Neurology Flashcards
(166 cards)
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
2
Q
List the sensory modalities that run along the spinothalamic system
A
3 modalities:
- Pressure / crude touch
- Pain
- Temperature
3
Q
List the sensory modalities that run along the dorsal column system
A
4 modalities:
- Fine touch
- Vibration
- Proprioception
- 2 point discrimination
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
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
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
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)
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
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
10
Q
Name the 3 major branches of the trigeminal nerve and which foramen they travel through
A
- Ophthalmic - superior orbital fissure (via cavernous sinus)
- Maxillary - foramen rotundum (via cavernous sinus)
- Mandibular - foramen ovale (via cavernous sinus)
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
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
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)
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
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
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
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
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
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
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
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
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
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
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
25
List some differentials for a sudden loss of consciousness
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
26
Briefly describe a coma and signs of impaired consciousness
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
27
List some differentials incoordination, gait disturbance and impaired balance
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
28
List some differentials for generalised hypokinesia (reduced movements)
Parkinsonism
Catatonia
Psychomotor depression
Arthritis
Hypocalcaemia (dystonia)
(not 100% sure)
29
List some differentials for hyperkinesia (increased movements)
Epilepsy
Tics, such as Tourette syndrome
Essential tremor
Huntington's disease (chorea)
Functional movement disorder
(not 100% sure)
30
List some differentials for focal neurological weakness
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
31
List some differentials for generalised neurological weakness
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
32
List some differentials for speech, swallow or language problems
- 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
33
List some differentials for urinary incontinence
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
34
List some differentials for faecal incontinence
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
35
List some differentials for reduced cognition
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
36
List some differentials for behaviour or personality change
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
37
List some differentials for neuropathic pain syndromes (central, peripheral, mixed)
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
38
Describe neuropathic pain and list some positive features and negative features of neuropathic pain
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
39
List some differentials for sensory disturbances
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
40
List some differentials for transient motor and sensory disturbances
- TIA
- Seizure
- Raised ICP
- Migraine (with aura)
- MS
- Electrolyte abnormalities
- Psychiatric disorders e.g. panic disorder, schizophrenia
41
List some potential causes of ICP
Vascular:
- Aneurysm
- Intracranial haemorrhage / stroke
- Hydrocephalus
Infection:
- Meningitis / encephalitis
- Intracranial abscess
Neoplasm / neurological:
- Tumours
Trauma:
- Head trauma
42
Outline how raised ICP can present
- Headache
- Diplopia / blurred vision
- N&V
- Behavioural changes
- Reduced conscious level
- Seizures
Cushing's triad: bradycardia, hypertension, irregular breathing
43
Outline some initial investigations and first line management steps for raised ICP
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
44
Outline how a subarachnoid haemorrhage can present
- Thunderclap headache during episode of strenuous activity
- Neck stiffness
- Photophobia
- N&V
- Neurological symptoms e.g. visual changes, dysphasia, focal weakness, seizures, reduced consciousness
45
Outline some initial investigations and first line management steps for subarachnoid haemorrhage
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
46
List some causes of subarachnoid haemorrhage
70% = berry aneurysms
10% = HTN
10% = AV malformation
5% = idiopathic
+ trauma
47
Outline how meningitis / encephalitis can present
- Fever
- Non-blanching purpuric rash if bacterial meningitis
- Headache, stiff neck, photophobia
- N&V
- Reduced conscious level
- Seizures
48
Outline some initial investigations and first line management steps for meningitis / encephalitis
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
49
Outline the recognised definition of status epilepticus
- Over 5 minutes of single continuous seizure
- OR 2 or more discrete seizures between which there is incomplete recovery of consciousness
50
Outline some initial investigations and first line management steps for status epilepticus
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
51
List some aftercare management steps post-status epilepticus (and investigations)
- 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*
52
Outline 2 diagnostic indicator assessment that can be used for suspected stroke
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
53
Outline some initial investigations an acute stroke
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)
54
Outline first line management steps for an acute stroke of the following categories
- TIA
- Minor ischaemic / TIA
- Major ischaemic
- Haemorrhagic
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
55
Outline some initial investigations and first line management steps for cauda equina / spinal cord compression
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)
56
Outline some initial investigations and first line management steps for head trauma
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
57
Outline how acute respiratory distress can present
Acute onset (within 1 week)
- Dyspnoea
- Tachypnoea
- Tachycardia
- Reduced O2 sats
58
Outline some initial investigations and first line management steps for acute respiratory distress
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
59
Giant cell arteritis (GCA) - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigation
- Management
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
60
List some complications of giant cell arteritis (including complications related to medications)
- Vision loss (often irreversible)
- Stroke
Steroid-related complications e.g., weight gain, diabetes and osteoporosis
61
Bulbar palsy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
62
Outline the main causes of bulbar palsy
- Brainstem stroke
- Brainstem tumours
- Guillain Barre syndrome
- Various genetic conditions
63
State the 3 parameters that doing the 'Romberg's test' will test
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
64
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
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
65
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)
Muscle mass = mildly decreased
Muscle strength = mildly decreased
Muscle tone = increased (spasticity)
Reflexes = increased (hyperreflexia)
Fasciculations (not present)
66
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)
Muscle mass = significantly decreased
Muscle strength = significantly decreased
Muscle tone = decreased (flaccid)
Reflexes = decreased (hyporeflexia)
Fasciculations (present)
67
State the 2 structures within the basal ganglia
1. Striatum (receives input from cortex)
2. Globus pallidus (sends output back to cortex)
68
Outline the main role of the basal ganglia and cerebellum
Basal ganglia = determine the most appropriate set of movements for a required task
Cerebellum = determine the ORDER of sequence for these movements
69
Outline the cardinal signs of Parkinson's disease
- Bradykinesia
- Tremor
- Rigidity
+ postural instability
70
Outline the cerebellar signs (think of mnemonic)
DANISH - cerebellar signs
Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
71
Outline whether damage to the following structures will produce ipsilateral or contralateral symptoms
- Basal ganglia lesion
- Cerebellar lesion
Basal ganglia lesion = contralateral signs
Cerebellar lesion = ipsilateral signs
72
List some functions of the frontal lobe
- Higher cognition / personality
- Motor (primary motor cortex)
- Express speech (Broca's area)
- Eye movements
- Continence
73
List some functions of the parietal lobes
- Sensation (somatosensory cortex)
- Formulate speech (Wernicke's area)
- Calculation and writing
- Attention to external environment
- Body image
(contains superior optic radiations)
74
List some functions of the temporal lobes
Special sensory!
- Hearing (primary auditory cortex)
- Smell (primary olfactory cortex)
- Memory
- Emotion
(contains optic radiations to visual cortex)
75
Outline the main role of the left and right sides of the brain
Left:
- Maths / logic
- Language
Right:
- Emotion
- Music
- Visuospatial awareness
- Body image
76
For Broca's area, state its location, main role and clinical picture if area becomes damaged
Location: inferior lateral frontal lobe
Role: production of speech
Damage presentation: unable to get words out easily (expressive aphasia)
77
For Wernicke's area, state its location, main role and clinical picture if area becomes damaged
Location: superior temporal lobe
Role: interpretation of speech
Damage presentation: speaking fine but making no sense (fluent aphasia)
78
Outline the 3 parameters of the glasgow coma scale
1. Motor movement
2. Verbal
3. Eye movement
79
For the 3 parameters of the glasgow coma scale, outline the scoring system
1. Motor movement
2. Verbal
3. Eye movement
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
Outline the possible GCS score range
3 (worst) to 15 (perfect)
81
List some risk factors for stroke (non-modifiable and modifiable)
Non-modifiable:
- Increased age
- Polycythaemia vera + other clotting disorders
- Atrial fibrillation
- Previous stroke / TIA
Modifable:
- Smoking
- HTN
- Hyperlipidaemia
- Diabetes
- Excess alcohol
- COCP
82
Outline some potential presenting features of an anterior cerebral artery stroke
- Contralateral limb weakness
- Contralateral sensory deficit
+ urinary incontinence
+ risk of alien hand syndrome
+ may have frontal lobe features e.g. personality change
83
Outline some potential presenting features of a (proximal) middle cerebral artery stroke
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
Outline some potential presenting features of a (distal) middle cerebral artery stroke
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
Outline some potential presenting features of a lenticulostriate artery stroke
(Variable presentation, varying in significance)
Purely motor deficit OR purely sensory deficit
86
Outline some potential presenting features of an posterior cerebral artery stroke
- Contralateral sensory loss (thalamus involvement)
- Contralateral homonymous hemianopia
87
Outline some potential presenting features of a cerebellar artery stroke
Ipsilateral DANISH symptoms
Dysdiadodyskinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
+ Contralateral sensory deficit
+ Ipsilateral Horner's syndrome
88
Outline signs seen in total anterior circulation (TAC) strokes
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
Outline signs seen in partial anterior circulation (PAC) strokes
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
Outline signs seen in posterior circulation (PoC) strokes
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
Epilepsy - state the following:
- Pathophysiology
- Investigations
- Management (very general long term)
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
State the definition of a seizure
Transient episodes of abnormal electrical activity in the brain
93
List some types of epileptic seizures in adults (and some more common in children)
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
Describe the presentation / features of a generalised tonic-clonic seizure
- 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
Describe the presentation / features of a partial (focal) seizure
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
Describe the presentation / features of a myoclonic seizure
- Sudden, brief muscle contractions (jump or jolt), limb, trunk, or face
- Remain awake
97
Describe the presentation / features of a tonic seizure
Only a few seconds-minutes
- Entire body stiffens (sudden onset of increased muscle tone)
- Patient usually falls if standing (backwards)
98
Describe the presentation / features of an atonic seizure (drop attacks)
- Sudden loss of muscle tone, often resulting in a fall
- Usually aware during episodes
Only last briefly
99
Describe the presentation / features of an absence seizure
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
List some differentials for seizures
- Pseudoseizures (non-epileptic attacks)
- Vasovagal syncope (fainting)
- Cardiac syncope (e.g. arrhythmias)
- Hypoglycaemia
- Hemiplegic migraine
- TIA / stroke
- Panic disorder
101
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)
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
List some side effects of sodium valproate
- Teratogenic
- Hair loss
- Tremor
- Reduce fertility
- Liver damage / hepatitis
103
Outline the key points from DVLA guidance for epilepsy
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
Migraine - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
List some potential triggers for migraines
- Stress
- Hormonal changes
- Changes in weather
- Certain foods
- Certain medications e.g. oral contraceptive
106
List some diagnostic factors to be able to diagnose migraines (ICHD criteria) in ABCDE format
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
State some differentials for migraines
- Other primary headache disorders e.g.tension-type headache, cluster headache
- Medication overuse headache
- Subarachnoid hemorrhage
- Giant cell arteritis
108
List the most common prophylactic medications for migraines
- Propranolol
- Amitriptyline
- Topimerate (anticonvulsant)
109
State the 5 criteria to fulfil for migraines
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
List the advice that should be given to a patient with overuse medication headaches
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
Idiopathic Parkinson's disease - state the following:
- Pathophysiology
- Presentation (3 cardinal features)
- Investigations
- Management
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
List some peripheral and central side effects of Levodopa medication for Parkinson's disease
Peripheral:
- Postural hypotension
- N&V
(Reduced by peripheral dopa decarboxylase inhibitor e.g. Carbidopa)
Central:
- Hallucinations / psychosis
- Confusion
- Dyskinesia (involuntary, erratic, writhing movements)
113
State some motor and non-motor features of Parkinson's disease
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
Outline the difference between Parkinson’s tremor
and benign essential tremor
- Asymmetrical vs symmetrical
- Frequency
- Worse when...
- Improved when...
- Change with alcohol
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
List some Parkinsonism conditions (not Parkinson's disease)
- Vascular parkinsonism
- Drug-induced parkinsonism
- Dementia with Lewy bodies
- Multiple system atrophy (MSA)
- Progressive supranuclear palsy
- Corticobasal degeneration
116
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
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
Motor neurone disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
List some subtypes of motor neurone disease
- Amyotrophic lateral sclerosis (ALS) = most common
- Progressive bulbar palsy
- Progressive muscular atrophy
- Primary lateral sclerosis
119
State the usual life expectancy for patients diagnosed with motor neurone disease
Less than 5 years from diagnosis - usually dying from respiratory complications
120
State what medications can be used in the management of motor neurone disease
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
Guillain Barre syndrome (GBS) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline some infections commonly associated with Guillain Barre syndrome (GBS)
- Epstein-Barr virus (EBV)
- Cytomegalovirus (CMV)
- Campylobacter jejuni
123
Suggest the general prognosis for Guillain Barre syndrome (GBS)
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
Myasthenia gravis (MG) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline a myasthenic crisis, how it might present and how it is managed
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
Muscular dystrophy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Multiple sclerosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
State the 3 main patterns of MS disease
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
List some potential risk factors that have been identified for multiple sclerosis (MS)
- Female (F:M = 2:1)
- Family history
- Vitamin D deficiency / latitude
- Smoking
- Obesity
- EBV (glandular fever)
130
List the most common presenting symptoms for multiple sclerosis (how they could present to GP)
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
Bell's palsy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline some risk factors / potential causes of idiopathic Bell's palsy
- History of recent infection (EBV, herpes zoster, herpes simplex)
- Diabetes mellitus
- HTN
- Sarcoidosis
133
List some differential diagnoses for Bell's palsy = unilateral facial weakness and paralysis
- 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
Dementia - state the following:
- Definition
- 4 main types (in order of frequency)
- Presentation
- Investigations
- Management
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
Carpal tunnel syndrome - state the following:
- Pathophysiology
- Presentation
- Special tests and investigations
- Management
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
Cubital tunnel syndrome - state the following:
- Pathophysiology
- Presentation
- Investigation and special tests
- Management
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
List some risk factors for carpal tunnel syndrome
Most commonly idiopathic
- Repetitive activities
- Pregnancy
- Obesity
- Diabetes
- Acromegaly
- Hypothyroidism
- Rheumatoid arthritis
138
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
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
Diabetic neuropathy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Cervical spondylosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Lumbar spondylosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline an essential tremor, including typical features of the tremor
- 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
Outline some differentials for a tremor
- Essential tremor
- Parkinson’s disease
- Huntington’s chorea
- Hyperthyroidism
- Multiple sclerosis
- Fever
- Anxiety
- Dopamine antagonists e.g. antipsychotics
144
Outline how an essential tremor is managed and 2 medications that can be used
No definitive treatment (not harmful and does not require treatment, unless causing functional or psychological problems)
Medications:
- Propranolol
- Primidone (anti-epileptic)
145
Outline some potential causes for the following types of tremor:
- Essential tremor (benign)
- Resting tremor
- Intention tremor (cerebellar)
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
For the following types of tremor:
- Essential tremor (benign)
- Resting tremor (Parkinson's)
- Intention tremor (cerebellar)
State...
1. Worse on
2. Better on
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
Radiculopathy - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
List some causes of radiculopathy
- 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
List some red flag conditions to consider in a patient presenting with radiculopathy symptoms
- Cauda equina syndrome
- Malignancy / metastatic disease
- Fracture
- Infection e.g. abscess
150
Subacute combined degeneration of the cord - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
State some complications if subacute combined degeneration of the cord is left untreated
- Neurological complications e.g. paraplegia or quadriplegia
- Bladder / bowel incontinence
- Congestive heart failure (from ongoing anaemia stress)
152
Outline what cranial nerves are affected in cavernous sinus syndrome and therefore how it presents
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
Pituitary tumours - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Wernicke-Korsakoff Syndrome - state the following:
- Pathophysiology
- Presentation
- Management
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
Describe an Argyll Robertson pupil and in which disease it is seen in
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
List the 4 main types of Creutzfeldt-Jakob disease
1. Sporadic (most common)
2. Variant (mad cow disease)
3. Familial (inherited)
4. Iatrogenic (contaminated cataracts / blood products)
157
Outline the pathophysiology of Creutzfeldt-Jakob disease and the main presenting symptoms
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
List 3 types of gliomas (from least malignant to most malignant)
1. Ependymoma
2. Oligodendroglioma
3. Astrocytoma (the most common and aggressive form is glioblastoma)
159
List 4 hormones that are usually secreted by pituitary tumours (functional tumours) and the conditions it leads to
1. Prolactin = hyperprolactinaemia
2. ATCH = Cushing's disease
3. GHRH = acromegaly
4. TSH = thyrotoxicosis
160
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
Generally:
- Transsphenoidal surgery
- Radiotherapy
Prolactin (hyperprolactinaemia):
- Bromocriptine to block excess prolactin
GHRH = acromegaly:
- Somatostatin analogues to block excess GH
161
Lambert-Eaton syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations
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
Charcot-Marie-Tooth Disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
List causes of peripheral neuropathy (ABCDE)
Alcohol
B12 deficiency
CKD and Cancer
Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
Every vasculitis
164
List some investigations to consider for patietns presenting with peripheral neuropathy
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
Normal pressure hydrocephalus - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline some of the management options for Huntington's disease
- Tetrabenazine (chorea)
- SSRIs (depression)
- Antipsychotics (psychosis)
- Supportive care (physical and emotional support)
