes
  • Malignancy
  • IV drug use
124
Q

What is the classic triad of meningitis symptoms?

A

Headache, neck stiffness and fever

125
Q

What is the clinical presentation of acute bacterial meningitis?

A
  • Onset is typically sudden
  • Papilloedema: swelling of optic disc on fundoscopy, usually bilateral, can occur over hours to weeks, caused by raised ICA
  • Usually intense malaise, fever, rigors, severe headache, photophobia and vomiting within hours or minutes
  • Patient is irritable and prefers to lie still
  • Neck stiffness, positive Kernig’s and Brudzinski’s sign can appear within hours
  • Meningococcal septicaemia is associated with a non-blanching and purpuric skin rash
  • Altered mental state (reduced GCS) with high fever (often absent though)
  • Seizures and focal CNS signs
  • Progressive drowsiness, materialising signs and CN lesions indicate a complication (e.g. venous sinus thrombosis, severe cerebral oedema or cerebral abscess)
126
Q

What is the clinical presentation of viral meningitis?

A
  • Benign, self-limited condition lasting 4-10d

- Headache may follow for some months

127
Q

What is the clinical presentation of chronic meningitis?

A
  • Mycobacterium tuberculosis
  • Long history and vague symptoms of headache, anorexia and vomiting
  • Signs of meningeal triad are often absent or late
128
Q

What are the differential diagnoses of meningitis?

A
  • Aseptic meningitis (due to tumour)
  • Subarachnoid haemorrhage (headache is more sudden)
  • Encephalitis (altered mental state is the predominant symptom)
129
Q

How is meningitis diagnosed?

A
  • Blood cultures before lumbar puncture
  • Blood tests: FBC, U&E, CRP, serum glucose
  • CT head to exclude lesions e.g. tumour
  • CT before lumbar puncture if aged >60y, history of a CNS disease, papilloedema, immunocompromised, focal neurological signs, decreasing consciousness levels
  • Throat swabs (bacterial and viral)
  • Pneumococcal and meningococcal serum PCR
  • If meningococcal septicaemia (non-blanching rash or purpuric rash) then immediate IV benzylpenicillin or IV cefotaxime
130
Q

How is meningitis managed?

A
  • Start antibiotics immediately
  • IV cefotaxime or IV ceftriaxone (can give IV chloramphenicol if severe anaphylaxis)
  • Add IV amoxicillin if >50y or immunocompromised
  • Steroids e.g. oral dexamethasone to reduce cerebral oedema
  • IV vancomycin for return travellers
  • Prophylaxis for contacts: oral ciprofloxacin
131
Q

What is the aetiology of encephalitis?

A
  • Mainly viral (herpes simplex virus 1&2, varicella zoster, EBV, cytomegalovirus, HIV, mumps, measles)
  • Non viral = bacterial meningitis, TB, malaria
132
Q

What is the pathophysiology of encephalitis?

A

Disease which mostly affects the frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs

133
Q

What are the risk factors of encephalitis?

A
  • Extremes of age

- Immunocompromised

134
Q

What us the clinical presentation of encephalitis?

A
  • Whole brain affected – problems with consciousness compared to meningitis
  • Onset can be insidious (over days) or abrupt
  • CLASSIC TRIAD: fever + headache + altered mental state
  • May have signs of meningitis ( = meningo-encephalitis and consists of inflammation of meninges and brain parenchyma)
  • May have a history of travel and/or an animal bite
  • Begins with features of a viral infection: fever, headaches, myalgia, fatigue and nausea

PROGRESSES:

  • Personality and behavioural changes (common early manifestation)
  • Decreased consciousness, confusion and drowsiness
  • Focal neurological deficit (hemiparesis and dysphagia)
  • Seizures
  • Raised ICP and midline shift may occur, resulting in coning
  • Coma
135
Q

What are the differential diagnoses of encephalitis?

A
  • Meningitis
  • Stroke
  • Brain tumour
136
Q

How is encephalitis diagnosed?

A
  • MRI shows area of inflammation and swelling and may have midline shifting
  • Electroencephalography shows periodic sharp and slow wave complexes
  • Lumbar puncture: CSF shows elevated lymphocyte count, also used to viral detection
  • Blood and CSF serology is usually helpful
137
Q

How is encephalitis managed?

A
  • If viral, then immediate treatment with an anti-viral e.g. IV aciclovir (before test results are available)
  • Anti-seizure medication e.g. primidone
  • If meningitis is suspected, then emergency IM benzylpenicillin
138
Q

What is the aetiology of herpes voster (shingles)?

A

Reactivation of varicella zoster virus, usually within the dorsal root ganglia

139
Q

What is the pathophysiology of herpes voster (shingles)?

A
  • Viral infection affecting peripheral nerves
  • When latent virus is reactivated in the dorsal root ganglia it travels down the affected nerve via the sensory root in dermatomal distribution over a period of 3-4d, resulting in perineural and intramural inflammation
  • In immunocompromised patients, the most frequent site of reactivation is the thoracic nerves followed by the ophthalmic division of the trigeminal nerve
  • Can also affect the cervical, lumbar and sacral nerve roots
  • Person with weeping shingles rash can cause chickenpox in non-immune person after close contact
140
Q

What are the risk factors of herpes zoster (shingles)?

A
  • Increasing age
  • Immunocompromised
  • HIV, Hodgkin’s lymphoma and bone marrow transplants
141
Q

What is the clinical presentation of herpes zoster (shingles)?

A
  • Pain and paraesthesia in dermatomal distribution priced rash for days
  • Malaise, myalgia, headache and fever can be present
  • Can be over a week before eruption appears
  • Rash consists of papules and vesicles restricted to the same dermatome (neuritis pain, crust formation and drying occurs over the next week with resolution within 2-3w)
  • Patients are infectious until lesions are dried
  • Rash does not extent outside dermatome
142
Q

What are the differential diagnoses of herpes zoster (shingles)?

A
  • Cholecystitis or renal stones (before rash appears, the pain may come from the chest/ abdominal)
  • Cluster headaches or migraine
  • Atopic eczema, contact dermatitis or herpes simplex or impetigo
143
Q

How is herpes zoster (shingles) diagnosed?

A
  • Clinical diagnosis

- Eruption of rash is virtually diagnostic

144
Q

How is herpes zoster (shingles) managed?

A
  • Oral antiviral therapy within 72h of rash onset
  • Oral aciclovir 5x daily or oral valaciclovir/ famciclovir 2x daily
  • Topical antibiotic treatment for secondary bacterial infection
  • Analgesia e.g. ibuprofen for pain

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