neuro top tier Flashcards

1
Q

what investigation can be done to assess type of stroke

what does this affect

A

CT stroke - allows you to see if haemorrhagic.

if not (=embolic) then lytic medicine given so embolus broken down and damage reduced. but if it is haemorrhagic, then lytic medicine should be avoided as this would increase the bleed

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2
Q

effect on ischaemia to broca’s area

A

expressive dysphasia (motor)

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3
Q

effect on ischaemia to wernicke’s area

A
receptive dysphasia (sensory) - misinterpret own speaking and you think it is wrong
\+ can't understand other people's communication
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4
Q

is someone more likely to recover from a large ischaemic (embolic) or haemorrhagic stroke?

A

haemorrhagic

in haemorrhagic- the axons are disturbed (lenticular striate arteries cross internal capsule) but cell bodies are not affected- so necrosis. so as the haemorrhage resolves (With macrophages ), the pressure on axons decreases allowing recovery

with embolic blockage- there is necrosis of cell bodies. these are unable to regenerate and so are non-recoverable

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5
Q

in terms of the motor homunculus- which areas are supplied to which arteries (and so which areas would suffer from a stroke blockage in this artery)

A

anterior cerebral arteries = medial of cerebrum and homunculus
– lower limb

middle cerebral arteries = lateral of cerebrum
– upper limb and face

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6
Q

which is more common, embolic or haemorrhagic stroke?

A

85% embolic

15% haemorrhagic

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7
Q

which side of the brain is more likely to be affected by embolus from heart / carried in heart and why

A

right brain

R common carotid comes of before L from arch of aorta

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8
Q

name 3 significant causes of embolic stroke

A

1 heart failure (AF –> stasis –> embolus –> ejected when sinus rhythm returns)
2 blood pressure (stretches artery /longer –> turbulent blood flow –> clot embolus)
3 also kidney/lung/liver failure

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9
Q

what drugs may be given to AF patient for stroke prophylaxis

A

warfarin - prevent clot formation

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10
Q

where may a clot form with AF

A

in auricular appendage of atria in heart (Stasis of blood)

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11
Q

where does external carotid supply

A

dura
skull
face
neck

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12
Q

where does internal carotid supple

A

circle of willis

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13
Q

which vessels lie extradurally

A

meningeal arteries

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14
Q

which vessels lie subdurally

A

bridging veins

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15
Q

which vessels lie subarachnoidly

A

circle of willis

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16
Q

what symptoms is associated with a subarachnoid haemorrhage

A

thundeclap headache

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17
Q

what is the main cause of a subarachnoid haemorrhage

A

berry anerysrm in circle of willis

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18
Q

which haemorrhage type would cause dura to be pushed away from bone

A

extradural - meningeal

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19
Q

which groups are more suscpetible to subdural haemorrhage

A

elderly
children
alcoholics

they have brains smaller than their ckulls

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20
Q

epidemioloogy of migraines

A

common
f>m
<40y. most have 1st in adolescence

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21
Q

epidemiology of tension headaches

A

very common

f>m

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22
Q

epidemiology of cluster headaches

A

m>f
<40y
disabling

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23
Q

triggers for migraine

A

chocolate:

chocolate
hangover
orgasm
cheese
oral contraceptuve
lie ins
alcohol
tumult
exercise
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24
Q

triggers for tension headache

A
stress
sleep deprivation
bad posture
hunger
eyestrain
anxiety
noise
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25
red flags for headaches patient
``` thunderclap headache seizure+ new headache red eye (gllaucoma) immunosuppressed prev malignancy recent trauma fever neck stiffness papilloedema - swollen optic discs ```
26
classification of headaches
Primary (migraine, cluster, tension) Secondary (meningitis, subarachnoid haemorrhage, Giant cell arteritis, idiopathic intracranial HTN, medication overuse headache) painful cranial neuroptahies, facial pains and othe headaches (trigeminal neuralgia)
27
pathophysiology of migraines
Changes in brainstem blood flow → unstable trigeminal nerve nucleus and nuclei in the basal thalamus → release of vasoactive peptides (CGRP and substance P)→ inflammation, vasodilation and plasma protein extravasation
28
migraine severity features uni/bilateral
moderate to severe ``` aura disrupt daily activity naus/vom photo/phonophobia throbbing ``` unilateral
29
tension severity features uni/bilateral
mild-modeate. continue with activities squeezing/tightening no naus/vom none/one of phot/phonophobia scalp tenderness bilateral
30
cluster severity features uni/bilateral
v/ severe ``` pain around eye/ temporal cranial autonomic features, ipsilateral --red eye --- lactimation --swollen lid -- facial flushing -- blocked nose -rhinnorhea agitated frequent but short may but nocturnal- wake u up ``` unilateral
31
rhinnorhea
= blocked nose
32
trigeminal neuralgia uni/bilateral features
unilateral facial pain severe electric shock/shooting/stabbing triggor= eating, talking
33
trigeminal neuralgia treatment
carbamazepine
34
non pharmocological headache management
lifestyle modification trigger management psychological and behaviour treatment surgical treatment (rare)
35
migraine preventative treatment
B blocker- propanolol acupuncutre topiramate - anticonvulsant botulinum toxin injections Riboflavin (vit B2) amitriptyline- tricyclic antidepressant BAT BRA
36
migraine relief treatment
triptan (eg sumatriptan) + NSAID | antiemetics (naus/vom)
37
what should NOT be given to headache patients
opioids/ergots
38
tension headaches treatment
``` analgesics - aspirin, NSAIDs tricylci antidepressant (amitryptilline) ```
39
cluster headaches treatment for acute attack
triptan - sumatriptan - (zolmitriptan) 100% oxygen
40
cluster headache prevention treatment
verapamil (CCB) corticosteroids avoid alcohol lithium
41
visual fortification spectra
visual patterns seen withiin aura of migraine - zig zags - lines - flashing lights non-visual aura experiences do exist -- tingling, weakness, dysphasia
42
meningitis management that is not to do with patient
notify public health
43
how is neisseria meningitidis spread
droplet
44
glasgow coma scale
a measure of consciousness | eye/verbal/motor response
45
neonatal causes of menigitis
e coli strep b listeria
46
infant causes of menigitis
hemophilius influenzae b neisseria menigitidis strep pneumonia
47
adults causes of meningitis
neisseria meningitidis strep pneumoniae listeria if immunocompromised
48
name some complications of meningitis
``` death amputation scars (from rash) seizures hearing loss (from brain swelling) brain damage, neurological dysfunction ```
49
meningitis and encephalitis risk factors
immunosuppression | travel
50
name 2 causes of chronic meningitis
TB syphillis cryptococcal -- fungus! parasitic
51
what are non-infective causes of meningitis and encephalitis
cancer drug side effects autoimmune - vasculitis, SLE
52
what is different about the presentation of chronic menigitis (compared to acute)
triad = absent/ late | anorexia
53
menigitis triad other symptoms
headache stiff neck fever ``` photophobia rash malaise, vomitting irritable wants to lie still papilloedema -- due to increased ICP -- usuaully bilateral ```
54
encephalitis symptoms
preceding - flu like illness (headache, sore throat, myalgia, malaise, runny nose) ``` then: - fever altered GCS - seizures - memory loss - headache ``` +/- meningism
55
kernigs sign
resistnace to extension of the leg while hip flexed (thigh at 90 degrees and calf straightened) sign of menigism - specific but not sensitive
56
brudzinki's sign
neck in lifted (flexion) and there is reflex flexion of hips and knees in response (in order to relieve meninges discomfort) sign of menigism - specific but not sensitive
57
CSF biochemistry results for menigitis
bacteru, TB, cryptococcus (fungus): - HIGH in protein and LOW in glucose virus: - HIGH in protein and NORMAL in glucose (virus does not use glucose in order to replicate whereas the others do)
58
antibiotic treatment for bacterial meningitis
most = cefotaxime and ceftriaxone (3rd gen cephlosporin) listeria = amoxycillin
59
non antibiotic treatment for menigitis
steroids - IV dexamethosone --> reduces brain swelling call public health
60
treatment for encephalitis
mainly supportive - fluid/nutrients - protect, keep on wards - painkillers - physio and neuro rehab antiobiotics for potential menigitis if herpes simplex virus or varicella zoster virus --> ACICLOVIR
61
when is aciclovir given to encephalitis
if the cause is herpes simplex virus or varicella-zoster virus
62
which prophylactic antibiotics are given to close contacts of meningitis
ciprofloxacin | rifampicin
63
what might GP have to get meningitis started on treatment asap
IM benzylpenicillin (long shelf life)
64
varicella zoster virus -- shingles - cause - preeruptive - eruptive phase - investigation - treatment
varicella zoster virus reactivated after lying dormant in the sensory nervous system. when flares up, travels down affected nerve no skin lesion. but burning and itching in one dermatome eruption 2 days later: skin lesions appear - red, swellen plaques. rash within dermatome. these lesions are infectious sample fluid --> culture. + history and symptoms oral aciclovir
65
watershed stroke
due to low BP -low cerebral blood flow vulnerable areas of brain at the water shed area between arterial territories are the first to be deficient in perfusion lead to infarcts
66
what is obstructive hydrocephalus
complication... Blood (haemorrhagic stroke), pus (meningitis) or mass (tumour) around the brainstem/cerebellum - squashes /covers 4th ventricle and exiting foramen .... raise ICP!!!
67
long term stroke treatment
clopidogrel (antiplatelet) secondary prevention -- statin, warfarin (if AF) antihypertensives
68
haemorrhagic stroke treatment
monitor GCS reverse any anticoagulants (vit k for warfarin) control hypertesnion manual and medical decompression of high ICP (diuretics, raise head etc)
69
how do you reverse warfarin
vitamin K)
70
contraindication for thrombolysis for ischaemic stroke. name 5
``` 1 Recent surgery (3m) 2 Recent arterial puncture 3 History of active malignancy 4 Brain ansyursm 5 Patient is on anticoagulation 6 Severe liver disease 7. Acute pancreatitis 8 Clotting disorder 9 If time of onset not unknown. Don't give thrombolysis -- give aspirin for 2w than clopidogrel after ```
71
ischaemic stroke treatment
``` thrombolysis tissues plasminogen activator = ALTEPLASE antiplatelet therapy = CLOPIDOGREL/ASPIRIN ```
72
general stroke supportice treatment
oxygen | hydration inc glucose
73
CHADVASC=
calculates risk of stroke for patients with AF
74
ABCD score
calculates risk of stroke for TIA patients ``` age diabetes high BP clinical features (of TIA/stroke) duration (longer than 1h = 2 points, less =1) ```
75
calculates risk of stroke for TIA patients
ABCD score
76
calculates risk of stroke for patients with AF
CHADVASC=
77
stroke investigation
** CT/MRI head -- see if haemorrhagic or ischemic (ischaemi = less dense) look for AF - pulse, BP, ECG look for thrombocytopenia/polycythaemia (highrbc) -- FBC look for hypoglycaemia -- serum glucose can also do doppler ultrasound of carotid
78
lenticulostriate artery haemorrhagic stroke
- these are small vessels off the anterior cerebral artery that supply mid brain, and cross internal capsule - theyre prone to rupture due to thin adventitia - this disturbs all motor and sensory axons - cant transmit (internal capsule) - but the cellbodies are not affected so there is no necrosis. this means there is the possibility of recovery as pressure on axons decreases
79
amaurosis fugax
transient visual distubrance - sudden temporary sight loss in one or both eyes. painless (stroke/TIA) ``` Due to atherosclerosis / thromboembolism in Internal carotid artery Ophthalmic artery Retinal artery -leading to temporary retinal hypoxia ```
80
symptoms of PCA stroke
Visual issues - peripheral vision, face recognition, colour naming, can’t interpret what they can see, cortical blindness Headache --Rare in ischaemic stroke! Think PCA!
81
symptoms of MCA stroke
upper limb and face face droop hemianopia if L stroke: brocas (expressive dysphasia) wernickes (receptive dysphasia + cant understand others)
82
symptoms of ACA
``` lower limb -- gait incontinence drowsiness decrease in spontaneous speech and movement ```
83
why is necrosis of cell bodies in stroke so bad?
no regeneration of these -- non-recoverable
84
internal and external carotid supply where?
internal --> brain external --> head and neck except for brain (neck, dura, skull, face)
85
causes of hemorrhagic stroke
Trauma Aneurysm rupture Thrombolysis, Anticoagulation Carotid artery dissection
86
how does high blood pressure contribute to stroke
Blood pressure → stretches artery → longer → turbulent blood flow → clot → emboli
87
causes of ischaemic stroke
thromboembolism: ``` AF (stasis) infective endocarditis valve disease mural thrombosis from the damaged ventricle hypoperfusion fat emboli after a long bone fracture ``` venous sinus thrombosis liver/lung/kidney failure
88
where is clot likely to go after leaving the heart
arch of aorta --> brachiocephalic --> R common carotid (R brain)
89
risk factors for stroke, name 5
``` 1 Age ---Increases with age --Uncommon under 40 2 Race --Asian --Black African 3 Hypertension 4 Past TIA 5 Family history 6 Smoking 7 obesity 8 Diabetes 9 Alcohol 10 Heart disease (AF, valvular, infective endocarditis) 11 Blood clotting disorders (thrombophilia, polycythemia (high RBC)) --Combined pill 12 Hypercholesterolemia ```
90
are embolic or hemorrhagic strokes more common
85% embolic | 15% hemorrhagic
91
male or female more likely for strokes and what age group and what ethnicities
male older Asian, black African
92
``` what blood vessels are between: skull and dura dura and arachnoid arachnoid and pia pia and brain ```
skull and dura -- meningeal vessels dura and arachnoid -- bridging veins arachnoid and pia -- the circle of Willis pia and brain -- no veins. pia forms part of the blood-brain barrier, cannot separate
93
complication of TIA
stroke! assess with ABCD score
94
what in your liefstyle is adjusted after TIA
``` no driving for 4w smoking weight activity alcohol ```
95
pharm treatment for TIA
``` antiplatelet -ASPIRIN (or clopidogrel) statins long term anticoagulant if AF (warfarin0 control diabetes control CV with antihypertensives ```
96
TIA investigations
``` hisotyr can be diagnostic Bloods --FBC - polycythemia --ESR- raised in vasculitis --Glucose - hypoglycaemia --Creatinine --Electrolytes --Cholesterol Doppler US/MRI/CT angiography - look for stenosis + determine extent ECG/ echo/ Cardiac monitoring - AF, MI , other heart problems ```
97
TIA symptoms sudden or gradual
sudden
98
are more TIAs anterior or posterior circulation and what vessels do each refer to
90% anterior circ -- carotid artery 10% posterior circ -- vertebrobasilar artery
99
anterior circ TIA symptoms
- amauris fugax - aphasia (production /comprehension of speech- brocas/wernickes) - hemiparesis (unilateral weakenss) - hemisensory loss
100
posterior circ TIA symptoms
- diplopia (double vision) - vertigo - vomitting - choking, dysarthia (speech -muscular) - ataxia - hemisensory loss - hemianopia - tetraparesis (muscle weakness in all 4 extremeties) - transient confusion
101
what is pathophysiological diff between stroke and TIA
TIA ischaemia is short lived WITHOUT infarction so it resolves before irreversible cell death TIA- small vessel occlusion
102
TIA causes
Microemboli - - From carotid - - Cardiac embolus (IE, AF, valve issue) Hyperviscosity - - Polycythaemia - - Sickle cell anaemia - - V raised wbc - - Meyloma Hypoperfusion - - Esp young people - - Postural hypertension - - Atherosclerosis - reduced flow - - Cardiac dysrhythmia
103
risk factors of TIA. name 5
``` 1. age 2 gender - m>f 3 race: black = :/ 4 CV - hypertension, heart disease, PAD 5 past TIA 6 combined pill 7 alcohol 8 hyperlipidaemia 9 diabetes 10 blood - raised packed cell volume, clotting disorder, polycythaemia ```
104
2 complications of epilepsy
status epilepticus = continuous seizure without recoevery of conciousness - - emergency!! risk CV/resp failure - - causes : alcohol abuse, anti-epileptic therapy poor compliance inc abrupt cessation sudden unexpected death - more common if nocturnal and if uncontrolled epilepsy
105
treatment of epilepsy - pharmacological
anti-epileptics - carbamazepine - lamotrigine - sodium valproate (not if preggers)
106
surgical epilepsy treatment
remove part of brain implant electrical device to control seizure - vagus nerve/ deep brain stimulation
107
epilepsy investigations
Diagnosis = 2 or more seizures, 24h+ apart --Video telemetry EEG - -Electrical impulses in brian measured to detect unusual activity (even when not having stroke) - -Not diagnostic, supports diagnosis - -May help determine type of seizure Image brain - CT/MRI/PET - -Check for bleeds/ underlying cause/ lesions (tumour) / rule out differentials - -Image hippocampus Neural examination(behaviours, skills, functionS) Bloods - - FBC, electrolytes, renal/liver function - -Discover comorbidities - -Rule out infection/metabolic causes - -Genetic conditions associated with epilepsy ECG
108
what does prodrome mean
change in modd/behavious hour/days before epileptic seizure
109
how long does epileptic seizure last
30s - 2min
110
what does postictally mean? give charactheristics too
this is the state after a epileptic seizure | - headache, sore tongue, myalgia, confusion, weakness, dysphasia
111
Generalised tonic-clonic seizure (grand mal)
No aura Loss of consciousness Tonic phase = rigid, stiff (may fall) Clonic phase = generalised bilateral rhythmic muscle jerking Second-minutes Maybe incontinence Followed by drowsiness, confusion, coma (postically) this is a primarily generalised type
112
Typical absence seizure (petit mal)
Usually childhood Cease activity and stare pale (eg stop talking mid sentence) Few seconds Unaware of attack May go on to develop generalised tonic-clonic seizures as an adult this is a primarily generalised type
113
myoclonic seizure
sudden isolated jerk (limb, face trunk) (inc fall) this is a primarily generalised type
114
tonic seizure
sudden body stiff (tonic) but not followed by jerking
115
atonic seizure
sudden loss of tone (floppy ) --> fall
116
Simple partial seizure
Not affecting consciousness / memory. With awareness Temporal lobe - deja vu, fear, olfactory, auditory and gustatory hallucinations Occipital lobe - auras Frontal lobe - conjugate gaze (eyes not working together), jacksonian march (spread of seizure along motor homunculus starting in face / thumb) partial/focal type
117
Complex partial seizure inc features, where
Impaired awareness (before, during or after) Commonly temporal lobe - automatisms eg rubbing hands, smacking lips, chewing, fiddling Less commonly frontal lobe - peddling legs Often preceded by auras Postictal confusion partial/focal type
118
Partial seizure with secondary generlisation
Often, electrical disturbance starts focally spreads wider, causing secondary generalised seizure - typically convulsive
119
primarily generalised vs partial/focal seizures
generliased= electrical discharge throughout whole cortex, both sides --> bilateral manifestations associated with loss of conciousness/awareness focal = electrical discharge limited to one part of one hemisphere so focal onset with features referable to one part of one hemisphere
120
how does syncope differ from epilepsy
Hypoperfusion to brain Lasts shorter - typically <30s Rarely occurs in sleep. much more likely when standing Pre-syncope symptoms = nausea, sweating, seeing stars, noises distorted, dizzy, light-headed May also have limb jerks, eye closed
121
how does non epileptic seizure NES differ from epilepsy
``` Gradual onset Longer duration - 1-20min Associated with Trigger. Protective Eyes closed Crying + speaking History of psychiatric illness ```
122
name 5 epilepsy risk facotrs
``` 1 family history 2 premature babies + small for age 3 childhood febreile convulsion 4 abnormal brain blood vessels 5 alzeimers/dementia 6 trauma 7stroke /TIA 8 drugs- cocaine 9 alcohol withdrawal ```
123
epilepsy age for onset=
most = before 20 or after 60
124
complications of PD
- - psychiatric -- depression, anxiety, phobias - - dementia - -autonomic problems - constipation, increased urinary frequency - - drugs wear off - painful dystonic posturing + loss of mobility
125
surgical treatment of PD
ablation of overactive basal ganglia
126
non pharmacological PD treatment
physiotherpay | - balance and speech and gait disturbance do not respons to medication !
127
gold standard PD treatment - what is it - what else is given - effect - over time?
L dopa = levodopa = dopamine precursor (dopamine cannot cross blood brain barrier) given alongside decarboxylase inhibitor(co- beneldopa, co-careldopa, carbidopa) -- to stop peripheral conversion of L dopa to dopamine (maximise amount that enters brain) symptom releif. no help with disease progression effect decreases over time (5-10y)
128
why is dopamine not given for PD
dopamine cannot cross blood brain barrier)
129
what is given instead of L dopa and why
L dopa saved for late on as effect decreases. instead... dopamine agonist (ropinrole) MAO-B (-giline) / COMT (-capone) inhibitors - enzyme inhibiterer prevent dopamine breakdown so active for longer anticholinergics (amantadine)- treat tremor
130
L dopa s/e | name 3
``` dyskinesia, painful dystonia, psychosis, hallucinations, nausea, vom, a rrhythmias ```
131
PD investigation
observe cardinal signs imaging (cT/MRI/PET) - see substantia nigra atrophy and rule out other things eg tumour confirm with levodopa response
132
3 cardinal PD signs
``` BRADYKINESIA/ AKENISA Slow movement Low amplitude on repetition Deteriorated walking- foot drag, slower hands, smaller writing, expressionless face, soft indistinct speech, reduced blink rate, reduced gait arm swing Difficulty with buttons Difficulty swallowing is a late feature ``` ``` RESTING TREMOR At rest. Improved by voluntary movements Unilateral/asymmetrical ‘Pill-rolling’- thumb over fingers Made worse by anxiety Made worse by repetitive hand movements ``` ``` RIGIDITY (HYPERTONIA) Pain Reduced mobility Resists movement throughout the movement (unlike UMN lesion where resistance falls away as the movement continues (clasp knife) - spasticity) Characteristic stoop ```
133
before motor symtpoms develop for PD ...
``` Anosmia (smell) Depression /anxiety Aches, pains REM sleep disorders Urinary urgency Hypotension Constipation ```
134
HOW do the triad of PD signs present
gradual onset unilateral -worse on one side often mild presentation at beginning (reduced dexterity- difficulty with buttons/ unilateral foot drop / depression)
135
pathophysiology of PD
Neurodegenerative loss of dopamine-secreting cells (dopaminergic neurons) from the substantia nigra (substantia nigra produces dopamine) - -So less striatal dopamine levels - -So thalamus inhibited - -So decreased of movement
136
Causes oF PD
``` enviromental (pesticides, MPTP in illegal opiates) and genetic (parkin gene, alpha synuclein gene) ``` results from oxidative stress and mitochondrial dysfunction
137
accumulation of what in PD
There is an Abnormal accumulation of lewy bodies (contains protein aggregates. alpha-synuclein bound to ubiquitin) in cytoplasm These become more widespread as the condition progresses (lower brainstem → midbrain → cortex)
138
cerebellar ataxia (cerebellar atrophy)
Clumsy Intention tremor Broad based gait
139
generalised dystonia
=sustained muscle contraction Onset in childhood, family history No cell death Twisting, repetitive movement, abnormal posture
140
essential tremor - pathology - commonness - features - treatment
No pathology -- benign Common Action tremor- worse on movement, rare at rest treatment - B blockers (Unless asthmatic/diabetes) - Antiepileptic treatment
141
name 5 risk factors for PD
``` 1 Age 2 Male 3 Family history - Parkin gene - Alpha synuclein gene 4 NON smoker 5 Environmental factors - Pesticides - MPTP , in illegal opiates ```
142
how long does it take kernig sign to develop in sub arach haemor
6h
143
diplopia =
double vision
144
hydrocephalus =? complication of?
blockage of arachnoid granulations (where CSF drains into venous system) Need drainage SAH
145
name 5 SAH complications
``` CVA cerebrovascular accident = stroke Raised ICP Rebleed Cerebral ischemia may results in permanent deficit (common morbidity) Seizures Hyponatraemia Hydrocephalus ```
146
SAH surgical treatments
endovascular coiling = best (promotes thrombosis and ablation of aneurysm) clipping (leaving collapsed sac) stenting
147
SAH medical treatmebts
maintain cerebral perfusion (BP, IV fluids- replace salt) CCB (nimodipine) - reduce vasospasm so reduce risk of cerebral ischaemia corticosteroid (dexamethasone) to reduce inflammation if cerebral oedema
148
what do you do when there is cerebral oedema
corticosteroid (dexamethasone) - reduces inflammation and presh
149
SAH investigation
CT - gold standard - - star shaped lesion - - CT angiography to see extent of anyeursm if confirmed ABG- exclude hypoxia Lumbar puncture (if cT normal) - bloody early on then yellow (xanthochromia - degradation products) later on
150
SAH symptoms
often asymptomatic until rupture. may have 'warning headaches' (sentinel headaches) days before due to small leak from aneurism - sudden intense, persistent thunderclap headache - sudden - severe - ussualy at back- occipital ``` nausea seizure collapse coma, drowsy, lower level of conciousness vision loss/diplopia ```
151
SAH signs
neck stiffness - kernig and brudsinkis signs papiloedema (swollen /dilated optic disc) marked increase in bP (reflex) retinal/subhyaloid/vitresou bleeds (eye ) - terson's syndrome - increased mortality
152
how to differentiate migraine from SAH
SAH has neck stiffness usually
153
causes of SAH
spontaneous bleeding - no trauma mainly due to berry aneurism(s) (at branching point of circle of willis) congential arteriovenous malformation rupture ``` encephalitis vasculitis tumour bleeding disorder acute meningitis ```
154
risk factors of SAH
``` Smoking Alcohol misuse Increased BP Bleeding disorders Family history known anyerusm .. .... increased risk of anyeyrsm if - ehlers danlos syndrome - aortic coactation - kidney disease ```
155
what proportion of strokes are SAH
5%
156
age most common for SAH
35-65
157
complication of subdural haem
coning/hernia of cerbrum | - this then compresses brainstem --> coma
158
subdrual haem management
stabilise patient surgery -- burr hole craniotomy (irrigation, draingage, decompress) mannitol IV - reduced ICP addresss cause of trauma
159
subdural haem inv
CT - crescent shaped blood over 1 hemisphere - midline features are shifter - MRI good for subacute/smaller hematomas
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symtpoms/signs of subdural haem name 6
May have large interval between injury and symptoms - Headache - Drowsy, sleepy - Confusion - Loss of consciousness - Naus, vom - Raised ICP - Seizures - Personality change - Unsteadiness - Focal sensory loss - Unequal pupils
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where is the rupture in subdural haem then what
bridging veins -- these run subdurally from hemisphere to feed into saggital sinus (in dura) bleed--> hematoma increase in oncotic/osmotic pressure so water is sucked out of blood vessels into the hematoma ICP rises gradually
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risk factors/causes for subdural haem
when brain smaller than skull, bridging veins are more vulnerable - children - elderly - alcholics - dementia trauma -- minor : falls may be months after the incident! anticoagulation dural metastases DM
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extradural management
stabilise - ventilation surgical drainage, decompression, ligation, clot removal mannitol IV- reduces ICP
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extradural inv
CT - convex lens (lemon) hyperdense midline shift away from bleed Xray - fracture lines crossing meningeal artery course
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extradural presentation
Unconscious Lucid recovery for few days = typical of extradural ``` Rapid deterioration-- Loss of consciousness (GCS) Focal neurological signs Severe headaches vomiting Confusion Seizures hemiparesis ```
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most common age for extradural haemor
young adults
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causes of extradural haemor
trauma - fractured skull - temporal /parietal bone due to any tear in dural venous sinus
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what does the term positive ictal symptoms mean?
feeling things that are not there | eg hallucination, feeling things etc
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spastic =
continual contraction of muscles
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MS age?
young | 20-40y
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MS gender?
f>m (as other autoimmune) - and hits f sooner except primary progressive MS is m>f
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MS pathophysiology
T cell mediated (autoimmune) :T cells activate B cells to produce antibody against myelin. So demyelination at multiple sites (+ loss of oligodendrocytes) Affects white matter (axons). This disrupts conduction. Sclerosis along neurones → slowed/blocked conduction → impaired movement / sensation Myelin sheath regenerates but new myelin is less efficient and is much worse in high heat - -This healing is what is observed with remissions - -This is why heat exacerbates it (Uhthoff’s phenomenon) Especially at : perivenular sites (around vein /ventricle ) - -Optic nerves (optic neuritis) - -Corpus callosum - -Brainstem - -Spinal cord
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types of MS
Benign - - Few relapses - - Little disability Relapsing and remitting - -Most common - -Onset = days (sudden). Recovery (partial/fully) = weeks Secondary progressive MS - -Follows on from relapsing and remitting, normally after 35 years - late stage MS - -Gradually worsening symptoms with fewer remissions Primary progressive MS - -Gradually worsening disability without relapses or remission - -Typically presents later - -Associated with fewer inflammatory changes on MRI
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Lhermitte’s sign
tingling (electric shock) down back into limb on the flex of the neck (head forward) seen in MS
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Uhthoff’s sign
symptoms worse after heat seen in MS
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in what way do MS symptoms present
Initially monosymptomatic Progressive disability Symptoms worsen with - Heat (= Uhthoff’s phenomenon) - Exercise Symptoms relapse and remit
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3 broad presentations of MS
SPINAL CORD (weak, spastic, stiff, reduced movement, tingly/numb/painful, tremor) OPTIC NEURITIS (pain on eye movement and reduced central vision blurred) BRAINSTEM DEMYELINATION (diplopia, vertigo, facial numbness/weakness, dysarthria, dysphagia, nystagmus, clumsy)
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spinal cord MS symptoms
weakness (motor) - -Often leg - -Spasticity (continual contraction) → stiffness/tightness - -Movement / function impaired eg speech slurred, gait - - Intention tremor numbness/ tingling (Sensory) / pain --Often limbs
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optic neuritis
Plaques collect around optic nerve in MS - -Pain in eye on movement - -Reduced central vision- blurred
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brainstem demyelination in MS (symptoms)
``` Diplopia Vertigo Facial numbness/weakness Dysarthria Dysphasia Nystagmus Brainstem or spinal tract plaque -- Clumsy / poor proprioception ```
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other MS symptoms (other than spinal cord, optic or brainstem)
- cerebellar -- ataxia - constipation - amnesia - cognitive decline - brown sequard - sexual dysfunction (erectile dysfunction) - bladder dysfunction (LUTS)
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diagnosis of MS critera
requires 2 or more attack affecting different parts of CNS
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MS investigations (4)
bloods to exclude differentials MRI brain +spinal cord - looking for periventricular plaques /lesions /white matter abnormalities - exclude other things eg spinal compression lumbar puncture = raised cell count and oligoclonal IgG bands on electrophoresis (not in serum) suggesting CNS inflammation (but this is not specific) electrophysiology - delayed nerve conduction
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MS lifestyle management
``` Reduce stress Stop smoking Vit D/ sun exposure Avoid triggers Avoid infections Regular exercise Physiotherapy inc speech and language Occupational therapy education ```
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MS treatment for acute relapse
IV methylprednisolone Used during relapse. Shortens relapse Try to use infrequently
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MS treatment: disease modifying therapies for aggressive MS
SC inferon IB/IA (anti-inflammatory cytokines) Monoclonal antibodies - Alemtuzumab (targets T cells) - Natalizumab (reduces number of immune cells that cross the blood brain barrier so less damage in CNS. and increases the activity of T regulator/suppressor cells) - Dimethyl fumarate these reduce number of relapses so are good for frequent relapse patients stem cell transplant
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symptoms relief for MS
Antispasticity = Baclofen (GABA analogue) or gabapentin or tizanidine Neuropathic pain = Gabapentin (blocks GABA breakdown) Tremor = Botox (botulinum injections (reduce ACh in neuromuscular junction) -- Transient effect LUTS urgency/frequency ---Self catheterisation ----Tolterodine (anticholinergic) Incontinence Doxazosin (Alpha blocker)
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MS complications
disease progresses - more areas of disease with reduced function reduced life expectancy 5-10y (dysphagia, pneumonia) GU - overactive bladder, incomplete emptying
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race relation to MS
more common in white more risk if further from equator (Esp if higher eg uk, usa)
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how is MS related to virus
If CNS share epitope to virus then , T lymphocytes attack (and B cells --> antibodies)
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what is MND prognosis
very poor. most die within 3 y from respiratory failure
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treatment for MND symptoms
palliative care Drooling - amitriptyline (tricyclic antidepressant) or propantheline (anti-muscarinic) Spasticity - baclofen (GABA agonist) Joint pain - analgesia respiratory failure - non-invasive ventilator and feeding tube Dysphasia - blend food/ NG feeding tube Speech : physiotherapy Occupational therapy
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MND disease-altering treatment
Riluzole Sodium channel blocker → Inhibits glutamate release (anti-glutaminergic) Prolongs life by a few months
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MND investigations
clinical mainly -UMN/LMN signs EMG- electromyography : denervation of muscles due to degeneration of LMN NCS - nerve conduction studies Exclude other diagnoses - -- Lumbar puncture - excludes inflammatory causes - --MRI - excludes structural causes
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umn/lmn signs
``` UMN -- everything upped increased muscle tone --> spasticity hyper-reflexes increased plantar (minimal muscle atrophy ) positive babinksi sign(big toe goes up rather than down when sole is stroked) ``` ``` LMN - everything lowered! muscle atrophy (wasting) hypo- reflexia reduced muscle tone --> flaccid fasciculation (brief spontaneous contraction) negative babinski sign ```
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what is definite / probable/ possible/suspected MND
Definite = LMN+UMN in 3 regions Probable = LMN +UMN in 2 regions Possible = LMN + UMN in 1 region Suspected = LMN or UMN in 1 region
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UMN presentation
No sensory loss No sphincter disturbance No eye movements affected muscular atrophy (weakness and wasting) and spasticity (increased tone, stiffness) - reduced dexterity - stumbling spastic gait - foot/wrist drop - speech (slurred, hoarse, nasal) /swallowing disturbed (choking) (bulbar palsy) - fasciculation - dementia
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what distinguishes MND from differential diagnosis
No sensory loss No sphincter disturbance No eye movements affected ---These distinguish from MS and polyneuropathies. Myasthenia gravis : eye movements are affected MRI to rule out structural causes lumbar puncture to rule out infective causes
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types of MND - which is most common and most rare - do they affect LMN/UMN - particular features of the type
amyotophic lateral sclerosis (ALS) - most common - UMN and LMN (loss of motor neurones in motor cortex and anterior horn) progressive bulbar and pseudobulbar palsy - LMN - affects CN9-12 only so involved in dysarthria, dysphagia (inc choking), nasal regurgitation of fluids and fasciculating tongue, jaw progressive muscular atrophy - LMN only (anterior horn lesion) - affects distal groups before proximal - starts in one place and gradually affects more primary lateral sclerosis - rare - UMN only (loss of Betz cells in motor cortex) - affects groups of muscles rather than individual muscles - no cognitive decline - Upper limb - flexors > extensors - Lower limb - extensors> flexors
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UMN pathophysiology
Destruction of upper motor neurons (namely motor cortex) and anterior horn cells (this is where LMN are) in the CNS and motor cranial nerve nuclei (also LMN) Causes LMN and UMN dysfunction → mixed picture of muscular paralysis motor only!!
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MND epidemiology - gender? - common? - age? - genetic?
m>f uncommon 60 - middle aged there is a familial link
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pyramidal pattern of weakness characteristic pattern of limb muscle weakness in UMN pathology
Upper limb - flexors > extensors - proximal > distal Lower limb - extensors> flexors - distal >proximal
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parkinsons disease vs parkinsonism
parkinsonism = drug induced movement disorder, non-progressive parkinsons disease = neurodegenerative disease (not drug induced)
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what is co-careldopa?
carbidopa (prevent premature breakdown of levodopa) and levodopa (dopamine precursor) PD first line treatment
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What score of CHADVASC is significant and what does this mean
risk of stroke if AF | 2 + ---> anticoagulant
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MND speed of onset
gradual