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MY PHASE 2A MEDICINE > NEURO > Flashcards

NEURO Flashcards

1
Q

Define syncope.

A

Insufficient blood or oxygen supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes.

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2
Q

Give 5 signs that a transient loss of consciousness is due to syncope.

A
  1. Situational.
  2. 5-30s in duration.
  3. Sweating.
  4. Nausea.
  5. Pallor.
  6. Dehydration.
  7. more likely with exertion
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3
Q

Give 5 causes of transient loss of consciousness.

A
  1. Syncope.
  2. Epileptic seizures.
  3. Non-epileptic seizures.
  4. Intoxication e.g. alcohol.
  5. Ketoacidosis/hypoglycaemia.
  6. Trauma.
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4
Q

What can be the causes of syncope?

A

Drop in blood pressure (assytolly)

Non-epileptic seizure

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5
Q

Give a definition for a non-epileptic seizure.

A

Mental processes associated with psychological distress cause paroxysmal changes in behaviour, sensation and cognitive processes.

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6
Q

Give 5 signs of a non-epileptic seizure.

A
  1. Situational.
  2. 1-20 minutes in duration (longer than epileptic).
  3. Eyes closed.
  4. Crying or speaking.
  5. Pelvic thrusting.
  6. History of psychiatric illness.
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7
Q

Which is likely to last for longer, an epileptic or a non-epileptic seizure?

A

A non-epileptic seizure can last from 1-20 minutes whereas an epileptic seizure lasts for 30-120 seconds.

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8
Q

Give some of the causes of syncope

A
  1. structural/congenital heart defects
  2. hypovolaemia ( V&D, addisons)
  3. postural
  4. orthostatic stress (standing up in hot crowds)
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9
Q

In what ways are epilepsy different from syncope?

A

Epilepsy = Tongue biting, head turning, muscle pain, loss of consciousness,
cyanosis, post-ictal symptoms

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10
Q

Give a definition for an epileptic seizure.

A

Excessive, unsynchronised neuronal discharges in the brain cause paroxysmal changes in behaviour, sensation or cognitive processes.

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11
Q

Give 5 signs of an epileptic seizure.

A
  1. 30-120s in duration.
  2. ‘Positive’ symptoms e.g. tingling and movement.
  3. Tongue biting.
  4. Head turning.
  5. Muscle pain.
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12
Q

Give 5 causes of epilepsy.

A
  1. Flashing lights.
  2. Cerebrovascular disease e.g. stroke.
  3. Genetic predisposition.
  4. CNS infection e.g. meningitis.
  5. Trauma.
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13
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

This is likely to be an epileptic seizure.

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14
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

This is likely to be due to a blood circulation problem e.g. syncope.

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15
Q

What 2 categories can epileptic seizures be broadly divided into?

A
  1. Focal epilepsy - only one portion of the brain is involved.
  2. Generalised epilepsy - the whole brain is affected.
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16
Q

Give 3 examples of focal epileptic seizures.

A
  1. Simple partial seizures with consciousness.
  2. Complex partial seizures without consciousness.
  3. Secondary generalised seizures.
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17
Q

Give 3 examples of generalised epileptic seizures.

A
  1. Absence seizures.
  2. Myoclonic seizures.
  3. Generalised tonic clonic seizures.
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18
Q

Describe a generalised tonic clonic seizure.

A

Sudden onset rigid tonic phase followed by a convulsion (clonic phase) in which the muscles jerk rhythmically.

The episode lasts up to 120s and is associated with tongue biting and incontinence.

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19
Q

Give 2 features of absence seizures.

A
  1. Commonly present in childhood.

2. Child ceases activity and stares for a few seconds.

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20
Q

Describe a myoclonic seizure.

A

Isolated muscle jerking.

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21
Q

What is the treatment for focal epileptic seizures?

A

Carbamazepine.

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22
Q

How does carbamazepine work as an AED?

A

It inhibits pre-synaptic Na+ channels and so prevents axonal firing.

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23
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valporate.

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24
Q

What is the major side effect of sodium valporate?

A

It is teratogenic!

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25
Q

Give 4 potential side effects of AED’s e.g. sodium valporate and carbamazepine.

A
  1. Cognitive disturbances.
  2. Heart disease.
  3. Drug interactions.
  4. Teratogenic.
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26
Q

What features might be present in the history of a headache that make you suspect meningitis?

A
  1. Pyrexia.
  2. Photophobia.
  3. Neck stiffness.
  4. Non-blanching purpura rash.
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27
Q

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

A
  1. Bloods.
  2. Blood cultures.
  3. Throat swab.
  4. Blood for serology and PCR.
  5. CT head.
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28
Q

Name 3 organisms that can cause meningitis in adults.

A
  1. N.meningitidis (g-ve diplococci).
  2. S.pneumoniae (g+ve cocci chain).
  3. Listeria monocytogenes (g+ve bacilli).
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29
Q

Name 3 organisms that can cause meningitis in children.

A
  1. E.coli (g-ve bacilli).
  2. Group B streptococci e.g. s.agalactiae.
  3. Listeria monocytogenes.
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30
Q

Give 5 symptoms of meningitis.

A
  1. Non-blanching petechial rash.
  2. Neck stiffness.
  3. Headache.
  4. Photophobia.
  5. Papilloedema.
  6. Fever.
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31
Q

How would you describe the rash that is characteristic of meningitis?

A

Non-blanching petechial rash

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32
Q

When is a child vaccinated against meningitis B?

A

At 8 weeks and 16 weeks.

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33
Q

When is a child vaccinated against meningitis C?

A

At 12 weeks and 1 year.

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34
Q

When is a child vaccinated against meningitis ACWY?

A

14 years old

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35
Q

For which bacteria is meningitis prophylaxis effective against?

A

N. Meningitidis

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36
Q

What can be given as prophylaxis against N.meningitidis infection?

A

Ciprofloxacin.

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37
Q

What is the most common cause of viral meningitis?

A

Enterovirus

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38
Q

What is the colour of the CSF in someone with bacterial infection?

A

Cloudy

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39
Q

In what group of people is encephalitis common?

A

The immunocompromised.

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40
Q

Give 4 symptoms of encephalitis.

A
  1. Fever.
  2. Headache.
  3. Lethargy.
  4. Behavioural change.
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41
Q

A lumbar puncture is done and a CSF sample is obtained from someone who is suspected to have encephalitis. Describe what the lymphocyte, protein and glucose levels would be like in someone with encephalitis.

A
  • Lymphocytosis (raised lymphocytes).
  • Raised protein.
  • Normal glucose.
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42
Q

What is meningitis?

A

Inflammation of the Pia and arachnoid mater.

Infection of the CSF

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43
Q

What is encephalitis?

A

Inflammation of the cerebral cortex

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44
Q

What are the viral causes of encephalitis?

A
  1. HERPES SIMPLEX
  2. Varicella zoster
  3. Parvovirus
  4. HIV
  5. Mumps
    (Ask about travel!!!)
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45
Q

How would you treat meningitis in the community/ in hospital?

A 
Community = IM benzylpenicillin
Hospital = cefotaxime

Also prescribe STEROIDS - > reduced neurological sequelae and therefore reduce morbidity (particularly with strep. Pneumoniae)

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46
Q

Describe the pathophysiology of meningitis

A
  1. Bacteria enter CSF; and can be isolated from immune cells due to BBB, replication
  2. Blood vessels become leaky
  3. Meningeal inflammation +/- brain swelling
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47
Q

What is the management plan for when a patient enters hospital with meningitis?

A
  1. Assess GCS (Glasgow Coma Score)
  2. Blood cultures
  3. Broad spectrum antibiotics
  4. Steroids (IV dexamethasone)
  5. Lumbar puncture (more specific antibiotics)
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48
Q

What are contraindications for carrying out a lumbar puncture?

A
  1. Abnormal clotting (platelets/coagulation)
  2. Petechial rash
  3. Raised intracranial pressure
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49
Q

What are the two ‘non-clinical’ procedures you have to do with a patient who has meningitis?

A
  1. Provide prophylaxis for ‘close contacts’

2. Notify PUBLIC HEALTH ENGLAND

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50
Q

What would a likely clinical picture be for encephalitis?

A

Hours to days:
Preceding “flu-like” illness

Then:
1. Altered GCS: confusion, drowsiness, coma
2. Fever
3. Seizures
4. Memory loss
(+/- meningism)
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51
Q

What is meningism?

A
  1. Neck stiffness
  2. Photophobia
  3. Headache
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52
Q

What is the investigation pathway for a patient with suspected encephalitis?

A
  1. MRI head +/- EEG
  2. Lumbar puncture after
    • Lymphocytic CSF
    • Viral PCR
  3. DO A HIV TEST!
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53
Q

How do you treat encephalitis?

A
  1. Mostly supportive

2. Aciclovir if HSV or VZV

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54
Q

How do you contract tetanus?

A

Inoculation through skin with Clostridium tetani spores (GRAM POSITIVE ANAEROBE found globally in soil)

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55
Q

What toxin is produced that causes clinical tetanus?

A

Tetanospasmin

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56
Q

What is the pathophysiology of tetanus?

A
  1. Interferes with neurotransmitter release
  2. increased neuron firing
  3. unopposed muscle contraction and spasm
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57
Q

Give 3 symptoms of tetanus.

A
  1. Trismus (lockjaw).
  2. Sustained muscle contraction.
  3. Facial muscle involvement.
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58
Q

Is rabies a bacterial or viral infection?

A

Viral

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59
Q

What is the pathophysiology of herpes zoster?

A
  1. Infected with Varicella zoster = chicken pox
  2. Dormant in dorsal root ganglion
  3. Reactivation = shingles
  4. Pain in dermatomal distribution that doesn’t cross midline
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60
Q

How do you treat encephalitis caused by herpes zoster?

A

Oral acyclovir

Herpes simplex = Iv acyclovir

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61
Q

Define dementia.

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language. There is a progressive decline in cognitive function.

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62
Q

What is the epidemiology of dementia?

A

10% of people over 65 and 20% of people over 80 have dementia.

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63
Q

Give 3 causes of dementia.

A
  1. Alzheimer’s disease (65%).
  2. Fronto-temporal.
  3. Vascular.
  4. Lewy bodies.
  5. Vitamin deficiency e.g. B12.
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64
Q

Frontal lobe atrophy is seen on an MRI. What kind of dementia is this patient likely to have?

A

Fronto - temporal

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65
Q

Give 3 functions of the temporal lobe.

A
  1. Hearing.
  2. Language comprehension.
  3. Memory.
  4. Emotion.
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66
Q

What lobe of the brain is affected in Alzheimer’s disease?

A

Temporal lobe

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67
Q

Give 4 symptoms of Alzheimer’s disease.

A
  1. Selective attention.
  2. Language impairments - difficulty in naming and understanding.
  3. Apraxia.
  4. Global deficits.
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68
Q

What is the 6CIT?

A

Six Item Cognitive Imapirment Test

  • Dementia screening tool
    1. What year is it?
    2. What month is it?
    3. Give an address with 5 parts (John, Smith, 42, High, St, Bedford)
    4. Count 20-1
    5. Say months of year in reverse
    6. Repeat address
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69
Q

What is often the first cognitive marker of AD?

A

Short term memory impairment.

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70
Q

Give 2 histological signs of AD.

A
  1. Amyloid plaques

2. Neuronal reduction

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71
Q

How is AD diagnosed?

A

When criteria (Braak staging) for intermediate or high likelihood AD are met AND the patient has a clinical history of dementia.

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72
Q

25% of all patients with AD will develop what?

A

Parkinsonism

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73
Q

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

A
  1. Good history of symptoms.
  2. 6CIT.
  3. Blood tests.
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74
Q

Why might you do a blood test in someone who you suspect has dementia?

A

To look at the vitamin levels that may suggest a reversible cause e.g. dementia due to B12 deficiency.

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75
Q

Dementia: what secondary care investigation could you do to look at brain structure?

A

Brain MRI

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76
Q

What secondary care investigation could you do to look at the pathology of dementia?

A

Amyloid and tau histopathology.

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77
Q

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

A

Braak staging.

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78
Q

Describe Braak staging.

A
  • Stage 5/6 - high likelihood of AD.
  • Stage 3/4 - intermediate likelihood.
  • Stage 1/2 - low likelihood.
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79
Q

Give 5 ways in which dementia can be prevented.

A
  1. Stop smoking.
  2. Healthy diet.
  3. Regular exercise.
  4. Healthy weight.
  5. Low alcohol intake.
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80
Q

What medications might you use in someone with dementia?

A

Acetylcholine esterase inhibitors.

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81
Q

What are the differentials for dementia?

A
  1. Parkinsons
  2. Depression
  3. Huntingtons disease
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82
Q

Give 5 psychiatric changes in Alzheimers dementia

A
  1. APATHY
  2. Subtle behaviour changes: inattentiveness, social and emotional withdrawal, agitation
  3. Psychotic symptoms: delusions or hallucinations
  4. Agitation, anxiety.
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83
Q

How would you differentiate between dementia and depression?

A
  1. Dementia attempts to answer Qs, depression distressed and may answer ‘ don’t know’
  2. Dementia vague, insidious onset, depression may be sudden with traumatic event
  3. Dementia attempt to hide problems + confusion in evenings, depression subjective memory loss
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84
Q

Give 5 red flags for suspected brain tumour in a patient presenting with a headache.

A
  1. New onset headache and history of cancer.
  2. Cluster headache.
  3. Seizure.
  4. Significantly altered consciousness, memory, confusion.
  5. Papilloedema (swollen optic disc).
  6. Other abnormal neuro exam.
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85
Q

What are the 3 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP.
  2. Progressive neurological deficit.
  3. Seizures
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86
Q

What are the most frequent brain tumour?

A

GLIOMA

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87
Q

Give 3 symptoms of raised ICP.

A
  1. Headache.
  2. Drowsiness.
  3. +/- vomiting.
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88
Q

You ask a patient with a brain tumour about any factors that aggravate their headache. What might they say?

A
  1. Worst first thing in the morning.

2. Worst when coughing, straining or bending forward.

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89
Q

What is the cardinal physical sign of raised ICP?

A

Papilloedema.

Due to obstruction of venous return from the retina.

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90
Q

Where might secondary brain tumours arise from?

A
  1. Lung (NSCC).
  2. Breast.
  3. Malignant melanoma.
  4. Kidney.
  5. Gut.
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91
Q

Describe the treatment for secondary brain tumours.

A
  1. Surgery and adjuvant radiotherapy.
  2. Chemotherapy.
  3. Supportive care.
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92
Q

From what cell do primary brain tumours originate?

A

Glial cells:

  • Astrocytoma (90%).
  • Oligodendroglioma (<5%).
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93
Q

Describe the WHO glioma grading.

A
  1. Grade 1: benign paediatric tumour.
  2. Grade 2: pre-malignant tumour.
  3. Grade 3: ‘anaplastic astrocytoma’ - cancer.
  4. Grade 4: glioblastoma multiforme (GBM).
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94
Q

Describe the epidemiology of grade 2 gliomas.

A

Disease of young adults

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95
Q

What is often the first symptom that someone with a grade 2 glioma presents with?

A

Seizures

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96
Q

Describe the treatment for High grade glioma.

A

HGG:

  1. steroids (reduce oedema)
  2. resect tumour (relieve pressure, improves prognosis, better diagnosis)
  3. radical radiotherapy
  4. chemotherapy (temozolomide).

(prognosis 6 without or 18 months with)

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97
Q

Describe the treatment for low grade glioma

A

LGG:

  1. early resection/biopsy (awake craniotomy)
  2. radio and chemotherapy improves long term survival.
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98
Q

How can raised ICP lead to death?

A
  1. As tumour grows -> downward displacement of the brain
  2. pressure on the brainstem (drowsiness) -> respiratory depression
  3. coma -> death
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99
Q

What could a tumour in the spinal cord lead to?

A

Spinal cord compression/cauda equina

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100
Q

What nerve is affected in carpal tunnel syndrome?

A

Median nerve

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101
Q

Give 3 risk factors for carpal tunnel syndrome.

A
  1. Pregnancy.
  2. Obesity.
  3. RA.
  4. Hypothyroidism.
  5. Acromegaly.
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102
Q

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

A
  1. Tinel’s test
    - Tap over carpal tunnel with finger
    - If patient develops tingling in the thumb and radial two and a half fingers this is suggestive of median nerve irritation and compression
  2. Phalen’s test.
    - Ask patient to hold their wrist in complete and forced flexion (pushing the dorsal surfaces of both hands together) for 60 seconds
    - If the patient’s symptoms of carpal tunnel syndrome are reproduced then the test is positive (e.g burning, tingling or numb sensation in the thumb, index, middle and ring fingers)
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103
Q

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol.

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104
Q

Give an example of an acute neuroapthy.

A

Guillan - Barre syndrome (Demyelinating / Axonal motor / Axonal sensorimotor)

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105
Q

What can cause Guillain-barré syndrome?

A

Often post-infection e.g. following CMV, EBV, campylobacter jejuni infection.

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106
Q

Describe the symptoms seen in Guillain-barré syndrome.

A

ASCENDING muscle weakness, changes in sensation/pain.

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107
Q

How would you treat GB syndrome

A

IV IG in ITU

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108
Q

What is the most common type of peripheral neuropathy?

A

Sensori - motor

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109
Q

What type of neuropathy does vasculitis cause?

A

asymmetrical sensori - motor

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110
Q

Name a disease that is associated with NMJ damage.

A

Myasthenia Gravis

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111
Q

What is myasthenia gravis characterised by?

A

Weakness and fatigability of

  • ocular (ptosis)
  • bulbar (dysphasia + dysarthria - brainstem minus midbrain, plus cerebellum)
  • proximal limb muscles
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112
Q

What antibodies would be detected in the serum of someone with myasthenia gravis?

A
  1. Autoantibodies to nicotinic acetylcholine receptors (anti-AChR antibodies)
  2. MuSK (muscle specific tyrosine kinase)

Also ask patient to count to 50!

113
Q

A 40 year old woman has weakness, fatiguability of ocular (-> Ptosis), bulbar (dysphasia, dysarthria) and proximal limbs but their conditions improve after rest.

A

Myasthenia gravis

114
Q

What is the pathophysiology of MG?

A

Myasthenia gravis is an autoimmune disorder.

  1. Auto-antibodies (IgG) attach to Ach receptors at post synaptic membrane and destroy them
  2. Fewer action potentials fire -> muscle weakness and fatigue.
115
Q

What condition is often also present in patient with MG?

A

10% have thymic tumour

116
Q

Which drugs aggravate MG?

A

BETA BLOCKERS
lithium
some AbX

117
Q

How would you treat MG?

A
  1. ANTICHOLINESTERASES
    - Pyridostigmine
  2. Immunosupressants
    - Prednisolone, azathioprine
  3. Plasmapheresis
  4. IVIG used in myasthenic crisis
  5. Thymectomy
118
Q

If a patient has aphasia what region in the brain has been affected?

A

Brocas area

119
Q

If a patient has receptive dysphasia what region in the brain has been affected?

A

Werncikes area

120
Q

Name 3 intra-cranial haemorrhages.

A
  1. Extra-dural.
  2. Sub-dural.
  3. Sub-arachnoid.
121
Q

What can cause a sub-arachnoid haematoma?

A

Rupture of a berry aneurysm around the circle of willis

  • Origin of anterior communicating artery
  • Joining of posterior communicating artery with ICA
122
Q

Give 5 symptoms of a sub-arachnoid haemorrhage.

A
  1. Sudden onset ‘thunderclap’ headache.
  2. Photophobia.
  3. Reduced conciousness.
  4. Neck stiffness.
  5. Nausea and vomiting.
123
Q

What investigations might you do to see if someone has a sub-arachnoid haemorrhage?

A
  1. CT scan of head - would show blood in sulci(white star)
  2. Lumbar puncture (wait 12 hours!)
  3. MRA.
124
Q

What is the treatment for a sub-arachnoid haematoma?

A
  1. Nimodipine -> decreases cerebral artery vasospasm so prevents cerebral ischaemia
  2. Surgery – coiling (endovascular obliteration) preferred to clipping
125
Q

What would a lumbar puncture of a patient with SAH show?

A

AFTER 12 HOURS
LP result shows xanthochromia (yellowing)
- Breakdown of RBCs -> increased bilirubin

126
Q

What are RF for having a SAH?

A
  1. Smoking, alcohol
  2. HTN
  3. bleeding disorders
  4. Marfan + ED syndromes
  5. autosomal dominant PKD
127
Q

What would small warning bleeds prior to the onset of SAH cause?

A

Sentinel headache (headache, dizziness, orbital pain) in 3 weeks prior

128
Q

Describe the natural history of a sub-dural haematoma.

A

Latent period after the head injury. 8-10 weeks later the clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up into the haematoma -> signs and symptoms develop. There is a gradual rise in ICP.

129
Q

What causes water to be sucked up into a sub-dural haematoma 8-10 weeks after a head injury?

A

The clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up by osmosis into the haematoma.

130
Q

Give 3 symptoms of a SUB-DURAL haematoma.

A
  1. Headache.
  2. Drowsiness.
  3. Confusion.
    (increased ICP)
131
Q

Why are elderly and alcoholics most likely to be affected by sub/extra dural haematomas?

A
  1. Brain atrophy
  2. Vein stretching
  3. Increased likelihood to fall
132
Q

How does the cause of bleeding differ in sub/ extra dural haematomas?

A

SUB = Rupture of bridging veins running from cortex to venous sinuses

EXTRA = Fracture of temporal bone leading to tear of middle meningeal artery

133
Q

What do the ventricles do to prolong survival in someone with an extra-dural haemorrhage?

A

The ventricles get rid of their CSF to prevent the rise in inter-cranial pressure.

134
Q

How do the levels of consciousness differ in a patient with sub/extra dural haematoma?

A

SUB = Fluctuating levels of consciousness but ICP gradually rises over some weeks

EXTRA= Brief period of unconsciousness, then a lucid interval of improvement, then condition rapidly deteriorates as ICP increases

135
Q

How would you manage a sub/ extra dural haematoma?

A
  1. ABCDE
  2. Osmotic diuresis with mannitol (lower ICP)
  3. Surgery
    - SDH = emergency evacuation via Burr hole craniotomy
    - EDH = clot evacuation +/- ligation of bleeding vessel
136
Q

How would you distinguish between an EDH and SDH on CT?

A

Egg shaped = Extra dural

Sickle shaped = Sub dural

137
Q

Why is lumbar puncture contraindicated in EDH and SDH?

A

CONING

138
Q

Give 2 primary causes of intra-cerebral haemorrhage.

A
  1. Hypertension -> Berry or Charcot-Bouchard aneurysms -> rupture.
  2. Lobar (amyloid angiopathy).
139
Q

Give 5 secondary causes of intra-cerebral haemorrhage.

A
  1. Tumour.
  2. Arterio-venous malformations (AVM).
  3. Cerebral aneurysm.
  4. Anticoagulants e.g. warfarin.
  5. Haemorrhagic transformation infarct.
140
Q

What is the likely cause of bleeds in the basal ganglia, pons and/or cerebellum?

A

Hypertension

141
Q

Describe the treatment for anti-coagulant related intra-cerebral haemorrhage.

A
  1. Control BP: B-blocker
  2. BERIPLEX (works faster than vit K)
  3. Clot evacuation
142
Q

Define stroke.

A

Rapid onset of neurological deficit which is the result of a vascular lesion and is associated with infarction of central nervous tissue.

143
Q

What can cause a stroke?

A
  1. Cerebral infarction due to embolism or thrombosis (85%).

2. Intracerebral or sub-arachnoid haemorrhage (15%).

144
Q

Give 4 modifiable RF for strokes

A
  1. HTN
  2. smoking
  3. hyperlipidaemia
  4. obesity
145
Q

Give 4 non-modifiable RF for strokes

A
  1. DM
  2. male
  3. vasculitis
  4. hypotension
146
Q

Give 5 signs of an ACA stroke.

A
  1. Lower limb weakness and loss of sensation to the lower limb.
  2. Gait apraxia (unable to initiate walking).
  3. Incontinence.
  4. Drowsiness.
  5. Decrease in spontaneous speech.
147
Q

Give 5 signs of a MCA stroke.

A
  1. Upper limb weakness and loss of sensation to the upper limb.
  2. Hemianopia.
  3. Aphasia.
  4. Dysphasia.
  5. Facial drop.
148
Q

Give 5 signs of a PCA stroke.

A
  1. Visual field defects.
  2. Cortical blindness.
  3. Visual agnosia.
  4. Prosopagnosia.
  5. Dyslexia.
  6. Unilateral headache.
149
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information.

150
Q

What is prosopagnosia?

A

An inability to recognise a familiar face.

151
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

MCA

152
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

ACA

153
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

PCA

154
Q

What investigation could you do to determine whether someone has had a haemorrhagic or an ischaemic stroke?

A

CT head

155
Q

What is the treatment for an ischaemic stroke?

A

1st line – thrombolysis (IV alteplase)

2nd line – aspirin 300mg for 2 weeks then clopidogrel 75mg OD

156
Q

What non pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units.
  2. Swallowing and feeding help.
  3. Physiotherapy.
  4. Home modifications.
157
Q

What is the Bamford stroke classification divided into?

A
  1. Total anterior circulation syndrome (TACS)
  2. Partial anterior circulation stroke (PACS)
  3. Lacunar syndrome (LACS)
  4. Posterior circulation syndrome (POCS)
158
Q

How would you diagnose TACS?

A

Large cortical stroke in ACA/MCA territories
ALL 3 OF:
1. Contralateral weakness (and/or sensory deficit) of face, arm + leg
2. Homonymous hemianopia
3. Higher dysfunction – dysphasia, visuospatial disorder

159
Q

How would you diagnose PACS?

A

Cortical stroke in ACA/MCA territories
2 OF:
1. Contralateral weakness (and/or sensory deficit) of face, arm + leg
2. Homonymous hemianopia
3. Higher dysfunction – dysphasia, visuospatial disorder

160
Q

How would you diagnose LACS?

A

Subcortical stroke due to small vessel disease
1 OF:
1. Pure motor stroke – contralateral weakness of face, arm, leg, or all 3
2. Ataxic hemiparesis – ipsilateral weakness + clumsiness (mostly affects legs)
3. Pure sensory stroke – contralateral numbness, tingling, pain, or burning
4. Mixed sensorimotor stroke
5. Clumsy hand dysarthria

161
Q

How would you diagnose POCS?

A

1 OF:

  1. Cerebellar / brainstem syndrome – e.g. quadriplegia, locked in syndrome
  2. LoC
  3. Isolated homonymous hemianopia
  4. Cranial nerve palsy AND contralateral motor/sensory deficit
162
Q

What is a Transient Ischaemic Attack?

A

TIA = sudden onset global neurological deficit lasting <24h with complete clinical recovery” (usually 5-15m)

163
Q

What are the features of a carotid/anterior blockage in a TIA? (80% of strokes)

A
  1. Hemiparesis – unilateral weakness (and/or hemisensory loss)
  2. AMOUROSIS FUGAX -> descending loss of vision in one eye (ipsilateral retinal/ophthalmic artery embolism)
  3. Broca’s (expressive) dysphasia
164
Q

What are the features of a vertebrobasilar/posterior blockage?

A
  1. Hemisensory symptoms
  2. Diplopia, vertigo, vomiting, dysarthria (leading to slurred speech), ataxia
  3. Hemianopia (ophthalmic cortex) or bilateral visual loss
165
Q

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

A

Assess their risk of having a stroke in the next 7 days - ABCD2 score.

166
Q

What is the ABCD2 score?

A

It is used in patients who have had TIA’s to assess their risk of stroke in the next 7 days.
1. Age > 60.

  1. BP > 140/90mmHg.
  2. Clinical features:
    - Unilateral weakness = 2 points
    - Speech disturbance without weakness = 1 point
  3. Duration?
    >60 mins = 2 points
    10 - 59 mins = 1 point
  4. Diabetes?
167
Q

What would indicate that a patient who has had a TIA is now at high risk of a stroke?

A
  1. ABCD2 ≥4
  2. > 1 TIA/week
  3. AF
  4. On anticoagulant
168
Q

What is the managements for patients at high risk of having a stroke after a TIA?

A
  1. Antiplatelet – aspirin 300mg (or clopidogrel 300mg) unless on anticoagulant therapy
  2. Statin – simvastatin 40mg
  3. If on anticoagulant therapy – admit for imaging to rule out haemorrhagic stroke
169
Q

What is dopamine produced from?

A

Tyrosine -> L-dopa -> dopamine.

170
Q

What is the pathophysiology of Parkinson’s disease?

A
  1. Decrease of dopamine secreting cells of substantia nigra (so it lightens in colour)
  2. Decrease of dopamine transported to striatum
  3. Decrease in neuronal transmission from basal ganglia to cortex
171
Q

What are the textbook signs of Parkinson’s disease?

A
  1. Bradykinesia – slowness of movement
  2. Resting tremor – starts unilaterally, improved by voluntary movement
  3. Rigidity (cog-wheel) – increased tone and spasticity
172
Q

What are additional features patients with PD may display?

A
  1. Micrographia
  2. Postural changes - stoop, shuffling + festinant (hurrying) gait
  3. Non-motor features – decreased sense of smell, constipation, frequency/urgency
173
Q

What are the differentials for Parkinson’s?

A
  1. Benign essential tremor
  2. Parkinson-plus syndromes – VIVID
  3. Drugs – antipsychotics, metoclopramide, prochlorperazine
  4. Rarer causes – trauma (e.g. boxing), Wilson’s disease, HIV
174
Q

You ask a patient who you suspect might have PD to walk up and down the corridor so that you can assess their gait. What features would be suggestive of PD?

A
  • Stooped posture.
  • Asymmetrical arm swing.
  • Small steps.
  • Shuffling.
175
Q

What drugs could you use to increase dopamine supply?

A
  1. LDOPA (powerful! Make use of different preparations)
  2. Dopamine receptor agonists -> ropinirole/rotigotine
    (SE = tiredness, gambling, hyper sexuality)
176
Q

What drug could you use to decrease dopamine breakdown?

A

MAO-B inhibitor -> rasagiline/selegiline

least powerful but least amount of SE

177
Q

What drugs could you prescribe to help control the tremor of a patient with PD? why would you be hesitant to prescribe?

A

Anti- cholinergics

- SE = cognition/confusion/systemic

178
Q

Give 2 conditions that also present alongside/as a result go Parkinson’s?

A
  1. DEPRESSION (20-40%)

2. Dementia (20%)

179
Q

Give 3 signs of normal pressure hydrocephalus.

A
  1. Magnetic gait.
  2. Incontinence.
  3. Dementia.
180
Q

Describe the treatment for essential tremor.

A
  • Beta blockers.

- Primidone.

181
Q

Give 2 features which can distinguish between essential tremor and PD

A
  1. PD = tremor at rest (ET = exaggerated with action)

2. PD = unilateral (ET = bilateral)

182
Q

Describe the inheritance pattern seen in huntington’s disease.

A

Autosomal Dominant

183
Q

In huntington’s disease, what area of the basal ganglia and what neurotransmitter are affected?

A

Atrophy of the STRIATUM leads to depletion of GABA

184
Q

Give 2 histopathological signs of Parkinson’s disease.

A
  1. Lewy bodies.

2. Loss of dopaminergic neurones in the substantia nigra.

185
Q

Give an example of a dopamine agonist.

A

Ropinirole, cabergoline.

186
Q

Give an example of a MAO inhibitor.

A

Selegiline.

187
Q

What triplet code is repeated in Huntington’s disease?

A

CAG triplet repeat.

> 39 repeats = HD.

188
Q

Give 2 early signs of Huntington’s disease.

A
  1. Irritability.
  2. Depression.
  3. Personality change.
189
Q

Give 3 later signs of Huntington’s disease.

A
  1. Chorea - fidgety.
  2. Psychiatric problems.
  3. Dementia.
190
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs.
  2. Aurus.
  3. Ictal.
  4. Post-ictal - often drowsy and confused.
191
Q

Give 3 differentials for Huntington’s Chorea

A
  1. Sydenham’s chorea
  2. benign hereditary chorea
  3. drug induced (e.g. L-DOPA)
  4. other dyskinesias, other causes of dementia
192
Q

What is the pathophysiology of Huntington’s chorea?

A
  1. GABA releasing cells in the striatum degenerate
  2. Less inhibitory GABA acting on substantia nigra
  3. Dopamine release is not inhibited
  4. Increased movement and activation of indirect pathway
193
Q

What is generalised dystonia?

A

Dystonia is syndrome of sustained muscle contraction, frequently causing twisting and repetitive movements as well as abnormal posture

194
Q

How would you manage Huntington’s?

A
  1. Symptomatic
    - Treat chorea symptoms (benzodiazepines, sodium valproate)
  2. Genetic counselling.
195
Q

Give examples of 5 causes for polyneruopathy

A 
DAVID!
Diabetes
Alcohol
Vitamin deficiency (B12) 
Infective (GB)
Drugs (isoniazid)
196
Q

What is aphasia?

A

Inability (or impaired ability) to understand or produce speech, as a result of brain damage.

197
Q

What is arthralgia?

A

Difficult or unclear articulation of speech that is otherwise linguistically normal

198
Q

Give an example of a primary headache.

A
  1. Migraine.
  2. Tension headache.
  3. Cluster headache.
199
Q

Give an example of a secondary headache

A
  1. Meningitis.
  2. Subarachnoid haemorrhage.
  3. Giant cell arteritis.
  4. Medication overuse headache.
200
Q

How can migraines be subdivided?

A
  1. Episodic with (20%)/without (80%) aura.

2. Chronic migraine.

201
Q

Describe the treatment for migraines.

A
  1. Avoid triggers + stop pill
  2. Mild attack -> aspirin/ibuprofen +/- anti-emetic (e.g. metoclopramide)

Severe attack -> sumatriptan + NSAID/paracetamol

202
Q

What are the methods used for prophylaxis of a migraine? x3

A
  1. Propranolol or topiramate
  2. Acupuncture
  3. Amitriptyline / pizotifen
203
Q

Give 5 triggers for a migraine

A
  1. CHOCOLATE
  2. Orgasms
  3. Cheese
  4. Oral contraceptive pill
  5. Alcohol
  6. Exercise
204
Q

How would you diagnose a migraine WITHOUT aura?

A
  1. ≥5 attacks
  2. Lasting 4-72h
  3. ≥2 of the following 4:
    - Unilateral
    - Pulsating
    - Moderate/severe pain
    - Aggravation by (or avoidance of) routine physical activity
  4. ≥1 of the following:
    - Nausea and/or vomiting
    - Photophobia and phonophobia
205
Q

How would you diagnose a migraine WITH aura?

A
  1. ≥1 reversible aura symptom
    - Visual – zigzags, spots
    - Unilateral sensory – tingling, numbness
    - Speech – aphasia
    - Motor weakness (known as “hemiplegic migraine” so rule out stroke & TIA)

≥2 of the following 4:

  • ≥1 aura symptom spreads gradually over ≥5m and/or ≥2 aura symptoms occurring in succession
  • Each aura symptom lasts 5-60m
  • ≥1 aura symptom is unilateral
  • Aura accompanied/followed within 60m by headache
206
Q

What is the most common type of primary headache?

A

Tension headache

207
Q

What could a red eye accompanying a headache suggest?

A

Acute glaucoma

208
Q

Give 6 questions that are important to ask when taking a history of headache.

A
  1. Time: onset, duration, frequency, pattern.
  2. Pain: severity, quality, site and spread.
  3. Associated symptoms e.g. nausea, vomiting, photophobia, phonophobia.
  4. Triggers/aggravating/relieving factors.
  5. Response to attack: is medication useful?
  6. What are symptoms like between attacks?
209
Q

What is Kernigs sign?

A

Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

210
Q

What are the two types of tension headaches?

A
  1. Episodic TH – <15d per month

2. Chronic TH – >15d per month, can be medication induced, also associated with depression

211
Q

How long do tension headaches usually last for?

A

From 30 minutes to 7 days.

212
Q

Describe the pain of a tension headache.

A
  1. Bilateral.
  2. Pressing/tight.
  3. Mild/moderate pain.
  4. Not aggravated by physical activty.
213
Q

What is the most common type of secondary headache?

A

Medication overuse headache

214
Q

What is the diagnostic criteria for medication overuse headache?

A
  1. Headache present for >15 days/month.
  2. Regular use for >3 months of >1 symptomatic treatment drugs.
  3. Headache has developed or markedly worsened during drug use.
215
Q

Describe the pain of a cluster headache.

A
  1. Severe/very severe pain.
  2. Pain around the eye/temporal area.
  3. Unilateral.
  4. Headache is accompanied by cranial autonomic features.
216
Q

When do patients tend to get cluster headaches?

A

AFTER REM SLEEP

  1. middle of night
  2. early morning hours
217
Q

How long do cluster headaches usually last for?

A

15 minutes to 3 hours.

218
Q

Name a type of headache that is accompanied with cranial autonomic features.

A

Cluster headache

219
Q

What cranial autonomic features would you get in a cluster headache and why?

A

Parasympathetic hyperactivity ->

  1. ipsilateral eye lacrimation and redness
  2. ipsilateral nasal congestion (rhinorrhoea)
  3. ipsilateral miosis and/or ptosis
220
Q

How would you manage a cluster headache?

A

Prevention:
- Verapamil

Treatment:

  • 100% O2 `(non-rebreathable mask)
  • SC Sumatriptan at onset
221
Q

What is Giant Cell Arteritis?

A

granulomatous inflammation of blood vessel walls (vasculitis)

222
Q

What are the secondary causes of GCA?

A
  1. SLE
  2. RA
  3. HIV
223
Q

What investigations would you carry out on a patient with suspected GCA?

A
  1. Bloods - inc ESR
  2. Temporal artery biopsy - GOLD STANDARD
    ( shows necrotising arteritis with inflammation)
224
Q

What is the treatment for GCA?

A
  1. High dose steroids - IV methylprednisolone/oral prednisolone
  2. aspirin 75mg
225
Q

What other drugs normally need to be prescribed alongside steroids?

A
  1. PPI (gastric protection)

2. bisphosphonate (bone protection)

226
Q

What is the general criteria for diagnosing GCA?

A 
3 of these 5 criteria present:
• Age>50
• New headache or new type of localised pain.
• Temporal artery abnormality:
- tenderness
- decreased pulsation
• ESR elevated > 50
• Biopsy abnormal
227
Q 
60yr old female
New onset headache, doesn’t go away with painkillers
Tenderness when brushing hair
Pain in jaw when eating
Loss of vision in 1 eye
Pain and stiffness in shoulders

Most likely diagnosis?

A

GCA!

loss of vision in eye = amaurosis fugax

228
Q

86 yr old female
Severe electric shock sensation over jaw
Occurs when brushing teeth
Lasts only a few seconds

Most likely diagnosis?

A

TRIGEMINAL NEURALGIA

229
Q

In trigeminal neuralgia, which branch of the trigeminal nerve is normally afftected?

A

Mandibular branch of trigeminal nerve

230
Q

What is the epidemiology of trigeminal neuralgia?

A

Presents in people >75yrs

More common in women

231
Q

What are the triggers for trigeminal neuralgia?

A
  1. Eating
  2. Shaving
  3. Washing
232
Q

How would you investigate the cause and confirm the diagnosis of trigeminal neuralgia?

A
  1. Ix - MRI head
  2. Causes
    - Idiopathic
    - Secondary:
    • Tumour
    • AV malformation
    • MS
233
Q

How would you treat trigeminal neuralgia? Why?

A

CARBEMAZEPINE
- acts as a membrane stabilizer and reduces the frequency of spontaneous nerve impulses within the nerve

(hence its use in focal epilepsy!)

234
Q

What is multiple sclerosis?

A

A chronic auto-immune disorder of the CNS. It is an inflammatory and demyelinating disease characterised by progressive disability.

235
Q

Describe the epidemiology of MS.

A
  • Presents between 20-40 y/o.
  • Females > males.
  • Rare in the tropics.
236
Q

Describe the aetiology of MS

A
  1. AUTOIMMUNE DEMYELINATION (T cell mediated)
  2. Low vit D exposure
  3. Environment e.g. EBV infection is shown to be associated.
237
Q

Where would MS plaques be seen histologically?

A

Around blood vessels: perivenular.

238
Q

Does myelin regenerate in someone with MS?

A

Yes but it is much thinner which causes inefficient nerve conduction.

239
Q

Give 3 major features of an MS plaque.

A
  1. Inflammation.
  2. Demyelination.
  3. Axon loss.
240
Q

Describe the relapsing/remitting course of MS.

A

The patient has random attacks over a number of years. Between attacks there is no disease progression.

241
Q

Describe the chronic progressive course of MS.

A

Slow decline in neurological functions from the onset.

242
Q

What can exacerbate the symptoms of MS?

A

Heat - typically a warm shower.
(URTHOFF’S SIGN)

Symptoms can be relieved by cool temperatures.

243
Q

What is the diagnostic criteria for MS?

A
  1. > 2 CNS lesions disseminated in time and space.

2. Exclusion of conditions that may give a similar clinical presentation.

244
Q

Name 3 conditions in the differential diagnosis of MS.

A
  1. SLE.
  2. Sjögren’s.
  3. AIDS.
245
Q

Where are common sites for neuronal damage in MS?

A
  1. Optic nerves
  2. Brainstem - dysarthria/ vertigo/ nystagmus
  3. Cervical spinal cord - weakness/ paraplegia/ spasticity/ incontinence/ sexual dysfunction
246
Q

What are typical symptoms for MS?

A
  1. Eye - optic neuritis/ nystagmus/ double vision/ vertigo

2. CNS - spasticity/ Lhermitte’s sign/bladder and sexual dysfunction

247
Q

What is Lhermitte’s sign?

A

Electric shock like feeling down spine and into legs upon flexion of neck

248
Q

What investigations might you do in someone to see if they have MS?

A

Diagnosis:

  1. one clinical attack + multiple plaques on MRI disseminated in time and space
  2. IgG olicoglonal bands on LP
  3. Visual evoked potential (VEP) – visual pathway lesions
249
Q

How would you manage a patient with MS?

A

Acute
Steroids = Methylprednisolone

Chronic
1st line = Beta Interferon, Glatiramer acetate
2nd line = Natalizumab

Symptom management
Tremor = BB, Spasticity = Baclofen

250
Q

What might electrophoresis of CSF show for someone with MS?

A

Oligoclonal IgG bands.

251
Q

What medication might you give to someone to reduce the relapse severity of MS?

A

Short course steroids e.g. methylprednisolone.

252
Q

Describe the non-pharmacological treatment for MS.

A
  1. Psychological therapies and counselling.
  2. Speech therapists.
  3. Physiotherapy and occupational therapy.
253
Q

Briefly describe the pathophysiology of cauda equina syndrome.

A

Spinal compression at or distal to the L1 nerve root disrupts sensation and movement. It is a surgical emergency.

254
Q

Give 5 signs of cauda equina syndrome.

A
  1. Bilateral sciatica (pain radiates down the leg to the foot).
  2. Saddle anaesthesia.
  3. Bladder/bowel dysfunction.
  4. Erectile dysfunction.
  5. Variable leg weakness.
255
Q

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

A

MRI of spine.

256
Q

What is the most common cause of spinal cord compression?

A

Secondary malignancy from lung, breast, prostate, kidney etc.

257
Q 
What drug is prescribed in sub-arachnoid haematoma to prevent arterial spasm and subsequent ischaemia? 
What class of drugs does this come from?
A

Nimodipine – CCB.

258
Q

Define myelopathy.

A
  1. Injury to spinal cord due to severe compression
  2. Effecting UMN.
  3. Surgery is often indicated to prevent deterioration.
259
Q

Define radiculopathy.

A
  1. Spinal nerve root disease
  2. LMN problem.
  3. conservative management
260
Q

Is myelopathy or radiculopathy an UMN problem?

A

Myelopathy is a spinal cord disease and therefore is an UMN problem.

261
Q

Is myelopathy or radiculopathy a LMN problem?

A

Radiculopathy is a spinal nerve root disease and therefore is a LMN problem.

262
Q

What is the most common type of radiculopathy?

A

SCIATICA

  • unilateral pain w/out neurological signs
  • Mx = physio + NSAIDs
263
Q

Give 3 diseases that are associated with motor neurone damage.

A
  1. Motor neurone disease.
  2. Spinal atrophy.
  3. Poliomyelitis.
  4. Spinal cord compression.
264
Q

Define weakness.

A

Impaired ability to move a body part in response to will.

265
Q

Define paralysis.

A

The ability to move a body part in response to will is completely lost.

266
Q

Define ataxia.

A

Willed movements are clumsy and uncontrolled.

267
Q

Define involuntary movements.

A

Spontaneous movement independent of will.

268
Q

Define apraxia.

A

The ability to carry out familiar purposeful movements is lost in the absence of paralysis or other sensory or motor impairments.

269
Q

Give 3 pathologies that are associated with ventral spinal root damage

A
  1. Tumours.
  2. Prolapsed intervertebral discs.
  3. Cervical/lumbar spondylosis (wear and tear).
270
Q

What investigations could you do to see if someone has damage to their LMN’s?

A
  1. EMG (electromyography)
  2. MRI.
  3. Muscle enzymes.
  4. Lumbar puncture -> CSF.
271
Q

What is the function of muscle spindles?

A

Muscle spindles control muscle tone and tell you how much a muscle is stretched.

272
Q

What would common features of UMN damage be?

A
  1. Hyper-reflexia
  2. Hyper-tonia
  3. Spasticity
  4. Babinski +ve
273
Q

What would common features of LMN damage be?

A
  1. Hypo-reflexia
  2. Hypo-tonia
  3. Denervation atrophy
  4. Babinski -ve
  5. Fasciculations
274
Q

Describe the pathophysiology of MND

A
  1. Motor neurones destroyed, namely anterior horn cells of the spinal cord and motor cranial nuclei
  2. LMN and UMN dysfunction
  3. Mixed picture of muscular paralysis
275
Q

What is a characteristic feature of MND?

A

FASCICULATIONS

276
Q

What is the treatment for MND?

A

RILUZOLE

- Na+ channel blocker works on Glutamate

277
Q

In Brown-Sequard syndrome, which tracts are affected?

A
  1. Lateral corticospinal tract
  2. Dorsal columns
  3. Lateral spinothalamic tract
278
Q

What is the clinical picture seen in Brown-Sequard syndrome?

A
  1. Ipsilateral spastic paresis below lesion
  2. Ipsilateral loss of proprioception and vibration sensation
  3. Contralateral loss of pain and temperature sensation
279
Q

What spinal tract is affected in Neurosyphillis?

A

Dorsal column

- resulting in loss of proprioception and vibration sensation

MY PHASE 2A MEDICINE (14 decks)

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