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Phase 3A Sam Harper > Neurology > Flashcards

Neurology Flashcards

1
Q

Name the excitatory neurotransmitters

A

Acetylcholine, noradrenaline, adrenaline, serotonin, dopamine, glutamate, aspartate

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2
Q

Name the inhibitory neurotransmitters

A

GABA, histamine and glycine

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3
Q

Name the inhibitory/excitatory neuropeptides

A

Vasopressin, ACTH, opioid peptides, ATP, AMP

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4
Q

What area of the brain is affected in aphasia

A

left frontal lobe

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5
Q

What area of the brain is affected in hemiparesis

A

internal capsule

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6
Q

What cranial nerve is affected in Bells palsy

A

12th

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7
Q

What is the effect of a destructive cortical lesion in the frontal lobe (either side)

A

Intellectual impairment, personality change, Urinary incontinence, Mono or hemiparesis

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8
Q

What is the effect of a destructive cortical lesion in the left frontal lobe

A

Brocas aphasia

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9
Q

What is the effect of a destructive cortical lesion in the left tempero-parietal lobe

A

Acalculia, Alexia, Agraphia, Wernickes aphasia, Right-left disorientation, homonymous field defect

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10
Q

What is the effect of a destructive cortical lesion in the right temporal lobe

A

Confusional state, homonymous field defect, cant recognise faces

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11
Q

What is the effect of a destructive cortical lesion in the parietal lobe (either side)

A

Contralateral sensory loss, Agraphaesthesia, Homonymous field defect

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12
Q

What is the effect of a destructive cortical lesion in the right parietal lobe

A

Dressing apraxia, failure to recognise faces

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13
Q

What is the effect of a destructive cortical lesion in the left parietal lobe

A

Limb apraxia

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14
Q

What is the effect of a destructive cortical lesion in the occipital/occipitoparietal lobe

A

Visual field defects, visuospatial defects, disturbance of visual recognition

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15
Q

What is the effect of an irritative cortical lesion in the frontal lobes

A

Partial seizures, focal motor seizures of the contralateral limb, Conjugate deviation of the head and eyes away from the side of the lesion

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16
Q

What is the effect of an irritative cortical lesion on the temporal lobes

A

Formed visual hallucination, complex partial seizures, memory disturbance

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17
Q

What is the effect of an irritative cortical lesion in the parietal lobe

A

Partial seizures-focal sensory seizures of the contralateral limb

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18
Q

What is the effect of an irritative cortical lesion in the parieto-occipital lobe

A

Crude visual hallucinations

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19
Q

What is the effect of an irritative cortical lesion in the occipital lobe

A

Visual disturbance (e.g. flashing)

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20
Q

What is Brocas aphasia

A

Damage in the left frontal lobe causes reduced speech fluency but preserved comprehension - cant construct sentences but know what they want to say

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21
Q

What is Wernickes aphasia

A

Left temporo-parietal damage leaves fluency of language but words are muddled - patients describe finding speech unintelligible

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22
Q

What is nominal aphasia

A

Difficulty in naming objects. An early feature in all types of aphasia

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23
Q

What is global aphasia

A

Combo of expressive problems of Brocas and loss of comprehension seen in Wernickes. Loss of language production and understanding

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24
Q

What is Dysarthria

A

Disordered articulation - slurred speech

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25
Q

Causes of anosmia

A

head injury, tumour (meningioma), URTI, Parkinsons

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26
Q

What causes mononuclear field loss

A

Complete optic nerve lesion

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27
Q

What causes bitemporal hemianopia

A

chiasmal lesion

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28
Q

What causes homonymous hemianopia

A

optic tract lesion

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29
Q

What causes homonymous quadrantanopia

A

temporal or parietal lesion

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30
Q

What causes homonymous hemianopia with macular sparing

A

occipital cortex or optic radiation

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31
Q

What causes homonymous hemianopia (hemiscotoma)

A

Occipital pole lesion

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32
Q

What is papilloedema

A

Swelling of the optic disc

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33
Q

Explain afferent pupillary defect (APD)

A

Complete optic nerve lesion causes a dilated pupil and APD. Pupil is unreactive to light (absent direct reflex) and the consensual reflex is absent. The consensual reflex is preserved when light is shone into the affected eye

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34
Q

Explain relative afferent pupillary defect (RAPD)

A

Incomplete damage to one optic nerve relative to the other. Direct and indirect reflexes are intact but differ in relative strength. When light is swung the left will dilate slightly when illuminated and constrict slightly when right is illuminated (consensual reflex stronger than direct)

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35
Q

What can disrupt blood supply in an ischaemic stroke

A

thrombus or embolus, atheroscleosis, shock, vasculitis

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36
Q

What is a transient ischaemic attack

A

temporary neurological dysfunction lasting less than 24 hours causing by ischaemia but without infarction. Rapid onset of Sx and often resolve before a pt is seen. May precede a stroke

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37
Q

What is a Crescendo TIA

A

Two or more TIA’s in a week and indicates a high risk of stroke

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38
Q

Are stroke symptoms symmetrical or asymmetrical

A

Asymmetrical

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39
Q

Common stroke Sx

A

Limb weakness, Facial weakness, Dysphasia, Visual field defect, Sensory loss, Ataxia and vertigo

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40
Q

RF for Stroke

A

Previous stroke or TIA, AF, Carotid artery stenosis, HTN, Diabetes, Raised cholesterol, FHx, Smoking, Obesity, Vasculitis, Thrombophilia, COCP

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41
Q

What is the FAST tool

A

Face, Arm, Speech, Time

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42
Q

What is the emergency room tool for stroke

A

ROSIER - Recognition of stroke in the emergency room. A score of one or more indicates a possible stroke

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43
Q

Management of a TIA

A

Aspirin 300mg daily

Refer for specialist assessment within 24 hours

Diffusion weighted MRI

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44
Q

Initial management of stroke

A

Exclude hypoglycaemia, Immediate CT head to exclude haemorrhage, Aspirin 300mg daily and admit to stroke centre

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45
Q

What is given once haemorrhage is excluded in stroke

A

Thrombolysis with alteplase

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46
Q

Alteplase class and moa

A

Tissue plasminogen activator that rapidly breaks down clots

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47
Q

Within how many hours can alteplase be given

A

4.5 hours

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48
Q

Who is considered for thrombectomy

A

Pt with confirmed blockage of the proximal anterior circulation or proximal posterior circulation and within 24 hours of onset alongside thrombolysis

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49
Q

Explain the assessement for the underlying cause of a stroke

A

Investigate for carotid artery stenosis and AF with carotid imaging and ECG. GIve anticoag if Dx with AF. Surgical interventions for carotid artery stenosis such as carotid endarterectomy, angioplasty and stenting

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50
Q

Secondary prevention for stroke

A

Clopidogrel 75mg once daily, atorvastatin 20-80mg, BP and diabetes control, address modifiable RF

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51
Q

Rehab for stroke pt

A

MDT approach
Stroke physicians, nurses, SALT, dietician, Physio, OT, Social services, Psych, Orthotics

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52
Q

What is an extradural haemorrhage

A

Bleeding between the skull and the dura

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53
Q

What is a subdural haemorrhage

A

Bleeding between the dura and arachnoid

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54
Q

What is an Intracerebral haemorrhage

A

Bleeding into the brain tissue

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55
Q

What is a subarachnoid haemorrhage

A

Bleeding in the subarachnoid space

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56
Q

RF for intracranial haemorrhage

A

Head injury, HTN, Aneurysm, Ischaemic stroke, tumour, thrombocytopenia, Bleeding disorder, Anticoags

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57
Q

Presentation of intracranial bleed

A

Sudden onset headache, seizures, vomiting, reduced consciousness, focal neuro Sx

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58
Q

What GCS score warrant airway support

A

8/15

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59
Q

What usually causes an extradural haemorrhage

A

rupture of the middle meningeal artery in the temporoparietal region or fracture of the temporal bone

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60
Q

Shape of extradural haemorrhage

A

Bi-convex shape limited by the cranial sutures

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61
Q

Typical Hx for an extradural haemorrhage

A

young pt with traumatic head injury and ongoing headache. Period of improved Sx followed by rapid decline as haematoma compresses intracranial contents

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62
Q

Cause of subdural haemorrhage

A

Rupture of bridging veins in the outermost meningeal layer

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63
Q

Subdural haemorrhage shape

A

crescent shape and not limited by cranial sutures

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64
Q

Subdural haemorrhage typical patient

A

elderly and alcoholic pt who have more atrophy in their brains

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65
Q

Intracerebral haemorrhage presentation

A

similar to a stroke with sudden onset focal neurological symptoms such as limb, facial weakness, dysphasia and vision loss

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66
Q

Where can intracerebral haemorrhage occur

A

anywhere in the brain e.g. lobar, deep, intraventricular, basal ganglia, cerebellar

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67
Q

Cause of subarachnoid haemorrhage

A

ruptured cerebral aneurysm

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68
Q

Subarachnoid haemorrhage presentation

A

Sudden-onset occiptal headache during strenuous activity, thunderclap headache description

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69
Q

Immediate investigation for intracranial bleed

A

CT head

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70
Q

Initial management of intracranial bleed

A

Admission to specialist stroke unit, consider surgery, consider intubation/vent/ICU, correct any clotting abnormality (eg platelets or vit K), correct severe HTN but avoid hypo

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71
Q

Surgical options for intracranial bleeds

A

Craniotomy, Burr holes

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72
Q

Mortality of subarachnoid haemorrhage

A

30%

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73
Q

RF for subarachnoid haemorrhage

A

Aged 45-70, women, black ethnicity

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74
Q

General RF for Subarachnoid Haemorrhage

A

HTN, smoking, excessive alcohol intake

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75
Q

What is subarachnoid haemorrhage associated with

A

FHx, Cocaine use, Sickle cell, connective tissue disorder, Neurofibromatosis, Autosomal dominant PKD

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76
Q

Presentation of Subarachnoid Haemorrhage

A

Neck stiffness, Photophobia, Vomiting, Neuro Sx

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77
Q

Ix for Subarachnoid Haemorrhage

A

CT head, blood will cause hyperattenuation in the subarachnoid space

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78
Q

Secondary Ix for subarachnoid haremorrhage

A

LP after 12 hours as bilirubin takes time to accumulate

Sample will show: Raised red cells, Xanthochromia

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79
Q

Management of Subarachnoid Haemorrhage

A

Specialist, intubate/vent, surgical intervention for aneurysm (endovascular coiling, clipping), give nimodipine to prevent vasospasm

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80
Q

Management for the complications of subarachnoid haeomorrhage

A

Hydrocephalus: LP, External ventricular drain, VP shunt

Treat seizures with antiepileptics

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81
Q

What is MS

A

A chronic and degenerative autoimmune condition involving demyelination in the CNS. Immune system attacks myelin sheath of myelinated neurones

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82
Q

Typical MS patient

A

Young adults under 50, more common in women

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83
Q

What cells provide myelin in the CNS and PNS

A

CNS - Oligodendrocytes
PNS - Schwann cells

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84
Q

Explain the characteristic pattern in MS

A

Lesions vary in location, meaning affected sites and Sx change over time. The lesions are described as ‘disseminated in time and space’. Early in the disease remyelination occurs and Sx can resolve but this stops in later stages with remyelination being incomplete

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85
Q

Causes of MS

A

Genetic
EBV
Low Vit D
Smoking
Obesity

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86
Q

Onset of Sx in MS

A

Progress over more than 24 hours. Sx last days to weeks at first presentation and then improve

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87
Q

What is the most common presentation in MS

A

Optic neuritis - demyelination of the optic nerve - presents with unilateral reduced vision

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88
Q

Key features of optic neuritis

A

Central scotoma, Pain with eye movement, Impaired colour vision, Relative afferent pupillary defect

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89
Q

What are some other causes of optic neuritis

A

Sarcoidosis, SLE, Syphilis, Measles and mumps, Neuromyelitis Optica, Lyme

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90
Q

Tx for optic neuritis

A

High dose steroids

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91
Q

What lesions cause double vision (diplopia) and nystagmus?

A

Lesions to CN3, CN4 and CN6

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92
Q

Where is the lesion in internuclear opthalmoplegia

A

Medial longitudinal fasciculus

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93
Q

Explain internuclear opthalmoplegia

A

The nerve fibres of the medial internuclear fasciculus connect the CN nuclei that control eye movements. A lesion here causes impaired adduction on the same side as the lesion and nystagmus in the contralateral abducting eye

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94
Q

What does a lesion in CN6 cause?

A

Conjugate lateral gaze disorder

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95
Q

What is conjugate lateral gaze disorder

A

Both eyes look laterally to the left or right, when looking laterally in the direction of the affected eye then the affected eye will not be able to abduct

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96
Q

Examples of focal weakness seen in MS

A

Incontinence, Horners, Facial nerve palsy, Limb paralysis

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97
Q

Examples of focal sensory Sx in MS

A

Trigeminal Neuralgia, Numbness, Paraesthesia, Lhermittes sign

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98
Q

What is Lhermittes sign

A

Electric shock sensation that travels sown the spine into the limbs when flexing the neck. Indicates disease in the dorsal column

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99
Q

What is transverse myelitis

A

A site of inflammation in the spinal cord

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100
Q

Explain sensory ataxia

A

Due to loss of proprioception. This results in a +ve Rombergs test (lose balance when standing with their eyes closed) and can cause pseudoathetosis (involuntary writhing movements). A lesion in the dorsal columns of the spine can cause sensory ataxia

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101
Q

What is Clinically isolated syndrome in MS

A

First episode of demyelination and neuro Sx. Patients may never have another episode or go on to develop MS. MRI lesions can suggest whether they are likely to progress to MS

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102
Q

What is Relapsing-Remitting MS?

A

Most common pattern. Characterised by episodes of disease and Sx and then recovery. The Sx occur in different areas with each episode

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103
Q

Classification of relapsing-remitting MS

A

Active or Worsening:
Active: new Sx are developing or new lesions on MRI
Not Active: No new Sx or MRI lesions
Worsening: Overall worsening of disability over time
Not Worsening: no worsening of disability over time

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104
Q

What is secondary progressive MS?

A

Where there is relapsing-remitting disease but now there is a progressive worsening of Sx and incomplete remission. Sx become increasingly permanent

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105
Q

What is Primary progressive MS?

A

Involves worsening disease and neuro Sx from the point of diagnosis without relapses or remission

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106
Q

Investigations to support the diagnosis of MS

A

MRI shows lesions and LP can detect oligoclonal bands in the CSFe

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107
Q

Tx for MS

A

MDT led. Disease modifying therapies aim to induce long term remission. Relapses treated with steroids (500mg oral for 5 days or 1g IV daily for 3-5 days)

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108
Q

Symptomatic Tx for MS

A

Exercise, Treat fatigue with amantidine/modafinil/SSRI, Neuropathic pain management, Depression treat with SSRI, Urge incontinence with antimuscs (solifenacin), Spasticity with baclofen or gabapentin, Oscillopsia with gabapentin or memantine

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109
Q

What is MND

A

Encompasses a variety of specific disease that affect the motor nerves. It is progressive and eventually fatal

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110
Q

Name the types of MND

A

Amyotrophic Lateral Sclerosis, Progressive Bulbar Palsy, Progressive Muscular dystrophy and primary lateral sclerosis

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111
Q

What muscles are affected in progressive bulbar palsy

A

Muscles of talking and swallowing (bulbar muscles)

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112
Q

Causes of MND

A

FHx, smoking, heavy metal exposure, Pesticide

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113
Q

Typical MND pt

A

late middle-aged (60 yo) man possibly with an affected relative

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114
Q

Typical onset of Sx in MND

A

Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech. Typical is limb first. Clumsiness, dropping things and tripping, slurred speech

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115
Q

Signs of LMN disease

A

Muscle wasting, reduced tone, fasciculations, reduced reflexes

116
Q

Signs of UMN disease

A

Increased tone and spasticity, Brisk reflexes, Upgoing plantar reflexes

117
Q

Diagnosis of MND

A

Clinical, made by a specialist when there is certainty

118
Q

Management of MND

A

Riluzole can slow the progression of the disease and extend survival by several months in ALS. NIV to support breathing

119
Q

Holistic management of MND

A

Breaking bad news, MDT input, Symptom control (baclofen for muscle spas, Antimusc for excessive saliva), Benzos for breathlessness from anxiety, Advanced directives, EOL care

120
Q

What is Parkinsons

A

Disease of progressive reduction in dopamine in the basal ganglia leading to a disorder in movement

121
Q

Symptom symmetry in Parkinsons

A

Asymmetrical

122
Q

Typical Parkinsons Pt

A

Older man, around 70 with gradual onset of Sx

123
Q

Classic triad in Parkinsons

A

Resting tremor, Rigidity, Bradykinesia

124
Q

Hertz of Parkinsons tremor

A

4-6 hertz frequency

125
Q

Describe the tremor in parkinsons

A

Worse on one side, pill rolling, worse when resting and improves with voluntary movement, worse when distracted

126
Q

Describe the rigidity seen in Parkinsons

A

Resistance to passive movement of the joint, Tension gives way in small increments, this jerking resistance is termed ‘cogwheel rigidity’

127
Q

Effects of bradykinesia

A

Handwriting gets smaller and smaller (micrographia), Small steps when walking (shuffling gait), Rapid frequency of steps to compensate (festinating gait), Hard to initiate movement, Difficulty turning when standing, reduced facial movements and expressions (hypomimia)

128
Q

Other features of Parkinsons

A

Depression, Sleep disturbance and insomnia, Loss of sense of smell, Postural instability, Cognitive/memory impairment

129
Q

What is multi system atrophy

A

A Parkinsons plus syndrome where the neurones in various systems degenerate. can lead to autonomic (postural Hypo, constipation, sweating, sexual dysfunction) and cerebellar dysfunction

130
Q

What is Dementia with Lewy Bodies

A

Parkinsons plus syndrome. Progressive cognitive decline, associated Sx of visual hallucinations, delusions, REM sleep disorder, fluctuating consciousness

131
Q

Name the two other Parkinsons Plus syndromes

A

Progressive supranuclear palsy, Corticobasal degenerative

132
Q

Diagnosis of Parkinsons

A

Clinical

133
Q

What are the four treatment options for Parkinsons

A

Levodopa, COMT inhibitors, Dopamine agonists, Monamine oxidase-B inhibitors

134
Q

Explain Levodopa therapy

A

It is a synthetic form of dopamine taken orally. It is usually combined with a peripheral decarboxylase inhibitor (e.g. carbidopa or benserazide) which stops it being metabolised in the body before it reaches the brain. It become less effective over time and is often reserved for when other tx arent working

135
Q

Common combination drugs of levadopa

A

Co-beneldopa (levadopa + benserazide) and Co-careldopa (Levodopa + carbidopa)

136
Q

SE of Levodopa

A

Dyskinesia (abnormal movements associated with excessive motor activity) e.g. dystonia, chorea and athetosis

137
Q

Tx for dyskinesia associated with Levodopa

A

Amantadine (glutamate antagonist)

138
Q

What are COMT inhibitors

A

E.g. entacapone. Inhibit catechol-o-methyltransferase. The COMT enzyme metabolises levodopa so a COMT inhibitor slows the breakdown of levodopa

139
Q

Explain dopamine agonists

A

Mimic the action of dopamine. Less effective than Levodopa so are used to delay the use of Levodopa and then used in combo

140
Q

Examples of dopamine agonists

A

Bromocriptine, Pergolide, Cabergoline

141
Q

SE of Dopamine agonists

A

Pulmonary fibrosis

142
Q

Explain the use of Monamine oxidase-B inhibitors

A

Blocks the action of MOA-B enzyme (breaks down dopamine, serotonin and adrenaline). They are more specific to dopamine. Used to delay the use of Levodopa and then in combo

143
Q

Examples of MOA-B inhibitors

A

Selegiline and Rasagiline

144
Q

Summarise benign essential tremor

A

Affects voluntary muscles commonly in hands, head, jaw and voice. Symmetrical, 6-12 hertz, improved by alcohol, absent in sleep

145
Q

DDx for benign essential tremor

A

Parkinsons, MS, Huntingtons, Hyperthyroid, Fever, Dopamine antagonist (antipsychotics)

146
Q

Tx for benign essential tremor

A

Propranolol
Primidone (a barbituate antiepileptic)

147
Q

What is Epilepsy

A

Characterised by seizures (transient episodes of abnormal electrical activity)

148
Q

Types of seizures

A

Generalise tonic-clonic, Partial, Myoclonic, Tonic, Atonic, Absent, Febrile, Infantile spasm

149
Q

Explain tonic-clonic seizures

A

muscle tensing and jerking associated with loss of consciousness, aka grand mal, before the patient may experience an aura, may be tongue biting, incontinence, groaning and irregular breathing, after the seizure there is a prolonged post-ictal period

150
Q

What are partial seizures

A

Occur in an isolated area of the brain often in the temporal lobes, affect hearing, speech, memory and emotions. Patient remains awake. They are aware in simple partial and not in complex

151
Q

Symptoms associated with partial seizures

A

Deja vu, Strange smells/taste/sight or sound, unusual emotions, abnormal behaviour

152
Q

What are myoclonic seizures

A

Sudden, brief muscle contraction like an abrupt jolt or jump. can occur as part of juvenile myoclonic epilepsy in children

153
Q

What are tonic seizures

A

Sudden onset of increased muscle tone, where the body stiffens. Results in a fall if standing

154
Q

What are atonic seizures

A

Drop attacks, sudden loss of muscle tone, may be indicative of Lennox-Gastuat syndrome

155
Q

What are absence seizures

A

Seen in children, pt becomes blank and stares into space, they are unaware of surroundings and dont respond

156
Q

What are infantile spasms

A

AKA west syndrome. Rare disorder starting at 6mo. presents with clusters of full body seizures. Hypsarrhythmia is a characteristic EEG finding, poor prognosis and developmental delay

157
Q

Tx for Infantile spasms

A

ACTH and Vigabatrin

158
Q

DDx for epilepsy

A

Vasovagal syncope, Pseudosizures, Cardiac syncope, Hypoglycaemia, Hemiplegic migraine, TIA

159
Q

IX for Epilepsy

A

EEG, MRI brain, ECG, Serum electrolytes, Blood glucose, Cultures

160
Q

Tx for tonic clonic for men and women who cant have children and women who are able to have children

A

Sodium valproate for men and women who cant have children

Lamotrigine or Levetiracetam for women who can have children

161
Q

Tx for partial seizures for men and women who cant have children and women who are able to have children

A

Lamotrigine or Levetiracetam for both groups

162
Q

Tx for Myoclonic seizures for men and women who cant have children and women who are able to have children

A

Sodium valproate for men and women who cant have children

Levitiracetam for women who can have children

163
Q

Tx for tonic and atonic seizures for men and women who cant have children and women who are able to have children

A

Sodium valproate for men and women who cant have seizures

Lamotrigine for women who can have children

164
Q

Tx for Absence seizures

A

Ehtosuximide

165
Q

Other less commonly used anti-epileptics

A

Carbamazepine, Phenytoin, Topiramate

166
Q

Summarise Sodium valproate

A

Works by increasing the activity of GABA

SE: Teratogenic, Liver damage, hair loss, Tremor, reduced fertility

167
Q

What is status epilepticus

A

A seizure lasting more than five minutes or multiple seizures without regaining consciousness between them

168
Q

Management of status epilepticus

A

ABCDE (secure airway, give O2, Check blood glucose, Gain IV acces)

Medical Tx: Benzodiazapine, after 2 doses of benzo give IV Levetiracetam, phenyotin or sodium valproate, third line is phenobarbital or anaethesia

169
Q

What is Allodynia

A

When pain is experienced with sensory inputs that dont usually cause pain e.g. light touch

170
Q

Which two groups of pain fibres transmit pain, explain

A

C fibres - transmit signals slowly and produce dull and diffuse pain sensations

A-delta fibres - Transmit signals fast and produce sharp and localised pain sensations

171
Q

Explain the analgesic ladder

A

Step 1: non-opioid such as NSAID and Paracetamol
Step 2: weak opiate e.g. codeine and tramadol
Step 3: Strong opiate e.g. morphine, oxycodone, fentanyl and buprenorphine

172
Q

SE of NSAIDS

A

Gastritis, Ulcers, exacerbate asthma, HTN, renal impairment, Coronary artery disease

173
Q

SE of Opioids

A

Constipation, Skin itching, Nausea, Altered mental state, resp depression

174
Q

Typical features of neuropathic pain

A

numbness, tingling, burning and pins and needles

175
Q

Common cause of neuropathic pain

A

Post-herpetic neuralgia, nerve damage, MS, Diabetic neuralgia, Trigeminal neuralgia, Complex regional pain syndrome

176
Q

Questionnaire for neuropathic pain

A

DN4

177
Q

First line Tx for Neuropathic pain

A

Amitriptyline - a TCA
Duloxetine - SNRI
Gabapentin - anticonvulsant
Pregabalin - anticonvulsant

178
Q

First line for trigeminal neuralgia

A

Carbamazepine

179
Q

What is facial nerve palsy

A

isolated dysfunction of the facial nerve and presents with unilateral facial weakness

180
Q

What are the five branches of the facial nerve

A

Temporal, Zygomatic, Buccal, Marginal mandibular and Cervical

181
Q

Facial nerve motor function

A

Facial expression, Stapedius, Posterior digastric, Stylohyoid, platysma

182
Q

Facial nerve sensory function

A

Taste for anterior 2/3 of tongue

183
Q

Facial nerve parasympathetic function

A

Submandibular and sublingual salivary glands, lacrimal glands

184
Q

UMN vs LMN facial nerve palsy urgency

A

UMN could be a stroke so its urgent and LMN can be managed less urgently

185
Q

Forehead sparing in facial nerve palsy

A

Forehead is spared in an UMN lesion so patient can move forehead on the affected side. Not spared in LMN

186
Q

Where do unilateral UMN lesions occur

A

Stroke and tumours

187
Q

Where do bilateral UMN lesions occur

A

Pseudobulbar palsies
MND

188
Q

Summarise Bells palsy

A

Common
Idiopathic
Unilateral LMN facial palsy
Use prednisolone 50mg for 10 days
Lubricating eye drops to prevent eye drying out

189
Q

Summarise Ramsay-Hunt syndrome

A

Caused by VZV
Unilateral LMN facial nerve palsy
Painful tender vesicular rash in the ear canal, pinna and around ear
Tx with aciclovir and prednisolone and eye drops

190
Q

Infectious causes of LMN facial nerve palsy

A

Otitis media, Otitis externa, HIV, Lyme

191
Q

Systemic causes of LMN facial nerve palsy

A

Diabetes, Sarcoidosis, Leukaemia, MS, Guillain-Barré

192
Q

Tumour causes of LMN facial palsy

A

Acoustic neuroma, Parotid tumour, Cholesteatoma

193
Q

Trauma causes of LMN facial nerve palsy

A

Direct nerve trauma, Surgery, Base of skull fracture

194
Q

How do brain tumours often first present

A

Sx of raised ICP

195
Q

Causes of Intracranial HTN

A

Brain tumour, Intracranial haemorrhage, Idiopathic intracranial HTN, Abscesses or infection

196
Q

In patients with headache what are the concerning features that may suggest raised intracranial HTN

A

Constant headache, Nocturnal, Worse on waking, worse on coughing or straining, Vomiting, Papilloedema

197
Q

Summarise Papilloedema

A

Swelling of the optic disc secondary to raised ICP
Raised CSF pressure flows into the optic nerve sheath and causing optic disc to bulge forwards
Seen on fundoscopy as: Blurring of the optic disc margin, Elevated optic disc, Loss of venous palpation, Engorged retinal veins, Patons lines

198
Q

Name the three glial cells

A

Astrocytes, Oligodendrocytes and ependymal cells

199
Q

What are the three main types of glioma

A

Atrocytoma (glioblastoma is the most common and aggressive)
Oligodendroglioma
Ependymoma

200
Q

Summarise meningioma

A

Tumours growing from the cells of the meninges. Usually benign however they take up space which can lead to raised ICP

201
Q

What cancers most often spread to the brain

A

Lung, Breast, RCC, Melanoma

202
Q

What hormone deficiencies or excesses are caused by pituitary tumours

A

Acromegaly, Hyperprolactinaemia, Cushings and Thyrotoxicosis

203
Q

Tx of Pituitary tumours

A

Trans-sphenoidal surgery, Radiotherapy, Bromocriptine to block excess prolactin, Somatostatin analogues

204
Q

What cells are acoustic neuromas associated with

A

Schwann cells

205
Q

What are bilateral acoustic neuromas associated with

A

Neurofibromatosis type 2

206
Q

Typical clinical picture in acoustic neuroma

A

Patient is a 40-60 year old with gradual onset of unilateral sensorineural hearing loss, unilateral tinntius, dizziness and imbalance, sensation of fullness in the ear and facial nerve palsy

207
Q

Management options for acoustic neuroma

A

Conservative, surgery to remove the tumour and radiotherapy to reduce the growth

208
Q

General management for brain tumour

A

Surgery, chemo, radio, palliative

209
Q

Huntingtons inheritance and mutations

A

Autosomal dominant. It is a trinucleotide repeat disorder involving mutations on the HTT gene on chromosome 4 which codes for huntingtin (HTT) protein

210
Q

When do symptoms begin in Huntingtons

A

30-50 yo

211
Q

What is anticipation

A

A feature of trinucleotide repeat disorders where successive generations have more repeats in the gene resulting in earlier age of onset and increased severity of the disease

212
Q

Sx in Hungtingtons

A

Insidious progressive worsening of Sx. Begins with cognitive, psychiatric and mood problems followed by the development of movement disorders. Chorea, dystonia, rigidity, eye movement disorders, dysarthria, dysphagia

213
Q

Diagnosis of Huntingtons

A

Genetic testing

214
Q

Tx for Huntingtons

A

Breaking bad news, Genetic counselling, MDT, Physio, SALT, Tetrabenazine for chorea, Antidepressants, Advanced directives, EOLC

215
Q

Prognosis for Huntingtons

A

Life expectancy is 10-20 years after onset of Sx. as the disease progresses the pt becomes more frail and susceptible to illness (e.g. infections, weight loss, falls and pressure ulcers), Death is often due to aspiration pneumonia or suicide

216
Q

What is Myasthenia Gravis

A

An autoimmune condition affecting the neuromuscular junction

217
Q

General Sx of MG

A

Muscle weakness that progressively worsens with activity and improves with rest

218
Q

Typical MG pt

A

Affects women under 40 and men over 60

219
Q

What tumour is strongly associated with MG

A

Thymoma - 10-20% of pt with MG have a thymoma

220
Q

What antibodies are involved in MG

A

Acetylcholine receptor (AChR) antibodies, Muscle-specific kinase (MuSK), Low-density lipoprotein receptor-related protein 4 (LRP4)

221
Q

What muscles are mainly affected in MG

A

Proximal muscles of the limbs and small muscles of the head

222
Q

Sx and difficulties has by pt with MG

A

Difficulty climbing stairs, standing from a seat, raising hands above head
Diplopia
Ptosis
Facial movement weakness
Difficulty swallowing
Fatigue in jaw
Slurred speech

223
Q

Ways to elicit muscle weakness in MG

A

Repeated blinking makes ptosis worse, Prolonged upward gaze worsens diplopia, repeated abduction of arm causes weakness

224
Q

Ix for MG

A

Antibody tests looking for AchR, MuSK, LRP4

CT or MRI of the thymus

Edrophonium test

225
Q

What is an edrophonium test

A

Pt given Iv edrophonium chloride. Normally, cholinesterase enzymes in the NMJ break down acetylcholine, edrophonium blocks these enzymes reducing the breakdown of acetylcholine. as a result the levels of Ach in the NMJ rise which relieves muscle weakness which is suggestive of MG

226
Q

Tx for MG

A

Pyridostigmine - cholinesterase inhibitor that prolongs action of Ach and improves Sx
Immunosuppression (pred or azathioprine) suppresses prod of Ab
Thymectomy
Rituximab

227
Q

Explain myasthenic crisis

A

Causes acute worsening of Sx often triggered by another illness, resp muscles weaken and lead to resp failure. Patients may require NIV or mechanical vent

Tx with IV Ig and plasmapheresis

228
Q

What is Lambert-Eaton Myasthenic Syndrome

A

Similar to MG except the symptoms are more insidious and less pronounced. in most cases it is paraneoplastic occurring alongside small-cell lung cancer. Can occur as a primary condition

229
Q

Sx of Lambert Eaton and how they differ from MG

A

Proximal muscle weakness, Autonomic dysfunction, Reduced or absent tendon reflexes. Sx improve after periods of muscle contraction.

230
Q

Management of Lambert Eaton

A

Exclude underlying malignancy

Amifampridine works by blocking voltage-gated potassium chanells in the presynaptic membrane, which prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action

Other: Pyridostigmine, Immunosuppress, IV Ig, Plasmapharesis

231
Q

What is Charcot-Marie-Tooth Disease

A

Inherited disease that affects the peripheral motor and sensory neurones. Causes myelin or axon dysfunction. Majority of mutations are autosomal dominant

232
Q

Symptom onset of CMT

A

Usually start to appear before aged 10 but can be delayed until 40 or later

233
Q

Classical features of CMT

A

High foot arches (pes cavus)
Distal muscle wasting causing “inverted champagne bottle legs”
Lower leg weakness, particularly loss of ankle dorsiflexion (with high stepping gait due to foot drop)
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

234
Q

Other causes of Peripheral neuropathy

A

ABCDE
A - Alcohol
B - B12 def
C - Cancer (e.g. myeloma) and CKD
D - Diabetes and drugs
E - Every vasculitis

235
Q

What drugs cause peripheral neuropathy

A

Isoniazid, Amiodarone, Leflunomide, Cisplatin

236
Q

Management of CMT

A

There is no cure or treatment to prevent progression. Neuro and genetics made a Dx, Physio, OT, Podiatrists, Analgesia, Ortho surg

237
Q

What is Guillain-Barré syndrome

A

An acute paralytic polyneuropathy that affects the PNS

238
Q

Patten of illness in GBS

A

Acute, symmetrical, ascending weakness and can also cause sensory Sx

239
Q

GBS causative organisms

A

Campylobacter jejuni, CMV and EBV

240
Q

GBS pathophysiology

A

molecular mimicry. B cells of the immune system create Ab against the antigens on the triggering pathogen and these Ab match proteins on the peri neurones causing damage to nerve cells, myelin sheath and nerve axon

241
Q

Presentation of Sx in GBS

A

Usually start within four weeks of the triggering infection. Begin in the feet and progress upwards, peak at 2-4 weeks then recovery. Reduced reflexes. Neuropathic pain. May spread to CN and cause facial weakness. Autonomic dysfunction may lead to urinary retention , ileus and heart arrhythmias

242
Q

What criteria tool is used to diagnose GBS

A

Brighton criteria

243
Q

What Ix can support a Dx of GBS

A

Nerve conduction studies (show reduced signal through the nerves) and LP (raised protein)

244
Q

Management of GBS

A

Supportive, VTE prophylaxis, IV Ig, Plasmapheresis

Resp failure: intubate, ventilate, admit to ICU

245
Q

Prognosis for GBS

A

Recovery can take months to years, most eventually fully recover or are left with minor Sx. Mortality is 5%

246
Q

What is neurofibromatosis

A

A genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system. They are benign but can cause neurological and structural problems. Type 1 is more common than type 2

247
Q

Neurofibromatosis type 1 genetics

A

Gene found on chromosome 17. Codes for a protein called neurofibramin which is a tumour suppressor protein. Autosomal dominant inheritance

248
Q

Features of Neurofibromatosis Type 1

A

CRABBING:
C - Cafe-au-lait spots
R - Relative with NF1
A - Axillary or inguinal freckling
BB - Bony dysplasia such as Bowing of the long vone or sphenoid wing dysplasia
I - Iris hamartomas
N - Neurofibromas
G - Glioma of the optic pathway

249
Q

What are neurofibromas

A

Skin-coloured, raised nodules or papules with a smooth, regular surface, two or more is signficicant

250
Q

Management of NF1

A

No treatment for the underlying disease, genetic tests are useful, monitor and manage Sx and complications

251
Q

Complications of NF1

A

Migraines, Epilepsy, Renal artery stenosis, Learning disability, Behavioural problems, Scoliosis, vision loss, Malignant peripheral nerve sheath tumours, GI stromal tumours, Brain tumours, Spinal cord tumours, Increased cancer risk

252
Q

Summarise NF2

A

On chromosome 22. Codes for merlin. Schwannomas are associated, autosomal dominant, NF2 is associated with acoustic neuromas

253
Q

What is tuberous sclerosis

A

autosomal dominant genetic condition that affects multiple systems

254
Q

Characteristic feature of tuberous sclerosis

A

Hamartomas which are benign growths. Commonly affect the skin, brain, lungs, heart, kidneys and eyes

255
Q

Tuberous sclerosis mutations

A

TSC1 gene on chromosome 9 which codes for hamartin
TSC2 gene on chromosome 16 that codes for tuberin

256
Q

Features of tuberous sclerosis

A

Ash leaf spots (depigmented areas of skin shaped like ash leaf), Shagreen patches (thickened, dimpled, pigmented patches), Angiofibromas (nose and cheek papules), Ungual fibromas (lumps in nail bed), Cafe-au-lait spots, Poliosis (patch of white hair on head, eyebrows

257
Q

Neurological features of Tuberous Sclerosis

A

Epilepsy, Learning disability, Brain tumours

258
Q

Other features of Tuberous Sclerosis

A

Rhabdomyomas, Angiomyolipoma, Lymphangioleiomyomatosis, Subependymal giant cell astrocytoma, Retinal hamartoma

259
Q

Management of tuberous sclerosis

A

No treatment for gene defect, management is supportive and tx complications. In some circumstances mTOR inhibitors (e.g. everolimus or sirolimus) may be used to suppress the growth of brain, lung or kidney tumours

260
Q

Red flags for headaches

A

Fever, photophobia or neck stiffness (Meningitis, enceph)

New neuro Sx (haemorrhage or tumour)

Visual disturbance (GCA, Glaucoma, tumour)

Sudden onset occipital headache (SAH)

Worse on coughing or straining (Raised ICP)

Postural, worse on standing, lying or bent over (raised ICP)

Vomiting (Raised ICP or CO poisoning)

Hx of trauma (Haemorrhage)

Hx of cancer (met)

Pregnancy (pre-eclampsia)

261
Q

Tx for chronic or frequent tension headaches

A

Amitriptyline

262
Q

Tx for prolonged case of sinusitis

A

steroid nasal spray or antibiotics (phenoxymethylpenicillin)

263
Q

When do hormonal headaches occur

A

Two days before and the first three days of the menstrual period. In the perimenopausal period and in early pregnancy

264
Q

Tx for hormonal headaches

A

Triptans and NSAID’s

265
Q

What is cervical spondylosis

A

Caused by degenerative changes in the cervical spine. Causes neck pain, made worse by movement and presents with headaches

266
Q

What is Trigeminal Neuralgia

A

Causes intense facial pain and 90% is unilateral pain. Described as electric shock like, shooting, stabbing, burning, can be triggered by touch, talking, eating, shaving and cold

267
Q

Tx for Trigeminal neuralgia

A

Carbamazepine

268
Q

What condition is trigeminal neuralgia more common in

A

MS

269
Q

Four main types of migraines

A

Migraine wiith aura, without aura, silent migraine (aura but no headache), Hemiplegic migraine

270
Q

Five stages of migraine

A

Permonitory/Prodromal stage, Aura, Headache, Resolution and Postdromal/Recovery

271
Q

Typical features of migraine

A

Unilateral, Moderate-Severe intensity, Pounding or throbbing, Photophobia, Phonophobia, Osmophobia, Aura, N/V

272
Q

What is an aura

A

Visual Sx most common, sparks in vision, blurred vision, lines across vision, loss of visual fields, tingling or numbness, dysphagia

273
Q

What is a hemiplegic migraine

A

Unilateral limb weakness, ataxia and impaired consciousness. Familial hemiplegic migraine is an autosomal dominant genetic condition. Can mimic a stroke or TIA

274
Q

Triggers of migraine

A

Stress, bright lights, Strong smells, Certain foods, Dehydration, Menstruation, Disrupted sleep, Trauma

275
Q

Acute management of migraine

A

NSAID’s. Paracetamol, Triptans, Antiemetics

276
Q

Explain Triptans

A

Serotonin receptor agonists and cause cranial vasoconstriction, Inhibit pain signals, Inhibit release of inflammatory neuropeptides

277
Q

Contraindications of triptans

A

HTN, Coronary artery disease, previous stroke

278
Q

Prophylactic medications for migraines

A

Propanolol, Amitriptyline, Topiramate

279
Q

Other options for migraine management

A

CBT, Meditation, Acupuncture, Vitamin B2

280
Q

Prophylactic triptans for menstrual migraines

A

Frovatriptan or zolmitriptan

281
Q

What is a cluster headache

A

Unbearable unilateral headache usually centered around the eye. Occur in clusters of attacks and then disappear

282
Q

Typical cluster headache pt

A

30-50 year old male smoker

283
Q

Sx of Cluster headaches

A

Red, swollen watering eye
Pupil constriction
Eyelid drooping
Nasal discharge
Facial sweating

284
Q

Management for cluster headaches

A

Triptans
high flow 100% O2

285
Q

Prophylaxis options for cluster headaches

A

Verapamil, Occipital nerve block, Prednisolone, lithium

Phase 3A Sam Harper (4 decks)

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