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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the most common types of dementia?

A
  1. Alzheimer’s
  2. Vascular
  3. Dementia with Lewy-body
  4. Frontotemporal dementia (a.k.a Pick’s disease)
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2
Q

Describe the pathophysiology of Alzheimer’s

A
  • Mostly affects temporal lobes
  • Senile plaques (deposits of beta-amyloid outside of neurons)
  • Neurofibrillary tangles (aggregation of hyperphosphorylated tau proteins inside neurons which cause necrosis of neural tissue)
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3
Q

What are key clinical features of Alzheimer’s?

A
  • Early impairment of memory
  • Short-term memory loss/difficultly learning new information
  • 4 A’s = amnesia, aphasia, agnosia, apraxia
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4
Q

What are investigations for Alzheimer’s?

A
  • Cognitive assessment
  • Memory assessment
  • Bloods (TFTs/B12)
  • CSF Tau studies
  • CT/MRI
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5
Q

What medications can be used for patients with dementia?

A

Mostly for Alzheimer’s:
- Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine, galantamine
- N-methyl-D-aspartic acid receptor antagonists (NMDA) e.g. memantine (for memory loss)
- Antipsychotics

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6
Q

What is the difference between dementia and delirium?

A

Dementia = slowly progressive changes with limited fluctuation. Attention is usually intact and very early memories may be preserved

Delirium = acute, transient and usually reversible changes. Often an associated acute illness

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7
Q

What are the clinical features of delirium?

A
  • Acute onset
  • Fluctuating symptoms
  • Disturbance in awareness and attention
  • Disturbance in cognition
  • Evidence of an organic cause
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8
Q

What are clinical features of hypoactive delirium?

A
  • Lethargy
  • Apathy
  • Excessive sleeping
  • Inattention
  • Withdrawn
  • Motor retardation
  • Drowsy
  • Unrousable
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9
Q

What are clinical features of hyperactive delirium?

A
  • Agitation
  • Aggression
  • Restlessness
  • Rapidly distracted
  • Wandering
  • Delusions
  • Hallucinations
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10
Q

What are the investigations for delirium?

A
  • Bloods (FBC/U&Es/TFTs/LFTs/B12 and folate/coagulation and INR/calcium/glucose/blood cultures)
  • Urine dipstick
  • MRI/CT
  • CXR
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11
Q

What criteria is used for delirium?

A

DSM-5 criteria:
- Disturbance in awareness
- Acute onset
- Disturbance in cognition
- Not better explained by a pre-existing established or evolving neurocognitive disorder
- Absence of severely reduced GCS
- Evidence of organic cause

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12
Q

What is the management for delirium?

A
  • Determine/treat underlying cause
  • Rapid tranquilisation (benzodiazepines e.g. lorazepam/antipsychotics e.g. haloperidol, olanzapine)
  • De-escalation methods (maintain adequate distance/move to safe, low-stimulant environment/use non-threatening verbal and non-verbal techniques/involve relatives or people close to patient)
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13
Q

Describe the pathophysiology of vascular dementia

A
  • Subcortical VD (disease affected small vessels of brain)
  • Stroke-related VD (following large cortical stroke)
  • Single/multi-infarct VD (following single/multiple small strokes)
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14
Q

Describe the pathophysiology of Lewy-Body dementia

A
  • If dementia symptoms 12 months before motor symptoms
  • Histopathological findings of intracytoplasmic inclusions (Lewy bodies) that contain alpha-synuclein
  • Lewy bodies lead to reduced levels of acetylcholine and dopamine in the brain
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15
Q

Describe the pathophysiology of frontotemporal dementia

A
  • Tissue deposition of aggregated proteins (phosphorylated tau or transactive response DNA-binding protein 43)
  • Atrophy around frontal/temporal lobes
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16
Q

What are general clinical features of dementia?

A
  • Slow onset sx
  • Lack of insight
  • Cognitive impairment
  • Behavioural and psychological sx
  • Decreased ability to carry out ADLs
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17
Q

What are key clinical features of vascular dementia?

A
  • Stepwise decline in function
  • Gait/attention/personality changes
  • Focal neurological symptoms e.g. aphasia/weakness
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18
Q

What are key clinical features of Lewy-Body dementia?

A
  • Fluctuating cognitive impairment
  • Parkinsonism sx (tremor/rigidity/bradykinesia/postural instability)
  • Falls/syncope/hallucinations
  • Sleep disturbances/restlessness at night
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19
Q

What are key clinical features of frontotemporal dementia?

A
  • Personality changes and behavioural disturbances (disinhibition)
  • Memory and perception relatively preserved
  • Stereotypical, repetitive, compulsive behaviour/emotional blunting/abnormal eating/language problems
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20
Q

What is sundowning?

A

Increase in certain symptoms (e.g. distress/agitation/hallucinations/delusions) in dementia patients that often occur in the late afternoon/evening

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21
Q

What are investigations for dementia?

A
  • Exclude alternative diagnoses
  • Cognitive assessments
  • Bloods
  • ECG
  • Virology
  • Syphilis testing
  • CXR
  • CT/MRI head
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22
Q

What are some differential diagnoses for dementia?

A
  • Depression
  • Drugs with anticholinergic effects
  • Delirium
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23
Q

What is the management for dementia?

A
  • Assess capacity
  • Inform DVLA
  • Cognitive stimulation therapy
  • Cognitive rehabilitation
  • Reminiscence work
  • Admiral nurses
  • Reduce risk factors (e.g. for VD) - stop smoking/exercise/statins/etc.
  • Medications
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24
Q

What are risk factors for Parkinson’s?

A
  • Age
  • Male
  • Pesticide exposure
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25
Q

Describe the pathophysiology of Parkinson’s

A
  • Basal ganglia responsible for coordinating habitual movements
  • Substantia nigra = part of basal ganglia that produce dopamine (needed for functioning of basal ganglia)
  • Parkinson’s = gradual fall in production of dopamine
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26
Q

What are the clinical features of Parkinson’s?

A
  • Unilateral symptoms (bilateral suggests drug-induced)
  • Resting ‘pill rolling’ tremor better on voluntary movement
  • Cogwheel rigidity
  • Bradykinesia (shuffling gait/small handwriting/hypomimia)
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27
Q

What investigation can differentiate Parkinson’s Disease and benign essential tremor?

A

DAT scan:
- Normal in tremor

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28
Q

What is the management for Parkinson’s?

A
  • FIRST LINE = Levodopa + peripheral decarboxylase inhibitors (Carbidopa/benserazide)
  • Catechol-o-methyltransferase (COMT) inhibitors e.g. entacapone
  • Dopamine agonists e.g. bromocriptine/cabergoline/pergolide
  • Monoamine oxidase-B inhibitors e.g. selegiline/rasagiline
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29
Q

What are the side effects of excess dopamine?

A
  • Dyskinesias (dystonia/chorea/athetosis)
  • Treat with amantadine (glutamate antagonist)
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30
Q

What is an essential tremor and what is it associated with?

A

A type of action tremor (fine tremor) associated with older age

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31
Q

What are the clinical features of essential tremor?

A
  • Fine tremor in hands/head/jaw/vocals
  • Symmetrical
  • More prominent with voluntary movement
  • Worse when tired/stressed/caffeine
  • Improved by alcohol
  • Absent during sleep
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32
Q

What is the management for essential tremor?

A
  • No treatment required if not causing issues
  • Symptomatic relief = propranolol, primidone
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33
Q

Describe the pathophysiology of Huntington’s disease

A
  • Autosomal dominant
  • Increased CAG repeats on Huntington (HTT) gene on chromosome 4
  • Caudate nucleus atrophy
  • Inhibitory neurones in corpus striatum degenerate
  • Lack of GABA
  • Anticipation (successive generations have more repeats)
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34
Q

What are the clinical features of Huntington’s disease?

A
  • Typically presents around 30-50
  • Chorea
  • Eye movement disorders
  • Dysarthria
  • Dysphagia
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35
Q

What are the investigations for Huntington’s disease?

A
  • Genetic test
  • MRI/CT = loss of striatal volume
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36
Q

What is the management for Huntington’s disease?

A

Symptomatic relief:
- Antipsychotics e.g. olanzapine
- Benzodiazepines e.g. diazepam
- Dopamine-depleting agents e.g. tetrabenzine

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37
Q

What are the complications of Huntington’s disease?

A
  • Life expectancy = approx. 15-20 years after onset of sx
  • Death due to respiratory disease
  • Suicide
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38
Q

What are the most common types of motor neurone disease and what are the risk factors?

A
  • Amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy
  • Genetics
  • Smoking
  • Exposure to heavy metals
  • Pesticides
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39
Q

Describe the pathophysiology of motor neurone disease

A
  • Loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells
  • ALS = motor cortex, anterior horn (UMN + LMN)
  • PBP = CN IX-XII (UMN + LMN)
  • Progressive muscular atrophy = Anterior horn (LMN)
  • Primary lateral sclerosis = UMN
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40
Q

What are the clinical features of motor neurone disease?

A
  • No sensory sx
  • Progressive weakness of muscles in limbs/trunk/face/speech –> clumsiness
  • Often first noted in upper limbs
  • Increased fatigue when exercising
  • Dysphagia/chewing difficulties
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41
Q

What are the specific clinical features of upper and lower motor neurone disease?

A

Upper MND = hypertonia/spasticity, clonus, brisk reflexes

Lower MND = muscle wasting, hypotonia, fasciculations, reduced reflexes

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42
Q

What is the management for motor neurone disease?

A
  • ALS = riluzole (slows progression)
  • Non-invasive ventilations
  • End of life care
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43
Q

What are risk factors for multiple sclerosis?

A
  • Female
  • Genetics
  • Epstein-Barr virus
  • Low vitamin D
  • Smoking
  • Obesity
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44
Q

Describe the pathophysiology of multiple sclerosis

A
  • Affects CNS (oligodendrocytes)
  • Inflammation and infiltration of immune cells damages myelin
  • Causes demyelination
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45
Q

What are the clinical features of multiple sclerosis?

A
  • Optic neuritis due to demyelination of optic nerve (reduced vision, central scotoma, pain on movement, impaired colour vision, pupil defect)
  • Eye movement abnormalities due to lesions in abducens nerve (diplopia, internuclear ophthalmoplegia, conjugate lateral gaze disorder)
  • Weakness (Bell’s palsy, Horner’s, limb paralysis, incontinence)
  • Sensory sx (trigeminal neuralgia, numbness, MS hug, paraesthesia, Lhermitte’s sign (electric shock))
  • Ataxia
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46
Q

What is optic neuritis?

A

Inflammatory optic neuropathy affecting one or both optic nerves
- Typical (a.k.a demyelinating) is the most common type

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47
Q

What are the clinical features of optic neuritis?

A
  • Reduced acuity
  • RAPD (relative afferent pupillary defect)
  • Dyschromatopsia (colour blindness where 2/3 fundamental colours seen)
  • Typical patient = Young, Caucasian woman presenting with acute unilateral vision loss associated with painful eye movements and colour desaturation
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48
Q

What are the investigations for multiple sclerosis?

A
  • McDonald’s criteria
  • MRI = lesions/areas of T2 hyperintensity
  • LP = oligoclonal bands in CSF
  • Fundoscopy = often normal but may show optic disc swelling (optic neuritis)
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49
Q

What is McDonald’s criteria?

A

For MS diagnosis
- 2+ attacks, 2+ lesions
- 1+ attacks,1 lesion, dissemination in space on MR
- 1 attack, 2 lesions, dissemination in time on MR
- 1 attack, 1 lesion, dissemination in space and time
- 1 year of disease progression, at least 2 out of 3 criteria (dissemination in space in the brain/dissemination in space in the spinal cord based on 2 or more T2 lesions/positive CSF)

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50
Q

What does disseminated in space mean for McDonald’s criteria (MS)?

A

In different regions = juxtacortical, subcortical, infratentorial and spinal cord

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51
Q

What is the management for multiple sclerosis?

A
  • Steroids
  • Interleukins/inflammatory cytokines/immune cells
  • Symptomatic relief (amitriptyline/antidepressants/anticholinergics e.g. tolterodine, oxybutynin/anti-spasticity e.g. baclofen/gabapentin)
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52
Q

What is given to patients experiencing a relapse of MS?

A

500mg methylprednisolone orally for 5 days or IV for 3 days

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53
Q

What does myasthenia gravis have an association with?

A

Thymomas (tumours of thymus gland)

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54
Q

Describe the pathophysiology of myasthenia gravis

A
  • Acetylcholinesterase receptor (Ach-R) antibodies
  • Muscle-specific kinase (MuSK) antibodies
  • Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies
  • Antibodies affect acetylcholine receptors and prevent uptake of the neurotransmitter acetylcholine
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55
Q

What are the clinical features of myasthenia gravis?

A
  • Fatiguability
  • Weakness that worsens with activity and improves with rest
  • Proximal muscles more commonly affected
  • Diplopia/ptosis/facial weakness
  • Swallowing/chewing difficulty
  • Slurred speech
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56
Q

What are the investigations for myasthenia gravis?

A
  • Check fatiguability (repeated blinking/upward gazing/abduction of arm)
  • Antibodies
  • Edrophonium test
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57
Q

What is the edrophonium test?

A
  • Investigation for myasthenia gravis
  • IV dose of edrophonium chloride given
  • Blocks enzymes that break down acetylcholine - Symptoms briefly relieved
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58
Q

What is the management for myasthenia gravis?

A
  • Acetylcholinesterase inhibitors e.g. pyridostigmine, neostigmine (long-acting)
  • Prednisolone/azathioprine
  • Monoclonal antibodies e.g. rituximab, eculizumab
  • Thymectomy
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59
Q

What is a complication of myasthenia gravis?

A

Myasthenia crisis:
- Acute worsening of symptoms often triggered by another illness
- Can lead to respiratory failure
- Management = IV immunoglobulins and plasmapheresis +/- ventilation

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60
Q

When does Guillain-Barre syndrome typically occur?

A

Following an infection (e.g. gastroenteritis) - associated with C. Jejuni, CMV, EBV

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61
Q

What are the clinical features of Guillain-Barre syndrome?

A
  • History of recent infection
  • Symmetrical ascending weakness
  • Reduced reflexes
  • Peripheral loss of sensation
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62
Q

What are the investigations for Guillain-Barre syndrome?

A
  • Nerve conduction studies = reduced
  • LP for CSF = raised protein, normal cell count/glucose
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63
Q

What is the management for Guillain-Barre syndrome?

A
  • IV immunoglobulins
  • Supportive care
  • Plasmapheresis (alternative to IV Ig)
  • VTE prophylaxis
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64
Q

What are the complications of Guillain-Barre syndrome?

A
  • PE –> respiratory failure
  • Locked-in syndrome
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65
Q

What are the most common causes of viral meningitis?

A

Viral meningitis more common and less severe
- Enteroviruses e.g. echovirus, coxsackie
- HSV
- Mumps virus

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66
Q

What are the most common causes of bacterial meningitis?

A

Bacterial meningitis less common and more severe
- Neonates = group B strep (strep. agalactiae), E. coli, listeria meningitis
- N. meningitis (a.k.a meningococcus), strep. pneumoniae

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67
Q

What are other causes of meningitis?

A

Fungal = cryptococcus, candida

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68
Q

What are the risk factors for meningitis?

A
  • Student
  • Recent travel
  • Immunocompromised
  • Pregnancy
  • Extremes of ages
  • Unvaccinated
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69
Q

What are the clinical features of meningitis?

A
  • Fever
  • Neck stiffness/pain
  • N+V
  • Headache
  • Photophobia
  • Altered consciousness
  • Seizures
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70
Q

What is the main feature of meningococcal septicaemia?

A
  • Non blanching rash –> infection has caused DIC and subcutaneous haemorrhage
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71
Q

What are the investigations for meningitis?

A
  • LP for CSF
  • Bloods/blood culture
  • Kernig’s test
  • Brudzinski’s test
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72
Q

How do you differentiate between viral and bacterial meningitis?

A

LP for CSF
- Appearance = cloudy (bacterial) or clear (viral)
- Protein = very high (bacterial), high/normal (viral)
- Glucose = low (bacterial), normal (viral)
- WCC = high neutrophils (bacterial), high lymphocytes (viral)
- Culture = bacteria (bacterial), negative (viral)

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73
Q

What is Kernig’s test?

A

Investigation for meningitis
- Patient lies on back with hip flexed and knee bent to 90 degrees
- Slowly try to extend knee whilst keeping hip flexed
- Meningitis = spinal pain/resistance to movement

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74
Q

What is Brudzinski’s test?

A

Investigation for meningitis
- Patient lies on back
- Lift head and neck off bed and flex chin to chest
- Positive = involuntarily flexion of hip and knees

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75
Q

What is the management for viral meningitis?

A

Aciclovir

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76
Q

What is the management for bacterial meningitis?

A
  • Meningococcal septicaemia = IM/IV benzylpenicillin
  • <3 months = cefotaxime + amoxicillin/ampicillin
  • > 3 months = ceftriaxone
  • Post exposure prophylaxis = ciprofloxacin/rifampicin
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77
Q

What is the most common complication of bacterial meningitis?

A

Sensorineural hearing loss - due to damage to the cochlear nerve or inner ear structures during inflammation

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78
Q

What are the most common causes of encephalitis?

A
  • HSV (neonates = HSV-2, children = HSV-1)
  • VZV
  • CMV
  • EBV
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79
Q

What are the clinical features of encephalitis?

A
  • Fever
  • Headache
  • Encephalopathy
  • Altered consciousness
  • Altered cognition/behaviour
  • Focal seizures
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80
Q

What are the investigations for encephalitis?

A
  • LP for CSF
  • CT/MRI
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81
Q

What is the management for encephalitis?

A
  • HSV/VZV = aciclovir
  • CMV = ganciclovir
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82
Q

What are the main components of a seizure?

A
  • Prodrome = precedes seizures by hours to days - weird feeling
  • Aura = right before - deja vu/strange smells/flashing lights
  • Post-ictal = after seizure - headache/confusion/sore tongue/post-ictal Todd’s palsy (temporary weakness in motor cortex)
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83
Q

What are the features of a non epileptic seizure?

A
  • Occurs in abnormal metabolic circumstances e.g. low Na+, hypoxia
  • Last longer than epileptic seizures
  • Do not occur in sleep
  • No incontinence/tongue biting
  • No muscle pain
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84
Q

What blood test can differentiate true seizures from pseudoseizures?

A

Prolactin - raised in true seizures

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85
Q

What is required for a diagnosis of epilepsy?

A
  • At least 2 unprovoked seizures occurring more than 24 hours apart
  • 1 unprovoked seizure and a high probability of further seizures
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86
Q

What are the investigations for seizures?

A
  • EEG
  • MRI
  • ECG
  • Bloods/electolytes/glucose/cultures/LP
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87
Q

What is the management for seizures/epilepsy?

A

Acute:
- Recovery position
- Place something soft under head
- Remove things that could cause injury
- Note start/end time of seizures
- Call ambulance if seizure lasts >5 mins

Medication:
- Sodium valproate/lamotrigine/carbamazepine/levetiracetam/ethosuximide

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88
Q

When is a diagnosis of epilepsy remission given?

A

Individuals who:
- Had an age-dependent epilepsy syndrome but are now past the applicable age
- Have remained seizure-free for at least 10 years off anti-seizure medications, provided that there are no known risk factors associated with high probability of future seizures

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89
Q

What is the main complication of seizures/epilepsy?

A

Status epilepticus - when seizure lasts >5 minutes or 2+ seizures without regaining consciousness
Management:
- ABCDE
- Community = buccal midazolam/rectal diazepam
- FIRST LINE = benzodiazepine - IV lorazepam
- After 2 attempts of benzodiazepine = IV phenytoin/sodium valproate/levetiracetam
- Third line = phenobarbital/general anaesthesia

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90
Q

What is sodium valproate used for and what are the side effects?

A

Epilepsy and bipolar disorder/mania
- Teratogenic
- Liver damage
- Hair loss
- Tremor

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91
Q

What is carbamazepine used for and what are the side effects?

A

Epilepsy and bipolar disorder/mania
- Agranulocytosis
- Aplastic anaemia

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92
Q

What is ethosuximide used for and what are the side effects?

A

Epilepsy
- Night tremors
- Rash
- N+V

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93
Q

What is lamotrigine used for and what are the side effects?

A

Epilepsy and bipolar disorder/mania
- DRESS syndrome = drug reaction with eosinophilia and systemic symptoms
- Leukopenia
- Stevens-Johnson syndrome (rare, severe skin reaction)

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94
Q

Describe tonic clonic seizures

A

A.k.a grand mal seizures
- Loss of consciousness
- Tonic (muscle tensing) and clonic (muscle jerking)
- Tongue biting/incontinence/groaning/irregular breathing
- First line management = sodium valproate
- Second line management = lamotrigine/carbamazepine

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95
Q

Describe myoclonic seizures

A
  • Sudden brief muscle contractions
  • Patient usually conscious
  • Often happens in children as part of juvenile myoclonic epilepsy
  • First line management = sodium valproate
  • Second line management = Lamotrigine/levetiracetam/topiramate
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96
Q

Describe tonic seizures

A
  • Sudden onset of increased muscle tone (entire body stiffens) - fall if patient standing
  • Usually only lasts a few seconds
  • First line = sodium valproate
  • Second line = lamotrigine
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97
Q

Describe atonic seizures

A

A.k.a drop attacks
- Brief lapses in muscle tone
- Sudden loss of muscle strength
- Part/all of body becomes limp
- Usually last <3 minutes
- First line management = sodium valproate
- Second line management = lamotrigine

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98
Q

Describe absence seizures

A
  • Common in children
  • Blank expression/staring into space
  • Abrupt return to normal
  • Unaware of surroundings and won’t respond during episode
  • Typically last 10-20 seconds
  • Management = sodium valproate/ethosuximide
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99
Q

Describe temporal lobe seizures

A
  • Affect hearing/speech/memory/emotions
  • Hallucinations/memory flashbacks/deja vu/anxiety/automatisms
  • First line management = lamotrigine/carbamazepine
  • Second line management = sodium valproate/levetiracetam
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100
Q

Describe frontal lobe seizures

A
  • Motor disturbances
  • Jacksonian march
  • Remains conscious
  • Post-ictal Todd’s palsy
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101
Q

What are febrile convulsions and what are the risk factors?

A
  • Seizures that occur in children whilst they’re febrile (only between ages of 6 months and 5 years)
  • Fhx
  • Socio-economic class
  • Winter season
  • Zinc/iron deficiency
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102
Q

What are the clinical features of febrile convulsions?

A

Simple:
- Generalised tonic-clonic seizures
- Last <15 minutes
- Only occur once during febrile illness
Complex:
- Focal seizures
- Last >15 minutes
- Occur multiple times during febrile illness

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103
Q

What is associated with subarachnoid haemorrhages?

A

Autosomal dominant polycystic kidney disease - berry aneurysms

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104
Q

What are the clinical features of a subarachnoid haemorrhage?

A
  • History of trauma
  • Sudden onset
  • ‘Thunderclap’ headache
  • Loss of consciousness
  • N+V
  • Confusion
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105
Q

What are the investigations for subarachnoid haemorrhages?

A
  • CT = hyper-attenuation around circle of Willis (‘5 pointed star’ appearance) - suggests aneurysm –> follow with CT angiogram - if more peripheral, suggests due to trauma
  • LP = xanthochromia (yellow due to bilirubin breakdown)
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106
Q

What is the management for subarachnoid haemorrhages?

A
  • Immediately stop antiplatelets/anticoagulants
  • Endovascular coiling +/- neurosurgical clipping
  • IV mannitol for high ICP
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107
Q

What are subdural haemorrhages and what are the risk factors?

A

Bleeding into subdural space due to ruptured bridging vein
- Anticoagulants
- Accident prone = dementia/elderly/alcoholics/epileptics
- Babies (shaken baby syndrome)

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108
Q

What are the clinical features of a subdural haemorrhage?

A
  • History of trauma
  • N+V
  • Confusion
  • Fluctuating consciousness/drowsiness
  • Headache
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109
Q

How can you tell if a bleed in the brain is acute or chronic?

A

CT:
- Acute - hyperdense (brighter)
- Chronic - hypodense (darker)

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110
Q

What are the investigations for subdural haemorrhages?

A

CT:
- Haematoma
- Crescent shaped
- Unilateral
- Midline structures shift away
- Cross sutures

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111
Q

What is the management for subdural haemorrhages?

A
  • Immediately stop antiplatelets/anticoagulants
  • Clot evacuation to remove haematoma
  • Craniotomy
  • Burr hole washout
  • IV mannitol for high ICP
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112
Q

What are epidural haemorrhages and who are they more common in?

A

Bleeding into extradural space due to ruptured middle meningeal artery
- Males
- Young people

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113
Q

What are the clinical features of an epidural haemorrhage?

A
  • History of trauma
  • Skull fracture
  • Lucid interval = initial drowsiness/unconsciousness –> recovery –> rapid deterioration
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114
Q

What are the investigations for epidural haemorrhages?

A

CT:
- Bi-convex
- Unilateral
- Do not cross sutures
- Midline shift

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115
Q

What is the management for epidural haemorrhages?

A
  • Immediately stop antiplatelets/anticoagulants
  • Clot evacuation
  • Ligation of bleeding vessel
  • IV mannitol for high ICP
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116
Q

What are the clinical features of an intracerebral haemorrhage?

A

Sudden onset focal neurological symptoms
- Limb/facial weakness
- Dysphasia
- Vision/sensory loss

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117
Q

What are the investigations for intracerebral haemorrhages?

A
  • CT = hyper- attenuation in brain parenchyma, commonly in middle if patient has HTN
  • Often associated with subarachnoid haemorrhage as pia is very thin
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118
Q

Which type of stroke is more common?

A

Ischaemic

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119
Q

What are the risk factors for strokes?

A

Same as CVD
- Age
- Male
- HTN/hyperlipidaemia
- Diabetes
- Smoking
- Previous TIA
- Heart disease/AF
- COC (ischaemic)

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120
Q

What are the clinical features of a stroke?

A
  • Sudden limb/facial weakness
  • Dysphasia
  • Visual/sensory loss
  • N+V
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121
Q

What are the investigations for haemorrhagic strokes?

A
  • FIRST LINE = CT
  • Diffusion-weighted MRI
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122
Q

What is the management for haemorrhagic strokes?

A

Acute:
- Neurosurgery - evacuate blood
- IV mannitol for high ICP
- Stop anticoagulants

Secondary:
- Anticoagulant
- BP aim of 140/90
- External ventricular drain (if hydrocephalus)
- Rehabilitation (SALT/PT/OT)

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123
Q

What type of infarcts occur in ischaemic strokes?

A

Cerebral:
- More common
- Occlusion of large blood vessel to cerebrum (e.g. internal carotid artery/middle cerebral artery)

Lacunar:
- Infarcts of smaller blood vessels
- Affected smaller areas e.g. internal capsule/basal ganglia/thalamus/pons
- Produce more specific symptoms

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124
Q

What are the investigations for ischaemic strokes?

A
  • FIRST LINE = Bloods and CT
  • Diffusion-weighted MRI
  • Carotid USS
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125
Q

What is the Bamford classification?

A

Categorises ischaemic strokes based on initial presenting features
- Total anterior circulation stroke
- Partial anterior circulation stroke
- Lacunar syndrome
- Posterior circulation syndrome
- Lateral medullary syndrome (Wallenberg’s syndrome)
- Weber’s syndrome
- Basilar artery

126
Q

What is the Bamford classification criteria for total anterior circulation stroke?

A

ALL THREE:
- Unilateral weakness (and/or sensory deficit of face/arm/leg)
- Homonymous hemianopia
- Higher cerebral dysfunction (e.g. dysphasia/visuospatial disorder)

127
Q

What is the Bamford classification criteria for partial anterior circulation stroke?

A

TWO:
- Unilateral weakness (and/or sensory deficit of face/arm/leg)
- Homonymous hemianopia
- Higher cerebral dysfunction (e.g. dysphasia/visuospatial disorder)

128
Q

What is the Bamford classification criteria for lacunar syndrome?

A

ONE OF:
- Pure sensory stroke
- Pure motor stroke
- Sensorimotor stroke
- Ataxic hemiparesis

129
Q

What is the Bamford classification criteria for posterior circulation syndrome?

A

ONE OF:
- CN palsy and a contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (e.g. gaze palsy)
- Cerebral dysfunction (e.g. ataxia/nystagmus/vertigo)
- Isolated homonymous hemianopia/cortical blindness

130
Q

What is the Bamford classification criteria for lateral medullary syndrome?

A
  • Ipsilateral ataxia/nystagmus/dysphagia/facial numbness/CN palsy e.g. Horner’s syndrome
  • Contralateral limb sensory loss
131
Q

What is the Bamford classification criteria for Weber’s syndrome?

A
  • Ipsilateral CN III palsy
  • Contralateral weakness
132
Q

What is the Bamford classification criteria for a basilar artery stroke?

A

‘Locked in’ syndrome

133
Q

What is the management for ischaemic strokes?

A

Acute:
- Exclude haemorrhagic stroke
- Oral/rectal aspirin 300mg
- Thrombolysis = IV alteplase (within 4.5 hours of sx onset)
- Mechanical thrombectomy (within 6 hours)

  • Aspirin 300mg daily for 2 weeks then clopidogrel
  • Warfarin/apixaban
  • Rehabilitation (SALT/OT/PT)
134
Q

What is Wallenberg syndrome/lateral medullary syndrome?

A

Stroke due to blockage of posterior inferior cerebellar artery
- Causes ischaemia in lateral part of medulla oblongata in brainstem
- Involvement of lateral spinothalamic tract
- Ipsilateral facial pain and loss of temperature sensation
- Contralateral limb/torso pain and loss of temperature sensation
- Ataxia
- Nystagmus

135
Q

What is lateral pontine syndrome?

A

Stroke due to blockage of anterior inferior cerebellar artery
- Artery supplies the pons
- Similar presentation to lateral medullary syndrome
- Ipsilateral facial paralysis
- Ipsilateral deafness

136
Q

What are the clinical features of a stroke affecting the anterior cerebral artery?

A
  • Contralateral hemiparesis and sensory deficits
  • Lower extremities worse affected
137
Q

What are the clinical features of a stroke affecting the middle cerebral artery?

A
  • Contralateral hemiparesis
  • Upper extremities worse affected
  • Contralateral homonymous hemianopia
  • Aphasia
138
Q

What are the clinical features of a stroke affecting the posterior cerebral artery?

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia

Weber’s syndrome = branches of the posterior cerebral artery that supply the midbrain
- Ipsilateral CN III palsy (eye points down and out)
- Contralateral weakness of upper/lower extremities

139
Q

What are the clinical features of a stroke affecting the retinal/ophthalmic artery?

A

Amaurosis fugax

140
Q

What are the clinical features of a stroke affecting the basilar artery?

A

Locked-in syndrome

141
Q

Describe lacunar strokes

A
  • Strong association with HTN
  • Common sites = basal ganglia/thalamus/internal capsule
  • Isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
142
Q

What are causes of transient ischaemic attacks?

A
  • Thromboemboli
  • Hypoviscosity
  • Hypoperfusion
  • Vasculitis
143
Q

What is a crescendo TIA?

A
  • 2 or more TIAs in 1 week
  • High risk factor for stroke
144
Q

What are the clinical features of a transient ischaemic attack?

A
  • Last <24 hours without infarction (typically resolve within 10 minutes)
  • Sudden facial/limb weakness
  • Dysphasia
  • Sensory/visual loss
  • N+V
145
Q

What are the investigations for transient ischaemic attacks?

A
  • Blood glucose (hypoglycaemia can cause focal neurological symptoms)
  • CT
  • Diffusion-weighted MRI
  • Carotid doppler
  • ACBD2 risk score (age/BP/clinical features/duration/diabetes)
146
Q

What is the management for transient ischaemic attacks?

A
  • Aspirin (acute)
  • Clopidogrel and atorvastatin (long term prophylaxis)
147
Q

What are triggers for migraines?

A

CHOCOLATE:
- Chocolate
- Hangovers
- Orgasms
- Cheese
- Oral contraceptives
- Lie ins
- Alcohol
- Tumult (loud noise)
- Exercise

148
Q

What are the clinical features of migraines?

A
  • Aura (visual disturbances/somatosensory sx)
  • Unilateral pain
  • Throbbing-type pain
  • Moderate to severe intensity
  • Motion sensitivity
  • Nausea/vomiting
  • Photophobia/phonophobia
149
Q

What are the investigations for migraines?

A
  • Diagnosis using sx
  • CT/MRI
  • LP
150
Q

What is the management for migraines?

A

Acute:
- Triptans (sumatriptan)
- NSAIDs (naproxen)
- Paracetamol
- Anti-emetics (prochlorperazine)

Secondary:
- Beta blockers (propranolol)
- Anti-convulsants (topiramate)
- TCAs (amitriptyline)

151
Q

What are the risk factors for cluster headaches?

A
  • Male
  • Genetics
  • Smoker
  • Alcohol
152
Q

What are the clinical features of cluster headaches?

A
  • Rapid onset of excruciating pain around eye/temples/forehead
  • Unilateral and localised pain
  • Pain rises to crescendo over a few minutes and lasts for 15-160 minutes
  • Watery/bloodshot eyes
  • Facial flushing
  • Rhinorrhoea
  • Miosis
  • Ptosis
153
Q

What is the management for cluster headaches?

A

Acute:
- Analgesics ineffective
- 15L 100% O2 for 15 mins via non-rebreather mask
- Triptans (sumatriptan)

Secondary:
- Calcium channel blocker (verapamil)
- Prednisolone
- Reduce alcohol intake/stop smoking

154
Q

What are triggers of tension headaches?

A
  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger
  • Eyestrain
  • Anxiety/depression
  • Noise
  • Dehydration
  • Alcohol
155
Q

What are the clinical features of tension headaches?

A
  • Come on and resolve gradually
  • No visual changes/aura
  • No vomiting
  • No sensitivity to head movement
  • Pressure behind eyes
156
Q

What is the management for tension headaches?

A
  • Avoidance of triggers
  • Basic analgesia (aspirin/paracetamol/ibuprofen)
  • Relaxation techniques
  • Hot towels to local area
157
Q

What are triggers of trigeminal neuralgia?

A
  • Cold weather
  • Spicy food
  • Caffeine
  • Citrus fruits
158
Q

What causes trigeminal neuralgia?

A

Compression of trigeminal nerve and its branches (ophthalmic/maxillary/madibular)

159
Q

What are the clinical features of trigeminal neuralgia?

A
  • Intense facial pain that comes on spontaneously
  • Lasts between a few seconds to hours
  • Electricity-like shooting pain
  • Majority are unilateral
160
Q

What is the management for trigeminal neuralgia?

A
  • Carbamazepine
  • Surgery to decompress trigeminal nerve
161
Q

What are the clinical features of idiopathic intracranial hypertension?

A

Typical patient:
- Obese, young female with headaches and blurred vision
- N+V
- Often eases throughout the day
- Worsens when patient bends down

162
Q

What does temporal (giant cell) arteritis affect?

A

The aorta and/or its major branches (carotid and vertebral arteries)

163
Q

What are the clinical features of temporal arteritis?

A
  • Unilateral headache over temporal area
  • Scalp tenderness
  • Jaw claudication
  • Visual disturbances (blurred vision, diplopia, amaurosis fugax)
164
Q

What are the investigations for temporal arteritis?

A
  • USS = halo sign of temporal and axillary arteries
  • Temporal artery biopsy (gold standard) = shows giant cells and granulomatous inflammation
165
Q

What is the management for temporal arteritis?

A

High dose glucocorticoid stat e.g. prednisolone 40mg-60mg

166
Q

Describe the pathophysiology and clinical features of Horner’s syndrome

A

Dysfunction of oculosympathetic nerve
- Unilateral ptosis
- Unilateral miosis
- Unilateral anhidrosis
- Enophthalmos

167
Q

What are the investigations for Horner’s syndrome?

A
  • Examination = visual fields/facial sensation/extra-ocular movements
  • Eye drops to make pupils dilated = sympathetically denervated pupil will dilated poorly
  • CT/MRI
168
Q

What is a squint and what are some common causes of it?

A

Misalignment of the eye a.k.a strabismus
- Hydrocephalus
- Cerebral palsy
- Space-occupying lesions e.g. retinoblastoma
- Trauma

169
Q

What are the different types of squint?

A
  • Concomitant (difference in control of extraocular muscles)
  • Paralytic (paralysis in one/more of extraocular muscles)
  • Esotropia/exotropia (inward/outward positioned)
  • Hyper/hypotropia (upward/downward)
170
Q

What is amblyopia?

A

In squint, lazy eye becomes progressively more passive and has reduced function

171
Q

What is the main feature of a squint?

172
Q

What are the investigations for squints?

A
  • Fundoscopy/eye movements/visual acuity
  • Hirschberg’s test (pen torch shone and observe reflection in cornea)
  • Cover test (cover one eye and observe when moved to other eye)
173
Q

What is the management for squints?

A
  • Occlusive patch over good eye
  • Atropine drops in dominant eye (causes blurred vision)
174
Q

What is Bell’s palsy?

A

Acute, unilateral facial nerve weakness/paralysis

175
Q

What is the facial nerve (CN VII) responsible for?

A
  • Motor = facial expression, stapedius in inner ear, posterior digastric/stylohyoid/platysma muscles
  • Sensory = taste from anterior 2/3 of tongue
  • Parasympathetic = submandibular/sublingual salivary gland, lacrimal gland
176
Q

What is the management for Bell’s palsy?

A

-Often self limiting over several weeks/months
- Prednisolone 50mg for 10 days or 60mg for 5 days followed by 5 day reducing regime
- Lubricating eye drops

177
Q

What is Ramsay-Hunt syndrome?

A
  • Shingles infection that has affected the facial nerve
  • Painful vesicular rash in ear canal/pinna/around ear (may extend to anterior 2/3 of tongue and hard palate)
  • Unilateral lower motor neurone facial nerve palsy
178
Q

What are some risk factors for cerebral palsy?

A
  • Antenatal = maternal infection/trauma during pregnancy
  • Perinatal = birth asphyxia (HIE)/pre-term birth
  • Postnatal = meningitis/severe neonatal jaundice/head injury
179
Q

Describe the pathophysiology of the different types of cerebral palsy

A
  • Spastic = UMN damage
  • Dyskinetic = basal ganglia damage
  • Ataxic = cerebellar damage
  • Mixed = all
180
Q

What are the clinical features of spastic cerebral palsy?

A
  • Hypertonia
  • Reduced function
181
Q

What are the clinical features of dyskinetic cerebral palsy?

A
  • Problems controlling muscle tone
  • Hypertonia/hyptonia
  • Athetoid movements (abnormal, involuntary movements)
  • Oro-motor problems
182
Q

What are the clinical features of ataxic cerebral palsy?

A

Problems with coordinated movement

183
Q

What are the clinical features of cerebral palsy in development?

A
  • Failure to meet milestones
  • Hypertonia/hypotonia
  • Hand preference below 18 months
  • Problems with coordination/speech/walking
  • Problems with feeding/swallowing
  • Learning difficulties
184
Q

What are the investigations for cerebral palsy?

A

Neurological examination:
- Hemiplegic/diplegic gait
- Extended legs with plantarflexion of feet/toes
- Coordination problems
- Hypertonia/brisk reflexes/reduce power (UMN signs)
- Athetoid movements

185
Q

What is the management for cerebral palsy?

A
  • SALT/PT/OT/dieticians
  • Surgery (release contractures/lengthen tendons)
  • Muscle relaxants e.g. baclofen
  • Anti-epileptics
  • Glycopyrronium bromide (for excessive drooling)
186
Q

What are causes of hypoxic ischaemic encephalopathy?

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord
  • Nuchal cord (wrapped around baby’s neck)
187
Q

How are the clinical features of hypoxic ischaemic encephalopathy graded?

A

Sarnat Staging Grades:
- Mild = poor feeding/general irritability/hyper-alert/resolves within 24 hours
- Moderate = poor feeding/lethargic/hypotonic/seizures/can take weeks to resolve
- Severe = reduced consciousness/apnoeas/flaccid, reduced or absent reflexes

188
Q

What is the management for hypoxic ischaemic encephalopathy?

A

Supportive care:
- Neonatal resuscitation
- Ventilation
- Circulatory support
- Nutrition
- Acid base balance
- Treatment of seizures
- Therapeutic hypothermia

189
Q

What are the most common types of muscular dystrophy and when do they present?

A
  • Duchenne’s = 3-5 years
  • Becker’s = 8-12 years
  • Myotonic dystrophy
  • Facioscapulohumeral muscular dystrophy
  • Oculopharyngeal muscular dystrophy
  • Limb-girdle muscular dystrophy
  • Emery-Dreifuss muscular dystrophy
190
Q

Describe the pathophysiology of Duchenne’s/Becker’s muscular dystrophy

A
  • X linked recessive
  • Defective gene for dystrophin (protein that helps to hold muscles together)
  • Becker’s = gene less severely affected than Duchenne’s
191
Q

What are the clinical features of muscular dystrophy?

A
  • Gower’s sign (stand up from lying down using a specific technique)
  • Progressive weakness
  • Waddling gait
  • Language delay
  • Pseudohypertrophy of calves
  • Slow/clumsy
192
Q

What is Gower’s sign?

A

Specific technique used by patients with proximal muscle weakness (muscular dystrophy) to stand up from lying position:
- Get on hands and knees and push hips up and backwards
- Weight shifted backwards and hands moved to knees
- Legs kept mostly straight and hands walk up legs to get upper body erect

193
Q

What is the management for Duchenne’s/Becker’s muscular dystrophy?

A
  • Exercise
  • Night splints/passive stretching
  • Oral steroids
  • Creatinine supplementation
194
Q

What is the life expectancy of Duchenne’s muscular dystrophy?

A
  • 25-35 years
  • Usually due to cardiac/respiratory complications
195
Q

What are the clinical features of a brain abscess?

A
  • Pain
  • Headache
  • Fever
  • Fluctuating consciousness
  • Visual disturbance
  • Unilateral weakness
  • N+V
  • Seizures
  • Personality changes
  • Confusion
  • Difficulty moving/speaking
  • Neck/back stiffness
196
Q

What are the investigations for a brain abscess/herniation?

A
  • Bloods
  • MRI/CT
197
Q

What is the management for a brain abscess?

A
  • Abx (cephalosporin + metronidazole)
  • Steroids
  • Surgery
198
Q

What are the clinical features of a brain herniation?

A
  • Seizures
  • Decreased level of consciousness/coma
  • Mydriasis
  • Irregular/slow pulse
  • Respiratory/cardiac arrest
  • Loss of brainstem reflexes (blinking/gagging/pupillary reflex)
  • Fever
199
Q

What is the management for a brain herniation?

A
  • Osmotic diuretics
  • Paracetamol (fever)
  • Sedation/paralytic agents
  • Prophylactic anticonvulsants
  • Surgery - decompressive craniectomy
  • Hypertonic saline bolus (to decrease ICP)
200
Q

What is Herpes Zoster?

A

A.k.a shingles
An infection caused by the reactivation of VZV within dorsal root or cranial nerve ganglia

201
Q

What is herpes zoster ophthalmicus?

A

When it affects the ophthalmic branch (V1) of the trigeminal nerve (CN V)

202
Q

What are the clinical features of shingles?

A
  • Fever
  • Headache/photophobia
  • Malaise
  • Paraesthesia/pain along affected dermatome
  • Painful/itchy unilateral maculopapular rash –> vesicular rash –> dries and scabs over
  • Hutchinson’s sign
203
Q

What is Hutchinson’s sign?

A

Sign of shingles
- Cutaneous lesions on tip/side/root of nose
- Indicates involvement of V1 nasal branch
- Strong predictor of ocular involvement

204
Q

What are the investigations for shingles?

A
  • Ophthalmological examination (acuity/vision/anterior segment/slit lamp/fundoscopy/extra-ocular muscles)
  • Neurological examination (eyelid erythema, oedema/retinitis, optic neuritis/CN palsy/reduced corneal sensation)
  • Swabs for viral PCR
205
Q

What is the management for shingles?

A
  • Antiviral therapy = oral aciclovir 800mg 5x a day for 7-10 days (should be given within 72 hours of rash onset)
  • Oral steroids
  • Supportive management (cold compress/analgesia/topical lubricants)
206
Q

What is the main complication of shingles?

A

Postherpetic neuralgia (PHN):
- Pain that persists in areas where the rash once was located and continues for >90 days after rash onset

207
Q

What is Ramsay-Hunt syndrome and what are the clinical features?

A
  • Reactivation of varicella zoster virus in the facial nerve (Herpes Zoster Oticus)
  • Otalgia
  • Hearing loss
  • Facial paralysis
208
Q

What is the cause of malaria and how is it spread?

A

Plasmodium family of protozoan parasites spread via bites from female anopheles mosquitos

209
Q

What are the types of malaria?

A
  • Plasmodium falciparum = most common and most severe
  • Plasmodium vivax and ovale (can lie dormant for up to 4 years)
  • Plasmodium malariae
  • Plasmodium knowlesi
210
Q

What are the clinical features of malaria?

A
  • Fever/sweats/rigors
  • Fatigue/myalgia
  • Headache
  • N+V
  • Pallor
  • Hepatosplenomegaly
  • Jaundice
211
Q

What are the investigations for malaria?

A

Malaria blood film
- In order to exclude malaria = require 3 negative samples taken over 3 consecutive days

212
Q

What is the management for uncomplicated malaria?

A
  • Notify public health
  • FIRST LINE = artemether + lumefantrine (Riamet)
  • Quinine + doxycycline
  • Quinine + clindamycin
  • Proguanil + atovaquone (Malarone)
  • Chloroquine
  • Primaquine
213
Q

What is chloroquine used for and what are the side effects?

A

Uncomplicated malaria and malaria prophylaxis
- Increasing rates of resistance

214
Q

What is primaquine used for and what are the side effects?

A

Uncomplicated malaria
- Can cause severe haemolysis in patients with G6PD deficiency

215
Q

What is the management for complicated malaria?

A
  • Notify public health
  • HDU/ICU admission
  • FIRST LINE = IV artesunate
  • IV quinine dihydrochloride
216
Q

What is prophylactic management for malaria?

A
  • Mosquito spray/nets/barriers
  • Antimalarial medication:
  • Proguanil + atovaquone (malarone)
  • Doxycycline
  • Mefloquine
  • Chloroquine + proguanil
217
Q

What is mefloquine used for and what are the side effects?

A

Prophylactic management of malaria
- Risk of psychiatric side effects e.g. anxiety/depression/abnormal dreams/psychosis/seizures

218
Q

What is artesunate used for and what are the side effects?

A

Complicated malaria
- Haemolysis

219
Q

What is an acoustic neuroma?

A

A.k.a vestibular schwannoma
- Benign tumour of Schwann cells surrounding the vestibulocochlear nerve (CN VIII)

220
Q

What are the clinical features of an acoustic neuroma?

A
  • Gradual onset
  • Unilateral sensorineural hearing loss
  • Unilateral tinnitus
  • Dizziness/imbalance
  • Sensation of fullness in ear
  • Loss of corneal reflex
  • Facial nerve palsy (if large)
221
Q

What are the investigations for acoustic neuromas?

A
  • Audiometry = sensorineural hearing loss
  • MRI/CT
222
Q

What is the management for acoustic neuromas?

A
  • Conservative management
  • Surgery
  • Radiotherapy
223
Q

Describe the epidemiology of brain tumours

A
  • Leading cause of childhood cancer deaths in UK
  • Almost always primary in children
224
Q

Which cancers are most likely to metastasise to the brain?

A
  • Lung
  • Breast
  • Renal cell carcinoma
  • Melanoma
  • Colon
225
Q

What is a meningioma?

A
  • Brain tumour growing from cells of meninges
  • Usually benign
226
Q

What is a glioma?

A
  • Tumour of glial cells in brain/spinal cord
  • Astrocytoma (astrocytes) - glioblastoma is most malignant
  • Oligodendroglioma (oligodendrocytes)
  • Ependymoma (ependymal cells)
227
Q

What are the clinical features of brain tumours?

A
  • Can be asx
  • Progressive focal neurological symptoms (depending on location) = limb weakness/balance and coordination issues/memory loss/speech disturbance/behaviour and personality changes/visual disturbances
  • Raised ICP (headache worse on waking, coughing, straining, bending forward/vomiting/papilloedema)
228
Q

What are clinical features of a pituitary tumour?

A
  • Bitemporal hemianopia
  • Acromegaly (excess GH)
  • Hyperprolactinaemia
  • Cushing’s disease (excess ACTH/cortisol)
  • Thyrotoxicosis (excess TSH/T3/T4)
229
Q

What are the investigations for brain tumours?

A
  • CT/MRI
  • Biopsy
  • Fundoscopy
  • Glioma grading (1-4 where 4 is most malignant e.g. glioblastoma multiforme)
230
Q

What is the investigation for papilloedema (due to raised ICP)?

A

Fundoscopy:
- Blurring of optic disc margin
- Elevated optic disc
- Loss of venous pulsation
- Engorged retinal veins
- Haemorrhages around optic disc
- Paton’s line

231
Q

What is the management for brain tumours?

A
  • Surgery
  • Chemotherapy/radiotherapy
  • Palliative care
232
Q

What is the management for pituitary tumours?

A
  • Trans-sphenoidal surgery
  • Radiotherapy
  • Bromocriptine (blocks excess prolactin)
  • Somatostatin analogue e.g. octreotide (blocks excess GH)
233
Q

What are the clinical features of cerebellar disease?

A

VANISHED:
- Vertigo
- Ataxia
- Nystagmus
- Intention tremor
- Slurred speech
- Hypotonia
- Exaggerated broad based gait
- Dysdiadochokinesis

234
Q

What is cauda equina syndrome?

A

Compression of nerve roots of the cauda equina - collection of nerve roots that travel through the spinal canal after the spinal cord terminates at L2/L3:
- Provides sensory innervation to lower limbs/perineum/bladder/rectum
- Provide motor innervation to lower limbs/anal and urethral sphincters
- Provides parasympathetic innervation to bladder/rectum

235
Q

What are the clinical features of cauda equina syndrome?

A
  • Saddle anaesthesia
  • Loss of sensation in bladder/rectum
  • Urinary/faecal retention/incontinence
  • Bilateral sciatica
  • Bilateral/severe motor weakness in legs
  • Reduced anal tone
236
Q

What are the clinical features of spinal cord commpression?

A
  • Myelopathy
  • Back/neck/spine pain
  • Limb weakness
  • Difficulty walking
  • Sensory changes e.g. numbness/paraesthesia
  • Urinary/faecal retention/incontinence
237
Q

What are the investigations for spinal cord compression/cauda equina syndrome?

A
  • X-ray/MRI/CT (urgent - within 24 hours)
  • Biopsy
238
Q

What is the management for spinal cord compression/cauda equina syndrome?

A
  • NSAIDs
  • Steroid injections
  • High dose steroids
  • Abx
  • Chemotherapy/radiotherapy
  • Surgery (lumbar decompression)
  • Acupuncture/chiropractic care
  • PT
239
Q

What is anterior cord syndrome and what are common causes?

A

Incomplete spinal cord injury to the anterior 2/3 of spinal cord
- Anterior spinal artery ischaemia
- Disc herniation
- Trauma
- Tumour
- Epidural collection

240
Q

What are the clinical features of anterior cord syndrome?

A
  • Weakness/paralysis
  • Loss of pain/temperature sensation
  • Autonomic dysfunction (orthostatic hypotension)
  • Bladder/bowel/sexual dysfunction
  • NORMAL 2 point discrimination/proprioception/vibratory senses
241
Q

What are the investigations and management for anterior cord syndrome

A
  • MRI
  • Supportive treatment (poor prognosis)
242
Q

What is neurofibromatosis?

A

Genetic condition that causes benign nerve tumours (neuromas) to develop throughout the nervous system

243
Q

Describe the pathophysiology of neurofibromatosis?

A

Type 1:
- More common
- NF1 gene found on chromosome 17
- Codes for a protein called neurofibromin (tumour suppressor protein)
- Autosomal dominant
Type 2:
- Associated with acoustic neuromas
- NF2 gene found on chromosome 22
- Codes for a protein called merlin (tumour suppressor protein - important in Schwann cells)
- Mutations lead to schwannomas
- Autosomal dominant

244
Q

What are the clinical features of neurofibromatosis?

A

Type 1 - CABBING
- Café-au-lait spots
- Axillary/inguinal freckling
- BB = bony dysplasia (e.g. bowing of long bone/sphenoid wing dysplasia)
- Iris hamartomas (Lisch nodules - yellow/brown spots on iris)
- Neurofibromas (skin-coloured raised nodules/papules with smooth regular surface)
- Glioma of optic pathway

245
Q

What are the investigations and management for neurofibromatosis?

A
  • Genetic testing
  • Monitoring/managing symptoms/treating complications
246
Q

What is chronic fatigue syndrome also known as?

A

Myalgic encephalomyelitis

247
Q

What are the risk factors for chronic fatigue syndrome?

A
  • Female
  • Infections
  • Immune system problems
  • Hormone imbalance
  • Genetics
248
Q

What are the clinical features of chronic fatigue syndrome?

A
  • Extreme tiredness all the time
  • Long recovery time following physical activity
  • Insomnia
  • Thinking/memory/concentration difficulties
  • Muscle/joint pain
  • Headaches
  • Sore throat/flu-like symptoms
  • Dizziness/nausea
  • Palpitations
249
Q

What is the criteria for a diagnosis of chronic fatigue syndrome?

A
  • Severe tiredness lasting >6 months
  • Other medical conditions have been ruled out
  • > 4 symptoms present
250
Q

What is the management for chronic fatigue syndrome?

A
  • Symptomatic relief
  • CBT
  • Energy management
  • Diet changes/vitamin supplements
  • Medications for pain/sleeping
251
Q

What is narcolepsy and what is it associated with?

A

Primary sleep disorder in which the brain loses its normal ability to regulate the sleep-wake cycle - strong association with certain HLA-subtypes

252
Q

Describe the pathophysiology of narcolepsy

A

Type 1:
- Low levels of orexin (hypocretin) in CSF
- This is a neurotransmitter involved in the regulation of sleep/wakefulness/appetite
- Loss of orexin-secreting neurons in the hypothalamus = narcolepsy

253
Q

What are the clinical features of narcolepsy?

A
  • Insomnia
  • Vivid dreams
  • Excessive daytime sleepiness
  • Cataplexy (type 1)
  • Hypnagogic/hypnopompic hallucinations (dream-like hallucinations)
  • Sleep paralysis
254
Q

What are the investigations for narcolepsy?

A
  • Multiple sleep latency testing EEG (MSLT)
  • Polysomnography (PSG)
  • CSF orexin levels
255
Q

What is multiple sleep latency testing EEG (MSLT)?

A

Investigation for narcolepsy - EEG
- Sleep latency = time taken to fall asleep
- SOREM = sleep-onset REM - REM sleep occurring within 15 minutes of sleep onset (usually occurs over an hour after falling asleep)

256
Q

What is the management for narcolepsy?

A
  • Scheduled naps
  • CNS stimulants e.g. modafinil/dexamphetamine/methylphenidate/pitolisant
  • Antidepressants (for cataplexy) e.g. clomipramine, SSRIs, venlafaxine
  • Sodium oxybate (sedative)
  • Social support
257
Q

What is cataplexy?

A

Sudden loss of muscle tone whilst conscious leading to weakness and a loss of voluntary muscle control

258
Q

What are risk factors for cataplexy?

A
  • Fhx
  • Brain injury
    Associated with certain conditions:
  • Type 1 narcolepsy
  • Prader-Willi syndrome
  • Angelman syndrome
  • Niemann-Pick type C disease
259
Q

What are common triggers for cataplexy?

A

Sudden, strong emotions e.g. laughter/fear/anger/stress/excitement

260
Q

What are the clinical features of cataplexy?

A

ALWAYS FULLY CONSCIOUS - vary in severity:
- Minor = slight drooping of eyelids
- Severe = total body collapse with inability to move/speak/keep eyes opem

261
Q

What is Wernicke’s encephalopathy?

A

Acute neurological condition characterised by a triad of confusion, ataxia and oculomotor dysfunction

262
Q

What is Korsakoff syndrome?

A

Chronic amnesia syndrome characterised by defects in both anterograde and retrograde memory

263
Q

What are the causes of Wernicke’s encephalopathy?

A

Thiamine/vitamin B1 deficiency due to:
- Chronic alcoholism
- Prolonged fasting/starvation
- Anorexia nervosa
- Hyperemesis gravidarum
- Systemic malignancy
- End-stage renal failure
- GI disease/malabsorption

264
Q

What are the causes of Korsakoff syndrome?

A

Untreated Wernicke’s encephalopathy

265
Q

What are clinical features of Wernicke’s encephalopathy?

A
  • Ataxia
  • Delirium/confusion
  • Ophthalmoplegia/nystagmus
266
Q

What are clinical features of Korsakoff syndrome?

A
  • Irreversible short term memory loss
  • Confabulation
  • Time disorientation
267
Q

How is Wernicke’s encephalopathy/Korsakoff syndrome treated?

A

IV pabrinex

268
Q

What are the complications of Wernicke’s encephalopathy?

A
  • Permanent horizontal nystagmus
  • Inability to walk
  • Deficit in learning/memory
269
Q

What are the complications of Korsakoff syndrome?

A

Permanent neurological damage - recovery is rare
- Progressive reduced level of consciousness
- Coma
- Death

270
Q

What is Meniere’s disease?

A

Balance disorder caused by excess fluid in a part of the inner ear (labyrinth)

271
Q

What are some causes of Meniere’s disease?

A
  • Allergies
  • Abnormal immune system response
  • Abnormal fluid drainage (due to blockage)
  • Head injury
  • Genetic risk
  • Migraines
  • Viral infection
272
Q

Describe the pathophysiology of Meniere’s disease

A
  • Labyrinth made up of bony labyrinth and membranous labyrinth
  • Membranous labyrinth encased in bone and contains endolymph
  • When head moves, endolymph moves
  • Excess endolymph build-up = vertigo and affect hearing
273
Q

What are the clinical features of Meniere’s disease?

A
  • Vertigo (sweating, N+V)
  • Tinnitus
  • Loss/reduced hearing
  • Loss of ability to hear low frequencies
  • Pressure in affected ear
  • Loss of balance
  • Headaches
274
Q

What are the investigations for Meniere’s disease?

A
  • Hearing test
  • Balance t7est
  • MRI
  • Electrocochleography (ECOG - measures electrical activity of inner ear)
275
Q

What is the management for Meniere’s disease?

A
  • No curative treatment
  • Surgery
  • Medication (allergies/reduce fluid build up/relieve symptoms/improve circulation in inner ear)
  • Hearing aids
276
Q

Describe the pathophysiology of hydrocephalus

A

Obstruction leading to blocked CSF flow

Aqueductal stenosis:
- Cerebral aqueduct that connects third and fourth ventricles is narrowed
- CSF build-up in lateral/third ventricles

Arnold-Chiari malformation:
- Cerebellum herniates downwards through foramen magnum to block CSF outflow

Babies <2:
- Cranial bones not fused at sutures
- Skull able to expand to fit cranial contents
- Hydrocephalus causes outward pressure on cranial bones

277
Q

What are the clinical features of hydrocephalus?

A
  • Gait changes
  • Poor balance
  • Mood changes/depression
  • Confusion/memory changes
  • Difficulty responding to questions
  • Loss of bladder control
278
Q

What are the clinical features of hydrocephalus in babies <2?

A
  • Enlarged/rapidly increasing head circumference (occipito-frontal circumference)
  • Bulging anterior fontanelle
  • Poor feeding/vomiting
  • Poor tone
  • Sleepiness
279
Q

What is normal pressure hydrocephalus?

A

Increased CSF in the ventricles without raised ICP - there is no physical obstruction of CSF, the ventricles just dilated

280
Q

What are the characteristic clinical features of normal pressure hydrocephalus?

A
  • Confusion
  • Ataxia
  • Urinary incontinence
281
Q

What is communicating hydrocephalus and what are common causes?

A

Build up of CSF not due to obstruction but due to an inability if the arachnoid granulations to absorb the CSF
- Meningitis
- SAH
- Cancer

282
Q

What are the clinical features of raised ICP?

A
  • Reduced alertness/consciousness
  • Severe headaches (usually worse in the morning and wake patients up, worse on coughing/straining/bending forward)
  • Blurred vision
  • N+V
  • Changes in behaviour
  • Weakness/problems moving/talking
  • Lack of energy
283
Q

What would the observations be in a patient with raised ICP?

A

Cushing’s triad:
- Widening pulse pressure
- Bradycardia
- Irregular breathing

284
Q

What are the investigations for hydrocephalus?

A
  • CT/MRI (FIRST LINE)
  • LP for CSF (not if raised ICP suspected - contraindicated)
  • Temporary drain (see if symptoms improve)
285
Q

What are normal ICP values?

A

Adults = 10-15mmHg
Infants = 5-20mmHg

286
Q

What is the management for hydrocephalus?

A
  • Osmotic diuretics
  • Prophylactic anticonvulsants
  • Surgery (remove lesion)
  • Surgery (decompressive craniectomy)
  • VP shunt
287
Q

What is a VP shunt?

A

Ventriculoperitoneal shunt - used for hydrocephalus
- Inserted into ventricle in brain and passed under skin from head through to abdomen
- Extra CSF shunted to abdomen where it is absorbed

288
Q

Describe mononeuropathy

A
  • Only one nerve affected
  • Nerve compression due to tumour/cast/prolonged posture/etc.
  • E.g. cubital tunnel syndrome = neuropathy of ulnar nerve
  • E.g. carpal tunnel syndrome = neuropathy of median nerve
289
Q

What are the most common non-compression causes of peripheral neuropathy?

A

DAVID
- Diabetes mellitus
- Alcoholism
- Vitamin B12 deficiency
- Infection/inherited (GBC/Charcot-Marie-Tooth)
- Drugs

290
Q

What are the clinical features of peripheral neuropathy?

A
  • Numbness/tingling/loss of sensation in hands/feet
  • Burning/stabbing/shooting pain in affected areas
  • Loss of balance/coordination
  • Muscle weakness
291
Q

What are the investigations for peripheral neuropathy?

A
  • CT/MRI
  • Nerve conduction studies
292
Q

How are peripheral nerve injuries classified?

A

Sunderland classification system:
- First degree = reversible, local block, no surgery required, usually recovers within hours-weeks
- Second degree = loss of continuity of axons, no surgery required
- Third degree = damage to axons and supporting structures, neurolysis/grafting required
- Fourth degree = damage to axons and surrounding tissues to create scarring that prevents nerve regeneration, surgery/grafting required
- Fifth degree = nerve divided into 2, surgery required

293
Q

What is the management for peripheral neuropathy?

A
  • Acupuncture/massage therapy
  • Medication
  • Orthotics
  • PT/rehab
  • Weight loss
  • Surgery/neurolysis/grafting
  • Lifestyle changes (better control of diabetes)
294
Q

What is a radiculopathy and which type is the most common?

A

Compression of the nerve roots as they exit the spinal cord and spinal column - lumbar radiculopathy is most common

295
Q

What are common causes of radiculopathies?

A
  • Stenosis (spinal stenosis/foraminal stenosis)
  • Bone spurs (OA/trauma/degenerative conditions)
  • Disc herniation
  • Injury
  • Gradual degeneration with age
296
Q

What is sciatica?

A

A lumbar radiculopathy involving the sciatic nerve (L4-S3)

297
Q

Describe the anatomy of the sciatic nerve

A
  • Divides into tibial and common peroneal nerve at knee
  • Supplies sensation to lateral lower leg and foot
  • Supplies motor function to posterior thigh, lower leg and foot
298
Q

What are the clinical features of radiculopathies?

A
  • Sharp pain in affected area
  • Weakness/loss of reflexes
  • Numbness/paraesthesia
  • Poor coordination/difficulty walking
299
Q

What are the clinical features of sciatica?

A
  • Unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet
  • ‘Electric/shooting’ pain
  • Paraesthesia/numbness
  • Motor weakness
  • Affected reflexes
  • Bilateral sciatica = red flag for cauda equina
300
Q

What are the investigations for radiculopathies?

A
  • X-ray
  • CT/MRI
  • Nerve conduction studies
301
Q

What is the investigation for sciatica?

A

Sciatic stretch test:
- Patient lies on back with leg straight
- One leg lifted from ankle with knee extended until limit of hip flexion
- Ankle dorsiflexed
- Sciatica-type pain in buttock/posterior thigh indicates sciatic nerve root irritation
- Symptoms improve with knee flexion

302
Q

What is the management for radiculopathies?

A
  • NSAIDs/opioids/muscle relaxants
  • Steroid injections
  • Maintain healthy weight
  • Good posture whilst sitting/playing sports/exercise/lifting heavy objects
  • Lifestyle changes
  • PT
  • Surgery - laminectomy (remove small section of bone to relieve pressure)
303
Q

What causes neuroleptic malignant syndrome?

A
  • Adverse reactions to antipsychotics
  • Abrupt withdrawal of dopaminergic medication
304
Q

What are the clinical features of neuroleptic malignant syndrome?

A
  • Rigidity
  • Hyperthermia
  • Altered mental status
  • Autonomic instability
305
Q

What are the investigations for neuroleptic malignant syndrome?

A
  • Bloods (raised CK/WCC, deranged LFTs/U&Es, metabolic acidosis)
  • CT/MRI head
  • Infection screen (culture/LP)
306
Q

What is the management for neuroleptic malignant syndrome?

A
  • Withdraw causative medication
  • Supportive treatment
  • Dantrolene may be used
  • Dopamine agonist (bromocriptine) may be used
307
Q

What is the main complication of neuroleptic malignant syndrome?

308
Q

What is the difference between myopathy and myelopathy?

A

Myopathy - any disease affecting muscles

Myelopathy - nerve damage inside spinal cord

309
Q

What pattern of weakness is typically associated with myopathies?

A

Proximal and asymmetrical

310
Q

What are the most common causes of delirium?

A

PINCH ME:
- Pain
- Infection
- Nutrition
- Constipation
- Hydration
- Medication
- Environment

Phase 3a (21 decks)

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