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YEAR 3 MED > Module 3C Neurology and Vision - Conditions DONE > Flashcards

Module 3C Neurology and Vision - Conditions DONE Flashcards

1
Q

Basic pain pathway

A
  • Nociceptors (pain receptors) at the end of nerves detect damage to tissues
  • Nerve signals are transmitted along the afferent nerves to the spinal cord
  • The signal then travels in the CNS, up the spinal cord (mainly in the spinothalamic tract and spinoreticular tract) to the brain (thalamus) where it is interpreted as pain (somatosensory cortex)
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2
Q

Two types of nerve fibres

A
  • C fibres (unmyelinated) - transmit signals slowly and produce dull and diffuse pain sensations
  • A-delta fibres (myelinated) - transmit signals fast and produce shapr and localised pain sensations
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3
Q

Headaches - red flags

A

-Fever, photophobia or neck stiffness (meningitis, encephalitis or brain abscess)
- New neurological symptoms (haemorrhage or tumours)
- Visual disturbance (giant cell arteritis, glaucoma or tumours)
- Sudden-onset occipital headache (subarachnoid haemorrhage)
- Worse on coughing or straining (raised intracranial pressure)
- Postural, worse on standing, lying or bending over (raised intracranial pressure)
- Vomiting (raised intracranial pressure or carbon monoxide poisoning)
- History of trauma (intracranial haemorrhage)
- History of cancer (brain metastasis)
- Pregnancy (pre-eclampsia)

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4
Q

What does papilloedema on fundoscopy indicate?

A

Suggests raised intracranial pressure

  • brain tumour
  • benign intracranial hypertension
  • intracranial bleed
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5
Q

Tension headache - typical presentation + what is it associated with?

A
  • mild ache or pressure in a band-like pattern around the head
  • develop gradually and do not produce visual changes
    .
    Associated with:
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
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6
Q

What is defined as a chronic tension-type headache?

A

TTH occurring on more than 15 days per month for at least 3 months

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7
Q

Tension (or tension-type) headache - Management

A
  1. Reassurance +/- simple analgesia
  2. Amitriptyline - 1st-line for chronic TTH
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8
Q

Sinusitis - presentation

A
  • usually following a recent viral URTI
  • tenderness and swelling on palpation of the affected areas
  • usually resolves in 2-3 weeks
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9
Q

Sinusitis - management of prolonged cases

A
  1. steroid nasal spray
  2. antibiotics (phenoxymethylpenicillin 1st line)
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10
Q

Medication-overuse headache - treatment

A
  1. withdrawal of the analgesia
    (challenging in pts with chronic pain)
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11
Q

Hormonal headache (menstrual migraines) - presentation

A

Related to low oestrogen
- unilateral, pulsatile headache associated with nausea

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12
Q

Hormonal headache (menstrual migraine) - treatment

A
  1. Triptans and NSAIDs (eg. mefenamic acid)
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13
Q

Trigeminal neuralgia - treatment

A
  1. Carbamazepine 1st-line
  2. Surgical options can be considered if symptoms persist
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14
Q

Types of migraine

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (migraine with aura but without a headache)
  • Hemiplegic migraine
  • Chronic migraine - pt experiences for more than 15 days per month for at least 3 months
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15
Q

Migraine - clinical features

A

Symptoms can last up to 72hrs, typical features are:
- Severe, unilateral, throbbing headache - pounding/throbbing in nature
- Aura (can last up to 60 mins)
- Photophobia/phonophobia/osmophobia - pts usually go toa darkened, quiet room during an attack
- nausea and vomiting

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16
Q

Migraines - what is aura

A

Aura can affect vision, sensation, or language - visual symptoms are the most common:
- sparks in vision
- blurred vision
- lines across vision
- loss of visual fields (eg. scotoma)
.
- Sensation changes - tingling/numbness
- Language changes - dysphasia

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17
Q

What is a hemiplegic migraine and what should be ruled out?

A

Migraine with hemiplegia (unilateral limb weakness)
- other symptoms may include ataxia and impaired consciousness
- note: can mimic a stroke/TIA - so it is important to rule this out

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18
Q

Migraine - triggers

A
  • stress
  • sensory stimuli - eg. bright lights, loud noises, strong smells
  • sleep disturbances - eg. insomnia, irregular sleep patterns
  • Dietary factors - eg. caffeine, alcohol
  • Hormonal changes - eg. menstruation, menopause
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19
Q

Migraines - Acute management

A

(pts may develop strategies for managing symptoms - eg. going into a dark, quiet room)
1. Oral triptan (eg. sumatriptan) +/- NSAID +/- paracetamol
2. Anti-emetic (eg. metoclopramide)

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20
Q

What medication should NOT be given to pts with migraines (eg. acute attack)

A

Opiates - can make condition worse

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21
Q

Migraines - Prophylactic management

A

(a headache diary can help identify triggers and access response to treatment)
1. Propranolol OR Topiramate OR Amitriptyline
(menstrual migraine treatment - frovatriptan or zolmitriptan as “mini-prophylaxis”)

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22
Q

Who should not take topiramate (an option of medication used in migraine prophylaxis)?

A

Women of childbearing age - teratogenic + can reduce the effectiveness of hormonal contraception

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23
Q

Cluster headaches - Clinical features

A
  • Severe pain - stabbing pain around one eye
  • typically occurs once or twice a day - each episode lasting 15 mins to 2hrs
  • “clusters” typically last 4-12 weeks
  • red, swollen, and watering eye
  • +/- miosis and ptosis
    (note: alcohol can be a trigger)
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24
Q

Cluster headache - Acute treatment

A
  1. High-flow 100% oxygen
  2. Subcutaneous triptan
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25
Q

Cluster headache - Prophylaxis

A
  1. Verapamil
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26
Q

What is the most common viral cause of encephalitis?

A

Herpes simplex virus (HSV)
- Children - HSV-1 from cold sores
- Neonates - HSV-2 from genital herpes, contracted during birth

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27
Q

Encephalitis - clinical features

A

Rapid onset of symptoms:
- fever
- headache
- altered consciousness
- +/- neurological deficits

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28
Q

Encephalitis - investigations

A
  • Lumbar puncture - send CSF for viral PCR testing
  • (CT scan if LP contraindicated - -eg. GCS < 9, hemodynamically unstable, active seizures or post-ictal)
  • MRI brain - after LP
  • EEG - not routinely required
  • HIV testing is recommended
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29
Q

Encephalitis - Management

A
  1. IV antiviral
    - Aciclovir for HSV and VZV
    - Ganciclovir for CMV
  2. Supportive care - fluids, monitor ICP, +/- manage seizures
  3. Repeat lumbar puncture - to ensure successful treatment prior to stopping antivirals
    (4. Follow-up and rehab - manage any complications)
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30
Q

Meningitis - Aetiology

A

Usually bacterial or viral:

  1. Bacterial
    - Neisseria meningitidis - gram -ve diplococcus (meningococcal meningitis)
    - Strep. pneumoniae
    - Haemophilus influenzae
    - Listeria monocytogenes, E. coli, and group B Strep (neonates)
  2. Viral
    - Enteroviruses (eg. coxsackievirus) - most common
    - Herpes simplex virus (HSV)
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31
Q

Meningitis - Pathophysiology (invasion –> survival –> replication and tissue damage)

A
  1. Invasion
    - Pathogen colonises nasopharynx
    - pathogen then invades bloodstream
    - bacteria then cross the blood-brain barrier (BBB)
  2. Survival
    - bacteria evades immune responses to survive and proliferate
    - various mechanisms - antigenic variation, inhibition of complement activation, intracellular survival inside phagocytes, production of immunomodulatory molecules, and formation of biofilms
  3. Replication and Tissue damage
    - bacteria multiply in the subarachnoid space - leading to increased ICP
    - Inflammatory response leads to damage of neuronal tissue and the BBB - results in symptoms
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32
Q

Meningitis - Clinical features

A

(a prodromal phase often precedes the classic symptoms - malaise, headache, myalgia, and low-grade fever)
.
Classic symptoms:
- Fever - moderate to high grade
- Neck stiffness - worse with passive flexion of neck
- Altered mental state

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33
Q

Meningococcal septicaemia - what is it and what symptom is often associated with it?

A
  • When the meningococcus bacterial infection is in the bloodstream
  • non-blanching rash
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34
Q

Meningitis - additional signs that there is meningeal irritation are Kernig’s sign and Brudzinski’s sign, what are these? (aka. Kernig’s and Brudzinski’s test)

A
  • Kernig’s sign - pt in supine position with hips and knees flexed at 90 degrees, pain on straightening the knee suggests meningeal irritation (causes a stretch in the meninges)
  • Brudzinski’s sign - pt supine, use your hands to lift their head and neck off the bed and flexing their chin to their chest - +ve sign is when this causes the pt to flex their hips and knees involuntarily
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35
Q

Meningitis - Investigations

A
  • Blood cultures - to help identify causative organism
  • FBC - elevated WCC
  • CRP and ESR - often raised in bacterial infections
  • Blood glucose - important for comparison with CSF glucose lvls
  • Lumbar puncture - essential for confirming a diagnosis (culture, viral PCR, CSF glucose and protein)
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36
Q

Meningitis - using a lumbar puncture (CSF analysis) to differentiate between bacterial and viral cause

A

Think about what is going on:
- bacteria swimming in the CSF will release proteins and use up glucose
- Viruses may release a small amount of protein and do not use up glucose
- The immune system releases more neutrophils with bacteria and lymphocytes with viruses

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37
Q

Meningitis - Bacterial meningitis management

A

Ideally blood cultures and a LP should be performed before starting antibx, however don’t delay antibx if pt is acutely unwell (once causative organism identified - start specific antibx)

  1. Ceftriaxone + amoxicillin (to cover Listeria)
    (cefotaxime - if under 3 months)
  2. +/- Acyclovir (only if HSV encephalitis is suspected)
  3. +/- Vancomycin (if there is a risk of penicillin-resistant pneumococcal infection - eg. recent foreign travel or prolonged antibx exposure)
  4. Steroids (eg. dexamethasone) - to reduce hearing loss complications
  5. Close monitoring for complications - raised ICP, seizures, neuro deficits
  6. Supportive care - analgesics/antipyretics/antiemetics +/- fluids +/- oxygen
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38
Q

Is bacterial meningitis a notifiable disease?

A

YES
- notify the UK Health Security Agency

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39
Q

What is the most common complication of bacterial meningitis?

A

Hearing loss
- Sensorineural hearing loss can occur due to cochlear damage

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40
Q

Meningitis - Post-exposure prophylaxis

A

If close contact - give a single dose of ciprofloxacin as prophylaxis

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41
Q

Brain tumours - Clinical features

A

May be asymptomatic (particularly when small in size)

  • headaches - persistent, morning, worse on lying down, +/- nausea and vomiting
    Seizures - focal or generalised
  • Progressive focal neuro symptoms (depending on location) - cognitive, motor, sensory, vision, speech, personality changes
  • Raised ICP signs
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42
Q

Raised intracranial pressure - Signs and symptoms

A
  • constant headache
  • nocturnal
  • worse on waking
  • worse on coughing, straining, or bending forward
  • nausea and vomiting
  • papilloedema on fundoscopy

more signs:
- altered mental state
- visual field defects
- seizures
- unilateral ptosis
- 3rd and 6th nerve palsies

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43
Q

Raised ICP - why does it cause papilloedema?

A

Papilloedema = swelling of the optic disc secondary to raised ICP
- the sheath around the optic nerve is connected with the subarachnoid space
- the raised CSF pressure flows into the optic nerve sheath, increasing the pressure around the optic nerve behind the optic disc causing the optic disc to bulge forward

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44
Q

Name some types of brain tumour

A
  1. Gliomas (can be benign or malignant) - tumours of the glial cells in brain or spinal cord
    - Glioblastoma - most common primary brain tumour in adults
    - Pilocystic astrocytoma - most common primary brain tumour in children
  2. Meningiomas (typically benign) - tumours growing from the cells of the meninges, cause symptoms by compression not invasion
  3. Secondary metastases (bad) - most common form of brain tumours, often multiple lesions
  4. Pituitary adenoma (benign tumours) - can be hormone secreting or non-secreting
  5. Vestibular schwannoma (or acoustic neuroma) - benign tumour of the Schwann cells that surround the 8th cranial nerve (vestibulocochlear)
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45
Q

Which tumours most commonly spread to the brain to cause secondary metastases?

A
  • Lung (most common)
  • Breast
  • Bowel
  • Skin (melanoma)
  • Kidney (renal cell carcinoma)
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46
Q

Glioma - which type is the most malignant and also the most common primary tumour in adults?

A

Glioblastoma multiforme

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47
Q

What type of visual field defect do pituitary adenomas cause if they grow large enough?

A

Bitemporal hemianopia
- pituitary sits close to the optic chiasm

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48
Q

Pituitary adenomas - presentation

A

They can cause hromone deficiencies (hypopituitarism) or excessive release of hormones, leading to:
- Acromegaly (excessive GH)
- Hyperprolactinaemia (excessive prolactin)
- Cushing’s disease (excessive ACTH and cortisol)
- Thyrotoxicosis (excessive TSH and thyroid hormones)

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49
Q

Pituitary adenomas - management

A
  1. Trans-sphenoidal surgery (thorugh the nose and sphenoid bone)
  2. Radiotherapy
  3. Bromocriptine (blocks excess prolactin)
  4. Somatostatin analogues (eg. octreotide) - to block excess GH
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50
Q

What do Schwann cells do?

A

provide the myelin sheath around neurones of the peripheral NS

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51
Q

Where do vestibular schwannomas (or acoustic neuromas) occur?

A

the cerebellopontine angle
(arises from the 8th cranial nerve - vestibulocochlear)

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52
Q

Vestibular schwannoma (or acoustic neuroma) - presentation

A
  • Unilateral sensorineural hearing loss (often first symptom)
  • unilateral tinnitus
  • dizziness or imbalance
  • sensation of fullness in the ear
  • facial nerve palsy (if tumour grows large enough to compress the facial nerve)
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53
Q

Brain tumours - General management (include investigations)

A
  • MRI brain
  • Biopsy - gives defintive histological daignosis
    .
    Management depends on type and, grade - guided by MDT:
    1. Surgery
    2. Chemotherapy
    3. Radiotherapy
    4. Palliative care
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54
Q

How are brain tumours classified / graded?

A

Grades 1 to 4 - where 1 is least aggressive and 4 is most aggressive, based off:
- cellular appearance
- mitotic activity (how quickly cells are dividing)
- necrosis (dead tissue within the tumour)
- vascular proliferation

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55
Q

Which lobe would the tumour be in if the pt has an unusual change in personality and behavior?

A

Frontal lobe
- the frontal lobe is responsible for personality and higher-level decision-making

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56
Q

Brain abscesses - aetiology (where do they usually originate from)

A
  • Contiguous spread of infection - sinusitis, otitis media, or dental infections
  • Haematogenous spread from distant sources - eg, endocarditis, pulmonary infections
  • Direct inoculation - trauma or neurosurgical procedures

(risk factors - immunocompromised, IV drug use)

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57
Q

Symptoms and signs of brain abscesses are usually quite non-specific and hard to localise, what investigations would you do for a suspected brain abscess or to rule it out?

A
  • Neuroimaging - MRI (with gadolinium) and CT both have roles
  • Stereotactic needle aspiration - can aid diagnosis and serve as treatment

(note: lumbar puncture is contraindicated due to risk of brain herniation)

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58
Q

Brain abscesses - Management

A
  1. Surgery - craniotomy –> abscess cavity debrided
  2. IV antibiotics
  3. Intracranial pressure management (eg. dexamethasone)
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59
Q

2 causes of ischaemic strokes

A
  • Thrombotic - eg. atherosclerosis (ruptured plaque)
  • Embolic - eg. AF
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60
Q

Oxford classification of stroke (Bamford classification)

A
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61
Q

Risk factors for a stroke

A
  • Main –> smoking, AF, hx of previous stroke or TIA
  • Other –> hypertension, hypercholesterolemia, obesity, family hx, vasculitis, combined oral-contraceptive pill

(stroke is associated with co-morbidities such as cardiovascular disease and vascular disease –> share the same risk factors)

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62
Q

Definition of stroke, TIA, crescendo TIAs

A
  • Stroke = a clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal neurological deficit lasting more than 24hrs and thought to be of vascular origin
  • TIA = neurological signs/symptoms that are consistent with a stroke that resolve within 24hrs
  • Crescendo TIAs = two or more TIAs within a week and indicate a high risk of stroke
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63
Q

Common symptoms of a stroke

A
  • One-sided muscle weakness (hemiparesis)
  • Dysphasia (speech disturbance)
  • Aphasia (expressive/receptive/global)
  • One-half visual field defects (hemianopia) - often lose one-half of visual field in each eye which results in neglect on one side of the body
  • Sensory loss
  • Ataxia and vertigo
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64
Q

Does stroke always affect the contralateral side of the body?

A

Not always –> if cerebellum affected then ipsilateral presentation

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65
Q

Label the cerebral arteries.
- Which arteries supply anterior brain
- Which arteries supply posterior brain

A
  • Blood is delivered to brain through 4 main arteries, two internal carotid arteries (anterior supply), and two vertebral arteries (posterior supply to the brain)
  • Anterior supplied by internal carotid arteries which form the ACA and MCA
  • Anterior connects with Posterior via posterior communicating artery
  • Posterior supplied by vertebral arteries which combine to form the Basilar artery

(The brain also has a venous drainage system which drain into the venous sinuses)

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66
Q

Which arteries form the Circle of Willis?
- What is function of Circle of Willis?

A
  • Formed by basilar artery, internal carotid artery, and middle cerebral artery
  • Safeguards the oxygen supply from interruption by arterial blockage
  • For example, if there is stenosis in one artery then other source arteries to the Circle of Willis can provide an alternative blood flow (collateral circulation)
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67
Q

The limbic system is made up of the hippocampus and amygdala, what are their functions?

A

Limbic system is involved in behavioural and emotional responses (survival, fight or flight)

  • Hippocampus –> memory centre, spatial orientation, neurogenesis occurs here (key brain structure for learning new things)
  • Amygdala –> central role in emotional responses (pleasure, pain, fear, anxiety, anger), attaches emotional content to memories
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68
Q

Functions of frontal lobe, parietal lobe, temporal lobe, and occipital lobe

A
  • Frontal lobe –> higher executive function (emotions, planning, reasoning, problem-solving), primary motor cortex (responsible for voluntary movement)
  • Parietal lobe –> sensory info (touch, temp., pressure, pain), two-point discrimination can be used to assess
  • Temporal lobe –> sensory info (hearing, recognising language, forming memories), primary auditory cortex (can understand what we hear), making sense of complex visual info (faces and scenes), hippocampus (memory, learning, emotions)
  • Occipital lobe –> Primary visual cortex (major visual processing centre in the brain)
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69
Q

MCA infarct:
- locations affected?
- symptoms associated

A
  • Locations affected –> frontal, parietal, and temporal lobes

Symptoms:
- hemiparesis –> arm worse than leg
- Sensory loss
- Facial weakness –> facial droop/dysarthria
- Dysphasia –> expressive, receptive, global
- Hemianopia –> without macula sparing

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70
Q

Broca’s aphasia vs Wernicke’s aphasia

A
  • Broca’s –> expressive dysphasia (pt can understand what is said but cannot express with words, difficult to speak)
  • Wernicke’s –> receptive dysphasia (pt doesn’t understand what is being said, but can still talk normally, but it doesn’t make any sense)
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71
Q

If a right-hand dominant patient has Broca’s or Wernicke’s aphasia then which side is the stroke?

A
  • Left MCA
  • Broca’s and Wernicke’s area are found in the dominant cerebral hemisphere
  • left side for right-handed
  • right side for left-handed
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72
Q

ACA infarct:
- locations affected?
- symptoms associated

A
  • Locations affected –> frontal and parietal lobes

Symptoms:
- hemiparesis –> leg worse than arm
- Apathy –> lack of interest, enthusiasm, or concern
- incontinence
- Disinhibition –> lack of restraint in social scenarios (affects motor, emotional, cognitive, instinctual, and perceptual behaviours)
- Mutism

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73
Q

Lacunar stroke:
- locations affected?
- symptoms associated

A

Locations affected –> Lenticulostriate arteries (small penetrating arteries that supply deep structures
(susceptible to injury secondary to uncontrolled hypertension)

Symptoms:
- Pure motor –> hemiparesis or hemiplegia, dysrthria, dysphagia
- Pure sensory –> numbness/tingling/pain on one side of body
- Sensorimotor –> hemiparesis or hemiplegia with contralateral sensory impairment

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74
Q

What are the watershed zones?
- Symptoms for each

A

Watershed zones are prone to infarction as they receive blood supply from two arteries

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75
Q

PCA infarct:
- locations affected?
- symptoms associated

A

Locations affected –> mainly occipital, parts of temporal

Symptoms:
- Hemianopia –> with macular sparing
- Amnesia
- Sensory loss (thalamus)
- Thalamic pain

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76
Q

Where does basilar artery supply and if basilar artery is affected in a stroke, what is the serious condition that can result? + what structure is damaged to cause this

A
  • Supplies lower midbrain, pons, and medulla (and occipital lobe)
  • Infarction causes locked-in syndrome –> individual has full consciousness but is paralysed
  • due to damage to corticospinal tracts (quadriplegia)
  • Respiratory muscles also paralysed so individual has to be ventilated –> resp. failure and coma/death can be result
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77
Q

Acute stroke management

A
  • Non-contrast CT is mainstay investigation
  • Thrombectomy –> Can be done together with IV thrombolysis if within 4.5hrs onset –> CT perfusion or CT angiography used to assess salvageable brain tissue
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78
Q

Contraindications for thrombolysis

A
  • pt on DOAC or Warfarin (check INR)
  • Hx of surgery, Hx of bleeding (external/internal)
  • Uncontrolled hypertension –> BP > 180/120mmHg
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79
Q

What investigation should be done 24hrs after onset of a stroke

A

Repeat CT head to check for haemorrhagic transformation

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80
Q

Longer-term management of ischaemic stroke

A
  • Aspirin 300mg daily –> for 2 weeks (start aspirin 24hrs after thrombolysis and once repeat CT confirms no haemorrhage)
  • After the 2 weeks –> Clopidogrel 75mg –> lifelong
  • Atorvastatin 20-80mg (after 48hrs) –> lifelong
  • Address modifiable risk factors –> smoking, diabetes control, AF control (if ECG showed AF to be the cause), exercise
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81
Q

Indications for carotid endarterectomy

A
  • If carotid artery doppler ultrasound confirms > 50% carotid stenosis
  • (risk of clot embolising and causing stroke)
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82
Q

ROSIER score
(recognition of stroke in the emergency room)

A

Exclude hypoglycaemia first then assess the following:

  • a stroke is likely if > 0
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83
Q

FAST tool for stroke

A

simple way to identify stroke in the community

F – Face
A – Arm
S – Speech
T – Time to call 999

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84
Q

NIH stroke scale (NIHSS) + criteria for no stroke/mod stroke/mod-sev/severe

A

NIH Stroke Scale (NIHSS)  used as an initial assessment of the patient for suspected stroke and gives a rough idea of how severe the stroke is
(used in secondary care)
- < 5 –> no stroke/minor
- 5-15 –> moderate
- 16-20 –> moderate-severe
- 21-42 –> severe

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85
Q

Vascular territories

A
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86
Q
A

Dense MCA sign –> visible immediately, shows the responsible arterial clot

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87
Q

Warfarin reversal agents

A

Vitamin K and prothrombin complex concentrate

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88
Q

Heparin/LMWH reversal

A

Protamine sulfate

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89
Q

Dabigatran reversal agent

A

Idarucizunab

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90
Q

Apixaban, edoxaban, and rivaroxaban reversal agent

A

Andexanet alfa

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91
Q

For patient’s on anticoagulant therapy, what is the INR target range? + what value indicates a risk of bleeding?

A
  • 2.0-3.0
  • > 4.9 is high risk of bleeding
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92
Q

Complications of stroke (hospital problems)

A
  • dysphagia/aspiration pneumonia –> most common cause of death pst-stroke in hospital setting –> SLT assessment + fluids
  • DVT/PE –> normal pt (antiplatelets), stroke pt (mechanical stockings –> we don’t want to turn an ischaemic stroke into a haemorrhagic stroke)
  • UTI –> stroke can cause bowel/bladder issues
  • spasticity
  • shoulder subluxation
  • depression
  • nutrition
  • pressure sores –> look for bruising on pressure areas of body
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93
Q

How would you manage a patient who has had an ischaemic stroke and they have atrial fibrillation?

A

Anticoagulants should not be started until brain imaging has excluded haemorrhage, and not until 14 days after the onset of an ischaemic stroke

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94
Q

Cerebellar stroke symptoms

A
  • Problems with moving/walking –> balance (cerebellum is part of brain responsible for balance)
  • Vertigo –> ‘room spinning’
  • muscle weakness or tremors
  • headache
  • nausea and vomiting
  • hearing and vision problems
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95
Q

Management of crescendo TIAs

A

Aspirin 300mg and review in TIA clinic within 24hrs

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96
Q

Stroke/TIA –> DVLA guidelines for car drivers

A
  • Must stop driving immediately
  • Must stop for 1 month
  • Must inform DVLA if after 1 month you still have –> weakness in arms or legs, eyesight problems (visual filed loss or double vision), or problems with balance, memory, or understanding –> or if doctor says not safe to drive
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97
Q

Stroke/TIA –> DVLA guidelines for bus/lorry drivers

A
  • stop driving immediately
  • Must stop driving for at least one year, can only restart when doctor says it is safe
98
Q

Most common cause of a lacunar stroke

A

Long-standing hypertension

99
Q

Homonymous hemianopia in PCA vs MCA

A
  • PCA –> macular sparing due to occipital dual blood supply
  • MCA –> without macular sparing
100
Q

Facial nerve - pathway and its 5 branches

A
  • facial nerve exits brainstem at the cerebellopontine angle
  • on its journey to the face it passes through the temporal bone and parotid gland
  • it then branches off into its 5 divisions
101
Q

Facial nerve function - what are its motor functions, sensory function, and parasympathetic supply?

A
  • Motor - facial expression, stapedius (in inner ear), posterior digastric, stylohyoid, and platysma muscles
  • Sensory - taste from anterior 2/3 of tongue
  • Parasympathetic supply - submandibular and sublingual salivary glands + lacrimal gland
102
Q

Facial nerve palsy (Bell’s palsy) - Clinical features

A

Unilateral facial paralysis
- unable to wrinkle forehad and close eye fully
- loss of nasolabial fold, drooping of mouth
- +/- loss of taste in anterior 2/3 of tongue

103
Q

Facial nerve palsy (Bell’s palsy) - Investigations

A

It is a diagnosis of exclusion
- however, symptoms can be similar to an UMN leison (stroke) so it is important that stroke is ruled out

104
Q

Facial nerve palsy (bell’s palsy) - Management

A

Most pts recover over several weeks:

  1. Prednisolone (if pt present within 72hrs of onset) +/- antivirals
  2. Lubricating eye drops (to prevent eye from drying out)

(if eye pain - refer to ophthalmology for potential exposure keratopathy)

105
Q

A patient presents with a unilateral LMN facial nerve palsy, they have a painful and tender vesicular rash in and around the ear on the affected side - what condition is this describing + what is the management

A

Ramsay-Hunt Syndrome
- Treatment - aciclovir + prednisolone +/- lubricating eye drops

106
Q

Subarachnoid haemorrhage - aetiology

A
  • Traumatic SAH (head injury)
  • Spontaneous SAH (intracranial aneurysm - saccular “berry” aneurysms)
107
Q

Subarachnoid haemorrhage - Clinical features

A
  • Sudden-onset occipital headache (“thunderclap” or “hit with a baseball bat”) - typically peaking in intensity within 1-5 mins
  • may be a hx of a less severe ‘sentinel’ headache a few days before
  • Nausea and vomiting
  • meningism - photophobia +/- neck stiffness
  • Neuro symptoms (eg. visual changes, dysphasia, focal weakness, seizures, reduced consciousness)
108
Q

Subarachnoid haemorrhage - Investigations

A
  • Non-contrast CT head is first-line (ideally within 6hrs of onset)
    (Note: if CT head is done within 6hrs of onset and is normal, then don’t do an LP and consider another diagnosis)
  • Lumbar puncture - should be done at least 12hrs after onset to allow for development of xanthochromia (RBC breakdown - eg. bilirubin) - xanthochromia helps to distinguish true SAH from a ‘traumatic tap’
    .
  • CT intracranial angiogram (to identify a vascular lesion - eg. aneurysm)
109
Q

Subarachnoid haemorrhage - Acute management

A
  1. Refer to neurosurgery - endovascular coiling OR neurosurgical clipping to repair aneurysm
  2. Supportive: analgesia +/- reversal of anticoagulation
110
Q

Subarachnoid haemorrhage - Management of complications that can occur:

  1. Vasospasm - resulting in brain ischaemia
  2. Hydrocephalus
  3. Seizures
A
  1. Vasospasm - Nimodipine (Ca-channel blocker)
  2. Hydrocephalus - LP, external ventricular drain, VP shunt
  3. Seizures - anti-epileptic drugs
111
Q

Intracranial bleeds - Presentation

A

Sudden-onset headache
- seizures
- nausea and vomiting
- reduced consciousness
- focal neurological symptoms (eg. weakness)

112
Q

Glasgow Coma Scale (GCS) - what is measured + scores given and what score would indicate intubation?

A

GCS measures level of consciousness
- GCS < 8 –> intubation (needs airway support as risk of airway obstruction or aspiration, leading to hypoxia and brain injury)

113
Q

Intracranial bleeds - principles of management

A
  • CT head - to establish diagnosis
  • Bloods - FBC (platelets) + coagulation screen
    1. Refer to neurosurgery
    2. Consider intubation, ventilation, and intensive care (if reduced GCS)
    3. Correct any clotting abnormality (eg. platelet transfusion or reversal agents for blood thinners)
    4. Correct severe hypertension, but avoid hypotension
    (5. Surgical options (for extradural OR subdural) - Craniotomy OR Burr holes)
114
Q

Main causes of raised intracranial pressure

A
  • Brain tumours
  • Intracranial haemorrhage
  • Idiopathic intracranial hypertension
  • Abscesses or infection
115
Q

Idiopathic intracranial hypertension - Risk factorsdd

A

As the name suggests, the cause is unknown, risk factors include:
- Female (90%)
- Obesity (often associated with recent weight gain)
- Pregnancy

116
Q

Idiopathic intracranial hypertension (IIH) - Clinical features (symptoms and signs)

A

Symptoms (gradual and progressive)
- Headache +/- nausea and vomiting
- Transient visual obscurations
- Pulsatile tinnitus
- Photopsia (seeing flashes of light)
- Back pain + Retrobulbar pain
.
Signs:
- Papilloedema - typically bilateral and symmetrical
- Visual field loss - typically peripheral
- 6th nerve pasly
- RAPD

117
Q

IIH - main principle of investigation

A

To rule out a secondary cause of intracranial hypertension
- MRI brain
- LP (once intracranial mass lesions have been ruled out - cranial herniation)

118
Q

IIH - Management

A
  1. Conservative - weight loss
  2. Acetazolamide
    (3. Topiramate may be used as an alternative + aids in weight loss)
  3. Refractory cases: Loop diuretics + repeated LPs (as a holding measure)
  4. Analgesia - paracetamol/NSAIDs (for head or back pain)
  5. Surgery - optic nerve sheath fenestration or CSF shunting
119
Q

Hydrocephalus - symptoms (under 2yrs)

A
  • Enlarged and rapidly increasing head circumference (occipito-frontal circumference)
  • bulging anterior fontanelle
  • poor feeding and vomiting
120
Q

Mainstay of treatment for hydrocephalus

A

Ventriculoperitoneal shunt (VP shunt)
- drains CSF from ventricles into another body cavity (peritoneal cavity usually used)

121
Q

What is Wernicke’s encephalopathy?

A

acute thiamine (vitamin B1) deficiency
- associated with chronic alcoholics, but can occur due to malnutrition

122
Q

Wernicke’s encephalopathy - Clinical features

A
  • Classic triad - confusion, ophthalmoplegia, and ataxia
123
Q

Wernicke’s encephalopathy - Management

A
  1. Parenteral (not oral) thiamine - minimum of 5 days
  2. Continue oral thiamine
124
Q

Which vein is most commonly affected by central venous thrombosis?

A

Sagittal sinus thrombosis
- thrombus/occlusion of cerebral vein or sinus leads to deoxygenated blood pooling within the brain parenchyma - causes an increase in cerebral venous pressure

125
Q

Central venous thrombosis - management

A
  1. acute antithrombotic therapy - LMWH
  2. treat symptoms:
    - raised ICP - mannitol or hypertonic saline
    - seizures - anticonvulsants
    - infection/inflammation - antibx/glucorticoids
  3. long-term - anticoagulation (Warfarin)
126
Q

What is multiple sclerosis?

A
  • chronic and progressive autoimmune condition involving demyelination in the central nervous system (oligodendrocytes)
  • the immune system attacks the myelin sheath of the myelinated neurons
127
Q

What cells produce myelin in the…

  • central nervous system
  • peripheral nervous system
A
  • CNS - Oligodendrocytes
  • PNS - Schwann cells
128
Q

What are the 3 main patterns of multiple sclerosis?

A
  1. Relapsing-remitting MS (RRMS)
    - 85% of cases
    - relapses are followed by periods of neurological stability between episodes
    - RMMS often progresses to SPMS
  2. Secondary progressive MS (SPMS)
    - A progressive neurological disability after an initial RRMS course
  3. Primary progressive MS (PPMS)
    - Steady progressive worsening of neurological symptoms from onset
129
Q

Multiple sclerosis - clinically isolated syndrome (CIS)

A
  • CIS describes the dirst episode of demyelination and nuro signs/symptoms
  • Pts with CIS may never have another episode or may go on to develop MS
130
Q

Multiple sclerosis - Clinical features

A
  • Optic neuritis (most common presentation) - unilateral reduced vision (central scotoma, pain with eye movement, impaired colour vision, RAPD)
  • Focal weakness - incontinence, Horner’s, facial nerve palsy, limb paralysis
  • Focal sensory symptoms - trigeminal neuralgia, numbness, paraesthesia, Lhermitte’s sign
  • Ataxia - Sensory (due to loss of proprioception) OR Cerebellar (due to loss of coordination/balance)
  • Sexual dysfunction - most common complaint in men
  • Depression and anxiety
131
Q

Multiple sclerosis - what is Lhermitte’s sign?

A

describes an electric shock sensation that travels down the spine and into the limbs when flexing the neck

132
Q

Multiple sclerosis can present with sensory ataxia - what test can test proprioception and balance?

A

Romberg’s test
- lose balance when standing with eyes closed

133
Q

Multiple sclerosis - Investigations/diagnosis

A
  • MRI scans - demonstrate typical lesions
  • Lumbar puncture - oligoclonal bands in CSF
134
Q

Multiple sclerosis - Management

A

Specialist MDT manages MS:
1. Acute relapse - High-dose steroids IV or oral for 5 days (also improves optic neuritis)
2. Reducing long-term remission - DMARDS (eg. natalizumab, ocrelizumab)

Specific problems:
3. Spasticity - baclofen or gabapentin
4. Fatigue - amantadine
5. Oscillopsia - gabapentin
6. Depression - antidepressants (eg. SSRIs)

135
Q

Motor neurone disease - which neurones are affected?

A

Motor neurones (upper and lower)
- the sensory neurones are spared

136
Q

2 most common types of motor neurone disease

A
  1. Amyotrophic lateral sclerosis (ALS) - Stephen Hawking had this type
  2. Progressive bulbar palsy - primarily affects the muscles of talking and swallowing (the bulbar muscles)
137
Q

Motor neurone disease - Clinical features (include upper/lower MND)

A
  • insidious, progressive weakness of the muscles throughout the body (limbs, trunk, face, and speech)
  • absence of sensory signs/symptoms
  • typically a 60-70yr old man
    .
    Lower MND signs:
  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes
    .
    Upper MND signs:
  • increased tone/spasticity
  • brisk reflexes
  • upgoing plantar reflex
138
Q

Motor neuron disease - Management

A

There are no effective treatment for halting or reversing the progression of the disease
1. Riluzole - can slow progression of the disease (used in ALS)

  1. Respiratory care - NIV (BiPAP) used at night
  2. Palliative care

Symptom control:
4. Spasticity - baclofen
5. Excess saliva - antimuscarinic
6. Breathlessness (worsened by anxiety) - benzodiazepines

139
Q

What do pts with MND usually die of?

A

Respiratory failure (due to weakened resp. muscles) or Pneumonia

140
Q

Cervical spondylitic myelopathy - Clinical features

A

Cervical spondylosis is a degenerative condition affecting the cervical spine (ie. OA of the cervical vertebral bodies)
- Motor weakness, sensory loss and bladder/bowel dysfunction

141
Q

Cervical spondylitic myelopathy - investigations

A

MRI cervical spine is gold-standard

142
Q

Cervical spondylitic myelopathy - Management

A
  1. Urgent referral to neurosurgery/orthopaedic spinal surgery
  2. Decompressive surgery is only effective treatment
143
Q

Friedrich’s ataxia - what is it + genetic inheritance

A
  • most common early-onset hereditary ataxias
  • autosomal recessive
144
Q

Friedrich’s ataxia - Clinical features

A
  • typical age of onset is 10-15yrs old
  • Gait ataxia and kyphoscoliosis
145
Q

Subacute combined degeneration of spinal cord (SCD) - what is it + aetiology

A
  • SCD = rare neuro condition that affects the dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts of the spinal cord
  • caused by vitamin B12 deficiency
146
Q

Subacute combined degeneration of spinal cord (SCD) - treatment

A
  1. High-dose vitamin B12 supplementation
147
Q

Contraindications for performing a lumbar puncture

A
  1. Raised ICP (risk of cranial herniation)
  2. Recent seizures
  3. Brain tumours
  4. Coagulopathy or Anticoagulation (risk of spinal haematoma)
  5. Local infection at puncture site
148
Q

Describe what generalised tonic-clonic seizures (aka. grand mal seizures) involve.

A
  • involve tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness
  • typically the tonic phase comes before the clonic phase
  • before the seizure, pts may experience aura
  • there may be tongue biting, incontinence, groaning, and irregular breathing
  • after the seizure, there is a prolonged post-ictal period, where the person is confused, tired, and irritable
149
Q

Describe what partial (or focal) seizures involve.

A
  • occur in an isolated brain area (often in the temporal lobes)
  • they affect hearing, speech, memory, and emotions
    .
    Pts remain awake during partial seizures:
  • Focal aware seizures (simple partial):
    pts remain aware
  • Focal impaired awareness seizures (complex partial): pts lose awareness
    .
    Symptoms associated:
  • Deja vu
  • strange smells/tastes/sight/sound sensations
  • unusual emotions
  • abnormal behaviours
150
Q

Describe what myoclonic seizures involve

A
  • present with sudden, brief muscle contracts - like an abrupt jump or jolt
  • they remain awake
  • can occur as part of juvenile myoclonic epilepsy in children
151
Q

Describe what tonic seizures involve

A
  • involve a sudden onset of increased muscle tone, where the body stiffens
  • this results in a fall if the pt is standing, usually backwards
  • only last a few seconds to a minute
152
Q

Describe what atonic seizures involve

A
  • “drop attacks” - involve a sudden loss of muscle tone, often resulting in a fall
  • only last briefly and pts are usually aware during the episodes
  • often begin in childhood - may be indicative of Lennox-Gastaut syndrome
153
Q

Describe what absence seizures involve

A
  • usualyl seen in children
  • pt becomes blank, stares into space, and then abruptly returns to normal
  • during the episode, they are unaware of their surroundings and do not respond
  • typically last a few seconds
  • most pts stop having absence seizures as they get older
154
Q

Describe what infantile spasms (aka. West syndrome) involve

A
  • very rare disorder, starting at around 6 months of age
  • presents with clusters of full-body spasms
  • Hypsarrhythmia is a characteristic EEG finding
  • associated with developmental regression and poor prognosis
  • treatment is with ACTH and vigabatrin
155
Q

Describe what febrile convulsions involve

A
  • tonic-clonic seizures that occur in children during a high fever
  • do not usually cause any lasting damage and are no serious, but can increase risk of developing epilepsy
156
Q

Describe the following epilepsy syndromes:

  • Childhood Absence Epilepsy (CAE)
  • Juvenile myoclonic epilepsy (JME)
  • Dravet syndrome
  • Lennox-Gastaut syndrome
A
  • Childhood Absence Epilepsy (CAE): Characterised by typical absence seizures, with onset usually between 4-10 years
  • Juvenile Myoclonic Epilepsy (JME): Marked by myoclonic jerks, typically shortly after waking
  • Dravet Syndrome: Severe epilepsy beginning in infancy, initially presenting as prolonged seizures with fever
  • Lennox-Gastaut Syndrome: Characterised by multiple seizure types, cognitive dysfunction, and a specific EEG pattern
157
Q

Seizures/Epilepsy - differential diagnosis

A
  • Syncope: eg. Vasovagal syncope
  • Psychogenic Nonepileptic Seizures (PNES)
  • Cardiac syncope (e.g., arrhythmias or structural heart disease)
  • Hypoglycaemia
  • Hemiplegic migraine
  • Transient ischaemic attack
  • Alcohol withdrawal seizures: occurs in pts with a hx of chronic alcohol use who stop their alcohol intake too abruptly
158
Q

Seizures/Epilepsy - Investigations

A
  • EEG (electroencephalogram) - can do prolonged EEG monitoring
  • MRI brain: used to diagnose structural pathology (eg. tumours)
  • ECG: rule out arrhythmias
  • Serum electrolytes: Na+, K+, Ca2+, Mg2+
  • Blood glucose: rule out hypogylcaemia and diabetes
  • Blood cultures, urine cultures, and LP: where sepsis, encephalitis, or meningitis is suspected
159
Q

Epilepsy/Seizures - Chronic management

A
  • DVLA: license removed until specific criteria met (eg. seizure-free for 1 year)
  • Showers not baths: due to risk of drowning
  • Caution with swimming, heights etc.
    .
    (Note: carbamazepine can be used as 2nd line in generalised tonic-clonic seizures and focal seizures, BUT may exacerbate absence seizures and myoclonic seizures)
160
Q

Epilepsy/Seizures - Acute management

A

(most seziures terminate spontaneously - if not terminated after 5-10 mins then it is appropriate to administer medication)

  1. Benzodiazepines (eg. diazepam)
  2. If a pt continues to fit despite such measures then they are termed to have status epilepticus
161
Q

How does sodium valproate work (MOA)?
+ what is the main side effect to be aware of?

A
  • Increases activity of GABA (gamma-aminobutyric acid), which has a calming effect on the brain
  • Teratogenic (harmful in pregnancy)
162
Q

What is status epilepticus?

A
  • a seizure lasting more than 5 minutes
  • multiple seizures without regaining consciousness in the interim
163
Q

Status epilepticus - Management

A
  1. ABCDE: secure airway, give oxygen, check blood glucose lvls, gain IV access (cannula)

Medical treatment:
2. Benzodiazepine (eg. midazolam, diazepam, lorazepam)
3. (after 2 doses of benzos) IV levetiracetam, phenytoin, or sodium valproate

164
Q

What are Psychogenic non-epileptic seizures (PNES)?

A

PNES = a type of seizure caused by psychological factors (not abnormal electrical activity in the brain)

165
Q

Psychogenic non-epileptic seizures (PNES) VS Epilepsy seizures

A

PNES have NO:
- EEG changes associated with epilepsy
- Autonomic symptoms
- Post-ictal confusion
.
PNES does:
- have emotional triggers +/- hx of psychological trauma
- forced eye closure

166
Q

Psychogenic non-epileptic seizures (PNES) - Management

A
  1. Once confirmed PNES and no epilepsy –> educate the pt
  2. CBT + other mental health management
167
Q

What is SUDEP?

A

Sudden unexpected death in epilepsy:
- exact cause remains unknown but possible mechanisms include cardiac arrhythmias, respiratory dysfunction, and cerebral depression post-seizure
- good seizure control can reduce the potential risk of SUDEP

168
Q

What is myasthenia gravis + how does it typically affect women and men?

A

Myasthenia gravis = a chronic autoimmune neuromuscular disease, characterised by muscle weakness that progressively worsens with activity and improves with rest

  • Typically affects women under 40yrs and men over 60yrs
169
Q

What condition is myasthenia gravis strongly associated with (10-20% of pts have this)?

A

thymomas (thymus gland tumours)

170
Q

Myasthenia gravis - Pathophysiology

A

General info:
- Motor neurones communicate with muscles via the neuromuscular junction
- the axons release a neurotransmitter called acetylcholine from the presynaptic membrane - acetylcholine travels across the synapse and attaches to receptors on the postsynaptic membrane –> simulating muscle contraction
.
1. Acetylcholine receptor (AChR) antibodies are found in most patients with myasthenia gravis - these bind to postsynaptic acetylcholine receptors, blocking them and preventing stimulation by acetylcholine
.
2. The more the receptors are used during muscle activity, the more they become blocked)
- there is less effective stimulation of the muscle with increased activity - with rest, the receptors are cleared and symptoms improve
.
3. These antibodies (AChR antibodies) also activate the complement system within the NMJ - leading to cell damage at the postsynaptic membrane, further worsening symptoms
.
4. Two other antibodies (MuSK and LRP4) are affected - they are important proteins for the creation and organisation of the acetylcholine receptor
- destruction of these proteins leads to inadequate acetylcholine receptors

171
Q

Myasthenia gravis - Clinical features (symptoms + ways to exacerbate fatiguability in the muscles + O/E)

A

Symptoms:
- weakness that worsens with muscle use and improves with rest
- typically best in morning and worst at end of the day
- symptoms most affect proximal muscles of the limbs and small muscles of the head and neck (ocular muscles in 50% of pts)
.
Ways to exacerbate fatiguability in the muscles:
- repeated blinking –> ptosis
- prolonged upward gazing –> diplopia
- repeated abduction of one arm 20 times –> unilateral weakness
.
O/E:
- check for thymectomy scar
- test forced vital capacity (FVC)

172
Q

Why is forced vital capacity (FVC) monitored in myasthenia gravis?

A

To monitor respiratory muscle function - risk of respiratory failure

173
Q

Myasthenia gravis - Investigations

A
  1. Antibody tests:
    - AChR antibodies (present in about 85% of pts with generalised MG and 50% with ocular MG)
    - MuSK antibodies (anti-muscle-specific kinase)
    - LRP4 antibodies (anti-lipoprotein-related protein 4)
  2. Electrophysiological studies:
    - repetitive nerve stimulation
    - single-fiber electromyography
  3. CT or MRI of thymus - to look for a thymoma
  4. Edrophonium test
174
Q

How does the edrophonium test work as an investigation for myasthenia gravis?

A
  1. Pts are give IV edrophonium chloride
    - normally, cholinesterase enzymes in the NMJ break down acetylcholine
    - edrophonium blocks these enzymes, reducing the breakdown of acetylcholine
  2. As a result, the level of acetylcholine at the NMJ rises, temporarily relieving the weakness
  3. A positive results suggests a diagnosis of myasthenia gravis
175
Q

Myasthenias gravis - Management

A
  1. Acetylcholinesterase inhibitors: eg. Pyridostigmine (prolongs action of acetylcholine)
  2. Immunosuppression: eg. prednisolone or azathioprine (suppresses antibody production)
  3. Surgery: Thymectomy (can improve symptoms even in pts without a thymoma)
  4. Rituximab (monoclonal antibody against B cells) - consider if other treatments fail
176
Q

What is a myasthenic crisis + what is the management?

A
  • Myasthenic crisis is an acute worsening of symptoms, often triggered by another illness (eg. respiratory tract infection)
  • Respiratory muscle weakness can lead to respiratory failure
    .
    Management:
    1. IV immunoglobulins and plasmapheresis
    2. +/- NIV or mechanical ventilation
177
Q

What is Parkinson’s disease?

A

a chronic, condition where there is a progressive reduction in dopamine in the basal ganglia - leading to disorders of movement

178
Q

Parkinson’s disease - Clinical features

A

Classic triad of symptoms (usually asymmetrical):
- Resting tremor (“pill-rolling tremor”): worse at rest
- Muscle rigidity: resistance to passive movement of a joint (jerking resistance - “cogwheel rigidity”)
- Bradykinesia: movements get slower and smaller (eg. micrographia, “shuffling” gait)

Other symptoms (non-motor):
- Autonomic (urinary incontinence, constipation)
- Depression, anxiety, and cognitive impairment
- Sleep disturbances (acting out in sleep)
- Loss of smell (anosmia)

179
Q

Parkinson’s disease VS Benign Essential Tremor

A
180
Q

Parkinson’s disease, describe each of the below…

  • Multiple system atrophy
  • Dementia with Lewy bodies
A

Multiple system atrophy:
- where neurones of various systems in the brain degenerate, including the basal ganglia
- degeneration in the basal ganglia leads to a Parkinson’s presentation
- degeneration in other areas leads to autonomic dysfunction and cerebellar dysfunction (causing ataxia)
.
Dementia with Lewy bodies:
- type of dementia associated with features of Parkinsonism
- causes a progressive decline

181
Q

What criteria is used to diagnose Parkinson’s disease?

A

UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria

182
Q

Parkinson’s disease - Management

A

No cure - treatment is aimed at controlling symptoms:
1. Levodopa + carbidopa
(Carbidopa is given along with levodopa (Co-careldopa) as it reduces the breakdown of levodopa peripherally, leading to a better therapeutic effect)

  1. Monoamine oxidase-B (MAO-B) inhibitors
  2. Dopamine agonists
  3. Adjuvant therapy: physiotherapy + speech therapy + occupational therapy
183
Q

How does levodopa and carbidopa work in the management of Parkinson’s disease?

A
  • Levodopa is a precursor to dopamine - converted in both CNS and periphery
  • Carbidopa is a dopamine decarboxylase inhibitor - reduces the amount that is converted in periphery, thus increasing the amount available in the CNS (brain)
184
Q

How do monoamine oxidase-B inhibitors (eg. Selegiline, Rasagiline) work in the management of Parkinson’s disease?

A

inhibitors of MAO-B, which are responsible for degrading dopamine, therefore increasing the amount of dopamine available
- Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline
- Monoamine oxidase-B is more specific to dopamine

185
Q

How do dopamine agonists (eg. Bromocriptine, cabergoline, pergolide) work in the management of Parkinson’s disease?

A

mimic the action of dopamine in the basal ganglia, stimulating the dopamine receptors

186
Q

Benign essential tremor - Clinical features

A
  • Fine tremor (6-12Hz)
  • Symmetrical/bilateral
  • “Action tremor” - exacerbated on voluntary movements
  • worse when tired/stressed/after caffeine
  • improved by alcohol
187
Q

Differential diagnosis of a tremor

A
  • Parkinson’s disease
  • Multiple sclerosis
  • Huntington’s chorea
  • Benign essential tremor
  • Hyperthyroidism
  • Fever
  • Dopamine antagonists (e.g., antipsychotics)
188
Q

Benign essential tremor - Management

A

Medications that may improve symptoms:

  1. Propranolol (a non-selective beta blocker)
  2. Primidone (a barbiturate anti-epileptic medication)
189
Q

What is Huntington’s disease (Huntington’s chorea)?

  • include genetic inheritance pattern and genetic mutation
A
  • Huntington’s = an inherited autosomal dominant genetic condition, it causes progressive neurological dysfunction
  • trinucleotide repeat disorder - genetic mutation in the HTT gene on chromosome 4, which codes for the Huntingtin (HTT) protein
190
Q

Huntington’s disease displays something called genetic anticipation, this is a feature of trinucleotide repeat disorders. What is anticipation?

A

Where successive generations have more repeats in the gene, resulting in:
- Earlier age of onset
- Increased severity of disease

191
Q

Huntington’s disease (Huntington’s chorea) - Clinical features

A

Usually develops age 30-50yrs, presents with an insidious, progressive worsening of symptoms:
Typically begins with cognitive, psychiatric, or mood problems - followed by development of movement disorders:
- Chorea (involuntary, random, irregular, and abnormal body movements)
- Dystonia (abnormal muscle tone, leading to abnormal postures)
- Rigidity (increased resistance to the passive movement of a joint)
- Eye movement disorders (saccadic eye movements)
- Dysarthria (speech difficulties)
- Dysphagia (swallowing difficulties)

192
Q

How is a diagnosis of Huntington’s disease (Huntington’s chorea) made?

A

Genetic testing
- identifies the CAG trinucleotide repeat expansion in the HTT gene on chromosome 4

193
Q

Huntington’s disease (Huntington’s chorea) - Management

A

Management involves an MDT approach, there is no treatment for slowing or stopping the progression of the disease:
1. Tetrabenazine: used for chorea symptoms
2. Antidepressants (eg. SSRIs): for depression

(MDT: Physio, SLT, OT, palliative care)

194
Q

What % chance does a child of somebody with Huntington’s disease have of inheriting the faulty gene?

A

50% chance
- Huntington’s is an autosomal dominant condition

195
Q

Huntington’s disease (Huntington’s chorea) - Prognosis

A

Progressive condition, life expectancy is around 10-20yrs after othe nset of symptoms
- death is often due to aspiration pneumonia or suicide

196
Q

What is Lamber-Eaton myasthenic syndrome + what condition does it usually occur with?

A
  • an autoimmune condition affecting the NMJ
  • usually occurs with small-cell lung cancer
197
Q

Lambert-Eaton myasthenic syndrome - Pathophysiology

A
  1. Antibodies against voltage-gated calcium channels (often produced in response to small cell lung cancer)
  2. they target and damage voltage-gated calcium channels in the presynaptic membrane of the NMJ
  3. Voltage-gated calcium channels are responsible for assisting in the release of acetylcholine into the synapse of the NMJ
    - acetylcholine travels across the synapse and attaches to receptors on the postsynaptic membrane, stimulating muscle contraction
  4. When the voltage-gated calcium channels are destroyed, less acetylcholine is released into the synapse - resulting in a weaker signal and reduced muscle contraction
198
Q

Lambert-Eaton myasthenic syndrome - Clinical features

A

Symptoms improve after repeated muscle contractions (reverse of what is seen in myasthenia gravis) + ocular symptoms are not commonly a feature (unlike in myasthenia gravis):
- Proximal muscle weakness (causing difficulty climbing stairs, standing from a seat, or raising arms overhead)
- Autonomic symptoms (dry mouth, blurred vision, impotence, and dizziness)
.
O/E:
- Reduced or absent tendon reflexes (hyporeflexia)

199
Q

Lambert-Eaton myasthenic syndrome - Investigations

A

EMG - incremental response to repetitive electrical stimulation

200
Q

Lambert-Eaton myasthenic syndrome - Management

A
  1. Treatment of underlying cancer
  2. Amifampridine (3,4-diaminopyridine): works by blocking voltage-gated potassium channels which in turn increases duration of action potential so calcium channels can be open for a longer time
  3. immunosuppression (eg. prednisolone or azathioprine)
  4. IV immunoglobulin and plasma exchange - may be beneficial
201
Q

What is Charcot-Marie-Tooth disease?

A
  • an inherited disease that affects the peripheral motor and sensory neurones (hereditary peripheral neuropathy)
202
Q

Charcot-Marie-Tooth disease - Clinical features

A

(Peripheral neuropathy - “stocking-glove” distribution)
- High foot arches (pes cavus)
- Distal muscle wasting - causing “inverted champagne bottle legs”
- Lower leg weakness, particularly loss of ankle dorsiflexion (with a high stepping gait due to foot drop)
- Weakness in the hands + distal muscle atrophy
- Reduced tendon reflexes (hyporeflexia)
- Reduced muscle tone
- Peripheral sensory loss

203
Q

Charcot-Marie-Tooth disease is a peripheral neuropathy, name some other causes of peripheral neuropathy.

A
  • A – Alcohol
  • B – B12 deficiency
  • C – Cancer (e.g., myeloma) and Chronic kidney disease
  • D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
  • E – Every vasculitis
204
Q

Charcot-Marie-Tooth disease - Management

A

Management is supportive (cannot stop progression) and requires an MDT approach:
1. MDT: neurologists + geneticists, physio, OT, podiatrist
2. Analgesia - for neuropathic pain (eg. amitriptyline)
3. Orthopaedic surgeons - for severe joint deformities

205
Q

What is Guillain-Barre syndrome (GBS) + what usually triggers it?

A
  • GBS = an acute paralytic polyneuropathy that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms
  • usually triggered by an infection and is particularly associated with to Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).
206
Q

Guillain-Barre syndrome - Clinical features

A
  • Progressive, symmetrical, and ascending weakness of all 4 limbs
  • Reduced reflexes (hyporeflexia)
    .
  • +/- cranial nerve involvement (facial weakness)
  • +/- autonomic involvement (eg. urinary retention, diarrhoea)
207
Q

Guillain-Barre syndrome - Investigations

A

Diagnosis is primarily clinical (Brighton criteria), supported by investigations:
- Nerve conduction studies: shows reduced signal through nerves
- Lumbar puncture: raised protein with a normal WCC and glucose

208
Q

Guillain-Barre syndrome - Management

A
  1. Supportive care
  2. VTE prophylaxis (pulmonary embolism is a leading cause of death)
  3. IV immunoglobulins (IVIG) first-line
  4. Plasmapheresis (is an alternative to IVIG)
  5. If resp. failure: intubation, ventilation, and admission to ICU
    (FVC regularly to monitor respiratory function)
209
Q

Guillain-Barre syndrome - Prognosis

A
  • Recovery can take months to years
  • Pts can continue regaining function five years after the acute illness
  • Most pts eventually make either a full recovery or are left with minor symptoms
  • Some are left with significant disability
  • Mortality is around 5%, - mainly due to respiratory or CVD complications
210
Q

What is neurofibromatosis and which type is more common?

A
  • a genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system - these tumours are benign but can cause neurological and structural problems
  • Neurofibromatosis type 1 is more common than neurofibromatosis type 2
211
Q

Neurofibromatosis type 1 - Genetic inheritance + genetic mutation

A
  • Mutations in this gene are inherited in an autosomal dominant pattern (but can occur de novo)
  • NF1 gene is found on chromosome 17 - it codes for a protein called neurofibromin, which is a tumour suppressor protein
212
Q

Neurofibromatosis type 1 - Clinical features

A

“CRABBING”:
- C – Café-au-lait spots (more than 15mm diameter is significant in adults)
- R – Relative with NF1
- A – Axillary or inguinal freckling
- BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
- I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
- N – Neurofibromas
- G – Glioma of the optic pathway

213
Q

Neurofibromatosis type 1 - Management/complications

A

ManaInvolves monitoring, managing symptoms, and treating complications:
- Lots of complications, two unique ones for NF1 are malignant peripheral nerve sheath (MPNST) and gastrointestinal stromal tumours (GIST)

214
Q

Neurofibromatosis type 2 - genetics (inheritance and genetic mutation)

A
  • autosomal dominant inheritance pattern
  • NF2 gene is found on chromosome 22 - codes for a protein called merlin (tumour suppressor protein important in Schwann cells)
215
Q

What type of tumours is neurofibromatosis type 2 particularly associated with?

A

Acoustic neuromas (tumours of the auditory nerve that innervates the inner ear)
- Note: an exam pt with bilateral acoustic neuromas almost certainly has NF type 2

216
Q

Tuberous sclerosis is an autosomal dominant condition that affects multiple systems.

  1. What genetic mutations occur?
  2. What is the characteristic feature of this condition?
A
  1. mutations in either:
    - TSC1 gene on chromosome 9, which codes for hamartin
    - OR TSC2 gene on chromosome 16, which codes for tuberin
    (Hamartin and tuberin interact with each other to control the size and growth of cells - abnormalities in one of these proteins lead to abnormal cell size and growth)
  2. The characteristic feature is the development of hamartomas, which are benign tissue growths - hamartomas cause problems based on the location of the lesion
217
Q

Tuberous sclerosis - Skin features, neuro features, and other features

A

Skin features:
- Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
- Shagreen patches (thickened, dimpled, pigmented patches of skin)
- Angiofibromas (small skin-coloured or pigmented papules that occur over the nose and cheeks)
- Ungual fibromas (circular painless lumps that slowly grow from the nail bed and displace the nail)
- Cafe-au-lait spots (light brown “coffee and milk” coloured flat pigmented lesions on the skin)
- Poliosis (an isolated patch of white hair on the head, eyebrows, eyelashes or beard)
.
Neuro features:
- Epilepsy
- Learning disability/Autism
- Brain tumours
.
Other features:
- Angiomyolipoma in the kidneys
- Lymphangioleiomyomatosis in the lungs (affects women)
- Rhabdomyomas in the heart

218
Q

What are the key clinical features of cerebellar disorders?

A
  • Motor: ataxia, dysmetria, dysdiadochokinesia
  • Speech: scanning dysathria
  • Eye movement: Nystagmus
  • Intention tremor
  • Postural instability
  • Hypotonia
219
Q

What are some key tests to detect cerebellar dysfunction?

A
  • Finger-to-nose and heel-to-shin tests (assess dysmetria).
  • Rapid alternating movements (for dysdiadochokinesia).
  • Observation of gait and stance (wide-based gait, Romberg test negative).
220
Q

What is the mnemonic for cerebellar disorder features?

A

DANISH:
- D: Dysdiadochokinesia
- A: Ataxia
- N: Nystagmus
- I: Intention Tremor
- S: Scanning Speech
- H: Hypotonia

221
Q

Alzheimer’s disease - pathology

A
  • Amyloid plaques (beta-amyloid)
  • Neurofibrillary tangles: caused by abnormal aggregation of hyperphosphorylated tau protein
  • Neuroinflammation
  • Brain atrophy
  • reduced cholinergic activity
222
Q

Alzheimer’s disease - Clinical features

A

Insidious onset (over months/years), concerns from family members often prompt the pt to seek help
- Cognitive impairment: memory loss (progressive episodic), reasoning and comms problems, decision-making/executive function, nominal dysphasia
- Behavioural and psychological symptoms: depression, agitation, psychosis, apathy, disinhibition
- Difficulties with ADLs

223
Q

Alzheimer’s disease - Investigations

A
  1. Cognitive testing:
    - eg. MoCA
    - eg. Addenbrooke’s cognitive examination III (ACE-III)
  2. Blood tests (to exclude a physical cause before referring to memory clinic): FBC, electroyltes, LFTs, TFTs, vit B12, folate
  3. Imaging: MRI brain to exclude other cerebral pathology
    (note: in AD, atrophy usually seen in the medial temporal lobe structures)
224
Q

What 5 domains are tested in the Addenbrooke’s Cognitive Examination-III (ACE-III) and what score /100 indicates possible dementia?

A
  • Attention
  • Memory
  • Language
  • Visuospatial function
  • Verbal fluency
    .
  • a score of 88 or less - indicates possible dementia
225
Q

Alzheimer’s disease - Management

A

There is no cure, but symptoms can be managed:
1. Acetylcholinesterase inhibitors: eg. donepezil, rivastigmine, or galantamine)
2. Memantine (NMDA receptor antagonist)

(Note: it is important to plan ahead (eg. lasting power of attorney, advanced decisions, planning future care)

226
Q

4 main differentials for dementia

A
  1. Alzheimer’s disease
  2. Vascular dementia
  3. Lewy Body dementia
  4. Frontotemporal dementia
227
Q

3 main subtypes of vascular dementia

A
  1. Stroke-related VD - multi-infarct or single-infarct dementia
  2. Subcortical VD - caused by small vessel disease
  3. Mixed dementia - the presence of both VD and Alzheimer’s disease
228
Q

Risk factors for vascular dementia (same a CVD)

A
  • History of stroke or (TIA)
  • Atrial fibrillation
  • Hypertension
  • Diabetes mellitus
  • Hyperlipidaemia
  • Smoking
  • Obesity
  • Coronary heart disease
  • Family hx of stroke or CVD
229
Q

What is Lewy body dementia characterised by (pathology) and what additional clinical features does it have?

A
  • alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas
  • Parkinsonism +/- visual hallucinations
230
Q

Does frontotemporal dementia usually affect the younger or older population?

A

rarer type of dementia that notably affects people at a younger age (starting aged 40-60)

231
Q

What are the typical clinical features of frontotemporal dementia?

A

typically involves abnormalities in behaviour, speech and language

232
Q

Parkinson medication side effects (edit this card)

A
  • chorea
  • hypersexual, gambling, addiction
233
Q

Parkinson plus syndromes:

A

.

234
Q

What drugs can cause Parkinsonism (drug-induced Parkinson’s)

A

.

235
Q

What is Holmes-Adie syndrome?

A

Holmes-Adie pupil + absent ankle and knee reflexes

236
Q

light reflex pathway

A

.

237
Q

What inheritance pattern do Duchenne’s and Becker’s muscular dystrophy have + therefore which sex is affected?

A

X-linked recessive - primarily affects males

238
Q

What gene is affected in Duchenne’s and Becker’s muscular dystrophy?

A

Dystrophin gene

239
Q

What is the difference between Duchenne’s and Becker’s muscular dystrophy in terms of clinical features (severity) and age of onset?

A
  • Duchenne’s: more severe and earlier onset

Clinical features:
- Proximal muscle weakness
- Gower’s sign
- Waddling gait (weakness in pelvic muscles)
- Calf pseudohypertrophy
- Intellectual impairment

240
Q

Duchenne’s and Becker’s Muscular Dystrophy - Investigations and Management

A

Investigations:
- Creatine kinase (CK): raised (due to muscle breakdown)
- Genetic testing: dystrophin gene

Management:
- MDT + managing complications (dilated cardiomyopathy, resp. failure)
- Corticosteroids (to improve muscle function)

241
Q

Cerebral palsy:

  • What is it?
  • Clinical features
  • Management
A
  • Cerebral palsy: a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain (antenatal cause)
  • Spastic (hemiplegia, diplegia, or quadrariplegia) +/- learning difficulties/epilpesy/squints

Management:
- MDT approach
- For spasticity: oral diazepam, baclofen, botulinum toxin, surgery
- (anticonvulsants + analgesia as required)

242
Q
A

YEAR 3 MED (9 decks)

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