Neuro conditions Flashcards
1
Q
describe a transient ischaemic attack (TIA)
A
sudden onset, brief neurological deficit due 2 temporary focal cerebral ischaemia (no infarction)
- lasts <24hrs- Sxs usually last 10-15 mins
2
Q
what are the 2 arteries involved in a TIA
A
90%- carotid artery (anterior circulation)
10%- vertebral artery (posterior circulation)
3
Q
list 7 risk factors for a TIA
A
HTN
AF
VSD (ventricular septal defect)
smoking
DMT2
obesity
male + black
4
Q
what are general presentations of a TIA
A
Sxs= maximal @ onset 10-15 mins
amaurosis fugax= transient unilateral sudden vision loss, due 2 retinal artery occlusion
hemiparesis- 1sided weakness/paralysis
hemisensory loss
hemianopia vision loss
syncope + dizziness + ataxia + vertigo
5
Q
what are area specific signs of a TIA
A
ACA- weak, numb contralateral leg
MCA-
weak, numb contralateral side of body
face drooping with forehead sparing
dysphagia
PCA- vision loss= contralateral homonymous hemianopia with macular sparing
vertebral- cerebellar syndrome
pneumonic= DANISH
Dysdiadochokinesis (can’t do rapid, alternating movements)
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
6
Q
investigations for a TIA
A
clinical Dx
FAST- face, arms, speech, time
1st= FBC- look for polycythaemia, glucose, increased ESR, PT
GOLD= Sx last 10-15 mins + no infarction
7
Q
management of TIA
A
1st=
aspirin 300mg (antiplatelet therapy) + referral to specialist + diffuse weighted MRI
2ndary prevention=
clopidogrel 75mg daily
atorvastatin (20-80mg 48hrs after)
control modifiable risk factors
if AF- anticoagulant eg warfarin
8
Q
how can you differentiate between a TIA and a stroke
A
after recovery:
TIA= Sx usually resolve within mins + always <24hrs w. no infarct
Stroke= Sx last +24hrs w. infarct
9
Q
what are the 2 types of stroke
A
ischaemic and haemorrhage
10
Q
describe an ischaemic stroke
(what percentage of strokes)
A
rapid onset neurological deficit lasting 24hrs+
-due to blood clot blocking blood supply to brain causing ischaemia + infarction
(85% of strokes)
11
Q
list 8 risk factors for ischaemic strokes
A
HTN (biggest)
past TIA
smoking
obesity
T2DM
heart disease (IHD, AF, valve diseases)
combined oral contraceptive oill
clotting disorder
12
Q
what are the four areas infarcts can occur in ischaemic strokes
A
cerebral infarcts
brainstem infarcts
cerebellar infarcts
lacunar infarcts
13
Q
presentation of cerebral infarct in an ischaemic stroke
A
contralateral sensory loss
contralateral hemiplegia (paralysis- usually flaccid then spastic)
UMN facial weakness (forehead sparing)
dysphagia (speech)
homonymous hemianopia
visuo-spatial defecit
14
Q
presentation of a brain stem infarct in an ischaemic stroke
A
quadriplegia
facial numbness + paralysis
vision disturbances
dysarthria + speech imparement
vertigo
n+v
15
Q
presentation of a cerebellar infarct in an ischaemic stroke
A
palatal paralysis + diminished gag reflex
incoordination
ataxia
n+v
dizziness + unsteadiness
horizontal nystagmus
16
Q
what is a lacunar stroke/infarct and how does it present
A
blockage of blood vessels causing ischaemia to deep parts of brain (e.g basal ganglia, internal capsule, thalamus, pons)
sensory loss
unilateral weakness
ataxic hemiparesis
dysarthria
17
Q
investigations for an ischaemic stroke
A
urgent non contrast CT scan (NCCT) of head- 2 distinguish between ischaemic + haemorrhagic & shows site of infarct
Bloods=
FBC- thrombocytopenia, polycthaemia
ESR- raised in vasculitis
PT/INR- if on warfarin
U&Es, cholesterol, lipid profile, PT
ECG- look for AF, MI
other= diffusion weighted MRI scan
18
Q
management of an ischaemic stroke
immediate treatment + secondary prevention
A
once haemorrhagic excluded- 300mg aspirin straight after CT
thrombolysis within 4-5 hrs of Sxs using IV alteplase 2 dissolve blood clots
other option= mechanical thrombectomy (endovascular removal of thrombus)
antiplatelet therapy= aspirin 300mg for x2 weeks
THEN
clopidogrel 75mg daily, long term
prophylaxis= atorvastatin, ramipril, warfarin 4 AF
19
Q
describe a hemorrhagic stroke
A
rapid onset neurological defect lasting 24hrs+
-caused by bleeding into brain due to ruptured blood vessel in/around vein= infarction
20
Q
describe the 2 types of hemorrhagic stroke
A
intracerebral haemorrhage=
rupture of bv within brain- O2 deprivation + infarction- pooling of blood > raised ICP
subarachnoid haemorrhage=
spontaneous bleed into subarachnoid space between arachnoid mater and Pia mater
21
Q
list 6 risk factors for hemorrhagic strokes
A
(mainly the same as ischaemic)
HTN (biggest)
thrombolysis
anticoagulation
arteriovenous malformations
smoking
diabetes
22
Q
presentation of hemorrhagic strokes
A
Sxs last 24hrs+:
raised ICP Sxs
severe headache
limb+ facial weakness
visual or sensory loss
dysphagia
23
Q
investigations for hemorrhagic strokes
A
urgent NCCT of head
- shows hyper dense blood, distinguishes ischaemic from hemorrhagic + shows site of stroke
FBC- look for polycythemia, thrombocytopenia
other = GCS
24
Q
management of a hemorrhagic stroke
A
stop any blood thinning meds eg warfarin, aspirin
neurosurgery referral
IV mannitol 2 reduce ICP
25
name 4 spaces haemorrhages can occur in
extradural
subdural
subarachnoid
intra-cerebral
26
where does an extradural haemorrhage occur and how does one occur
extradural space between dura mate and skull
cause-
trauma 2 temple> fracture 2 temporal/parietal bone > rupture of middle meningeal artery
27
what age group do extradural haemorrhages most commonly occur in
young adults
-as age increases, risk decreases as dura more firmly adhered to skull
28
what is the classic presentation of an extradural hemorrhage
initial head trauma 2 temple/pterion >
lucid interval ('I feel fine'- short episode of drowsiness/unconsciousness)>
sudden rapid deterioration (old blood clot becomes haemolysed)
Sxs due to increased ICP
-rapidly declining GCS
-increasingly severe headache
-vomiting
-seizures
29
what are signs of an extradural haemorrhage
UMN signs
ipsilateral pupil dilation
hemiparesis + bilateral limb weakness
coma
30
what does Cushing's triad indicate and what are the signs
Cushing's triad indicates raised ICP
-decreased heart rate
-wide pulse pressure
-irregular respiration
31
investigations for an extradural hemorrhage
NCCT head= haematoma
-biconvex lens-shaped (lemon)
-hyperdense
-doesn't cross suture lines
-unilateral
-midline drift
skull x-ray- for fractures
32
management of an extradural hemorrhage
urgent surgery > clot evacuation, ligation of bleeding vessel, burr hole craniotomy
IV mannitol 2 reduce ICP
33
where does a subdural haemorrhage occur and what causes one
bleeding into subdural space between dura mater and arachnoid mater
-due 2 rupture of bridging vein
34
list 5 risk factors for a subdural haemorrhage
shaken baby syndrome
shearing deceleration injuries
dural metastases
epilepsy
brain atrophy- dementia/elderly, alcoholics
35
how does a subdural haemorrhage occur
bleeding from bridging vein in subdural space= haematoma
weeks/months later- haematoma autolysis= massive increase in oncotic + osmotic pressure > H20 sucked into haematoma + increase in ICP
36
presentation of a subdural haemorrhage
gradual onset with latent period:
headache + confusion
fluctuating consciousness
seizures
signs of raised ICP= cushing triad
focal neurology occurs later eg unequal pupils, hemiparesis
physical + intellectual slowing
personality change
memory loss
37
investigations for a subdural haemorrhage
NCCT head- crescent (banana) shaped haematoma
crosses suture lines
unilateral
midline shift
acute= hyper dense blood
subacute= isodense
chronic= hypodense (darker than brain)
38
management of a subdural haemorrhage
surgery= clot evacuation, craniotomy, Burr hole washout
IV mannitol to reduce ICP
antiepileptics- phenytoin
address cause of trauma eg childabuse
39
where does a subarachnoid hemorrhage occur and what are 2 causes
spontaneous bleeding into subarachnoid space
causes=
Berry aneurysm (70-80%, mc. @ ACA)
traumatic injury
arteriovenous malformations
idiopathic
40
list 7 risk factors for subarachnoid haemorrhages
HTN
PKD!!!!!
known/previous aneurysm @ SA
trauma
FHx
bleeding disorders
connective tissue disorders
41
symptoms of subarachnoid haemorrhages
occipital THUNDER CLAP HEADACHE
n+v
collapse + loss of consciousness
neck stiffness
sentinel headache (throbbing occipital pain preceding main rupture
42
signs of subarachnoid haemorrhages
meninges inflammation:
-kernig sign (pain on passive extension of leg when knee is flexed)
-Brudzinksi sign (when neck elevated, hip + knee automatically flex)
- (symptom= neck stiffness)
bleeds into eye eg retinol or vitreous
focal neurological signs eg 3rd nerve palsy (fixed + dilated pupil)
low GCS
43
describe the Glasgow coma scale (GCS)
used to measure a person's level of consciousness
out of 15:
eye 4, verbal 5, motor 6
15= normal
8= comatose
3= unresponsive
44
investigations for a subarachnoid haemorrhage
urgent brain CT- looking for subarachnoid and/or intraventricular blood aka. 'star sign'
positive star sign- CT angiography 2 see extent of rupture
negative- lumbar puncture after 12hrs - xanthochromia confirms subarachnoid (yellowish CSF filled w. breakdown products of RBCs)
| PKD= U&E- hyperkalaemia + hyponatremmia
45
management of a subarachnoid haemorrhage
immediate neurosurgical referral
- endovascular/surgical coiling if aneurysm
IV fluids- maintain cerebral perfusion
nimodipine (CCB)- to decrease vasospasm + BP
46
describe an intra-cerebral haemorrhage and its causes
sudden bleeding into brain tissue due 2 rupture of a blood vessel within the brain (10% of strokes)
causes=
HTN- stiff & brittle vessels prone to rupture
2ndary to ischaemic stroke- bleeding after reperfusion
head trauma, arteriovenous malformations, brain tumours, carotid artery dissection
47
list 6 risk factors for an intra-cerebral haemorrhage
HTN
anticoagulation
thrombolysis
alcohol
smoking
diabetes
48
what happens in an intra-cerebral haemorrhage
rupture of blood vessel within brain= O2 deprivation + infarction
-pooling of blood= raised ICP
raised ICP> puts pressure on skull + brain + blood vessels= tissue death
tissue herniation (hydrocephalus) + midline shift + tentorial herniation + coning (brainstem compression)
49
presentation of an intra-cerebral haemorrhage
Sxs last 24hrs+:
sudden onset severe headache
facial + limb weakness
dysphagia
visual/sensory loss
increased ICP
n+v
syncope
loss of consciousness
50
investigations for an intra-cerebral haemorrhage
urgent NCCT of head- distinguish between haemorrhagic + ischaemic and shows site of haemorrhage
-hyperdense blood on CT
Bloods=
FBC- polycythemia, thrombocytopenia
PT/INR if on warfarin
ECG- look for AF, MI
GCS
51
management of intra-cerebral haemorrhages
urgent lowering of BP
IV mannitol 2 decrease ICP
urgent anticoagulation reversal- clotting factor replacement
52
what is syncope
temporary unconsciousness due to a disruption of blood flow to the brain- often leads to a fall
53
what are primary and secondary causes of syncope
primary=
dehydration, missed meals, standing for ages, vasovagal response 2 stimuli eg blood, pain, surprise
secondary=
hypoglycaemia
anaemia
infection
anaphylaxis
arrhythmias
valvular heart disease
hypertrophic cardiomyopathy
54
what happens in syncope
vagus nerve receives strong stimulus > stimulates parasympathetic nervous system
>vasodilation of blood vessels in brain > BP in cerebral circulation decreases = hypo perfusion of brain tissue- loss of consciousness & fainting
55
presentation of syncope
prodrome=
hot or clammy
sweating
dizzy/lightheaded
vision going blurry
headache
56
investigations for syncope
history + clinical examination
ECG (arrhythmias, long QT syndrome)
echo
bloods- FBC =anaemia
electrolytes
bad glucose
57
list 4 primary types of headaches
migrane
cluster
tension
drug OD
58
list 6 secondary causes of headaches
giant cell arteritis
infection
subarachnoid haematoma
trauma
cerebrovascular disease
59
describe a migrane
recurrent throbbing headache- often preceded by aura + associated with n+v and visual changes
60
triggers of migraines using CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraception
Lie ins
Alcohol
Tumult eg loud noises
Excercise
61
what are 3 stage of a migrane
prodrome (days)- yawning, cravings, mood/sleep changes
aura (mins b4 attack)- visual disturbances eg dots, lines, zigzags
somatosensory eg pins and needles
throbbing headache (4-72 hrs)
62
presentation + diagnostic criteria for a migrane
@least 2 of:
unilateral pain (4-72hrs)
throbbing pain
moderate to severe intensity
motion sensitivity
plus @ least 1 of:
n+v
photophobia/phonophobia
-must be a normal neurological exam, no other attributable cause
63
management of migraines
1st= oral triptans eg sumatriptan or aspirin 900mg
NSAIDs= naproxen
anti-emtic= metoclopramide
prevention= required if 2+ attacks per month or require acute meds +2 times a week
BB (propanol), tricyclic antidepressants (amitriptyline), anti-convulsant (topiramate - CI if preggo)
64
describe a cluster headache
clusters of episodic headaches lasting from 7 days up to 1year
-usually 2-3 weeks w. pain free periods inbetween
65
presentation of cluster headaches
rapid onset of excruciating pain around eye + sometimes temples and forehead
-pain rises to a crescendo over a few mins and last 15mins-3hrs, 1-2 times a day
strictly unilateral + localised to 1 area
ipsilateral autonomic:
watery, bloodshot eye
facial flushing
blocked nose
pupil constriction
ptosis
66
investigations and management of cluster headaches
Dx= @ least 5 similar attacks + rule out other causes (brain MRI, ESR, pituitary function tests)
Tx=
acute attack-
15L 100% O2 for 15 mins via nonrebreather mask
triptans eg sumatriptan
prevention-
verapamil (CCB)
no smoking/alcohol
67
describe a tension headache
bilateral generalised pain, radiates 2 neck
mc. headache
can be episodic= <15 days/month
or chronic= >15 days/month for @ least 3 months
68
list 7 triggers of tension headaches
STRESS
sleep deprivation
hunger
eyestrain
anxiety
noise
overexertion
69
presentation of a tension headache
rubber band tight round head
bilateral pain, mild/moderate intensity
+/- scalp tenderness
-no aura, vomiting, photophobia or motion sickness
70
describe trigeminal neuralagia
facial pain in 1 or more branches of the trigeminal nerve : ophthalmic, maxillary, mandibular
-usually unilateral
71
what are 3 risk factors for trigeminal neuralagia
x20 times mc. in multiple sclerosis
increasing age
female
caused by trigeminal nerve compression
72
list 7 triggers of trigeminal neuralagia
eating
shaving
talking
caffeine
brushing teeth
cold weather
spicy food
73
presentation and investigations for trigeminal neuralagia
spontaneous electric shock pain (up to 2mins) in U1/2/3
Dx= clinical- 3+ attacks with the same presentation of Sxs
74
management of trigeminal neuralagia
carbamazepine (anticonvulsant)
surgery 2 decompress nerve if nothing else works
75
who is the typical person presenting with giant cell arteritis and what are their symptoms
50 y/o Caucasian woman presents with
-unilateral tender scalp
-intermittent jaw claudication
-amaurosis fugax
76
investigations for giant cell arteritis
temporal artery biopsy= granulomatous + giant cells & skip lesions
+ raised ESR/CRP
+ normocytic, normochromic anaemia of chronic disease
77
management of giant cell arteritis
prednisolone
- if any signs of amaurosis fugal/vision changes- high dose IV methylprednisolone ASAP
78
what is a seizure
transient episode of abnormal brain activity
79
what are 3 things that only occur in an epileptic seizure vs non-epileptic
epileptic=
-eyes open
-synchronous movements
-can occur in sleep
80
list 6 risk for seizures
FHx
dementia- 10x more likely
alcohol withdrawl
tumours
strokes
cortical scarring
81
describe the pathology of a seizure
GABA= inhibitory
glutamate= excitatory
norm balance between GABA and glutamate shifts towards glutamate
- more glutamate stimulation + more GABA inhibition= more excitatory
82
criteria for diagnosis of epilepsy
1 of :
@ least 2 unprovoked seizures occurring more then 24hrs apart
1 unprovoked seizure + probability of future seizures (>60% risk in 10yrs)
diagnosis of an epileptic syndrome
83
describe the prodrome phase of an epileptic seizure
weird feeling/change in mood days or hrs b4 seizure
84
describe the aura phase of an epileptic seizure
minutes B4:
automatisms (lip smacking, rapid blinking)
strange feeling in gut
deja vu
strange smells
85
describe the post-ictal period of an epileptic seizure + Todd's paralysis
post-ictal period= after seizure:
headache
confusion
myalgia
sore tongue- often bitten
amnesia
dysphagia (temporal lobe)
Todd's paralysis occurs of motor cortex affected- may have temporary paralysis + musc weakness
86
what kind of seizure involves both sides of the brain and always results in unconsciousness
generalised seizures
87
name and describe the 6 types of generalised seizures
TONIC= high musc tone, rigid, stiff limbs- will fall to floor if standing
CLONIC= rhythmic muscle jerking
TONIC-CLONIC (grand-mal)= combo of tonic & clonic
+ up gazing open eyes, incontinence, tongue bitten
MYOCLONIC= isolated jerking of a limb/face/trunk, 'disobedient limb' or 'thrown to the floor'
ATONIC= opp of tonic- lack of musc tone, floppy
ABSCENCE (petit Mal) = mc. in childhood, go pale + stare blankly into space for a few secs- min, then carry on where left off
++ will have a 3Hz spike on EEG
88
what are focal/partial seizures
seizures mainly confined to 1 region/lobe eg temporal
-may progress later 2 generalised seizures
89
how does a simple partial seizure present
no loss of consciousness, patient awake + aware
just uncontrollable muscle jerking
+ sensory/autonomic/physic Sxs depending on which lobe is affected
90
how does a complex partial seizure present
loss of consciousness
post itical period positive
91
what are the different presentations of focal neurologies affecting the temporal, frontal, parietal and occipital lobes
TEMPORAL= aura, dysphagia, memory, emotion, speech
FRONTAL= Todd's palsy + Jacksonian march (simple partial seizure spreads from distal part of limb 2 ipsilateral side of face- seizures march up and down motor homunculus)
PARIETAL= parathesia
OCCIPITAL= visual phenomena eg spots, lines, zigzags
92
investigations for epileptic seizures + GS
electroencephalogram (EEG)
-supportive not diagnostic, can determine type of epileptic syndrome eg 3Hz spike in absence seizure
head MRI/CT- examine hippocampus + rule out other causes eg tumour, bleeding
bloods- rule out metabollic causes + infection
GOLD= clinical diagnosis (@least 2 seizure more than 24hrs apart) + EEG (determine type of seizure
93
management of generalised seizures
usually only started after 2nd epileptic episode
1st= sodium valporate- males + women not childbearing age as highly teratogenic
women child bearing age (15-45)= lamotrigine
if absence- enosuximide
94
management of focal seizures
1st= lamotrigine/carbamazepine
2nd= sodium valproate/levetrivacetam
95
what is status epilepticus
status epilepticus= comp of epilepsy, 3+ seizures in 1hr/seizure lasting longer than 5 mins
Tx= IV/rectal benzodiazepines eg lorezapam or diazepam, if not working give phenytoin
96
what is Parkinson's a loss of
loss of dopaminergic neurones from substantia nigra pars compacts in basal ganglia
97
list 5 risk factors for parkinsons
FHx
males
increasing age
encephalitis
pesticide exposure
98
what are the basal ganglia responsible for
coordination of habitual movements eg walking, controlling voluntary motions, learning specific movements patterns
99
what does the substantia nigra pars compacta produce and how does it initiate movement
produces dopamine, essential for correct functioning of basal ganglia
2 initiate movement:
substantia nigra pars compacta signals 2 striatum to stop firing to substantia nigra pars reticula - therefore stopping inhibition of movement
if substantial nigra pars compact= degenerated- decreased dopamine production and input= harder to initiate movement
100
what are the cardinal presentations of Parkinson's
bradykinsesia (slowness of movement)
resting tremor
rigidity
postural instability
often asymmetrical
101
signs of parkinsons
impaired dexterity
fixed facial expressions
foot drag
shuffling gate w. arm swing on 1 side
pill rolling thumb (rolling thumb + finger back and forth)
cogwheel/lead pipe rigidity (resistance to motion either stop or start or constant)
stooped posture + forward tilt
102
symptoms of parkinsons
dementia
depression
urinary frequency
constipation
disturbed sleep
fatigue
loss of sense of smell
103
what are the 3 steps of diagnosis for parkinsons
1. Dx of Parkinsonium syndrome= bradykinesia + 1 of : rigidity, resting tremor, postural instability
2. exclusion criteria (can't have any)
- Hx of stroke
- repeat head injury
-neuroleptic Tx
-unilateral features after 3 yrs
3. supportive criteria (3+ required)
-unilateral onset
-rest tremor present
-progressive
-excellent response to L-dopa
-visual hallucinations
104
management of parkinsons
moderatly/severely= levodopa (L-dopa) + peripheral decarboxylase inhibitor eg beneldopa
problem= body can become resistant 2 L-dopa
-therefore give COMT inhibitor alongside L-dopa to prevent wearing off eg entacapone
105
what is dementia
neurodegenerative disorder- decrease in cognition (memory, judgement, lang) overtime
106
name 4 kinds of dementia
alzheimers
vascular
Lewy body
fronto-temporal
107
list 4 risk factors for Alzheimers
Down's
ApoE4 allele homozygosity in familial alzheimers
depression/loneliness
increasing age
108
describe the pathology of alzheimers
extracellular deposition of:
beta-amyloid plaques + tau-containing intracellular neurofibrillary tangles
- accumulation of above= reduction in information transmission and eventually death of brain cells
also occur=
damaged synapses, atrophy, cortical scarring, decreased Ash neurotransmitter
109
presentation of Alzheimers (including x3 signs)
memory- episodic & semantic (lang difficulty, gen knowledge, fact recall)
lang- difficulty understanding/finding words + dysphagia
attention + concentration issues
physics changes eg personality change, withdrawal, delusions, apathy
disorientation (time + surroundings)
signs=
agnosia- can't recognise things
apraxia- can't do basic motor skills
aphasia- speech issues
110
1st line + GOLD investigations for alzheimers
1st= MMSE (mini mental state exam)
score out of 30
>25 = normal
18-25 = impared
<18 = severely impaire
bloods= FBC, U&E- rule out other causes
GOLD= brain MRI- temporal lobe + cortical atrophy
111
management of Alzheimer's
supportive therapy
-carers, adapt home, help w. daily activities
meds for Sxs= anti cholinesterase inhibitors eg donepezil, rivastigme, galantamine, memantine
112
describe vascular dementia
chronic progressive decline due 2 loss of brain parenchyma from cerebrovascular events eg infarction caused by stroke
113
list 7 risk factors for vascular dementia
history of TIAs
AF
HTN
CHD
hyperlipidemia
smoking
obesity
114
presentation of vascular dementia
stepwise progression
= periods of stable Sxs followed by sudden increase in severity
visual disturbances
UMN signs
difficulty solving problems
apathy
disinhibtion
poor attention
emotional disturbances
mood changes
115
investigations for vascular dementia (including GOLD)
Hx of TIA/stroke?
bloods 2 rule out other causes
MMSE
CT/MRI to look for previous infarcts
GOLD= dementia diagnosis + sign of cerebrovascular event
116
management of vascular dementia
1st=
antiplatelet therapy : aspirin or clopidogrel
OR
anticoagulation therapy= warfarin, rivaroxaban
supportive therapy + lifestyle changes
SSRIs or antipsychotics eg sertraline or lorazepam
117
what causes Lewy body dementia
abnormal deposits of a protein called alpha-synuclein (Lewy bodies)
neurodegenerative w. parkinsonium
118
what would Lewy body dementia 1st and then Parkinsonism be called
vs
what would Parkinsonism as presenting complaint be called
dementia 1st then Parkinsonism= Lewy body dementia w. parkinsonism
parkinsonism as presenting complaint= Parkinson dementia
119
presentation of Lewy body dementia (+ Parkinsonism Sxs)
often dementia presents initially:
memory loss
spatial awareness difficulties
loss of cog fucntion
behavioural problems
visual hallucinations
sleep disorders
parkinsonism:
bradykinesia (slowness of movement)
rigidity
resting tremor
change in gait
120
investigations for Lewy body dementia (+ GOLD)
MMSE
bloods- rule out other causes
Brain MRI- generalised atrophy
GOLD= international criteria-
1. prescence of dementia with 2 of
-fluctuating attention/concentration
-recurrent visual hallucinations
-spontaneous parkinsonism
2. if only one core feature- Dx can be made w. SPECT or PET scan, showing decreased dopamine transporter uptake in basal ganglia
121
management of Lewy body dementia
supportive therapy- cog. stimulation, exercise programmes, @ home care
cholinesterase inhibitors- donezepil, rivastigmine
122
describe frontotemporal dementia
progressive dementia common in under 65s
-atrophy of frontal + temporal lobes with loss of neurones but no plaque formation
123
list 2 risk factors for frontotemporal dementia
autodom inheritance
- change in Tau protein on chromosome 17
FHx of MND
124
presentations of frontotemporal dementia
behavioural issues= issues w. empathy, understanding words, recognising objects/faces
progressive aphasia= slow, difficult speech w. grammatical errors
semantic dementia= issues w. vocal, understanding words, recognising objects/ phases
parkinsonism= memory impairment, disorientation
125
investigations for frontotemporal dementia (including GOLD)
MMSE
bloods 2 rule out other causes
GS= Brain MRI (frontal + temporal atrophy)
126
management of frontotemporal dementia
supportive therapy= carers, speech + lang therapy
SSRIs eg sertraline, citalopram 4 behavioural Sxs
levodopa 4 Parkinsonism Sxs
127
what is huntington's and what mutation causes it
auto dom condition causing progressive degeneration of the nervous system
-100% penetrance, all genotypes will express phenotype
caused by trinucleotide expansion repeats
- CAG repeats on Huntingtons gene on chromosome 4
>35 CAG repeats= Huntington's
128
describe anticipation in huntingtons
successive generations have more CAG repeats in HTT gene on chromosome 4= earlier onset + greater severity of the disease
129
presentation of huntingtons
HYPERKINESIA
chorea (involuntary/irregular unpredictable muscle movements)
dystonia (abnormal muscle tone= musc spasm + abnormal posture)
uncoordination
depression
physch issues
cognitive imparement
behavioural difficulties
psychosis
eye movement disorders
dysarthria (diff talking due 2 weak speech muscles)
dysphagia
130
investigations for huntingtons
clinical diagnosis + FHX + genetic testing (35+ CAG repeats on chromosome 4)
-MRI/CT brain shows loss of striatal vol
131
management of Huntingtons
no treatment, manage Sxs
chorea= antiphychotics (olanzapine), benzodiazepines (diazepam), dopamine antagonists (tetrabenazine)
psychosis= antipsychotics (haloperidol)
depression= SSRIs (citalopram)
132
ethics around Huntingtons + testing for it
poor prognosis= 15-20 yrs from onset
- suicide= 2nd mc cause of death
child of affected adult has 50% chance of inheriting disease
can take a genetic test when 18 yrs
133
describe the 4 kinds of hypersensitivity reactions
T1= IgE antibodies
basophils>mast cells - release histamine
-anaphylaxis, food + drug allergies, bee stings
T2= IgG/IgM
cytoxic/antibody mediated
-haemolytic react (eg blood transfusion)
good pasture's
T3= IgG/IgM/immune complex mediated
immune complex deposition
hypersensitivity pneuomnitis
SLE
polarteritis nodosa
T4= T cell mediated/delayed
contact dermatitis, T1DM, MS
134
describe multiple sclerosis (MS)
Type 4 hypersensitivity autoimmune condition
-characterised by repeated episodes of inflammation of the nervous tissue of brain + spinal cord
= results in demyelination of CNS neurones (oligodendryte destruction)
135
list 4 risk factors for MS
female 20-40yrs
FHx
autoimmune conditions
EBV
136
name and describe the 3 types of MS
relapsing- remitting MS:
-Sxs come and go w. good health inbtwn.
2ndary progressive MS:
-flows from relapsing-remitting to gradually worsening Sxs w. fewer remissions over time
primary progressive MS:
-from the beginning- Sxs gradually develop & worsen over time w.out remission
137
name and describe the most common presentation of MS
optic neuritis- demyelination of optic nerve causing unilateral reduced vision + loss of colour vision
relative afferent pupillary defect:
light shone in affected eye= no pupil change, light in unaffected eye- affected eye will show pupil constriction
also may have eye movement abnormalities- due 2 6th CN palsy (abducens)
138
in multiple sclerosis, describe the presentation of
4 focal neurological weaknesses
&
4 focal neurological sensory Sxs
focal weakness=
Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis
focal sensory Sxs=
Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign (UMN sign- electric shock felt down spine, into limbs due 2 flexion of neck)
139
what is the classic triad associated with MS
Charcot's triad:
-nystagmus
-intention tremor
-dysarthria
140
investigations for MS
1st= (bloods should be norm)
lumbar puncture- may show oligoclonal IgG bands in CSF
GS= McDonald criteia- 2≤ attacks disseminated in time (separate events) + space (diff parts of CNS affected)
Dx tool= MRI brain + spinal cord
oligodendrytes in CNS
141
describe the non-pharm management of MS + management of acute flares
gen managment= MDT care, supportive therapy, legal obligation to inform DVLA
acute flares= IV methylprednisolone
142
describe management of the 3 different types of MS
relapsing-remitting MS=
interferon beta (CI preggo)
DMARDs- IV natalizumab
immunomodulator (oral fingolimod)
2ndary progressive MS=
Siponimod (DMT) or methylprednisolone
primary progressive MS=
ocrelizumab (DMT)
143
what is Motor neurone disease (MND)
group of diseases involving progressive degeneration of UMN + LMN (sensory neurones spared)
144
describe the presentations of upper VS lower motor neurone lesions
UMN vs LMN
-hypertonia -hypotonia
-hypereflexia -hyporeflexia
-no fasciculation -fasciculetinous
-Babinski positive -babinski negative
-powers. -gen. reduced power
arms=flexors>
extensors
legs=extensors>
flexors
MIXED UMN + LMN- THINK MND!!!
145
what mutation is associated with MND
SOD-1 mutation
146
what are 2 things MND never affects
1. eye muscles (MS + myasthenia gravis do)
2. sensory func (MS + polyneuropathies do)
147
what are the four subtypes MND can be classed as
ALS (mc) amyotrophic lateral sclerosis
-UMN + LMN
PMA, progressive muscular atrophy
-LMN only
PLS, primary lateral sclerosis
-UMN only
PBP, progressive bulbar palsy
-CN 9-12 affected
-worst prognosis + highest chance of rest failure
148
what are the key presentations of MND
mixed UMN + LMN presentations
onset in limb= atypical presentation
-wrist/foot drop
-gait disorders/tripping
-wasting of hands
-excessive fatigue
149
investigations for MND
1st= nerve conduction studies- electromyogram
GOLD= clinical diagnosis- presence of UMN + LMN degeneration & absence of evidence of other diseases
150
management of MND
MDT care
supportive therapy- speech + lang therapy + physio
riluzole (antiglutaminergic)
quinine/baclofen (cramps)
comps= aspiration pneumoniae, resp failure, swallowing failure
prognosis= 2-4 yrs
151
what is meningitis
inflammation of the meninges lining the brain + spinal cord due 2 viral, bacterial or fungal infection
-notifiable disease
152
what are the viral, bacterial and fungal causes of meningitis
viral= mumps, herpes, influenza, HIV, measles, enteroviruses (coxsackie)
bacterial= N.meningitidis, E.coli, listeria, haemophiliac, influenza B, s.pneumonia, klebsiella, TB
Fungal= cryptococcus, candida, histoplasma
153
name 4 risk factors for meningitis
immunocompromised
extremes of age
not vaxed
crowded environment (uni!)
154
what most commonly causes neonatal meningitis
group B strep- gram pos diplococcus in chains
-mc. causing neonatal jaundice bc colonises maternal vag.
155
presentation of meningitis
stiff neck
photophobia
headache
fever
raised ICP Sxs
kernig sign- can't extend knee when hip flexed w.out pain
Brudzinksi sign- when neck flexed, knees + hips automatically flex
meningococcus only= non-blanching purpuric rash
156
what are signs of raised ICP
decreased GCS
Cranial nerve palsy
focal deficits
seizures
157
investigations for meningitis
lumbar puncture (@L3/4) + CSF analysis
to ID cause of meningitis (look up table of Investigations)
158
management of meningitis
1st= empirical Abxs
bacterial meningits:
w. rash= benzylpenicilin IV
w. out rash= cefotaxime IV
+ steroids (dexamethasone)
add vancomycin if s.pneumoniae suspected
add amoxicillin if listeria suspected
no spec Tx for viral- analgesia, antipyretics, hydration
159
what prophylaxis should be given to the household/contacts of someone w meningitis ( + what are some comps of meningitis)
prophylaxis= 1 off dose of ciprofloxacin
comps= DIC (disseminated intravascular coagulation)
waterhouse friedrichsen syndrome
160
what is encephalitis and what is it most commonly caused by
viral infection causing inflammation of brain parenchyma
-mc. caused by HSV-1- herpes simplex virus
others= CMV, EBV, Lyme disease, toxoplasmosis
161
presentation of encephalitis
fever
headache
altered mental status
rash
increased ICP
focal neurology- mc. affects temporal lobe= aphasia
meningitis Sxs=
-neck stiffness
-photophobia
-vomiting
-headache
reduced consciousness
162
investigations for encephalitis
bloods-
FBC= raised WBC
U&Es= hyponatraemia
lumbar puncture + CSF analysis- use viral PCR to detect virus
GOLD= MRI brain > swelling of brain, normally unilateral + primarily affecting temporal lobe
163
management of encephalitis
acyclovir
non-viral encephalitis= Abxs (IV benzylpenicilin)
164
what are glial cells
name the 3 kinds of glial cells
what are gliomas
glial cells= surround + support the neurones
3 types=
-oligodendrytes
-astrocytes
-ependymal cells
gliomas= tumours of glial cells, these are PRIMARY brain tumours
165
what are the 3 types of glioma and how are they graded
graded 1-4 (4= most malignant)
Astrocytoma (the most common and aggressive form is glioblastoma multiforme)
Oligodendroglioma
Ependymoma
166
what are meningiomas
tumour of meninges- usually benign but can cause raised ICP + neurological issues
167
where do secondary brain tumours mc. metastasise from
non-small cell lung cancers (mc.)
small cell lung cancer
breast
melanoma
RCC
gastric cancer
168
presentation of a brain tumour
raised ICP:
-cushing triad
-CN6 palsy
-papilloedema (swollen of the optic disc- Dx w. fundoscopy)
focal neurology
epileptic seizures
lethargy + wt. loss
169
investigations for a brain tumour
MRI to locate tumour then > biopsy to determine grade (1-4, 4= worst, glioblastoma)
170
what investigation must you not do If someone has raised ICP
raised ICP = DO NOT LUMBAR PUNCTURE
- can cause brain herniation
171
management of a brain tumour
surgery to remove tumour if possible
+ chemo b4 after and during surgery
dexamethasone + mannitol 2 reduce ICP
palliative care
172
what does hemiplegia vs paraplegia indicate
hemiplegia= 1 side of body > BRAIN lesion
paraplegia= both legs > CORD lesion
173
list the number of vertebrae in each section of the spinal column
spinal column:
C1-7= cervical
T1-12= thoracic
L1-5= lumbar
S1-5= sacral
174
which vertebrae does spinal cord compression (myelopathy) occur between and what are some causes
compression of spinal cord from C1-L1/2
causes=
-vertebral body tumours (mc. mets from lung, breast,, prostate)
-trauma
-prolapsed disc
-epidural haematoma
-infection
175
what are red flag signs for spinal cord compression + other Sxs
RED FLAGS=
progressive limb weakness + UMN signs in lower limbs (eg contralateral hyperreflexia, Babinski sign positive, spasticity
sensory loss below lesion
loss of bladder function/control
paraplegia
back pain
176
investigations for spinal cord compression
MRI whole spine ASAP
-chest x-ray if malignancy suspected
177
management of spinal cord compression
1st= dexamethasone until Tx plan confirmed
surgical decompression (laminectomy, microdiscetomy)
chemo if needed
178
what is caudal equina syndrome and what do the nerve provide innervation for
surgical emergency
nerver roots of caudal equina @ end of spinal cord= compressed L2/3 downwards
nerve roots of caudal equina provide motor + sensory innervation to:
-lower limbs
-perineum
-bladder + urethral sphincters
-rectum
179
what are 4 causes of caudal equina
lumbar herniation @ L4/5 or L5/S1 level
tumours
trauma
infection/abscess
180
presentation of caudal equina syndrome
sudden onset
leg weakness w. LMN signs eg ipsilateral hypotonia, hyporeflexia, loss of ankle reflex
saddle anaesthesia > perianal numbness
bladder/bowel dysfunction + sphincter involvement (incontinence)
181
investigations and management for cauda equina syndrome
urgent MRI spine (diagnostic) + testing nerve roots and reflexes > absent ankle reflex L5-S1
Tx= surgical decompression ASAP
182
what is damaged in foot drop and what are some causes of this damage
foot drop= difficulty lifting front part of foot= dragging of the toes
caused by damage 2 common peroneal nerve L4-S2 via:
-injury
-lower back damage
-cauda equina syndrome
-tumour
-hip replacement
-multiple sclerosis
183
how would you manage foot drop
brace/splint
physiotherapy
specialised shoes
nerve stimulation
surgery if needed
184
what is brown sequard syndrome and what is the classic presentation
hemisection of the spinal cord (mc. cervical region)
1. ipsilateral hemiplegia (corticospinal tract)
2. ipsilateral loss of proprioception, fine touch and vibration (DCML tract)
3. contralateral pain + temp sensation defects (spinothalamic)
185
investigations + management for brown sequard syndrome
1st- bloods
plain radiographs for penetrating/blunt trauma
GOLD= MRI spine + neurological examination 2 see extent of injury eg checking reflexes
Tx=
surgery- spine immobilisation, decompression
steroids to reduce swelling (IV methylprednisolone)
physio/occupational therapy
186
list 3 reflexes and where the nerve that innervate them originate from
L3/4= knee jerk
L5= big toe jerk
S1= ankle jerk
187
what are peripheral neuropathies + name 5 causes
damage to peripheral nerves resulting in transmission blockages between CNS & PNS
causes=
DMT2
demyelination > Guillian- barre, B12 def
infection eg shingles
alcohol excess
surgery
188
name 5 mechanisms that cause peripheral neuropathy
demyelination
axonal damage
nerve compression
vasa nervosum infarction
wallerian degeneration (nerve= cut + distally dies)
189
describe mononeuropathy, mononeuritis complex and polyneuropathy
mononeuropathy= single nerve affected
mononeuritis complex= several individual nerves- causes = WARDS PLC
polyneuropathy= diffuse, often symmetrical pathology
190
what is the pneumonic for causes of mononeuritis complex
WARDS PLC
Wegner's vasculitis
AIDS/amyloidosis
RA
DMT2
Sarcoidosis
Polyarteritis nodosa
Leprosy
carcinomas
191
describe carpal tunnel syndrome
mononeuropathy
-compression of median nerve (C6-T1) passing thru carpal tunnel
median nerve provides innervation 2 palmar side of hand:
thumb + index + middle finger + half of ring finger
motor innervation of thenar muscles
192
what are some risk factors/causes of carpal tunnel syndrome
female
acromegaly
hypothyroidism
RA
pregnancy
obesity
repeat strains
193
presentation of carpal tunnel syndrome
gradual onset-
weakness of grip + aching hand and forearm > worse @ night, relieved by hanging hand over side of bed (wake + shake)
parathesia of hand
wasting of thenar eminence
194
investigations and management of carpal tunnel syndrome
Dx= clinical based on Sxs
Phalen test= make fist + flex wrist for 1 min
positive> pain + parathesia
Tinel test= tapping wrist > causes tingling
Electromyogram> diagnostic if above tests uncertain
Tx= wrist splint @ night + steroid injections
last resort > surgery 2 decompress
195
describe wrist drop
radial nerve palsy > C5-T1, innervates forearm extensor muscles
Sxs= wrist drop + loss of sensation in dorsal hand & lateral 3.5 fingers
Tx= splint + simple analgesia
196
describe claw hand
ulnar nerve palsy>C8-T1, motor innervation to part of forearm + most of hand
Sxs= claw hand, difficulty straightening fingers, numbness along forearm, wrist, ring + little finger
Tx = splint + simples analgesia
197
what is sciatica and what are causes of it
lower back pain + Sxs associated w. irritation of the sciatic nerve: L4-S3
causes:
spinal= disc herniation/prolapse
non-spinal= piriformis syndrome, tumours, pregnancy
198
presentation of sciatica
unilateral pain from buttock > down lateral leg > pinky toe
weak plantar flexion + absent ankle jerk reflex
leg weakness
199
investigations and management of sciatica
Dx=
1st- SOCRATES + physical examination (no ankle reflex + can't do straighten leg raise test w.out pain)
GOLD= MRI spinal cord
Tx= analgesia - NSAIDS/amitriptyline
+ physio
surgery- decompression
200
what are causes of motor and sensory polyneuropathies
polyneuropathies= glove + stocking presentation
MOTOR= mc Guillian Barre
SENSORY= mc. diabetic neuropathy
other causes= vasculitis, malignancy, B12 def, RA
201
what are cranial nerve lesions and where do CN 3-12 stem from
damage to a nerve via trauma, compression, infection> results in interruption of axonal continuing
nerves 3-12 come from brainstem
therefore brainstem pathology = cause
eg trauma, tumour, multiple sclerosis
202
describe lesions of cranial nerves 1-6
1. olfactory= impared/loss of sense of smell
2. optic= blindness, visual field defects
3.occulomotor= ptosis, down + out eye, fixed and dilated pupil
4. trochlear= diplopia looking down
5. trigeminal= jaw deviates to 1 side, loss of corneal reflex, causes= trigeminal neuralagia: sensory/motor jaw pain in v1/2/3
6. abducens= adducted eye, inability 2 look laterally > sign of raised ICP
203
describe lesions of cranial nerves 7-12
7. facial= facial droop w. forehead sparing
causes= Bell's palsy + parotid inflammation
8. vestibulocochlear= loss of hearing + balance
causes= skull changes (eg Paget's) compression, middle ear disease
9. glossopharyngeal= impaired gag reflex
10. vagus= impared gag reflex, swallowing, respiration, vocal issues
causes= jugular foramen lesion
11. accessory= can't shrug shoulders or turn head against resistance
12. hypoglossal= tongue deviation towards affected side
204
describe myasthenia gravis
autoimmune condition causing disorders of neuromuscular transmission > due 2 binding of autoantibodies to components of the neuromuscular junction
-mc. acetylcholine receptor
(antibodies destroy the connections between nerves and muscles= weakness in skeletal muscles)
205
describe the pathology of myasthenia gravis and what is condition related to in females/males
1. autoantibodies bind to post-synaptic receptor> competitively inhibit Ach binding
2. more receptors blocked during exertion - leads 2 more muscles weakness
3. autoantibodies activate compliment system > damages cells at post-synaptic membrane
females- related 2 autoimmune disease
males- related to thyoma
206
presentation of myasthenia gravis
Sxs get worse throughout the day:
musc weakness- worse w. exercise, better w. rest- starts @ head and neck > progresses to lower body
weak eye muscles- diplopia, ptosis
weakness more marked in proximal muscles
jaw fatiguability
swallowing difficulty
myasthenia snarl > difficulty smiling , looks creepy
(DDx= Lambert Eaton syndrome BUT Sxs improve w. exertion)
207
investigations for myasthenia gravis
GOLD= clinical diagnosis + serology:
-detection of Acetylcholine receptor antibodies (ACh-R)
-detection of MuSK (Muscle-specific kinase antibodies)
208
management of myasthenia gravis
1st= acetycholinesterase inhibitors eg pyridostigmine or neostigmine
2nd= immunosuppression (steroids> prednisolone)
209
what is a myasthenic crisis + treatment
acute Sxs worsening + acute respiratory weakness
Tx= plasma exchange + IVIg + BiPAP ventilation 4 resp failure
210
describe Guillain barre and who does it mc affect
acute polyneuropathy causing rapid damage to peripheral nerves = in demyelination + axonal degeneration
mc. males: peak ages
15-35
50-75
211
what is mc common cause of Guillain barre and what is the underlying pathology
GB mc. presents post GI infection
-CAMPYLOBACTER JEJUNI
also can be caused by EBV, CMV, HIV
path=
B cells create antibodies against antigens on pathogen that caused infection
- these antibodies also match proteins on the nerve cells
>therefore they may target proteins on the myelin sheath of the motor nerve cell or axon
212
presentation of Guillain Barre
post infection, presents w/:
ascending asymmetrical weakness + paralysis (from nose 2 toes)
parathesia
loss of deep tendon reflexes
peripheral loss of sensation or neuropathic pain
cranial nerve facial weakness
absent reflexes (LMN sign)
+in 50%- autonomic nervous system involvement >decreased sweating + heat intolerance, urinary hesitation
+ in 35% > resp failure
213
investigations for Guillain Barre
1st=
Bloods- FBC (normal WCC), U&Es, LFT (raised AST + ALT)
lumbar puncture @L3/4= raised protein + normal WCC > inflammation + no infection
nerve conduction studies > decreased conduction velocities, downward conduction block
spirometry + resp func test
GOLD= Brighton criteria>
> clinical Sxs + lumbar puncture CSF analysis + nerve conduction studies
214
management of Guillain Barre
IVIg for 5 days with plasma exchange (CI in IgA def patients- allergic reaction)
DVT prohylaxis- LMWH
215
describe wernicke's encephalopathy
reversible acute emergency due to severe B1 (thiamin) deficiency
cause= mainly alcohol
Sxs= ataxia, confusion, ophthalmoplegia (paralysis/weakness of extra-ocular muscles)
Dx= clinical Dx, supported w. microcytic anaemia + deranged LFTs
Tx= pabrinex 5 days
oral thiamine prohylaxis
216
describe Duchenne Muscular dystrophy (including Sxs + who is normally affected)
x-linked recessive condition- characterised by progressive musc. wasting + weakness
muscle replaced with adipose
only affects boys
217
presentation, diagnosis and management of Duchenne muscular dystrophy
difficulty getting up (gower's sign)
skeletal deformities eg scoliosis
Dx=
raised serum creatinine kinase
musc. biopsy w. assay for dystrophin protein
GOLD= genetic analysis
Tx= purely supportive
218
what is Charcot Marie tooth disorder
autodom mutation causing damage to myelin or axons causing PNS polyneuropathy
childhood> adulthood onset
219
presentation, diagnosis and management of Charcot Marie tooth disorder
Sx=
foot drop, stork legs (v. thin calves), hammer toes (toes always curled up), feet- pes cars (high foot arch), reduction in deep tendon reflexes
Dx= nerve conduction studies, genetic testing
Tx=orthotics + physio
220
define depression and name 4 risk factors
persistent low mood, loss of interest and enjoyment + reduced energy causing social and occupational dysfunction
RFs= postnatal status, FHx, dementia, stress
221
investigations for depression
need 5/9 Sxs most of the day, nearly everyday:
1.persistent low mood
2.lack of interest/pleasure
3.wt. loss/gain
4.inability to sleep/oversleeping
5.physcomotor agitation
6.fatigue
7.feelings of guilt/worthlessness
8.lack of concentration
9.thoughts of death/suicide
b. Sx cause sig stress in daily life
c. not due to sub. or other med conditions
d. Sx cannot be explained by another mental disorder
e. no mania episodes
222
management of depression
non-pharm= physical activity, healthy diet, physcotherapy, CBT
antidepressants=
SSRIs eg citalopram
manomine oxidase inhibitors eg isocarboxazid
tricyclic antidepressants eg amitriptyline
