Neuro Flashcards
(191 cards)
1
Q
What structure is damaged in Bell’s palsy?
A
Cranial nerve 7 (facial)
2
Q
What is the presentation of Bell’s palsy?
A
Weakness of the facial muscles responsible for expression
3
Q
LMN presentation vs UMN presentation
bells palsy vs stroke
A
LMN - no forehead sparing
UMN - forehead sparing ie can wrinkle forehead
4
Q
What is the management for Bell’s palsy?
A
Steroids
Surgery if there is residual symptoms 6-9 months after initial symptoms
5
Q
Bulbar palsy vs Peudobulbar palsy
A
Bulbar palsy - lower motor neurone dysarthria (difficult/unclear articulation of speech) and dysphagia (difficulties swallowing)
Pseudobulbar palsy - upper motor neurone dysarthria and dysphagia
6
Q
What is the aetiology of Bulbar palsy?
A
Diphtheria Poliomyelitis Motor neurone disease Cerebrovascular event Brainstem tumours Gullain-Barre syndrome
7
Q
Aetiology of Pseudobulbar palsy?
A
Cerebrovascular event demyelinating disorders motor neurone disease head injuries neurosyphillis high brainstem tumours
8
Q
What are the investigations for bulbar/pseudobulbar palsy?
A
CT/MRI
electropalatography
electromagnetic articulography
9
Q
What is the management for bulbar/pseudobulbar palsy?
A
Treat directing cause
SALT
Baclofen for spasticity, anticholinergics for drooling
Dietician
10
Q
What is cerebral palsy?
A
A brain disease causing paralysis
Lesion in an immature brain any time up to the postnatal period
11
Q
What causes cerebral palsy?
A
Vascular hypoxic-ischaemic teratogenic exposure to radiation infection ie meningitis toxins metabollic problems trauma ie head injury
12
Q
What are the different characteristics of cerebral palsy?
A
- Spastic (70% of types): scissor gait
- Dyskinetic: hyperkinesia - dystonia and chorea
- Ataxic: without order/control
13
Q
Epidemiology of cerebral palsy?
A
More likely in new borns <2500g
14
Q
What are the risk factors for cerebral palsy?
A
- antenatal: preterm birth, intrauterine infections, multiple births
- perinatal: low birth weight, neonatal sepsis, chorioamnionitis
- postnatal: meningitis, intracranial haemorrhage, seizures
15
Q
Presentation of cerebral palsy?
A
- associated with low Apgar score
- delay in reaching developmental milestones
- abnormal tone
- excessively fidgety
- feeding difficulties
- emotional and behavioural difficulties in later childhood
- epilepsy
- sleep disturbance
16
Q
Investigations for cerebral palsy?
A
Neuroimaging: USS, CT, MRI, PET
17
Q
Managment for cerebral palsy?
A
Treat/support symptoms: wheelchairs, splints, physio
medical treatment: diazepam/baclofen for spastic pain
Surgical treatment
18
Q
What is churg-strauss/Eosinophilic Granulomatosis with Polyangiitis ?
A
diffuse vasculitic disease affecting coronary, pulmonary, cerebral, abdominal and visceral circulations
19
Q
what’s the aetiology of churg-strauss?
A
unknown - thought to be autoimmune and have a genetic factor
drugs known to cause churg-strauss: mesalazine, leukotriene receptor antagonists
20
Q
What are the 3 features that characterise churg strauss?
A
eosinophillia
asthma
peripheral neuropathy
*can also have paranasal sinusitis
21
Q
Presentation of churg strauss..
A
depends on the system affected
peripheral neuropathy presents as mononeuritis multiplex,
pulmonary system presents as asthma,
cardiac: heart failure, myocarditis, mi.
renal: glomerulonephritis
general symptoms include: fatigue, malaise, weight loss, fever
22
Q
Investigations of churg strauss
A
antineutrophil cypoplasmic antibodies
bloods: eosinophillia, raised inflammatory markers
23
Q
Management of churg strauss?
A
high dose steroids
cyclophosphamide for severe/life threatening disease
IVIg, interferon-alpha, plasma exchange
rituximab
24
Q
What is Horner’s syndrome?
A
Lesion which affects the sympathetic nervous supply to the eye.
TRIAD: partial ptosis, miosis and hemifacial anhidrosis
25
What are some of the causes of Horner's syndrome
```
Anything that can cause a lesion to the sympathetic nervous system
Apical lung tumours
cerebrovascular accidents
cluster headaches/migraines
internal carotid artery dissection
+ many more
```
26
What is the presentation of Horner's syndrome?
TRIAD: miosis, partial ptosis, hemifacial anhidrosis
| pain
27
What are the investigations for Horner's syndrome?
guided by suspected underlying aetiology
CXR for suspected lung tumour
CT/MRI for suspected cerebrovascular event
Ct angiography for suspected carotid artery dissection
28
Management for Horner's syndrome?
treat underlying cause
29
What is hydrocelphalus?
an increase in CSF in the cerebral ventricles.
due to impaired absorption or increased secretion.
obstructive vs communicating
30
Epidemiology of hydrocephalus?
occurs in neonates
| -absence of neonatal care, maternal hypertension during pregnancy, alcohol use during pregnancy
31
Presentation of hydrocephalus
Acute onset: headache and vomiting, papilloedema
gradual onset: unsteady gait, large head
cognitive deterioration, neck pain, blurred/double vision, incontinence
32
investigations for hydrocephalus?
HEAD CT
33
Management for hydrocephalus?
lumbar puncture (once ct is done and if hydrocephalus is communicating)
furesomide - inhibits further csf secretion
surgery - shunt and venrticular drain
34
What is a mononeuropathy?
a local lesion that causes focal involvement of a nerve
35
What is the aetiology of mononeuropathies?
```
mechanical ie compression, constriction, trauma
entrapment
diabetes mellitus
hypothyroidism
rheumatoid arthritis
vasculitis
pregnancy
sarcoidosis
amyloidosis
```
36
How does carpal tunnel present?
- lesion of the median nerve
- caused by excessive use of the wrist, obesity, tenosynovitis
- presents with NOCTURNAL PARASTHESIA affecting the thumb, index and middle fingers
- in severe cases: wasting of abductor pollicis brevis
37
How does ulnar nerve palsy present?
- lesion of the ulnar nerve
- also known as claw hand
- causes complete paralysis and sensory loss in 4th/5th fingers, wasting and weakness of the small muscles of the hands
38
How does radial nerve palsy present?
- saturday night palsy (occurs after a night out if slept on a chair and compressed raidal nerve against the humerus)
- wrist and finger drop
- variable parasthesia
39
How does common peroneal nerve present?
- foot drop
- commonly caused by surgery or trauma
- weakness on the everting foot
- inability to extend the toes
- parastheisa over the dorsum of the foot
40
What are the investigations for a mononeuropathy?
- nerve conduction studies
- electromyography
- ultrasounds
- MRI
- nerve biopsy
41
What is the conservative management for a mononeuropathy?
NSAIDS
Splints
local steroid injections
(done if there is no history of trauma, if the onset is sudden, if there are no or few sensory findings and no motor deficit)
42
What is the surgical management for a mononeuropathy?
decompression
| -done in carpal tunnel if conservative management is ineffective
43
What is narcolepsy?
chronic neurological condition producing abnormal disruption in normal sleep patterns
44
What is cataplexy?
sudden loss of muscle tone and power in response to strong emotion
-always occurs alongside narcolepsy
45
What is the epidemiology of narcolepsy?
onset is usually in adulthood
usually affects males
genetic component
46
What is the pathology behind narcolepsy?
- patients enter REM sleep a lot faster than usual
| - REM sleep intrudes into wakefulness
47
What's the presentation of narcolepsy?
- excessive daytime sleepiness (napping during daytime activities ie eating and talking)
- cataplexy (attacks can be triggered by emotion and last from seconds to minutes)
- hypnagogic hallucinations (at onset of sleep)
- sleep paralysis
48
Investigations for narcolepsy?
CLINICAL DIAGNOSIS: >3 months excessive daytime sleepiness, cataplexy, hypersomnia not attributive to another condition, biomarkers present in tests
Epsworth sleepiness scale
Sleep studies
Brain MRI
49
Management of narcolepsy?
inform the DVLA
referral to sleep services
good sleep hygeine, regular exercise, strategic day time naps
drug treatment: modafinil, antidepressants, benzodiazapines (at night)
50
What is neurofibromatosis?
lesions on the skin, nervous system and skeleton
- genetic disorder (autosomal dominant)
- NF1 - most common causing skin lesions
- NF2 - CNS tumours
- schwannomatosis - benign nerve sheath tumour
51
what is the epidemiology of neurofibromatosis?
NF1>NF2
white caucasion
autosomal dominantly inherited
(50% of new cases do not have a family history)
52
presentation of NF1?
at least 2/7 of the following:
- >6 cafe-au-lait spots or hyperpigmented macules
- Axillary or inguinal freckles
- >2 typical neurofibromas or one plexiform neurofibroma (from nervous tissue)
- Optic nerve glioma
- >2 iris hamartomas - Lisch nodules
- Sphenoid dysplasia
- First degree relative with NF1
53
presentation of NF2
at least 1/3 of the following:
- Bilateral 8th nerve masses on MRI scan
- 1st degree relative with NF2 for a unilateral 8th nerve mass
- 1st degree relative with NF2 with at least 2 of the following: Meningioma, Glioma, Schwannoma, Juvenile cataracts
54
What are the investigations for neurofibromatosis?
plain x ray
ct/mri head
genetic testing
histology
55
Management for neurofibramotosis?
monitor for malignant change
monitor multisystem involvement
surgical management for compression of tumours on other structures
pain management
56
What is non-epileptic attack disorder?
Attacks that have no epileptical activity in the brain
| are usually pscyhologically related - known as dissociative seizures
57
How do non-epileptic attacks present?
- often longer than 2 minutes
- flapping movements (like a fish out of water)
- eyes closed
- have limited information about the event
- gradual onset
- if collapse (dramatic fall, won't hurt themselves, legs collapse)
- fluctuating course
- pelvic thrusting
- asynchronous movements (no symmetry involved)
- can identify a trigger in some cases ie emotions
58
Investigations for non-epileptic attack?
- exclude epilepsy (eeg studies)
- mri
- investigate other physiological causes of attacks ie syncope
- psychiatric assessment
59
management for non-epileptic attack disorder?
- education
- anti-anxiety and antidepressant medications
- psychological therapies ie cbt
60
What is normal pressure hydrocephalus?
-ventricular dilatation in the absence of increased csf pressure
61
What is the aetiology of normal pressure hydrocephalus?
- idiopathic
- SAH
- meningitis
- head injury
- CNS tumour
62
How does normal pressure hydrocephalus present?
TRIAD:
gait disturbance - dilated ventricles cause distrubance to corona radiata
sphincter disturbance - urinary incontinence > bowel incontinence
dementia - memory loss, inattention, slow progression
63
investigations for normal pressure hydrocephalus?
CT/MRI - dilated ventricles
lumbar puncture - csf pressure should be normal
intraventricular pressure monitoring
64
management of normal pressure hydrocephalus
short term management: carbonic anhydrase inhibitors, repeated lumbar puncture
surgical management: CSF shunt
65
What is a polyneuropathy?
a general degeneration of peripheral nerves that spreads towards the centre of the body.
chronic and generally slow progression
66
what are the common causes of peripheral neuropathy?
diabetes
alcohol
leprosy (worldwide)
67
presentation of diabetic neuropathy?
parasthesiae, numbness, burning pain
| may not have symptoms and signs picked up on check up - loss of sensation
68
What are examples of motor polyneuropathies?
guillain-barre syndrome
charcot-marie-tooth syndrome
-lead poisoning
-diphtheria
69
What are examples of painful peripheral neuropathies?
- alcoholic neuropathy
- diabetic myotrophy
- vitamin b1 and b12 deficiency
70
examples of causes of peripheral neuropathies?
- diabetic neuropathy
| - nutritional deficiencies ie alcohol, vit b1/b12 deficiency,
71
What are some other causes of polyneuropathies?
- heavy metal poisoning
- infection
- chronic vascular disease
- iatrogenic
- idiopathic
72
investigations for polyneuropathy?
-distal and proximal nerve stimulation tests
-immunology
-nerve biopsy
VASCULITIS SCREEN:
-glucose
-rheumatoid factors, anca
-inflammatory markers
-fbc (anaemia)
-b12
-U&Es, LFTs
-paraneoplastic antibodies and PET scan
73
management of polyneuropathies?
- treat underlying cause
- foot care, weight reduction, sensible footwear and foot orthoses
- OT/PT
- chronic inflammatory demyelinating polyneuropathy: steroids, IVIg, plasma exchange
74
What is a common cause of mononeuritis multiplex?
VASCULITIS
75
What are radiculopathies?
- nerve root compression
| - C6/C7 and L5/S1 are usually affected
76
What cause radiculopathies?
- degenerative disc disease = disc prolapse
- osteoarthritis
- facet joint degeneration
77
How do patients describe a radiculopathic pain?
SHARP AND SHOOTING, radiating down a limb commonly in the pattern of a dermatome
78
Presentation of C6/C7 radiculopathy?
affects the thumb and middle finger
79
presentation of L5/S1 radiculopathy?
dorsum of foot/big toe and the ankle, lateral aspect of the foot and the sole
80
What are the investigations for radiculopathy?
MRI
| nerve conduction studies
81
management for radiculopathy?
physio
| surgery for herniated discs if appropriate
82
What is shingles?
a rash that occurs in a dermatomal pattern following immunosuppression allowing the dormant herpes virus to flare up
83
what are the risk factors for shingles?
- increasing age
| - immunocomprimisation
84
How does shingles present?
1. Pre-eruptive phase: no skin lesion, parastheisa in a dermatome, generally unwell, malaise, tender dermatome
2. eruptive phase: skin lesions with acute neuritic pain, crust formation and drying around 7-10 days
3. chronic phase: persistent and recurring pain lasting for 30 days
85
Investigations of shingles
clinical diagnosis
| if presentation is atypical ie extending beyond one dermatome- investigate for immunodeficiency
86
management of shingles?
general: keep area clean and dry, when the rash isn't covered, weeping - stay at home
Oral anti-viral therapy: aciclovir (shortens symptom duration and severity)
analgesia and fluids
87
What is a stroke?
a clinical syndrome caused by a disruption of blood supply to the brain causing focal and/or global disturbance or cerebral function
-lasts for more than 24 hours and can be fatal
88
What are the different types of stroke?
ischaemic (75%) and haemorrhagic (25%)
89
What causes ischaemic infarctions?
-thromboembolisms and atheromas
| can rarely be caused by trauma, infection or malignancy
90
What are haemorrhagic stroke features?
meningism
severe headache
coma within hours
91
what signs indicate ischaemic stroke?
carotid bruits
af
past tia
92
What are the risk factors for stroke?
- hypertension
- smoking
- diabetes mellitus
- heart disease - valvular, ischaemic and AF
- peripheral artery disease
- post tia
- carotid artery occlusion
- combined oral contraceptive pill
- hyperlipidaemia
- excess alcohol
- family history
- age
- gender: female
93
Presentation of cerebral hemisphere infarcts:
- ~2/3 of strokes occur from the middle cerebral artery
- contralateral hemiplegia
- facial weakness
- contralateral sensory loss
- homonymous hemianopia
- dysphasia, dysphagia
94
Presentation of posterior circulation infarct?
```
motor deficit: ipsilateral weakness, lack of coordination
ipsilateral cranial nerve dysfunction
sensory deficit contralaterally
ataxia
vertigo +nausea/vomiting
diplopia
dysphagia
```
95
investigations for stroke?
- glucose
- ECG
- head ct
- carotid duplex ultrasound
- echo
- bloods
96
management of stroke
General: blood pressure and blood sugar managment
Ischaemic: aspiring or thrombolysis (once haemorrhage has been excluded), thrombectomy (to push clot out), long term antiplatelet therapy
haemorrhagic: clot evacuation, burr hole
REHABILLITATION with PT/OT
97
indications for thrombolysis:
- within 4.5 hours of initial onset of symptoms
| - haemorrhagic stroke has been excluded
98
What is a subarachnoid haemorrhage?
spontaneous arterial bleeding into the subarachnoid space usually caused by a rupture of berry aneurysms
99
what are the clinical features of a SAH?
-thunder clap headache
nausea and vomiting
sometimes there can be a loss of consciousness
o/e focal neurological signs, papilloedema, meningeal irritation
100
investigations for SAH?
```
CT scan
lumbar puncture (12 hours after onset of symptoms if ct is clear) - XANTHOCHROMIA
```
101
management of SAH?
```
Bed rest
supportive measures ie control hypertension
NIMODIPINE - control artery spasms
IV Saline if hyponatraemic
neurosurgery referral?
```
102
What is a subdural haematoma?
a bleed into the subdural space caused by a rupture of bridging veins
usually caused by a head injury a few weeks previously
elderly and alcoholics are most at risk
103
clinical symptoms of subdural haematoma?
headaches
drowsiness
fluctuating confusion
104
how is subdural bleeds diagnosed?
CT head - long crescent shaped white bleed
105
treatment of subdural
surgery if chronic.
106
what is an extradural haematoma?
a bleed in the extradural space - usually caused by trauma causing the underlying middle meningeal artery
107
what is the history of an extradural haematoma?
-head injury with brief loss of consciousness, lucid interval recovery and then rapid deterioration focal neurological signs
108
what does an extraduarl haematoma look like on CT?
lens shaped
109
how is an extradural haematoma treated?
surgical drainage
110
What is temporal arteritis?
systemic immune-mediated vasculitis usually affecting the carotid artery and it's extracranial branches
111
Epidemiology of temporal arteritis?
women are commonly affected
112
risk factors for temporal arteritis?
european
peak incidence 60-80
genetic factors
113
Presentation of temporal arteritis?
- temporal headache with scalp tenderness - usually noticed when combing hair
- transient visual symptoms
- jaw/tongue claudication
- systeic features: fatigue, malaise, anorexia, fever
114
Investigations for temporal arteritis?
ESR - elevated
temporal artery biopsy
colour duplex ultrasonography
115
Management for temporal arteritis
- steroids
| - low dose aspirin
116
What are myopathies? What is a common type of muscular dystrophy?
a disease of the muscle
| Duchenne's muscular dystrophy
117
Aetiology of myopathies?
inherited: Duchenne's
Acquired: immmunologically mediated ie RA, SLE
non-inflammatory mediated: hyper/hypothyroidism, Cushings
toxic: drugs - steroids, statins
infection: hiv, influenza, LYME DISEASE
118
Clinical features of myopathies?
Weakness: usually proximally
variation of strength with exercise
difficulties rising from a chair, climbing stairs, combing hair
119
investigations for myopathy
```
blood and urine tests: creatinine kinase, renal function,
ecg
muscle biopsy
electromyopgraphy
mri
genetic testing
```
120
management of myopathies?
treat underlying cause ie treat infection, stop/change drugs
physiotherapy
physical aids
dietary advice
121
what is wernicke korsakoff's syndrome?
a sprectrum of disease resulting from thiamine deficiency
| triad: mental confusion, ataxia, ophthalmoplegia
122
epidemiology of wernicke korsakoff's syndrome?
alcoholics
| higher prevalence in lower socioeconomic groups
123
pathogenesis wernicke korsakoffs?
chronic alcohol misuse = inadequate thiamine intake, decreased absorption, impaired thiamine usage in cells
124
presentation of wernicke korsakoffs?
- confusion,
- nausea and vomiting
- weakness and loss of muscle coordination
- eye problems: diplopia, nystagmus, eye movement abnormalities
125
investigations for wernicke korsakoffs??
clinical diagnosis - treat is suspicions are high
bloods - fbc, u&es, lfts, glucose, serum thiamine levels
ct scan
abg
126
management of wernicke korsakoffs?
management of alcohol
oral thiamine replacement
dietician input
127
What are the acute causes of headaches?
- infection: meningitis/encephalitis
- haemorrhage: SAH, extradural
- venous sinus thrombosis
- sinusitis
- low pressure headache: csf leak
- acute glaucoma
128
what are the causes of chronic headache?
- tension headaches
- migraine
- cluster headaches
- trigeminal neuralgia
- raised icp
- medication overuse headache
- giant cell arteritis
129
what are the triggers for a migraine?
- Chocolate
- Hangovers
- Orgasms
- Cheese
- Oral contraceptives
- Lie ins
- Alcohol
- Tumult (loud noises)
- Exercise
130
Treatment for acute migraine?
NSAIDs, triptans
131
Prevention for migraine?
beta blockers
amitriptyline
topiramate
132
presentation of a cluster headache?
unilateral pain around the eye, watery/bloodshot eye, clusters of headaches - followed by pain free periods for months
133
management of a cluster headache?
oxygen, sumatriptan
134
what's the management for trigeminal neuralgia
MRI
carbamazepine
microvascular decompression
135
what's the definition of a TIA?
stroke symptoms lasting less than 24 hours
136
TIA management?
```
reduce blood pressure
reduce cholesterol
control diabetes
control other lifestyle factors
DVLA - can't drive for 1 month
CLOPIDOGREL
carotid endarectomy
```
137
What are the causes of seizures?
- epilepsy
- febrile convulsions
- alcohol withdrawal seizures
- psychogenic non epileptic seizures
- brain injury
- infection
- trauma
- metabolic disturbance
138
What are the different partial types of seizures?
Focal/partial: seizure activity is limited to one part of a hemisphere
Complex/partial: disturbance of consciousness or awareness
eg. frontal lobe seizure: usually occur from waking, 4-shape, drawing an arrow. very fast recovery
139
what are the different generalised types of seizures?
Absence: brief episode where patient appears blank/staring
Tonic-clonic: muscle rigidity followed by repeated contraction and relaxation
Myoclonic: brief, rapid muscle jerks
Atonic: 'drop attacks', lose muscle tone and drop to ground
140
Treatment for generalised seizures?
- Sodium valproate
| - lamotrigine, carbamazepine
141
Treatment for partial/focal seizures?
- Carbamazepine
| - leveritacetam (keppra)
142
treatment for absence seizures?
- sodium valproate
| - ethosuximide
143
what is multiple sclerosis?
cell mediated demyelination in the cns
144
how does ms present?
- Visual: optic neuritis, optic atrophy, uhtoff's phenomenon
- sensory: numbness, tingling, trigeminal neuralgia
- motor: spastic weakenss
- cerebellar: ataxia, diplopia, intention tremor
- urinary incontinence
- sexual dysfunction
- intellectual deterioration
145
epidemiology of ms?
- 20-40 year old females
| - temperate climate with low vit d levels
146
how is ms investigated?
MRI - demyelinated plaques
147
types of ms progression?
Relapsing-remitting
Primary progressive
Secondary progressive
148
MS management?
Steroids for acute relapses
Disease modifying drugs: beta-interferon, alemtuzimab
Treat symptoms
149
parkinsons pathophysiology?
degeneration of dopaminergic neurones in the substantia nigra
150
parkinsons presentation?
TRIAD: bradykinesia, cogwheel ridigity, resting tremor
- postural instability
- asymmetrical pattern
- shuffling gait with reduced arm swing
- difficulty initiating movement
151
What are the histiological findings in parkinsons?
lewy bodies
152
management of parkinsons?
- dopamine receptor agonists (bromocriptine, ropinirole)
- levodopa and dopa-decarboxylase inhibitor (carbadopa)
- MAO-B inhibitors: selegilline
- anticholinergics: orphenadrine
- COMT inhibitors: entacapone
153
what is huntington's disease?
-inherited (autosomal dominant) - defect in huntingtin gene, repeated CAG neurodegenerative, progressive
movement disorder
-loss of GABA mediated inhibition
154
prodrome features of huntingtons?
- personality changes
- lack of coordination
- chorea
- dystonia/hypotonia
- intention/tremor
- fits
- intellectual impairment
- progressive dementia
155
investigations fo huntingtons disease
genetic testing
156
management of huntingtons?
MDT approach: genetic counselling, salt, dieticians, physio, ot, psychologists
symptom control: dopamine antagonists
157
what is motor neurone disease?
a degenerative condition that affects motor neurones
- no sensory involvement or cerebellar signs
- no effect on eye movements
158
what are the different types of motor neurone disease?
- ALS: amyotrophic lateral sclerosis (most common type - both)
- progressive bulbar palsy (Both)
- progressive muscular atrophy (LMN)
- primary lateral sclerosis (UMN)
159
presentation of MND:
LMN signs: progressive limb weakness, wasting of thenar/tibialis anterior, fasciculations
UMN signs: hypertonia, brisk reflexes, upgoing plantars, spasticity
CLASSICALLY: stumbling spastic gait, foot drop, proximal myopathy, weak grip, associate with frontotemporal dementia
160
investigations for mnd:
nerve conduction studies
| mri (exclude cervical cord compression, ms, myelopathy
161
management of mnd:
```
feeding and respiratory support
mdt approach
RILUZOLE
BACLOFEN
ANTIDEPRESSANTS
```
162
What is gullain-barre syndrome?
acute inflammatory demyelinating polyenuropathy
163
how does guillaine-barre syndrome present?
```
post-infection: campylobacter
symmetrical ascending weakness
no or little sensory signs
areflexia
cranial nerve dysfunction ie diplopia
autonomic dysfunction: sweating, tachycardia, arrhythmias, urinary retention
```
164
investigations for guillain barre?
nerve conduction studies: slow
csf: raised protein, normal wcc
anti-gm1 antibodies
165
management for guillain barre?
IVIg
| Plasma exchange
166
What is myasthenia Gravis?
autoimmune neuromuscular disease causing weakness of the muscles
167
pathology of myasthenia gravis?
antibodies to post-synaptic nicotinic ACh receptors which interferes with muscular transmission causing fatiguability. This is because of the fewer receptors at the NMJ.
168
what antibodies would be present in myasthenia gravis?
ACh-R
| MuSK - Muscle-specific receptor tyrosine kinase
169
epidemiology of myasthenia gravis?
females
30-50 year old
other autoimmune conditions
associated with a thymic tumour
170
presentation of myasthenia gravis?
- increasing muscular fatigue (especially at the end of the day)
- in order: extra-ocular (ptosis, diplopia), bulbar (swallowing, chewing, dysphonia) face, neck, limbs (proximal), girdle, trunk
- normal tendon reflexes
171
What are 2 classic myasthenic signs?
- Peek sign: After 30 seconds of sustained forced eyelid closure, he is unable to keep the lids fully closed.
- Myasthenic snarl: may occur when patients try to smile. The snarl follows contraction of the middle portion of the upper lip while the upper mouth corners fail to contract.
172
investigations for myasthenia gravis?
antibodies: anti-AChR, MuSK
CT Thorax: thymus
Ice test
Tensilon test (short acting antiacetylcholinesterase which improves muscle strength after administration)
173
treatment for myasthenia gravis?
- acetylcholineesterase inhibitors: PYRISTIGMINE
- immunosuppressants for relapses: prednisolone
- Thymectomy
174
what is myasthenic crisis?
- weakness of the respiratory muscles
- may need intubation and ventilation
- treated with plasmapharesis/IVIg
- treat trigger ie infection, medications, post-op
175
What are some examples of types of dementia?
- alzheimers
- vascular
- lewybody
- frontotemporal
- huntingtons, CJD
176
What are some treatable types of dementia?
- Hypothyroid
- Addisons
- B12/Folate deficiency
- Low thiamine
- Syphillis
- Brain tumour
- Normal pressure hydrocephalus
- Subdural haematoma
- Depression
- Drugs
177
Assessment tools for dementia?
```
Adenbrookes cognitive examination - less than 84 indicates dementia. poor memory and fluency inidicates alzheimers
Abbreviated mental test score (AMTS)
6CIT - 6 item cognitive impairment test
GPCOG- GP assessment of cognition
MMSE - (less than 24/30)
```
178
What is alzheimer's disease?
progressive global cognitive impairment
179
what is the pathology of alzheimer's?
beta-amyloid plaques
cerebral atrophy in the cortex and hippocampus
defecit in acetylcholine
180
what are the features of alzheimers?
```
memory loss
decrease in visuospatial skills
verbal abilities decline
reduction in executive function
lack of insight
```
181
management of alzheimers?
- specialist memory service
| - acetylcholineesterase inhibitors: rivistigmine, donepezil, galantamine, memantine (late stages)
182
describe vascular dementia, its associations and management
- cumulative effect of many small strokes, stepwise progression
- associated with: past history of stroke, hypertension, AF, diabetes, smoking, coronary heart disease, obesity
- management: modify risk factors, treat symptoms
183
describe lewybody dementia, its features and management
- lewybody: alpha-synuclein cytoplasmic inclusions in brainstem and neocortex
- features: progressive cognitive impairment, parkinsonism, visual hallucinations
- management: avoidance of neuroleptics, AChesterase inhibitors,
184
What is dysarthria?
difficult or unclear articulation of speech that is otherwise linguistically normal
185
what is dysphonia
- difficulty in speaking due to a physical disorder of the mouth, tongue, throat or vocal cords
- sounds like donald duck
186
what is dysphagia?
difficulties swalloing
187
what is dysphasia?
| what are the different types of dysphasia?
- difficulty communicating
- expressive dysphasia: difficulties with speech - broken sentences that is comprehensible once they've said what they want (BROCAS)
- receptive dyspahsia: difficulties with comprehension. what they say won't make sense (WERNICKES)
- NOTE: aphasia and dysphasia are used interchangably
188
what is akinesia?
loss or impairment of the power of voluntary movement
189
what is ataxia?
- lack of voluntary coordination of muscle movements
| - includes: gait abnormality, speech changes, eye movement abnoralities
190
what is apraxia?
difficulty with the motor planning to perform tasks or movements when asked (provided that the request or command is understood and he/she is willing to perform the task.)
191
what is agnoisa?
inability to interpret sensations and therefore recognise things ie not recognising people
