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Phase1c Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Definition of Bell’s Palsy?

A

Unilateral peripheral facial nerve palsy with unremarkable physical examination and history
-Facial nerve aetiolgoy

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2
Q

Which motor neurones are affected in Bell’s Palsy?

A

CN VII, lower motor neurones, affecting both contralateral and ipsilateral motor cortices
Equal distribution of facial weakness across facial zones

Note: Does not spare the forehead

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3
Q

What are the symptoms of Bell’s Palsy?

A

Absence of nasolabial fold
Drooping of the eyelid and mouth
- Drooling, difficulty eating/drinking

-Keratoconjunctivitis sicca (dry eye) with parasympathetic dysfunction of the lacrimal gland
Hyperacusis
Dysgeusia- loss of taste on anterior 2/3rd of the tongue

Post-auricular pain

Symptoms fully evolve in 72 hours

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4
Q

How is Bell’s Palsy diagnosed?

A

Clinical diagnosis

Consider electroneuronography - >90% decrease in compound muscle action potential.

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5
Q

Which infectious diseases can cause facial nerve palsies?

A

Borella burgdorefi - Lyme disease
EBV
HSV-1
VZ

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6
Q

What is the palpebral-oculogyric reflex in Bell’s Palsy?

A

• Attempted eyelid closure  Upward eye deviation (when eye remains open).

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7
Q

What should be examined to exclude Ramsay Hunt Syndrome in Bell’s Palsy?

A

Otoscopy - vesicular rash in the auditory canal suggests RHS.

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8
Q

What is the treatment for Bell’s Palsy?

A

High dose 50mg OM Prednisolone within 72 hours of onset

Protection of the cornea with artificial tears

surgery - Lateral tarssorrhaphy is established corneal damage

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9
Q

What is the management for Ramsay Hunt Syndrome?

A

Corticosteroid + Acyclovir

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10
Q

What are the complications of Bells Palsy?

A

Keratoconjunctivitis Sicca
Contracture and synkinesis
Crocodile tears

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11
Q

What is the definition of a cluster headache?

A

Severe headache characterised by unilateral pain persisting 15-180 minutes untreated occurring at a cyclical pattern

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12
Q

What is the distribution of pain in cluster headaches?

A

Phantom of the opera mask distribution of pain pattern

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13
Q

What are the symptoms of cluster headaches?

A

Conjunctival redness and/or lacramation

Nasal congestion or rhinorrhoea

Eyelid oedema

Flushing and facial swelling

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14
Q

What are the risk factors for cluster headaches?

A

Male sex
Family history
Cigarette smoking and heaving drinking (+ sleep disruption)

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15
Q

Which reflex is thought to be implicated in the aetiology of cluster headaches?

A

Trigeminal autonomic reflex

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16
Q

Which brain structure is responsible for regulating circadian rhythms and is linked to the cyclical pattern of cluster headaches?

A

Hypothalamus

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17
Q

What is the presentation of cluster headaches?

A 
Forehead and facial sweating
Miosis or ptosis 
A sense of restlessness or agitation 
Photophobia, phonophobia
Frequency of headache 1-8-per day (diurnal pattern)
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18
Q

What is the average number of daily headaches in Cluster headaches?

A

4

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19
Q

What are the two types of cluster headaches?

A

Episodic

Chronic

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20
Q

What are episodic cluster headaches?

A

occurring in periods lasting 7 days - separate by pain-free periods lasting a month or longer

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21
Q

What are chronic cluster headaches?

A

Occurring for 1 year without remissions or with short-lived remissions of less than a month

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22
Q

What is the pattern of occurrence in cluster headaches?

A

Cluster headaches last 4-12 weeks (Interval between bouts tend to be the same)

Occur once ever year or every two years - seasonal pattern

Headaches typically occur at night, 1-2 hours after falling sleep

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23
Q

Describe the onset of cluster headaches?

A

10 minutes

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24
Q

Describe the pain of cluster headaches?

A

Intense, sharp and penetrating centered around the eye, temple or forehead with a unilateral presentation

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25
Q

How long does a cluster headache typically last?

A

45-90 minutes (Range 15 minutes-3 hours)

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26
Q

What is the definition of motor neurone disease?

A

A neurodegenerative disorder of cortical, brain stem and spinal neurones (Lower and upper motor neurones) characterised by progressive muscle weakness

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27
Q

What is ALS?

A

• Amyotrophic lateral sclerosis (ALS): Combined degeneration of UMN and LMN.

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28
Q

What is progressive bulbar palsy variant of MND?

A

Dysarthria and dysphagia + atrophied fasciculating tongue (LMN) and brisk jaw jerk (UMN).

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29
Q

Which mutation is associated with motor neurone disease?

A

SOD1 mutation

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30
Q

What is the aetiology of motor neurone disease?

A

Free radical damage and glutamate excitotoxicity have been implicated in familial motor neurone disease
-Progressive motor neurone degeneration and death with gliosis replacing lost neurones

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31
Q

What is the presentation of motor neurone disease?

A

Upper limb weakness –> Difficulty with ADLs
Stiffness with poor coordination and balance
Spasticity
Dysarthria
Dysphagia

LMN signs

  • painful muscle spasms
  • Foot drop
  • Muscle atrophy
  • Slurred speech and dysphonic speech
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32
Q

What are the LMN examination features in MND?

A

Muscle wasting
Fasciculations
Flaccid weakness
Reduced or absent reflexes

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33
Q

What are the upper motor neurone features in MND?

A

Spastic weakness
Brisk reflexes
Hypertonia
Extensor plantar (Babinski’s sign)

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34
Q

What investigations are performed to diagnose MND?

A

Electromyography (EMG)
-Features of chronic and acute denervation with giant motor unit action potentials in more than 1 limb.

MRI -used to exclude cord or root compression and brainstem lesion

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35
Q

What pharmacological therapy is implicated in the management of MND?

A

Riluzole

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36
Q

What is Riluzole?

A

Inactivator of voltage-gated sodium channels, and indirect inhibitor of glutamate release - reduces motor neurone firing and prolongs survival

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37
Q

What are the symptomatic treatment for MND?

A

Spasticity (baclofen), salivation (anticholinergics), dyspnoea and anxiety (opiates, benzodiazepines).

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38
Q

What are the end of life management options for MND?

A

End of life management
Consider percutaneous endoscopic gastrostomy (PEG) and non-invasive ventilation.
• Consider hospice care in terminal stages.

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39
Q

What are the complications associated with MND?

A
  • Depression
  • Emotional lability
  • Frontal-type dementia
  • Weight loss and malnutrition (resulting from dysphagia)
  • Immobility-related problems: DVT, aspiration pneumonia.
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40
Q

What is the main cause of death in MND disease?

A

Respiratory failure because of respiratory muscle weakness

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41
Q

Define multiple sclerosis?

A

An inflammatory demyelinating disease of the central nervous system

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42
Q

What is the most common form of multiple sclerosis?

A

Relapsing-remitting MS - Characterised by clinical attacks of demyelination with complete recovery in between attacks

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43
Q

What is primary progressive MS?

A

Gradual accumulation of disability with no clear relapsing-remitting pattern

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44
Q

What is the aetiology of MS?

A

Autoimmune degeneration of CNS myelin results in impaired conduction of electrical impulses along axons

Associated grey matter atrophy and T-cell mediated phagocytosis of oligodendrocytes

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45
Q

What are the risk factors for MS?

A

Female Sex (Presents at 20-40 years)
Family history of MS
Genes encoding for HLA-DR2
EBV exposure

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46
Q

What is the presentation of MS?

A

Optic neuritis
Sensory systems
Motor - limb weakness, spasms, stiffness, heaviness (Foot dragging)
Autonomic - Urinary urgency, hesitancy, incontinence and impotence
Psychological: Depression and psychosis

Paraesthesia (Loss of vibration and join position)

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47
Q

What is optic neuritis in MS?

A

Unilateral deterioration in visual acuity and colour perception + pain in eye movement

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48
Q

What is Uhthoff’s phenomenon?

A

Transient increase or recurrence of symptoms due to conduction block precipitated by a rise in body temperature

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49
Q

What is Charcot’s neurological triad?

A

Dysarthria - Plaques in the brain stem
Nystagmus - Plaques on the optic nerve
Intention tremor - Plaques along motor pathways

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50
Q

How is optic neuritis examined in MS?

A

Fundoscopy revealing swollen optic nerve head (optic atrophy in chronic disease)

Visual field testing - Central scotoma (optic nerve affected) or field defects (optic radiations affected)

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51
Q

What visual abnormalities are detected on examination in MS?

A

Relative afferent pupillary defect
-Using swinging torch test - both pupils contract when light is shone on the unaffected side

Both pupils dilate when the light is swung go the diseased eye

Optic neuritis

Internuclear ophthalmoplegia
-Lateral horizontal gaze - Failure of adduction on the contralateral eye

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52
Q

What are the cerebellar signs in MS?

A 
Limb ataxia 
Intention tremor
Past-pointing 
Dysmetria on finger-nose test
Dysdiadochokinesis
Ataxic wide-based gait, scanning speech
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53
Q

What is Lhermitte’s phenomenon?

A

Electric shock-like sensation in arms and legs precipitated by neck flexion.

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54
Q

What are the investigations to diagnose MS?

A

MRI -Gadolinium contrast
-Plaque detection is highlighted as high-signal lesions
Hyperintensities in the periventricular white matter (plaques with myelin)

Diagnosis is based on two or more CNS lesions with corresponding symptoms separated in time and space (McDonald Criteria)

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55
Q

What criteria is used in the diagnosis of MS?

A

McDonald Criteria

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56
Q

What signs are seen on a lumbar puncture in MS?

A

Positive oligoclonal banding

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57
Q

What is the acute management of MS?

A

Corticosteroids- IV methylprednisolone

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58
Q

What is the chronic management of relapsing remitting MS?

A

β-Interferon or glatiramer SC injections may reduce relapse frequency.
Natalizumab (Monoclonal antibody – prevents T-cell movement into the CNS) – reduces relapse & disability progression.
Cladribine/Fingolomid – Shown to be superior to B-interferon.

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59
Q

What is the first-line management for cluster headaches?

A

100% oxygen, and subcutaneous triptan

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60
Q

What is the prophylaxis for cluster headaches?

A

Verapamil

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61
Q

What is myasthenia gravis?

A

An autoimmune disease affecting the post-synaptic membrane of a neuromuscular junction - resulting in weakness off skeletal muscles

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62
Q

Which antibodies are involved with myasthenia Gravis?

A

Nicotinic acetylcholine receptor antibodies

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63
Q

What is the paraneoplastic subtype of myasthenia Gravis?

A

Lambert-Eaton Myasthenic syndrome- caused by autoantibodies against presynaptic calcium ion channels

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64
Q

What is strongly associated with myasthenia gravis?

A

Thymoma development

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65
Q

What is the presentation of myasthenia gravis?

A

Progressive muscle weakness is worsened with repetitive use.

Ocular symptoms: Drooping eyelids, diplopia,

Bulbar symptoms: Facial weakness (myasthenic snarl) , disturbed hypernasal speech, difficulty in similing, chewing or swallowing

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66
Q

What is the pattern of muscle weakness with repeated use in Lambert-Eaton Syndrome?

A

Improves after repeated use

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67
Q

What is the pattern of muscle weakness in myasthenia gravis?

A

Worsens with repeated use

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68
Q

What are the ocular symptoms in myasthenia gravis?

A

Drooping eyelids, diplopia

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69
Q

What are the bulbar symptoms in myasthenia gravis?

A

Facial weakness (myasthenic snarl), disturbed hypernasal speech, difficulty in smiling, chewing or swallowing

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70
Q

On examination of the eyes, what findings are present in myasthenia gravis?

A

Bilateral ptosis
Complex ophthalmoplegia
Test for ocular fatigue

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71
Q

What test is used to identify ptosis in myasthenia gravis?

A

Ice on eyes test

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72
Q

What is the ice on eyes test in myasthenia gravis?

A

Ice packs are placed on closed eyelids for 2 minutes, improving neuromuscular transmission, reducing ptosis.

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73
Q

What investigations are used to diagnose myasthenia gravis?

A

Serum acetylcholine receptor antibodies
MuSk antibodies

Tensilon test

Nerve conduction study - repetitive stimulation demonstrates decrements of the muscle action potential

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74
Q

What is the Tensilon test in myasthenia gravis?

A

Short-acting anti-cholinesterase (Edrophonium) increases acetylcholine levels by inhibiting acetylcholinesterase activity

Transient improvement in clinical features

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75
Q

What does a nerve conduction study reveal in myasthenia gravis?

A

Repetitive stimulation demonstrates decrements of the muscle action potential

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76
Q

What is the acute treatment of myasthenia gravis?

A

Intravenous immunoglobulin and plasma exchange (rapid immunosuppression)

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77
Q

What is the symptomatic treatment of myasthenia gravis?

A

Cholinesterase inhibitors (Pyridostigmine, neostigmine)

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78
Q

What are the side effects associated with cholinesterase inhibitors?

A

Risk of bradycardia and diarrhoea

Cholinergic crisis

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79
Q

What should be monitored and measured in myasthenia gravis?

A

Vital capacity to assess the risk of respiratory failure

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80
Q

Which immunosuppressants are recommended in myasthenia gravis?

A

Prednisolone
Azathioprine
Ciclosprin

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81
Q

What are the complications of myasthenia gravis?

A

Myasthenic crisis - respiratory failure, requiring intubation and mechanical ventilation

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82
Q

What is a subarachnoid haemorrhage?

A

An arterial haemorrhage in the subarachnoid space

-Predominantly caused due to a rupture of saccular aneurysms at the base of the brain

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83
Q

Which vessels are predominantly implicated in a subarachnoid haemorrhage?

A

Circle of Willis

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84
Q

What are the risk factors for developing a subarachnoid haemorrhage?

A

Hypertension
Smoking
Excess alcohol intake

Polycystic kidney disease
Marfan’s syndrome
Pseudoaxanthoma elasticum
Ehler’s Danlos syndrome

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85
Q

What is the presentation of a subarachnoid haemorrhage?

A

Sudden onset severe headache in the occipital region

Thunderclap headache

-Nausea and vomiting
Neck stiffness
Photophobia
Decreased level of consciousness

Symptoms of meningism

Signs of raised intracranial pressure

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86
Q

What type of headache is associated with a subarachnoid haemorrhage?

A

Thunderclap headache, peaking within 1-5 minutes

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87
Q

What is the site of headache in a subarachnoid haemorrhage?

A

Occipital region

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88
Q

What is kernig’s sign?

A

Pain on knee extension when the hip is flexed

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89
Q

What are the signs of raised intracranial pressure?

A

Papilloedema, IV or III cranial nerve palsies, hypertension and bradycardia

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90
Q

Why do focal neurological signs occur in a subarachnoid haemorrhage?

A

Develop on the second day and are caused by ischaemia from vasospasm and reduced brain perfusion

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91
Q

What is the main investigation for subarachnoid haemorrhage?

A

Emergency non-contrast CT scan

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92
Q

What does an emergency non-contrast CT scan reveal in a subarachnoid haemorrhage?

A

Hyperdense areas in basal regions of the skull (within the subarachnoid space)

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93
Q

What does a lumbar puncture reveal in a subarachnoid haemorrhage?

A

CSF opening pressure is increased

Red cells, xanthochromia

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94
Q

What is xanthochromia is a subarachnoid haemorrhage lumbar puncture?

A

Straw-coloured CSF due to breakdown of haemoglobin, confirm using spectrophotometry

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95
Q

What drug is prescribed in a subarachnoid haemorrhage?

A

Nimodipine

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96
Q

What role does nimodipine play in the management of a subarachnoid haemorrhage?

A

A calcium channel antagonist - reducing vasospasm

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97
Q

what is the surgical management for a subarachnoid haemorrhage?

A

Endovascular coiling (Platinum) of the aneurysm

Clipping or wrapping

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98
Q

What are the complications with a subarachnoid haemorrhage?

A

Obstructive hydrocephalus (CSF backflow within the ventricles)

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99
Q

What is a subdural haemorrhage?

A

A subdural haemorrhage is defined as an accumulation of blood between the dura and arachnoid layers of the brain

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100
Q

What defines an acute subdural haemorrhage?

A

Symptoms occurring within 72 hours

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101
Q

What defines a subacute subdural haemorrhage?

A

Symptoms within 3-20 days

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102
Q

What defines a chronic subdural haemorrhage?

A

After 3 weeks

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103
Q

What is the aetiology of a subdural haemorrhage?

A

Trauma- shear forces cause a disruption to the bridging cortical veins emptying into the dural venous sinuses

brain atrophy - Room for the haematoma to enlarge before causing symptoms

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104
Q

What is the presentation of a subdural haemorrhage?

A

History of trauma with head injury - patient has a decreased conscious level

Subacute - worsening headache 7-14 days after injury

Chronic

  • Headache
  • Confusion
  • Cognitive impairment
  • Psychiatric symptoms
  • Gait deterioation
  • Focal weakness (Aniscoria - unequal pupil size- sign of brainstem herniation)
  • Seizures
  • Diminished motor response
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105
Q

What are the examination findings in a subdural haemorrhage?

A

Decreased GCS
Anisocoria - Large haematomas result in a midline shift - ipsilateral fixed dilated pupil (Compression of the third nerve parasympathetic fibres)

Raised ICP - Decreased consciousness bradycardia, irregular breathing and widened pulse pressure

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106
Q

What is the definitive investigation for a subdural haemorrhage?

A

CT head

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107
Q

What is revealed in a CT head in a patient with a subdural haemorrhage?

A

Crescent-shaped, concave bleed over the brain surface.

Ct appearances change with time - acute haemorrhages –> Hyperdense

Become isodense over 1-3 weeks, effacement of sulci and midline shift, ventricular compression present

Chronic subdural - hypodense

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108
Q

What prophylactic anti-epileptics are administered in subdural haemorrhage?

A

Phenytoin or levetiracetam

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109
Q

How is coagulopathy corrected in subdural haemorrhage?

A

Reverse or stop anti-coagulant treatment

Correction involves administration of vitamin-K, FFP, platelets, cryptoprecipitate or protamine

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110
Q

What is the first-line management of a raised ICP?

A

Head elevation and consider osmotic diuresis with mannitol or hypertonic saline

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111
Q

What is the surgical management in symptomatic subdural haemorrhage?

A

Burr-hole or craniotomy and drainage

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112
Q

What is the Wernicke’s Encephalopathy?

A

A neurological emergency resulting from a thiamine deficiency with varied neurocognitive manifestations.
• Changes in mental state status
• Gait and oculomotor dysfunction.

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113
Q

What is the aetiology of wernicke’s?

A

Thiamine deficiency can occur because of reduced intake, increased demand, and malabsorption

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114
Q

What are the risk factors of Wernicke’s?

A
  • Alcohol dependence – Low storage capacity of the liver, decreased intestinal absorption and impaired thiamine metabolism.
  • AIDs
  • Cancer and treatment with chemotherapeutic agents
  • Malnutrition
  • History of gastrointestinal surgery – Bariatric surgery procedures for Class III obesity may predispose to thiamine malabsorption.
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115
Q

What is the presentation of Wernicke’s?

A
  • Cognitive dysfunction: Mental slowing, impaired concentration, and apathy.
  • Frank confusion: Presenting manifestation in emergency departments and in patients who misuse alcohol.
  • Ocular motor findings: Gaze palsies, sixth nerve palsies, and impaired vestibulo-ocular reflexes + Nystagmus, unequal pupils, nonreactive pupils.
  • Mild irritability
  • Delirium
  • Acute psychosis
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116
Q

What are the triad of symptoms?

A

Ophthalmoplegia, ataxia, , and confusion

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117
Q

What are the investigations of Wernickes?

A

A therapeutic trial of parenteral thiamine – Clinical response to treatment.
N.B: Diagnosis is predominantly based on history and examination.
• FBC: High MCV is a common feature amongst alcoholics.
• U&Es: Exclude metabolic imbalances as a cause of confusion
• Glucose
• ABG: Hypercapnia and hypoxia can cause confusion.

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118
Q

What is the management of Wernicke’s?

A

Stabilisation/resuscitation + thiamine + magnesium + multivitamins.
• Intravenous 250-500mg Thiamine
• Magnesium sulphate
• Multivitamin.

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119
Q

What is Korsakoff’s psychosis?

A

• Korsakoff’s Psychosis: May present as profound anterograde amnesia with limited retrograde amnesia (Degeneration of mamillary bodies).
Confabulation – Fabrication of memories to mask memory deficit.

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120
Q

What is Meniere’s disease?

A

Meniere’s disease is an auditory disease characterised by an episodic sudden onset of vertigo, low-frequency roaring tinnitus and sensation of fullness in the affected ear.

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121
Q

What are endolymphatic hydrops?

A

• Endolymphatic hydrops Over-production or impaired absorption of endolymph – Excessive pressure causes distension and rupture of Reisner’s membrane.

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122
Q

What is the presentation of Meniere’s disease?

A
  • Vertigo – Recurrent episodes – spinning sensation lasting minutes – hours; usually associated with nausea and vomiting.
  • Hearing loss- Fluctuating and worsens during or around the vertigo spells.
  • Tinnitus- Unilateral in the affected ear.
  • Aural fullness – May increase prior to an attack.
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123
Q

What is positive Romberg’s sign?

A

Swaying or falling when asked to stand with feet together and eyes closed

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124
Q

What is Fukuda’s stepping test?

A

Turning towards the affected side when asked to march in place with eyes closed.

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125
Q

What is tandem walk?

A

Inability to walk in a straight line (heel-toe)

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126
Q

What is the first-line investigation for Meniere’s disease?

A

Pure-tone audiometry

Air-bone conduction is equal- indicates the underlying pathology is in the cochlear or the auditor nerve

Unilateral sensorineural hearing loss - Inner ear is affected - low frequency

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127
Q

What are otoacoustic emissions?

A

The measure of outer hair cell dysfunction: Absence of measurable OAE in frequency range affected by MD.

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128
Q

What is the management of MD?

A

Dietary changes and lifestyle modification: Restrict salt intake (prevent-sodium related water retention and redistribution into the endolymphatic system).
• Limit caffeine intake, reduce alcohol consumption, smoking cessation and stress management to minimise triggers.

Diuretic: For symptomatic vertigo.

Vestibular suppressant, anti-emetic, or corticosteroid
• Antihistamines (Meclozine, dimenhydrinate, promethazine)
• Benzodiazepines (Diazepam and phenothiazines) – Used in acute attacks only.
• Oral corticosteroids: Used to treat acute attacks of vertigo, especially when accompanied by acute hearing loss and tinnitus.

Persistent hearing loss: Hearing aid or assistive listening device.

Surgical (Failure of therapies): Endolymphatic sac surgery.

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129
Q

What is the definition of a stroke?

A

A stroke is a rapidly developing focal disturbance of brain function due to cerebrovascular insult lasting >24 hours.
Can be subdivided based on:
• Location: Anterior v Posterior circulation
• Pathological process: Infarction v haemorrhage.

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130
Q

what is the most common type of stroke?

A

Ischaemic stroke

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131
Q

What is the common cause of embolic stroke?

A

Carotid dissection, carotid atherosclerosis, atrial fibrillation

Venous blood clots

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132
Q

What is the presentation of a stroke?

A

Stroke affects 5 core functions: Motor, sensation, speech, balance, and vision.
• Sudden onset (Deterioration within seconds).
• Weakness
• Sensory, visual, or cognitive impairment
• Impaired coordination
• Impaired consciousness
• Head or neck pain (If carotid or vertebral artery dissection).

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133
Q

What are the symptoms of an ACA stroke?

A
  • Hemiparesis – Contralateral lower limb weakness (Topographic organisation of the primary motor cortex).
  • Confusion
  • Abulia: Disturbance of intellect, executive function, and judgement.
  • Loss of appropriate social behaviour (Disinhibition)
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134
Q

What are the symptoms of an MCA stroke?

A

The MCA primarily supplies a portion of the frontal lobe and the lateral surface of the temporal and parietal lobes.
• Contralateral hemiplegia – Topographically affecting the upper limb + Facial weakness.
• Contralateral hemisensory deficits – Primary somatosensory cortex is affected.
• Hemineglect
• Hemianopia
• Apraxia
• Aphasia (In a left-sided lesion)  Broca’s and Wernicke’s area is affected.
• Quadrantanopia (If superior or inferior optic radiations are affected).

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135
Q

What are the symptoms of a PCA stroke?

A

The PCA is largely responsible for supplying the occipital lobe, in addition to the inferior region of the temporal lobe.
• Homonymous hemianopia (one side) and visual agnosia (Inability to recognise objects).
• Prosopagnosia – A cognitive disorder of facial recognition.

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136
Q

What are the symptoms of an anterior-inferior cerebellar stroke?

A

Vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness

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137
Q

What are the symptoms of a posterior inferior cerebellar stroke?

A 
Vertigo
Ipsilateral ataxia
Ipsilateral Horner's syndrome
Ipsilateral hemisensory loss
Dysarthria
Contralateral spinothalamic sensory loss
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138
Q

What are lacunar infarcts?

A

Affecting the internal capsule or pons (pure sensory or motor deficit)

Affecting the thalamus or the basal ganglia.

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139
Q

What are the investigations for a stroke?

A 
Urgent non-contrast CT 
Blood glucose
U&Es
Clotting screen
ECG
Echocardiogram
Carotid Doppler Ultrasound
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140
Q

What is the management of a hyperacute stroke <4.5 hours?

A

Intravenous thrombolysis
Alteplase (IV tPA)

Do not administer aspirin within the first 24 hours of presentation

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141
Q

What is the management of an acute ischaemic stroke beyond 4.5 hours?

A

2 weeks of 300mg Asipirin and 75mg lifelong clopidogrel

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142
Q

What is the surgical management for a stroke?

A

Carotid endarterectomy within 2 weeks of stroke

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143
Q

What is a TIA?

A

Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours.

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144
Q

What is the most common cause of a TIA?

A

Embolic causes - carotid atherosclerosis

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145
Q

What is the first-line management of a TIA?

A

300mg aspirin

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146
Q

How long do TIAs typically last?

A

10-15 minutes

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147
Q

What are the global events that occur in a TIA?

A

Syncope and dizziness (typical of ECG)

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148
Q

What is amaurosis fugax?

A

Painless fleeting loss of vision caused by retinal ischaemia

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149
Q

What investigations are performed in a patient presenting with a TIA?

A

300mg Aspirin
Clopidogrel 300mg then 75mg thereafter
Atorvastatin 20-80mg

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150
Q

What are the indications for performing a carotid endarcetectomy?

A

> 70% stenosis at the origin of the ICA

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151
Q

What is the definition of a migraine?

A

A migraine is defined as a severe episodic headache that is associated with a prodrome of focal neurological symptoms and systemic disturbance.

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152
Q

What are classic migraines?

A

Migraines with an aura

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153
Q

What are the typical prodromal symptoms in a migraine?

A 
Changes in mood
Urination
Fluid retention
Food craving
Yawning
Aura
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154
Q

What are auras in migraines?

A

Visual disturbances can develop

Sensory disturbances (numbness, paraesthesia)

Positive symptoms: Scintilating scotomas - zig-zag crescent

Negative symptoms: Blind spots and visual occlusions

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155
Q

Describe a migraine headache?

A

Pulsating hemicranial nausea and photophobia with headache

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156
Q

What is the typical duration of a migraine?

A

3-12 hours

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157
Q

What are the triggers of a migraine?

A

: Stress, exercise, lack of sleep, oral contraceptive pill, food (caffeine, alcohol, cheese, chocolate), and pattern of analgesic use.

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158
Q

What is the first-line management of a migraine?

A

Tiprants - Sumatripain
NSAIDs
Metoclopramide

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159
Q

What is the prophylactic treatment of a migraine?

A

Beta-blockers (Propranolol)

Topiramate (Contraindicated in asthma)

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160
Q

What are tension headaches?

A

Generalised throughout the head, with a predilection involving the frontal and occipital regions

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161
Q

How does a tension headache feel?

A

Tight band around the head

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162
Q

How often do episodic Tension headaches occur?

A

<15 days per month

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163
Q

Which sex experiences tension headaches more?

A

Women

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164
Q

What is the presentation of a tension headache?

A

A generalised headache that is moderate in severity
• Pressure around the head (Tight band).
• Non-pulsatile, bilateral pain.
• Often a relationship with the neck
• Can be disabling for a few hours but does not have specific associated symptoms.
• Gradual onset
• Variable duration
• Usually responsive to over-the-counter medication.

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165
Q

What is the management of a tension headache?

A
  • Reassurance
  • Address triggers (Stress, anxiety)
  • Advice on avoiding medications that can cause medication-induced headaches (opioids).
  • Simple analgesia (Ibuprofen, paracetamol, aspirin)
  • Tricyclic antidepressants may be considered in frequency recurrent episodic tension headaches or chronic tension headaches.
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166
Q

Define trigeminal neuralgia?

A

Trigeminal neuralgia (TN) is a facial pain syndrome in the distribution of the trigeminal nerve divisions, characterised by a paroxysm of sharp, stabbing, intense pain lasting up to 2 minutes

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167
Q

What is the most common aetiology of trigeminal neuralgia?

A

Compression of the trigeminal nerve root at the root entry zone by an aberrant vascular loop (Mainly the superior cerebellar artery).

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168
Q

What is the presentation of trigeminal neuralgia?

A

Sudden, unilateral, brief, stabbing pain in the distribution of one or more of the branches of the trigeminal nerve.

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169
Q

How long does the pain last for trigeminal neuralgia?

A

Few seconds to a couple of minutes

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170
Q

How is the pain described in trigeminal neuralgia?

A

Shock-like pain

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171
Q

What are the triggers of trigeminal neuralgia?

A 
Vibration
Skin contact- washing, shaving
Eating
Dental prostheses
Brushing teeth
Exposure to wind
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172
Q

What investigations are performed in trigeminal neuralgia?

A

Note: Diagnosis is predominantly based on clinical presentation

Consider performing an MRI to visualise abnormal vessel loop in association with the trigeminal nerve.

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173
Q

What is the first-line therapy for trigeminal neuralgia?

A

Anti-convulsant - Carbamazepine

Baclofen - if unresponsive to anti-convulsant treatment

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174
Q

What is Guillain Barre Syndrome?

A

An acute inflammatory neuropathy characterised by motor difficulty, absence o tendon reflexes and paraesthesia

Antibodies following a recent infection react with self-antigen on myelin on neurones

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175
Q

What is the pattern of motor difficulty in GBS?

A

Progressive symptoms of muscle weakness, initially affecting the lower extremities

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176
Q

Presentation of GBS

A
  • Muscle weakness – usually affecting the lower extremities before upper extremities and proximal muscles.
  • Paraesthesia- In hands and feet, preceding the onset of weakness.
  • Back/leg pain – May precede muscle weakness.
  • Respiratory distress – Include dyspnoea on exertion and shortness of breath.
  • Speech problems – Facial weakness and slurred speech
  • Areflexia/hyporeflexia
  • Facial weakness
  • Bulbar dysfunction
  • Extra-ocular muscle weakness
  • Facial droop
  • Diplopia
  • Dysarthria
  • Dysphagia
  • Dysautonomia
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177
Q

On examination what are the features of GBS?

A

Hypotonia
Flaccid paralysis
Areflexia

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178
Q

What triad is associated with Miller-Fischer Synrome?

A

Ataxia
Areflexia
Opthalmoplegia

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179
Q

What are the investigations in GBS?

A

Nerve conduction studies
Lumbar puncture
Blood
Spirometer

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180
Q

What is spirometry performed in GBS?

A

Reduced vital capacity and maximal inspiratory/expiratory pressures - indicating type 2 respiratory failure due to paralysis of respiratory muscles

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181
Q

What would a lumbar puncture reveal in GBS?

A

Elevated CSF protein

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182
Q

What antibodies are associated with Miller-Fischer Variant of GBS?

A

Anti-ganglioside antibodies

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183
Q

What is the first-line management of GBS?

A

Intravenous immunoglobulin

Plasma exchange with IVIG

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184
Q

Define epilepsy

A

A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in the part of the brain, manifesting as seizures (paroxysmal synchronised cortical electrical discharge).
• > 2 seizures for epilepsy to be diagnosed.

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185
Q

What are the two main categories of seizures?

A

Partial

Generalised

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186
Q

What are the two types of partial seizures?

A

Complex

Simple

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187
Q

What are partial seizures?

A

Focal onset seizure localised to specific cortical regions

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188
Q

What is a complex partial seizure?

A

Consciousness is affected

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189
Q

What is a simple partial seizure?

A

Consciousness is not affected

190
Q

What is a generalised seizure?

A

Seizures that affect the whole of the brain - also affects consciousness

191
Q

What are the four types of seizures?

A

Tonic-clonic
Absence
Myoclonic
Atonic

192
Q

What are tonic-clonic seizures?

A

Limbs stiffen (tonic) then jerk (clonic)

193
Q

What are absence seizures?

A

Brief pauses

194
Q

What are myoclonic seizures?

A

Sudden jerk of a limb, face or trunk

195
Q

What are atonic seizures?

A

Sudden loss of muscle tone causing fall

196
Q

What is the presentation of a frontal motor seizure?

A 
Motor convulsions
Jacksonian March (Muscular spasm caused by simple partial seizure spreads from affecting the distal part of the limb towards the ipsilateral face)

Post-ictal flaccid weakness (Todd’s paralysis)

197
Q

What is a Jacksonian March?

A

Muscular spasms caused by simple partial seizures spread from affecting the distal part of the limb towards the ipsilateral face

198
Q

What is the presentation of a temporal lobe seizure?

A

Aura - visceral or psychic symptoms

Hallucinations (Olfactory or affecting taste)

199
Q

Olfactory hallucinations are associated with which type of seizure?

A

Temporal lobe seizures

200
Q

Lip-smacking is associated with which type of seizure?

A

Temporal lobe seizures

201
Q

What lobe specific symptoms are associated with a parietal lobe seizure?

A

Sensory -Paraesthesia

202
Q

What is the presentation of a tonic-clonic seizure?

A

Tonic phase - generalised muscle spasms

Clonic phase - Repetitive synchronous jerks

Faecal/urinary incontinence

Tongue biting

203
Q

What is associated in the post-ictal phase of a tonic-clonic seizure?

A

Impaired consciousness, lethargy, confusion, headache back pain and stiffness

204
Q

What is the presentation of an absence seizure?

A
  • Onset in childhood
  • Loss of consciousness but maintained posture
  • The patient will appear to stop talking and stare into space for a few seconds
  • No post-ictal phase.
205
Q

What investigation is used to confirm the diagnosis of epilepsy?

A

EEG

206
Q

What is status epilepticus?

A

A seizure lasting >30 minutes or repeated seizures without recovery and regain consciousness in between

207
Q

What is the first-line management of status epilepticus?

A

IV lorazepam or IV/pr diazepam - repeat again after 10 minutes

208
Q

If seizures recur despite lorazepam management, what management should be considered?

A

IV phenytoin

209
Q

What is the first-line therapy for generalised seizures?

A

Sodium valproate
Lamotrigine
Ethosuximide

210
Q

What is the first-line therapy for partial seizurs?

A

Carbamazepine

211
Q

Which anti-epileptic drug should be used in women of child-bearing age?

A

lamotrigine

And folic acid

212
Q

What are the complications of lamtorigine?

A

Steven-Johnson Syndrome

213
Q

What are the complications of carbamazepine?

A

Neutropenia and osteoporosis

214
Q

What is BPPV?

A

BPPV is a peripheral vestibular disorder (labyrinth and/or vestibulocochlear nerve) that manifests as sudden, short-lived episodes of vertigo elicited by specific head movements.

215
Q

what is the average duration of a BPPV episode?

A

30 seconds

216
Q

What is the average age of onset of BPPV?

A

55 Years

217
Q

What is the pathophysiology of BPPV?

A

Otoliths from the utricle are detached from the maculae and are dislodged into the semi-circular canals.
• Otoliths stimulate a larger endolymph flow when the head is in motion, thus facilitating the movement of the head will be processed by the brain as bigger and faster than perceived.
• Settle into the posterior semi-circular canal – Most gravity-dependent regions of the vestibular labyrinth.
• The posterior semi-circular canal has an impermeable barrier that enables otolith particles to be trapped as opposed to the lateral and anterior semi-circular canal.

218
Q

What repositioning manoeuvres are associated with improving vertigo in BPPV?

A

Epley

Sermont

219
Q

Which semi-circular canal is most affected in BPPV?

A

Posterior semi-circular canal

220
Q

What is the presentation of BPPV?

A

Brief duration of vertigo <30 seconds

Associated symptoms : Nausea, imbalance, and light-headedness
Episodic vertigo

221
Q

What are the associated symptoms with BPPV?

A

Nausea, imbalance and light-headedness

222
Q

Which manoeuvre can be used to diagnose BPPV?

A

Hallpike

  • Positive supine lateral head turn
  • Rotatory nystagmus
223
Q

What is the management for BPPV?

A

Epley Manoeuvre

• Teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation for example Brandt-Daroff exercises.

N.B: Good prognosis – Resolves spontaneously within a few weeks to months.

224
Q

What is epistaxis categorised into?

A

Posterior and anterior bleeds

225
Q

Which plexus is associated with anterior nose bleeds?

A

Kiesselbach’s plexus

226
Q

Where do the majority of nose bleeds occur?

A

Little’s area of the anterior septum

227
Q

What are the causes of secondary epistaxis?

A
  • Alcohol
  • Antiplatelet drugs (Clopidogrel)
  • Aspirin and NSAIDs
  • Anticoagulants (Warfarin)
  • Coagulopathy (Haemophilia, von Willebrand’s disease)
  • Trauma (Nasal fracture)
  • Tumours
  • Surgery
  • Septal perforation
  • Cocaine use – Septum may look abraded or atrophied – inquire about drug use. Cocaine is a potent vasoconstrictor and repeated use can cause obliteration of the septum.
  • Juvenile angiofibroma – Benign tumour that is highly vascularized (Seen in adolescent males).
  • Hereditary haemorrhagic telangiectasia
228
Q

What is the presentation of epistaxis?

A

Blood at one nostril or on both sides of the nose
Septal deviation
Recurrent epistaxis - common in children

Bleeding starting at the nares - anterior bleed causes blood in the pharynx

229
Q

What is the first-line management of nose bleeds?

A

Inform the patient to sit with their torso forward and mouth open (Avoid lying down)
Decreases blood flow to the nasopharynx and allows the patient to spit out any blood

pinch the soft area of the nose firmly for a minimum of 20 minutes

230
Q

How long should the nose be pinched for in an acute nosebleed?

A

20 minutes

231
Q

What treatment is available in recurrent nose bleeds?

A

Nasal cautery
Silver nitrate sticks
Nasal packing

232
Q

What is the definition of tonsillitis?

A

Refers to the intense acute inflammation of the tonsils - an infection of the parenchyma of the palatine tonsils

Associated with a purulent exudate

233
Q

What is the predominant causative organism in tonsilitis?

A

Streptococcus pneumoniae

234
Q

What is bacterial tonsilitis associated with?

A

Cervical lymphadenopathy

235
Q

What symptoms are associated with viral tonsilitis?

A

Associated with headache, apathy and abdominal pain

236
Q

What is the CENTOR criteria?

A

Gives an indication of the likelihood of a sore throat being due to a bacterial infection

  1. Tonsillar exudate
  2. Tender anterior cervical lymphandenopathy
  3. Fever over 38
  4. Absence of cough
237
Q

What is the presentation of tonsilitis?

A
  • Pain on swallowing
  • Fever >38
  • Tonsillar exudate
  • Sudden onset sore throat
  • Headache
  • Nausea and vomiting
  • Tonsillar erythema and enlargement
238
Q

What investigations are performed in bacterial tonsilitis?

A

Throat culture

Rapid streptococcal antigen test

239
Q

What is the first-line management for bacterial tonsitilitis?

A

Penicillin V 500 mg PO QDS for 5-10 days

240
Q

What are the indications for a tonsillectomy?

A

If a patient suffers more than 5 episodes of tonsillitis per year for 2 years and interferes with daily life  Refer for tonsillectomy.

241
Q

Define Rhino-sinusitis

A

Acute sinusitis is a symptomatic inflammation of the mucosal lining of the nasal cavity and paranasal sinuses – Presenting with purulent nasal drainage accompanied by nasal obstruction, and facial pain <4 weeks.

242
Q

What are the two key features of rhino-sinusitis?

A

Nasal congestion

Nasal discharge

243
Q

What are the predisposing factors for rhinosinusitis?

A

Nasal obstruction - Septal deviation or nasal polyps

Recent local infection: Rhinitis or dental extraction

Swimming/diving

Smoking

244
Q

What are the predominant causative infectious organisms in rhinosinusitis?

A

Streptococcus pneumoniae, Haemophilus influenzae and rhinovirus.

245
Q

What is the presentation of rhinosinusitis?

A

Purulent nasal discharge
Nasal obstruction
Facial pain/pressure - Frontal Pain which is worse on bending forward

246
Q

What is the management for rhinosinusitis?

A

Conservative management
• Analgesia
• Intranasal corticosteroids if symptoms persist > 10 days.
• Intranasal decongestants or nasal saline

Severe presentations (Antibiotics) 
•	Phenoxymethylpenicillin first-line
247
Q

What is obstructive sleep apnoea?

A

OSA is characterised by episodes of complete or partial upper airway obstruction during sleep

248
Q

What are the predisposing factors of OSA?

A

Obesity
Macroglossia - Acromegaly, hypothyroidism, amyloidosis

Large tonsils
Marfan's syndrome
Micrognathia
Neuromuscular disease
Alcohol
249
Q

What is the presentation of OSA?

A 
Excessive daytime sleepiness
Lack of concentration
Chronic snoring
Restless sleep
Insomnia 
Irritability/personality change
Episodic gasping
250
Q

What investigations are performed in OSA?

A

Polysomnography

251
Q

How many episodes/hour on the Apnoea-Hypopnea diagnose for OSA?

A

> 15 episodes

252
Q

How is sleepiness assessed?

A

Epworth Sleepiness Scale

253
Q

What is the first-line management of OSA?

A

Continuous positive airway pressure (CPAP)

254
Q

What are the complications of OSA?

A
  • Impaired glucose metabolism
  • Cardiovascular disease
  • Depression
  • Motor vehicle accidents
  • Cognitive dysfunction
  • Increased mortality
255
Q

What is Parkinson’s Disease?

A

A neurodegenerative disorder of the dopaminergic neurones of the Substantia nigra.

256
Q

Which part of the brain is affected in Parkinson’s disease?

A

Substantia Nigra

257
Q

What is the pattern of symptoms presented in Parkinson’s disease?

A

Asymmetrical

258
Q

What is the triad of symptoms in Parkinson’s disease?

A

Bradykinesia
Rigidity
Resting tremor

259
Q

What is bradykinesia?

A

Slowness of small movements

260
Q

What tremor is associated with Parkinson’s disease?

A

Pill-rolling tremor starting in one hand.

261
Q

Which neurones are affected in PD?

A

Dopaminergic neurones

262
Q

What is drug-induced PD?

A

Concerns a rapid onset and bilateral character of symptoms

Rigidity and rest tremor are uncommon

263
Q

Which drugs can induce PD?

A

Anti-psychotics

Anti-emetics - Metoclopramide

264
Q

What is the onset of PD?

A

Insidious

265
Q

What frequency is the pill-rolling resting tremor in PD?

A

3-5 Hz

266
Q

When is the pill-rolling tremor most marked?

A

At rest

267
Q

When is the pill-rolling tremor worse?

A

When stressed or tired, improves with involuntary movement

268
Q

What kind of rigidity is associated with PD?

A

lead pipe

Cogwheel

269
Q

What are the symptoms of PD?

A 
•	Insidious Onset
•	Resting tremor (Mainly in hands) – Asymmetrical 
-	Most marked at rest, 3-5 Hz
-	Worse when stressed or tired – Improves with voluntary movement
-	Pill-rolling – Thumb and index finger 
•	Bradykinesia 
-	Stiffness and slowness of movements
-	Poverty of movement (Hypokinesia)
-	Akinesia: Difficulty initiating movements
•	Rigidity
-	Lead pipe 
-	Cogwheel: Due to superimposed tremor
-	Enhanced by distraction 
•	Frequent falls
•	Micrographic – Smaller handwriting 
•	Insomnia
•	Mental slowness (Bradyphemia)
•	Subtle: Sense of smell reduced, constipation, visual hallucinations, frequency/urgency, dribbling of saliva, depression.
270
Q

What face is seen in a patient with PD?

A

Hypomimic face - Expressionless, mask-like

271
Q

What gait is seen in PD?

A

Shuffling gait

272
Q

What are the investigations for PD?

A

Diagnosis is confirmed based on history and examination

Levodopa trial –> Improvement in symptoms (Indicated in patients presenting with atypical features)

273
Q

What investigation is performed to differentiate between essential tremor and Parkinson’s disease?

A

I-FP-CIT single proton emission computed tomography (SPECT)

274
Q

What is the first-line management for Parkinson’s disease?

A

Levodopa (If motor symptoms are affecting quality of life)

275
Q

If motor functions are not affecting the patient’s quality of life in PD, what drug can be adminsitered?

A

Oral monoamine oxidase-B inhibitors

-• Selegiline, rasagiline or safinamide

276
Q

What are the common complications of PD medication?

A

Acute akinesia, neuroleptic malignant syndrome

277
Q

What is encephalitis?

A

Inflammation of the brain parenchyma associated with neurological dysfunction

278
Q

What are the initial symptoms of encephalitis?

A

Pyrexia and headache

279
Q

What is the most common viral cause of encephalitis?

A

HSV

280
Q

What is the presentation of encephalitis?

A
  • Fever
  • Seizures
  • Vomiting
  • Headache
  • Behavioural changes/Mental state alteration – Confusion
  • History of seizures
  • Focal neurological symptoms: Dysphagia, hemiplegia, aphasia (Hallmark feature)

Signs of meningism- neck stifness and photophobia

281
Q

What are the hallmark features of encephalitis?

A

Focal neurological symptoms: Dysphagia, hemiplegia, aphasia

Behavioural changes/Mental stage alteration

282
Q

What examination findings are evident in encephalitis?

A

Reduced consciousness, deteriorating GCS

Seizures
Pyrexia
Neck stiffness
Photophobia
Kernig test positive

Signs of Raised ICP - Cushing’s Triad

Vesicular eruption

283
Q

What investigations are performed in encephalitis?

A

CSF - lymphocytosis and elevated protein

MRI/CT

FBC

Lumbar puncture

284
Q

What does a Lumbar puncture reveal in encephalitis?

A 
High lymphocytes
High monocytes
High protein
Normal or low glucose
Viral PCR - 95% specific for HSV-1
285
Q

Which part of the brain is affected by HSV encephalitis?

A

Temporal lobe

286
Q

What is the first-line management of encephlalitis?

A

Intravenous acyclovir

287
Q

What is a brain abscess?

A

Suppurative collection of microbes within a gliotic capsule occurring within the brain parenchyma

288
Q

What are the risk factors of a brain abscess?

A
  • Sinusitis
  • Otitis media
  • Recent dental procedure or infection
  • Recent neurosurgery
  • Meningitis
  • Congenital heart disease
  • Endocarditis
  • Diverticular disease
  • Hereditary haemorrhage telangiectasia
  • HIV
289
Q

What is the presentation of a brain abscess?

A
  • Meningismus
  • Headache- Often dull, persistent.
  • Cranial nerve palsy- Third or sixth palsies, anisocoria, and papilledema (Secondary to raised ICP).
  • Positive Kernig or Brudzinski sign
  • Fever
  • Neurological deficit
  • Infants: Bulging fontanelles, and increased head circumference
290
Q

What investigations are performed in a brain abscess?

A

CT scan - ring-enhancing lesions

FBC -leukocytosis

291
Q

What is the management of a brain abscess?

A

A craniotomy is performed, and the abscess cavity is debrided

IV antibiotics - Cephalosporin + metronidazole

292
Q

What drug can be used to manage intracranial pressure in a brain abscess?

A

Dexamethasone

293
Q

What is carpal tunnel syndrome?

A

Compression of the median nerve in the carpal tunnel

294
Q

Which nerve is affected in carpal tunnel syndrome?

A

Median nerve

295
Q

What is the aetiology of carpal tunnel syndrome

A

Repetitive stress injury in susceptible people  Inflammation  Oedema  Fluid in narrow space compresses structures  Nerve injury.

296
Q

What are the causes of carpal tunnel syndrome?

A

Tendonitis
Oedema
Repetitive stress injury

297
Q

What are the risk factors for carpal tunnel syndrome?

A
  • Obesity
  • Pregnancy
  • Underlying conditions (Rheumatoid arthritis)
  • Trauma
  • Genetic predisposition
  • Occupation
298
Q

What is the presentation of carpal tunnel syndrome?

A
  • Numbness of hands – Dominant hand is usually affected (Fingers affected: Thumb, index, middle finger).
  • Night-time worsening – Waking up at night with paraesthesia/pain in hand/wrist and shaking the hand to relieve symptoms.
  • Symptoms are intermittent
  • Gradual onset
  • Weakness of hand
  • Clumsiness
  • Aching and pain in the arm
299
Q

Which three fingers are affected in Carpal tunnel syndrome?

A

Thumb, index and middle finger

300
Q

When are the symptoms of carpal tunnel syndrome worse?

A

During the night

301
Q

What is Tinel’s sign in carpal tunnel syndrome?

A

Tapping causes paraesthesia

302
Q

What is Phalen’s Sign in carpal tunnel syndrome?

A

Flexion of the wrist causes symptoms (Pressing of upper hands together when flexing wrists induces pain)

303
Q

What is the treatment of carpal tunnel syndrome?

A

Corticosteroid injections to decrease inflammation

Wrist splints at night

Surgical decompression

304
Q

Define Erb Palsy?

A

A brachial plexus birth palsy, encountered because of a delivery complicated by shoulder dystocia

305
Q

Which nerve roots are involved in Erb Palsy?

A

C5 and C6

306
Q

Which peripheral nerves are affected in erb palsy?

A

Axillary
Musculocutaneous
Suprascapular

307
Q

What is neuropraxia in Erb Palsy?

A

A stretch injury of the axon that does not cause division of the neural tissue

  • Conduction block
  • Resolves quickly
308
Q

What is the presentation of Erb palsy?

A

Paralysis of an arm - Lack of movement. of an affected extremity

Decreased motion of an arm

The abnormal posture of the arm

309
Q

What investigations are performed in Erb Palsy?

A

X-ray of chest and affected upper extremity

Ultrasound scan of the shoulder to detect dislocation

310
Q

What is the treatment of Erb Palsy?

A

Physiotherapy

Surgical nerve repair/reconstruction

311
Q

What is Klumpke Paralysis?

A

a type of brachial plexus affecting the lower brachial plexus nerve roots c8-T1

312
Q

Which nerve roots are affected in Klumpke paralysis?

A

C8-T1

313
Q

What is the presentation of Klumpke Paralysis?

A

Claw hand

Intrinsic hand muscle atrophy

Sensation loss in the medial side of the upper arm, upper arm weakness

Horner syndrome

314
Q

What is Horner’s syndrome?

A

Ptosis (Drooping eyelid)

Enopthalmos (Deep set eye)

Miosis (Constricted pupil)

Anhidrosis

315
Q

What is Alzheimer’s Dementia?

A

Alzheimer’s dementia is a chronic neurodegenerative disease with progressive and (Slow cognitive decline) and an insidious onset.
• Most common type of dementia (60-70%)
• Characterised by memory impairment.

316
Q

Which extracellular protein is associated with AD?

A

Amyloid precursor protein

317
Q

Which intracellular protein is associated with AD?

A

Neurofibrillary tangles -Tau proteins

318
Q

Which part of the brain is affected predominantly in AD?

A

Hippocampus, amygdala, basalis of Meynert

AcH deficiency

319
Q

Which neurotransmitter is deficient in AD?

A

Acetylcholine

320
Q

What are the symptoms of AD?

A
  • Amnesia – Loss of short-term memory
  • Anomia – Inability to name objects
  • Apraxia – Loss of dexterity
  • Agnosia – Inability to recognise things, unable to understand the function of objects
  • Aphasia – inability to talk
  • Decline in ADLs
  • Personality change – Exaggeration of premorbid traits with coarsening of affect and egocentricity.
  • Behavioural disturbances: Aggression, wandering, explosive temper, sexual disinhibition, incontinence, excessive eating, and searching behaviour.
321
Q

What investigations are performed in suspected AD?

A 
Mini-Mental State Examination (MMSE) 
•	Impaired recall
•	Dysphagia
•	Disorientation 
•	Impaired executive functioning

Metabolic panel
• Exclude abnormal sodium calcium and glucose
• TFTs

MRI
• Generalised atrophy with medial temporal lobe and later parietal lobe

322
Q

What does an MRI suggest? in a patient with AD?

A

• Generalised atrophy with medial temporal lobe and later parietal lobe

323
Q

What is the first-line treatment of AD?

A

Acetylcholinesterase inhibitors

Donepezil

324
Q

What is the mechanism of action of Donepezil, galantamine, and rivastigmine?

A

Acetylcholinesterase inhibitors

325
Q

What is the mechanism of action of memantine?

A

NMDA receptor antagonist

326
Q

What is vascular demntia?

A

Vascular dementia is associated with reduced blood supply to the brain due to diseased vessels and multiple infarcts within the minor blood vessels of the brain – Associated with cardiovascular disorders.

The executive functions of the brain affected more > memory – Underlying damages to both grey and white matter.

327
Q

What type of progression is seen in vascular dementia?

A

Stepwise progression

328
Q

What are the risk factors for vascular dementia?

A

Age > 60 years
Obesity
Hypertension
Cigarette smoking

329
Q

What is the presentation of vascular dementia?

A

Cognitive-executive decline - Increased time to process information and formulate thoughts and structured communication

Personality changes - low mood, emotionally sensitive, or less environmentally withdrawn
-Frontal cognitive syndrome - apathy

Motility - Difficulty in walking/stability/gait

330
Q

What is the management for vascular dementia?

A

Antiplatelet therapy + lifestyle modification

Aspirin
Cholinesterase inhibitor
Statin therapy
Carotid endarterectomy

331
Q

What is Lewy-body dementia?

A

Defined as progressive cognitive decline - interfering with ADLs and is characterised by three of the following:

Fluctuating cognition
Recurrent visual hallucinations
REM sleep behavioural disorder

332
Q

What are the triad of symptoms associated with Lewy-Body dementia?

A
  1. Fluctuating cognition
  2. Recurrent visual hallucinations
  3. REM sleep behaviour disorder
333
Q

What other features are associated with Lewy-Body dementia?

A

Parkinsonism
Bradykinesia
Rest tremor or rigidity

334
Q

What is the aetiology of Lewy-body dementia?

A

Is associated with aberrant deposits of alpha-synuclein protein with the brain - predominantly within the primary motor cortex

335
Q

Which part of the brain is predominantly affected in LB dementia?

A

Primary motor cortex

336
Q

Which deposits are associated with LB dementia?

A

Alpha-synuclein protein

337
Q

What is the presentation of LB dementia?

A

• Cognitive fluctuations

  • Cognition
  • Attention
  • Arousal

• Visual hallucinations
- Well formed

  • Motor symptoms
  • REM sleep behavioural disturbance
338
Q

What is the first-line management for LB dementia?

A

Cholinesterase inhibitors (Donepezil)

339
Q

What is frontotemporal dementia?

A

Associated with neuronal atrophy of the frontal and temporal lobes due to the presence of abnormal proteins within them – Phosphorylated tau orTDP-43.
• Appear in mid-life with average age of onset between 45-65 years.

340
Q

What are the symptoms of front-temporal dementia?

A 
Symptoms
•	Coarsening of personality, social behaviour and habits 
-	Slovenly appearance
-	Impatience
-	Irritability 
-	Argumentativeness
-	Impulsiveness
  • Progressive loss of language fluency or comprehension
  • Development of memory impairment, disorientation, or apraxia
  • Progressive self-neglect
341
Q

What is meningitis?

A

Refers to the inflammation of the meninges (dura mater, arachnoid mater and pia mater)

342
Q

What are the common bacterial causes of meningitis?

A
  • Streptococcus pneumoniae (pneumococcus)
  • Neisseria meningitides (meningococcus)
  • Haemophilus influenzae
  • Listeria monocytogenes
343
Q

What is the presentation of meningitis?

A
  • Headache
  • Fever
  • Neck stiffness
  • Photophobia
  • Nausea and vomiting
  • Focal neurology
  • Seizures
  • Reduced conscious level
  • Features of sepsis (non-blanching petechial rash of impending DIC)
344
Q

What is Kernig;s sign?

A

Pain in the lower back or back of the thigh on the extension of the knee when the hip is flexed to a right angle.

345
Q

What is Brudzinkski’s sign?

A

Forced flexion of the neck elicits a reflex flexion of the hips

346
Q

What investigations should be performed in meningitis?

A

Blood cultures within 1 hour of arrival at the hospital and prior to administering antibiotics.

Serum pneumococcal and meningococcal PCR

FBC
• Leucocytosis, anaemia, and thrombocytopenia

Serum urea, creatinine, and electrolytes
• In severe bacterial meningitis – metabolic acidosis, hypokalaemia, hypocalcaemia, and hypomagnesemia.

Cerebrospinal fluid (Lumbar puncture)

347
Q

What is the first-line management of meningitis?

A

IM benzylpenicillin and urgent hospital transfer

348
Q

What is raised intracranial pressure?

A

The brain and ventricles are enclosed by a rigid skull having a limited ability to accommodate additional volume.
• Additional volume: Haematoma, tumour, excessive CSF – Lead to a rise in intracranial pressure.

349
Q

What are the causes of raised ICP?

A
  • Idiopathic intracranial hypertension
  • Traumatic head injuries
  • Infection: Meningitis
  • Tumours
  • Hydrocephalus
350
Q

What is the presentation of raised ICP?

A
  • Headache
  • Vomiting
  • Reduced levels of consciousness
  • Papilledema

Cushing’s triad
• Widening pulse pressure
• Bradycardia
• Irregular breathing

351
Q

What is Cushing’s triad?

A

Widening pulse pressure
Bradycardia
Irregular breathing

352
Q

How is ICP monitored?

A

A catheter is placed into the lateral ventricle of the brain to monitor the pressure

353
Q

What neuroimaging is performed in raised ICP?

A

CT/MRI

354
Q

What is the management of raised ICP?

A

Head elevation to 30 degrees
IV mannitol or hypertonic saline

Controlled hyperventilation

Removal of CSF

355
Q

What is essential tremor?

A

Essential tremor is a symmetrical and rhythmic involuntary oscillation movement disorder of the hands and forearms.
• Absent at rest
• Present during posture and intentional movements

356
Q

What is the pattern of tremor in essential tremor?

A

Symmetrical

Absent at rest

357
Q

When is an essential tremor evident?

A
  • Postural or kinetic (A postural tremor occurs when you attempt to hold parts of your body still against gravity).
  • Tremor amplitude increases with time
  • Patients have trouble with writing, eating, holding objects, and doing fine motor tasks.
358
Q

What is the first-line management of essential tremor?

A

Propanolol

359
Q

What investigations are performed in radiculopathy?

A

Spinal X-ray - narrowing of vertebral openings or disc injury

CT scan to visualise spinal cord

Nerve conduction studies

360
Q

What is temporal arteritis?

A

Temporal arteritis is a large vessel vasculitis that overlaps with polymyalgia rheumatica (PMR), predominantly affecting branches of the external carotid artery.
• Occurs in people aged >50 years and is more common in women.

361
Q

What is often coexistent with temporal arteritis?

A

Polymylagia rheuamtica

362
Q

Which artery is predominantly affected in temporal arteritis?

A

Branches of the external carotid artery

363
Q

What are the symptoms of temporal arteritis?

A

• Headache
- Associated with scalp tenderness (Noticed when brushing hair)
• Aching and stiffness
- Aching and stiffness in the neck, shoulders, hip, and proximal extremities that worsens after a period of inactivity and with movement.
- Symptoms of polymyalgia rheumatica
• Limb claudication
• Loss of vision
- Amaurosis fugax: Transient monocular blindness, described as a dark curtain descending vertically.
- Blurring
- Double vision
• Jaw and tongue claudication
• Arterial tenderness, thickening or nodularity
• Absent pulse
• Abnormal fundoscopy

364
Q

What is the pattern of stiffness in temporal arteritis?

A

Neck, shoulder, hip and proximal extremities that worsens after a period of inactivity and with movement

365
Q

What visual impairments are associated with temporal arteritis?

A

Amaurosis fugax
Blurring
Double vision

366
Q

What is Amaurosis fugax?

A

Transient monocular blindness, described as a dark curtain

367
Q

Which inflammatory markers is raised in temporal arteritis?

A

ESR >50 mm/hr

368
Q

What is the definitive diagnostic investigation in temporal arteritis?

A

Temporal artery biopsy

-Skip lesions in the artery

369
Q

What is the first-line treatment in temporal arteritis?

A

Prednisolone high dose 60 mg OD

Bisphosphonates and PPIs to reduce osteoporosis and gastric ulcer risk

370
Q

What should be administered in temporal arteritis if there is visual loss?

A

Methylprednisolone

371
Q

What is an extradural haemorrhage?

A

A collection of blood that resides between the skull and dura, predominantly caused by trauma

372
Q

Which artery is predominantly affected in an extradural haemorrhage?

A

Middle meningeal artery

373
Q

Which part of the skull is susceptible to fracture?

A

Pterion

374
Q

What is the initial presentation of an extradural haemorrhage?

A

Brief loss of consciousness followed by a lucid interval

Deterioration of consciousness and headache

Fixed and dilated pupil due to compression of the third cranial nerve

375
Q

What is the lucid interval in an extradural haemorrhage

A

• Brief loss of consciousness, followed by regaining of normal consciousness level (Lucid interval).

The lucid interval is lost eventually due to the expanding haematoma and brain herniation; as it expands, the uncus of the temporal lobe herniates around the tentorium cerebelli.

376
Q

What visual changes occur in extradural haemtoma?

A

Fixed dilated pupil

377
Q

What is the definitive imaging in an extradural haemorrhage?

A

CT head

378
Q

What does a CT head reveal in an extradural haemorrhage?

A

Biconcave (lentiform) and hyperdense collection around the surface of the brain

379
Q

What is the definitive treatment of an extradural haemorrhage?

A

Craniotomy and evacuation of the haematoma

380
Q

What are the symptoms of a cerebellar stroke?

A

Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
Ataxia (a broad-based, unsteady gait)
Nystagmus (involuntary eye movements)
Intention tremor (seen when the patient is asked to perform the ‘finger-nose test’)
Slurred speech
Hypotonia

381
Q

What is Weber’s syndrome?

A

A midbrain stroke characterised by a third cranial nerve palsy and contralateral motor weakness (hemiparesis)

382
Q

Which cranial nerve is affected in Weber’s syndrome?

A

Third cranial nerve

383
Q

What is the main cause of basal ganglia haemorrhages?

A

Hypertension

384
Q

What type of aneurysms are associated with a subarachnoid haemorrhage?

A

Charcot-Bouchard

Berry aneurysm - Predominantly

385
Q

Which class of drugs are associated with worsening Myasthenia Gravis?

A

beta-blockers

386
Q

What is the first stage of thiamine deficiency in chronic alcoholism?

A

Wet/Dry beriberi

387
Q

Which factor is associated as a worse prognosis for a patient with MS?

A

Male sex

388
Q

Which anti-epileptic drug is administered in a tonic-clonic seizure?

A

Lamotrigine

389
Q

When should a patient take Sumatriptan during a migraine?

A

Once the headache starts and not during the aura phase

390
Q

What is the first-line prophylactic management of a migraine?

A

Propranolol or amitriptyline or topiramate (Tetatrogenic)

391
Q

Which migraine prophylaxis is contraindicated in women of child bearing age?

A

Topiramate

392
Q

A mid-shaft humeral fracture is associated with injury to which peripheral nerve?

A

Radial nerve (runs along the radial groove)- causes wrist drop

393
Q

A radial nerve palsy causes what?

A

Wrist drop

394
Q

Tension headaches are associated with what type of tenderness?

A

Scalp muscle

395
Q

Which gaze is associated with a progressive supranuclear palsy?

A

Vertical gaze - inability to look in vertical direction

396
Q

A lesion to which artery is associated with Locked-in syndrome?

A

Basilar artery

397
Q

In malignancy-associated spinal cord compression what i the management?

A

Dexamethasone

398
Q

Which antibody is most common in myasthenia gravis?

A

Nicotinic acetylcholine receptor antibodies

399
Q

A ring-enhancing lesion on a CT with a history of immunosuppressants is associated with what?

A

brain abscess

400
Q

Lip-smacking is associated with what type of focal seizure?

A

Temporal lobe

401
Q

What is the management of a warfarin-induced intracranial bleed?

A

Vitamin K 5mg IV and prothrombin complex concentrate

402
Q

Hemiballism is associated with a lesion to which basal ganglia structure?

A

Sub-thalamic nucleus

403
Q

Which part of the brain is an acoustic neuroma best visualised?

A

Cerebellopontine angle

404
Q

What is the classical presentation of an acoustic neuroma?

A

The classical history of vestibular schwannoma includes a combination of vertigo, hearing loss, tinnitus and an absent corneal reflex. Features can be predicted by the affected cranial nerves:
cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy

405
Q

The absent corneal reflex associated with tinnitus and vertigo is associated with what diagnosis?

A

Acoustic neuroma

406
Q

What radiological imaging should be conducted in an acoustic neuroma?

A

MRI of the cerebellopontine angle

407
Q

Which part of the ear is more sensitive to air conduction?

A

The inner ear is more sensitive to sound via air conduction than bone conduction

408
Q

What tuning fork is used for the Rhinnes and Weber test?

A

512Hz

409
Q

If a patient has unilateral conductive hearing loss, Weber’s test would lateralise to which ear?

A

The affected ear

410
Q

If a patient has unilateral sensorineural hearing loss, Weber’s test would lateralise to which ear?

A

The normal ear

411
Q

What is Rinne’s test normal?

A

Air louder than Bone

Rinne’s Positive

412
Q

What is Rinne’s negative?

A

Bone louder than Air (Conductive hearing loss)

413
Q

What are the common causes of conductive hearing loss?

A

cerumen impaction, otitis media, and otosclerosis.

414
Q

What is normal Weber test?

A

Sound is heard in the midline

415
Q

Why is the COCP contraindicated in migraines?

A

Significantly increased risk for developing a stroke

416
Q

What categories are associated with a partial anterior circulation stroke?

A

Two of the following:
Contralateral motor deficit
Homonymous hemianopia
Higher cortical dysfunction

417
Q

What categories are associated with a total anterior circulation stroke?

A
  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
418
Q

A III cranial nerve palsy with an enlarged pupil is associated with what type of cause?

A

surgical third nerve palsy, most likely caused by external compression due to a tumour

419
Q

What is the definition of multiple sclerosis?

A

A chronic inflammatory multifocal demyelinating disease of the central nervous system.

-Loss of myelin and oligodendroglian and aonal pathology

420
Q

What is the most common type of multiple sclerosis?

A

Relapsing remitting

421
Q

What are the signs of multiple sclerosis?

A 
Optic neuritis
Sensory disturbance
Hemiparesis/hemisensory loss
Motor weakness 
Fatigue
Lhermitte's sign 
Hyperreflexia and spasticity
Urinary urgency and incontinence
Diplopia
Vertigo 
Visual feed defect
Dysarthria
422
Q

What CSF findings are associated with MS?

A

Oligoclonal bands

423
Q

What scan is used for MS?

A

Gadolinium contrast scan

424
Q

What autoantibodies are associated with myasthenia gravis?

A

Against AChR at NMJ

425
Q

What is associated with myasthenia gravis (manifestation)?

A

Thmus association
Thymic hyperplasia
Thymoma

426
Q

What is the presentation of MG?

A 
Ptosis
Diplopia
Dysarthria
Dysphagia
SOB
Fatigable muscles
Normal reflexes

Muscle fatigue with use

427
Q

What is elevated in MG BLOOD?

A

Anti ACHr And anti-Musk antibodies

428
Q

What does an EMG reveal in MG?

A

Decline in amplitude with repetitive use of muscle

429
Q

What antibodies are associated w Lambert Eaton Mysathetnic syndrome?

A

autoantibodies against presynaptic VGCC at NMJ

430
Q

What is the presentation of LEMS?

A

Difficulty walking
Weakness in upper arms and shoulder

Dry mouth
Constipation
Incontinence

Muscle weakness improves with use

Hyporeflexia

Associated with small cell lung cancer

431
Q

LEMs is associated with which type of lung cancer?

A

Small cell lung cancer

432
Q

What are the symptoms of MND?

A

Progressive muscle weakness
Dysphagia
Shortness of breath
Sparing of oculomotor, sensory and autonomic function

-Wasting of thenar muscles and tongue base

433
Q

Signs of uMn Lesion

A

Spasticity
Hyper-reflexia
Clonus
Positve Babinski’s sign

434
Q

Sign of LMN

A

Hyporeflexia
Hypotonia
Muscle atrophy
Fasciculations and fibrillations

435
Q

What is Parkinson?

A

Loss of dopaminergic neurones in the substania nigra (Midbrain)

436
Q

What is the triad of parkinsons

A

Bradykinesia
Resting tremor and
Rigidity

437
Q

Which drugs can cause Parkinsonian features?

A

Anti-emetics

Anti-pyschotics

438
Q

What are the 6Ms of Parkinon’s?

A 
Monotonous hypotonic speech
Micrographia
March a petit pas
Misery (depression)
Memory loss (dementia)
HypoMesis
439
Q

What gait is associated with Parkinson’s?

A

Shuffling gait

440
Q

What palsy is associated with progressive supranuclear palsy?

A

Vertical gaze

441
Q

Where does Huntington;’s disease affect?

A

Straitum (caudate and putamen)

442
Q

Inheritance pattern of Huntington’s Disease?

A

Autosomal dominant pattern

CAG trinucleotide

443
Q

Symptoms of Huntington’s Disease

A

Chorea
Athetosis - slow involuntary and writhing movements

Dysphagia
Ataxia

Cognitinve
-Depression
-Personality changes
Lack of concentration
Dementia
444
Q

What genetic testing is done in Huntington’s Disease?

A

CAG repeat testing

445
Q

Triad of Wernicke’s

A

Ataxia
Eye signs - opthahlmoplegua, nystagmus, diplopia and ptoss
Confusion

446
Q

Common cause of encephalitis (Virus)

A

Herpes simplex virus

447
Q

Management of stroke within 4.5 hours?

A

Thrombolysis (IV atelplase) and thrombectomy

448
Q

Management of stroke within 6 hours

A

Thrombectomy

449
Q

Middle finger dermatome

A

C7

450
Q

Management of Parkinson’s if motor function is affecting QoL?

A

Levodopa

451
Q

Cause of non-communicating hydrocephalus

A

Arnold-chiari malformation

452
Q

Main features of Neuroleptic malignant syndrome

A

rigidity, hyperthermia, autonomic instability (hypotension, tachycardia) and altered mental status (confusion)

453
Q

What are the causes of pre-chiasmal visual field defects (One eye is affected, ipsilatearl)

A 
Optic neuritis
Amaurosis fugax
Optic atrophy
Retrobulbar optic neuropathy
Trauma
454
Q

What are the main causes of bitemporal hemianopia?

A

Pituitary adenoma

Suprasellar aneurysm

455
Q

What are the causes of homonymous contralateral hemianopia?

A

Stroke
Tumour
Trauma

456
Q

Which interocular muscles are innervated by the oculomotor nerve?

A

Superior rectus
Inferior rectus
Medial rectus
Inferior oblique

457
Q

Which extra-ocular muscle is innervated by the trochlear nerve?

A

Superior oblique

458
Q

Which extra-ocular muscle is innervated by the abducens nerve?

A

Lateral rectus

459
Q

What is the presentation of an oculomotor palsy?

A

Ptosis
Mydriasis
Down and out

460
Q

What is the presentation of a trochlear nerve palsy?

A

Prevents moving inwards and down

461
Q

What is the presentation of an abducens nerve palsy?

A

Prevents movement outwards

462
Q

Which virus is associated with Ramsay Hunt syndrome?

A

Reactivation of varicella zoster

463
Q

What is the triad of Horner’s syndrome?

A

Miosis
Partial ptosis
Anhidrosis

464
Q

What tumour is associated with Horner syndrome?

A

Pancoast tumour

465
Q

Which chromosome is associated with neurofibromatosis type 1?

A

Chromosome 17

Mutation in neurofibromin

466
Q

What skin manifestation is associated with NF?

A

Cafe au lait macules

467
Q

What is the presentation of neurofibromatosis?

A

Signs of hydrocephalus, brain tumours
Cerebellor abmnormalities
Seizures

468
Q

What is the investigation for neuroplastic spinal cord compression?

A

Urgent Spinal MRI

469
Q

What is a significant complication of spinal mets?

A

Neuroplastic spinal cord compression

470
Q

What is the treatment for neuroplastic spinal cord compression?

A

High-dose oral dexamethasone

Phase1c Medicine (11 decks)

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