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Year 4 > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the risk factors for MS?

A
  • Female sex
  • Age 25-35
  • Family history
  • Latitude
  • EBV
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2
Q

Describe the two main types of MS

A

1) Relapsing/remitting - clear relapses followed by recovery (can become secondary progressive)
2) Primary progressive (about 10%)

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3
Q

Describe the potential clinical features of MS

A
  1. Sensory (most common presentation, first symptom in 40% people)
    - Numbness/coldness/pin and needles
    - Swelling/tightness
    - Vibration and proprioception loss
    - Lhermitte’s phenomenon
    - Optic neuritis
    - Pain on eye movement
    - Relative afferent pupillary defect
    - Uhtoff’s phenomenon
    - Leg weakness/paraplegia
    - UMN signs
    - Bladder/bowel/sexual dysfunction
    - Tremors
    - Double vision/nystagmus
    - Cranial nerve palsies
    - Dizziness
    - Dysarthria
    - Gait abnormalities/ataxia/impaired ambulation
    - Fatigue
    - Minor cognitive impairment
    - Epilepsy
    - Depression
    - Hallucinations/psychosis
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4
Q

How would you diagnose MS?

A

Two separate episodes of CNS demyelination separated in space and time - can be clinical diagnosis or imaging (MRI brain/spine, CSF)

Diagnosis is made using the McDonald Criteria 2017.

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5
Q

What would you expect to see in the lumbar puncture of a patient with MS?

A
  • Oligoclonal bands from antibodies

- Slightly elevated WCC

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6
Q

What condition may you suspect if there was oligoclonal bands present in the CSF but NOT the serum?

A

MS

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7
Q

What condition may you suspect if there was oligoclonal bands present in the CSF and the serum?

A
  • Neurosyphilis
  • Lyme disease
  • Behcet’s disease
  • SLE
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8
Q

What conditions would produce plaque lesions visible on MRI?

A 
MS
Old age
Cerebral ischaemia
Sarcoidosis
Behcet's syndrome
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9
Q

What differentials would you consider in a patient with suspected MS?

A

Optic neuritis
Spinal cord syndromes e.g. compression, vitamin B12 deficiency, HTLV-1 myelopathy, ALS
Brain stem syndromes e.g. tumour, encephalitis
Inflammatory disease e.g. SLE, sarcoid, Behcet’s
Infection e.g HIV, Lyme disease, syphilis

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10
Q

How would you assess the level of disability in a patient with MS?

A

Kurtzke disability status scale

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11
Q

What treatments could you consider for symptomatic relief in a patient with MS?

A

Accelerate recovery after relapse: IV methylprednisolone for 3 days
Relieve pain and treat depression: amitriptyline, Gabapentin
Reduce Lhermitte’s phenomenon or trigeminal neuralgia: Carbamazepine
Reduce tremor: stereotactic thalamotomy
Maximise function and reduce spasticity: physiotherapy/OT/speech therapy
Reduce spasticity: baclofen, dantrolene, tizanidine, botox
Reduce fatigue: amantadine, pemoline, modafinil
Reduce ataxia: isoniazid
Reduce unstable bladder symptoms: intermittent self-catheterisation
Reduce uncoordinated bladder symptoms: oxybutynin, tolterdoine
Treat erectile dysfunction: sildenafil
Constipation: bulking agents and stool softeners

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12
Q

What disease-modifying treatments could you consider in a patient with MS?

A 
Beta-inteferons 
Natalizumab
Glatiramer acetate
Daclizumab
Alemutzumab
Dimethyl fumarate
Teriflunomide
Fingolimod
Cladribine
Ocrelizumab
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13
Q

What monitoring would you do on a patient with MS being treated with beta-interferon?

A

LFTs

FBC

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14
Q

What are the side effects of beta-interferon?

A

Local irritation
Flu-like symptoms
Deranged LFTs

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15
Q

What are the side effects of Natalizumab?

A 
Dizziness
Itch
Rash
Shivering
Infection
PML
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16
Q

What MS treatments can cause PML?

A

Natalizumab
DImethyl fumarate
Fingolimod

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17
Q

What monitoring would you do on a patient with MS being treated with Natalizumab?

A 
FBC
LFT
U&E
JCV antibody ttest
MRI scan
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18
Q

What are the side effects of Glatiramer acetate?

A

Injection site reaction, lipoatrophy

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19
Q

What monitoring would you do on a patient with MS being treated with Glatiramer acetate?

A

None

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20
Q

What are the side effects of Daclizumab?

A

New autoimmune disease

Infection

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21
Q

What are the side effects of dimethyl fumarate?

A

Flushing
GI upset
Lymphopenia
PML

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22
Q

What monitoring would you do on a patient with MS being treated with Dimethyl fumarate?

A

FBC
LFTs
U&Es
MRI scan

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23
Q

What are the side effects of Teriflunomide?

A

GI upset
Hair thinning
Rash

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24
Q

What monitoring would you do on a patient with MS being treated with Teriflunomide?

A

FBC

LFTs

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25
Q

What are the side effects of Fingolimod?

A 
Bradycardia
Heart block
Infection
Lymphopenia
Liver dysfunction
PML
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26
Q

What monitoring would you do on a patient with MS being treated with Fingolimod?

A 
VZV screen
FBC
LFTs
BP
Eye and skin examination
MRI scan
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27
Q

What are the side effects of Cladribine?

A

Lymphopenia

Headache

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28
Q

What monitoring would you do on a patient with MS being treated with Cladribine?

A

FBC
LFT
TB, HIV, Hep B, VZV screen
MRI scan

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29
Q

What are the side effects of Alemutzumab?

A

Infusion reaction
Infection
Thyroid problems
Clotting disorders

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30
Q

What monitoring would you do on a patient with MS being treated with Alemutzumab?

A 
FBC
U&E
TFTs
VZV antibody
HPV, Hepatitis, FB screening
MRI scan
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31
Q

What are the side effects of Ocrelizumab?

A

Infusion reaction
Chest infection
Herpes infection

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32
Q

What monitoring would you do on a patient with MS being treated with Ocrelizumab?

A

FBC

Hep B screen

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33
Q

Which factors would indicate a better prognosis in a patient with MS?

A

Relapsing-remitting disease
Female sex
Sensory symptoms or optic neuritis at onset

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34
Q

Risk factors for stroke

A 
Hypertension
Diabetes
Smoking
Family history
High cholesterol
Excess alcohol intake
COCP
Obesity
Depression
Heart disease e.g. AF, MI, left ventricular dilatation
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35
Q

Define a stroke

A

A clinical syndrome characterised by acute onset neurological deficit due to dysfunction of the brain, caused by a problem with the blood supply, which does not resolve within 24 hours

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36
Q

What percentage of strokes are ischaemic?

A

85%

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37
Q

Define a TIA

A

A clinical syndrome characterised by acute onset neurological deficit due to dysfunction of the brain, caused by a problem with the blood supply, which resolves within 24 hours

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38
Q

What are the causes of intracerebral haemorrhage

A

Hypertension
Charcot-Bouchard aneurysms
Arteriovenous malformation
Bleeding disorders

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39
Q

Where do intracerebral haemorrhages most commonly occur?

A

Basal ganglia (50%)
Lobar white matter (20%)
Pons (10%)
Cerebellum (10%)

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40
Q

Which features in a history would make you suspect a patient had a TACI stroke?

A 
Rapid onset
Hemiparesis affecting face, arm and leg
Homonymous hemianopia
Drowsiness
Complete aphasia (if dominant side affected)
Inattention/neglect (if non-dominant side affected)
Transient dysarthria
Impaired swallowing
Incontinence
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41
Q

Which features in a history would make you suspect a patient had a PACI stroke?

A

MCA inferior branch infarction:
Hemianopia
Wernicke’s aphasia (if dominant side affected)
Constructional aphasia (if non-dominant side affected)

MCA superior branch infarction:
Hemiparesis
Broca’s aphasia (if dominant side affected)
Neglect (if non-dominant side affected)

MCA distal branch infarction:
Weakness of one limb
Isolated higher function deficit

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42
Q

Which features in a history would make you suspect a patient had a POCI stroke?

A

Large vessel syndrome:
Contralateral hemisensory homonymous hemianopia
Contralateral hemisensory loss
Higher function disturbance

Basilar artery occlusion:
Locked in state

Vertebral artery occlusion:
No deficit OR
Nystagmus
Dysarthria
Diplopia
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43
Q

Which features in a history would make you suspect a patient had a LACI stroke?

A

Internal capsule lesion:
Face, arm and leg weakness

Posterior internal capsule, midbrain or pons lesion:
Motor hemiparesis with cerebellar type ataxia on ipsilateral side

Thalmic lesion:
Hemisensory loss

Dysarthria
Tongue/face weakness
Hand clumsiness

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44
Q

Which features in a history would make you suspect a patient had an anterior circulation TIA?

A

Amaurosis fungax (fleeting blindness in one eye)
Aphasia
Dyslexia
Dysgraphia
Unilateral weakness or sensory loss in face, arm or leg

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45
Q

Which features in a history would make you suspect a patient had a posterior circulation TIA?

A

Homonymous visual field loss
Dysarthria
Combined brain stem symptoms
Bilateral or unilateral weakness or sensory loss in face, arm or leg

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46
Q

What investigations would you consider in a patient with a suspected stroke?

A

1) MRI/CT SCAN

2) Risk factors for atheroma:
- BP
- Blood glucose
- Cholesterol
- TFTs
- LFTs

3) Sources of embolism
- ECG
- Echo
- Blood cultures
- 24-hour tape
- Carotid doppler, angiogram or MRI angiography

4) Causes of thrombosis
- FBC
- Thrombophilia screen
- Sickle cell screen

5) Causes of inflammatory vascular disease
- ESR
- ANA, anticardiolipin antibodies
- Syphilis serology
- Temporal artery biopsy

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47
Q

Which factors worsen the outcome for a stroke patient?

A

Hypoxia
Hyperglycaemia
Over-hydration

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48
Q

What might you find on examination and investigation of a patient with a TIA?

A

No neurological abnormality

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49
Q

What would you do if a patient presented with a suspected stroke?

A

1) CT/MRI scan (within an hour)
2) Thrombolysis with alteplase within 4 hours
3) CT angiogram
4) Consider thrombectomy within 6 hours of onset
5) Aspirin 300mg

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50
Q

What are the indications for doing a CT/MRI scan in a patient with a suspected stroke?

A
  • Indication for thrombolysis or early anticoagulant treatment
  • On anticoagulants
  • Known bleeding tendency
  • GCS <13
  • Unexplained progressive or fluctuating symptoms
  • Papilloedema, neck stiffness or fever
  • Severe headache at onset of symptoms
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51
Q

What are the contra-indications to treating a stroke patient with alteplase?

A
  • Surgery within 2 weeks
  • Ischaemic stroke within 3 months
  • Significant trauma
  • INR >1.5
  • On anticoagulants
  • No motor deficit
  • Symptom onset >4 hours
  • Impaired consciousness
  • Recent eplieptic seizure
  • History of intra-cranial haemorrhage
  • Pregnant or delivered within 15 days
  • Lumbar puncture or ABG within 7 days
  • BP >185/110
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52
Q

What are the indications for a decompressive hemicraniectomy in a stroke patient?

A
  • Age <60
  • Clinical deficits suggestive of MCA infarction, NIHSS score >15
  • Decrease in consciousness
  • Signs of infarct of >50% of MCA territory on CT scan
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53
Q

How would you prevent a second stroke?

A
  • Smoking cessation
  • Reduce alcohol intake
  • Aspirin 300mg for 2 weeks + clopidogrel/dipyridamole
  • Anticoagulation (Apixiban)
  • Antihypertensives
  • Good glycaemic control
  • Lower cholesterol (statin)
  • Symptomatic Carotid endarectectomy
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54
Q

Complications of stroke

A 
Raised intracranial pressure and herniation
Aspiration pneumonia
Contractures
DVT
Bed sores
UTI
Constipation
Depression
Epilepsy
Thalmic pain
Social problems
Financial problems
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55
Q

What screening tests could you use in a patient with confusion?

A
  • Addenbrooke’s Cognitive Assessment (ACE-III)
  • Mini-Mental State Examination
  • Clock Drawing Test
  • Mini-Cog
  • Time and Change
  • 7-Minute Screen
  • Abbreviated Mental Test
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56
Q

What investigations would you consider in a patient with confusion/delirium?

A

1) Evidence of biological derangement
- FBC
- U&Es
- TFTs
- B12/folate levels
- LFTs
- Inflammatory markers
- Syphilis/HIV screen
- Glucose
- ABG

2) Infection screen
- Urine/sputum culture

3) Radiology
- CXR
- CT/MRI head

4) Specialised blood tests
- Autoimmune/vasculitis screen
- Paraneoplastic onconeural antibodies
- Autoimune encephalitic antibodies (VGKC and NMDA receptor)

5) EEG
6) Lumbar Puncture

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57
Q

List some potential causes of delirium

A
  • Hyper/hyponatremia
  • Hypercalcemia
  • Hypoglycaemia
  • Hepatic failure
  • Hypothyroidism
  • Drugs - antiparkinsonian medications, recreational drugs, alcohol, alcohol withdrawal
  • Infection - sepsis, UTI, meningitis, encephalitis, pneumonia, malaria
  • Epilepsy
  • SLE
  • Limbic encephalitis
  • Stroke
  • Subarachnoid haemorrhage/subdural haematoma
  • Trauma
  • Hydrocephalus
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58
Q

What are the 4 defining features of delirium

A 
1) Acute onset and fluctuating symptom course
AND
2) Inattention
AND
3) Disorganised thinking
OR
4) Altered level of consciousness
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59
Q

List the clinical features of delirium

A 
Alterations in arousal
Fluctuating attention
Distracted
Disorganised thinking
Slow responses, going off on tangents
Slurred speech
Hallucinations
Disputed sleep
Slow movements
Short-term memory loss
Emotional instability
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60
Q

What differentials would you consider in a patient with suspected delirium?

A
  • Dementia
  • Aphasia
  • Schizophrenia/psychosis
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61
Q

List the 3 key features of dementia

A

1) Progressive decline
2) Acquired widespread loss of mental function in >1 cognitive domain
3) in clear consciousness

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62
Q

List the clinical features of dementia

A
  • Memory loss
  • Language impairment
  • Disorientation
  • Abstract thinking
  • Personality changes
  • Psychiatric symptoms
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63
Q

What investigations would you consider in a patient with suspected dementia?

A
  • CT/MRI head (loss of tissue, wide sulk, large ventricles)
  • FBC and ESR
  • LFTs
  • U&Es
  • TFTs
  • Vitamin B12 and folic acid
  • Syphilis serology
  • Neuropsychological assessment
  • EEG
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64
Q

Describe the pathophysiology of Alzheimer’s disease

A
  • 70% of all dementias
  • Insidious onset and progressive gradual decline
  • Extracellular neuritic beta amyloid plaques
  • Intracellular neurofibrillary tangles
  • Cholinergic system degerneation and neuron loss
  • Cerebral atrophy, particularly in the temporal lobes
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65
Q

List the 3 stages that Alzheimer’s disease commonly presents with

A

1) Memory disturbance
2) Global cognitive decline with relatively intact personality
3) Severe global decline with disorders of social behaviour and function

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66
Q

List the clinical features of Alzheimer’s disease

A
  • Short-term memory loss
  • Language difficulties
  • Praxis
  • Visuospatial difficulties
  • Executive functioning difficulties
  • Behavioural changes
  • Anosognia
  • Depression
  • Delusions/hallucinations
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67
Q

What might you find on examination of a patient with Alzheimer’s disease

A

Gegenhalten pattern of increased tone

Relapse of primitive reflexes

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68
Q

What treatment could you consider in a patient with Alzheimer’s disease?

A
  • Central cholinesterase inhibitors (donepezil, galantamine, rivastigmine)
    OR
  • NMDA-receptor antagonists (Memantine)
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69
Q

Risk factors for vascular dementia

A
  • Smoking
  • AF
  • Diabetes
  • Hypertension
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70
Q

List the 5 sub-types of front-temporal dementia

A
  1. Behavioural variant FTD
  2. Primary progressive aphasia
  3. Semantic dementia
  4. Progressive non-fluent aphasia
  5. FTD-MND
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71
Q

List the clinical features of fronto-temporal dementia

A
  • Behaviour and personality changes
  • Lack of insight
  • Progressive memory deficit
  • Variable movement disorders
  • Language impairment
  • Hyperorality
  • Perservation
  • Hypersexual behaviour
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72
Q

Describe the pathology of Lewy Body dementia

A

Lewi bodies in the cerebral cortex

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73
Q

Clinical features of Lewy Body dementia

A
  • Fluctuations in mental state
  • Early delusions and hallucinations
  • Mild extrapyramidal signs
  • Neuroleptic hypersensitivity
  • Unexplained falls/transient changes in consciousness
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74
Q

List the risk factors for a patient with Parkinson’s developing dementia

A
  • Age >70
  • Depression
  • Confusion/psychosis on Levadopa
  • Facial masking at presentation
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75
Q

List some potentially reversible causes of dementia

A
  • Drug toxicity
  • Metabolic disturbance
  • Autoimmune/paraneoplastic encephalopathy
  • Mass/lesions
  • Infection (meningitis, syphilis)
  • Inflammatory disorders (SLE, sarcoid)
  • Endocrine disorders (thyroid, parathyroid)
  • Nutritional disease (B12, thiamine, folate)
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76
Q

List the clinical features of Horner’s syndrome

A
  • Ptosis (may be partial)
  • Miosis
  • Anhydrosis
  • Enopthalmos (eye looks sunken)
  • (different colour pupils - only in congenital Horner’s or lesions in young children)
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77
Q

Describe the pathology of Horner’s syndrome

A

A lesion in the sympathetic trunk

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78
Q

List the causes of Horner’s syndrome

A
  • Idiopathic
  • Pancoast tumours
  • Neuroblastoma (paediatric)
  • Neck/eye/cerebellar tumours
  • Stroke
  • Migraine/cluster headache
  • Internal carotid dissection/thrombosis
  • Birth trauma to shoulder/neck
  • Arnold-Chiari malformation
  • Demyelinating disease - MS, Guillain-Barre syndrome
  • Inflammatory disease
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79
Q

What investigations would you consider in a patient with suspected Horner’s syndrome?

A
  • CXR
  • CT/MRI head
  • Carotid doppler
  • Bloods
  • Cerebral angiogram
  • LP
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80
Q

What is the treatment for Horner’s syndrome?

A

No treatment available - treat underlying disease

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81
Q

Describe the pathophysiology of Parkinson’s disease

A

Loss of dopaminergic cells in the substantia nigra caused by Lewy bodies

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82
Q

Which drugs can induce Parkinsonism?

A
  • Chlorpromazine/prochlorperazine
  • Phenothiazines
  • Antipsychotics
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83
Q

Describer the 4 cardinal features of Parkinson’s

A
  1. Resting tremor
  2. Rigidity
  3. Bradykinesia
  4. Postural instability
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84
Q

Describe the clinical features of Parkinson’s disease

A
  • Insidious onset and gradually progressive symptoms
  • Often unilateral at presentation
  • Resting tremor (coarse and slow, usually affecting the hands, pill-rolling tremor)
  • Cogwheel rigidity
  • Bradykinesia
  • Postural instability - stooped posture with flexed elbows
  • Difficulty in fine movement e.g. writing
  • Fatigue
  • Lack of facial expression
  • Slowed blink rate
  • Dysrathria - monotonous voice which trails off
  • Micrographia
  • Loss of arm swing
  • Shuffling gait
  • Difficulty starting or stopping movements
  • Altered higher function
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85
Q

What differentials would you consider in a patient with suspected Parkinson’s disease

A
  • Drug-induced Parkinson’s
  • Essential tremor (not present at rest, more prominent on sustained posture or movement)
  • Wilson’s disease (in younger patients)
  • Lewy Body dementia (in patients with loss of higher function and prominent hallucinations on low dose therapy)
  • Unilateral hemiparesis
  • Depression
  • Diffuse cerebrovascular disease
  • Normall pressure hydrocephalus
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86
Q

How would you diagnose Parkinson’s disease?

A

Clinical diagnosis - Bradykinesia, rigidity, tremor, postural instability

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87
Q

What investigations could you consider in a patient with suspected Parkinson’s disease with diagnostic uncertainty?

A
  • CT/MRI head (look for normal pressure hydrocephalus or small vessel disease)
  • Trial of dopaminergic drugs
  • DAT scan
  • Test eye movements and standing/lying BP
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88
Q

How would you treat a patient with Parkinson’s who was under 70 years old?

A

1) Amantadine OR selegiline/rasagiline
2) Dopamine agonists (Bromocriptine, lisuride, pergolide OR carbergoline, apomorphine, ropinirole, pramipexole, rotigotine)

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89
Q

How would you treat a patient with Parkinson’s who was over 70 years old?

A

1) Amantadine OR selegiline/rasagiline

2) Levodopa preparations (Sinemet or Madopar)

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90
Q

Side effects of Sinemet or Madopar

A
  • Wearing off
  • Dyskinesia
  • Impulsive/compulsive behaviour
  • GI upset e.g. nausea
  • Hypotension
  • Psychological problems
  • Withdrawal
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91
Q

What anti-emetic would you use to treat nausea in a patient with Parkinson’s?

A

Domperidone

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92
Q

Side effects of dopamine agonists (bromocriptine, carbergoline)

A
  • Cardiac valvular fibrosis, pulmonary fibrosis, abdominal fibrosis (requires monitoring)
  • Nausea
  • Dizziness
  • Confusion
  • Sudden bouts of sleepiness
  • Altered behaviour e.g. gambling, hyper-sexuality
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93
Q

Side effects of dopamine-releasing agents (amantadine)

A
  • Dizziness, falls
  • Dry mouth
  • Peripheral oedema
  • GI upset
  • Insomnia
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94
Q

Side effects of monoamine oxidase B inhibitors (Selegiline, Rasagiline)

A
  • Dizziness, falls
  • Dry mouth
  • Peripheral oedema
  • GI upset
  • Insomnia
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95
Q

Benefits of Amantadine or selegiline/rasagiline

A

Smooth out delivery of levodopa

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96
Q

Side effects of Co-methyl transferase (COMT) inhibitors e.g. Entacapone

A
  • Behavioural disturbances
  • Stiff muscles
  • Fever, sweating
  • Tachycardia
  • Tremors
  • Diarrhoea
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97
Q

What is an effective treatment option for patients with tremor caused by Parkinson’s?

A

Anticholinergics (Procyclidine or benzotropine)

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98
Q

Benefits of anticholinergics in Parkinson’s disease

A
  • Effective in mild, early tremor

- Effective in salivary drooling

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99
Q

Side effects of anticholinergics (procyclidine or benzotropine)

A
  • Drowsiness
  • Dry mouth
  • Dizziness
  • GI upset
  • Flushing
  • Blurred vision
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100
Q

List 3 complications of long-term treatment of Parkinson’s disease

A

1) Fluctuations
2) Dyskinesia
3) Drug failure

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101
Q

How could you deal with fluctuations in control of Parkinson’s disease?

A
  • Increase dose frequency
  • Add selegiline, COMT inhibitor or a dopamine agonist
  • Change to a controlled release form of Levodopa
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102
Q

How would you deal with a dyskinesia caused by treating Parkinson’s disease?

A
  • Add selegiline/rasagiline, dopamine agonist or amantidine

- Reduce dose of levodopa

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103
Q

Name 2 common forms of ‘Parkinson’s plus syndromes and their symptoms

A

1) Multisystem atrophy - autonomic failure, cerebellar signs, UMN signs
2) Progressive supranuclear palsy/Steele-Richardson syndrome - reduced ability to move eyes voluntarily, loss of postural reflexes and dsyrrthria

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104
Q

Diagnostic criteria for a TACS stroke

A

ALL of

1) Total hemiparesis and/or hemiparathesis
2) Higher function dysfunction e.g. cognitive impairment, dysphasia, visuo-spatial defects (visual neglect, tactile neglect)
3) Homonymous hemianopia

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105
Q

Diagnostic criteria for a PACS stroke

A

2 of:

1) Total hemiparesis and/or hemiparathesis
2) Higher function dysfunction e.g. cognitive impairment, dysphasia, visuo-spatial defects (visual neglect, tactile neglect)
3) Homonymous hemianopia

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106
Q

Diagnostic criteria for a LACS stroke

A

1 of:

1) Total hemiparesis and/or hemiparathesis
2) Higher function dysfunction e.g. cognitive impairment, dysphasia, visuo-spatial defects (visual neglect, tactile neglect)
3) Homonymous hemianopia

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107
Q

Diagnostic criteria for a POCS stroke

A

Signs of:

1) Cerebellar signs
2) Cranial neuropathy
3) Isolated hemianopia
4) Bilateral motor/sensory loss
5) Conjugate eye movements

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108
Q

What is the most common cause of headache seen in general neurology clinic?

A

Chronic daily headache syndrome with angles excess

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109
Q

How would you treat an acute migraine attack?

A

1) 300-900mg of aspirin at start of attack

2) Triptan (if not relieved by aspirin)

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110
Q

How could you prevent migraines?

A

1) Propanolol
2) Topiramate
3) Amitryptilline
4) Nortriptylline
5) Candesartan
6) Botulin toxin
7) Sodium valproate in men

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111
Q

Risk factors for functional disorders

A
  • Female
  • Young
  • History of abuse/trauma
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112
Q

Which features in a history would make you suspect a functional disorder?

A
  • Long list of symptoms
  • History of previous functional symptoms
  • Dissociative symptoms
  • Emotional symptoms
  • History of deliberate self-harm or drug overdose
  • ‘Belle indifference’
  • Collapsing weakness
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113
Q

What general features should you ask about in a patient with suspected functional disorder?

A
  • Pain
  • Fatigue
  • Sleep disturbance
  • Memory and concentration problems
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114
Q

Describe the main features which would differentiate a pseudo-seizure from an epileptic seizure?

A
  • Semi-purposeful thrashing
  • No cyanosis
  • Normal respiration
  • No tongue biting
  • No incontinence
  • Feeling ‘crazy’
  • Numbness and tingling
  • Sweating
  • Shortness of breath
  • Heart racing
  • Chest pain
  • Gradual onset
  • Asynchronous limb movements
  • Side to side head shaking
  • Closed eyelids, resistant to opening
  • Retained pupillary light reflex
  • Convulsions >2 mins
  • Quick post-ictal recovery
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115
Q

What investigations would you consider to diagnose pseudo-seziures?

A

1) EEG during attack - must be NORMAL

2) Post-seizure prolactin - will be raised 15-20 mins after a tonic-clonic epileptic seizure

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116
Q

Which features would differentiate functional paralysis from true paralysis?

A
  • Inconsistency of power in formal testing and during general use
  • Collapsing weakness
  • Co-contraction
  • Slow and jerky arm drop test
  • Positive Hoover’s sign
  • Normal plantar response
  • Normal movement restored when using hypnosis or sedatives
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117
Q

Clinical features of functional weakness of the face

A
  • Persistently depressed eyebrow
  • Variable inability to elevate frontalis
  • Over-activity of orbicular
  • Photophobia
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118
Q

What are the general features common to all functional movement disorders?

A
  • Rapid onset
  • Variability in frequency, amplitude or distribution
  • Improvement with distraction/worsening with attention
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119
Q

How would you make a diagnosis of functional movement disorder?

A
  • Complete remission demonstrated after admission of general anaesthetic
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120
Q

What are the general features of a functional gait disturbance?

A
  • Variability
  • Improvement with distractions
  • Excessive slowness
  • Falling towards/away from the doctor
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121
Q

Describe the typical patterns of functional gait disturbance

A
  • ‘Walking on ice’ pattern - cautious, broad base, decreased stride length and height, stiff knees and ankles, arms abudcuted)
  • Uneconomic postures with waste of muscle energy (flexed knees/hips)
  • Sudden knee buckling
  • Pseudo-ataxia (crossed legs, unsteady gait, sudden side steps)
  • Dragging gait
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122
Q

What are the general features of a functional sensory loss?

A
  • Non-recognisable pattern
  • Complete sensory loss in all modalities
  • Inconsistencies in repeat testing
  • Discrepancies in functional loss
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123
Q

Describe the clinical features of hemi-sensory syndrome

A
  • Intermittent visual blurring in ipsilateral eye
  • Ipsilateral hearing problems
  • Chronic generalised and regional pain
  • ‘Midline splitting’ of sensory loss
  • Differences in sensation at sternum
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124
Q

Describe the main clinical feature of functional visual loss

A

‘Tube’ field loss

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125
Q

Describe the clinical features of physiologically-induced bodily sensations or the physical symptoms of anxiety

A
  • Dizziness/light-headedness
  • Tingling in hands, feet and around mouth
  • Some visual disturbances
  • Loss of consciousness
  • Reduced breath holding time
  • Symptoms reproduced on forced hyperventilation
  • Tremor
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126
Q

Describe the clinical features of chronic fatigue syndrome

A
  • Female
  • Sore throat
  • Low-grade fever
  • Joint and muscle pain
  • Headache
  • Poor concentration
  • Sleep disturbances
  • Features of depression
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127
Q

Define chronic fatigue syndrome

A

Disabling fatigue lasting >6 months where no other medical cause has been found

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128
Q

How would you treat chronic fatigue syndrome?

A
  • Tricyclic antidepressants
  • Graded exercise
  • CBT
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129
Q

Describe the clinical features of fibromyalgia

A
  • Prominent muscle aching
  • Fatigue
  • Arthralgia
  • Malaise
  • Sleep disturbances
  • Headache
  • No abnormality on examination except some muscle tenderness
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130
Q

How would you treat fibromyalgia?

A
  • Tricyclic antidepressants
  • Graded exercise
  • CBT
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131
Q

Define a seizure

A

Paroxysmal neurological event caused by abnormal discharge of neurons

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132
Q

Define epilepsy

A

Tendency to recurrent seizures

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133
Q

List the 4 types of focal seizures

A

1) Simple partial
2) Complex partial (with loss of consciousness)
3) Secondary generalised
4) Focal status epilepticus

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134
Q

Describe the typical clinical features of a generalised seizure

A
  • Usually starts in childhood/adolesence

Clusters of tonic-clonic, absence and myclonic jerks

  • Generalised stiffness (tonic)
  • Repeated generalised jerking (clonic)
  • Intermittent symmetrical jerks (myoclonic)
  • Absence with no focal symptoms
  • Atonic drop attacks

Characteristic EEG signature

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135
Q

Describe the typical clinical features of a focal seizure

A
  • Occurs at any age
  • May be associated with structural brain disease
  • May be post-ictal confusion and automatisms
  • Inter-ictal EEG may show localised spikes or sharp waves
  • Focal limb jerking (motor cortex)
  • Focal tingling (somatosensory cortex)
  • Olfactory or gustatory hallucination (temporal lobe)
  • Visual hallucination (occipital lobe)
  • Limb posturing (supplementary motor area)
  • Swallowing/chewing movements (temporal lobe/insula)
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136
Q

What can provoke a seizure?

A
  • Metabolic disturbance e.g. renal/liver failure
  • Drugs
  • Alcohol
  • Alcohol withdrawal
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137
Q

What differentials would you consider in a patient presenting with suspected epilepsy?

A
  • Vasovagal syncope
  • Dissociative attacks
  • Sleep disorders
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138
Q

Define status epilepticus

A

Seizures occurring for >30 minutes without recovery (either continuously or intermittently)

(>5 minutes of continuous seizure or >2 seizures without complete resolution in between)

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139
Q

What are the potential secondary manifestations of status epilepticus?

A
  • Hypoxia
  • Acidosis
  • Myoglobulinuria
  • Renal failure
  • Disseminated intravascular coagulation
  • Hyperthermia
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140
Q

What are the indications for further investigation in a patient who has had a single seizure?

A

> 20 years old
Younger patients with clinical or EEG evidence of focal seizures
Seizures which are difficult to control

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141
Q

What investigation would you perform (if indicated) in a patient with a single seizure?

A

CT/MRI head

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142
Q

How would you diagnose epilepsy?

A
  • Clinical diagnosis - 2 or more spontaneous seizures

- May be supported with EEG (but mainly for classification)

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143
Q

When can a patient with epilepsy safely drive again?

A

After they have been seizure free for 2 years

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144
Q

When would you commence patients on anti-epileptic therapy?

A

When a person has suffered two or more seizures within 2 years

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145
Q

What treatment would you recommend for focal epilepsy?

A

1) Lamotrigine

2) Carbamazepine or Levetiracetam

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146
Q

Side effects of lamotrigine

A
  • Sedation
  • Diplopia
  • Ataxia
  • Rash
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147
Q

Benefit of lamotrigine

A

Lower risk of teratogenicity

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148
Q

Side effects of Carbamazepine

A
  • Sedation
  • Diplopia
  • Ataxia
  • Rash
  • GI upset
  • Weight gain
  • Teratogenicity
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149
Q

When is Carbamazepine contra-indicated?

A
  • Women of child-bearing age
  • Not well tolerated in the elderly
  • Hepatic enzyme inducer (increases COCP elimination)
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150
Q

Side effects of Levetiracetam

A
  • Sedation

- Mood disturbance

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151
Q

What treatment would you recommend for a patient with general epilepsy?

A

1) Sodium valproate OR lamotrigine

2) Topiramate OR lecetiracetam

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152
Q

Side effects of sodium valproate

A
  • Sedation
  • GI upset
  • Weight gain
  • Reversible hair loss
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153
Q

Side effects of lamotrigine

A
  • Sedation
  • Diplopia
  • Ataxia
  • Rash
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154
Q

When would sodium valproate be contra-indicated?

A

Women of child-bearing age

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155
Q

Benefits of sodium valproate

A

Favoured in the elderly as lower risk of ataxia and falls (than Carbamazepine)

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156
Q

Side effects of Topiramate

A
  • Sedation

- Weight loss

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157
Q

When would topiramate be conta-indicated

A

Women of child-bearing age

also a hepatic enzyme inducer

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158
Q

Which epilepsy patients would you consider neurosurgery in?

A

Patients with:

  • Focal onset seizures
  • Not controlled by medication
  • Epilepsy demonstrated to originate in single part of brain which could be removed without any major neurological deficit
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159
Q

How would you treat status epilepticus?

A

1) Benzodiazepam e.g. Lorazepam/Diazepam IV OR diazepam PR or midazolam buccal
2) Repeat benzodiazepine
3) Loading dose of Phenytoin IV OR sodium valproate IV
4) Admit to ITU

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160
Q

What features in a history would make you suspect a diagnosis of tension headache?

A
  • Continuous or episodic pain
  • Tight, dull band pain/pressure around the head
  • Pain lasts 30 mins-7 days
  • Triggers: stress, fatigue
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161
Q

What features in a history would make you suspect a diagnosis of medication overuse headache?

A
  • Chronic headache >15 days per month

- Regular overuse >3 months of codeine, triptans, caffeine, paracetamol

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162
Q

What features in a history would make you suspect a diagnosis of migraine?

A
  • Episodic unilateral throbbing headache over the temples
  • Lasts 4-72 hours
  • Relieved by sleep
  • Triggers: cheese, chocolate, coffee, red wine, lying in, relaxation/stress relief, hormonal changes, COCP, menstruation
  • Worsened by activity
  • Associated symptoms: nasa, photophobia, phonophobia, aura
  • Premonitory symptoms 24 hours before headache - mood swings, hunger, drowsiness
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163
Q

What features in a history would make you suspect a diagnosis of cluster headache?

A
  • Severe unilateral retro-orbital pain
  • Lasts 15 mins-3 hours
  • Occurs once or more per day for several weeks before subsiding
  • Associated symptoms: red eye, lacrimation, nasal stuffiness, ptosis, Horner’s syndrome, restlessness, forehead/facial sweating
  • Triggered by alcohol
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164
Q

What features in a history would make you suspect a diagnosis of sinusitis?

A
  • Tender frontal and maxillary sinuses

- Associated symptoms: fever, nasal discharge

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165
Q

What features in a history would make you suspect a diagnosis of trigeminal neuralgia?

A
  • Sudden severe pain lasting seconds-minutes followed by a dull ache
  • Occurs in bouts many times each day
  • Triggers: touch, movement (brushing teeth, eating, speaking), cold
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166
Q

How would you treat a tension headache?

A
  • Relaxation exercises

- Amitryptilline

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167
Q

How would you treat medication overuse headache?

A
  • Withdraw analgesics
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168
Q

How would you treat cluster headaches?

A

1) Oxygen
2) Sumatriptan injections
3) Steroids
4) Verapamil

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169
Q

How would you treat trigeminal neuralgia?

A

1) Carbamazepine
2) Glycerol injections, electrical lesion
3) Surgical decompression

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170
Q

What features in a history would make you suspect a diagnosis of subarachnoid haemorrhage?

A
  • Sudden severe headache at back of head, lasting >1 hour

- Associated symptoms: loss of consciousness, seizures, focal neurological signs, neck stiffness, vomiting

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171
Q

What features in a history would make you suspect a diagnosis of temporal arteritis?

A
  • Typical patient >50 years old, female, associated with PMR
  • Insidious onset
  • Bitemporal pain
  • Associated symptoms: jaw claudication, scalp tenderness
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172
Q

What features in a history would make you suspect a diagnosis of meningitis?

A
  • Progressive headache developing over hours/days

- Associated symptoms: fever, neck stiffness, rash, impaired consciousness

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173
Q

What features in a history would make you suspect a diagnosis of raised intra-cranial pressure?

A
  • Generalised headache triggered/worsened by coughing, bending over or lying down
  • Headache worse in morning
  • Associated symptoms: vomiting, false localising signs (nerve palsies), papilloedema, altered consciousness
  • Varying time course
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174
Q

What features in a history would make you suspect a diagnosis of idiopathic intracranial hypertension?

A
  • Young, obese women
  • Caused by tetracycline
  • Generalised headache triggered/worsened by coughing, bending over or lying down
  • Associated symptoms: machinery noise in the ears
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175
Q

What features in a history would make you suspect a diagnosis of cranial venous sinus thrombosis?

A
  • Causes: COCP, dehydration, clotting abnormalities, ear infections
  • Generalised headache worsened/triggered by coughing, bending over, lying down
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176
Q

What features in a history would make you suspect a diagnosis of carotid arterial dissection?

A
  • Sudden onset head or neck pain
  • Associated Horner’s syndrome
  • Associated TIA/stroke
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177
Q

What investigations would you do in a case of suspected subarachnoid haemorrhage, and what would they show?

A
  • Fundoscopy (papilloedema)
  • CT
  • CT angiography
  • Lumbar puncture - elevated RBC, WCC and bilirubin (after 12 hours)
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178
Q

What investigations would you do in a case of suspected temporal arteritis, and what would they show?

A
  • Inflammatory markers - elevated CSR

- Temporal artery biopsy

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179
Q

What investigations would you do in a case of suspected idiopathic intracranial hypertension, and what would they show?

A
  • MRI
  • MR venography
  • Lumbar puncture - increased ICP with normal CSF constituents
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180
Q

What investigations would you do in a case of suspected cranial venous sinus thrombosis, and what would they show?

A
  • MR venography
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181
Q

How would you treat a patient with suspected idiopathic intracranial hypertension

A
  • Lumbar puncture
  • Acetazolamide
  • Weight loss
  • Surgical drainage through lumboperitoneal drainage
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182
Q

How would you treat a patient with suspected cranial venous sinus thrombosis?

A
  • Anticoagulants
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183
Q

What features in a history would make you suspect a diagnosis of subarachnoid haemorrhage?

A
  • 40-60 years old
  • Sudden severe generalised headache - ‘hit by bat on back of head’
  • Transient loss of consciousness, drowsiness or coma
  • Vomiting
  • Neck stiffness
  • Focal neurological signs
  • Hypertension
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184
Q

Describe the pathophysiology os subarachnoid haemorrhage

A
  • Most result from ruptured saccular intracranial haemorrhage in the circle of Willis
  • 5% caused by arteriovenous malformation
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185
Q

What differentials would you consider in a patient with suspected subarachnoid haemorrhage?

A
  • Thunderclap headache

- Meningitis

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186
Q

What investigations would you request in a patient with suspected subarachnoid haemorrhage?

A

1) CT head
1a) Lumbar puncture at least 6 hours after onset (if CT negative) - would be blood stained with xanthochromic supernatant
2) 4-vessel cerebral angiogram OR MRI/CT angiography

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187
Q

How would you manage a patient with subarachnoid haemorrhage?

A

1) Transfer to neurosurgical centre
2) Frequent neurological observations
3) Endovascular occlusion of the aneurysm OR surgical clipping
4) Sustained hypervolaemia (3l of normal saline per day) + nimodipine (to prevent ischaemic complications caused by vasospasm)

Fludrocortisone OR hypertonic saline to treat hyponatremia
Drainage used to treat hydrocephalus

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188
Q

Which group of drugs are contra-indicated in patients with a subarachnoid haemorrhage

A

Anti-hypertensives

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189
Q

Complications of subarachnoid haemorrhage

A
  • Re-bleeding from a ruptured aneurysm
  • Cerebral ischaemia
  • Hydrocephalus
  • Hyponatremia
  • Neurogenic pulmonary oedema
  • Cardiac arrhythmias
  • Bedrest complications: DVT, aspiration/basal pneumonia
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190
Q

How would complications of a subarachnoid haemorrhage present?

A
  • Deterioration in consciousness and focal neurological signs
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191
Q

How would you investigate a patient with suspected subarachnoid haemorrhage complications

A

Repeat CT head

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192
Q

Define vertigo

A

One, or more, of the following:

1) A distortion of static gravitational orientation
2) An erroneous perception of movement of the sufferer
3) An erroneous perception of movement of the environment

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193
Q

What tests can be used to distinguish between peripheral and central vertigo?

A

1) Unidirectional nystagmus
- Positive in peripheral lesion
- Negative in central lesion

2) Vor/head impulse test
- Impaired in peripheral lesion
- Normal in central lesion

3) Suppression of nystagmus
- Positive in peripheral lesion
- Negative in central lesion

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194
Q

Describe the clinical features of acute idiopathic unilateral peripheral vestibulopathy

A
  • 30-60 year olds
  • May precede URTI
  • Severe rotary vertigo
  • Accompanying vertigo disturbances e.g. imbalance, vomiting
  • Symptoms exacerbated by head movement
  • Symptoms last around a week
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195
Q

What would you expect to find on examination of a patient with acute idiopathic unilateral peripheral vestibulopathy?

A
  • Unidirectional nystagmus
  • Fast phase to unaffected ear
  • No deafness or other features
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196
Q

How would you treat a patient with acute idiopathic unilateral peripheral vestibulopathy?

A

1) Reassurance and explanation
- Gradual full recovery or compensation
- Good prognosis - vertigo on sudden head movements may persist

2) Symptomatic drug treatment
- Nausea - anti-emetics
- Vertigo - vestibular suppressants (cinnarizine, cyclizine)

3) ?corticosteroids

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197
Q

What red flag symptom would make you suspect a central lesion in a patient presenting with vertigo?

A
  • Deafness or other neurological features
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198
Q

Describe the clinical features of benign paroxysmal positional vertigo

A
  • Mainly >40s
  • Female
  • Attacks of rotational vertigo lasting 10-20 seconds
  • Symptoms provoked by positional changes
  • Brief nausea
  • Other symptoms rare
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199
Q

What features would you see on examination of a patient with BPPV?

A
  • Delayed torsional nystagmus on positional testing, which spontaneously resolves and is fatiguable
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200
Q

How would you manage a patient with BPPV?

A

1) Reassurance and explanation
- May resolve spontaneously but may recur

2) Particle repositioning manoeuvres

Medication is ineffective

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201
Q

Describe the triad of Meniere’s disease

A

1) Vertigo
2) Hearing Loss
3) Tinnitus

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202
Q

Describe the typical clinical features of Meniere’s disease

A
  • 30-50 year olds

Typical attack lasts a few hours with classic evolution:

  1. Sensation of fullness in ear
  2. Reduced hearing
  3. Occurrence/increases tinnitus
  4. Rotational vertigo
  5. Postural imbalance
  6. Nystagmus
  7. Nausea
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203
Q

Risk factors for MND

A
  • Age >50

- Family history - 5% of cases are familial

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204
Q

3 main patterns of MND

A

1) Amyotrophic lateral sclerosis
2) Progressive bulbar palsy
3) Progressive muscular atrophy

205
Q

What must be normal to make a diagnosis of MND?

A

Sensation

206
Q

What investigations could you consider in a patient with suspected MND?

A
  • Nerve conduction studies - exclude neuropathy
  • Electromyography - confirm denervation and show fasciculations
  • MRI brain/neck - exclude other causes, may show corticospinal degenertion
207
Q

Clinical features of ALS

A
  • Stiff and weak hands
  • Muscle cramps and discomfort
  • Onset may be more proximal and resemble plexopathy or foot drop

Progresses to:
- Widespread patch weakness affecting many muscles (extra-ocular muscles spared)

Progresses to:
- Weakness spreads to truncal and bulbar muscles

208
Q

Which muscles are spared in ALS?

A

Extra-ocular muscles

209
Q

What would you expect to see on examination of a patient with ALS?

A
  • Hands severely wasted
  • Interosseous fasciculations
  • Normal muscle tone
  • Patchy weakness
  • Brisk reflexes
  • Extensor plantars
210
Q

What differentials would you consider in a patient with suspected ALS?

A
  • Cervical myeloradiculopathy
211
Q

Clinical features of progressive bulbar palsy

A
  • Progressive dysarthria
  • Dysphagia
  • Rapid weight loss
  • Repeated aspiration pneumonias
  • Emotional lability
212
Q

What features would you see on examination of a patient with progressive bulbar palsy?

A
  • Tongue wasting and fasciculations
  • Tongue spasticity
  • Sagging facial muscles
  • Brisk facial and jaw reflexes
213
Q

What differentials would you consider in a patient with suspected progressive bulbar palsy?

A
  • Myasthenia Gravis
  • Brain stem lesions
  • Cerebrovascular disease
  • MS
  • X-linked bulbospinal neuronopathy
214
Q

Clinical features of progressive muscular atrophy

A
  • Slow progressive muscle wasting, usually symmetrical in both hands
  • Progresses to proximal muscles and legs
215
Q

What would you see on examination of a patient with progressive muscular atrophy?

A
  • Fasciculations
216
Q

What differentials would you consider in a patient with suspected progressive muscular atrophy?

A
  • Multifocal motor neuropathy with conduction block
  • Inherited spinal muscular atrophy
  • Post-polio syndrome
217
Q

Describe the potential treatment options for patients with MND

A
  • Spasticity - baclofen
  • Bulbar involvement (maintaining nutrition and preventing aspiration pneumonia) - percutaneous endoscopic gastrostomy tube (PEG)
  • Respiratory weakness, fatigue or headache - nocturnal or diurnal respiratory support
  • Riluzole (glutamate antagonist) - shown to improve 18 month survival by 7%
218
Q

Describe the clinical features of polio/post-polio syndrome

A
  • Foreign travel
  • Expousre to nappies of babies who have recently received oral, live attenuated polio vaccine
  • Mild upper respiratory tract infection symptoms
  • Meningitis or encephalitis symptoms
  • Severe muscle weakness developing over 24 hours affecting any pattern of muscles
  • Atrophic muscles which do not recover - subsequent skeletal development impaired and muscles flaccid and small
219
Q

Describe the features of inherited spinal muscular atrophies

A
  • LMN symptoms
  • Variable inheritance, all forms are allelic variations of the same gene
  • 3 forms:
    1) rapidly fatal infantile/Werdnig-Hoffman syndrome
    2) slowly progressive juvenile/Kugelberg-Welander syndrome
    3) adult onset
220
Q

Describe the features of hereditary spastic paraparesis

A
  • Autosomal dominant
  • Leg spasticity
  • Compensatory hypertrophy in arms
221
Q

Describe the features of Adrenoleucodystrophy

A
  • X-linked recessive
  • Mixed UMN and LMN signs
  • Mild adrenal insufficiency
222
Q

Describe the features of X-linked bulbospinal neuronopathy

A
  • X-linked
  • Defect in androgen receptor
  • Much better prognosis than MND
  • Bulbar palsy
  • Pronounced action-induced fasciculations
  • Diabetes
  • Gynaecomastia
  • Infertility
  • Mild neuropathy
223
Q

A monocular blindness would suggest a lesion in the…

A

Optic nerve

224
Q

A bitemporal hemianopia would suggest a lesion in the…

A

Optic chiasm

225
Q

A left nasal hemianopia would suggest a lesion in the…

A

Left lateral optic chiasm

226
Q

A right homonymous hemianopia would suggest a lesion in the…

A

Left optic tract

227
Q

A homonymous superior quadrantanopia would suggest a lesion in the…

A

Contralateral temporal lobe (inferior optic radiation

228
Q

An inferior homonymous quadrantanopia would suggest a lesion in the…

A

Contralateral parietal lobe (superior optic radiation)

229
Q

Differentials for sudden-onset monocular visual loss

A
  • Retinal detachment
  • Virtuous haemorrhage
  • Retinal vein thrombosis
230
Q

The pupil response will be normal in disease of the … but impaired in disease of the …

A

Eye

Optic nerve

231
Q

Differentials for progressive monocular visual loss

A
  • Senile macular degeneration
  • Diabetic retinopathy
  • Chronic (open angle) glaucoma
  • Compression of optic nerve by meningioma or glioma
232
Q

Clinical features of amaurosis fugax

A
  • Caused by embolism from the ipsilateral carotid artery to the retinal artery
  • Middle-aged to elderly
  • Sudden reversible vision loss lasting up to 30 mins with complete and rapid recovery (‘curtain coming down over one eye’)
  • May have associated TIA symptoms
  • Examination: no ocular signs/no abnormalities between episodes, cholesterol plaques, carotid bruit
233
Q

Clinical features of retinal migraine

A
  • Occasionally occurs in younger patients
  • Gradual vision loss and slower recovery
  • Typical migraine headache
234
Q

Clinical features of acute glaucoma

A
  • Young to middle aged
  • Transient painful visual loss associated with coloured halos in vision preceding loss
  • Examination: no abnormalities between episodes, normal visual acuity, dilated pupils during episodes, long-sightedness, raised intra-ocular pressure
  • Diagnosis requires ophthalmological assessment
235
Q

Clinical features of optic neuritis

A
  • Usually occurs in young adults
  • Visual loss that evolves over 3-10 days then gradually improves over days-weeks
  • Associated with: retro-orbital pain, flashing lights on eye movement
  • Other MS symptoms
  • Examination: pink or pale atrophic optic disc, reduced colour vision, reduced visual acuity, afferent pupillary defect
236
Q

Clinical features of acute anterior ischaemic optic neuropathy

A
  • Caused by atheromatous disease in <55s
  • Caused by giant cell arteritis in >55s
  • Middle-aged to elderly
  • Altitudinal field defect evolving over minutes-days
  • Associated with: headache, weight loss, malaise
  • Examination: reduced visual acuity, relative afferent pupil defect, optic nerve head swelling, fundal haemorrhages, elevated ESR
  • Treat with 60-80mg prednisolone
237
Q

Clinical features of a bilateral optic nerve lesion

A
  • Causes: optic neuritis, idiopathic intracarnial hypertension
  • Examination: reduced visual acuity, optic atrophy, incongrous field defects with central scotomas which cross the midline, colour desaturation and abnormal pupil response
238
Q

Differentials for acute bilateral vision loss

A
  • Pituitary lesions
  • Temporal arteritis
  • Acute demyelinating diseases
  • Leber’s optic atrophy
  • Bilateral intra-ocular disease (anterior uveitis)
  • Bilateral occipital infarction (cortical blindness)
239
Q

Differential for bitemporal hemianopia

A
  • Chiasmal lesions e.g. pituitary tumour

- Associated with: reduced visual acuity, optic atrophy

240
Q

Differentials for symmetrical anterior visual pathway disturbance

A
  • Vitamin B12 deficiency
  • Folate deficiency
  • Tobacco-alcohol amblyopia
  • Retinitis pigmentosa
241
Q

Clinical features of an optic nerve tumour

A
  • Examination: reduced visual acuity, relative afferent pupillary defect, optic atrophy or papilloedema
242
Q

Clinical features of open angle glaucoma

A
  • Middle-aged to elderly

- Examination: normal visual acuity, normal pupil response, cupped optic disc

243
Q

Clinical features of a pituitary tumour

A
  • Middle-aged to elderly
  • Bitemporal hemianopia
  • Associated endocrine abnormalities or extra-ocular nerve palsies
  • Examination: initially normal visual acuity, optic atrophy or papilloedema
244
Q

Clinical features of a optic radiation infarct

A
  • Middle-aged to elderly
  • Hemiparesis, hemi-sensory loss, dysphasia
  • Examination: hemianopia or quadrantanopia
245
Q

Clinical features of a bilateral occipital infarct

A
  • Middle-aged to elderly
  • Brain stem symptoms
  • Vision loss
  • Examination: blind, normal pupil response, possible brain stem signs
246
Q

How would you investigate a patient with suspected amaurosis fugax?

A
  • Bloods: FBC, glucose, lipids, ESR

- Carotid Doppler

247
Q

How would you investigate a patient with suspected glaucoma?

A
  • Ocualr pressure
248
Q

How would you investigate a patient with suspected optic neuritis?

A
  • Visual evoked potentials
  • CSF
  • MRI
249
Q

Clinical features of an intra-cranial tumour

A

1) Progressive focal neurological deficit

2) Symptoms of raised intracranial pressure
- Headache which is worse on lying down, bending or straining (initially may be present each morning and clear after rising)
- Associated symptoms: nausea, vomiting, unsteadiness, fatigue, drowsiness
- On examination: gait ataxia, papilloedema, failure of up gaze and 3rd/6th cranial nerve palsies
(- May cause ventricular obstruction - sudden onset severe headache with collapse of loss of consciousness)

3) Focal seizures
4) Endocrine disturbances

250
Q

Differentials for a patient with a suspected intracranial tumour

A
  • Chronic subdural haematoma
  • Intracranial abscess
  • Giant aneurysm
  • Obstructive hydrocephalus from non-malignant cause
251
Q

How would you investigate a patient with a suspected intracranial tumour?

A
  • MRI head

- Intracranial biopsy

252
Q

How would you manage the symptoms of an intracranial tumour

A
  • Cerebral oedema - dexamethasone OR IV mannitol (for rapid but transient reduction in critically raised intracranial pressure)
  • Maintain arterial blood pressure - IV fluids
  • Cerebral hypoperfusion - artificial ventilation with hyperventilation
  • Seizures - IV phenytoin
  • Obstructive hydrocephalus - ventriculoperitoneal shunts or ventriculostomy
253
Q

Clinical features of pituitary adenomas

A
  • Endocrine malfunction
  • Infertility
  • Amenorrhoea
  • Loss of libido
  • Hypothyroidism
  • Lactation
  • Acromegaly
  • Cushing’s syndrome
  • Diabetes insipidus
  • Hypoadrenalism
  • Bitemporal hemianopia
  • Reduced acuity
  • Papilloedema or optic atrophy
  • Headache
254
Q

Clinical features of pituitary apoplexy

A
  • Acute visual disturbances
  • Headache
  • Malaise
  • Systemic collapse
255
Q

How would you investigate a patient with suspected pituitary adenoma?

A
  • Serum prolactin
  • MRI/CT head
  • Endocrine assessment e.g. TFTs, LH, FSH
256
Q

How would you manage a patient with a pituitary tumour

A

1) Dopamine agonists e.g. bromocriptine, carbergoline
2) Surgery
3) Radiotherapy

257
Q

Clinical features of craniopharyngiomas

A
  • Children
  • Endocrine disturbance
  • Headache
  • Bitemporal hemianopia
  • Mental dulling
  • Diabetes insipidus
  • Eating disorders
  • Disturbances of thermoregulation
  • Hydrocephalus
258
Q

Clinical features of cerebellopontine angle tumours/acoustic nerve Schwannomas

A
  • Progressive deafness in one ear
  • Ipsilateral face weakness
  • Facial sensory loss
  • Ataxia
  • Headache
  • Neurological deficit in the limb may occur later with brain stem compression
259
Q

What investigations would you carry out in a patient presenting with unilateral sensorineural hearing loss (and to rule out what diagnosis)?

A
  • MRI head and audiometry

- To rule out acoustic nerve Schwannoma

260
Q

How would you treat an acoustic nerve Schwannoma?

A
  • Surgical resection via suboccipital transmeatal micro-dissection
  • Monitor function with facial nerve electromyography and auditory evoked potentials
261
Q

Clinical features of pineal region tumours

A
  • Visual disturbances
  • Headache
  • Parinaud’s syndrome
  • Hydrocephalus
  • Papilloedema
262
Q

Features of Parinaud’s syndrome

A
  • Failure of up gaze
  • Eyelid retraction
  • Dilated unreactive pupils
  • Conervergence-retraction nystagmus
263
Q

How would you investigate a patient with suspected pineal tumour?

A
  • CT/MRI head

- A-fetoprotein or beta-human chorionic gonadotrophin

264
Q

Clinical features of malignant meningitis

A
  • History of: adenocarcinoma, lymphoma, leukaemia and melanoma
  • Symptoms evolving over a few weeks
  • Headache
  • Radicular pain
  • Multiple cranial nerve palsies
  • Polyradiculopathy in the limbs
265
Q

How would you investigate a patient with suspected malignant meningitis?

A
  • Clinical diagnosis
  • CSF examination for malignant cells
  • MRI head (if 2 negative LPs)
266
Q

Clinical features of neurofibromatosis I

A
  • Optic nerve glioma (children)
  • Cortical dysgenesis
  • Mental retardation
  • Seizures
  • Syringomyelia
  • Hydrocephalus
  • Peripheral nerve neurofibromas
  • Epidermal molluscum fibrosum
  • Cafe au Lait patches
  • Massive plexiform neurofibromas
  • Axillary freckles
  • Pigmented Lisch nodules in iris by age 5
  • Bone cysts
  • Precocious puberty
  • Phaeochromocytoma
267
Q

Clinical features of neurofibromatosis II

A
  • Bilateral acoustic Schwannoma
  • Multiple spinal neurofibroma
  • Multiple menigioma, glioma
  • Few cutaneous lesions
268
Q

Clinical features of Tuberous Sclerosis

A
  • Seizures
  • Mental retardation
  • Cortical dysplasia and tubers
  • Hypomelanotic regions
  • Adenoma sebaceum
  • Subungal fibromalas
  • Shagreen patches
269
Q

Clinical features of Von Hippel-Lindau

A
  • CNS haemangioblastomas, especially cerebellum, spinal cord and retina
270
Q

Clinical features of cerebellar degeneration (paraneoplastic syndrome)

A
  • History of bronchus/breast/female genital tract cancer/lymphoma
  • Progressive cerebellar syndrome over weeks/months
  • Sometimes myoclonus, diplopia, hearing loss
  • Anti-Purkinje cell antibodies
271
Q

Clinical features of Limbic Encephalitis

A
  • History of malignancy
  • Personality change
  • Subacute confusion
  • Seizures
  • Movement disorders
  • K+ channel antibodies
272
Q

Clinical features of myasthenia gravis

A
  • Females aged 15-30 OR males aged 50-70
  • Variable muscle weakness with fatiguability
  • Weakness of eye movements, eyelid, facial, neck and bulbar muscles, proximal arm muscles, respiratory muscles
  • Ptosis
  • Diplopia
  • Normal muscle appearance, tone, reflexes and sensation
  • Reduced muscle power on examination
273
Q

Describe a myasthenia crisis

A

Bulbar or respiratory failure, precipitated by intercurrent illness or drugs

274
Q

How would you manage a patient at risk of myasthenia crisis

A
  • Measure FVC every hour - an FVC <2 is borderline and an FVC <1.5 may require ventilation.
  • Consider NG feeding - bulbar failure may cause aspiration pneumonia
275
Q

Differentials for myasthenia gravis

A
  • Chronic progressive external ophthalmoplegia
  • Midbrain lesions
  • Guillain-Barre syndrome
  • MND
276
Q

How would you investigate a patient with suspected myasthenia gravis?

A
  • ACh receptor antibody detection
  • Electromyography - may show typical decrement on repetitive stimulation
  • Single-fibre EMG - may show increased jitter
  • Edrophonium test - give a short-acting cholinesterase inhibitor to overcome symptoms for 2-3 minutes
  • CT/MRI head (identify associated thymus disease)
277
Q

What are the risks of an edrophonium test, and how would you reduce these risks?

A
  • Overactivity at cardiac muscarinic receptors –> bradycardia
  • May tip over-treated patients into respiratory failure
  • Risks reduced by pre-dosing with atropine
278
Q

How would you manage a patient with myasthenia gravis?

A

1) Pyridostigmine or neostigmine (cholinesterase inhibitors) for symptomatic relief
2) Corticosteroids/azathiorprine/methotrexate to reduce production of abnormal antibodies

279
Q

Side effects of pyridostigmine/neostigmine

A
  • Diarrhoea (treated with anti-muscarinics e.g. atropine, propantheline)
  • Cholinergic crisis
280
Q

Side effects of corticosteroids in myasthenia gravis treatment

A
  • Paradoxical deterioration in condition in first 7-10 days of treatment - need to monitor patients closely
281
Q

How would you treat a patient with myasthenia gravis who was acutely unwell?

A
  • IV immunoglobulins or plasmapheresis
282
Q

When would you consider thymectomy in a patient with myasthenia gravis?

A
  • Patient <40

- Older patient with thyme enlargement

283
Q

What drugs are contra-indicated in myasthenia gravis?

A
  • Sedatives
  • Calcium channel blockers
  • Beta-blockers
  • Aminoglycoside antibiotics
  • Erythromycin
  • Benzodiazepines
  • Curare-type muscle relaxants
284
Q

Clinical features of Lambert-Eaton Myasthenia Syndrome

A
  • Usually male
  • History of lung/breast/prostate/stomach cancer/lymphoma
  • Subacute proximal weakness
  • Sensory disturbances
  • Autonomic disturbances e.g. dry mouth

(Bulbar and ocular muscles are rarely affected)

285
Q

Describe the investigations and findings you would see in a patient with Lambert-Eaton Myasthenia syndrome

A
  • EMG - low amplitude muscle action potentials, increment at high stimulation frequencies
  • Single fibre EMG - increases jitters
  • Presence of anti-voltage-gated calcium channel antibodies
286
Q

How would you manage a patient with Lambert-Earton Myasthenic syndrome

A
  • 3,4-diaminopyridine (symptomatic relief)

- Immunosuppression and plasmapheresis

287
Q

List the 4 normal phenomena which occur in sleep

A

1) Dreams/nightmare
2) Sleep talking
3) Hypnic jerks
4) Sleep paralysis

288
Q

What features would you want to include in a sleep history?

A
  • What time they go to bed
  • How long it takes them to fall asleep
  • When they wake up
  • How often they wake through the night
  • What they do when they wake
  • How they feel on waking in the morning
  • Whether they sleep again through the day (when, where and how long)
  • If and when they fall asleep
  • Parallel history from a sleep partner (movement and snoring)
289
Q

Which factors can interfere with sleep?

A
  • Previous sleep history
  • Work pattern/domestic circumstances
  • Exercise
  • Psychiatric history
  • Alcohol
  • Caffeine
  • Medication
  • Pain/medical conditions
  • Nocturia
  • Daytime naps
290
Q

General clinical features of a sleep disorder

A
  • Lethargy
  • Poor concentration
  • Memory loss
  • Depression
  • Personality changes - irritability
291
Q

Features of disrupted sleep

A
  • Caused by non-neurological problems
  • Difficulty sleeping
  • Excess daytime sleepiness
  • Repeated awakening
  • Periodic limb movement during sleep
  • Sleep apnoea
  • Treated by treating the underlying disorder/factors
292
Q

Describe the pathophysiology and treatment of insomnia

A
  • Disrupted sleep, poor sleep hygiene and idiopathic insomnia
  • Treated with eliminate sleep disruption and improve sleep hygiene (avoiding naps, optimising time of sleep and sleeping environment).
  • Nocturnal sedatives can be used if there is a short-term reversible cause for poor sleep but should be avoided for long-term use
293
Q

3 causes of excessive sleepiness

A

1) Obstructive sleep apnoea
2) Disrupted sleep
3) Narcolepsy

294
Q

Most common cause of excessive sleepiness

A
  • Obstructive sleep apnoea
295
Q

Risk factors for obstructive sleep apnoea

A
  • Obesity
  • Upper airways disorder
  • Neuromuscular disorders
  • Neurodegenerative disease
  • Sedative medication
296
Q

Clinical features of obstructive sleep apnoea

A
  • Patients report they sleep well but wake feeling drowsy
  • Headache on waking
  • Fall asleep easily throughout the day
  • Snoring and other apnoea spells
297
Q

How would you diagnose a patient with obstructive sleep apnoea?

A
  • Overnight oximetry - frequent dips corresponding to apnoeic spells are recorded.
  • If this is not diagnostic, more formal sleep studies (EEG monitoring, recording of respiratory function)
298
Q

Treatment of obstructive sleep apnoea

A
  • Weight loss
  • Continuous positive airway pressure therapy delivered via a face mask
  • Modafinil
  • Driving is restricted until symptoms are controlled
299
Q

Clinical features of narcolepsy

A
  • Excessive daytime sleepiness - bouts of uncontrollable sleepiness and refreshing naps of 20-60 mins
  • Cataplexy
  • Hypnagogic hallucinations
  • Sleep paralysis
300
Q

How would you diagnose a patient with narcolepsy?

A
  • Multiple sleep latency test - mean time to fall asleep is measured on a series of occasions throughout the day
  • Patients with narcolepsy fall asleep in <8 minutes and progress rapidly to REM sleep
  • Hypocretin levels in CSF will be low (not a routine test)
301
Q

Treatment of narcolepsy

A
  • Modafenil
  • Fluoxetine or clomipramine are useful to control cataplexy
  • Dexamphetamine or sodium oxybate can be used if ineffective
302
Q

Clinical features of sleep terrors

A
  • Usually brief
  • Patient typically sits up and screams/appears bewildered then goes back to sleep
  • Occurs in first hour after going to sleep
  • No recollection the next day
303
Q

Clinical features of sleep walking

A
  • Associated with more complex automatic behaviours (e.g. going to fridge and eating)
304
Q

Treatment options for sleep walking

A

1) Avoid sleep deprivation

2) Benzodiazepines

305
Q

Clinical features of hyping jerks

A
  • Brief generalised jerks on falling asleep
306
Q

Clinical features of ‘exploding head syndrome’

A
  • Sensation of painless explosion on falling asleep
307
Q

Clinical features of periodic limb movements of sleep

A
  • Brief repeated movements, predominantly of the lower limb

- Often associated with restless leg syndrome and daytime sleepiness

308
Q

Treatment for Periodic limb movements of sleep

A

1) Dopamine agonists e.g. Ropinirole or Pramipexole

309
Q

Clinical features of REM sleep disorder

A
  • Elderly patients
  • Associated with altered development of Parkinson’s or dementia
  • Limited recall of a dream but complain of injuries sustained during the night
  • Partner reports episodes vigorous/violent purposeful behaviour
310
Q

Treatment of REM sleep disorder

A

1) Clonazepam

311
Q

Clinical features of nocturnal seizures

A
  • Tongue biting
  • More sterotyped than parasomnias
  • Generally brief (<2 mins)
  • Occur at any stage of sleep
312
Q

Causes of sleep occurring at the wrong time

A
  • Jet lag
  • Delayed-phase sleep disorder (run on 25 hour internal clock)
  • Advanced-phase sleep disorder (23-hour internal clock)
313
Q

Causes of bacterial meningitis

A

Neonates

  • E.Coli
  • Group B strep

Adults

  • Haemophilus influenzae
  • Neisseria meningitidis
  • Strep. pneumoniae

Developing countries
- Tuberculous meningitis

314
Q

Risk factors for meningitis

A
  • Overcrowding

- Poverty

315
Q

Clinical features of bacterial meningitis

A
  • Headache
  • Fever
  • Neck stiffness
  • Photophobia
  • Positive Kernig’s sign
  • Purpuric rash (meningococcal meningitis)
  • Altered consciousness
  • Seizures
  • Focal signs
316
Q

How would you investigate a patient with suspected bacterial meningitis

A

1) Blood cultures
2) CT/MRI head - rule out contra-indications for lumbar puncture
3) Lumbar puncture

317
Q

When would a lumbar puncture be contra-indicated in a patient with bacterial meningitis?

A
  • Severely ill children - may lead to deterioration

- Evidence of raised intra-cranial pressure on CT head

318
Q

Normal CSF constituents

A
  • <5 cell count
  • lymphocytes
  • <0.45 protein
  • Glucose >60% blood glucose
319
Q

CSF appearance in bacterial meningitis

A
  • Cell count >200
  • Polymorphs
  • Protein >1.5
  • Glucose <40%
320
Q

CSF appearance in viral meningitis

A
  • Cell count 50-200
  • Lymphocytes
  • Protein <1
  • Normal glucose
321
Q

CSF appearance in tuberculous meningitis

A
  • Cell count 50-500
  • Lymphocytes
  • Protein >1
  • Glucose <40%
322
Q

CSF appearance in partially treated bacterial meningitis

A
  • Cell count 50-500
  • Mainly lymphocytes
  • Variable protein
  • Normal or reduced glucose
323
Q

Treatment of bacterial meningitis

A

IV ceftriaxone + IV dexamethasone + IV amoxicillin

324
Q

Most common complications of bacterial meningitis

A

1) Hearing loss
2) Higher function deficits
3) Epilepsy

325
Q

Most common cause of viral meningitis

A

Enterovirus

326
Q

Clinical features of viral meningitis

A
  • Less severe headache
  • Fever
  • Less severe neck stiffness
327
Q

Define aseptic meningitis

A
  • Patients with a clinical and CSF picture of meningitis but without bacterial culture from the CSF
328
Q

Clinical features of tuberculous meningitis

A
  • More insidious onset
  • General malaise
  • Progressive headache
  • Multiple lower cranial nerve palsies
  • Multiple radiculopathies
329
Q

What investigations would you do in a patient with suspected tuberculous meningitis, and what would they show?

A
  • Lumbar puncture - CSF will show lower levels of lymphocyte pleocytosis, raised protein and low glucose
  • Culture - culture of Mycobacterium tuberculosis takes 6 weeks
  • PCR
330
Q

Treatment for tuberculous meningitis

A
  • Rifampicin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
  • Treat once diagnosis is suspected
  • Treat for 9 months
331
Q

Causes of viral encephalitis

A
  • HSV - typically affects the temporal lobes
  • EBV
  • Adenovirus
  • Arbovirus
  • Rabies
332
Q

Clinical features of viral encephalitis

A
  • History of prodromal infection
  • Fever
  • Altered behaviour
  • Seizures
  • Confusion
  • Coma
  • Temporal lobe symptoms - behavioural changes, speech disturbances, hemiplegia, seizures (HSV)
333
Q

How would you investigate a patient with suspected viral encephalitis, and what would they show?

A
  • Lumbar puncture - CSF will show slightly lymphocytic pleocytosis, elevated protein and normal glucose
  • CT/MRI head - usually normal
  • Serum PCR or virus culture
  • EEG - slow and cannot distinguish between infective and other encephalopathies
334
Q

How would you manage a patient with viral encephalitis?

A
  • IV aciclovir (to cover possibility of HSV)
335
Q

Most common and disabling sequelae of HSV viral encephalitis

A
  • Short-term memory loss
336
Q

Clinical features of cerebral abscess

A
  • Progressive headache
  • Focal neurological symptoms and signs
  • Fever
  • Seizures
  • Features of primary infection or markers of systemic infection
337
Q

Main differential for a cerebral abscess

A

Cerebral tumour

338
Q

How would you investigate a patient with a suspected cerebral abscess, and what would it show?

A
  • CT/MRI head - one or more ring enhancing lesions with associated oedema
339
Q

Treatment for cerebral abscess

A
  • IV ceftriaxone AND metronidazole PO AND surgical drainage
340
Q

Name a common complication of cerebral abscess

A
  • Epilepsy
341
Q

Clinical features of subacute sclerosing panencphalitis

A
  • Presents in late childhood/early adolescence
  • Presents after measles
  • Progressive intellectual deterioration
  • Seizures
  • Myoclonus
  • Progressive tetra-paresis
342
Q

Clinical features of Whipple’s disease

A
  • GI upset
  • Supra-nuclear gaz disorder
  • Bizarre rhythmical movements of the eyes and mouth
343
Q

Clinical features of CJD

A
  • 50-70 year olds
  • Family history (5%)
  • Dementia
  • Myoclonus
  • Typical EEG changes
  • Median survival <1 year
344
Q

Clinical features of new-variant CJD

A
  • Young people
  • Symptoms progress over months
  • Psychiatric disturbances
  • Dementia
  • Ataxia
  • Dystonia
  • No myoclonus or typical EEG changes
345
Q

Clinical features of HTLV-1

A
  • Common in West Indies, Africa and South America, and immigrants from these areas
  • Progressive weakness and stiffness in the legs
  • Sensory symptoms
  • Prominent bladder symptoms
  • Arms early affected
346
Q

How would you investigate a patient with suspected HTLV-1 infection, and what would it show?

A
  • Lumbar puncture - oligoclonalbands
347
Q

Clinical features of a pyogenic infection/epidural abscess

A
  • Back pain
  • Fever
  • Progressive radicular pain
  • Symptoms/signs of spinal cord/cauda equina involvement
348
Q

How would you investigate a patient with suspected pyogenic infection/epidural abscess?

A
  • Urgent spinal MRI
349
Q

Clinical features of shingles

A
  • Usually affecting thoracic spine
  • Rash affecting one dermatome
  • Neuralgic pain
  • If it occurs in unusual or more than one dermatome, consider underlying causes of immunosuppression
350
Q

How would you manage a patient with shingles?

A
  • Shorten illness and reduce frequency of post-herpetic neuralgia –> oral aciclovir (acyclovir eye drops in ophthalmic zoster)
  • Neuralgic pain–> carbamazepine and amitryptilline
351
Q

When would you be concerned about a patient with shingles?

A
  • When it occurs in the ophthalmic branch of the trigeminal nerve - this innervates the cornea, and corneal ulcers can occur
352
Q

4 neurological syndromes of syphilis infection, and how they would present

A

1) Meningeal syphilis (6-12 months after infection)
- Chronic meningitis
- Multiple cranial nerve palsies

2) Meningovascular syphilis (5-10 years after infection)
- Young stroke

3) Tabes Dorsalis (15+ years after infection)
- Lightening pain in the legs
- Loss of sensation in the legs
- Charcot joints
- Wide-based, high stepping gait

4) Paretic syphilis (15+ years after infection)
- Progressive dementia
- Prominent delusions
- Personality changes
- Weakness
- Gait disturbance

353
Q

How would you investigate a patient with suspected neurological syphilis?

A

1) Blood serology - TPHA, VDRL, FTA

2) Lumbar puncture - CSF examination of cell count, protein and VDRL titre

354
Q

Treatment of syphilis

A

21 days of supervised IM penicillin

355
Q

Potential neurological complications of HIV infection

A
  • Chronic demyelinating neuropathies
  • Gillain-Barre syndrome
  • Facial weakness
  • Opportunistic infection e.g. toxoplasmosis, CMV, PML, cryptococcus, HSV, HZ
  • Tumours e.g. primary CNS lymphoma
356
Q

Clinical features of toxoplasmosis

A
  • Immunocompromised patients
  • Symptoms develop over a few weeks
  • Focal neurological deficit
  • Headache
  • Seizures
357
Q

How would you investigate a patent with suspected toxoplasmosis, and what would it show?

A
  • CT/MRI head- single or multiple ring-enhancing masses with oedema
358
Q

How would PML appear on MRI head?

A
  • Non-enhancing lesions without mass effect limited to the white matter
359
Q

Which region does PML usually affect?

A

Occipitoparietal region

360
Q

Clinical features of cryptococcal meningitis

A
  • Immunocompromised patient
  • Headache
  • Malaise
  • Confusion
  • multiple cranial nerve palsies
361
Q

How would you investigate a patient with suspected cryptococcal meningitis?

A
  • Lumbar puncture with India ink staining and antigen detection
362
Q

Treatment of cryptococcal meningitis

A
  • Amphotericin B
  • Flucytosine
  • Fluconazole
363
Q

Treatment for CMV

A
  • Ganciclovir and foscarnet
364
Q

Clinical features of HIV encephalopathy

A
  • Immunocompromised patient
  • Apathy
  • Behavioural abnormalities
  • Marked memory problems
  • Brisk reflexes
  • Prominent frontal withdrawal signs
365
Q

What would you see on investigation of a patient with HIV encephalopathy?

A
  • Cerebral atrophy

- Multinucleate giant cells with myelin pallor and gliosis

366
Q

Most common cause of head injury in <15s and >65s

A

Falls

367
Q

Most common cause of head injury in 15-65s

A

Assault

368
Q

Clinical features of uncal herniation

A
  • Typically occurs after a squamous temporal bone injury which tears the middle meningeal artery
  • Headache
  • No loss of consciousness
  • Contralateral limb weakness
  • Dilated pupils on ipsilateral side
  • Reduced consciousness
  • Cushing’s response (increasing BP with decreasing HR)
  • May progress to bilateral pupillary dilation
369
Q

Treatment for uncal herniation

A
  • Immediate surgical evacuation (before development of bilateral fixed pupils)
370
Q

Clinical features of skull fractures

A
  • Raccoon eyes/periorbital bruising
  • Battle’s sign
  • Auditory and facial nerve damage
  • Blood behind ear drum or in external ear
  • CSF rhinorrhoea
371
Q

If a patient had clear fluid leaking from their nose, how would you test if it was mucus or CSF?

A
  • Glucose (in CSF, not mucus)

- Isotransferrin - more specific but takes longer

372
Q

Indicators of severity of a head injury

A
  • GCS
  • Signs indicative of a basal skull fracture
  • Pupil reactions
  • Focal neurological signs
  • Duration of post-traumatic amnesia
  • Imaging - fractures, penetrating injuries, haemorrhage, oedema, brain stem or deep brain involvement
373
Q

Define a mild head injury

A
  • GCS >12
  • Post-trauamtic amnesia <24 hours
  • Loss of consciousness <30 min
374
Q

Define a moderately severe head injury

A
  • GCS 9-12
  • Post-trauamtic amnesia 1-7 days
  • Loss of consciousness <24 hours
375
Q

Define a severe head injury

A

GCS <9

  • Post-trauamtic amnesia >7 days
  • Loss of consciousness >24 hours
376
Q

What patients with a head injury can you send home with a responsible adult?

A
  • Mild head injury
  • No loss of consciousness or loss of consciousness <5 mins
  • Normal neurological examination
  • No skull fracture
377
Q

Indications for admitting a patient with a head injury to hospital

A
  • Amnesia
  • Brief or impact seizure
  • Coagulation or bleeding diathesis
  • Drowsiness, headache, irritability, lethargy
  • Intoxication
  • Loss of consciousness >5-10 mins
  • No responsible carer at home
  • Persistant episodes of vomiting
  • Suspicion of base of skull fracture
  • Unreasonable time/distance from home
378
Q

Indications for an urget CT/MRI head in a patient with a head injury

A
  • GCS <14
  • GCS <15 2 hours after injury
  • Focal neurological signs or symptoms
  • Focal or sustained seizure
  • Suspicion of compound/depressed skull fracture
  • Penetrating skull injury
379
Q

Indications for a skull x-ray in a patient with a head injury

A
  • Age 1 unless trivial mechanism of injury
  • Suspicion of non-accidental injury
  • Full thickness laceration
  • Large boggy swelling
380
Q

Aims of treatment for a patient with a head injury

A

Avoid hypotension
Maintain oxygenation
Avoid raised intracranial pressure
- Head elevation
- Reduce temperature
- Surgical procedures o evacuate intracranial haematoma
- Surgical shunt for hydrocephalus
- Medical interventions with mannitol, mechanical ventilation and forced hyperventilation
- Monitor with intracranial pressure monitors
Rehabilitation

381
Q

Complications of a head injury

A

Post-traumatic syndromes

  • Anxiety, difficulty sleeping, poor concentration
  • Recollections of the accident
  • Behavioural changes e.g. avoiding driving
  • Migraine-like headaches (usually spontaneously improve over 2 years)

Permanent anosmia

Post-traumatic vertigo

Post-traumatic epilepsy

382
Q

Clinical features of a lesion in the corticospinal tract

A
  • Weakness and unsteadiness in walking
  • Stiffness on walking
  • Spontaneous leg spasms
  • Increased tone and reflexes
  • Extensor plantar responses
383
Q

Clinical features of a lesion in the dorsal column

A
  • Ataxia
  • Clumsiness in the hands
  • Loss of joint position and vibration senses
384
Q

Clinical features of a lesion in the spinothalamic tract

A
  • Loss or altered cutaneous sensation and pain sensation

- Painless injuries/burns and secondary deformities (Charcot joints)

385
Q

Clinical features of a lesion in the lateral columns

A
  • Altered sphincter function
386
Q

Clinical features of a total spinal transection

A
  • Loss of all function below the level of the lesion
  • Urinary retention
  • Constipation
387
Q

Clinical features of Brown-Sequard syndrome

A
  • Ipsilateral spasticity
  • Ipsilateral loss of vibration and proprioception
  • Contralateral loss of fine touch and pain
388
Q

Clinical features of a central cord lesion

A
  • Constipation
  • Urinary retention
  • Bilateral loss of fine touch and pain sensation
  • Muscle wasting
  • Weakness
  • Areflexia
  • Spasticity
389
Q

Clinical features of anterior cord syndrome

A
  • Loss of all functions
    EXCEPT
  • Preservation of proprioception and vibration sense
390
Q

What investigation would you use in a suspected myelopathy?

A
  • MRI spine
391
Q

How would you treat cervical spondylosis?

A
  • Posterior laminectomy OR
  • Excision of disc material OR
  • Anterior cervical decompression and fusion with iliac crest grafts
392
Q

How would you treat non-infective inflammatory causes of spinal cord compression

A

High dose corticosteroids

393
Q

Common primary malignancies which metastasise to the vertebrae

A
  • Bronchus
  • Breast
  • Myeloma
  • Lymphoma
  • Prostate
394
Q

Causes of inflammatory spinal cord disease

A
  • MS
  • Sarcoidosis
  • Sjogren’s syndrome
  • SLE
395
Q

Infective causes of spinal cord disease

A
  • Paraspinal/epidural abscesses
  • Brucellosis
  • Syphilis
  • HIV
  • HTLV-1
396
Q

What is the most common presentation of vascular spinal cord syndrome

A
  • Sudden onset of anterior spinal cord syndrome at 8-T11

- Symptoms exacerbated by exercise

397
Q

Most common cause of spinal cord compression

A

Degenerative cervical disc disease

398
Q

Clinical features of vitamin B12/folate deficiency

A
  • Sudden myelopathy affecting dorsal columns
  • Megaloblastic anaemia
  • Mental slowing
  • Cerebellar ataxia
  • Peripheral neuropathy
399
Q

Clinical features of Freidreich’s Ataxia

A
  • Symptoms onset at 8-15 years
  • Loss of reflexes (axonal neuropathy)
  • Optic atrophy
  • Cardiomyopathy
  • Wheelchair bound by 40
400
Q

Clinical features of familial spastic paraparesis

A
  • Severe spasticity of the legs

= Relative preservation of power and compensatory hypertrophy in the arms

401
Q

Clinical features of syringomyelia

A
  • History of congenital abnormality (Chiari malformation), tumour or trauma
  • Constipation
  • Urinary retention
  • Bilateral loss of fine touch and pain
  • Muscle wasting, weakness and areflexia
  • Muscle spasticity
  • May have lower cranial nerve signs (syringobulbia)
402
Q

Most common causes of radiculopathy

A
  • Displaced intervertebral discs (in young people with history of recent injury/straining)
  • Degernative spine disease (spondylosis in older adults)
  • Tumours (breast, bronchus, kidney, thyroid, lymphoma)
  • Inflammation (e.g. shingles)
403
Q

Clinical features of radiculopathy

A
  • Pain radiating from spine in distribution of affected nerve root
  • Constant pain
  • Pain exacerbated by moving the limb
  • Movements painful and limited
  • Weakness in distribution of affected nerve root
  • Muscle wasting or fasciculations
  • Areflexia
  • Sensory loss in a dermatomal distribution
  • In disc prolapse: acute onset and related to physical exertion
  • In mechanical causes: pain worsened by coughing, sneezing or straining
404
Q

What investigations would you consider in a patient with a suspected radiuclopathy?

A
  • MRI spine of relevant level
  • EMG - may show ridiculer pattern of denervation
  • Nerve conduction studies - exclude neuropathy
  • Lumbar puncture (in multiple radiculopathies with evidence of systemic illness)
405
Q

How would you manage a patient with lumbar disc disease?

A

1) Period of rest
2) Mobilisation and education about avoiding back strain/injury
3) Surgical management e.g. microdiscectomy, laminectomy (consider earlier if neurological deficit present)

406
Q

How would you manage a patient with cervical disc protrusions

A

1) Physiotherapy, soft collar or traction

2) Surgery e.g. single level discectomy, anterior disc removal and bone grafts

407
Q

Clinical features of lumbar central disc prolapse

A

MEDICAL EMERGENCY

  • Severe back pain radiating into both legs (usually sciatic distribution)
  • Bilateral foot drop
  • Bilateral hip and knee flexor weakness
  • Sphincter disturbance
  • Loss of ankle jerk and sacral reflex
  • Sensory loss in feet
  • Saddle anaesthesia
408
Q

Management of lumbar central disc prolapse

A

Urgent surgical decompression

409
Q

Clinical features of lumbar canal stenosis

A
  • Increasing leg weakness on walking (neurogenic claudication)
  • Stooped posture
  • Symptoms ease on walking uphill
  • No neurological signs
410
Q

Management of lumbar canal stenosis

A

Surgical decompression

411
Q

Clinical features of normal pressure hydrocephalus

A
  • Urinary incontinence
  • Gait ataxia
  • Dementia
412
Q

Clinical features of Korsakoff’s psychosis

A
  • Retrograde amnesia

- Confabulations

413
Q

Clinical features of Wernicke’s encephaloapthy

A
  • Confusion
  • Ataxia
  • Nystagmus
  • Opthamoplegia
  • Peripheral neuropathy
414
Q

Driving advice for a patient with a single unprovoked seizure or blackout with seizure markers

A

Licence revoked for 1 year (6 months if ECG and scan are normal)

415
Q

Driving advice for a patient with a single provoked seizure

A

Inform DVLA and await guidance before driving again

416
Q

Driving advice for a patient with recurrent seizures

A

License revoked until seizure free for 1 year

417
Q

Driving advice for a patient with seizures in sleep only

A

May drive despite continuing seizures providing all seizures have been in sleep for at least 3 years

418
Q

Driving advice for a patient with a single TIA

A

Can drive 1 month after episode

419
Q

What investigations would you do in a patent with suspected syncope?

A
  • Fasting glucose
  • 24-hour ECG
  • Echocardiogram
  • Tilt table test
420
Q

What investigations would you do in a patient with a suspected seizure?

A
  • MRI/CT head
  • EEG
  • 24-hour EEG
  • Serum calcium
421
Q

Define coma

A

A state of unconsciousness in which a person

  • Can not be awakened
  • Fails to respond normally to painful stimuli, light or sound
  • Lacks a normal sleep/wake pattern
  • Does not initiate voluntary actions
422
Q

Equal pinpoint pupils would make you think of a diagnosis of…

A
  • Opiate overdose

- Pontine lesion

423
Q

Equal small/mid-sized, reactive pupils would make you think of a diagnosis of…

A
  • Metabolic encephalopathy
424
Q

Equal mid-sized, unreactive pupils would make you think of a diagnosis of…

A
  • Midbrain lesion
425
Q

Equal large pupils would make you think of a diagnosis of…

A
  • Drug overdose - cocaine, ecstasy, anti-depressants, cholinesterase inhibitors
426
Q

Unequal small, reactive pupils would make you think of a diagnosis of…

A
  • Horner’s syndrome with partial ptosis
427
Q

Unequal large, unreactive pupils would make you think of a diagnosis of…

A
  • 3rd nerve palsy (ptosis and dilated pupil) - can be caused by herniation
428
Q

What would you look for on examination of a patient in a a coma

A

Vital signs

  • BP
  • Pulse
  • Respiratory rate

External signs of trauma

  • Battle’s sign
  • Evidence of injections
  • Bitten tongue
  • Neck stiffness

Neurological examination

  • GCS
  • Pupillary examination
  • Doll’s head eye movements
  • Fundoscopy
  • Facial/limb asymmetry
  • Tone, posture and repsonse to pain
  • Reflex/plantar response asymmetry
429
Q

What investigations would you do to determine the cause of coma?

A

Bloods:

  • FBC
  • Glucose
  • U&Es
  • LFTs
  • Toxicology screen
  • Ammonia
  • Red cell transketolase

ABG

CT/MRI head

Lumbar puncture

EEG

430
Q

Differentials for a patient in a suspected coma

A
  • Locked in syndrome (high midbrain lesion or severe generalised neuropathy) - normal consciousness, eyes open, normal sleep-wake pattern
  • Catatonia - psychiatric state of unresponsiveness
  • Vegetative state (diffuse bihemispheric disease but normal brain stem function) - open eyes and normal sleep-wake pattern
431
Q

What supportive management would you provide a patient in a coma?

A
  • Intubation and ventilation
  • IV fluids and inotropes as required
  • NG tube
  • TED stockings
  • Urinary catheter
432
Q

How would you investigate/manage a patient with coma, neck stiffness and fever?

A

1) Broad-spectrum antibiotics to cover meningitic organisms

2) MRI/CT head and lumbar puncture

433
Q

How would you investigate a patient with coma and neck stiffness?

A

1) CT brain

434
Q

How would you investigate/manage a patient with coma and focal signs?

A

1) CT/MRI head
2) Mannitol infusion
3) Dexamethasone
4) Intubation and hyperventilation

435
Q

How would you manage a patient with coma caused by hyponatremia?

A

Slow correction to avoid pontine myelinolysis

436
Q

How would you manage a patient with coma caused by encephalitis

A

Antiviral therapy

437
Q

How would you manage a patient with coma caused by hypoglycaemia?

A

25-50ml glucose OR 250-500ml 5% IV dextrose

438
Q

How would you manage a patient with coma caused by opiate overdose?

A

Naloxone 800micrograms

439
Q

How would you manage a patient with coma caused by benzodiazepine overdose?

A

Flumazenil 400mg

440
Q

How would you manage a patient with coma caused by Wernicke’s encephalopathy?

A

Pabrinex IV

441
Q

How would you manage a patient with coma caused by Addisonian crisis?

A

Steroids

442
Q

The 3 elements of brain stem death in the UK

A

1) Cause of failure known to be irreversible
2) Absence of cerebral function, patient is unresponsive and unreceptive
3) Absence of brain stem function

443
Q

How would you test brainstem function to confirm brainstem death

A
  • Correct metabolic abnormalities
  • Allow time for sedative medication to clear
  • Tests undertaken by two senior physicians on two occasions

No response must be found to any of the following:

  • Pupillary response
  • Doll’s head eye movements
  • Eye movements on caloric testing
  • Corneal responses
  • Gag responses
  • Response to painful stimuli
  • Respiratory response to hypercapnia
444
Q

Risk factors for peripheral neuropathy

A
  • Diabetes
  • Malignancy
  • Connective tissue disease
  • Sarcoidosis
  • Rheumatoid arthritis
  • SLE
  • AIDS
  • Uraemia
  • Hypothyroidism
  • Critical illness
  • Thiamine deficiency
  • Niacin deficiency
  • B6 deficiency
  • B12 deficiency
  • Folate deficiency
  • Vitamin E deficiency
  • Alcohol excess
  • Industrial toxins
  • Drugs - amiodarone, cisplatin, dapsone, gold, isoniazid, metronidazole, thalidomide, vincristine
445
Q

What investigations could you consider to help you diagnose a peripheral neuropathy and its cause?

A
  • Nerve conduction studies
  • Lumbar puncture
  • Molecular genetics
  • Nerve biopsy
  • Formal autonomic testing
446
Q

Most common cause of peripheral neuropathy

A

Diabetes

447
Q

Clinical features of diabetic neuropathy

A
  • Poor glycaemic control
  • Predominantly symmetrical sensory symptoms e.g. painful parasthesia or numbness
  • Autonomic nervous system involvement e.g. postural hypotension, tachycardia, nausea/vomiting, intermittent diarrhoea/constipation, urinary retention/overflow, impotence, disordered sweating
  • Can lead to foot ulcers and neuropathic arthropathies (Charcot joints)
  • May present with asymmetrical painful proximal muscle weakness in the legs
448
Q

Clinical features of nutritional deficiency neuropathies

A
  • Painful, predominantly sensory distal symmetrical axonal neuropathy
  • Vitamin B12 deficiency often has associated myelopathy - progressive prominent distal paraparesis, loss of proprioception and associated dementia
449
Q

How would you diagnose a vitamin B12 deficiency neuropathy?

A
  • Vitamin B12 measurement
  • Demonstration of anti parietal cell antibodies
  • Demonstration of malabsorption
450
Q

Clinical features of toxic neuropathy

A
  • Sensorimotor distal symmetrical peripheral neuropathy (except lead, predominantly motor)
451
Q

Clinical features of Lyme disease neuropathy

A
  • Facial nerve neuropathy
  • Radiculopathies
  • Lymphocytic meningitis
  • Later presents with distal symmetrical neuropathy
452
Q

Clinical features of Charcot-Marie-Tooth disease

A
  • Insidious onset
  • Minor symptoms with more marked signs
  • Distal symmetrical neuropathy
  • Preferential atrophy of distal leg muscles (‘inverted champagne bottle legs’)
453
Q

Most common inherited neuropathy

A

Charcot-Marie-Tooth disease

454
Q

Clinical features of Guillain-Barre syndrome

A
  • Any age
  • History of illness - typically Campylobacter jejune, CMV or EBV
  • Symptoms develop over days to 4 weeks
  • Affects limbs and cranial nerves
  • Mild sensory symptoms and signs
  • Significant weakness
  • Areflexia
  • Autonomic nervous system involvement e.g. arrhythmia, hypo/hypertension
455
Q

Clinical features of Miller-Fisher variant of Guillain-Barre syndrome

A
  • Areflexia
  • Opthalmoplegia
  • Ataxia
456
Q

How would you diagnose Guillain-Barre syndrome

A
  • Clinical diagnosis

Supported by

  • Neurophsyiological studies
  • Lumbar puncture - shows raised CSF protein
457
Q

Treatment for Guillain-Barre syndrome

A

Plasma exchange OR IV immunoglobulin

and supportive measures

458
Q

Main risk factor for vasculitis neuropathies

A

Systemic vascular disease

  • Wegener’s granulomatosis
  • Polyarteritis nodosa
  • RA
  • Sjogren’s syndrome
459
Q

Clinical features of neuralgic amyotrophy

A
  • Uncommon
  • History of infection or vaccination
  • Severe neuralgic pain in one arm followed by weakness
  • Pain eases after a few weeks and patient notices muscle weakness
  • Typically affects shoulder girdle - winging of the scapula
  • Sensory loss in lateral aspect of upper arm
460
Q

Risk factors of median nerve neuropathy

A
  • Pregnant
  • Rheumatoid arthritis
  • Hypothyroidism
  • Diabetes
  • Acromegaly
  • Myeloma
  • Female sex
  • Age 40-60
461
Q

Most common mononeuropathy

A

Median nerve

462
Q

Clinical features of Carpal Tunnel Syndrome

A
  • Age 40-60
  • Dominant hand affected first
  • Patient awoken with tingling or pain in hand - progresses to occur throughout the day
  • Pain relieved by shaking/dangling hand
  • Weakness of prolonged grip/clumsy hands
  • Abductor pollicus brevis wasting
  • Sensory changes in median nerve distribution
  • Positive Tinel’s test
  • Positive Phalen’s test
463
Q

How would you diagnose a mononeuropathy?

A
  • Nerve conduction studies
464
Q

Management of carpal tunnel syndrome

A

1) Wrist splints
2) Corticosteroid injections into carpal tunnel
3) Surgical decompression

465
Q

Factors which indicate a poor prognosis for surgical decompression in carpal tunnel syndrome

A
  • Duration of symptoms >6 months
  • Increasing age
  • Pre-op muscle atrophy
  • Poor response to corticosteroid injections
466
Q

Clinical features of ulnar nerve lesion

A
  • Injury/compression/bony deformities at the elbow
  • Numbness/tingling in pinky finger
  • Arm pain
  • Hand weakness
  • Weakness and wasting of interpose and long flexors of ring and pinky finger
  • Sensory loss in ring and pinky finger
467
Q

Management of ulnar nerve lesion

A
  • Avoidance of further compression

- Surgical decompression or transposition

468
Q

Clinical features of radial nerve lesion

A
  • Deep sleep/unconsciousness
  • Humeral shaft fracture
  • Weakness of wrist and finger extension
  • Impaired triceps reflex
  • Sensory loss at base of thumb
469
Q

Management of a radial nerve lesion

A
  • Most improve spontaneously

- Lively splint

470
Q

Clinical features of a common peroneal nerve lesion

A
  • External pressure or trauma to the fibula
  • Foot drop
  • Tibilais anterior wasting
  • Weakness of ankle dorsiflexion, toe extension and foot eversion
  • Sensory loss down lateral aspect of leg and top of foot
471
Q

Management of a common peroneal nerve lesion

A
  • Foot drop splint

- Surgical decompression or transposition

472
Q

Clinical features of a lateral cutaneous nerve of the thigh lesion

A
  • Related to weight changes

- Burning/numbness on the lateral aspect of the thigh

473
Q

How would you investigate and manage a lateral cutaneous nerve of the thigh lesion?

A
  • No investigation

- No treatment - self-limiting

474
Q

Clinical features of a femoral nerve lesion

A
  • Diabetes
  • Weakness and wasting of the quadriceps
  • Sensory loss on inner aspect of thigh
475
Q

Clinical features of raised intracranial pressure

A
  • Headache
  • Ataxia
  • Confusion
  • Drowsiness
  • Coma
  • Papilloedema
  • Sixth nerve palsy
  • 3rd nerve palsy (temporal lobe herniation)
  • Failure of up gaze (mid brain compression)
  • Rise in systolic BP (medullary involvement)
  • Fall in pulse (medullary involvement)
476
Q

Causes of reduced intracranial pressure

A

CSF leakage through torn meninges caused by:

  • trauma
  • iatrogenic
  • tumours
477
Q

Clinical features of reduced intracranial pressure

A
  • Headache on standing

- CSF rhinorrhoea

478
Q

Clinical features of spontaneous intracranial hypotension

A
  • Generalised headache, worse on standing and improved on lying flat
  • 6th nerve palsy
479
Q

What would you see on imaging of a patient with spontaneous intracranial hypotension?

A
  • On MRI scanning with gadolinium you would see marked dural enhancement reflecting engorged normal veins (as CSF is reduced)
480
Q

Features of tectorial herniation

A
  • Unilateral 3rd nerve palsy involving the pupils
  • Coma
  • Bilateral pupil changes
  • Tetraparesis
  • Occipital infarct - worsens herniation
481
Q

Features of foramen magnum herniation

A
  • Severe neck pain
  • Erratic breathing
  • Progressive tetraparesis
  • Coma
482
Q

Causes of a asymmetrical gait abnormality

A
  • Orthopaedic problems e.g. fixed hip joint, shortened limbs
  • Pain

Neurological abnormalities (usually reflect unilateral weakness or abnormal tone)

  • Hemi-Parkinsonian gait - arm swing reduced on one side, posture is slightly stiff and gait is hesitant
  • Hemiplegic/circumducting gait - one leg is swift and swung out and around, often catching the toes
  • Foot drop - high stepping gait where the heel is brought up to avoid catching toe, usually a slap as the foot is brought down
483
Q

Causes of a symmetrical gait abnormality with broad-based gait

A
  • Loss of proprioception (sensory ataxia) - usually have a positive Romberg’s test
  • Loss of coordination (ataxia) caused by midline cerebellar ataxia or widespread cerebellar disease
484
Q

Symmetrical gait with narrow-based gait

A
  • Parkinsonism - short-paced, stooped, poor arm swing. May have difficulty stopping and starting. When walking they appear to be falling froward, often trying to catch up with themselves (festinant gait)
  • Marche a petit pas - small steps, upright posture, good arm swings - caused by cerebellar disease
485
Q

Cause of scissoring gait

A
  • Bilateral leg spasticity with circumlocution from both legs e.g. spinal cord disease or bilateral hemisphere disease
486
Q

Causes of bizarre gait

A
  • Chorea - Huntingtons, Parkinsons treatments
  • Multiple diseases
  • Functional disorder
487
Q

Cause of apraxia (great difficulty in starting, with a broken up gait pattern)

A
  • Normal pressure hydrocephalus

- Diffuse cerebral disease

488
Q

Causes of high stepping gait

A
  • Sensory ataxia

- Peripheral neuropathy

489
Q

Cause of a waddling gait (patient with marked hip movement abnormalities with prominent hip rotation on walking)

A
  • Hip disease

- Proximal pelvis weakness

490
Q

Causes of marche a petit pas

A
  • Diffuse cerebrovascular disease
491
Q

Causes of cerebellar syndromes

A
  • MS (most common cause in younger patients)
  • Stroke (most common cause in older patients)
  • Tumour
  • Trauma
  • Degeneration
  • Metabolic e.g. hypothyroidism
  • Paraneoplastic
  • Toxic e.g. anti-convulsnats and alcohol
492
Q

Main 3 features of cerebellar disease

A
  • Clumsiness
  • Incoordination
  • Ataxia
493
Q

Most common inherited muscle disease

A

DMD

494
Q

Clinical features of Duchenne Muscular Dystrophy

A
  • Weakness of lower limb girdle by age 3-6
  • Gower manoeuvre
  • Weakness spreads to other muscles in arms and legs
  • Pseudohyertrophy of the calves (rubbery)
  • Low IQ
495
Q

How would you diagnose a patient with DMD?

A
  • Muscle creatinine kinase - highly elevated
  • Muscle biopsy - no fibre staining for dystrophin
  • ECG
496
Q

Clinical features of myotonic syndrome

A
  • Stiffness
  • Limitation of movement
  • Weakness
  • Contractions provoked by cold or direct muscle stimulation
497
Q

Clinical features of dystrophic myotonia

A
  • Muscle cramps triggered by the cold
  • Hand weakness
  • Difficulty releasing grip
  • Characteristic facial appearance - frontal balding, severe temporals and sternocleidomastoid muscle wasting, bilateral ptosis, facial weakness
  • Limb weakness worse distally
  • Areflexia
498
Q

Treatment options for myotonia

A
  • Phenytoin
  • Procainamide
  • Quinine
499
Q

Complications of myotonia

A
  • Cardiac conduction abnormalities
  • Impaired respiratory drive
  • Diabetes
  • Hypothyroidism
  • Cataracts
  • Male infertility
  • Bowel dysmotility
  • Mental retardation
500
Q

Causes of acquired muscle disease

A
  • Renal/hepatic failure
  • Hypocalcaemia
  • Hypokalemia
  • Hypomagnesaemia
  • Hypo/hyperthyroidism
  • Cushing’s syndrome
  • Addison’s disease
  • Polymyositis
  • Dermatomyositis
  • Vasculitis
  • Acute viral myositis
  • Sarcoidosis
  • Drugs e.g. statins, tyrptophan, zidovudine
  • Parasites
501
Q

Clinical features of polymyositis

A
  • Woman
  • Age 30-60
  • Proximal limb, trunk, neck,, pharyngeal, oesophageal weakness
  • Painful muscles
  • Elevated CK
  • EMG shows myopathic changes with increased spontaneous activity
502
Q

How would you diagnose polymyositis?

A
  • Diagnosed confirmed by demonstrating inflammatory changes on muscle biopsy
503
Q

Treatment for polymyositis

A
  • Corticosteroids and immunosuppression

- Treatment response monitored using CK levels

504
Q

Clinical features of dermatomyositis

A
  • Children
  • Purple heliotrope rash round the eyes
  • Gottron’s papules
505
Q

Dermatomyositis and polymyositis are associated with an increased risk of…

A

Lymphoma and ovarian cancer

506
Q

Clinical features of Bell’s palsy

A
  • Ipsilateral loss of control of facial muscles
  • Symptoms come on over 48 hours
  • Ptosis
  • Change in taste
  • Pain around the ear
  • Phonophobia
  • Inability to show teeth or raise eyebrows (forehead NOT spared)
507
Q

Risk factors for Bell’s palsy

A
  • Diabetes
  • URTI
  • Pregnancy
508
Q

Management options for a patient with Bell’s palsy

A

1) Eyedrops or an eyepatch
2) Corticosteroids
3) Antiviral medication

Year 4 (11 decks)

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