Neurology Flashcards

1
Q

Define cerebrovascular event (stroke)

A

A clinical syndrome caused by disruption of blood supply to the brain (due to infarction or haemorrhage), characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death

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2
Q

Define ischemic stroke

A

An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction (cell death due to lack of blood supply)

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3
Q

What are the 5 types of ischemic stroke?

A
  • Large vessel disease (atherosclerosis/thrombosis)
  • Small vessel disease (microathermoma, lacunes)
  • Cardioembolic (caused by AF, endocarditis, mural thrombus)
  • Other (rare causes e.g. vasculitis, venous thrombosis, carotid dissection)
  • Undefined
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4
Q

Define stroke due to primary intracerebral haemorrhage

A

Rapidly developing clinical signs of neurological dysfunction because of a focal collection of blood within the brain parenchyma or ventricular system, which is not caused by trauma
*secondary intracerebral haemorrhage = due to trauma, blood thinners etc.

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5
Q

Define stroke due to subarachnoid haemorrhage

A

Rapidly developing signs of neurological dysfunction and/or headache (thunderclap) because of bleeding into the subarachnoid space, which is not caused by trauma

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6
Q

What are the risk factors for strokes?

A

Lifestyle factors:
- smoking
- alcohol misuse
- physical inactivity
- poor diet
Established CVD:
- hypertension
- AF
- infective endocarditis
- IHD
- congestive heart failure
- structural defects (valve disease)
Other medical conditions:
- migraine
- hyperlipidaemia
- diabetes mellitus
- hypercoagulable disorders
- connective tissue disorders
- taking combined oral contraceptive
Non-modifiable factors:
- older age
- male sex
- personal/family history of stroke/TIA
- lower level of education

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7
Q

What are the signs/symptoms of a stroke in the anterior circulation?

A

Either hemisphere (symptoms contralateral):
- hemiparesis (upper limb = MCA, lower limb = ACA)
- hemisensory loss (upper limb = MCA, lower limb = ACA)
- visual field defect

Dominant hemisphere (usually LEFT hemisphere)
- language dysfunction (expressive/receptive dysphasia, dyslexia, dysgraphia)

Non-dominant hemisphere (usually RIGHT hemisphere)
- visuospatial dysfunction (geographical agnosia, dressing apraxia, constructional apraxia)
- anosognosia (impaired understanding of their illness, neglect of paralysed limb, denial of weakness)

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8
Q

What are the signs/symptoms of a stroke in the posterior circulation?

A
  • Vertigo
  • Ataxia, unsteadiness, imbalance
  • Visual disturbance (homonymous hemianopia, diplopia)
  • Slurred speech
  • Disorder of perception
  • Headache
  • Nausea and/or vomiting
  • Motor and sensory dysfunction
  • Cranial nerve dysfunction
  • Dysarthria/dysphasia
  • Others e.g. memory loss, confusion, reduced consciousness
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9
Q

What investigations are needed for a stroke?

A
  • CT head (1ST LINE, without contrast, ideally within 1 hour)
  • MRI brain with diffusion weighted imaging (GOLDSTANDARD)
  • Blood tests (FBC, U&E, ESR, TFTs, glucose, lipids, HIV, syphilis: to asses general health and exclude other causes)
  • ECG (look for arrhythmias and cardiac causes)
  • ECHO (may show mural thrombus, valvular lesions)
  • Carotid Doppler ultrasound, or CT/MRI angiogram if thrombectomy indicated (asses carotid artery stenosis and location of occlusion)
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10
Q

What are the treatments for an ischemic stroke?

A

General:
- ABCDE
- maintain oxygen, hydration, blood pressure and glucose
- assess swallow

Antiplatelets:
- only once haemorrhagic stroke is ruled out
- aspirin 300mg (or clopidogrel)

Thrombolysis:
- only within 4.5 hours of onset and once haemorrhagic stroke is ruled out
- most effective in 1st 90 mins
- using alteplase (tissue plasminogen activator)
- CI if uncertain timing, recent head injury/surgery, cerebral neoplasm, recent GI surgery, BP >180/110, on anticoagulant, seizure, hypodensity on CT

Surgical:
- thrombectomy (for confirmed large vessel occlusions, within 6 hours of symptom onset)
- decompressive hemicraniectomy (for large MCA infarcts with severe deficits, within 48 hours of symptom onset)

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11
Q

What is the primary prevention for strokes?

A

Control risk factors:
- asses and screen for hypertension, DM, hyperlipidaemia, cardiac disease (QRISK)
- smoking cessation
- exercise
- dietary advice
- weight management
- avoid alcohol excess

Drug treatment:
- control hypertension
- aspirin + statin following MI
- DOAC in AF (with high risk CHADS-VASc score)
- warfarin in valvular disease/replacement

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12
Q

What is the secondary prevention for a stroke?

A
  • Lifestyle changes
  • Investigate and treat risk factors: hypertension, hyperlipidaemia, cardiac disease, carotid artery stenosis, etc.
  • Short term antiplatelets: aspirin 300mg for 2 weeks
  • Long term antiplatelets: clopidogrel
  • Anticoagulants if cardiac cause: warfarin/DOAC
  • Statin (if evidence of atherosclerosis)
  • Surgical: carotid endarterectomy or stenting (if carotid stenosis)
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13
Q

Define TIA

A

Transient (less than 24 hours) neurological dysfunction caused by focal cerebral, spinal, or retinal infarction

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14
Q

What are the signs/symptoms of TIA?

A

*symptoms come on suddenly and usually resolve after 1 hour but can persist up to 24 hours
Focal neurological defects:
- unilateral weakness/sensory loss
- dysphasia
- ataxia, vertigo, loss of balance
Cranial nerve defects
Amaurosis fugax (sudden transient loss of vision in one eye)

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15
Q

What is the management of a TIA?

A
  • Lifestyle changes
  • Assess and control cardiovascular risk factors (blood pressure, lipids, glucose)
  • Antiplatelets: short-term aspirin, long-term = clopidogrel
  • Anticoagulants (warfarin/DOAC) is cardiac cause
  • Carotid endarterectomy/stenting (reduce stenosis)
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16
Q

Describe an extradural haemorrhage

A

Bleeding between the dura and bone (usually skull, but may be spine), usually with a traumatic cause due to fractures temporal/parietal bone damaging the middle meningeal artery

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17
Q

What are the clinical features of an extradural haemorrhage?

A
  • May present with traumatic injuries
  • Can have a ‘lucid period’ lasting hours-days
  • Symptoms of headache, nausea/vomiting, seizures, reduced GCS, CSF leak
  • Signs of bradycardia +/- hypotension (raised ICP), unequal pupils, facial nerve injury, focal neurological deficits
  • Features of cord compression if haematoma in the spinal column (weakness, numbness, altered reflexes, incontinence)
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18
Q

How does an extradural haemorrhage appear on a CT scan?

A
  • Acute (fresh) blood appearing hyperdense (bright wight)
  • Convex - does not conform to surface of the brain, limited by dural attachments
  • Involves compression of the brain (midline shift of falx cerebri, compression of lateral ventricles)
  • Skull fracture may be seen (or picked up on X-ray)
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19
Q

What is the management of an extradural haemorrhage?

A
  • ABCDE
  • IV mannitol or hypertonic saline to reduced ICP
  • Conservative management for small bleeds
  • Burr hole craniotomy for larger bleeds
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20
Q

Describe a subdural haemorrhage

A

Bleeding between the dura and arachnoid, usually with a traumatic cause due to rupture of the bridging cranial veins by shearing forces (e.g. acceleration-declaration in RTA), with risk factors being older age (cerebral atrophy), alcoholism, non-accidental injury in infants, and anticoagulant use

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21
Q

What are the clinical features of subdural haemorrhage?

A
  • presentation may be acute, or gradual in chronic SDH (2-3 weeks after trauma)
  • Symptoms of headache, nausea/vomiting, confusion, drowsiness, poor balance, weakness, numbness
  • Acute SDH may have loss of consciousness
  • Chronic SDH may have insidious progression of physical or cognitive decline
22
Q

How does a subdural haemorrhage appear on a CT scan?

A
  • Acute (fresh) blood appears hyperdense (white) and chronic (old) bleed appears hypodense (dark)
  • Concave - conforms to surface of the brain as bleeding is not limited by dural attachments
  • Involves compression of the brain (midline shift of falx cerebri, compression of lateral ventricles)
23
Q

What is the management of a subdural haemorrhage?

A
  • ABCDE
  • IV mannitol or hypertonic saline to reduce ICP
  • Conservative management for small bleeds
  • Burr hole craniotomy for chronic SDH
  • Trauma craniotomy for large acute SDH
24
Q

Describe a subarachnoid haemorrhage

A

Bleeding between the arachnoid and pia (arachnoid space), which occurs due to trauma, or spontaneously due to rupture of a berry aneurysm or arterio-venous malformations, with risk factors being hypertension, smoking, and family, history

25
Q

What are the clinical features of a subarachnoid haemorrhage?

A
  • Sudden-onset excruciating headache (thunder-clap)
  • Other symptoms: nausea/vomiting, photophobia, collapse, seizures, neck stiffness, or focal neurology (pupil changes, hemiparesis)
  • May have reduced level of consciousness
26
Q

How does a subarachnoid haemorrhage appear on CT? (+other investigations)

A
  • Acute (fresh) bleed is hyperdense (bright white), seen in fissures and cisterns +/- ventricles
  • Lumbar puncture performed at least 12 hours after onset shows xanthochromia (CSF stained yellow die to infiltration of blood)
27
Q

What is the management of a subarachnoid haemorrhage?

A
  • ABCDE
  • Calcium channel blocker (nimodipine): reduces cerebral artery vasospasm
  • Neurosurgery: endovascular coiling/clipping of aneurysm
  • Venous drainage for secondary hydrocephalus
28
Q

Describe an intracerebral haemorrhage (definition, cause, features, CT)

A
  • Bleeding into the brain parenchyma, categorised as primary (haemorrhagic stroke), or secondary (due to trauma, blood thinners, etc.) spontaneous rupture of aneurysm/vessel
  • Clinical features: determined by size and location of bleed - weakness (facial/limbs), seizure, coma
  • CT: acute hyperdense blood, within substance of brain, with mass effect (midline shift) if large
29
Q

Describe essential tremor

A
  • Involuntary rhythmic movement of a body part (usually hand/arm), which is not caused by an underlying disease, but associated with a family history
  • Occurs with maintained posture (e.g. carrying cup, writing etc.) but not present at rest
  • May progress to affect both sides, legs, jaw/face
  • Improves with alcohol
  • Treatment includes propranolol, primidone, or surgery (deep brain stimulation)
30
Q

Define motor neuron disease

A

A neurodegenerative disorder that affects the upper and lower motor neurons, most commonly due to amyotrophic lateral sclerosis, leading to progressive paralysis and eventual death

31
Q

Describe the different types of motor neuron disease

A
  • Amyotrophic lateral sclerosis - loss of neurons in motor cranial nuclei and anterior horn cells, causing UMN and LMN symptoms
  • Progressive bulbar palsy - affects cranial nerves IX-XII, causing difficulties with talking, chewing, swallowing
  • Primary lateral sclerosis - loss of neurons from the motor cortex, causing UMN symptoms
  • Progressive muscular atrophy - anterior horn cell lesion, causing LMN symptoms
32
Q

What are the symptoms of motor neuron disease?

A

Limb symptoms:
- weakness (drop objects, difficulty manipulating objects in hands, difficulty rising from chair/climbing stairs, tendency to trip)
- wasting (noticeable change in appearance of hands)
- fasciculations
- wrist/foot drop

Bulbar symptoms:
- dysarthria (slurring of speech due to muscle weakness)
- wasting and fasciculations of the tongue
- dysphagia (difficulty swallowing causing choking, nasal regurgitation)
- weakness of muscles of facial expression
- emotional lability (pseudobulbar palsies)

Respiratory symptoms:
- breathlessness
- orthopnoea
- repeated chest infection from aspiration
- disturbed sleep (waking, morning headaches, daytime sleepiness)

33
Q

What are the causes of motor neuron disease?

A
  • Unknown cause
  • 5-10% have an inherited genetic cause
  • May be due to abnormal mitochondrial function causing oxidative stress in motor neurons
34
Q

What are the signs seen in motor neuron disease?

A

Lower motor neuron dysfunction:
- weakness
- atrophy
- fasciculations
- hyporeflexia

Upper motor neuron dysfunction:
- weakness (arm extensors, leg flexors)
- hypertonia
- hyperreflexia (upgoing plantar reflex, exaggerated jaw jerk)

  • no sensory signs or sphincter involvement
35
Q

What investigations are needed for motor neuron disease?

A

Diagnosis is clinical after ruling out other causes:
- blood tests to exclude vitamin B12/folate deficiency, HIV, thyroid/parathyroid disease, lead poisoning, elevated serum paraproteins
- brain/spinal cord CT/MRI: exclude structural causes
- lumbar puncture: exclude infectious causes
- muscle biopsy: exclude myopathic conditions
EMG: shows fibrillation and fasciculations

36
Q

What is the management of motor neuron disease?

A

Non-pharmacological:
- physio/OT
- exercise programs
- speech and language
- dietician
- non-invasive ventilation (bilateral positive airway pressure, overnight)

Disease modifying drugs:
- riluzole (neuroprotective glutamate-release inhibitor)

Symptomatic management:
- quinine for muscle cramps
- baclofen for muscle stiffness
- anti-muscarinic for drooling of saliva
- antidepressants
- opioids for dyspnoea/respiratory distress

37
Q

Define multiple sclerosis

A

A chronic auto-immune inflammatory condition affecting the brain and spinal cord, causing demyelination and neuronal damage throughout the central nervous system

38
Q

Describe the different types of multiple sclerosis

A
  • Relapsing-remitting (85%): exacerbations of disease followed by compete or partial recovery, and periods of stability
  • Secondary progressive: often comes after relapsing-remitting disease, where recovery is incomplete and there is cumulative loss of function and disability
  • Primary progressive: steady progression and worsening of disease from onset without remissions
39
Q

What are the risk factors for multiple sclerosis?

A
  • Genetics
  • Female
  • Vitamin D deficiency
  • Higher latitude
  • Smoking
  • Diet and obesity in early life
  • Viruses (VZV, HSV, EBV)
40
Q

What are the clinical features of multiple sclerosis?

A
  • Early vague symptoms: fatigue, headache, depression, myalgia
  • Sensory symptoms: numbness, paraesthesia, tightness/burning, pain traveling down back when neck flexed (Lhermitte’s sign)
  • Motor symptoms: weakness (typically arm extensors and leg flexors), spasticity, increased tendon reflexes
  • Visual symptoms: acute optic neuritis (unilateral vision loss and pain), diplopia, horizontal nystagmus
  • Other symptoms: vertigo, ataxia, sphincter disturbance (urgency, frequency, incontinence, or retention), impotence, mood changes, cognitive decline
41
Q

What investigations are needed for multiple sclerosis?

A
  • Electrophysiology: visual evoked potential studies (detects demyelination, characteristic delay)
  • Lumbar puncture: increased total protein and concentration of immunoglobulin, with oligoclonal bands on electrophoresis
  • MRI: shows white matter abnormalities and focal demyelination plaques
42
Q

What is the management of multiple sclerosis?

A

Non-pharmacological:
- lifestyle advice
- physio
- speech and language
- counselling

Acute relapse treatment:
- methylprednisolone (oral, or IV if severe)

Disease modifying treatment:
- interferon beta
- glatiramer acetate
- dimethyl fumarate
- monoclonal antibodies

Symptomatic management:
- control pain
- baclofen/dantrolene for spasticity
- anticholinergics for urinary urgency
- desmopressin for nocturia
- laxatives/suppositories
- antidepressants
- propranolol/primidone for tremor

43
Q

Define myasthenia gravis

A

An autoimmune condition of the neuromuscular junction, characterised by fatigable weakness of muscle groups

44
Q

Describe the pathophysiology of myasthenia gravis

A
  • In most cases, IGI antibodies against acetylcholine receptors destruct the receptor sites on the post-synaptic membrane of the neuromuscular junction
  • In other cases, this is caused by MuSK antibodies
45
Q

What are the clinical features of myasthenia gravis?

A

Extra-ocular weakness:
- ptosis
- diplopia

Bulbar weakness:
- dysphagia and nasal regurgitation
- weak chewing
- dysarthria (worse after continued speech)
- nasal/slurred speech
- reduced facial expressions, horizontal smile

Limb weakness:
- commonly deltoids, triceps, and small muscles of hands
- fatigued after exercise/repeated testing
- proximal is more effected, usually symmetrical
- normal tone, reflexes, and sensation

Severe symptoms:
- weakness of muscles of ventilation can cause acute respiratory distress
- seizures

46
Q

What things trigger the symptoms of myasthenia gravis?

A
  • Pregnancy
  • Infection
  • Over-treatment
  • Change of climate
  • Emotion
  • Exercise
  • Hypokalaemia
  • Drugs (gentamicin, macrolides, tetracycline, beta-blockers, opiates, lithium, statins)
47
Q

What investigations are needed for myasthenia gravis?

A
  • Antibodies: ACh-R, or MuSK
  • EMG: decremental muscle response to repetitive nerve stimulation, and many have increased single-fibre jitter
  • CT/MRI of thymus: check for enlargement
    MRI of brain: exclude structural brain disease
    Ice pack test: >2mm improvement of ptosis after 2mins
  • Tensilon test: administer short-acting acetylcholinesterase inhibitor to see transient improvement of muscle strength
48
Q

What is the management of myasthenia gravis?

A
  • Acetylcholinesterase inhibitors (pyridostigmine)
  • Immunosuppression (corticosteroids, azathioprine)
  • Thymectomy (if thymoma present, reduces compression symptoms and immunosuppressive)
  • Immunoglobulins (in exacerbations)
  • Plasma exchange (in myasthenic crisis)
49
Q
A
50
Q
A