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Phase 3a > Neurology > Flashcards

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

Posterior cerebral artery:
- contralateral homonymous hemianopia
- visual agnosia (difficulty recognising objects visually)

Posterior inferior cerebellar artery:
- ipsilateral facial and contralateral limb pain and temperature loss
- ataxia
- nystagmus

Anterior inferior cerebellar artery:
- ipsilateral facial and contralateral limb pain and temperature loss
- ipsilateral facial paralysis and deafness
- ataxia
- nystagmus

Basilar artery:
- ‘locked-in’ syndrome

Other symptoms:
- vertigo
- disorder of perception
- headache
- nausea and/or vomiting
- cranial nerve dysfunction
- dysarthria/dysphasia
- 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? (non-pharmacological and pharmacological)

A

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

(Pharmacological):
- 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
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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)
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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
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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

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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
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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)
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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
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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
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29
Q

Describe essential tremor (inc. treatment)

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)
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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

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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
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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)

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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
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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
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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

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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

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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

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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
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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)
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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
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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
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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

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43
Q

Define myasthenia gravis

A

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

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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
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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:
- patient complains of difficulty typing, walking, etc.
- 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

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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)
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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
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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)
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49
Q

Define muscular dystrophy

A

Inherited progressive disorders of the muscle associated with abnormalities in the dystrophin-associated glycoprotein complex, causing weakness due to muscle fibre necrosis

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50
Q

Describe the inheritance of Duchenne and Becker muscular dystrophy

A
  • Point mutations and deletions affecting the dystrophin gene on the X chromosome
  • When occurring at the terminal domains, causes more severe phenotype of Duchenne’s
  • When occurring with the central rod, causes milder phenotype of Becker’s
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51
Q

What are the clinical features of Duchenne muscular dystrophy?

A
  • Delayed early motor development (between 1-3 years)
  • Scoliosis
  • Pseudohypertrophy of the muscle (e.g. calf)
  • Gower’s sign (walks hands up body to stand, sign of pelvic girdle weakness)
  • Waddling gait, or toe walking
  • Inability to run, hop, jump
  • Eventual loss of ambulation (by 12 years)
  • General fatigue
  • May have global developmental delay
  • Anaesthetic complications (myoglobinuria, rhabdomyolysis, malignant hyperthermia)
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52
Q

What investigations are needed for Duchenne muscular dystrophy?

A
  • Creatine kinase: raised by 10-100 times (from birth)
  • Genetic analysis: identifies most mutations
  • Muscle biopsy with assay for dystrophin protein
  • EMG: shows severe myopathy
  • ECG: shows conduction disorders
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53
Q

What are the clinical features of Becker muscular dystrophy?

A
  • May have delayed walking
  • Muscle cramps on exercise
  • Struggling with school sports
  • Muscle weakness (mostly proximal muscles, difficulty climbing stairs, lifting heavy objects)
  • Loss of walking ability (usually 40-60, but can be 20-30)
  • Hypertrophy of muscles (e.g. calf)
  • Cardiomyopathy may be first presentation
  • Learning difficulties
  • Anaesthetic complications (hyperthermia-like reaction)
  • Myoglobinuria
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54
Q

What are the investigations needed for Becker muscular dystrophy?

A
  • Creatine kinase: raised 5-50 times
  • Genetic analysis
  • Muscle biopsy with array for dystrophin gene
  • Monitoring for cardiomyopathy
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55
Q

What is the management for Duchenne and Becker muscular dystrophy? (early stages and late stages)

A

Early stages (while still walking):
- genetic counselling
- physiotherapy
- orthoses may prolong walking
- optimise bone health (vitamin D, bisphosphonates if vertebral fractures occur)
- corticosteroids (improve muscle strength and function in Duchenne’s)

Late stages:
- mobility adaptations
- orthopaedic care (for scoliosis and contractures)
- cardiac and respiratory treatment (non-invasive ventilation, assisted coughing, airway clearance, screening for cardiomyopathy, treatment of arrhythmias/heart failure)
- family support
- end of life care

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56
Q

What are the muscular dystrophies associated with certain patterns?

A
  • Facioscapulohumeral (face, scapula, humerus, proximal lower limbs)
  • Scapuloperoneal (proximal upper and lower limbs, foot drop)
  • Distal (upper and lower limbs)
  • Emery-Dreifuss (contractures of spine, elbows, ankles, proximal muscle weakness)
  • Oculopharyngeal (ocular muscle weakness, dysphagia, may have limb weakness)
  • Limb-girdle (group of conditions with progressive weakness around shoulder and hip girdle)
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57
Q

Define Huntington’s disease

A

An inherited neurodegenerative disorder characterised by movement disorder and neuropsychiatric changes

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58
Q

Describe the pathophysiology of Huntington’s disease

A
  • Autosomal dominant inheritance caused by a increased length of CAG triplet repeat in a gene called huntingtin on chromosome 4
  • Neuronal loss in the basal ganglia causes a deficiency of GABA and acetylcholine
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59
Q

What are the clinical features of Huntington’s disease?

A
  • Chorea (may be initial symptom, progresses from small fidgetiness to gross involuntary movements)
  • Personality changes, behavioural problems, and depression
  • Progressive rigidity
  • Dysarthria and dysphagia
  • Cognitive impairment (subcortical dementia)
60
Q

What investigations are needed for Huntington’s disease?

A
  • MRI: loss of striatal volume, increase size of frontal horns of lateral ventricles
  • Genetic testing with counselling
  • Testing for other movement disorders
61
Q

What is the management for Huntington’s disease?

A
  • Symptomatic treatment only (no effect on disease progression
  • Physio, OT, speech and language therapy
  • SSRIs for depression
  • Tetrabenazine for chorea
  • Atypical antipsychotics for psychosis
  • Deep brain stimulation
62
Q

Define mononeuropathy

A

Disease of a single peripheral or cranial nerve, which may be caused by entrapment (e.g. soft tissue swelling), or associated with systemic diseases (diabetes, sarcoidosis, vasculitis, leprosy)

63
Q

Describe axillary nerve neuropathy (nerve root, supplies, damaged by, results in)

A
  • Nerve root: C5/6
  • Supplies deltoid and teres minor muscles
  • Damaged by shoulder dislocation or relocation, brachial neuritis
  • Results in weakness of shoulder abduction between 15-90 degrees, and sensory loss of outer aspect of shoulder
64
Q

Describe radial nerve neuropathy (nerve root, supplies, damaged by, results in)

A
  • Nerve root: C5-T1
  • Supplies sensation to dorsum of the hand and posterior muscles of arm and wrist/hand extensors
  • Damaged by fractured humerus, prolonged pressure, intramuscular injection, soft tissue tumour
  • Results in wrist drop, loss of sensation of dorsum of hand, loss of triceps reflex
65
Q

Describe median nerve neuropathy (nerve root, supplies, damaged by, results in)

A
  • Nerve root: C5-T1
  • Supplies sensation to palmar surface of radial border of hand, and muscle of flexion of the wrist/hand
  • Damaged by injury in axilla, shoulder dislocation, compression in carpal tunnel syndrome
  • Results in weakness of pronation, flexion of thumb and index finger, and abduction and opposition of the thumb, sensory loss in distribution, thenar eminence wasting, paraesthesia (often at night)
66
Q

Describe ulnar nerve neuropathy (nerve root, supplies, damaged by, results in)

A
  • Nerve root: C8 and T1
  • Supplies sensation to palmar and dorsum of the ulnar border of the hand, and small muscles of the hand and flexors of the wrist
  • Damaged by injury (dislocation) or entrapment (cubital tunnel syndrome) at the elbow or wrist (ulnar tunnel syndrome)
  • Results in muscle weakness causing claw hand, sensory loss in distribution
67
Q

Describe sciatic nerve neuropathy (nerve root, supplies, damaged by, results in)

A
  • Nerve root: L4-S3
  • Supplies hamstring muscles, and sensation to outer aspect of the leg
  • Damaged by hip dislocation, penetrating injuries, misplaced intramuscular injection, entrapment, systemic causes
  • Results in weakness of hamstrings, loss of knee flexion, loss of ankle reflex, sensory loss
68
Q

Describe deep peroneal nerve neuropathy (supplies, damaged by, results in)

A
  • Nerve root: L4-S1
  • Supplies muscles of anterior compartment of leg and intrinsic muscle of foot, and sensation to dorsum of foot
  • Damaged by trauma to head of fibula, pressure from kneeling/crossing legs, systemic causes
  • Results in weakness of dorsiflexion causing foot drop, sensory loss of dorsum of foot
69
Q

Describe inflammatory myopathy

A
  • Polymyositis: muscle pain, proximal muscle weakness, may involve pharyngeal, respiratory, or cardiac muscle
  • Dermatomyositis: violet skin rash, periorbital oedema, proximal muscle weakness
  • Inclusion body myositis: asymmetrical distal weakness
  • Associated with malignant disease: neoplasm may present before or after
  • Associated with autoimmune vascular disorders: SLE, rheumatoid arthritis
  • Associated with infection: toxoplasmosis, HIV, coxsackie virus, influenza
70
Q

Describe the endocrine causes of myopathy

A
  • Pituitary: acromegaly
  • Parathyroid: hyperparathyroidism, osteomalacia
  • Adrenal: Addison’s disease, hyperaldosteronism, Cushing’s syndrome, excessive exogenous steroids
  • Thyroid: hyper or hypothyroid
71
Q

What are the clinical feature of proximal myopathy?

A

Patient complains of difficulty with…
- climbing stairs
- walking up hills
- walking slower than others
- rising from chairs
- combing hair

Signs…
- symmetrical weakness (difficulty with single leg squat)
- normal sensation and reflexes
- atrophy is a late sign

72
Q

Define polyneuropathy

A

The most common disorder of the peripheral nervous system affecting both peripheral and cranial nerves, due to axonal degeneration or demyelination, categorised as…
- acute or chronic
- motor, sensory, autonomic, or mixed

73
Q

Describe the acute causes of peripheral neuropathy

A
  • Inflammatory: e.g. Guillain Barre syndrome, motor and autonomic disturbance due to demyelination
  • Infection: e.g. Diphtheria (cranial nerve onset, mixed motor/sensory),
74
Q

Describe the chronic causes of peripheral neuropathy

A

Asymmetrical:
- infections (leprosy, HIV)
- vasculitis (polyarteritis nodosa)

Symmetrical:
- metabolic/endocrine (diabetes, uraemia, hypothyroidism, acromegaly: causes distal sensorimotor disturbance)
- nutritional deficiencies (thiamine: sensory with burning mixed, vitamin B12: sensory, alcoholic: motor and autonomic)
- malignant (paraneoplastic: sensorimotor, infiltration: multifocal)
- inherited (Charcot-Marie-tooth disease: motor)
- drug induced (antibiotics, oncology drugs, HIV drugs)
- toxin induced (solvents, heavy metals)

75
Q

Define diabetic peripheral neuropathy

A
  • Most common cause of peripheral neuropathy, with motor, sensory, and autonomic neuropathy
  • Peripheral nerve damage due to poor control of diabetes caused by metabolic disturbance or occlusion of the vessels supplying nerves
76
Q

What are the clinical features of diabetic neuropathy?

A

Chronic peripheral neuropathy:
- predominantly sensory loss, signs often develop before symptoms
- large fibre (loss of touch, vibration, and proprioception in glove and stocking distribution)
- small fibre (rare, loss pain and temperature)

Autonomic neuropathy:
- pupil abnormalities
- loss of sweating
- orthostatic hypotension
- resting tachycardia
- gastroparesis
- nausea and vomiting
- diarrhoea
- impotence

Diabetic amyotrophy:
- rare motor manifestation
- rapidly developing severe pain and paraesthesia in upper legs
- wasting of thigh muscles
- associated with very poor glycaemic control

77
Q

What is the management of diabetic neuropathy?

A
  • Improve control of diabetes
  • Regular surveillance for sings of neuropathy
  • Prevention of foot trauma and disease
  • Control pain with amitriptyline, gabapentin, pregabalin, duloxetine
  • Control cardiac effects of autonomic neuropathy (e.g. ACEi, b-blockers, diuretics)
  • Treat erectile dysfunction
  • Fludrocortisone for postural hypotension
  • Metoclopramide to increase gastric emptying
78
Q

What are the risk factors for diabetic neuropathy?

A
  • Smoking
  • Age over 40
  • History of poor glycaemic control
  • Increased duration of diabetes
  • Presence of diabetic nephropathy and retinopathy
  • Hypertension
  • Coronary heart disease
  • Dyslipidaemia
79
Q

What are the causes of spinal cord/root compression?

A

Trauma:
- history of car accidents, falls, sports injuries
- usually vertebral fracture or facet joint dislocation
- complete transection of the cord may occur, or hemisection (Brown-Sequard syndrome)

Tumours:
- can be benign or malignant, primary or metastatic, bone, myeloma, meningioma, neurofibroma

Prolapsed intervertebral disc:
- L4-5 and L5-S1 are most common, or cervical
- can causes cauda equina syndrome

Haematoma:
- epidural or subdural
- may be spontaneous or traumatic

Infection:
- acute (usually bacterial) or chronic (usually TB or fungal)
- can lead to epidural abscess

Cervical spondylosis:
- aging process leading to osteophytes, disc herniation, thickened ligamentum flavum

Spondylothesis:
- degenerative disease causes one vertebral body to shift forward

80
Q

Define radiculopathy

A

A clinical syndrome affecting the nerve roots, resulting in impaired nerve function (neuropathy), characteristic pain, muscle weakness, and paraesthesia

81
Q

What are the clinical features of radiculopathy? (C6, C7, L5, S1)

A
  • Radiating pain, sensory loss/paraesthesia, and weakness (along entire dermatome of affected nerve root)
  • C6: pain radiating to thumb, numbness/tingling over front of upper arm and thumb, weakness of biceps (elbow flexion), loss of biceps reflex
  • C7: pain radiating to middle finger, numbness/tingling over back of arm and back of hand/wrist, weakness of triceps (elbow extension), loss of triceps reflex
  • L5: pain radiating to top of foot, numbness/tingling over this area, weakness of dorsiflexion (foot drop, dragging feet)
  • S1: pain radiating to sole of foot and little toe, weakness of plantarflexion (struggles with pedals)
82
Q

Describe cauda equina syndrome (definition, causes, features)

A
  • A type of radiculopathy caused by lesions below the cauda equina
  • Most commonly caused by lumbar disc herniation, but can be other causes of cord compression
  • Clinical features include bilateral radiating leg pain and weakness, sensory loss over saddle area (can’t feel when wiping/scratching), loss of bladder function, faecal incontinence, impotence
83
Q

Define myelopathy

A
  • Any neurological deficit related to lesions of the spinal cord itself, most commonly due to osteophytes or disc herniation (but may be other causes of cord compression)
  • Most common in the cervical region, but may be thoracic or lumbar
84
Q

What are the clinical features of myelopathy?

A

*signs develop before symptoms
- Weakness and wasting of muscles at level of lesion (e.g. C5=biceps)
- Increased tone (spasticity)
- Positive Babinski and Hoffman’s reflex
- Ankle clonus
- Clumsy hands (loss of fine finger movements)
- Gait disturbance
- Vertebral pain
- Sensory loss
- Bladder/bowel dysfunction (late sign)

85
Q

What investigations are used for spinal cord and root compression?

A

MRI: sagittal view of the whole spine, with T1 and T2 weight images

86
Q

What is the management of spinal cord and root compression?

A

Tumours:
- steroids
- biopsy
- radiotherapy
- decompression surgery

Infection:
- decompressive surgery
- abscess drainage
- TB treatment

Disc problems:
- conservative (analgesia, avoid lifting/bending, cervical collar)
- percutaneous decompression of the disc space
- decompression surgery (laminectomy, discectomy, microdiscectomy)
- prosthetic intervertebral disc replacement
- lumbar fusion

87
Q

Describe the causes of spinal cord injuries

A

Primary injury:
- vertical compression (e.g. object falling on head/jump from height, causes burst fracture)
- hinge injury (e.g. weight falling on back, anterior wedge fracture, can damage ligaments)
- hyperextension (anterior longitudinal ligament rupture)
- shearing injury (e.g. RTA and rotational forces, causes dislocation and ligament damage)
- penetrating injuries (e.g. weapon, bullet)

Secondary injury:
- arterial disruption
- thrombosis
- hypoperfusion in shock

88
Q

Describe the pattern of clinical features in spinal cord injury

A

Complete cord injury:
- loss of all motor and sensory function below the level of injury

Anterior cord syndrome:
- variable paralysis below the level of injury
- loss of pain and temperature sensation

Brown-Sequard’s syndrome:
- contralateral loss of pain and temperature
- ipsilateral spastic paresis and loss of proprioception and vibration sense

Central cord syndrome:
- greater motor weakness in upper and distal extremities than lower and proximal
- variable sensory loss (more likely affects pain and temperature) with sacral sparing

Posterior cord syndrome:
- loss of proprioception and vibration sense
- motor and pain/temperature sensation is preserved

Spinal shock:
- immediate flaccidity, paralysis, areflexia, and loss of sensation below the level of injury
- becomes hyperreflexia in days-weeks

89
Q

What is the management of spinal cord injury?

A
  • ABCDE resuscitation
  • Stabilisation and immobilisation of the spine
  • Emergency decompression
  • Surgical fixation
  • MDT approach to rehabilitation
90
Q

Define Guillain Barre syndrome

A

An acute inflammatory polyneuropathy, associated with a preceding viral or bacterial infection (e.g. influenza, EBV, VZV, campylobacter jejuni, cytomegalovirus, HIV, SARS-CoV-2, hepatitis A/B/C/E), which can lead to axonal degeneration and demyelination of peripheral nerves and roots

91
Q

What are the clinical features of Guillain-Barre syndrome?

A
  • Sensory loss/paraesthesia (usually first symptom, feet then hands)
  • Weakness (progressive, ascending, symmetrical, can affect bulbar and respiratory muscles)
  • Reduced or absent reflexes
  • Pain (neuropathic pain in legs, or back)
  • Autonomic symptoms (reduced sweating, heat intolerance, labile blood pressure, tachycardia, ileus, urinary retention)
  • Reduced forced vital capacity (risk of respiratory failure due to diaphragmatic paralysis)
92
Q

What investigations are needed for Guillain-Barre syndrome?

A
  • Lumbar puncture: raised CSF protein, raised opening pressure, normal cell count and glucose
  • Nerve conduction studies: normal initially, then evidence of demyelination
  • Other: viral/bacterial serology, neuroimaging, antibody screen, electrolytes (for SIADH)
93
Q

What is the management of Guillain-Barre syndrome?

A
  • Supportive care and prevention of respiratory failure (monitored with repeat FVC)
  • Plasma exchange or IV immunoglobulins
  • VTE prophylaxis
94
Q

Describe the causes of headaches

A

Primary:
- migraine
- cluster
- tension

Secondary:
- sinusitis
- glaucoma
- arterial dissection
- post-traumatic
- infection (meningitis, encephalitis, TB)
- hydrocephalus
- haemorrhage (acute, or chronic subdural)
- intracranial tumour
- idiopathic intracranial hypertension
- temporal arteritis
- medication overuse
- drugs/toxins (vasodilators)
- cervical spondylosis

95
Q

Describe a tension headache (features, duration, treatment)

A
  • Dull, aching, band-like headache associated with feeling of tension but no other physical symptoms
  • May last hours-days, be infrequent or daily, and persist over many years
  • Treatment: reduce psychological stress, simple analgesia, prophylactic amitriptyline or beta-blockers
96
Q

Describe a migraine headache (features, duration, triggers treatment)

A
  • Unilateral throbbing headache, may have aura (visual, sensory, or motor symptoms, worsened by bright light and movement, associated with nausea/vomiting
  • Onset in childhood or early adulthood, may last hours-days, recurrent
  • Triggered by alcohol, chocolate, cheese, stress, hormonal changes
  • Prevention: avoid triggers, prevention = propranolol, topiramate, or amitriptyline, candesartan, botox, CGRP blockers (monoclonal antibodies, gipants)
  • Treatment of acute attack = oral triptans (CI: in cardio/cerebrovascular disease), paracetamol, NSAIDs, aspirin, anti-emetics
97
Q

Describe cluster headaches (features, duration, triggers, treatment)

A
  • Severe, sharp, unilateral pain around the eye, associated lacrimation, rhinorrhoea, red eyes, drooping eye lids, and restlessness/agitation
  • Short lasting (15mins - 2 hours), episodic, often at same time in the day
  • Triggered by alcohol, histamine, heat, exercise, disturbed sleep pattern
  • Prevention: avoid triggers, prevention = verapamil, lithium, topiramate, prednisolone (10 day course)
    Treatment for acute attack = high-flow oxygen, nasal or s/c triptan
98
Q

Define giant cell arteritis

A

An autoimmune condition of medium an large vessel vasculitis affecting the external cranial branches of the aorta, with an unknown cause but associated with polymyalgia rheumatica

99
Q

Describe the clinical features of giant cell arteritis

A
  • Headache: new-onset, severe, unilateral or bilateral
  • Temporal artery abnormality: tenderness, thickening, nodularity
  • Visual disturbances: loss of vision, diplopia, changes to colour vision
  • Jaw claudication: pain in jaw when chewing, swallowing, talking
  • Systemic symptoms: fatigue anorexia, weight loss, myalgia
  • Neurological features: mononeuropathy, polyneuropathy, cranial nerve palsies, TIA or stroke
100
Q

What are the investigations needed for giant cell arteritis?

A
  • ESR: raised
  • FBC: anaemia, thrombocytosis
  • LFTs: raised alkaline phosphate
  • Biopsy of temporal artery
  • Colour duplex ultrasound
101
Q

What is the management of giant cell arteritis?

A
  • High dose prednisolone (60mg, weaned over weeks)
  • If visual complications have occurred, IV methylprednisolone
  • Tocilizumab (monoclonal antibody, glucocorticoid-sparing therapy)
102
Q

Describe the features of a headache due to raised intracranial pressure

A
  • Generalised pain, gradually progresses in severity
  • Aggravated by bending or coughing
  • Worse in the morning, may wake patient from sleep
  • Vomiting (in later stages, or acute rise)
  • Transient loss of vision with sudden change in posture
  • Eventual impairment in consciousness
  • May have papilloedema
103
Q

What are the causes of raised intracranial pressure?

A
  • Idiopathic intracranial hypertension
  • Expanding mass (tumour, haematoma, abscess)
  • Increased brain water content (cerebral oedema)
  • Increased cerebral blood volume (vasodilation, or venous outflow obstruction)
  • Increased CSF (impaired absorption/drainage, excessive secretion)
104
Q

What is the management of raised intracranial pressure?

A
  • Definitive treatment: treat the cause
  • IV mannitol: buys time before further treatment
  • CSF withdrawal: immediately reduces ICP, but will rise again
  • Sedation: propofol, barbiturates
  • Controlled hyperventilation: lowers PCO2 which reduces ICP
  • Steroids: treats oedema
  • Decompressive craniectomy
  • For idiopathic intracranial hypertension: acetazolamide
105
Q

Define trigeminal neuralgia

A

A chronic neuropathic disorder of the 5th cranial nerve, with sensory disturbance to the ophthalmic, maxillary, and/or mandibular regions of the face, and disruption to the muscles of mastication

106
Q

What are the causes of trigeminal neuralgia?

A
  • Compression of the trigeminal nerve by vasculature
  • Compression by a tumour
  • Trauma
  • Demyelination in MS
  • Systemic conditions (diabetes, SLE)
107
Q

What are the clinical features of trigeminal neuralgia?

A
  • Unilateral, sharp, stabbing, shooting pain in the ophthalmic, maxillary, or mandibular region
  • Intermittent episodes of short and sudden attacks, can last days, weeks, or months
  • Provoked by light touch to the face (e.g. shaving, washing, brushing teeth), eating, cold, vibrations
  • No neurological deficit
108
Q

What is the management of trigeminal neuralgia?

A
  • Carbamazepine (high dose until pain subsides)
  • If not effective: lamotrigine, gabapentin, baclofen
  • Surgical: microvascular decompression, peripheral nerve block, radiofrequency thermocoagulation
109
Q

Define Horner’s syndrome

A

A rare condition resulting from disruption of the sympathetic nerve supply, with a triad of symptoms:
- partial ptosis
- miosis (pupillary constriction)
- hemifacial anhidrosis (absence of sweating)

110
Q

What are the causes of Horner’s syndrome?

A

First order lesion (between hypothalamus and spinal cord):
- stroke
- MS
- tumour (pituitary, skull base, spinal cord)
- meningitis
- neck trauma

Second order lesion, preganglionic (between spinal cord and sympathetic chain at C3-4 level)
- apical lung tumour (Pancoast’s syndrome)
- lymphadenopathy
- lower brachial plexus trauma
- neck or chest trauma/surgery
- neuroblastoma
- dental abscess

Third order lesion, postganglionic (between sympathetic chain and eye)
- cluster headaches and migraines
- herpes zoster infection
- internal carotid artery dissection
- temporal arteritis
- tumour, granuloma

111
Q

Define meningitis and its causes

A

Inflammation of the meninges, due to…
- bacterial (Neisseria meningitidis, Strep. pneumoniae, Haemophilus influenzae, Listeria, gram -ve bacilli e.g. Klebsiella)
- viral (enteroviruses, EBV, HSV, HIV, mumps, measles, influenzas)
- other infections (TB, syphilis, leptospirosis, fungal, parasitic)
- non infectious (infiltration of malignant cells, medication, sarcoidosis, SLE)

112
Q

What are the clinical features of meningitis?

A
  • Non-specific lethargy, anorexia, respiratory symptoms, arthralgia
  • Fever
  • Headache
  • Photophobia
  • Neck stiffness
  • Non-blanching purpuric/petechial rash (meningococcal meningitis)
  • Shock (tachycardia, hypotension, increased CRT)
  • Reduced GCS
  • Focal neurological signs (cranial nerves, paresis, dysphasia)
  • Seizures
113
Q

What investigations are needed for meningitis?

A
  • Bloods: cultures, FBC, U&E, glucose, CRP, procalcitonin
  • Nose and throat swabs: for culture and PCR
  • CT (if any focal neurology, reduced GCS aged >60, immunocompromised, history of CNS disease, seizures)
  • Lumbar puncture (microscopy and culture of CSF): bacterial = cloudy, neutrophils, high protein, low glucose, viral = clear, lymphocytes, high protein, normal glucose
114
Q

What is the management of meningitis?

A

Bacterial:
- in GP = IM/IV benzylpenicillin, urgent transfer to hospital
- supportive care = hydration, analgesia, antipyretic
- initial therapy = ceftriaxone (or cefotaxime + amoxicillin if risk factors for listeria)
- IV dexamethasone (initially, then continue in pneumococcal or Hib)

Viral:
- self-limiting, supportive care only
- acyclovir is not needed unless suspicion of HSV encephalitis

115
Q

Describe cerebral malaria

A
  • Caused by plasmodium falciparum
  • Infected red blood cells adhere to vascular endothelium and block microcirculation
  • Features: confusion, focal signs, seizures, coma
  • Treatment: IV chloroquine, exchange transfusion, supportive care
116
Q

Define encephalitis and its causes

A

Inflammation of the brain parenchyma, due to…
- viral infection (HSV, mumps, VZV, HIV)
- bacterial infection (TB, listeria, all causes of bacterial meningitis)
- others (fungal, parasitic, tick borne, autoimmune)

117
Q

What are the clinical features of encephalitis?

A
  • Initial flu-like illness
  • Symptoms of meningitis (fever, headache, neck stiffness, vomiting)
  • Altered consciousness, confusion, drowsiness, seizures, coma
  • Focal signs (motor/sensory dysfunction, autonomic dysfunction, ataxia, dysphasia, cranial nerve palsies)
118
Q

What investigations are needed for encephalitis?

A
  • Lumbar puncture: raised proteins and lymphocytes, normal glucose, PCR confirms organism
  • CT: rule out space-occupying lesion and raised ICP
  • MRI: sensitive detection of demyelination and oedematous changes
  • EEG: generalised slowing with periodic discharges, determines localisation
119
Q

What is the management of encephalitis?

A
  • Supportive care (fluids, sedatives, ventilation)
  • Immediate acyclovir
  • Broad spectrum antibiotics for secondary bacterial infections
120
Q

What are the potential causes of a cerebral abscess?

A
  • Chronic otitis media/mastoiditis
  • Infected dental caries
  • Basal fracture
  • Frontal sinusitis
  • Compound skull fracture
  • Haematogenous spread (bacterial endocarditis, congenital heart disease, bronchiectasis, pulmonary abscess)
121
Q

What are the clinical features of a cerebral abscess?

A
  • Systemic toxicity: fever, malaise
  • Raised intracranial pressure: headache, vomiting, reduced GCS
  • Focal damage: paresis, dysphasia, ataxia, nystagmus, seizures
  • Signs of infectious source: discharging ear, tender mastoid, cardiac murmurs, splenomegaly
122
Q

What investigations are needed for a cerebral abscess?

A
  • CT: abscess has central low density with marked ring enhancement, surrounding oedema, midline shift due to mass effect
  • MRI: will detect changes earlier
123
Q

What is the management of a cerebral abscess?

A
  • Empirical antibiotics (ceftriaxone + metronidazole + vancomycin)
  • Anticonvulsant
  • Dexamethasone
  • Surgical evacuation/decompression
124
Q

Define epileptic seizures

A

A paroxysmal event in which changes of
behaviour, motor function, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain

125
Q

Define epilepsy

A

A neurological disorder of recurrent seizures, caused by one of many epileptic syndromes (or another disorder e.g. structural abnormalities, genetics, SOL)

126
Q

Describe focal epileptic seizures

A

Seizures begin focally from a single location in one hemisphere, classified by site of onset and severity…
- Focal aware seizures (simple): consciousness preserved, no post-ictal symptoms
- Focal impaired awareness seizures (complex): consciousness is impaired, with post-ictal confusion, most commonly temporal lobe origin
- Focal to bilateral convulsive seizures: disturbance starts focally then becomes widespread to cause a generalised seizure

127
Q

Describe the clinical features of each focal lobe seizure

A
  • Frontal: arising from motor cortex, clonic movement in hands/face, weakness may persist for a few hours
  • Parietal: arising from sensory cortex, paraesthesia in an extremity or face, limb weakness, may have visual, auditory, or autonomic features
  • Temporal: characterised by complex aura, impaired consciousness, visceral, memory, motor, or affective disturbances, post-ictal confusion and headache
  • Occipital: uncommon, visual hallucination prior to tonic-clonic seizure
128
Q

Describe generalised epileptic seizures

A

Arising from subcortical structures and involving both hemispheres…
- Tonic-clonic seizures: muscle stiffening (tonic), then jerking (clonic), lasting <5mins, LOC, post-ictal confusion/drowsiness
- Absence seizures: brief pauses (<10s) in activity, can happen in clusters, worse with coming in/out of sleep, presents in childhood, induced by hyperventilation
- Myoclonic seizures: sudden jerking of limb, face and/of trunk, can be thrown to floor
- Tonic seizures: sudden muscle stiffness, may cause fall, extended neck, open eyes, stop breathing, rare in adults
- Atonic seizures: all muscles relax, causing sudden fall, head drops forwards, knees sag, only brief LOC, rare in isolation

129
Q

What investigations are needed for epilepsy?

A
  • MRI: look for structural causes
  • EEG: identifies abnormal patterns, but low yield (increased by sleep deprivation or ambulatory)
  • ECG: rule out cardiac abnormalities causing syncope
  • Neuropsychological assessment
  • Genetic testing
  • Metabolic testing (glucose, U&Es, calcium, LFTs)
130
Q

What is the management of epilepsy?

A

Anticonvulsant medications:
- monotherapy were possible, polytherapy only when monotherapy fails
- initiation and withdrawal by specialist
- focal epilepsy = lamotrigine, levetiracetam, carbamazepine, topiramate
- generalised epilepsy = sodium valproate (teratogenic), lamotrigine, levetiracetam, ethosuximide (absence seizures)

Other:
- psychological interventions
- driving regulations (6 months from first seizure if normal MRI and EEG, or 1 year from last attack)
- vagal nerve and deep brain stimulation
- surgical resection

131
Q

What are the common side effects of anticonvulsant medications?

A
  • Levetiracetam: irritability, weight gain
  • Sodium valproate: abdominal pain, weight gain, thrombocytopenia, tremor
  • Lamotrigine: rash (Stevens-Johnson syndrome), drowsiness
  • Carbamazepine: rash, drowsiness, ataxia, hyponatraemia, diplopia, interaction with oral contraceptives and warfarin
132
Q

Describe seizures in pregnancy

A
  • Women may experience their first seizure during pregnancy due to tumour or arteriovenous malformation enlargement, or eclampsia in later stages
  • Women with epilepsy who become pregnant should continue anticonvulsant medications and take folic acid (preconception)
  • Sodium valproate should not be given to women of child bearing age unless no other treatment is effective, and the pregnancy prevention programme is met
133
Q

What are the feature of a non-epileptic seizure?

A
  • Prolonged seizure (>5 mins)
  • Gradual onset
  • Symptoms wax and wane throughout seizure, fluctuating course
  • Violent thrashing of arms or pelvic thrusts
  • Eyes are usually closed
134
Q

Describe the pathology of intracranial tumours

A

Neuroepithelial
- astrocytoma: most common primary brain tumour, 4 different grades, most malignant is called glioblastoma
- oligodendroglioma: usually slow growing and less infiltrating
- ependymoma: arises from lining of ventricles or spinal canal, common in paediatrics, can infiltrate through CSF pathways
- pineocytoma/blastoma: extremely rare, latter is more malignant
- ganglioglioma: rare tumour containing ganglion cells, varying degrees of malignancy

Meninges
- meningioma: arises from arachnoid granulations, mostly benign, compress the brain rather than invade

Nerve sheath cells
- schwannoma: arises from Schwann cells of cranial or peripheral nerves, non-invasive
- neurofibroma: also arises from Schwann cells or peripheral or spinal nerve roots, more likely to be malignant

Sellar region
- pituitary adenoma: usually benign, secretes hormones, likely to affect upper visual quadrant
- craniopharyngioma: benign tumour usually arise from above the pituitary gland, likely to affect lower visual quadrant

Other
- germ cell tumours: germinoma, teratoma
- haemangioblastoma: arises from blood vessels in the spinal cord or cerebellar parenchyma

135
Q

Describe the clinical features of brain tumours?

A

Features of raised intracranial pressure and mass effects…
- headache: worse in mornings, worse with Valsalva, change in pattern or frequency
- nausea and/or vomiting
- papilloedema
- reduced consciousness

Focal damage…
- frontal lobe: personality changes, expressive dysphasia (Broca’s area), contralateral hemiparesis
- parietal lobe: hemisensory loss, sensory inattention, dysgraphia, dyscalculia, loss or stereognosis
- temporal lobe: epilepsy, receptive dysphasia (Wernicke’s), emotional changes, memory changes
- occipital lobe: visual changes (contralateral homonymous hemianopia)
- cerebellar: ataxia, nystagmus, dysarthria, intention tremor, dysdiadochokinesis
- midbrain/brainstem: unequal pupils, cranial nerve lesion, long tract signs, reduced consciousness

136
Q

What investigations are needed for brain tumours?

A
  • Bloods: FBC, CRP etc
  • CT: shows site of lesion, size, mass effect
  • MRI: better detail, especially for skull bass and brain stem tumours
137
Q

What is the management of brain tumours?

A
  • Steroids: reduces oedema around tumour
  • Surgery: for biopsy, decompression, partial, or total removal (craniotomy, burr hole, transsphenoidal route)
  • Radiotherapy and chemotherapy
138
Q

What are the common primary tumours that metastasise to the brain?

A
  • Bronchus
  • Breast
  • Kidney
  • Thyroid
  • Stomach
  • Prostate
  • Testis
  • Melanoma
139
Q

Describe neurofibromatosis type 1

A
  • Most common type, autosomal dominant inheritance
  • Caused by localised overgrowth of mesodermal (meninges, vascular system) or ectodermal (skin, viscera, nervous system)
  • Clinical features: café au lait spots, subcutaneous neurofibromas, Lisch nodules of the iris, scoliosis, sphenoid dysplasia
140
Q

Describe neurofibromatosis type 2

A
  • Less common, autosomal inheritance, associated with reduced life expectancy
  • Characterised by bilateral vestibular schwannomas on the 8th cranial nerve, presenting as tinnitus, balance problems, hearing loss, seizures
  • Other intracranial or intraspinal neoplasms may occur (e.g. meningioma, glioma, neurofibroma)
141
Q

Describe acoustic neuromas

A
  • Tumours of the vestibulocochlear nerve (8th cranial nerve), arising from Schwann cells
  • Typically benign and slow-growing
  • Presents with unilateral hearing loss or tinnitus, impaired facial sensation (involvement of trigeminal nerve), balance problems (cerebellar compression)
  • Treated conservatively or with surgical removal
142
Q

Describe Bell’s Palsy (definition, cause, features, treatment)

A
  • Acute paralysis of the face related to inflammation of the facial nerve within the facial canal
  • Uncertain cause but association with viral infections (HSV, VZV)
  • Features: usually bilateral weakness, variable pain, impairment of taste and salivation
  • Treatment: eye care, high dose prednisolone
143
Q

What are the clinical features of cerebellar disease?

A
  • Ataxia (unsteady gait)
  • Dysmetria (overshooting of motor tasks)
  • Intention tremor
  • Dysdiadochokinesia
  • Nystagmus
  • Dysarthria
  • Titubation (head nodding)
  • Involuntary movements (myoclonic jerks, chorea)
144
Q

What are the causes of cerebellar dysfunction?

A
  • Developmental: agenesis, or other malformations
  • Demyelination: MS, acute disseminated encephalomyelitis
  • Degenerative: cerebellar degeneration, multi system atrophy, spinocerebellar ataxia
  • Neoplastic: astrocytoma, haemangioblastoma, metastasis, paraneoplastic
  • Infectious: abscess, acute cerebellitis
  • Metabolic: hypoxia, hypoglycaemia, alcohol, inborn disorders of metabolism
  • Vascular: haemorrhage, infarction
  • Drugs/toxins: alcohol, phenytoin, carbamazepine
145
Q

Describe Meniere’s syndrome (definition, cause, features, treatment)

A
  • Disorder of the inner ear caused by changes in fluid volume in the labyrinth
  • Unknown cause, but risk factors include allergy, autoimmunity, genetics, metabolic disturbance, vascular factors, viral infection
  • Clinical features: acute attacks of vertigo, tinnitus, hearing loss, and sensation of aural pressure
  • Treatment: acute relief with prochlorperazine, cyclizine, promethazine, prophylaxis with betahistine

Phase 3a (10 decks)

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