Neuro Flashcards

1
Q

Alzheimers pathophysiology

A

neurofibrillary triangles and amyloid plaque deposits in hippocampus and temporal cortex
reduced acetylcholine production
global progressive impairment of brain function and intellect

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2
Q

Alzheimers genetics

A

risk factor- epsilon 4 of apolipoprotein E gene
early onset- APP, PSEN1, PSEN2

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3
Q

normal pressure hydrocephalus

A

apathy, inattention
urinary incontinence
gait apraxia
reversible dementia
50-70y/o

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4
Q

prion disease presentation

A

myoclonic jerks, seizures
cerebellar ataxia
starts < 50y
rapid onset and progression

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5
Q

alzheimer’s management

A

cholinesterase inhibitors for mild-mod disease to improve behaviour and cognition- donepezil, rivastigmine, galantamine

NMDA antagonist memantine for mod-severe

avoid TCAs and anticholinergics

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6
Q

types of amyloidosis

A

AL- most common, associated with myeloma
AA- assoc w/ inflammatory arthropathies and IBD
ATTR- auto dom

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7
Q

amyloidosis treatment

A

AL- chemo melphalan then stem cell
AA- control underlying condition

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8
Q

amyloidosis presentation

A

bruising, SOB, oedema, peripheral neuropathy, autonomic symptoms

AA- kidney, liver, spleen deposits. nephrotic syndrome or renal dysfunction
AL- SOB, weakness, proteinuria, nephrotic syndrome, renal dysfunction, cardiomyopathy, HF

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9
Q

amyloidosis poor prognostic factors

A

heart involvement
requirement of dialysis

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10
Q

amyloidosis investigation

A

serum immunofixation monoclonal protein
urine immunofixation
Ig free light chain assay raised kappa lambda
bone marrow clonal plasma cells
beta 2 microglobulin
congo red staining

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11
Q

kernig sign

A

pain and resistance on passive knee extension with hips flexed

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12
Q

brudzinski sign

A

hip flex on bending head forward

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13
Q

meningitis predisposing factors

A

influenza A
asplenia
complement deficiencies

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14
Q

meningitis most common organisms

A

children > 3 months:
neisseria meningitidis
strep pneumoniae
hib

neonates < 1 month:
strep agalactiae
ecoli
strep pneumoniae
listeria

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15
Q

cushings reflex

A

bradycardia
hypertension
irregular respiration
assoc w/ cerebral herniation in meningitis

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16
Q

LP results in bacterial meningitis

A

opening pressure > 180
WBC 10-10 000 mostly neutrophils
glucose < 0.4
protein > 0.45

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17
Q

abx for meningitis

A

non blanching rash:
benpen ASAP (300/600/1200mg) (<1y/1-9y/>9y)

without non blanching rash:
ceftriaxone or benpen or cefotaxime or chloramphenicol
vanc if foreign travel

ciproflox for prophylaxis for contacts

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18
Q

behcet’s presentation

A

recurrent oral ulcers
and at least two of:
genital ulcers
erythema nodosum, acne lesions
uveitis, hypopyon
positive pathergy test (papule/pustule after skin prick)
GI symptoms
DVT, thrombophlebitis
seizures, CN palsies, dizziness, memory problems

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19
Q

behcets treatment

A

ulcers:
topical steroids
colchicine, oral steroids, azathioprine
TNF alpha inhibitors

eyes:
pred + azathio
pred + monoclonal ab

GI/CNS:
pred + monoclonal ab

major vasc:
pred + ciclosporin

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20
Q

ischaemic stroke cerebral infarction pathophysiology

A

necrotic pathway w/ rapid cytoskeletal breakdown
apoptotic pathway
reduced cerebral blood flow results in death of brain tissue within 4-10 mins

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21
Q

left vs right hemisphere stroke symptoms

A

left:
aphasia, R sensory and motor loss, R visual field defects, dysarthria, dyscalculia, dysgraphia

right:
L sensory and motor loss, left gaze disturbance, dysarthria, aphasia, spatial disorientation

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22
Q

stroke management

A

thrombolysis with alteplase if presenting within 4.5 hours
aspirin 24h after thrombolysis
thrombectomy if presenting within 6h
load with aspirin if not thrombolysed

2 week follow up:
start clopi or aspirin + dipyrimidole

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23
Q

haemorrhagic stroke BP targets

A

rapidly lower BP if within 6h onset and SBP 150-220
rapidly lower BP if beyond 6h onset but SBP > 220

target SBP 130-140

do not offer rapid BP lowering therapy for pt with structural cause, GCS < 6 or planning early neurosurgery

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24
Q

when to admit TIA?

A

more than one in a week
ongoing neuro symptoms
severe cardiac stenosis
suspected cardio embolic cause
bleeding disorder or on anticoag
no one at home in case of further symptoms

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25
TIA management
300mg aspirin 2/52 stroke doctor within 24h switch aspirin to clopi 75mg after 2/52 add statin 40mg stroke clinic within 7 days if TIA happened over a week ago
26
decompressive hemicraniotomy criteria
within 48h ischaemic stroke clinical deficits suggest MCA territory reduced consciousness infarct of at least 50% of MCA territory infarct volume > 145cm
27
NIHSS scoring
1a level of consciousness (/3) 1b level of consciousness questions (/2) 1c commands (/2) 2 best gaze (/2) 3 visual defects (/3) 4 facial palsy (/3) 5a,b motor arm (/4) 6a,b motor leg (/4) 7 limb ataxia /2 8 sensory /2 9 aphasia 10 dysarthria 11 extinction and inattention
28
ABCD2 score stroke
total score /7 age > 60y BP > 140/90 diabetes uni weakness (2) speech impairment > 60 mins (2) 10-15 mins (1)
29
botulism toxins
7 neurotoxins A, B, E cause disease in humans metalloproteinase cleaves SNARE proteins at NMJ
30
botulism presentation
symmetrical descending flaccid paralysis absent deep tendon reflexes urinary retention, constipation, postural hypotension, dry mouth normal sensory nerve studies reduced muscle action potentials
31
botulin antitoxin
human for infants horse derived heptavalent antitoxin for adults
32
chronic vs episodic cluster headache
clusters > 1y or remission < 1 month
33
cluster prophylaxis
verapamil topiramate, valproate, lithium second line
34
cerebral mets- most common source
lung breast bowel melanoma renal cell
35
glioblastoma multiforme
regional heterogeneity within single lesion highly anaplastic glial cells vascular proliferation and thrombosis necrosis greyish ill defined mass with areas of necrosis and haemorrhage
36
anaplastic astrocytoma
nuclear atypia, diffusely infiltrating astrocytes no microvascular proliferation or necrosis round rubbery lobulated mass firmly attached to dura white ill defined mass calcification not uncommon sometimes whorls and lobules or sheets of spindles
37
presentation of function pituitary tumours
GH excess- acromegaly ACTH excess- cushings PRL excess- galactorrhoea TSH excess (rare)- hyperthyroidism
38
micro vs macroadenoma
micro < 10mm macro > 10mm
39
commonly used MRI sequences for brain tumours
T1 weighted- CSF low signal (dark) T2 weighted- CSF high signal (white) FLAIR for periventricular lesions STIR
40
stereotactic RTX indications
small target < 3cm AVM lesions not amenable to clipping or coiling vestibular schwannoma/acoustic neuroma mets
41
curative resection is not possible for what types of primary brain tumour?
glioblastoma anaplastic astrocytoma
42
indications for surgery for pituitary tymours
non functional w/ mass effect cushings acromegaly acute visual deterioration pituitary apoplexy
43
dementia w/ Lewy bodies
alpha synuclein aggregates in brainstem and cortex neurotransmitter deficiencies, predominantly cholinergic and dopaminergic fluctuating levels of arousal REM sleep disorder
44
treating dementia w/ lewy bodies
cholinesterase inhibitors for cognitive symptoms dopaminergics for parkinsonism dopaminergics can worsen confusion and hallucinations
45
parkinsonism
bradykinesia and at least one of: tremor/rigidity/gait disturbance
46
encephalitis most common causative organism in UK
HSV 1
47
causes of encephalitis (infectious)
HSV, VZV, enterovirus, adenovirus, parechovirus, HIV TB, listeria, strep pneumoniae, neisseria meningitidis, syphilis crypto neoformans, toxoplasma, rickettsiae, fungal
48
causes of antibody associated encephalitis
paraneoplastic non paraneoplastic hashimotos
49
CSF findings in CNS infections
normal: opening pressure 10-20 0.45g protein 50-66% glucose bacterial: raised opening pressure 100-50000 cells (neutrophils) 1g protein 40% glucose (low) viral: normal opening pressure 5-1000 cells (lymphocytes) 0.5-1.0g protein 50-66% glucose (normal) TB: high or v high pressure 5-500 cells (lymphocytes) 1-5g protein glucose 33% (v low) fungal: v high opening pressure 0-1000 cells (lymphocytes) 0.5-2g protein 30-50% glucose
50
encephalitis management
IV aciclovir also IV ben pen to cover for meningitis add broad spec abx if bacterial encephalitis is suspected
51
neuological manifestations of eosinophilic granulomatosis w/ polyangiitis (churg strauss)
peripheral neuropathy/mononeuritis multiplex stroke
52
management of epilepsy in pregnancy
5mg folic acid preconception and first 3/12 pregnancy fetal anomaly scan 19-20 weeks if on phenytoin, give vit K from 36 weeks (to counteract coagulopathy) increased clearance of antiepileptics in pregnancy
53
epilepsy predisposing factors
premature birth head injury complicated febrile seizures genetic conditions FHx structural abnormalities incl stroke and trauma infections (TB, malaria, HIV, zika) metabolic e.g. uraemia immune mediated (anti NMDA encephalitis, anti LG1 encephalitis) dementia and neurodegenerative conditions
54
seizure pathophysiology
influx of extracellular calcium and depolarisation neural membrane > Na channels open > influx of Na > repetitive action potential > hyperpolarisation of GABA receptors/K channels (spike on EEG)
55
eliptogenesis
transformation of normal neuronal network into one that is chronically hyper excitable
56
focal impaired awareness seizure anatomy
medial temporal (mostly hippocampal) focus
57
focal impaired awareness seizure features
impaired or loss of consciousness aura automatism post ictal confusion
58
DVLA and seizures
inform after first episode stop for 6 months after first seizure with normal EEG stop for 12 months if abnormal report can drive if seizure free (and aura free) for one year or if nocturnal only for the past 3 years for vocational group 1 or group 2 license, needs to be seizure free, not on antiepileptics and no continuing liability for 10 years
59
epilepsy referral to tertiary services
poor control w/ medication within 2y or 2 drugs
60
resolution of epilepsy is defined as?
seizure free for 10 years no antiepileptic drugs for at least 5y
61
tonic clonic treatment
sodium valproate carbamazepine lamotrigine
62
focal seizure treatment
carbamazepine lamotrigine
63
absence seizure treatment
ethosuxamide
64
management of status epilepticus
pre hospital: 10-20mg PR diazepam or PO midaz and repeat every 15 mins 0-10 mins: IV loraz 0.1mg/kg and repeat once after 10-20 mins 0-160 mins: phenytoin infusion 15-18mg/kg or phosphenytoin infusion or phenobarbital bolus refractory: GA (propofol/midaz/thiopental) continued for 12-24h after last seizure, then taper
65
management of status in children
5 min: PO 0.5mg/kg midaz or 0.1mg/kg loraz 15 min: 0.1 mg/kg loraz 25 min: phenytoin 20mg/kg infusion or phenobarbital if on regular phenytoin 45 min: RSI thiopental 4mg/kg
66
postural tremor
occurs when limb is raised against gravity essential tremor anxiety alcohol wilsons disease
67
essential tremor management
propranolol or primidone deep brain stimulation, radiofrequency thalamotomy
68
friedreich's ataxia
auto rec GAA repeat expansion of frataxin most common cause of death is congestive HF and arrhthymias life expectancy 40-50y symptoms begin 5-20y affected areas: spinocerebellar tracts and dorsal columns in spinal cord pyramidal tracts in cerebellum and medulla
69
friedreich's ataxia presentation
typically more slowly progressive than other dementias progressive ataxia absence of deep tendon reflexes spasticity peripheral sensory neuropathy dysarthria, dysphagia muscle weakness, progressive kyphoscoliosis pes cavus, hammer toes HOCM, fibrosis, CCF, arrhythmias DM, optic atrophy, hearing loss
70
frontotemporal dementia pathophysiology
1/2: tau (Pick's bodies) 1/2: TDP 43 transactive response DNA binding protein 43 genes: C9orf72, MAPT, GRN associated w/ progressive supranuclear palsy PSP, corticobasal degeneration CBD, familial MND
71
types/syndromes of frontotemporal dementia
behavioural variant primary progressive aphasia semantic
72
semantic dementia
syndrome of frontotemporal dementia loss of vocabulary and loss of recognition of familiar faces or objects fluency of speech maintained
73
histoplasmosis risk factor
caving (bat dropping)
74
guillain barre
most have preceding URTI or UTI campylobacter is most common organism ascending paralysis flaccid tone, hypo/areflexia raised protein in CSF delayed conduction velocities > IVIG and plasma exchange most make full recovery 20% have long term weakness/paraesthesia/fatigue
75
headache urgent referral criteria
new/sudden/severe/unexpected progressive/persistent fever neck pain/stiffness photophobia papilloedema atypical or new onset aura and on COCP visual disturbance or vomiting unless clearly migraine contacts with similar symptoms head trauma within last 3/12 worse on standing or lying down pregnancy malignancy history HIV or immunosuppression
76
Holmes Adie syndrome
holmes adie pupil and absent deep tendon reflexes absent/slow response to light but normal accommodation 80% unilateral
77
holmes adie syndrome pathophysiology
mostly idiopathic, assoc w/ syphilis, tumours, trauma, post op damage to ciliary ganglion > interrupted parasympathetic supply to ciliary body and iris damage to dorsal root ganglion > loss of deep tendon reflexes
78
Ross syndrome
variant of holmes adie holmes adie pupil, loss of tendon reflexes and hypohidrosis
79
horner syndrome
ptosis + miosis + anhidrosis interruption of sympathetic pupillomotor fibres
80
causes of horner syndrome
central: anhidrosis of face, arm and trunk - syringomyelia, MS, encephalitis, brain tumours, lateral medullary syndrome preganglionic: anhidrosis of face - cervical rib, thyroid cancer or removal, bronchogenic pancoast tumour, trauma, thoracic aortic aneurysm post ganglionic: no anhidrosis - cluster headache, carotid artery dissection or aneurysm, carvenous sinus thrombosis, middle ear infection
81
pupilloconstrictor and pupillodilator pathway
constrictor: Edinger Westphal nucleus in midbrain > orbit on CNIII dilator: 1st order from posterior hypothalamus through brainstem to ciliospinal centre of Budge C8-T2 2nd order preganglionic neurones from cord to paravertebral sympathetic chain to superior cervical ganglion 3rd order postganglionic fibres traverse with internal carotid into skull to orbit
82
ptosis is caused by paralysis of...
superior tarsal muscle
83
testing for Horners syndrome
cocaine eye drops > lack of dilatation apraclonidine hydrochloride beta adrenergic receptor agonist eye drops > affected eye more dilated hydroxyamphetamine test to differentiate between 1st/2nd/3rd order (dilation occurs in 1st and 2nd order)
84
huntingtons genetics
CAG repeat expansion chromo 4
85
pharmacalogical management of chorea for huntingtons
anti dopaminergics e.g. tetrabenazine
86
medications associated w/ IIH
lithium cimetidine tetracycline tamoxifen vit A nitrofurantoin
87
IIH diagnostic criteria
neuro exam normal except cranial nerves (may have 6th nerve palsy horizontal diplopia) papilloedema normal neuroimaging CT/MRI normal CSF composition opening pressure > 25
87
conditions associated w/ IIH
thyroid, cushings IDA chronic renal conditions lyme
88
management of IIH
weight reduction acetazolamide topiramate steroids for acute severe headache and papilloedema series of LPs ventriculoperitoneal shunt for recurrent disease optic nerve sheath fenestration
89
lambert eaton myaesthenic syndrome
presynaptic autoantibodies to P/Q calcium channels treat with 3,4 diaminopyridine and/or pyridostigmine, steroids, plasma exchange, IVIG assoc w/ small cell lung, ovarian, breast, lymphoproliferative ca, T1DM, thyroid disorders
90
migraine prophylaxis
propranolol 80-160mg topiramate 50-100mg amitriptyline botulinum or CGRP agent if refractory to 2 or more prophylactic drugs
91
managing mitochondrial disorders
coenzyme Q amino acids and vitamins physical exercise
92
lebers hereditary optic neuropathy
mito disorder defective complex 1 NADH coQ oxidoreductase > optic nerve degeneration
93
kearns sayre
mito disorder degeneration of retinal pigments > ophthalmoplegia, painful eyes, cardiac conduction defects defects in ragged red fibres
94
MELAS syndrome
mitochondrial encephalopathy lactic acidosis stroke syndrome energy deficiency, angiopathy, nitric oxide deficiency
95
MERF
myoclonic epilepsy w/ ragged red fibres mito disorder
96
maternally inherited deafness and diabetes MIDD
mito disorder 3242 tRNA mutation defective insulin secretion and cochlear hearing loss age 30-40y
97
pearson syndrome
mito disorder DNA deletions sideroblastic anaemia, pancreatic dysfunction
98
leigh syndrome
mito disorder bilateral symmetric necrotising lesions spongy changes and microcysts in basal ganlia, thalamus, brainstem, cord
99
mitochondrial neurogastrointestinal encephalopathy MNGIE
pseudo obstruction TYMP mutation
100
causes of mononeuritis multiplex
diabetes B12 deficiency sarcoidosis vasculitis RA, SLE HNPP lyme, leprosy
101
MND features
asymmetrical UMN and LMN muscle weakness, wasting , fasciculation brisk reflexes, spasticity ALS- bulbar, arm and leg UMN and LMN signs. upper limb > lower limb. PBP- facial weakness, dysphagia, progressive dysarthria, upper and lower limb weakness, emotional lability PMA- LMN only, poor prognosis PLS- progressive spastic weakness arms and legs, spastic dysarthria, sensation intact. aggressive course
102
causes of MND
infections (polio, tetanus, lyme) lead paraneoplastic plasma cell dyscrasia metabolic conditions hyperlipidaemia genetic
103
MND treatment
positive pressure ventilation riluzole (bone marrow suppression and deranged LFTs)
104
Kennedy disease
X linked spinobulbar muscular atrophy CAG expansion LMN progressive weakness and wasting, no spasticity slight sensory neuropathy assoc w/ gynaecomastia and reduced fertility
105
MS risk factors
HLA DRB1 EBV vit D deficiency smoking relapses- stress, post partum, infection
106
MS 4 key areas of demyelination
periventricular cortical/juxtacortical infratentorial spinal cord
107
Kurtzke Disability Status Score
used to monitor MS disease status 0- no signs/symptoms 10- death
108
primary and secondary progressive MS treatment
primary- ocrelizumab secondary- siponimod
109
MS drugs safe in pregnancy
interferon glatiramer acetate natalizumab glucocorticoids or plasma exchange for acute episodes during pregnancy
110
muscular dystrophy genetics
auto rec- some limb girdle auto dom- myotonic dystrophy, fascioscapulohumeral, oculopharyngeal, some limb girdle X linked- duchenne, becker, emery dreifuss
111
emery dreifuss MD
uncommon x linked muscular dystrophy presents in teenage years contractures and cardiomyopathy death from first degree AV block
112
muscular dystrophy pathophysiology
Duchenne and Becker- dystrophin gene mutation (Xp21) > leakage of creatine phosphokinase CPK other types- mutation of dystrophin associated glycoprotein complexed
113
muscular dystrophy medication
steroids, creatine ataluren for DMD above 5y who can still walk ACEi, beta blockers
114
myaesthenia gravis pathophysiology
90% cases nicotinic acetylcholine receptor 10% cases muscle specific tyrosine kinase MuSK 75% associated w/ thymus abnormalities HLA B8, HLA DR3 HLA DR1 (ocular)
115
myaesthenia gravid presentation
ophthalmoplegia (ptosis, diplopia, weakness of eyelid closure) muscle weakness (esp shoulder) myaesthenic snarl dysarthria, dysphagia, dysphonia (fatiguable) breathing difficulty
116
most common CNS infections in advanced HIV
toxoplasmosis cryptococcal meningitis, TB meningitis PML (JC virus) CMV encephalitis neurosyphilis CMV retinitis
117
features of cryptococcal and TB meningitis
cryptococcal- subacute over 1-2 weeks, often also disorientation and confusion TB- subacute over several weeks, also constitutional symptoms
118
secondary causes of normal pressure hydrocephalus
intraventricular or subarach haemorrhage meningitis Paget achondroplasia
119
features of normal pressure hydrocephalus
gait disturbance urinary frequency/urgency/incontinence cognitive impairment UMN in lower extremities
120
predictors of improvement after shunting for normal pressure hydrocephalus
good- gait disorder as most prominent symptom, shorter duration of symptoms, clinical response from CSF removal unfavourable- dementia early appearance, no gait disorder or appearing after dementia, alcoholism, marked white matter disease on MRI
121
features of parkinsons plus syndromes
reduced response to Ldopa dysarthria autonomic dysfunction supranuclear gaze palsy
122
parkinsons plus syndromes
multiple system dystrophy dementia w/ lewy bodies progressive supranuclear palsy corticobasal degeneration
123
medications causing parkinsonism
antipsychotics metoclopramide prochlorperazine tetrabenazine sodium valproate lithium
124
adverse effects of ergot derived dopamine agonists e.g. cabergoline, pergolide
cardiac fibrosis
125
parkinsons drug treatment
- Ldopa + decarboxylase inhibitor - dopamine agonist (pramipexole, ropinirole, rotigotine) adjuvants: - MAOBi - COMTi- for people who have developed dyskinesia or motor fluctuations - amantadine (dyskinesia) - SC apomorphine- advanced disease
126
features of corticobasal degeneration
starts on one side of body then becomes bilateral parkinsons symptoms + behavioural and cognitive changes
127
phenytoin toxicity
ataxia, nystagmus, dysarthria, confusion, impaired coordination, seizures, hypoglycaemia hypotension, bradycardia, asystole can > DRESS, TEN, SJS no antidote
128
drugs causing polyneuropathies
isoniazid- subacute pyridoxine- sensory chemo- may start after stopping CTx lead- may be acute, motor
129
CJD histopathology findings
vacuolar degeneration
130
CJD investigations
EEG: periodic sharp wave complexes in sporadic CJD LP: high levels of proteins 14-3-3 and S100B MRI: hyperintense signal change in basal ganglia and cortex tissue diagnosis: gold standard but high morbidity and mortality EEG and LP less sensitive in variant CJD (mad cow)
131
SAH ECG changes
QT prolongation Q waves dysrhthymias ST elevation
132
SAH management
0.9% NaCl to prevent hyponatraemia 3L or more per day to keep intravascular compartment filled inotropes or vasopressors to prevent vasospasm and ischaemia antihypertensives to keep SBP < 180 surgery- clipping, coiling, clot evacuation LP or ventricular drainage of hydrocephalus
133
SAH most common cause
trauma then aneurysm
134
ct within 1h head inury
GCS <13 GCS < 15 at 2h suspected open/depressed skull # signs of basal skull # focal neuro deficit post trauma seizure > 1 vomit children: LOC > 5 mins drowsiness 3 or more vomits dangerous mechanism amnesia > 5 mins children < 1y w/ bruising, swelling or lacerations > 5cm on head CT within 8 hours if no risk factors but on anticoagulants
135
subdural haematoma on imagine
acute and chronic will be seen on non contrast CT subacute need MRI or CT with contrast
136
early vs late syphilis
early: < 2y post infection primary, secondary, early latent late: > 2y post infection late latent (confirmed infection in absence of current clinical features), tertiary
137
syphilis treatment
early: - procaine penicillin 750mg IM OD for 10 days - ben penicillin 2.4mg IM for 1-2 doses 1 week apart - PO azithromycin if pen allergic or doxy 14/7 late: - ben pen IM 3 doses week apart - amox PO + probenecid 500mg QDS 28 days - doxy if pen allergic
138
causes of trigeminal neuralgia
90% caused by vascular compression of trigeminal n MS AV malformations tumours skill base abnormalities
139
coma anatomy
interruption of ascending reticular activating system in midbrain and pons projecting to thalamus and cortex causes: - damage to reticular activating system at level of midbrain - destruction to large surface of both cerebral hemispheres - suppression of reticulocerebral functions by drugs/toxins/metabolic disturbances
140
brainstem reflexes and localising lesions
pupils normal- above thalamus and below pons pupils pinpoint- opioid or pontine lesion fixed midpoint pupils- midbrain dilated pupils- CN3 or midbrain, sympathomimetics
141
ocular movements and localising causes of coma
roving eye/conjugate lateral nystagmus- intact brainstem. metabolic or bilateral hemisphere damage skew deviaion- posterior fossa oculocephalic dolls eye reflex- cerebral hemisphere corneal reflex- eyelids will close if pons is intact. upward movement and eyelid closure if pons and midbrain are intact
142
breathing patterns and localising coma
cheyne stoke- most common deep breathing- acidosis yawning or hiccups- brainstem regular shallow- OD
143
brain death
brainstem reflexes, motor responses, resp drive are absent irreversible widespread brain lesion of known cause with satisfactory oxygenation, temp, no hypercapnia or sedation
144
causes of central and peripheral visual field loss
central: ARMD, macular holes optic neuropathy lebers optic atrophy retinal a occlusion peripheral: glaucoma retinal detachment retinitis pigmentosa chorioretinitis branch of retinal a occlusion
145
optic chiasm lesions
before chiasm: ipsilateral defect central, asymmetrical, unilateral e.g. optic neuritis, optic atrophy, glaucoma, trauma can also cause small defect in upper temporal field of other eye at chiasm: bitemporal hemianopia pituitary tumour worse in upper field craniopharyngioma worse in lower field after chiasm: homonymous defect main optic radiation > complete homo hemi w/ macular sparing (e.g. stroke, MCA) temporal radiation > upper quad homo hemi parietal radiation > inferior quad homo hemi anterior visual cortex- contra homo hemi w/ macula sparing (e.g. posterior cerebral a) macular cortex > homo macular defect
146
wernickes pathophysiology
petechial haemorrhages in mammillary bodies
147
Wilsons disease
auto rec ATP7B mutation high levels of free copper (impaired binding and impaired excretion into bile) reduced caeruloplasmin, increased urine copper > fibrosis children present more with liver disease adults present more with neuro and eye signs
148