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Phase 2A revision > neuro to work on > Flashcards

neuro to work on Flashcards

1
Q

Name 2 types of secondary headache

A

Underlying cause

  1. Meningitis
  2. Subarachnoid haemorrhage
  3. Giant cell arteritis
  4. Idiopathic intracranial hypertension
  5. Medication overuse headache
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2
Q

Briefly describe the pathophysiology of migraines

A
  1. Cerebrovascular constriction –> aura, dilation –> headache
  2. Spreading of cortical depression
  3. Activation of CN V nerve terminals in meninges and cerebral vessels
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3
Q

what are the differential diagnoses for a migraine?

A
  1. Other headache type
  2. Hypertension
  3. TIA
  4. Meningitis
  5. Subarachnoid haemorrhage
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4
Q

How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

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5
Q

Give 3 causes of trigeminal neuralgia

A
  1. Compression of trigeminal nerve by a loop of vein or artery
  2. Aneurysms
  3. Meningeal inflammation
  4. Tumours
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6
Q

What is the treatment for trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery

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7
Q

What does a small response on an nerve conduction study suggest?

A

There is axon loss

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8
Q

What does a slow response on an nerve conduction study suggest?

A

There is myelin loss

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9
Q

Name 2 organisms that can cause meningitis in immunocompromised patients

A
  1. CMV
  2. Cryptococcus
  3. TB
  4. HIV
  5. herpes simplex
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10
Q

what are the signs of meningitis

A

Kernig’s sign = unable to straighten leg more than 135 degrees without pain when hip is flexed to 90 degrees

Brudzinski’s sign = severe neck stiffness cause hip and knees to flex when neck is flexed

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11
Q

What investigations might you do in someone you suspect has meningitis?

A
  1. Blood cultures (pre LP)
  2. Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
  3. Lumbar puncture (contraindicated with raised ICP)
  4. CT head - exclude lesions
  5. Throat swabs - bacterial and viral
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12
Q

What is the treatment of bacterial meningitis?

A
  • ABCDE + support
  • Empirical therapy = IV Benzylpenicillin
    Assess GCS
  • First line = Ceftriaxone / Cefotaxime
  • Add IV Benzylpenicillin for rash
  • Penicillin allergy = Chloramphenicol
  • Immunocompromised ( Risk of Listeria) = Amoxicillin / Ampicillin

oral dexamethasone to reduce cerebral oedema

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13
Q

What is the treatment of viral meningitis?

A

Watch and wait

acyclovir

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14
Q

What is the treatment for meningococcal septicaemia?

A

IV BENZYLPENICILLIN (in community)

IV CEFOTAXIME (in hospital)

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15
Q

Give 4 reasons why a lumbar puncture might be contraindicated

A
  1. Thrombocytopenia
  2. Delay in Abx admin
  3. Signs of raised ICP
  4. Unstable cardio or resp systems
  5. Coagulation disorder
  6. Infections at LP site
  7. Focal neurological signs
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16
Q

what are the non-viral causes of encephalitis

A
  1. Bacterial meningitis
  2. TB
  3. Malaria
  4. Lyme’s disease
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17
Q

What investigations might you do on someone with encephalitis?

A
  • MRI - shows areas of inflammation, may be midline shifting
  • EEG - periodic sharp and slow wave complexes
  • lumbar puncture
  • blood and CSF serology
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18
Q

what are the causes/risk factors of MS?

A 
Unknown
Environment and genetic components
- exposure to EBV in childhood
- low levels of sunlight and vitamin D
- female
- white
- living far from equator
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19
Q

what are the symptoms of MS?

A

TEAM

  • Tingling
  • Eye = optic neuritis
  • Ataxia
  • Motor - spastic paraparesis, pyramidal weakness (UL = extensors, LL = flexors)
  • swallowing disorders
  • bladder incontinence
  • dizziness, falls
  • constipation
  • fatigue
  • cognitive impairment, depression
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20
Q

what are the signs of MS?

A
  • Lhermitte sign - electric jolt felt down the spine when flexing neck
  • Uhthoff phenomenon - symptoms worse with heat, e.g. hot bath/exercise
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21
Q

Name 3 differential diagnosis’s of MS

A
  1. SLE
  2. Sjogren’s
  3. AIDS
  4. Syphilis
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22
Q

Describe the pharmacological treatment for MS

A

acute relapse
- steroids = IV METHYLPREDNISOLONE

chronic/frequent relapse

  • biological - SC BETA INTERFERON (contraindicated in pregnancy)
  • DMARDs - IV alentuzumab, IV natalizumab
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23
Q

What symptomatic treatments can you give to those with MS?

A

Spasticity

  • BACLOFEN (GABA analogue, reduces Ca2+ influx)
  • TIZANIDINE (alpha-2 agonist)
  • BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

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24
Q

Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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25
Q

Define epileptic seizure

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excess, hypersynchronous neuronal discharge in the brain

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26
Q

Give 5 causes of epilepsy

A
  1. Idiopathic (2/3)
  2. cortical scarring
  3. tumour
  4. stroke
  5. alzheimers dementia
  6. alcohol withdrawal
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27
Q

What is the treatment for focal epileptic seizures?

A 
Lamotrigine = 1st line
Carbamazepine = 2nd line
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28
Q

How do lamotrigine and Carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

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29
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valproate = 1st line

Lamotrigine = 2nd line

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30
Q

How does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

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31
Q

Give 4 potential side effects of anti-epileptic drugs (AED’s)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
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32
Q

Give 4 differential diagnosis’s of epilepsy

A
  1. Syncope
  2. Non-epileptic seizure
  3. Migraine
  4. Hyperventilation
  5. TIA
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33
Q

Define non-epileptic seizure

A

Mental processes associated with psychological distress causes paroxysmal changes in behaviour, sensation and cognitive processes
1-20 minute duration
Closed eyes and mouth

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34
Q

Name 3 intra-cranial haemorrhages

A
  1. Sub-arachnoid haemorrhage
  2. Sub-dural haemorrhage
  3. Extra-dural haemorrhage
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35
Q

What can cause a subarachnoid haemorrhage?

A
  • Traumatic injury
  • Berry aneurysm rupture
    (70-80%) - at common points round Circle of Willis
  • Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins
  • Idiopathic (15-20%)
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36
Q

Give 3 risk factors for a subarachnoid haemorrhage

A

Hypertension
Known aneurysm
Previous aneurysmal SAH

Smoking
Alcohol
Family history
Bleeding disorders

  • associated with berry aneurysms:
    • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
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37
Q

Briefly describe the pathophysiology of a subarachnoid haemorrhage

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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38
Q

Describe the treatment for a subarachnoid haemorrhage

A
  • NIMODIPINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
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39
Q

Give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
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40
Q

Give 3 risk factors of a subdural haematoma?

A
  1. Elderly - brain atrophy, dementia
  2. Frequent falls - epileptics, alcoholics
  3. Anticoagulants
  4. babies - traumatic injury (“shaking baby syndrome”)
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41
Q

Name 3 differential diagnosis’s of a subdural haematoma

A
  1. Stroke
  2. Dementia
  3. CNS masses (tumour vs abscess)
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42
Q

What is the treatment for a subdural haematoma?

A

SURGERY

  • 1* = irrigation via burr-hole craniostomy
  • 2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

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43
Q

Give 3 things that modulate LMN action potential transmission to effectors

A
  1. Cerebellum
  2. Basal ganglia
  3. Sensory feedback
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44
Q

Give 3 disease that are associated with motor neurone damage

A
  1. Motor neurone disease
  2. Spinal atrophy
  3. Poliomyelitis
  4. Spinal cord compression
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45
Q

Give 3 pathologies that are associated with ventral spinal root damage

A
  1. Prolapsed intervertebral disc
  2. Tumours
  3. Cervical or lumbar spondylosis
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46
Q

Describe the pyramidal pattern of weakness in the upper limbs

A

Flexors are stronger than extensors

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47
Q

Describe the pyramidal pattern of weakness in the lower limbs

A

Extensors are stronger than flexors

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48
Q

Give 3 causes of UMN weakness

A
  1. MS
  2. Brain tumour
  3. Stroke
  4. MND
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49
Q

Give 4 sites of UMN damage

A
  1. Motor cortex lesions
  2. Internal capsule
  3. Brainstem
  4. Spinal cord
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50
Q

Define motor neurone disease (MND)

A

A group of neuro degenerative disorders that selectively affect the motor neurons

Most in the anterior horn, cells of the spinal cord and the motor cranial nuclei

There are no sensory problems

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51
Q

What is the clinical presentation of MND?

A
  • results in mixed UMN and LMN presentation (LMN symptoms predominate)
  • wrist drop/foot drop
  • change in appearance of hands - wasting
  • gait disorders/tendencies to trip
  • excessive fatigue
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52
Q

What investigations might you do in someone you suspect to have MND?

A 
Head/spine MRI
Blood tests = muscle enzymes, autoantibodies 
Nerve conduction studies 
EMG
Lumbar Puncture
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53
Q

What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

  1. Presences of LMN and UMN degeneration and progressive history
  2. Absence of other disease processes
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54
Q

What is the treatment for MND?

A
  • MDT care
  • anti-glutaminergic drugs - ORAL RILUZOLE - Na+ channel blocker, inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
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55
Q

Give 3 limb onset symptoms of MND

A
  1. Weakness
  2. Clumsiness
  3. Wasting of muscles
  4. Foot drop
  5. Tripping
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56
Q

Give 3 respiratory onset symptoms of MND

A
  1. Dyspnoea
  2. Orthopnoea
  3. Poor sleep
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57
Q

What are the 4 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP –> headache, decrease GCS, n+v, papilloedema
  2. Progressive neurological deficit –> deficit of all major functions (motor, sensory, auditory, visual) + personality change
  3. Epilepsy
  4. lethargy/tiredness - caused by pressure on brainstem
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58
Q

Name 2 differential diagnosis’s for a brain tumour

A
  1. Aneurysm
  2. Abscess
  3. Cyst
  4. Haemorrhage
  5. Idiopathic intracranial hypertension
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59
Q

Where might secondary brain tumours arise from?

A
  1. non-small cell lung cancer
  2. small cell lung cancer
  3. breast
  4. melanoma
  5. renal cell carcinoma
  6. GI
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60
Q

Give 3 causes of dementia

A
  1. Alzheimer’s disease (50%)
  2. Vascular dementia (25%)
  3. Lewy body dementia (15%)
  4. Fronto-temporal (Pick’s)
  5. Huntington’s
  6. Liver failure
  7. Vitamin deficiency - B12 or folate
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61
Q

Give 3 risk factors of dementia

A
  1. Family history
  2. Age
  3. Down’s syndrome
  4. Alcohol use, obesity, HTN, hyperlipidaemia, DM
  5. Depression
  6. ? Head injury
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62
Q

what is the clinical presentation of Alzheimer’s Disease

A 
● Memory - episodic and semantic
● Language - difficulty understanding or
finding words
● Attention and concentration issues
● Psychiatric changes, e.g. withdrawal,
delusions
● Disorientation, e.g. time and surroundings
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63
Q

What does vascular dementia often present with?

A

● Characterised by stepwise progression - Periods of stable symptoms, followed by a sudden increase in severity
● Presentation varies massively but can include:
- Visual disturbances,
- UMN signs (e.g. muscle weakness, overactive reflexes, clonus),
- attention deficit,
- depression,
- incontinence,
- emotional disturbances
○ If infarct was subcortical, then expect to see dysarthria and parkinsonisms

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64
Q

Describe the pathophysiology of Lewy body dementia

A

● Characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex
● Also see substantia nigra depigmentation and amyloid deposits

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65
Q

what are the clinical features of Lewy body dementia

A

● Dementia is often presented initially
○ Memory loss, spatial awareness difficulties,
loss of cognitive function
● Parkinsonisms, e.g. tremor, rigidity, change in gait
● Visual hallucinations
● Sleep disorders, restless leg syndrome

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66
Q

Give 3 symptoms of Fronto-temporal dementia

A

● Onset tends to be insidious and progressive
● Present with 3 main symptoms:
○ Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning
○ Progressive aphasia, e.g. slow, difficult speech, grammatical errors
○ Semantic dementia, e.g. loss of vocabulary, problems understanding

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67
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in absence of an organic cause

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68
Q

What investigations can you do in primary care to determine whether someone might have dementia?

A
  1. Good history of symptoms
  2. 6 item cognitive impairment test (6CIT)
  3. Blood tests - FBC, liver biochemistry, TFTs, vitamin B12 and folate
  4. Mini mental state examination = screening
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69
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
  3. Give an address with 5 parts
  4. Count backwards from 20
  5. Say the months of the year in reverse
  6. Repeat the address
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70
Q

Name the staging system that classifies the degree of pathology in AD

A

Braak staging
Stage 5/6 = high likelihood of AD
Stage 3/4 = intermediate likelihood
Stage 1/2 = low likelihood

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71
Q

Give 3 ways in which dementia can be prevented

A
  1. Smoking cessation
  2. Healthy diet
  3. Regular exercise
  4. Low alcohol
  5. Engaging in leisure activités
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72
Q

What support should be offered to patients with dementia?

A

Social suport
Cognitive support
Specialist memory service

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73
Q

What medications might you use in someone with dementia?

A 
Acetylcholinesterase inhibitors - increase ACh = donepezil, rivastigmine
Control BP (ACEi) to reduce further vascular damage
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74
Q

what are the causes/risk factors for myasthenia gravis?

A

If <50 = associated with other AI conditions (pernicious anaemia, SLE, RA) and more common in women
If >50 = associated with thymic atrophy, thymic tumour, SLE and RA and more common in men

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75
Q

what are the clinical features of myasthenia gravis?

A
  1. Muscle weakness
  2. Increasing muscular fatigue
  3. Ptosis
  4. Diplopia
  5. Myasthenic snarl
  6. Tendon reflexes normal but fatigable
● Weakness is more marked in proximal muscles
● Weakness might be seen in:
    ○ Small muscle of the hands
    ○ Deltoid and triceps muscles
    ○ Bulbar muscles
    ○ Muscles involved in chewing
● No muscle wasting, sensation is unimpaired
● Seizures can occur
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76
Q

What muscle groups are affected in myasthenia gravis?

A

muscle groups affected in order:

  • extra-ocular
  • bulbar - chewing and swallowing
  • face
  • neck
  • trunk
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77
Q

What can weakness due to myasthenia gravis be worsened by?

A 
Pregnancy
Hypokalaemia
Infection 
Emotion
Exercise 
Drugs (opiates, BB, gentamicin, tetracycline)
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78
Q

What investigations might you do to see if someone has myasthenia gravis?

A
  • mostly clinical examination
  • positive tensilon test
  • anti-AChR antibodies
  • TFTs
  • EMG
  • CT of thymus
  • crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis
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79
Q

Give 3 possible differential diagnosis’s for myasthenia gravis

A
  1. MS
  2. Hyperthyroidism
  3. Acute Guillain-Barre syndrome
  4. Lamert-Eaton myasthenia syndrome
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80
Q

What is treatment for myasthenia gravis?

A

Anti-cholinesterase = pyridostigmine
Immunosuppression = prednisolone (with alendronate - bisphosphonate)
Steroids can be combined with azathioprine or methotrexate
Thymectomy

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81
Q

Give a complication of myasthenia gravis

A

Myasthenic crisis
Weakness of respiratory muscle during relapse
Treatment = plasmapheresis and IV immunoglobulin

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82
Q

Describe the pathophysiology of Parkinson’s disease

A

destruction of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms
Lewy body formation in basal ganglia

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83
Q

What is the 3 cardinal symptoms for Parkinsonism?

A

resting tremor
rigidity
bradykinesia
postural instability

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84
Q

what are the clinical features of Parkinson’s disease

A

● Often an insidious onset

  • impaired dexterity,
  • fixed facial expressions,
  • foot drag

● Common associated symptoms:

  • dementia,
  • depression,
  • urinary frequency,
  • constipation,
  • sleep disturbances
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85
Q

You ask a patient who you suspect to have Parkinson’s disease to walk up and down the corridor to assess their gait, what features would be suggestive of PD?

A

Stooped posture
Asymmetrical arm swing
Small steps
Shuffling

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86
Q

What investigations might you do in someone you suspect to have PD?

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

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87
Q

Describe the pharmacological treatment for Parkinson’s disease

A

young onset + fit

  • Dopamine agonist (ropinirole)
  • MAO-B inhibitor (rasagiline)
  • L-DOPA (co-careldopa)

frail + co-morbidities

  • L-DOPA (co-careldopa)
  • MAO-B inhibitor (rasagiline)
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88
Q

How do dopamine agonists work in the treatment of PD and give an example of one?

A

Reduced risk of dyskinesia
First line in patient <60
Ropinirole, pramipexole

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89
Q

How do MAO-B inhibitors work in the treatment of PD and give an example of one?

A

Inhibit MAO-B enzymes which breakdown dopamine -> increases amount of dopamine available
Rasagiline, selegiline

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90
Q

How do COMT inhibitors work in the treatment of PD and give an example of one?

A

Inhibit COMT enzymes which breakdown dopamine

Entacapone, tolcapone

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91
Q

What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

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92
Q

Define Huntington’s disease

A

Neurodegenerative disorder characterised by the lack of inhibitory neurotransmitter GABA - too much dopamine
autosomal dominant - 100% penetrance

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93
Q

Briefly describe the pathophysiology of Huntington’s disease

A

Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)

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94
Q

Name the cardinal features of Huntington’s disease

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

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95
Q

Name 3 signs of Huntington’s disease

A
  1. Abnormal eye movements
  2. Dysarthria
  3. Dysphagia
  4. Rigidity
  5. Ataxia
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96
Q

What investigations might you do in someone you suspect to have Huntington’s disease?

A

● MRI/CT - loss of striatal volume

● Genetic testing

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97
Q

Describe the treatment of Huntington’s disease

A

poor prognosis - no treatment
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis

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98
Q

what are the causes/risk factors of carpal tunnel syndrome

A
  1. Pregnancy
  2. Obesity
  3. RA
  4. DM
  5. Hypothyroidism
  6. Acromegaly
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99
Q

What investigations might you do in someone who you suspect to have carpal tunnel syndrome?

A

clinical diagnoses based on symptom presentation

EMG = slowing conduction velocity in median sensory nerves
Phalen’s test = 1 min maximal wrist flexion –> symptoms
Tinel’s test = tapping over nerve at wrist –> tingling

USS or MRI if other damage is suspected

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100
Q

What can cause Guillain-Barre syndrome?

A

Bacteria

  • Camplylobacter jejuni
  • Mycoplasma

Viruses

  • CMV
  • EBV
  • HIV
  • Herpes zoster
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101
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Same antigens on infectious organisms as Schwann cells (PNS) –> autoantibody mediated nerve cell damage -> via molecular mimicry
Schwann cell damage consists of demyelination, which results in a reduction in peripheral nerve conduction –> causes acute polyneuropathy

spreads from proximal to distal

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102
Q

what are the clinical features of Guillain-Barre syndrome

A 
Breathing problems
Back pain 
Sensory disturbance
Sweating
Urinary retention
  1. Ascending symmetrical muscle weakness 1-3 weeks post-infection (proximal muscles most affected - trunk, respiratory, CN) TOES TO NOSE WEAKNESS
  2. Pain in legs, back is rare
  3. sensory loss in lower extremities
  4. Reflexes lost early on (LMN sign)
  5. Autonomic features =
    • reduced sweating
    • reduced heat tolerance
    • paralytic ileus - intestinal obstruction w/o blockage
    • urinary hesitancy
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103
Q

What investigations might you do in someone you suspect has Guillain-Barre syndrome?

A
  • Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
  • Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
  • bloods - FBC, U&E, LFT, TFT
  • Spirometry = respiratory involvement
  • ECG
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104
Q

Describe the treatment for Guillain-Barre syndrome

A
  • If FVC <1.5L/80% = ventilate and ITU monitoring
  • IV immunoglobulin (IvIg) for 5 days = decrease duration and severity of paralysis
  • Plasma exchange
  • Low molecular weight heparin (LMWH) - SC ENOXAPARIN
  • Analgesia
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105
Q

What are the causes of an ischaemic stroke?

A
  • small vessel occlusion by thrombus
  • atherothromboembolism (e.g. from carotid artery)
  • cardioembolism (post MI, valve disease, IE)
  • hyper viscosity
  • hypoperfusion
  • vasculitis
  • fat emboli from a long bone fracture
  • venous sinus thrombosis
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106
Q

What are the causes of an haemorrhagic stroke

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
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107
Q

what are the risk factors for ischaemic stroke?

A
  1. Age
  2. Male
  3. Hypertension
  4. Smoking
  5. Diabetes
  6. Recent/past TIA
  7. Heart disease - IHD, AF, valve disease
  8. Combined oral contraceptive
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108
Q

Give 3 signs of an ACA stroke

A
  1. Leg weakness - contralateral
  2. Sensory disturbance in legs
  3. Gait apraxia
  4. Incontinence
  5. Drowsiness
  6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
  7. truncal ataxia - can’t sit or stand unsupported
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109
Q

Give 3 signs of a MCA stroke

A
  1. Contralateral arm and leg weakness and sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
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110
Q

Give 3 signs of a PCA stroke

A

visual issues

  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
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111
Q

Give 3 differential diagnosis’s for a stroke

A
  1. Hypoglycaemia
  2. Intracranial tumour
  3. Head injury +/- haemorrhage
112
Q

What is the treatment for an ischaemic stroke?

A

Immediate management:

  • CT/MRI to exclude haemorrhagic stroke
  • aspirin 300mg

Antiplatelet therapy

  • aspirin 300mg for 2 weeks
  • clopidogrel daily long term

Anticoagulation (e.g. warfarin) for AF

thrombolysis

  • within 4.5 hrs of onset
  • IV alteplase
  • lots of contraindications (can cause massive bleeds)

mechanical thromboectomy
- endovascular removal of thrombus

113
Q

How does alteplase work?

A

Converts plasminogen –> plasmin

So promotes breakdown of fibrin clot

114
Q

What is primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
115
Q

What is secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

116
Q

Give 3 causes of a TIA

A
  1. Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
  2. Cardioembolism - in AF, after MI, valve disease/prosthetic valve
  3. Hyperviscosity - polycythaemia, sickle cell, high WBCC
  4. hypoperfusion - postural hypotension, decreased flow
117
Q

what are the signs of a carotid TIA?

A
  1. Amaurosis fugax = retinal artery occlusion –> vision loss
  2. Aphasia
  3. Hemiparesis
  4. Hemisensory loss
  5. hemianopia
118
Q

what are the signs of a vertebrobasilar TIA?

A
  1. Diplopia, vertigo, vomiting
  2. Choking and dysarthria
  3. Ataxia
  4. Hemisensory loss
  5. Hemianopic/bilateral visual loss
  6. tetraparesis
  7. loss of consciousness
119
Q

what are the differential diagnosis’s for a TIA

A
  1. Migraine aura
  2. Epilepsy
  3. Hypoglycaemia
  4. Hyperventilation
  5. retinal bleed
  6. syncope - due to arrhythmia
120
Q

What investigations would you do in someone who you suspect to have a TIA?

A

first line = diffusion weighted MRI or CT

second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found)

Bloods

  • FBC - look for polycythaemia
  • ESR - raised in vasculitis
  • U&Es, glucose

ECG

echocardiogram

121
Q

What is it essential to do in someone who has had a TIA?

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

122
Q

What is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

  • age
  • BP
  • clinical features - unilateral weakness, speech disturbance
  • duration of TIA
  • presence of diabetes mellitus
123
Q

What classifies as a high risk stroke patient?

A
  • have ABCD2 score >4
  • have AF
  • > 1 TIA in a week
124
Q

What is the treatment for a TIA?

A

immediate treatment = aspirin 300mg and refer to specialist within 24hrs

control CV risk factors

  • BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
  • smoking cessation
  • statin - SIMVASTATIN
  • no driving for 1 month

antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily

anticoagulation (e.g. WARFARIN) for patients with AF

carotid endarterectomy

  • if >70% carotid stenosis
  • reduces stroke/TIA risk by 75%
125
Q

Give 3 causes of spinal cord compression

A
  • trauma,
  • tumours - most common spinal metastases are
    breast, prostate and lung cancer
  • central disc protrusion,
  • prolapsed disc (L4-5 and L5-S1 most common),
  • epidural haematoma,
  • infection,
  • cervical spondylitic myelopathy
126
Q

Give 3 signs and symptoms of spinal cord compression

A 
Red flag signs:
- Loss of bladder or bowel function, 
- UMN signs in the lower limbs (e.g. clonus, hyperreflexia), 
- LMN signs in the upper
limbs (e.g. atrophy)

● Symptoms depend on the injury type and site

  • Can include paraplegia,
  • pain,
  • paraesthesia,
  • changes to tendon reflexes
127
Q

What is the treatment for spinal cord compression?

A

● Acute spinal cord compression is a neurosurgical emergency
● Dexamethasone until treatment plan confirmed
● Catheterisation
● Analgesia
● Surgical decompression if indicated
● Chemotherapy if indicated

128
Q

Give 3 causes of cauda equina syndrome

A
  1. Lumbar disc herniation at L4/5 or L5/S1
  2. Tumour
  3. Trauma
  4. Infection
  5. late-stage ankylosing spondylitis
  6. post-operative haematoma
  7. sarcoidosis
129
Q

what are the clinical features of cauda equina syndrome

A 
● Sudden onset - hours
● Saddle paraesthesia
● bilateral sciatica
● Bladder/bowel dysfunction
● erectile dysfunction
● Motor problems
● Lower back pain
● Bilateral LMN weakness, absent ankle reflex (flaccid and areflexic)
130
Q

What investigations might you do to see if someone has cauda equina syndrome?

A

● Medical emergency
- immediate referral
● Rectal exam - loss of anal tone/sensation
● MRI spine
● knee flexion (L5-S1) and ankle plantar flexion (S1-S2)

131
Q

How do you treat cauda equina syndrome?

A 
● Surgical decompression is essential
● Immobilise spine
● Anti-inflammatory agents
● Antibiotics if infection present
● Chemotherapy if indicated
  • Microdiscectomy - removal of part of the disc - may tear dura!
  • Epidural steroid injection - more effective for leg pain
  • Surgical spine fixation - if vertebra slipped
  • Spinal fusion - reduces pain from motion and nerve root inflammation
132
Q

Define spondyloisthesis

A

Slippage of vertebra over the one below

133
Q

Define spondylosis

A

Degenerative disc disease

134
Q

what are the risk factors for Alzheimer’s disease?

A
  • Down’s syndrome,
  • ApoE E4 allele homozygosity,
  • reduced cognitive activity,
  • depression/loneliness
135
Q

what is the pathophysiology of frontotemporal dementia?

A

● Atrophy of the frontal and temporal lobes
● Loss of neurons, but no plaque formation
● Tau +ve or TDP-43 +ve inclusions

136
Q

what are the risk factors for frontotemporal dementia?

A

50% dominant inheritance

137
Q

what is the treatment for frontotemporal dementia?

A

● No cure
● Supportive therapy, e.g. carers, help setting up a stable routine, home changes for motor difficulties, speech and language therapy
● SSRIs - help with behaviour symptoms
● Levodopa/carbidopa if Parkinson’s symptoms present
● Stopping exacerbating drugs

138
Q

what are the risk factors for vascular dementia?

A 
smoking, 
history of TIAs, 
AF,
hypertension, 
DMT1, 
hyperlipidaemia, 
obesity,
coronary heart disease
139
Q

what is the treatment for vascular dementia?

A

● Supportive therapy, e.g. carers, home changes,
routine help, cognitive simulation programmes
● No pharmacological treatment for the dementia
itself
● SSRIs or anti-psychotics to control symptoms,
e.g. lorazepam
● Prognosis is 3-5 years from diagnosis

140
Q

what are the investigations for Lewy Body dementia?

A

● MMSE or 6-item cognitive impairment test (6-CIT)
● Bloods - B12, TFTs, U&E, MRI (?other cause)
● MSU to check for urine infection

141
Q

what is the diagnostic criteria for Lewy Body dementia?

A

○ Presence of dementia with 2 of:

- fluctuating attention and concentration, 
- recurrent well-formed visual hallucinations, 
- spontaneous Parkinsonism

○ If there is only 1 of the 3 core features, diagnosis can also be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia

142
Q

what is the treatment for Lewy Body dementia?

A

● Refer to a specialist
● Supportive therapy - cognitive stimulation, exercise programmes, at-home care
● Cholinesterase inhibitors, e.g. rivastigmine suggested to treat cognitive decline
● Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe
sensitivity reactions

143
Q

what are the other causes of Parkinson’s disease?

A
  • Drug induced Parkinsonism - caused by dopamine
    antagonists, e.g. clozepine
  • encephalitis
  • exposure to certain toxins, e.g. manganese dust
144
Q

what is the 3 step diagnostic pathway for diagnosing Parkinson’s disease?

A

1) Diagnosis of Parkinsonian syndrome
○ Bradykinesia (required) plus one of rigidity, resting tremor, or postural instability

2) Exclusion criteria (none to be met)
○ History of stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, babinski’s sign, early severe dementia, negative response to large L-dopa dose

3) Supportive criteria (3 or more required)
○ Unilateral onset, rest tremor present, progressive, excellent response to L-dope (70-100%), visual hallucinations

145
Q

Damage to which nerve causes foot drop?

A

Caused by damage to the common peroneal nerve - L4-S1 (also called common fibular
nerve)

146
Q

what are the causes of foot drop?

A 
injury, 
lower back damage,
tumour, 
hip replacement, 
cauda equina syndrome, 
multiple sclerosis
147
Q

what are the investigations for foot drop?

A

● Foot drop itself can be a clinical diagnosis
● Need to find the underlying cause:
○ X-ray, USS, CT, MRI
○ Nerve conduction study

148
Q

what is the treatment for foot drop?

A 
● Brace or splint
● Physiotherapy
● Specialised shoes - prevent foot drop when walking
● Nerve stimulation
● Surgery if indicated
149
Q

what are the risk factors for TIA?

A
  • age
  • hypertension
  • smoking
  • diabetes
  • heart disease - AF
  • combined oral contraceptive pill
  • hyperlipidaemia
  • peripheral artery disease
  • clotting disorder
  • vasculitis
150
Q

what are the differential diagnoses for TIA?

A 
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis
Syncope - E.g. due to an arrythmia
Retinal bleed
151
Q

what are lacunar infarcts (ischaemic stroke)?

A
  • Small infarcts
  • From occlusion of a single small perforating artery supplying a subcortical area
  • Can happen in:
    • Internal capsule
    • Basal ganglia
    • Thalamus
    • Pons
152
Q

what is the clinical presentation of lacunar infarcts (ischaemic stroke)?

A

Depends on the area affected

One of:

  • Sensory loss
  • Weakness (unilateral)
  • Ataxic hemiparesis
  • Dysarthria
  • Motor speech problems
153
Q

which areas of the brain can be affected by lacunar infarcts (ischaemic stroke)?

A

Internal capsule
Basal ganglia
Thalamus
Pons

154
Q

what is the clinical presentation of brainstem infarcts (ischaemic stroke)?

A
  • Quadriplegia
  • Facial numbness & paralysis
  • Gaze & vision disturbances
  • Dysarthria & speech impairment
  • Vertigo, nausea, vomiting
  • Cerebellar signs
  • Palatal paralysis & diminished gag reflex
  • Altered consciousness
  • Locked-in syndrome
  • Coma
155
Q

what are the investigations for ischaemic stroke?

A
  • urgent head CT before treatment
    - shows site
  • pulse, BP and ECG
    • look for AF and MI
  • bloods
    • FBC - look for polycythaemia
    • glucose - rule out hypoglycaemia
    • ESR - raised in vasculitis
    • cholesterol
    • INR - if on warfarin
    • U&Es
  • MRI
    • more sensitive but may be negative in first few hours after infarct
    • indicated if diagnosis is uncertain
156
Q

what are the contraindications of thrombolysis (IV alteplase)?

A
  • Recent surgery last 3 months
  • Recent arterial puncture
  • History of active malignancy (highly vascular thus increased
    bleeding risk)
  • Evidence of brain aneurysm
  • Patient on anticoagulation
  • Severe liver disease (abnormal clotting)
  • Acute pancreatitis
  • Clotting disorder
157
Q

what is the treatment for haemorrhagic stroke?

A
  • frequent GCS monitoring
  • anticoagulants are contraindicated (any anticoagulants should be reversed with vitamin K)
  • control hypertension
  • decompression of raised ICP - MANNITOL
  • surgery may be required
158
Q

what are the causes of intracerebral haemorrhages?

A
  • Hypertension
    • Stiff & brittle vessels, prone to rupture
    • Microaneurysms
  • Secondary to ischaemic stroke
    • Bleeding after reperfusion
  • Head trauma
  • Arteriovenous malformations
  • Vasculitis
  • Vascular tumours
  • Brain tumours
  • Cerebral amyloid angiopathy
  • Carotid artery dissection
159
Q

what is the clinical presentation of intracerebral haemorrhage?

A

similar to ischaemic stroke

pointers to haemorrhage:

  • sudden loss of consciousness
  • severe headache
  • meningism
  • coma
160
Q

what is the management for intracerebral haemorrhage?

A
  • stop anticoagulants immediately
    • effects reversed with clotting factor replacement
  • control of BP - IV drugs
  • reduce ICP
    • mechanical ventilation
    • IV mannitol
  • refer for neurosurgical intervention if:
    • hydrocephalus
    • coma
    • brainstem compression
161
Q

what are the differential diagnoses for subarachnoid haemorrhages?

A
  • headache - migraine, cluster headache
  • meningitis
  • intracerebral haemorrhage
  • cortical vein thrombosis
  • carotid/vertebral artery dissection
162
Q

what are the investigations for migraines?

A
  • usually made with little/no investigations, however if there are red flags further investigation is required
  • always examine eyes, BP, head and neck (muscles, scalp, temporal arteries)
  • lab tests e.g. CRP, ESR
  • CT/MRI
  • LUMBAR PUNCTURE
163
Q

what are the red flag indications for CT/MRI in migraines?

A
  • worst/severe headache i.e. “thunderclap”
  • change in pattern of migraine
  • abnormal neurological exam
  • onset > 50yrs
  • epilepsy
  • posteriorly located headache
164
Q

what are the red flag indications for a lumbar puncture in migraines?

A
  • thunderclap headache

- severe, rapid onset headache / progressive headache / unresponsive headache

165
Q

when are triptans contraindicated?

A

in ischaemic heart disease, coronary spasm and uncontrolled high BP

family history of CVD, stroke, DM and high cholesterol

166
Q

what are the side effects of triptans?

A
  • arrhythmias
  • angina +/- MI
  • recurrence of migraines - higher frequency
167
Q

what are the risk factors of cluster headaches?

A

Smoker
Alcohol
Male
Genetics - autosomal dominant gene has a link

168
Q

what are the preventative measures for cluster headaches?

A
  • 1st line = verapamil (CCB)
  • prednisolone
  • reduce alcohol consumption and stop smoking
169
Q

what are the triggers for tension headaches?

A
  • stress
  • sleep deprivation
  • bad posture
  • hunger
  • eyestrain
  • anxiety
  • noise
170
Q

what is wernicke’s encephalopathy caused by?

A

depletion of thiamine (vitamin B1)

171
Q

what is the clinical presentation of wernicke’s encephalopathy?

A
  • classic triad
    • confusion
    • ataxia
    • ophthalmoplegia
  • sign
    • asterixis (liver flap) - general sign of metabolic encephalopathy
172
Q

what diseases does wernicke’s encephalopathy occur in?

A
  • chronic alcoholism
  • severe starvation
  • prolonged vomiting
173
Q

what are the investigations for wernicke’s encephalopathy?

A
  • diagnosed via clinical examination
174
Q

what is the management for wernicke’s encephalopathy?

A
  • pabrinex - IV B-vitamins (including thiamine)
175
Q

what are the complications of wernicke’s encephalopathy?

A

if not managed appropriately

  • fatal in 20%
  • can progress to korsakoff’s syndrome
176
Q

what is korsakoff’s syndrome?

A
  • irreversible
  • long term brain damage due to vitamin B1 deficiency
  • symptoms = decreased ability to acquire new memories, retrograde amnesia, confabulation (invented memories)
177
Q

what are the causes and risk factors of MND?

A
  • usually sporadic and unknown cause

- 5-10% are familial = SOD-1 mutation

178
Q

what are the 4 different types of MND? do they affect LMN or UMN?

A

amyotrophic lateral sclerosis (ALS) - UMN + LMN

progressive muscular atrophy (PMA) - LMN only

progressive bulbar palsy (PBP) LMN only

primary lateral sclerosis (PLS) UMN only

179
Q

what is the clinical presentation of ALS?

A

● Presents with signs of degeneration of upper and
lower motor neurons
● progressive paralysis and eventual respiratory failure
● Asymmetric onset
● Babinski sign +ve
● Fasciculations of the tongue
● Any corticobulbar signs indicate a worse prognosis:
○ Brisk jaw reflex
○ Dysarthria (difficulty speaking)
○ Dysphagia (difficulty swallowing)
○ Sialorrhoea (excess salivation)

180
Q

what are the clinical features of progressive bulbar palsy (PBP) in MND?

A

CN 9-12

  • LMN in the brain stem
  • pharyngeal muscle weakness
  • progressive loss of speech (hoarse, quiet, nasal)
  • tongue atrophy (flaccid)
181
Q

what are the clinical features of primary lateral sclerosis (PLS) in MND?

A
  • UMN of the arm, legs and face
  • movements become slow
  • progressive tetraparesis
182
Q

what are the clinical features of progressive muscular atrophy (PMA) in MND?

A
  • LMNs only
  • muscle wasting
  • clumsy hand movements
  • fasciculations
  • muscle cramps
183
Q

what are the side effects of pyridostigmine used to treat myasthenia gravis?

A
  • increased salivation
  • lacrimation
  • sweats
  • vomiting
  • miosis (excessive pupillary constriction)
  • diarrhoea
184
Q

what is the treatment for myasthenic crisis?

A
  • monitor FVC
  • plasmapheresis and IV immunoglobulin
  • identify and treat trigger of relapse e.g. infection, medications
185
Q

where are MS demyelination plaques commonly found?

A
  • optic nerves
  • around ventricles of the brain
  • brainstem and cerebellar connections
  • corpus callosum
  • cervical cord (corticospinal tract and dorsal columns)
186
Q

what are the lumbar puncture results for meningitis caused by bacteria?

A
  • cells = polymorphs
  • proteins = raised
  • glucose = low
  • CSF = turbid colour
187
Q

what are the lumbar puncture results for meningitis caused by TB?

A
  • cells = lymphocytes
  • proteins = raised
  • glucose = normal/low
188
Q

what are the lumbar puncture results for meningitis caused by viruses?

A
  • cells = lymphocytes
  • proteins = normal
  • glucose = normal
189
Q

what antibiotic is used in meningitis if S. Pneumoniae is suspected?

A

vancomycin

190
Q

what antibiotic is used in meningitis if listeria is suspected?

A

ampicillin (or amoxicillin) and gentamycin

191
Q

what is the treatment for viral meningitis?

A

no specific treatment
analgesia
antipyretics
hydration

192
Q

what are the risk factors for meningitis?

A
  • immunosuppression
  • elderly
  • pregnant
  • crowding (university)
  • diabetes
  • malignancy
  • IV drug use
  • sickle cell anaemia
  • adrenal insufficiency
193
Q

what are the risk factors for epilepsy?

A

FHx
Premature babies, especially if they are small for their gestational age
Abnormal cerebral blood vessels
Drugs eg. cocaine

194
Q

what are simple focal (partial) seizures?

A
  • No affect on consciousness or memory
  • Awareness unimpaired but will have focal motor, sensory, autonomic or psychic symptoms depending on the affected lobe
  • No post-ictal symptoms
195
Q

what are complex focal (partial) seizures?

A

Memory/awareness is affected before, during or immediately after the seizure

Most commonly arises from the temporal lobe > affects speech, memory & emotion

Post-ictal confusion is common if temporal lobe, whereas recovery is often swift if the frontal lobe is affected

196
Q

what are the characteristics of temporal lobe specific seizures?

A

Aura (80%); deja-vu, auditory hallucinations, funny smells, fear

  • Anxiety, out-of-body experiences
  • Automatisms eg. lip smacking
197
Q

what are the characteristics of frontal lobe specific seizures?

A

Motor features eg. posturing, peddling movements of leg

JACKSONIAN MARCH – seizures march up/down the motor homunculus

Post-Ictal Todd’s palsy

Starts distally in a limb & works its way upwards to the face

198
Q

what is the emergency treatment for epilepsy?

A
  • ABCDE
  • check glucose
  • RECTAL/IV DIAZEPAM or LORAZEPAM
  • IV PHENYTOIN loading
  • mechanical ventilation
199
Q

what is the treatment for generalised tonic-clonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

200
Q

what is the treatment for generalised tonic/atonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

201
Q

what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

202
Q

what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

203
Q

what are the side effects of sodium valproate?

A
  • weight gain
  • hair loss
  • liver failure
204
Q

what are the side effects of lamotrigine?

A

maculopapular rash
blurred vision
vomiting

205
Q

what are the side effects of carbamazepine?

A 
diplopia
rashes
leucopenia
impaired balance
drowsiness
206
Q

what are the side effects of ethosuximide?

A

rashes

night terrors

207
Q

what are the investigations for trigeminal neuralgia?

A
  • In order to diagnose needs to be at least 3 attacks with unilateral facial pain
  • Clinical diagnosis based on criteria above and based on history
  • MRI to exclude secondary causes or other pathologies
  • Not attributed to another disorder
208
Q

what are brainstem lesions caused by?

A
  • Tumour
  • MS
  • Trauma
  • Aneurysm
  • Vertebral artery dissection resulting in infarction
  • Infection - cerebellar abscess from ear
209
Q

what are the signs of a CN3 palsy?

A
  • Ptosis - dropping eyelids
  • Fixed dilated pupil - loss of PARASYMPATHETIC outflow from EDINGER
    WESTPHAL NUCLEUS which supply pupillary sphincter and ciliary bodies -
    lens accommodation
  • Eye down and out
210
Q

what are the causes of CN3 palsy?

A
  • Raised ICP
  • Diabetes
  • Hypertension
  • Giant cell arteritis
211
Q

what are the signs of a CN4 palsy?

A

Innervate superior oblique muscle and results in a head tilt to correct the
extortion that results in diplopia on looking down e.g. walking downstairs

212
Q

what are the causes of a CN4 palsy?

A

Trauma to the orbit - rare

213
Q

what are the causes of CN6 palsy?

A
  • MS
  • Wernicke’s encephalopathy
  • Pontine stroke - presents with fixed small pupils +/- quadriparesis
214
Q

what are the causes of CN3,4,6 palsy?

A
  • Storke
  • Tumours
  • Wernicke’s encephalopathy
215
Q

what are the signs of CN5 palsy?

A
  • Jaw deviates to side of lesion

- Loss of corneal reflex

216
Q

what are the causes of CN5 palsy?

A

trigeminal neuralgia (pain but no sensory loss),
herpes zoster,
nasopharyngeal cancer

217
Q

what are the signs of CN7 palsy?

A

Facial droop and weakness

218
Q

what are the causes of CN7 palsy?

A

• Bells palsy is the most common lesion of the facial nerve - will see
dribbling out the side of mouth
• Fractures of the petrous bones
• Middle ear infections
• Inflammation of the parotid gland - which facial nerve passes through

219
Q

what are the signs of CN9,10 palsy?

A
  • Gag reflex issues
  • Swallowing issues
  • Vocal issues
220
Q

what are the causes of CN9,10 palsy?

A

jugular foramen lesion

221
Q

which conditions are associated with berry aneurysms?

A
  • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
222
Q

give an example of an SSRI

A

citalopram
fluoxetine
sertraline

223
Q

what are the side effects of SSRIs?

A
  • GI disturbance
  • appetite and weight disturbance
  • hypersensitivity reactions
  • hyponatraemia
  • suicidal thoughts
  • seizures
  • prolonged QT interval
224
Q

what are the contraindications of SSRIs?

A
  • contraindicated with other monamine oxidase inhibitors -> may cause serotonin syndrome
  • other drugs that cause prolonged QT interval
  • increase bleeding when used with anticoagulants
225
Q

what are the indications for using tricyclic antidepressants?

A

As a second line treatment for moderate to severe depression where SSRIs
are ineffective

226
Q

what is the mechanism of action for tricyclic antidepressants?

A
  • inhibits neuronal uptake of serotonin and noradrenaline from the synaptic cleft -> increase availability for neurotransmission
227
Q

why do tricyclic antidepressants have extensive side effects?

A
  • they block a wide range of receptors
228
Q

what are the side effects of tricyclic antidepressants?

A
  • dry mouth
  • constipation
  • urinary retention
  • blurred vision
  • sedation
  • hypotension
  • arrhythmias
  • QT and QRS prolongation
  • hallucinations
  • sexual dysfunction
229
Q

when are tricyclic antidepressants contraindicated?

A
  • with other monoamine oxidase inhibitors
230
Q

what are the indications for using a benzodiazepine

A
  • First line treatment of seizures and status epilepticus
  • Management of alcohol withdrawal reactions
  • SHORT TERM treatment of severe anxiety or insomnia
231
Q

what is the mechanism of action for benzodiazepines?

A
  • Benzodiazepines target the GABA-a receptor, which is a chloride channel that opens in response to binding by GABA (the main INHIBITORY NEUROTRANSMITTER)
  • opening the channel allows chloride to enter making the cell more resistant to depolarisation
  • They facilitate the enhanced binding of GABA to GABA-a receptors and have a widespread depressant effect on synaptic transmission
232
Q

what are the side effects of benzodiazepines?

A

cause dose dependent drowsiness, sedation and coma

233
Q

when are benzodiazepines contraindicated?

A
  • in elderly
  • those with respiratory or hepatic impairment
  • neuromuscular disease
  • has sedative effects with alcohol, opioids and CYP450 inhibitors
234
Q

what are the side effects of carbamazepine?

A
  • GI disturbance
  • dizziness
  • ataxia
  • hypersensitivity rash
  • oedema
  • hyponatraemia
235
Q

when is carbamazepine contraindicated?

A
  • prior anti-epileptic hypersensitivity syndrome

- caution in hepatic, renal and cardiac disease

236
Q

what is the mechanism of action for gabapentin and pregabalin?

A

it is closely related to GABA

  • It binds voltage sensitive Ca2+ channels, where it prevents inflow of Ca2+ and thus inhibits neurotransmitter release
  • interfering with synaptic transmission and reducing neuronal excitability
237
Q

what are the side effects of gabapentin and pregabalin?

A
  • drowsiness
  • dizziness
  • ataxia
238
Q

what are the contraindications of gabapentin and pregabalin?

A
  • renal impairment

- other sedating drugs

239
Q

what are the side effects of levo-dopa?

A 
nausea
drowsiness
confusion
hallucinations
hypertension
240
Q

what are the contraindications for levo-dopa?

A
  • take care in elderly

- caution in CVS disease

241
Q

why is levo-dopa always given alongside a decarboxylase inhibitor (Co-Careldopa)?

A
  • reduce levo-dopa’s peripheral conversion before it is able to enter the brain
    this reduces nausea and lowers dose required
242
Q

give an example of a dopamine deleting drug

A

reserpine

243
Q

what are the indications for using a dopamine depleting drug (reserpine)?

A
  • treat dyskinesia in Huntington’s

- can be used as antipsychotic and antihypertensive drug

244
Q

what is the mechanism of action for dopamine depleting drugs (reserpine)?

A
  • irreversibly blocks vescicular monoamine transporter (VMAT)
245
Q

what are the side effects of dopamine depleting drugs (reserpine)?

A
  • nasal congestion
  • GI disturbance
  • drowsiness/dizziness
  • hypotension
  • bradycardia
246
Q

what are the contraindications for dopamine depleting drugs?

A
  • asthma

- CVS disease

247
Q

give an example of MAO inhibitor?

A

selegiline

rasagiline

248
Q

what are the contraindications of MAO inhibitors?

A
  • aged cheese and alcohol -> can cause hypertensive crisis

- antidepressants and adrenaline

249
Q

give an example of ACh inhibitor

A

rivastigmine

donepezil

250
Q

what are the indications for ACh inhibitors?

A
  • alzheimers
  • Lewy body dementia
  • parkinsons
  • myasthenia gravis
251
Q

what is the mechanism of action for ACh inhibitors

A

inhibits ACh breakdown by blocking site of acetylcholinesterase

252
Q

what are the side effects of ACh inhibitors?

A
  • bradycardia
  • hypotension
  • hypersecretion
  • bronchoconstriction
  • GI tract hyper motility
  • prolonged muscular contraction
253
Q

what are the contraindications of ACh inhibitors?

A

urinary retention

CVS disease

254
Q

what are the causes of primary syncope?

A

Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

255
Q

what is the treatment for Bell’s palsy?

A
  • prednisolone
  • eye care
  • ?antivirals
256
Q

what are the characteristics of cushing’s triad?

A
  • bradycardia
  • irregular respirations
  • widened pulse pressure
257
Q

what is cushing’s reflex?

A
  • nervous system response to increased ICP
  • as ICP increases cerebral perfusion pressure (CPP) decreases, resulting in reduced cerebral perfusion
  • sympathetic nervous system is activated which increases BP
258
Q

what are the clinical presentation of cushing’s reflex?

A
  • cushing’s triad - bradycardia, irregular respirations and widened pulse pressure
  • hypertension
  • headache
  • vomiting
  • blurred vision
259
Q

what are the investigations for cushing’s reflex?

A
  • measure ICP - lumbar puncture or continuous monitoring via catheter in ventricle of brain
  • CT/MRI
260
Q

what is the treatment for cushing’s reflex?

A
  • mannitol
  • duiretics - furosemide
  • steroids - methylprednisolone
  • sedatives - propofol
  • hyperventilation
  • elevate head to 30 degrees (reverse trendelenburg position)
  • drain CSF
  • craniotomy
261
Q

what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

262
Q

what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

263
Q

what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

264
Q

what are the clinical features of horner’s syndrome?

A

MAPLE

  • Miosis
  • Anhydrosis
  • Ptosis
  • Loss of ciliospinal reflex
  • Endophthalmos (sunken eyeball)
265
Q

what is the treatment for horner’s syndrome?

A

treat underlying cause

266
Q

what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

267
Q

what is the presentation of brown-sequard syndrome?

A
  • DCML = ipsilateral loss of proprioception and vibration sensation
  • spinothalamic = contralateral loss of temperature and pain sensation
  • corticospinal = ipsilateral spastic paralysis below lesion
268
Q

what are the signs of lateral medullary syndrome in ischaemic stroke?

A

Sudden vomiting and vertigo

Ipsilateral Horner’s syndrome = reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia

269
Q

what are the causes of status epilepticus?

A
  • Abruptly stopping anti epileptic treatment
  • Alcohol abuse
  • Poor compliance to therapy
270
Q

give one differential diagnosis for huntington’s disease

A

Sydenham’s chorea (Rheumatic fever)

271
Q

what are the secondary causes of syncope?

A 
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
272
Q

what are the clinical features of syncope?

A 
Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache
273
Q

`what are the investigations for syncope?

A

Full history and examination

ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome

24 hour ECG if paroxysmal arrhythmias are suspected

Echocardiogram if structural heart disease is suspected

Bloods, including a FBC (anaemia), U&E (arrhythmias and seizures) and blood glucose (diabetes)

274
Q

what is the management for syncope?

A

avoid triggers in primary syncope.

management of underlying pathology

275
Q

what preventative measures should be taken for migraines?

A
  • beta blockers - propranolol
  • TCA - amitrityline
    anticonvulsant - topiramate
  • acupuncture

Phase 2A revision (38 decks)

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