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3a neuro/geriatrics > Neurology > Flashcards

Neurology Flashcards

1
Q

What is Stroke

A

a cerebrovascular accident

can either be
- Ischaemia (85%) or haemorrhage (15%)

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2
Q

What is Intracranial Haemorrhage

A

bleeding within the brain

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3
Q

What are 4 types of Intracranial haemorrhages

A

Extradural haemorrhage
Subdural haemorrhage
Intracerebral haemorrhage
Subarachnoid haemorrhage

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4
Q

what is a Intracerebral haemorrhage

A

bleeding into brain tissue

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5
Q

What is Subarachnoid haemorrhage

A

bleeding in the subarachnoid space from ruptured circle of willis

where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane

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6
Q

What is a Extradural haemorrhage

A

bleeding between the skull and dura mater

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7
Q

What is a Subdural haemorrhage

A

bleeding between the dura mater and arachnoid mater

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8
Q

What are RF for Intracranial Haemorrhage

A

Head injuries
Hypertension
Aneurysms
Ischaemic strokes (progressing to bleeding)
Brain tumours
Thrombocytopenia (low platelets)
Bleeding disorders (e.g., haemophilia)
Anticoagulants (e.g., DOACs or warfarin)

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9
Q

How do Intracerebral haemorrhag present

A

sudden-onset focal neurological symptoms, such as limb or facial weakness, dysphasia or vision loss.

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10
Q

What is most common cause of extradural haemorrhage

A

rupture of the middle meningeal artery in the temporoparietal region

fracture of temporal bone

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11
Q

How does Extradural haemorrhage present on CT

A

bi-convex shape and are limited by the cranial sutures

lemon shaped

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12
Q

what is typical presentation of Extradural haemorrhage

A

young patient with a traumatic head injury and an ongoing headache.
They have a period of improved neurological symptoms and consciousness, followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents

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13
Q

What is most common cause of subdural haemorrhage

A

rupture of the bridging veins in the outermost meningeal layer

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14
Q

How does subdural haemorrhage present on CT

A

a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).

moon shaped

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15
Q

what is typical presentation of subdural haemorrhage

A

elderly and alcoholic patients, who have more atrophy in their brains, making the vessels more prone to rupture.

or shaken baby

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16
Q

What is most common cause of Subarachnoid haemorrhage

A

ruptured cerebral aneurysm.
berry aneurysm ACA

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17
Q

what is typical presentation of Subarachnoid haemorrhage

A

sudden-onset occipital headache during strenuous activity

“thunderclap headache” description.

Neck stiffness
Photophobia
Vomiting
Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)

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18
Q

What is 1st line investigation for Subarachnoid haemorrhage

A

NCCT head

hyper-attenuation in the subarachnoid space
Star shaped

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19
Q

What is GS investigation for Subarachnoid haemorrhage and what will it show

A

Lumbar puncture

Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
Xanthochromia (a yellow colour to the CSF caused by bilirubin)

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20
Q

How is source of bleeding located in Subarachnoid haemorrhage

A

CT angiography

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21
Q

How are cerebral aneurysms surgically managed

A

endovascular coiling
neurosurgical clipping,

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22
Q

WHat is a complication of Subarachnoid haemorrhage and how is it managed

A

Vasospasm - brain ischaemia

Nimodipine is a calcium channel blocker

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23
Q

How are Intracranial Haemorrhages investigated

A

Immediate imaging (e.g., CT head) is required to establish the diagnosis.

Bloods should include a full blood count (for platelets) and a coagulation screen.

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24
Q

How are Intracranial Haemorrhage initially managed

A
  • Admission to a specialist stroke centre
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and intensive care if they have reduced consciousness
  • Correct any clotting abnormality (e.g., platelet transfusions or vitamin K for warfarin)
  • Correct severe hypertension but avoid hypotension

ABCDE

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25
Q

What are surgical options for treating an extradural or subdural haematoma

A

Craniotomy (open surgery by removing a section of the skull)
Burr holes (small holes drilled in the skull to drain the blood)

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26
Q

What GCS requires airway support

A

8/15

minimum score 3/15

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27
Q

How is Glasgow Coma Scale (GCS) scored

A

eyes, verbal response and motor response

motor /6
verbal /5
eyes /4

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28
Q

What is Ischaemia

A

inadequate blood supply

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29
Q

What is infarction

A

tissue death due to ischaemia

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30
Q

What can cause blood supply to brain to become disrupted

A

A thrombus or embolus
Atherosclerosis
Shock
Vasculitis

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31
Q

What is Transient ischaemic attack (TIA)

A

temporary neurological dysfunction caused by ischaemia but without infarction

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32
Q

What are symptoms of TIA

A

rapid onset and often resolve before the patient is seen

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33
Q

What are Crescendo TIAs

A

two or more TIAs within a week and indicate a high risk of stroke

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34
Q

How is TIA investigated

A

diffusion weighted MRI

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35
Q

what is the long term management of TIA

A
  • first 21 days after attack = clopidogrel + Aspirin
  • after 21 days = Clopidogrel
  • if high lipids then + a high-intensity statin (atorvastatin)
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36
Q

what prophylaxis medication is given with aspirin

A

PPI

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37
Q

How is TIA managed initially

A

aspirin 300mg
review within 24 hours

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38
Q

How does stroke present

A

sudden onset of neurological symptoms suggests a vascular cause (e.g., stroke)
typically asymmetrical

  • Limb weakness
  • Facial weakness
  • Dysphasia (speech disturbance)
  • Visual field defects
  • Sensory loss
  • Ataxia and vertigo (posterior circulation infarction)
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39
Q

How strokes classified

A

Oxford Stroke Classification (Bamford)

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40
Q

What criteria is assessed in Bamford classification

A
  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
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41
Q

What is Total anterior circulation infarcts (TACI, c. 15%)

A

3/3
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia

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42
Q

What do Total anterior circulation infarcts involve

A

involves middle and anterior cerebral arteries

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43
Q

What is Partial anterior circulation infarcts (PACI, c. 25%)

A

and 2/3
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia

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44
Q

What do Partial anterior circulation infarcts involve

A

involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

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45
Q

What is Lacunar infarcts (LACI, c. 25%)

A

presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

subcortical stroke

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46
Q

what is Posterior circulation infarcts (POCI, c. 25%)

A

involves vertebrobasilar arteries

damage to cerebellum and brainstem.

presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia

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47
Q

What are associated effects of anterior cerebral artery stroke

A
  • lower limb > upper affected and no face or speech impairment
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48
Q

What are associated effects of middle cerebral artery stroke

A
  • upper >lower limb + speech impaired, contralateral homonymous hemianopia
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49
Q

What are associated effects of posterior cerebral artery stroke

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia
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50
Q

What are associated effects of Lateral medullary syndrome (PICA)

A
  • ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  • contralateral: limb sensory loss
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51
Q

What are associated effects of Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain) stroke

A
  • Ipsilateral CN III palsy
  • Contralateral weakness of upper and lower extremity
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52
Q

what is CN III palsy

A

eye turns down and out
double vision

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53
Q

What are associated effects of Basilar artery stroke

A

‘Locked-in’ syndrome

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54
Q

What are Rf for ischaemic stroke

A

age
hypertension
smoking
hyperlipidaemia
diabetes mellitus
atrial fibrillation

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55
Q

What are Lacunar infarcts

A

small infarcts around the basal ganglia, internal capsule, thalamus and pons

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56
Q

What are Rf for Haemorrhagic stroke

A

age
hypertension
arteriovenous malformation
anticoagulation therapy

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57
Q

What increases the risk of stroke in patients on Combined contraceptive pill

A

migraines with aura, smokers over 34 years or those with a history of stroke or TIA.

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58
Q

What is FAST tool

A

used in community to ID stroke

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

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59
Q

What is ROSIER tool

A

(Recognition Of Stroke In the Emergency Room) gives a score based on the clinical features and duration.

Stroke is possible in patients scoring one or more.

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60
Q

what is CHA2D2VASC

A

the risk of stroke in AF patients.

  • congestive heart failure
  • hypertension
  • age ≥75 (doubled)
  • diabetes (doubled)
  • vascular disease
  • age 65 to 74
  • sex category (female).
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61
Q

What is ORBIT

A

RF for bleeding

  • older (75 years or older)
  • reduced haemoglobin
  • bleeding history
  • insufficient kidney function (eGFR < 60 mg/dL/1.73 m2)
  • treatment with an antiplatelet agent
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62
Q

What is ABCD2

A

used to determine the risk for stroke in the days following a transient ischemic attack

age
BP
clinical features
DM
Duration of Sx

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63
Q

What is the first line radiological investigation for suspected stroke

A

non-contrast CT head scan

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64
Q

How do acute ischaemic strokes present on CT

A

‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately

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65
Q

How do acute haemorrhagic strokes appear on CT

A

typically show areas of hyperdense material (blood) surrounded by low density (oedema)

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66
Q

What is the initial management of ischaemic stroke

A

Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
Admission to a specialist stroke centre

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67
Q

How is Ischaemic stroke treated if presenting within 4.5 24

A

Thrombolysis with alteplase

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68
Q

What is alteplase

A

tissue plasminogen activator

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69
Q

What should blood pressure be lowered to before thrombolysis

A

185/110 mmHg

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70
Q

How is Ischaemic stroke treated WITHIN 6hrs hours

A

Thrombectomy

if also under 4.5hr then IV thrombolysis

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71
Q

How is Ischaemic stroke treated WITHIN 24hrs hours

A

Thrombectomy

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72
Q

Where does a thrombus/embolus have to be located to use Thrombectomy

A

proximal anterior circulation or proximal posterior circulation

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73
Q

When is High blood pressure treatment indicated in stroke treatment

A

only in hypertensive emergency

with ischaemic stroke lowering the blood pressure can worsen the ischaemia

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74
Q

How are patients assessed for underlying causes in stroke

A

carotid artery stenosis and atrial fibrillation with:

Carotid imaging (e.g., carotid duplex ultrasound, or CT or MRI angiogram)
ECG or ambulatory ECG monitoring

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75
Q

How is Afib managed

A

Anticoagulation –> Apixaban

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76
Q

How is carotid artery stenosis managed

A

Carotid endarterectomy (if the stenosis > 50%)
Angioplasty and stenting

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77
Q

What is Secondary Prevention for stroke

A
  • Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
  • Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
  • Blood pressure and diabetes control
  • Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
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78
Q

What people are involved in stroke rehabilitation MDT

A

Stroke physicians
Nurses
Speech and language (SALT) to assess swallowing
Dieticians in those at risk of malnutrition
Physiotherapy
Occupational therapy
Social services
Optometry and ophthalmology
Psychology
Orthotics

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79
Q

how does pontine haemorrhage present

A

reduced GCS, paralysis and bilateral pin point pupils

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80
Q

What is dementia

A

progressive and irreversible impairment in memory, cognition, personality and communication

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81
Q

what is early onset dementia

A

when the symptoms start before aged 65.

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82
Q

what is Mild cognitive impairment

A

a deficit in cognition and memory that is greater than expected with age but not significant enough for a diagnosis of dementia

usually live independently

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83
Q

What is Alzheimers dementia

A

MC type of dementia

progressive degenerative disease of the brain

pathophysiology involves brain atrophy, amyloid plaques, reduced cholinergic activity and neuroinflammation

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84
Q

What is Vascular dementia

A

2nd MC type of dementia

vascular damage and impaired blood supply to the brain.

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85
Q

WHat are RF for vascular dementia

A

History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

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86
Q

What is Dementia with Lewy bodies

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

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87
Q

What are associated symptoms of Dementia with Lewy bodies

A

visual hallucinations, delusions, REM sleep disorders and fluctuating consciousness.

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88
Q

What are the macroscopic pathological changes associated with Alzheimers

A

widespread cerebral atrophy, particularly involving the cortex and hippocampus

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89
Q

What are the microscopic pathological changes associated with Alzheimers

A
  • cortical plaques due to deposition of type A-Beta-amyloid protein
  • intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
  • hyperphosphorylation of the tau protein
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90
Q

What are the biochemical pathological changes associated with Alzheimers

A

deficit of acetylcholine from damage to an ascending forebrain projection

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91
Q

What happens to tau proteins in AD

A

Neurofibrillary tangles; filaments made from protein called tau

excessively phosphorylated, impairing its function

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92
Q

What are the main subtypes of VD

A

Stroke-related VD - multi-infarct or single-infarct dementia
Subcortical VD - caused by small vessel disease
Mixed dementia - the presence of both VD and Alzheimer’s disease

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93
Q

How do patients with vascular dementia present

A

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

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94
Q

What are symptoms of Vascular dementia

A

Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

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95
Q

What could an MRI show for vascular dementia

A

infarcts and extensive white matter changes

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96
Q

How can Lewy body dementia be differentiated from Parkinsons

A

LBD = progressive cognitive impairment typically occurs before parkinsonism symptoms

PD = motor symptoms typically present at least one year before cognitive symptoms

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97
Q

What special investigation can be used for Lewy body dementia with high specificity

A

single-photon emission computed tomography (SPECT)

DaTscan.

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98
Q

What are 3 classic features of Parkinsons

A

Bradykinesia
Tremor (pill rolling)
Rigidity (lead pipe, cog wheel)

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99
Q

What medication should be avoided in Lewy body dementia

A

neuroleptics aka antipsyhotics as v sensitive and can cause irreversible parkinsonism

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100
Q

What type of medication can have cognitive impairment, memory impairment or personality changes.

A

Medications with an anticholinergic effect,

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101
Q

Name 3 types of medication with an anticholinergic effect

A

Anticholinergic urological drugs (e.g., oxybutynin, solifenacin and tolterodine)
Antihistamines (e.g., chlorphenamine and promethazine)
Tricyclic antidepressants (e.g., amitriptyline)

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102
Q

What are psychiatric DDx for dementia

A

Depression
Psychosis
Delirium (e.g., secondary to infection)

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103
Q

What are neurological DDx for dementia

A

Brain tumours (particularly affecting the frontal lobes)
Parkinson’s disease
Huntington’s disease
Progressive supranuclear palsy

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104
Q

What are endocrine DDx for dementia

A

Hypothyroidism
Adrenal insufficiency
Cushing’s syndrome
Hyperparathyroidism (causing hypercalcaemia)

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105
Q

What are nutritional DDx for dementia

A

Vitamin B12 deficiency
Thiamine deficiency (causing Wernicke-Korsakoff syndrome)

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106
Q

What are modifiable Risk Factors for dementia

A

Exercise
Mental stimulation (e.g., a more mentally challenging job)
Maintaining a healthy weight (obesity increases the risk)
Blood pressure control (hypertension increases the risk)
Blood glucose control (diabetes increase the risk)

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107
Q

What are early symptoms of dementia

A

Forgetting events
Forgetting names
Difficult remembering words
Repeatedly asking the same questions
Impaired decision making
Reduced flexibility

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108
Q

What are features of advanced dementia

A
  • Inability to speak or understand speech (aphasia)
  • Swallowing difficulties (dysphagia), which can lead to aspiration and pneumonia
  • Appetite and weight loss
  • Incontinence
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109
Q

what are memory screening testes that can be used at the initial presentation

A

Six Item Cognitive Impairment Test (6CIT)
10-point Cognitive Screener (10-CS)
Mini-Cog
General Practitioner Assessment of Cognition (GPCOG)
Montreal Cognition Assessment (MoCA)

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110
Q

What additional blood tests can be ordered to exclude dementia DDx

A

Full blood count
Urea and electrolytes
Liver function tests
Inflammatory markers (e.g., CRP and ESR)
Thyroid profile
Calcium
HbA1c
B12 and folate

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111
Q

What investigations can be ordered to exclude dementia DDx

A

Mid-stream urine (MSU) if infection is suspected
Chest x-ray (if lung cancer is suspected)
MRI brain) to exclude structural pathology.

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112
Q

What 5 domains are tested in Addenbrooke’s Cognitive Examination-II

A

Attention
Memory
Language
Visuospatial function
Verbal fluency

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113
Q

What score indicate possible dementia in Addenbrooke’s Cognitive Examination-II

A

88 or less

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114
Q

What plannung steps can be taken for patient with dementia

A
  • Lasting power of attorney
  • Advanced decisions
  • Planning future care, including places and end-of-life care
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115
Q

What are medication options for Alzheimers

A
  • Acetylcholinesterase inhibitors (e.g., donepezil, rivastigmine or galantamine)
  • Memantine, which works by blocking N-methyl-D-aspartic acid (NMDA) receptors
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116
Q

Name 3 Acetylcholinesterase inhibitors

A

donepezil, rivastigmine or galantamine

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117
Q

What behavioural and psychological symptoms of dementia (BPSD) include

A

Depression
Anxiety
Agitation
Aggression
Disinhibition (e.g., sexually inappropriate behaviour)
Hallucinations
Delusions
Sleep disturbance

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118
Q

What initial steps can be taken to manage behavioural and psychological symptoms of dementia

A

Treating underlying causes (e.g., pain, constipation or urinary retention)
Environmental factors (e.g., providing a calming setting and removing triggers)
Appropriately trained carers
Appropriate supervision (one-to-one observation may be required)
Music therapy

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119
Q

What are common features of frontotemporal lobar dementias

A

initial presentation typically involves abnormalities in behaviour, speech and language

Relatively preserved memory

early onset 40-60

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120
Q

What medication can be taken to manage behavioural and psychological symptoms of dementia

A

SSRI antidepressants for depressive symptoms
Antipsychotic drugs (typically risperidone first-line)
Benzodiazepines (only for crisis management)

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121
Q

What factors favor delirium over dementia

A
  • acute onset
  • impairment of consciousness
  • fluctuation of symptoms: worse at night, periods of normality
  • abnormal perception (e.g. illusions and hallucinations)
  • agitation, fear
  • delusions
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122
Q

What can cause delirium

A

Constipation
Hypoxia
Infection
Metabolic disturbance
Pain
Sleeplessness

Prescriptions
Hypothermia/pyrexia
Organ dysfunction (hepatic or renal impairment)
Nutrition
Environmental changes
Drugs (over the counter, illicit, alcohol and smoking)

CHIMPS PHONED

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123
Q

What are features of hyperactive delirium

A

Agitation
Delusions
Hallucinations
Wandering
Aggression

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124
Q

What are features of hypoactive delirium

A

Lethargy
Slow
Sleepy
Inattention

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125
Q

What are investigations are included in a confusion screen

A

Blood tests:
FBC (e.g. infection, anaemia, malignancy)
U&Es (e.g. hyponatraemia, hypernatraemia)
LFTs (e.g. liver failure with secondary encephalopathy)
Coagulation/INR (e.g. intracranial bleeding)
TFTs (e.g. hypothyroidism)
Calcium (e.g. hypercalcaemia)
B12 + folate/haematinics (e.g. B12/folate deficiency)
Glucose (e.g. hypoglycaemia/hyperglycaemia)
Blood cultures (e.g. sepsis)

Urinalysis:
UTI

CT head: if there is concern about intracranial pathology (bleeding, ischaemic stroke, abscess)
Chest X-ray: may be performed if there is concern about lung pathology (e.g. pneumonia, pulmonary oedema)

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126
Q

clinical signs/investigations that suggest delirium

A

Vital signs (e.g. fever in infection, low SpO2 in pneumonia)
Level of consciousness (e.g. GCS/AVPU)
Evidence of head trauma
Sources of infection (e.g. suprapubic tenderness in urinary tract infection)
Asterixis (e.g. uraemia/encephalopathy)

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127
Q

WHat is 1st line medication option for delirium

A

Haloperidol (oral, IV or IM)

If benzodiazepines are to be used, lorazepam is first-line

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128
Q

What steps can be taken to prevent episodes of delirium

A
  • Avoid drugs known to precipitate delirium (e.g. opiates and benzodiazepines)
  • Identify patients at higher risk of developing delirium and observe them closely for early signs of delirium
  • Assess other factors which may induce or exacerbate delirium (e.g. pain control, drugs etc)6
  • Employ supportive/environmental management approaches for all patients, regardless of delirium risk
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129
Q

What are environmental adaptation management strategies to manage delirium

A

access to a clock and other orientation reminders
familiar objects where possible
Involve the family, friends and/or carers
control the level of noise, temperature and light

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130
Q

What are general supportive adaptation management strategies to manage delirium

A

consistent nursing and medical team
patient has access to aids
Enable the patient to do what they can for themselves

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131
Q

What is Parkinson’s disease

A

progressive reduction in dopamine in the substantia nigra pars compacta, leading to disorders of movement

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132
Q

Are parkinsons symptoms symmetrical or asymmetrical

A

asymmetrical

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133
Q

What is the parkinsons triad

A

Resting tremor (a tremor that is worse at rest)
Rigidity (resisting passive movement)
Bradykinesia (slowness of movement)

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134
Q

What does someone with parkinsons look like when walking

A

maks like face
stooped posture
forward tilt
reduced arm swinging
shuffling gair

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135
Q

What is the basal ganglia responsible for

A

coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patterns.

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136
Q

What are features of a Parkinson’s Tremor

A

Asymmetrical
4-6 hertz (cycles 4-6 times a second
Worse at rest
Improves with intentional movement
No change with alcohol

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137
Q

How can Bradykinesia present in Parkinsons

A

Handwriting gets smaller and smaller (micrographia)
Small steps when walking (“shuffling” gait)
Rapid frequency of steps to compensate for the small steps and avoid falling (“festinating” gait)
Difficulty initiating movement (e.g., going from standing still to walking)
Difficulty in turning around when standing and having to take lots of little steps to turn
Reduced facial movements and facial expressions (hypomimia)

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138
Q

What are other features of Parkinsons

A

Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Postural instability (increasing the risk of falls)
Cognitive impairment and memory problems

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139
Q

What is “cogwheel” rigidity describe

A

jerking resistance to movement

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140
Q

What are features of a Benign Essential Tremor

A

Symmetrical
6-12 hertz
Improves at rest
Worse with intentional movement
No other Parkinson’s features
Improves with alcohol

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141
Q

What are DDx of a tremor

A

Parkinson’s disease
Multiple sclerosis
Huntington’s chorea
Hyperthyroidism
Fever
Dopamine antagonists (e.g., antipsychotics)

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142
Q

What medication can improve symptom of benign essential tremor

A

Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)

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143
Q

What are Parkinson’s-Plus Syndromes

A

Multiple system atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration

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144
Q

What is Multiple System Atrophy

A

Parkinsonism with associated autonomic disturbance (atonic bladder, postural hypotension)

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145
Q

How is Parkinson’s disease diagnosed

A

diagnosed clinically based on the history and examination findings

UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.

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146
Q

What is the diagnostic criteria from UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria Diagnosis of a Parkinsonian syndrome

A

presence of bradykinesia

plus at least one of the following:

  • Muscular rigidity
  • Resting tremor (4-6 Hz frequency)
  • Postural instability (not caused by a visual, vestibular, cerebellar or proprioceptive dysfunction)
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147
Q

In addition to Parkinsonian syndrome criteria what also must be included for Parkinsons diagnosis

A
  • Exclusion criteria –> Hx of stroke, encephalitis, head injury…
  • Supportive positive criteria –> response to med, unilateral onset, progressive disease…
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148
Q

What is the diagnostic criteria from the ‘International Parkinson and Movement Disorder Society’ for diagnosis of benign essential tremor

A
  • Isolated tremor consisting of bilateral upper limb action tremor, with no other significant motor abnormalities
  • Greater than 3 years in duration
  • With/without tremor in other locations (e.g. head, voice, trunk, lower limbs)
  • Absence of other neurological signs (e.g. dystonia, ataxia, parkinsonism
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149
Q

What are signs of autonomic dysfunction

A

postural hypotension, constipation, abnormal sweating and sexual dysfunction

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150
Q

WHat is the first-line treatment for parkinsons if the motor symptoms are affecting the patient’s quality of life

A

levodopa

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151
Q

WHat is the first-line treatment for parkinsons if the motor symptoms are NOT affecting the patient’s quality of life

A

dopamine agonist or monoamine oxidase B (MAO-B) inhibitor

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152
Q

What are adverse side event of Dopamine receptor agonists

A

excessive sleepiness, hallucinations and impulse control disorders

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153
Q

Name an example of a Dopamine receptor agonists

A

Ropinirole

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154
Q

WHat are common SE of Levodopa

A

dyskinesia
dry mouth
anorexia
palpitations
postural hypotension
psychosis

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155
Q

What medication is Levodopa often combined with

A

peripheral decarboxylase inhibitors

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156
Q

Name 2 peripheral decarboxylase inhibitors

A

carbidopa and benserazide)

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157
Q

Why is Levodopa often combined with peripheral decarboxylase inhibitors

A

tops it from being metabolised in the body before it reaches the brain.

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158
Q

What are examples of Dyskinesia in levodopa users

A
  • Dystonia (where excessive muscle contraction leads to abnormal postures or exaggerated movements)
  • Chorea (abnormal involuntary movements that can be jerking and random)
  • Athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)
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159
Q

How is dyskinesia associated with levodopa managed

A

Amantadine (glutamate antagonist)

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160
Q

What medication is used to extend the effective duration of the levodopa.

slow the breakdown of the levodopa in the brain

A

COMT Inhibitors (e.g., entacapone)

catechol-o-methyltransferase (COMT)

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161
Q

How do dopamine agonists work

A

mimic the action of dopamine in the basal ganglia, stimulating the dopamine receptors.

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162
Q

What are side effects of Dopamine agonists with prolonged use

A

Pulmonary fibrosis

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163
Q

Give an example of Dopamine agonists

A

Bromocriptine
Pergolide
Cabergoline

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164
Q

What do Monoamine oxidase enzymes do

A

break down neurotransmitters such as dopamine, serotonin and adrenaline.

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165
Q

What medication is used to delay/extend the use of levodopa

A

Dopamine agonists
Monoamine oxidase-B inhibitors
COMT Inhibitors

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166
Q

What are examples of Monoamine oxidase-B inhibitors

A

Selegiline
Rasagiline

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167
Q

How is Parkinson’s disease diagnosed

A

diagnosed clinically based on the history and examination findings.

UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.

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168
Q

What is Epilepsy

A

chronic neurological disorder characterised by recurrent, unprovoked seizures due to abnormal and excessive neuronal activity in the brain

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169
Q

What are the two general categorizations of epilepsy

A
  • focal (originating from a specific region)
  • or generalised (involving both hemispheres)
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170
Q

What are classifications of seizure types

A

tonic-clonic, absence, myoclonic, atonic, and tonic

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171
Q

What are causes of Epilepsy

A
  • genetic predisposition
  • structural brain abnormalities
  • metabolic disorders
  • immune conditions
  • infectious diseases like meningitis or encephalitis
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172
Q

What is tonic

A

muscle tensing

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173
Q

What is clonic

A

muscle jerking

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174
Q

How do Generalised tonic-clonic seizures present generally

A

Before patients might experience aura

involve tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness

After the seizure, there is a prolonged post-ictal period, where the person is confused, tired, and irritable or low.

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175
Q

What are associated symptoms with Generalised tonic-clonic seizures

A

tongue biting, incontinence, groaning and irregular breathing

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176
Q

Where do Partial seizures (or focal seizures) commonly occur

A

temporal lobe

affect hearing, speech, memory and emotions.

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177
Q

What symptoms are associated with temporal lobe focal seizures

A
  • Often stay awake
  • Déjà vu
  • typically a rising epigastric sensation
  • automatisms (e.g. lip smacking/grabbing/plucking)
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178
Q

What are DDx for seizures

A

Vasovagal syncope (fainting)
Pseudoseizures (non-epileptic attacks)
Cardiac syncope (e.g., arrhythmias or structural heart disease)
Hypoglycaemia
Hemiplegic migraine
Transient ischaemic attack

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179
Q

How do Myoclonic seizures present

A

sudden, brief muscle contractions, like an abrupt jump or jolt. They remain awake

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180
Q

How do Tonic seizures present

A

sudden onset of increased muscle tone, where the entire body stiffens. This results in a fall if the patient is standing, usually backwards. They last only a few seconds, or at most a few minutes.

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181
Q

How do Atonic seizures present

A

sudden loss of muscle tone, often resulting in a fall.

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182
Q

How do Absence seizures present

A

usually seen in children. The patient becomes blank, stares into space, and then abruptly returns to normal. During the episode, they are unaware of their surroundings and do not respond. These typically last 10 to 20 seconds.

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183
Q

How do Infantile spasms present

A

West syndrome
presents with clusters of full-body spasms
associated with developmental regression and has a poor prognosi

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184
Q

What is characteristic EEG finding of Infantile spasm

A

Hypsarrhythmia

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185
Q

WHat is treatment for infantile spasms

A

ACTH and vigabatrin

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186
Q

What are Febrile convulsions

A

tonic-clonic seizures that occur in children during a high fever

not caused by epilepsy

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187
Q

How is epilepsy investigated

A

electroencephalogram (EEG)
MRI brain -> structural pathology

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188
Q

What Additional investigations can be ordered for epilepsy

A
  • ECG
  • Serum electrolytes, including sodium, potassium, calcium and magnesium
  • Blood glucose for hypoglycaemia and diabetes
  • Blood cultures, urine cultures and lumbar puncture where sepsis, encephalitis or meningitis is suspected
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189
Q

What safety precautions can be taken for epilepsy

A

The DVLA will remove their driving licence until specific criteria are met (e.g., being seizure-free for one year)
Taking showers rather than baths (drowning is a major risk in epilepsy)
Particular caution with swimming, heights, traffic and dangerous equipment

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190
Q

What is first line management for male and non child bearing women with generalised tonic-clonic

A

Sodium valproate

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191
Q

What is first line management for male and non child bearing women with Partial (or focal)

A

Lamotrigine or Levetiracetam

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192
Q

What is first line management for male and non child bearing women with Myoclonic

A

Sodium valproate

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193
Q

What is first line management for male and non child bearing women with Tonic and atonic

A

Sodium valproate

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194
Q

What is first line management for male and non child bearing women with Absence

A

Ethosuximide

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195
Q

What is first line management for child bearing women with Generalised tonic-clonic

A

Lamotrigine or Levetiracetam

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196
Q

What is first line management for child bearing women with Partial (or focal)

A

Lamotrigine or Levetiracetam

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197
Q

What is first line management for child bearing women with Myoclonic

A

Levetiracetam

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198
Q

What is first line management for child bearing women with Tonic and atonic

A

Lamotrigine

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199
Q

What is first line management for child bearing women with Absence

A

Ethosuximide

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200
Q

How does Sodium Valproate work

A

increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brai

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201
Q

What are SE of Sodium Valproate

A

Teratogenic (harmful in pregnancy)
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

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202
Q

What is Status Epilepticus

A

medical emergency defined as either:

  • A seizure lasting more than 5 minutes
  • Multiple seizures without regaining consciousness in the interim
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203
Q

What is the immediate management of status epilepticus

A

Securing the airway
Giving high-concentration oxygen
Checking blood glucose levels
Gaining intravenous access (inserting a cannula)

ABCDE approach

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204
Q

What is the Medical treatment of status epilepticus

A
  1. benzodiazepine - PR diazepam or buccal midazolam or IV lorezapam
  2. repeated benzodiazepine 5-10 minutes if the seizure continues
  3. (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
  4. general anaesthesia
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205
Q

What needs to be monitored in phenytoin

A

cardiac

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206
Q

What are benzodiazepine options for status epilepticus

A

Buccal midazolam (10mg)
Rectal diazepam (10mg)
Intravenous lorazepam (4mg)

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207
Q

What is cerebral palsy

A

non progressive permanent neurological problems resulting from damage to the brain around the time of birt

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208
Q

What are antenatal causes of cerebral palsy

A
  • Maternal infections –> rubella, toxoplasmosis, CMV
  • Trauma during pregnancy
  • Placental abruption
  • cerebral malformation
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209
Q

What are intrapartum causes of cerebral palsy

A

Birth asphyxia
Birth Trauma
Pre-term birth

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210
Q

What are postnatal causes of cerebral palsy

A

Meningitis
Severe neonatal jaundice
Head injury
intraventricular haemorrhage

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211
Q

what is spastic cerebral palsy

A

hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones

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212
Q

What are the 4 types of cerebral palsy

A

Spastic
Dyskinetic
Ataxic
Mixed

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213
Q

what is dyskinetic cerebral palsy

A

problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems.

This is the result of damage to the basal ganglia and the substantia nigra

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214
Q

what is ataxic cerebral palsy

A

problems with coordinated movement resulting from damage to the cerebellum

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215
Q

what is mixed cerebral palsy

A

a mix of spastic, dyskinetic and/or ataxic features

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216
Q

what is another name for Spastic CP

A

pyramidal CP

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217
Q

what is another name for Dyskinetic CP

A

athetoid CP and extrapyramidal CP.

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218
Q

What is Monoplegia CP

A

one limb affected

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219
Q

What is Hemiplegia CP

A

one side of the body affected

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220
Q

What is Diplegia CP

A

four limbs are affects, but mostly the legs

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221
Q

What is Quadriplegia CP

A

four limbs are affected more severely, often with seizures, speech disturbance and other impairments

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222
Q

What are signs and symptoms of cerebral palsy during development

A

Failure to meet milestones
Increased or decreased tone, generally or in specific limbs
Hand preference below 18 months is a key sign to remember for exams
Problems with coordination, speech or walking
Feeding or swallowing problems
Learning difficulties

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223
Q

What gait is associated commonly with CP

A

hemiplegic or diplegic gait

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224
Q

How does CP gait present

A

The leg will be extended with plantar flexion of the feet and toes.

This means they have to swing the leg around in a large semicircle when moving their leg from behind them to in front

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225
Q

How will CP present on examination

A

Like UMN lesion

good muscle bulk, increased tone, brisk reflexes and slightly reduced power

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226
Q

What are complications and associated conditions with CP

A

Learning disability
Epilepsy
Kyphoscoliosis
Muscle contractures
Hearing and visual impairment
Gastro-oesophageal reflux

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227
Q

What is the management for cerebral palsy

A

MDT team approach
Physiotherapy
Occupational therapy
Speech and language therapy
Dieticians
Orthopaedic surgeons
Paediatricians
Social workers
Charities and support groups

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228
Q

What medication can be involved in CP care

A

Muscle relaxants (e.g. baclofen) for muscle spasticity and contractures
Anti-epileptic drugs for seizures
Glycopyrronium bromide for excessive drooling

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229
Q

What is motor neuron disease

A

erm that encompasses a variety of specific diseases affecting the motor nerves.

progressive condition where eventually neurons stop working

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230
Q

What does motor neuron disease NOT affect

A

no effect on the sensory neurones.

Sensory symptoms suggest an alternate diagnosis.

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231
Q

Name two types of Motor Neurone Disease

A

amyotrophic lateral sclerosis - MC
progressive bulbar palsy - 2nd MC
progressive muscular atrophy

232
Q

What are the bulbar muscles

A

muscles of talking and swallowing

233
Q

What are RF for MND

A

FH
Smoking
heavy metals
pesticide

234
Q

What is typical presentation of MND

A

late middle-aged (e.g., 60) man
insidious, progressive weakness of the muscles throughout the body, affecting the limbs, trunk, face and speech (dysarthria)
increased fatigue when exercising.
complain of clumsiness,

235
Q

What are signs of lower motor neurone disease

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

236
Q

What are signs of upper motor neurone disease

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

237
Q

How is MND diagnosed

A

clinical
diagnosis of exclusion

238
Q

What should MND show on nerve conduction study

A

normal motor conduction

239
Q

How is MND managed

A

Riluzole –> can slow the progression of the disease and extend survival by several months in ALS.

Non-invasive ventilation (NIV)

PEG feedng tube

240
Q

How can MND poatients be supported

A

Breaking bad news effectively and supportively
Multidisciplinary team (MDT) input to support and maintain their quality of life
Symptom control (e.g., baclofen for muscle spasticity and antimuscarinic medical for excessive saliva)
Benzodiazepines may help breathlessness worsened by anxiety
Advanced directives to document their wishes as the disease progresses
End-of-life care

241
Q

How will most MND patients die

A

respiratory failure or pneumonia.

242
Q

What is MND prognosis

A

50% of patients die within 3 years

243
Q

What is multiple sclerosis

A

inflammatory demyelinating disease, clinically defined by two episodes of neurological dysfunction (brain, spinal cord or optic nerves) separated in space and time.

T4 autoimmune rxn

oligodendroctyes CNS

244
Q

What cell myelinates nerves in the CNS

A

Oligodendrocytes in the central nervous system

245
Q

What cell myelinates nerves in the PNS

A

Schwann cells in the peripheral nervous system

246
Q

does Multiple sclerosis affect CNS or PNS

A

CNS

247
Q

What does “disseminated in time and space” mean in MS

A

lesions vary in location, meaning that the affected sites and symptoms change over time

248
Q

What factors influence MS

A

Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity

249
Q

How do MS symptoms onset presents

A

Symptoms usually progress over more than 24 hours.

Symptoms tend to last days to weeks at the first presentation and then improve

250
Q

What is Optic neuritis

A

demyelination of the optic nerve and presents with unilateral reduced vision, developing over hours to days.

251
Q

WHat are key features of Optic neuritis

A

Central scotoma (an enlarged central blind spot)
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect

252
Q

What are DDx for Optic neuritis

A

Neuromyelitis optica
Sarcoidosis
Systemic lupus erythematosus
Syphilis
Measles or mumps

Lyme disease

253
Q

How is Optic neuritis managed

A

acute loss of vision –> urgent ophthalmology input.

treated with high-dose steroids.

MRI to monitor progression to MS

254
Q

WHat is relative afferent pupillary defect

A

the pupil in the affected eye constricts more when shining a light in the contralateral eye than when shining it in the affected eye

255
Q

How does optic neuritis when testing the direct pupillary reflex

A

reduced pupil response to shining light in the eye affected by optic neuritis.

However, the affected eye has a normal pupil response when testing the consensual pupillary reflex.

256
Q

What focal weakness symptoms may MS present with

A

Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis

257
Q

What focal sensory symptoms symptoms may MS present with

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

258
Q

What is Lhermitte’s sign

A

electric shock sensation that travels down the spine and into the limbs when flexing the neck

259
Q

What is affected in Lhermitte’s sign

A

cervical spinal cord in the dorsal column

260
Q

What is Uhthoff sign

A

worsening of neurological function lasting less than 24 hours that can occur in multiple sclerosis patients due to increases in core body temperature

261
Q

What is Sensory ataxia

A

due to loss of proprioception

262
Q

What positive test does sensory ataxia result in

A

Romberg’s test

they lose balance when standing with their eyes closed)

263
Q

Where would a lesion in MS causing sensory ataxia be located

A

dorsal columns

264
Q

What is Cerebellar ataxia

A

problems with the cerebellum coordinating movement, indicating a cerebellar lesion

265
Q

What are disease patterns in MS

A

Clinically isolated syndrome
Relapsing-remitting
Secondary progressive
Primary progressive

266
Q

What is Clinically isolated syndrome MS

A

first episode of demyelination and neurological signs and symptoms. Patients with clinically isolated syndrome may never have another episode or may go on to develop MS

267
Q

What is Relapsing-remitting MS

A

MC

episodes of disease and neurological symptoms followed by recovery

can be further classified based on whether the disease is active or worsening

268
Q

What is Active Relapsing-remitting MS

A

new symptoms are developing, or new lesions are appearing on the MRI

269
Q

What is Not Active Relapsing-remitting MS

A

no new symptoms or MRI lesions are developing

270
Q

What is Worsening Relapsing-remitting MS

A

there is an overall worsening of disability over time

271
Q

What is not Worsening Relapsing-remitting MS

A

there is no worsening of disability over time

272
Q

What is Secondary progressive MS

A

where there was relapsing-remitting disease, but now there is a progressive worsening of symptoms with incomplete remissions.

273
Q

What is Primary progressive MS

A

worsening disease and neurological symptoms from the point of diagnosis WITHOUT relapses and remission

274
Q

How can progressive MS be further categorized

A

active or progressing

275
Q

What investigations can support MS diagnosis

A

MRI scans can demonstrate typical lesions
Lumbar puncture can detect oligoclonal bands in the cerebrospinal fluid (CSF)

276
Q

How can spasticity be managed in MS

A

Baclofen and gabapentin are first-line

277
Q

What is the criteria is used to diagnose MS

A

McDonald criteria

278
Q

What is McDonald criteria

A

≥ 2 clinical attacks desiminted in time and space and objective clinical evidence of ≥ 2 lesions

279
Q

What is DDx for MS

A

Migraine
TIA Stroke
Giant Cell Arteritis
Fibromyalgia
Neuromyelitis optica

280
Q

How is Acute relapse MS managed

A

High-dose steroids (e.g. oral or IV methylprednisolone)

oral 500mg
1g IV

281
Q

What Disease modifying drugs are given for MS

A

natalizumab - 1st line
ocrelizumab
fingolimod

282
Q

How can fatigue be managed in MS

A

modafinil or SSRI

283
Q

How can Neuropathic pain be managed in MS

A
  • amitriptyline
  • duloxetine
  • gabapentin
  • pregabalin
284
Q

How can urge incontinence be managed in MS

A

Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin

285
Q

Who would be part of a specialist multidisciplinary team (MDT) for MS

A

including neurologists, specialist nurses, physiotherapists and occupational therapists.

286
Q

Name two types of Muscular dystrophy

A

Duchennes muscular dystrophy
Beckers muscular dystrophy
Myotonic dystrophy

287
Q

What is Gower’s Sign

A

Children with proximal muscle weakness use a specific technique to stand up from a lying position.

using their hands on their legs to help them stand up

288
Q

What is Duchennes muscular dystrophy

A

defective gene for dystrophin on the X-chromosome

289
Q

What is dystrophin

A

protein that helps hold muscles together at the cellular level.

290
Q

Who is most affected by Duchennes muscular dystrophy boys or girls

A

boys

291
Q

What is the inheritance pattern of Duchennes muscular dystrophy

A

X-linked recessive

292
Q

If a mother is a carrier (meaning she has one faulty gene) of Duchennes muscular dystrophy and she has a child what is the chance of having the condition if she has a girl or boy

A
  • 50% change of being a carrier if they female
  • 50% change of having the condition if they are male
293
Q

How does Duchennes Muscular Dystrophy present

A

present around 3 – 5 years with weakness in the muscles around their pelvis
delayed motor milestones
progressive to all muscles
calf pseudohypertrophy
symmetrical proximal muscle wasting
life expectance of around 25 – 35 years

294
Q

How can Duchennes Muscular Dystrophy be managed pharmacuetically

A

Oral steroids have been shown to slow the progression of muscle weakness by as much as two years.
Creatine supplementation can give a slight improvement in muscle strength.

295
Q

How is Duchennes Muscular Dystrophy diagnosed

A

genetic testing
GS muscle biopsy

296
Q

What are complications of Duchennes Muscular Dystrophy

A

cardiomyopathy
heart failure
scoliosis
resp failure

297
Q

What are Complications seen secondary to longterm corticosteroid use

A

osteoporosis
impaired glucose tolerance
obesity
Addisonian crisis triggered by suddenly stopping steroids or intercurrent illness

298
Q

How is Muscular Dystrophy managed

A

occupational therapy, physiotherapy and medical appliances (such as wheelchairs and braces) as well as surgical and medical management of complications

299
Q

What is Beckers muscular dystrophy

A

similar to Duchennes, however the dystrophin gene is less severely affected and maintains some of its function

300
Q

When is typical presentation age for Beckers muscular dystrophy

A

Symptoms only start to appear around 8 – 12 years

wheelchair late 20s-30s

301
Q

WHat is the difference between Beckers and Duchennes mutation

A

Duchennes = frameshift
Beckers = missense

302
Q

What would bloods show for muscular dystrophy

A

inc CK

303
Q

What does a patient that is unable to let go after shaking someones hand indicate

A

Myotonic dystrophy

304
Q

What is key feature of myotonic dystrophy

A

prolonged muscle contraction.

305
Q

WHat is the inheritance pattern of Huntington’s disease

A

autosomal dominant

306
Q

WHat is Huntington’s disease

A

progressive neurological dysfunction.

It is a trinucleotide repeat disorder involving a genetic mutation in the HTT gene on chromosome 4, which codes for the huntingtin (HTT) protein.

autosomal dominant

307
Q

what are other examples of trinucleotide repeat disorders

A

Fragile X syndrome
Spinocerebellar ataxia
Myotonic dystrophy
Friedrich ataxia

308
Q

What does inheritance of Huntington’s display in successive generations

A

genetic anticipation

resulting in:
Earlier age of onset
Increased severity of disease

309
Q

How does Huntington’s typically present initially

A

cognitive, psychiatric or mood problems

310
Q

what movement disorders are associated with Huntington’s

A
  • Chorea (involuntary, random, irregular and abnormal body movements)
  • Dystonia (abnormal muscle tone, leading to abnormal postures)
  • Rigidity (increased resistance to the passive movement of a joint)
  • Eye movement disorders
  • Dysarthria (speech difficulties)
  • Dysphagia (swallowing difficulties)
311
Q

How is Huntington’s diagnosed

A

genetic testing

312
Q

How is Huntington’s managed

A
  • no treatment options
  • Breaking bad news effectively and supportively
  • Genetic counselling regarding relatives, pregnancy and children
  • Multidisciplinary team (MDT) input to support and maintain their quality of life
  • Physiotherapy to improve mobility, maintain joint function and prevent contractures
  • Speech and language therapy where there are speech and swallowing difficulties
  • Advanced directives to document their wishes as the disease progresses
  • End-of-life care
313
Q

What medication can be used for chorea symptoms

A

Tetrabenazine

314
Q

What percent chance does a child of someone wth Huntington’s have to develop condition

A

50%

315
Q

What is the prognosis of Huntington’s

A

Life expectance is around 10-20 years after the onset of symptoms

316
Q

WHat is common cause of death in Huntington’s

A

aspiration pneumonia
Suicide

317
Q

What are Migraines

A

complex neurological condition causing episodes or attacks of headache and associated symptoms

318
Q

What are 4 types of Migraines

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

319
Q

what factors influcence the pathophysiology of Migraines

A

combination of structural, functional, chemical, vascular and inflammatory factors.

320
Q

What are the 5 stages of Migraine

A
  • Premonitory or prodromal stage (can begin several days before the headache)
  • Aura (lasting up to 60 minutes)
  • Headache stage (lasts 4 to 72 hours)
  • Resolution stage (the headache may fade away or be relieved abruptly by vomiting or sleeping)
  • Postdromal or recovery phase
321
Q

What are typical features of Migraine headaches

A

Usually unilateral but can be bilateral
Moderate-severe intensity
Pounding or throbbing in nature
Photophobia
Phonophobia
Osmophobia
Aura
Nausea and vomiting

322
Q

what are typical visual symptoms of Migraine aura

A

Sparks in the vision
Blurred vision
Lines across the vision
Loss of visual fields (e.g., scotoma)

323
Q

What is main feature of Hemiplegic Migraine

A

hemiplegia (unilateral limb weakness)

ataxia (loss of coordination) and impaired consciousnes

324
Q

what are causes of Hemiplegic Migraine

A

Familial hemiplegic migraine is an autosomal dominant

325
Q

what are DDx for Hemiplegic Migraine

A

stroke or TIA.

326
Q

What are Migraine triggers

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

327
Q

What is acute management of Migraine

A

Triptans (e.g., sumatriptan)

NSAIDs (e.g., ibuprofen or naproxen)
Paracetamol
Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)

328
Q

what is Migraine prophylactic medication

A

Propranolol (a non-selective beta blocker)
Amitriptyline (a tricyclic antidepressant)
Topiramate (teratogenic and very effective contraception is needed)

329
Q

What class of medication is Triptans

A

5-HT receptor agonists (they bind to and stimulate serotonin receptors

330
Q

What are the mechanisms of action of Triptans

A

Cranial vasoconstriction
Inhibiting the transmission of pain signals
Inhibiting the release of inflammatory neuropeptides

331
Q

What is a common side-effect of triptan use

A

Tightness of the throat and chest

332
Q

What are DDx for headache

A

Tension headaches
Migraines
Cluster headaches
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Venous sinus thrombosis
Subarachnoid haemorrhage
Medication overuse
Hormonal headache
Cervical spondylosis
Carbon monoxide poisoning
Trigeminal neuralgia
Raised intracranial pressure
Brain tumours
Meningitis
Encephalitis
Brain abscess
Pre-eclampsia

333
Q

What could Fever, photophobia or neck stiffness headache indicate

A

meningitis, encephalitis or brain abscess

334
Q

What could New neurological symptoms with headache indicate

A

haemorrhage or tumours

335
Q

What could Visual disturbance with headache indicate

A

giant cell arteritis, glaucoma or tumours

336
Q

What could Sudden-onset occipital headache indicate

A

subarachnoid haemorrhage

337
Q

What could headache Worse on coughing or straining indicate

A

raised intracranial pressure

338
Q

What could Vomiting with headache indicate

A

raised intracranial pressure or carbon monoxide poisoning

339
Q

What could Postural, worse on standing, lying or bending over headache indicate

A

raised intracranial pressure

340
Q

What could History of trauma with headache indicate

A

intracranial haemorrhage

341
Q

What could History of cancer with headache indicate

A

brain metastasis

342
Q

what could headache with pregnancy indicate

A

pre-eclampsia)

343
Q

What does Papilloedema suggest

A

raised intracranial pressure, which may be due to a brain tumour, benign intracranial hypertension or an intracranial bleed.

344
Q

What are tension headaches

A

cause a mild ache or pressure in a band-like pattern around the head. They develop and resolve gradually and do not produce visual changes.

345
Q

What may tension headaches be associated with

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

346
Q

how are tension headaches managed

A

Reassurance
Simple analgesia (e.g., ibuprofen or paracetamol)

347
Q

What is first line medication for chronic or frequent tension headache

A

Amitriptyline

348
Q

what is Sinusitis

A

inflammation of the paranasal sinuses

349
Q

How does Sinusitis present

A

causes pain and pressure following a recent viral upper respiratory tract infection. There may be tenderness and swelling on palpation of the affected areas.

350
Q

What is first line treatment for Sinusitis

A

Most cases are caused by a viral infection and resolve within 2-3 weeks.

Prolonged cases (over 10 days) may be treated with a steroid nasal spray or antibiotics (phenoxymethylpenicillin first-line).

351
Q

What is Hormonal Headache

A

related to low oestrogen.

352
Q

When do hormonal headaches occur

A

Two days before and the first three days of the menstrual period
In the perimenopausal period
Early pregnancy (headaches in the second half of pregnancy should prompt investigations for pre-eclampsia)

353
Q

How are Hormonal Headache treated

A

NSAIDS (e.g., mefenamic acid) and triptans

354
Q

WHat are features of Hormonal Headache

A

similar features to migraines, with a unilateral, pulsatile headache associated with nausea

355
Q

What is Trigeminal Neuralgia

A

excruciating shooting or stabbing facial pain followed by a burning ache.

It is caused by either neurovascular compression from a neighboring vessel or nerve damage resulting from an underlying condition such as multiple sclerosis.

356
Q

WHat are the three branches of the Trigeminal nerve

A

Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)

357
Q

what can trigger Trigeminal Neuralgia

A

touch, taking, eating, shaving or cold. Attacks may worsen over time.

358
Q

What is first line medication for Trigeminal Neuralgia

A

carbamazepine

359
Q

What are Cluster headaches

A

Severe and unbearable unilateral headaches, usually centred around the eye.

360
Q

What is the frequency of Cluster headaches

A

come in clusters of attacks and then disappear for extended periods.

clusters typically last 4-12 weeks

Attacks last between 15 minutes and 3 hours.

361
Q

What are triggers to Cluster headaches

A

alcohol, strong smells or exercise

362
Q

What are Cluster headache associated symptoms

A

Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating

363
Q

How are acute Cluster headaches managed

A

Triptans (e.g., subcutaneous or intranasal sumatriptan)
High-flow 100% oxygen (may be kept at home)

364
Q

What is prophylaxis for Cluster headaches

A

1st line = Verapamil

alt
Occipital nerve block
Prednisolone (e.g., a short course to break the cycle during clusters)
Lithium

365
Q

What is Giant cell arteritis (GCA)

A

aka temporal arteritis. It is a type of systemic vasculitis affecting the medium and large arteries.

366
Q

What is Giant cell arteritis strongly linked to

A

polymyalgia rheumatica.
older white patients.

367
Q

How does Giant cell arteritis present

A

Unilateral headache severe and around the temple and forehead.

Scalp tenderness (e.g., noticed when brushing the hair)
Jaw claudication
Blurred or double vision
Loss of vision if untreated

368
Q

How may Giant cell arteritis present on examination

A

temporal artery may be tender and thickened to palpation, with reduced or absent pulsation.

369
Q

What are associated features with Giant cell arteritis

A

Symptoms of polymyalgia rheumatica (e.g., shoulder and pelvic girdle pain and stiffness)
Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
Muscle tenderness
Carpel tunnel syndrome
Peripheral oedema

370
Q

How is Giant cell arteritis investigated

A

Clinical presentation
Raised inflammatory markers, particularly ESR (usually more than 50 mm/hour)
Temporal artery biopsy
Duplex ultrasound

371
Q

In giant cell arteritis occlusion of what artery causes anterior ischemic optic neuropathy

A

posterior ciliary artery

372
Q

How does Giant cell arteritis present on biposy

A

showing multinucleated giant cells

skip lesions

373
Q

How does Giant cell arteritis present on US

A

showing the hypoechoic “halo” sign and stenosis of the temporal artery

374
Q

How does Giant cell arteritis present on Fundoscopy

A

swollen pale disc and blurred margins

375
Q

How is Giant cell arteritis initially managed

A

steroids started before Dx to reduce risk of vision loss

  • 40-60mg prednisolone daily with no visual symptoms or jaw claudication
  • 500mg-1000mg methylprednisolone daily with visual symptoms or jaw claudication
376
Q

What medication is involved in Giant cell arteritis management longer term

A

steroids weaned over 1-2 years

Aspirin 75mg daily decreases vision loss and strokes
Proton pump inhibitor (e.g., omeprazole) for gastroprotection while on steroids
Bisphosphonates and calcium and vitamin D for bone protection while on steroids

377
Q

What people may be involved in management of Giant cell arteritis

A

Rheumatology for specialist diagnosis and management
Vascular surgeons for a temporal artery biopsy
Ophthalmology review for visual symptoms

378
Q

WHat are complications of Giant cell arteritis

A

Visual loss ** = irreversible
Steroid-related complications (e.g., weight gain, diabetes and osteoporosis)
Cerebrovascular accident (stroke)

379
Q

WHat is Myasthenia gravis

A

autoimmune condition affecting the neuromuscular junction. It causes muscle weakness that progressively worsens with activity and improves with rest.

380
Q

who does Myasthenia gravis typically affect

A

ffecting women under 40 and men over 60.

381
Q

What is the pathophysiology of Myasthenia gravis

A

Acetylcholine stimulates muscle contraction

Acetylcholine receptor (AChR) antibodies in MG

bind to the postsynaptic acetylcholine receptors, blocking them and preventing stimulation by acetylcholine

more the receptors are used during muscle activity, the more they become blocked.

382
Q

How does Myasthenia gravis present

A

weakness that worsens with muscle use and improves with rest

Difficulty climbing stairs, standing from a seat or raising their hands above their head
diplopia
ptosis
facial weakness
jaw fatigue
weak swallow
Slurred speech

383
Q

What part of the body does Myasthenia gravis most affect

A

affect the proximal muscles of the limbs and small muscles of the head and neck, with:

384
Q

What ways can Myasthenia gravis symptoms be elicited

A

Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

385
Q

What further examination steps can be taken in Myasthenia gravis

A

Checking for a thymectomy scar
Testing the forced vital capacity (FVC)

386
Q

What condition is Myasthenia gravis strongly linked with

A
  • thymomas (thymus gland tumours)
  • 10-20% of patients with myasthenia gravis have a thymoma.
  • 30% of patients with a thymoma develop myasthenia gravis.
  • autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
  • thymic hyperplasia in 50-70%
387
Q

What do antibody tests for Myasthenia gravis look for

A

AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)

388
Q

What further investigations can be down for Myasthenia gravis

A

A CT or MRI of the thymus gland is used to look for a thymoma.

The edrophonium test can be helpful where there is doubt about the diagnosis.

389
Q

What is a edrophonium test for Myasthenia gravis

A

Patients are given intravenous edrophonium chloride

Edrophonium blocks enzymes in the neuromuscular junction that break down acetylcholine = level of acetylcholine at the neuromuscular junction rises, temporarily relieving the weakness

390
Q

How is Myasthenia gravis treated

A
  • Pyridostigmine a long acting acetylcholinesterase inhibitor that prolongs the action of acetylcholine and improves symptoms
  • Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies
  • Thymectomy can improve symptoms, even in patients without a thymoma
  • Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail
391
Q

What is a Myasthenic crisis

A

life-threatening complication of myasthenia gravis
often triggered by another illness
Respiratory muscle weakness can lead to respiratory failure.

392
Q

How is Myasthenic crisis treated

A

non-invasive ventilation or mechanical ventilation.

Treatment is with IV immunoglobulins and plasmapheresis.

393
Q

What is Guillain-Barré Syndrome

A

acute paralytic polyneuropathy that affects the peripheral nervous system

acute, symmetrical, ascending weakness and can also cause sensory symptoms.

394
Q

What is Guillain-Barré Syndrome associated with

A

Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).

395
Q

What is pathophysiology of Guillain-Barré Syndrome

A

molecular mimicry

target proteins on the myelin sheath or the nerve axon of PNS

396
Q

How does Guillain-Barré Syndrome present

A

Symptoms within four weeks of the triggering infection

begin in the feet and progress upward.

The characteristic features are:
Symmetrical ascending weakness
Reduced reflexes
peripheral loss of sensation
neuropathic pain

397
Q

How is Guillain-Barré Syndrome diagnosed

A

clinically with Brighton criteria suppoted by nerve conduction study and LP

anti-GM1 antibodies

398
Q

What would Guillain-Barré Syndrome show on nerve conduction studies

A

showing reduced signal through the nerves

399
Q

WHat would Guillain-Barré Syndrome show on lumbar puncture

A

showing raised protein with a normal cell count and glucose

400
Q

How is Guillain-Barré Syndrome managed

A
  • Supportive care
  • VTE prophylaxis
  • IV immunoglobulins (IVIG) first-line
  • Plasmapheresis is an alternative to IVIG

with respiratory failure may require intubation, ventilation and admission to the intensive care unit.

401
Q

How is main complication of Guillain-Barré Syndrome

A

pulmonary embolism is a leading cause of death

402
Q

What is prognosis for Guillain-Barré Syndrome

A

Recovery can take months to year
Most full recovery
Some are left with significant disability

Mortality is around 5%

403
Q

What is Peripheral Neuropathy

A

reduced sensory and motor function in the peripheral nerves, typically affecting the feet and hands (“stocking-glove” distribution).

404
Q

What are causes of Peripheral Neuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis

405
Q

What does facial nerve pass through

A

temporal bone and parotid gland.

406
Q

What are 5 branches of the facial nerve

A

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

407
Q

WHat is the motor function of the facial nerve

A

Facial expression
Stapedius in the inner ear
Posterior digastric, stylohyoid and platysma muscles

408
Q

what is the sensory function fo the facial nerve

A

taste from the anterior 2/3 of the tongue.

409
Q

what si the parasympathetic supply of the facial nerve

A

Submandibular and sublingual salivary glands
Lacrimal gland (stimulating tear production)

410
Q

How is UMNv LMN lesion distingiushed

A

UMN= stroke
LMN= palsy

UMN = forehead spared = move forehead

411
Q

When do Bilateral upper motor neurone lesions occur

A

Cerebrovascular accidents (strokes)
Tumours

412
Q

when do unilater upper motor neurone lesions occur

A

Pseudobulbar palsies
Motor neurone disease

413
Q

how is bells palsy treated

A

if within 72 hours of developing symptoms: prednisolone

50mg for 10 days
60mg for 5 days followed by a 5-day reducing regime, dropping the dose by 10mg per day

+ lubricating eye drops

414
Q

What is Ramsay-Hunt syndrome

A

caused by the varicella zoster virus (VZV).

415
Q

How does Ramsay-Hunt syndrome present

A
  • unilateral LMN facial nerve palsy.
  • painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side.
416
Q

How is Ramsay-Hunt syndrome treated

A

aciclovir and prednisolone. Patients also require lubricating eye drops.

417
Q

What are Systemic disease causes of LMN facial nerve palsy

A

Diabetes
Sarcoidosis
Leukaemia
Multiple sclerosis
Guillain–Barré

418
Q

What are tumor causes of LMN facial nerve palsy

A

Acoustic neuroma
Parotid tumour
Cholesteatoma

419
Q

What are benign brain tumors

A

meningiomas

420
Q

what are malignant brain tumors

A

glioblastomas

421
Q

How do brain tumors present

A

progressive focal neurological symptoms

symptoms and signs of raised intracranial pressure (intracranial hypertension)

422
Q

What are causes of raised ICP

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection

423
Q

What are symptoms of raised ICP

A

Constant headache
Nocturnal (occurring at night)
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
Papilloedema on fundoscopy

424
Q

What are signs of raised ICP

A

Altered mental state
Visual field defects
Seizures (particularly partial seizures)
Unilateral ptosis (drooping upper eyelid)
Third and sixth nerve palsies

425
Q

What is Papilloedema

A

swelling of the optic disc secondary to raised intracranial pressure.

426
Q

How does Papilloedema present on fundoscopy

A

Blurring of the optic disc margin
Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
Loss of venous pulsation
Engorged retinal veins
Haemorrhages around the optic disc
Paton’s lines, which are creases or folds in the retina around the optic disc

427
Q

How do retinal vessels cross disc in Papilloedema

A

Vessels can travel straight across a flat surface, whereas they will curve over a raised disc.

428
Q

What are gliomas tumors of

A

glial cells in the brain or spinal cor

429
Q

What are types of Glial cells

A

astrocytes, oligodendrocytes and ependymal cells

430
Q

what are three main tyoes of Gliomas

A

Astrocytoma (the most common and aggressive form is glioblastoma)
Oligodendroglioma
Ependymoma

431
Q

is a grade 1 Gliomas most benign or malignant

A

benign

432
Q

What cells do meningiomas grow from

A

meninges

433
Q

What cancers spread to brain

A

Lung
Breast
Renal cell carcinoma
Melanoma

434
Q

What visual field defect do pit tumors cause

A

bitemporal hemianopia, with loss of the outer half of the visual fields in both eyes.

435
Q

WHat hormones conditions can Pituitary Tumours cause

A

Acromegaly (excessive growth hormone)
Hyperprolactinaemia (excessive prolactin)
Cushing’s disease (excessive ACTH and cortisol)
Thyrotoxicosis (excessive TSH and thyroid hormone)

436
Q

How can Pituitary Tumours be managed

A

Trans-sphenoidal surgery (through the nose and sphenoid bone)
Radiotherapy
Bromocriptine to block excess prolactin
Somatostatin analogues (e.g., octreotide) to block excess growth hormone

437
Q

What are Acoustic Neuroma

A

tumor of schwann cells that surround the auditory nerve (vestibulocochlear nerve) that innervates the inner ear.

provide myelin sheath of PNS

438
Q

what is another name for Acoustic neuromas

A

vestibular schwannomas.

439
Q

What angle do Acoustic Neuroma occur are
and what is the investigation of choice

A

cerebellopontine angle

Ix = MRI of the cerebellopontine angle

440
Q

What are bilateral Acoustic Neuroma associated with

A

neurofibromatosis type 2.

441
Q

How do Acoustic Neuroma present

A

Unilateral sensorineural hearing loss (often the first symptom)

classic combination of vertigo, hearing loss, tinnitus and an absent corneal reflex.

Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)

442
Q

How are Acoustic Neuroma managed

A

Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate
Surgery to remove the tumour (partial or total removal)
Radiotherapy to reduce the growth

443
Q

What is 1st line investigation in patients with possible brain tumor

A

MRI brain

444
Q

How is the definitive diagnosis of brain tumors given

A

Biopsy

definitive histological diagnosis,

445
Q

What are treatment options for brain tumors

A

Surgery
Chemotherapy
Radiotherapy
Palliative care

446
Q

What is Stevens-Johnson syndrome and and toxic epidermal necrolysis (TEN)

A

spectrum of disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of ski

447
Q

What is difference between SJS and TEN

A

SJS affects less that 10% of body surface area whereas TEN affects more than 10% of body surface area.

448
Q

What medication causes SJS

A

Anti-epileptics
Antibiotics
Allopurinol
NSAIDs

449
Q

what infections causes SJS

A

Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV

450
Q

How does SJS present

A

non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. They then develop a purple or red rash that spreads across the skin and starts to blister.

451
Q

How is SJS managed

A

medical emergencies
cease medication stat
IV fluids
steroids, immunoglobulins and immunosuppressant

452
Q

What are complications of SJS

A

secondary infection
permanent skin damage
visual complications

453
Q

what is Neurofibromatosis

A

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

enign but can cause neurological and structural problems.

454
Q

what is MC Neurofibromatosis

A

type 1

455
Q

Where is the gene for Neurofibromatosis type 1 found

A

chromosome 17.

456
Q

what does Neurofibromatosis gene code for

A

neurofibromin
tumour suppressor protein.

457
Q

what is the inheritance pattern of Neurofibromatosis

A

auto dom

458
Q

What is the diagnostic criteria for Neurofibromatosis type 1

A

C – Café-au-lait spots (more than 15mm diameter is significant in adults)
R – Relative with NF1
A – Axillary or inguinal freckling
BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
N – Neurofibromas
G – Glioma of the optic pathway

CRABBING

459
Q

How is Neurofibromatosis managed

A

iagnostic criteria. Genetic testing can be helpful.

no treatment

460
Q

What are complications of Neurofibromatosis type 1

A
  • malignant peripheral nerve sheath (MPNST)
  • gastrointestinal stromal tumours (GIST).
  • Migraines
  • Epilepsy
  • Renal artery stenosis, causing hypertension
  • Learning disability
  • Behavioural problems (e.g., ADHD)
  • Scoliosis of the spine
  • Vision loss (secondary to optic nerve gliomas)
  • Brain tumours
  • Spinal cord tumours with associated neurology (e.g., paraplegia)
  • Increased risk of cancer (e.g., breast cancer and leukaemia)
461
Q

where is the gene for Neurofibromatosis type 2 located

A

chromosome 22

462
Q

what does the affected gene in Neurofibromatosis type 2 code for

A

merlin, a tumour suppressor protein important in Schwann cells

463
Q

what is Neurofibromatosis type 2 associated with

A

acoustic neuromas, which are tumours of the auditory nerve that innervates the inner ear.

464
Q

What does a palsy in the third cranial nerve (the oculomotor nerve) cause

A

Ptosis (drooping upper eyelid)
Dilated non-reactive pupil
Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye

465
Q

the 3rd cranial nerve supplies all extraocular muscles except …

A

lateral rectus and superior oblique

466
Q

What does a third nerve palsy that does not affect the pupil (sparing of the pupil) suggest

A

microvascular… parasympathetic fibres are spared.

Diabetes
Hypertension
Ischaemia

467
Q

what can cause a full third nerve palsy

A
  • Vasulitis
  • DM
  • Cavernous sinus thrombosis
  • Posterior communicating artery aneurysm –> Painful CN3
  • Raised intracranial pressure –> causung trans-tentorial, or uncal, herniation.
  • Weber’s syndrome:
468
Q

what is horner sydnrome triad

A

Ptosis
Miosis
Anhidrosis (loss of sweating)

469
Q

in horners syndrome what does anhidrosis of the arm, trunk and face indicate

A

Central lesions (occurring before the nerves exit the spinal cord)

470
Q

what causes horners sydnrome

A

damage to the sympathetic nervous system supplying the face.

471
Q

in horners syndrome what does anhidrosis of the face indicate

A

Pre-ganglionic lesions

472
Q

what are central lesion causes of horners syndrome

A

Central lesions:

S – Stroke
S – Multiple Sclerosis
S – Swelling (tumours)
S – Syringomyelia (cyst in the spinal cord)

473
Q

what are Pre-ganglionic lesion causes of horners syndrome

A

T – Tumour (Pancoast tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib and clavicle)

474
Q

what are post-ganglionic lesion causes of horners syndrome

A

C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache

475
Q

what is Argyll-Robertson Pupil

A

neurosyphilis

it accommodates but does not react

476
Q

causes of dilated pupil

A

Congenital
Stimulants (e.g., cocaine)
Anticholinergics (e.g., oxybutynin)
Trauma
Third nerve palsy
Holmes-Adie syndrome
Raised intracranial pressure
Acute angle-closure glaucoma

477
Q

causes of constricted pupil

A

Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine

478
Q

What is Meningitis

A

inflammation of the meninges, the lining of the brain and spinal cord.

479
Q

What are causes of bacterial Meningitis

A

Neisseria meningitidis
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae
Group B streptococcus (GBS) (particularly in neonates as GBS may colonise the vagina)
Listeria monocytogenes (particularly in neonates)

480
Q

What type of bacteria is Neisseria meningitidis

A

gram-negative diplococcus bacteria

481
Q

what is Meningococcal septicaemia

A

meningococcus bacterial infection is in the bloodstream

(non blanching rash)

482
Q

what is Meningococcal meningitis

A

bacteria infects the meninges and the cerebrospinal fluid.

483
Q

what are mc causes of viral Meningitis

A

Enteroviruses (e.g., coxsackievirus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)

484
Q

how is viral Meningitis tested

A

Viral PCR testing

485
Q

how is Herpes simplex virus (HSV) and Varicella zoster virus (VZV) Meningitis treated

A

Aciclovir

486
Q

How does Meningitis present

A

Fever
Neck stiffness
Vomiting
non-blanching rash
Headache
Photophobia
Altered consciousness
Seizures

487
Q

What non specific symptoms can babies and neonates with Meningitis present with

A

hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle

488
Q

What are the special tests to do for Meningitis

A

Kernig’s test
Brudzinski’s test

489
Q

what is Kernig’s test

A

A positive test is the elicitation of pain or resistance with passive extension of the patient’s knee

490
Q

what is Brudzinski’s test

A

Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed

491
Q

where is needle inserted for lumbar puncture

A

L3-L4 or L4/L5 intervertebral space

492
Q

what would CSF sample for bacterial Meningitis show

A

Appearance = cloudy
Protein = high
Glucose = low
WCC = high neutrophils
Culture = bacteria

493
Q

what would CSF sample for viral Meningitis show

A

Appearance = clear
Protein = mild to normal
Glucose = normal
WCC = high lymphocytes
Culture = negative

494
Q

How is Meningitis managed in GP

A

benzylpenicillin (IM or IV)

Under 1 year – 300mg
1-9 years – 600mg
Over 10 years – 1200mg

495
Q

How is Meningitis managed in hospital

A

Under 3 months – cefotaxime plus amoxicillin (amoxicillin is to cover listeria)
Above 3 months – ceftriaxone

496
Q

how are close contacts of Meningitis treated

A

single dose of ciprofloxacin

497
Q

What should be added to Meningitis treatemnt if risk of penicillin-resistant pneumococcal infection

A

Vancomycin

498
Q

Is Meningitis a notifiable disease

A

yes

499
Q

What are complications of Meningitis

A

Hearing loss (a key complication)
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits, such as limb weakness or spasticity

500
Q

what can be given to prevent hearing loss with Meningitis

A

Steroids (e.g., dexamethasone) a

501
Q

When is LP contraindicated

A
  • signs of raised ICP
  • GCS below 9
  • haemodynamically unstable
  • active seizures or post-ictal.
502
Q

What investigations can be ordered for meningitis

A

blood cultures and a lumbar puncture

503
Q

what is Encephalitis

A

inflammation of the brain. This can be the result of infective or non-infective causes

NI = autoimmune

504
Q

what is the MC cause of Encephalitis

A

herpes simplex virus (HSV).

type 1 in children (cold sores)
type 2 in neonates (genital herpes)

505
Q

how does Encephalitis present

A
  • fever, headache, psychiatric symptoms, seizures, vomiting
  • focal features e.g. aphasia
506
Q

what are lab investigations for Encephalitis

A

Lumbar puncture, sending cerebrospinal fluid for viral PCR
Blood tests
Serology
Autoimmune antibody panel

507
Q

what is imaging investigation of chocie for Encephalitis

A

CT or MRI scan (better)
areas of inflammation or oedema

508
Q

What does imaging for HSV encephalitis show

A

temporal lobe changes (hypodensities on CT, or hyperintensities on MRI) and bilateral temporal lobe changes

509
Q

How is Encephalitis managed

A
  • IV Aciclovir treats herpes simplex virus (HSV) and varicella zoster virus (VZV)
  • IV Ganciclovir treat cytomegalovirus (CMV)
510
Q

what are complications of Encephalitis

A

Lasting fatigue and prolonged recovery
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance

511
Q

How does brain abscess present

A

headache
focal neurological deficits
fever
signs of raised ICP

512
Q

how is brain abscess diagnosed

A

GS = MRI
CT for detetcing complications
needle aspiration

513
Q

How is brain abscess managed

A

IV antibiotics: IV 3rd-generation cephalosporin (ceftriaxone) + metronidazole

drainage or debridement

ICP management = dexamethasone

514
Q

What causes brain abscess

A

contiguous spread of infection from sinusitis, otitis media, or dental infections

haematogenous spread from distant sources (e.g., endocarditis, pulmonary infections)

direct inoculation from trauma or neurosurgical procedures.

515
Q

What are the complications of a brain abscess

A

seizures, meningitis, ventriculitis, hydrocephalus, cerebral oedema, and herniation

516
Q

What is hydrocephalus

A

cerebrospinal fluid (CSF) building up abnormally within the brain and spinal cord.

This is a result of either over-production of CSF or a problem with draining or absorbing CSF.

517
Q

where is CSF created

A

created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles

518
Q

where is CSF absorbed

A

into the venous system by the arachnoid granulations.

519
Q

WHat are the 4 ventricles in the brain

A

two lateral ventricles, the third and the fourth ventricles

520
Q

What is the MC cause of hydrocephalus

A

aqueductal stenosis

cerebral aqueduct that connects the third and fourth ventricle is stenosed (narrowed).

causing CSF to build up in the lateral and third ventricles.

521
Q

What are other causes of hydrocephalus

A
  • Arachnoid cysts can block the outflow of CSF if they are large enough
  • Arnold-Chiari malformation is where the cerebellum herniates downwards through the foramen magnum, blocking the outflow of CSF
  • Chromosomal abnormalities and congenital malformations can cause obstruction to CSF drainage.
522
Q

how is Normal pressure hydrocephalus investigated

A

CT

hydrocephalus with an enlarged fourth ventricle
in addition to the ventriculomegaly there is typically an absence of substantial sulcal atrophy

523
Q

How does Normal pressure hydrocephalus present

A
  • urinary incontinence
  • dementia and bradyphrenia (slow thinking)
  • gait abnormality (may be similar to Parkinson’s disease)
524
Q

what is Normal pressure hydrocephalus associated with

A

subarachnoid haemorrhage or meningitis

525
Q

How is hydrocephalus treated

A

Ventriculoperitoneal Shunt

CSF from the ventricles into another body cavity Usually the peritoneal cavity i

526
Q

what are complications of VP shunts

A
  • Intraventricular haemorrhage during shunt related surgery
  • Infection
  • Blockage
  • Excessive drainage
  • Outgrowing them (they typically need replacing around every 2 years as the child grows)
527
Q

What is Hypoxic-ischaemic encephalopathy

A

neurological condition resulting from inadequate cerebral oxygen supply.

528
Q

WHat is primary energy failure in Hypoxic-ischaemic encephalopathy

A

occurs immediately during the hypoxic-ischaemic event, leading to anaerobic metabolism, lactic acidosis, and cytotoxic oedem

529
Q

what is secondary energy failure in Hypoxic-ischaemic encephalopathy

A

ccurring hours to days later, is characterised by renewed accumulation of toxic metabolites and free radicals causing further neuronal death

530
Q

How does Hypoxic-ischaemic encephalopathy present

A
  • altered consciousness levels ranging from lethargy to coma
  • seizures
  • abnormal tone and reflexes.
531
Q

How is Hypoxic-ischaemic encephalopathy managed

A

supportive care such as maintaining normal body temperature and blood glucose levels alongside seizure control.

therapeutic hypothermia

532
Q

What are causes of Hypoxic-ischaemic encephalopathy

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
533
Q

How is Hypoxic-ischaemic encephalopathy investiagted

A

Blood gas analysis
complete blood count
serum electrolytes and glucose
LFT

US = 1st line
MRI = GS

534
Q

How is Hypoxic-Ischaemic Encephalopathy Graded

A

Sarnat Staging

535
Q

WHat is Ménière’s disease

A

long-term inner ear disorder that causes recurrent attacks of vertigo

536
Q

What is Ménière’s disease triad

A

Hearing loss
Vertigo
Tinnitus

537
Q

How is Ménière’s disease diagnosed

A

clinical, based on the signs and symptoms
ENT
audiology assessment

538
Q

How are acute Ménière’s disease attacks managed

A

acute attacks: buccal or intramuscular prochlorperazine

Antihistamines (e.g., cyclizine, cinnarizine and promethazine)

539
Q

What is Ménière’s disease prophylaxis

A

Betahistine

540
Q

what causes Ménière’s disease

A

excessive buildup of endolymph in the labyrinth of the inner ear, causing a higher pressure than normal and disrupting the sensory signal

541
Q

WHat are features of Wernicke’s encephalopathy

A

Confusion
Ataxia
Nystagmus
Ophthamoplegia
PEripheral
Neuropathy

542
Q

WHat are features of Korsakoff syndrome

A
  • anterograde amnesia: inability to acquire new memories
  • retrograde amnesia
  • confabulation
543
Q

how is Wernicke’s encephalopathy treated

A

IV thiamine

544
Q

what is Cauda Equina

A

surgical emergency where the nerve roots of the cauda equina at the bottom of the spine are compressed

545
Q

What is the sensory supply of the Cauda Equina

A

lower limbs, perineum, bladder and rectum

546
Q

What is the motor supply of the Cauda Equina

A

lower limbs and the anal and urethral sphincters

547
Q

What is the parasympathetic supply of the Cauda Equina

A

bladder and rectum

548
Q

what are causes of cauda equina

A

Herniated disc (the most common cause)
Tumours, particularly metastasis
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Abscess (infection)
Trauma

549
Q

What are red flag signs of cauda equina

A
  • Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus)
  • Loss of sensation in the bladder and rectum (not knowing when they are full)
  • Urinary retention or incontinence
  • Faecal incontinence
  • Bilateral sciatica
  • Bilateral or severe motor weakness in the legs
  • Reduced anal tone on PR examination
550
Q

How is cauda equina investigated

A

Emergency MRI scan to confirm or exclude cauda equina syndrome

551
Q

how is cauda equina managed

A

lumbar decompression surgery

552
Q

how can cauda equina be differentiated from metastatic spinal cord compression

A

cauda equina = LMN signs(reduced tone and reflexes)

MSSC = UMN signs (inc tone, reflxes and plantar reflex

553
Q

How is metastatic spinal cord compression managed

A

High dose dexamethasone (to reduce swelling in the tumour and relieve compression)
Analgesia
Surgery
Radiotherapy
Chemotherapy

554
Q

What makes MSSC pain worse

A

worse on coughing or straining.

555
Q

what is Anterior Cord Syndrome

A

Damage to the anterior part of the spinal cord resulting in

LOSS of motor function and pain and temperature sensation,

but preservation of proprioception and touch.

556
Q

what are signs of autonomic dysreflexia

A

severe hypertension and flushing and sweating above the level of injury
full bladder

can only occur if the spinal cord injury occurs above the T6 level

557
Q

what causes autonomic dysreflexia

A

spinal cord injury at, or above T6

MC triggered by faecal impaction or urinary retention

558
Q

what is Syringomyelia

A

cyst or cavity forms within the spinal cord leading to collection of CSF within the spinal cord.

559
Q

how does Syringomyelia present

A

cape-like loss of pain and temperature sensation

due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine

560
Q

what are complications of spinal injuries

A

pressure sores, urinary tract infections, deep vein thrombosis and autonomic dysreflexia

561
Q

what is Brown-Séquard Syndrome

A

damage to one half of the spinal cord.

  • ipsilateral weakness below lesion
  • ipsilateral loss of proprioception and vibration sensation
  • contralateral loss of pain and temperature sensation
562
Q

What is malaria

A

disease caused by Plasmodium protozoa which is spread by the female Anopheles mosquito

563
Q

name 3 types of malaria

A
  • Plasmodium falciparum (the most common and severe form)
  • Plasmodium vivax
  • Plasmodium ovale
  • Plasmodium malariae
    *
564
Q

what is dormnat malaria called

A

hypnozoites

565
Q

where do malaria mature

A

liver

566
Q

what is malaria travelling in RBc called

A

merozoites

567
Q

when merozoites rupture RBc what dot hey cause

A

haemolytic anaemia.

568
Q

what are malaria symptoms

A

Fever (up to 41ºC) with sweats and rigors
Fatigue
Myalgia (muscle aches and pain)
Headache
Nausea
Vomiting

569
Q

what are malaria signs on examination

A

Pallor due to the anaemia
Hepatosplenomegaly
Jaundice (bilirubin is released during the rupture of red blood cells)

570
Q

how is malaria investigated

A

malaria blood film
schizonts on a blood film

571
Q

what is required to exclude a malaria diagnosis

A

Three negative samples taken over three consecutive

572
Q

how is uncomplicated malaria managed

A

1st - oral artemisinin-based combination therapies

eg artemether plus lumefantrine
artesunate plus amodiaquine

573
Q

how is severe malaria manahed

A

1st - IV Artesunate is the usual first choice (haemolysis is a common side effect)

574
Q

what are complications of malaria

A

Cerebral malaria
Seizures
Reduced consciousness
Acute kidney injury
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death

575
Q

what is antimalarial medication with least side effects

A

Proguanil / atovaquone (Malarone)

3a neuro/geriatrics (3 decks)

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