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Year 4 - 5. Neurology & Special Senses > Neurology > Flashcards

Neurology Flashcards

1
Q

State which nerves and vessels run through the cavernous sinus

A

Nerves:
- CN3 (oculomotor)
- CN4 (trochlear)
- CN5 (V1 + V2, trigeminal ophthalmic and maxillary sinus)
- CN6 (abducens)

Vessels:
- Internal carotid artery

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2
Q

List the sensory modalities that run along the spinothalamic system

A

3 modalities:
- Pressure / crude touch
- Pain
- Temperature

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3
Q

List the sensory modalities that run along the dorsal column system

A

4 modalities:
- Fine touch
- Vibration
- Proprioception
- 2 point discrimination

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4
Q

What investigations are needed if you suspect a peripheral nerve entrapment vs a central (spinal) cause

A

Peripheral nerve entrapment = nerve conduction studies
Central (spinal) cause = MRI

If you’re not sure, can refer for both nerve conduction studies and MRI +/- blood tests

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5
Q

Cranial nerve 1 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Olfactory

Aetiology of damage (causes):
- URTI
- Trauma / facial damage
- Anterior cranial fossa tumours

Role of nerve:
- Sense of smell

Sensory / motor / both:
- Sensory

How to assess:
- Cover one nostril and ask about sense of smell

Presenting features of damaged cranial nerve:
- Hyponosmia / anosmia

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6
Q

Cranial nerve 2 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Optic

Aetiology of damage (causes):
- Any disease affecting optic nerve e.g. optic neuritis, anterior optic neuropathy

Role of nerve:
- Vision

Sensory / motor / both:
- Sensory

How to assess:
1. Snellen chart
2. Ophthalmoscopy
3. Pupil size and response to light

Presenting features of damaged cranial nerve:
1. Blurred or absent vision
2. Evidence of pathology on ophthalmoscope
3. Abnormalities in pupil size or response to light

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7
Q

Cranial nerve 3 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Oculomotor

Aetiology of damage (causes - ischaemia or compressive):
Microvascular causes
- Microvascular ischaemia (pupil spared)
Compressive causes
- Head injury
- Raised ICP = tentorial herniation
- Aneurysm of posterior communicating artery

Role of nerve:
- Move 4/6 eye muscles
- Pupil size and reflex
- Eyelid position

Sensory / motor / both:
- Motor
- Parasympathetic

How to assess:
- Assess position of eye at rest / eye movements
- Assess position of eyelid at rest
- Pupil size and response to light

Presenting features of damaged cranial nerve:
DOWN and OUT
- Down and out appearance to eye
- Ptosis
- Pupil may / may not be affected (affected if compressive cause)

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8
Q

Cranial nerve 4 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Trochlear

Aetiology of damage (causes - congenital or acquired):
Congenital
Acquired
- Microvascular ischaemia
- Trauma (thin nerve)
- Tumour

Role of nerve:
- Innervate superior oblique extraocular muscle

Sensory / motor / both:
- Motor

How to assess:
- Assess position of eye at rest / eye movements
- Assess position of head at rest (head tilt)

Presenting features of damaged cranial nerve:
UP and IN
- Up and inward appearance to eye
- May be a head tilt
- Diplopia

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9
Q

Cranial nerve 5 - state the following:
- Name and 3 main branches
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name and 3 main branches:
Trigeminal
1. Ophthalmic
2. Maxillary
3. Mandibular

Aetiology of damage (causes):
- Orbital / mandibular fracture
- Tumour in posterior cranial fossa (close to pons)
- Trigeminal neuralgia
- Shingles (in trigeminal distribution)

Role of nerve:
- Sensory to face and scalp
- Motor muscles of mastication

Sensory / motor / both:
- Sensory
- Motor

How to assess:
- Sensory tests on face in 3 areas (sharp and soft)
- Test strength of muscles of mastication

Presenting features of damaged cranial nerve:
- Sensory deficits on face in 3 areas
- Weakness of muscles of mastication

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10
Q

Name the 3 major branches of the trigeminal nerve and which foramen they travel through

A
  1. Ophthalmic - superior orbital fissure (via cavernous sinus)
  2. Maxillary - foramen rotundum (via cavernous sinus)
  3. Mandibular - foramen ovale (via cavernous sinus)
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11
Q

Cranial nerve 6 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Abducens

Aetiology of damage (causes):
- Microvascular ischaemia
- Trauma (thin nerve)
- Raised ICP (most commonly affected, steep upward route)

Role of nerve:
- Innervate lateral rectus muscle

Sensory / motor / both:
- Motor

How to assess:
- Assess position of eye at rest / eye movements

Presenting features of damaged cranial nerve:
- Inability to abduct eye laterally to affected side

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12
Q

Cranial nerve 7 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Facial

Aetiology of damage (causes):
- Parotid disease e.g. parotitis / parotid gland tumour
- Inflammation in facial canal e.g. Bell’s palsy, Ramsey Hunt syndrome
- Damage to petrous bone / lesions around internal acoustic meatus

Role of nerve:
- Innervate muscles of facial expression
- Taste from anterior 2/3 of tongue
- Innervate glands (lacrimal, salivary and nasal)

Sensory / motor / both:
- Motor
- Sensory
- Parasympathetic

How to assess:
- Test muscles of facial expression (raise eyebrows, screw up eyes, blow out cheeks, smile)

Presenting features of damaged cranial nerve:
- Unilateral facial droop
- Inability to carry out facial movements

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13
Q

Outline the difference between Bell’s palsy / facial nerve injury and a stroke, in terms of presentation

A

Bell’s palsy / facial nerve injury:
- Forehead not spared (CAN’T raise eyebrows)

Stroke:
- Forehead spared (CAN raise eyebrows)

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14
Q

Cranial nerve 8 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Vestibulocochlear

Aetiology of damage (causes):
- Basal skull petrous bone fracture
- Vestibular schwannoma
- Damage to labyrinthine artery (in a stroke)

Role of nerve:
- Hearing
- Balance

Sensory / motor / both:
- Sensory

How to assess:
- Gross whisper
- Tuning fork testing

Presenting features of damaged cranial nerve:
- Hearing loss
- Vertigo (dizziness)
- Tinnitus

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15
Q

Cranial nerve 9 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Glossopharyngeal

Aetiology of damage (causes):
- Carotid endarterectomy
- Posterior cranial fossa tumours
- Brainstem lesions

Role of nerve:
- Sensation to oral cavity
- Sensory to posterior 1/3 tongue
- Innervate parotid gland

Sensory / motor / both:
- Sensory
- Parasympathetic

How to assess:
- Gag reflex

Presenting features of damaged cranial nerve:
- Dysphagia

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16
Q

Cranial nerve 10 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Vagus

Aetiology of damage (causes):
- Recurrent laryngeal nerve (thyroid disease/surgery, superior thorax disease/surgery)
- Posterior cranial fossa tumours
- Brainstem lesions

Role of nerve:
- Innervate larynx / pharynx
- Sensation to larynx / pharynx
- Parasympathetic to many tissues!

Sensory / motor / both:
- Sensory
- Motor
- Parasympathetic

How to assess:
- ‘Ahhh’
- Gag reflex

Presenting features of damaged cranial nerve:
- Dysphagia
- Weak cough
- Hoarse voice

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17
Q

Cranial nerve 11 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Accessory

Aetiology of damage (causes):
- Posterior triangle lesions/surgery
- Posterior cranial fossa tumours
- Brainstem lesions

Role of nerve:
- Innervate trapezius muscle
- Innervate sternocleidomastoid muscle

Sensory / motor / both:
- Motor

How to assess:
- Shrug shoulders (trapezius)
- Turn head into hands (sternocleidomastoid)

Presenting features of damaged cranial nerve:
- Weakness in shrugging shoulders
- Weakness in turning head into hands

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18
Q

Cranial nerve 12 - state the following:
- Name
- Aetiology of damage (causes)
- Role of nerve
- Sensory / motor / both
- How to assess
- Presenting features of damaged cranial nerve

A

Name:
- Hypoglossal

Aetiology of damage (causes):
- Posterior cranial fossa tumours
- Carotid endarterectomy
- Brainstem lesions

Role of nerve:
- Tongue movements (speech and eating)

Sensory / motor / both:
- Motor

How to assess:
- Stick tongue out front
- Tongue movements

Presenting features of damaged cranial nerve:
- Tongue deviation out front to affected side (lick your wounds)
- Tongue weakness

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19
Q

Outline which structures the sympathetic and parasympathetic nervous systems innervate in the head and neck
- Eyes
- Glands
- Smooth muscle

A

Sympathetic nervous system:
Eyes:
- Dilator pupillae
- Superior tarsal muscle
Glands:
- Sweat glands
Smooth muscle:
- Blood vessels

Parasympathetic nervous system:
Eyes:
- Sphincter pupillae
- Cilliary body
Glands:
- Lacrimal
- Salivary
- Mucosal
Smooth muscle:
- Respiratory tract
- GI tract

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20
Q

Outline Horner’s syndrome, including the main 3 features

A

Horner’s syndrome occurs from pathology in the lung apex or carotid artery (& branches) and disruption to the sympathetic chain
- Leads to autonomic dysfunction and unopposed parasympathetic stimulation

Ipsilateral symptoms:
1. Partial ptosis
2. Miosis (constricted pupil)
3. Anhidrosis

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21
Q

Outline some investigations to do with someone presenting with Horner’s syndrome

A
  • Cocaine eye drops (normally causes pupil dilation)
  • CT or MRI head and neck
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22
Q

List some differentials for headaches

A

Primary:
- Tension headaches
- Migraines
- Cluster headaches

Secondary:
- Intracranial haemorrhage
- Medication overuse
- Raised ICP e.g. tumours
- Giant cell arteritis / TMJ dysfunction / trigeminal neuralgia / acute glaucoma
- Infection e.g. meningitis, encephalitis
- Referred pain from H&N pathology e.g. otitis media, tonsillitis
- Hypoxia e.g. carbon monoxide poisoning

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23
Q

List some differentials for seizures (fits) / convulsions

A
  • Epilepsy
  • Non-epileptic attack
  • Vasovagal syncope
  • Electrolyte disturbances e.g. hypoglycemia, hypocalcemia
  • Acute toxic effects e.g. antidepressant overdose
  • Acute withdrawal e.g. Ethanol, Benzodiazepines
  • Sepsis
  • Increased ICP e.g. malignancy, hydrocephalus
  • Febrile seizures
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24
Q

List some differentials for an unconscious patient (structural / systemic / psychogenic)

A

Structural:
- Trauma / traumatic brain injury
- Cerebrovascular disease
- Tumours / malignancy
- Infection / inflammation e.g. meningitis
- Haemorrhages

Systemic:
- Seizures
- Intoxication e.g. alcohol, illicit drug use
- Metabolic causes e.g. hypoglycaemia, electrolyte abnormalities, hepatic encephalopathy
- Adrenal crisis
- Neuroleptic malignant syndrome

Psychogenic:
- Catatonia
- Severe depression
- Non-epileptic attacks

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25
Q

List some differentials for a sudden loss of consciousness

A

Vascular:
- Stroke (ischaemic or haemorrhagic) / TIA
- Cardiac arrest / arrhythmias
- Volume depletion e.g. blood loss, anaphylaxis

Infection:
- Meningitis / encephalitis
- Sepsis

Neoplasm / neurological:
- Vasovagal response
- Migraines (associated with syncope in some people)
- Epilepsy
- Non-epileptic attacks

Drugs:
- Intoxication

Trauma

Endocrine:
- Hypoglycaemia

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26
Q

Briefly describe a coma and signs of impaired consciousness

A

A coma is a profound and occasionally extended state of unconsciousness

Signs of impaired consciousness:
- Reduced alertness
- Diminished wakefulness
- Decreased awareness of oneself and environment

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27
Q

List some differentials incoordination, gait disturbance and impaired balance

A

Neurological:
- MS
- Cerebral palsy
- GBS
- Stroke (posterior circulation)
- Cerebellopontine angle lesions
- Space-occupying lesions
- Neurodegenerative e.g. Parkinson’s disease, dementia, amyotrophic lateral sclerosis

Other:
- Alcohol / drugs / medications e.g. alcohol, Lithium
- Infectious e.g. neurosyphilis
- Metabolic e.g. B12 deficiency, Wilson disease, secondary to peripheral neuropathy

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28
Q

List some differentials for generalised hypokinesia (reduced movements)

A

Parkinsonism
Catatonia
Psychomotor depression
Arthritis
Hypocalcaemia (dystonia)

(not 100% sure)

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29
Q

List some differentials for hyperkinesia (increased movements)

A

Epilepsy
Tics, such as Tourette syndrome
Essential tremor
Huntington’s disease (chorea)
Functional movement disorder

(not 100% sure)

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30
Q

List some differentials for focal neurological weakness

A

Local:
- Nerve / tissue injury
- Disorders of a single nerve or nerve group e.g. carpal tunnel syndrome
- Spinal root entrapment
- Spinal cord compression

Neurological / systemic:
- Degenerative nerve illness e.g. MS
- Infections e.g. meningitis or encephalitis
- Stroke / TIA
- Brain tumor
- Cerebral palsy

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31
Q

List some differentials for generalised neurological weakness

A

Diseases:
- Myasthenia gravis or Lambert-Eaton syndrome
- Hereditary muscle disorders e.g. muscular dystrophy
- Polymyositis or dermatomyositis

  • Deconditioning due to inactivity (disuse atrophy)
  • Sepsis / severe illness
  • Critical illness myopathy / paralytic agents in critical care
  • Electrolyte abnormalities e.g. hypocalcemia
  • Common myopathies e.g. alcohol myopathy, corticosteroid myopathy
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32
Q

List some differentials for speech, swallow or language problems

A
  • Trauma e.g. brain injury e.g. hypoxic brain injury
  • Infection e.g. epiglottitis, tonsillitis, GORD
  • Neoplasia e.g. tumors / malignancy
  • or neurological e.g. degenerative neurological diseases e.g. ALS, MS, MND and Huntington disease, bulbar palsy, neuromuscular disorders e.g. muscular dystrophy
  • Drugs e.g. intoxication, anti-muscarinics
  • Endocrine?
  • Vascular e.g. stroke / TIA
  • Reduced conscious level
  • Autism spectrum disorder
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33
Q

List some differentials for urinary incontinence

A

Urological:
- Urge / stress incontinence
- UTI
- Prostatitis

Neurological:
- Spinal cord damage e.g. cauda equina / spinal cord compression
- Spina bifida
- MS / Parkinson’s disease
- Stroke / TIA
- Hydrocephalus
- Diabetes

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34
Q

List some differentials for faecal incontinence

A

Gastro:
- Trauma / surgery to anal sphincter
- Overflow constipation
- IBD / IBS / chronic diarrhoea or constipation
- Severe haemorrhoids / rectal prolapse
- Congenital problems e.g. Hirschprung’s disease or anal atresia

Neurological:
- Spinal cord damage e.g. cauda equina / spinal cord compression
- Spina bifida
- MS / Parkinson’s disease
- Stroke / TIA
- Hydrocephalus
- Diabetes

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35
Q

List some differentials for reduced cognition

A

Neurological:
- Alzheimer disease
- Stroke
- Parkinson disease / Huntington disease
- MS
- Lewy body dementia
- Tumour / malignancy

Other:
- Developmental disorders e.g. Down syndrome
- Severe depression / anxiety / catatonia
- Delirium
- Head injury
- Meningitis
- Sepsis
- Intoxication e.g. alcohol, drugs, toxins
- Wernicke Korsakoff syndrome

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36
Q

List some differentials for behaviour or personality change

A

Organic:
- Stroke
- Tumour / malignancy
- Dementia
- Postictal (after seizure)
- Meningitis / encephalitis
- Sepsis (hallucinations)
- MS / Parkinson’s / Huntington’s

Non-organic:
- Pain / tiredness
- Delirium
- Metabolic causes e.g. hypoglycaemia
- Severe depression / anxiety / catatonia / bipolar
- Intoxication e.g. alcohol, illicit drugs or withdrawal

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37
Q

List some differentials for neuropathic pain syndromes (central, peripheral, mixed)

A

Central:
- After spinal cord injury
- After stroke
- MS

Peripheral:
- Painful neuropathy e.g. diabetic neuropathy, post-chemotherapy neuropathy
- Radiculopathy
- Injury to nerve itself (trauma)
- Nerve compression e.g. carpal tunnel syndrome
- Post-surgical e.g. post-mastectomy, post-thoracotomy

Mixed:
- Complex regional pain syndromes
- Chronic back pain
- Cancer-related pain

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38
Q

Describe neuropathic pain and list some positive features and negative features of neuropathic pain

A

Neuropathic pain = painful condition caused by neurological lesions or diseases

Positive features = extra sensation perceived by the patient
- Pain
- Paresthesia
- Numbness
- Tingling

Negative features = loss of functions
- Sensory deficits
- Motor deficits
- Cognitive deficits

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39
Q

List some differentials for sensory disturbances

A

Metabolic:
- Diabetes mellitus
- Vitamin B12 / folate deficiency
- Nutritional deficiencies

Immune-mediated:
- SLE
- Sarcoidosis
- Sjögren syndrome
- Coeliac disease

Toxic:
- Chemotherapy
- Drug-induced
- Alcohol

Hereditary:
- Ehlers-Danlos syndrome
- Haemochromatosis

Infectious:
- Syphilis
- Leprosy
- HIV

Other
- Idiopathic
- Fibromyalgia
- Vasculitis

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40
Q

List some differentials for transient motor and sensory disturbances

A
  • TIA
  • Seizure
  • Raised ICP
  • Migraine (with aura)
  • MS
  • Electrolyte abnormalities
  • Psychiatric disorders e.g. panic disorder, schizophrenia
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41
Q

List some potential causes of ICP

A

Vascular:
- Aneurysm
- Intracranial haemorrhage / stroke
- Hydrocephalus

Infection:
- Meningitis / encephalitis
- Intracranial abscess

Neoplasm / neurological:
- Tumours

Trauma:
- Head trauma

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42
Q

Outline how raised ICP can present

A
  • Headache
  • Diplopia / blurred vision
  • N&V
  • Behavioural changes
  • Reduced conscious level
  • Seizures
    Cushing’s triad: bradycardia, hypertension, irregular breathing
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43
Q

Outline some initial investigations and first line management steps for raised ICP

A

Investigations:
- Fundoscopy (optic disc swelling)
- CT / MRI head

Management:
- Elevate head to 30 degrees
- IV Mannitol or hypertonic saline
- Neurological observations every 15 mins
- Involve seniors and contact ICU

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44
Q

Outline how a subarachnoid haemorrhage can present

A
  • Thunderclap headache during episode of strenuous activity
  • Neck stiffness
  • Photophobia
  • N&V
  • Neurological symptoms e.g. visual changes, dysphasia, focal weakness, seizures, reduced consciousness
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45
Q

Outline some initial investigations and first line management steps for subarachnoid haemorrhage

A

Investigations:
- CT head within 6 hours of headache onset (hyper-attenuation in the subarachnoid space), after 24 hrs the sensitivity significantly reduces
- Consider lumbar puncture after 12 hours (raised RBC count and yellow colour from bilirubin)
- CT angiography later to confirm site of bleeding

Management:
- Oral Nimodipine 60mg 4 hourly (prevent vasospasm)
- Elevate head
- Hourly neuro observations
- Reverse any anticoagulants
- Analgesia / antiemetics
- Refer for neuro bed and discuss with neurosurgeons

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46
Q

List some causes of subarachnoid haemorrhage

A

70% = berry aneurysms
10% = HTN
10% = AV malformation
5% = idiopathic
+ trauma

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47
Q

Outline how meningitis / encephalitis can present

A
  • Fever
  • Non-blanching purpuric rash if bacterial meningitis
  • Headache, stiff neck, photophobia
  • N&V
  • Reduced conscious level
  • Seizures
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48
Q

Outline some initial investigations and first line management steps for meningitis / encephalitis

A

Investigations:
- FBC, U&E, glucose, LFT, CRP, clotting, lactate
- Blood cultures, throat swab and skin swab
- Meningococcal and pneumococcal PCR
- Lumbar puncture (CT head first if signs of brain shift)

Management:
- Isolate patient
- IV Ceftriaxone 2g immediately and continued every 12-hours initially
- If bacterial suspected, also give IV Dexamethasone 10mg every 6 hours
- Intravenous fluids and oxygen if required
- Inform public health

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49
Q

Outline the recognised definition of status epilepticus

A
  • Over 5 minutes of single continuous seizure
  • OR 2 or more discrete seizures between which there is incomplete recovery of consciousness
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50
Q

Outline some initial investigations and first line management steps for status epilepticus

A

Investigations:
- Take bloods when gaining access (FBC, U&Es, LFTs, bone profile, magnesium, CRP, VBG, coagulation)
- CBG
- Bloods for levels of any anti seizure medications

Management:
- Early involvement senior staff
- Secure airway and high flow 15L O2
- Immediate IV access
- After first 5 mins, IV Lorazepam (or buccal Midazolam)
- If continuing after next 5 mins, IV Lorazepam 2nd dose
- If continuing after next 5 mins, IV Phenytoin
- Call 2222

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51
Q

List some aftercare management steps post-status epilepticus (and investigations)

A
  • Place in recovery position
  • Monitor for respiratory depression, wean off O2
  • Give anti-epileptic to prevent seizure recurrence (Levetiracetam, Sodium valproate or Phenytoin)

Investigations:
- Investigate any injuries e.g. shoulder dislocations
- Consider CT head

Request specialist neurology assessment - same/next day

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52
Q

Outline 2 diagnostic indicator assessment that can be used for suspected stroke

A

FAST test (community idenitifiation)
Face
Arm
Speech
Time (act fast and call 999)

The ROSIER scale = Recognition Of Stroke In the Emergency Room
- Score based on the clinical features and duration
- Stroke is possible in patients scoring 1 or more

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53
Q

Outline some initial investigations an acute stroke

A

Investigations:
- CT head
- Bloods (FBC, clotting profile, INR, U&Es, LFTs, CRP, bone profile, creatine kinase, lipids, TFTs, magnesium, HbA1c and HIV serology)
- CBG
- ECG (atrial fibrillation)

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54
Q

Outline first line management steps for an acute stroke of the following categories
- TIA
- Minor ischaemic / TIA
- Major ischaemic
- Haemorrhagic

A

General:
- A-E assessment (ensure patent airway, O2 sats and haemodynamically stable)
- Transfer to stroke unit
- Urgent non-contrast CT head
- Give Aspirin 300mg (if not haemorrhagic)

TIA:
- Aspirin 300 mg oral loading dose
- Clopidogrel 600mg oral loading dose
- Diffusion-weighted MRI scan
= can be managed in community with TIA clinic

Minor ischaemic:
- Aspirin 300 mg oral loading dose
- Clopidogrel 600mg oral loading dose
+ subsequently lifestyle advice
= can be managed in community with minor stroke clinic

Major ischaemic:
- IV thrombolysis with Alteplase if within 4.5 hours (Aspirin 300mg loading dose if thrombolysis contraindicated)
- Consider surgical thrombectomy (proximal anterior circulation or proximal posterior circulation)

Haemorrhagic:
- Reversal of any anticoagulation (anticoagulants, antiplatelets, NSAIDs)
- Lower BP to 140mmHg if high
- Consider surgical management

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55
Q

Outline some initial investigations and first line management steps for cauda equina / spinal cord compression

A

Investigations:
- Bloods (FBC, U&Es, LFTs, CRP, Group & Save, clotting screen)
- Urgent whole spine MRI

Management:
- IV access
- Analgesia
- Urgent surgical decompression (chemotherapy/radiotherapy or steroids in malignant cord compression)

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56
Q

Outline some initial investigations and first line management steps for head trauma

A

Approach depends on GCS score = blue light to Nottingham if GCS < 9

Investigations:
- CT head (based on risk factor list)

Management:
- Stabilise neck if indicated
- Regular neuro obs
- Analgesia / antiemetics
- Consider reversing anticoagulation / consider tranexamic acid
- Consider referral to neurosurgeons

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57
Q

Outline how acute respiratory distress can present

A

Acute onset (within 1 week)
- Dyspnoea
- Tachypnoea
- Tachycardia
- Reduced O2 sats

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58
Q

Outline some initial investigations and first line management steps for acute respiratory distress

A

Investigations:
- O2 sats
- ABG
- Chest x-ray (bilateral opacities)
- Sputum culture / blood culture

Management:
Supportive control e.g. preventing DVT
- High flow O2 15L
- Consider prone positioning
- Mechanism ventilation with low tidal volume
- Antibiotics if suspect bacterial cause

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59
Q

Giant cell arteritis (GCA) - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Systemic vasculitis affecting medium and large arteries
- Key complication is vision loss, is often irreversible

Typical patient:
- Over 50
- Caucasian female
- Strong association with polymyalgia rheumatica

Presentation:
- Severe unilateral temporal headache
- Scalp tenderness
- Jaw claudication
- Vision changes (blurred or double vision)
- Systemic symptoms e.g. fever, muscle aches, fatigue, loss of appetite
- Temporal artery can be tender or thickened +/- reduced pulsation

Investigation:
- Bloods including ESR
- Temporal artery biopsy (multinucleated giant cells)
- Duplex ultrasound (“halo” sign and stenosis of the temporal artery)

Management:
- High dose steroids!!
no vision loss = Prednisolone
vision loss = Methylprednisolone
- Daily Aspirin (reduce vision loss and stroke risk)
If vision changes - same day referral to ophthalmologist
If no vision changes - discuss with specialist and refer using GCA fast-track pathway
Continue on steroids until symptoms have resolved, can take years

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60
Q

List some complications of giant cell arteritis (including complications related to medications)

A
  • Vision loss (often irreversible)
  • Stroke

Steroid-related complications e.g., weight gain, diabetes and osteoporosis

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61
Q

Bulbar palsy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Impaired function of cranial nerves (CN9, 10, 11 and 12)
- Variety of causes which damage the bulbar aspect of the brainstem
- Progressive or non-progressive

Presentation:
- Dysphagia, absent gag reflex, difficulty chewing, drooling
- Dysphonia, dysarthria, slurred speech
- Atrophy of tongue, jaw muscles, facial muscles
- Aspiration e.g. aspiration pneumonia

Investigations:
- MRI (for stroke / tumour)
- Lumbar puncture and CSF analysis (MS)

Management:
If acute presentation, secure airway (A-E approach)
No known treatment, supportive measures:
- Medications for drooling
- NG tube / feeding tube for swallowing difficulties
- Speech and language therapy

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62
Q

Outline the main causes of bulbar palsy

A
  • Brainstem stroke
  • Brainstem tumours
  • Guillain Barre syndrome
  • Various genetic conditions
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63
Q

State the 3 parameters that doing the ‘Romberg’s test’ will test

A
  1. Vision = removed during the test
  2. Proprioception
  3. Vestibular function (inner ear)

If abnormal test, do Unterberg’s test where the patient marches (removing proprioception) to decide whether there is an issue with proprioception or vestibular function
If damage to vestibular system, will turn torwards side of the lesion

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64
Q

For the following brain arteries, state what areas of the brain they supply
- Vertebral arteries
- Pontine arteries
- Lenticulostriate arteries
- Posterior cerebral arteries
- Middle cerebral arteries
- Anterior cerebral arteries

A

Vertebral/basilar arteries
- Anterior 2/3 of spinal cord
- Cerebellum
- Midbrain

Pontine arteries (branch off basilar artery):
- Pons

Lenticulostriate arteries = deep nuclei:
- Basal ganglia
- Internal capsule

Posterior cerebral arteries = posterior areas:
- Occipital lobe
- (inferior) temporal lobe
- Midbrain and thalamus

Middle cerebral arteries = lateral areas:
- (lateral) frontal lobe incl. primary motor cortex
- (lateral) parietal lobe incl. somatosensory cortex
- (superior) temporal lobe

Anterior cerebral arteries = medial areas:
- (medial) frontal lobe
- (medial) parietal lobe
- Corpus callosum

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65
Q

For upper motor neurones lesions, state the results for the following (increase or decrease):
- Muscle mass
- Muscle strength
- Muscle tone
- Reflexes
- Fasciculations (present/not present)

A

Muscle mass = mildly decreased
Muscle strength = mildly decreased
Muscle tone = increased (spasticity)
Reflexes = increased (hyperreflexia)
Fasciculations (not present)

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66
Q

For lower motor neurones lesions, state the results for the following (increase or decrease):
- Muscle mass
- Muscle strength
- Muscle tone
- Reflexes
- Fasciculations (present/not present)

A

Muscle mass = significantly decreased
Muscle strength = significantly decreased
Muscle tone = decreased (flaccid)
Reflexes = decreased (hyporeflexia)
Fasciculations (present)

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67
Q

State the 2 structures within the basal ganglia

A
  1. Striatum (receives input from cortex)
  2. Globus pallidus (sends output back to cortex)
68
Q

Outline the main role of the basal ganglia and cerebellum

A

Basal ganglia = determine the most appropriate set of movements for a required task

Cerebellum = determine the ORDER of sequence for these movements

69
Q

Outline the cardinal signs of Parkinson’s disease

A
  • Bradykinesia
  • Tremor
  • Rigidity
    + postural instability
70
Q

Outline the cerebellar signs (think of mnemonic)

A

DANISH - cerebellar signs

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

71
Q

Outline whether damage to the following structures will produce ipsilateral or contralateral symptoms
- Basal ganglia lesion
- Cerebellar lesion

A

Basal ganglia lesion = contralateral signs
Cerebellar lesion = ipsilateral signs

72
Q

List some functions of the frontal lobe

A
  • Higher cognition / personality
  • Motor (primary motor cortex)
  • Express speech (Broca’s area)
  • Eye movements
  • Continence
73
Q

List some functions of the parietal lobes

A
  • Sensation (somatosensory cortex)
  • Formulate speech (Wernicke’s area)
  • Calculation and writing
  • Attention to external environment
  • Body image
    (contains superior optic radiations)
74
Q

List some functions of the temporal lobes

A

Special sensory!
- Hearing (primary auditory cortex)
- Smell (primary olfactory cortex)
- Memory
- Emotion
(contains optic radiations to visual cortex)

75
Q

Outline the main role of the left and right sides of the brain

A

Left:
- Maths / logic
- Language

Right:
- Emotion
- Music
- Visuospatial awareness
- Body image

76
Q

For Broca’s area, state its location, main role and clinical picture if area becomes damaged

A

Location: inferior lateral frontal lobe
Role: production of speech
Damage presentation: unable to get words out easily (expressive aphasia)

77
Q

For Wernicke’s area, state its location, main role and clinical picture if area becomes damaged

A

Location: superior temporal lobe
Role: interpretation of speech
Damage presentation: speaking fine but making no sense (fluent aphasia)

78
Q

Outline the 3 parameters of the glasgow coma scale

A
  1. Motor movement
  2. Verbal
  3. Eye movement
79
Q

For the 3 parameters of the glasgow coma scale, outline the scoring system
1. Motor movement
2. Verbal
3. Eye movement

A
  1. Motor movement
    6 = obey commands
    5 = localise to pain
    4 = withdraw from pain
    3 = flexor response to pain
    2 = extensor response to pain
    1 = no response to pain
  2. Verbal
    5 = orientated
    4 = confused conversation
    3 = inappropriate words
    2 = noises (not words)
    1 = no response
  3. Eye movement
    4 = spontaneous eye opening
    3 = eye opening in response to voice
    2 = eye opening in response to pain
    1 = no eye opening
80
Q

Outline the possible GCS score range

A

3 (worst) to 15 (perfect)

81
Q

List some risk factors for stroke (non-modifiable and modifiable)

A

Non-modifiable:
- Increased age
- Polycythaemia vera + other clotting disorders
- Atrial fibrillation
- Previous stroke / TIA

Modifable:
- Smoking
- HTN
- Hyperlipidaemia
- Diabetes
- Excess alcohol
- COCP

82
Q

Outline some potential presenting features of an anterior cerebral artery stroke

A
  • Contralateral limb weakness
  • Contralateral sensory deficit
    + urinary incontinence
    + risk of alien hand syndrome
    + may have frontal lobe features e.g. personality change
83
Q

Outline some potential presenting features of a (proximal) middle cerebral artery stroke

A

Early on = most damage
- Contralateral limb weakness (usually hemiparesis - internal capsule affected)
- Contralateral sensory deficit (match with sensory homunculus area)
- Vision issues (contralateral homonymous hemianopia)
- Speech problems if left sided lesion (Brocas and Wernickes)
+ risk of neglect syndrome

84
Q

Outline some potential presenting features of a (distal) middle cerebral artery stroke

A

Superior division affected:
- Contralateral limb weakness
- Speech problems if left sided lesion (Brocas)

Inferior division affected:
- Contralateral sensory deficit
- Speech problems if left sided lesion (Wernickes)
- Vision problems if radiations affected (homonymous hemianopia or quadrantanopia)

85
Q

Outline some potential presenting features of a lenticulostriate artery stroke

A

(Variable presentation, varying in significance)

Purely motor deficit OR purely sensory deficit

86
Q

Outline some potential presenting features of an posterior cerebral artery stroke

A
  • Contralateral sensory loss (thalamus involvement)
  • Contralateral homonymous hemianopia
87
Q

Outline some potential presenting features of a cerebellar artery stroke

A

Ipsilateral DANISH symptoms
Dysdiadodyskinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

+ Contralateral sensory deficit
+ Ipsilateral Horner’s syndrome

88
Q

Outline signs seen in total anterior circulation (TAC) strokes

A

All 3 of:
1. Unilateral weakness of face, arm and leg +/- sensory deficit
2. Homonymous hemianopia
3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder

89
Q

Outline signs seen in partial anterior circulation (PAC) strokes

A

2 / 3 of:
1. Unilateral weakness of face, arm and leg +/- sensory deficit
2. Homonymous hemianopia
3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder

90
Q

Outline signs seen in posterior circulation (PoC) strokes

A

Only 1 / 5 of:
1. Bilateral motor / sensory deficit
2. Homonymous hemianopia (macular sparing)
3. Cranial nerve palsy + contralateral motor/sensory deficit
4. Cerebellar dysfunction
5. Conjugate eye movement disorder

91
Q

Epilepsy - state the following:
- Pathophysiology
- Investigations
- Management (very general long term)

A

Pathophysiology:
- Tendency to have seizures

Investigations:
- EEG
- Consider video-EEG telemetry
- To rule out other causes e.g. U&Es, ECG, blood glucose, MRI brain, blood cultures, urine cultures and lumbar puncture

Management (very general long term):
- Inform DVLA of driving ban
- Showers rather than baths
- Avoid heights e.g. cliff edges
- Anti-epileptics, depends on type

92
Q

State the definition of a seizure

A

Transient episodes of abnormal electrical activity in the brain

93
Q

List some types of epileptic seizures in adults (and some more common in children)

A

Adults:
- Generalised tonic-clonic seizures
- Partial seizures (focal seizures)
- Myoclonic seizures
- Tonic seizures
- Atonic seizures (drop attacks)

Children:
- Absence seizures
- Febrile seizures
- Infantile spasms

94
Q

Describe the presentation / features of a generalised tonic-clonic seizure

A
  • Muscle tensing (tonic) and jerking (clonic) movements, with tonic generally coming before clonic
  • Complete loss of consciousness
  • Pre-seizure aura
    + tongue biting
    + incontinence
    + groaning
    + irregular breathing

Prolonged post-ictal period (confused, tired, and irritable or low)

95
Q

Describe the presentation / features of a partial (focal) seizure

A

Simple partial seizure = aware throughout
Complex partial seizure = unaware throughout
Sensory modalities affected e.g. hearing, speech, memory and emotions
- Déjà vu
- Strange smells, tastes, sight or sound sensations
- Unusual emotions
- Abnormal behaviours

Can evolvie to a bilateral, convulsive seizure (generalised tonic clonic)

96
Q

Describe the presentation / features of a myoclonic seizure

A
  • Sudden, brief muscle contractions (jump or jolt), limb, trunk, or face
  • Remain awake
97
Q

Describe the presentation / features of a tonic seizure

A

Only a few seconds-minutes
- Entire body stiffens (sudden onset of increased muscle tone)
- Patient usually falls if standing (backwards)

98
Q

Describe the presentation / features of an atonic seizure (drop attacks)

A
  • Sudden loss of muscle tone, often resulting in a fall
  • Usually aware during episodes

Only last briefly

99
Q

Describe the presentation / features of an absence seizure

A

Usually seen in children
- Patient becomes blank, stares into space, and then abruptly returns to normal
- Unaware of surroundings during episode and do not respond

Last 10-20 seconds

100
Q

List some differentials for seizures

A
  • Pseudoseizures (non-epileptic attacks)
  • Vasovagal syncope (fainting)
  • Cardiac syncope (e.g. arrhythmias)
  • Hypoglycaemia
  • Hemiplegic migraine
  • TIA / stroke
  • Panic disorder
101
Q

For the following types of seizure, outline the first line antiepileptic medication that is recommended for men/women who can’t have children and medication for women of childbearing age
- Generalised tonic-clonic
- Partial (focal)
- Myoclonic
- Tonic and atonic
- Absence (both)

A

Generalised tonic-clonic:
Men & no child women: Sodium valproate
Childbearing women: Lamotrigine / Levetiracetam

Partial (focal):
Men & no child women: Lamotrigine / Levetiracetam
Childbearing women: Lamotrigine / Levetiracetam

Myoclonic:
Men & no child women: Sodium valproate
Childbearing women: Levetiracetam
(avoid Carbamazepine as it may worsen myoclonic seizures)

Tonic and atonic:
Men & no child women: Sodium valproate
Childbearing women: Lamotrigine

Absence
Both: Ethosuximide

102
Q

List some side effects of sodium valproate

A
  • Teratogenic
  • Hair loss
  • Tremor
  • Reduce fertility
  • Liver damage / hepatitis
103
Q

Outline the key points from DVLA guidance for epilepsy

A

Reapply after 6 months for a one-off seizure
(reapply after 1 year for multiple seizures)

However for bus/coach/lorry licence = reapply after 5 years for a one-off seizure if no anti-epileptic medications (reapply after 10 seizure-free years for multiple seizures)

104
Q

Migraine - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Neurological disorder characterised by severe headaches, usually unilateral and pulsating
- Often preceded by an aura such as visual or sensory symptoms
- Exact cause is unknown but likely a combination of genetic and environmental factors

Presentation:
F>M (3:1), peak age 30-39
Pain lasts for 4-72 hours
- Severe, unilateral, pulsating/throbbing headache
- N&V
- Photophobia
- Phonophobia
+ preceding ‘aura’

Investigations:
Primarily based on the history and examination
- Neuroimaging (MRI or CT) or blood tests (ESR, CRP) may be considered to rule out other more sinister causes

Management:
- Avoid triggers if possible
- In dark room
- Paracetamol or NSAIDs (best taken at start of attack)
- May need Triptan drugs e.g. Sumatriptan
- Prophylaxis with Propranolol, Amitriptyline, Topiramate if having significant effect on QOL or not responding to treatment
*Avoid COCP

105
Q

List some potential triggers for migraines

A
  • Stress
  • Hormonal changes
  • Changes in weather
  • Certain foods
  • Certain medications e.g. oral contraceptive
106
Q

List some diagnostic factors to be able to diagnose migraines (ICHD criteria) in ABCDE format

A

A = > 5 attacks
B = attacks lasting 4–72 hours
C = at least 2/4 following characteristics: unilateral location, pulsating, moderate / severe pain, interfering with daily activity
D = at least 1 of: N&V, photophobia or phonophobia
E = not better accounted for by another diagnosis

107
Q

State some differentials for migraines

A
  • Other primary headache disorders e.g.tension-type headache, cluster headache
  • Medication overuse headache
  • Subarachnoid hemorrhage
  • Giant cell arteritis
108
Q

List the most common prophylactic medications for migraines

A
  • Propranolol
  • Amitriptyline
  • Topimerate (anticonvulsant)
109
Q

State the 5 criteria to fulfil for migraines

A
  1. At least 5 attacks
  2. Lasts 4-72 hours
  3. Typical features of headache (unilateral, throbbing, moderate-severe intensity, prevents regular activity)
  4. At least 1 of the following: N&V, photophobia or phonophobia
  5. No other diagnosis better accounted for
110
Q

List the advice that should be given to a patient with overuse medication headaches

A

Explain headache will be worse initially, but frequency of the headaches will reduce (but not for weeks - may need time off work)

The simple analgesia = stopped abruptly for at least 6 weeks
Codeine = withdrawn more slowly over 2-4 weeks

After 6 weeks, reintroduce but no more than 10-15 days per month

111
Q

Idiopathic Parkinson’s disease - state the following:
- Pathophysiology
- Presentation (3 cardinal features)
- Investigations
- Management

A

Pathophysiology:
- Neurodegenerative disorder, with accumulation of ‘Lewy bodies’
- Thought to lead to neuronal death in the dopaminergic cells of the substantia nigra (basal ganglia)
- Predominantly affects adults > 65 years
- Characterised by triad of: tremor, bradykinesia and rigidity

Presentation:
Triad of
1. Asymmetrical, resting tremor (3-5Hz ‘pill-rolling’)
2. Bradykinesia
3. Lead-pipe rigidity

Investigations:
Primarily a clinical diagnosis, supported by positive response to Parkinson’s treatment (absolute failure to respond to Levodopa basically excludes a diagnosis)

Management:
Depends on effect that the motor symptoms have on QOL
- Oral Levodopa PLUS peripheral decarboxylase inhibitors (first line if impact on QOL)
- Dopamine agonists e.g. Ropinirole (if no impact on QOL)
- Monoamine oxidase‑B (MAO‑B) inhibitors e.g. Selegiline (if no impact on QOL)

112
Q

List some peripheral and central side effects of Levodopa medication for Parkinson’s disease

A

Peripheral:
- Postural hypotension
- N&V
(Reduced by peripheral dopa decarboxylase inhibitor e.g. Carbidopa)

Central:
- Hallucinations / psychosis
- Confusion
- Dyskinesia (involuntary, erratic, writhing movements)

113
Q

State some motor and non-motor features of Parkinson’s disease

A

3 core features:
1. Bradykinesia
2. Asymmetric 3-5Hz “pill-rolling” tremor (worse on activity)
3. Lead pipe rigidity

Other motor features:
+ Parkinsonian gait (shuffling small steps, difficulty with initiation and turning)
+ cog wheel rigidity
+ micrographia
+ forward leaning posture
+ reduced arm swing
+ hypomimic facies (reduced facial expression)

Non-motor features:
- Sleep disorders
- Autonomic dysfunction (constipation, postural hypotension and erectile dysfunction)
- Olfactory loss
- Psychiatric features including depression, anxiety, and hallucinations

Early and prominent cognitive dysfunction = think dementia with Lewy bodies

114
Q

Outline the difference between Parkinson’s tremor
and benign essential tremor
- Asymmetrical vs symmetrical
- Frequency
- Worse when…
- Improved when…
- Change with alcohol

A

Parkinson’s Tremor:
- Asymmetrical
- 4-6 hertz
- Worse at rest
- Improves with intentional movement
- No change with alcohol

Benign Essential Tremor:
- Symmetrical
- 6-12 hertz
- Improves at rest
- Worse with intentional movement
- Improves with alcohol

115
Q

List some Parkinsonism conditions (not Parkinson’s disease)

A
  • Vascular parkinsonism
  • Drug-induced parkinsonism
  • Dementia with Lewy bodies
  • Multiple system atrophy (MSA)
  • Progressive supranuclear palsy
  • Corticobasal degeneration
116
Q

For the following Parkinsonism conditions (not Idiopathic Parkinson’s disease), give a brief description of how they present differently to Parkinson’s disease:
- Vascular parkinsonism
- Drug-induced parkinsonism
- Dementia with Lewy bodies
- Multiple system atrophy (MSA)
- Progressive supranuclear palsy
- Corticobasal degeneration

A

Vascular parkinsonism:
- Occurs after a stroke, sudden onset (rather than gradual and insidious)

Drug-induced parkinsonism:
- Associated with specific medications e.g. neuroleptic drugs and resolves once medication is withdrawn/changed

Dementia with Lewy bodies:
- Memory loss and confusion
- Visual hallucinations (small children and furry animals)

Multiple system atrophy (MSA)
- Autonomic problem e.g. orthostatic hypotension are a significant feature
- Urinary incontinence

Progressive supranuclear palsy:
- Limited vertical eye movements
- Significant balance problems / falls

Corticobasal degeneration:
- Jerking movements and muscle tightness
- Dystonia (abnormal hand and feet postures)

117
Q

Motor neurone disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Umbrella which encompasses a variety of diseases affecting the motor nerves (ALS is most common)
- Progressive degeneration of both upper and lower motor nerves (NO effect on sensory nerves)
- Exact cause is unclear, however genetic links

Presentation:
Typically 60’s man
- Insidious, progressive weakness of muscles throughout body (usually upper body noticed first)
- Dysarthria (slurred speech)
- Increased fatigue when exercising
- Clumsiness

Investigations:
- Clinical but made by a specialist, when other causes are ruled out (thyroid function tests, nerve conduction studies, proteinelectrophoresis for paraproteinaemias, MRI of brain and spinal cord)

Management:
No effective treatments for halting or reversing progression
- MDT / psychosocial support for individual and family
- Symptom control e.g. Baclofen (muscle spasticity), antimuscarinic (excessive saliva)
- Non-invasive ventilation (NIV) when respiratory muscles weaken
- Riluzole can help in ALS
- EOL care when needed (respiratory failure or pneumonia)

118
Q

List some subtypes of motor neurone disease

A
  • Amyotrophic lateral sclerosis (ALS) = most common
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
119
Q

State the usual life expectancy for patients diagnosed with motor neurone disease

A

Less than 5 years from diagnosis - usually dying from respiratory complications

120
Q

State what medications can be used in the management of motor neurone disease

A

Riluzole - disease modifying but only extends life by 3 months

+ Baclofen / botox injections for muscle spacicity
+ anticholingerics for drooling

Other:
+ non-invasive ventilation in patients in type 2 respiratory failure

121
Q

Guillain Barre syndrome (GBS) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Acute paralytic polyneuropathy that affects the peripheral nervous system
- Underlying pathology thought to be due to molecular mimicry
- B cells create antibodies against the antigens on invading pathogen, but antibodies also match proteins on peripheral neurones (myelin sheath or the nerve axon itself)

Presentation:
Symptoms usually appear within 1 month of triggering infection, with a peak at 2-4 weeks after
However, recovery can last months-years
- Symmetrical ascending weakness
- Reduced reflexes
+ peripheral sensory deficit or neuropathic pain
+ facial weakness
+ autonomic dysfunction e.g. urinary retention, paralytic ileus or arrythmias

Investigations:
Clinical diagnosis with ‘Brighton criteria’ supported by investigations
- Nerve conduction studies (reduced signalling)
- Lumbar puncture (raised protein, with a normal cell count and glucose)

Management:
Supportive care and monitor FVC daily (risk of respiratory depression)
- IV immunoglobulins (IVIG)
- Plasmapheresis (alternative to IVIG)
+ VTE prophylaxis (PE is a leading cause of death)

122
Q

Outline some infections commonly associated with Guillain Barre syndrome (GBS)

A
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Campylobacter jejuni
123
Q

Suggest the general prognosis for Guillain Barre syndrome (GBS)

A

Recovery can take months - years (up to 5 years)

Most patients eventually make either a full recovery or are left with minor symptoms

However some are left with significant disability

Mortality ~ 5% (respiratory / cardiovascular complications)

124
Q

Myasthenia gravis (MG) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Autoimmune condition where there are antibodies directed against the neuromuscular junction, specifically postsynaptic nACh receptors
- Leads to reduced muscle contractility
- Improves with rest, as the receptors are cleared
- Strong link with thymomas (thymus gland tumours)

Presentation:
Symptoms vary between patients (from mild to life-threatening)
Typically affects women < 40 and men > 60
- Proximal muscle weakness e.g. difficulty climbing stairs, standing from a seat
- Diplopia (extraocular muscle weakness)
- Ptosis (eyelid weakness)
- Weakness in facial movements
- Dysphagia
- Fatigue in the jaw when chewing
- Slurred speech
All symptoms worse at the end of the day

Investigations:
- Antibody test for nAChR antibodies
- CT / MRI thymus gland (thymoma in 10-20% patients)
- Any doubt, give IV Neostigmine

Management:
- Pyridostigmine (cholinesterase inhibitor)
- Immunosuppression e.g. Prednisolone or Azathioprine
- Thymectomy can improve symptoms, even in patients without a thymoma
- Rituximab as last line option

125
Q

Outline a myasthenic crisis, how it might present and how it is managed

A

Outline:
- Potentially life-threatening complication of myasthenia gravis
- Often triggered by another illness e.g. respiratory tract infection

Presentation:
- Acute worsening of myasthenia symptoms

Management:
- May need NIV or mechanical ventilation
- IV immunoglobulins and plasmapheresis

126
Q

Muscular dystrophy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- X-linked recessive mutation in the dystrophin protein (which joins muscles)
- Initially causes muscle regeneration
- However over time, there is muscle atrophy (with cell death and fat accumulation in the muscle)
- Also affects the heart due to dystrophin

Presentation:
- Progressive proximal muscle weakness
- Waddling gait
- Calf pseudohypertrophy
- Gower’s sign
- Wheelchair in later stages

Investigations:
- Creatine kinase
- Muscle biopsy
- Genetic testing

Management:
- MDT approach, mainly PT/OT
- Oral corticosteroids
- Creatine supplements

127
Q

Multiple sclerosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Autoimmune condition attacking myelin sheath of the central nervous system (brain and spinal cord)
- Demyelination leads to motor, sensory and cognitive problems
- Lesions vary in location, meaning that the affected sites and symptoms change over time
- In early disease, remyelination can occur, however in later stages remyelination is incomplete and symptoms become more permanent gradually

Presentation:
Symptoms vary significantly, F>M (2:1) and typically 20-40 years
Symptoms usually progress over >24 hours, last days-weeks and then improve
- Optic neuritis
- Diplopia and abnormal eye movements
- Focal neurological symptoms e.g. limb weakness, Horner’s syndrome, facial palsy, incontinence
- Focal sensory symptoms e.g. numbness, paraesthesia
- Lhermitte’s sign (shooting pain when neck bent forward)
- Balance and gait issues (ataxia = sensory or cerebellar)

Investigations:
- Clinical diagnosis by neurologist based on symptoms
- MRI scans (lesions)
- Lumbar puncture (oligoclonal bands in CSF)

Management:
MDT approach, plus symptomatic management e.g. depression, incontinence
- Steroids for flares of disease activity (oral or IV if severe)
- Ongoing treatment can use injectables e.e interferon beta
*Inform that they need to inform the DVLA

128
Q

State the 3 main patterns of MS disease

A
  1. Relapsing remitting
    - Flares, with mostly recovery (but some residual deficit)
    - However between episodes of flares, no change
  2. Secondary progressive MS
    - Starts off as relapsing remitting
    - However over time, develops into gradual continuous deterioration, with no specific ‘flares’
  3. Primary progressive
    - Starts off as a gradual continuous deterioration, with no specific ‘flares’
129
Q

List some potential risk factors that have been identified for multiple sclerosis (MS)

A
  • Female (F:M = 2:1)
  • Family history
  • Vitamin D deficiency / latitude
  • Smoking
  • Obesity
  • EBV (glandular fever)
130
Q

List the most common presenting symptoms for multiple sclerosis (how they could present to GP)

A

Often aged under 50, with symptoms that have evolved over more than 24 hours (persist over several days or weeks) and then improve

Most common:
- Loss / reduction of vision in one eye
- Diplopia
- Nystagmus (horizontal jerking)
- Focal sensory disturbance e.g. paraesthesia, numbness
- Focal weakness
- Facial weakness (Bells palsy)
- Lhermitte’s sign (shooting pain when neck bent down)
- Progressive difficulties with balance and gait

+ vertigo, vomiting, headache
+ cognitive issues
+ Urinary urgency and frequency (with incontinence)

131
Q

Bell’s palsy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Inflammation / damage to facial nerve (CN7)
- Acute, unilateral facial nerve weakness or paralysis of rapid onset (< 72 hours) and unknown cause
- Diagnosis can only be made when no other causitive medical condition is found

Presentation:
Symptoms generally begin suddenly, worsening over 24 hours - almost always unilateral
Variety from mild weakness to total paralysis
- Unilateral eyelid drooping, mouth drooping and loss of nasolabial fold
- Pain behind ear / unilateral hyperacusis
- Difficulty with speech / drinking or eating
- Unilateral dry eye
- Unilateral dry mouth
- Loss of taste (anterior 2/3 tongue)

Investigations:
- CT / MRI (rule out stroke / TIA / brain tumour)

Management:
Improvements seen after 2-3 weeks, most cases resolve completely after 4 months
- Consider Prednisolone if presented within 72 hours
- Eye lubricating drops for affected eye

132
Q

Outline some risk factors / potential causes of idiopathic Bell’s palsy

A
  • History of recent infection (EBV, herpes zoster, herpes simplex)
  • Diabetes mellitus
  • HTN
  • Sarcoidosis
133
Q

List some differential diagnoses for Bell’s palsy = unilateral facial weakness and paralysis

A
  • Stroke (forehead spared)
  • Brain tumour
  • Traumatic injury to facial nerve
  • Iatrogenic e.g. damage during surgery
  • Local tumours e.g. parotid tumours / facial nerve tumour / skin cancer
  • Infectious causes e.g. syphilis, mastoiditis, Ramsay Hunt syndrome
  • MS
134
Q

Dementia - state the following:
- Definition
- 4 main types (in order of frequency)
- Presentation
- Investigations
- Management

A

Definition:
- Progressive decline in cognitive functioning, affecting different areas of function

4 main types (in order of frequency):
- Alzheimer’s
- Vascular
- Frontotemporal dementia
- Lewy Body or Parkinson’s with Dementia

Presentation:
Depends on type of dementia
- Cognitive impairment e.g. problem solving
- Memory loss
- Confusion
- Mood changes e.g. agitation
- Difficulties with ADLs

Investigations:
Mainly a clinical diagnosis - MMSE (mini mental state exam)
- May want to rule out other causes e.g. CT/MRI head

Management:
- Alzheimer’s = Cholinesterase inhibitors
- Vascular = modify risk factors

135
Q

Carpal tunnel syndrome - state the following:
- Pathophysiology
- Presentation
- Special tests and investigations
- Management

A

Pathophysiology:
- Compression of the median nerve at the carpal tunnel
- Compression comes from narrowing of the tunnel or swelling of the contents e.g. tendon sheaths

Presentations:
Gradual onset of sensory and motor symptoms in the distribution of the median nerve, bilateral in approx. 75% cases
Sensory symptoms:
- Neuropathic pain (burning, paresthesia, numbness) in palmar digital cutaneous branch distribution
- Palmar surface spared
Motor symptoms:
- Atrophied thenar muscles
- Weakness of thumb abduction and fine movements
- Reduced grip strength
Symptoms can wake patients at night

Investigation and special tests:
- Nerve conduction studies
- Tinnel’s test (tapping)
- Phalen’s test (60 sec)

Management:
- Rest
- Activity modification (avoid repetitive movements)
- Splinting (holds in neutral position)
- Steroid injection
- Surgery to cut flexor retinaculum to release pressure

136
Q

Cubital tunnel syndrome - state the following:
- Pathophysiology
- Presentation
- Investigation and special tests
- Management

A

Pathophysiology:
- Compression of the ulnar nerve at the cubital tunnel
- Commonly associated with cyclists due to repetitive compression

Presentations:
Gradual onset of sensory and motor symptoms in the distribution of the ulnar nerve
Sensory symptoms:
- Neuropathic pain (burning, paresthesia, numbness) in ulnar nerve distribution
Motor symptoms:
- Hand of Benediction
- Atrophied hypothenar muscles
- Reduced dexterity
- Reduced grip strength

Investigation and special tests:
- Nerve conduction studies
- Tinnel’s test (tapping)
- Consider USS of elbow

Management:
- Rest
- Activity modification (avoid repetitive compression)
- Nocturnal elbow splinting (holds in 45 degree position)
- Steroid injection
- Surgery

137
Q

List some risk factors for carpal tunnel syndrome

A

Most commonly idiopathic
- Repetitive activities
- Pregnancy
- Obesity
- Diabetes
- Acromegaly
- Hypothyroidism
- Rheumatoid arthritis

138
Q

State the 2 sites at which the ulnar nerve is commonly compressed and which syndromes occur when this happens and for each type, list some causes for both together

A
  1. Elbow (more common)
    = cubital tunnel syndrome
  2. Wrist (less common)
    = Guyon’s canal syndrome / ulnar tunnel syndrome

Causes:
- Repetitive compression e.g. cycling (cyclists palsy)
- Trauma / fractures
- Swelling
- Vascular / bony abnormalities

139
Q

Diabetic neuropathy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Most common chronic complication of diabetes
- Presence of peripheral nerve dysfunction (diagnosed after the exclusion of other causes)
- Pain is the outstanding complaint in most patients, but many patients are completely asymptomatic

Presentation:
- Glove and stocking distribution of a loss of: touch, pain, temperature, sensation and proprioception
- Loss of reflexes (ankle then knee)
(hands are only affected in severe long-standing neuropathy)

Investigations:
Mainly a clinical diagnosis
- Fasting blood glucose
- HbA1c
- Serum TSH / B12 and folate / urea and electrolytes

Management - based on pain vs no pain
No pain
- Improve glycaemic control (underlying condition)
- Supportive measures e.g. foot care
Pain
- Pregabalin / gabapentin and/or Duloxetine

140
Q

Cervical spondylosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Osteoarthritis of the spine, degenerative age-related wear and tear of either intervertebral discs or facet joints
- Most common complication is radiculopathy = compression of nerve root (next common after this is myelopathy = compression of spinal cord)

Presentation:
Can be asymptomatic (incidental finding)
Most commonly C5-7 levels
- Neck pain (worse on movement)
- Reduced range of motion of neck / stiffness
- Tenderness (poorly localised)
- Crepitus
- Neurological changes in upper limbs (weakness, numbness or tingling)
- Referred pain (occiput, between the shoulder blades, upper limbs)
- Hyporeflexia at affected muscles

Investigations:
Mostly clinical diagnosis
- May need a MRI spine

Management:
Reassurance for first 3-4 weeks
- Keep active and continue normal activities (including work)
- Caution with driving if restricted neck movements
- Simple analgesia (Paracetamol, Ibuprofen, Codeine), can consider Gabapentin etc.
- Physiotherapy if symptoms persist after 1 month
- Consider MRI if neurological signs or present > 6 weeks
- Consider surgery if progressive neurological deficits, intractable pain or if MRI shows compression

141
Q

Lumbar spondylosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Osteoarthritis of the lumbar spine, degenerative age-related wear and tear of either intervertebral discs or facet joints
- Most common complication is radiculopathy = compression of nerve root (next common after this is myelopathy = compression of spinal cord)

Presentation:
Can be asymptomatic (incidental finding)
Most commonly C5-7 levels
- Neck pain (worse on movement)
- Reduced range of motion of neck / stiffness
- Tenderness (poorly localised)
- Crepitus
- Neurological changes in upper limbs (weakness, numbness or tingling)
- Referred pain (occiput, between the shoulder blades, upper limbs)
- Hyporeflexia at affected muscles

Investigations:
Mostly clinical diagnosis
- May need a MRI spine

Management:
Reassurance for first 3-4 weeks
- Keep active and continue normal activities (including work)
- Caution with driving if restricted neck movements
- Simple analgesia (Paracetamol, Ibuprofen, Codeine), can consider Gabapentin etc.
- Physiotherapy if symptoms persist after 1 month
- Consider MRI if neurological signs or present > 6 weeks
- Consider surgery if progressive neurological deficits, intractable pain or if MRI shows compression

142
Q

Outline an essential tremor, including typical features of the tremor

A
  • Common condition, associated with older age
  • Fine tremor of voluntary muscles, most notable in the hands (but can affect head, jaw and vocal cords)

Features:
- Symmetrical
- Fine tremor (6-12 Hz)
- Better with: alcohol and beta blockers
- Worse with movements e.g. picking up cup of tea, caffeine or stress
- Tremor not present during sleep

143
Q

Outline some differentials for a tremor

A
  • Essential tremor
  • Parkinson’s disease
  • Huntington’s chorea
  • Hyperthyroidism
  • Multiple sclerosis
  • Fever
  • Anxiety
  • Dopamine antagonists e.g. antipsychotics
144
Q

Outline how an essential tremor is managed and 2 medications that can be used

A

No definitive treatment (not harmful and does not require treatment, unless causing functional or psychological problems)

Medications:
- Propranolol
- Primidone (anti-epileptic)

145
Q

Outline some potential causes for the following types of tremor:
- Essential tremor (benign)
- Resting tremor
- Intention tremor (cerebellar)

A

Essential tremor (benign):
- Older age
- Familial

Resting tremor:
- Parkinson’s disease
- Parkinsonism
- Supranuclear palsy
- Basal ganglia affecting drugs e.g. antipsychotics

Intention tremor:
- Cerebellar disease (DANISH symptom)
- MS
- Chronic alcohol abuse (cerebellar damage)

146
Q

For the following types of tremor:
- Essential tremor (benign)
- Resting tremor (Parkinson’s)
- Intention tremor (cerebellar)
State…
1. Worse on
2. Better on

A

Essential tremor (benign)
- Worse on activity, caffeine, stress
- Better with rest, alcohol, beta blockers

Resting tremor (Parkinson’s)
- Worse on resting
- Better on movement / activity

Intention tremor (cerebellar)
- Worse on movement / activity
- Better on resting

147
Q

Radiculopathy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Mostly compression of the nerve root, leading to motor and sensory deficits
- Lots of causes (discussed in another card)

Presentation:
- Motor weakness in affected myotome
- Sensory deficit (paraesthesia) in affected dermatome
- Radicular pain (deep, burning, strap like)

Investigations:
Mostly clinical diagnosis
- Can consider nerve conduction studies

Management:
Depends on the underlying cause
- Analgesia (WHO then consider neuropathic analgesia e.g. Amitriptyline first line)
- Physiotherapy

148
Q

List some causes of radiculopathy

A
  • Intervertebral disc prolapse
  • Degenerative diseases of the spine (spinal canal stenosis)
  • Vertebral fracture
  • Malignancy (most commonly metastatic)
  • Infection e.g. spinal TB, extradural abscess or osteomyelitis
149
Q

List some red flag conditions to consider in a patient presenting with radiculopathy symptoms

A
  • Cauda equina syndrome
  • Malignancy / metastatic disease
  • Fracture
  • Infection e.g. abscess
150
Q

Subacute combined degeneration of the cord - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Degeneration of the spinal cord, secondary to B12 deficiency
- Demyelination predominantly affects dorsal column, but also lateral columns

Presentation:
Combination of peripheral and CNS signs, triad:
1. Extensor planar response
2. Brisk knee reflex
3. Absent ankle reflex
Dorsal column degeneration = sensory deficits / paresthesia
Lateral column degeneration = motor weakness, hyperreflexia and spasticity
Spinothalamic column degeneration = ataxia / gait disturbance
+ signs of anaemia

Investigations:
- Bloods (FBC, B12 and folate, LFTs, TFTs, GGT)
- Blood film (hypersegmented neutrophils)

Management:
- IM Hydroxocobalamin (B12) injection (on alternate days) until there is no further improvement
- Thereafter, injection every 2 months

151
Q

State some complications if subacute combined degeneration of the cord is left untreated

A
  • Neurological complications e.g. paraplegia or quadriplegia
  • Bladder / bowel incontinence
  • Congestive heart failure (from ongoing anaemia stress)
152
Q

Outline what cranial nerves are affected in cavernous sinus syndrome and therefore how it presents

A

CN3 - oculomotor
CN4 - trochlear
CN5 - trigeminal (V1 and V2)
CN6 - abducens
+ internal carotid artery

Presentation:
- Headache
- Diplopia
- Paralysis of eye muscles (ophthalmoplegia)
- Sensory loss in V1 and V2 distribution
- Horner’s syndrome
- Proptosis

153
Q

Pituitary tumours - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Tumours of the pituitary gland (mostly benign = pituitary adenomas)
- 2 main categories: non-hormone producing (non-functioning) and hormone producing (functioning)
- Can be microadenoma or macroadenoma

Presentation:
Can be incidental finding on CT/MRI
- Homonymous hemianopia
- Headache
- N&V
- Seizures

Investigations:
- CT / MRI
- Bloods for hormone disturbance (prolactinomas are most common hormone secreting tumours)

Management:
- Active monitoring if asymptomatic or minimal impact
- Transsphenoidal surgery
- If prolactinoma, Cabergoline

154
Q

Wernicke-Korsakoff Syndrome - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Caused by a thiamine (vitamin B1 deficiency)
- Alcohol reduces the absorption of thiamine, reduces stores in the liver and reduces enzyme activity that converts thiamine into an active state
- Generally caused by alcoholic disease but can also be caused by malnutrition
- Wernicke syndrome occurs first in an acute phase and if left untreated, will progress to chronic irreversible Korsakoff syndrome

Presentation:

Wernicke syndrome (triad)
1. Confusion / mental state changes
2. Ataxia
3. Eye movement dysfunction

Korsakoff syndrome:
- Memory impairment, specifically short-term memory loss (sometimes also have long-term memory loss)

Management:
- Thiamine replacement therapy (either prophylactically or as treatment)
- Alcohol abstinence
- Improved nutrition
If caught early, Wernicke’s syndrome can be reserved fully

155
Q

Describe an Argyll Robertson pupil and in which disease it is seen in

A

Description:
Gradual onset over years
- Bilateral small irregular pupils that fail to constrict in response to bright light
- But exhibit constriction during accommodation

Seen in advanced stages of syphilis (occurs due to invasion of the CSF by syphilis)

156
Q

List the 4 main types of Creutzfeldt-Jakob disease

A
  1. Sporadic (most common)
  2. Variant (mad cow disease)
  3. Familial (inherited)
  4. Iatrogenic (contaminated cataracts / blood products)
157
Q

Outline the pathophysiology of Creutzfeldt-Jakob disease and the main presenting symptoms

A

Pathophysiology:
- Abnormal infectious ‘prion’ protein
- Causes other proteins to form ‘prion’ proteins in a chain reaction
- Leads to loss of grey mater in the brain
- Rapidly progressive and always fatal, most patients will die within a year

Presentation:
- Cognitive impairment
- Personality changes
- Ataxia
- Slurred speech
- Vision problems and blindness
- Chorea

158
Q

List 3 types of gliomas (from least malignant to most malignant)

A
  1. Ependymoma
  2. Oligodendroglioma
  3. Astrocytoma (the most common and aggressive form is glioblastoma)
159
Q

List 4 hormones that are usually secreted by pituitary tumours (functional tumours) and the conditions it leads to

A
  1. Prolactin = hyperprolactinaemia
  2. ATCH = Cushing’s disease
  3. GHRH = acromegaly
  4. TSH = thyrotoxicosis
160
Q

Generally for pituitary tumours (functional tumours), state how they can be managed as well as specific management for the types below
Prolactin = hyperprolactinaemia
GHRH = acromegaly

A

Generally:
- Transsphenoidal surgery
- Radiotherapy

Prolactin (hyperprolactinaemia):
- Bromocriptine to block excess prolactin

GHRH = acromegaly:
- Somatostatin analogues to block excess GH

161
Q

Lambert-Eaton syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations

A

Pathophysiology:
- Autoimmune condition affecting the neuromuscular junction (similar to myasthenia gravis)
- Specifically the voltage-gated Ca channels of the pre-synaptic membrane, leading to less ACh release
- Usually a paraneoplastic syndrome from a small-cell lung cancer, but can also occur as a primary autoimmune disorder with no SCLC
- Symptoms are more insidious and less pronounced than MG

Presentation:
- Proximal muscle weakness
- Autonomic dysfunction e.g. dry mouth, blurred vision, impotence and dizziness
- Reduced or absent tendon reflexes
Symptoms improve after periods of muscle contraction (opposite to MG)

Investigations:
- Exclude underlying malignancy (SCLC) with chest x-ray

162
Q

Charcot-Marie-Tooth Disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Inherited disease, affecting peripheral motor and sensory nerves
- Various types, causing myelin or axon dysfunction
- Mostly autosomal dominant, symptoms usually appear before age 10

Presentation:
- High foot arch
- Peripheral sensory loss
- Distal muscle wasting (champagne legs)
- Lower leg weakness (esp. loss of ankle dorsiflexion and foot drop)
- Distal weakness (hands)
- Reduced tendon reflexes
- Reduced muscle tone

Investigations:
Mostly clinical diagnosis with some genetic testing
- Nerve conduction test / EMG
- Genetic testing

Management:
No cure or treatment - MDT management
- Analgesia for neuropathic pain (e.g. Amitriptyline)
- Physiotherapists (maintain strength and joint ROM)
- Occupational therapists
- Podiatrists (foot symptoms)
- May require surgery if severe joint deformities

163
Q

List causes of peripheral neuropathy (ABCDE)

A

Alcohol
B12 deficiency
CKD and Cancer
Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
Every vasculitis

164
Q

List some investigations to consider for patietns presenting with peripheral neuropathy

A

B - CBG
L - FBC, U&Es, TFTs, B12 and folate, HbA1C, ANA and ANCA (vasculitis)
I - MRI brain and spinal cord
P - nerve conduction studies, +/- nerve biopsy

165
Q

Normal pressure hydrocephalus - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Excess CSF accumulates in the ventricles, causing them to enlarge
- Called normal pressure as the CSF pressure on lumbar puncture is often normal

Presentation:
Classic triad
- Dementia
- Incontinence
- Magnetic gait
“Wet, Wacky and Wobbly”

Investigations:
- CT or MRI (dilated lateral ventricles)
- Lumbar puncture

Management:
- Therapeutic lumbar puncture (removes CSF from the system to relieve the pressure)
- Ventriculoperitoneal shunt (if unresponsive to lumbar puncture treatment)

166
Q

Outline some of the management options for Huntington’s disease

A
  • Tetrabenazine (chorea)
  • SSRIs (depression)
  • Antipsychotics (psychosis)
  • Supportive care (physical and emotional support)

Year 4 - 5. Neurology & Special Senses (7 decks)

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