Neuro Flashcards
(298 cards)
1
Q
Name the causes of epilepsy
A
Idiopathic
Genetics
Brain trauma
Strokes
Infectious diseases
Developmental disorders
2
Q
Name the types of focal seizures
A
Simple-no LOC
Complex-Impaired consciousness
Secondary generalised-evolves into generalised
3
Q
Name the types of generalised seizures
A
Absence-<10 seconds
Tonic clonic-stiffening and jerkin of limbs
Myoclonic-sudden jerking of lib, trunk or face
Atonic-sudden loss of muscle tone, patient falls but no LOC
4
Q
Name some differentials for epilepsy
A
Syncope
TIA
Migraines
Panic disorder
5
Q
Name some investigations used to diagnose epilepsy
A
Clinical history
Neuro exam
EEG
CT/MRI
Video EEG telemetry may be used in some cases
6
Q
When are anti-epileptics generally started
A
Following second epileptic seizure
7
Q
Under what circumstances might antiepileptics be started after the first seizure
A
Neurological deficit
Brain imaging shows a structural abnormality
EEG shows unequivocal epileptic activity
Patient/family or carers consider risk of having further seizure unacceptable
8
Q
Describe the treatment for generalised tonic clonic seizures in males
A
Sodium valproate
9
Q
Describe the treatment for generalised tonic clonic seizures in females
A
Lamotrigine or levetiracetam
10
Q
What is the first line treatment for focal seizures?
A
Lamotrigine or levetiracetam
11
Q
What is the second line treatment for focal seizures
A
Carbamazepine
Oxcarbazepine
Zonisamide
12
Q
What is the first line treatment for absence seizures?
A
Ethosuximide
13
Q
What is the second line treatment for absence seizures
A
Male-sodium valproate
Female-Lamotrigine or levetiracetam
14
Q
Which medication can exacerbate absence seizures?
A
Carbamazepine
15
Q
What is the treatment for myoclonus seizures in men?
A
Sodium valproate
16
Q
What is the treatment for myoclonic seizures in females
A
Levetiracetam
17
Q
What is the treatment for tonic/a tonic seizures in males?
A
Sodium valproate
18
Q
What is the treatment for tonic/atomic seizures in females
A
Lamotrigine
19
Q
Name some complications of epilepsy
A
Status epilepticus-lasts >5 minutes
Psychiatric conditions
Sudden unexpected death in epilepsy(SUDEP)
20
Q
What are the side effect of topiramate
A
Abdo pain
Cognitive impairment
Confusion
Mood changes
Muscle spasm
Nausea and vomiting
Neohrolithiasis
Tremor
Weight loss
21
Q
Name some side effects of lamotrigine
A
Blurred vision
Arthralgia
Ataxia
Diarrhoea
Dizziness
Headache
Insomnia
Rash
Tremor
22
Q
What are the side effects of carbamazepine
A
Ataxia
Blood disorders
Blurred vision
Fatigue
Hypo stream is
Skin problems
23
Q
What are the side effects of sodium valproate
A
Ataxia
Anaemia
Confusion
Gastric irritation
Haemorrhage
Hyponatraemia
Tremor
Weight gain
24
Q
How long do you have to wait to drive after a one off seizure?
A
6 months
24
What are the side effects of phenytoin
Acne
Anorexia
Constipation
Dizziness
Gingival hypertrophy
Hirsutism
Insomnia
Rash
Tremor
25
How long do you have to wait to drive after more than one seizure?
1 year
26
How long doo you have to wait to drive after a change in anti-epileptic medication?
6 months
27
How long do you have to wait to drive a bus/coach/lorry after a one off seizure?
5 years
28
How long do you have to wait to drive a bus/coach/lorry for multiple seizures
10 seizure free yearss
29
Define essential tremor
Chronic neurological condition that typically manifests as an involuntary shaking or trembling
30
Describe the epidemiology of essential tremor
Highly prevalent
Incidence increases with age
Age of onset earlier in those with a family history
31
Describe the aetiology of essential tremor?
Genetic and environmental factors
32
Describe the inheritance pattern in the majority of essential tremor cases
Autosomal dominant
33
What effect does alcohol have on the symptoms of essential tremor?
Alcohol can temporarily improve the tremor
34
Describe the symptoms of essential tremor
Main: postural or kinetic tremor which predominantly effects the upper limbs distally
Less commonly effects the head, lower limbs, voice, tongue, face and trunk
Increased tremor amplitude over time-difficulty with ADL’s
Exacerbation of tremor during ties of stress, anxiety and social interaction
35
Name some differentials for essential tremor
Parkinson’s
Hyperthyroidism associated tremor
Dystonic tremor
36
What investigations should be done in someone presenting with essential tremor?
Mainly clinical diagnosis
Rule out other causes e.g. with Neuro imaging or TFT’s
Evaluation of functional and psychosocial disabilities performed to determine need for pharmacotherapy
37
Describe the pharmacological management of essential tremor
Propranolol
Primidone
Topiramate
Gabapentin
Clonazepam
38
Describe the surgical management of essential tremor
DBS
Focused ultrasound thalamtomy
Radiosurgical (gamma knife) thalamotomy
39
Describe the epidemiology of Parkinson’s disease
Second most common Neuro degenerative disorder
40
Describe the aetiology and pathophysiology of Parkinson’s
Accumulation of Lewy bodies that lead to neuronal death of the dopaminergic cells of the substantia nigra of the basal ganglia
41
What are Lewy bodies?
Intracellular inclusions primarily composed of misfolded alpha synuclein
42
What is the triad of Parkinson’s?
Bradykinesia
Tremor
Lead pipe rigidity
43
Describe the tremor associated with Parkinson’s
Asymmetric 3-5Hz ‘pill-rolling’ tremor
44
Describe a Parkinsonian gait
Small shuffling steps, slow movement especially on initiating and turning, flexed posture
Asymmetric tremor
45
What is cogwheeling?
Jerkiness felt when testing a patient’s muscle tone
Seen in Parkinson’s
46
Name some non-motor features of Parkinson’s disease?
Autonomic dysfunction (constipation, postural hypotension erectile dysfunction)
Olfactory loss
Sleep disorders like REM behavioural disorders
Psychiatric features-depression anxiety, hallucinations
47
What is hypomimic facies and what condition is it seen in?
Reduced facial expression
Parkinson’s
48
In a patient with features of Parkinson’s and early and prominent autonomic dysfunction what condition should be considered
Multiple System Atrophy
49
In a patient with features of Parkinson’s an early and prominent cognitive dysfunction what condition should b considered?
Dementia with Lewy bodies
50
Name some key differentials of Parkinson’s disease
Multiple System Atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasilar degeneration
Wilsson’s disease
Dementia pugilistica
51
How is Parkinson’s disease diagnosed?
Clinical diagnosis, supported by positive response to treatment trials
MRI head/dopamine transporter scan(DaT scan) in atypical cases
52
What can exclude a diagnosis of idiopathic Parkinson’s disease?
Absolute failure to respond to 1-1.5g of levodopa daily
53
What are the main medications used to treat Parkinson’s disease?
Levodopa
Dopamine agonists
MAO-B Inhibitors
COMT inhibitors
Amantadine
Anticholinergic agents
54
Name the peripheral side effects of levodopa
Postural hypotension
Nausea and vomiting
55
How can peripheral side effects from levodopa treatment be reduced?
Co-administration of a peripheral dopa decarboxylase inhibitor like
CARBIDOPA
56
57
What can be used to treat nausea from levodopa therapy?
Domperidone
Acts as a peripheral dopamine antagonist
58
Name the central side effects of levodopa therapy
Hallucinations
Confusion
Dyskinesia
Psychosis
59
60
Why is levodopa treatment for parkinson’s problematic?
Can become less effective
End-of-dose effects: motor activity progressively declines as previous dose wear off
On-off phenomenon: random fluctuations in drug effect
60
Name some dopamine agonists
Ropinirole
Rotigotine
Apomorphine
61
How long does it typically take to develop complete loss of response too levodopa
2-5 years
62
Why is cabergoline less commonly used now?
Associated with lung fibrosis
63
What needs to be monitored for in patients on dopamine agonists?
Autoimmune haemolytic anaemia-regular FBC’s and DAT scans
64
What is the most potent dopamine agonist and how is it given?
Apomorphine
Given subcutaneously
65
Name some examples of MAO-B inhibitors
Selegiline
Rasagiline
66
How do MAO-B inhibitors work for patients with Parkinson’s disease?
Reduce dopamine breakdown peripherally so increase the central uptake of levodopa-often used in conjunction
67
What should you be cautious of in patients on MAO-B inhibitors?
Serotonin syndrome
68
Name some COMT inhibitors
Entacapone
Tolcapone
69
How do COMT inhibitors work for patients with Parkinson’s
Extend the use of levodopa
70
What drug class is amantadine
NMDA receptor antagonist
71
Give some examples of anticholinergic agents
Procyclidine
Trihexyphenydil
72
Describe the surgical management of parkinson’s
DBS: typically done by implanting a stimulating device into a target area of the brain, often thalamus or subthalamus
73
Describe the prognosis of those with Parkinson’s
Little to no change in life expectancy
Some will have significant disability, others will not progress as fast
74
What are motor neurone diseases?
Groups of progressive neurological disorders that destroy motor neurones
75
Describe the epidemiology of MND
Slight 2:1 mile predominance
Mean onset: 50-60 years
90% of cases are sporadic, 10% familial
76
What condition has a notable overlap in genetics with MND?
Frontotemporal dementia
77
78
Name some upper motor neurone signs
Spasticity
Hypereflexia
78
Describe the aetiology of MND
Misfolding of TDP-43 protein in many cases
Can be an inherited condition
2% of cases associated with a mutation in the SOD-1 gene
78
Name some lower motor neurone signs
Fasciculations
Muscle atrophy
Hyporeflexia
78
Describe the main features of ALS
Typically LMN signs in arms and UMN signs in legs
Familial cases: gene lies on chromosome 21
78
What are the types of MND?
Amyotrophic lateral sclerosis
Primary lateral sclerosis
Progressive multiple atrophy
Progressive bulbar palsy
78
Describe the features of progressive bulbar palsy
Palsy of the tongue, uncles of chewing/swallowing and facial muscles due to loss of function f brain stem motor nuclei
Carries the worst prognosis
78
Are eye and sphincter muscles typically involved in MND?
No-usually spared until late in disease course
78
What is the most common type of MND
ALS-50% of patients
78
Name some differentials of MND
Thyrotoxicosis syndrome
Paraprotinemias
Brain stem lesions
Cervical spondylopathy
Myasthenic syndromes
Chronic inflammatory demyelinations polyneuropathy
Multi focal mononeuropathy
78
Describe the features of primary lateral sclerosis
UMN signs only
78
Describe thee features of progressive muscular atrophy
LMN signs only
Affects distal muscles before proximal
Carries best prognosis
79
Name some investigations for MND
TFT’s
Protein electrophoresis: rule out paraproteinaemias
MRI of brain/spinal cord-rule out brain stem lesions or cervical spondylopathy
EMG and nerve conduction studies
80
Describe the management of MND
Riluzole-only disease modifying drug but only extends life expectancy by 3 months
Non invasive ventilation in patients with type 2 reps failure
Anticholinergics for drooling
Supporting feeding via NG/PEG feeding for bulbar diseaseAdvanced care plan in advance
81
Describe the prognosis for MND
Poor-life expectancy from diagnosis less than 5 years
Most patients die from respiratory complications
82
What is an extradural haematoma?
Collection of blood between the dura mater(outermost meningeal layer) and the inner surface of the skull
83
Which blood vessel is most commonly involved in an extradural haematoma and why?
Middle meningeal artery->thin skull at the pterion overlies the middle meningeal artery
84
Describe the epidemiology of an extradural haematoma?
Young patients
Head injury e.g. from sports or road traffic accident
85
Describe the characteristic clinical presentation/history of an extradural haematoma
1)Initial, brief loss of consciousness post initial trauma
2)Lucid interval(regained consciousness and apparent recovery)
3)Subsequent deterioration of consciousness and headache onset
86
What is the pathology behind the lucid interval in an extradural haematoma?
The dura mater underneath tears, the pressure falls temporarily & the patient regains consciousness. The pressure then rebuilds = LOC.
87
Describe the pathophysiology behind what happens after the lucid interval of an extradural haematoma
Haematoma expands->uncus of temporal lobe herniates around the tentorium cerebelli
88
What finding may be seen on physical examination of a patient with an extradural haematoma and why?
Fixed dilated pupil
Parasympathetic fibres of CN3 compressed by herniation of the uncus of the temporal lobe around the tentorium cerebelli
89
Name some differentials of an extradural haemorrhage
Subdural haematoma
SAH
Intracerebral haemorrhage
Cerebral contusion
90
What investigations should be carried out to diagnose an extradural haematoma?
CT scan
91
What would you expect to see on a CT head of a patient with an extradural haematoma
Biconvex/lentiform, hyperdense collection limited by the suture lines of the skull
Most commonly unilateral and supratentorial
92
Describe the management of a patient with an extradural haemorrhage
No neurological deficit: conservative management->supportive therapy, radiological observation
Definitive: craniotomy and evacuation of haematoma
93
What is a subdural haemorrhage?
Accumulation of venous blood in the potential space between the dura mater and the arachnoid mater of the brain
94
What percentage of subdural haemorrhages are bilateral?
Adults: 15%
Infants: 80%
95
Describe the difference in time frame of acute, subacute and chronic subdural haemorrhages
Acute: symptoms develop within 48 hour post injury-rapid neurological deterioration
Subacute: Days-weeks post injury-gradual progression
Chronic: Weeks to months-may not remember specific head injury
96
Describe the epidemiology of a subdural haematoma
Mostly elderly individuals :>65 years
97
Name some risk factors for developing a subdural haemorrhage
>65 years
Anticoagulants
Chronic alcohol use
Young infants-shaken baby syndrome
Recent trauma
98
Why are the elderly and alcoholics more at risk of a subdural haemorrhage?
Brain atrophy-> fragile, taut bridging veins
99
What is the pathological process that causes a subdural heamorrhage?
Rupture of bridging veins within the subdural space
100
Describe the classical history of a patient presenting with a subdural haemorrhage
History of head trauma-> lucid interval-> fluctuation and eventual decline in consciousness
101
What neurological signs/symptoms might a patient with a subdural haemorrhage have?
Altered/fluctuating mental status
Focal neurological deficits
Headaches
Memory loss
Seizures
Personality changes
Cognitive impairment
102
What examination findings might be present in a patient with a subdural haematoma?
Signs of increased ICP:
-Papilloedema
-Cushing's triad: bradycardia, widened pulse pressure, irregular respirations
Others:
-Gait abnormalities
-Hemiparesis/hemiplegia-midline shift and mass effect
-Pupillary changes-unilateral dilated pupil-CNS compression
103
What investigation should be used to diagnose a subdural haemorrhage?
CT scan head
104
What would you expect to see on a CT scan of a patient with a subdural haemorrhage?
Crescent shaped, not restricted by suture lines
Hyperacute(<1hour)-isodense
Acute(<3 days)-hyperdense
Subacute(3 days-3 weeks)-isodense
Chronic(>3 weeks)-hypodense
105
Describe the management of a subdural haemorrhage?
Conservative-monitor ICP
Acute: decompressive craniotomy
Chronic: burr holes
106
What is a subarachnoid haemorrhage?
Blood within the subarachnoid space(under arachnoid mater)
107
Describe the epidemiology of subarachnoid haemorrhage
Mc in females
Peak incidence: 40-50 years
108
What is the most common cause of subarachnoid haemorrhage?
Head injury
109
What is the most common cause of spontaneous subarachnoid haemorrhage?
Berry aneurysm-85%
110
Name some risk factors for a Berry aneurysm
Hypertension
Adult polycystic kidney disease
EDS
Coarctation of aorta
111
Name some causes of a SAH besides a Berry aneurysm
AVM's
Pituitary apoplexy
Mycocytic(infective) aneurysms
112
Describe the symptoms of a SAH
Sudden onset 'thunderclap' headache
History of previous less severe sentinel headache
Altered consciousness
Nausea and vomiting
Seizures
Meningism: photophobia, neck stiffness
113
Name some signs that may be seen on physical examination of a patient with a SAH
Fundoscopy-> retinal haemorrhage
Positive Kernig's/Brudzinski's sign
Focal neurological deficits (CN3, 4, 6 compression-diplopia, visual disturbances, aphasia, hemiparesis/plagia)
114
What is the first line investigation used to diagnose a SAH?
Non contrast head CT
115
What would you expect to see on a CT scan of a patient with a SAH?
Hyperdense blood in basal cisterns/sulci
116
Name some other investigations used to diagnose a SAH besides CT head
LP: done >12 hours post symptoms onset if CT done >6hrs symptoms onset was normal
Will show xanthochromia(RBC breakdown), may have high opening pressure
CT angiogram to diagnose aneurysm or vascular abnormalities
117
What is the treatment for a SAH?
Oral nimodipine to prevent vasospasm and prevent ischaemic damage
Coiling, stenting, clipping of aneurysm by neurosurgeons/neuroradiologists
118
Name some complications of a SAH
Re bleeding
Hydrocephalus
Vasospasm
Hyponatraemia from SIADH
Seizures
119
Describe the prognosis of untreated SAH
50% mortality if untreated
Of those who survive past the 1st month-50% will be dependent on others for activities of daily living
120
Name some predictive factors of prognosis for patients with a SAH
Age
Consciousness level on admission
Amount of blood visible on CT head
121
Name some ECG changes that may be seen in a SAH
Transient ST elevation
Secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
122
Define a TIA
Sudden on set focal neurological deficit with a vascular aetiology typically lasting less than 1 hour, completely resolves within 24 hours
123
Describe the epidemiology of a TIA
230/100,000
Peak: 70 years
More common in males
124
Describe the pathology of a TIA
Transient disruption of blood flow to a specific region of the CNS resulting in ischaemia and focal neurological deficit
125
Name some causes of a TIA and which is the most common
Mc: Embolism-mostly atherosclerotic plaques from the heart
Lacunar
Haemodynamic compromise(often stenosis of major artery)
126
Describe the presentation of a patient presenting with a TIA
Any focal neurological deficits that completely resolve in <24 hours, most commonly lasting <1 hour
Aphasia/dysarthria
Unilateral weakness/sensory loss
Ataxia, vertigo, balance issues
Visual: amaurosis fugax, diplopia, homonymous hemianopia
127
What is the main investigation done when investigation a TIA
MRI-ischaemia, haemorrhage, vascular abnormalities, any other pathologies
128
Name the investigations done to diagnose a TIA
MRI-ischaemia, haemorrhage, vascular abnormalities
Carotid doppler US-atherosclerosis
Echocardiogram-cardiac thrombus
24 hour ECG-A fib
Bloods-glucose, lipid profile, clotting
129
Describe the immediate management of a patient with a TIA
Immediate antithrombotic therapy-aspirin 300mg unless CI
Specialist review
<24 hour if TIA in last 7 days
<7 days if TIA in over 7 days
Admission considered if crescendo TIA or cardioembolic source
130
Describe the secondary management of a patient with a TIA
Risk factor modification
Antiplatelet therapy-clopidogrel
Lipid modification-atorvastatin 20-80mg daily
Carotid endartectomy if severe carotid stenosis
131
When should you not give aspirin to a patient with a suspected TIA
If any contraindications:
-Already on low dose daily aspirin
-Haemorrhagic stroke not ruled out
-Bleeding disorders
132
Describe the driving rules post a TIA
Can't drive until seen by specialist
Once seen by specialist, dr is happy, and no lasting effects:
-1 month for cars
-1 year for bus/lorries
133
Where do Berry aneurysms most commonly occur?
Bifurcation points in the Circle of Willis
Anterior circle of Willis
Anterior communicating artery
Middle cerebral artery
134
Which area of the brain does the anterior cerebral artery supply?
Middle of the brain-middle cerebral cortex
135
How would an anterior cerebral artery occlusion present?
Contralateral loss of sensation and motor control to LOWER body
136
Which area of the brain does the middle cerebral artery supply?
Sides-lateral cerebral cortex
137
How would a middle cerebral artery occlusion present?
Contralateral loss of sensation and motor control to face and upper limbs
Broca's aphasia
138
Which area of the brain is supplied by the posterior cerebral artery?
Back-posterior cerebral cortex
Occipital lobe, thalamus etc
139
How would a posterior cerebral artery occlusion present?
Contralateral homonymous hemianopia
140
How would a basilar artery occlusion present and why?
Locked in syndrome
Bilateral loss of corticospinal tracts
141
How would an anterior inferior cerebellar artery occlusion present?
Lateral pontine syndrome:
-Ipsilateral CN3 palsy
-Ipsilateral vertigo/nystagmus/deafness
-Ipsilateral poor coordination/tone/balance
Contralateral loss of pain and temperature sensation
142
What is posterior inferior cerebellar stroke also known as?
Wallenberg's syndrome
143
How would a posterior inferior cerebellar artery occlusion present?
Horner's syndrome:
-Ipsilateral ptosis, miosis, anhidrosis
Ipsilateral loss of pain and temp sensation in face
Contralateral loss of pain and temp sensation in trunk and limbs
Ipsilateral cerebellar signs: nystagmus, vertigo
Ipsilateral bulbar muscle weakness: dysphagia, dysarthria
Diplopia
144
Which arteries are involved in a total anterior circulation stroke?
Middle cerebral/anterior cerebral
145
What is the criteria for diagnosing a total anterior circulation stroke?
3/3 of:
-Unilateral weakness and/or sensory deficit of face, arm, leg
-Homonymous hemianopia
-Higher cerebral dysfunction(dysphagia, visuospatial disorder)
146
What arteries are involved in a partial anterior circulation stroke?
Only part of the anterior circulation: Anterior cerebral/middle cerebral
147
What is the criteria to diagnose a partial anterior circulation stroke?
2/3 of:
-Unilateral weakness and/or sensory deficit of face, arm ,leg
-Homonymous hemianopia
-Higher cerebral dysfunction(dysphasia, visuospatial disorder)
OR
Higher cerebral dysfunction on its own
148
Which arteries are involved in a posterior circulation stroke?
Vertebrobasilar arteries
149
Which parts of the brain are affected by posterior circulation strokes?
Cortical
Brainstem
Cerebellum
150
What criteria can be used to diagnose a posterior circulation stroke?
1/5 of:
-Cranial nerve palsy and contralateral motor/sensory deficit
-Bilateral motor/sensory deficit
-Conjugate eye movement disorder(like horizontal gaze palsy)
-Cerebellar dysfunction (vertigo, nystagmus, ataxia etc)
-Isolated homonymous hemianopia
151
Describe the pathology of a lacunar stroke
Subcortical damage secondary to small vessel disease
152
What distinguishes a lacunar stroke from other strokes?
NO loss of higher cerebral function e.g. dysphagia
153
What criteria can be used to diagnose a lacunar stroke?
1/4 of:
-Pure sensory stroke
-Pure motor stroke
-Sensori-motor stroke
-Ataxic hemiparesis
154
What is Weber's syndrome?
Stroke: upper basilar and proximal posterior cerebral
Causes ipsilateral CN3 palsy and contralateral hemiparesis
155
Define a stroke
Sudden onset focal neurological deficit of vascular aetiology with symptoms lasting over 24 hours
156
What are the 2 types of ischaemic stroke?
Thrombotic
Embolic
157
What percentage of strokes are ischaemic and haemorrhagic?
Ischaemic: 85%
Haemorrhagic: 15%
158
Describe the pathology behind ischaemic strokes
Decrease in blood flow->decreased delivery of oxygen and glucose-> energy failure and disruption of cellular ion haemostasis->excitotoxicity, oxidative stress, inflammation and apoptosis-> irreversible neuronal damage
Can also lead to cerebral oedema-> increased ICP-> secondary neuronal damage
159
Name the strong risk factors fro having a stroke
Age
Male
Family history of stroke
Hypertension
Smoking
Diabetes
Afib
160
Name the weak risk factors for having a stroke
Hypercholesterolaemia
obesity
poor diet
oestrogen containing therapy
migraines
161
What investigations are done to diagnose a stroke?
ROSIER score
Non contrast CT head-areas of low density-takes longer to appear, and hyperdense artery sign visible immediately
162
Describe the ROSIER score
-LOC/syncope: -1
-Seizure activity: -1
New, acute onset of:
-Asymmetric facial weakness: +1
-Asymmetric arm weakness: +1
-Asymmetric leg weakness: +1
-Speech disturbance: +1
-Visual field defect:+1
Stroke likely if >0
163
Describe the acute management of a stroke
Once haemorrhagic stroke ruled out:
-Aspirin 300mg orally/rectally
-Thrombolysis
-Mechanical thrombectomy
164
What is used for stroke thrombolysis?
IV alteplase-tissue plasminogen activator
165
In what time frame can thrombolysis be done?
<4.5 hours from symptoms onset
166
Name some contraindications to thrombolysis for stroke
Previous haemorrhage/current bleeding, GI bleed, recent surgery, hypertension, increased INR etc
167
When can mechanical thrombectomy be done?
Offered within 6 hours of symptoms onset for patients with proximal anterior circulation occlusion seen on CTA/MRA
Done in conjunction with thrombolysis if <4.5 hours
Can be done on certain patients with proximal posterior circulation
168
Describe the long term treatment of strokes
Clopidogrel 75mg (If AF was cause-warfarin/rivaroxaban)
Atorvastatin 20-80mg daily
Hypertension management
Diabetes management
Smoking cessation
Surgery-carotid endartectomy
169
What surgery may be offered in some patients post stroke with carotid stenosis?
Carotid endartectomy
170
Define Bell's Palsy
Acute, unilateral, idiopathic facial nerve paralysis
171
Describe the epidemiology of Bell's palsy
Peak incidence: 15-45 years
More common in pregnant women
172
Describe the aetiology of Bell's Palsy
Unknown
Linked to HSV1
Also linked to EBV, VZV
173
Describe the presentation of a patient with Bell's Palsy
Acute onset of unilateral LMN facial weakness-no forehead sparing
Post-auricular otalgia
Hyperacusis
Nervus intermedius-altered taste, dry eyes/mouth
174
Is there forehead sparing in patients with Bell's Palsy? Why?/Why not?
NO forehead sparing
Bilateral supply to forehead from both sides of the brain
175
Name some differentials for Bell's Palsy
Ramsay-Hunt-prominent otalgia, vesicular rash
Stroke-forehead sparing
Guillain-Barre
Acute otitis media
Herpes zoster
Lyme disease
176
How is Bell's palsy diagnosed?
Mostly clinical-investigations to rule out other causes/assess extent of damage
FB, CRP, ESR
Viral serology-HSV, VZV etc
Lyme serology
Otoscopy
EG
MIR/CT
177
Describe the management of Bell's Palsy
50mg oral prednisolone once daily for 10 days, then taper
Aciclovir for attempted patients
Supportive therapy-artificial tears/ocular lubricants, eye tape
PT, Psychological support
178
Describe what referrals should be made if a patient with Bell's palsy isn't improving
3 weeks: Urgent ENT referral
If long standing weakness(months)-plastic surgery referral
179
Describe the prognosis for a patient with Bell's palsy
Complete recovery in 70-80% of adults in a few weeks- months
If untreated, 15% of patients have permanent moderate-severe weakness
180
What are some risk factors for poorer prognosis in a patient with Bell's palsy?
Older
More severe initial facial weakness
181
Describe the epidemiology of essential tremor
Common
Peak 40-50 years
182
Describe the aetiology of essential tremor
50% of cases are autosomal dominant inheritance
183
Describe the pathophysiology of essential tremor
GABA-ergic dysfunction->increased activity in cerebellar-thalamic-cortical circuit
184
What are some of the symptoms of essential tremor plus?
Difficulty with tandem gait
Mild cognitive impairment
Slight resting tremor alongside action tremor
185
How is essential tremor diagnosed?
Clinical diagnosis
-Bilateral upper lib action tremor
->3 years
-No other tremor elsewhere or other neurological signs
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Name some differentials for essential tremor
Parkinson's disease
Hyperthyroidism associated tremor
Dystonic tremor
Spasmodic dysphonia
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What can exacerbate essential tremor?
Anxiety, excitement etc
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What can improve essential tremor?
Alcohol-temporarily
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What happens to the amplitude of essential tremor over time?
Increases
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Describe the 1st line pharmacological management of essential tremor
Propranolol
Primidone
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Describe the 2nd line pharmacological management of essential tremor
Gabapentin
Topiramate
Nimodipine
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Describe the surgical management of essential tremor?
DBS
Botulinum toxin type A injections
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Describe the prognosis of essential tremor
Typically worsens with increasing age
Can remain isolated or can spread, e.g. to head, voice over years
Can cause major disability
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What is myasthenia gravis?
Autoimmune disease affecting the NMJ causing muscle weakness the progressively worsens with activity and improves with rest
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Describe the epidemiology of myasthenia gravis
Affects males and females equally
Bimodal distribution: highest prevalence in F<40yrs and M>60 yrs
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Name some risk factors for myasthenia gravis
Thymomas
Thymic hyperplasia
Other autoimmune disorders
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What are the autoantibodies in myasthenia gravis?
AChR antibodies(nicotinic acetylcholine receptor antibodies)
MuSk(muscle specific kinase)
LRP4(low-density lipoprotein receptor related protein)
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What are MuSK and LRP4 antibodies responsible for?
Creation and organisation of AChR-inadequate AChR
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Describe the normal action of ACh at the NMJ
Axons release ACh from the presynaptic membrane->travels across the synapse->attaches to ACh receptors on postsynaptic membrane, stimulating muscle contraction
200
Describe the pathophysiology of myasthenia gravis
AChR antibodies bind to postsynaptic AChR, blocked them and preventing stimulation by ACh
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Why does muscle weakness worsen with activity in patients with myasthenia gravis?
The more the ACh receptors are used during muscle activity, the more they become blocked-> less effective stimulation of the muscle with increased activity.
With rest, receptors are clears and symptoms improve
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Which muscles are most commonly affected by myasthenia gravis? What symptoms can these cause?
Ocular-ptosis, diplopia
Bulbar-dysarthria, dysphagia
Limb-proximal limb weakness weakness
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Name some drugs that can exacerbate myasthenia gravis
Beta blockers
lithium
phenytoin
Antibiotics
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Name some bedside tests that can be used to indicate myasthenia gravis
Ice pack test-ice will reduce ptosis
Encourage lots of blinking-> ptosis will worsen
Prolonged upward gazing will exacerbate diplopia
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
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How is myasthenia gravis diagnosed?
Serology: AChR antibodies(85%), MuSK and LRP4 antibodies in small proportion
CT/MRI chest->thymoma/thymic hyperplasia
Edrophonium test-ACh inhibitor-> rapid, transient increase in muscle strength indicates MG
206
Name some differentials for myasthenia gravis
Lambert-Eaton syndrome
MS
Polymyosits/dermatomyositis
Graves ophthalmoplegia
Botulism
Brainstem gliomas
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Describe the management o myasthenia gravis
ACh Inhibitors-pyridostigmine, neostigmine
Immunosuppression-steroids, azathioprine
Thymectomy
Rituximab if severe
In crisis: plasma exchange and IVIG
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Name some prognostic factors for myasthenia gravis
Age of onset
Antibody subtype
Thymus histology
response to treatment
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What is a myasthenic crisis?
Life threatening, acute worsening of symptoms, often triggered by another illness/infection like a URTI
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What is the main danger when someone has a myasthenic crisis?
Respiratory muscle failure
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When should patients with myasthenia gravis be considered for mechanical ventilation?
When FVC<15mL/kg
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What is the treatment for someone in a myasthenic crisis?
IVIG and plasmapheresis
Usual meds
213
Define chronic fatigue syndrome
Chronic, disabling condition characterised by profound fatigue and impairment following minimal physical/cognitive effort
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Describe the epidemiology of chronic fatigue syndrome
Peak: 30-40 years
2:1 ratio-more common in females
215
Describe the aetiology of chronic fatigue syndrome
Unknown
Triggers like EBV, psychological stress
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Describe the signs and symptoms of chronic fatigue syndrome
Extreme fatigue
Post exertional malaise
Sleep disturbances and unrefreshing sleep
Cognitive impairment
Orthostatic intolerance
Immune, neurological, autonomic, psychiatric manifestations
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Name some differentials for chronic fatigue syndrome
Fibromyalgia
Depression
Hypothyroidism
AI disorders
218
How is chronic fatigue syndrome diagnosed?
Mostly clinical-rule out other causes
Bloods-
TFT's
inflammation
infection
blood cell abnormalities
Present >3 months AND significant decrease in ability to engage in activities from before
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Describe the management for chronic fatigue syndrome
Refer to CFS service if >3 months
Energy conservation
Physical activity and exercise(graded exercise therapy no longer recommended)
Symptom control (pain, sleep etc)
CBT
220
What is encephalitis?
Inflammation of the brain parenchyma
221
Describe the epidemiology of encephalitis
Peak in >70years, <1 year
Affects males and females equally
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What is the most common cause of encephalitis?
HSV1
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Name some causes of encephalitis
HSV1/2
CMV
EBV
VZV
HIV
Autoimmune
224
Describe the pathophysiology of autoimmune encephalitis
NMDA receptor antibody associated encaphilitis
225
Which part of the brain is typically affected by HSV1 encephalitis
Temporal and inferior frontal lobes
226
Describe the presentation of a patient with encephalitis
Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features like aphasia
Flu-like prodromal illness
227
Name some differentials for encephalitis
Hypoglycaemia
DKA
HE
Uremic/drug induced encephalopathy
228
What investigations should be done to diagnose encephalitis?
Routine blood
CSF testing and PCR analysis
CT
MRI-better than CT
EEG
229
What would be seen on a CSF sample of a patient with encephalitis
Lymphocytosis
Increased protein
Viral PCR analysis
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What could be seen on a CT of a patient with encephalitis?
medial temporal and inferior frontal changes
-Most commonly bilateral multifocal petechial haemorrhages
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What might be seen in the EEG of a patient with encephalitis?
Lateralised periodic charges at 2Hz
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Describe the treatment of encephalitis
10mg/kg acyclovir TDS for 2 weeks
Broad spectrum antimicrobial cover, eg ceftriaxone 2g
Supportive treatment-such as seizure treatment
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Name some side effects of acyclovir
GI changes
Photosensitivity
Rash
Acute renal failure
Hepatitis
234
Describe the prognosis of encephalitis
If treatment started promptly: 10-20% mortality
Untreated: 80% mortality
235
Define meningitis
Inflammation of the meninges(dura, arachnoid, pia). Infective and non infective causes
236
Describe the epidemiology of meningitis
Viral(enteroviruses) most common and least severe
Bacterial: high morbidity and mortality
Fungal/parasitic-> rare except in immunosuppressed
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Name some non infective causes of meningitis
Malignancies-leukaemia, lymphoma
Drugs-NSAIDs, trimethoprim
Systemic inflammatory diseases-sarcoidosis, SLE, Bechet's
238
Name some symptoms of meningitis
Headache
Fever
nausea and vomiting
seizures
photophobia
neck stiffness
decreased consciousness
239
Name some signs that might be seen in meningitis
Non-blanching petechial/purpuric rash->impending DIC
Kernig's sign-?pain and resistance on knee extension
Brudzinski's sign-passive neck flexion results in involuntary hip and knee flexion
240
Name some differentials for meningitis
Encephalitis
SAH
Brian abscess
Sinusitis
Migraines
241
When might typical signs of meningitis be absent
In infants with bacterial meningitis
242
Name some investigations used to diagnose meningitis
Bloods-FBC,CRP, coag screen, cultures, PCR, glucose
ABG
CT head
lP for CSF analysis
243
When should an LP not be done?
If there are signs of raised ICP
244
Where in the spine is an LP done
L3/L4
245
What would you expect in CSF analysis of a patient with bacterial meningitis?
High opening pressure
Cloudy/yellow
Low glucose vs serum(<50%)
High protein (>1g/L)
Neutrophilia
246
What would you expect in CSF analysis of a patient with viral meningitis?
Normal opening pressure
Clear/cloudy
High glucose vs serum(>60%)
Normal protein
Lymphocytosis
247
What would you expect in CSF analysis of a patient with fungal/TB meningitis?
High opening pressure
Cloudy and fibrous
Low glucose vs serum (<50%)
High protein (>1g/L)
Lymphocytosis
248
Describe the treatment in primary care of a patient with suspected meningitis
IM benzylpenicillin and urgent hospital transfer
249
Describe the treatment for bacterial meningitis
IV cefotaxime/ceftriaxone (3rd gen cephalosporin) and IV dexamethasone
250
What antibiotic should be added in in patients at age extremes with suspected meningitis and why?
Amoxicillin-covers for listeria
251
Describe the treatment for viral meningitis
Nothing if enteroviruses
Acyclovir if HSV/VZV
252
What prophylaxis should be given to close contacts of someone with bacterial meningitis
One off oral ciprofloxacin -if in close contact up to 7 days before
253
Name some complications of meningitis
Sepsis
DIC
Coma
SIADH
Seizures
Death
254
Name some delayed complications of meningitis
Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness
255
What is Waterhouse Friedrichsen Syndrome and what can cause it?
Adrenal insufficiency caused by intraadrenal haemorrhage from DIC
256
What are the most common bacteria that can cause meningitis in neonates?
Group B strep
E.Coli
Gram negative bacilli
Listeria
S.pneumoniae
257
What are the most common bacteria that can cause meningitis in 3month-6years ols?
S. pneumonia
n.meningitidis
H.influenzae
258
What are the most common bacteria that can cause meningitis 6-60 year olds?
S.pneumonia
N.meningitidis
259
What are the most common bacteria that can cause meningitis in those over 60 years?
S.pneumoniae
N.meningitidis
Listeria
Gram negative bacili
260
What kind of bacteria is n.meningitidis?
Gram negative diplococcus
261
Which meningitis causing bacteria is there a vaccine for?
N.meningitidis
262
Which meningitis causing bacteria causes a non-blanching purpuric rash?
N.meningitidis
263
What kind of bacteria is S.pneumoniae?
Gram positive diplococcus in chains
264
What kind of bacteria is Group B strep?
Gram positive coccus in chains
265
What age group is group B strep most common in and why?
Neonates
Colonises in the maternal vagina
266
What kind of bacteria is listeria monocytogenes?
Gram positive bacillus
267
What groups are most likely to get meningitis cause by listeria monocytogenes?
Extremes of age
pregnancy
268
What is neurofibromatosis?
Genetic condition that causes nerve tumours(neuromas) to develop in the nervous system. Benign but can cause structural and neurological problems
269
Which type of neurofibromatosis is more common?
neurofibromatosis type 1
270
What is neurofibromatosis type 1 also called?
von Recklinghausen's syndrome
271
HOW IS neurofibromatosis inherited?
autosomal dominant
272
Describe the aetiology of neurofibromatosis type 1
Mutation on chromosome 17 which codes for neurofibrin->tumour suppressor protein
273
Name the symptoms of neurofibromatosis type 1
CABBING
CAFE AU LAit spots
Relative with nf1
bony dysplasia, bowing of long bone or sphenoid wing dysplasia
iris hamartomas(lisch nodules)
neurofibromas(>2 is singificant, or >1 plexiform)
glioma of optic pathway
274
How is nf type 1 treated?
monitor and manage complications
275
What are the 2 most significant complications of nf type 1?
malignant peripheral nerve sheath tumours(MPNST)
Gastrointestinal stronal tumour(GIST)
276
Name some complications of nft1
migraines
epilepsy
hypertension from renal artery stenosis
learnign disability
scoliosis
brain tumours
spinal tumours
increased cancer risk
277
Describe the aetiology of neurofibromatosis type 2
mutation on chromosome 22-> merlin-> tumour suppressor protein important in schwann cells->schwannomas
278
What is the main complication of neurofibromatosis type 2
Acoustic neuromas
BILATERAL ACOUSTIC NEUROMAS->THINK NF2
279
What is giant cell arteritis also known as?
Temporal arteritis
280
What is temporal arteritis?
Vasculitis of unknown cause that affects medium to large size of vessel arteries, particularly at the temmples
281
What condition overlaps with temporal arteritis?
polymyalgia rheumatica
282
Describe the epidemiology of temporal arteritis
most common primary vasculitis
>50 years, peak in 70s
M:F-1:3
283
Describe the aetiology of temporal arteritis
genetics
environmental
age
sex
ethnicity(caucasian-scandinavian)
284
describe the presentation of a patient with temporal arteritis
temporal headache
jaw claudication
amaurosis fugax
tender, palpable temporal artery, scalp tenderness
50% have PMR features-morning, proximal muscle weakness
285
What investigations shoud be done to diagnose temporal arteritis
Inflammatory markers-ESR and CRP raised
LFTs and FBC
Temporal artery biopsy
Doppler ultrasound
286
