Neurology Flashcards

1
Q

STROKE

What is it?

A

Ischaemic infarction or brain haemorrhage

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2
Q

STROKE

Risk factors?

A
  • HTN
  • DM
  • HD
    -PVD
    Previous TIA
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3
Q

STROKE

Cause?

A
  • Vessel occlusion
  • Cardiac Emboli
    CNS bleeds e.g. aneurysm rupture
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4
Q

STROKE

Number of deaths?

A

1 per 1000 per year

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5
Q

Clinical Presentation of ACA Stroke

A

1) Leg weakness
2) Sensory disturbances in leg
3) incontinence
4) Gait apraxia (can move lying down but cant walk)
5) drowsiness

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6
Q

Clinical Presentation of MCA Stroke

A

1) Contralateral arm+leg weakness
2) Contralateral sensory loss
3) hemianopia
4) Aphasia (language impairment)
5) Dysphagia
6) facial droop

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7
Q

Clinical Presentation of PCA Stroke

A

1) contralateral hemianopia
2) Cortical blindness
3) Visual agnosia (inability to process sensory information)
4) facial blindness
5) Facial droop

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8
Q

Clinical Presentation of Lateral Medullary Infarct occlusion of PICA (brainstem)

A

1) ipsilateral horner’s syndrome
2) Vomiting
3) Vertigo (environment or you are spinning)
4) Cerebellar signs
5) Facial numbness

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9
Q

What is Horner’s syndrome characterised by?

A

classic triad of miosis (ie, constricted pupil), partial ptosis, and loss of hemifacial sweating (ie, anhidrosis).

Miosis
Ptosis
Anhidrosis

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10
Q

STROKE

tests?

A

ACT FAST

  • CT/MRI
  • ECG for MI/AF
  • CXR FOR LVH
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11
Q

STROKE

Posterior circulating stroke features?

A
  • Vomit/vertigo/nausea
  • Dysarthria/ speech impairment
  • motor deficit
  • locked in
  • visual disturbances
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12
Q

STROKE

Acute treatment? within 1 hour

A
  • protect airway

- check pulse, BP, ECG

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13
Q

STROKE

Within 4.5 hours?

A

thrombolysis (IV alteplase)

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14
Q

STROKE

how should a patient by hydrated?

A

IV so no choking.

food assistance and TED stockinga

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15
Q

STROKE

Primary prevention?

A
  • Reduce Risk Factors

statins, smoking, DM, HTN, exercise

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16
Q

STROKE

Secondary prevention

A
  • Antiplatelet (clopidogrel)
    + Aspirin
    + AF/BP treatment
  • Warfarin if cause was AF
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17
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Cause?

A

1) microemboli- which then lyse, from atheromas or thrombus

2) Temporary decrease in cerebral perfusion

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18
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Risk Factors?

A
  • HTN
  • DM
  • Smoking
  • Hyperlipidaemia
  • Obesity
  • High alcohol
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19
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

What is the definition?

A
  • Sudden onset focal neurological deficit with symptoms that are maximal at onset and usually resolve within 15 minutes
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20
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

carotid Symptoms?

A
  • Amaurosis Fugax (emboli in retinal artery)
  • Aphasia (language impairment)
  • Hemiparesis (one side weakness)
  • Hemisensory loss
  • Hemianopia visual loss
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21
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Vertebrobasilar symptoms?

A
  • Diplopia (double vision)
  • Vertigo/ vomit
  • Ataxia (lack of voluntary coordination of muscle movements)
  • tetraplegia
  • Hemisensory loss
  • choking and dysarthria (hard to speak)
  • hemianopia visual loss
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22
Q

What is Amaurosis Fugax?

A
  • progressive visual loss in one eye. ‘curtain descending’
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23
Q

TRANSIENT ISCHAEMIC ATTACK (TIA)

Investigation?

A
  • FBC, ESR, Glucose, lipids, U+E

CXR

ECG

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24
Q

What is a ABCD2 score?

A

Determines time frame needed to investigate a stroke (score of 6+ means 35.5% of stroke in next week)

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25
list the different reasons to get a point for the ABCD2 score?
- Age >60 = 1 point - BP >140/90 = 1 point - Unilateral weakness = 2 points - speech problems + weakness = 1 point - Duration >1 hour = 2 points <1 hour = 1 point - diabetes = 1 point
26
What investigations need to be done for a high/low ABCD2 score?
high = MRI & carotid doppler ultrasound within 24 hours low = same but within a week
27
treatment of TIA?
- control CVS risks - Aspirin + Clopidogrel - Carotid Endarterectomy if necessary within 2 weeks
28
SUBARACHNOID HAEMORRHAGE What is it?
spontaneous bleeding in sub-arachnoid space and they account for 5% of all strokes
29
SUBARACHNOID HAEMORRHAGE most common causes?
- berry aneurysm rupture 70% - arterio-venous malformations 15% - idiopathic 15%
30
Common sites for berry aneurysms?
1) bifurcation of middle cerebral 2) Junction of posterior and internal carotid 3) Junction of anterior communicating and anterior cerebral
31
SUBARACHNOID HAEMORRHAGE Symptoms?
- sudden onset of worst headache 'ever' - Vomit / nausea - loss of conciousness
32
SUBARACHNOID HAEMORRHAGE Signs
- Kernig's (inability to straighten knee when hip flexed 90 degrees) - Brudzinski's- neck stiffness - flex neck and knee+hip flex too
33
SUBARACHNOID HAEMORRHAGE Investigations?
CT (Blood in sulci) if negative do LP 12hrs after blood becomes yellow due to bilirubin and oxyhaemoglobin degradation ( Xanthochromia)
34
SUBARACHNOID HAEMORRHAGE Treatment?
- bed rest + supportive care - CCB's and control of HTN surgeon may be able to coil/ clip aneurysm
35
What is a subdural haemorrhage?
Bleeding from bridging veins between cortex and sinuses (below dura)
36
What is an extra-dural haemorrhage?
tear in dural venous sinus due to fractured temporal/parietal bone
37
How long do sub/extra dural haemorrhages take to develop? why do they take this long?
can take a very long time 1) pressure change is small 2) clot degrades 3) increased osmotic pressure - enlarges due to H20
38
investigation and treatment of sub/extra dural haemorrhages?
clot evacuation CT shows haematoma treatment - Surgery
39
INTRACEREBRAL STROKE Types? and what is the percentage of intracerebral out of all strokes?
Hypertensive Lobar 15% of all strokes
40
INTRACEREBRAL STROKE Clinical features?
1) Loss o consciousness 2) Stroke features 3) severe headache
41
Cause of hypertensive bleed?
Charcot-Bouchard aneurysm due to longstanding HTN Leaking due to microbleeds across the brain = bad prognosis
42
What are Lobar bleeds associated with?
dementia (B-amyloid deposition in vessel walls)
43
Features and location of hypertensive bleedas?
deep and small bleeds in the basal ganglia, pons and cerebellum
44
INTRACEREBRAL STROKE Investigations?
ABC and CT of head
45
what is Hydrocephalus?
blood in ventricles and clots them off small vessels become blocked so more ischaemia = immediate neurosurgery
46
INTRACEREBRAL STROKE Treatment?
BP control labetolol + GTN spray immediately
47
EPILEPSY Different types of seizures?
``` generalised Tonic-Clonic Seizure Absence Seizure Myotonic/clonic Akinetic/Atonic Motor seizure temporal Frontal occipital parietal ```
48
Describe a generalised tonic-clonic seizure
1) Period of ridgity (tonic) followed by rhythmical jerks (clonic) 2) Then drowsy/coma for a few minutes
49
describe an absence seizure
Cessation of activity and staring for a few seconds
50
describe a Clonic seizure
Isolated muscle jerking
51
Describe a Tonic Seizure
Stiffness of body
52
Describe an Atonic Seizure
loss of moving = falling and loss of consciousness
53
What happens if a partial seizure becomes a generalised seizure?
still classes as partial
54
describe a motor seizure
Motor cortex - jerky movements to contralateral limbs of seizure may be paralysis few hours later
55
What is the post-ictal state
After seizure headache, confusion, myalgia, weakness
56
Temporal Seizure effects?
visual/olfactory hallucinations. Deja vu Jemais vu - things feel unfamiliar
57
Frontal seizure effects?
speech/motor movement loss
58
EPILEPSY Cause?
unknown | flashing lights possibly
59
EPILEPSY Signs of EPILEPTIC?
- tongue bite - cyanosis - incontinence - head turn - less than 5 min - drowsy and muscle pain
60
EPILEPSY Signs of Syncope?
- Upright position, sweating and vomit before/after
61
EPILEPSY Signs of NON-EPILEPTIC?
- eyes closed - talking - crying - long duration
62
EPILEPSY Investigations?
MRI and video EEG
63
EPILEPSY Treatment of generalised TOnic-clonic?
Sodium Valproate or Lamitrigine
64
EPILEPSY Treatment of PArtial?
Carbomazepine
65
EPILEPSY Treatment of Absence?
same as GTC + ethosuximide Sodium valproate or Lamitrigine + ethosuximide
66
EPILEPSY treatment of tonic/ Myotonic/ Atonic
sodium valproate or Lamitrigine (avoid carbamazepine)
67
treatment of severe EPILEPSY?
surgery 1) lobe removal/ removal of problematic area | 2) Vagal Nerve stimulation
68
How does carbamezapine work?
1) Blocks Na+ channels = decreased firing of neurones and glutamate
69
Side effects of Carbamezapine?
``` Nausea vomiting drowsy double vision dizziness ```
70
how does valproate work?
1) Blocks transmembrane Na+ -stabilises neuronal membranes
71
Side effects of valproate?
hepatotoxicity hair loss increased appetite
72
When should you avoid using Valproate?
pregnant and hepatic disease patients
73
DEMENTIA What is the percentage change of someone to get dementia at the following ages : >65 >80 >100
5-10% >65 20%>80 70%>100
74
DEMENTIA Aetiology?
- Alzheimer's (65%) - vascular (25%) - lewy bodies (15-25%)
75
DEMENTIA What is inevitable for someone with Down's Syndrome?
Alzheimer's disease
76
DEMENTIA | Clinical Features of Alzheimer's?
1) Decrease in neurone number 2) neurofibrillary tangles 3) accumulation of B-amyloid plaques
77
DEMENTIA Symptoms of Alzheimer's?
INITAL = Memory loss over months/years progressions 1) All aspects of cerebral function 2) Decrease in language 3) Intellect, verbal and memory loss 4) Agnosia (cant recognise things) 5) Visuospacial skills lost
78
DEMENTIA General non cognitive symptoms?
- Aggression - Depression - Hallucinations - Agitation - Apathy
79
DEMENTIA tests?
MMSE CT for young patient Good history/ timeline required bloods- FBC, thyroid, LFTs, B12/folate (exclude other causes)
80
DEMENTIA treatment?
- Donepazil - Rivastigmine - SSRI's (depression)
81
When is Vascular Dementia common and how is it characterised?
Common after strokes characterised by periods of stability then sharp decline
82
what is Lewy Body Dementia?
- fluctuating cognition with variation of attention
83
Clinical features of Lewy Body Dementia?
- Hallucinations 2) Parkinson's 3) Sleep problems 4) Depression - may not have memory loss early on!
84
MULTIPLE SCLEROSIS Types?
- relapsing-remitting - primary Progressive (no Rx) - Secondary progressive
85
MULTIPLE SCLEROSIS Epidemiology?
1/1000 F:M 3:1
86
MULTIPLE SCLEROSIS Risk factors?
- Epstein-barr Virus - urban western living - low vitamin D - Female - Genetics
87
MULTIPLE SCLEROSIS pathology?
1) Antigens against CNS made due to exposure to a similar antigen (e.g. EBV) 2) T-lymphocytes cause problems when they cause the blood-brain barrier
88
MULTIPLE SCLEROSIS Cause?
- Demyelination of oligodendrocytes and axonal damage - Myelin recovers whereas the axons don't - Shorter gaps between the Nodes of Ranvier due to thin myelin = slow conduction
89
MULTIPLE SCLEROSIS Where is inflammation likely to be found?
Brain = Ventricles Spinal Cord = Posterior column
90
MULTIPLE SCLEROSIS clinical Features?
1) Optic neuritis 2) Pain 3) Spasticity 4) paraesthesia (pins and needles) 5) Bladder/sexual dysfunction 6) Nystagmus (involuntary eye movement) 7) vertigo 8) Diplopia (double vision)
91
MULTIPLE SCLEROSIS Exacerbating factors?
- STRESS | - HOT TEMP
92
MULTIPLE SCLEROSIS diagnosis?
- >2 CNS symptoms disseminated in time and space - MRI shows plaques/inflammatory lesions around ventricles IgG monoclonal bands
93
MULTIPLE SCLEROSIS Treatment of Acute relapse?
Steroids Vit D and stress free
94
MULTIPLE SCLEROSIS Treatment?
1) Interferon beta (prevents immune activation) 2) glatiramer acetate (similar to myelin) 3) Natalizumab prevents t-lymphocytes crossing blood-brain barrier
95
MULTIPLE SCLEROSIS Lifestyle adaptations?
- vit D supplements and stress free
96
MULTIPLE SCLEROSIS medicine for Spasticity?
baclofen
97
MULTIPLE SCLEROSIS medicine for Tremors?
Beta blockers
98
MULTIPLE SCLEROSIS Medicine for incontinence
Tolterodine Oxybutynin
99
PARKINSON'S Pathology?
- Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones In the substantia nigra pars compacta - Synuclein deposition leads to Lewy bodies and decreased dopamine
100
PARKINSON'S Aetiology?
Mitochondrial DNA dysfunction and oxidation stress Idiopathic
101
PARKINSON'S Risk Factor genes?
SNCA and PRKN genes
102
PARKINSON'S Cardinal Triad?
1) Tremor 2) Ridgity 3) Bradykinesia
103
PARKINSON'S Describe the Tremor
- worse at rest - 'pill rolling' of thumb over fingers - asymmetrical and gradual
104
PARKINSON'S Describe the Ridgity
- Cogwheel ridgity - Whole ROM is rigid - Felt especially through rapid pronation/supination
105
PARKINSON'S Describe Bradykinesia>
- slow initiation of movements - Shuffle steps - Decreased arm swing - Freezing at obstacles - Slow blinking
106
PARKINSON'S Postural Effects?
- Shuffle - Stoop - Decreased arm swing - poor balance
107
PARKINSON'S Non motor effects?
- Depression - constipation - Micrographia (abnormally small, cramped handwriting) - Dementia
108
PARKINSON'S tests?
Ct to exclude other causes
109
PARKINSON'S treatment?
1) Postural Exercises 2) L-Dopa and Carbidopa 3) Dopamine Agonists 4) MAO-B Inhibitors 5) COMT inhibitors
110
Give an example of a Dopamine Agonist
Ropinirole
111
Give an example of a MAO-B inhibitor
Rasagiline
112
Give an example of a COMT inhibitor
Entacapone
113
What is the function of COMT and MAO-B enzymes?
convert Dopamine into DOPAC + HVA. To treat Parkinson's we need as much dopamine as possible therefore these enzymes need to be inhibited
114
BRAIN TUMOURS Name some different types and their percentage of occurrence
Primary Malignant (35%) Benign (15%) Metastases (50%)
115
BRAIN TUMOURS Of Primary malignant BT's, how many are Astrocytomas and how many are oligodendrogliomas?
Astrocytomas (90%) oligodendrogliomas (5%)
116
BRAIN TUMOURS a brain tumour will cause an increased intra-cranial pressure, what effects would this pressure increase have
Headache + confusion headache worsens: 1) Morning 2) leaning forward 3) cough/straining
117
BRAIN TUMOURS Pathology of an increased ICP
1) brain displaced downwards 2) Pressure on brainstem 3) drowsiness and respiratory depression
118
BRAIN TUMOURS Clinical presentation? (apart from raised ICP)
- neurological deficit (depending where the tumour is) | - focal epilepsy (need a CT to exclude a tumour if someone has a new seizure)
119
BRAIN TUMOURS Tests?
CT/MRI and PET scan
120
BRAIN TUMOURS Treat?
Surgery/radiotherapy
121
BRAIN TUMOURS what is given for rapid relief of symptoms?
IV Dexamethasone
122
What does Dexamethasone do?
reduce cerebral oedema
123
Where the most common sites of Mets to the brain?
- lung - breast - colon - skin - kidney
124
BRAIN TUMOURS Any associated mutations?
50% of tumours have methylated MGMT mutation
125
BRAIN TUMOURS What does having a methylated MGMT mutation mean?
Sensitive to Temozolomide so a better prognosis
126
BRAIN TUMOURS What may mean a good prognosis for someone with a brain tumour?
- under 50 IDH mutation MGMT mutation
127
What may mean a bad prognosis for someone with a brain tumour?
- over 50 | - no IDH or MGMT mutation
128
What is Kernig's and brudzinski's signs?
- Kernig's (inability to straighten knee when hip flexed 90 degrees) - Brudzinski's- neck stiffness - flex neck and knee+hip flex too
129
MENINGITIS cause?
Meningococcus or Pneumococcus immunocompromised = Cryptococcus Unvaccinated = H.influenzae Elderly = S.pneumoniae
130
MENINGITIS Early Clinical Features?
1) Headache 2) Fever 3) kernig's sign 4) brudzinksi's sign
131
MENINGITIS later Clinical Features?
- Decreased consciousness - Stiff neck - Photophobia - Non-blanching petechial rash - Seizures
132
MENINGITIS Investigations?
1) Blood cultures 2) Lumbar Puncture 3) IV cefotaxime 4) Head CT 5) Bacterial + viral throat swabs 6) PCR for meningococcus and Pneumococcus
133
MENINGITIS When should you not do a lumbar puncture
When there is a risk of cerebral coning
134
MENINGITIS When should a CT be done first?
If raised ICP
135
MENINGITIS How would bacterial lumbar puncture look?
- cloudy - high neutrophils - low CSF - high protein
136
MENINGITIS How would a viral Lumbar Puncture look?
- Clear - high lymphocytes - normal CSF - Normal to high protein
137
MENINGITIS Which is more serious bacterial or viral?
bacterial, there is also no rash with viral
138
MENINGITIS treat?
IMMEDIATELY = IV Cefotaxime and ampicillin also IV Dexamethasone
139
ENCEPHALITIS What is it?
Inflammation of brain parenchyma
140
ENCEPHALITIS Clinical features?
- Altered mental state - motor and sensory deficits 1) fever 2) headache 3) loss of consciousness 4) lethargy PROGRESSES into seizures
141
ENCEPHALITIS Cause?
Usually virally by Herpes Simplex Virus immunocompromised are at risk
142
ENCEPHALITIS investigation|?
1st- CT | 2nd- LP for viral findings
143
ENCEPHALITIS Treatment?
IV acyclovir IMMEDIATELY
144
What is Shingles?
reactivation of dormant Herpes zoster virus in dorsal root ganglion
145
Features of Shingles?
dermatome distribution of pain and a rash (papules and vesicles)
146
Treatment of shingles?
PO Acyclovir
147
Headache red flags?
1) papilloedema (optic disc swelling that is caused by increased intracranial pressure) 2) seizure 3) Cancer history
148
Urgent referrals for headache?
- suspected Meningitis - thunderclap headache - Red eye (glaucoma)
149
What is Aura?
Patient knows about a seizure e.g. strange feeling in gut
150
Migraine Diagnostic Criteria without Aura?
1) >5 attacks 2) they last 4-72 hours 3) Nausea/Vomiting 4) unilateral/Pulsating 5) aggravated by movement
151
20% of migraines have aura, what may this be?
1) Flashing lights (visual) 2) tingling (sensory) 3) Dysphagia (speech)
152
Partial triggers of headaches? (50%)
``` Chocolate Hangovers Orgasm Cheese Oral contraceptives Lie ins Alcohol Tumult (loud noise) Exercise ```
153
abortive treatment of headaches?
NSAIDs/paracetamol | + PO rizatriptan (migraines)
154
Preventative treatment for migraines?
1st- propranolol or amitriptyline or topiramate 2nd- valproate/Botulinum toxin type A
155
How do migraines happen?
1) changes in brainstem blood flow = unstable trigeminal nuclei 2) Inflammatory mediators released 3) These impact on trigeminal nerve nucleus
156
MOTOR NEURONE DISEASE characteristics?
- Relentless and unexplained destruction of: - UMN - anterior horn cells cranial nerve nuclei
157
MOTOR NEURONE DISEASE what does it never affect?
- Sensory - Ocular movement (eye) - sphincters
158
MOTOR NEURONE DISEASE What will most people die of if they have MND within 3 years?
Respiratory failure - bulbar palsy / pneumonia
159
MOTOR NEURONE DISEASE Cause?
oxidative stress and free radicals
160
What is Oxidative stress
Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants
161
MOTOR NEURONE DISEASE Clinical features of Amyotrophic lateral Sclerosis (50%)
- Lateral corticospinal tracts and anterior horn cells affected; 1) Progressive spastic tetraplegia 2) Split hand sign; thumb side of hand appears separated due to excessive wasting (thenar muscles disproportionately wasted as compared to the hypothenar muscles)
162
MOTOR NEURONE DISEASE what does Progressive muscle Atrophy affect (10%)
- LMN lesion - distal 1st to be affected - NO UMN signs
163
MOTOR NEURONE DISEASE what does Progressive Bulbar Palsy affect (10%)
Cn 9-12 affected LMN lesion of: tongue (fasciculations) speech - dysarthria swallowing dysphagia
164
MOTOR NEURONE DISEASE give examples of UMN signs?
- Spasticity - brisk reflexes - Upgoing plantars (Babinski reflex) SEE TABLE IN NOTES
165
What is the Babinski reflex?
when the sole of the foot is stimulated with a blunt instrument. The reflex can take one of two forms. In normal adults, the plantar reflex causes a downward response of the hallux. An upward response of the hallux is known as the Babinski response
166
MOTOR NEURONE DISEASE LMN signs?
- Wasting - tongue fasciculations - abdo,back,thigh fasciculations SEE TABLE IN NOTES
167
MOTOR NEURONE DISEASE Investigations?
1) EMG - shows muscle degeneration (electromyography) | 2) MRI + LP (exclude inflammatory types)
168
MOTOR NEURONE DISEASE treatment? ``` Drug dysphagia Resp failure Drooling spasticity ```
``` 1) Riluzole (blocks Na+ channels = less glutamate) PEG feeding - Dysphagia ventilatory support -resp failure amitriptyline - Drooling Baclofen - spasticity ```
169
MYASTHENIA GRAVIS Epidemiology?
40-60s, mainly women
170
MYASTHENIA GRAVIS Pathology>
- Autoimmune disease mediated by A-bodies to nicotinic ACh receptors - both T/B cells involved - Depletion of Post-synaptic receptors
171
MYASTHENIA GRAVIS Associations?
50 years - Thymic hyperplasia / atrophic / tumour
172
MYASTHENIA GRAVIS Clinical Features?
Fatigability of muscle on sustained activity that gets better with rest Ocular muscles affected 1st then moves down speech chewing swallowing breathing
173
MYASTHENIA GRAVIS Specific features?
- ptosis (eye-lid droop) - diplopia (double - vision) - Voice fade
174
MYASTHENIA GRAVIS Diagnostic test?
ask patient to hold up arms and they will fall
175
MYASTHENIA GRAVIS Scientific investigations?
- Autoantibodies to AChR in 90% of cases - Autoantibodies to MuSK - CT of thymus - See if ptosis improves by 2mm when ice applied for >2 mins
176
MYASTHENIA GRAVIS treatment?
1st - symptom control - Pyridostigmine (anticholinesterase) 2nd - Steroids (prednisolone) 3rd- thymectomy
177
TENSION HEADACHES Cause?
Depression and anxiety
178
TENSION HEADACHES Diagnostic Criteria?
1) >10 2) Last 30 mins - 7 days 3) 2 of: bilateral pain, pressing/tightening 4) mild/moderate 5) Not triggered by exercise
179
TENSION HEADACHES treat?
paracetamol/NSAIDs - not overusing analgesia
180
CLUSTER HEADACHES Diagnostic Criteria
1) >5 2) Severe 3) unilateral 4) temporal/orbital pain 5) 15-180 mins 6) Restlessness and agitation 7) Occurs every other day, as many as 8 each day
181
CLUSTER HEADACHES Acute Treatment?
100%O2 for 15 mins | Subcutaneous Sumatriptan
182
TRIGEMINAL NEURALGIA What is it?
Compression on trigeminal root e.g. aneurysm or tumour
183
TRIGEMINAL NEURALGIA Diagnostic criteria
- Severe, stabbing pain lasting seconds-mins | - Precipitated by stimuli to the face
184
TRIGEMINAL NEURALGIA Treat?
carbamazepine
185
CAUDA EQUINA SYNDROME Where does the spinal cord end
L1/L2
186
CAUDA EQUINA SYNDROME cause?
Lumbar disc prolapse - L4-L5 and L5-S1
187
CAUDA EQUINA SYNDROME associated with?
bladder and bowel dysfunction | and perianal numbness (saddle paraesthesia)
188
CAUDA EQUINA SYNDROME Signs?
1) back pain 2) leg weakness 3) Numbness 4) decreased reflexes
189
CAUDA EQUINA SYNDROME treat?
MRI of spine and surgical decompression
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NEUROPATHIES Cause?
acute compression and entrapment
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NEUROPATHIES Common mononeuropathies?
median ulnar common peroneal radial- (wrist drop)
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POLYNEUROPATHIES Sensory Symptoms?
- Pins and needles - Numbness - Pain in extremities - Tingling 'glove and stocking' - numbness in distal areas (hands and feet)
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POLYNEUROPATHIES Motor symptoms?
weakness
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POLYNEUROPATHIES Autonomic Symptoms?
- Postural Hypotension - erectile dysfunction - Sweating - diarrhoea
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POLYNEUROPATHIES Causes?
``` Diabetes Alcohol Vit B12 deficiency Infections (Guillain-Barre) Drugs (isoniazid) ```
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POLYNEUROPATHIES treatment?
- weak opiates - SSRI's/TCAs - treat cause - Physiotherapy
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CARE OF UNCONCIOUS PATIENT What are the severity ranges on the Glasgow coma score?
mild >13 moderate 9-12 severe <8
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CARE OF UNCONCIOUS PATIENT What cant they do?
1) gag 2) Circulating depression 3) cant maintain airway 4) No protection
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CARE OF UNCONCIOUS PATIENT 1st line treatment?
basic life support
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CARE OF UNCONCIOUS PATIENT Acute life support is made up of?
1) Intubation 2) IV fluids 3) Drugs to maintain circulation 4) venous access
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CARE OF UNCONCIOUS PATIENT Intensive care?
same as acute ,life support +: - catheter - tracheal suction - nutrition - pressure sore prevention
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GIANT CELL ARTERITIS who is it common in?
elderly
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GIANT CELL ARTERITIS Symptoms?
1) Scalp tenderness 2) headache 3) Amaurosis Fugax (blind in 1 eye)
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GIANT CELL ARTERITIS Extracranial symptoms?
1) Dyspnoea 2) Morning stiffness 3) Unequal weak pulses
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GIANT CELL ARTERITIS Investigations?
RAISED- ESR, CRP, platelets, Alkaline phosphate - low Hb - temporal Artery Biopsy
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GIANT CELL ARTERITIS treatment?
immediate prednisolone | delay the risk of irreversible bilateral vision loss
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HUNTINGTON'S Features of Huntington's?
- Chorea (involuntary movements) - personality change - Dementia -
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HUNTINGTON'S what is it and what are its genetic components
-Incurable neurodegenerative disorder - Autosomal dominant - expansion of CAG repeat on chromosome 4 that produces mutant Huntington protein
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HUNTINGTON'S How does someone die of Huntington's?
loss of basal ganglia neurones/ GABA/ ACh until death
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SPINAL CORD COMPRESSION Aetiology?
- Secondary malignancy in spine from (breast, kidney, lung, prostate, thyroid) BKLPT
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SPINAL CORD COMPRESSION features?
weak legs sensory loss spinal pain arm weakness often less severe
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SPINAL CORD COMPRESSION Signs?
Look for motor sensory and reflexes 1) normal above the lesion 2) LMN signs at the level of the lesion 3) UMN signs below the level of the lesion
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SPINAL CORD COMPRESSION Investigations?
Instant MRI screening bloods and biopsy CXR to check for lung malignancy
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SPINAL CORD COMPRESSION Treatment?
Malignant = IV Dexamethasone while waiting for Chemo/Radio
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GUILLAIN-BARRE SYNDROME | What is it?
Acute inflammatory demyelinating polyneuropathy
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GUILLAIN-BARRE SYNDROME key clinical feature?
Progressive symmetrical ascending weakness (starting at the feet and moving up the body) Reduced reflexes There may be peripheral loss of sensation or neuropathic pain It may progress to the cranial nerves and cause facial nerve weakness
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GUILLAIN-BARRE SYNDROME Cause?
Infective triggers (commonly post campylobacter gastroenteritis or EBV/CMV) cause antibodies to attack nerves
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GUILLAIN-BARRE SYNDROME How may death occur?
autonomic neuropathy = cardiac arrest
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GUILLAIN-BARRE SYNDROME Investigation?
1) lumbar puncture - rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66% 2) nerve conduction studies may be performed - decreased motor nerve conduction velocity (due to demyelination) - prolonged distal motor latency - increased F wave latency
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GUILLAIN-BARRE SYNDROME treatment?
IV immunoglobulins for 5 days and plasma exchange
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What is Hydrocephalus?
abnormal build up of CSF (cerebrospinal fluid) in the cavities (ventricles) of the brain. The build-up is often caused by an obstruction that prevents proper fluid drainage
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What does interferon beta do?
prevents immune activation1) Interferon beta (prevents immune activation
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What is glatiramer acetate similar to?
Myelin
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what does Natalizumab do?
prevent t-lymphocytes crossing the blood-brain barrier
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classic triad of Meningitis?
- Photosensitivity - Stiff neck - Headache